Futurity.org – Obesity related deaths hit 1-in-5 Americans

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“Obesity has dramatically worse health consequences than some recent reports have led us to believe,” says first author Ryan Masters, who conducted the research as a Robert Wood Johnson Foundation Health Society Scholar at Columbia University’s Mailman School of Public Health.

“We expect that obesity will be responsible for an increasing share of deaths in the United States and perhaps even lead to declines in US life expectancy.”

While there have been signs that obesity is in decline for some groups of young people, rates continue to be near historic highs. For the bulk of children and adults who are already obese, the condition will likely persist, wreaking damage over the course of their lives. The study is published online in the American Journal of Public Health.

In older Americans, the rising toll of obesity is already evident. Masters and his colleagues documented its increasing effect on mortality in white men who died between the ages of 65 and 70 in the years 1986 to 2006. Grade one obesity (body mass index of 30 to less than 35) accounted for about 3.5 percent of deaths for those born between 1915 and 1919—a grouping known as a birth cohort. For those born 10 years later, it accounted for about 5 percent of deaths. Another 10 years later, it killed off upwards of 7 percent.

Straight from the Source

Read the original study

DOI: 10.2105/AJPH.2013.301379

When the obesity epidemic hit in the 1980s, it hit across all age groups, so older Americans have lived through it for a relatively short period of time. But younger age groups will be exposed to the full brunt for much longer periods.

“A 5-year-old growing up today is living in an environment where obesity is much more the norm than was the case for a 5-year-old a generation or two ago. Drink sizes are bigger, clothes are bigger, and greater numbers of a child’s peers are obese,” explains co-author Bruce Link, professor of epidemiology and sociomedical sciences at Columbia University’s Mailman School of Public Health. “And once someone is obese, it is very difficult to undo. So it stands to reason that we won’t see the worst of the epidemic until the current generation of children grows old.”

New way to look at a growing problem

This study is the first to account for differences in age, birth cohort, sex, and race in analyzing Americans’ risk for death from obesity.

“Past research in this area lumped together all Americans, but obesity prevalence and its effect on mortality differ substantially based on your race or ethnicity, how old you are, and when you were born,” says Masters. “It’s important for policy-makers to understand that different groups experience obesity in different ways.”

The researchers analyzed 19 waves of the National Health Interview Survey linked to individual mortality records in the National Death Index for the years 1986 to 2006, when the most recent data are available. They focused on ages 40 to 85 in order to exclude accidental deaths, homicides, and congenital conditions that are the leading causes of death for younger people.

The study builds on earlier research by Masters that found, contrary to conventional wisdom, that risk for death from obesity increases with age. The new study is also influenced by previous work by co-authors Eric Reither, associate professor at Utah State University, and Claire Yang, associate professor at the University of North Carolina at Chapel Hill, which showed significant cohort differences in US obesity rates.

Effects by sex and race

In the groups studied, black women had the highest risk of dying from obesity or being overweight at 27 percent, followed by White women at 21 percent. Obesity in black women is nearly twice that of white women. White men fared better at 15 percent, and the lowest risk for dying from being obese was 5 percent, for black men.

While white men and black men have similar rates of obesity, the effect of obesity on mortality is lower in black men because it is “crowded out” by other risk factors, from high rates of cigarette smoking to challenging socioeconomic conditions. There were insufficient data to make estimates for Asians, Hispanics, and other groups due to the highly stratified nature of the methodology.

In sum, by using a new, more rigorous approach, the new research shows that obesity is far more consequential than previously recognized, that the impact of the epidemic is only beginning to be felt, and that some population groups are affected much more powerfully than others.

The Robert Wood Johnson Foundation funded the study.

Source: Columbia University

Could a Gene Help Make You Obese? – WebMD

Could a Gene Help Make You Obese?

