A RARE, SEVERE FORM OF EPILEPSY CALLED INFANTILE SPASMS CAN STRIKE BABIES IN THE FIRST MONTHS OF LIFE. RELATIVELY LITTLE IS KNOWN ABOUT THE CAUSES OF THE DISORDER IN SUCH CHILDREN OR ABOUT HOW TO TREAT IT EFFECTIVELY, SO TO LEARN MORE, RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE AND THE UNIVERSITY OF CHICAGO HAVE LAUNCHED A REGISTRY FOR CHILDREN WITH THE DISORDER AND THEIR PARENTS. JIM DRYDEN HAS THE STORY ...

INFANTILE SPASMS IN VERY YOUNG CHILDREN ARE SOMETHING THAT PEDIATRIC NEUROLOGISTS ENCOUNTER FROM TIME TO TIME, BUT THEY DON’T SEE THE DISORDER ALL THAT OFTEN, ACCORDING TO ALEX PACIORKOWSKI, A PEDIATRIC NEUROLOGIST AT WASHINGTON UNIVERSITY AND ST. LOUIS CHILDREN’S HOSPITAL.

(act) :14 o/c their computer

This project is, really, designed with parents at the center.
If they have a computer at home and if they have access to
the Internet, if they want to participate in the study; they
can pretty much do everything that they need to do just from
their computer.

TO BECOME PART OF THE REGISTRY, PARENTS WILL NEED THEIR LOCAL DOCTOR TO SEND THEIR CHILD’S BRAIN-WAVE SCANS, CALLED EEGs. BUT PACIORKOWSKI SAYS PARENTS CAN DO MOST EVERYTHING ELSE ON THEIR OWN.

(act) :15 o/c research basis

It takes about 10 or 15 minutes, and we’re able to get good,
quality data that’s important for the registry. And then the
additional thing is we’re collecting a blood sample from the
children and the parents for specific genetic tests that we
can offer on a research basis.

ONE OF THE CONFUSING THINGS ABOUT INFANTILE SPASMS IS THAT THEY CAN SOMETIMES AFFECT DIFFERENT CHILDREN DIFFERENTLY. AND PACIORKOWSKI SAYS THERAPIES SOMETIMES DON’T WORK WELL IN PARTICULAR CHILDREN. DOCTORS HAVE DIFFFICULTY PREDICTING WHO WILL RESPOND IN WHAT WAYS, SO THE IDEA OF THE REGISTRY IS TO DEVELOP A BIG ENOUGH DATABASE TO LEARN WHETHER THE DISORDER COMES IN VARIOUS SUB-TYPES AND TO FIGURE OUT WHICH TREATMENTS MIGHT HELP WHICH KIDS THE MOST.

(act) :28 o/c those kids

One of the mysteries is that some children develop infantile
spasms and are clearly neurologically very challenged after
that. They have developmental delay. They have other seizure
problems that just continue. There’s a percentage of children
who have autism. But then there is this other population of
children who develop infantile spasms, they receive medication,
they recover, and they never have any of those problems. And
we don’t understand, really, what separates some of those kids.

PACIORKOWSKI SAYS THE MODEL FOR THIS APPROACH COMES FROM PEDIATRIC CANCER. BY COMBINING RESOURCES AND DATA FROM AROUND THE COUNTRY, ONCOLOGISTS WHO TREAT CHILDREN HAVE BEEN ABLE TO LEARN A GREAT DEAL ABOUT EFFECTIVE DIAGNOSIS AND TREATMENT OF PEDIATRIC FORMS OF CANCER.

(act) :19 o/c there though

How well they’ve done looking even at relatively rare pediatric
cancers. So if we could carry neurology and pediatrics somewhere
along that way, I think that would be a good step and be able to
give people that information: We can tell which medicine will
help your child the most. I think that would be a goal. It’s
going to take a lot of work to get there though.

AND HE SAYS EARLY RESPONSE TO THE REGISTRY HAS BEEN VERY GOOD.

(act) :23 o/c that going

We have had an overwhelming response. Parents have contacted
me after hearing about the study from a friend, hearing about
it from their doctor, hearing about it through various other
parent support groups. And it’s really something that we hoped
would happen. Now every study has, at the beginning, a wave
of interest in it, and the challenge is going to be to keep
that going.

ALREADY, HE SAYS, FAMILIES FROM ALL OVER NORTH AMERICA HAVE SIGNED UP. I’M JIM DRYDEN…

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IT’S NOT ALL THAT COMMON, BUT INFANTILE SPASMS CAN BE SEVERE. PEDIATRIC NEUROLOGISTS SEE YOUNG CHILDREN WITH THE DISORDER, BUT MOST DON’T SEE VERY MANY, ACCORDING TO ALEX PACIORKOWSKI, A PEDIATRIC NEUROLOGIST AT WASHINGTON UNIVERSITY AND ST. LOUIS CHILDREN’S HOSPITAL. HE SAYS THERAPIES SOMETIMES DON’T WORK WELL IN THESE CHILDREN, SO HE HAS HELPED LAUNCH A REGISTRY FOR AFFECTED CHILDREN AND THEIR PARENTS. THE IDEA IS TO DEVELOP A BIG ENOUGH DATABASE TO LEARN WHETHER THE DISORDER COMES IN VARIOUS SUB-TYPES AND WHICH TREATMENTS MIGHT HELP WHICH KIDS THE MOST.

(act) :14 o/c there though

So if we could carry neurology and pediatrics somewhere along
that way, I think that would be a good step and be able to
give people that information: We can tell which medicine will
help your child the most. I think that would be a goal. It’s
going to take a lot of work to get there though.

PACIORKOWSKI SAYS IF PARENTS OF CHILDREN WITH INFANTILE SPASMS HAVE AN INTERNET CONNECTION, THEY CAN PARTICIPATE. AND HE SAYS EARLY RESPONSE HAS BEEN OVERWHELMING, WITH FAMILIES FROM ALL OVER NORTH AMERICA BECOMING PART OF THE REGISTRY. I’M JIM DRYDEN…

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THERE HAVE BEEN STORIES FOR YEARS ABOUT HOW AUNT MINNIE OR UNCLE HARRY WERE NEVER THE SAME AFTER THEIR OPERATION. AND DOCTORS AND THEIR OLDER PATIENTS OFTEN FEAR THAT SENIORS MAY EXPERIENCE DECLINES IN COGNITIVE ABILITY FOLLOWING SURGERY, BUT A NEW STUDY FROM WASHINGTON UNIVERSITY RESEARCHERS FOUND NO EVIDENCE OF LONG-TERM DECLINES THAT COULD BE LINKED TO SURGERY OR ILLNESS. JIM DRYDEN REPORTS…

THE NOTION THAT SURGERY AND LONG-TERM COGNITIVE PROBLEMS ARE LINKED GOES BACK A LONG WAY. A GOOD DEAL OF PAST RESEARCH CONNECTS SURGERY WITH LATER COGNITIVE DIFFICULTIES, ACCORDING TO WASHINGTON UNIVERSITY ANESTHESIOLOGIST MICHAEL AVIDAN.

(act) :09 o/c common concern

A lot of elderly people do need to undergo surgery, and certainly,
from my experience as an anesthesiologist, this is a very common
concern.

BUT AVIDAN AND FELLOW INVESTIGATOR ALEX EVERS WEREN’T CONVINCED THAT THOSE COMMON CONCERNS WERE LEGITIMATE. PAST RESEARCH TENDED TO MEASURE A PERSON’S COGNITIVE PERFORMANCE RIGHT BEFORE SURGERY AND THEN AGAIN IN THE MONTHS AFTERWARDS. ALTHOUGH THOSE STUDIES HAD OFTEN NOTED DECLINES, EVERS SAYS THEY DIDN’T REALLY HAVE ENOUGH INFORMATION. FOR THIS STUDY, EVERS AND AVIDAN LOOKED AT PEOPLE WITH AND WITHOUT COGNITIVE PROBLEMS WHO HAD BEEN FOLLOWED FOR SEVERAL YEARS BY WASHINGTON UNIVERSITY’S ALZHEIMER’S DISEASE RESEARCH CENTER. EVERS SAYS BY LOOKING AT LONG-TERM TRAJECTORIES BEFORE AND AFTER SURGERY OR ILLNESS, THEY FOUND THAT THERE WAS NO LINK BETWEEN SURGERY AND LONG-TERM COGNITIVE DECLINE.

(act) :12 o/c cognitive decline

Comparing groups of patients who had surgery to patients who had
major medical illness to patients who had neither of the above,
what we found is we could not detect any evidence of a long-term
cognitive decline.

ANOTHER COMMON CONCERN, HE SAYS, IS THAT SURGERY CAN EXACERBATE SYMPTOMS OF ALZHEIMER’S DISEASE IN THOSE PEOPLE WHO HAVE ALREADY BEEN DIAGNOSED.

(act) :16 o/c widely-held assumption

We were also able to examine that in this study, and we also found
when doing appropriate time courses, using appropriate controls and
statistics, that we could also not find evidence of exacerbation of
Alzheimer’s disease, again challenging that widely-held assumption.

EVERS AND AVIDAN SAY THERE CAN BE SHORT-TERM DECLINES, BUT PEOPLE TEND TO BOUNCE BACK. OR IF THEY DON’T BOUNCE BACK, IT TENDS TO HAVE MORE TO DO WITH THE FACT THAT THEY ARE SICK, RATHER THAN WITH THE FACT THAT THEY HAVE HAD SURGERY OR BEEN EXPOSED TO ANESTHESIA. AVIDAN SAYS THE NEW STUDY IS NOT THE LAST WORD ON THE SUBJECT, AND HE SAYS THERE MAY BE SOME PEOPLE WHO DO HAVE LONG-TERM COGNITIVE PROBLEMS FOLLOWING SURGERY, BUT AT THIS POINT, IT’S UNCLEAR WHY THEY ARE AT RISK.

(act) :35 o/c more vulnerable

It’s important to look at whether there are some people who are
especially vulnerable, depending on the type of surgery they have
or depending on their pre-existing characteristics. It’s important
to find out whether there are early markers of which people might
go on to have long-term deterioration. Are these the people who are
confused or have delirium shortly after their surgery? Are these the
people who have a marked inflammatory response to surgery or injury?
What is it about certain people that might make them more vulnerable?

AND EVERS SAYS THE STUDY SUGGESTS THAT FOR MOST OLDER PEOPLE, A RETURN TO THEIR PREVIOUS LEVEL OF COGNITIVE FUNCTION WILL BE THE NORM.

(act) :11 o/c of cognition

If you’re going to have a major surgery, your expectation should
be that within six months to a year, you should expect to have a
return to your previous level of cognition.

EVERS AND AVIDAN REPORTED THEIR FINDINGS IN THE JOURNAL ANESTHESIOLOGY. I’M JIM DRYDEN…

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PAST RESEARCH LOOKED AT A PERSON’S COGNITIVE PERFORMANCE RIGHT BEFORE SURGERY AND THEN AGAIN IN THE MONTHS AFTERWARDS, AND THOSE STUDIES HAD OFTEN NOTED DECLINES, BUT WASHINGTON UNIVERSITY RESEARCHER ALEX EVERS SAYS THOSE STUDIES OFTEN DIDN’T HAVE ENOUGH INFORMATION. WITH COLLEAGUE MICHAEL AVIDAN, EVERS LOOKED AT PEOPLE WITH AND WITHOUT COGNITIVE PROBLEMS WHO HAD BEEN FOLLOWED FOR YEARS BY WASHINGTON UNIVERSITY’S ALZHEIMER’S DISEASE RESEARCH CENTER. EVERS SAYS BY LOOKING AT LONG-TERM TRAJECTORIES BEFORE AND AFTER SURGERY OR ILLNESS, THEY FOUND THAT THERE WAS NO LINK BETWEEN SURGERY AND LONG-TERM COGNITIVE DECLINE.

(act) :16 o/c cognitive decline

And when we did appropriate statistics using each patient as
their own control, and then comparing groups of patients who
had surgery to patients who had major medical illness to patients
who had neither of the above, what we found is we could not
detect any evidence of a long-term cognitive decline.

EVEN IN PATIENTS ALREADY DIAGNOSED WITH ALZHEIMER’S DISEASE, THERE WAS NO EVIDENCE THAT SURGERY OR ILLNESS MADE SYMPTOMS ANY WORSE. I’M JIM DRYDEN…

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THE BEST WAY TO TREAT DIABETES IS TO PREVENT IT IF POSSIBLE, AND DIABETES RESEARCHERS FROM AROUND THE COUNTRY HAVE FOUND THAT LIFESTYLE CHANGES AIMED AT MODEST WEIGHT LOSS APPEAR TO REDUCE THE RISK OF DEVELOPING DIABETES IN PEOPLE WHO ARE AT RISK FOR THE DISORDER. JIM DRYDEN HAS MORE…

THE RESEARCHERS FOLLOWED PEOPLE FOR AT LEAST 10 YEARS. ACTUALLY, THIS STUDY FOLLOWED THE ORIGINAL DIABETES PREVENTION PROGRAM, OR DPP STUDY, THAT WAS COMPLETED IN 2001. IN THAT ORIGINAL, 3-YEAR TRIAL INVOLVING MORE THAN 3200 OVERWEIGHT AND OBESE ADULTS, RESEARCHERS HAD FOUND THAT A PROGRAM THAT ENCOURAGED REGULAR EXERCISE, CUT FAT FROM THE DIET AND REDUCED CALORIES COULD SIGNIFICANTLY LOWER THE RISK OF DEVELOPING DIABETES. IN THIS FOLLOW-UP STUDY, CALLED THE DIABETES PREVENTION PROGRAM OUTCOMES STUDY, THE RESEARCHERS CONTINUED TO FOLLOW THOSE PEOPLE AND FOUND THAT THEIR RISK WAS CUT BY 34 PERCENT. WASHINGTON UNIVERSITY ENDOCRINOLOGIST NEIL WHITE RAN THE ST. LOUIS ARM OF THE STUDY.

(act) :19 o/c at risk

The rate of development of diabetes has been reduced by the
ongoing lifestyle intervention, so it at least appears that
the interventions that we have been able to implement in the
DPP and subsequently continue, after 10 years now, to significantly
reduce the development of diabetes in a population at risk.

WHITE SAYS THE AVERAGE AGE OF STUDY PARTICIPANTS WAS ABOUT 50, AND THEY HAD BEEN ENROLLED IN THE STUDY BECAUSE THEY WERE KNOWN TO BE AT HIGH RISK FOR DEVELOPING DIABETES BECAUSE THEY HAD ELEVATED BLOOD GLUCOSE AND OTHER RISK FACTORS.

(act) :20 o/c a year

They were overweight or obese, and they had high blood
sugars – sugars that were not high enough to make them
diabetic, but they did have blood sugars that were higher
than normal – and we know that they, from that information,
that they were at risk to get diabetes, and indeed, those
who were in the control group developed diabetes at a
rapid rate of about 11 percent a year.
OTHERS IN THE STUDY TOOK THE DIABETES DRUG METFORMIN. THEY ALSO LOWERED THEIR RISK, BUT NOT QUITE AS MUCH AS THE PEOPLE WHO EXERCISED AND ATE HEALTHIER DIETS. WHITE SAYS THE CHANGES SEEMED TO HELP EVERYONE, REGARDLESS OF ETHNIC BACKGROUND, RACE OR AGE.

(act) :23 o/c older subjects

It would appear that the interventions the lifestyle intervention
in particular, is going to be effective at any age. Now when I say
any age, we don’t know in pediatrics, but we presume it’s going to
be true in pediatrics as well. But this study did not include any
children, and so when I say any age, I’m saying any adult age. The
lifestyle intervention was effective at any age and was a little bit
more effective in the older subjects.

HE SAYS NOT EVERYONE IS AT RISK FOR DIABETES, BUT PRETTY MUCH EVERYONE COULD STILL BENEFIT FROM EATING HEALTHIER AND EXERCISING MORE.

(act) :29 o/c get it

So it would be important that everybody try to maintain a
healthy lifestyle to prevent the development of one of the
major risk factors for diabetes, and also for heart disease
and stroke, which would be obesity and high blood pressure.
And healthy lifestyle, including exercise and not gaining
weight, would all lead in the direction of preventing those
from developing, and then, perhaps, a group of people such
as yourself or myself will never have to find out if they
are at risk for diabetes because even if they were, they
might not get it.

WHITE AND COLLEAGUES FROM 26 U.S. SITES REPORTED THEIR FINDINGS IN THE ONLINE EDITION OF THE LANCET. I’M JIM DRYDEN…

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RESEARCHERS FOLLOWED PEOPLE OF DIFFERENT AGES AND ETHNIC BACKGROUNDS FOR AT LEAST 10 YEARS. THE ONE THING THAT ALL OF THE PEOPLE IN THE STUDY HAD IN COMMON WAS THAT THEY WERE AT RISK FOR DIABETES. THOSE PEOPLE WERE PUT ON A PROGRAM THAT ENCOURAGED REGULAR EXERCISE, CUT FAT FROM THEIR DIETS AND REDUCED THE NUMBER OF CALORIES THEY CONSUMED. WASHINGTON UNIVERSITY ENDOCRINOLOGIST NEIL WHITE RAN THE ST. LOUIS ARM OF THE STUDY.

(act) :21 o/c older subjects

The interventions, the lifestyle intervention in particular, is
effective at any age. Now when I say any age, we don’t know in
pediatrics, but we presume it’s going to be true in pediatrics as
well. But this study did not include any children, and so when I
say any age, I’m saying any adult age. The lifestyle intervention
was effective at any age and was a little bit more effective in
the older subjects.

WHITE SAYS OTHERS IN THE STUDY TOOK THE DIABETES DRUG METFORMIN. THEY ALSO LOWERED THEIR RISK, BUT NOT AS MUCH AS THE PEOPLE WHO EXERCISED AND ATE HEALTHIER DIETS. WHITE AND COLLEAGUES FROM 26 U.S. SITES REPORTED THEIR FINDINGS IN THE ONLINE EDITION OF THE LANCET. I’M JIM DRYDEN…

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BETWEEN ALCOHOLISM, DEPRESSION AND OTHER PSYCHIATRIC DISORDERS, CURRENT ESTIMATES ARE THAT ONE IN THREE AMERICANS WILL NEED HELP FROM A MENTAL HEALTH PROFESSIONAL AT SOME POINT IN THEIR LIVES. OF COURSE, NOT EVERYONE GETS THAT HELP, AND TWO WASHINGTON UNIVERSITY PSYCHIATRISTS ARE HOPING THAT THEIR NEW BOOK, ENTITLED DEMYSTIFYING PSYCHIATRY, WILL EXPLAIN WHAT’S AVAILABLE AND MAKE PSYCHIATRY LESS MYSTERIOUS AND THREATENING FOR THOSE WHO NEED IT. JIM DRYDEN HAS MORE…

IT ISN’T A TEXTBOOK. IT’S DESIGNED FOR CONSUMERS, PATIENTS AND THEIR FAMILIES, TO BETTER EXPLAIN THE FIELD OF PSYCHIATRY, WHERE IT’S GOING, WHAT ILLNESSES PSYCHIATRISTS TREAT AND HOW THEY DO IT. CHUCK ZORUMSKI HEADS THE PSYCHIATRY DEPARTMENT AT WASHINGTON UNIVERSITY. WITH VICE-CHAIR EUGENE RUBIN, HE SAYS THEY WROTE THE BOOK TO EXPLAIN WHAT PSYCHIATRY IS AND WHAT PSYCHIATRISTS DO,

(act) :24 o/c be understandable

The book actually comes from many conversations we’ve had with
people in the community and individuals in our own families who
not only misunderstand psychiatric illnesses but don’t understand,
necessarily, who psychiatrists are and how the fit into healthcare
delivery. And so the impetus behind writing the book was to try
to bring those things out in a fashion that we thought would
be understandable.

HE SAYS PSYCHIATRY IS ARGUABLY THE LEAST UNDERSTOOD BRANCH OF MEDICINE, AND PSYCHIATRISTS OFTEN ARE THOUGHT OF AS PART PHYSICIAN, PART CONFESSOR, PART POLICE OFFICER AND PART SHAMAN. RUBIN SAYS THAT’S BECAUSE THERE ARE DIFFERENT APPROACHES FOR DIFFERENT PROBLEMS. IT’S NOT AS SIMPLE AS GIVING SOMEONE A PILL TO PEP THEM UP WHEN THEY’RE DEPRESSED OR PUTTING THEM INTO DETOX IF THEY’RE AN ALCOHOLIC OR A DRUG ADDICT. IN FACT, RUBIN SAYS, ONE OF THE ISSUES THEY DEVOTE A LOT OF PAGES TO IN THIS BOOK IS THE IDEA THAT ALTHOUGH TREATING PSYCHIATRIC ILLNESSES DOES HELP PEOPLE, THOSE TREATMENTS RARELY CURE PSYCHIATRIC PROBLEMS.

(act) :22 o/c psychiatric illnesses

There are no full cures in much of medicine, including psychiatry.
Medications can sometimes help – not as much as, sometimes, we’re
led to believe – to help people feel somewhat better. But there is
no “quick fix” when we’re dealing with something as complex as
significant psychiatric illnesses.

ZORUMSKI SAYS THAT PSYCHIATRISTS, LIKE ENDOCRINOLOGISTS OR CARDIOLOGISTS, OFTEN MANAGE DISORDERS. THEY DON’T ACTUALLY ELIMINATE THEM.

(act) :30 o/c common illnesses

About a third of the population has a significant psychiatric
disorder. It doesn’t matter whether we’re talking about major
depression, a very common psychiatric illness, or we’re talking
about high blood pressure or diabetes, those illnesses are not
cured either, and they’re managed over time. And that’s one of
the things we really want consumers and those who have the
illnesses to understand: The expectation that a pill or a form
of treatment is going to cure you is really inappropriate, just
as it is inappropriate with high blood pressure and the other
common illnesses.

RUBIN SAYS CURE OR NOT, IT’S IMPORTANT TO DIAGNOSE AND TREAT THESE PROBLEMS BECAUSE THEY ARE TREATABLE, AND WITHOUT THERAPY, THEY CAN BE EXTREMELY DISABLING.

(act) :20 o/c severe hypertension

Psychiatric illnesses are among, in fact they are, the most
disabling group of illnesses in the world today, and I personally
believe that not recognizing a severe depression or not addressing
severe alcoholism is tantamount to avoiding or ignoring diabetes
or severe hypertension.

THEIR NEW BOOK IS CALLED DEMYSTIFYING PSYCHIATRY. IT’S PUBLISHED BY OXFORD UNIVERSITY PRESS. I’M JIM DRYDEN…

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THEY WROTE THE BOOK TO EXPLAIN WHAT PSYCHIATRY IS AND WHAT PSYCHIATRISTS DO, AS WELL AS TO HELP PATIENTS AND THEIR FAMILIES UNDERSTAND THE STATE OF THE SCIENCE AND THE TYPES OF THERAPY NORMALLY USED TO TREAT PSYCHIATRIC ILLNESS. CHUCK ZORUMSKI HEADS THE PSYCHIATRY DEPARTMENT AT WASHINGTON UNIVERSITY. HE SAYS ABOUT ONE-THIRD OF THE POPULATION SUFFERS WITH A PSYCHIATRIC ILLNESS AT SOME POINT DURING THEIR LIVES. MANY WILL NEVER BE DIAGNOSED. OTHERS WON’T GET EFFECTIVE TREATMENTS. ZORUMSKI’S VICE CHAIR, EUGENE RUBIN, SAYS THAT’S A BIG PUBLIC HEALTH PROBLEM BECAUSE PSYCHIATRIC ILLNESSES CAN BE SO DISABLING.

(act) :18 o/c severe hypertension

In fact they are the most disabling group of illnesses in the world
today, and I personally believe that not recognizing a severe
depression or not addressing severe alcoholism is tantamount to
avoiding or ignoring diabetes or severe hypertension.

BUT ZORUMSKI AND RUBIN SAY THERE ARE NO “MAGIC PILLS,” AND PSYCHIATRIC ILLNESSES, JUST LIKE DIABETES AND HYPERTENSION, TEND TO BE MANAGED RATHER THAN CURED. I’M JIM DRYDEN…

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DEPRESSION IN HEART PATIENTS HAS BEEN LINKED TO RISK FOR SUBSEQUENT HEART ATTACKS AND TO SUDDEN CARDIAC DEATH. TO TREAT DEPRESSION IN THOSE PATIENTS, WASHINGTON UNIVERSITY RESEARCHERS TRIED ADDING OMEGA-3 FATTY ACIDS TO ANTIDEPRESSANT DRUGS. BUT ALTHOUGH PAST STUDIES HAD SHOWN OMEGA-3 COULD HELP BOTH CARDIOVASCULAR FUNCTION AND DEPRESSION, THE COMBINATION THERAPY DIDN’T SEEM TO HELP DEPRESSED HEART PATIENTS. JIM DRYDEN HAS MORE…

WASHINGTON UNIVERSITY BEHAVIORAL MEDICINE RESEARCHERS HAVE BEEN LOOKING FOR EFFECTIVE WAYS TO RELIEVE DEPRESSION IN HEART PATIENTS IN HOPES THAT BY TREATING DEPRESSION, THEY CAN BOTH IMPROVE CURRENT QUALITY OF LIFE AND LOWER THE RISKS OF FUTURE HEART PROBLEMS. SO THEY GAVE DEPRESSED HEART PATIENTS ANTIDEPRESSANT MEDICATION, AND SOME ALSO GOT OMEGA-3 FATTY ACIDS. PRINCIPAL INVESTIGATOR ROBERT CARNEY SAYS THAT PAST STUDIES SUGGESTED OMEGA-3, WHICH IS FOUND IN FISH OIL, MIGHT HELP WITH DEPRESSION AND HEART PROBLEMS.

(act) :15 o/c heart disease

Because our diets have changed so radically in the last 100 years
or so, people may not be getting enough of this very important
substance, and it may be responsible for things like depression,
as well as some difficulties related to heart disease.

CARNEY SAYS ALL OF THE 122 DEPRESSED HEART PATIENTS IN THIS STUDY GOT AN ANTIDEPRESSANT. AND HALF OF THEM ALSO GOT OMEGA-3.

(act) :13 o/c corn-oil treatment

Patients in both groups did a very good job of taking both
the medications and the either the omega-3 or placebo. We
found that there was no difference between the patients who
received omega-3 and those who received the corn-oil treatment.

PATIENTS WHO TOOK OMEGA-3 DIDN’T IMPROVE ANY MORE THAN THOSE WHO TOOK ONLY ANTIDEPRESSANT DRUGS.

(act) :13 o/c oil placebo
The majority of patients actually responded, to some extent,
to the antidepressant treatment. So overall, patients did
improve, but there was no difference in improvement between
the patients who received omega-3 and those who received the
corn-oil placebo.

CARNEY SAYS MANY PATIENTS GOT A LITTLE BETTER, BUT THE ANTIDEPRESSANTS DIDN’T WORK FOR EVERYBODY. HE SAYS HE WAS SURPRISED AND DISAPPOINTED BY THE RESULTS, BUT HE SAYS PERHAPS OMEGA-3 FATTY ACIDS WILL BE MORE BENEFICIAL IN A LONGER STUDY – THIS ONE LASTED ONLY 10 WEEKS – OR MAYBE A HIGHER DOSE WOULD BE MORE EFFECTIVE.

(act) :33 o/c no effect
The American Heart Association advises people to at least eat
some fish each week. And for patients who have heart disease,
they advise that these patients actually may take supplements,
or should take supplements, of omega-3 as well. So there’s
certainly evidence that omega-3 can benefit cardiovascular
functioning, and again, there was this suggestive evidence that
it also may improve depression. Now, I certainly wouldn’t say
that it won’t improve depression. What I would say is that at
the dose that we tried at least, and for the 10-week period
that we ran our trial, there was no effect.

BUT CARNEY SAYS THE REAL ISSUE IS THAT ANTIDEPRESSANT DRUGS AREN’T EFFECTIVE IN ENOUGH HEART PATIENTS, SO HE’S INVESTIGATING NON-DRUG THERAPIES FOR DEPRESSION TO SEE WHETHER THEY’LL WORK ANY BETTER.

(act) :29 o/c try again
Most of the antidepressants that are presently on the market
– and most of the ones that I’m aware of, at least in the early
studies – that are about to come on the market, are all pretty
close to the same, in terms of effectiveness. They’re better than
placebo, but not a lot better. And I don’t see anything, anytime
soon, that’s likely to change that. But again, there are a number
of treatments that are being studied, and we always hope for a
big breakthrough. We were hoping for one here. We didn’t see it,
but again, we may need to do it a little differently and try again.

CARNEY AND COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION. I’M JIM DRYDEN…

DEPRESSION IS COMMON IN HEART PATIENTS AND HAS BEEN LINKED TO RISK FOR A SECOND HEART ATTACK AND TO SUDDEN CARDIAC DEATH. FOR MANY YEARS, WASHINGTON UNIVERSITY BEHAVIORAL MEDICINE RESEARCHERS HAVE BEEN LOOKING FOR EFFECTIVE WAYS TO RELIEVE DEPRESSION IN HEART PATIENTS IN HOPES THAT BY TREATING DEPRESSION, THEY CAN BOTH IMPROVE CURRENT QUALITY OF LIFE AND LOWER THE RISKS OF FUTURE HEART PROBLEMS. SO THEY GAVE DEPRESSED HEART PATIENTS ANTIDEPRESSANT MEDICATION, AND SOME ALSO GOT OMEGA-3 FATTY ACIDS. IN PAST STUDIES OMEGA-3, WHICH IS FOUND IN FISH OIL, HAS BEEN SHOWN TO HELP BOTH WITH DEPRESSION AND WITH CARDIAC FUNCTION. BUT IN THIS STUDY, RESEARCHER ROBERT CARNEY SAYS PATIENTS WHO TOOK OMEGA-3 DIDN’T DO ANY BETTER THAN THOSE WHO TOOK ONLY ANTIDEPRESSANTS.

(act) :07 o/c corn-oil placebo

Overall, patients did improve, but there was no difference in
improvement between the patients who received omega-3 and
those who received the corn-oil placebo.

AND ALTHOUGH MANY PATIENTS GOT A LITTLE BETTER, THE ANTIDEPRESSANTS DIDN’T WORK FOR EVERYBODY. CARNEY SAYS PERHAPS NON-DRUG THERAPIES WILL WORK BETTER. HIS TEAM IS NOW STUDYING COGNITIVE BEHAVIOR THERAPY IN DEPRESSED CARDIAC PATIENTS. I’M JIM DRYDEN…

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WHEN WE’RE IN BRIGHT LIGHT, PHOTORECEPTOR CELLS IN OUR EYES, CALLED CONE CELLS, ALLOW US TO SEE. THEY ALSO HELP US ADAPT TO SUDDEN LOSS OF LIGHT. NOW VISION SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE LEARNED A BIT MORE ABOUT HOW THOSE CELLS ARE ABLE TO QUICKLY ADAPT BOTH TO BRIGHT LIGHT AND TO LOW LIGHT. JIM DRYDEN HAS THE STORY…

EARLIER THIS YEAR WORKING IN SALAMADER EYES, THIS TEAM OF SCIENTISTS DEMONSTRATED THAT A VISUAL PATHWAY IN THE RETINA ALLOWED CONE CELLS TO FUNCTION IN BRIGHT LIGHT AND TO ADAPT TO DARKNESS. THE OTHER TYPE OF PHOTORECEPTORS, CALLED ROD CELLS, CAN’T FUNCTION IN BRIGHT LIGHT, AND THEY ADAPT TO DARKNESS MUCH MORE SLOWLY. FIRST, LIGHT-SENSING MOLECULES BIND TOGETHER TO MAKE UP VISUAL PIGMENTS. THEN WHEN THE RETINA IS EXPOSED TO LIGHT, CONE CELLS RELEASE THOSE PHOTOPIGMENTS. AND BEFORE THE CELLS CAN FUNCTION AGAIN, THOSE PIGMENTS MUST BE REBUILT, OR RECYCLED. VISION SCIENTISTS HAVE LONG KNOWN THAT PIGMENT MOLECULES IN A PART OF THE EYE CALLED THE RETINAL PIGMENT EPITHELIUM CAN HELP CONE CELLS RELOAD WITH PHOTOPIGMENTS, BUT THAT’S A RELATIVELY SLOW PROCESS. IN THE SALAMANDER, WASHINGTON UNIVERSITY RESEARCHER VLADIMIR KEFALOV AND COLLEAGUES HAD FOUND THAT THE CONES ALSO COULD GET PIGMENT FROM CELLS IN THE RETINA ITSELF, CALLED MüLLER CELLS, WITHOUT HAVING TO RELY ONLY ON THE SLOWER PATHWAY THROUGH THE PIGMENT EPITHELIUM.

(act) :22 o/c this pathway

We discovered that, indeed, if we take an isolated salamander
retina and expose it to very bright light, in rods the visual
pigment will remain destroyed and will never regenerate in the
absence of pigment epithelium. Whereas in cones, the visual
pigment eventually will regenerate, and we later on showed
that glial cells in the retina called Müller cells, are a
key component of this pathway.

NOW THEY’VE FOUND THAT CONES IN MICE, PRIMATES AND HUMANS CAN DO THE SAME THING.

(act) :16 o/c including humans

Indeed, the mouse and, later on, the primate and human retina are
also able to drive cone dark adaptation independently of the pigment
epithelium indicating that this pathway is, indeed, present and
functional in higher mammals including humans.

KEFALOV SAYS THE THE NEWLY IDENTIFIED PATHWAY INVOLVING MüLLER CELLS IN THE RETINA SPEEDS UP THE PROCESS CONSIDERABLY AND EXPLAINS WHY CONES, BUT NOT ROD CELLS, CAN FUNCTION AS THEY DO. AND JUST TO ENSURE THAT THE PATHWAY WAS, IN FACT, RUNNING THROUGH THOSE MULLER CELLS, KEFALOV’S LABORATORY DID AN EXPERIMENT WHERE THOSE CELLS WERE SELECTIVELY DISABLED.

(act) :19 o/c high rate

We performed, again, experiments in mouse, and what we found
was that when we inhibited the function of the Müller cells,
we saw a significant reduction in the range of light intensities
over which cones are able to function, presumably by regenerating
enough visual pigment so that the cones can remain functional
even in very bright light, which destroys their pigment at a
very high rate.

KEFALOV SAYS UNDERSTANDING HOW THIS PATHWAY WORKS, AND CONFIRMING THAT IT OPERATES IN HUMANS, COULD HAVE IMPLICATIONS IN UNDERSTANDING EYE DISEASES, SUCH AS AGE-RELATED MACULAR DEGENERATION.

(act) :18 o/c macular degeneration

Age-related macular degeneration could also be modulated, perhaps,
by this pathway. Presumably, deficiencies in this pathway will affect,
selectively, the cones as well. And it’s possible that over time, this
will result in degeneration of our cone photoreceptors. One classic
example of this would be age-related macular degeneration.

KEFALOV REPORTS HIS FINDINGS IN THE JOURNAL CURRENT BIOLOGY. I’M JIM DRYDEN

RUNS 2:56

VISION SCIENTISTS HAVE LONG KNOWN THAT PIGMENT MOLECULES IN PART OF THE EYE CALLED THE RETINAL PIGMENT EPITHELIUM COULD HELP RELOAD CONE CELLS IN THE RETINA WHEN THEY’RE EXPOSED TO LIGHT AND USE THEIR OWN PIGMENTS. WITHOUT THOSE PIGMENTS THE CELLS CAN’T FUNCTION PROPERLY. IN THE SALAMANDER EYE, WASHINGTON UNIVERSITY RESEARCHER VLADIMIR KEFALOV AND COLLEAGUES HAD FOUND THAT THE CONES ALSO COULD GET PIGMENT FROM CELLS IN THE RETINA ITSELF, CALLED MüLLER CELLS. NOW THEY’VE FOUND THAT CONES IN MICE, PRIMATES AND HUMANS CAN DO THE SAME THING.

(act) :15 o/c in humans

The mouse and, later on, the primate and human retina are also
able to recycle their chromophore and drive cone dark adaptation
independently of the pigment epithelium indicating that this
pathway is, indeed, present and functional.

KEFALOV SAYS THE NEW STUDY HELPS WITH THE UNDERSTANDING OF HOW OUR CONES WORK, AND THAT COULD HAVE IMPLICATIONS FOR UNDERSTANDING EYE DISEASES, SUCH AS AGE-RELATED MACULAR DEGENERATION. HE REPORTS HIS FINDINGS IN THE JOURNAL CURRENT BIOLOGY. I’M JIM DRYDEN

RUNS :59

YOUR AGE WHEN YOU FIRST BEGIN TO DRINK ALCOHOL CAN BE A RISK FACTOR FOR ALCOHOL DEPENDENCE LATER IN LIFE. THE YOUNGER THAT AGE AT FIRST DRINK, THE HIGHER THE RISK OF PROBLEMS DOWN THE ROAD. NOW WASHINGTON UNIVERSITY RESEARCHERS HAVE FOUND THAT WHEN VERY YOUNG PEOPLE BEGIN DRINKING, IT MAY INCREASE THEIR RISK BY INFLUENCING GENES THAT ARE LINKED TO ALCOHOLISM. JIM DRYDEN HAS MORE…

THE RESEARCHERS STUDIED MORE THAN 6,000 TWINS FROM AUSTRALIA. SINCE TWINS SHARE A GREAT DEAL OF THEIR DNA – 100 PERCENT OF IT FOR IDENTICAL TWINS – IT’S POSSIBLE TO LEARN WHETHER GENES OR ENVIRONMENT ARE EXERTING MORE INFLUENCE ON VARIOUS BEHAVIORS, INCLUDING DRINKING. THE WASHINGTON UNIVERSITY RESEARCHERS FOUND THAT AMONG THESE AUSTRALIAN TWINS, THE YOUNGER A PERSON WAS AT FIRST DRINK, THE GREATER THEIR RISK FOR ALCOHOL DEPENDENCE AND THE MORE PROMINENT THE ROLE PLAYED BY GENETIC FACTORS. LEAD AUTHOR ARPANA AGRAWAL SAYS RESEARCHERS KNEW AN EARLIER START TO DRINKING WAS LINKED TO LATER PROBLEMS, AND SHE SAYS THERE WERE TWO MAIN EXPLANATIONS OF WHY.

(act) :20 o/c common factors

One is that there are common genetic and environmental factors
that motivate people to start drinking at a young age – and that’s
part of a cluster of non-normative behaviors – and that that
genetic predisposition is actually correlated with subsequently
developing alcohol dependence. So it’s all part of a set of
common factors.

THE OTHER HYPOTHESIS, SHE SAYS, WAS THAT EARLY DRINKING MIGHT ACTUALLY INCREASE GENETIC RISKS, AND SHE SAYS THIS STUDY FOUND SOME EVIDENCE THAT MIGHT SUPPORT THAT.

(act) :14 o/c in them

Early drinkers were more likely to have alcohol dependence
and have more symptoms, but their alcohol dependence was
just more heritable. So if you think of heritability in
terms of lots of genes, there seemed to be a greater genetic
loading in them.

AGRAWAL SAYS THAT ALTHOUGH SHE DOESN’T HAVE ANY GENE EXPRESSION DATA TO PROVE THIS, IT DOES SEEM THAT PERHAPS STARTING TO DRINK AT A YOUNGER AGE MAY CAUSE SOME GENES TO BECOME MORE OR LESS ACTIVE AND THUS, INCREASE THE RISKS FOR ALCOHOLISM.

(act) :20 o/c look at

Adolescents have a very susceptible brain, if you will, and
perhaps early-onset drinking – especially if it’s frequent or
heavy, which it can be – could that have an effect on the
developing brain? Perhaps. I think neuro-imaging studies,
gene expression assays should certainly look at.

SHE SAYS SOME OF THE PEOPLE IN THIS STUDY REPORTED STARTING TO DRINK AT AGES AS YOUNG AS 3 OR 4. FOR THE PURPOSES OF COMPARISON, THE RESEARCHERS DEFINED EARLY DRINKING AS HAVING A FIRST DRINK BEFORE THE AGE OF 15, AND AGRAWAL SAYS IN THOSE VERY YOUNG DRINKERS, GENETIC FACTORS CONTRIBUTED TO RISK FOR ALCOHOL DEPENDENCE AT RATES AS HIGH AS 90 PERCENT. BUT SHE SAYS THIS FINDING DOESN’T MEAN THAT PEOPLE WHO START DRINKING VERY YOUNG ARE SOMEHOW DOOMED TO BECOME ALCOHOLICS.

(act) :21 o/c completely protected

So I don’t think at any point in this trajectory is it determined,
or pre-determined, whether an individual, who has a genetic loading
and starts drinking at an early age, will definitively become alcohol
dependent or have more symptoms. It’s also not the case that individuals
who don’t start drinking at a young age are completely protected.

SHE SAYS THOSE WHO DON’T DRINK UNTIL THEY ARE OLDER STILL CAN BECOME ALCOHOLIC, DEPENDING ON HOW MUCH AND HOW OFTEN THEY DRINK. HER TEAM REPORTED ITS FINDINGS IN THE JOURNAL ALCOHOLISM: CLINICAL & EXPERIMENTAL RESEARCH. I’M JIM DRYDEN

RUNS 2:54

THE RESEARCHERS STUDIED MORE THAN 6,000 TWINS FROM AUSTRALIA AND FOUND THAT THE YOUNGER A PERSON WAS AT FIRST DRINK, THE GREATER THEIR RISK FOR ALCOHOL DEPENDENCE AND THE MORE PROMINENT THE ROLE PLAYED BY GENETIC FACTORS. LEAD AUTHOR ARPANA AGRAWAL SAYS ALCOHOLISM RESEARCHERS KNEW THAT YOUNGER AGE AT FIRST DRINK WAS LINKED TO LATER PROBLEMS, AND SHE SAYS THERE WERE TWO MAIN HYPOTHESES TO EXPLAIN WHY.

(act) :20 o/c common factors

One is that there are common genetic and environmental factors
that motivate people to start drinking at a young age – and that’s
part of a cluster of non-normative behaviors – and that that
genetic predisposition is actually correlated with subsequently
developing alcohol dependence. So it’s all part of a set of
common factors.

THE OTHER HYPOTHESIS WAS THAT EARLY DRINKING MIGHT ACTUALLY HELP INCREASE GENETIC RISKS. AGRAWAL SAYS HER TEAM FOUND THAT IN TWINS WHO STARTED DRINKING EARLY, GENETIC FACTORS CONTRIBUTED TO RISK FOR ALCOHOL DEPENDENCE AT RATES AS HIGH AS 90 PERCENT FOR THE YOUNGEST DRINKERS. I’M JIM DRYDEN

RUNS :58

BEE VENOM CONTAINS TOXINS THAT CAN FIGHT INFECTION AND KILL CANCEROUS TUMORS. THE PROBLEM, UNTIL RECENTLY, HAS INVOLVED HOW TO GET TOXINS TO TUMORS WITHOUT KILLING PATIENTS. NOW, WORKING IN MICE, WASHINGTON UNIVERSITY RESEARCHERS MAY HAVE FOUND A SOLUTION: NANOBEES. JIM DRYDEN HAS MORE…

NANOBEES ARE ONE OF THE LATEST VARIATIONS OF NANOPARTICLES, MICROSCOPIC SPHERES THAT CAN DELIVER DRUGS AND IMAGING AGENTS TO TUMORS, CARDIAC BLOCKAGES AND OTHER SICK PARTS OF THE BODY. IN THE CASE OF CANCER THERAPY, THE IDEA IS TO DELIVER CANCER DRUGS TO KILL TUMOR CELLS, WHILE PRESERVING HEALTHY TISSUE THAT SURROUNDS TUMORS, ACCORDING TO WASHINGTON UNIVERSITY RESEARCHER SAMUEL WICKLINE. HE SAYS TINY NANOPARTICLES ALLOW THAT TO HAPPEN.

(act) :11 o/c appropriate address

The point is to include them on a nanoparticle, which is a small
carrier of drugs that will deliver them – like the Post Office –
directly to the appropriate address.

WICKLINE SAYS IN RECENT EXPERIMENTS, HE AND HIS COLLEAGUES DELIVERED A TOXIN FROM BEE VENOM, CALLED MELITTIN, IN MICROSCOPIC NANOPARTICLES, TO TUMOR CELLS IN MICE. WHEN MELITTIN IS ATTACHED TO NANOPARTICLES, THE RESEARCHERS CALL THOSE STRUCTURES NANOBEES. WICKLINE SAYS SCIENTISTS HAVE KNOWN FOR SOME TIME THAT MELITTIN COULD KILL CANCER CELLS, BUT IT HAS BEEN VIRUTALLY IMPOSSIBLE TO SAFELY DELIVER THE TOXIN.

(act) :25 o/c therapeutic agent

It now can be put onto one of these little particle carriers,
where it is safely conveyed in the bloodstream to the tumor,
without harming other tissues. And so we’ve basically replicated
what the bee is able to do, by carrying this toxin. And we know
how to make this in the laboratory, and so we don’t have to ask
bees to make it. So when we make it, we can then make it and
include it in our nanoparticles as a therapeutic agent.

