Health and Fitness Blog

PARIS (AFP) -
Teams of doctors on Sunday said they had uncovered genetic flaws that separately boost the risk of a common form of leukaemia and bowel disease in children and may also influence obesity and fertility.

The work is reported in three different studies, published by the journals Nature Genetics and Nature Medicine.

A team led by Richard Houlston of Britain’s Institute of Cancer Research found six genetic variants that increase vulnerability to chronic lymphocytic leukaemia (CLL), which accounts for roughly a quarter of all leukaemia cases.

The variants occur in genes that play a role in the proliferation of so-called B cells, a type of white blood produced in the bone marrow.

Individually, these variants each contribute to a modest increase in the risk of CLL, but a person with all six faces an eight-fold increase.

Meanwhile, investigators in the United States found that a gene switched on by leptin — a hormone that tells the brain when the body has sufficient nutrition — is involved in appetite disorder and infertility.

The discovery was found in the brain of mice, but there are likely to be strong similarities in humans, the authors said.

“This gene is crucial to the daisy chain of signals that run between body fat and brain,” lead researcher Marc Montminy of the Clayton Foundation Laboratories for Peptide Biology, said in a press release.

“It likely plays a pivotal role in how much we, as humans, eat and whether we have offspring.”

Variations of the gene, called TORC1, could play a part in obesity and infertility, as they could send the wrong signals to the brain as to whether food is needed and whether the body has sufficient energy stores for reproduction.

A third study, entailing a trawl through the genetic code of thousands of people, netted two new genes involved in childhood inflammatory bowel disease (IBD), a painful condition that includes Crohn’s disease and ulcerative colitis.

Genomics — as genetic analysis is called — is one of the most eagerly explored frontiers of medicine today.

Finding genes that cause or amplify a disease opens up pathways for diagnostic tools to help identify people at risk from the ailment.

It also, more distantly, opens up avenues for potential drugs to block or reverse the gene’s malfunction.

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WEDNESDAY, Aug. 27 (HealthDay News) — Fat cells in obese people
are “sick” compared to those in lean people, a new study shows.

Published in the September issue of Diabetes, a group of
researchers from the Temple University School of Medicine analyzed fat
samples from the upper thighs of six lean and six obese people.

They found significant differences in the fat cells of the obese
participants compared with the lean participants.

“The fat cells we found in our obese patients were deficient in several
areas,” study author Guenther Boden, the Laura H. Carnell Professor of
Medicine and chief of endocrinology, said in Temple press release.

Boden said that the obese people’s fat cells showed stress on the
endoplasmic reticulum (ER), which helps cells synthesize proteins and
monitor how they are folded. When the ER is stressed, Boden explained, it
produces several proteins that ultimately lead to insulin resistance.
Insulin resistance, in turn, plays a major role in the development of
obesity-related conditions.

The differences in the fat cells between obese and lean people may help
explain the link between obesity and a higher risk of diabetes, heart
disease, and stroke, Boden theorized.

More information

The National Heart, Lung, and Blood Institute has more about overweight and obesity.

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WASHINGTON (Reuters) -
Researchers studying people with a
rare genetic disorder have identified a brain chemical that may
play a role in appetite and obesity, a finding they say could
lead to new drugs to help some obese people.

Previous animal studies had pointed to this chemical, known
as BDNF, as helping to regulate appetite and weight, but the
new study published on Wednesday in the New England Journal of
Medicine is the first to show such a role in people.

“The importance of the finding is that it opens up another
avenue for us to develop treatments that might help folks with
obesity,” said Dr. Jack Yanovski of the Eunice Kennedy Shriver
National Institute of Child Health and Human Development, part
of the U.S. National Institutes of Health.

A number of substances naturally occurring in the body,
including the hormone leptin and neuropeptide Y, are known to
affect appetite and obesity, and the findings about BDNF add to
the understanding of factors underpinning obesity, he added.

BDNF, which stands for brain-derived neurotrophic factor,
is already known to play a role in long-term memory.

“We’re looking at a small part of what is really a large
and complex puzzle,” Yanovski, who helped lead the study, said
in a telephone interview. “We guess there are probably about
300 genes that affect body weight in some form or another.”