By Dennis Thompson

HealthDay Reporter

MONDAY, July 15 (HealthDay News) — Researchers have discovered a potential genetic explanation for why some people overeat and run a greater risk for obesity.

People who carry two copies of a variant form of the “FTO” gene are more likely to feel hungry soon after eating a meal, because they carry higher levels of the hunger-producing hormone ghrelin in their bloodstream, an international team of scientists found.

What’s more, brain scans revealed this double FTO gene variant changes the way in which the brain reacts to food and ghrelin. People with the double variant displayed different neural responses in the brain region known to regulate appetite and the pleasure/reward center that normally responds to alcohol and recreational drug use.

About one in every six people carries two copies of this FTO gene variant. These folks are 70 percent more likely to become obese than people who carry other versions of FTO gene, according to background information in the study published July 15 in the Journal of Clinical Investigation.

“We’ve known for a while that variations in the FTO gene are strongly linked with obesity, but until now we didn’t know why,” said lead author Dr. Rachel Batterham. “What this study shows us is that individuals with two copies of the obesity-risk FTO variant are biologically programmed to eat more.”

Evolution may be responsible for the existence of this double variant in so many people.

“For the majority of the time that humans have existed food has been scarce. Having this genetic variant would have conferred a survival advantage,” said Batterham, head of obesity and bariatric services and director of Center for Obesity Research at University College London Hospitals.

The researchers first asked a group of 20 men — 10 with the double variant, and 10 with a version of the FTO gene linked to lower obesity risk — to rate their hunger before and after a meal. Blood samples were taken to test their levels of ghrelin, a hormone secreted by the stomach that stimulates appetite.

Ghrelin levels normally increase before meals and fall afterward, but researchers found the men with the double FTO variant had much higher ghrelin levels after a meal and felt hungrier after eating than men who had the variation that carries lower obesity risk.

In the next step, the research team used functional MRI to measure how the brain responds to food images and ghrelin levels before and after a meal, using a different group of 24 men.

MRI scans revealed altered brain activity in the double-variant men, both in the appetite-controlling hypothalamus and the brain’s “reward” regions, which are known to respond to alcohol and recreational drugs. The altered activity occurred in response to food images and to the ghrelin in their bloodstream.

How 'obesity gene' triggers weight gain

FTO picture no labels

An international team of researchers
has discovered why people with a variation of the FTO gene that affects one in six
of the population are 70 per cent more likely to become obese.

A new study led by scientists
at UCL, the Medical Research Council (MRC) and
King’s College London Institute of Psychiatry shows that people with the
obesity-risk FTO variant have higher circulating levels of the ‘hunger hormone’,
ghrelin, in their blood. This means they start to feel hungry again soon after
eating a meal.

Real-time brain imaging
reveals that the FTO gene variation also changes the way the brain responds to ghrelin,
and to images of food, in the regions linked with the control of eating and reward.

Together these findings explain
for the first time why people with the obesity-risk variant of the FTO gene eat
more and prefer higher calorie foods compared with those with the low-risk
version, even before they become overweight. The research, funded by the MRC
and the Rosetrees Trust, is published today in the Journal of Clinical Investigation.

Individuals with two copies of the obesity-risk FTO variant are biologically programmed to eat more. Not only do these people have higher ghrelin levels and therefore feel hungrier, their brains respond differently to ghrelin and to pictures of food – it’s a double hit.

Dr Rachel Batterham, UCL metabolism Experimental Therapeutics

Previous studies have revealed
that single ‘letter’ variations in the genetic code of the FTO gene are linked
with an increased risk of obesity, and this behaviour is present even in
preschool children.

Using a unique study design, scientists
led by Dr Rachel Batterham (UCL Metabolism and Experimental Therapeutics) recruited 359 healthy male volunteers to examine the
‘real life’ effects of the FTO variation in humans.