CANCER CHEMOTHERAPY OFTEN INVOLVES THE INFUSION OF INTRAVENOUS DRUGS THAT KILL TUMOR CELLS, BUT THOSE DRUGS ALSO CAN KILL HEALTHY TISSUE. IN THE CASE OF THIS BEE VENOM TOXIN, WICKLINE SAY INTRAVENOUS DELIVERY OF THE TOXIN WOULD RESULT IN WIDESPREAD DESTRUCTION OF RED BLOOD CELLS. BUT IN MICE, WICKLINE AND COLLEAGUES WERE ABLE TO DELIVER LOTS OF THE TOXIN WITHOUT CAUSING TOXIC SIDE EFFECTS.

(act) :29 o/c side effects

We delivered about four times the dose that would normally
kill a small animal, without having any toxic side effects
at all, and so the real promise of this delivery system is
that, not only does it make the drug able to go to the site
where it’s supposed to be active, but it protects the other
tissues against harmful side effects to an incredible extent,
in fact. So much so that you could use four times the lethal
dose and have absolutely no side effects.

BUT THE NANOBEES DID HAVE THE DESIRED EFFECT. TUMORS STOPPED GROWING AND EVEN GOT SMALLER. WICKLINE SAYS THE TOXIN MAY KILL MANY DIFFERENT TYPES OF TUMOR CELLS BECAUSE IT DOESN’T NEED TO BIND TO SPECIFIC RECEPTORS ON PARTICULAR TUMORS AS MANY OTHER CHEMOTHERAPY AGENTS DO.

(act) :15 o/c of cancers

It doesn’t rely on specific binding at specific sites,
but once it gets there, it can then kill the cancer cell,
generically, by just poking a hole in it. And so, as long
as it’s able to be delivered to a cell, it would be useful
for many different kinds of cancers.

WICKLINE’S TEAM REPORTED ITS FINDINGS IN THE JOURNAL OF CLINICAL INVESTIGATION. I’M JIM DRYDEN

RUNS 3:00

THE SOLUTION IS TO DELIVER THE BEE TOXIN, CALLED MELITTIN, IN MICROSCOPIC SPHERES CALLED NANOPARTICLES. WHEN MELITTIN IS ATTACHED TO NANOPARTICLES, THE RESEARCHERS FOUND IT’S POSSIBLE TO DELIVER THE VENOM DIRECTLY TO TUMORS WITHOUT CAUSING SIDE EFFECTS. IN THE CASE OF THIS BEE VENOM TOXIN, WASHINGTON UNIVERSITY INVESTIGATOR SAMUEL WICKLINE SAY INTRAVENOUS DELIVERY OF THE DRUG WOULD RESULT IN WIDESPREAD DESTRUCTION OF RED BLOOD CELLS. BUT IN MICE, WICKLINE AND COLLEAGUES WERE ABLE TO DELIVER LOTS OF THE TOXIN WITHOUT CAUSING TOXIC SIDE EFFECTS.

(act) :19 o/c side effects

The real promise of this delivery system is that not only
does it make the drug able to go to the site where it’s
supposed to be active, but it protects the other tissues
against harmful side effects to an incredible extent, in
fact, so much so that you could use four times the lethal
dose and have absolutely no side effects.

BUT THE SO-CALLED NANOBEES DID HAVE THE DESIRED EFFECT. TUMORS STOPPED GROWING AND EVEN GOT SMALLER. I’M JIM DRYDEN

RUNS :59

WHEN YOU DO THE SAME THINGS EVERY DAY, IT CAN BE EASY TO REMEMBER TO DO IT, BUT HARDER TO REMEMBER WHETHER YOU DID IT. THAT’S A BIG PROBLEM FOR MANY OLDER ADULTS WHO TAKE MEDICINE EVERY DAY. AFTER A WHILE THE DAYS RUN TOGETHER, AND IT CAN BE HARD FOR A PERSON TO REMEMBER WHETHER HE OR SHE TOOK THEIR PILLS. BUT A TEAM OF PSYCHOLOGISTS AT WASHINGTON UNIVERSITY IN ST. LOUIS SAYS THE SOLUTION MAY BE AS SIMPLE AS A PAT ON THE HEAD. JIM DRYDEN HAS THE STORY…

REMEMBERING TO DO SOMETHING IN THE FUTURE IS WHAT PSYCHOLOGISTS CALL PROSPECTIVE MEMORY. THINGS LIKE REMEMBERING TO GO TO YOUR DOCTOR’S APPOINTMENT ON THURSDAY OR TO A LUNCHEON ON SATURDAY ARE EXAMPLES OF PROSPECTIVE MEMORY. BUT SOME FUTURE EVENTS ARE HABITUAL, ACCORDING TO WASHINGTON UNIVERSITY PSYCHOLOGIST MARK MCDANIEL, AND HE SAYS THOSE HABITUAL FUTURE EVENTS, LIKE TAKING YOUR DAILY MEDICINE, CAN BE DIFFICULT FOR OLDER ADULTS.

(act) :31 o/c or not

As you repeatedly perform a task, on any particular day,
for example in medication taking, you may start to get
confused about whether you’ve taken that medication that
day or not. A lot of older adults use external cues. So
they’ll use a pill box, and when the pill is out of the
box, it’s clear that you’ve taken the pill. So I’m talking
about a situation where there are no external “crutches”
as it were. We thought it might be the case that older
adults would become confused about whether they had taken
the medication that particular moment or not.

MCDANIEL’S TEAM DEVISED A LABORATORY EXPERIMENT WHERE THEY ASKED PEOPLE TO DO A SERIES OF TASKS, AND IN THE MIDST OF THOSE TASKS, THE PEOPLE IN THE STUDY WERE ASKED TO DO SOMETHING VERY SIMPLE.

(act) :17 o/c trial block

Our idea was to get people busily involved in an ongoing task
and, in addition, try to have them perform this habitual,
prospective memory task. And the task was very simple. It was
simply remembering to press a particular key on the keyboard
sometime in the midst of their ongoing trial block.
HE SAYS OLDER ADULTS MADE A LOT OF MISTAKES, AND THEY TENDED TO REMEMBER TO PERFORM THE TASK BUT NOT TO REMEMBER WHEN THEY ALREADY HAD DONE IT.

(act) :13 o/c task again

Initially, older and younger adults were performing about
equivalently, but later, older adults, they would remember
to do the prospective memory task and then later within that
block do the prospective memory task again.

ONCE THE EXPERIMENTAL TASK BECAME A HABIT, ABOUT 50 PERCENT OF OLDER PEOPLE REPEATED IT. IN THE REAL WORLD, MCDANIEL SAYS, THAT RAISES CONCERNS ABOUT OLDER PEOPLE WHO TAKE DAILY MEDICATION.

(act) :13 o/c it again

Older adults might tend to over-medicate in a medication-taking
situation because they may forget whether or not they’ve
taken their medication on that day, and in forgetting whether
or not they’ve taken it, they may take it again.

HE SAYS THE SOLUTION TO WHETHER OLD PEOPLE HAVE TAKEN THEIR MEDICATION MAY BE AS CLOSE AS THE ENDS OF THEIR ARMS. AT LEAST THAT’S WHAT THEY FOUND IN THE LABORATORY WHERE THEY ASKED OLDER PEOPLE TO PERFORM HABITUAL MEMORY TASKS, AND THEY ALSO ASKED THEM TO TOUCH THEIR HEADS.

(act) :23 o/c declined substantially

This task was designed to create an additional motor movement
and thus cause people to pay attention to the fact that they had
done the prospective memory task. And it worked. Older adults who
were asked to put their hand on their head when they were also
making the prospective memory task appeared to remember having
made that task, and the repetition errors declined substantially.

MCDANIEL SAYS OTHER UNUSUAL ACTIONS PROBABLY WORK, TOO. THE KEY, HE SAYS, IS TO DO SOMETHING DIFFERENT, SO THAT YOUR BRAIN TAKES NOTE. HE REPORTED ON THE STUDY IN THE JOURNAL AGING, NEUROPSYCHOLOGY AND COGNITION. I’M JIM DRYDEN

RUNS 2:57

HABITUAL ACTIONS CAN BECOME AUTOMATIC, AND IT SOMETIMES TAKES A SECOND TO REMEMBER WHETHER YOU LOCKED THE CAR OR UPLUGGED THE IRON. THOSE AUTOMATIC ACTIONS CAN BE ESPECIALLY DIFFICULT FOR OLDER PEOPLE TO REMEMBER, AND IF THE ACT INVOLVES DAILY MEDICATION, IT CAN BE JUST AS DANGEROUS TO TAKE A DRUG A SECOND TIME AS TO FORGET TO TAKE IT ALTOGETHER. STUDYING OLDER ADULTS IN THE LABORATORY, WASHINGTON UNIVERSITY PSYCHOLOGIST MARK MCDANIEL FOUND THAT IF THEY PATTTED THEMSELVES ON THE HEADS WHILE PERFORMING A TASK, OLDER PEOPLE TENDED TO BETTER REMEMBER THOSE HABITUAL MEMORY TASKS.

(act) :12 o/c declined substantially

Older adults who were asked to put their hand on their head when
they were also making the prospective memory task appeared to
remember having made that task, and their repetition errors
declined substantially.

MCDANIEL RECOMMENDS EXTERNAL TOOLS LIKE PILL BOXES TO MAKE SURE, BUT HE SAYS IT MAY BE POSSIBLE TO BETTER REMEMBER TAKING MEDICINE IF THE PILL GOES WITH A PAT ON THE HEAD, OR SOME OTHER UNUSUAL ACTION. I’M JIM DRYDEN

RUNS :59

SCIENTISTS FROM EUROPE AND THE UNITED STATES HAVE IDENTIFIED TWO NEW GENETIC RISK FACTORS FOR ALZHEIMER’S DISEASE. THESE GENES INCREASE THE RISK FOR THE MORE COMMON, LATE-ONSET FORM OF ALZHEIMER’S. JIM DRYDEN HAS MORE…

THE GROUP, LED BY INVESTIGATORS FROM THE SCHOOL OF MEDICINE AT CARDIFF IN THE UNITED KINGDOM, INCLUDED ALZHEIMER’S RESEARCHERS FROM WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS. THEY SCANNED THE ENTIRE HUMAN GENOME FOR MARKERS OF ALZHEIMER’S RISK, LOOKING AT MORE THAN 600,000 COMMON DNA MARKERS IN A TOTAL OF MORE THAN 19,000 OLDER ADULTS FROM THE UNITED STATES AND EUROPE. WASHINGTON UNIVERSITY RESEARCHER ALISON GOATE SAYS TWO GENES SEEMED TO CONTRIBUTE TO ALZHEIMER’S. ONE IS KNOWN AS THE APOJ, OR CLUSTRIN GENE, THE OTHER IS CALLED PICALM.

(act) :16 o/c in 1993

This is the first time two genes have been so significant
in a dataset. Based on this, there’s good evidence that
these may be novel risk factors, the first novel risk
factors since APOE in 1993.

SOME GENE MUTATIONS ACTUALLY CAUSE EARLY-ONSET ALZHEIMER’S DISEASE, BUT THESE GENES, LIKE THE APOE GENE IDENTIFIED PREVIOUSLY, CONTRIBUTE TO RISK FOR THE MORE COMMON, LATE-ONSET FORM OF ALZHEIMER’S. HOWEVER, GOATE SAYS LIKE APOE, THESE NEWLY IDENTIFIED GENE VARIANTS DON’T GUARANTEE A PERSON WILL DEVELOP ALZHEIMER’S.

(act) :18 o/c develop disease

Genes where the mutations cause the disease, we can accurately
predict who is going to get disease. With genes like APOE, APOJ,
PICALM, these are risk factors, and just because you carry the
risk factor doesn’t mean you will develop disease.
GOATE SAYS ALTHOUGH THESE GENES DO CONTRIBUTE TO ALZHEIMER’S RISK, THEIR EFFECTS APPEAR TO BE RELATIVELY MINOR. SHE SAYS RESEARCHERS ONLY WERE ABLE TO IDENTIFY THEM AS RISK FACTORS BECAUSE THEY WERE ABLE TO STUDY SO MANY OLDER ADULTS, WITH AND WITHOUT ALZHEIMER’S DISEASE.

(act) :21 o/c big dataset

This is the largest genetic study that’s been published on
Alzheimer’s disease to date. It’s certainly comparable in size
to some of the earlier studies in diabetes and some of the
cancer genetics projects. And the size is really important.
We would not have made these observations without such a
big dataset.

GOATE SAYS IT’S NOT CLEAR EXACTLY HOW THESE GENES MAY WORK TO CONTRIBUTE TO ALZHEIMER’S RISK. SHE SAYS IT APPEARS THE PICALM GENE MAY AFFECT SYNAPSES, THOSE ARE THE PATHWAYS THROUGH WHICH BRAIN CELLS COMMUNICATE WITH ONE ANOTHER. HOW THE OTHER GENE, CALLED APOJ OR CLUTRIN, MAY BE AFFECTING THE RISK IS A BIT BETTER UNDERSTOOD.

(act) :25 o/c the brain

David Holtzman at Washington University had, actually,
previously done mouse studies where he demonstrated that
APOE and APOJ cooperatively influence amyloid deposition
in a mouse model. That suggests that this APOJ gene, or
clustrin, that it’s affecting the deposition of amyloid
in the brain.

AMYLOID MAKES UP THE SENILE PLAQUES THAT CHARACTERIZE ALZHEIMER’S DISEASE IN THE BRAIN. GOATE AND COLLEAGUES FROM THE UK, GREECE, IRELAND, GERMANY, BELGIUM AND THE UNITED STATES, REPORTED THEIR FINDINGS IN THE JOURNAL NATURE GENETICS. I’M JIM DRYDEN…

RUNS 2:59

THE GROUP WAS LED BY INVESTIGATORS FROM THE SCHOOL OF MEDICINE AT CARDIFF IN THE UNITED KINGDOM AND INCLUDED ALZHEIMER’S RESEARCHERS FROM WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS. THEY LOOKED AT MORE THAN 600,000 COMMON DNA MARKERS IN A TOTAL OF MORE THAN 19,000 OLDER ADULTS. WASHINGTON UNIVERSITY RESEARCHER ALISON GOATE SAYS THE TEAM FOUND EVIDENCE THAT A PAIR OF GENES SEEMED TO BE CONTRIBUTING TO ALZHEIMER’S. ONE IS KNOWN AS THE APOJ, OR CLUSTRIN GENE, THE OTHER IS CALLED PICALM.

(act) :21 o/c in 1993

This is the first time two genes have been so significant
in a dataset that they’re still significant when you
correct for those very large number of tests. And so
based on this, there’s good evidence that these may be
novel risk factors, the first novel risk factors since
APOE in 1993.

ALL OF THOSE GENES CONTRIBUTE TO RISK FOR LATE-ONSET ALZHEIMER’S DISEASE. THE RESEARCHERS REPORTED THEIR FINDINGS IN THE JOURNAL NATURE GENETICS. I’M JIM DRYDEN

RUNS 1:00

SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT INSUFFICIENT LEVELS OF VITAMIN D SEEM TO PREVENT PEOPLE WITH DIABETES FROM PROCESSING CHOLESTEROL NORMALLY. AND THAT MAY BE THE MECHANISM THAT INCREASES THE RISK OF CARDIOVASCULAR DISEASE IN THOSE PATIENTS. JIM DRYDEN HAS MORE…

IT’S KNOWN THAT PEOPLE WITH DIABETES HAVE AN INCREASED RISK FOR CARDIOVASCULAR PROBLEMS. BUT IT’S NOT CLEAR EXACTLY WHY THAT IS. NOW, SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE IDENTIFIED VITAMIN D AS A POSSIBLE LINK. THEY FOUND THAT DIABETICS WITH LOW LEVELS OF VITAMIN D CAN’T PROCESS CHOLESTEROL NORMALLY. RESEARCHER CARLOS BERNAL-MIZRACHI SAYS WHEN IMMUNE SYSTEM CELLS CALLED MACROPHAGES DON’T GET ENOUGH VITAMIN D, THEY CAN BECOME CLOGGED WITH CHOLESTEROL.

(act) :16 o/c of atherosclerosis

What we found was that with macrophages with vitamin D deficiency,
they accelerate eating cholesterol, and they cannot get rid of it.
So they stay in the macrophage, and that’s what is called foam cells.
And that’s the earliest stage for the development of atherosclerosis.

BERNAL-MIZRACHI SAYS PAST ATTEMPTS TO LOWER THE RISK OF CARDIOVASCULAR DISEASE IN PEOPLE WITH DIABETES HAVE CONCENTRATED ON TIGHTLY CONTROLLING BLOOD SUGAR LEVELS. BUT HE SAYS THAT HASN’T WORKED VERY WELL.

(act) :24 o/c with diabetes

Most of the studies have been linked to glucose, but despite the
fact that we intensively control the glucose, the cardiovascular
disease hasn’t been significantly decreased. So we looked at other
risk factors, and it seems like vitamin D, mechanistically and by
association and correlations, may be a key risk factor for the
development of atherosclerosis in patients with diabetes.

SO BERNAL-MIZRACHI HAS BEEN CONCENTRATING ON THE ROLE OF VITAMIN D. THE MAIN WAY OUR BODIES MAKE VITAMIN D IS THROUGH EXPOSURE TO THE SUN. PEOPLE ALSO CAN TAKE VITAMIN D SUPPLEMENTS, BUT IT TURNS OUT MOST OF US DON’T GET VERY MUCH EXPOSURE TO THE SUN, AND WE END UP WITH INSUFFICIENT AMOUNTS OF THE VITAMIN. AND THAT GETS WORSE AS WE GET OLDER

(act) :19 o/c of atherosclerosis

After a year or two or three or four, or whatever, that we don’t
get exposed to the sunlight, we’re going to start becoming deficient.
We can make a big impact in public health with supplementations of
vitamin D. I’m not saying it will cure, but it may take out the
potential risk factor for the development of cardiovascular disease.

BUT BERNAL-MIZRACHI ISN’T SUGGESTING THAT WE ALL START SPENDING LOTS OF TIME IN THE SUN WITHOUT PROTECTION. THAT WOULD INCREASE THE RISKS FOR SKIN CANCER. INSTEAD, HE’S CURRENTLY STUDYING THE EFFICACY OF ORAL SUPPLEMENTS OF VITAMIN D. AND HE SAYS IT MAY SOMEDAY WORK OUT THAT SHORT PERIODS OF SUN EXPOSURE WILL BE COMBINED WITH ORAL SUPPLEMENTS, AS A WAY TO INCREASE VITAMIN D LEVELS.

(act) :31 o/c sun exposure

Ten, 15 minutes of sun exposure – maybe hands and face
without sun protection – 10, 15 minutes may be enough for
you to achieve good levels during the summer that will hold
during the winter. That’s an area that is very difficult because
it’s clearly known that sun exposure may produce skin cancer,
so we have to put it in a balance in the future: oral pills to
replace the amounts, and/or the sun exposure.

BERNAL-MIZRACHI AND HIS COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL CIRCULATION. I’M JIM DRYDEN…

RUNS 2:53

THE MAIN WAY OUR BODIES MAKE VITAMIN D IS THROUGH EXPOSURE TO THE SUN. PEOPLE ALSO CAN TAKE VITAMIN D SUPPLEMENTS, BUT IT TURNS OUT MOST OF US END UP WITH INSUFFICIENT AMOUNTS OF THE VITAMIN. AND THAT SEEMS TO CAUSE REAL PROBLEMS FOR PEOPLE WITH DIABETES, ACCORDING TO WASHINGTON UNIVERSITY RESEARCHER CARLOS BERNAL-MIZRACHI. HE SAYS WHEN IMMUNE SYSTEM CELLS CALLED MACROPHAGES DON’T GET ENOUGH VITAMIN D, THEY TEND TO BECOME CLOGGED WITH CHOLESTEROL.

(act) :14 o/c of atherosclerosis

With macrophages with vitamin D deficiency, they accelerate
eating cholesterol, and they cannot get rid of it. So they stay
in the macrophage, and that’s what is called foam cells. And
that’s the earliest stage for the development of atherosclerosis.

BERNAL-MIZRACHI SAYS MANY STUDIES LOOKING AT WAYS TO LOWER CARDIOVASCULAR RISK FOR DIABETIC PATIENTS INVOLVE TRYING TO TIGHTLY CONTROL BLOOD SUGAR LEVELS, BUT HE SAYS THAT’S NOT THE ENTIRE PROBLEM. HE SAYS FINDING WAYS TO SUPPLEMENT VITAMIN D LEVELS ALSO WOULD APPEAR TO BE AN IMPORTANT TREATMENT STRATEGY FOR THOSE PATIENTS. I’M JIM DRYDEN…

RUNS :59

TYPICAL PRESCHOOLERS CAN BE MOODY AND PRONE TO TANTRUMS. JUST TRY TAKING ONE TO THE GROCERY STORE. BUT SOME VERY YOUNG CHILDREN HAVE GREATER PROBLEMS THAN JUST THE OCCASIONAL TANTRUM. UP TO 2 PERCENT OF U.S. PRESCHOOLERS ARE CLINICALLY DEPRESSED, AND RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT, LIKE ADULTS, DEPRESSED KIDS ARE LIKELY TO BATTLE THE DISORDER FOR A LONG, LONG TIME. JIM DRYDEN HAS MORE…

STUDYING CHILDREN AS YOUNG AS 3, WASHINGTON UNIVERSITY CHILD PSYCHIATRIST JOAN LUBY FOUND THAT KIDS WHO ARE DEPRESSED TEND TO STAY THAT WAY, OR AT LEAST TO GET DEPRESSED AGAIN. ALMOST TWO-THIRDS STILL HAD DEPRESSION 6 MONTHS AFTER AN INITIAL DIAGNOSIS. 40 PERCENT WERE STILL DEPRESSED TWO YEARS LATER.

(act) :14 o/c later life
And surely when something has longitudinal stability, it
does underscore its importance for treating early. But we, as
infant/preschool psychiatrists, like to treat disorders early
regardless of what implications that has for later life.

LUBY SAYS ALTHOUGH IMPROVING LONG-TERM OUTCOMES IS AN IMPORTANT GOAL, HER TOP PRIORITY IS WORKING TO HELP PRESCHOOLERS FEEL BETTER QUICKLY. FOR A LONG TIME DOCTORS THOUGHT IF VERY YOUNG CHILDREN WERE DEPRESSED, THAT DEPRESSION MIGHT MANIFEST ITSELF AS A STOMACH ACHE OR SOME OTHER PHYSICAL SYMPTOM. BUT LUBY’S TEAM HAS FOUND THAT IN GENERAL, DEPRESSION IN VERY YOUNG CHILDREN LOOKS PRETTY MUCH LIKE DEPRESSION IN OLDER CHILDREN AND ADULTS.

(act) :18 o/c be depression
It’s not just a transient developmental blip that’s going to
spontaneously go away. And it’s not a non-specific precursor
of some later type of problem. It appears to be very true to
form – or what we call homotypic continuity – that it goes on
to continue to be depression.

LUBY’S TEAM HAS SHOWN THAT IT’S POSSIBLE TO DETECT DEPRESSION IN PRESCHOOLEERS AS THEY EXPERIENCE THE CHRONIC DISORDER’S EARLIEST MANIFESTATIONS.
(act) :21 o/c detecting it
So it’s not like we’re saying, “Now preschoolers are depressed,
and they didn’t get depressed 50 years ago.” We’re saying, “We’re
now detecting depression in preschoolers, and it’s very likely that
this has been going on for as long as we’ve known about depression.”
It’s just we now have more sensitive and developmentally appropriate
ways of detecting it.

AND LUBY SAYS THAT’S GOOD NEWS BECAUSE EARLY DETECTION OPENS UP THE POSSIBILITY OF EARLY TREATMENT.

(act) :16 o/c it early
Many disorders, and mental disorders in particular, are more
treatable when the brain is more changeable and neuroplastic,
so that’s why we’re hopeful that if we identify the disorder
early, we could have more success treating it early.

LUBY BELIEVES THAT FOR THE BEST, POSSIBLE OUTCOMES, IT’S IMPORTANT TO TREAT CHILDREN AS SOON AS POSSIBLE. BUT SHE’S NOT PROPOSING PUTTING PRESCHOOLERS ON PROZAC.

(act) :21 o/c and child
That is not, in any way, what this work is supporting or
suggesting. It makes absolutely no statement whatsoever
about treatment. So we definitely do not recommend treatment
with antidepressants, and in fact, we are investigating early
dyadic play psychotherapeutic treatments with the caregiver
and child.

HER GROUP IS NOW COMPARING THE INTERVENTION FOR KIDS AND THEIR CAREGIVERS TO EDUCATION PROVIDED BY A DEVELOPMENTAL PSYCHOLOGIST. SHE SAYS THE INVESTIGATIONAL INTERVENTION FOR KIDS HAS SHOWN SOME PROMISE, BUT MORE RESEARCH IS NEEDED.

(act) :13 o/c is effective
We’ve completed the first phase of the study, and it appears
to be robustly effective. But we’ll await the comparison between
the active treatment and the education/control condition to
really know whether the treatment is effective.

SHE REPORTED THESE FINDINGS IN THE ARCHIVES OF GENERAL PSYCHIATRY. I’M JIM DRYDEN…

RUNS 3:00

CHILD PSYCHIATRIST JOAN LUBY AND HER COLLEAGUES HAVE BEEN STUDYING DEPRESSION IN PRESCHOOLERS FOR MANY YEARS. THIS TIME, THEY FOLLOWED MORE THAN 300 CHILDREN BETWEEN 3 AND 6 FOR UP TO 2 YEARS. 75 OF THOSE KIDS WERE DEPRESSED, AND ALMOST TWO-THIRDS OF THOSE CHILDREN EITHER REMAINED DEPRESSED OR HAD RECURRENT DEPRESSION 6 MONTHS AFTER THEIR INITIAL ASSESSMENT. 40 PERCENT STILL HAD DEPRESSION TWO YEARS LATER.

(act) :14 o/c later life

And surely when something has longitudinal stability, it
does underscore its importance for treating early. But we, as
infant/preschool psychiatrists, like to treat disorders early
regardless of what implications that has for later life.

LUBY SAYS ALTHOUGH IMPROVING LONG-TERM OUTCOMES IS AN IMPORTANT GOAL, HER TOP PRIORITY IS WORKING TO HELP PRESCHOOLERS FEEL BETTER QUICKLY. ABOUT 2 PERCENT OF U.S. PRESCHOOLERS MAY HAVE DEPRESSION, AND LUBY SAYS IT’S IMPORTANT TO RECOGNIZE IT EARLY. HOW TO BEST TREAT IT ISN’T YET KNOWN. SHE SAYS SHE’S NOT ADVOCATING ANTIDEPRESSANTS FOR PRESCHOOLERS, BUT SHE SAYS IT IS IMPORTANT TO INVESTIGATE AND DEVELOP TREATMENTS FOR THOSE WHO ARE DEPRESSED. I’M JIM DRYDEN

RUNS 1:00

RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE DISCOVERED THAT, AT LEAST IN MICE, SOME NERVE CELLS IN THE SPINAL CORD SEEM TO BE SPECIFIC TO THE SENSATION OF ITCH. IT’S POSSIBLE TO KNOCK OUT AN ANIMAL’S ITCH RESPONSE WITHOUT AFFFECTING ITS ABILITY TO SENSE PAIN. JIM DRYDEN HAS MORE…

THIS RESEARCH TEAM PREVIOUSLY HAD DISCOVERED THAT CERTAIN NEURONS HAD A GENE, CALLED GRPR, ACTIVATED BY THINGS THAT MADE MICE ITCHY. IN THIS STUDY THEY WANTED TO LEARN WHETHER NEURONS WITH THAT GRPR GENE WERE ITCH-SPECIFIC, SO THEY USED A TOXIC SUBSTANCE THAT BOUND WITH GRPR TO SELECTIVELY DESTROY THOSE NEURONS. ZHOU-FENG CHEN IS THE RESEARCH TEAM’S PRINCIPAL INVESTIGATOR.

(act) :10 o/c pruritogenic stimuli

They have a profound deficiency in their scratching response to all
sorts of pruritogenic stimuli.

IN OTHER WORDS, THINGS THAT MAKE MICE SCRATCH. CHEN SAYS WHEN HIS TEAM SELECTIVELY KNOCKED OUT SPINAL CORD NEURONS WITH GRPR, THEY ENDED UP WITH MICE THAT BEHAVED NORMALLY, EXCEPT THAT THEY SCRATCHED VERY LITTLE IN RESPONSE TO THOSE STIMULI THAT MADE HEALTHY MICE SCRATCH LIKE CRAZY.

(act) :18 o/c spinal cord

In contrast, those mice responded normally to all sorts of
noxious stimuli. So this is a very, very striking result
because those results suggest there is an itch-specific
neuronal pathway in the spinal cord.

THAT’S IMPORTANT BECAUSE FOR YEARS MANY SCIENTISTS THOUGHT OF ITCH AS A LESS INTENSE SENSATION OF PAIN. CHEN SAYS THESE FINDINGS WOULD SUGGEST OTHERWISE.

(act) :22 o/c itch sensation

The simplest explanation is that those are distinct
sensations are relayed by different types of neurons.
But so far it has been very, very difficult to find such
kinds of neurons. So therefore, our study has shown in
the spinal cord, there’s a specific, labeled line for the
itch sensation.

AND CHEN SAYS KNOWING THAT IT’S POSSIBLE TO BLOCK ITCH SIGNALS WITHOUT BLOCKING PAIN SIGNALS HAS MAJOR IMPLICATIONS FOR THERAPY.

(act) :20 o/c chronic itch

We’ve shown those neurons are critical for the itch sensation,
which means they may contain other itch-specific receptors or
signaling molecules, which can be explored or identified in the
future for treatment, or for management, of chronic itch.

CHEN’S RESEARCH TEAM REPORTED ITS FINDINGS ONLINE IN THE JOURNAL SCIENCE EXPRESS. I’M JIM DRYDEN

RUNS 2:17

THIS RESEARCH TEAM PREVIOUSLY HAD DISCOVERED THAT CERTAIN NEURONS HAD A GENE, CALLED GRPR, ACTIVATED BY THINGS THAT MADE MICE ITCHY. IN THIS STUDY THEY FOUND THAT IF THEY SELECTIVELY KNOCKED OUT SPINAL CORD NEURONS THAT HAD THE GRPR GENE, THEY ENDED UP WITH MICE THAT BEHAVED NORMALLY, EXCEPT THAT THEY SCRATCHED VERY LITTLE IN RESPONSE TO STIMULI THAT MADE HEALTHY MICE SCRATCH LIKE CRAZY. PRINCIPAL INVESTIGATOR ZHOU-FENG CHEN SAYS ALTHOUGH THE MICE DON’T SCRATCH, THEY DO SEEM TO SENSE PAIN THE SAME WAY AS NORMAL MICE DO.

(act) :09 o/c spinal cord

So this is a very, very striking result because those results
suggest there is an itch-specific, neuronal pathway in the
spinal cord.

THAT’S IMPORTANT BECAUSE FOR YEARS MANY SCIENTISTS THOUGHT OF ITCH AS A LESS INTENSE SENSATION OF PAIN. THESE FINDINGS, CHEN SAYS, WOULD SUGGEST OTHERWISE. HE REPORTED THE FINDINGS IN THE ONLINE JOURNAL SCIENCE EXPRESS. I’M JIM DRYDEN

RUNS 1:00

A STUDY OF MALE AND FEMALE SOCCER PLAYERS HAS UNCOVERED DIFFERENCES IN THE WAYS MEN AND WOMEN KICK. STUDYING COLLEGE SOCCER PLAYERS, SPORTS MEDICINE SPECIALISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS AND THE HOSPITAL FOR SPECIAL SURGERY IN NEW YORK HAVE FOUND THAT THERE ARE DIFFERENCES IN HOW MEN AND WOMEN USE MUSCLES IN THE HIP AND ELSEWHERE THAT MAY HELP EXPLAIN DIFFERENCES IN INJURY RISK BETWEEN MEN AND WOMEN. JIM DRYDEN HAS MORE…

FEMALE ATHLETES HAVE A MUCH HIGHER RISK FOR KNEE INJURIES TO THE ANTERIOR CRUCIATE LIGAMENT, OR ACL. TO LEARN ABOUT THOSE DIFFERENCES IN SOCCER PLAYERS, A TEAM OF RESEARCHERS OBSERVED COLLEGE MEN AND WOMEN KICKING A SOCCER BALL. WASHINGTON UNIVERSITY SPORTS MEDICINE SPECIALIST ROBERT BROPHY.

(act) :17 o/c injury differences

We had done a study where we looked at kicking in collegiate male
soccer players, and we wanted to do the same in collegiate female
soccer players and then compare the differences between the genders
and see if there were any differences in terms of which muscles were
activated, and how the lower extremity lined up, that may be related
to some of these injury differences.

BROPHY SAYS THE RESEARCH TEAM DID VIDEO-BASED MOTION STUDIES OF MEN AND WOMEN KICKING A BALL IN A COUPLE OF DIFFERENT WAYS – KICKS THAT USED THE INSTEP OF THE FOOT AND KICKS USING THE SIDE OF THE FOOT.

(act) :22 o/c two genders

The motion analysis laboratory has the ability to track all the
muscle activation and at the same time use motion analysis
cameras to capture the movement of the entire body. So we had
them line up in the lab and then do a variety of kicks into a
small goal about five yards away. And, again, it was the same
thing we had done in the males. We then repeated it in the
females and then compared the two genders.

HE SAYS THE MEN USED MUSCLES IN BOTH THE SUPPORTING LEG AND THE KICKING LEG DIFFERENTLY THAN THE WOMEN.
(act) :20 o/c used it

Men tended to use their hip abductor, their gluteus medius,
of the supporting leg much more. They also tended to use
the medial inter-quad muscle much more in that leg compared
to the women. And then in the kicking leg, the males used
their iliacus, or the hip flexor, much more than the females
used it.

BROPHY SAYS EVEN NOTING THESE DIFFERENCES DOESN’T BEGIN TO EXPLAIN THE POTENTIAL DIFFERENCES IN INJURY RISK BETWEEN MEN AND WOMEN. THESE WERE, AFTER ALL, ARTIFICIAL LABORATORY STUDIES RATHER THAN MEN AND WOMEN GIVING IT THEIR ALL ON A SOCCER FIELD. SO IT DOESN’T EVEN CONSIDER ALL OF THE POTENTIAL RISKS, BUT…

(act) :29 o/c that injury

The women had a weaker hip abductor, a weaker muscle, on that
leg that they use to support. And that was weaker than the other
hip abductor. That difference was not found in the male players.
So there does seem to be some patterning, and then some result,
of this that the women are a little bit weaker in that muscle.
That muscle may be protective against injuries such as an ACL
tear, and so the fact that they are weaker in these hip abductors
may put women more at risk for that injury.

BROPHY, WHO ALSO SERVES AS THE TEAM DOCTOR FOR THE ST. LOUIS ATHLETICA OF THE WOMEN’S PROFESSIONAL SOCCER LEAGUE, SAYS HE BELIEVES THAT CHANGING SOME OF THE PATTERNS THEY OBSERVED IN THIS STUDY MAY HELP PROTECT AND PREVENT SOME INJURIES.

(act) :22 o/c of injury

The hip collapses, on that supporting side, when the women
kick, and that makes sense. The hip abductor is what prevents
the hip from collapsing, so they had less activation of that
muscle, and therefore, their hip collapsed more than the male
players. So one of those things may just be that they have to
concentrate on thinking about that – as they do kicking, as they
do running, jumping, stopping – try to maintain that proper
posture and alignment, which may help also reduce the risk
of injury.

BUT, BROPHY SAYS, MORE RESEARCH WILL BE NEEDED TO PROVE THAT. I’M JIM DRYDEN…

RUNS 2:59

FEMALE ATHLETES HAVE A GREATER RISK THAN THEIR MALE COUNTERPARTS FOR INJURIES TO THE ANTERIOR CRUCIATE LIGAMENT, OR ACL, IN THE KNEE. IN AN ATTEMPT TO LEARN ABOUT DIFFERENCES IN SOCCER PLAYERS, A TEAM OF RESEARCHERS OBSERVED COLLEGE MEN AND WOMEN KICKING A BALL IN THE LABORATORY. WASHINGTON UNIVERSITY SPORTS MEDICINE SPECIALIST ROBERT BROPHY SAYS THEY FOUND THAT MEN AND WOMEN USED DIFFERENT MUSCLES IN THEIR NON-KICKING LEGS.

(act) :21 o/c used it

Men tended to use their hip abductor, their gluteus medius,
of the supporting leg much more than the women. They also
tended to use the medial inter-quad muscle much more in
that leg compared to the women. And then in the kicking leg,
the males used their iliacus, or the hip flexor, much more
than the females used it.

BROPHY SAYS THAT MAY HELP EXPLAIN DIFFERENCES IN RISK FOR KNEE, AND OTHER INJURIES, AND HE SAYS TRAINING FEMALE SOCCER PLAYERS TO KICK THE BALL A BIT DIFFERENTLY MAY BE ABLE TO PROTECT THEM, BUT HE SAYS MORE RESEARCH WILL BE NEEDED TO PROVE THAT. I’M JIM DRYDEN

RUNS 1:00

SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE DISCOVERED A SUBSTANCE MADE IN THE BODY THAT SEEMS TO ACTIVATE ANOTHER MOLECULE THAT HELPS CONTROL FATS AND SUGARS. THE SCIENTISTS SAY THE DISCOVERY COULD LEAD TO BETTER TREATMENTS FOR LIPID DISORDERS AND OTHER METABOLIC PROBLEMS. JIM DRYDEN REPORTS…

THE MOLECULE THAT METABOLIZES FATS AND GLUCOSE IS CALLED PPAR-ALPHA. AND IT CAN BE ACTIVATED WITH DRUGS, BUT SCIENTISTS KNEW THAT THE BODY HAD TO HAVE A WAY TO ACTIVATE IT, TOO. THEY JUST DIDN’T KNOW WHAT IT WAS. METABOLISM RESEARCHER CLAY SEMENKOVICH AND HIS COLLEAGUES WERE STUDYING MICE THAT CAN’T MAKE A SUBSTANCE CALLED FATTY ACID SYNTHASE IN THE LIVER, AND THEY FOUND THAT THOSE ANIMALS ALSO COULDN’T REGULATE FATS AND SUGARS IN A NORMAL FASHION.

(act) :20 o/c fixed ‘em

We made an animal that was missing fatty acid synthase in the liver,
and it acted just like an animal that was also missing PPAR-alpha.
And we could correct the way the animal acted by giving back a
single dose of a pharmacologic activator of PPAR-alpha, in essence
the same kind of drug that people take to lower triglycerides. And
it fixed ‘em.

SEMENKOVICH SAYS THAT MADE THE TEAM LOOK TO FATTY ACID SYNTHASE FOR THE ACTIVATOR, OR LIGAND, THAT TURNED ON PPAR-ALPHA. AND THEY IDENTIFIED A SUBSTANCE THAT ALSO HAPPENS TO BE A VERY COMMON FOOD ADDITIVE.

(act) :22 o/c treat disease

It’s phosphatidylcholine, and so a common name for that is
lecithin. And it’s actually found at a high concentration in egg
whites, not the yolk, and so at least one potential extension of
this work is that it may be possible to modify the composition of
] egg whites or other dietary supplements to actually treat disease.

ANOTHER RESEARCHER ON THE TEAM, IRFAN LODHI, SAYS LEARNING HOW THE BODY ACTIVATES PPAR-ALPHA MAY MAKE IT POSSIBLE TO DELIVER MORE EFFECTIVE THERAPIES WITH FEWER SIDE EFFFECTS.

(act) :12 o/c be delivery

I think if you can manipulate the pathways that synthesize
endogenous ligand, I think you can minimize some of the side
effects. Obviously, the next challenge is going to be delivery.

AND SEMENKOVICH SAYS IT’S LIKELY THAT PEOPLE WITH LIPID DISORDERS MAY SOMEDAY BE ABLE TO SIT DOWN WITH A PLATE OF FOOD THAT CAN HELP THEM CONTROL THEIR METABOLIC PROBLEMS.

(act) :19 o/c are coming

An extremely common compound appears to be binding to this
protein that is also the target of drugs. And that common
compound, that information could be exploited to make better
drugs and to even develop what, you know, sometimes people refer
to as nutriceuticals – you know, nutrients that can have
pharaceutical-like properties. And I think those are coming.

HE SAYS PPAR-ALPHA ALSO IS INVOLVED WITH INFLAMMATION, WHICH IS ANOTHER KEY FACTOR IN PROBLEMS LIKE DIABETES, HYPERTENSION AND HEART DISEASE.

(act) :29 o/c the cell

People who get insulin resistance probably have defects in
many of these PPAR-alpha-dependent pathways, and curiously,
fatty acid synthase is one of the most important insulin-
responsive proteins. So if you are looking at a system and
want to make sure it responds to insulin, you make sure that
when you give insulin, fatty acid synthase goes up a lot.
So there’s a good chance that these lipid disorders that one
sees in insulin-resistance syndromes may, in fact, be
modulated by fatty acid synthase inside the cell.

SEMENKOVICH, LODHI AND COLLEAGUES REPORTED ON THEIR FINDINGS ABOUT THE RELATIONSHIP BETWEEN PPAR-ALPHA, FATTY ACID SYNTHASE AND LECITHIN IN THE JOURNAL CELL. I’M JIM DRYDEN

RUNS 2:57

THE PRIMARY MOLECULE THAT SEEMS TO CONTROL FATS AND GLUCOSE IS CALLED PPAR-ALPHA. AND IT CAN BE ACTIVATED WITH DRUGS, BUT SCIENTISTS KNEW THAT THE BODY HAD TO HAVE A WAY TO ACTIVATE IT, TOO. BUT STUDYING MICE THAT CAN’T MAKE FATTY ACID SYNTHASE IN THEIR LIVERS, METABOLISM RESEARCHER CLAY SEMENKOVICH AND HIS COLLEAGUES FOUND THAT THOSE ANIMALS ALSO COULDN’T REGULATE FATS AND SUGARS IN A NORMAL FASHION.

(act) :18 o/c lower trigylerides

We made an animal that was missing fatty acid synthase in the liver,
and it acted just like an animal that was also missing PPAR-alpha.
And we could correct the way the animal acted by giving back a
single dose of a pharmacologic activator of PPAR-alpha, in essence
the same kind of drug that people take to lower triglycerides.

THAT MADE THEM LOOK AT FATTY ACID SYNTHASE TO FIND AN ACTIVATOR FOR PPAR-ALPHA. AND THEY EVENTUALLY ISOLATED A COMPOUND COMMONLY CALLED LECITHIN. IT’S USED AS A FOOD ADDITIVE, BUT IT ALSO SEEMS TO PLAY A ROLE IN ACTIVATING PPAR-ALPHA AND THUS IN THE METABOLISM OF FATS AND SUGARS. I’M JIM DRYDEN

RUNS 1:00

TUMORS WITH PARTICULAR GENETIC DEFECTS CAN BE RESISTANT TO RADIATION THERAPY, AND RESEARCHERS AT THE SITEMAN CANCER CENTER AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE AND BARNES-JEWISH HOSPITAL IN ST. LOUIS HAVE NOW DISCOVERED HOW THE MUTATIONS MAKE THE TUMOR CELLS RESISTANT TO RADIATION. JIM DRYDEN REPORTS…

RADIATION ONCOLOGY RESEARCHER TEJ PANDITA FOCUSES HIS EFFORTS ON HOW TO MAKE RADIATION THERAPY MORE DEADLY TO TUMOR CELLS.

(act) :12 o/c adjacent tissue

We are trying to understand how best we can specifically kill
tumor cells and save the normal, adjacent tissue.

PANDITA’S TEAM HAS BEEN TRYING TO FIGURE OUT WHY SOME TUMOR CELLS ARE DESTROYED BY RADIATION, BUT OTHER CANCER CELLS CAN BE RESISTANT TO THE THERAPY. THE DIFFERENCE SEEMS TO INVOLVE A GENE CALLED PTEN THAT CAN BE DEFECTIVE IN MANY TYPES OF CANCEROUS TUMORS. MUTATIONS IN THE PTEN GENE OFTEN MAKE THE CELLS RESISTANT TO RADIATION, ACCORDING TO PANDITA. HE HAS FOUND THAT WHEN TUMOR CELLS ARE DEFICIENT IN PTEN, THEY TEND TO HAVE DEFECTIVE CELL CHECKPOINTS, WHICH HE COMPARES TO CARS WITH DEFECTIVE BRAKES.

(act) :29 o/c the damage

Those checkpoints are like, you have the brakes on a car.
When the car is running if your brakes are not working well,
the car can keep on moving. In a similar way if the cell does
not have this PTEN program working and it is challenged by
some agent, which causes damage to it, what it does is it
allows the cell to keep on going, accumulating the damage.

