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

RUNS :59

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 LOW AND OVER BOTH SHOULDERS, CAN HELP. SO CAN USING A DIFFERENT KIND OF BACKPACK.

(act) :32 o/c the school
You know, backpacks that have the waist-belt support, which
reduces compression or weight load carried on the spine, and
also to teach the students – especially at a young age – to
wear their backpacks lower so that the weight is on the lower
back, and not carried up around the upper back and neck area.
The other things I always recommend is try to use a rolling
backpack. I’ve gotten a lot of feedback from families that
the rolling backpacks, at many schools, actually are not
allowed, and they, apparently, take up more space, and they
have trouble fitting them into lockers. So these are often,
sort of, banned from the school.

DOBBS SAYS REDUCING THE WEIGHT OF BACKPACKS, GETTING RID OF EXCESS MATERIAL OTHER THAN BOOKS, USING MORE ELECTRONIC MATERIALS AND EVEN GIVING KIDS A SECOND SET OF BOOKS — ONE FOR SCHOOL AND ONE FOR HOME — CAN HELP AVOID PROBLEMS THAT SEEM TO ESPECIALLY AFFECT MIDDLE SCHOOL CHILDREN.

(act) :12 o/c 8th graders
So they’re often, in 7th and 8th grade, carrying the same
amount of books that a high school student will carry. And
obviously, a high school student is going to weigh more,
so you often run into this percentage weight problem much
more often in the 7th and 8th graders.

DOBBS SAYS MANY SCHOOLS AND SCHOOL DISTRICTS DON’T SEEM TO BE TOO CONCERNED WITH THE PROBLEM, SO HE SAYS IT’S UP TO PARENTS TO HAVE THEIR KIDS’ BACKS. TO I’M JIM DRYDEN…

RUNS 2:49

WITH LABOR DAY IN THE REARVIEW MIRROR, MOST KIDS ARE BACK IN SCHOOL. AND MOST OF THEM ARE CARRYING BOOKS FROM HOME TO SCHOOL AND BACK AGAIN. AND THE VAST MAJORITY USE A BACKPACK TO TRANSPORT THE BOOKS. BACKPACKS ARE SUPPOSED TO BE CONVENIENT, BUT MORE THAN 7,000 CHILDREN ARE INJURED DUE TO OVERLOADED BACKPACKS. WASHINGTON UNIVERSITY ORTHOPEDIST MATTHEW DOBBS TREATS SOME OF THOSE KIDS AT ST. LOUIS CHILDREN’S HOSPITAL. HE SAYS TO BE SAFE, BACKPACKS SHOULD ONLY WEIGH ABOUT 10 TO 15 PERCENT OF A CHILD’S BODY WEIGHT, SO A 90-POUND CHILD SHOULDN’T BE CARRYING MORE THAN 9 TO 13 POUNDS OF BOOKS.

(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.

HE SAYS WEARING BACKPACKS PROPERLY, DOWN LOW AND OVER BOTH SHOULDERS, CAN HELP. SO CAN THE USE OF ROLLING BACKPACKS. I’M JIM DRYDEN…

RUNS 1:00

PARENTS HAVE A TREMENDOUS INFLUENCE OVER THE KINDS OF FOOD THAT THEIR PRESCHOOLERS EAT. SO IN ORDER TO COMBAT THE GROWING PROBLEM OF CHILDHOOD OBESITY, RESEARCHERS AT THE GEORGE WARREN BROWN SCHOOL OF SOCIAL WORK AT WASHINGTON UNIVERSITY IN ST. LOUIS ARE LOOKING FOR WAYS TO TEACH PARENTS HOW TO CREATE ENVIRONMENTS WHERE CHILDREN WILL REACH FOR A BANANA INSTEAD OF POTATO CHIPS. THE EFFORT IS WORKING WELL FOR SOME FAMILIES WITH PRESCHOOLERS. JIM DRYDEN REPORTS… …

DIETS THAT INCLUDE LOTS OF FRUITS AND VEGETABLES ARE ASSSOCIATED WITH A LOWER RISK FOR OBESITY, SO THE RESEARCHERS’ GOAL HAS BEEN TO GET KIDS TO EAT MORE OF THOSE FOODS. TEAMS OF INVESTIGATORS, LED BY WASHINGTON UNIVERSITY SOCIAL-WORK RESEARCHER DEBRA HAIRE-JOSHU, VISITED FAMILIES WITH PRESCHOOLERS IN RURAL, SOUTHEASTERN MISSOURI AS PART OF THE PARENTS AS TEACHERS PROGRAM.

(act) :23 o/c like that

To teach them about modeling good dietary and activity
behaviors and feeding their child with appropriate foods
and, as importantly, we taught the parent how to change
the home environment so that the child had access to healthy
foods, had access to fruits and vegetables on a regular
basis, as opposed to access to other foods that they
would learn to like: potato chips, sweetened drinks, things
like that.

HAIRE-JOSHU SAYS THE RESEARCHERS STUDIED AN INTERVENTION CALLED HIGH 5 FOR KIDS. IT USES BOOKS-ON-TAPE, COLORING BOOKS AND OTHER METHODS TO TEACH PRESCHOOLERS ABOUT FRUITS AND VEGETABLES. THE RESEARCHERS ALSO WORKED WITH PARENTS AND FOUND THAT WHEN PARENTS INCREASED THEIR FRUIT AND VEGETABLE CONSUMPTION, SO DID THEIR CHILDREN.

(act) :10 o/c a serving

If we got the parents to increase their fruit and vegetable
consumption by even one fruit or vegetable a day, the child’s
intake improved as well, by at least a half a serving.

BUT IT’S IMPORTANT THAT PRESCHOOLERS DEVELOP HEALTHY EATING HABITS EARLY IN LIFE BECAUSE IN THEIR 5-YEAR STUDY, HAIRE-JOSHU’S TEAM FOUND THAT THEY DIDN’T SUCCEED AS WELL WITH KIDS WHO ALREADY WERE OVERWEIGHT.

(act) :16 o/c as healthy

Preschool children who were already overweight, we did not see
that happen, and we think it’s because they’re already overweight
at preschool age. They already are learning patterns, from their
parents more than likely, that they’re starting to learn to like
foods that are not as healthy.

SHE SAYS USING TOOLS LIKE THE COLORING BOOKS SEEMS TO WORK MUCH BETTER TO PREVENT UNHEALTHY EATING THAN IT DOES TO CORRECT BAD EATING HABITS THAT ALREADY HAVE BEGUN.

(act) :14 o/c address that

We went in with the idea of preventing obesity, preventing
excess weight through good dietary patterns. Children who
are already overweight – and their families that are working
with them – would probably need a more intensive or a different
kind of intervention to address that.

HAIRE-JOSHU SAYS SOME RESEARCHERS BELIEVE THAT ONCE A CHILD HAS REACHED AGE 2 OR 3, IT’S ALREADY TOO LATE TO GET THEM TO PREFER HEALTHY FOOD OVER SUGARY OR SALTY SNACKS. BUT SHE SAYS THERE IS OTHER EVIDENCE SUGGESTING THAT ALTHOUGH IT’S HARDER TO CHANGE HABITS, EVEN IN VERY YOUNG CHILDREN, IT IS POSSIBLE.

(act) :28 o/c nutritious foods

We tried to identify the very colorful fruits and vegetables
and talked a lot about the green, leafy vegetables and the
bright-colored fruits to try to introduce the kids, colorwise,
to get them inclined to want to eat those kinds of foods. So
the intervention had things for the parents. We had the books
on tape for the kids, then the parents could also read the books
with the kids, which tried to reinforce the idea that the bright
colors tend to have the more nutritious foods.

HAIRE-JOSHU’S RESEARCH TEAM REPORTED ITS FINDINGS IN THE JOURNAL PREVENTIVE MEDICINE. I’M JIM DRYDEN…

RUNS 2:52

DIETS THAT INCLUDE LOTS OF FRUITS AND VEGETABLES ARE ASSSOCIATED WITH A LOWER RISK FOR OBESITY, SO THE RESEAERCHERS’ GOAL HAS BEEN TO GET KIDS TO EAT MORE OF THOSE FOODS. VISITING FAMILIES WITH PRESCHOOLERS AS PART OF THE PARENTS AS TEACHERS PROGRAM, THE RESEARCHERS STUDIED AN INTERVENTION CALLED HIGH 5 FOR KIDS. IT USES BOOKS-ON-TAPE, COLORING BOOKS AND OTHER METHODS TO TEACH PRESCHOOLERS ABOUT FRUITS AND VEGETABLES. THE RESEARCHERS ALSO WORKED WITH PARENTS. WASHINGTON UNIVERSITY SOCIAL-WORK RESEARCHER DEBRA HAIRE-JOSHU SAYS THE RESEARCHERS FOUND THAT WHEN PARENTS INCREASED THEIR FRUIT AND VEGETABLE CONSUMPTION, SO DID THEIR CHILDREN.

(act) :10 o/c a serving

If we got the parents to increase their fruit and vegetable
consumption by even one fruit or vegetable a day, the child’s
intake improved as well, by at least a half a serving.

SHE SAYS IT’S IMPORTANT TO GET CHILDREN ACCUSTOMED TO HEALTHY FOODS EARLY IN LIFE BECAUSE ROUTINE EXPOSURE TO GOOD FOODS WILL HELP PRESCHOOLERS DEVELOP HEALTHIER LIFETIME EATING HABITS. HAIRE-JOSHU’S RESEARCH TEAM REPORTED ITS FINDINGS IN THE JOURNAL PREVENTIVE MEDICINE. I’M JIM DRYDEN…

RUNS 1:00

ENDURANCE EXERCISE SEEMS TO MAKE THE HEARTS OF OLDER PEOPLE BEHAVE MORE LIKE THE HEARTS OF YOUNGER PEOPLE. CARDIOLOGY RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT FOLLOWING EXERCISE TRAINING, OLDER HEARTS USED MORE GLUCOSE DURING PERIODS WHEN THE HEART NEEDED EXTRA ENERGY. JIM DRYDEN REPORTS…

AS WE GET OLDER, OUR HEARTS GET LESS EFFICIENT, AND OUR RISK FOR HEART DISEASE INCREASES. SOME OF THAT MAY BE BECAUSE AS WE GET OLDER, WE TEND TO BE LESS ACTIVE, ACCORDING TO WASHINGTON UNIVERSITY CARDIOLOGY RESEARCHER PABLO SOTO.

(act) :20 o/c those changes

Even if you don’t develop any heart disease, the heart function
deteriorates, and people, even if they otherwise stay healthy,
tend to develop heart failure as they get into extreme old age.
So we wanted to look at some of the changes that occurred in the
heart as you get older and see if there was the potential to
reverse some of those changes.

ONE OF THOSE CHANGES INVOLVES HOW THE HEART USES ENERGY. A HEALTHY HEART GETS ABOUT 70 PERCENT OF ITS ENERGY FROM FATTY ACIDS AND ABOUT 30 PERCENT FROM GLUCOSE. THEN WHEN IT’S SUBJECTED TO THE STRESS OF EXERCISE, THE HEART RAMPS UP ITS USE OF BOTH FATTY ACIDS AND GLUCOSE. BUT SOTO SAYS OLDER HEARTS ARE MUCH LESS LIKELY TO INCREASE GLUCOSE METABOLISM THAN THEIR YOUNGER COUNTERPARTS. HIS TEAM STUDIED HEALTHY-BUT-SEDENTARY OLDER ADULTS. A GROUP OF 6 OLDER MEN AND 6 OLDER WOMEN DID 11 MONTHS OF ENDURANCE EXERCISE TRAINING.

(act) :16 o/c exercise training

All individuals across both genders improved their glucose use
to levels that were very similar to what we saw in our previous
study with young individuals. This indicated to us that at least
the metabolic changes associated with aging could be, potentially,
reversed with exercise training.

SOTO SAYS HE’S NOT CERTAIN WHAT THE FINDINGS MEAN TO THE RISK FOR HEART PROBLEMS BECAUSE ALL OF THE PEOPLE IN THE STUDY WERE OLDER AND SEDENTARY, BUT THEY DIDN’T HAVE HEART DISEASE.
(act) :12 o/c those individuals

Results of the study might have been different if we were studying
patients that had heart disease already and had a heart attack or
had bypass surgery. But other investigators have shown that exercise
is also beneficial for those individuals.

SOTO SAYS A POSSIBLE EXPLANATION FOR THE DIFFERENCES IN THE HEART’S GLUCOSE METABOLISM BETWEEN OLDER AND YOUNGER PEOPLE COULD BE THAT THE OLDER PEOPLE HAVE DEVELOPED THE VERY BEGINNINGS OF HEART FAILURE, WHICH WON’T DEVELOP FULLY UNTIL THEY REACH THEIR 80s OR 90s. HE PLANS TO STUDY THAT IDEA BY LOOKING AT THE EFFECTS OF EXERCISE ON THE HEART’S GLUCOSE METABOLISM IN PEOPLE WHO ALREADY HAVE BEEN DIAGNOSED WITH HEART FAILURE.

(act) :30 o/c beneficial effect

Older individuals, the way we see it, even though their heart’s
pumping well, the pattern of their metabolism suggests that heart
failure is starting to develop. So what we suspect is that if we
do this same study in individuals that already have heart failure
from other reasons, perhaps we can improve their metabolic profile.
So, indeed, other investigators that have not looked at metabolism
have showed that exercise is beneficial for individuals with heart
failure, but the big question is why? What is it that has the
beneficial effect?