They studied two groups of participants
– those with two copies of the high obesity-risk FTO variant (AA group) and
those with the low obesity-risk version (TT group). They matched the volunteers
perfectly for body weight, fat distribution and social factors such as
educational level to ensure that any differences they saw were linked to FTO,
and not to other physical or psychological characteristics.

A group of 20 participants
(10 AA and 10 TT) were asked to rate their hunger before and after a standard meal,
while blood samples were taken to test levels of ghrelin – a hormone released
by cells in the stomach that stimulates appetite.

Normally ghrelin levels rise before
meals and fall after eating, but in this study men with the AA variation had much
higher circulating ghrelin levels and felt hungrier after the meal than the TT
group. This suggests that the obesity-risk variant (AA) group do not suppress ghrelin
in a normal way after a meal.

The researchers then used functional
magnetic resonance imaging (fMRI) in a different group of 24 participants to
measure how the brain responds to pictures of high-calorie and low-calorie food
images, and non-food items, before and after a meal. Again they took blood
samples and asked the participants to rate on a scale how appealing the images
were.

Individuals with the obesity-risk
FTO variant rated pictures of high-calorie foods as more appealing after a meal
than the low-risk group. In addition, the fMRI study results revealed that the
brains of the two groups responded differently to food images (before and after
a meal) and to circulating levels of ghrelin. The differences were most
pronounced in the brain’s reward regions (known to respond to alcohol and
recreational drugs) and in the hypothalamus – a non-conscious part of the brain
that controls appetite.

Finally, the scientists
looked at mouse and human cells to uncover what causes increased ghrelin production
at a molecular level. They over-expressed the FTO gene and found that this altered
the chemical make-up of ghrelin mRNA (the template for the ghrelin protein) leading
to higher levels of ghrelin itself. Blood cells taken from the obesity-risk
group also had higher levels of FTO gene expression and more ghrelin mRNA than
the low-risk group.

Dr Rachel Batterham from UCL
and University College London Hospitals, who led the study, said: “We’ve known for a while that
variations in the FTO gene are strongly linked with obesity, but until now we
didn’t know why. What this study shows us is that individuals with two copies
of the obesity-risk FTO variant are biologically programmed to eat more. Not
only do these people have higher ghrelin levels and therefore feel hungrier,
their brains respond differently to ghrelin and to pictures of food – it’s a
double hit.

“At a therapeutic level this
arms us with some important new insights to help in the fight against the
obesity pandemic. For example, we know that ghrelin (and therefore hunger) can
be reduced by exercise like running and cycling, or by eating a high-protein
diet. There are also some drugs in the pipeline that suppress ghrelin, which might
be particularly effective if they are targeted to patients with the
obesity-risk variant of the FTO gene.”

Professor David Lomas, Chair
of the MRC’s Population and Systems Medicine Board, said: ““Large scale population
studies have done an excellent job at highlighting FTO as a key obesity gene.
Here scientists have used an innovative combination of human studies and more
basic biology to finally give us the ‘smoking gun’ linking FTO variations,
hunger and weight gain.

“The brain imaging adds a fascinating insight into the
role of the nervous system in obesity, which is becoming increasingly clear. This
work will contribute to more targeted treatments and better outcomes for obese
patients in the future.”

Richard Ross, Chairman of the
Rosetrees Trust, said: “Rosetrees is delighted to be
able to support cutting-edge research carried out by outstanding researchers
such as Dr Batterham, which has such a direct human impact. Rosetrees supports
over 200 projects, helping researchers to make breakthroughs across all the
major illnesses.”

The research was led by UCL, Professor
Dominic Withers in the MRC Clinical Sciences Centre at Imperial College London,
and Dr Fernando Zelaya at King’s College London Institute of Psychiatry in
collaboration with a host of international partners.

It was funded by the MRC,
Rosetrees Trust, the National Institute for Health Research University College
London Hospitals Biomedical Research Centre (NIHR BRC) and the Wellcome Trust.