The study involved 33 people with WAGR (pronounced wagger)
syndrome, a rare genetic condition that puts one at high risk
for eye problems, certain cancer types and mental retardation.

Normally a person has two copies of the gene that controls
BDNF. But the researchers found that most of the WAGR syndrome
patients — 19 of them — were missing one copy of the gene,
and thus had low blood levels of BDNF.

Every one of the 19 was obese by age 10 and had a strong
tendency to overeat. The 14 other people who had two working
copies of the gene were no more likely than the general
population to be obese or overeat, the researchers said.

This strongly suggests BDNF is involved in controlling
appetite and thus obesity, they said. The release of BDNF in
the hypothalamus, a brain structure involved in regulating
appetite, may be triggered indirectly by leptin, they added.

Yanovski said drugs that are based on improving low levels
of BDNF could help certain obese people who have not had
success with other treatments.

(Editing by Julie Steenhuysen and Cynthia Osterman)

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EDINBURG, Texas - A nearly half-ton Texas woman charged in the death of her toddler nephew couldn’t have beaten the boy to death because of her limited movement from weight problems, her attorney said Tuesday.

Mayra Rosales, who weighs nearly 1,000 pounds, was indicted last week on capital murder charges in the death of Eliseo Gonzalez Jr. Prosecutors said the 2-year-old boy died after being struck at least twice in the head while in the care of Rosales, who is bedridden.

Jamie Rosales, the boy’s 20-year-old mother, believes the death was possibly caused by the morbidly obese woman rolling onto the toddler, said Oscar Vega, her attorney. She faces one felony count of injury to a child, which carries a life sentence and 10,000 in fines.

“She doesn’t believe her sister intentionally did anything to her child,” Vega told The Associated Press.

A state district judge put Mayra Rosales, 27, under house arrest Monday because the county jail lacks a large enough cell or necessary medical resources. She is required to wear a global-positioning tracker until her trial.

Sergio Valdez, Mayra Rosales’ attorney, said she lacks the movement in her arms to have killed the child, calling it an “impossibility.”

“She is not physically capable of having committed those acts,” Valdez said.

Valdez said Rosales suffers from a thyroid problem that has caused her to put on hundreds of pounds over the past three to four years and has been bedridden for more than a year.

The stress of the arrest and charges has exacerbated the poor health of Mayra Rosales, who also suffers from a “life-threatening” ailment he would not disclose, Valdez said.

“This whole ordeal has taken a very negative effect on her, emotionally and physically,” Valdez said. “She wants this to be over. She wants to be vindicated.”

Vega said Jamie Rosales has a learning disability and will plead not guilty.

He declined to say where his client was the day of her son’s death, but said he knew of no order forbidding the boy to be watched by his aunt.

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COLUMBUS, Ohio - A death row inmate who says he’s too fat to be executed received poor legal help during his trial and later when he appealed the death sentence, his lawyers said Monday during a clemency hearing.

It’s the second time that Richard Cooey, convicted of killing two University of Akron students in 1986, has asked the state for mercy. The Ohio Parole Board denied a similar request five years ago, and Cooey came within a day of being executed in 2003 before a federal judge issued a reprieve.

In a lawsuit filed this month, his lawyers said that executioners would have trouble finding Cooey’s veins and that his weight could diminish the effectiveness of one of the lethal injection drugs.

Cooey stands 5 feet 7 and weighs 267 pounds. His execution is scheduled for Oct. 14. It would be the first execution in the state since the end of a moratorium while the U.S. Supreme Court reviewed Kentucky’s lethal injection procedure.

Cooey didn’t attend Monday’s clemency hearing, and neither side argued the merits of the obesity lawsuit.

His lawyers said that Cooey’s original defense team didn’t properly present evidence about the effect of beatings he received as a child, as well as the impact of Cooey’s alcohol abuse.

Cooey, 41, isn’t the same person who committed the murders and is remorseful to the point of self-loathing, said Dana Cole, a University of Akron law professor who represented Cooey at the parole board hearing.

“If he’s killed on Oct. 14, we will kill a changed man,” Cole said. “He’s not the same man who committed these crimes.”