BUT CONTINUING TO GROW AND DIVIDE AT A TIME WHEN NORMAL PTEN GENES WOULD WANT THE CELL TO DIE…LIKE WHEN IT’S EXPOSED TO RADIATION. PANDITA SAYS THE CELLS WITH FAULTY CHECKPOINTS SEEM TO BE RESISTANT TO RADIATION BECAUSE THEY’RE RESISTANT TO APOPTOSIS, OR PROGRAMMED CELL DEATH, IN WHICH THE DAMAGED CELL KILLS ITSELF.

(act) :08 o/c to apoptosis

Cells in which this PTEN protein is absent, they are resistant
to apoptosis.

PANDITA SAYS TO MAKE TUMOR CELLS MORE VULNERABLE TO RADIATION THERAPY IT WILL BE NECESSARY TO CORRECT THEIR FAUTLY CHECKPOINTS BY SOMEHOW IMPROVING PTEN FUNCTION.

(act) :29 o/c normal tissue

So what we need to do is to make the cells have a normal PTEN
function, either by using a genetic engineering approach or by
using different chemical approaches. And we are trying to find
out how we can restore the function in the tumor where the tumor
becomes very, very resistant to the radiation so that we can
cure tumor with a moderate radiation dose, and we can save the
normal tissue.

PANDITA AND HIS COLLEAGUES REPORTED THEIR FINDINGS EARLIER THIS MONTH IN THE JOURNAL CELL CYCLE. I’M JIM DRYDEN…

RUNS 2:32

DEFECTS IN THE GENE CALLED PTEN ARE FOUND IN MANY TYPES OF CANCEROUS TUMORS, AND THOSE TUMORS, WITH MUTATIONS IN THE PTEN GENE, ARE OFTEN RESISTANT TO RADIATION, ACCORDING TO RADIATION ONCOLOGY RESEARCHER TEJ PANDITA. WHEN TUMOR CELLS ARE DEFICIENT IN PTEN, THEY WILL TEND TO HAVE DEFECTIVE CELL CHECKPOINTS, WHICH HE COMPARES TO A CAR WITH DEFECTIVE BRAKES.

(act) :21 o/c the damage

You have the brakes in a car. When the car is running, if your
brakes are not working well, the car can keep on moving. In a
similar way, if the cell does not have this PTEN protein working,
what it does, it allows the cell to keep on going, accumulating
the damage.

AND CONTINUE GROWING AND DIVIDING AT A TIME WHEN A NORMAL PTEN GENE WOULD WANT THE CELL TO DIE…LIKE WHEN IT’S EXPOSED TO RADIATION TREATMENTS. PANDITA SAYS TO MAKE THOSE TUMOR CELLS MORE VULNERABLE TO RADIATION THERAPY, IT WILL BE NECESSARY TO CORRECT THEIR FAULTY CHECKPOINTS. I’M JIM DRYDEN…

RUNS :59

SEVERAL YEARS AGO, SCIENTISTS COMPLETED THE FIRST MAP AND SEQUENCE OF THE HUMAN GENOME. IT CONTAINS THE INFORMATION ABOUT ALL OF THE HUMAN GENES THAT DETERMINE WHETHER WE’RE SICK OR HEALTHY. BUT RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS ARE NOW PART OF AN EFFORT TO USE GENETIC SEQUENCING TECHNIQUES TO BETTER UNDERSTAND THE MICROBES THAT INHABIT THE HUMAN BODY. JIM DRYDEN REPORTS…

OUR BODIES ARE FILLED WITH CELLS: BLOOD CELLS, SKIN CELLS, NERVE CELLS, BONE CELLS. BUT BELIEVE IT OR NOT, WE’VE GOT MORE VISITING MICROBES IN THE BODY RIGHT NOW THAN ALL OF THOSE CELLS PUT TOGETHER.

(act) :26 o/c is huge

It’s slowly become appreciated that we actually have 10
times more microbial cells in our body than we have human
cells, and the number of microbial genes that those microbes
encode for is, maybe, 100 times as many genes as we carry in
our own genome. So the amount of gene activity, and therefore
functional activity, that the microbes are contributing to
our body, is huge.

THAT’S WASHINGTON UNIVERSITY GENETICS RESEARCHER GEORGE WEINSTOCK. HE IS LEADING WORK AT WASHINGTON UNIVERSITY, THAT’S BEING DONE, IN CONJUNCTION WITH RESEARCHERS AT 12 OTHER INSTITUTIONS IN THE U.S., CALLED THE HUMAN MICROBIOME PROJECT. WEINSTOCK SAYS THE PROJECT SEEKS TO CATALOG THE BACTERIA, VIRUSES, FUNGI AND OTHER MICROORGANISMS THAT NATURALLY COEXIST WITH HUMAN CELLS.

(act) :31 o/c culture ‘em

People discovered that they could sequence a part of the
microbial genome called the ribosomal RNA gene, and this is
like a bar code. Every microorganism, every species has this
gene. Once we learned that, we could take these microbial
communities, and we could just pull out these ribosomal RNA
genes and sequence them and then take a census, basically, of
what are all the microbes that were there and how many of each
one that were there, without actually having to culture ‘em.

THAT WAS THE FIRST STEP, AND WEINSTOCK SAYS ADVANCES IN THE SPEED AND EFFICIENCY OF SEQUENCING TECHNOLOGY ALSO HAVE MADE THIS WORK POSSIBLE.

(act) :18 o/c of dollars

The Human Genome Project, which was the real breakthrough
project in DNA sequencing, can now be done in a day at a
single genome center for 50 thousand dollars, whereas the
original project, of course, took five centers several years
and cost hundreds of millions of dollars.

WEINSTOCK SAYS THE MICROBIOME PROJECT ULTIMATELY HOPES TO LEARN HOW THESE NON-HUMAN MICROBES AFFECT HUMAN HEALTH AND DISEASE.

(act) :20 o/c can happen

When conditions change in your body, you may have a microbe
that was a minor organism suddenly overgrow. Or you may have
a microbe that was a major organism – and protecting you against
other ones – suddenly diminish in numbers. Or even more complicated
poly-microbial changes can happen.

WEINSTOCK AND THE OTHER RESEARCHERS AROUND THE UNITED STATES WILL SURVEY SEVERAL HUNDRED PEOPLE AND TAKE SAMPLES FROM MANY SITES THROUGHOUT THE BODY THAT CAN STORE VISITING MICROBES.

(act) :14 o/c be off

Each person will be sequenced at 15 or 18 sites, depending
on whether they’re a boy or a girl, and this will generate
altogether about 12,000 specimens. And based on that initial
benchmarking, we’ll be off!

WASHINGTON UNIVERSITY RECENTLY RECEIVED 4 GRANTS TOTALING 19 MILLION DOLLARS IN FUNDING TO HELP LEAD THE MICROBIOME PROJECT. THE EFFORT IS EXPECTED TO CONTINUE FOR SEVERAL YEARS. I’M JIM DRYDEN

RUNS 2:57

IT’S CALLED THE HUMAN MICROBIOME PROJECT, AND IT SEEKS TO CATALOG THE BACTERIA, VIRUSES, FUNGI AND OTHER MICROORGANISMS THAT NATURALLY COEXIST WITH HUMAN CELLS IN OUR BODIES. WASHINGTON UNIVERSITY GENETICS RESEARCHER GEORGE WEINSTOEK SAYS MICROBES MAKE A HUGE CONTRIBUTION TO WHO WE ARE, BUT IT’S BEEN HARD TO STUDY THEM IN THE PAST BECAUSE MOST OF THE MICROBES COULDN’T BE GROWN IN A CULTURE DISH. THAT ROADBLOCK WAS REMOVED, HE SAYS, ABOUT FIVE YEARS AGO.

(act) :24 o/c culture ‘em

People discovered that they could sequence a part of the
microbial genome called the ribosomal RNA gene, and this
is like a bar code. Once we learned that, we could take
these microbial communities, and we could just pull out
these ribosomal RNA genes and sequence them and then take
a census, basically, without actually having to culture ‘em.

WASHINGTON UNIVERSITY RECEIVED 4 GRANTS TOTALING 19 MILLION DOLLARS TO HELP LEAD 12 U.S. INSTITUTIONS WORKING ON THE MICROBIOME PROJECT. I’M JIM DRYDEN

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SOMETIMES WHEN A PERSON HAS A DEFECTIVE HEART VALVE, SURGEONS CAN REPLACE THE BAD VALVE WITH A VALVE TAKEN FROM A PIG. BUT HEART SURGEONS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE AND BARNES-JEWISH HOSPITAL IN ST. LOUIS FOUND THAT SOME OF THOSE VALVES HAVE FAILED EARLIER AND MORE OFTEN THAN EXPECTED. SO THEY’VE STOPPED USING THEM UNTIL FURTHER NOTICE. JIM DRYDEN HAS THE STORY…

PEOPLE WHO HAVE HEART VALVE PROBLEMS ARE CANDIDATES FOR SURGERY TO EITHER REPAIR OR REPLACE THEIR DEFECTIVE VALVE. THAT CAN MEAN SURGERY TO IMPLANT A MECHANICAL VALVE, OR OFTEN SURGERY TO REPLACE THE DEFECTIVE VALVE WITH ONE TAKEN FROM A COW OR A PIG, ACCORDING TO WASHINGTON UNIVERSITY HEART SURGEON JENNIFER LAWTON.

(act) :25 o/c very quickly

The failure in these patients was typically a heart failure or
difficulty breathing, and it was manifested by the valve not
opening properly, recurrence of the narrowing of the valve itself.
Not enough blood was going through the opening of the valve, and
it became stenotic, or narrowed. And in these patients, the new
valve became stenotic, or narrowed, very quickly.

LAWTON SAYS THE REPLACMENT VALVES FROM PIGS WOULD BE EXPECTED TO LAST FOR 10 TO 15 YEARS, BUT THE VALVES IN THIS STUDY TENDED TO FAIL IN A MATTER OF MONTHS. ONE OF THEM FAILED…

(act) :10 o/c valve lasted

Three months after implantation. So that was the main thing
that was very alarming to us was the short amount of time in
which the valve lasted.

LAWTON SAYS THE VALVES FROM PIG TISSUE NORMALLY DO VERY WELL, AND IN FACT, MORE THAN 95 PERCENT OF THE VALVES IMPLANTED AT BARNES-JEWISH HOSPITAL BETWEEN 2001 AND 2005 ARE STILL FUNCTIONING. BUT SHE SAYS THE FAILURE RATE IS STILL TOO HIGH. PATIENTS WHOSE VALVES FAIL NEED ANOTHER OPERATION, SO HER GROUP OF CARDIAC SURGEONS HAS STOPPED USING THE PIG VALVES. LAWTON SAYS THE PIG VALVES CURRENTLY CARRY RISK THAT OTHER TYPES OF REPLACEMENT VALVES DON’T.

(act) :11 o/c that valve

At our institution, we probably won’t implant them again until
we would be comfortable that they would not fail again. To us,
it was too high to continue to use that valve.

SO LAWTON AND HER COLLEAGUES ARE NOW USING MECHANICAL VALVES AND VALVES TAKEN FROM COWS WHEN PATIENTS NEED REPLACEMENT SURGERY. SHE SAYS IF SHE NEEDED TO HAVE VALVE SURGERY, SHE PROBABLY WOULD OPT FOR ONE OF THOSE OPTIONS, BUT SHE SAYS THOSE PATIENTS WHO ALREADY RECEIVED PIG VALVES DO HAVE A CHANCE TO DO JUST FINE. BUT SHE RECOMMENDS CAREFUL MEDICAL FOLLOW-UP.

(act) :27 o/c the valve

And anytime you have a valve replacement, whatever type of
valve that may be, you should follow regularly with your doctor.
And that means periodically obtaining an echocardiogram, and if
you’re not having any symptoms, then you could follow up regularly
with your doctor. If you begin to have symptoms of difficulty
breathing or lower extremity swelling or chest pain, then you
would need to see your doctor and, perhaps, get an echocardiogram,
which would detect this problem with the valve.

SHE REPORTED ON THE VALVE FAILURES IN THE JUNE ISSUE OF THE JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY. I’M JIM DRYDEN

RUNS 2:36

THE RESEARCHERS NOTICED THAT 4 OF 106 PATIENTS WITH PIG VALVES DEVELOPED SEVERE IMPAIRMENT AFTER LESS THAN FOUR YEARS. NORMALLY, ACCORDING TO LEAD AUTHOR AND HEART SURGEON JENNIFER LAWTON, SUCH VALVES WOULD BE EXPECTED TO LAST FOR 10 TO 15 YEARS, BUT SHE SAYS THE VALVES THAT FAILED TENDED TO DO SO IN A MATTER OF MONTHS. ONE OF THEM FAILED…

(act) :10 o/c valve lasted

Three months after implantation. So that was the main thing
that was very alarming to us was the short amount of time in
which the valve lasted.

LAWTON SAYS THAT MEANT ANOTHER VALVE REPLACEMENT OPERATION WAS REQUIRED. BECAUSE OF THE FAILURES, LAWTON SAYS THE PIG VALVES CURRENTLY CARRY RISKS THAT OTHER TYPES OF REPLACEMENT VALVES DON’T.

(act) :07 o/c fail again

At our institution, we probably won’t implant them again until
we would be comfortable that they would not fail again.

SHE REPORTED ON THE VALVE FAILURES IN THE JUNE ISSUE OF THE JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY. I’M JIM DRYDEN

RUNS :56

THE MINIMUM DRINKING AGE IN THE UNITED STATES WAS SET AT 21 YEARS OLD ABOUT TWO DECADES AGO. SINCE THEN, THERE HAS BEEN A REDUCTION IN BINGE DRINKING. WASHINGTON UNIVERSITY RESEARCHERS HAVE FOUND THAT SINCE 1979, BINGE DRINKING RATES HAVE DECLINED SUBSTANTIALLY AMONG YOUNG PEOPLE…WITH ONE EXCEPTION: COLLEGE STUDENTS. JIM DRYDEN HAS MORE…

THE RESEARCHERS WENT BACK TO LOOK AT DATA GATHERED OVER THE LAST 30 YEARS OR SO. THE INFORMATION CAME FROM MORE THAN 500 THOUSAND SUBJECTS, AND THE RESEARCHERS WERE ABLE TO DIVIDE THEM INTO GROUPS, ACCORDING TO AGE, SEX, ETHNICITY AND WHETHER OR NOT THEY ATTENDED COLLEGE. PRINCIPAL INVESTIGATOR RICHARD GRUCZA.

(act) :18 o/c going up

On the whole, binge drinking is down. Young men tend to
account for the majority of binge drinking, and their rates
have dropped substantially. However, at the same time, there’s
been, kind of, this closing gender gap in terms of alcohol and
drug use. Women, you know, their rates of alcohol use have been
going up.

THE OTHER BIG ISSUE IS WHETHER A YOUNG PERSON GOES TO COLLEGE.

(act) :09 o/c college campuses

These positive trends – the tendency for binge drinking to go
down in society – has not permeated college campuses.

GRUCZA’S TEAM FOUND THAT ALTHOUGH KIDS OF COLLEGE AGE ARE GENERALLY DOING LESS BINGE DRINKING, THOSE ON COLLEGE CAMPUSES ARE BUCKING THAT TREND. GRUCZA SAYS AMONG 18-TO 20-YEAR-OLD MEN, BINGE DRINKING DECLINED BY MORE THAN 30 PERCENT AMONG THOSE NOT IN COLLEGE, WHILE REMAINING STATISTICALLY UNCHANGED AMONG COLLEGE STUDENTS. FOR WOMEN 21 TO 23, BINGE DRINKING INCREASED ABOUT 20 PERCENT AMONG NON-STUDENTS BUT ROSE MORE THAN 40 PERCENT AMONG WOMEN IN COLLEGE.

(act) :09 o/c a bit

Basically, if you look at college age in total, the rates
were down for people who were not in college, but in college,
the rates were about the same, perhaps even going up a bit.

HE SAYS IT’S FAIRLY CLEAR THAT INCREASING THE DRINKING AGE TO 21 HAS DRAMATICALLY CUT RATES OF BINGE DRINKING AMONG HIGH-SCHOOL STUDENTS. AND GRUCZA ASSUMES PART OF THE REASON IS THAT WHEREAS ONCE 18-YEAR-OLDS COULD LEGALLY OBTAIN ALCOHOL AND SHARE IT WITH THEIR YOUNGER FRIENDS, THERE ARE NOW FEWER STUDENTS IN HIGH SCHOOL WITH FRIENDS WHO CAN PURCHASE AND POSESS ALCOHOL. BUT THAT’S NOT THE CASE ON COLLEGE CAMPUSES. THAT’S WHY A NUMBER OF COLLEGE PRESIDENTS HAVE PROPOSED LOWERING THE DRINKING AGE AGAIN, WITH THE IDEA THAT FEWER STUDENTS WOULD BINGE DRINK – THAT IS, FEWER WOULD HAVE AT LEAST 5 DRINKS AT A TIME – IF THEY WERE ALLOWED TO DRINK IN MODERATION AT COLLEGE AND UNIVERSITY EVENTS. THAT PROPOSAL IS KNOWN AS THE AMETHYST INITIATIVE, AND GRUCZA SAYS IN SOME WAYS, THE IDEA MAKES GOOD SENSE.

(act) :16 o/c age increases

You know, that’s an argument that makes a lot of common sense,
but for which there is absolutely no evidence to support. The
number of binge-drinking episodes or the number of fatal car
crashes or other adverse, alcohol-related outcomes, they all
tend to come down as the drinking age increases.

GRUCZA SAYS LOWERING THE DRINKING AGE WOULD HAVE NEGATIVE PUBLIC HEALTH CONSEQUENCES.

(act) :15 o/c public health

There is no public-health benefit to a lower drinking age. There’s
lots of good, libertarian, philosophical arguments about why the
drinking age should be lower, and we can’t address those. But we
know what the public-health consequences are. The higher drinking
age has been good for public health.

GRUCZA SAYS OVERALL, THE LOWER RATES OF BINGE DRINKING MAKE THE HIGHER DRINKING AGE WORTHWHILE, BUT HE SAYS IT’S CLEAR SOMETHING NEEDS TO BE DONE TO BRING COLLEGE STUDENTS INTO LINE WITH THEIR PEERS WHO DON’T ATTEND COLLEGE. HE REPORTED HIS FINDINGS IN THE JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY. I’M JIM DRYDEN…

RUNS 2:58

THE RESEARCHERS FOUND THAT ALTHOUGH POLICY INITIATIVES AIMED AT LOWER RATES OF UNDERAGE DRINKING GENERALLY HAVE BEEN SUCCESSFUL AND THAT BINGE DRINKING IS DOWN AMONG YOUNG PEOPLE OVERALL, IT REMAINS A PROBLEM ON COLLEGE CAMPUSES. RESEARCHER RICHARD GRUCZA’S TEAM WENT BACK TO THE 1970s TO STUDY RATES OF BINGE DRINKING AND FOUND THAT ALTHOUGH RATES HAVE DECLINED IN MOST YOUNG PEOPLE. ALMOST 40 PERCENT OF COLLEGE-AGE WOMEN AND MORE THAN HALF OF COLLEGE-AGE MEN REPORTED BINGE DRINKING.

(act) :06 o/c college campuses

The tendency for binge drinking to go down in society has not
permeated college campuses.

GRUCZA SAYS AMONG 18-TO 20-YEAR-OLD MEN, BINGE DRINKING DECLINED BY MORE THAN 30 PERCENT AMONG THOSE NOT IN COLLEGE WHILE REMAINING STATISTICALLY UNCHANGED IN COLLEGE STUDENTS. FOR WOMEN 21 TO 23, BINGE DRINKING INCREASED ABOUT 20 PERCENT AMONG NON-STUDENTS BUT ROSE MORE THAN 40 PERCENT AMONG WOMEN IN COLLEGE. GRUCZA SAYS IT’S CLEAR SOMETHING NEEDS TO BE DONE TO BRING COLLEGE STUDENTS INTO LINE WITH THEIR PEERS WHO DON’T GO TO COLLEGE. I’M JIM DRYDEN

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BEDTIME CAN BE VERY STRESSFUL FOR PEOPLE WHO CAN’T SLEEP, BUT STRESS ISN’T THE ONLY THING THAT CAUSES INSOMNIA. LIKE MANY DISORDERS, THE PROBLEM INVOLVES BOTH GENETIC AND ENVIRONMENTAL FACTORS. AND AS JIM DRYDEN REPORTS, WASHINGTON UNIVERSITY SCIENTISTS HAVE DEVELOPED A LINE OF FRUIT FLIES THAT MAY BE ABLE TO SHED SOME LIGHT ON THE MECHANISMS THAT CAUSE INSOMNIA IN HUMANS…

ALL OF US HAVE TROUBLE SLEEPING FROM TIME TO TIME. A BIG TEST IN THE MORNING OR AN IMPORTANT BUSINESS MEETING CAN LEAVE YOU TOSSING AND TURNING. SO CAN A FIGHT WITH YOUR SIGNIFICANT OTHER. BUT THOSE TYPES OF SLEEPLESS NIGHTS AREN’T THE SAME THING AS INSOMNIA. WASHINGTON UNIVERSITY NEUROBIOLOGIST PAUL SHAW SAYS MOST OF US WILL EXPERIENCE A FEW SLEEPLESS NIGHTS EVERY SO OFTEN. AND SOME PEOPLE ACTUALLY NEED LESS SLEEP THAN OTHERS. BUT FOR MANY, LACK OF SLEEP IS A BIG PROBLEM. THOSE ARE THE PEOPLE WHO SUFFER FROM CHRONIC INSOMNIA. SHAW SAYS IT’S A VERY TOUGH DISEASE TO STUDY IN ANIMALS, BUT HIS TEAM OF RESEARCHERS NOW HAS FOUND A GOOD MODEL ORGANISM: THE FRUIT FLY. IN THESE DAYS OF GENETIC ENGINEERING, SHAW’S BRED THESE FLIES TO HAVE INSOMNIA IN THE WAY THAT BOTANISTS IN THE MIDDLE AGES MIGHT HAVE MADE A NEW TYPE OF ROSE, OR DOG BREEDERS MIGHT HAVE CREATED A CHIHUAHUA. FIRST, THEY OBSERVED THE BEHAVIOR OF THE FLIES. THEN THEY MATED THOSE THAT DIDN’T SLEEP MUCH WITH OTHER FLIES THAT ALSO TENDED TO SLEEP LESS.

(act) :17 o/c messed up

They had difficulty going to sleep. They had difficulty
staying asleep. They looked hyperactive. Just looking at a
wild-type population of flies, some flies sleep great. Some flies
just can’t, and we thought, “Well, God, what if we take all of
these flies, and we breed them together over successive generations?
Can we get a fly that is really messed up?”

EVENTUALLY, SHAW’S TEAM CREATED A LINE OF FRUIT FLIES THAT SLEEPS FOR ONLY ABOUT AN HOUR PER DAY. AND HE SAYS IT TURNS OUT THAT THE FLIES HAVE MANY OF THE SAME PROBLEMS AS HUMANS WITH INSOMNIA.

(act) :36 o/c them anyway

We have these insomnia-like flies that they don’t sleep very
much. They fall down. It’s worth remembering that flies have
six legs, but yet, they still can’t maintain their balance.
And that seemed strange to us. We thought that maybe these
flies had some degenerative problem, and so we sent our flies
to experts in the field of degeneration to see if they could
identify problems with their brain. And they looked, and they
came back with a clean bill of health, no serious problems.
And it wasn’t until a couple of months, maybe a year, later
that I was reading a review article, and I found a reference
showing that human insomniacs also have difficulty maintaining
their balance. So here we created a line of insomniac flies.
We didn’t necessarily know all of the features we should be
looking for, and we found them anyway.

THAT SUGGESTS TO SHAW THAT HIS TEAM IS ON THE RIGHT TRACK. HE SAYS HUMANS WITH INSOMNIA DON’T HAVE PROBLEMS THAT ARE AS PRONOUNCED AS WHAT HIS TEAM HAS OBSERVED IN THE FLY. HE SAYS THERE ARE MANY PEOPLE WHO DON’T SLEEP VERY MUCH, BUT ONLY THOSE WITH INSOMNIA EXPERIENCE PROBLEMS AS A RESULT.

(act) :12 o/c fundamentally impaired

If you’re a human, and you’ve got insomnia, you’re cognitively
impaired on certain tasks. And so we have an assay in the fly
that measures short-term memory. We ask, “Can our flies learn
this task?” and they can’t. So they’re fundamentally impaired.

HE SAYS BECAUSE THESE ARE FLIES WHO REPRODUCE RAPIDLY, IT’S POSSIBLE TO QUICKLY LEARN ABOUT UNDERLYING GENETIC MECHANISMS THAT MAY BE CONTRIBUTING TO SLEEP PROBLEMS.

(act) :19 o/c altered state

Stress disrupts sleep. We know that to be true, but insomnia
is not solely a case of people being stressed. We’ve created
a line of flies that they don’t lose sleep because they’re
stressed. They lose sleep because they can’t sleep. It more
closely resembles what we see in humans, as opposed to some
other animal studies where you have to artificially induce
some kind of altered state.

SHAW’S TEAM REPORTED ITS FINDINGS IN THE JOURNAL OF NEUROSCIENCE. I’M JIM DRYDEN…

RUNS 3:00

IN THESE DAYS OF GENETIC ENGINEERING, THE WASHINGTON UNIVERSITY SCIENTISTS BRED THESE FLIES TO HAVE INSOMNIA IN THE WAY THAT BOTANISTS IN THE MIDDLE AGES MIGHT HAVE BRED A NEW TYPE OF ROSE, OR DOG BREEDERS MIGHT HAVE CREATED A CHIHUAHUA. FIRST, THE RESEARCHERS OBSERVED THE BEHAVIOR OF FLIES. THEN THEY MATED THE FLIES THAT DIDN’T SLEEP MUCH WITH OTHER FLIES THAT ALSO TENDED TO SLEEP LESS. THE RESULT, SAYS PRINCIPAL INVESTIGATOR PAUL SHAW, WAS A LINE OF FRUIT FLIES THAT SLEPT FOR ONLY ABOUT AN HOUR A DAY.

(act) :15 o/c going on

They had difficulty going to sleep. They had difficulty
staying asleep. They looked hyperactive, and we thought,
“Well, God, what if we take all of these flies, and we
breed them together over successive generations? Can we
get a fly that is really messed up? And if we can, then
what can we find out about what might be going on?”

IT TURNS OUT, SHAW SAYS, THAT THE FLIES HAVE MANY OF THE SAME PROBLEMS AS HUMANS WHO HAVE INSOMNIA. THEY HAVE TROUBLE CONCENTRATING AND LEARNING, DIFFICULTY WITH BALANCE AND OTHER SIMILARITIES THAT HE SAYS MAKE THEM A GOOD MODEL ORGANISM FOR STUDYING INSOMNIA. I’M JIM DRYDEN

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CHILDREN WITH ECZEMA ARE AT MUCH HIGHER RISK FOR ASTHMA THAN THOSE WHO DON’T HAVE THE SKIN DISEASE. BUT WHY THIS SKIN RASH SHOULD INCREASE THE RISK OF LUNG INFLAMMATION HASN’T BEEN CLEAR. NOW, WORKING IN A MOUSE MODEL, A TEAM OF WASHINGTON UNIVERSITY RESEARCHERS MAY HAVE FIGURED OUT THE CONNECTION. JIM DRYDEN REPORTS…

ECZEMA INVOLVES ITCHY PATCHES ON THE SKIN. THE CONDITION IS ASSOCIATED WITH ASTHMA IN CHILDREN. ACCORDING TO WASHINGTON UNIVERSITY SCIENTIST RAPHAEL KOPAN, THOSE WHO DEVELOP ECZEMA ON THE SKIN ARE AT MUCH HIGHER RISK OF DEVELOPING ASTHMA IN THE LUNGS.

(act) :13 o/c we generated

The history of eczema give you a 10-fold higher likelihood of
developing asthma. So the question became a) why is that? and
b) can we address that by looking at a colony of animals that
we generated?

KOPAN SAYS SOME SCIENTISTS EXPLAINED THE RELATIONSHIP BETWEEN ECZEMA AND ASTHMA BY PRESUMING THAT BOTH PROBLEMS RESULTED FROM A SIMILAR GENETIC DEFECT. OTHERS BELIEVED THAT WHEN PEOPLE SCRATCHED THEIR ITCHY SKIN, THEY WOULD BECOME EXPOSED TO ALLERGENS RELEASED BY THE SCRATCHING THAT COULD THEN CAUSE THEM TO DEVELOP ASTHMA. BUT KOPAN SAYS NEITHER SEEMS TO EXPLAIN THE PHENOMENON THAT SCIENTISTS CALL ATOPIC MARCH, THAT IS HOW A SKIN DISEASE CAN INCREASE THE RISK OF A LUNG DISEASE. WORKING IN MICE, KOPAN’S GROUP STARTED WITH AN ASSUMPTION ABOUT THE IMMUNE SYSTEM: THAT AN ATTACK ANYWHERE WOULD LEAD TO INCREASED ACTIVITY EVERYWHERE.

(act) :21 o/c the lung

Imagine that you, you know, are a country at was, and you
are surrounded by a border. If there’s a breach in the north,
the people in the south are still going to be more vigilant,
assuming that there might be an attack from all directions.
So with that logic, then perhaps some product the skin secretes
would be read by the lung, creating a hypersensitive condition
in the lung
THAT SUBSTANCE — FOUND BOTH IN THE SKIN OF PEOPLE WITH ECZEMA AND IN THE LUNGS OF THOSE WITH ASTHMA — IS CALLED TSLP. DAMAGED SKIN SECRETES IT AND ACTIVTATES AN IMMUNE RESPONSE. KOPAN SAYS HIGH LEVELS OF TSLP IN THE LUNG CAN MAKE ASTHMA MORE LIKELY. HIS TEAM ENGINEERED MICE THAT DEVELOP A CONDITION SIMILAR TO ECZEMA. THE RESEARCHERS THEN TESTED WHAT HAPPENED WHEN THOSE MICE WITH SKIN DEFECTS INHALED AN ALLERGEN.

(act) :10 o/c the allergen

The animals that had a high level of TSLP immediately develop
asthma-like symptoms. The animals that don’t have TSLP do not,
even though everybody saw the allergen.

KOPAN SAYS IT’S LIKELY THAT BECAUSE THE IMMUNE SYSTEM IS VERY SENSITIVE IN THOSE WITH ECZEMA, THE LUNGS CAN RESPOND BADLY WHEN EXPOSED TO ALLERGENS THAT CAN CONTRIBUTE TO ASTHMA. HE SAYS IT’S NOT CLEAR THAT TSLP IS THE SUBSTANCE DRIVING THE CASCADE IN HUMANS, BUT HE SAYS THE CONNECTION BETWEEN SKIN AND LUNGS IN HUMANS LOOKS SIMILAR TO WHAT HIS TEAM HAS OBSERVED IN MICE. AND HE SAYS THAT MEANS IT MAY BE POSSIBLE TO PREVENT SOME CASES OF ASTHMA BY TREATING CASES OF ECZEMA WITH MORE VIGILANCE.

(act) :18 o/c of asthma

We now are looking at the skin as the instigator, and thus, we
propose if you were to take care of treating an eczema patient
aggressively so that they don’t develop this chronic “alarm
system” – that you can turn the alarm off, whatever its molecular
nature – that will reduce the incidence of asthma.

KOPAN’S TEAM REPORTED ITS FINDINGS IN THE JOURNAL PUBLIC LIBRARY OF SCIENCE: BIOLOGY. I’M JIM DRYDEN

RUNS 2:55

THE PROGRESSION FROM ECZEMA TO ASTHMA IS WHAT SCIENTISTS CALL THE ATOPIC MARCH. SOME HAD HYPOTHESIZED THAT BOTH ECZEMA AND ASTHMA WERE CAUSED BY THE SAME GENETIC DEFECT. OTHERS FIGURED THAT WHEN A CHILD WITH ECZEMA SCRATCHED HIS OR HER ITCHY SKIN, PERHAPS THAT RELEASED PARTICLES THAT COULD TRAVEL TO THE LUNGS AND CONTRIBUTE TO ASTHMA. BUT IN MICE, IT TURNS OUT THAT THE CONNECTION IS A SUBSTANCE CALLED TSLP. IT’S FOUND BOTH IN THE SKIN AND IN LUNG TISSUE. WASHINGTON UNIVERSITY SCIENTIST RAPHAEL KOPAN SAYS WHEN A CHILD GETS ECZEMA, THE IMMUNE SYSTEM REACTS AS IF IT WERE PROTECTING A BORDER DURING WARTIME.
(act) :14 o/c the lung

If there’s a breach in the north, the people in the south
are still going to be more vigilant. So with that logic,
then perhaps some product the skin secretes would be read
by the lung, creating a hypersensitive condition in the lung.

KOPAN SAYS IN MICE, THAT HYPERAROUSAL OF THE IMMUNE SYSTEM MAKES THE ANIMALS MORE VULNERABLE TO THE ALLERGANS THAT CAN CONTRIBUTE TO ASTHMA. KOPAN’S TEAM REPORTED ITS FINDINGS IN THE JOURNAL PUBLIC LIBRARY OF SCIENCE: BIOLOGY. I’M JIM DRYDEN

RUNS 1:00

IN RECENT YEARS, RATES OF OBESITY HAVE SKYROCKETED IN THE UNITED STATES AND OTHER DEVELOPED COUNTRIES. THAT’S LED TO A LOT MORE DIETING, EXERCISING AND WEIGHT-LOSS SURGERY. AND SOME PEOPLE HAVE MANAGED TO LOSE THAT EXCESS WEIGHT. THE PROBLEM IS WHEN SOMEONE LOSES A LOT OF WEIGHT, THAT PERSON OFTEN IS LEFT WITH A LOT OF EXCESS SKIN, SO PLASTIC SURGEONS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS ARE SPENDING MORE OF THEIR TIME HELPING THE FORMERLY OBESE LOOK MORE NORMAL BY SURGICALLY REMOVING THAT SKIN. JIM DRYDEN HAS MORE…

IF YOU LOSE 10 POUNDS, YOUR SKIN IS ELASTIC ENOUGH TO SHRINK A BIT AND TIGHTEN UP, BUT WHAT IF YOU LOSE 80, OR 100 OR 200? WASHINGTON UNIVERSITY PLASTIC SURGEON TERRY MYCKATYN.

(act) :19 o/c out skin

They’re typically patients who have lost at least 80 to
90 pounds, and in many cases, I would say the average is
more like 100 to 120 pounds that we see. And in those
individuals, you have this tremendous amount of extra skin,
and so you’re basically looking at cutting out skin.

MYCKATYN SAYS ALTHOUGH THIS TYPE OF SURGERY OFTEN IS CONSIDERED TO BE COSMETIC, THERE ARE SOME IMPORTANT HEALTH COMPLICATIONS THAT EXCESS SKIN CAN CONTRIBUTE TO.

(act) :21 o/c treat this

The major issues with that are, there’s one is the weight.
It can cause back pain, for example, and also that skin can
become irritated. You can get dermatitis or, basically skin
irritation or infection. Some people actually get infections
to the point where there are patients who have to actually go
to E/R’s to get intravenous antibiotics to treat this.

ONE OF MYCKATYN’S PATIENTS, KELLY VALENTINE, RECENTLY LEFT A GOOD DEAL OF SKIN BEHIND. FOLLOWING GASTRIC BYPASS SURGERY SEVERAL YEARS AGO, VALENTINE LOST 240 POUNDS. SHE HAD WAY TOO MUCH SKIN FOR IT TO CONFORM TO HER NEW, THINNER BODY. IN FACT, MYCKATYN REMOVED MORE THAN 18 POUNDS OF SKIN FROM HER BELLY, HER ARMS, BREASTS, THIGHS AND BACK.
(act) :11 o/c for me

Before I had the skin-removal surgery, I still looked
overweight. I still looked chunky because I had all of
this extra skin hanging there, so I’d have to buy bigger
clothes, and he fixed that for me.

VALENTINE SAYS THE SURGERY IMPROVED HER APPEARANCE, BUT IT DID MORE THAN THAT.

(act) :21 o/c weight back

I noticed lately, like within the last year or two, that I
was getting like skin rashes underneath the folds. There was
boils. You would get boils in, like, your upper thigh area
because the skin just hung over, rashes, yeast infections.
So I thought, “Well, I guess it’s time to go under the knife
and get it taken off.” It’s either that or stop exercising,
and I didn’t want to gain the weight back.

MYCKATYN SAYS THESE TEND TO BE LONG OPERATIONS, AND THERE ARE SOME RISKS OF INFECTION, CLOTTING OR BLEEDING. PLUS, COMPARED TO OTHER COSMETIC PROCEDURES, THESE OPERATIONS HAVE THE POTENTIAL TO LEAVE LONGER OR MORE NOTICEABLE SCARS.

(act) :21 o/c have surgery

But what we try to do is we try to hide those incisions. Around
the belly, we put it in a place that could be concealed by a
bathing suit or underwear. On the arm, we put it on the inside
of the arm. In the thighs, we put it up high in the groin or
in the inside of the thigh. We work very hard to conceal the
scars, but there are a fair number of them. Scars are definitely
a variable any time you have surgery.

BOTH THE SURGEON, MYCKATYN, AND THE PATIENT, VALENTINE, SAY THE SURGERY TO REMOVE EXCESS SKIN CAN CHANGE A PATIENT’S LIFE ALMOST AS MUCH AS THEIR ORIGINAL WEIGHT-LOSS. AND BOTH BELIEVE THAT AS MORE AND MORE EXTREMELY OBESE PEOPLE MAKE THE DECISION TO LOSE WEIGHT, THERE WILL BE A GREATER AND GREATER DEMAND FOR THESE TYPES OF OPERATIONS. I’M JIM DRYDEN…

RUNS 2:56

IF YOU LOSE 10 POUNDS, YOUR SKIN IS ELASTIC ENOUGH TO SHRINK A BIT AND TIGHTEN UP, BUT WHAT IF YOU LOSE 80, OR 100 OR 200? WASHINGTON UNIVERSITY PLASTIC SURGEON TERRY MYCKATYN SAYS IN THOSE PEOPLE THERE’S TOO MUCH SKIN LEFTOVER TO SHRINK BACK INTO PLACE.

(act) :06 o/c out skin

You have this tremendous amount of extra skin, and so you’re
basically looking at cutting out skin.

THAT’S WHAT MCKATYN DID FOR KELLY VALENTINE. SHE LOST 240 POUNDS FOLLOWING GASTRIC BYPASS SURGERY, BUT SHE DIDN’T END UP LOOKING THIN BECAUSE THERE WAS SO MUCH EXCESS SKIN LEFT ON HER BODY.

(act) :11 o/c it’s nice

I still looked overweight. I still looked chunky because I
had all of this skin hanging there. So I’d have to buy
bigger clothes, and he fixed that for me. And now I can
buy regular clothes and shop in regular stores, so it’s nice.

IN ALL MYCKATYN REMOVED ALMOST 18 POUNDS OF EXTRA SKIN FROM VALENTINE’S BODY. SO NOW SHE NOT ONLY LOOKS THINNER, BUT SHE ALSO GETS FEWER SKIN RASHES, BOILS AND YEAST INFECTIONS WHERE THAT EXTRA SKIN USED TO BE. I’M JIM DRYDEN…

RUNS :59

SCIENTISTS AT 19 SITES AROUND THE COUNTRY HAVE LEARNED THAT A NON-SURGICAL TECHNIQUE CAN ELIMINATE THE POTENTIALLY SERIOUS CONDITION CALLED BARRETT’S ESOPHAGUS IN THE MAJORITY OF PATIENTS. IN THE PAST, MAJOR SURGERY OFTEN WAS PRESCRIBED FOR THESE PATIENTS. JIM DRYDEN HAS MORE ON THE STORY…

THOSE WHO HAVE THE SEVERE HEARTBURN CALLED ACID REFLUX ALSO CAN DEVELOP A MORE SERIOUS DIFFICULTY CALLED BARRETT’S ESOPHAGUS, ACCORDING TO WASHINGTON UNIVERSITY GASTROENTEROLOGIST STEVEN EDMUNDOWICZ.
(act) :16 o/c develop Barrett’s

We do believe that chronic, long-term acid reflux actually is
necessary to cause Barrett’s esophagus. Now there may be some
genetic predisposition to this as well because some people with
long-standing reflux never develop Barrett’s.

THE BARRETT’S ESOPHAGUS CONDITION CAN SOMETIMES BE A PRECURSOR TO CANCER, BUT RESEARCHERS HAVE NOW FOUND THAT THEY CAN ELIMINATE BARRETT’S ESOPHAGUS IN MANY PATIENTS WITH A TREATMENT THAT USES HEAT GENERATED FROM RADIO WAVES AND REQUIRES NO INCISIONS. EDMUNDOWICZ AND HIS COLLEAGUES AROUND THE COUNTRY TREATED PATIENTS ENDOSCOPICALLY, INSERTING TOOLS THROUGH THE MOUTH TO DESTROY ABNORMAL TISSUE IN THE LINING OF THE ESOPHAGUS, WHICH, HE SAYS, IS THE HALLMARK OF BARRETT’S ESOPHAGUS.
(act) :17 o/c the wall

It’s clearly not a tumor, and in fact, most patients with
Barrett’s esophagus never develop a tumor of the esophagus.
It just looks like a different color or appearance of the
lining. You could imagine it if you were looking at a wall
in a room, it would be a different texture or color of paint
of the wall.

BUT INSTEAD OF ESOPHAGUS CELLS, THE CELLS LOOK LIKE THOSE THAT LINE THE INTESTINES, AND WHEN THE DISORDER ADVANCES TO THE POINT WHERE PATIENTS HAVE WHAT’S CALLED DYSPLASIA, BARRETT’S ESOPHAGUS CAN SOMETIMES PROGRESS INTO CANCER.
(act) :22 o/c very low

Esophageal cancer does develop, and in patients that have
gotten to a stage of high-grade dysplasia, as many as 6 or
10 percent of them a year will then progress to a cancer.
And once you have cancer of the esophagus – unless it’s a
very superficial cancer – if it starts to grow into the
wall of the esophagus, the chance of actually curing that
patient of cancer is actually very low.

TO PREVENT THE CONDITION FROM BECOMING CANCER, PATIENTS OFTEN WERE REFERRED TO SURGEONS WHO WOULD REMOVE ALL, OR MOST OF THE ESOPHAGUS IN A RADICAL SURGERY THAT WORKED BUT THAT POSED ALL OF THE RISKS THAT ANY MAJOR SURGERY POSES. EDMUNDOWICZ SAYS THE RADIO WAVES SEEM TO WORK BETTER FOR MOST PATIENTS. PLUS THE DEVICE DOCTORS USE, TAKES ADVANTAGE OF A BALLOON THAT INFLATES THE ESOPHAGUS AND ALLOWS FOR THE DELIVERY OF MORE CONSISTENT ENERGY TO GET RID OF THE UNUSUAL TISSUE IN MORE THAN 80 PERCENT OF PATIENTS WHO RECEIVED THE TREATMENT.
(act) :16 o/c acid reflux

Because we give patients acid-lowering medicines, we take away
the acid reflux, and instead of re-growing a Barrett’s lining,
they grown back the normal, esophageal lining that they had
before the acid reflux.

THE ONLY REAL SIDE EFFECTS SEEN IN THE STUDY WERE SOME PAIN IN THE CHEST FOR A FEW DAYS AFTER TREATMENT AND SOMETIMES A BIT OF DIFFICULTY SWALLOWING, BUT THAT ALSO RESOLVED QUICKLY. EDMUNDOWICZ SAYS, HOWEVER, THAT IT’S TOO EARLY TO TELL WHETHER MOST PATIENTS WERE ACTUALLY CURED.
(act) :12 o/c maybe longer

This study is very key, but it only reports follow-up at one
year, and what we really need to see is how the patients that
have been treated with this device behave at two years, five
years and maybe longer.

EDMUNDOWICZ AND COLLEAGUES REPORTED THEIR FINDINGS IN THE NEW ENGLAND JOURNAL OF MEDICINE. I’M JIM DRYDEN…

RUNS 3:00

THE RESEARCHERS TREATED BARRETT’S ESOPHAGUS PATIENTS ENDOSCOPICALLY, INSERTING TOOLS THROUGH THE MOUTH TO DESTROY ABNORMAL TISSUE IN THE LINING OF THE ESOPHAGUS, WHICH ACCORDING TO WASHINGTON UNIVERSITY RESERCHER STEVEN EDMUNDOWICZ IS THE HALLMARK OF THE CONDITION.
(act) :17 o/c the wall

It’s clearly not a tumor, and in fact, most patients with
Barrett’s esophagus never develop a tumor of the esophagus.
It just looks like a different color or appearance of the
lining. You could imagine it if you were looking at a wall
in a room, it would be a different texture or color of paint
of the wall.

BUT INSTEAD OF ESOPHAGUS CELLS, THE CELLS LOOK LIKE THOSE THAT LINE THE INTESTINE. WHEN THE CONDITION PROGRESSES, ABOUT 6 TO 10 PERCENT OF PATIENTS CAN GO ON TO DEVELOP CANCER OF THE ESOPHAGUS.
(act) :10 o/c very low

And once you have cancer of the esophagus, if it starts to
grow into the wall of the esophagus, the chance of actually
curing that patient of cancer is actually very low.