-Ends-


Media contact: David Weston

Image caption: Key brain regions that
regulate eating, reward and motivation show altered response to the hunger
hormone ghrelin in subjects with the obesity-risk FTO variant. (Credit: UCL)


Links:

Whole Health Source: The Genetics of Obesity, Part II

Rodents Lead the Way


The study of obesity genetics dates back more than half a century.  In 1949, researchers at the Jackson Laboratories identified a remarkably fat mouse, which they determined carried a spontaneous mutation in an unidentified gene.  They named this the “obese” (ob/ob) mouse.  Over the next few decades, researchers identified several other genetically obese mice with spontaneous mutations, including diabetic (db/db) mice, “agouti” (Avy) mice, and “Zucker” (fa/fa) rats.

At the time of discovery, no one knew where the mutations resided in the genome.  All they knew is that the mutations were in single genes, and they resulted in extreme obesity.  Researchers recognized this as a huge opportunity to learn something important about the regulation of body fatness in an unbiased way.  Unbiased because these mutations could be identified with no prior knowledge about their function, therefore the investigators’ pre-existing beliefs about the mechanisms of body fat regulation could have no impact on what they learned.  Many different research groups tried to pin down the underlying source of dysfunction: some thought it was elevated insulin and changes in adipose tissue metabolism, others thought it was elevated cortisol, and a variety of other hypotheses.

At the same time, several groups were researching a fascinating new “anti-lipogenic factor” (also “satiety factor”) they had identified by literally fusing together obese and normal rats, allowing their circulation to (very slowly) communicate (1).  Their results suggested the existence of a previously unidentified, powerful circulating factor that regulates food intake and body fatness, and they were able to rule out insulin, glucose, fatty acids, cortisol, and a variety of other potential contenders.  Furthermore, their findings suggested that ob/ob mice lack the anti-lipogenic factor, db/db mice lack its receptor, and the factor acts primarily in a brain region called the hypothalamus (2).  Yet the identity of the factor remained unknown until 1994.

Realizing that a full understanding of obesity in ob/ob mice would require identifying the mutation, a research team led by Dr. Rudolf Leibel set out to identify it through a laborious process called positional cloning.  In 1994, this led to the cloning and sequencing of the ob gene (3), which encoded a previously unknown protein of 16 kilodaltons.  They named it leptin, after the Greek word “leptos”, meaning “thin”.  Here is the full abstract of the paper:

The mechanisms that balance food intake and energy expenditure determine who will be obese and who will be lean. One of the molecules that regulates energy balance in the mouse is the obese (ob) gene. Mutation of ob results in profound obesity and type II diabetes as part of a syndrome that resembles morbid obesity in humans. The ob gene product may function as part of a signalling pathway from adipose tissue that acts to regulate the size of the body fat depot.

Further work confirmed that leptin is produced primarily by fat cells and acts in the brain to constrain food intake and body fatness (4).  Remarkably, all of the original single-gene mutations that cause rodent obesity ended up being in the leptin signaling pathway.  ob/ob mice lack leptin, db/db mice and fa/fa rats lack the leptin receptor, and Avy mice have a mutation that mimics the effects of leptin deficiency in the brain.  The obesity, elevated insulin, and alterations in fat cell metabolism in these models were all downstream consequences of defects in the leptin signaling pathway– via the brain.

Humans Follow


Shortly after the cloning of the leptin gene, researchers identified a family of humans that also lacked leptin function (5), providing “the first genetic evidence that leptin is an important regulator of energy balance in humans”.  Not only were they obese, with an abnormally large appetite, but treating them with leptin normalized their appetite and returned them to a normal weight (6), as shown in the photo to the left (6b).  As of 2013, a number of human families with obesity due to single-gene mutations have been identified.  If we consider only those mutations that cause obesity without causing significant developmental abnormalities, all of them turned out to be in the leptin signaling pathway– either in leptin, the leptin receptor, or the brain circuits that respond to leptin and related signals (7)*.  As was the case in rodents, spontaneous mutations in humans pointed to the leptin-brain axis as the primary regulator of body fatness.