SOTO REPORTED HIS FINDINGS IN THE AMERICAN JOURNAL OF PHYSIOLOGY, HEART AND CIRCULATORY PHYSIOLOGY. I’M JIM DRYDEN…

RUNS 2:47

A HEALTHY HEART GETS ABOUT 70 PERCENT OF ITS ENERGY FROM FATTY ACIDS AND ABOUT 30 PERCENT FROM GLUCOSE. THEN WHEN IT’S SUBJECTED TO THE STRESS OF EXERCISE, THE HEART RAMPS UP ITS USE OF BOTH FATTY ACIDS AND GLUCOSE. BUT ACCORDING TO WASHINGTON UNIVERSITY CARDIOLOGY RESEARCHER PABLO SOTO, OLDER HEARTS TEND TO INCREASE FATTY ACID USE, BUT THEY DON’T METABOLIZE MORE GLUCOSE, AT LEAST NOT WITHOUT EXERCISE. STUDYING HEALTHY-BUT-SEDENTARY OLDER ADULTS, SOTO AND HIS COLLEAGUES FOUND THAT 11 MONTHS OF EXERCISE TRAINING MAKES THOSE HEARTS BEHAVE MORE LIKE YOUNGER HEARTS. THEY STUDIED THE EFFECTS OF EXERCISE ON 6 OLDER WOMEN AND 6 OLDER MEN.

(act) :16 o/c exercise training

All individuals across both genders improved their glucose use
to levels that were very similar to what we saw in our previous
study with young individuals. This indicated to us that at least
the metabolic changes associated with aging could be, potentially,
reversed with exercise training.

HE REPORTED HIS FINDINGS IN THE AMERICAN JOURNAL OF PHYSIOLOGY, HEART AND CIRCULATORY PHYSIOLOGY. I’M JIM DRYDEN…

RUNS 1:00

MOST OF US KNOW THAT HIGH CHOLESTEROL IS BAD FOR YOU. IT CAN CLOG YOUR ARTERIES AND INCREASE THE RISKS OF A HEART ATTACK OR A STROKE. MOST PEOPLE WITH HIGH CHOLESTEROL CHANGE THEIR DIETS AND TAKE CHOLESTEROL-LOWERING DRUGS, BUT THOSE TREATMENTS DON’T WORK FOR EVERYONE. NOW WASHINGTON UNIVERSITY LIPID RESEARCH SPECIALISTS ARE OFFERING THOSE PATIENTS A TREATMENT THAT LITERALLY FILTERS BAD CHOLESTEROL OUT OF THEIR BLOOD.
JIM DRYDEN REPORTS…

THE TECHNIQUE IS CALLED LDL APHERESIS. IT’S A BIT LIKE DIALYSIS THERAPY FOR PATIENTS WITH KIDNEY FAILURE, AND TO WATCH A PATIENT RECEIVE THE CHOLESTEROL-LOWERING THERAPY, YOU MIGHT THINK YOU WERE WATCHING A PERSON DONATE BLOOD PLATELETS AT THE BLOOD BANK. WASHINGTON UNIVERSITY LIPID RESEARCH SPECIALIST ANNE GOLDBERG SAYS THE TREATMENT USES A FILTER CONTAINING A SUBSTANCE THAT CAN ATTACH TO A PROTEIN FOUND ON LDL, THE SO-CALLED BAD CHOLESTEROL.

(act) :22 o/c the patient

It actually picks up particles containing a certain protein,
a protein found on LDL cholesterol, the bad cholesterol. And
it essentially removes LDL directly from the blood by grabbing
on to it, and what happens is that the plasma that’s had the
LDL removed is then put back together with the patient’s own
red blood cells, and then it gets back into the patient.

GOLDBERG SAYS THE THERAPY IS BEING OFFERED TO PEOPLE WHO HAVE VERY HIGH CHOLESTEROL LEVELS THAT AREN’T SUFFICIENTLY LOWERED WITH STANDARD THERAPIES. SHE SAYS THE LDL APHERESIS TECHNIQUE CAN LOWER BAD CHOLESTEROL BY MORE THAN HALF.

(act) :10 o/c of treatment

So you can see the bad cholesterol, the LDL cholesterol, going
down from about 200 to around 70 or 80 after a couple hours
of treatment.

BUT IT’S NOT A TREATMENT FOR JUST ANYBODY WITH HIGH CHOLESTEROL. IN PEOPLE WHO HAVE DIAGNOSED CARDIOVASCULAR DISEASE, LDL LEVELS HAVE TO BE AT 200 OR HIGHER, AND THE PERSON HAS TO BE ON CHOLESTEROL-LOWERING THERAPY. IN THOSE WHO DON’T HAVE DIAGNOSED CARDIOVASCULAR DISEASE, THE LDL LEVEL HAS TO BE AT LEAST 300.

(act) :26 o/c the blood

So these are people where normal therapy either isn’t
working well enough, or they can’t tolerate enough therapy
to get the levels down. And most of these people are people
who have the severe, genetic type of cholesterol problem,
Familial Hypercholesterolemia. And that involves an abnormality
in a protein, which is used to remove LDL, the bad cholesterol,
from the blood.

GOLDBERG SAYS IT ISN’T UNUSUAL TO SEE VERY BIG DROPS IN LDL LEVELS FOLLOWING THE BLOOD-FILTERING THERAPY. BUT SHE SAYS THOSE LOWER CHOLESTEROL LEVELS DON’T LAST FOREVER.

(act) :12 o/c up again

This is done, usually, every other week. Generally, you’d
like to do it at least 20 times a year, and what happens is
that once you do this removal, the bad cholesterol is lowered
a lot, but then the levels build up again.

GOLDBERG SAYS BECAUSE LDL IS REMOVED FROM THE BLOOD, SOME PEOPLE COMPARE THIS KIND OF THERAPY TO THE DIALYSIS TREATMENT THAT KIDNEY PATIENTS RECEIVE. BUT SHE SAYS THERE ARE SEVERAL KEY DIFFERENCES BETWEEN THE TWO TREATMENT STRATEGIES.

(act) :17 o/c is LDL

In dialysis, you’re trying to remove all sorts of impurities
from the blood, and people often have imbalances in things
like potassium and sodium and stuff. That isn’t the situation
here. We’re not doing anything to any of those things. Basically,
the only thing we’re taking out of the blood is LDL.

THERE IS SOME PRELIMINARY EVIDENCE THAT REGULAR TREATMENT WITH LDL APHERESIS CAN IMPROVE THE HEALTH OF BLOOD VESSESLS IN THESE PATIENTS, BUT GOLDBERG SAYS MORE RESEARCH IS NEEDED TO PROVE THAT. I’M JIM DRYDEN…

RUNS 2:59

THE TECHNIQUE IS CALLED LDL APHERESIS. IT INVOLVES TAKING BLOOD OUT OF THE BODY, FILTERING OUT THE LDL, OR SO-CALLED BAD CHOLESTEROL, AND THEN RETURNING THE BLOOD TO THE BODY. THE THERAPY IS BEING OFFERED TO PEOPLE WHO HAVE VERY HIGH CHOLESTEROL LEVELS THAT AREN’T SUFFICIENTLY LOWERED WITH STANDARD THERAPIES. WASHINGTON UNIVERSITY LIPID RESEARCH SPECIALIST ANNE GOLDBERG SAYS THE LDL APHERESIS TECHNIQUE CAN LOWER BAD CHOLESTEROL BY MORE THAN HALF.

(act) :10 o/c of treatment

So you can see the bad cholesterol, the LDL cholesterol, going
down from about 200 to around 70 or 80 after a couple hours
of treatment.

UNFORTUNATELY, PEOPLE HAVE TO COME BACK FOR THE TREATMENT EVERY COUPLE OF WEEKS BECAUSE LDL CHOLESTEROL BEGINS TO BUILD UP AGAIN IN THE BLOODSTREAM. SHE SAYS MOST CANDIDATES FOR THIS PROCEDURE ARE PEOPLE WITH GENETIC ABNORMALITIES THAT CAUSE THEIR LDL CHOLESTEROL LEVELS TO BE EXTREMELY HIGH. I’M JIM DRYDEN…

RUNS :55

INHERITED FORMS OF ALZHEIMER’S DISEASE ARE RARE, BUT LEARNING HOW THE DISEASE DEVELOPS IN THESE RARE FORMS CAN HELP SCIENTISTS LEARN MORE ABOUT WHAT TO EXPECT IN THE MORE COMMON, SPORADIC FORMS OF THE DISEASE. NOW, WASHINGTON UNIVERSITY’S ALZHEIMER’S DISEASE RESEARCH CENTER IS LEADING A 6-YEAR, INTERNATIONAL RESEARCH EFFORT DESIGNED TO HELP INVESTIGATORS BETTER UNDERSTAND INHERITED FORMS OF THE DISEASE. JIM DRYDEN REPORTS…

WHEN A PARENT HAS ALZHEIMER’S DISEASE, THE CHILD’S RISK INCREASES. WHEN A PARENT HAS A RARE, GENETIC MUTATION THAT CAUSES ALZHEIMER’S DISEASE, THE CHILD’S RISK GOES WAY UP. A NEW RESEARCH EFFORT CALLED THE DOMINANTLY INHERITED ALZHEIMER’S NETWORK, OR DIAN, AIMS TO FOLLOW A LARGE NUMBER OF FAMILIES WITH GENETIC MUTATIONS THAT CAUSE ALZHEIMER’S. THE RESAERCH EFFORT WILL BE LED BY SCIENTISTS AT WASHINGTON UNIVERSITY’S ALZHEIMER’S DISEASE RESEARCH CENTER. CENTER DIRECTOR AND PRINCIPAL INVESTIGATOR FOR DIAN, JOHN MORRIS SAYS PAST WASHINGTON UNIVERSITY STUDIES OF THE ADULT CHILDREN OF ALZHEIMER’S PATIENTS MADE THE UNIVERSITY A NATURAL TO LEAD THIS NEW EFFORT.

(act) :30 o/c have Alzheimer’s

Because our work, including the Adult Children Study, is really
the model for all of this. If you have a parent who has Alzheimer’s,
your chances of getting Alzheimer’s are increased quite dramatically.
But our hypothesis was that even in middle age, it’s possible that
the initial changes in the brain begin, and we would be able to detect
that by comparing the children of parents who had Alzheimer’s with
those whose parents didn’t have Alzheimer’s.

MORRIS SAYS THE RISKS INCREASE EVEN MORE WHEN ONE, OR BOTH, PARENTS HAVE AN INHERITED FORM OF ALZHEIMER’S DISEASE.

(act) :23 o/c for Alzheimer’s

Of the children of a parent who has a known mutation, roughly
half will carry the mutation, and roughly half won’t. So right
away,we can compare those who carry the gene mutation with those
who don’t have it and see if any of these biomarkers or imaging
studies of personality measures or cognitive tests vary. And that
would give us a potential way to develop tests for Alzheimer’s.
KNOWING THAT SOME PEOPLE EVENTUALLY ARE DESTINED TO DEVELOP ALZHEIMER’S DISEASE, AS IS THE CASE IN PEOPLE WITH INHERITED GENETIC MUTATIONS, WILL ALLOW MORRIS AND OTHER RESEARCHERS TO START STUDYING THE CHILDREN OF THOSE WITH INHERITED FORMS OF ALZHEIMER’S AT A VERY YOUNG AGE.

(act) :15 o/c Alzheimer’s begins

We’re actually going to start testing these people at age 21
because we’re going to find out which one of these biomarkers
goes wrong first, so we’ll learn something about the chronology
of the disease. And that will tell us about the mechanisms by
which Alzheimer’s begins.

ONE OTHER ADVANTAGE OF THE DIAN STUDY WILL INVOLVE VALIDATING THE USUAL ASSUMPTIONS THAT IN STUDYING PEOPLE WITH GENETIC FORMS OF ALZHEIMER’S DISEASE, SCIENTISTS ARE LEARNING NOT ONLY ABOUT THOSE TYPES OF ALZHEIMER’S, BUT ABOUT THE MORE COMMON, SPORADIC FORMS OF THE ILLNESS.

(act) :25 o/c of Alzheimer’s

Once the people in this special group of families that have
this mutation actually develop the dementia – they reach age
45; they’ve got the mutation; they develop dementia – we’re
going to characterize that dementia because this is the rarest
form of Alzheimer’s, and what we learn from these people we
want to know is it going to be applicable to the much more
common late-onset. In other words, do they have the same type
of Alzheimer’s?

IN ADDITION TO THE CENTER AT WASHINGTON UNIVERSITY, THE DIAN EFFORT WILL INCLUDE RESEARCHERS AT HARVARD, BROWN, COLUMBIA, INDIANA UNIVERSITY, UCLA AND CENTERS IN ENGLAND AND AUSTRALIA. I’M JIM DRYDEN…

RUNS 3:00

KNOWING THAT SOME PEOPLE EVENTUALLY ARE DESTINED TO DEVELOP ALZHEIMER’S DISEASE, AS IS THE CASE IN PEOPLE WITH INHERITED GENETIC MUTATIONS, SHOULD GIVE SCIENTISTS CLUES ABOUT THE EARLIEST CLINICAL EVIDENCE OF DISEASE. PRINCIPAL INVESTIGATOR JOHN MORRIS SAYS RESEARCHERS WILL LOOK CLOSELY AT THE ADULT CHILDREN OF THOSE WITH GENETIC FORMS OF ALZHEIMER’S, AND BECAUSE THE DISEASE IS INHERITED, IT SHOULD BE POSSIBLE TO START TARGETING THOSE ADULT CHILDREN AT A VERY YOUNG AGE.

(act) :14 o/c Alzheimer’s begins

We’re actually going to start testing these people at age 21.
We’re going to find out which one of these biomarkers goes
wrong first, so we’ll learn something about the chronology of
the disease. And that will tell us about the mechanisms by which
Alzheimer’s begins.