EDMUNDOWICZ AND COLLEAGUES AT 19 CLINICAL SITES IN THE UNITED STATES FOUND THAT USING THE RADIOFREQUENCY ABLATION TECHNIQUE OVER 12 MONTHS ELIMINATED THE CONDITION IN MORE THAN 80 PERCENT OF THE PATIENTS IN THE STUDY. I’M JIM DRYDEN…

RUNS 1:00

SUMMERTIME IS SUNBURN TIME FOR MANY AMERICANS. POOLS ARE NOW OPENING IN MOST OF THE COUNTRY, AND THAT MEANS SUNSCREEN SALES ARE SOARING, TOO. A WASHINGTON UNIVERSITY DERMATOLOGIST SAYS FREQUENT APPLICATION OF SUNSCREEN, WEARING PROTECTIVE CLOTHING AND FINDING SHADE FROM TIME TO TIME REMAINS THE BEST WAY TO APPROACH SUMMER AND TO PROTECT YOUR SKIN FROM BURNING, AGING AND EVEN SKIN CANCER. JIM DRYDEN REPORTS…

IN MUCH OF THE COUNTRY, SUMMERTIME IS WHEN PEOPLE WORK IN THE GARDEN, LOUNGE AT THE POOL, BARBECUE ON THE DECK AND DO OTHER THINGS OUTSIDE THAT THEY DON’T DO DURING THE REST OF THE YEAR. WE ALSO TEND TO HAVE MORE SKIN EXPOSED TO SUNLIGHT AND TO SPEND MORE TIME OUTDOORS. THAT INCREASES THE RISK FOR SUNBURNS AND FOR OTHER PROBLEMS RELATED TO SUN EXPOSURE, ACCORDING TO WASHINGTON UNIVERSITY DERMATOLOGIST LYNN CORNELIUS. THE BIGGEST RISK RELATED TO SUN EXPOSURE IS SKIN CANCER, AND THE WORST OF THE SKIN CANCERS IS MELANOMA. BUT, CORNELIUS SAYS OTHER TYPES OF SKIN CANCER ARE MORE COMMON.

(act) :27 o/c not heal

And they are also the least serious of the skin cancers in
general. There are basal cell cancers, which are the most
common of the non-melanoma skin cancers, and squamous cell
cancers, which are very related to ultraviolet light exposure.
Basal cell carcinomas occur on sun-exposed areas, areas that
are usually pink or skin-colored, maybe ulcerated but areas
that are small and may not heal.

SHE SAYS THOSE SKIN CANCERS USUALLY CAN BE SURGICALLY EXCISED. MELANOMA, HOWEVER, IS USUALLY HARDER TO TREAT. UNLIKE LESS SERIOUS CANCERS, MELANOMA LESIONS TEND TO HAVE MORE COLOR.

(act) :15 o/c watch our for

I think the biggest thing for people to recognize is evolution,
or a changing lesion, and something that’s changing that just
doesn’t look like a normal mole, or a mole that has taken on
new characteristics. That’s something to watch out for.

THE DEATH RATE FROM MELANOMA HAS INCREASED BY ABOUT 4 PERCENT PER YEAR SINCE 1973. IT REPRESENTS ONLY ABOUT 47 THOUSAND OF THE ALMOST 2 MILLION CASES OF SKIN CANCER ANNUALLY, BUT IT CAUSES ALMOST 80 PERCENT OF SKIN CANCER DEATHS. CORNELIUS SAYS IT’S BETTER TO TRY AND PREVENT THE CANCER IN THE FIRST PLACE. THAT’S WHERE SUNSCREENS COME IN.

(act) :14 o/c of ultraviolet

Sunscreens are getting better and better. We can group the
sunscreens many different ways. One is into UVA protection –
or the longer wave-length of ultraviolet light – and UVB
protection, which is the shorter, or burning, rays of
ultraviolet.

THE SPF RATING MEANS REFERS TO PROTECTION FROM ULTRAVIOLET-B. IF YOU NORMALLY WOULD GET PINK SKIN IN ONE MINUTE, AN SPF RATING OF 30 MEANS THAT IF YOU APPLIED THAT SUNSCREEN, YOU COULD THEORETICALLY REMAIN IN THE SUN FOR 30 MINUTES WITHOUT GETTING A SUNBURN.

(act) :08 o/c longer wavelength

It’s very important to protect from both the short wavelength,
or ultraviolet B, ultraviolet exposure as well as ultraviolet A,
or the longer wavelength.

AND THERE ARE OTHER COMMON-SENSE WAYS TO PROTECT YOURSELF, TOO.

(act) :16 o/c includes clothing

What we like to tell people is it’s not just about sunscreen or
sunblock. It’s also about sun protection – seeking shade, using a
hat – it’s a whole way of protection that includes sunscreen, but
it also includes clothing.

AND SHE SAYS THOSE PEOPLE WHO THINK THEY LOOK THEIR BEST WHEN THEY HAVE A SUNTAN SHOULD THINK ABOUT USING A SPRAY-ON PRODUCT RATHER THAN LAYING OUT BY THE POOL. I’M JIM DRYDEN

RUNS 2:51

SUNSCREENS DO PROTECT YOU FROM SUNBURN. THAT’S WHAT THE SPF RATING MEANS. IF YOU NORMALLY WOULD GET PINK SKIN IN ONE MINUTE, AN SPF RATING OF 30 MEANS THAT IF YOU APPLY THAT SUNSCREEN, YOU CAN THEORETICALLY REMAIN IN THE SUN FOR 30 MINUTES WITHOUT GETTING BURNED. BUT WASHINGTON UNIVERSITY DERMATOLOGIST LYNN CORNELIUS SAYS A DEBATE IS SIMMERING ABOUT THE ROLE LOWER-ENERGY ULTRAVIOLET LIGHT PLAYS IN SKIN DAMAGE AND WHETHER MANY CURRENT SUNSCREENS PROVIDE ADEQUATE PROTECTION. SHE SAYS IT’S IMPORTANT TO USE A SUNSCREEN THAT PROTECTS AGAINST BOTH TYPES OF ULTRAVIOLET LIGHT.

(act) :15 o/c of ultraviolet

Sunscreens are getting better and better. We can group the
sunscreens many different ways. One is into UVA protection –
or the longer wave-length of ultraviolet light – and UVB
protection, which is the shorter, or burning, rays of
ultraviolet.

CORNELIUS SAYS SINCE BOTH TYPES OF UV RADIATION ARE RELATED TO SKIN CANCER, SUNSCREENS THAT PROTECT AGAINST ONLY ONE DON’T OFFER COMPLETE PROTECTION. I’M JIM DRYDEN

RUNS :56

NOT EVERYONE WITH A MEDICAL PROBLEM RESPONDS TO THERAPY EXACTLY THE SAME WAY: ONE PATIENT MAY BE ALLERGIC TO A PARTICULAR DRUG, ANOTHER SIMPLY MAY NOT RESPOND, WHILE A THIRD DOES WELL AND GETS BETTER. NOW RESEARCHERS AT WASHINGTON UNIVERSITY AND ST. LOUIS CHILDREN’S HOSPITAL ARE LOOKING AT CHARACTERISTICS IN CHILDREN THAT MAY HELP PREDICT WHICH ONES WILL RESPOND BEST TO ASTHMA THERAPY. JIM DRYDEN REPORTS…

THE RESEARCHERS RE-EXAMINED DATA FROM A STUDY THAT ORIGINALLY WAS DESIGNED TO LEARN WHETHER EARLY TREATMENT MIGHT PREVENT THE DEVELOPMENT OF ASTHMA IN CHILDREN AT HIGH RISK. THAT DIDN’T WORK, BUT IN LOOKING AGAIN AT THE DATA, THE RESEARCHRS HAVE FOUND THAT THE CHILDREN WHO RESPONDED BEST TO TREATMENT WITH INHALED STEROIDS TENDED TO BE THOSE WHO HAD THE HIGHEST RISK OF MORE SEVERE ASTHMA, ACCORDING TO LEAD AUTHOR LEONARD BACHARIER, AN ASTHMA AND ALLERGY SPECIALIST AT WASHINGTON UNIVERSITY AND ST. LOUIS CHILDREN’S HOSPITAL

(act) :10 o/c significant disease

It turns out that the children who did best while receiving the
inhaled steroid were the ones who had markers of more significant
disease.

FOR EXAMPLE, BACHARIER SAYS BOYS TENDED TO HAVE A BIGGER RESPONSE THAN GIRLS. AND CAUCASIANS RESPONDED BETTER THAN NON-WHITES.

(act) :27 o/c the therapy

Children who had allergy to one of the inhalent allergens
did better than children who had no evidence of allergy.
Children who were seen at an emergency department or a
hospital the year before the study did better than children
who weren’t. So all of those factors identify groups of children
who actually have more active disease, more significant disease,
and those are the children who derived the greatest benefit
from the therapy.

HE SAYS IT ISN’T THAT NO GIRLS RESPONDED TO THERAPY OR NO NON-ALLERGIC KIDS DID WORSE, BUT ON AVERAGE CERTAIN GROUPS HAD A BIGGER RESPONSE TO THE INHALED STEROID MEDICATION. BACHARIER CALLS THE FINDINGS FROM THE STUDY INTERESTING, BUT HE SAYS SINCE THE ORIGINAL STUDY WASN’T SET UP TO ANSWER QUESTIONS ABOUT WHICH PATIENTS WOULD RESPOND BEST TO WHAT KIND OF THERAPY, MORE STUDY WILL BE NEEDED.

(act) :28 o/c from therapy

That being said, if you see children who have these characteristics,
we think that this work has identified the ones who are at highest
likelihood of having a clinical improvement. But if you’re seeing
a three-year-old boy who’s been in the emergency room, been in the
hospital, has allergy to inhalent allergens, you could presume that
that child will derive a substantial, clinical benefit from therapy.

AND BACHARIER EMPHASIZES THAT EVEN WHEN STUDIES FIND THAT CERTAIN GROUPS OF PATIENTS RESPOND TO THERAPY BETTER OR WORSE THAN OTHERS, THAT INFORMATION SHOULDN’T BE USED AS A REASON NOT TO TREAT AN INDIVIDUAL PATIENT. HE SAYS MANY STUDIES LOOK AT HOW AN AVERAGE PATIENT MIGHT RESPOND TO A DRUG, BUT HE SAYS THERE’S REALLY NO SUCH THING AS AN AVERAGE PATIENT.

(act) :25 o/c best outcomes

Because there are therapies that work very well in one group of
people that don’t work in another. And we should be able to
identify those patient characteristics and then make a good
treatment decision that’s individualized, as opposed to treating
all patients with asthma as if they have the exact same disease,
as if they’re the “average” patient because that’s really not
the best way to achieve the best outcomes.

HE SAYS KNOWING WHICH PATIENTS MIGHT RESPOND BEST COULD HELP DOCTORS TAILOR THERAPY TO THOSE WHO WILL BENEFIT MOST. BACHARIER AND HIS COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY. I’M JIM DRYDEN

RUNS 2:58

THE RESEARCHERS HAVE RE-EXAMINED DATA FROM A STUDY THAT ORIGINALLY WAS DESIGNED TO LEARN WHETHER EARLY TREATMENT MIGHT PREVENT THE DEVELOPMENT OF ASTHMA IN CHILDREN AT HIGH RISK. THEY COULDN’T DO THAT, BUT IN LOOKING AGAIN AT THE DATA, THEY FOUND THAT THE CHILDREN WHO RESPONDED BEST TO TREATMENT WITH INHALED STEROIDS TENDED TO BE THE CHILDREN WHO HAD THE HIGHEST RISK OF MORE SEVERE ASTHMA. LEAD AUTHOR LEONARD BACHARIER IS AN ASTHMA AND ALLERGY SPECIALIST AT WASHINGTON UNIVERSITY AND ST. LOUIS CHILDREN’S HOSPITAL

(act) :21 o/c who weren’t

It turns out that the children who did best were the ones
who had markers of more significant disease: Children who
had allergy to one of the inhalant allergens did better than
children who had no evidence of allergy. Children who were
seen in an emergency department or hospital the year before
the study did better than children who weren’t.

BACHARIER SAYS KNOWING WHICH PATIENTS MIGHT RESPOND BEST COULD HELP DOCTORS TAILOR THERAPY TO THOSE WHO WILL BENEFIT MOST. HE REPORTED HIS FINDINGS IN THE JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY. I’M JIM DRYDEN

RUNS 1:00

IT’S BEEN KNOWN FOR YEARS THAT RED WINE CAN BE GOOD FOR YOU. PAST STUDIES HAVE FOUND THAT REGULAR RED WINE DRINKERS OFTEN HAVE LESS RISK OF CARDIOVASCULAR PROBLEMS AND OTHER DISEASES ASSOCIATED WITH AGING. NOW RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS ARE STUDYING THE ACTIVE INGREDIENT IN RED WINE TO SEE WHETHER IT MIGHT HELP SLOW AGING. JIM DRYDEN REPORTS…

THE ACTIVE INGREDIENT IN RED WINE IS CALLED RESEVERATROL. IT’S A COMPOUND THAT’S FOUND IN GRAPES AND BERRIES AND IN SOME SEEDS. ANIMAL STUDIES HAVE FOUND THAT THE COMPOUND MAY HELP SLOW AGING, PERHAPS BY INTERACTING WITH A GENETIC PATHWAY THAT INVOLVES GENES CALLED SIR2 AND SIRT1. NOW, LED BY WASHINGTON UNIVERSITY NUTRITION RESEARCHER SAMUEL KLEIN, INVESTIGATORS ARE LOOKING AT THE EFFECTS OF RESVERATROL ON ASPECTS OF HUMAN METABOLISM THAT ARE ASSOCIATED WITH AGING.

(act) :25 o/c with aging

And so as we get older, we reduce our insulin sensitivity.
We’ll be looking at insulin action in both liver, adipose
tissue and muscle tissue. We’ll be looking at the expression
of genes in various tissues – fat tissue and muscle tissue –
because differences in gene expression occur during aging.
And we’ll be looking at mitochondrial function as well
because the mitochondria, that are the energy-producing
components of our cells also become affected with aging.

IN THE STUDY, KLEIN SAYS PEOPLE TAKING RESVERATROL IN PILL FORM WILL BE COMPARED TO OTHERS WHO WILL CONTINUE LIVING AS THEY HAVE BEEN. A THIRD ARM OF THE STUDY WILL EMPLOY CALORIE RESTRICTION – A DIET THAT CUTS CALORIES BY 25 PERCENT AND THAT ALSO HAS BEEN LINKED TO SLOWER AGING.

(act) :14 o/c resveratrol therapy

If we understand the mechanism at the cellular level that’s
responsible for what we see whole-body, we will do further
studies to help hone down and narrow down the mechanism that’s
responsible for the beneficial effect of reseveratrol therapy.

KLEIN SAYS SUBJECTS IN THE 12-WEEK STUDY WILL RECEIVE DOSES OF RESVERATROL THAT ARE SIMILAR TO WHAT THEY WOULD GET FROM DRINKING QUITE A BITE OF WINE.

(act) :20 o/c clinical trials

Red wine does contain resveratrol, but the amount contained in
red wine is actually quite small compared to what you can get
in the pill forms that are being made for these different
studies evaluating the effect of resveratrol. It’s estimated
that you would really need to drink about 600 bottles of wine
per day to get the dose that’s being used in some of these
clinical trials.

KLEIN SAYS IT’S TOO EARLY TO SAY WHETHER RESVERATROL WILL HAVE THE DESIRED EFFECTS ON INSULIN SENSITIVITY AND FAT METABOLISM RELATED TO AGING. AND HE SAYS IT’S ALSO TOO EARLY TO SAY FOR SURE HOW MUCH OF THE SUBSTANCE MAY BE BENEFICIAL. IT’S NOT ALWAYS THE CASE THAT MORE IS BETTER. PERHAPS, HE SAYS, THE RESEVERATROL FROM 100 BOTTLES OF WINE MIGHT BE MORE BENEFICIAL THAN THE AMOUNT FROM 600. THEY’RE JUST TRYING TO MATCH THE AMOUNTS OF RESVERATROL THAT SEEMED TO AFFECT AGING IN ANIMALS.

(act) :22 o/c healthful benefits

More is not always better, and that’s also true with resveratrol
potentially, but it does look like in some of the animal studies
that have been done now, that larger doses are needed to get the
metabolic effects of this compound and that the very low doses
will not give you those same metabolic effects. This doesn’t
mean though, that drinking a couple of glasses of red wine
every day doesn’t have healthful benefits.

FOR NOW, KLEIN SAYS INVESTIGATORS ARE STUDYING ONLY POST-MENOPAUSAL WOMEN IN THIS TRIAL, BUT IF THE RESULTS SHOW PROMISE, THEY WILL EXPAND THE POOL OF THOSE WHO ARE ELIGILBE TO PARTICIPATE IN FUTURE STUDIES. I’M JIM DRYDEN…

RUNS 2:56

RESEVERATROL IS A COMPOUND FOUND IN GRAPES AND BERRIES. ANIMAL STUDIES HAVE FOUND THAT THE COMPOUND MAY INFLUENCE A GENETIC PATHWAY INVOLVED IN AGING. NOW, LED BY WASHINGTON UNIVERSITY NUTRITION RESEARCHER SAMUEL KLEIN, INVESTIGATORS ARE LOOKING AT THE EFFECTS OF RESVERATROL ON ASPECTS OF HUMAN METABOLISM THAT ARE ASSOCIATED WITH AGING. PEOPLE TAKING RESVERATROL IN PILL FORM WILL BE COMPARED TO OTHERS WHO CONTINUE LIVING AS THEY HAVE BEEN, WHILE A THIRD ARM OF THE STUDY WILL EMPLOY CALORIE RESTRICTION – A DIET THAT CUTS CALORIES BY 25 PERCENT AND THAT HAS ALSO BEEN LINKED TO SLOWER AGING.

(act) :14 o/c resveratrol therapy

If we understand the mechanism at the cellular level that’s
responsible for what we see whole-body, we will do further
studies to help hone down and narrow down the mechanism that’s
responsible for the beneficial effect of reseveratrol therapy.

FOR NOW, INVESTIGATORS ARE STUDYING ONLY POST-MENOPAULSAL WOMEN, BUT IF THE RESULTS SHOW PROMISE, THEY’LL EXPAND THE POOL OF THOSE WHO ARE ELIGILBE TO PARTICIPATE. I’M JIM DRYDEN…

RUNS :57

A GENETICALLY ENGINEERED STRAIN OF MOUSE HAS DEMONSTRATED THAT, AT LEAST IN MICE, OBESITY AND GALLSTONES AREN’T ALWAYS RELATED. THE MICE DON’T BECOME OBESE WHEN THEY EAT A DIET HIGH IN FAT, BUT THEY DO DEVELOP GALLSTONES. JIM DRYDEN HAS MORE…

GALLSTONES AFFECT BETWEEN 16 AND 22 MILLION AMERICANS. THE STONES, WHICH ARE DEPOSITS OF CHOLESTEROL OR CALCIUM SALTS THAT FORM IN THE GALLBLADDER OR BILE DUCTS, LEAD TO MORE THAN HALF A MILLION GALLBLADDER OPERATIONS EACH YEAR IN THE UNITED STATES. WASHINGTON UNIVERSITY GASTROENTEROLOGIST NICHOLAS DAVIDSON HAS BEEN STUDYING GALLSTONES IN A STRAIN OF MOUSE THAT HIS LABORATORY DEVELOPED. THE MICE DON’T MAKE A SUBSTANCE CALLED LIVER FATTY ACID BINDING PROTEIN. PREVIOUSLY, DAVIDSON HAD FOUND THAT MICE WHO DON’T MAKE THAT PROTEIN ALSO DON’T BECOME OBESE WHEN THEY EAT A HIGH-FAT DIET. AND SINCE OBESITY AND GALLSTONES OFTEN GO HAND IN HAND, HE THOUGHT THEY MIGHT NOT GET GALLSTONES EITHER.

(act) :20 o/c more susceptible

These mice are protected against high-fat-induced obesity, so we
had predicted that these mice would be, possibly, protected
against the development of gallstones when we put them on a
high-cholesterol, high-fat diet. And in fact to our surprise,
we found that they were dramatically more susceptible.

OBESITY IS A RISK FACTOR FOR GALLSTONES, AND DAVIDSON SAYS THERE ARE SEVERAL OTHERS THAT DOCTORS LOOK FOR, TOO.

(act) :07 o/c diabetic patients

Patients who’ve lost weight rapidly, patients who take estrogens,
and in diabetic patients.

ALTHOUGH MINIMALLY INVASIVE GALLBLADDER SURGERY IS NOW THE NORM, AND PEOPLE WHO HAVE HAD GALLSTONE PROBLEMS OFTEN CAN HAVE SURGERY AND QUICKLY RETURN TO THEIR NORMAL LIVES, DAVIDSON SAYS GALLSTONES DO REMAIN A MAJOR PUBLIC HEALTH PROBLEM IN THE UNITED STATES. THE STONES ARE MUCH MORE COMMON, AND THE COMPLICATIONS MUCH MORE SERIOUS, THAN MANY BELIEVE.

(act) :26 o/c of gallstones

In the vast majority of patients, the gallstones are clinically
silent. In a small percentage of patients who get them, the
clinical manifestations can be very dramatic. They can present
with gallstone pancreatitis. The gallstones can become obstructed
in the bile duct and then get infected and cause cholangitis.
So there are actually potentially very serious medical complications
of gallstones.

MOST GALLSTONES FORM WHEN CHOLESTEROL IS SECRETED IN HIGH CONCENTRATIONS. IN THIS STUDY, AFTER TWO WEEKS OF EATING A HIGH-FAT DIET, 6 OF THE 8 GENETICALLY ENGINEERED MICE DEVELOPED GALLSTONES, WHEREAS ONLY 1 IN 17 OF THEIR NORMAL LITTERMATES DID. DAVIDSON SAYS THE GENE THESE MICE WERE MISSING MAPS TO A REGION IN THE MOUSE GENOME THAT SEEMS RELATED TO GALLSTONE RISK. BOTH HUMANS AND MICE HAVE THE GENE.

(act) :08 o/c susceptibility gene

There is a genetic component to gallstone susceptibility.
So we think that this may be a gallstone-susceptibility gene.

HE SAYS IT’S CLEAR THAT THERE IS A GENETIC COMPONENT TO GALLSTONE RISK, BUT HOW IT ALL FITS TOGETHER IS STILL SOMETHING OF A MYSTERY.

(act) :15 o/c and unravel

You know, I think the mechanisms are complex. Alterations in
the trafficking of not only cholesterol but also bile salts
through the intestine and the liver, so I think that it’s
likely going to be a complex metabolic system to try and unravel.

DAVIDSON’S TEAM REPORTED ITS FINDINGS IN THE JOURAL OF LIPID RESEARCH. I’M JIM DRYDEN…

RUNS 3:00

OBESITY AND GALLSTONES OFTEN GO HAND IN HAND, SO THE INVESTIGATORS THOUGHT THAT SINCE THESE MICE DIDN’T GET FAT, THEY WOULDN’T DEVELOP GALLSTONES EITHER, ACCORDING TO WASHINGTON UNIVERSITY GASTROENTEROLOGIST NICHOLAS DAVIDSON.

(act) :20 o/c more susceptible

These mice are protected against high-fat-induced obesity, so we
had predicted that these mice would be, possibly, protected
against the development of gallstones when we put them on a
high-cholesterol, high-fat diet. And in fact to our surprise,
we found that they were dramatically more susceptible.

THE MICE WERE GENETICALLY ENGINEERED WITHOUT THE ABILITY TO MAKE A SUBSTANCE CALLED LIVER FATTY ACID BINDING PROTEIN. BOTH HUMANS AND MICE HAVE THE GENE FOR THAT PROTEIN.

(act) :10 o/c susceptibility gene

In addition to diabetes and obesity, there is a genetic component
to gallstone susceptibility. So we think that this may be a
gallstone-susceptibility gene.

DAVIDSON’S TEAM REPORTED ITS FINDINGS IN THE JOURAL OF LIPID RESEARCH. I’M JIM DRYDEN…

RUNS :57

AS WE GET OLDER, OUR BODY CLOCKS TEND TO CHANGE. AND THOSE CHANGES IN OUR CIRCADIAN RHYTHMS APPEAR TO BE LINKED BOTH TO THE AGING PROCESS ITSELF AND TO AGING-RELATED METABOLIC PROBLEMS SUCH AS INSULIN RESISTANCE AND TYPE 2 DIABETES. IN A NEW STUDY INVOLVING MICE, SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE AND NORTHWESTERN UNIVERSITY HAVE TIED ALL OF THOSE THINGS TOGETHER. JIM DRYDEN HAS MORE…

OUR CIRCADIAN CLOCKS CREATE DAILY OSCILLATIONS OF BODY TEMPERATURE, BRAIN ACTIVITY, HORMONE PRODUCTION AND METABOLISM. THEY’RE ALSO, APPARENTLY PLAYING A ROLE IN AGING, ACCORDING TO THIS NEW STUDY. THE MECHANISM SEEMS TO INVOLVE A COUPLE OF KEY PROTEINS, ACCORDING TO WASHINGTON UNIVERSITY AGING RESEARCHER SHIN IMAI. PREVIOUSLY, HE HAD DEMONSTRATED THAT A GENE CALLED SIRT1 WAS AT THE CENTER OF A NETWORK THAT REGULATES AGING. NOW, WITH RESEARCHERS FROM NORTHWESTERN, HE’S LEARNED THAT IN MICE, THE CIRCADIAN CLOCK IS LINKED TO SIRT1 THROUGH A KEY SUSBSTANCE CALLED NAD THAT REGULATES ENERGY METABOLISM.

(act) :16 o/c all organisms

This discovery basically connects energy metabolism and
aging through this novel enzymatic activity because SIRT
requires NAD. NAD is an essential currency for energy
metabolism in pretty much all organisms.

THE FAMILY OF SIRT PROTEINS REGULATES AGING IN LOWER ANIMALS, AND ALTHOUGH THIS LATEST FINDING DOESN’T PROVE THAT THE SIRT1 PROTEIN IS DOING THE SAME THING IN MAMMALS, IMAI SAYS THE EVIDENCE IS PRETTY STRONG BECAUSE THE MECHANISM THEY’VE DISCOVERED CONNECTS SIRT1 TO BOTH THE CIRCADIAN CLOCK AND TO METABOLISM.

(act) :21 o/c NAD itself

The key enzyme for NAD biosynthesis follows a circadian
oscillation in our body, at least in the mice. So the
expression of this protein is really oscillating, and
that creates the very interesting oscillation, circadian
oscillation, of NAD itself.

IMAI SAYS THE INTERACTIONS OF THE BODY CLOCK, SIRT1 AND NAD LINK TOGETHER NICELY TO PROVIDE A HYPOTHESIS THAT CONNECTS AGING AND METABOLISM.

(act) :18 o/c complete circle

All of the, you know, biological events are now linked. That
creates NAD oscillation. This NAD oscillation regulates SIRT1
activity, and then SIRT1 actually puts the regulation back to
the circadian clock mechanism. It’s almost like a complete circle.

IMAI SAYS HIS COLLEAGUES AT NORTHWESTERN ALREADY HAVE DEMONSTRATED THAT WHEN THE CIRCADIAN CLOCKS OF MICE GET OUT OF WHACK, SO DOES METABOLISM, AND THE ANIMALS DEVELOP PROBLEMS SIMILAR TO THE COMPLEX OF PROBLEMS THAT DOCTORS CALL THE METABOLIC SYMDROME, INVOLVING INSULIN DIFFICULTIES, OBESITY AND HIGH BLOOD PRESSURE AMONG OTHER THINGS. HE SAYS THIS NEW DISCOVERY SUGGESTS THAT SIRT1 AND NAD ARE THE SUBSTANCES THAT ARE INVOLVED IN THAT PROCESS.

(act) :27 o/c come true

Maybe when, you know, we get old, we might have some
problems somewhere in this NAD biosynthesis mechanism.
And maybe we can fix that problem by enhancing this NAD
biosynthesis process. And at least in the mice, we already
have preliminary results that this idea might come true.

THE RESEARCHERS REPORTED THEIR FINDINGS IN THE JOURNAL SCIENCE. I’M JIM DRYDEN…

RUNS 2:59

ALL ANIMALS HAVE AN INTERNAL, CIRCADIAN CLOCK, AND AS WE AGE, OUR CIRCADIAN RHYTHMS CHANGE. IN THIS NEW STUDY, SCIENTISTS ARE ZEROING IN ON HOW THINGS CHANGE. THE MECHANISM INVOLVES A COUPLE OF PROTEINS, ACCORDING TO WASHINGTON UNIVERSITY AGING RESEARCHER SHIN IMAI. PREVIOUSLY, HE HAD DEMONSTRATED THAT A GENE CALLED SIRT1 WAS AT THE CENTER OF A NETWORK THAT REGULATES AGING. NOW, WITH RESEARCHERS FROM NORTHWESTERN, HE’S LEARNED THAT IN MICE, THE CIRCADIAN CLOCK IS LINKED TO SIRT1 THROUGH A KEY SUSBSTANCE CALLED NAD THAT REGULATES ENERGY METABOLISM.

(act) :16 o/c all organisms

This discovery basically connects energy metabolism and
aging through this novel enzymatic activity because SIRT
requires NAD. NAD is an essential currency for energy
metabolism in pretty much all organisms.

THE RESEARCHERS REPORTED THEIR FINDINGS IN THE JOURNAL SCIENCE. I’M JIM DRYDEN…

RUNS :57

HEART PATIENTS WHO ARE DEPRESSED ARE MORE LIKELY TO HAVE FUTURE HEART ATTACKS, POOR QUALITY OF LIFE, EVEN MORE LIKELY TO DIE. BUT NOW WASHINGTON UNIVERSITY RESEARCHERS HAVE FOUND THAT IT’S POSSIBLE TO ALLEVIATE SYMPTOMS OF DEPRESSION FOR MANY CORONARY BYPASS SURGERY PATIENTS WITH COGNITIVE BEHAVIOR THERAPY, A NON-DRUG THERPY THAT HELPS PEOPLE IDENTIFY PROBLEMS AND DEVELOP COGNITIVE TECHNIQUES TO OVERCOME THEM. JIM DRYDEN HAS THE STORY…

DEPRESSION IS ESPECIALLY DIFFICULT TO TREAT IN HEART PATIENTS. ALTHOUGH ANTIDEPRESSANT DRUGS WORK PRETTY WELL FOR MANY MEDICALLY HEALTHY PEOPLE, RESEARCH HAS FOUND THAT THE DRUGS OFTEN MAKE LITTLE DIFFERENCE IN CARDIAC PATIENTS, SO WHEN WASHINGTON UNIVERSITY PSYCHOLOGIST KENNETH FREEDLAND AND HIS TEAM STUDIED MORE THAN 100 CORONARY BYPASS PATIENTS WITH DEPRESSION, THEY TESTED THE NON-DRUG TREATMENTS COGNITIVE BEHAVIOR THERAPY AND SUPPORTIVE STRESS MANAGEMENT.

(act) :16 o/c very effective

Antidepressant therapy helps many people, and there have been
antidepressants that have been tested in various cardiac patient
populations and have been shown to be safe, but there’s not great
evidence that they’re very effective.

ALTHOUGH IT’S WELL-KNOWN THAT DEPRESSION CAN MAKE HEART PROBLEMS WORSE, FREEDLAND AND OTHER RESEARCHERS HAVE BEEN UNABLE SO FAR TO PROVE THAT TREATING DEPRESSION MAKES THEM ANY BETTER. SO HE SAYS THE GOAL IN THIS STUDY HAD LESS TO DO WITH THE HEART HEALTH OF BYPASS PATIENTS AND MORE TO DO WITH ALLEVIATING THEIR DEPRESSION.

(act) :18 o/c doing enough

We allowed people to enroll in the study whether or not they
were already taking an antidepressant, and we found that about
half of the patients already were on an antidepressant, and yet,
they were still depressed. At lest for those people, we know
that whatever the antidepressant was doing for them, it wasn’t
doing enough.

FREEDLAND’S TEAM TESTED 12 WEEKS OF TREATMENT WITH COGNITIVE BEHAVIOR THERAPY OR SUPPORTIVE STRESS MANAGEMENT. AND THEY COMPARED THOSE TREATED PATIENTS TO A GROUP OF DEPRESSED CARDIAC BYPASS PATIENTS WHO RECEIVED WHAT THE INVESTIGATORS CALLED USUAL CARE — THAT IS, THEY RECEIVED ANTIDEPRESSANT DRUGS IF THE DRUGS WERE PRESCRIBED BY THEIR CARIOLOGIST OR OTHER PRIMARY CARE DOCTOR. BOTH COGNITIVE BEHAVIOR THERAPY AND SUPPORTIVE STRESS MANAGEMENT HELPED TO RELIEVE DEPRESSION IN THE MAJORITY OF PATIENTS, BUT COGNITIVE THERAPY WAS MOST EFFECTIVE.

(act) :20 o/c patients achieved

They improved the most, and their improvement was sustained over
nine months. They did not tend to relapse. The supportive stress
management people improved, but not quite as much. Their improvement
was also sustained, but they never really got down to the level the
CBT patients achieved.

NINE MONTHS AFTER TREATMENT 73 PERCENT OF THE BYPASS SURGERY PATIENTS WHO RECEIVED COGNITIVE BEHAVIOR THERAPY HAD EXPERIENCED REMISSION OF THEIR DEPRESSION, COMPARED WITH ONLY 35 PERCENT OF THOSE WHO RECEIVED THE CARE PRESCRIBED BY THEIR PRIMARY CARE DOCTOR. FREEDLAND SAYS WHEN IT COMES TO ALLEVIATING THEIR SYMPTOMS, PEOPLE WITH MAJOR DEPRESSION WHO GET USUAL CARE DON’T SEEM TO DO VERY WELL.

(act) :18 o/c called for

They’ll go to their primary care doctor. They’ll either get
an antidepressant, or they won’t. We now see that if you have
major depression after bypass surgery, that’s not a recipe for
a good outcome.

FREEDLAND SAYS CORONARY BYPASS PATIENTS WHO DECIDE TO TAKE ANTIDEPRESSANTS AFTER BYPASS SURGERY SHOULD WORK CLOSELY WITH THEIR DOCTORS TO MAKE SURE THEIR DEPRESSION ACTUALLY IMPROVES. HE REPORTED HIS FINDINGS IN THE ARCHIVES OF GENERAL PSYCHIATRY. I’M JIM DRYDEN…

RUNS 2:54

DEPRESSION IS DIFFICULT TO TREAT IN HEART PATIENTS. AND UNTREATED DEPRESSION IS LINKED TO FUTURE HEART PROBLEMS. WASHINGTON UNIVERSITY PSYCHOLOGIST KENNETH FREEDLAND STUDIED MORE THAN 100 HEART BYPASS PATIENTS WHO WERE DEPRESSED. SOME RECEIVED COGNITIVE THERAPY. OTHERS WERE FOLLOWED BUT RECEIVED NO STUDY TREATMENT, INSTEAD GETTING ONLY WHAT THEIR PRIMARY CARE DOCTORS PRESCRIBED. AND A THIRD GROUP RECEIVED AN INTERVENTION CALLED SUPPORTIVE STRESS MANAGEMENT. FREEDLAND DIDN’T STUDY ANTIDEPRESSANT DRUGS BECAUSE MANY HEART PATIENTS ALREADY TAKE A LOT OF OTHER MEDICATIONS, BUT THAT WASN’T THE ONLY REASON.

(act) :12 o/c very effective

There have been antidepressants that have been tested in various
cardiac patient populations and have been shown to be safe, but
there’s not great evidence that they’re very effective.

NINE MONTHS AFTER TREATMENT, 73 PERCENT OF BYPASS SURGERY PATIENTS WHO RECEIVED COGNITIVE BEHAVIOR THERAPY HAD EXPERIENCED REMISSION OF THEIR DEPRESSION, COMPARED WITH ONLY 35 PERCENT OF THOSE WHO RECEIVED THE CARE PRESCRIBED BY THEIR PRIMARY CARE DOCTORS. I’M JIM DRYDEN…

RUNS 1:00

ALZHEIMER’S DISEASE RESEARCHERS KNOW THAT A SUBSTANCE CALLED AMYLOID-BETA BUILDS UP IN THE BRAIN TO FORM THE PLAQUES THAT CHARACTERIZE THE ILLNESS. THEY ALSO KNOW THAT WHEN LEVELS OF THE SUBSTANCE IN THE SPINAL FLUID GET LOW, THERE’S A VERY GOOD CHANCE BRAIN PLAQUES ARE PRESENT. AND NOW SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE DEMONSTRATED THAT LOW LEVELS OF A-BETA IN THE SPINAL FLUID SEEM TO SIGNAL THE PRESENCE OF BRAIN DAMAGE CONNECTED TO ALZHEIMER’S DISEASE, EVEN IF THERE ARE NO DETECTABLE SYMPTOMS OF THE DISORDER. JIM DRYDEN HAS THE STORY…

AMYLOID PLAQUES BUILD UP IN THE BRAINS OF PEOPLE WITH ALZHEIMER’S DISEASE, AND AS THE AMYLOID COLLECTS IN THE PLAQUES, THERE SEEMS TO BE LESS OF IT IN THE FLUID THAT SURROUNDS THE BRAIN AND THE SPINAL CORD, CALLED THE CEREBROSPINAL FLUID OR CSF, ACCORDING TO WASHINGTON UNIVERSITY NEUROLOGIST DAVID HOLTZMAN.

(act) :17 o/c fluid analysis

It’s actually an outstanding marker for whether or not amyloid
plaques are building up. By combining imaging of amyloid with
looking at the spinal fluid, you can see that everyone who has
amyloid plaques in their brain is picked up by the spinal fluid
analysis.

HOLTZMAN, COLLEAGUE ANNE FAGAN, AND OTHERS MEASURED THE CEREBROSPINAL FLUID OF ADULTS AGES 60 TO 90 YEARS OLD. IN ADULTS OF THAT AGE, THEY EXPECTED SOME WOULD HAVE AMYLOID IN THE BRAIN, EVEN IF THEY DIDN’T HAVE CLINICAL SYMPTOMS OF ALZHEIMER’S. WHAT SURPRISED THEM, HOLTZMAN SAYS, WAS THAT THE BRAINS OF PEOPLE WITH LOW CSF LEVELS OF AMYLOID-BETA 42 HAD GOTTEN SMALLER.

(act) :19 o/c to atrophy

What that suggests is that if you have amyloid plaques in the
brain, your CSF A-beta 42 is lower, and those are the people
who had smaller brains. And that suggests that they probably
started with a larger brain, and then as amyloid plaques
developed in the brain, the brain started to atrophy.
HOLTZMAN SAYS AS NERVE CELLS DIE, OR BECOME DAMAGED, THEY CAN DISAPPEAR OR SIMPLY GET SMALLER AS THEY LOSE PARTS OF THE CELL THAT STRETCH OUT TO CONNECT TO OTHER CELLS.

(act) :12 o/c around anymore

Whether or not there’s actually cell death going on isn’t clear,
but it’s likely that there’s retraction of the cell extensions so
that there’s not as much of the nerve fibers around anymore.

HOLTZMAN SAYS IT WAS CLEAR THAT AMYLOID PLAQUES COULD DEVELOP PRIOR TO ALZHEIMER’S SYMPTOMS AND THAT LOW AMYLOID LEVELS IN THE CSF WERE A MARKER FOR PLAQUES IN THE BRAIN, BUT HE SAYS THIS NEW STUDY SHOWS THAT AMYLOID PLAQUES ARE RELATED TO BRAIN SHRINKING, EVEN BEFORE THE START OF CLINICAL SYMPTOMS.

(act) :19 o/c seem fine

Basically, showing that the atrophy, or the shrinking of the
brain correlates with the presence of amyloid plaques, that
was not shown before. And I think it argues that either the
amyloid plaques or something associated with the amyloid
plaques is damaging the brain, even when people seem fine.

HOLTZMAN SAYS ONE REASON THAT SIGNFICANT DAMAGE CAN OCCUR BEFORE SYMPTOMS APPEAR IS THAT THE BRAIN HAS BUILT-IN RESERVES AND CAN SUSTAIN A FAIR AMOUNT OF DAMAGE BEFORE COGNITIVE FUNCTIONS ARE IMPAIRED.

(act) :20 o/c already occurring

You’d still have normal function until you dropped down below
some critical number, and that’s probably the case in the brain
in general. So you may require a dropping out of, say, 50 or 60
percent of function of a particular network in the brain for
there to be symptoms, and until you hit that number, the person
seems fine even though damage is already occurring.

THE RESEARCHERS REPORTED THEIR FINDINGS IN THE ANNALS OF NEUROLOGY. I’M JIM DRYDEN…

RUNS 2:53

STRUCTURES CALLED PLAQUES BUILD UP IN THE BRAINS OF PEOPLE WITH ALZHEIMER’S DISEASE, AND THOSE PLAQUES ARE MADE OF A SUBSTANCE CALLED AMYLOID. BUT WHEN AMYLOID IS BUILDING UP IN THE BRAIN, THERE’S APPARENTLY LESS OF IT IN THE FLUID THAT SURROUNDS THE BRAIN AND THE SPINAL CORD, CALLED THE CEREBROSPINAL FLUID OR CSF. WASHINGTON UNIVERSITY ALZHEIMER’S RESEARCHERS HAD PREVIOUSLY SHOWN THAT LOW LEVELS OF AMYLOID-BETA 42 IN THE CSF WERE A MARKER FOR THE PRESENCE OF AMYLOID PLAQUES IN THE BRAIN. NOW, ACCORDING TO NEUROLOGIST DAVID HOLTZMAN, THE RESEARCHERS HAVE FOUND THAT EVEN WHEN THERE ARE NO CLINICAL SYMPTOMS OF ALZHEIMER’S DISEASE, THE BRAINS OF PEOPLE WITH LOW LEVELS OF AMYLOID-BETA IN THEIR SPINAL FLUID, SEEM TO HAVE SHRUNK.

(act) :17 o/c to atrophy

If you have amyloid plaques in the brain, your CSF A-beta 42
is lower, and those are the people who had smaller brains.
And that suggests that they probably started with a larger
brain, and then as amyloid plaques developed in the brain,
the brain started to atrophy.

HOLTZMAN, HIS COLLEAGUE ANNE FAGAN AND OTHERS REPORTED THEIR FINDINGS IN THE ANNALS OF NEUROLOGY. I’M JIM DRYDEN…

RUNS 1:00

SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE IDENTIFIED THE FIRST GENE THAT CONVINCES AILING NERVE CELL BRANCHES TO DESTROY THEMSELVES. AND THEY BELIEVE THE FINDING MAY EVENTUALLY PLAY A ROLE IN THE DEVELOPMENT OF MORE EFFECTIVE THERAPIES FOR THE PAINFUL CONDITION CALLED NEUROPATHY. JIM DRYDEN HAS THE STORY…

NEUROPATHY IS A POTENTIALLY PAINFUL CONDITION THAT COMES ABOUT WHEN PARTS OF NERVE CELLS, CALLED AXONS, DESTROY THEMSELVES, ACCORDING TO WASHINGTON UNIVERSITY DEVELOPMENTAL BIOLOGIST AARON DIANTONIO.

(act) :18 o/c self destruct

In many different diseases: trauma, sometimes with diabetes,
as a side effect of certain chemotherapeutics and certain
neurodegenerative diseases, the axon is injured, and when the
axon is injured, one thing that can happen is it can, basically,
decide to self destruct.

DEPENDING UPON HOW IT AFFECTS A PERSON, NEUROPATHY CAN CAUSE EXCRUTIATING PAIN, OR PERHAPS NUMBNESS. BUT DIANTONIO SAYS THE PROCESS, INVOLVING THE DEGENERATION OF NERVE AXONS, IS WHAT DRIVES THINGS.

(act) :14 o/c not enough

The sorts of problems one can have include pain, an inability
to control, say, in muscles in your arms or your legs, inability
to sense things normally – either because, you know, it hurts
too much or, maybe not enough.

DIANTONIO SAYS SCIENTISTS HAVE KNOWN ABOUT AXON DEGENERATION FOR MORE THAN 150 YEARS. THE PROCESS WAS FIRST DESCRIBED IN 1850. BUT IT TOOK UNTIL NOW FOR SCIENTISTS IN HIS LABORATORY TO IDENTIFY A GENE INVOLVED.

(act) :19 o/c the process

We discovered a couple of genes that seem to function together
to help make the decision… After an axon gets injured, it sort
of needs to decide: “Okay. I notice I’m injured. Is this bad
enough that I should start degenerating or not?” And so the
genes we found seem to be involved in that part of the process.
DIANTONIO HAD BEEN STUDYING THE DLK GENE IN FRUIT FLIES BECAUSE THEY FOUND IT WAS IMPORTANT IN SYAPSES — THE SPACES BETWEEN NERVE CELLS THAT TRANSMIT AND RECEIVE NERVE SIGNALS. WORKING WITH COLLEAGUE JEFFREY MILBRANDT AND GRADUATE STUDENT BRADLEY MILLER, DIANTONIO SAYS THEY WERE ABLE TO FIND THAT THE DLK GENE, AND A COMPANION MOLECULE CALLED JUNK, ARE INVOLVED IN THE CASCADE THAT LEADS NERVE AXONS TO DEGENERATE.