More recently, researchers have performed large-scale genetic screens on people who have severe or early-onset obesity to see if some cases can be attributed to variance in specific genes.  About 4 percent of severely obese people have a mutation in the melanocortin receptor 4 (MC4R) gene that causes it to lose function (8), and two recently published papers identified a loss-of function variant of the gene SIM1 in another subset of early-onset obese subjects (9, 10).  MC4R is a receptor for alpha-MSH**, the product of leptin-responsive POMC neurons, and SIM1 is an important protein for the development and function of the paraventricular nucleus of the hypothalamus, a major target of POMC neurons.  In other words, they are both part of the same system in the brain that regulates body fatness in response to leptin and other signals.  Both the MC4R and SIM1 variants cause an increase in food intake due to a defect in satiety (11).  For people with these variants, achieving real leanness is unlikely.  Other studies have also uncovered mutations in genes associated with the brain regulation of body fatness in severe early-onset obesity (11b).

So far, I’ve described rare mutations that lead to severe obesity.  These mutations only account for a very small fraction of the obese population.  To understand what genes are involved in common obesity, we’ll have to turn to another method: genome-wide association studies (GWAS).  The GWAS method takes advantage of the fact that everyone’s genome is a little bit different.  By sequencing these areas of difference between people***, they can associate them with specific traits, for example, obesity.  This allows researchers to “map” sites of particular importance to the trait in question, which tells us something about what biological processes are relevant to the trait.  For example, diabetes-linked regions are mostly associated with genes affecting the pancreas, as one would expect (12)  though some obesity genes do show up as well****.

The findings of obesity GWAS studies are basically consistent with the other evidence described above (12b).  For many of the identified regions, we don’t know which gene is involved.  For the genes that we have identified, most of them are involved in brain function, particularly the leptin-responsive hypothalamus.  Here’s a quote from a review paper that sums it up (13):

…when we look at the information gleaned from the past 15 years of molecular genetic activity we cannot avoid concluding that, as much as type 2 diabetes is clearly a disease in which pancreatic beta-cell dysfunction is a critical element, obesity is a condition in which inherent genetic predisposition is dominated by the brain.

That being said, GWAS studies have failed to identify the majority of the genetic differences that account for the 70 percent heritability of body fatness (less than 3% accounted for).  We have enough information to know what types of biological processes are involved in common obesity, but we don’t know all the details yet.  As the old saying goes, “more research is required”!

What does it Mean?

The genetic data converge powerfully with other fields such as neurobiology, endocrinology, and physiology, together demonstrating conclusively that:

  1. The brain is the main regulator of body fatness.
  2. The brain regulates body fatness in response to internal signals of energy stores, particularly leptin.
  3. Genetic variability in body fatness is likely predominantly determined by genetic differences in brain function, particularly the hypothalamus.

In the next post, I’ll explain why genes are not (usually) destiny.


* Those that do cause deformity also involve brain energy balance circuitry (14).

** Also AgRP, which is an inverse agonist at the MC4R and increases food intake.

*** Typically, single-nucleotide polymorphisms.

**** E.g., FTO, the #1 obesity GWAS hit.

Deep Brain Stimulation Studied as Last-Ditch Obesity Treatment …

Deep Brain Stimulation Studied as Last-Ditch Obesity Treatment

By Amy Norton

HealthDay Reporter

THURSDAY, June 13 (HealthDay News) — For the first time, researchers have shown that implanting electrodes in the brain’s “feeding center” can be safely done — in a bid to develop a new treatment option for severely obese people who fail to shed pounds even after weight-loss surgery.

In a preliminary study with three patients, researchers found that they could safely use the therapy, known as deep brain stimulation (DBS). Over almost three years, none of the patients had any serious side effects, and two even lost some weight — but it was temporary.