Larry Whitney, one of Cooey’s lawyers from the 1986 trial, said he and fellow defense attorney Roger Davidson did everything they could to present Cooey’s psychological makeup and background to the three-judge panel trying the case.

The judges “obviously felt that the mitigation we presented did not outweigh the aggravating factors in the case,” Whitney said.

Parole Board member Sandra Mack questioned whether Cooey has ever acknowledged his role in the crimes.

“This just does not sound like someone taking responsibility for the major part he played in killing these young women,” Mack said.

Summit County Prosecutor Sherri Bevan Walsh reviewed graphic details of the rape and murder of the two students. Cooey and his co-defendant met the victims after throwing chunks of concrete off an overpass and striking their car.

Walsh also reviewed Cooey’s unsuccessful attempt to escape from death row in 2005, when he used a homemade ladder constructed of rolled-up magazines and sheets to scale an outdoor recreation area wall.

“In the 22 years since the defendant committed these brutal acts, he has never demonstrated one second of genuine remorse for murdering these two young women,” Walsh said.

Cooey’s accomplice, Clinton Dickens, was not eligible for the death penalty because he was 17 at the time of the murders. He is serving a life sentence.

The parole board will make a recommendation to Gov. Ted Strickland on Tuesday. Strickland can follow the board’s ruling or make his own decision.

(This version CORRECTS that Dana Cole is representing Cooey at the parole board hearing but that she is not his defense attorney.)

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NEW YORK (Reuters Health) -
Metabolic syndrome, a cluster
of conditions that increases the risk of heart disease, stroke
and diabetes, in extremely obese patients can be cured by
gastric bypass surgery, according to the findings from a new
study.

“Reversibility of metabolic syndrome depends more on the
percentage of excess weight lost than on other clinical or
demographic characteristics,” the research team reports in the
journal, Mayo Clinic Proceedings.

To determine the effect of major weight loss on the
metabolic syndrome, Dr. Francisco Lopez-Jimenez and colleagues
evaluated patients being considered for bypass surgery at the
Mayo Clinic in Rochester, Minnesota, between 1990 and 2003.

All patients met at least three of the five criteria for
the metabolic syndrome - high levels of triglycerides (a “bad”
fat), low levels of high-density lipoprotein “good”
cholesterol, increased blood pressure, high blood sugar levels
and obesity.

The study group included 180 patients who underwent gastric
bypass and 157 patients who did not undergo the procedure,
either because they declined surgery, were denied coverage by
insurance providers, or did not maintain lifestyle
interventions during their evaluation. All patients received
medical and dietetic care and extensive counseling about the
importance of physical activity.

The mean body mass index (BMI) was 49 in the surgical group
and 44 in the nonsurgical group. A normal BMI is considered to
be between 18.5 and 24.9.

During an average follow-up of 3.4 years, the prevalence of
metabolic syndrome decreased from 87 percent to 29 percent in
the surgical group, and from 85 percent to 75 percent in the
control group. The authors estimate that the number of patients
needed to treat with bypass surgery to cure one patient of
metabolic syndrome was 2.1.

Weight loss averaged 44 lbs in the surgical group and 0.2
lbs in the nonsurgical group. Additional analysis showed that
the percentage of excess weight lost was the primary factor
that determined the resolution of the metabolic syndrome.

“Our study provides robust data to practicing clinicians
about the benefits of counseling weight reduction in metabolic
syndrome patients,” Lopez-Jimenez and his associates conclude.

They recommend “gastric bypass surgery should be considered
as a treatment option in patients with metabolic syndrome that
has not responded to conservative measures” in those eligible
for surgery.

SOURCE: Mayo Clinic Proceedings, August 2008.

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NEW YORK (Reuters Health) -
Use of cholesterol-lowering
statin drugs, especially long-term use, appears to raise the
risk of prostate cancer among obese men, according to findings
of a new study.

“Given the epidemic of obesity in the U.S. and the frequent
use of statins, the positive association we observed raises
substantial concern as to the safety of these widely prescribed
agents,” Dr. Janet L. Stanford of the Fred Hutchinson Cancer
Research Center in Seattle and colleagues wrote in the American
Journal of Epidemiology.