CALLED THE DOMINANTLY INHERITED ALZHEIMER’S NETWORK, OR DIAN, THE NEW RESEARCH EFFORT INVOLVES SCIENTISTS AT A CONSORTIUM OF CENTERS, INCLUDING WASHINGTON UNIVERSITY, HARVARD, BROWN, COLUMBIA UNIVERSITY, INDIANA, UCLA AND CENTERS IN ENGLAND AND AUSTRALIA. I’M JIM DRYDEN…

RUNS :59

CELLS IN OUR BODIES ARE DYING ALL THE TIME. SOMETIMES THEY’RE PROGRAMMED TO DIE DURING NORMAL GROWTH AND DEVELOPMENT, WHILE SOME OF OUR CELLS DIE AS A RESULT OF INFECTIONS OR INJURIES KILL CELLS. HOW THEY DIE IS IMPORTANT TO WHETHER OR NOT THE IMMUNE SYSTEM IS ACTIVATED, AND NOW RESEARCHERS AT WASHINGTON UNIVERSITY IN ST. LOUIS AND ST. JUDE’S IN MEMPHIS HAVE FIGURED OUT A REASON WHY. JIM DRYDEN HAS MORE…

HOW A CELL DIES IS VERY IMPORTANT IN DETERMINING WHAT HAPPENS NEXT IN THE BODY. THERE ARE TWO MAJOR TYPES OF CELL DEATH. PROGRAMMED CELL DEATH, OR APOPTOSIS, IS A NATURAL PART OF DEVELOPMENT. THAT TYPE OF CELL DEATH DOESN’T STIMULATE AN IMMUNE RESPONSE, WHEREAS A TYPE OF CELL DEATH CALLED NECROSIS DOES. THOMAS FERGUSON IS A WASHINGTON UNIVERSITY RESEARCHER.

(act) :07 o/c immune system

So what we’re trying to figure out is how these processes of
cell death signal, or don’t signal, the immune system.

FERGUSON SAYS THERE’S A KEY MOLECULE THAT’S RELEASED WHEN CELLS DIE THROUGH NECROSIS. IT’S CALLED HMGB1, AND IT SIGNALS THE IMMUNE SYSTEM. SCIENTISTS USED TO THINK THAT WHEN CELLS DIED THROUGH APOPTOSIS, THEY DIDN’T RELEASE THE MOLECULE, BUT THAT WAS WRONG.

(act) :36 o/c in another

The dogma, or the line, that had developed is that necrotic
cells release it. Apoptotic cells don’t. Our research, and also
other people’s research. was that in some cases, apoptotic cells
also release this. We had cells that whether they were apoptotic
or whether they were necrotic, they were releasing the protein.
But the cells that were undergoing apoptosis weren’t stimulatory
to the immune system. The cells that were necrotic were stimulatory
to the immune system. So the question is, the molecule’s the same.
Why is it stimulating the immune system in one situation and not
stimulating the immune system in another?

SO WHAT’S THE DIFFERENCE? WELL, FERGUSON SAYS A KEY DIFFERENCE INVOLVES THE RELEASE OF OXYGEN MOLECULES CALLED FREE RADICALS THAT CAN ALTER THE MAKE-UP OF THE MOLECULE THAT SIGNALS THE IMMUNE SYSTEM.
(act) :20 o/c this molecule

What we found was that during apoptosis, even though this
molecule is released, the process of apoptosis modifies that
protein, so it can’t stimulate the immune system. And the way
it does it is during apoptosis, reactive oxygen species, or
free radicals, are produced, and these free radicals actually
modify this molecule.

IN NECROSIS THERE ARE NO FREE RADICALS RELEASED, SO THE MOLECULE IS FREE SEND ITS SIGNAL TO THE IMMUNE SYSTEM UNIMPEDED. FERGUSON SAYS UNDERSTANDING HOW THIS SYSTEM WORKS MAY BE IMPORTANT IN AUTOIMMUNE DISEASES, SUCH AS ARTHRITIS OR DIABETES. IN THOSE CONDITIONS, THE IMMUNE SYSTEM IS ACTIVATED INAPPROPRIATELY AND CAN DESTROY HEALTHY TISSUE. ALTERING IMMUNE SIGNALLING IN THOSE CONDITIONS MIGHT BE A WAY TO TREAT THEM MORE EFFFECTIVELY. HE SAYS THE FINDING ALSO MIGHT HELP SCIENTISTS MAKE CANCER TREATMENTS MORE EFFECTIVE..

(act) :23 o/c as successful

For example, let’s say a chemotherapeutic agent kills a tumor,
but the tumor when it dies doesn’t release reactive oxygen. That
tumor might then be immunogenic, and the chemotherapy might be
more successful. If the tumor does make reactive oxygen, it’s
possible that it’s not as immunogenic, and therefore, the
chemotherapeutic might not be as successful.

FERGUSON AND HIS COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL IMMUNITY. I’M JIM DRYDEN…

RUNS 2:48

PROGRAMMED CELL DEATH, OR APOPTOSIS, IS A NATURAL PART OF DEVELOPMENT. CELLS ARE DYING ALL THE TIME FOR VARIOUS REASONS, BUT THAT CELL DEATH DOES NOT STIMULATE AN IMMUNE RESPONSE, WHEREAS A TYPE OF CELL DEATH CALLED NECROSIS DOES. THAT’S BECAUSE INFECTIONS CAN CAUSE NECROSIS. WASHINGTON UNIVERSITY RESEARCHER THOMAS FERGUSON SAYS NO MATTER HOW THEY DIE, CELLS RELEASE A CERTAIN MOLECULE THAT SIGNALS THE IMMUNE SYSTEM.

(act) :21 o/c immune system

During apoptosis, even though this molecule is released, the
process of apoptosis modifies that protein, so it can’t stimulate
the immune system. And the way it does it is during apoptosis,
reactive oxygen species, or free radicals, are produced, and
these free radicals actually modify this molecule and prevent
it from stimulating the immune system.

IN NECROSIS THERE’S NO FREE RADICALS RELEASED, SO THE MOLECULE CAN SEND ITS SIGNAL TO THE IMMUNE SYSTEM. THE FINDING IS IMPORTANT IN UNDERSTANDING PROBLEMS SUCH AS AUTOIMMUNITY AND ALSO MAY HELP MAKE SOME CANCER THERAPIES MORE EFFECTIVE. I’M JIM DRYDEN…

RUNS :59

AS NEWER DRUGS HAVE DRAMATICALLY REDUCED DEATH RATES AMONG PEOPLE WITH HIV INFECTION, SCIENTISTS HAVE NOTED THAT THOSE PATIENTS TEND TO DEVELOP OTHER COMPLICATIONS, SUCH AS CARDIOVASCULAR DISEASE, AT VERY HIGH RATES. AND WASHINGTON UNIVERSITY SCIENTISTS ARE JOINING OTHERS AROUND THE COUNTRY TO LOOK AT WHY THE RISKS INCREASE AND HOW THEY MIGHT BEST TREAT THE PROBLEM. JIM DRYDEN REPORTS…

THE DRUGS USED TO TREAT HIV INFECTION SEEM TO CONTRIBUTE TO SOME RISK FACTORS, SUCH AS ABNORMAL CHOLESTEROL, BUT OTHER RISK FACTORS APPEAR TO BE RELATED TO THE HIV VIRUS ITSELF, ACCORDING TO WASHINGTON UNIVERSITY RESEARCHER KEVIN YARASHESKI.

(act) :26 o/c add risk

There’s evidence to suggest that, yes, having HIV and having
all these cardio-metabolic risk factors is a little bit more
risky than not having HIV and all of these cardio-metabolic
risk factors. You’re at about a one-and-a-half to two-fold
greater risk if you have HIV and all of these risk factors
than if you don’t have HIV and these risk factors. So yeah,
the hypothesis that we’re going to test is does HIV, by
itself, add risk?

YARASHESKI WAS AMONG ABOUT A DOZEN WASHINGTON UNIVERSITY RESEARCHERS WHO MET THIS SUMMER WITH COLLEAGUES FROM AROUND THE COUNTRY TO DISCUSS THE NEXT STEPS IN THE BATTLE WITH HIV. NOW THAT HIV INFECTION IS NO LONGER A DEATH SENTENCE, YARASHESKI SAYS IT’S CLEAR MORE RESEARCH IS NEEDED INTO HOW HIV IS AFFECTING CARDIOVASCULAR RISK.

(act) :29 o/c risk profile

The hypothesis is, yeah, HIV adds to that. HIV is a chronic
infection. It’s going to cause inflammation in the body. We
know that inflammation is bad when it gets into the vessels.
We know that inflammation is bad when it gets into the heart
muscle. We know that inflammation is bad when it gets into
fat tissue, and we believe that that is one of the molecular-level
events that needs to be looked at in order to put this, this
entire picture together as to what is it about HIV infection
that adds risk to the standard cardiovascular risk profile?

YARASHESKI SAYS IT’S IMPORTANT THAT RESEARCHERS LOOK MORE CLOSELY AT WHAT’S GOING ON WITH HIV AND CARDIOVASCULAR DISEASE. HIS TEAM IS PLANNING TO USE SOPHISTICATED IMAGING TECHIQUES TO LOOK AT HOW THE HEART USES ENERGY AND WHETHER THE HIV VIRUS ALTERS THAT SOMEHOW.

(act) :22 o/c to happen

The question about cardiovascular disease in HIV-infected
people still needs a little more elucidation. How much more
risk, putting a number on it, how much more absolute risk
is there to having a cardiovascular event when you’re
HIV-positive versus not-HIV-positive? And then, yeah, what
are the molecular-level events that cause this to happen?

BUT WHILE WAITING FOR THE RESULTS OF NEW RESEARCH, YARASHESKI SAYS IT’S CLEAR THAT IT’S NOT ONLY THE VIRUS AND THE MEDICATION THAT ARE INCREASING THE RISK OF CARDIOVASCULAR PROBLEMS. HE SAYS ONE SURE WAY TO LOWER RISK WOULD BE TO HELP HIV-INFECTED PEOPLE STOP SMOKING.

(act) :32 o/c pharmaceutical interventions

Forty to 50 percent of the people who have HIV use tobacco, and we
know that tobacco is a great risk factor for cardiovascular disease,
so finding ways to stop smoking in the HIV population would probably
have the biggest impact on reducing cardiovascular disease, over and
above any of the statins or the glucose-lowering or the anti-hypertensive
drugs that we might want to give to HIV-infected people. So probably
smoking cessation would be step number one, and then you’d start thinking
about pharmaceutical interventions.

AND HOW TO DESIGN BETTER PHARMACEUTICAL INTERVENTIONS THAT ADDRESS WHAT’S REALLY GOING ON AT THE MOLECULAR LEVEL. I’M JIM DRYDEN…

RUNS 2:59

SOME RISK FACTORS, SUCH AS ABNORMAL CHOLESTEROL, MAY BE CAUSED BY HIV MEDICATIONS. BUT OTHER RISK FACTORS APPEAR TO BE RELATED TO THE HIV VIRUS ITSELF, ACCORDING TO RESEARCHER KEVIN YARASHESKI. HE WAS AMONG ABOUT A DOZEN WASHINGTON UNIVERSITY RESEARCHERS WHO MET WITH COLLEAGUES FROM AROUND THE COUNTRY TO DISCUSS THE NEXT STEPS NOW THAT HIV INFECTION IS NO LONGER A RAPID DEATH SENTENCE. YARASHESKI SAYS IT’S CLEAR MORE RESEARCH IS NEEDED INTO HOW HIV AFFECTS CARDIOVASCULAR RISK.

(act) :17 o/c looked at

HIV is a chronic infection. It’s going to cause inflammation
in the body. We know that inflammation is bad when it gets
into the vessels. We know that inflammation is bad when it
gets into the heart muscle. We know that inflammation is
bad when it gets into fat tissue, and we believe that that
is one of the molecular-level events that needs to be looked
at.

YARASHESKI SAYS HIS TEAM IS PLANNING TO USE SOPHISTICATED IMAGING TECHNIQUES TO LOOK AT HOW THE HEART USES ENERGY AND HOW THE HIV VIRUS MIGHT AFFECT THAT. BUT HE SAYS ONE SURE WAY TO QUICKLY LOWER RISK WOULD BE TO GET HIV-INFECTED PEOPLE TO STOP SMOKING. ABOUT 40 TO 50 PERCENT OF PEOPLE WITH HIV USE TOBACCO. I’M JIM DRYDEN…

RUNS 1:00

WEEKENDS CAN BE BAD FOR WEIGHT-LOSS PROGRAMS. STUDYING PEOPLE WHO WERE EXERCISING MORE OR EATING LESS, RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE FOUND THAT SATURDAYS ARE THE WORST ENEMY OF EXERCISE AND CALORIE RESTRICTION PROGRAMS. JIM DRYDEN HAS MORE…

LOSING WEIGHT IS ALWAYS HARD. KEEPING IT OFF IS EVEN HARDER. BUT ONE THING THOSE WHO DO LOSE WEIGHT TEND TO HAVE IN COMMEN IS THAT THEY MAINTAIN CONSISTENT DIET AND ACTIVITY PATTERNS OVER THE LONG TERM, ACCORDING TO WASHINGTON UNIVERSITY EXERCISE AND NUTRITION RESEARCHER SUSAN RACETTE.

(act) :28 o/c exercise programs

From day to day, weekends to weekdays, they follow a more regular
pattern that helps them to maintain a significant weight loss. So
we were interested in looking at this because another thing, in
the way of background, is that a lot of people when they’re trying
to lose weight – whether on their own or through a formal, research
study like ours – they don’t lose as much as is expected sometimes.
And so we were also curious in understanding what hinders adherence
to some of these diet and exercise programs.

SHE FOLLOWED ADULTS BETWEEN 50 AND 60 YEARS OLD WHO WERE EITHER EXERCISING OR RESTRICTING THEIR CALORIES. SOME SUBJECTS CUT CALORIE INTAKE BY 20 PERCENT. OTHERS INCREASED THEIR DAILY ACTIVITY BY 20 PERCENT. RACETTE SAYS BOTH THOSE WHO EXERCISED AND THOSE WHO RESTRICTED CALORIES HAD PROBLEMS MAINTAING THE PROGRAM ON WEEKENDS.

(act) :22 o/c stop losing

People were eating more, in particular on Saturdays, as
compared to the weekdays. Their exercise was higher on
Saturdays, lower on Sundays, but it was, you know, a bit
variable. But clearly, the energy intake contributed more
to the weight gain than the activity patterns, but even
during the intervention with the CR intervention, people
would lose weight nicely during the week, and then on the
weekend, they would stop losing.