“The first thing we needed to do was to see if this is safe,” said lead researcher Dr. Donald Whiting, vice chairman of neurosurgery at Allegheny General Hospital in Pittsburgh. “We’re at the point now where it looks like it is.”

The study, reported in the Journal of Neurosurgery and at a meeting this week of the International Neuromodulation Society in Berlin, Germany, was not meant to test effectiveness.

So the big remaining question is, can deep brain stimulation actually promote lasting weight loss?

“Nobody should get the idea that this has been shown to be effective,” Whiting said. “This is not something you can go ask your doctor about.”

Right now, deep brain stimulation is sometimes used for tough-to-treat cases of Parkinson’s disease, a movement disorder that causes tremors, stiff muscles, and balance and coordination problems. A surgeon implants electrodes into specific movement-related areas of the brain, then attaches those electrodes to a neurostimulator placed under the skin near the collarbone.

The neurostimulator continually sends tiny electrical pulses to the brain, which in turn interferes with the abnormal activity that causes tremors and other symptoms.

What does that have to do with obesity? In theory, Whiting explained, deep brain stimulation might be able to “override” brain signaling involved in eating, metabolism or feelings of fullness. Research in animals has shown that electrical stimulation of a particular area of the brain — the lateral hypothalamic area — can spur weight loss even if calorie intake stays the same.

The new study marks the first time that deep brain stimulation has been tried in that brain region. And it’s an important first step to show that not only could these three severely obese people get through the surgery, but they also seemed to have no serious effects from the brain stimulation, said Dr. Casey Halpern, a neurosurgeon at the University of Pennsylvania who was not involved in the research.

“That shows us this is a therapy that should be studied further in a larger trial,” said Halpern, who has done animal research exploring the idea of using deep brain stimulation for obesity.

“Obesity is a major problem,” Halpern said, “and current therapies, even gastric bypass surgery, don’t always work. There is a medical need for new therapies.”

Researchers Link Obsessive-Compulsive Behavior And Obesity

An experiment to probe brain circuits involved in compulsive behavior – where mice were bred missing a gene
suspected to be involved in compulsive behavior and obesity – resulted in offspring mice that were neither compulsive groomers nor obese.

Their Proceedings of the National Academy of Sciences (PNAS) paper suggests that the brain circuits that control obsessive-compulsive behavior are intertwined with circuits that control food intake and body weight.  

University of Iowa psychiatrists Michael Lutter, M.D., Ph.D. and Andrew Pieper, M.D., Ph.D., led the study, which included researchers from Stanford University School of Medicine, University of Texas Southwestern Medical Center, Beth Israel Deaconess Medical Center, and Harvard Medical School.

Pieper is interested in compulsive behavior. His mouse model of compulsivity lacks a brain protein called SAPAP3. These mice groom themselves excessively to the point of lesioning their skin, and their compulsive behavior can be effectively treated by fluoxetine, a drug that is commonly used to treat OCD in people. Lutter works with a mouse that genetically mimics an inherited form of human obesity. This mouse lacks a brain protein known a MC4R. Mutations in the MC4R gene are the most common single-gene cause of morbid obesity and over-eating in people.

“I study MC4R signaling pathways and their involvement in the development of obesity,” Lutter explains. “I’m also interested in how these same molecules affect mood and anxiety and reward, because it’s known that there is a connection between depression and anxiety and development of obesity.”

An old study hinted that in addition to its role in food intake and obesity, MC4R might also play a role in compulsive behavior, which got Lutter and Pieper thinking of ways to test the possible interaction.

“We knew in one mouse you could stimulate excessive grooming through this MC4R pathway and in another mouse a different pathway (SAPAP3) caused compulsive grooming,” Lutter says. “So, we decided to breed the two mice together to see if it would have an effect on compulsive grooming.”