In a population-based, case-control study, the researchers
matched 1,001 men with prostate cancer diagnosed between 2002
and 2005 with 942 age-matched cancer-free controls from King
County, Washington.

No overall association was observed between the risk of
prostate cancer and the current or past use of statin
treatment. Duration of statin use was also not associated with
prostate cancer risk.

“We also found no evidence that use of a statin was
associated with risk of developing more aggressive subtypes of
prostate caner,” Stanford said in an interview with Reuters
Health. “Overall we found no support for the current hypothesis
that statin use may reduce risk of prostate cancer.”

However, the results do suggest a significant increase in
the risk of developing prostate cancer associated with current
statin use and with longer durations of use among obese men
(defined as a body mass index of 30 greater).

“Among obese men,” Stanford told Reuters Health, “current
use of a statin was associated with a 50 percent increase in
risk of prostate cancer; and use for 5 or more years was
associated with an 80 percent increase in risk of the disease;
both of these risk estimates were statistically significant.”

These findings warrant further investigation, she said.

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WASHINGTON (Reuters) -
An epilepsy drug being tested for
use in treating addiction can help obese rats shed weight, U.S.
government researchers said on Wednesday.

Their findings point not only to an easy treatment for
obesity, but show it is similar to drug addiction, they said.

Even rats bred to be obese lost up to 19 percent of their
weight and normal rats lost 12 to 20 percent of their weight
after 40 days of injections of the drug, called vigabatrin or
GVG, the team at the U.S. Department of Energy’s Brookhaven
National Laboratory found.

“When we gave GVG, they would steadily lose weight, and
when we took them off GVG, they would steadily gain weight,”
Amy DeMarco, who worked on the study, said in a telephone
interview.

“It was like a roller coaster. It was also dose-dependent.
Rats given higher doses would lose more weight.” She added that
her team saw no side effects in the rats.

Vigabatrin, sold as Sabril in Canada and Mexico by
Deerfield, Illinois-based Ovation Pharmaceuticals Inc and in
Britain by Sanofi Aventis, is being tested in people now for
cocaine and methamphetamine addiction.

Writing in the journal Synapse, the researchers said the
drug stops the brain’s dopamine reward system, which underlies
addiction and overeating.

“For substance abusers, the number one cause of relapse is
environmental cues, triggers,” said Brookhaven’s Dr. Stephen
Dewey, who led the research.

“A fairly significant proportion of subjects who are obese
suffer from something called binge eating disorders. They
binge-eat based on cues. They see a cake, they smell a
hamburger and they crave and they start to eat. One of the
great things about this drug is it stops this,” Dewey added.

“Most drugs of abuse do the same thing to the brain. They
increase dopamine. GVG can prevent that increase of dopamine,”
DeMarco said.

Brookhaven has licensed its vigabatrin patents to Coral
Gables, Florida-based Catalyst Pharmaceutical Partners Inc,
which is testing the drug in phase II human trials for cocaine
and methamphetamine addiction.

The company also plans to test the drug, which it calls
CPP-109, for binge eating disorder and alcohol dependence.

Ovation is also testing the drug for use in cocaine and
methamphetamine dependence.

Dewey said he has been working with vigabatrin for decades.
“It was impossible to get any pharmaceutical company interested
in pursuing it for an addiction application,” he said.

Britain’s Royal College of Ophthalmologists reported in
March that the drug can affect sight, reducing peripheral
vision and limiting the field of vision in other ways, perhaps
irreversibly.

Dewey said these effects were seen with much heavier use of
the drug than might be indicated for weight loss.

(Reporting by Maggie Fox; Editing by Patricia Zengerle)

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PARIS (AFP) -
Scientists have found two genetic triggers for producing healthful “good” fat in mice, pointing the way to a new treatment for obesity, according to a pair of studies published Thursday.

Harvard University researchers also made the startling discovery that these so-called brown fat cells — which burn calories rather than store them — originate from the same immature stem cells that produce muscle.

While many people would prefer to have less of it, fat is essential for health. It helps regulate our metabolism, and keeps our bodies warm.

But there are two kinds of blubber.

White fat is composed of molecules that hoard calories, and has contributed to a worldwide crescendo of obesity with consequences ranging from diabetes to heart disease.