THIS WAS PART OF A BIGGER STUDY TO LEARN WHETHER WEIGHT LOSS MIGHT ELIMINATE SOME OF THE COMMON MARKERS OF AGING AND DISEASE. CALORIE RESTRICTION, IN PARTICULAR, IS KNOWN TO INCREASE THE LENGTH OF LIFE AND TO ELIMINATE DISEASE IN RATS. NOW RESEARCHERS ARE TRYING TO LEARN WHETHER IT HAS SIMILAR EFFECTS IN HUMANS, BUT RACETTE SAYS THERE IS AT LEAST ONE BIG DIFFERENCE.

(act) :27 o/c the weekdays

Rats don’t have weekends the way people do, and so we know that
on weekends, lifestyle patterns for a lot of people are very
different. We have social events, and so for example if you have
parties to go to, if you’re out at a bar, if you have family
gatherings where there’s a lot of food, if you have sports
events for your children, and you’re out at fields all day,
and you’re relying on concession stands; a lot of things are
just very different, and we’re less structured on weekends
than we generally are during the weekdays.

RACETTE SAYS ONE WAY TO TRY AND LIMIT THE NEGATIVE EFFECTS OF WEEKENDS IS TO PLAN AHEAD SO THAT YOU DON’T SHOW UP HUNGRY AT THE PARTY OR DRINK TOO MUCH ALCOHOL AT A FAMILY GATHERING. AND AS RACETTE AND OTHER INVESTIGATORS CONTINUE TO LOOK AT CALORIE RESTRICTION AND EXERCISE IN TIGHTLY CONTROLLED STUDIES, SHE ALSO RECOMMENDS THAT STUDY SUBJECTS PLAY TO WEIGH IN EVERY DAY.

(act) :21 o/c more careful

One of the recommendations for our intervention participants
is to do daily weights because it enables us to keep track more
closely. Instead of arriving, you know, on Wednesday and saying,
“Oh, my goodness! Look at my weight is so much up!” If they do
daily weights, it does help people adhere a little bit more on
the weekends and to be aware that, okay, Saturday I ate a little
too much or drank a little too much, so Sunday I need to be a
little more careful.

SHE REPORTED THE FINDINGS IN THE JOURNAL OBESITY. I’M JIM DRYDEN…

RUNS 3:00

THE RESEARCHERS WERE STUDYING ADULTS BETWEEN 50 AND 60 YEARS OLD WHO WERE EITHER EXERCISING OR RESTRICTING THEIR CALORIC INTAKE AS PART OF A STUDY TO LEARN WHETHER WEIGHT LOSS MIGHT ELIMINATE SOME OF THE COMMON MARKERS OF AGING AND DISEASE. SOME SUBJECTS CUT CALORIE INTAKE BY 20 PERCENT. OTHERS INCREASED THEIR DAILY ACTIVITY BY 20 PERCENT. FIRST AUTHOR SUSAN RACETTE SAYS BOTH THOSE WHO EXERCISED AND THOSE WHO RESTRICTED CALORIES HAD PROBLEMS MAINTAING THE PROGRAM ON WEEKENDS.

(act) :23 o/c stop losing

People were eating more, in particular on Saturdays, as
compared to the weekdays. Their exercise was higher on
Saturdays, lower on Sundays, but it was, you know, a bit
variable. But clearly, the energy intake contributed more
to the weight gain than the activity patterns, but even
during the intervention with the CR intervention, people
would lose weight nicely during the week, and then on the
weekend, they would stop losing.

RACETTE SAYS THE FINDINGS WERE NOT ALL THAT SURPRISING, BUT WHAT DID SURPRISE HER WAS HOW CONSISTENTLY THE STUDY PARTICIPANTS TENDED TO OVEREAT ON WEEKENDS. SHE REPORTED THE FINDINGS IN THE JOURNAL OBESITY. I’M JIM DRYDEN…

RUNS 1:00

ANIMALS HAVE A FASCINATION WITH WASTE PRODUCTS THAT MOST OF US HUMANS DON’T SHARE. BUT NEW RESEARCH FROM RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS DEMONSTRATES THAT IN THE CASE OF MICE, IT’S POSSIBLE FOR MALE MICE TO LEARN A LOT ABOUT FEMALES SIMPLY BY INVESTIGATING THEIR URINE, AND THE FINDING MAY EVEN PROVIDE SOME CLUES ABOUT HUMAN HEALTH AND BEHAVIOR. JIM DRYDEN HAS THE STORY...

WASHINGTON UNIVERSITY NEUROBIOLOGIST TIMOTHY HOLY IS FASCINATED WITH HOW MICE USE THEIR NOSES. HOLY HAS PREVIOUSLY FOUND THAT FEMALE MICE OR THEIR ODORS CAN CAUSE MALES TO BREAK INTO MOUSE SONG. NOW, HE’S FOCUSING ON ONE OF THE CHIEF TRANSMITTERS OF FEMALE MOUSE ODORS. THAT WOULD BE URINE.

(act) :03 o/c very informative

These waste products are, actually, often very informative.

HOLY SAYS THE URINE MAY ENCODE MESSAGES IN THE FORM OF CHEMICAL PHEROMONES. MICE HAVE WHAT’S KNOWN AS AN ACCESSORY OLFACTORY SYSTEM, AN ABILITY TO USE SMELL IN WAYS THAT HIGHER MAMMALS, LIKE HUMANS, CANNOT. AND HE CAN MEASURE THE ACTIVITY OF NERVE CELLS IN THIS ACCESSORY OLFACTORY SYSTEM TO FIND OUT WHAT THE CELLS DO IN RESPONSE TO CERTAIN SCENTS. THOSE CELLS SEEM PARTICULARLY TUNED IN TO SUBSTANCES FOUND IN MOUSE URINE CALLED SULFATED STEROIDS.

(act) :27 o/c sulfated steroids

And so what we decided to do is just simply take urine, the natural
stimulus, and start splitting it up into its component pieces. And
what we were very surprised to find is that a very large percentage
of the activity was really due to very few purified fractions, and
it turned out in the end to be because most of the activity seems
to be due to a set of compounds that are all very closely related
to each other, which are the sulfated steroids.

HOLY SAYS THE HORMONES IN THE URINE SEEM TO ACT A LITTLE LIKE A FIGERPRINT THAT CAN PROVIDE A LOT ABOUT THE ANIMAL’S HEALTH AND BEHAVIOR.

(act) :31 o/c information available

If you take a mouse, and you expose it to a brief restraint
stress, just by holding if for a few minutes, there’s a steroid,
corticosterone, that rises in the bloodstream under those conditions.
And we found that that also, specifically, rises in the urine,
whereas there are other sulfated steroids that don’t rise or don’t
rise as much as that. So it looks, both from the level of the ability
to detect individual compounds but also in how they’re affected by
the behavioral experience of the animal, that there’s probably going
to prove to be quite a lot of very specific information available.

TYPICALLY, WE THINK OF PHEROMONES AS SUBSTANCES THAT FACILITATE SEXUAL ATTRACTION, BUT HOLY SAYS THESE SULFATED STEROIDS SEEM TO HAVE A DIFFERENT ROLE.

(act) :22 o/c about you

Popularly, and perhaps even to a limited extent scientifically,
there’s sort of a view of pheromones as attractants, something
that draws an animal to you and makes it want to mate with
you. And I think this suggests it’s really kind of the opposite.
It’s that other animals are interested in evaluating who you are
and, perhaps, how good you are. They’re essentially collecting
information about you.

BUT HOW DO THESE FINDINGS APPLY TO US? AFTER ALL, WE DON’T EVEN HAVE THE ACCESSORY OLFACTORY ABILITY THAT THE MICE USE TO DETECT THE PRESENCE OF THESE SULFATED STEROIDS.

(act) :18 o/c mammalian physiology

If we find that the change in the levels of certain sulfated
steroids are correlated with very particular types of behavioral
conditions and that other mice care about those very particular
types of behavioral conditions, then I think there’s at least
some chance that we’ll discover some unexpected roles for steroids
in general in mammalian physiology.

HOLY AND HIS COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL OF NEUROSICENCE. I’M JIM DRYDEN…

RUNS 2:57

LED BY WASHINGTON UNIVERSITY NEUROBIOLOGIST TIMOTHY HOLY, THE REARCHERS STUDIED URINE EXCRETED BY FEMALE MICE. HOLY SAYS URINE IS LOCADED WITH CLUES ABOUT HEALTH.

(act) :03 o/c very informative

These waste products are, actually, often very informative.

HOLY SAYS URINE ALSO PROVIDES A WAY FOR MICE TO CLEAR STEROIDS FROM THEIR BODIES, AND SOME, CALLED SULFATED STEROIDS, APPEAR IMPORTANT IN COMMUNICATION BETWEEN MALE AND FEMALE. HOLY SAYS THE OLFACTORY SYSTEM IN THE MALE MOUSE IS UNUSUALLY ATTUNED TO THE PRESENCE OF THE STEROIDS.

(act) :15 o/c sulfated steroids

And so what we decided to do is just simply take urine, the
natural stimulus, and start splitting it up into its component
pieces. Most of the activity seems to be due to a set of
compounds that are all very closely related to each other,
which are the sulfated steroids.

HOLY SAYS THESE FINDINGS DEMONSTRATE THAT PHEROMONES DO MORE THAN JUST ATTRACT ONE ANIMAL TO ANOTHER. HE SAYS IT MAY BE THAT THESE SECRETIONS ARE MORE LIKE A MOUSE’S FINGERPRINT IN THAT THEY REVEAL QUITE A BIT ABOUT THE ANIMAL’S HEALTH AND PERSONAL TRAITS. I’M JIM DRYDEN…

RUNS :58

EVERY YEAR ON JULY 4TH, THOUSANDS OF PEOPLE ARE INJURED, AND A FEW EVEN DIE SETTING OFF FIREWORKS. IN TERMS OF THE RISK OF DEATH, FIREWORKS ARE MUCH LESS DANGEROUS THAN SAY, DRIVING A CAR ON THE INTERSTATE OVER THE HOLIDAY WEEKEND, BUT SOME PEOPLE HAVE TO TRAVEL, WHEREAS EMERGENCY MEDICINE SPECIALISTS AT WASHINGTON UNIVERSITY AND ST. LOUIS CHILDREN’S HOSPITAL SAY THERE’S NO GOOD REASON FOR PEOPLE TO SET OFF BACK-YARD FIREWORKS. JIM DRYDEN HAS THE STORY…

WASHINGTON UNIVERSITY EMERGENCY MEDICINE SPECIALIST BO KENNEDY SAYS HE’S HOPING THE EMERGENCY DEPARTMENT AT ST. LOUIS CHILDREN’S HOSPITAL WON’T BE BUSY ON JULY 4TH. BUT HE EXPECTS THE OPPOSITE WILL BE TRUE.

(act) :13 o/c very busy

Holidays tend to be quieter during the day, but in the
evening when people are beginning to settle down, or when
children are not being as closely watched and the serious
injuries occur, then they usually get very busy.

KENNEDY SAYS INDEPENDENCE DAY IS A DAY WHEN LOTS OF INJURIES OCCUR, FROM BEE STINGS AT PICNICS TO BURNS NEAR THE BARBECUE TO THE KINDS OF INJURIES PEOPLE GET WHEN FIREWORKS GO AWRY. JUST ABOUT EVERYBODY HAS A STORY ABOUT THAT TIME THE WICK ON THE BOTTLE ROCKET BURNED TOO QUICKLY, OR THE SPARKS FROM THE FIREWORKS FOUNTAIN CHASED THEM ACROSS THE YARD. FORTUNATELY, MOST OF THOSE STORIES ARE ABOUT NEAR MISSES. AND KENNEDY ADMITS THAT INJURIES FROM BACK-YARD FIREWORKS ARE RELATIVELY RARE…BUT

(act) :16 o/c serious injury

It’s more than just playing the odds, it’s what are the stakes?
The problem with fireworks is that the stakes are pretty high.
The odds are reasonably good that you’re not going to get hurt.
A lot of people shoot off fireworks and don’t get hurt, but when
they do get hurt, it tends to be a more serious injury.

THOSE CAN INCLUDE SERIOUS BURNS OR EVEN SOMETIMES THE SEVERE INJURY OR LOSS OF A FINGER. THE EYE ALSO IS A FREQUENT SITE OF INJURY.

(act) :20 o/c the eye
I think partly people are looking to see either what’s
wrong – why didn’t it go off? – when it does explode. Or
they want to see what kind of image or, you know, what it’s
going to cause. And so they’re looking directly at the
fireworks, and so when it does explode, things go in a
straight line, and if you’re looking at it, it tends to
go straight for the eye.

EVEN THOSE TYPES OF FIREWORKS THAT MANY THINK OF AS “SAFE” CAN CAUSE SERIOUS PROBLEMS. DATA FROM THE CENTERS FOR DISEASE CONTROL SHOWS SPARKLERS CAUSE THE HIGHEST NUMBER OF INJURIES IN CHILDREN UNDER THE AGE OF 5.

(act) :11 o/c deep burn

Sparklers are actually burning at more than 1,000 degrees,
and you get touched even briefly by a sparkler, and that
can be a very deep burn.

KENNEDY SAYS EVEN THOSE PARENTS WHO DON’T PLAN TO SET OFF BACK-YARD FIREWORKS SHOULD REMEMBER THAT THERE ARE PLENTY OF OTHER DANGERS ASSOCIATED WITH JULY 4TH, FROM ACCIDENTAL DROWNINGS IN THE POOL OR THE LAKE TO INJURIES FROM RIDING ATVs AND SERIOUS INJURIES THAT CAN OCCUR WHEN YOUNG CHILDREN DART OUT INTO TRAFFIC AFTER THE FIREWORKS FINALE.