(act) :11 o/c axon would

If you’re missing DLK, then injured axons are inhibited from
Degenerating, as if they don’t quite realize they were injured,
and so they don’t trigger the degeneration program like a
normal axon would.

IT SEEMS THAT DLK AND JUNK INTERACT TO LAUNCH THE PROCESS OF DEGENERATION. DIANTONIO SAYS A NUMBER OF DRUGS INHIBIT THE ACTIONS OF THE JUNK MOLECULE, AND HIS LABORATORY ALSO HAS FOUND THAT IN CELL CULTURE, THOSE DRUGS INHIBIT THE DEGENERATION OF NERVE AXONS.

(act) :19 o/c were protected

It protects axons from two different kinds of injury: traumatic
injury – just, basically when they get cut – but another one
that might be more clinically relevant is injury caused as a
side effect of chemotherapy. When we treated our axons with this
chemotherapeutic but added an inhibitor of this JUNK molecule,
then the axons were protected.

DIANTONIO SAYS MORE STUDY IS NEEDED BECAUSE THERE MAY BE BAD SIDE EFFECTS INVOLVED IN INHIBITING THESE MOLECULES, BUT HE SAYS THE FINDINGS DO PROVIDE AT LEAST SOME LONG-TERM HOPE FOR THE THOUSANDS WHO SUFFFER WITH NEUROPATHY. HIS TEAM REPORTED ITS FINDINGS IN THE JOURNAL NATURE NEUROSCIENCE. I’M JIM DRYDEN…

RUNS 2:58

NEUROPATHY CAN BE A SIDE EFFECT OF CHEMOTHERAPY, DIABETES OR OTHER CONDITIONS THAT DAMAGE PARTS OF NERVE CELLS CALLED AXONS. THE AXONS ARE LONG PROCESSES THAT RUN THROUGHOUT THE BODY. SINCE 1850, SCIENTISTS HAVE KNOWN THAT WHEN INJURED, AXONS CAN DESTROY THEMSELVES. BUT IT TOOK UNTIL THIS YEAR FOR SCIENTISTS IN THE LABORATORY OF AARON DIANTONIO TO IDENTIFY A GENE INVOLVED IN THAT PROCESS.

(act) :14 o/c the process

We discovered a couple of genes that seem to function together.
After an axon gets injured, it sort of needs to decide: “Is this
bad enough that I should start degenerating or not?” And so the
genes we found seem to be involved in that part of the process.

DIANTONIO SAYS THE GENE CALLED DLK INHIBITS AXON DEGENERATION, AND WITH A COMPANION MOLECULE, CALLED JUNK, COULD PROVIDE A TARGET FOR THERAPY.

(act) :08 o/c degeneration program

If you’re missing DLK, then injured axons are inhibited from
degenerating. They don’t trigger the degeneration program.

DIANTONIO’S TEAM REPORTED ITS FINDINGS IN THE JOURNAL NATURE NEUROSCIENCE. I’M JIM DRYDEN…

RUNS :58

AN MD/PhD STUDENT AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAS RECENTLY JOINED THE RANKS OF THOSE GOOD SAMARITANS WHO HAVE DONATED AN ORGAN TO A STRANGER. AND FOLLOWING THE OPERATIONS, BOTH THE KIDNEY DONOR AND RECIPIENT ARE DOING VERY WELL. JIM DRYDEN HAS THE STORY…

ACCORDING TO THE UNITED NETWORK FOR ORGAN SHARING, ALMOST 79 THOUSAND PEOPLE IN THE UNITED STATES ARE WAITING FOR A KIDNEY TRANSPLANT. SOMETIMES A FRIEND OR RELATIVE WILL OFFER TO DONATE, BUT IN RECENT YEARS, THERE HAVE BEEN MORE STORIES INVOLVING GOOD SAMARITANS WHO ELECT TO DONATE A KIDNEY TO SOMEONE THEY DON’T EVEN KNOW. CHUCK RICKERT WAS LISTENING TO THE RADIO ONE AFTERNOON WHILE WORKING IN THE LABORATORY OF WASHINGTON UNIVERSITY RESEARCHER ROBERT SCHREIBER. WHAT HE HEARD WAS A PROGRAM ABOUT KIDNEY DONATION ON NPR. AND ONE OF THE CALLERS SAID HE COULDN’T FIND A MATCH AMONG HIS FRIENDS OR RELATIVES, SO HIS ONLY OPTION WAS TO WAIT FOR SOMETHING TERRIBLE TO HAPPEN TO A YOUNG PERSON. THE COMMENT STUCK WITH RICKERT, AND HE DECIDED THAT SINCE HE REALLY ONLY NEEDED ONE KIDNEY, HE WOULD PART WITH THE OTHER ONE.

(act) :25 o/c the operation

This type of donation is still in its infancy in many ways. The
program in St. Louis has only been in existence since 2001. And
only around a dozen people, so far, have donated anonymously. So I
looked into the process, and about six months later, I was checking
into the hospital – with my family there in support and all of my
friends – and went through with the operation.

RICKERT SAYS THE PROCESS TOOK SOME TIME. IT’S IMPORTANT NOT ONLY TO SCREEN AN ANONYMOUS DONOR FOR BLOOD AND TISSUE TYPE BUT ALSO TO MAKE SURE THAT THE DONOR HAS HIS OR HER HEAD ON STRAIGHT AND HAS MADE THE DECISION FOR THE RIGHT REASONS. HE SAYS THE PROCESS WAS COMPLETELY ANONYMOUS. HE DIDN’T KNOW WHO WAS GETTING HIS KIDNEY, AND THE RECIPIENT DIDN’T KNOW WHO WAS DONATING.

(act) :24 o/c I donated

It was only after the operation that I found out that the
recipient was a 10-year-old girl who has a rare, genetic
disease that affects about one in a million individuals
and that this condition leads, ultimately, to both liver
and kidney failure, and she had, in fact, had a liver
transplant a couple of years prior to the kidney transplant,
in which she received the kidney I donated.

HE HAS NEVER SPOKEN TO THAT LITTLE GIRL WHO GOT HIS KIDNEY, BUT HE HAS LEARNED THAT SHE’S DOING WELL.

(act) :15 o/c 15 years

The goal is to have the kidney be useful to the recipient,
of course. You don’t know if it is always going to work out
that way. But, typically, it does. For living kidney donation,
the kidneys typically last around 12 to 15 years.

RICKERT HAD HEARD ABOUT KIDNEY DONATION IN MEDICAL SCHOOL, BUT HE HAD NEVER REALLY CONSIDERED IT UNTIL HE HEARD THAT RADIO PROGRAM. AND HE SAYS FOR A FEW WEEKS AFTER THE OPERATION, EVERY TIME HE FELT A LITTLE ACHE OR PAIN, PART OF HIM WONDERED WHETHER IT WAS RELATED TO HIS NEW STATUS AS A KIDNEY DONOR. AFTER DONATING HIS KIDNEY, HE WAS BACK AT WORK IN ABOUT TWO WEEKS, AND REALLY, HE SAYS, HE FOUND THAT IN TERMS OF HIS HEALTH, DONATING A KIDNEY WASN’T THAT BIG A DEAL.

(act) :15 o/c on my part

My lifestyle is exactly what it was before, and if anything,
I am more aware of my health in that I don’t take my good
health for granted. Really, it was, sort of, I feel a very
small sacrifice on my part.

I’M JIM DRYDEN…

RUNS 2:54

CHUCK RICKERT WAS LISTENING TO THE RADIO AND WORKING IN THE LABORATORY OF WASHINGTON UNIVERSITY RESEARCHER ROBERT SCHREIBER WHEN HE HEARD A PROGRAM ABOUT KIDNEY DONATION ON NPR. ONE OF THE CALLERS SAID HE COULDN’T FIND A MATCH AMONG FRIENDS OR RELATIVES, SO HIS ONLY OPTION WAS TO WAIT FOR SOMETHING TERRIBLE TO HAPPEN TO A YOUNG PERSON. THE COMMENT STUCK WITH RICKERT, AND A FEW MONTHS LATER, FOLLOWING A RIGOROUS SCREENING PROCESS, HE FOUND HIMSELF IN THE HOSPITAL, DONATING ONE OF HIS KIDNEYS.

(act) :21 o/c the operation

This type of donation is still in its infancy in many ways. The
program in St. Louis has only been in existence since 2001. So I
looked into the process, and about six months later, I was checking
into the hospital – with my family there in support and all of my
friends – and went through with the operation.

HE WAS BACK AT WORK IN THE LAB IN ABOUT TWO WEEKS. AND HE HAS SINCE LEARNED THAT A 10-YEAR-OLD GIRL WHO RECEIVED THE KIDNEY IS DOING VERY WELL, AND THAT, SAYS RICKERT, IS WHAT HE HAD HOPED FOR. I’M JIM DRYDEN…

RUNS :58

THERE HAVE BEEN NUMEROUS STUDIES CONDUCTED OVER MANY YEARS, WHICH SUGGEST THAT PHYSICAL ACTIVITY MAY LOWER THE RISK FOR COLON CANCER. AND NOW CANCER RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS AND HARVARD UNIVERSITY HAVE PUT TOGETHER THE RESULTS FROM THOSE STUDIES TO DETERMINE THAT, IN FACT, EXERCISE AND PHYSICAL ACTIVITY DO SIGNIFICANTLY LOWER COLON CANCER RISK. JIM DRYDEN HAS THE STORY…

COLORECTAL CANCER IS THE THIRD MOST COMMON TYPE OF CANCER. EVERY YEAR, MORE THAN 100 THOUSAND PEOPLE IN THE UNITED STATES ARE DIAGNOSED WITH COLON CANCER. ANOTHER 40,000 GET RECTAL CANCER. FOR THIS PROJECT, THE RESEARCHERS ANALYZED DATA FROM 52 STUDIES CONDUCTED SINCE THE 1980s AND FOUND THAT REGULAR EXERCISE OR JOB-RELATED ACTIVITY DID SEEM TO PROTECT PEOPLE FROM COLON CANCER. WASHINGTON UNIVERSITY AND SITEMAN CANCER CENTER RESEARCHER KATHLEEN WOLIN IS THE STUDY’S FIRST AUTHOR.

(act) :19 o/c least active

What we wanted to do is to take all of that data, bring it
together in s systematic way and provide a single, summary
estimate that takes advantage of the wealth of data that’s
out there, which is people who are most active have a 24 percent
lower risk of colon cancer than people who are least active.

WOLIN SAYS THE VARIOUS STUDIES HER GROUP REVIEWED LOOKED AT ALL KINDS OF DIFFERENT PHYSICAL ACTIVITY, FROM WALKING AND JOGGING TO LIFTING AND DIGGING. SO IT’S HARD TO SAY EXACTLY WHAT AN INDIVIDUAL PERSON MUST DO TO REDUCE THEIR COLON CANCER RISK.

(act) :28 o/c a week

One of the challenges of doing research like this is you
sort of end up with lines that are a little bit fuzzy, and
the most active group across each study is different. So
all we can really do is pull out an example of one of those
studies. So the previous study that we did, the most active
were people who were doing something that’s about equivalent
to walking five or six hours a week. And the least active
were people who were doing about the equivalent of brisk
walking a half hour a week.

SHE SAYS THE GOOD THING ABOUT AN ACTIVE LIFE IS THAT IT NOT ONLY LOWERS COLON CANCER RISK, BUT EXERCISE AND PHYSICAL ACTIVITY ALSO SEEM TO REDUCE THE RISKS FOR MANY OTHER PROBLEMS, FROM BREAST CANCER TO HEART DISEASE.

(act) :13 o/c of things

You know, one of the great things about something like
physical activity as a disease prevention intervention
is that you don’t just reduce your risk of one thing.
You are able to reduce your risk of lots of things.

AND PEOPLE SEEM TO GET THE BENEFIT FROM RELATIVELY MODEST INCREASES IN ACTIVITY.

(act) :23 o/c special equipment

There’s nothing in the data that says you need to be
running marathons. Some of these studies very specifically
looked at the benefits of walking. Generally speaking, we
recommend that people are doing something like a brisk walk,
not a vey leisurely stroll. You know, but walking is safe.
It’s pretty easy to do. It doesn’t require a special facility
or special equipment.

SOME OF THE PEOPLE IN THESE STUDIES LOWERED THEIR RISKS OF COLON CANCER BECAUSE THEY HAD ACTIVE JOBS, BUT WOLIN SAYS IT’S IMPORTANT TO REMEMBER THAT A JOB THAT MAKES YOU TIRED ISN’T NECESSARILY A JOB THAT’S AN ACTIVE ONE.

(act) :19 o/c physical activity

Someone who’s working in a retail environment and standing on
their feet all day long, and those are very exhausting – you’re
exhausted at the end of the day – but they’re actually not
physically active at work. So they do need to – even though
they’re tired at the end of the day – we do want them to go
out and get some physical activity.

WOLIN AND HER COLLEAGUES REPORTED THEIR FINDINGS IN THE BRITISH JOURNAL OF CANCER. I’M JIM DRYEN…

RUNS 2:57

COLORECTAL CANCER IS THE THIRD MOST COMMON TYPE OF CANCER. EACH YEAR, MORE THAN 100 THOUSAND PEOPLE IN THE UNITED STATES ARE DIAGNOSED WITH COLON CANCER. FOR THIS PROJECT, THE RESEARCHERS ANALYZED DATA FROM 52 STUDIES CONDUCTED SINCE THE 1980s. AND THEY FOUND THAT EXERCISES — SUCH AS WALKING, JOGGING, BIKING OR SWIMMING — AND JOB-RELATED ACTIVITIES — SUCH AS WALKING, LIFTING OR DIGGING — SEEMED TO PROTECT PEOPLE FROM COLON CANCER. WASHINGTON UNIVERSITY AND SITEMAN CANCER CENTER RESEARCHER KATHLEEN WOLIN IS THE STUDY’S FIRST AUTHOR.

(act) :14 o/c least active

What we wanted to do is to take all of that data and provide a
single, summary estimate, which is people who are most active
have a 24 percent lower risk of colon cancer than people who
are least active.

WOLIN AND HER COLLEAGUES REPORTED THEIR FINDINGS IN THE BRITISH JOURNAL OF CANCER. I’M JIM DRYEN…

RUNS :50

CATCHING CANCER EARLY, BEFORE IT CAN GROW AND SPREAD, IS IMPORTANT TO TREATMENT OR EVEN CURE. BUT A NEW STUDY FINDS THAT ANNUAL PROSTATE CANCER SCREENINGS DON’T APPEAR TO REDUCE DEATHS FROM PROSTATE CANCER, AT LEAST NOT IN MEN WHOSE LIFT EXPECTANCY IS LIMITED. RESEARCHERS, LED BY UROLOGIC SURGEONS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS, HAVE FOUND THAT ANNUAL PSA TESTSING AND DIGITAL RECTAL EXAMS DON’T APPEAR TO AFFECT SURVIVAL RATES. JIM DRYDEN REPORTS…

THE RESEARCHERS STUDIED MORE THAN 75,000 MEN BETWEEN THE AGES OF 55 AND 74. HALF WERE SCREENED WITH ANNUAL PSA BLOOD TESTS AND DIGITAL RECTAL EXAMS. THE OTHER HALF RECEIVED ROUTINE CARE, MEANING THEY WERE SCREENED ONLY IF THEIR PHYSICIANS RECOMMENDED IT. AFTER SEVEN YEARS, THERE WERE NO DIFFERENCES IN MORTALITY RATES, ACCORDING TO LEAD AUTHOR AND PRINCIPAL INVESTIGATOR GERALD ANDRIOLE, THE CHIEF OF UROLOGIC SURGERY AT THE SITEMAN CANCER CENTER AND WASHINGTON UNIVERSITY.

(act) :11 o/c rectal exam

We now know that for men who have a limited life expectancy,
it probably is not necessary for them to be screened each
year with a PSA and a digital rectal exam.

BUT ANDRIOLE SAYS IT’S NOT CORRECT TO SAY THAT ANNUAL PROSTATE SCREENINGS DON’T HELP ANYONE.

(act) :38 o/c prostate cancer

In this study, we followed all of our patients for at least
seven years, and through seven years of follow-up, there has
been no reduction in overall prostate cancer mortality. Now,
it could be that as we follow younger patients for longer and
longer, that a benefit will emerge. But I think the data are
pretty clear at this point, that if you’re a man and you have
a limited life expectancy – because of your age, because of
your other health status, in terms of heart disease and diabetes
and whatnot – at a certain point, it is no longer necessary for
you to be screened for prostate cancer.

PROSTATE CANCER KILLS 29 THOUSAND MEN IN THE UNITED STATES EACH YEAR. MORE THAN 186 THOUSAND ARE DIAGNOSED WITH THE DISEASE ANNUALLY. ANDRIOLE SAYS ABOUT 10 PERCENT OF THE MEN IN THIS STUDY DIED DURING ITS FIRST SEVEN YEARS. NOT ALL OF THEM DIED FROM PROSTATE CANCER, BUT SOME DID.

(act) :30 o/c rectal exam

It could be very premature to make generalizations about the
ultimate result of the trial. And remember, most of the men
who have died have been elderly to start with. So we are
particularly unable to say a lot about the youngest men in
this study – these were men in their 50s – it may well be that
given more time, that we will find out whether the younger
age groups of men do, in fact, benefit from PSA testing and
digital rectal exam.

FOR YOUNG MEN, HE SAYS, SCREENING MAY BE VERY HELPFUL. YOUNGER MEN TEND TO HAVE MORE AGGRESSIVE TUMORS THAN MEN WHO DEVELOP PROSTATE CANCER IN THEIR 70s OR 80s, AND THEY ALSO HAVE LONGER EXPECTED LIFESPANS.

(act) :27 o/c mortality benefit

For now, young men with a good life expectancy, those men should
continue to be screened. On the other hand, elderly men, men who
have significant co-morbid medical conditions, it’s probably not
necessary, but I would recommend that you have a face-to-face,
heart-to-heart conversation with your doctor. Unfortunately, for
the oldest age group, we have not been able to show a mortality
benefit.

ANDRIOLE AND HIS COLLEAGUES REPORT THEIR FINDINGS IN THE NEW ENGLAND JOURNAL OF MEDICINE. I’M JIM DRYEN…

RUNS 2:52

PROSTATE CANCER KILLS 29 THOUSAND MEN EACH YEAR IN THE UNITED STATES. MORE THAN 186 THOUSAND ARE DIAGNOSED WITH THE DISEASE ANNUALLY. SINCE THE 1980s, MANY HAVE BEEN SCREENED WITH PSA BLOOD TESTS, DESPITE A LACK OF EVIDENCE THAT THE TESTING ACTUALLY REDUCES DEATH RATES. NOW, A LARGE, NATIONAL STUDY HAS BEEN UNABLE TO FIND EVIDENCE THAT ANNUAL SCREENING HAS AN IMPACT ON SURVIVAL. LEAD AUTHOR AND PRINCIPAL INVESTIGATOR GERALD ANDRIOLE IS THE CHIEF OF UROLOGIC SURGERY AT THE SITEMAN CANCER CENTER AND WASHINGTON UNIVERSITY. HE SAYS 75,000 MEN WERE ENROLLED IN THE STUDY. HALF WERE SCREENED ANNUALLY WITH A PSA BLOOD TEST AND A DIGITAL RECTAL EXAM. BUT AFTER THE FIRST SEVEN YEARS OF THE STUDY, THERE WAS NO SIGNIFICANT DIFFERENCE IN SURVIVAL BETWEEN THE TWO GROUPS.

(act) :10 o/c rectal exam

For men who have a limited life expectancy, it probably is not
necessary for them to be screened each year with a PSA and a
digital rectal exam.

ANDRIOLE AND HIS COLLEAGUES REPORT THEIR FINDINGS IN THE NEW ENGLAND JOURNAL OF MEDICINE. I’M JIM DRYEN…

RUNS 1:00

SCIENTISTS HAVE KNOWN FOR MANY YEARS THAT DEPRESSION AND HEART DISEASE ARE CONNECTED. DEPRESSED HEART ATTACK PATIENTS ARE MORE LIKELY TO HAVE A SECOND HEART ATTACK. DEPRESSED HEART PATIENTS ARE MORE LIKELY TO HAVE DIFFICULTIES WITH HEART RATE. NOW A TEAM AT WASHINGTON UNIVERSITY IN ST. LOUIS AND THE VETERANS ADMINISTRATION HAVE FOUND THAT BEING DEPRESSED GREATLY INCREASES THE RISK OF A HEART EVENT, EVEN IN PEOPLE WITH VERY SIMILAR GENETIC AND ENVIRONMENTAL RISKS. JIM DRYDEN EXPLAINS…

THE RESEARCHERS STUDIED MORE THAN 1,200 MALE TWINS. ALL SERVED IN THE MILITARY DURING THE VIETNAM ERA, AND ALL WERE SURVEYED ABOUT A VARIETY OF HEALTH PROBLEMS IN 1992. THE RESEARCHERS ASSESSED THEM AGAIN IN 2005, AND WHEN THEY LOOKED TO SEE WHAT HAPPENED IN THE INTERVENING YEARS, THEY FOUND THAT THOSE WHO HAD DEPRESSION IN 1992 WERE TWICE AS LIKELY TO HAVE BEEN TREATED FOR ANGINA, HAD A HEART ATTACK OR NEEDED BYPASS SURGERY OR A STENT. VA AND WASHINGTON UNIVERSITY RESEARCHER JEFFREY SCHERRER.

(act) :33 o/c depression experience

Even after controlling for smoking and diabetes and hypertension
and all of these other significant predictors, depression remains
a significant contributor to incident heart disease. But other
studies have already shown that. What’s new here is that we can
say, after adjusting for all of these other risk factors, depression
remains a significant predictor after controlling for the genetic
vulnerability also, further evidence that there’s something unique
about the depression experience.

SCHERRER AND HIS COLLEAGUE HONG XIAN, AN ASSOCIATE PROFESSOR OF MATHEMATICS IN MEDICINE AT WASHINGTON UNIVERSITY AND A HEALTH SCIENCE SPECIALIST AT THE VA, GROUPED THE TWINS INTO SEVERAL CATEGORIES, REFLECTING A PERSON’S RELATIVE GENETIC AND ENVIRONMENTAL RISK FOR HEART DISEASE AND FOR DEPRESSION. XIAN SAYS THE STUDY WAS DESIGNED TO…

(act) :21 o/c group these

To see if the depression is a predictor of the disease outcome
after controlling for the traditional risk factors. We can tease
out the genetic effects or environmental effects by comparing
the groups: group one versus group two versus group three.

BY GROUPING THE TWINS IN THIS WAY, IT WAS POSSIBLE TO TEASE OUT VARIOUS FACTORS THAT ALSO CAN INCREASE RISK FOR HEART DISEASE OR DEPRESSION: THINGS LIKE SMOKING, OBESITY, SOCIAL SUPPORT GENETIC FACTORS. SHERRER SAYS EVEN WHEN ACCOUNTING FOR ALL OF THOSE RISK FACTORS, DEPRESSION STILL STOOD OUT.

(act) :09 o/c depressiogenic effect

So we’re hypothesizing that it requires both the genetic vulnerability
and, like a depressiogenic effect.

SCHERRER SAYS ONE MIGHT ALMOST COMPARE THESE RESULTS TO FINDINGS ABOUT ADDICTION. NO MATTER WHAT ONE’S GENETIC MAKEUP OR ENVIRONMENTAL RISK FACTORS, YOU WON’T BECOME AN ALCOHOLIC OR A DRUG ADDICT IF YOU NEVER DRINK OR USE DRUGS. IN THIS CASE, IT SEEMS THAT DEPRESSION ITSELF — AND NOT THE ASSOCIATED GENETIC AND ENVIRONMENTAL RISKS — IS WHAT’S CAUSING THE INCREASES IN HEART DISEASE RISK.

(act) :09 o/c for depression

It’s the expression of depression, or the exposure to depression.
that is the risk factor, not the genetic vulnerability for depression.

SCHERRER REPORTED HIS FINDINGS THIS MONTH AT THE ANNUAL MEETING OF THE AMERICAN PSYCHOSOMATIC SOCIETY IN CHICAGO. I’M JIM DRYEN…

RUNS 2:48

THE RESEARCHERS STUDIED MORE THAN 1,200 MALE TWINS. ALL HAD BEEN IN THE MILITARY DURING THE VIETNAM ERA, AND ALL HAD BEEN SURVEYED ABOUT A VARIETY OF HEALTH PROBLEMS BACK IN 1992. RESEARCHERS ASSESSED THEM AGAIN IN 2005. THEY FOUND THAT THOSE WHO HAD DEPRESSION IN 1992 WERE TWICE AS LIKELY TO HAVE BEEN TREATED FOR ANGINA, HAD A HEART ATTACK OR NEEDED BYPASS SURGERY OR A STENT. THAT WAS TRUE EVEN WHEN ONE TWIN, WITH ALMOST ALL OF THE SAME GENETIC AND ENVIRONMENTAL RISKS, WHO WAS NEVER DEPRESSED, WAS COMPARED TO HIS BROTHER WHO HAD BEEN DEPRESSED. VA AND WASHINGTON UNIVERSITY RESEARCHER JEFFREY SCHERRER.

(act) :08 o/c depressiogenic effect

So we’re hypothesizing that it requires both the genetic
vulnerability and, like a depressiogenic effect.

SCHERRER REPORTED HIS FINDINGS THIS MONTH AT THE ANNUAL MEETING OF THE AMERICAN PSYCHOSOMATIC SOCIETY IN CHICAGO. I’M JIM DRYEN…

RUNS :55

FOR MANY YEARS, THE DRUG METHADONE HAS BEEN USED AS A MAINSTAY IN THE TREATMENT OF ADDICITION TO OPIOID DRUGS SUCH AS HEROIN. IN RECENT YEARS, IT’S ALSO BEEN USED MORE AS A TREATMENT FOR PAIN, ESPECIALLY CANCER PAIN. NOW SCIENTISTS AT WASHINGTON UNIVERSITY IN ST. LOUIS AND THE UNIVERSITY OF WASHINGTON IN SEATTLE HAVE LEARNED THAT METHADONE ISN’T CLEARED FROM THE BODY THE WAY MOST HAD BELIEVED IT WAS. JIM DRYDEN HAS MORE ON THE STORY…

AS METHADONE HAS BEEN USED MORE OFTEN, THERE’S ALSO BEEN A BIG INCREASE IN ADVERSE EVENTS RELATED TO THERAPY. BETWEEN 1997 AND 2006, USE OF THE DRUG ROSE MORE THAN 1300 PERCENT! ADVERSE EVENTS ALSO INCREASED, BY 1800 PERCENT. AND DEATHS LINKED TO THE DRUG ROSE ABOUT 400 PERCENT. THOSE TRENDS MAY BEGIN TO CHANGE IN THE FUTURE, ACCORDING TO WASHINGTON UNIVERSITY RESEARCHER EVAN KHARASCH. HIS TEAM HAS FOUND THAT THE BODY DOES NOT CLEAR METHADONE THE WAY MOST HAD THOUGHT IT DID. CONVENTIONAL WISDOM STATED THAT THE DRUG INTERACTED WITH A PARTICULAR ENZYME CALLED P4503A.

(act) :28 o/c of methadone

And in fact, it appears that the enzyme P4503A is not involved in
the clinical elimination of methadone. The package insert for
methadone appears to be incorrect, or at least needs to be
reevaluated. It is possible that the incorrect extrapolation of
laboratory experiments, to patients, without having done the
clinical studies, may be responsible, in part, for some of the
adverse effects of methadone.

BECAUSE MANY PEOPLE TAKE METHADONE FOR CANCER OR FOR PROBLEMS RELATED TO HIV-AIDS, MOST OF THEM ALSO TAKE OTHER DRUGS ALONG WITH THE METHADONE. KHARASCH AND HIS COLLEAGUES STUDIED METHADONE WHEN TAKEN ALONG WITH CERTAIN PROTEASE INHIBITORS. THOSE ARE THE DRUGS THAT KEEP THE IMMUNE SYSTEMS OF HIV PATIENTS HEALTHY. SOME PROTEASE INHIBITORS ALSO INHIBIT THE ACTIONS OF THE P4503A ENZYME. SO ONE WOULD NORMALLY THINK THAT PATIENTS WOULD NEED LESS METHADONE BECAUSE IT WOULD BE CLEARED FROM THE BODY MORE SLOWLY. BUT THAT’S NOT WHAT KHARASCH FOUND. HE SAYS IT ISN’T IMPORTANT NECESSARILY TO SLOW DOWN OR SPEED UP CLEARANCE OF THE DRUG, BUT DOCTORS DO WANT TO BE ABLE TO PREDICT WHICH OF THOSE MAY OCCUR SO THAT THEY DON’T INADVERTENTLY OVER- OR UNDER-DOSE THEIR PATIENTS.

(act) :20 o/c side effects

We want to know how other drugs will influence the clearance
of methadone. If we know that another drug is going to slow
the elimination of methadone, we would cut the dosage. If we
don’t know and we keep the same dosing, we may have accumulation
of the drug and the potential for side effects.

KHARASCH SAYS THERE ARE A NUMBER OF SIMILAR ENZYMES RELATED TO DRUG CLEARANCE, AND THE ORIGINAL LABORATORY STUDIES DONE IN METHADONE SEEM TO HAVE IDENTIFIED THE WRONG ONE.

(act) :24 o/c clinical studies

All of the laboratory evidence we’ve developed so far suggests
that another one of the P450 enzymes, called P4502B, appears
responsible for the elimination of methadone. But we need to
confirm that, clinically in patients. Those studies are currently
underway. We have some in vitro evidence, but again, it needs to
be confirmed with clinical studies.

KHARASCH PLANS TO CONTINUE STUDYING HOW PATIENTS PROCESS AND CLEAR METHADONE FROM THEIR SYSTEMS. HE AND HIS COLLEAGUES REPORT THEIR FINDINGS IN STUDIES PUBLISHED IN THE JOURNALS ANESTHESIOLOGY AND DRUG AND ALCOHOL DEPENDENCE. I’M JIM DRYDEN…

RUNS 3:00

METHADONE HAS LONG BEEN USED TO TREAT ADDICTION, AND IN RECENT YEARS, DOCTORS HAVE BEEN PRESCRIBING IT MORE OFTEN FOR PAIN, ESPECIALLY CANCER PAIN. CONVENTIONAL WISDOM STATED THAT THE DRUG INTERACTED WITH A SPECIFIC ENZYME, SO WHEN DOCTORS PRESCRIBED OTHER MEDICATIONS THAT ALSO INTERACTED WITH THE ENZYME, THEY NEEDED TO BEWARE OF DRUG INTERACTIONS. BUT WASHINGTON UNIVERSITY RESEARCHER EVAN KHARASCH AND HIS COLLEAGUES HAVE FOUND THAT THE ENZYME IN QUESTION DOESN’T REALLY AFFECT METHADONE CLEARANCE. THAT MEANS DOCTORS COULD BE GIVING TOO MUCH OR TOO LITTLE OF THE DRUG, AND THAT CAN BE ESPECIALLY DANGEROUS WHEN PATIENTS FIRST BEGIN THERAPY.

(act) :16 o/c are available

The highest risk period for unintentional, adverse side effects
is in the first two weeks, where clinicians can only estimate a
starting dose based on the best information and dosing guidelines
which are available.

KHARASCH SAYS HIS RESEARCH SUGGESTS THE METHADONE PACKAGE INSERT NEEDS TO BE CHANGED AND THAT SCIENTISTS MUST QUICKLY DETERMINE WHICH ENZYMES REALLY CLEAR THE DRUG FROM THE BODY IN ORDER TO PREVENT SIDE EFFECTS. I’M JIM DRYDEN…

RUNS 1:00

IN RECENT YEARS, SCIENTISTS DOING BRAIN IMAGING STUDIES HAVE LEARNED THAT EVEN WHEN WE AREN’T DOING A PARTICULAR TASK, OUR BRAINS REMAIN BUSY WITH ACTIVITY IN A NETWORK OF BRAIN REGIONS. NOW, IN A NEW BRAIN IMAGING STUDY, WASHINGTON UNIVERSITY NEUROSCIENTISTS HAVE FOUND THAT IN DEPRESSED PEOPLE THis DEFAULT NETWORK IN THE BRAIN DOESN’T SEEM TO WORK THE SAME WAY AS IT DOES IN PEOPLE WHO AREN’T DEPRESSED. JIM DRYDEN HAS MORE…

SCIENTISTS USED TO THINK THAT WHEN WE WEREN’T DOING MUCH, OUR BRAINS WERE RESTING, TOO. THEY DON’T THINK THAT ANYMORE. A FEW YEARS AGO, WASHINGTON UNIVERSITY NEUROSCIENTISTS IDENTIFIED A NETWORK OF BRAIN REGIONS THAT’S ACTIVE WHEN WE’RE NOT. IT’S KNOWN AS THE DEFAULT MODE NETWORK, ACCORDING TO WASHINGTON UNIVERSITY PSYCHIATRIST YVETTE SHELINE.

(act) :20 o/c came to be

There were a number of regions that became active when you were
just lying there doing nothing. And then as a cognitive task had
to be accomplished, these regions, which had been active, shut
down. That’s why the term “default,” in other words, what you’re
doing when you’re doing nothing – default mode network – came
to be.

THE DEFAULT MODE NETWORK INVOLVES A GROUP OF BRAIN STRUCTURES, MOST OF WHICH SEEM TO BE MORE ACTIVE WHEN WE’RE LESS ACTIVE AND VICE VERSA. THAT GROUP OF BRAIN STRUCTURES WAS FIRST NAMED IN A 2001 SCIENTIFIC PAPER PUBLISHED BY WASHINGTON UNIVERSITY BRAIN IMAGING PIONEER MARCUS RAICHLE.

(act) :37 o/c forget yourself

It represents, as best we know, a group of functions that are very
much self-referential. Other parts of it have to do with making
judgments about the value of information that comes, not only from
our body but from the world around us: “Is this good, bad or indifferent?
Do I like it or I don’t?” And a lot of this is non-conscious. I’ve kind
of whimsically come to view this issue of its decrease in activity
along the lines of the notion that when I engage in very focused
activities, I, in a sense, lose myself in my work. If you really
engage in something, you kind of forget yourself.
ALTHOUGH RAICHLE HAS FOUND THAT THE DEFAULT MODE NETWORK BECOMES LESS ACTIVE WHEN WE DEVOTE OUR ATTENTION TO A PARTICULAR TASK, IT DOESN’T SEEM TO WORK THAT SAME WAY IN DEPRESSED PEOPLE. SHELINE PUT PEOPLE INTO MRI SCANNERS AND ASKED THEM TO LOOK AT SOME EMOTION-EVOKING PICTURES.

(act) :16 o/c on them

If they were supposed to deactivate, they didn’t deactivate as
much, so the activity was higher. They weren’t able to shut all
the way down in the way that a normal person could. And then,
if it was an emotionally active area, like amygdala, they were
more active, so the emotion had a larger effect on them.

SHELINE SAYS THIS STUDY DEMONSTRATES THAT THE BRAIN IS ACTIVE IN DIFFERENT WAYS IN DEPRESSED PEOPLE THAN IN THOSE WHO AREN’T DEPRESSED. NOW, SHE’S TRYING TO LEARN WHETHER THAT MIGHT BE REVERSIBLE. SHE’S LOOKING AGAIN AT THE BRAINS OF DEPRESSED PEOPLE AFTER THEY RECEIVE TREATMENT WITH ANTIDEPRESSANT DRUGS, AND SHE PLANS TO STUDY BRAIN ACTIVITY IN DEPRESSED PEOPLE WHO RECEIVE TALK THERAPY CALLED COGNITIVE BEHAVIOR THERAPY.

(act) :19 o/c of thinking

They’re kind of obsessing about this and turning it over and
over. Potentially, if you could stop that – teach people “stop!”
and stop the rumination – the hope would be that you could actually
deactivate some of these brain areas that are overactive and
keeping the person embroiled in this kind of thinking.

SHELINE, RAICHLE AND THEIR COLLEAGES REPORT THEIR FINDINGS ON-LINE IN THE EARLY EDITION OF THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. I’M JIM DRYDEN…

RUNS 2:51

SCIENTISTS USED TO THINK THAT WHEN WE WEREN’T DOING MUCH, OUR BRAINS WERE RESTING, TOO. THEY DON’T THINK THAT ANYMORE. A FEW YEARS AGO, WASHINGTON UNIVERSITY NEUROSCIENTISTS IDENTIFIED A NETWORK OF BRAIN REGIONS THAT’S ACTIVE WHEN WE’RE NOT, AND BECOMES LESS ACTIVE WHEN WE DEVOTE OUR ATTENTION TO A PARTICULAR TASK. BUT THAT SO-CALLED DEFAULT MODE NETWORK DOESN’T SEEM TO WORK THE SAME WAY IN DEPRESSED PEOPLE. WASHINGTON UNIVERSITY PSYCHIATRIST YVETTTE SHELINE PUT PEOPLE INTO MRI SCANNERS AND ASKED THEM TO LOOK AT SOME EMOTION-EVOKING PICTURES. IN HEALTHY PEOPLE, MUCH OF THE DEFAULT NETWORK BECOMES LESS ACTIVE WHEN LOOKING AT AND THINKING ABOUT THOSE PICTURES. NOT SO, SHELINE SAYS, FOR DEPRESSED PEOPLE.

(act) :12 o/c on them

If they were supposed to deactivate, they didn’t deactivate as
much. They weren’t able to shut all the way down. And then,
if it was an emotionally active area, like amygdala, they were
more active, so the emotion had a larger effect on them.

SHELINE AND COLLEAGUES, INCLUDING NEUROSCIENTIST MARCUS RAICHLE, WHO HELPED ORIGINALLY IDENTIFY THE DEFAULT NETWORK, REPORT THEIR FINDINGS ON-LINE IN THE EARLY EDITION OF THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. I’M JIM DRYDEN…

RUNS 1:00

MANY DISEASES TEND TO BE MORE VIRULENT WHEN THEY STRIKE EARLIER IN LIFE. THAT ALSO LOOKS TO BE THE CASE WITH ALCOHOL AND DRUG USE. A GOOD DEAL OF EVIDENCE SUGGESTS THAT WHEN A PERSON BEGINS DRINKING OR USING DRUGS AT A YOUNGER AGE, THEIR RISK FOR PROBLEMS AND DEPENDENCE INCREASES. A WASHINGTON UNIVERSITY RESEARCHER ADDRESSED THAT SUBJECT THIS MONTH AT THE ANNUAL GUZE SYMPOSIUM ON ALCOHOLISM. JIM DRYDEN HAS THE STORY…

SCIENTISTS CONSISTENTLY FIND THAT PEOPLE WHO DRINK, SMOKE OR USE ILLICIT DRUGS AT YOUNGER AGES, TEND TO HAVE HIGHER RISKS FOR PROBLEMS AND DEPENDENCE LATER IN LIFE.

(act) :16 o/c of problems

I mean, there’s probably been the most work done in this area
with alcohol, but very similar findings have emerged for nicotine
and also for cannabis and other illicit drugs. The earlier the
age of onset, it does seem, the higher the risk for a range of
problems.

THAT’S WASHINGTON UNIVERSITY RESEARCHER MICHAEL LYNSKY. HE SPOKE ABOUT THE RISKS ASSOCIATED WITH EARLY USE AT THE GUZE SYMPOSIUM ON ALCOHOLISM, AN ANNUAL EVENT HOSTED BY WASHINGTON UNIVERSITY AND THE MIDWEST ALCOHOLISM RESEARCH CENTER. LYNSKEY SAYS HOW EARLY USE AFFECTS LATER PROBLEMS ISN’T EXACTLY CLEAR. SOME SCIENTISTS BELIEVE THAT WHEN A PERSON BEGINS DRINKING AT, SAY, AGE 16 RATHER THAN AGE 26, IT MAY CAUSE CHANGES IN THE DRINKER THAT INCREASE THE RISK FOR DEPENDENCE.

(act) :17 o/c develop dependence

And with the still-developing, adolescent brain being more sensitive
to the effects of alcohol and other drugs, exposure to those drugs
at a young age does something to the brain if you like, which makes
someone more vulnerable to develop dependence.

BUT TAKING A FIRST DRINK, OR LIGHTING UP A FIRST CIGARETTE OR JOINT MAY ALSO BE A SYMPTOM OF OTHER PROBLEMS. LYNSKEY SAYS IT’S POSSIBLE THAT EARLY USE MAY NOT ACTUALLY BE A CAUSE. FOR EXAMPLE, WHEN A 15-YEAR-OLD SMOKES MARIJUANA, THE VERY FACT THAT HE OR SHE CAN OBTAIN THE DRUG SAYS SOMETHING ABOUT THEIR ENVIRONMENTAL RISKS. HE SAYS GENETIC AND ENVIRONMENTAL FACTORS LINKED TO DEPENDENCE ALSO MAY PREDISPOSE A PERSON TO EARLY SUBSTANCE USE.

(act) :34 o/c of necessarily causal

People who initiate use at a young age are going to be characterized
by a number of factors, which may be both genetic and environmental.
If you’ve been brought up in a family environment characterized by,
perhaps, a lot of early stress, then that may predispose an individual
both to start using drugs at a young age and also predispose them to
subsequently developing dependence. And in that way, although early use
is a marker for risk, it’s not necessarily causal.

LYNSKEY SAYS BETTER UNDERSTANDING OF THE FACTORS THAT LEAD TO EARLY SUBSTANCE USE AND TO SUBSEQUENT DEPENDENCE MAY MAKE MORE EFFECTIVE THERAPIES POSSIBLE. HE SAYS THOSE THERAPIES ARE NEEDED, PERHAPS ESPECIALLY FOR THOSE PEOPLE WHO BEGIN USING AT AN EARLY AGE BECAUSE ALCOHOL AND DRUG PROBLEMS, LIKE OTHER ILLNESSES, CAN BE MORE VIRULENT WHEN THEY BEGIN EARLIER.

(act) :16 o/c more severe

The duration of dependence is longer. The number of symptoms is
higher. So it’s not just that they’re more likely to meet these
criteria that we have in the DSM but also that the course of that
disorder is likely to be more prolonged and more severe.

LYNSKEY WAS ONE OF SEVERAL SCIENTISTS TO LECTURE AT THIS YEAR’S GUZE SYMPOSIUM ON ALCOHOLISM. I’M JIM DRYEN…

RUNS 2:57

SCIENTISTS CONSISTENTLY FIND THAT PEOPLE WHO DRINK, SMOKE OR USE ILLICIT DRUGS AT YOUNGER AGES, TEND TO HAVE HIGHER RISKS FOR PROBLEMS AND DEPENDENCE. WASHINGTON UNIVERSITY RESEARCHER MICHAEL LYNSKY SAYS HOW EARLY USE AFFECTS LATER PROBLEMS ISN’T CLEAR. SOME SCIENTISTS BELIEVE THAT WHEN A PERSON BEGINS DRINKING AT, SAY, AGE 16 RATHER THAN AGE 26, IT MAY CAUSE CHANGES IN THE BRAIN THAT INCREASE THE RISK FOR DEPENDENCE. LYNSKEY SAYS IT’S ALSO POSSIBLE THAT ALTHOUGH EARLY DRINKING IS ASSOCIATED WITH LATER PROBLEMS, IT MAY NOT ACTUALLY CAUSE THEM. HE SAYS PERHAPS THE GENETIC AND ENVIRONMENTAL FACTORS LINKED TO DEPENDENCE ALSO PREDISPOSE A PERSON TO EARLY SUBSTANCE USE.

(act) :10 o/c of problems

Alcohol, nicotine and also for cannabis and other illicit drugs,
the earlier the age of onset, it does seem, the higher the risk
for a range of problems.

LYNSKEY SAYS BETTER UNDERSTANDING OF THE FACTORS THAT LEAD TO EARLY SUBSTANCE USE AND TO SUBSEQUENT DEPENDENCE MAY MAKE MORE EFFECTIVE THERAPIES POSSIBLE. I’M JIM DRYEN…

RUNS 1:00

THE PHOTORECEPTOR CELLS IN OUR EYES CONVERT LIGHT INTO VISION, BUT THEY CAN’T DO THAT WITHOUT HELP FROM MOLECULES CALLED PHOTOPIGMENTS. THOSE PIGMENTS ALLOW THE RODS AND CONES TO FUNCTION, AND THEY HAVE TO BE MADE AND RECYLCLED IN A HURRY, ESPECIALLY WHEN WE ENCOUNTER VERY BRIGHT LIGHT OR SUDDEN DARKNESS. WASHINGTON UNIVERSITY VISION RESEARCHERS HAVE FOUND A NEW PATHWAY IN THE EYE’S RETINA THAT QUICKLY RECYCLES THOSE MOLECULES. JIM DRYDEN HAS MORE…

THE NEWLY DISCOVERED PATHWAY INVOLVES THE PHOTORECEPTOR CELLS CALLED CONES. THEY PROVIDE OUR DAYLIGHT VISION AND OUR COLOR VISION. RODS, THE OTHER CLASS OF PHOTORECEPTORS, QUICKLY BECOME SATURATED BY LIGHT AND STOP WORKING ALTOGETHER IN BRIGHT LIGHT.THEY ALSO CAN TAKE A LONG TIME TO ADAPT TO DARKNESS. BUT CONES CONTINUE WORKING IN VERY BRIGHT LIGHT, ACCORDING TO WASHINGTON UNIVERSITY VISION RESEARCHER VLADIMIR KEFALOV. AND HE SAYS HIS TEAM WANTED TO LEARN HOW THOSE CELLS WERE ABLE TO DO THAT.