Brown fat, more prevalent in infants than adults, is different — in fact far more different that scientists realised.

To find out what chemicals in the body trigger its production, a team of researchers led by Yu-Hua Tseng of the Joslin Diabetes Center at Harvard Medical School experimented with genetically modified mice.

They discovered that a protein called BMP7 was critical to the process: without it, brown fat cells failed to develop, causing the mice to die. Added in artificially high doses, BMP7 had the opposite effect.

But white fat, Tseng found, relied on different albeit related chemicals to develop.

More importantly, he proved that white and brown fat do not originate from the same precursor cells.

In the early phase of their development, the two types of fat cells appear to be identical, so most scientists had assumed they derive from a common source.

In the second study, Bruce Spiegelman of the Dana Farber Cancer Institute, also at Harvard, found out — to his “huge surprise” — that brown fat comes actually from the same stem cells that produce muscle tissue.

The key is a “master regulator” protein called PRDM16 that determines which way these adult stem cells will develop.

“I think we now have very convincing evidence that PRDM16 can turn cells into brown fat cells, with the possibility of combating obesity,” he said.

Though mature humans have relatively little brown fat, it is thought to play a critical metabolising role.

Spiegelman said that finding a new potential source for this “good” fat — the adult stem cells, or myoblasts, that exist to replace mature muscle cells — open a path for boosting its calorie-burning action to combat obesity.

Obesity is occurring at epidemic rates worldwide and is a major risk factor for type 2 diabetes and metabolic syndrome, a bundle of health problems including clogged arteries, heart attack and stroke.

Both studies were published in the British science and medical journal Nature.

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CHICAGO (Reuters) -
A new understanding of the origins of
brown fat cells — the “good” kind of fat that burns energy and
keeps us warm — may lead to new treatments for obesity, two
research teams reported on Wednesday.

Researchers at the Dana-Farber Cancer Institute in Boston
said they used a single molecular switch to turn immature
muscle cells into brown fat cells in the lab, suggesting that
brown fat may be more akin to muscle cells than conventional
white fat cells.

A second team from the Joslin Diabetes Center in Boston,
found a protein important for bone growth helped promote the
development of brown fat tissue in mice.

Both teams, reporting in the journal Nature, said their new
findings lend understanding about the origins of brown fat,
which releases energy, in contrast to conventional white fat,
which stores energy.

A person who is obese has large stores of white fat, and
researchers think if they can coax the body into making more
calorie-burning brown fat, this might help people obese people
lose weight.

Dana-Farber’s Bruce Spiegelman, who worked on the research,
said in a telephone interview that researchers have been trying
to find the genes that turn brown fat cells on.

Spiegelman said his team previously found that PRDM16, a
kind of genetic switch called a gene transcription factor,
appears to regulate the development of brown fat cells.

“What we show in this paper is kind of a big shock. We show
that brown fat is derived from a muscle-like cell, and that
brown fat and white fat are completely different,” he said.

When Spiegelman’s team removed PRDM16 from immature brown
fat cells in the lab, something strange happened.

“The dish filled up with muscle,” Spiegelman said. “What it
means is that muscle cells are precursor cells to brown fat
cells.”

Previously, his team also showed that PRDM16 could turn
conventional white fat cells into brown fat cells, but
Spiegelman thinks in living creatures, the muscle cell is a
natural cell type that gives rise to brown fat cells.

His team is now looking for a drug that could chemically
stimulate PRDM16 to make more brown fat cells, which would
shift the metabolism into more of a fat-burning mode.

In a separate finding, a team led by Yu-Hua Tseng of the
Joslin Diabetes Center found the protein BMP-7, known for
inducing bone growth, can also promote the development of brown
fat cells.

When Tseng’s team delivered this protein into mice through
a virus, the mice made more brown fat tissue.

And they found mice that developed extra brown fat tissue
gained less weight than other mice, suggesting a potential use
in weight loss.

The researchers were also able to get mice to develop extra
brown fat cells by pre-treating immature brown fat cells with
BMP-7 and transplanting them into the mice.

“We hope this study can be translated into applications to
help treat or prevent obesity,” Tseng said in a statement.

(Editing by Cynthia Osterman)

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