(act) :29 o/c we see

If parents are watching closely and paying attention to what
their children are doing, it’s very likely that they’ll prevent
them from getting into serious trouble. But parents are usually
quite busy with their friends. Perhaps alcohol is going on,
where the parents aren’t paying as much attention, and so,
for the child to step on the hot coals from the barbecue, that
have been dumped out of to step into traffic, darting out between
cars when it’s dark. These are some of the other types of
I injuries that we see.

NOT ALL ACCIDENTS CAN BE PREVENTED. BUT KENNEDY SAYS IF FAMILIES TAKE SOME PRECAUTIONS AND AVOID THINGS LIKE BACK-YARD FIREWORKS, IT’LL BE A MUCH BETTER BET THAT INDEPENDENCE DAY WILL BE A TIME FOR CELEBRATION, RATHER THAN AN OCCASION FOR INJURY. I’M JIM DRYDEN…

RUNS 2:58

JUST ABOUT EVERYBODY HAS A STORY ABOUT THAT TIME THE WICK ON THE BOTTLE ROCKET BURNED TOO QUICKLY, OR THE SPARKS FROM THE FIREWORKS FOUNTAIN CHASED THEM ACROSS THE YARD. FORTUNATELY, ACCORDING TO BO KENNEDY, A WASHINGTON UNIVERSITY EMERGENCY MEDICINE SPECIALIST AT ST. LOUIS CHILDREN’S HOSPITAL, INJURIES FROM BACK-YARD FIREWORKS ARE RELATIVELY RARE…BUT

(act) :16 o/c serious injury

It’s more than just playing the odds, it’s what are the stakes?
The problem with fireworks is that the stakes are pretty high.
The odds are reasonably good that you’re not going to get hurt.
A lot of people shoot off fireworks and don’t get hurt, but when
they do get hurt, it tends to be a more serious injury.

LIKE A BAD BURN OR A SERIOUS EYE INJURY. EVEN SO-CALLED “SAFE” FIREWORKS LIKE SPARKLERS CAN CAUSE BIG PROBLEMS. DATA FROM THE CENTERS FOR DISEASE CONTROL SHOWS SPARKLERS CAUSE THE HIGHEST NUMBER OF INJURIES IN CHILDREN UNDER THE AGE OF 5. SO KENNEDY ADVISES AGAIN THIS YEAR THAT RATHER THAN TAKING RISKS IN THE BACK YARD, PEOPLE SHOULD PLAN TO ATTEND A PROFESSIONAL FIREWORKS DISPLAY INSTEAD. I’M JIM DRYDEN…

RUNS :57

INJURIES ARE A FACT OF LIFE FOR FOOTBALL PLAYERS. MOST NFL SEASONS FEATURE INJURIES RANGING FROM BUMPS AND BRUISES TO SERIOUS CONCUSSIONS. NOW A TEAM OF RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS IS LOOKING AT NFL INJURY RECORDS TO SEE HOW MANY PLAYERS GET INJURED, THE MOST COMMON CAUSES OF THOSE INJURIES AND WHETHER SOME OF THEM MIGHT BE PREVETABLE. THEY BEGIN WITH A LOOK AT THE VERY COMMON INJURIES PLAYERS EXPERIENCE TO THEIR FINGERS AND HANDS. JIM DRYDEN REPORTS…

FROM 1996 THROUGH 2005, THERE WERE 1,385 HAND, FINGER AND THUMB INJURIES REPORTED AMONG NFL PLAYERS. UNLIKE A CONCUSSION OR A KNEE INJURY, MANY PLAYERS CAN CONTINUE PLAYING WITH HAND, FINGER AND THUMB INJURIES, ACCORDING TO WASHINGTON UNIVERSITY SPORTS MEDICINE SPECIALIST MATTHEW MATAVA, WHO ALSO IS A TEAM PHYSICIAN FOR THE NFL’S ST. LOUIS RAMS.

(act) :13 o/c was injured

A lot of these injuries are treated probably unbeknownst to
the general public. We’ll have a lot of players who wear
protective braces, protective casts, and the majority of
people, both at the game and on TV, didn’t even know the
player was injured.

MATAVA AND HIS COLLEAGUES WORKED WITH THE NFL’S SPORTS INJURY MONITORING SYSTEM TO LEARN HOW MANY PLAYERS HAD INJURIES INVOLVING THEIR HANDS DURING THE COURSE OF 10 SEASONS, HOW THEY SUSTAINED THOSE INJURIES AND WHAT POSITIONS THEY PLAYED. OFFENSIVE AND DEFENSIVE LINEMAN WERE THE MOST LIKELY TO HAVE HAND INJURIES. 80 PERCENT OF THE REPORTED HAND INJURIES INVOLVED BROKEN FINGERS. 28 PERCENT OF THE INJURIES OCCURRED DURING TACKLING. AND MATAVA SAYS THERE REALLY AREN’T MANY WAYS TO PROTECT SOME OF THESE PLAYERS FROM THESE KINDS OF INJURIES.

((act) :15 o/c certain level

We “buddy tape” fingers. We put splints on fingers, but at the
end of the day, certain positions: receiver, running back –
the so-called skill positions, quarterback, they need to have
their five digits essentially fairly mobile. Otherwise they’re
not able to function at a certain level.
MATAVA SAYS IT’S EASIER TO BRACE OR IMMOBILIZE THE HANDS AND FINGERS OF DEFENSIVE PLAYERS BECAUSE THEY DON’T NEED USUALLY NEED TO CATCH A FOOTBALL OR USE THEIR FINGERS THE WAY THAT BLOCKERS DO ON OFFENSE. BUT HE SAYS EVEN PUTTING A PLAYER IN A BRACE OR A CAST DOESN’T ALWAYS PREVENT THESE KINDS OF INJURIES ANYWAY.

(act) :23 o/c it happens

We are looking into preventive ways of dealing with this sort
of thing. We haven’t figured out or found a foolproof cast or
brace that’s going to allow a player to have complete mobility
of the joint or hand and still thoroughly prevent injury. So it’s
probably going to be one of those things where if you’re going
to play football, you are going to be at risk of certain injuries.
The purpose of this paper was to document what that risk is,
who it happens to and how often it happens.

MATAVA SAYS CLOSE STUDY OF THIS COMPREHENSIVE INJURY DATABASE NOT ONLY HELPS SPORTS MEDICINE SPECIALISTS KNOW WHAT HAS HAPPENED OVER THE YEARS IN THE NFL. HE SAYS THE DATA ALSO CONTAINS INFORMATION THAT MIGHT BE APPLIED IN COLLEGES AND HIGH SCHOOLS, TO PREDICT THE RISK OF INJURY AND TRY TO PREVENT THOSE INJURIES WHEN POSSIBLE.

(act) :26 o/c high school level

Some of the previous papers that have been written on this deal
with a hodge-podge of injuries, in other words “football injuries”
in general. There might be a paragraph on hand and wrist injuries,
not very comprehensive. There’s no breakdown by position, you know,
what sort of activity caused it and that sort of thing. So we hope
that this is the “gold standard” paper that addresses this particular
facet of football-related injuries and then that it, perhaps, will
trickle down to the NCAA level and to the high school level.

MATAVA AND HIS COLLEAGUES REPORTED THEIR FINDINGS IN THE AMERICAN JOURNAL OF SPORTS MEDICINE. I’M JIM DRYDEN…

RUNS 2:50

FROM 1996 THROUGH 2005, THERE WERE 1,385 HAND, FINGER AND THUMB INJURIES REPORTED AMONG NFL PLAYERS. SOME, LIKE LINEMEN, WERE ABLE TO KEEP PLAYING WITH CASTS OR BRACES ON FINGERS AND HANDS. OTHERS, SUCH AS QUARTERBACKS, MISSED PLAYING TIME. WASHINGTON UNIVERSITY SPORTS MEDICINE SPECIALIST MATTHEW MATAVA IS A TEAM PHYSICIAN FOR THE NFL’S ST. LOUIS RAMS. HE SAYS IT’S DIFFICULT TO PREVENT HAND AND FINGER INJURIES BECAUSE A LARGE NUMBER OF THEM, SOME 28 PERCENT, OCCUR DURING TACKLING, SOMETHING THAT’S KIND OF ESSENTIAL IN A FOOTBALL GAME.

((act) :14 o/c certain level

We “buddy tape” fingers. We put splints on fingers, but at the
end of the day, certain positions: receiver, running back,
quarterback, they need to have their five digits essentially
fairly mobile. Otherwise they’re not able to function at a
certain level.

MATAVA AND COLLEAGUES SAY THEY HOPE SOME OF THESE FINDINGS MAY BE APPLIED TO COLLEGE AND HIGH SCHOOL ATHLETES SO THAT DOCTORS AND TRAINERS KNOW WHAT SORTS OF INJURIES TO EXPECT…EVEN IF THERE’S NOT ALWAYS A GOOD WAY TO PREVENT THEM. I’M JIM DRYDEN…

RUNS :58

VARIATIONS IN A GENE THAT MANUFACTURES A PROTEIN FOUND IN LARGE AMOUNTS IN THE BRAINS OF ALZHEIMER’S DISEASE PATIENTS APPEAR TO BE RELATED TO AN EARLIER ONSET OF ALZHEIMER’S DISEASE SYMPTOMS. RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS SAY A DNA VARIATION IN A GENE THAT MAKE A PROTEIN CALLED TAU MAY HELP THEM UNDERSTAND WHY SOME ALZHEIMER’S PATIENTS DEVELOP SYMPTOMS MORE QUICKLY THAN OTHERS. JIM DRYDEN REPORTS …

THERE ARE TWO KEY PROTEINS THAT SCIENTISTS TALK ABOUT WHEN DISCUSSING ALZHEIMER’S DISEASE. ONE IS AMYLOID-BETA, WHICH MAKES UP THE SENILE PLAQUES THAT DOT THE BRAINS OF ALZHEIMER’S PATIENTS. THE OTHER PROTEIN IS CALLED TAU, AND IT’S FOUND PRIMARILY IN THE NEUROFIBRILLARY TANGLES THAT ALSO ARE LOCATED IN THE BRAIN’S OF PEOPLE WITH ALZHEIMER’S DISEASE. NOW, STUDYING DNA FROM MORE THAN 300 SUBJECTS AT WASHINGTON UNIVERSITY’S ALZHEIMER’S DISEASE RESEARCH CENTER, A TEAM OF SCIENTISTS HAS IDENTIFIED A KEY GENETIC VARIATION THAT AFFECTS LEVELS OF THE TAU PROTEIN. PRINCIPAL INVESTIGATOR ALISON GOATE SAYS IT’S POSSIBLE TO MEASURE LEVELS OF SOLUBLE TAU AND AMYLOID-BETA IN THE CEREBROSPINAL FLUID THAT SURROUNDS THE BRAIN. WHEN FLUID LEVELS OF TAU ARE HIGH AND AMYLOID-BETA LOW, THE PROGNOSIS USUALLY ISN’T GOOD.

(act) :18 o/c of dementia

So the ratio of those two is a pretty sensitive biomarker for
predicting, first of all, whether someone’s about to develop
disease, and also in people who have dementia, the ratio is
predictive of Alzheimer’s disease rather than other causes of
dementia.

IT’S FREQUENTLY TRUE THAT YEARS BEFORE THEY DEVELOP DEMENTIA, PATIENTS WILL HAVE AMYLOID-BETA IN THE BRAIN. GOATE’S TEAM FOUND THAT WHEN A PERSON HAS A PARTICULAR VARIANT OF THE TAU GENE, THEY END UP WITH HIGHER LEVELS OF THE TAU PROTEIN IN THE CEREBROSPINAL FLUID, BUT ONLY WHEN THEY ALSO HAVE AMYLOID-BETA PRESENT IN THE BRAIN.

(act) :19 o/c amyloid deposition

The association between the tau sequence variants and tau
protein levels in the CSF was only seen in people who had
amyloid deposition in the brain. These tau variants were
only having an impact on the levels of tau in the presence
of amyloid deposition.

GOATE SAYS THESE FINDING TENDS TO SUPPORT THE IDEA THAT WHEN AMYLOID-BETA BEGINS TO COLLECT IN THE BRAIN, TAU STARTS TO INFLUENCE THE DEVELOPMENT OF BOTH CLINICAL SYMPTOMS SUCH AS THE MEMORY LOSS AND OTHER COGNITIVE PROBLEMS AND DAMAGE TO NERVE CELLS.

(act) :23 o/c cell death

In the individuals who are releasing more tau, have higher
tau levels, you have more cellular damage. So there’s a worse
response to the amyloid deposition in the people that have
the higher tau levels. Having higher levels of tau may be
more prone to developing neurofibrillary tangles, and you have
more cell death.

GOAT SAYS FUTURE RESEARCH MAY REVEAL THE EXACT MECHANISMS THAT CAUSE THE DAMAGE. SHE SAYS IT’S POSSIBLE THAT BY BETTER UNDERSTANDING HOW THE TAU PROTEIN CONTRIBUTES TO DAMAGE, THEY MAY BE ABLE TO DELAY THE ONSET OF SOME ALZHEIMER’S DISEASE SYMPTOMS.

(act) :23 o/c of disease

I mean, that’s certainly what would appear from our results.
If you have higher levels of expression of tau, you have an
earlier age of onset in the face of amyloid deposition, compared
with someone who has lower levels of expression. So even in
someone you can already see amyloid deposition in their brain,
if you could lower their tau expression levels, you would
predict that you would delay the onset of disease.

GOATE’S TEAM REPORTED ITS FINDINGS IN THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. I’M JIM DRYDEN…

RUNS 2:59

THE REARCHERS ANALYZED DNA FROM MORE THAN 300 SUBJECTS AT WASHINGTON UNIVERSITY’S ALZHEIMER’S DISEASE RESEARCH CENTER, FOCUSING ON THE GENE THAT MAKES A PROTEIN CALLED TAU. TAU IS FOUND IN THE TANGLES THAT FORM IN THE BRAINS OF ALZHEIMER’S PATIENTS, ANOTHER SUBSTANCE, CALLED AMYLOID-BETA, IS FOUND IN THE PLAQUES THAT ALSO DOT THE BRAIN. PRINCIPAL INVESTIGATOR ALISON GOATE SAYS IT’S COMMON TO FIND AMYLOID PLAQUES BEFORE SYMPTOMS OF ALZHEIMER’S DISEASE ARE PRESENT, AND SHE SAYS CHANGES IN THE TAU GENE SEEM RELATED TO HOW ONE MOVES FROM HAVING AMYLOID IN THE BRAIN TO DEVELOPING SYMPTOMS OF THE DISEASE.