(act) :19 o/c all they need

A second, very important property of cones is their ability to
recover very quickly after exposure to really bright light, what
we call dark adaptation. The contrast between rods and cones is
striking. Rods can take up to an hour to dark adapt. Cones, in
contrast, dark adapt within several minutes. Three to five minutes
is all they need.

KEFALOV SAYS FOR MANY YEARS SCIENTISTS HAVE KNOWN ABOUT HOW SOME LIGHT-SENSING MOLECULES ARE RECYCLED WHEN THEY LEAVE THE RETINA AND TRAVEL TO ANOTHER PART OF THE EYE, CALLED THE PIGMENT EPITHELIUM. BUT THAT RECYCLINC PATHWAY ISN’T RAPID ENOUGH TO EXPLAIN HOW VISION WORKS IN VERY BRIGHT LIGHT OR HOW THE CONES CAN ADAPT TO DARKNESS SO QUICKLY. KEFALOV SAYS TRAVELLING TO AND FROM THE PIGMENT EPITHELIUM TAKES TOO LONG. HIS TEAM LOOKED AT A TYPE OF RETINAL CELLS CALLED MüLLER CELLS THAT SURROUND THE CONES. THEY ELIMINATED THE MüLLER CELLS WITH A TOXIC CHEMICAL AND FOUND THAT WITHOUT THE ACTIONS OF THOSE CELLS, THE CONES COULDN’T FUNCTION AS WELL IN BRIGHT LIGHT, NOR COULD THEY ADAPT TO DARKNESS AS QUICKLY WHEN THE LIGHT WAS REMOVED. THAT FINDING CONFIRMED THAT A SECOND PATHWAY IN THE RETINA SOMEHOW INVOLVED THOSE MüLLER CELLS. BUT THERE’S A CAVEAT TO THE FINDING. THAT ORIGINAL WORK WAS DONE IN SALAMANDER RETINAS.

(act) :29 o/c to study

The reason, mostly, is it’s a wonderful model. The photoreceptors
are much bigger, especially cones are much bigger and much more
robust than mammalian cones. And in fact, mouse cones have been
notoriously difficult to study physiologically because they are
only about 3 percent of the photoreceptors in the mouse retina.
So they are extremely hard to find, and they’re also very fragile.
The amphibians were just a wonderful starting point because those
photoreceptors have been extremely well characterized, and they are
relatively easy to study.

SO THE NEXT STEP WAS TO DEMONSTRATE THE SAME THING IN THE MOUSE RETINA, AND THAT’S EXACTLY WHAT KEFALOV’S TEAM DID. HE SAYS THE NEXT STEPS INVOLVE REPEATING THESE EXPERIMENTS IN PRIMATE AND HUMAN RETINAS, AND IF THE SECOND VISIUAL PATHWAY CAN STILL BE FOUND, HE SAYS IT MAY BE POSSIBLE TO USE THAT SECOND VISUAL PATHWAY TO TREAT AND IMPROVE SOME POTENTIALLY BLINDING RETINAL DISEASES.

(act) :11 o/c of diseases

So it provides better understanding to the human diseases
that affect the retina, including macular degeneration, and
on the other hand, potentially it opens opportunities for
treatment of diseases.

BUT FIRST THINGS FIRST. KEVALOV IS CURRENTLY LAUNCHING MORE STUDIES TO BETTER CHARACTERIZE WHAT’S GOING ON IN THAT SECOND PATHWAY IN THE RETINA. HE REPORTS HIS FINDINGS IN THE JOURNAL NATURE NEUROSCIENCE. I’M JIM DRYEN…

RUNS 2:57

THE NEWLY DISCOVERED PATHWAY INVOLVES PHOTORECEPTOR CELLS CALLED CONES. THEY PROVIDE OUR DAYLIGHT VISION. RODS, THE OTHER CLASS OF PHOTORECEPTORS, ARE FOR NIGHT VISION. THEY CAN QUICKLY BECOME SATURATED BY LIGHT AND CAN TAKE A VERY LONG TIME TO ADAPT TO DARK. BUT CONES CONTINUE WORKING IN VERY BRIGHT LIGHT AND QUICKLY ADAPT TO DARKNESS, ACCORDING TO WASHINGTON UNIVERSITY VISION RESEARCHER VLADIMIR KEFALOV. KEFALOV SAYS FOR MANY YEARS, SCIENTISTS HAVE KNOWN ABOUT HOW LIGHT-SENSING MOLECULES ARE RECYCLED WHEN THEY LEAVE THE RETINA AND TRAVEL TO ANOTHER PART OF THE EYE, CALLED THE PIGMENT EPITHELIUM. BUT WORKING IN SALAMANDER RETINA’S KEFALOV’S TEAM HAS FOUND THAT THERE’S ANOTHER RECYCLING PATHWAY IN THE RETINA ITSELF.

(act) :11 o/c of diseases

So it provides better understanding to the human diseases
that affect the retina, including macular degeneration, and
on the other hand, potentially it opens opportunities for
treatment of diseases.

KEFALOV ALSO DEMONSTRATED THAT THE PATHWAY EXISTS IN THE MOUSE RETINA, AND HE’S LOOKING IN PRIMATES AND HUMANS, TOO. I’M JIM DRYEN…

RUNS :59

OXYGEN IS ESSENTIAL TO LIFE. A LACK OF OXYGEN, CALLED HYPOXIA CAN DAMAGE CELLS AND EVEN KILL THEM. BUT SOME CELLS AND EVEN SOME ANIMALS HAVE FIGURED OUT HOW TO SURVIVE WITH LESS OXYGEN. RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS NOW HAVE IDENTIFIED PATHWAYS THAT ALLOW MICROSCOPIC WORMS TO SURVIVE IN A LOW-OXYGEN ENVIRONMENT. JIM DRYDEN REPORTS…

THE RESEARCH TEAM MANIPULATED GENES IN A WORM CALLED C. ELEGANS TO STUDY HOW THOSE GENES AFFECTED THE ANIMALS’ RESPONSE TO LOW OXYGEN, OR HYPOXIA. WASHINGTON UNIVERSITY NEUROBIOLOGIST MICHAEL CROWDER…

(act) :21 o/c lack oxygen

The reason why we’re studying hypoxia is that there’s major disease
processes where hypoxia is the primary problem, and those disease
processes are stroke and myocardial infarction. So in stroke and
myocardial infarction, cells die because they lack oxygen.

SO IF IT WERE POSSIBLE TO FIGURE OUT HOW SOME CELLS CAN SURVIVE WITH LESS OXYGEN, IT MIGHT BE POSSIBLE TO PREVENT SOME OF THE DAMAGE CAUSED BY STROKE AND HEART ATTACK. IN THIS STUDY, CROWDER IDENTIFIED A GENE RELATED TO THE MANUFACTURE OF NEW PROTEINS IN CELLS. ALTERING THE GENE MADE THE ANIMALS RESISTANT TO HYPOXIA. IN FACT, CUTTING PROTEIN BUILDING ABOUT IN HALF ALLOWED THE WORMS TO SURVIVE FOUR TIMES LONGER.

(act) :21 o/c modulate therapeutically

So us finding this gene, in and of itself, was not terribly
surprising. What was surprising is how big a “bang for your
buck” you get. Overall, it’s really a quite healthy animal.
Yet, it’s hypoxia resistant. That gives us hope that this pathway
really could be modulated therapeutically.

CROWDER SAYS IT MAY BE THAT THE PROCESS OF PROTEIN SYNTHESIS, CALLED TRANSLATION, USES LOTS OF ENERGY AND THUS NEEDS LOTS OF OXYGEN, SO ALTERING A GENE INVOLVED IN THAT PROCESS WOULD MEAN THAT THE WORM SIMPLY NEEDED LESS OXYGEN. BUT HE SAYS HE THINKS THERE’S MORE TO IT THAN THAT. A SECOND EXPERIMENT IN THE WORMS SHOWED THAT A PROCESS CALLED PROTEIN FOLDING ALSO IS IMPORTANT. WHEN PROTEINS ARE MADE, THEY MUST BE FOLDED INTO THE PROPER SHAPES SO THAT THEY CAN INTERACT WITH OTHER PROTEINS AND PERFORM VARIOUS FUNCTIONS IN A CELL.
(act) :16 o/c fold them

Hypoxia generates unfolded proteins. Perhaps the reason for
that is that protein folding is a very energetically, energy-
requiring process, and so it might be that the reason that you
get unfolded proteins is you just don’t have enough energy to
fold them.

IF THOSE ARE TOXIC, THEN CROWER SAYS ELIMINATING UNFOLDED PROTEINS MIGHT HELP CELLS SURVIVE, EVEN WITH LESS OXYGEN.

(act) :15 o/c what we saw

So what we predicted was if you mutate that process, the
unfolded protein response, that that would reduce the level
of resistance. And that’s what we saw.

CROWDER SAYS THE ABILITY TO PERHAPS ALTER A CELL’S UNFOLDED PROTEIN RESPONSE IS WHAT GIVES THESE DISCOVERIES THE BEST THERAPEUTIC POTENTIAL.

(act) :12 o/c therapeutic potential

Any time you can target process that’s induced by the disease process –
the response is induced by hypoxia – I think it has more therapeutic
potential.

BUT CROWDER SAYS MUCH WOR REIMANS BEFORE ANY HUMAN THERAPIES ARE POSSIBLE. HE REPORTED HIS FINDINGS IN THE JOURNAL SCIENCE. I’M JIM DRYEN…

RUNS 2:57

THE RESEARCH TEAM MANIPULATED GENES IN A WORM CALLED C. ELEGANS TO STUDY HOW THOSE GENES AFFECTED THE ANIMALS RESPONSE TO LOW OXYGEN, OR HYPOXIA. IN HEART ATTACK AND STROKE, CELLS DIE BECAUSE THEY DON’T GET ENOUGH OXYGEN. IN THE WORM, WASHINGTON UNIVERSITY NEUROBIOLOGIST MICHAEL CROWDER FOUND THAT A GENE RELATED TO THE MANUFACTURE OF NEW PROTEINS MADE THE ANIMALS RESISTANT TO HYPOXIA. IN FACT, CUTTING PROTEIN BUILDING ABOUT IN HALF ALLOWED THE WORMS TO SURVIVE FOUR TIMES LONGER IN LOW OXYGEN.

(act) :16 o/c modulate therapeutically

So us finding this gene, in and of itself, was not terribly
surprising. What was surprising is how big a “bang for your
buck” you get. That gives us hope that this pathway really
could be modulated therapeutically.

CROWDER SAYS THERAPIES MIGHT MAKE IT POSSIBLE FOR BRAIN CELLS OR HEART CELLS TO SURVIVE WITH LESS OXYGEN IN ORDER TO LIMIT DAMAGE FROM HEART ATTACK OR STROKE, BUT HE SAYS MUCH WORK REMAINS BEFORE SUCH THERAPIES BECOME A POSSIBILITY. I’M JIM DRYEN…

RUNS :59

A HERNIATED DISC IN THE NECK CAN CAUSE PAIN, NUMBNESS AND WEAKNESS. AND SPINE SURGEONS NORMALLY TRY TO RELIEVE THOSE SYMPTOMS BY REMOVING THE OFFENDING DISC AND THEN FUSING THE BONES TOGETHER AT THAT LOCATION IN THE SPINE. BUT NOW SPINE SUREGONS AT WASHINGTON UNIVERSITY AND AROUND THE COUNTRY HAVE BEEN STUDYING AN ARTIFICIAL DISC REPLACEMENT, AND THE RESULTS LOOK PROMISING. JIM DRYDEN HAS MORE…

NECK PAIN CAN BE A SIGN OF DISC DISEASE. SO CAN NUMBNESS IN THE FINGERS OR WEAKNESS IN THE ARMS. WASHINGTON UNIVERSITY CERVICAL SPINE SPECIALIST DAN RIEW RECOMMENDS PEOPLE WITH THOSE SYMPTOMS TRY EVERY OTHER OPTION BEFORE CONSIDERING SURGERY, BUT HE SAYS WHEN SURGERY IS UNAVOIDABLE, SOME PATIENTS MAY HAVE A NEW ALTERNATIVE. RIEW IS PART OF A NATIONAL TEAM THAT HAS BEEN STUDYING AN ARTIFICIAL DISC CALLED THE BRYAN CERVICAL DISC. IN MORE THAN 450 PATIENTS, THE SPONGY REPLACEMENT DISC WAS COMPARED TO SPINAL FUSION SURGERY, WHERE A DISEASED DISC IS REMOVED, AND THE BONES IN THE SPINE ARE FUSED TOGETHER.

(act) :23 o/c their motion

Half the people got the artificial disc. Half the people got fusion.
And what we found was that the patients who got the artificial
disc replacement either did equally as well as the patients who got
the fusion, or they did a little bit better. And the interesting
thing is that – and the most important thing, actually – is that
they were able to preserve all of their motion.

RIEW SAYS THOSE WHO GOT ARTIFICIAL DISCS ALSO RECOVERED MORE QUICKLY.

(act) :22 o/c to go

They tended to recover much faster. They didn’t require a
neck brace. If they had work, they returned to work faster.
And they often had resolution or their pain faster than
the patients who got the fusion because with a fusion,
you have to wait until the bone is fully incorporated, but
with an artificial disc replacement, as soon as that disc
is in, it’s good to go.

RIEW SAYS PATIENTS WITH ARTHRITIS PROBABLY ARE NOT GOOD CANDIDATES FOR AN ARTIFICIAL DISC. THE IDEAL PATIENTS, HE SAYS, WOULD BE THOSE WHO ARE YOUNGER AND ACTIVE.

(act) :29 o/c other levels

Say, somebody who is in their twenties and ruptures a disc and
has absolutely no arthritis. If we fuse that individual, then
the fusion adds a little bit of stress to the levels above and
below, makes it break down a little bit faster than it normally
would, and so that person – you know, 20 or 30 years down the line — is more likely to be looking at another operation. The hope with
an artificial cervical disc replacement is that since it doesn’t
take away motion, it doesn’t add any stress to the other levels.

THE BRYAN DISC IS ONE OF THREE DISC REPLACEMENT OPTIONS AVAILABLE. BUT RIEW SAYS THOSE DISCS AREN’T REALLY OPTIONS FOR MANY PATIENTS BECAUSE OF INSURANCE RESTRICTIONS. AND IF A PATIENT HAS TO HAVE SURGERY, RIEW SAYS IT’S PROBABLY BETTER THAT THEY GET IT DONE SOONER, RATHER THAN HOPING THEIR INSURANCE CARRIER MIGHT COVER THE ARTIFICIAL DISC PROCEDURE AT SOME POINT IN THE FUTURE.

(act) :17 o/c too long

Let’s say you had constant numbness in your thumb and index
finger on the right hand, but you said, “I’m going to wait
until insurance approves that artificial disc replacement.”
Let’s say it doesn’t happen for two years. At that point,
the artificial disc replacement, or even a fusion, is not
going to do anything for you because you’ve waited too long.

RIEW AND THE OTHER SURGEONS PARTICIPATING IN THE TRIAL REPORTED THEIR FINDINGS IN THE JOURNAL SPINE. I’M JIM DRYEN…

RUNS 2:50

WASHINGTON UNIVERSITY CERVICAL SPINE SPECIALIST DAN RIEW RECOMMENDS PEOPLE TRY EVERY OTHER OPTION BEFORE CONSIDERING SURGERY FOR DISC PROBLEMS IN THE NECK. BUT HE SAYS WHEN SURGERY CAN’T BE AVOIDED, IMPLANTING AN ARTIFICIAL DISC MAY BE A GOOD ALTERNATIVE FOR SOME PATIENTS. DISCS ARE LIKE SHOCK ABSORBERS BETWEEN THE BONES OF THE SPINE, AND RIEW HAS BEEN STUDYING AN ARTIFICIAL DISC CALLED THE BRYAN CERVICAL DISC TO SEE WHETHER REPLACING THE SPONGY DISC WITH THE ARTIFICIAL MATERIAL WILL WORK AS WELL AS REMOVING THE DISC AND FUSING VERTABRAE TOGETHER.

(act) :15 o/c their motion

The patients who got the artificial disc replacement either did
equally as well as the patients who got the fusion, or they did
a little bit better. And the most important things, actually, is
that they were able to preserve all of their motion.

RIEW SAYS PATIENTS WHO GOT ARTIFICIAL DISCS ALSO RECOVERED MORE QUICKLY AND WERE ABLE TO RETURN TO WORK SOONER THAN THOSE WHO RECEIVED FUSION SURGERY. I’M JIM DRYEN…

RUNS :57

ANTIDEPRESSANT DRUGS CALLED SSRIs NOT ONLY CAN HELP IMPROVE DEPRESSION, BUT THERE’S ALSO EVIDENCE SOME OF THOSE DRUGS CAN IMPROVE ANXIETY SYMPTOMS. ALMOST ONE IN 10 AMERICANS OVER 60 SUFFER FROM GENERALIZED ANXIETY DISORDER, AND A WASHINGTON UNIVERSITY MENTAL HEALTH RESEARCHER HAS FOUND THAT TREATMENT WITH AN SSRI DRUG CAN IMPROVE THEIR SYMPTOMS. JIM DRYDEN HAS THE STORY…

ALTHOUGH ANXIETY IS VERY COMMON IN OLDER ADULTS, MOST DON’T KNOW THEY HAVE A TREATABLE PROBLEM. WASHINGTON UNIVERSITY PSYCHIATRIST ERIC LENZE SAYS FOR PEOPLE WITH GENERALIZED ANXIETY DISORDER, WORRY IS A SERIOUS DIFFICULTY.

(act) :20 o/c anxiety attack

On average, it’s estimated that someone with Generalized
Anxiety Disorder spends about 40 hours a week worrying, so
in a sense it’s almost like having a full-time job spent
worrying. Certainly some patients with this problem, their
worries can evolve into a full-blown anxiety attack.

LENZE AND COLLEAGUES TREATED ANXIOUS PEOPLE OVER 60 WITH AN SSRI DRUG. AFTER 12 WEEKS, ABOUT TWO-THIRDS RESPONDED.

(act) :19 o/c itself causes

The kinds of things that older adults with this problem worry
about are their own health, their spouse’s health, problems
with disability, problems with finances, their children’s or
grandchildren’s status. Again, it’s the inability to put it
out of your mind and the amount of distress the worrying
itself causes.

ANXIETY DISORDERS CAN HARM QUALITY OF LIFE FOR OLDER PEOPLE AND MAKE IT HARDER FOR THEM TO FUNCTION DAY TO DAY. BUT LENZE SAYS MOST PEOPLE IN THIS STUDY RESPONDED WELL TO THE DRUG, WHICH IS KNOWN BY THE CHEMICAL NAME ESCITALOPRAM.

(act) :28 o/c of living

Sixty-eight percent of people who receive escitalopram
achieved response at some point during the study. The patients
who received escitalopram did better than those who received
placebo. So we found not only improvements in anxiety symptoms
and levels of worry but also in role functioning. So people felt
that they were less limited in their ability to carry our their
usual activities of living.

LENZE SAYS WORRY CAN CONTRIBUTE TO OTHER PROBLEMS, TOO. HE PREVIOUSLY HAD FOUND THAT OLDER ADULTS WITH GENERALIZED ANXIETY DISORDER ALSO TEND TO HAVE HIGHER LEVELS OF THE STRESS HORMONE CORTISOL, WHICH CAN AFFECT EVERYTHING FROM HEART DISEASE TO MEMORY FUNCTION. INTERESTINGLY, LENZE’S TEAM FOUND IN THIS STUDY THAT TREATMENT WITH THE SSRI DRUG IMPROVED BLOOD PRESSURE IN MANY PATIENTS.

(act) :24 o/c got better

We found that there was a greater drop, overall, in blood
pressure in folks receiving escitalopram than those who got
placebo. That blood pressure drop was, basically, entirely in
people who had high blood pressure to begin with. So if you
had normal blood pressure, the medication didn’t change that.
If you had high blood pressure, it got better.

LENZE SAYS THAT FINDING IS PRELIMINARY AND NEEDS MORE STUDY TO BE VERIFIED. HE IS NOW STUDYING WHETHER COMBINING THE DRUG WITH COGNITIVE BEHAVIOR THERAPY MIGHT IMPROVE THINGS EVEN MORE. HE REPORTED THESE FINDINGS IN THE JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION. I’M JIM DRYEN…

RUNS 2:47

IT WAS THE LARGEST STUDY TO LOOK AT THE ANTIDEPRESSANT DRUGS KNOWN AS SSRIs FOR TREATING OLDER ADULTS WITH GENERALIZED ANXIETY DISORDER. WASHINGTON UNIVERSITY PSYCHIATRIST ERIC LENZE AND COLLEAGUES GAVE ANXIOUS PEOPLE OVER 60 THE DRUG KNOWN AS LEXAPRO FOR 12 WEEKS, AND ABOUT TWO-THIRDS IMPROVED. LENZE SAYS THE THINGS THAT PEOPLE WITH THIS DISORDER WORRY ABOUT ARE NORMAL, BUT THE AMOUNT THEY WORRY IS NOT.

(act) :19 o/c itself causes

The kinds of things that older adults with this problem worry
about are their own health, their spouse’s health, problems
with disability, problems with finances, their children’s or
grandchildren’s status. Again, it’s the inability to put it
out of your mind and the amount of distress the worrying
itself causes.

THAT’S WHAT MAKES THE DISORDER SO POTENTIALLY DISABLING FOR OLDER PEOPLE. LENZE IS NOW STUDYING WHETHER COMBINING THE DRUG WITH COGNITIVE BEHAVIOR THERAPY MIGHT IMPROVE THINGS EVEN MORE. HE REPORTED THESE FINDINGS IN THE JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION. I’M JIM DRYEN…

RUNS :58

MOST BREAST CANCER DRUGS ATTEMPT TO REDUCE LEVELS OF THE HORMONE ESTROGEN, BUT A RESEARCH TEAM LED BY SITEMAN CANCER CENTER ONCOLOGISTS AT WASHINGTON UNIVERSITY AND BARNES-JEWISH HOSPITAL IN ST. LOUIS, REPORTS THAT IN SOME WOMEN WHOSE BREAST TUMORS HAVE SPREAD INTO OTHER PARTS OF THEIR BODIES, A DAILY DOSE OF ESTROGEN ACTUALLY MAY STOP TUMOR GROWTH AND EVEN CAUSE SOME TUMORS TO SHRINK. JIM DRYDEN REPORTS…

WHEN TUMOR CELLS SPREAD BEYOND THE BREAST, DRUGS SUCH AS TAMOXIFEN TEND TO KEEP THEM FROM GROWING BY LOWERING ESTROGEN LEVELS, BUT WASHINGTON UNIVERSITY ONCOLOGIST MATTHEW ELLIS SAYS AFTER MONTHS OR YEARS OF RESTRICTING ESTROGEN LEVELS, SOME TUMORS CAN BEGIN TO GROW AGAIN. AND AT THAT POINT, HE SAYS, IT MAY BE POSSIBLE TO TREAT THEM…WITH ESTROGEN. THE HORMONE WAS USED COMMONLY IN BREAST CANCER TREATMENT UNTIL ABOUT TWO DECADES AGO WHEN TAMOXIFEN BEGAN TO BE USED. BUT IN WOMEN WHOSE BREAST CANCER HAS METASTASIZED, OR SPREAD, INTO OTHER PARTS OF THE BODY, TUMORS CAN BEGIN TO GROW AGAIN EVEN IN AN ENVIRONMENT WHERE ESTROGEN LEVELS ARE VERY LOW. ELLIS SAYS SOME BASIC SCIENCE RESEARCHERS RECENTLY FOUND THAT REINTRODUCING ESTROGEN AT THAT POINT LOOKED LIKE A GOOD IDEA, AT LEAST IN THE TEST TUBE. SO ELLIS LED A MULTI-CENTER STUDY TO SEE WHETHER THE STRATEGY MIGHT WORK IN BREAST CANCER PATIENTS.

(act) :17 o/c preclinical findings

Breast cancer cells that had been grown in the near absence of
estrogen for long periods of time, estrogen would actually kill
them, those cells. And so we wanted to do a clinical trial to
address their preclinical findings.

ESTROGEN WASN’T AN ANSWER FOR EVERYONE, BUT IN SOME PATIENTS WHO HAD BEEN ON ESTROGEN-LOWERING DRUGS FOR MANY YEARS, ESTROGEN PILLS MADE A BIG IMPACT.

(act) :15 o/c tumor stabilizing

When you give those patients relatively low doses of estrogen –
which in this study was six milligrams daily – about a third of
the patients have very clear, clinical benefit from the therapy
with tumor regressions and tumor stabilizing.

ELLIS SAYS THE IDEA OF REINTRODUCING ESTROGEN MAY PROVIDE A NEW STRATEGY FOR TREATING WOMEN WITH METASTATIC BREAST CANCER.

(act) :30 o/c estrogen again

After the tumor progresses on the estrogen therapy, you can then
go back to the aromatase inhibitor therapy, and many patients
respond to the reintroduction of a drug that lowers estrogen levels.
So now you have an entirely new clinical strategy, where you first
use a drug that lowers estrogen levels. When the tumor becomes
resistant, you give estrogen so that you can then reuse the
aromatase inhibitor, and then when the aromatase inhibitor stops
working again, you can go back to estrogen again.

ELLIS SAYS CHEMOTHERAPY IS THE MOST COMMON TREATMENT IN THESE WOMEN, BUT FOR SOME, ESTROGEN MAY BE BETTER AT IMPROVING AND MAINTAINING QUALITY OF LIFE.

(act) :29 o/c tumor stabilizing

We’re not curing these ladies whether we give them chemotherapy
or endocrine manipulations, so the idea is to find ways to make
them feel better and to use drugs which don’t interfere with
quality of life. Chemotherapy always interferes with quality of
life, and so it’s a balance when you’re using those drugs. With
this hormonal manipulation approach, not only is it associated
with an improvement in their disease symptoms, but in addition,
there are some quality-of-life benefits.

FOR EXAMPLE, HOT FLASHES OR OTHER SYMPTOMS ASSOCIATED WITH LOW ESTROGEN MAY DISAPPEAR DURING TREATMENT. ELLIS REPORTED HIS FINDINGS LAST MONTH AT THE 31ST ANNUAL SAN ANTONIO BREAST CANCER SYMPOSIUM. I’M JIM DRYDEN…

RUNS 2:58

BEFORE THE DISCOVERY OF DRUGS LIKE TAMOXIFEN THAT LOWER ESTROGEN LEVELS, THE HORMONE ESTROGEN WAS USED COMMONLY TO TREAT BREAST CANCER. WASHINGTON UNIVERSITY ONCOLOGIST MATTHEW ELLIS SAYS IT MAY BECOME MORE COMMON WHEN TREATING WOMEN WITH METASTATIC BREAST TUMORS. CHEMOTHERAPY IS THE MOST COMMON TREATMENT IN THOSE WOMEN, BUT WHEN PRECLINICAL FINDINGS SHOWED ESTROGEN CPOULD KILL TUMOR CELLS IN THE TEST TUBE, ELLIS LED A MULTI-CENTER STUDY TO SEE WHETHER THE STRATEGY MIGHT WORK IN BREAST CANCER PATIENTS.

(act) :15 o/c tumor stabilizing

When you give those patients relatively low doses of estrogen –
which in this study was 6 milligrams daily – about a third of
the patients have very clear, clinical benefit from the therapy
with tumor regressions and tumor stabilizing.

ELLIS SAYS ESTROGEN TREATMENT DIDN’T WORK FOR EVERYONE, AND THESE FINDINGS STILL NEED TO BE REPLICATED IN MORE PATIENTS, BUT HE SAYS THE STRATEGY COULD IMPROVE QUALITY OF LIFE FOR SOME WOMEN WITH METASTATIC BREAST CANCER. HE REPORTED HIS FINDINGS LAST MONTH AT THE 31ST ANNUAL SAN ANTONIO BREAST CANCER SYMPOSIUM. I’M JIM DRYDEN…

RUNS 1:00

TOO MANY CALORIES, COMBINED WITH TOO LITTLE EXERCISE, IS A FORMULA FOR OBESITY WHETHER A PERSON LIVES IN AN URBAN CENTER OR A RURAL AREA, BUT RESEARCHERS AT WASHINGTON UNIVERSITY IN ST. LOUIS HAVE BEEN PAYING PARTICULAR ATTENTION TO SOME OF THE ISSUES THAT CONTRIBUTE TO OBESITY AMONG RURAL PEOPLE IN THE UNITED STATES. JIM DRYDEN HAS MORE…

PEOPLE IN SMALL TOWNS SPEND A LOT OF TIME IN THEIR CARS. THERE MAY NOT BE SIDEWALKS FOR WALKING OR BIKING. ACCESS TO FRESH FRUITS AND VEGETABLES ALSO MAY BE LIMITED. IT ISN’T THAT PEOPLE DON’T WANT TO EXERCISE OR TO EAT RIGHT, BUT ACTUALLY BEING PHYSICALLY ACTIVE OR EATING HEALTHY FOODS CAN BE DIFFICULT IN SOME RURAL COMMUNITIES, ACCORDING TO RESEARCHER ROSS BROWNSON, A FACULTY SCHOLAR AT WASHINGTON UNIVERSITY’S INSTITUTE FOR PUBLIC HEALTH.
(act) :25 o/c risk factors

Eating fast food led to about a 40 percent increased risk of
being obese. And another, important aspect was that having a
community that was pleasant for physical activity led to about
a 40 percent decreased risk of being obese. What’s important
about that is probably that we need to think broadly around the
entire community, not just about people’s individual-level risk factors.

ABOUT 30 PERCENT OF U.S. ADULTS ARE OBESE. THAT INCREASES THEIR RISK FOR PROBLEMS SUCH AS HIGH BLOOD PRESSURE, TYPE 2 DIABETES, HEART DISEASE AND STROKE. SO FINDING WAYS TO HELP PEOPLE MAKE HEALTHIER CHOICES COULD HAVE A BIG IMPACT ON PUBLIC HEALTH. BROWNSON STUDIED MORE THAN 1200 RANDOMLY SELECTED ADULTS IN 12 RURAL COMMUNITIES IN MISSOURI, ARKANSAS AND TENNESSEE. HE FOUND THAT LIMITED ACCESS TO HEALTHY FOODS AND OPPORTUNITIES TO EXERCISE DIDN’T NECESSARILY CAUSE PEOPLE TO BECOME OBESE, BUT HE SAYS PROBLEMS IN THE COMMUNITY ARE RELATED.
(act) :18 o/c healthy foods

Often eating at buffets led to about a 50 percent increased risk
of being obese in these rural communities. It’s important for
people to think about what a buffet means. It usually means
people use multiple plates and they fill up, sometimes multiple
times, and aren’t always eating the most healthy foods.

BUFFETS, WHERE MANY PEOPLE WILL CONTINUE TO EAT LONG AFTER THEIR APPETITE HAS SUBSIDED.
(act) :23 o/c buffet dinner

The human species is one of the few species on earth that will
still eat when we’re not hungry. Most other animals only eat
when they’re hungry, and I think the buffet is a good example
of where we’re over-stuffing ourselves when we’re eating when
we’re not hungry. And so it’s just something people should pay
attention to. It doesn’t mean that you should never eat at a
buffet, but try not to eat three-days-worth of a meal in one
sitting at a buffet dinner.

BROWNSON SAYS THIS STUDY POINTS OUT HOW IMPORTANT IT IS TO MAKE IT EASIER FOR PEOPLE TO MAKE HEALTHY CHOICES.
(act) :29 o/c local level

I like to think about a quote I like from the World Health
Organization: We need to make the healthy choice the easy
choice. What we’ve done so much in society is made being
healthy difficult. Making it more difficult to find fresh
fruits and vegetables or making it more difficult to walk
to work or to go to a bike ride after dinner in the evening.
And so we need to take better account of that, and I think
especially for this sort of issue, local policy, zoning
policy for example, can have a huge impact on people’s health
risks at the local level.

BROWNSON PUBLISHED HIS FINDINGS IN THE DECEMBER ISSUE OF THE JOURNAL PREVENTIVE MEDICINE. I’M JIM DRYDEN…

RUNS 2:50

IT ISN’T THAT PEOPLE DON’T WANT TO EXERCISE OR TO EAT HEALTHY FOODS, BUT ACTUALLY BEING PHYSICALLY ACTIVE OR EATING RIGHT CAN BE DIFFICULT IN MANY RURAL COMMUNITIES, ACCORDING TO RESEARCHER ROSS BROWNSON, A FACULTY SCHOLAR AT WASHINGTON UNIVERSITY’S INSTITUTE FOR PUBLIC HEALTH. BROWNSON STUDIED MORE THAN 1200 RANDOMLY SELECTED ADULTS IN 12 RURAL COMMUNITIES IN MISSOURI, ARKANSAS AND TENNESSEE,
(act) :20 o/c risk factors

Eating fast food led to about a 40 percent increased risk of
being obese. Having a community that was pleasant for physical
activity led to about a 40 percent decreased risk of being
obese. We need to think broadly around the entire community,
not just about people’s individual-level risk factors.

MANY OF THOSE SURVEYED REPORTED THAT THEY HAD LIMITED ACCESS TO FRUITS AND VEGETABLES. THEY ALSO WERE LIKELY TO THINK OF THEIR COMMUNITY AS UNPLEASANT FOR PHYSICAL ACTIVITY. BROWNSON PUBLISHED HIS FINDINGS IN THE DECEMBER ISSUE OF PREVENTIVE MEDICINE. I’M JIM DRYDEN…

RUNS 1:00

GLAUCOMA INVOLVES DEGENERATION OF THE OPTIC NERVE THAT CAN RESULT IN VISION LOSS AND BLINDNESS. TREATMENT IS ALWAYS DESIGNED TO LOWER PRESSURE IN THE EYE, AND DOCTORS AT WASHINGTON UNIVERSITY AND BARNES-JEWISH HOSPITAL IN ST. LOUIS ARE USING A NEW, LESS-INVASIVE SURGICAL DEVICE THAT LEAVES GLAUCOMA PATIENTS WITH SHORTER RECOVERY TIMES. JIM DRYDEN REPORTS…

THE SURGICAL DEVICE IS CALLED A TRABECTOME. WASHINGTON UNIVERSITY GLAUCOMA SPECIALISTS CARLA SIEGFRIED AND EDWARD BARNETT ARE USING THE TRABECTOME AS PART OF THEIR ARSENAL TO LOWER EYE PRESSURE IN PATIENTS WITH GLAUCOMA. SIEGFRIED SAYS ALL GLAUCOMA THERAPIES, FROM TOPICAL EYE DROPS TO LASERS TO SURGERY, WORK BY LOWERING PRESSURE IN THE EYE.

(act) :13 o/c our treatment

In most cases, but not all, the pressure inside the eye is the
culprit for this condition. And it’s always – at least at this
point in time – always the focus of our treatment.

SIEGFRIED SAYS EYE DROPS CAN LOWER PRESSURE VERY WELL IN THE EYE, BUT THEYAREN’T THE SOLUTION FOR EVERYONE. SOME PATIENTS CAN’T TOLERATE THE DROPS, AND OTHERS DON’T GET A GREAT ENOUGH REDUCTION IN PRESSURE TO MAKE A DIFFERENCE. THAT’S WHEN LASER TREATMENT AND SURGERY BECOME OPTIONS.

(act) :21 o/c advanced damage

Anyone in whom the treatment target is not reached by medications
or laser can be a candidate for surgery, so you do not have to
have severe damage. In fact, we like to catch people before they
have severe damage. But oftentimes, those individuals who end up
in the operating room are those who have more advanced damage.

SHE SAYS TRADITIONAL SURGERY IS DESINGED TO HELP GET FLUID OUT OF THE EYE AND ABSORBED BACK INTO THE SYSTEM. THE THEORY IS THAT TOO MUCH FLUID CAUSES PRESSURE TO RISE, SO GETTING THE FLUID OUT OF THE EYE WILL LOWER THE PRESSURE. SHE SAYS THE NEW TRABECTOME DEVICE OPERATES ON THE SAME PRINCIPLE, BUT UNLIKE TRADITIONAL SURGERY, IT ENHANCES THE EYE’S NATURAL DRAINAGE MECHANISM.

(act) :20 o/c electrical ablation

The Trabectome instrument is a new instrument that allows us to
actually remove the tissue that is causing resistance from the
fluid to exit the eye. So this tissue, the trabecular meshwork,
is removed by this instrument by ablation, by electrical ablation.

SIEGFRIED SAYS THE TRABECTOME DEVICE IS KIND OF LIKE OPENING A CLOGGED DRAIN, WHEREAS TRADITIONAL GLAUCOMA SURGERY IS MORE LIKE INSTALLING A NEW DRAINAGE SYSTEM.

(act) :19 o/c as well

The benefit of this procedure is that we’re looking at it in
a more physiological way. Rather than making a new drainage
output, we’re utilizing what nature gave us. And in that way,
it has less risk. It’s a more rapid procedure, with much more
rapid recovery time as well.

SHE SAYS IT CAN TAKE SEVERAL WEEKS TO RECOVER FROM STANDARD GLAUCOMA SURGERY, BUT AFTER THE NEW TECHNIQUE, PATIENTS RESUME NORMAL ACTIVITY IN ABOUT A WEEK. BUT IT’S NOT FOR EVERYBODY.

(act) :24 o/c of vision

This procedure does not give the same level of pressure
lowering. So not all patients are good candidates for this
procedure. It’s really the level of the disease that oftentimes
allows us to do this more simple procedure. Neither of these
procedures provide an improvement of vision. Our goal is to
stabilize their level of vision.

SIEGFIRED SAYS THE TRABECTOME IS BECOMING MORE POPULAR AT EYE CENTERS AROUND THE COUNTRY, AND SHE SAYS THE NUMBER OF CENTERS USING THE PROCEDURE HAS DOUBLED OVER THE PAST YEAR. I’M JIM DRYDEN…

RUNS 2:57

THE SURGICAL DEVICE IS CALLED A TRABECTOME. WASHINGTON UNIVERSITY GLAUCOMA SPECIALISTS CARLA SIEGFRIED AND EDWARD BARNETT ARE USING THE DEVICE TO LOWER EYE PRESSURE IN SOME PATIENTS WITH GLAUCOMA. SIEGFRIED SAYS WHERE TRADITIONAL GLAUCOMA SURGERY CREATES A NEW DRAINAGE SYSTEM IN THE EYE, THE TRABECTOME DEVICE WORKS BY ENHANCING FLUID DRAINAGE ALONG THE EYE’S NATURAL PATHWAY.

(act) :17 o/c as well

The benefit of this procedure is that we’re looking at it in
a more physiological way. Rather than making a new output,
we’re utilizing what nature gave us. And in that way, it has
less risk. It’s a more rapid procedure, with much more rapid
recovery time as well.

SIEGFRIED SAYS IT CAN TAKE SEVERAL WEEKS TO RECOVER FROM STANDARD GLAUCOMA SURGERY, BUT AFTER THE NEW TECHNIQUE, PATIENTS RESUME NORMAL ACTIVITY IN ABOUT A WEEK. SHE SAYS IT ALSO CARRIES A LOWER, LONG-TERM RISK OF INFECTION. BUT IT’S NOT FOR EVERYBODY. THE TRABECTOME WORKS BEST IN PATIENTS WHO DON’T NEED THEIR EYE PRESSURE LOWERED QUITE AS MUCH AS THOSE WHO NEED THE STANDARD SURGERY. I’M JIM DRYDEN…

RUNS :57

BRAIN CHANGES THAT ARE KEY TO ALZHEIMER’S DISEASE CAN DEVELOP MONTHS OR YEARS BEFORE THE DISEASE’S DEMENTIA AND COGNITIVE DECLINES ARE APPARENT. AND AN IMAGING TEST THAT CAN DETECT THOSE CHANGES HAS BOLSTERED THE IDEA THAT EDUCATION MAY HELP DELAY THE ONSET OF ALZHEIMER’S SYMPTOMS. JIM DRYDEN HAS THE STORY…

CAN PEOPLE WITH MORE ACTIVE INTELLECTUAL AND SOCIAL LIVES DELAY SOME OF THE SYMPTOMS OF ALZHEIMER’S DISEASE? PERHAPS, ACCORDING TO WASHINGTON UNIVERSITY ALZHEIMER’S RESEARCHER CATHY ROE. SHE SAYS THAT IN LOOKING AT THE BRAIN AFTER DEATH, MANY RESEARCHERS HAVE NOTICED THAT PEOPLE WITH ALZHEIMER’S DISEASE HAVE AMYLOID PLAQUES. IN FACT, THAT’S ONE OF THE WAYS THAT ALZHEIMER’S DISEASE IS DIAGNOSED. BUT SHE SAYS MANY PEOPLE WHO DIDN’T HAVE SYMPTOMS WHEN THEY DIED, DID HAVE PLAQUES IN THEIR BRAINS. SHE SAYS IT’S NOW POSSIBLE TO USE PET IMAGING TO FIND THOSE PLAQUES IN THE BRAIN OF A LIVING PERSON. AND HER TEAM HAS FOUND THAT PEOPLE WITH AND WITHOUT SYMPTOMS CAN HAVE PLAQUES IN THE BRAIN. SHE BOTH LOOKED AT BRAIN IMAGES AND CONDUCTED COGNITIVE TESTING ON OLDER ADULTS.

(act) :26 o/c dementia symptoms

The people who did not have plaques in their brain did really
well, and, basically, they were showing very few, if any, dementia
symptoms at all. But for people who did have plaques in their
brain, those people as a group were showing dementia symptoms,
and the degree to which they showed dementia symptoms depended
on how much education they had. So people who had more years of
education showed fewer dementia symptoms.

ALTHOUGH MOST PEOPLE WITH HIGH LEVELS OF AMYLOID PLAQUES DID POORLY ON COGNITIVE TESTS, THOSE WHO HAD DONE POST-GRADUATE WORK CONTINUED TO SCORE WELL IN THE TESTING. THEIR COGNITIVE ABILITIES HAD NOT DECLINED AS MUCH, AND THEY HAD NOT BECOME DEMENTED.
(act) :19 o/c watching TV

So education is one way of measuring that, but other ways of
measuring that are occupation, how intellectually active someone
is – so if they read the newspaper, if they read magazines, if they
do crossword puzzles. How socially engaged they are: do they get out?
Do they see friends and relatives? Or do they sit around watching TV?
ROE WANTS TO LOOK AT SOME OF THOSE THINGS IN FUTURE STUDIES, THE WAY SHE LOOKED AT EDUCATION LEVELS IN THIS STUDY. SHE SAYS IT WOULD BE NICE TO FIND OUT WHETHER PEOPLE COULD TAKE UP INTELLECTUAL PURSUITS AS A WAY TO FIGHT AGAINST ALZHEIMER’S.

(act) :20 o/c address that
We don’t know exactly what you can do when you’re an older adult
if that will help or not. But we do know that that’s just a healthy
way to live – to be intellectually active and take care of yourself.
So it can’t hurt, and I think in the next few years, you’ll start
to see results from studies that do address that.

ROE SAYS ALTHOUGH EDUCATION SEEMS TO BE RELATED TO A COGNITIVE RESERVE, NO ONE IS SURE EXACTLY HOW IT MIGHT HELP A PERSON AVOID THE SYMPTOMS OF ALZHEIMER’S DISEASE.

(act) :16 o/c dementia symptoms

But we do know that these things are associated with – things like
education and occupation and reading, and those sorts of things –
are associated with handling the plaques of Alzheimer’s disease
without showing dementia symptoms.

ROE SAYS THESE RESULTS BACK THE IDEA THAT WHEN IT COMES TO BRAIN FUNCTION, THERE MAY BE SOME TRUTH TO THE OLD CLICHÉ, “USE IT OR LOSE IT.” SHE REPORTED HER FINDINGS IN THE ARCHIVES OF NEUROLOGY. I’M JIM DRYDEN…

RUNS 2:54

THE IDEA IS THAT PEOPLE WITH MORE ACTIVE INTELLECTUAL AND SOCIAL LIVES MAY BE ABLE TO DELAY SOME OF THE SYMPTOMS OF ALZHEIMER’S DISEASE. WASHINGTON UNIVERSITY ALZHEIMER’S RESEARCHER CATHY ROE SAYS IT’S NOW POSSIBLE TO USE PET IMAGING TO FIND THE PLAQUES THE CHARACTERIZE ALZHEIMER’S DISEASE, AND SHE SAYS SOME PEOPLE WITH PLAQUES DON’T HAVE THE SAME COGNITIVE DECLINES THAT OTHERS WITH PLAQUES DEVELOP. THOSE PEOPLE WITH MILDER SYMPTOMS TEND TO HAVE MORE EDUCATION, SUPPORTING THE IDEA THAT USING YOUR BRAIN MORE MIGHT HELP PREVENT SOME OF THE SYMTPOMS OF ALZHEIMER’S.