(act) :14 o/c the risk

These tau variants were only having an impact on the levels
of tau in the presence of amyloid deposition, and therefore,
they might affect age of onset of Alzheimer’s disease rather
than the risk.

GOATE’S TEAM REPORTED ITS FINDINGS IN THE PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES. I’M JIM DRYDEN…

RUNS :57

METABOLIC SYNDROME CAN INVOLVE INSULIN RESISTANCE, ABNORMAL CHOLESTEROL AND ELEVATED BLOOD PRESSURE. PEOPLE WITH THE PROBLEM ARE AT INCREASED RISK FOR HEART DISEASE, DIABETES AND STROKE, AND NOW RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE IDENTIFIED SEVERAL GENETIC VARIATIONS THAT INFLUENCE THE RISK OF METABOLIC SYNDROME. JIM DRYDEN HAS THE STORY…

THEY FOCUSED ON VERY SMALL CHANGES IN A GENE CALLED CD36. THE PROTEIN MADE BY THAT GENE IS INVOLVED IN FATTY ACID AND LIPOPROTEIN METABOLISM, AND THE GENE ITSELF IS LOCATED ON A REGION OF CHROMOSOME 7 THAT APPEARS TO BE RELATED TO PROBLEMS LIKE DIABETES, HYPERTENSION AND OTHER CONDITIONS CLOSELY LINKED TO METABOLIC SYNDROME. FIRST AUTHOR LATISHA LOVE-GREGORY SAYS THE RESEARCH TEAM LOOKED AT SEVERAL VARIANTS IN THE GENE.

((act) :14 o/c protective effect

Five of those variants we found associated with increased risk
for metabolic syndrome, and one, in particular, associated with
a decreased risk, or suggested a protective effect.

LOVE-GREGORY AND HER COLLEAGUES ANALYZED DNA FROM AFRICAN-AMERICAN PATIENTS, NOT BECAUSE THOSE PATIENTS HAVE A HIGHER RISK FOR METABOLIC SYNDROME BUT BECAUSE THEY TEND TO HAVE MORE VARIATIONS IN THEIR CD36 GENE.

(act) :32 o/c in African-Americans

Subjects of African descent, as well as Asian descent, tend to
carry more changes in their CD36 gene. And this does not mean
that these subjects are any more at an increased risk for metabolic
syndrome than any other population. But what we did hypothesize is
that if there are more deleterious variants in the gene, then this
may, in some way, reflect why we’re seeing higher prevalences of,
say, diabetes of heart disease in African-Americans.

BUT LOVE-GREGORY SAYS HER FINDINGS SHOULD APPLY TO MEMBERS OF ANY RACIAL OR ETHNIC GROUP, PROVIDED THEY HAVE THE SAME GENETIC VARIANTS OR VARIANTS THAT ALTER THE PROTEIN IN THE SAME WAY. CO-INVESTIGATOR NADA ABUMRAD HAS BEEN INSTRUMENTAL IN LEARNING ABOUT HOW THE CD36 PROTEIN WORKS. SHE SAYS LINKING CHANGES IN THE PROTEIN TO METABOLIC SYNDROME IS EXCITING BECAUSE AS OUR NATION GETS MORE AND MORE OBESE, MORE AND MORE PEOPLE ARE SUSCEPTIBLE TO THE PROBLEM.

(act) :14 o/c that gene

It sort of was an important question to ask because we know
from previous data that the protein, the CD36 protein, is
highly polymorphic, that there are a lot of variations in
that gene.

ABUMRAD SAYS IF THE FINDINGS CAN BE REPLICATED, TYING CD36 TO INSULIN RESISTANCE AND TO CHANGES IN HDL, THE SO-CALLED GOOD CHOESTEROL, COULD HELP EXPLAIN A GREAT DEAL ABOUT A PERSON’S RISK FOR HEART DISEASE AND DIABETES.

(act) :14 o/c lipid abnormalities

There were a couple of studies that suggested a link between a
particular location on chromosome 7 where the gene for CD36 is
located and lipid abnormalities.

LOVE-GREGORY SAYS THE FINDINGS SO FAR SUGGEST THAT ALTERING THE CD36 GENE SO THAT PEOPLE MAKE LESS CD36 PROTEIN, SEEMS TO BE A GOOD THING.

(act) :08 o/c protective effect

Based on the data that we have, it does suggest that reduced
amounts of CD36 indicates a protective effect.

BUT ABUMRAD SAYS NOT HAVING ANY CD36 IS A BAD THING

(act) :06 o/c having problems

Your organs need a baseline amount, but then, in high amounts you
start having problems.

LOVE-GREGORY, ABUMRAD AND THEIR COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL HUMAN MOLECULAR GENETICS. I’M JIM DRYDEN…

RUNS 2:58

THE RESEARCHERS FOCUSED ON VERY SMALL CHANGES IN THE CD36 GENE. THE PROTEIN THAT GENE MAKES IS KNOWN TO BE INVOLVED IN FATTY ACID AND LIPOPROTEIN METABOLISM, AND THE GENE ITSELF IS LOCATED ON A REGION OF CHROMOSOME 7 THAT APPEARS TO BE RELATED TO PROBLEMS SUCH AS DIABETES, HYPERTENSION AND OTHER CONDITIONS CLOSELY RELATED TO METABOLIC SYNDROME. FIRST AUTHOR LATISHA LOVE-GREGORY SAYS THE RESEARCH TEAM LOOKED AT SEVERAL VARIANTS IN THE GENE.

(act) :14 o/c protective effect

And five of those variants we found associated with increased
risk for metabolic syndrome, and one, in particular, associated
with a decreased risk, or suggested a protective effect.

LOVE-GREGORY SAYS IT APPEARS SMALL REDUCTIONS IN CD36 LIMIT RISK OF METABOLIC SYNDROME, BUT GENETIC CHANGES THAT ELIMINATE THE PROTEIN ALTOGETHER ARE NOT A GOOD THING. HER TEAM REPORTED ITS FINDINGS IN THE JOURNAL HUMAN MOLECULAR GENETICS. I’M JIM DRYDEN…

RUNS :55

PHYSICAL ACTIVITY IS GOOD FOR YOU. IT CAN HELP STAVE OFF OBESITY, HEART DISEASE, DIABETES AND CANCER. CANCER RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS AND HARVARD UNIVERSITY HAVE FOUND THAT WOMEN WHO EXERCISE REGULARLY WHEN THEY ARE YOUNG HAVE A SUBSTANTIALLY LOWER RISK OF BREAST CANCER THAN THOSE WHO ARE NOT ACTIVE. JIM DRYDEN REPORTS…

REGULAR EXERCISE BETWEEN THE AGES OF 12 AND 22 SIGNIFICANTLY LOWERS THE RISK OF BREAST CANCER BEFORE MENOPAUSE, ACCORDING TO LEAD INVESTIGATOR GRAHAM COLDITZ, THE ASSOCIATE DIRECTOR OF PREVENTION AND CONTROL AT THE SITEMAN CANCER CENTER AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE AND BARNES-JEWISH HOSPITAL IN ST. LOUIS.

(act) :25 o/c been inactive

The women who were active from age 12 onwards had the greatest
reduction in their risk of breast cancer. The women who were
active from 12 to 22 and then continued on to be active through
their adult years, prevented about a quarter of the cases of
breast cancer that would have happened if they’d been inactive.

COLDITZ AND HIS COLLEAGUES STUDIED NEARLY 65 THOUSAND WOMEN AND FOUND THAT THOSE WHO DID THE EQUIVALENT OF WALKING FOR ABOUT TWO HOURS PER DAY OR RUNNING FOR HALF AN HOUR DAILY GOT THE BIGGEST REDUCTIONS IN BREAST CANCER PRIOR TO MENOPAUSE.

(act) :28 o/c more aggressive

Before menopause, the proportion of breast cancers that are
receptor-negative – that is, the breast cancer that’s estrogen
receptor-negative and progesterone receptor-negative – the proportion
is much higher. And that’s the breast cancer that we don’t have
any really good treatment for at the moment. On average, breast
cancer diagnosed before menopause is likely to be more aggressive.

COLDITZ SAYS THAT ALTHOUGH THIS STUDY SHOWS BENEFITS BEFORE MENOPAUSE, OTHER RESEARCH HAS SHOWN THAT EXERCISE AND ACTIVITY ALSO PAY DIVIDENDS AFTER MENOPAUSE.

(act) :20 o/c more treatable

Pre-menopausal it’s really the sustained activity, but the payoff
is, in some sense, greater because the disease is more aggressive.
Post-menopause, never too late to become active because the benefit
is there quite quickly, and the disease is typically more treatable.

AND ALTHOUGH THE BIGGEST BENEFITS WENT TO WOMEN WHO BEGAN REGULAR EXERCISE AT AROUND THE AGE OF 12, COLDITZ SAYS THERE IS ALWAYS SOME BENEFIT TO PHYSICAL ACTIVITY, REGARDLESS OF WHEN IT BEGINS.

(act) :19 o/c way through

We also looked at women who had been inactive from 12 to 22
and then become more active, and even those women who had
become more active in their 20s and 30s gained a benefit.
It just wasn’t as big a benefit as those who had been active
all the way through.

AND COLDITZ SAYS THE FACT THAT MORE YOUNG GIRLS PLAY SPORTS THAN EVER COULD END UP LOWERING RISKS EVEN MORE IN THE FUTURE, PROVIDED THAT THOSE GIRLS CONTINUE TO BE ACTIVE AS THEY GROW INTO ADULTHOOD.

(act) :19 o/c breast cancer

There’s been – at least in the U.S. – a major change in team
sport participation by young girls, adolescents, and that really
does translate, based on these data, into a substantial
reduction in the risk of pre-menopausal breast cancer.

COLDITZ AND HIS COLLEAGUES REPORT THEIR FINDINGS IN THE JOURNAL OF THE NATIONAL CANCER INSTITUTE. I’M JIM DRYDEN…

RUNS 2:58

THE REARCHERS STUDIED NEARLY 65 THOUSAND WOMEN, AND THEY FOUND THAT HIGH LEVELS OF PHYSICAL ACTIVITY BETWEEN THE AGES OF 12 AND 22 LOWERED THE RISK OF BREAST CANCER BEFORE MENOPAUSE. CANCERS THAT STRIKE BEFORE MENOPAUSE TEND TO BE MORE AGGRESSIVE AND HARDER TO TREAT THAN BREAST CANCER THAT STRIKES AFTER MENOPAUSE. GRAHAM COLDITZ IS THE ASSOCIATE DIRECTOR OF PREVENTION AND CONTROL AT THE SITEMAN CANCER CENTER AND WASHINGTON UNIVERSITY SCHOOL OF MEDICINE.

(act) :16 o/c been inactive

The women who were active from age 12 onwards had the greatest
reduction in their risk of breast cancer, prevented about a quarter
of the cases of breast cancer that would have happened if they’d
been inactive.

COLDITZ SAYS ALTHOUGH THE BENEFIT WASN’T QUITE AS LARGE, THERE WAS STILL A REDUCTION IN CANCER AMONG WOMEN WHO BECAME ACTIVE LATER IN LIFE. HE SAYS IT’S NEVER TOO LATE TO BENEFIT FROM PHYSICAL ACTIVITY. COLDITZ AND COLLEAGUES REPORT THEIR FINDINGS IN THE JOURNAL OF THE NATIONAL CANCER INSTITUTE. I’M JIM DRYDEN…

THERE’S A GREAT DEAL OF PHARMACEUTICAL RESEARCH TRYING TO DEVELOP DRUGS THAT MIMIC THE EFFECTS OF GENES, BUT A TEAM OF RESEARCHERS LED BY INVESTIGATORS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAS FOUND A GENETIC VARIATION THAT MIMICS THE EFFECTS OF A DRUG. THE VARIATION, WHICH IS COMMON IN AFRICAN-AMERICANS HELPS EXPLAIN WHY BETA BLOCKER THERAPY DOESN’T SEEM TO HELP AFRICAN-AMERICAN HEART FAILURE PATIENTS AS MUCH AS CAUCASIAN HEART FAILURE PATIENTS. JIM DRYDEN REPORTS…

IN HEART FAILURE, THE HEART BECOMES WEAK AND WORKS HARDER TO PERFORM THE SAME JOB. AFTER A WHILE, THE OVERWORKED HEART CAN’T DO IT ANYMORE, AND PATIENTS EITHER NEED A TRANSPLANT, OR THEY DIE. ABOUT 5 MILLION PEOPLE IN THE UNITED STATES HAVE HEART FAILURE, AND ABOUT 300 THOUSAND DIE FROM IT EACH YEAR. BETA BLOCKER THERAPY IMPROVES SURVIVAL AND QUALITY OF LIFE, BUT PAST RESEARCH HAS FOUND THAT AFRICAN-AMERICANS OFTEN DON’T GET AS MUCH BENEFIT AS CAUCASIANS, ACCORDING TO WASHINGTON UNIVERSITY GENETICS RESEARCHER GERALD DORN.

(act) :21 o/c racial disparities

The major, clinical trials that demonstrated the benefit of
beta blockers all showed a tremendous benefit in Caucasians
but little or no benefit in African-Americans. So we were
funded by the National Institutes of Health to explore the
reasons for racial disparities.

WORKING WITH COLLEAGUE STEPHEN LIGGETT FROM THE UNIVERSITY OF MARYLAND, DORN LOOKED AT DNA FOR THE REASONS, AND THEY IDENTIFIED A GENETIC VARIATION CARRIED BY 40 PERCENT OF AFRICAN-AMERICANS THAT MIMICS THE EFFECTS OF BETA BLOCKERS.

(act) :22 o/c do Caucasians

The reason that we are postulating the previous clinical trials
didn’t show as clear a benefit in the African-American population
as they did in the Caucasians – of whom only 4 percent carry the
gene – is that almost half of the African-Americans are already
protected. The ones who do not carry the variant get just as much
benefit from beta blockers as do Caucasians.

DORN SAYS IF THE HEART WERE A CAR, THEN BETA BLOCKERS WOULD PREVENT YOU FROM FLOORING THE GAS PEDAL. THE GENETIC VARIATION THEY IDENTIFIED INVOLVES A GENE CALLED GRK5. DORN SAYS UNLIKE BETA BLOCKERS, THE GENETIC VARIANT IS MORE LIKE A GOVERNOR THAT KEEPS THE ENGINE, OR HEART, FROM REVVING TOO HIGH.

(act) :15 o/c cardiac damage

Beta blockers protect the heart from that because, if you will,
you can’t ever mash on the gas pedal. The GRK variant that we
found still allows you to mash on the gas pedal. It’s just that
you can’t go so fast that you blow up your “engine,” that you
cause cardiac damage.

DORN SAYS THE REASON SOME AFRICAN AMERICANS HAVEN’T SEEMED TO BENEFIT FROM BETA BLOCKERS IS THAT IN THOSE WITH THE GENETIC VARIANT, THE DRUGS ARE SOMEWHAT REDUNDANT.

(act) :03 o/c clinical effect

The gene and the beta blocker have the same clinical effect.

BUT IN SPITE OF THE SIMILAR CLINICAL EFFECTS OF THE GENE AND OF BETA BLOCKERS, DORN SAYS HE WOULD NOT RECOMMEND TAKING AFRICAN-AMERICAN HEART FAILURE PATIENTS OFF OF THE DRUGS.

(act) :20 o/c the case

If you are on a beta blocker, you live twice as long if you
have heart failure and you don’t carry the gene. It is possible
that there is an additive benefit of drug-plus-gene that we did
not detect in this small cohort, and we are looking at a larger
cohort of 25 hundred patients right now to determine whether
that might be the case.

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

RUNS 2:52

IN HEART FAILURE, THE ORGAN BECOMES WEAK AND WORKS HARDER TO PERFORM THE SAME JOB. BETA BLOCKER THERAPY IMPROVES SURVIVAL AND QUALITY OF LIFE, BUT PAST RESEARCH HAS FOUND THAT AFRICAN-AMERICANS OFTEN DON’T GET AS MUCH BENEFIT AS CAUCASIANS, SO WASHINGTON UNIVERSITY GENETICS RESEARCHER GERALD DORN AND COLLEAGUE STEPHEN LIGGETT FROM THE UNIVERSITY OF MARYLAND, LOOKED AT DNA FOR THE REASON, AND THEY IDENTIFIED A GENETIC VARIATION CARRRIED BY 40 PERCENT OF AFRICAN-AMERICANS THAT MIMICS THE EFFECTS OF BETA BLOCKERS. DORN SAYS IF THE HEART WERE A CAR, THEN BETA BLOCKERS WOULD PREVENT YOU FROM FLOORING THE GAS PEDAL.

(act) :10 o/c your engine

If you will, you can’t ever mash on the gas pedal. The GRK
variant that we found still allows you to mash on the gas
pedal. It’s just that you can’t go so fast that you blow up
your “engine.”

DORN SAYS IT’S NOT THAT BETA BLOCKERS DON’T WORK FOR AFRICAN-AMERICANS...

(act) :04 o/c clinical effect

It’s that the gene and the beta blocker have the same clinical effect.

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

RUNS :57

IN MANY STUDIES OF ALCOHOLISM RATES, RESEARCHERS HAVE NOTICED THAT AMERICANS ARE STARTING TO HAVE PROBLEMS WITH DRINKING AT YOUNGER AGES. NOW, COMPARING DATA FROM STUDIES CONDUCTED 10 YEARS APART, WASHINGTON UNIVERSITY ALCOHOLISM RESEARCHERS HAVE FOUND BOTH THAT PEOPLE DO SEEM TO BE DEVELOPING PROBLEMS AT YOUNGER AGES AND THAT ALCOHOLISM RATES AMONG WOMEN ARE CLOSING THE GAP WITH RATES AMONG MEN. JIM DRYDEN HAS THE STORY …

THERE HAVE BEEN MANY MASSIVE CHANGES IN THE LAST 50 YEARS, AND WOMEN IN THE UNITED STATES HAVE MORE ECONOMIC, SOCIAL AND POLITICAL OPPORTUNITIES THAT EVER BEFORE. BUT WASHINGTON UNIVERSITY ALCOHOLISM RESEARCHER RICHARD GRUCZA SAYS WOMEN ALSO APPEAR TO BE CATCHING UP WITH MEN IN ANOTHER WAY. GRUCZA’S RESEARCH TEAM COMPARED ALCOHOL USE AND DEPENDENCE DATA GATHERED 10 YEARS APART. THE RESEARCHERS FOUND THAT MEN WHO WERE BORN IN THE 1950s HAD ABOUT THE SAME RATES OF DRINKING PROBLEMS AS MEN BORN LATER ON, BUT PROBLEMS AMONG WOMEN INCREASED.

(act) :22 o/c for women

The big change comes with women born, the group born between
1954 and 1963, compared with women who were born 10 years
earlier. There was a large increase in alcohol dependence,
and that increase remained for the next couple of birth
cohorts that we examined. So there was no return to “baseline”
after this initial spike in alcohol dependence for women.

GRUCZA SAYS HE DID THIS STUDY TO COMPARE RATES OF PROBLEMS AMONG PEOPLE WHO WERE THE SAME AGE WHEN THEY WERE STUDIED BUT WHO WERE BORN AT DIFFERENT TIMES. HE SAYS MANY PAST STUDIES OF DRINKING PREVALENCE HAVE LOOKED AT LARGE NUMBERS OF PEOPLE AT A SINGLE MOMENT IN TIME.

(act) :19 o/c in 2000

So we wanted to see what the data would look like when we
looked at people who were the same age but were born at
different times. That was made possible by the fact that
there were two surveys done, using very similar methods,
10 years apart. So the people who were 30 years old in
1990 could be compared to the people who were 30 years
old in 2000.
ALTHOUGH THIS STUDY FOUND THAT WOMEN ARE DEVELOPING MORE PROBLEMS AS MEN STAY RELATIVELY CONSTANT, GRUCZA SAYS ANOTHER BIG AREA OF CONCERN WAS A FINDING THAT HAS APPEARED IN MANY STUDIES OF DRINKING: RESEARCHERS OFTEN FIND THAT YOUNGER PEOPLE REPORT MORE LIFETIME PROBLEMS WITH ALCOHOL USE AND DEPENDENCE THAN OLDER PEOPLE DO. THAT’S SURPISING BECAUSE OLDER PEOPLE HAVE LIVED LONGER AND BY VIRTUE OF THAT FACT, THEY WOULD BE EXPECTED TO BE ABLE TO REPORT MORE ALCOHOL USE AND DEPENDENCE. HE SAYS PAST STUDIES SUGGESTED EITHER THAT THE GROUPS WERE PROVIDING FAULTY INFORMATION OR THAT ALCOHOLISM WAS BECOMING MUCH MORE COMMON.
(act) :19 o/c boomer women

In fact, it was both. You know, there was some inflation of
the prevalence estimates among younger people. There was a
tendency for younger people to sort of over-report their
problems, relative to older people. But even when you correct
for that, you still see this increase in dependence for the
post-World War II women, for the “baby boomer” women.

ANOTHER IMPORTANT FINDING, GRUCZA SAYS, INVOLVES THE IMPLICATIONS OF MORE WOMEN REPORTING ALCOHOL PROBLEMS. HE SAYS THESE SAMPLES OF THE GENERAL POPULATION IDENTIFY MORE PROBLEMS IN WOMEN, BUT THERE DOESN’T SEEM TO BE ANY CORRESPONDING EVIDENCE THAT MORE WOMEN ARE SEEKING TREATMENT FOR THOSE PROBLEMS.

(act) :09 o/c has not

My best answer is that there doesn’t seem to be, which, you
know, which is another problem because it looks like their
risk has increased, but their tendency to seek treatment
has not.

GRUCZA AND HIS COLLEAGUES REPORTED THEIR FINDINGS IN THE JOURNAL ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH. I’M JIM DRYDEN…

RUNS 2:56

STUDYING ALCOHOL USE, A TEAM LED BY WASHINGTON UNIVERSITY RESEARCHER RICHARD GRUCZA FOUND THAT YOUNGER PEOPLE ARE REPORTING MORE ALCOHOL PROBLEMS THAN THEY USED TO. THEY COMPARED PEOPLE OF THE SAME AGE WHO WERE BORN AT DIFFERENT TIMES, STUDYING DATA FROM A COUPLE OF STUDIES CONDUCTED 10 YEARS APART. THEY FOUND THAT MEN WHO WERE BORN IN THE 1950s HAD ABOUT THE SAME RATES OF DRINKING AND ALCOHOLISM AS MEN BORN IN THE 1960s, BUT PROBLEMS AMONG WOMEN INCREASED.

(act) :19 o/c initial spike

The big change comes with women born, the group born between
1954 and 1963, compared with women who were born 10 years
earlier. There was a large increase in alcohol dependence,
and that increase remained for the next couple of birth
cohorts that we examined. So there was no return to “baseline”
after this initial spike.

GRUCZA SAYS ALTHOUGH THE EVIDENCE SUGGESTS THAT MORE WOMEN HAVE DRINKING PROBLEMS, THERE DOESN’T APPEAR TO BE AN INCREASE IN THE NUMBER OF WOMEN SEEKING TREATMENT. HE REPORTED HIS FINDINGS IN THE JOURNAL ALCOHOLISM: CLINICAL AND EXPERIMENTAL RESEARCH. I’M JIM DRYDEN…

RUNS :56

AS PEOPLE AGE, THEY MAY BECOME UNSAFE DRIVERS, SO IT’S IMPORTANT TO HAVE A MECHANISM TO EVALUATE OLDER ADULTS WHEN THEIR DRIVING ABILITY HAS BEEN QUESTIONED. IT’S ALSO CRUCIAL TO HELP OLDER PEOPLE MAINTAIN THEIR INDEPENDENCE. SCIENTISTS FROM AROUND THE COUNTRY TALKED ABOUT THE ISSUE AT WASHINGTON UNIVERSITY IN ST. LOUIS, AND MOST AGREE THAT IT’S IMPORTANT TO COME UP WITH BETTER WAYS TO EVALUATE HOW FRAILTY OR COGNITIVE IMPAIRMENTS MAKE IT UNSAFE FOR SOME ELDERLY DRIVERS TO BE ON THE ROAD. JIM DRYDEN REPORTS …

THE SURGE OF BABY BOOMERS REACHING THEIR 70s MEANS THAT THERE WILL SOON BE MILLIONS MORE ELDERLY DRIVERS ON THE ROADS, AND THAT COULE RESULT IN MORE ACCIDENTS ATTRIBUTED TO OLDER ADULTS. WASHINGTON UNIVERSITY GERIATRICS RESEARCHER DAVID CARR SAYS AS WE AGE, SAFE DRIVING MAY BECOME AN ISSUE.

(act) :19 o/c driving skills

Although many older adults age gracefully and continue to be
in good shape cognitively and functionally, there’s a certain,
growing proportion that has been affected visually, cognitively
and/or from a motor standpoint. And at that time, it often can
impact driving skills.

CARR SAYS IT’S IMPORTANT TO REMOVE UNSAFE DRIVERS FROM THE ROADS, BUT IT’S ALSO IMPORTANT TO ALLOW OLDER PEOPLE TO KEEP DRIVING FOR AS LONG AS POSSIBLE, PROVIDED THEY REMAIN SAFE.

(act) :15 o/c transportation alternatives

A loss of license certainly means decreased social connectedness,
sometimes depression, isolation. For many frail, physically and/or
cognitively, older adults there’s just not a lot of viable
transportation alternatives.

SO HOW CAN WE DETERMINE WHEN SOMEONE IS NO LONGER ABLE TO DRIVE SAFELY?

(act) :22 o/c ideal battery

One option of method is to look at off-road tests – tests in the
physician/clinic setting, tests that performed by occupational
therapists (typically in driving clinics) – and to determine
whether a certain set of tests may be able to predict who is
safe to drive and who is not. Unfortunately, although we have a
few candidates, we haven’t come up, yet, with the ideal battery.

CARR SAYS A ROAD TEST WITH AN OCCUPATIONAL THERAPIST OR A DRIVING EVALUATOR IS ONE OF THE BEST WAYS TO ASSESS AN OLDER PERSON’S DRIVING ABILITY. BUT OFTEN THE DECK IS STACKED AGAINST PASSING A ROAD TEST. THE TESTS OCCUR IN A CAR THAT ISN’T THEIR OWN AND TYPICALLY ON A ROADWAY THAT IS UNFAMILIAR TO THE OLDER ADULT. ANXIETY AND LACK OF CONFIDENCE ALSO MAY IMPAIR PERFORMANCE DURING ON-ROAD TESTING. IN CASES WHERE THEY ARE EVALUATED IN THEIR OWN CARS BY HIGHWAY PATROL OFFICERS IT OFTEN IS DIFFFICULT FOR OLDER PEOPLE TO PASS DUE TO CONCERNS FROM THE EXAMINER AND THE FACT THAT THEY GIVE ELDERLY DRIVERS THE SAME TEST THAT’S USED FOR TEENAGERS.

(act) :13 o/c the physician

Their crash rate may be elevated. They’re having difficulty
with some of their driving skills. We do get those histories
often, that people will have an accident, or they’ll have
unsafe driving before it may even be recognized by the physician.