(act) :13 o/c crossword puzzles

So education is one way of measuring that, but other ways of
measuring that are occupation, how intellectually active someone
is – so if they read the newspaper, if they read magazines, if
they do crossword puzzles.

ROE SAYS IT’S NOT CLEAR WHETHER PEOPLE CAN TAKE UP INTELLECTUAL ACTIVITIES TO PROTECT THEMSELVES. SHE PLANS TO LOOK AT THAT QUESTION IN FUTURE RESEARCH. ROE REPORTED THESE FINDINGS IN THE ARCHIVES OF NEUROLOGY. I’M JIM DRYDEN…

RUNS :57

RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS ARE PART OF A NEW STUDY USING BRAIN IMAGING TECHNIQUES IN INFANTS TO LOOK FOR CHANGES IN THE BRAIN THAT MAY CONTRIBUTE TO AUTISM. THE RESEARCHERS BELIEVE IDENTIYING BRAIN CHANGES MAY LEAD TO EARLIER DIAGNOSIS AND INTERVENTION IN CHILDREN WHO HAVE THE DISORDER. JIM DRYDEN REPORTS…

AS AUTISM RATES CONTINUE TO INCREASE, SCIENTISTS HAVE BEEN ASKING BOTH WHY THE NUMBER OF AUTISTIC CHILDREN HAS RISEN AND WHAT THEY CAN DO ABOUT IT. THIS STUDY, WHICH INVOLVES INVESTIGATORS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE, THE UNIVERSITY OF NORTH CAROLINA, THE UNIVERSITY OF WASHINGTON IN SEATTLE AND CHILDREN’S HOSPITAL OF PHILADELPHIA — AS WELL AS AN IMAGE-PROCESSING SITE AT THE MONTREAL NEUROLOGIC INSTITUTE — WILL LOOK AT THE BRAINS OF BABIES AS YOUNG AS 6 MONTHS OLD TO SEE WHETHER IT’S POSSIBLE TO DETECT CHANGES IN THE BRAIN THAT CAN CONTRIBUTE TO AUTISM, A CONDITION THAT FIRST APPEARS IN EARLY CHILDHOOD. CHILD PSYCHIATRIST KELLY BOTTERON IS THE LEAD INVESTIGATOR AT THE WASHINGTON UNIVERSITY STUDY SITE. SHE’LL BE LOOKING AT BABIES WHO HAVE A SIBLING WITH AUTISM BECAUSE THOSE CHILDREN ARE AT AN INCREASED RISK FOR DEVELOPING THE DISORDER.

(act) :17 o/c developing autism
We don’t know much about early brain development in children who
have autism, or children who are at risk for autism, but yet, we
know that the symptoms start very early. And so we think it’s going
to be very important for us to learn about what changes happen in
early brain development that are associated with developing autism.

BUT EVEN THOUGH THESE BABIES HAVE A BIGGER RISK THAN MOST, IT’S STILL TRUE THAT THE VAST MAJORITY WILL NOT DEVELOP AUTISM. BUT BOTTERON SAYS IT’S IMPORTANT TO LOOK AT THIS GROUP OF CHILDREN BECAUSE THE ODDS ARE THAT SOME WILL.

(act) :25 o/c develop autism
Siblings of children with autism do have a higher risk of
developing autism, and so we do expect that probably somewhere
around 10 to 15 percent of the infants will actually go on
to develop autism. And so we will have infants in the study
that will develop autism. And then we can contrast the
differences in brain development between the infants who are
at risk but do not develop autism and the infants who do
develop autism.

BOTTERON AND HER COLLEAGUES ALSO WILL STUDY SOME CHILDREN WHO DON’T HAVE AN AUTISTIC BROTHER OR SISTER. SHE’LL USE MRI, FUNCTIONAL MRI IMAGING AND ANOTHER NON-INVASIVE TECHNIQUE CALLED DIFFUSION-TENSOR IMAGING IN BABIES AT 6 MONTHS, 12 MONTHS AND 24 MONTHS OF AGE. THE BABIES SLEEP IN THE MRI MACHINES WHILE THE INVESIGATORS GET BRAIN IMAGES. BOTTERON SAYS THEY’LL BE LOOKING IN PARTICULAR AT THE SIZE OF THE BRAIN.

(act) :20 o/c developing autism
Just from looking at the records of pediatricians, looking at
head-circumference records of infants who go on to develop
autism, they end up with slightly larger head size compared
to, just healthy contrast subjects. So overall brain size is
definitely one issue that we have some pretty good evidence is
probably associated with developing autism.

ULTIMATELY, BOTTERON SAYS THE GOAL OF THE STUDY IS TO FIND WAYS TO IDENTIFY AUTISM AT AN EARLIER STAGE IN LIFE, WHEN INTERVENTIONS AND TREATMENTS MIGHT BE MORE EFFECTIVE.

(act) :12 o/c such risk
From all of the studies that have been done so far, the
earlier the age of intervention, the better the potential
outcome. And so, we definitely hope that the study will
provide markers to detect such risk.

BOTTERON SAYS A PILOT STUDY WENT VERY WELL, AND THE INVESTIGATORS FOUND THAT THEY COULD PUT HEADPHONES ON SLEEPING BABIES TO KEEP THEM FROM WAKING UP IN NOISY MRI MACHINES DURING THE TESTING. THE STUDY ALSO INVOLVES SOME CLINICAL EVALUATION TO LOOK FOR DELAYED DEVELOPMENT THAT ALSO MAY BE RELATED TO AUTISM. I’M JIM DRYDEN…

RUNS 3:00

IT’S THE FIRST STUDY THAT WILL LOOK PROSPECTIVELY AT BOTH THE ONSET OF AUTISM SYMPTOMS AND AT BRAIN CHANGES THAT MAY OCCUR IN AUTISM. CHILD PSYCHIATRIST KELLY BOTTERON IS THE LEAD INVESTIGATOR AT THE WASHINGTON UNIVERSITY STUDY SITE. SHE’LL USE MRI, FUNCTIONAL MRI IMAGING AND ANOTHER NON-INVASIVE TECHNIQUE CALLED DIFFUSION-TENSOR IMAGING IN BABIES AT 6 MONTHS, 12 MONTHS AND 24 MONTHS OF AGE. THE BABIES, WHO HAVE A SIBLING WITH AUTISM, SLEEP IN THE MRI MACHINES WHILE THE INVESIGATORS GET BRAIN IMAGES. BOTTERON SAYS THEY’LL BE LOOKING IN PARTICULAR AT THE SIZE OF THE BABIES’ BRAINS.

(act) :14 o/c developing autism

They end up with slightly larger head size compared to, just
healthy contrast subjects. So overall brain size is definitely
one issue that we have some pretty good evidence is probably
associated with developing autism.

OTHER CENTERS INVOLVED IN THIS STUDY INCLUDE THE UNIVERSITY OF NORTH CAROLINA, THE UNIVERSITY OF WASHINGTON IN SEATTLE AND CHILDREN’S HOSPITAL OF PHILADELPHIA. I’M JIM DRYDEN…

RUNS :58

RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS WANT TO LEARN WHETHER AN INTERNET-BASED PROGRAM CAN HELP VERY YOUNG CHILDREN LOSE WEIGHT. CHILDREN AS YOUNG AS 2 ARE BECOMING DANGEROUSLY OVERWEIGHT AND OBESE, SO THE RESEARCHERS SAY IT’S IMPORTANT TO INTERVENE AND TRY TO PREVENT BIGGER PROBLEMS DOWN THE ROAD. JIM DRYDEN HAS THE STORY…

RATES OF OBESITY, AND OF OBESITY-RELATED DISEASES, ARE ON THE RISE IN JUST ABOUT EVERY DEMOGRAPHIC GROUP IN AMERICA, EVEN IN VERY YOUNG CHILDREN. ABOUT ONE IN FIVE KIDS IN THE U.S. IS OVERWEIGHT NOW WASHINGTON UNIVERSITY RESEARCHERS ARE HOPING TO USE THE INTERNET TO TRY AND REVERSE THE TREND. OBESITY RESEARCHER DENISE WILFLEY SAYS IT’S IMPORTANT TO INTERVENE WHEN KIDS ARE STILL YOUNG TO PREVENT PROBLEMS LATER IN LIFE.

(act) :21 o/c positive effect

Because obesity tracks into, you know, through childhood and
into adolescence then into adulthood, with mounting medical
complications the older the person gets and the longer the
persistence of the overweight, that if we can intervene earlier
when patterns and habits haven’t had as long a period of time
to establish, then we’re going to have a much more positive
effect.

WILFLEY AND HER COLLEAGUES ARE STUDYING AN INTERNET-BASED INTERVENTION CALLED “FOOD FOR THOUGHT.” IT’S THE FIRST PROGRAM OF ITS KIND TO TARGET VERY YOUNG CHILDREN, BETWEEN THE AGES OF 2 AND 6. BUT SHE SAYS IT’S NOT THE FIRST TIME SHE HAS LOOKED AT HOW THE INTERNET CAN HELP PEOPLE DEVELOP HEALTHIER HABITS.

(act) :17 o/c this young

I’ve certainly done work in Internet-based delivery of
interventions for prevention of eating disorders and
treatment of overweight in adolescents. And there’s been
studies done looking at using Internet-based technologies
for treatment of overweight in adults, but none with
children this young.

WILFLEY SAYS THE INTERNET PROGRAM CONCENTRATES ON HELPING PARENTS OF YOUNG CHILDREN TO MAKE AND SUSTAIN DIETARY AND LIFESTYLE CHANGES.

(act) :26 o/c child behavior

The program consists of 12 sessions delivered over a 16-week
period of time, and it focuses on systematically helping them
with providing specific knowledge about diet and physical
activity but also helping them with behavior change strategies
that’s going to help the parent not only change their own
behavior in terms of eating activity and managing their weight,
but also to help with parenting skills around changing the
child behavior.

KIDS AND PARENTS ARE EVALUATED AT THE START AND THE FINISH OF A 16-WEEK STUDY PERIOD, THEN EVALUATED AGAIN SIX MONTHS LATER TO SEE WHETHER THEY’VE BEEN ABLE TO MAINTAIN POSITIVE CHANGES IN WEIGHT AND LIFESTYLE. BUT BETWEEN VISITS TO THE DOCTOR’S OFFICE, PARENTS AND CHILDREN MAKE REGULAR VISITS TO THE HOUSEHOLD SCALE.

(act) :35 o/c so well

You know, if it’s gone up, then they look at the week and
try to evaluate what behavior patterns may have contributed
to weight gain. If they stay the same, you know that’s great.
You know, if the child’s not gaining weight, what are the
behavior patterns that they’re engaging in that helps the
child stabilize their weight? Of if they’re losing weight,
what are those behaviors? And so that that sort of data
point, their body weight, becomes a way to evaluate how
well they’re doing with making the behavior changes, and it’s
not looked at in a punitive way but just in a way to kind
of, you know, brainstorm with the family about either what’s
potentially working or not working so well.

WILFLEY SAYS IF THE INTERNET-BASED PROGRAM WORKS, IT MAY PROVIDE A WAY TO HELP LOWER THE RATES OF OBESITY-RELATED ILLNESSES THAT OTHERWISE WOULD AFFECT THESE CHILDREN AS THEY GET OLDER. I’M JIM DRYDEN…

RUNS 2:55

OBESITY CONTRIBUTES TO DIABETES, HIGH BLOOD PRESSURE AND CERTAIN TYPES OF CANCER. EVEN AMONG CHILDREN, RATES OF OVERWEIGHT AND OBESITY HAVE SKYROCKETED. ABOUT ONE IN FIVE KIDS IN THE U.S. IS OVERWEIGHT. WASHINGTON UNIVERSITY RESEARCHERS ARE STUDYING AN INTERNET-BASED PROGRAM CALLED “FOOD FOR THOUGHT” DESIGNED TO HELP SLIM DOWN KIDS BETWEEN 2 AND 6. WASHINGTON UNIVERSITY RESEARCHER DENISE WILFLEY SAYS IT’S THE FIRST PROGRAM OF ITS KIND FOR CHILDREN THIS YOUNG, AND IT ACTUALLY TARGETS PARENTS.

(act) :17 o/c this young

I’ve certainly done work in Internet-based delivery of
interventions for prevention of eating disorders and
treatment of overweight in adolescents. And there’s been
studies done looking at using Internet-based technologies
for treatment of overweight in adults, but none with
children this young.

WILFLEY SAYS IF THE INTERNET-BASED PROGRAM CAN HELP THESE YOUNG CHILDREN KEEP THEIR WEIGHT UNDER CONTROL, IT MAY PROVIDE A STRATEGY THAT COULD HELP LOWER THE RATES OF OBESITY-RELATED ILLNESSES THAT OTHERWISE WOULD AFFECT THESE CHILDREN AS THEY GET OLDER. I’M JIM DRYDEN…

RUNS 1:00

NEUROSCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT LOWERING BRAIN TEMPERATURE IN A MOUSE CAN PROTECT THAT ANIMAL’S DEVELOPING BRAIN FROM DAMAGE RELATED TO ANESTHETIC DRUG EXPOSURE. THAT CAN BE A PROBLEM FOR YOUNG CHILDREN WHO FACE SURGERY. JIM DRYDEN REPORTS…

THE RESEARCHERS PREVIOUSLY HAD LEARNED THAT EXPOSURE TO ANESTHETIC DRUGS, ALCOHOL AND ANTICONVULSANT MEDICATIONS COULD DESTROY LARGE NUMBERS OF BRAIN CELLS. THE DRUGS HAD THEIR EFFECT DURING A PERIOD OF RAPID BRAIN DEVELOPMENT, WHICH IN HUMAN CHILDREN RUNS FROM A FEW MONTHS BEFORE BIRTH TO THE AGE OF 3 OR 4. MANY KIDS REQUIRE SURGERY DURING THOSE YEARS.

(act) :34 o/c anesthetic effects

There are infants that absolutely need to have surgery and need to
be anesthetized, and if anesthetic drugs have the property, or run
the risk, of causing nerve cells to die, that’s a real dilemma. The
approach that we have taken is to see if we can develop some methods
that would prevent cell death but would not prevent the anesthetic
drug from having its beneficial, anesthetic effects.

THAT’S WASHINGTON UNIVERSITY NEUROSCIENTIST JOHN OLNEY. SINCE HIS INITIAL FINDINGS OF POTENTIAL HARM CAUSED BY ANESTHESIA, HIS TEAM HAS BEEN LOOKING FOR WAYS TO PREVENT THAT CELL DEATH. HE SAYS IN MICE AT A SIMILAR STAGE OF BRAIN DEVELOPMENT, COOLING THE BRAIN SEEMS TO WORK WELL.

(act) :19 o/c only temporary

We aren’t sure at the present time whether the cooling of the
brain temporarily suppresses it, but that’s what we’re currently
working on, to determine for sure whether the protection is
permanent and complete or partial and only temporary.

OLNEY SAYS A DRAWBACK IS COOLING THE BRAIN ALSO STOPS SOME OF THE HEALTHY NEURONAL DEATH THAT OCCURS IN THE DEVELOPING BRAIN, WHERE THERE IS QUITE A BIT OF REDUNDANCY BUILT IN.
(act) :19 o/c anesthetic drug

We hope that we’re only temporarily interfering with the process
by which nerve cells are naturally eliminated from the brain because
they’re not useful, and permanently preventing nerve cells from
dying because of the anesthetic drug.

OLNEY ALSO HAS FOUND THAT TREATMENT WITH OTHER DRUGS CAN STAVE OFF SOME OF THE DAMAGE CAUSED BY ANESTHESIA EXPOSURE. HE SAYS MORE RESEARCH IS NEEDED, BUT HE BELIEVES IT MAY SOON BE POSSIBLE TO PREVENT SOME OF THE DEVELOPMENTAL PROBLEMS THAT CAN RESULT FROM ANESTHESIA EXPOSURE AMONG VERY YOUNG CHILDREN WHO NEED SURGERY. HE SAYS FOR NOW, HOWEVER, THE BEST ADVICE HE CAN GIVE PARENTS IS TO TRY TO AVOID ANY ELECTIVE SURGERY FOR A CHILD UNTIL THAT CHILD IS A BIT OLDER.

(act) :22 o/c should be

We don’t know exactly what age surgery would be definitely
safe, but we do believe that the first two years or so,
there’s much higher risk than four years after birth. So if
the surgery can be postponed, we think it should be.

OLNEY REPORTED HIS FINDINGS AT THE ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE. I’M JIM DRYDEN…

RUNS 2:50

THE RESEARCH TEAM PREVIOUSLY HAD FOUND THAT DURING BRAIN DEVELOPMENT, EXPOSURE TO ANESTHESIA CAN KILL LARGE NUMBERS OF BRAIN CELLS. SINCE THOSE INITIAL FINDINGS, THE RESEARCHERS HAVE BEEN INVESTIGATING STRATEGIES TO PREVENT THAT CELL DEATH. NOW WASHINGTON UNIVERSITY RESEARCHER JOHN OLNEY AND HIS TEAM HAVE COOLED THE BRAINS OF INFANT MICE AND FOUND THAT EXPOSURE TO ANESTHESIA NO LONGER DESTROYS HEALTHY, DEVELOPING BRAIN CELLS. HE SAYS A POTENTIAL PROBLEM, HOWEVER, IS THAT COOLING THE BRAIN ALSO STOPS NORMAL CELL DEATH TO ELIMINATE UNHEALTHY OR REDUNDANT BRAIN CELLS.

(act) :17 o/c anesthetic drug

We hope that we’re only temporarily interfering with the process
by which nerve cells are naturally eliminated from the brain and
permanently preventing nerve cells from dying because of the
anesthetic drug.

OLNEY REPORTED HIS FINDINGS RECENTLY AT THE ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE. I’M JIM DRYDEN…

RUNS :58

A CLASS OF DRUGS THAT’S USED TO SPEED LUNG DEVELOPMENT IN PREMATURE NEWBORNS MAY ALSO CONTRIBUTE TO DEVELOPMENTAL DELAYS BY DAMAGING A KEY BRAIN STRUCTURE. SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT THE DRUGS DAMAGE THE BRAINS OF NEWBORN MICE. JIM DRYDEN REPORTS…

IT ONCE WAS RELATIVELY COMMON FOR DOCTORS TO TREAT PREMATURE INFANTS WITH A CLASS OF DRUGS CALLED GLUCOCORTICOIDS. THE DRUGS HELPED THE LUNGS MATURE, BUT DOCTORS ALSO NOTICED THAT SOME CHILDREN WHO GOT THEM DEVELOPED COGNITIVE AND MOTOR DIFFICULTIES. SO MOST DOCTORS STOPPED GIVING THOSE DRUGS TO BABIES AFTER THEY WERE BORN, BUT MANY STILL GAVE THE DRUGS PRENATALLY FOR THOSE BABIES AT HIGH RISK FOR PREMATURE BIRTH. WASHINGTON UNIVERSITY NEUROSCIENTIST KEVIN NOGUCHI WANTED TO SEE WHETHER THE NEW STRATEGY WAS SAFER THAN THE OLD, SO HE TESTED THE DRUGS IN NEWBORN MICE.

(act) :16 o/c administered glucocorticoid

We took neonatal mouse pups and exposed them at an age that
would roughly correspond to that of the prematurely born infant.
We administered a clinically relevant dose of dexamethasone, the
most commonly administered glucocorticoid.

NOGUCHI SAYS THE WASHINGTON UNIVERSITY SCIENTISTS FOUND SELECTIVE DAMAGE IN BRAIN CELLS LOCATED IN THE CEREBELLUM.

(act) :20 o/c see clinically

Glucocorticoids are actually causing a very selective degeneration
in a region called the external granule layer of the cerebellum.
The cerebellum is thought to be involved in neuro-motor function.
The deficits that you see postnatally are also neuro-motor function
deficits, so this seems to correlate with what we see clinically.

HE SAYS ALTHOUGH THE CEREBELLUM IS LINKED PRIMARILY TO MOTOR FUNCTION, MANY CHILDREN TREATED WITH GLUCOCORTICOIDS ALSO DEVELOPED COGNITIVE PROBLEMS. THAT’S TO BE EXPECTED SAYS CO-INVESTIGATOR NURI FARBER. HE SAYS THE CEREBELLUM LINKS TO MANY OTHER PARTS OF THE BRAIN, SO ALTHOUGH DAMAGE IS DONE TO CELLS IN THE CEREBELLUM, THAT WON’T AUTOMATICALLY LIMIT THE EFFECTS OF THAT DAMAGE TO THE BRAIN FUNCTIONS THAT NORMALLY ARE ASSOCIATED WITH THE CEREBELLUM.

(act) :10 o/c the brain

The cerebellum projects to these other, cortical regions, and
so in knocking off your cerebellar neurons, the granular cells
in your cerebellum, you could be affecting cognitive function in
non-motor regions of the brain.

AND NOGUCHI SAYS THE CELLS THAT ARE DAMAGED BY GLUCOCORTICOIDS TEND TO BE THE CELLS RESPONSIBLE FOR MAKING NEW NEURONS IN THE BRAIN.

(act) :16 o/c neuro-developmental deficits

The type of cells that are damaged are called neural progenitor cells,
and so you could imagine how if you actually kill off the cells
responsible for producing new neurons during neurodevelopment, you
could cause severe neuro-developmental deficits.

NOGUCHI SAYS IT OFTEN IS THE CASE THAT THESE PREMATURE BABIES NEED DRUG THERAPY TO HELP THEIR LUNGS IN SPITE OF POTENTIAL RISKS CAUSED BY THE GLUCOCORTICOID TREATMENT. AND FARBER SAYS IT’S IMPORTANT TO REMEMBER THAT GLUCORTICOIDS AND OTHER STEROID DRUGS CAN BE VERY USEFUL AS TREATMENTS FOR INFLAMMATION AND OTHER DIFFICULTIES.

(act) :14 o/c lung function

The glucocorticoids, in addition, are drugs like prednisone. They’re
used for arthritis or inflammation, things like that, so there’s lots
of reasons why you might use prednisone or dexamethasone or other
glucocorticoids, not necessarily for maturing lung function.

FARBER AND NOGUCHI REPORTED THEIR FINDINGS RECENTLY AT NEUROSCIENCE 2008, THE ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE. I’M JIM DRYDEN…

RUNS 2:58

IT USED TO BE COMMON FOR DOCTORS TO TREAT PREMATURE INFANTS WITH A CLASS OF DRUGS CALLED GLUCOCORTICOIDS. THE DRUGS HELPED THE LUNGS MATURE, BUT DOCTORS ALSO NOTICED THAT SOME CHILDREN WHO GOT THE DRUGS DEVELOPED COGNITIVE AND MOTOR PROBLEMS. SO MOST STOPPED GIVING THEM TO BABIES AFTER THEY WERE BORN, BUT GAVE THE DRUGS PRENATALLY IN THOSE AT HIGH RISK FOR EARLY BIRTH. WASHINGTON UNIVERSITY NEUROSCIENTIST KEVIN NOGUCHI SAYS WHEN MICE WITH COMPARABLY DEVELOPED BRAINS GET THOSE DRUGS, THEY END UP WITH DAMAGE IN A BRAIN STRUCTURE CALLED THE CEREBELLUM.

(act) :13 o/c see clinically

The cerebellum is thought to be involved in neuro-motor function.
The deficits that you see postnatally are also neuro-motor function
deficits, so this seems to correlate with what we see clinically.

NOGUCHI SAYS THE DRUGS ARE WORTH THE RISK IN PREMATURE INFANTS WHO PROBABLY WOULDN’T SURVIVE WITHOUT THEM, BUT THE BEST IDEA WOULD BE TO DEVELOP DIFFERENT DRUGS THAT MIGHT HELP THE LUNGS BUT SPARE THE BRAIN. I’M JIM DRYDEN…

RUNS 1:00

ONE OF THE MAJOR SIDE EFFECTS OF PAIN THERAPIES IS ITCHING. PEOPLE WHO TAKE PAIN-KILLING DRUGS, SUCH AS MORPHINE, OFTEN FIND THEMSELVES SCRATCHING IN EXCHANGE FOR THEIR RELIEF FROM PAIN. MANY SCIENTISTS, BELIEVING THAT ITCH WAS A LESS INTENSE FORM OF PAIN, FIGURED THAT TRADE-OFF WAS UNAVOIDABLE, BUT NEW FINDINGS FROM PAIN RESEARCHERS AT WASHINGTON UNIVERSITY IN ST. LOUIS SUGGEST PAIN AND ITCH RESPONSES CAN BE SEPARATED. JIM DRYDEN REPORTS…

PREVIOUSLY, THE RESEARCHERS HAD IDENTIFIED A GENE SPECIFIC TO THE ITCH RESPONSE, CALLED GRPR. WHEN MICE GENETICALLY ENGINEERED WITHOUT GRPR ARE EXPOSED TO AN ITCHY STIMULUS, THEY DON’T SCRATCH THE SAME WAY AS THEIR LITTERMATES THAT HAVE THE GENE. WASHINGTON UNIVERSITY PAIN CENTER RESEARCHER ZHOU-FENG CHEN SAYS THE GRPR GENE IS IMPORTANT FOR ITCH RESPONSE BUT IS NOT RELATED TO PAIN.

(act) :11 o/c pain transmission

Very interesting. We found GRPR was very important for itch
sensation, but it’s not involved in pain transmission.

CHEN SAYS IT HAS BEEN DIFFICULT TO SEPARATE PAIN AND ITCH BECAUSE THE NEURONS THAT TRANSMIT BOTH ARE LOCATED IN THE SAME AREA OF THE SPINAL CORD, AND SINCE MOST SCIENTISTS HAVE BELIEVED THAT PAIN AND ITCH WERE REALLY TWO MANIFESTATIONS OF THE SAME RESPONSE, MANY ASSUMED THAT PAIN AND ITCH OPERATED THROUGH THE SAME PATHWAY IN THE NERVOUS SYSTEM. THERE ALSO WAS THE EVIDENCE THAT THE DRUGS THAT RELIEVED PAIN, SUCH AS MORPHINE, OFTEN LED TO ITCHING. IF YOU BELIEVE THAT ITCH IS A LESS SEVERE FORM OF PAIN, THEN ITCHING CAN SEEM LIKE EVIDENCE THAT A PAIN DRUG IS WORKING — LESSENING THE PAIN RESPONSE DOWN TO THE LEVEL OF AN ITCH. BUT CHEN TOOK HIS FINDINGS ABOUT THE ITCH GENE, GRPR, TO PROVE THAT ITCHING WAS A SIDE EFFECT OF PAIN DRUGS. HE GAVE MICE A DRUG CALLED AN ANTAGOINST THAT BLOCKED THE ACTIVITY OF GRPR AND THEN GAVE THE MICE MORPHINE. THE MICE GOT RELIEF FROM PAIN, WITHOUT THE ITCH.

(act) :16 o/c of morphine
If you give the GRPR antagonist to mice, this antagonist can
actually block the itching. However, this antagonist won’t
interfere with the analgesic effect of morphine.

CHEN SAYS PAIN AND ITCH WERE SEPARATED IN BOTH MICE WITHOUT THE GENE AND IN MICE TREATED WITH THE ANTAGONIST DRUG,

(act) :17 o/c be separated

The mice still show a normal analgesic effect, but they don’t
scratch. So this is very interesting because it actually is a
perfect example showing that the analgesic effect and the
itching pathway can be separated.

AND CHEN SAYS IT’S POSSIBLE A STRATEGY THAT INVOLVES BLOCKING THE ACTIVITY OF THE GRPR GENE IN THE SPINAL CORD ALSO MIGHT WORK IN HUMANS.

(act) :16 o/c itch pathway

The genetic pathway of the itching sensation is conserved between
all mammals. There is GRPR in the human, so it’s conceivable if you
block GRPR activity in the spinal cord, you may block the itch pathway.

HE REPORTED HIS FINDINGS AT NEUROSCIENCE 2008, THE ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE. I’M JIM DRYDEN…

RUNS 2:37

PREVIOUSLY, THE WASHINGTON UNIVERSITY RESEARCHERS HAD IDENTIFIED A GENE SPECIFIC TO ITCHING, CALLED GRPR. WHEN MICE GENETICALLY ENGINEERED WITHOUT GRPR ARE EXPOSED TO AN ITCHY STIMULUS, THEY DON’T SCRATCH THE SAME WAY THEIR LITTERMATES DO. NOW PAIN CENTER RESEARCHERS ZHOU-FENG CHEN HAS FOUND THAT WHEN MICE WITHOUT THE GENE, OR MICE TREATED WITH A DRUG TO BLOCK THE GENE’S ACTIVITY, TAKE MORPHINE, THEY RECEIVE THE DRUG’S PAIN-RELIEVING BENEFITS, BUT THEY DON’T HAVE TO SCRATCH. THAT’S UNUSUAL BECAUSE CHEN SAYS SCRATCHING IS A COMMON SIDE EFFECT OF MORPHINE.

(act) :13 o/c be separated

They don’t scratch. So this is very interesting because it actually
is a perfect example showing that the analgesic effect and the
itching pathway can be separated.

CHEN SAYS HUMANS, LIKE MICE, HAVE THE ITCH GENE, AND HE SAYS THESE FINDINGS INDICATE IT MAY BE POSSIBLE TO TREAT CHRONIC ITCHING IN HUMANS BY BLOCKING THE ACTION OF THAT GENE IN THE SPINAL CORD. I’M JIM DRYDEN…

RUNS 1:00

MANY ANIMAL STUDIES HAVE SHOWN THAT CALORIE RESTRICTION CAN EXTEND LIFESPAN. NOW SCIENTISTS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT IF THEY GIVE DRUGS TO ROUNDWORMS THAT ROB THE ANIMALS OF THEIR SENSE OF SMELL, THOSE WORMS LIVE LONGER. THE EFFECT IS VERY SIMILAR WHAT IS SEEN WITH CALORIE RESTRICTION. JIM DRYDEN REPORTS…

WASHINGTON UNIVERSITY DEVELOPMENTAL BIOLOGIST KERRY KORNFELD SAYS THERE IS CLEAR EVIDENCE FROM MANY ANIMAL STUDIES THAT CALORIE RESTRICTION EXTENDS LIFE.

(act) :13 o/c in between

The most universal intervention that causes lifespan extension
is calorie restriction. It works in worms. It works in rodents,
where it was discovered, and it works in a whole host of animals
in between.

LOOKING FOR OTHER METHODS THAT MIGHT LENGTHEN LIFE, KORNFELD AND HIS COLLEAGUES GAVE ROUNDWORMS DRUGS THAT HUMANS TAKE TO PREVENT SEIZURES AND CONVULSIONS. AND THE ANIMALS LIVED LONGER, EVEN THOUGH THEY SEEMED TO EAT AS MUCH AS ANIMALS THAT DIDN’T GET THE DRUG.

(act) :22 o/c make eggs

The worms are eating robustly. They have relatively normal
reproduction. They make about the right number of eggs, and
that’s a very sensitive measure of how much animals are
eating. When animals are calorically restricted, they
invariably have a depression of their reproduction and
fairly dramatic reductions in their ability to make eggs.

KORNFELD SAYS THE DRUGS INTERFERE WITH THE ROUNDWORMS’ ABILITY TO SMELL. THEY CAN’T SENSE THE PRESENCE OF FOOD EVEN WHEN SURROUNDED WITH NUTRIENTS.

(act) :32 o/c of food

The information from the sensory system about the availability
of food is altered by the drugs, and we think that’s how they
work to extend lifespan. And it could be that in a real calorie
restriction example, animals both lack the perception of food
– because it’s not there – and they lack the ingestion of food
– because they’re being calorie restricted. And it’s some
combination of both of those that results in the lifespan extension.
And in our case, we may be getting the lifespan extension simply
by blocking perception of food in the environment without actually
blocking ingestion of food.

KORNFELD SAYS THE EVIDENCE FROM THE WORMS WOULD SUGGEST THAT WHAT ANIMALS EAT MAY HAVE LESS TO DO WITH LONGEVITY THAN ACTIVITY IN THE ANIMALS SENSORY SYSTEMS THAT ARE INVOLVED WITH EATING.

(act) :19 o/c different way

It may be that treating the animals with the medicines
ultimately results in changes in the animal that are similar
to the changes that might occur when it’s calorically
restricted, that there might be more than one way to achieve
these kinds of changes. Calorie restriction may be one way,
and the medicines may be a different way.

KORNFELD SAYS THE ADVANTAGE TO STUDYING WORMS IS THAT THEIR LIVES ARE SO SHORT THAT THIS TYPE OF RESEARCH CAN BE DONE QUICKLY. HE SAYS HE’D LIKE TO SEE WHETHER TREATMENT WITH THESE SAME TYPES OF DRUGS ALSO MIGHT LENGTHEN LIFESPAN IN OTHER ANIMALS. BUT HE SAYS THERE’S NO EVIDENCE THAT A SIMILAR STRATEGY WOULD WORK IN HUMANS, AND EVEN IF IT DID, POTENTIAL SIDE EFFECTS FROM THE DRUGS MIGHT MAKE TAKING THEM A BAD IDEA. BUT HE SAYS IT IS INTERESTING THAT THESE DRUGS ALSO IMPAIR SENSE OF SMELL IN THE HUMANS WHO TAKE THEM TO PREVENT SEIZURES AND CONVULSIONS.

(act) :11 o/c the food

A lot of the information that the body has about whether it’s
being calorie restricted or not may come from the sensation of
the environment, not the actual ingestion of the food.

KORNFELD REPORTED HIS FINDINGS IN THE JOURNAL PUBLIC LIBRARY OF SCIENCE GENETICS. I’M JIM DRYDEN…

RUNS 2:59

ANIMALS WHO EAT LOW CALORIE DIETS LIVE LONGER. NOW RESEARCHERS HAVE FOUND THAT IT’S POSSIBLE TO EXTEND THE LIFESPAN OF ROUNDWORMS BY IMPAIRING THEIR SENSE OF SMELL. WASHINGTON UNIVERSITY DEVELOPMENTAL BIOLOGIST KERRY KORNFELD GIVES THE WORMS ANTI-CONVULSANT DRUGS THAT INTERFERE WITH THEIR ABILITY TO SENSE THE PRESENCE OF FOOD. HE SAYS THE WORMS EAT AS MUCH AS THOSE WHO HAVE AN INTACT SENSE OF SMELL, BUT THEY LIVE AS LONG AS WORMS ON CALORIE RESTRICTION.

(act) :18 o/c different way

It may be that treating the animals with the medicines
ultimately results in changes in the animal that are similar
to the changes that might occur when it’s calorically
restricted, that there might be more than one way to achieve
these kinds of changes. Calorie restriction may be one way,
and the medicines may be a different way.

KORNFELD SAYS IT’S INTERESTING TO NOTE THAT MANY PEOPLE ON THESE DRUGS ALSO LOSE THEIR ABILITY TO SMELL, BUT THERE’S NO EVIDENCE THAT ANY OF THOSE PEOPLE LIVE ANY LONGER … YET. HE REPORTED HIS FINDINGS IN THE JOURNAL PUBLIC LIBRARY OF SCIENCE GENETICS. I’M JIM DRYDEN…

RUNS :59

VISION RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE DETERMINED THAT A PARTICULAR PROTEIN AND CELL TYPE FROM THE IMMUNE SYSTEM PLAY KEY ROLES IN THREE DIFFERENT BLINDING RETINAL DISEASES THAT INVOLVE DEVELOPMENT OF ABNORMAL BLOOD VESSELS IN THE RETINA. JIM DRYDEN REPORTS…

THE BLINDING DISEASES ARE AGE-RELATED MACULAR DEGENERATION, THE LEADING CAUSE OF BLINDNESS IN THE UNITED STATES IN PEOPLE OVER 50, DIABETIC RETINOPATHY, WHICH AFFECTS ABOUT 20 PERCENT OF THE 24 MILLION AMERICANS WITH DIABETES, AND RETINOPATHY OF PREMATURITY, A CONDITION THAT BLINDS 50 THOUSAND NEWBORN BABIES EACH YEAR. VISION RESEARCHERS, LED BY WASHINGTON UNIVERSITY RETINA SPECIALIST RAJENDA APTE SAYS IN ALL THREE DISORDERS, THE DEVELOPMENT OF ABNORMAL BLOOD VESSELS LEADS TO VISION LOSS. AND IN ALL THREE CONDITIONS, A SMALL, IMMUNE-SYSTEM PROTEIN CALLED INTERLEUKIN-10, AND IMMUNE CELLS CALLED MACROPHAGES, PLAY KEY ROLES.

(act) :17 o/c this process

All the mechanisms may not be the same in a premature baby
and a 70-year-old person, but it’s important to note that
the two key players, the macrophage and interleukin-10,
still play a very important role as prime movers in this
process.

APTE’S TEAM ORIGINALLY FOUND THAT IL-10 AND MACROPHAGES WERE CREATING ABNORMAL BLOOD VESSELS BENEATH THE RETINA IN AGE-RELATED MACULAR DEGENERATION. THE DEVELOPMENT OF THOSE VESSELS IS A PROCESS THAT SCIENTISTS CALL ANGIOGENESIS. NORMALLY, MACROPHAGES PROTECT AGAINST ANGIOGENESIS, BUT APTE’S TEAM FOUND THAT LARGE AMOUNTS OF IL-10 WERE CAUSING THOSE MACROPHAGE CELLS INSTEAD TO HELP PROMOTE THE GROWTH OF DAMAGING VESSELS.

(act_ :26 o/c to pro-angiogenic

The cytokine interleukin-10 seems to be pro-angiogenic
in that it skews these macrophages to promote growth of
abnormal blood vessels. The other thing that clearly has
an effect on promoting , or making, these macrophages
pro-angiogenic is age because as these macrophages age,
the levels of IL-10 go up in the eye, and under the
influence of IL-10, these macrophages switch from being
anti-angiogenic to proangiogenic.

AFTER THEY LEARNED THAT IL-10 AND MACROPHAGES WERE HELPING TO CREATE DAMAGE IN MACULAR DEGENERATION, APTE SAYS HE FIGURED THEY ALSO MIGHT CAUSE DAMAGE IN DIABETIC RETINOPATHY AND RETINOPATHY OF PREMATURITY BECAUSE BOTH OF THOSE DISEASES ALSO INVOLVE ABNORMAL BLOOD VESSEL DEVELOPMENT.

(act) :06 o/c bit different

The “offending” cell, so to speak, is the same, but the way
it’s causing the disease is, maybe, a little bit different.

APTE SAYS UNDERSTANDING WHAT IS HELPING TO DRIVE THE DISEASE PROCESS MAY MAKE IT POSSIBLE TO DEVELOP MORE EFFECTIVE THERAPIES. HE SAYS INTERFERING WITH IL-10 AND MACROPHAGES IN THE EYE WOULD BE AN OBVIOUS TREATMENT STRATEGY.

(act) :17 o/c therapeutic avenue

This is a local disease, so you wouldn’t want to affect systemic
processes, but, you know, local, targeted therapy that disrupts
these signaling pathways mediated by IL-10 or disrupts the
function of abnormal macrophages locally would clearly be an
attractive therapeutic avenue.

APTE AND HIS COLLEAGUES RECENTLY REPORTED THEIR FINDINGS IN THE JOURNAL PUBLIC LIBRARY OF SCIENCE: ONE. I’M JIM DRYDEN…

RUNS 2:51

THE VISION RESEARCHERS SAY A SMALL PROTEIN, CALLED INTERLEUKIN-10, AND IMMUNE CELLS CALLED MACROPHAGES, CONTRIBUTE TO ABNORMAL BLOOD VESSEL GROWTH BENEATH THE RETINA IN MACULAR DEGENERATION AND INSIDE THE RETINA IN DIABETIC RETINOPATHY AND IN RETINOPATHY OF PREMATURITY. MACULAR DEGENERATION IS THE LEADING CAUSE OF BLINDNESS IN THE UNITED STATES IN PEOPLE OVER 50, SOME 20 PERCENT OF THE 24 MILLION AMERICANS WITH DIABETES DEVELOP DIABETIC RETINOPATHY, AND RETINOPATHY OF PREMATURITY BLINDS 50 THOUSAND NEWBORN BABIES EACH YEAR. WASHINGTON UNIVERSITY RETINA SPECIALIST RAJENDA APTE.

(act) :17 o/c this process

All the mechanisms may not be the same in a premature baby
and a 70-year-old person, but it’s important to note that
the two key players, the macrophage and interleukin-10,
still play a very important role as prime movers in this
process.

THAT COULD HELP WITH THE DEVELOPMENT OF MORE EFFECTIVE THERAPIES. I’M JIM DRYDEN…

RUNS :57

JUST IN CASE YOU HAVEN’T NOTICED THE STORE DISPLAYS THAT HAVE BEEN UP SINCE JULY, HALLOWEEN IS COMING. AND IF THE PROSPECT OF GHOSTS AND GOBLINS AT THE FRONT DOOR ISN’T SCARY ENOUGH FOR YOU, HOW ABOUT THE PROSPECT OF THOSE SAME GHOSTS AND GOBLINS DARTING OUT FROM BETWEEN CARS INTO THE STREET? ON A FRIDAY NIGHT? THE COMBINATION OF CARS, KIDS AND DARKNESS PRESENTS THE BIGGEST DANGER OF HALLOWEEN, AND THAT COMBINATION COULD BE EVEN MORE DANGEROUS THIS YEAR. JIM DRYDEN REPORTS…

AT THIS TIME OF YEAR IT GETS DARKER EARLIER, AND ON HALLOWEEN, EXCITED, COSTUMED CHILDREN CAN BE DIFFICULT TO SEE, ESPECIALLY WHEN EXCITED ADULTS AND TEENAGERS ARE OFF TO THEIR OWN FRIDAY EVENING CELEBRATIONS. WASHINGTON UNIVERSITY PHYSICIAN BO KENNEDY, WHO WORKS IN THE EMERGENCY DEPARTMENT AT ST. LOUIS CHILDREN’S HOSPITAL, SAYS OVER THE YEARS, SOME PARENTS HAVE WORRIED ABOUT POISON CANDY OR RAZOR BLADES IN APPLES, BUT TAMPERING WITH TREATS IS EXTREMELY RARE.

(act) :23 o/c it’s raining

We worry about poison candies and razor blades in apples,
and things like that make the public awareness frequently.
But the real danger is from the cars striking the children
as they’re running about the streets. It’s a very difficult
situation for everybody, especially if the weather is bad
and if it’s raining.

KENNEDY SAYS THE STAFF IN THE EMERGENCY DEPARTMENT AT ST. LOUIS CHILDREN’S HOSPITAL WILL ALMOST CERTAINLY SEE A FEW KIDS THIS YEAR WHO HAVE BEEN HIT BY CARS. BUT PARENTS AND CHILDREN CAN TAKE SOME COMMON-SENSE STEPS TO AVOID THESE POTENTIALLY TRAGIC INJURIES.

(act) :32 o/c they’re running

The darkness is a big problem with Halloween, and carrying
flashlights is probably the most important way to help the
children be seen by the cars, as well as enable them to see
where they’re going. Additional things that are really
important are brightly-colored or reflective costumes and
masks that don’t cover the eyes. In fact, it’s much better
to paint the face with cosmetics than it is to cover with a
mask that may prevent the children from seeing where they’re
stepping or where they’re running.

KENNEDY SAYS THOSE WHO TURN ON THE PORCHLIGHT AND HAND OUT TREATS ALSO NEED TO KEEP CHILDREN SAFE. JACK O’ LANTERNS SHOULDN’T BE PLACED ON THE GROUND IN AREAS WHERE CHILDREN MIGHT BE AND WHERE CAPES OR OTHER PARTS OF FLOWING COSTUMES MIGHT COME INTO CONTACT WITH AN OPEN FLAME. IT ALSO MIGHT BE A GOOD IDEA TO KEEP THE DOG IN THE BASEMENT OR IN THE BACK OF THE HOUSE FOR A FEW HOURS.

(act) :15 o/c very real

Another problem that we have to worry about are pets.
People have to make sure that their dogs are kept out
of way. This is a time when lots of strangers are coming
around, as far as the pets are concerned, and the
potential for dog bites is very real.

TOO MUCH CANDY ALSO CAN BE A PROBLEM, BUT KENNEDY SAYS THE ENSUING STOMACH ACHE USUALLY PASSES RELATIVELY QUICKLY. OF COURSE, IT DOESN’T BECOME AN ISSUE AT ALL IF ADULTS MONITOR THE CANDY AND MAKE SURE THEIR CHILDREN DON’T STUFF THEMSELVES. HE SAYS PARENTAL SUPERVISION IS ONE OF THE KEYS TO A SAFE HALLOWEEN.