THAT COULD MEAN IMPAIRED DRIVING IS A MARKER FOR SOMEONE AT FUTURE RISK FOR ALZHEIMER’S DISEASE, RATHER THAN THE OTHER WAY AROUND. CARR SAYS AS RESEARCHERS WORK TO FIND WAYS TO IDENTIFY UNSAFE DRIVERS SOONER, HE ANTICIPATES MORE CLINICIANS AND CAREGIVERS WILL BE FACED WITH THE DIFFICULT ISSUE OF WHAT TO DO WITH ELDERLY DRIVERS.

(act) :11 o/c one step

Simply making people come in every few years to renew their
license in person is at least one step.

CARR SPOKE AT WASHINGTON UNIVERSITY’S 8TH ANNUAL FRIEDMAN CONFERENCE ON AGING. I’M JIM DRYDEN…

RUNS 2:51

WASHINGTON UNIVERSITY GERIATRICS RESEARCHER DAVID CARR SAYS IT’S IMPORTANT TO KEEP UNSAFE DRIVERS OFF OF THE ROAD, BUT IT’S ALSO IMPORTANT TO ALLOW OLDER PEOPLE TO KEEP DRIVING FOR AS LONG AS THEY REMAIN SAFE. HE SAYS THERE IS NO AGREED-UPON TEST OR SET OF TESTS TO IDENTIFY UNSAFE DRIVERS. BUT HE SAYS THE MAJORITY OF HEALTH PROFESSIONALS STUDYING MEDICAL FITNESS TO DRIVE AGREE THERE ARE STEPS TO KEEP UNSAFE DRIVERS OFF THE ROAD.
(act) :26 o/c one step

It is helpful to make people come in to renew their license
because there is a portion of the population that will say,
“You know what? I probably shouldn’t renew, and I’m not going
to.” Or when they show up, they’re so frail and impaired they’re
picked up by the driver’s license personnel. They’re referred in,
and they come off the road from that standpoint. Simply making
people come in every few years to renew their license in person
is at least one step.

CARR SPOKE AT WASHINGTON UNIVERSITY’S 8TH ANNUAL FRIEDMAN CONFERENCE ON AGING. I’M JIM DRYDEN…

RUNS :56

AN INTERNATIONAL TEAM OF SCIENTISTS, LED BY RESEARCHERS AT THE GENOME CENTER AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS, HAS COMPLETED A LOOK AT THE DNA OF ONE OF THE PLANET’S MOST UNUSUAL ANIMALS: THE DUCK-BILLED PLATYPUS. ALTHOUGH CLASSIFIED AS A MAMMAL, THE PLATYPUS SHARES TRAITS WITH BIRDS AND REPTILES, TOO, AND ITS DNA SEQUENCE ALSO APPEARS TO BE SOMETHING OF A MIXED BAG. JIM DRYDEN REPORTS …

THE DUCK-BILLED PLATYPUS HAS A COAT OF FUR LIKE A MAMMAL, BUT IT ALSO HAS A DUCK-LIKE BILL. PLUS, THE PLATYPUS HAS SEVERAL BIOLOGICAL TRAITS MORE COMMONLY FOUND IN REPTILES. WASHINGTON UNIVERSITY GENETICIST WES WARREN, WHO LED THE PROJECT, SAYS THE ANIMAL BRIDGES MANY BIOLOGICAL DIVIDES.

(act) :15 o/c in snakes

There’s unique aspects to the platypus that are just not
found in mammals, and the most striking one, of course, is
that they lay eggs. They also have venom, and they have a
venom-delivery system that is unique among all mammals and
very analogous to what we see in snakes.

REPORTING IN THE JOURNAL NATURE, WARREN AND GENOME SCIENTISTS FROM AROUND THE WORLD EXPLAIN THAT THE PLATYPUS IS A MIXED BAG, BOTH BIOLOGICALLY AND AT THE DNA LEVEL.

(act) :10 o/c the genome

And we refer to it as this mixture of reptilian and
mammalian features. And that mixture that we see in
the biology is also represented in the genome.

WARREN SAYS THE TEAM FOUND MANY GENES IN THE PLATYPUS THAT ALSO ARE SEEN IN REPTILES AND BIRDS. THEY ALSO FOUND GENES MORE COMMON TO MAMMALS. AND HE SAYS IT’S RARE FOR SUCH GENES TO BE FOUND IN THE SAME ORGANISM.

(act) :20 o/c genome-like features

The expectation is for, like, eggs you would have egg-yolk
proteins, and we actually find egg-yolk proteins. And at the
same time, we know that platypus animals lactate, and we see
the milk-protein genes that we expect to see. This is a
mixture at the genome level of reptile and mammal genome-like
features.

WARREN SAYS IN TERMS OF ITS SIZE, THE PLATYPUS GENOME IS CLOSER TO THAT OF A BIRD OR REPTILE. AN EARLIER EFFORT INVOLVING WASHINGTON UNIVERSITY GENOME SCIENTISTS HAD SEQUENCED CHICKEN DNA, AND THAT SEQUENCE WAS VERY SIMILAR IN SIZE TO THE PLATYPUS, AND MUCH SMALLER THAN GENOME SEQUENCES FROM THE CHIMPANZEE AND THE HUMAN.

(act) :18 o/c to 2.2

And if you look at the size of the genome, it’s actually
more similar in size to some reptiles and closer to the
bird. But it’s right in between because most of the
Eutherian genomes are close to 3 billion base pairs.
The platypus genome, our estimates are anywhere from 1.2
to 2.2.

WARREN SAYS THE SMALLER DNA SEQUENCE, FILLED WITH GENES SIMILAR TO REPTILES, BIRDS AND MAMMALS, HAD LED THE RESEARCHERS TO BELIEVE THAT THERE WOULD BE LESS REPETITIVE SEQUENCE IN THE PLATYPUS. REPETITITVE DNA SEQUENCE IS THE TERM GIVEN TO THE MOLECULAR DNA BASE-PAIRS THAT ARE NOT PART OF FUNCTIONING GENES. LITTLE IS KNOWN ABOUT HOW THIS SEEMINGLY “EXTRA” DNA FUNCTIONS, BUT THE RESEARCHERS HAD ASSUMED THAT LARGE NUMBERS OF GENES FROM DIFFERENT TYPES OF ANIMALS, COMBINED WITH A SMALLER NUMBER OF DNA BASE PAIRS, WOULD LEAD TO LESS REPETITIVE DNA SEQUENCE.

(act) :12 o/c somewhat surprising

We actually found that it’s the most repetitive genome that
we’ve sequenced thus far. It’s close to 50 percent total
repeat elements. So that was somewhat surprising.

WARREN SAYS THE PLATYPUS GENOME SHOULD TEACH SCIENTIST A GREAT DEAL ABOUT EVOLUTION AND ALSO MAY EVENTUALLY PROVIDE STRATEGIES FOR USING GENETIC TRAITS FROM OTHER ANIMALS TO TREAT DISEASEs IN HUMANS. I’M JIM DRYDEN…
RUNS 2:58

REPORTING IN THE JOURNAL NATURE, THE RESEARCHERS SAY THEY FOUND LOTS OF SEEMINGLY CONTRADICTORY GENES IN THE PLATYPUS. WASHINGTON UNIVERSITY GENETICIST WES WARREN, WHO LED THE PROJECT, SAYS THE PLATYPUS IS A BIOLOGICAL ANOMOLY THAT SEEMS TO BRIDGE BIOLOGICAL GAPS BETWEEN REPTILES, BIRDS AND MAMMALS.

(act) :10 o/c in snakes

There’s unique aspects to the platypus that are just not
found in mammals, and the most striking one, of course, is
that they lay eggs. They also have venom, very analogous to
what we see in snakes.

AND WARREN SAYS THE DNA SEQUENCE ALSO HAS GENES THAT COME FROM ALL OVER THE BIOLOGICAL MAP.

(act) :14 o/c to see

The expectation is for, like, eggs you would have egg-yolk
proteins, and we actually find egg-yolk proteins. And at the
same time, we know that platypus animals lactate, and we see
the milk-protein genes that we expect to see.

WARREN SAYS THE PLATYPUS GENOME WILL TEACH SCIENTIST A GREAT DEAL ABOUT EVOLUTION AND ALSO MAY EVENTUALLY PROVIDE STRATEGIES FOR USING GENETIC TRAITS FROM OTHER ANIMALS TO TREAT DISEASES IN HUMANS. I’M JIM DRYDEN…

RUNS 1:00

ALTHOUGH THE DISORDER WAS FIRST CHARACTERIZED MORE THAN 100 YEARS AGO, THERE’S STILL NOT MUCH KNOWN ABOUT WHAT CAUSES TOURETTE SYNDROME. BUT NOW RESEARCHERS AT WASHINGTON UNIVERSITY SCHOOL OF MEDICINE IN ST. LOUIS HAVE SPOTTED SOME IRREGULARITIES IN SOME OF THE NETWORKS THAT WORK TOGETHER IN THE BRAIN. AND THEY’RE USING SOPHISTICATED IMAGING TECHNIQUES TO TAKE A CLOSER LOOK. JIM DRYDEN HAS THE STORY …

THE RESEARCHERS HAVE FOUND THAT THE BRAINS OF ADOLESCENTS WITH TOURETTE SYNDROME DON’T FUNCTION IN QUITE THE SAME WAY AS IN ADOLESCENTS NOT AFFLICTED WITH THE DISORDER. A TEAM, LED BY WASHINGTON UNIVERSITY PEDIATRIC NEUROLOGIST BRADLEY SCHLAGGAR AND GRADUATE STUDENT JESSICA CHURCH, REPORTED THE DIFFERENCES LAST YEAR AT THE ANNUAL MEETING OF THE SOCIETY FOR NEUROSCIENCE.

(act) :19 o/c developing population

Adolescents with Tourette sydrome, with respect to networks
in the brain that are involved in attentional control, these
networks appear immature and, in some cases, just anomalous
in terms of their connections, compared to our well-characterized,
typically developing population.

WITH NEW FUNDING FROM THE TOURETTE SYNDROME ASSOCIATION, SCHLAGGAR AND CHURCH ARE USING MAGNETIC RESONANCE IMAGING TECHNIQUES TO LEARN MORE ABOUT HOW BRAIN NETWORKS FUNCTION AND DEVELOP IN KIDS WITH TOURETTE’S AND IN THOSE WHO DON’T HAVE TICS.

(act) :15 o/c given instant

We’re recognizing that to understand both typical and
atypical brain function, we have to stop focusing on’
just our “favorite” place in the brain, what it’s doing
during a task to truly understand who is listening to
that brain region at any given instant.

SCHLAGGAR SAYS HIS TEAM IS COLLABORATING WITH OTHER RESEARCHERS AT THE UNIVERSITY OF CALIFORNIA TO SEE HOW ATTENTION SYSTEMS WORK IN KIDS WITH TOURETTE’S. THE RESEARCHERS ALSO ARE EXPANDING THE NUMBER OF CHILDREN THAT THEY’LL STUDY. UNTIL NOW, THEY’VE LIMITED THEIR WORK TO KIDS BETWEEN 10 AND 15 YEARS OF AGE.

(act) :18 o/c isolated snapshots

So far, we’ve really focused on 10- to 15-year-olds with Tourette
syndrome. From a clinical standpoint, that was a natural place to
start for our initial investigations, but we believe that it’s
important to fully characterize the developmental trajectory and
not get isolated “snapshots.”

SCHLAGGAR SAYS THE EVENTUAL HOPE IS TO LEARN WHAT GOES WRONG IN THE STRUCTURE AND FUNCTION OF THE BRAIN IN PEOPLE WITH TOURETTE SYNDROME. ONE IDEA, HE SAYS, IS THAT THE BRAIN MAKES ITS CONNECTIONS IMPROPERLY DURING DEVELOPMENT.

(act) :27 o/c over time

Another hypothesis is that there will be catch-up, that there
is, sort of, a developmental lag, and as symptoms often improve
in Tourette syndrome in late adolescence, that perhaps we will see
a concomitant improvement in the maturation of these networks.
Or we might see an entirely atypical trajectory. Even though the
connections remain different than the normal population, that
there are other compensatory mechanisms that allow patients with
Tourette’s to improve over time.

AS SCHLAGGAR AND CHURCH EXPAND THEIR STUDIES. THEY ALSO PLAN TO LOOK AT WHAT EFFECT MEDICATIONS HAVE ON THE FUNCTION OF BRAIN NETWORKS. I’M JIM DRYDEN…

RUNS 2:33

THE RESEARCHERS REPORTED THEIR PRELIMINARY FINDINGS LAST YEAR TO THE SOCIETY FOR NEUROSCIENCE. NOW, WITH NEW FUNDING FROM THE TOURETTE SYNDROME ASSOCIATION, THE RESEARCHERS, LED BY PEDIATRIC NEUROLOGIST BRADLEY SCHLAGGAR AND GRADUATE STUDENT JESSICA CHURCH, ARE USING MAGNETIC RESONANCE IMAGING TECHNIQUES TO LEARN MORE ABOUT HOW THE BRAIN NETWORKS FUNCTION AND DEVELOP IN KIDS WITH TOURETTE’S. AS THEY STUDY HOW BRAIN NETWORKS FUNCTION, SCHLAGGAR SAYS THE RESEARCHERS HAVE NOTICED DIFFERENCES BETWEEN ADOLESCENTS WITH TOURETTE’S AND THOSE WHO DON’T HAVE THE DISORDER.

(act) :17 o/c developing population

With respect to networks in the brain that are involved in
attentional control, these networks appear immature and, in
some cases, just anomalous in terms of their connections,
compared to our well-characterized, typically developing population.

SCHLAGGAR AND CHURCH HAVE CONCENTRATED ON PATIENTS BETWEEN 10 AND 15 YEARS OLD, BUT THEY’RE EXPANDING THEIR STUDIES TO INCLUDE KIDS OF DIFFERENT AGES. AND THEY ALSO PLAN TO LOOK AT WHAT EFFECT MEDICATIONS HAVE ON THE FUNCTION OF THESE BRAIN NETWORKS. I’M JIM DRYDEN…

RUNS :58