(act) :11 o/c door to door

The best thing is to have your children go into neighborhoods
that you know, where you know the families and where the
parents are with them as they’re walking from door to door.

KENNEDY ALSO REMINDS THAT CHILDREN NEED TO STAY OUT OF THE STREET AND ONLY CROSS AT CORNERS AND DESIGNATED CROSSWALKS. EVEN A CAREFUL DRIVER MAY NOT BE ABLE TO STOP IF A CHILD DARTS INTO THE STREET FROM BETWEEN CARS. AND WITH THE HOLIDAY ON A FRIDAY NIGHT THIS YEAR, IT’S NOT A SURE BET THAT DRIVERS WILL BE ALL THAT CAREFUL. I’M JIM DRYDEN…

RUNS 2:58

IT’S BAD ENOUGH MOST YEARS, WHAT WITH KIDS OUT ON THE STREET, AFTER DARK, OFTEN WEARING MASKS THAT MAKE IT HARD FOR THEM TO SEE, EVEN IF THEY DO LOOK BOTH WAYS BEFORE CROSSING THE STREET. BUT THIS YEAR, ADD FRIDAY TO THE EQUATION, AND IT’S POTENTIALLY EVEN MORE DANGEROUS FOR KIDS, ACCORDING TO BO KENNEDY, A WASHINGTON UNIVERSITY PHYSICIAN WHO WORKS IN THE EMERGENCY DEPARTMENT AT ST. LOUIS CHILDREN’S HOSPITAL. HE RECOMMENDS FLASHLIGHTS, REFLECTIVE COSTUMES IF POSSIBLE. BUT THE MOST IMPORTANT WAY TO AVOID DANGERS ON HALLOWEEN, HE SAYS, IS FOR PARENTS TO GO FROM HOUSE TO HOUSE WITH THEIR CHILDREN.

(act) :11 o/c door to door

The best thing is to have your children go into neighborhoods
that you know, where you know the families and where the
parents are with them as they’re walking from door to door.

KENNEDY SAYS THE MAIN PROBLEM IS THAT EXCITED KIDS MAY GET HIT BY CARS. OTHER POTENTIAL DANGERS INCLUDE OPEN FLAMES IN JACK O’ LANTERNS, NERVOUS PETS AND TOO MUCH CANDY ALL IN ONE SITTING. I’M JIM DRYDEN…

RUNS :56

BREAST CANCER RESEARCHERS AT THE SITEMAN CANCER CENTER AT WASHINGTON UNIVERSITY AND BARNES-JEWISH HOSPITAL IN ST. LOUIS HAVE DEVELOPED A NEW PREDICTIVE MEASUREMENT, WHICH MAY BE ABLE TO BRING GOOD NEWS TO SOME WOMEN WITH BREAST CANCER. A LOW SCORE IN THE PREDICTIVE INDEX SEEMS TO INDICATE THAT A WOMAN WON’T NEED CHEMOTHERAPY FOLLOWING HER BREAST CANCER SURGERY. JIM DRYDEN HAS THE STORY …

ONCOLOGISTS NOW REALIZE THAT THE OLD STRATEGY FOR CANCER TREATMENT — BASICALLY GET RID OF IT AS QUICKLY AS YOU CAN — ISN’T ALWAYS THE BEST COURSE OF TREATMENT. FOR EXAMPLE, WASHINGTON UNIVERSITY ONCOLOGIST MATTHEW ELLIS NOW RECOMMENDS THAT HIS PATIENTS GET TREATED WITH DRUGS FOR SEVERAL MONTHS BEFORE A SURGEON OPERATES. THE REASON IS THAT MANY BREAST CANCER TUMORS RESPOND TO ANTI-ESTROGEN THERAPY WITH DRUGS SUCH AS TAMOXIFEN OR THE NEWER DRUG, LETROZOLE. ELLIS HAS FOUND THAT WHEN TREATED FIRST, MANY TUMORS ARE SMALLER AND LESS DANGEROUS WHEN PATIENTS FINALLY DO HAVE SURGERY. THE APPROACH ALSO HAS ALLOWED HIM TO DEVELOP A MEASUREMENT THAT CAN PREDICT WHETHER A WOMAN WILL DO WELL FOLLOWING SURGERY.

(act) :33 o/c prognostic index

In this particular setting of hormone receptor-positive breast
cancer, we shouldn’t immediately remove the cancer. We should
start one of these hormonal agents – and we know that’s a good
thing because that’ll shrink the cancer when you operate – but
also, we wanted to show that the obvious is true, which is,
tumors that shrink and stop growing will do better in the long
term than patients who have tumors that don’t shrink or show
evidence of continued growth. And that, essentially, is the
essence of the PEPI index: preoperative endocrine prognostic
index.

THE PEPI INDEX CAN HELP PREDICT WHICH WOMEN HAVE TUMORS THAT MAY RECUR AND CAUSE TROUBLE AND WHICH WOMEN’S TUMORS HAVE RESPONDED SO WELL TO PRE-OPERATIVE TREATMENT AND SURGERY THAT THEY REALLY DON’T NEED TO HAVE CHEMOTHERAPY.

(act) :23 o/c these agents

So, it’s been a long-standing question of how we can
come up with ways to predict which patients are going
to be cured, or at least do very well, and which
patients are in the unfortunate circumstances of having
a hormone receptor-positive breast cancer that does not
respond to these agents.

AFTER TREATING WOMEN WITH ANTI-ESTROGEN THERAPY FOR FOUR MONTHS, THE WOMAN THEN HAVE SURGERY. FOLLOWING SURGERY, ELLIS AND HIS COLLEAGUES MEASURE THE TUMOR’S SIZE, WHETHER IT HAS SPREAD INTO LYMPH NODES, AND WHETHER IT REMAINS HORMONE RECEPTOR-POSITIVE. THEY ALSO MEASURE SOMETHING CALLED THE TUMOR’S PROLIFERATION INDEX.

(act) :14 o/c do worse

A measurement of how fast the tumor is growing, not at the
beginning but after starting the hormonal therapy, and it
won’t surprise you to learn that tumors that are able to grow
despite the drug, do worse.

WHEN ALL OF THOSE FACTORS ARE COMBINED INTO THE SO-CALLED PEPI INDEX, ELLIS SAYS IT’S POSSIBLE TO PREDICT FAIRLY RELIABLY WHETHER A TUMOR LIKELY WILL RECUR OR WHETHER THE CHANCES OF RELAPSE ARE VERY SMALL.

(act) :18 o/c is unnecessary

The most favorable scenario is the tumor shrank, the proliferation
has stopped completely in the tumor and the tumor is still hormone
receptor-positive, and the nodes are negative. In two studies, we’ve
found there were no relapses in that group. None. So that would tell
you, if you’re lucky enough to be in that group, really chemotherapy
is unnecessary.

ELLIS REPORTED ON THE PEPI INDEX LAST MONTH IN THE JOURNAL OF THE NATIONAL CANCER INSTITUTE. I’M JIM DRYDEN…

RUNS 2:56

THE PREDICTIVE MEASUREMENT, CALLED THE PEPI SCORE, WAS DEVELOPED BY A TEAM LED BY WASHINGTON UNIVERSITY ONCOLOGIST MATTHEW ELLIS. PEPI STANDS FOR PREOPERATIVE ENDOCRINE PROGNOSITC INDEX. IT APPEARS TO BE USEFUL IN WOMEN WHOSE BREAST TUMORS ARE HORMONE-RECEPTOR POSITIVE. THOSE WOMEN ARE TREATED WITH ANTI-ESTROGEN THERAPY FOR FOUR MONTHS WITH A DRUG LIKE TAMOXIFEN OR LETROZOLE. THEN, AFTER SURGERY, ELLIS’S TEAM MEASURES THE TUMOR’S SIZE, WHETHER IT HAS SPREAD TO LYMPH NODES, AND WHETHER IT REMAINS A HORMONE RECEPTOR-POSITIVE TUMOR. THEY ALSO MEASURE SOMETHING CALLED THE TUMOR’S PROLIFERATION INDEX.

(act) :14 o/c do worse

A measurement of how fast the tumor is growing, not at the
beginning but after starting the hormonal therapy, and it
won’t surprise you to learn that tumors that are able to grow
despite the drug, do worse.

ELLIS SAYS WHEN ALL FOUR MEASUREMENTS ARE COMBINED, IT’S POSSIBLE TO PREDICT WHETHER A WOMAN MIGHT SUCCESSFULLY AVOID CHEMOTHERAPY. HE REPORTED ON THE PEPI INDEX LAST MONTH IN THE JOURNAL OF THE NATIONAL CANCER INSTITUTE. I’M JIM DRYDEN…

RUNS 1:00

DIABETES, HIGH BLOOD PRESSURE AND HEART DISEASE ARE JUST A FEW OF THE CONSEQUENCES OF OBESITY, BUT IT ISN’T ONLY OBESITY THAT’S CAUSING THOSE PROBLEMS. NEW RESEARCH FROM WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS SUGGESTS THAT BEING OVERWEIGHT IS NOT ENOUGH TO TRIGGER THOSE COMPLICATIONS. IT’S ALSO KEY THAT A PERSON HAS WHAT SCIENTISTS CALL NON-ALCOHOLIC FATTY LIVER DISEASE. JIM DRYDEN HAS THE STORY …

OBESITY IS CLOSELY LINKED TO FATTY LIVER DISEASE, BUT NOT EVERY OBESE PERSON WILL DEVELOP FATTY LIVER. WASHINGTON UNIVERSITY NUTRITION RESEARCHER SAMUEL KLEIN SAYS IN SOME CASES, FATTY LIVER DISEASE CAN PROGRESS TO LIVER INFLAMMATION AND EVEN TO CIRRHOSIS, BUT THE REALLY BIG DEAL IS THE CONDITION’S LINK TO PROBLEMS LIKE HEART DISEASE AND DIABETES.

(act) :18 o/c problem later

Since obesity is now becoming so much more prevalent in
children, we are now seeing a marked increase in fatty liver
disease in children, and this could have, then, serious
clinical consequences because developing this abnormality
so early in life gives you a longer duration of this insult
that can lead to serious problems later.

KLEIN’S TEAM COMPARED OBESE CHILDREN WITH AND WITHOUT FATTY LIVER AND USED ADVANCED TECHNIQUES TO MEASURE THEIR RISK FACTORS FOR METABOLIC PROBLEMS.

(act) :22 o/c fatty liver

And we found that those children with fat in the liver have
metabolic abnormalities – in terms of glucose metabolism and
fat metabolism, with resistance to insulin – compared to
those children who had normal fat in the liver. And so the
only difference you could tell between those two kids is really
fat in their liver, which was an important marker of metabolic
derangements in the obese children that had fatty liver.

HE SAYS THESE NEW FINDINGS ABOUT FATTY LIVER CAN BE VERY USEFUL TO DOCTORS TREATING OBESE KIDS. HE SAYS IF THEY KNOW WHICH KIDS HAVE FAT IN THEIR LIVERS, THEY ALSO SHOULD KNOW WHOM THEY TARGET WITH MORE INTENSIVE THERAPY.
(act) :18 o/c metabolic disease

So this could be a way to identify, potentially, which kids are
at increased risk for developing metabolic disease. And then focus
therapy on those children and maybe not focus as aggressive a therapy
in obese children that don’t have fatty liver because they’re not
at the same risk, potentially, for future metabolic disease.

KLEIN SAYS THESE FINDINGS ARE LINKED TO PREVIOUS RESEARCH THAT CARRYING FAT IN THE ABDOMEN IS WORSE THAN CARRYING IT IN THE HIPS OR THIGHS OR ELSEWHERE IN THE BODY, AND HE SAYS FAT IN THE LIVER IS CLOSELY CONNECTED WITH ABDOMINAL FAT.

(act) :31 o/c as well

But if you take people where it doesn’t track – where they
have fat in the liver and normal intra-abdominal fat and
vice versa, no fat in the liver and high intra-abdominal
fat – you find that the only thing that predicts metabolic
derangements is fat in the liver. So this also tells us
that the inability to put all of your fat in your fat cells,
but top have that fat “spill over” into other organs like
the liver, is a bad sign, and if you have that fat in the
liver, it’s associated with metabolic disease. And now we’re
trying to understand whether it actually causes the metabolic
disease as well.

THE GOOD NEWS IS THAT FATTY LIVER IS REVERSIBLE.

(act) :28 o/c liver fat

Completely reversible, so that if you lose weight, you
eliminate the fat in your liver. In fact, we have found
in another study that simply two days of calorie restriction,
cutting out 1,000 calories a day in an adult, causes a 25
percent reduction in your liver fat content. And at the same
time when you reduce the fat in your liver, you improve your
liver-insulin sensitivity simultaneously. So within two days
of calorie restriction, you improve your insulin sensitivity
in liver, and you reduce your liver fat.

KLEIN’S TEAM REPORTED ITS FINDINGS IN THE AMERICAN JOURNAL OF CLINICAL NUTRITION. I’M JIM DRYDEN…

RUNS 2:57

PART OF IT’S WHETHER A PERSON CARRIES FAT IN THE ABDOMEN OR IN OTHER PARTS OF THE BODY LIKE THE HIPS AND THIGHS, BUT AN EVEN MORE IMPORTANT INDICATOR OF PROBLEMS, SUCH AS DIABETES AND HEART DISEASE, IS THE PRESENCE OF FAT IN THE LIVER. THE WASHINGTON UNIVERSITY RESEARCHERS STUDIED A CONDITION CALLED NON-ALCOHOLIC FATTY LIVER DISEASE IN OBESE CHILDREN. SOME KIDS HAD FAT IN THE LIVER, BUT OTHER OBESE CHILDREN DIDN’T. SAMUEL KLEIN DIRECTS WASHINGTON UNIVERSITY’S CENTER FOR HUMAN NUTRITION, .

(act) :21 o/c fatty liver

Those children with fat in the liver have metabolic abnormalities –
in terms of glucose metabolism and fat metabolism, with resistance
to insulin – compared to those children who had normal fat in the
liver. And so the only difference you could tell between those
two kids is really fat in their liver, which was an important
marker of metabolic derangements in the obese children that had
fatty liver.

THE GOOD NEWS IS FATTY LIVER DISEASE IS REVERSIBLE, PROVIDED THAT PEOPLE RESTRICT THEIR INTAKE OF CALORIES. KLEIN’S TEAM REPORTED ITS FINDINGS IN THE AMERICAN JOURNAL OF CLINICAL NUTRITION. I’M JIM DRYDEN…

RUNS :59

FOR MANY YEARS, AFRICAN AMERICANS HAVE BEEN CONSIDERED TO BE AT HIGHER RISK FOR CERTAIN TYPES OF CANCER, MORE LIKELY BOTH TO BE DIAGNOSED WITH THE DISEASE AND TO DIE FROM IT. BUT RESEARCHERS AT THE SITEMAN CANCER CENTER AND WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE BEEN STUDYING RATES OF DIAGNOSIS AND DEATH FROM FOUR COMMON TYPES OF CANCER, AND THEY HAVE FOUND THAT THOSE DISPARITIES ARE DISAPPEARING. JIM DRYDEN HAS MORE …

THE RESEARCH TEAM LOOKED AT THE RATES AT WHICH FOUR COMMON CANCERS WERE DIAGNOSED IN BOTH AFRICAN AMERICANS AND IN WHITES, LOOKING AT LUNG, PROSTATE, BREAST AND COLON CANCER RATES. LEAD INVESTIGATOR MARIO SCHOOTMAN, CO-LEADER OF THE PREVENTION AND CONTROL PROGRAM AT THE SITEMAN CANCER CENTER, SAYS THERE HAVE BEEN HISTORICAL DISPARITIES BETWEEN THE RACES.

(act) :19 o/c been diagnosed

Historically, there have been quite a few disparities between
African Americans and whites, not only in Missouri but across
the nation. African Americans, for certain types of cancer, are
more likely to be diagnosed and in many instances are more likely
to die as well after having been diagnosed.

BUT LOOKING AT CANCER INCIDENCE IN THE STATE OF MISSOURI, SCHOOTMAN’S TEAM FOUND THAT GAPS IN THE RATES OF NEWLY DIAGNOSED CANCER CASES BETWEEN AFRICAN AMERICANS AND WHITES HAVE CLOSED IN RECENT YEARS.

(act) :30 o/c disappeared altogether

And so we looked, starting in 1996 where African Americans were
18 percent more likely to be diagnosed with new cancers. And then
we looked in 2003 again, and we found that the disparities between
African Americans and whites, in terms of new cancer diagnosis, was
only 6 percent higher. And then what we would expect in the year
2006 – data is not yet available from the Missouri cancer registry
– is that the disparities in new cancer diagnosis have disappeared
altogether.

HE SAYS THE TREND LOOKS SIMILAR WHEN IT COMES TO CANCER DEATH RATES, BUT THERE THE GAP HASN’T CLOSED QUITE AS RAPIDLY, AND THERE STILL IS A DISPARITY.

(act) :28 o/c being implemented

Disparities between African Americans and whites, in terms of cancer
death, have declined over time. In 1990, African Americans were 48
percent at increased risk of dying from cancer. By the year 2006, it
was reduced to 28 percent. However, even if those trends continue,
disparities will not be disappearing for the next few decades
unless more aggressive interventions are being implemented.

SCHOOTMAN SAYS THERE ALSO ARE SOME DIFFERENCES DEPENDING UPON THE TYPE OF CANCER. DIFFERENCES GOT SMALLER FOR LUNG AND PROSTATE CANCER, BUT FOR COLON AND BREAST CANCER … NOT SO MUCH.

(act) :23 o/c have increased

The differences between African Americans and whites, in terms of
lung cancer occurrence, new cancer diagnoses have declined over
time during 1996 through 2003. Also for prostate cancer, differences
between African Americans and whites became smaller. On the other
hand, differences between African Americans and whites, in terms
of colo-rectal cancer as well as breast cancer, have increased.

SCHOOTMAN SAYS IT’S IMPOSSIBLE TO SAY FROM THE DATA WHY RATES OF DEATH OR DIAGNOSIS MIGHT BE DIFFERENT BETWEEN AFRICAN AMERICANS AND WHITES, BUT HE SAYS IT’S RELATIVELY CERTAIN THAT FACTORS INVOLVING THE PATIENTS, THE PROVIDERS AND THE ENVIRONMENT ALL PLAY A ROLE. AND HE SAYS ALTHOUGH THIS STUDY LOOKED ONLY AT MISSOURI, RACIAL DISPARITY TRENDS SEEM TO BE SIMILAR IN OTHER PARTS OF THE COUNTRY. HE REPORTS HIS FINDINGS IN AN UPCOMING ISSUE OF THE JOURNAL MISSOURI MEDICINE. I’M JIM DRYDEN…

RUNS 2:58

STUDYING CANCER INCIDENCE AND DEATH RATES IN THE STATE OF MISSOURI, THE RESEARCHERS FOUND RATES OF NEWLY DIAGNOSED CANCER BETWEEN AFRICAN AMERICANS AND WHITES ARE ABOUT EQUAL. ALTHOUGH THERE HAVE BEEN HISTORICAL DISPARITIES BETWEEN AFRICAN AMERICANS AND WHITES, MARIO SCHOOTMAN, CO-LEADER OF THE PREVENTION AND CONTROL PROGRAM AT THE SITEMAN CANCER CENTER, FOUND THOSE DISPARITIES HAVE MOSTLY DISAPPEARED. SCHOOTMAN SAYS THE TRENDS ARE SIMILAR WHEN IT COMES TO DEATH RATES, BUT THERE IS STILL A GAP BETWEEN AFRICAN AMERICANS AND WHITES.

(act) :19 o/c few decades

Disparities, in terms of cancer death, have declined over time.
In 1990, African Americans were 48 percent at increased risk of
dying. By the year 2006, it was reduced to 28 percent. However,
even if those trends continue, disparities will not be disappearing
for the next few decades.

SCHOOTMAN’S TEAM STUDIED INCIDENCE AND DEATH RATES RELATED TO LUNG, PROSTATE, COLON AND BREAST CANCER. THEY REPORT THEIR FINDINGS IN AN UPCOMING ISSUE OF THE JOURNAL MISSOURI MEDICINE. I’M JIM DRYDEN…

RUNS :58

ADDICTION RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE COMPLETED THE FIRST GENOME-WIDE ASSOCIATION STUDY OF DNA CHANGES THAT MAY BE LINKED TO ADDICTION. IDENTIFYING FACTORS RELATED TO ALCOHOL DEPENDENCE OR OTHER ADDICTIONS MAY, ONE DAY, MAKE IT POSSIBLE TO IDENTIFY PEOPLE AT RISK AND TO TREAT THOSE WHO DEVELOP ADDICTIONS. JIM DRYDEN HAS MORE...

THE RESEARCHERS ARE LOOKING AT GENETIC FACTORS AS PART OF THE 48 MILLION DOLLAR GENEVA PROJECT OF THE NATIONAL INSTITUTES OF HEALTH. THE PROJECT WAS DESIGNED TO LEARN MORE ABOUT THE INTERPLAY OF GENES AND ENVIRONMENT IN THE DEVELOPMENT OF DISEASE. WASHINGTON UNIVERSITY PSYCHIATRIC GENETICIST LAURA BIERUT IS HEADING UP THE PROJECT’S ADDICTION STUDIES. SHE HAS COMPLETED LOOKING AT ONE MILLION GENETIC VARIANTS THROUGHOUT THE HUMAN GENOME TO SEE HOW THOSE TINY DIFFERENCES IN DNA MIGHT MAKE A PERSON MORE OR LESS LIKELY TO DEVELOP ALCOHOL DEPENDENCE. AND HER TEAM IS POSTING THAT GENOME-WIDE STUDY ON THE INTERNET TO GIVE ALL INTERESTED SCIENTISTS ACCESS.

(act) :24 o/c by NIH

One million genetic variants have been tested across this
sample. We’re getting ready to release this data to the
scientific community because these genome-wide association
studies are a resource, really, for the entire scientific
community. So it’s released not only to the investigative
team that developed it. It’s released on this national
website sponsored by NIH.

BIERUT SAYS THIS FIRST PASS THROUGH THE GENOME DOESN’T DO MUCH TO TELL THEM WHICH GENES ARE DOING WHAT. BUT SHE SAYS UPCOMING STUDIES WILL BE ABLE TO MATCH MANY OF THESE GENETIC VARIANTS WITH RISK FOR ADDICTION.

(act) :21 o/c additional samples
So what’s interesting is the data gets released before
you’ve really had a chance to analyze it. There are some
intriguing areas that are novel. It’s a discovery phase,
and I think that’s really the most important. It’s a
discovery phase to generate hypotheses, which then get
tested in additional samples.

BIERUT SAYS FOR THIS STUDY, THE INVESTIGATORS HAVE BEEN LOOKING PRIMARILY AT PEOPLE WHO ARE ALCOHOL DEPENDENT, BUT SHE SAYS THESE FINDINGS ALSO MAY PROVIDE CLUES ABOUT OTHER TYPES OF ADDICTION, TOO.
(act) :26 o/c to alcoholism

So we were comparing people with alcohol dependence with
those individuals who are not dependent on alcohol or
other illicit drugs, but we know that alcoholism frequently
is affected with smoking and other drug use. So that is
going to be one of our second steps that we start to look
at is how do the other addictions relate to alcoholism?

AND BIERUT SAYS THIS STUDY IS ONLY LOOKING AT HALF OF THE ADDICTION EQUATION. LATER ON, IT WILL BE IMPORTANT TO CONNECT GENETIC FACTORS WITH ENVIRONMENTAL ONES.

(act) :10 o/c as strong

We’re born with our genetic variants, but can we learn
more about our environment so that we could modify
these risk factors so that they are not as strong.

BIERUT SAYS HER TEAM NOW PLANS TO ANALYZE THIS RAW DATA, LOOKING FOR ASSOCIATIONS THAT CONNECT THESE TINY GENETIC DIFFERENCES TO THE RISK FOR ALCOHOL DEPENDENCE. I’M JIM DRYDEN…

RUNS 2:40

THE TEAM IS LOOKING AT GENETIC FACTORS AS PART OF THE 48 MILLION DOLLAR GENEVA PROJECT OF THE NATIONAL INSTITUTES OF HEALTH. THE OVERALL PROJECT IS LOOKING AT THE INTERPLAY OF GENES AND ENVIRONMENT IN THE DEVELOPMENT OF DISEASE. WASHINGTON UNIVERSITY PSYCHIATRIC GENETICIST LAURA BIERUT IS HEADING UP THE PROJECT’S ADDICTION STUDIES. SHE HAS COMPLETED LOOKING AT ONE MILLION GENETIC VARIANTS THROUGHOUT THE HUMAN GENOME TO SEE HOW THOSE TINY DIFFERENCES MIGHT MAKE A PERSON MORE OR LESS LIKELY TO DEVELOP ALCOHOL DEPENDENCE.

(act) :14 o/c to alcoholism

Alcoholism frequently is affected with smoking and other
drug use, so that is going to be one of our second steps
that we start to look at is how do the other addictions
relate to alcoholism?

THE DATA IS POSTED ON THE INTERNET TO GIVE ALL INTERESTED SCIENTISTS ACCESS BIERUT SAYS HER TEAM NOW PLANS TO ANALYZE THIS RAW DATA, LOOKING FOR ASSOCIATIONS THAT CONNECT THESE TINY GENETIC DIFFERENCES TO ALCOHOLISM. I’M JIM DRYDEN…

RUNS :55

INVESTIGATORS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE MADE THE SURPRISING DISCOVERY THAT ALCOHOLIC WOMEN TEND TO HAVE CHILDREN LATER IN LIFE THAN WOMEN WHO ARE NOT ALCOHOLIC. THAT’S SURPRISING BECAUSE ALCOHOL USE DURING THE TEEN YEARS CAN LEAD TO SUBSEQUENT PROBLEMS WITH ALCOHOL LATER IN LIFE, AS WELL AS TO RISKY SEXUAL BEHAVIOR AND UNPLANNED PREGNANCIES. JIM DRYDEN HAS THE STORY …

THE STUDY WAS THE FIRST TO LOOK SPECIFICALLY AT ALCOHOL’S EFFECTS ON CHILDBEARING ACROSS THE YEARS. LED BY WASHINGTON UNIVERSITY ALCOHOLISM RESEARCHER MARY WALDRON, THE SCIENTISTS ANALYZED DATA GATHERED FROM TWO GROUPS OF AUSTRALIAN TWINS, SOME OF WHOM WERE BORN MORE THAN 100 YEARS AGO. WALDRON FOUND THE LINK BETWEEN ALCOHOL DEPENDENCE AND DELAYED CHILDBEARING, REGARDLESS OF WHEN THE WOMEN WERE BORN.

(act) :14 o/c not expected

Alcoholism predicts delayed childbearing, primarily for women.
Across reproductive development, alcoholism is associated with
an overall delay or reduction in childbearing, which was very
interesting and not expected.

WALDRON SAYS IT ALSO WAS SURPRISING BECAUSE OF EARLY DRINKING’S RELATIONSHIP BOTH TO ALCOHOL DEPENDENCE AND TO RISKY SEXUAL BEHAVIOR.

(act) :22 o/c with delay

Early drinking is associated with a range of, kind of, risky
sexual behaviors that would predict early, and often unplanned,
pregnancy and child bearing. And we also know that early use is
one of our strongest predictors of future alcohol problems,
including alcohol dependence, so it was really interesting that,
in fact, the opposite was found, that alcohol dependence was
associated with delay.

WALDRON SAYS OLDER ALCOHOLICS ALSO TEND TO ENGAGE IN RISKIER SEXUAL BEHAVIOR THAN THOSE WHO AREN’T ALCOHOL DEPENDENT.

(act) :17 o/c much later

Adults are actually having very similar, risky sexual behaviors,
adult alcoholics. You know, they have sex more frequently. They
have more casual partners, and all of those behaviors are predictive
of unplanned pregnancy, too. However, at least according to our
study, they’re having kids much later.

SHE SAYS THE STUDY FOUND EVIDENCE THAT ALCOHOL IMPAIRS FERTILITY IN BOTH MEN AND WOMEN, BUT SHE SAYS MEN NEED TO DRINK LARGER AMOUNTS OF ALCOHOL THAN WOMEN BEFORE THESE EFFECTS BECOME SIGNIFICANT.

(act) :20 o/c and miscarriage

There’s some research to suggest that alcohol does impair your
reproductive functioning. The effects are stronger for women, so
for example, women who drink, even at moderate levels, tend to
have disruptions in their menstrual cycle, and they tend to have
other gynecological and obstetric problems that include infertility
and miscarriage.

IN ADDITION TO THOSE BIOLOGICAL FACTORS, WALDRON SAYS IT’S POSSIBLE SOME SOCIAL FACTORS ALSO ARE INVOLVED IN DELAYED CHILDBEARING AMONG WOMEN WHO DRINK.

(act) :24 o/c reproductive opportunities

There are probably many social factors going on. Even though we
controlled for a range of, kind of, socio-demographic risks, we
think that, you know, alcoholics don’t make great partners, and
so there’s a lot of interpersonal difficulties and relationship
instability among alcoholic individuals. And so it may be an
absence of stable partnerships that kind of limit reproductive
opportunities.

WALDRON AND HER COLLEAGUE REPORT THEIR FINDINGS IN THE JOURNAL ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH. I’M JIM DRYDEN…

RUNS 2:40

THE FINDING IS SURPRISING BECAUSE ALCOHOL USE AT A YOUNG AGE IS ONE OF THE CHIEF PREDICTORS OF ALCOHOLISM. DRINKING AT A YOUNG AGE ALSO IS ASSOCIATED WITH RISKY SEXUAL BEHAVIOR AND WITH UNWANTED PREGNANCIES. BUT STUDYING THOUSANDS OF TWINS FROM AUSTRAILIA, WASHINGTON UNIVERSITY ALCOHOLISM RESEARCHER MARY WALDRON FOUND THAT ALCOHOL DEPENDENCE MADE IT LIKELY WOMEN WOULDN’T HAVE CHILDREN UNTIL AFTER THYE GOT OLDER..

(act) :22 o/c with delay

Early drinking is associated with a range of, kind of, risky
sexual behaviors that would predict early, and often unplanned,
pregnancy and child bearing. And we also know that early use is
one of our strongest predictors of future alcohol problems,
including alcohol dependence, so it was really interesting that,
in fact, the opposite was found, that alcohol dependence was
associated with delay.

WALDRON SAYS ALCOHOL CAN INTERFERE WITH MENSTRUATION AND CONTRIBUTE TO MISCARRIAGE, WHICH MAY PARTLY EXPLAIN THE FINDING. ANOTHER POSSIBILITY,
SHE SAYS, IS THAT ALCOHOLICS DON’T MAKE VERY GOOD PARTNERS, SO THEY DON’T GET THE OPPORTUNITY TO HAVE CHILDREN. I’M JIM DRYDEN…

RUNS 1:00

WHEN LABORATORY ANIMALS EAT ABOUT 25 PERCENT LESS, THEY LIVE ABOUT 50 PERCENT LONGER. THAT’S LED SOME PEOPLE TO ADOPT CALORIE RESTRICTION DIETS, NOT AS A MEANS OF LOSING WEIGHT BUT AS A WAY TO EXTEND THEIR LIVES. BUT A NUTRITION RESEARCHER AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS SAYS THAT IDEA MAY NOT WORK AS WELL IN PEOPLE AS IT DOES IN RATS AND MICE UNLESS THEY ALSO LIMIT THEIR PROTEIN INTAKE. JIM DRYDEN REPORTS …

ANIMALS ON CALORIE RESTRICTION LIVE LONGER THAN THEIR LITTERMATES. THOSE ANIMALS APPEAR TO LIVE LONGER BECAUSE OF CHANGES IN PATHWAYS INVOLVING INSULIN AND A GROWTH FACTOR CALLED IGF-1. SOME BELIEVE PEOPLE ON CALORIE RESTRICTION DIETS COULD LIVE TO BE 130 OR EVEN OLDER, BUT IT TURNS OUT THAT PEOPLE WHO CUT THEIR CALORIES BY 25 PERCENT OR MORE, DON’T SEEM TO HAVE THE SAME CHANGES IN THE IGF-1 PATHWAY, ACCORDING TO WASHINGTON UNIVERSITY NUTRITION RESEARCHER LUIGI FONTANA.

(act) :19 o/c no differences

In CR mice and rats on chronic CR, you have a reduction of about 30 to
40 percent in IGF-1, in circulating IGF-1. And it’s stable. So we said,
“What happens in humans?” So we are following this cohort of people who
are the CR Society members, and we measured IGF-1. No difference.

FONTANA SAYS ONE REASON MAY INVOLVE PROTEIN IN THE DIET. MANY MEMBERS OF THE CR SOCIETY, WHO PRACTICE CALORIE RESTRICTION WITH OPTIMAL NUTRITION AND CALL THEMSELVES CRONIES, EAT A LOT OF PROTEIN TO MAKE UP FOR SOME OF WHAT THEY LOSE IN CALORIES. FONTANA ALSO STUDIED IGF-1 LEVELS IN PEOPLE WHO DID CR FOR ONE YEAR AS PART OF A STUDY, AND THEIR IGF-1 LEVELS DIDN’T CHANGE MUCH EITHER.

(act) :19 o/c on CR

So we have the intervention data, and we have the long-term
data on these people that have been doing severe calorie
restriction. So that was puzzling because, you know, this was
the first time that we didn’t see an agreement between mice
and rats on CR and humans on CR.

THERE’S ANOTHER UNUSUAL GROUP THAT FONTANA ALSO FOLLOWS. THEY ARE STRICT VEGANS. AND ALTHOUGH THEY DON’T RESTRICT CALORIES AS MUCH AS CRONIES DO, THE VEGANS DO TEND TO EAT LESS PROTEIN. THEY HAVE LOWER LEVELS OF IGF-1.

(act) :21 o/c circulating IGF-1

And so we have this special population of vegan people. They have
low protein intake, and we compared them with the CRONies, with
the CR people. And we found that, in fact, these people, even if
they were heavier than the CR people, they have less, significantly
les, circulating IGF-1.

FONTANA SAYS MANY OF US EAT MORE PROTEIN THAN THE RECOMMENDED DAILY ALLOWANCE, OR RDA. AND HE SAYS THAT MAY BE THE REASON THAT IGF-1 LEVELS REMAIN HIGH FOR MANY PEOPLE, EVEN THOSE WHO PRACTICE CALORIE RESTRICTION. TO MAKE SURE, HE ASKED SOME MEMBERS OF THE CR SOCIETY TO CHANGE THEIR DIETS AND TO EAT LESS PROTEIN. THE RESULT WAS LOWER LEVELS OF IGF-1.

(act) :14 o/c lower IGF-1

After three weeks, IGF-1 dropped. So even if they were on a
severe calorie-restricted diet, high protein intake was, basically,
preventing them from having lower IGF-1.

HE SAYS CONSUMING ADQUATE PROTEIN IS IMPORTANT, BUT TOO MUCH MAY NEGATE SOME OF THE POSITIVE EFFECTS OF CALORIE RESTRICTION. HE REPORTS HIS FINDINGS IN THE JOURNAL AGING CELL. I’M JIM DRYDEN…

RUNS 2:56

ANIMALS ON CALORIE RESTRICTION LIVE UP TO 50 PERCENT LONGER THAN THEIR LITTERMATES. APPLYING THAT TO HUMANS, SOME BELIEVE PEOPLE ON CALORIE RESTRICTION DIETS COULD LIVE TO BE 130 OR OLDER. BUT THERE’S A POTENTIAL “FLY IN THE OINTMENT,” SAYS WASHINGTON UNIVERSITY NUTRITION RESEARCHER LUIGI FONTANA. FONTANA SAYS PART OF THE INCREASE IN MAXIMAL LIFESPAN FOR ANIMALS APPEARS RELATED TO A PATHWAY INVOLVING INSULIN AND A GROWTH FACTOR CALLED IGF-1.

(act) :17 o/c no difference

In CR mice and rats, you have a reduction of about 30 to 40 percent
in IGF-1, in circulating IGF-1. So we said, “What happens in humans?”
So we are following this cohort of people who are the CR Society
members, and we measured IGF-1. No difference.

BUT FONTANA FOUND LOWER IGF-1 LEVELS IN PEOPLE WHO ATE LESS PROTEIN. HE ALSO FOUND THAT WHEN THOSE ON CALORIE RESTRICTION DIETS CUT BACK ON PROTEIN, THEIR IGF-1 DROPPED SIGNIFICANTLY IN ONLY THREE WEEKS. I’M JIM DRYDEN…

RUNS :59

IT’S POSSSIBLE TO HELP OBESE PATIENTS LOSE WEIGHT WITH SURGERY, BUT IT MAY SOON BE POSSIBLE TO HELP THEM LOSE A SIGNIFICANT NUMBER OF POUNDS WITH A STAPLING TECHNIQUE THAT DOESN’T REQUIRE INCISIONS. PHYSICIANS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS RECENTLY BECAME THE FIRST IN THE UNITED STATES TO USE THE NON-SURGICAL PROCEDURE. JIM DRYDEN REPORTS...

AS THE NUMBER OF OBESE AMERICANS CONTINUES TO INCREASE, THE NEED FOR BETTER THERAPIES BECOMES MORE OBVIOUS. FOR THOSE OBESE PEOPLE WHO CAN’T SEEM TO EXERCISE OR DIET THEIR WAY TO WEIGHT LOSS, THERE ARE SURGICAL OPTIONS, AND THE “GOLD STANDARD” FOR OBESITY SURGERY IS THE GASTRIC BYPASS, ACCORDING TO WASHINGTON UNIVERSITY GI SPECIALIST SREENI JONNALAGADDA. IN THE PAST THAT MEANT BIG WEIGHT LOSS, BUT IT ALSO MEANT BIG INCISIONS. FOR SEVERAL YEARS, HOWEVER, IT’S BEEN POSSIBLE TO DO THESE OPERATIONS LAPAROSCOPICALLY, THROUGH VERY SMALL INCISIONS.

(act) :30 o/c of obesity

Now, while these laparoscopic procedures are far superior
to the open surgery, in that they do not require large
incisions, and the recovery period is shorter, there is
still a significant time period after the surgery is
performed before the patient actually goes home. All of
these patients, in the post-surgical period, are susceptible
to wound infections as well as blood clots. As such, there is,
clearly, room for improvement even those these procedures are
fairly well-established in the management of obesity.

JONNALAGADDA SAYS IF SMALL INCISIONS ARE GOOD, PERHAPS NO INCISIONS WILL BE EVEN BETTER. WITH WASHINGTON UNIVERSITY BARIATRIC SURGEON CHRISTOPHER EAGON, JONNALAGADDA RECENTLY WAS PART OF THE FIRST TEAM IN THE UNITED STATES TO DO AN ENDOSCOPIC TECHNIQUE TO HELP AN OBESE PATIENT LOSE WEIGHT BY SENDING A STAPLING DEVICE INTO THE STOMACH WITHOUT THE NEED FOR INCISIONS.
(act) :18 o/c the mouth

We are now able to consider doing procedures by a trans-
oral route. The new device, called the TOGA device – which,
essentially, stands for Trans Oral GAstroplasty – allows a
gastric stapling to be performed via the mouth.

JONNALAGADDA ISN’T EXPECTING THE SO-CALLED TOGA PROCEDURE TO PROVIDE RESULTS AS DRAMATIC AS THE CURRENTLY AVAILABLE GASTRIC BYPASS PROCEDURE, BUT HE SAYS IT DOES OFFER SOME THINGS GASTRIC BYPASS DOES NOT, SUCH AS QUICKER RECOVERY.

(act) :25 o/c few days

A small pouch is created into which food enters, and the person
feels full after eating very small amounts of food. The big
advantages of this procedure are, obviously, that it does not
require any incisions. The recovery period is much shorter, as
well as the hospital stay is much shorter. Typically, patients,
after undergoing the TOGA procedure, go home the day following
the procedure and are able to return to work within a few days.

HE SAYS THE STUDY IS DESIGNED TO DETERMINE BOTH WHETHER THE TOGA PROCEDURE IS SAFE AND WHETHER IT CAN HELP OBESE PATIENTS LOSE ENOUGH WEIGHT TO MAKE IT WORTHWHILE. WITH GASTRIC BYPASS…

(act) :24 o/c band procedures

… patients can, at one year, have an excess weight loss of
up to 70 percent. The lap band procedure and the vertical
band gastroplasty achieve weight loss of the order of about
45 percent of excess weight loss at one year. The preliminary
data from Belgium regarding the TOGA procedure, shows that it
achieves weight loss similar to the lap-band procedures.

JONNALAGADDA SAYS IT’S IMPORTANT TO MAKE SURE THE TOGA PROCEUDRE IS SAFE AND THAT IT REALLY DOES HELP PATIENTS LOSE WEIGHT. I’M JIM DRYDEN…

RUNS 3:00

THE “GOLD STANDARD” FOR OBESITY SURGERY REMAINS THE GASTRIC BYPASS. FOLLOWING THAT SURGERY, OBESE PATIENTS TEND TO LOSE AROUND 70 PERCENT OF THEIR EXCESS BODY WEIGHT WITHIN A YEAR. THE INVESTIGATORS USING THE NON-SURGICAL, TOGA TECHNIQUE AREN’T EXPECTING RESULTS QUITE THAT DRAMATIC, BUT THEY SAY PATIENTS COULD LOSE 40 OR 50 PERCENT OF THEIR EXCESS WEIGHT, AND THEY’LL SPEND LESS TIME RECOVERING, ACCORDING TO WASHINGTON UNIVERSITY GI SPECIALIST SREENI JONNALAGADDA, WHO WITH SURGEON CHRISTOPHER EAGON, PERFORMED THE FIRST NON-SURGICAL TOGA PROCEDURE IN THE UNITED STATES.

(act) :13 o/c the mouth

We are now able to consider doing procedures by a trans-oral
route. The new device allows a gastric stapling to be performed
via the mouth.

JONNALAGADDA SAYS HIS TEAM AND TEAMS AT SEVERAL OTHER CENTERS IN THE UNITED STATES WILL SPEND THE NEXT SEVERAL MONTHS COMPARING THE INVESTIGATIONAL PROCEDURE TO ENDOSCOPIC EXAMINATIONS OF THE STOMACH THAT DON’T DEPLOY THE STAPLING DEVICE. I’M JIM DRYDEN…

RUNS 1:00

BACKPACKS ARE SUPPOSED TO BE CONVENIENT. PUT ALL OF YOUR SCHOOLBOOKS IN ONE PLACE AND TOTE THEM AROUND. BUT THEY ALSO CAN BE A SOURCE OF PAIN AND INJURY FOR THE CHILDREN WHO LUG THEM FROM CLASS TO CLASS. SOME 7,000 CHILDREN ARE INJURED ANNUALLY DUE TO OVERLOADED BACKPACKS. JIM DRYDEN REPORTS...

MOST KIDS ARE BACK IN SCHOOL NOW THAT LABOR DAY HAS COME AND GONE. AND MOST OF THOSE ARE CARRYING THEIR SCHOOLBOOKS IN BACKPACKS. UNFORTUNATELY, SOME OF THOSE KIDS GET INJURED CARRYING THOSE HEAVY BACKPACKS, ACCORDING TO WASHINGTON UNIVERSITY PEDIATRIC ORTHOPEDIST MATTHEW DOBBS.

(act) :19 o/c upper-back pain
This is most common in, sort of grade levels starting
grade 7, through high school. And probably most common
in that 7th and 8th grade level when the kids are a little
bit smaller but still carrying equally heavy backpacks.
It’s associated with – heavy backpack use – with mid- and
upper-back pain.

DOBBS, WHO TREATS PATIENTS AT ST. LOUIS CHILDREN’S HOSPITAL, SAYS KIDS CARRY A LOT OF BOOKS, BUT THEY ALSO CARRY OTHER HEAVY THINGS. AS MUCH AS 10 TO 30 PERCENT OF A BACKPACK’S WEIGHT CAN BE NON-SCHOOL-RELATED MATERIALS. BUT HOW MUCH WEIGHT IS TOO MUCH WEIGHT?

(act) :14 o/c body weight
The recommendations right now – and there’s some debate over
that – but the recommendations are somewhere between 10 to 15
percent of body weight. It should not exceed that, and probably
the safest thing to do is to recommend around 10 percent of
body weight.

SO A 90-POUND CHILD SHOULDN’T BE CARRYING MORE THAN 9 TO 13 POUNDS OF STUFF IN THEIR BACKPACK, BUT MANY MIDDLE-SCHOOLERS HAVE INDIVIDUAL BOOKS THAT WEIGH THAT MUCH. DOBBS SAYS THE INJURIES AREN’T USUALLY PERMANENT, AND MOST HEAL WITH REST. BUT SOME KIDS HURT THEIR BACKS BADLY ENOUGH THAT THEY ACTUALLY HAVE TO MISS DAYS OF SCHOOL.
(act) :08 o/c from it
They are mainly temporary injuries, so this is soft-tissue,
sort of, muscle pain. But, you know, it’s, again, enough of
an issue that kids can miss school from it.

DOBBS SAYS WEARING BACKPACKS PROPERLY, DOWN LO