The experiment proved their original hypothesis — knocking out the MC4R protein in the OCD mouse normalized grooming behavior in the animals. In addition, chemically blocking MC4R in the OCD mice also eliminated compulsive grooming. The rescued behavior is mirrored by normalization of a particular pattern of brain cell communication linked to compulsive behavior.

However, the breeding experiment revealed another totally unexpected result. Loss of the SAPAP3 protein from the mice that were obese due to lack of MC4R produced mice of normal weight.

“We had this other, completely shocking finding — we completely rescued body weight and food intake in the double null mouse,” Lutter says. “So, not only were we affecting the brain regions involved in grooming and behavior, but we also affected the brain regions involved in food intake and body weight.”

Although obesity and obsessive-compulsive behavior may seem unrelated, Lutter suggests that the connection may be rooted in the evolutionary need to eat safe, clean food in times of a food abundance, and to lessen this drive when food is scarce.

“Food safety has been an issue through the entire course of human evolution – refrigeration is a relatively recent invention,” he says. “Obsessive behavior, or fear of contamination, may be an evolutionary protection against eating rotten food.”

Oils and fats have lots of calories and nutrients but they also spoil much more easily than less nutrient- and calorie-dense foods like potatoes, onions, or apples.

“I think this circuit that we have uncovered is probably involved in determining whether or not people should eat calorically dense foods,” he says.

Lutter suggests that slight perturbations in this system might lead, on one hand, to disorders that link anxiety and obsessive behavior to limited food selection or intake, such as anorexia nervosa, Tourette syndrome, or OCD, and on the other hand, to obesity, where people over-consume high-fat foods and may have decreased obsessive behavior and anxiety.

“The next step will be to determine how these two pathways communicate with one another, in hopes of identifying new ways to develop drugs to treat either of these disorders,” says Pieper.

Futurity.org – Amino acid linked to asthma, obesity combo

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The relationship between asthma and obesity is in many ways a conundrum, says the study’s lead author, Fernando Holguin, associate professor in the Division of Pulmonary, Allergy and Critical Care Medicine at University of Pittsburgh School of Medicine, and co-director of the Asthma Institute.

Straight from the Source

Read the original study

DOI: 10.1164/rccm.201207-1270OC

A person who has severe asthma may require frequent steroid treatments and limit his or her activity, resulting in weight gain; in others, obesity seems to aggravate or even initiate asthma symptoms.

“Obese asthma patients tend to have worse symptoms, more frequent episodes of breathing difficulty, and don’t respond as readily to conventional treatments,” says Holguin, whose findings appear in the American Journal of Respiratory and Critical Care Medicine.

“Our study supports the premise that asthma is a multifactorial condition that can be triggered by a variety of underlying problems.” Interventions to improve clinically meaningful outcomes may need to be personalized to the type of asthmatic condition that patient has.

Patients who are obese and develop asthma as adults tend to exhale lower levels of nitric oxide (NO), a compound that relaxes blood vessels and is thought to play a similar role in airways.

The researchers collected blood samples from 155 adults, nearly half of whom had severe asthma and half of whom were obese. The team found that compared to early-onset asthma patients, late-onset obese asthma patients had lower plasma levels of the amino acid arginine and higher levels of an arginine metabolite called ADMA, which interferes with NO production.

“In healthy people, a balance is maintained between arginine and ADMA ensuring normal levels of airway NO,” Holguin says.

“But in obese, adult-onset asthma, the lower arginine and higher ADMA reduces airway NO levels. This finding is promising because it suggests that increasing arginine could restore NO levels and its positive effect on airways.” This might translate into patients having less wheezing and shortness of breath.

Arginine is readily available over the counter as a dietary supplement, but it is rapidly metabolized by the body and reduces its practicality as a treatment, he says. Another supplement called citrulline is known to enhance arginine production, and can be taken in high doses without ill effects.

“We will soon begin a small pilot study to see whether citrulline supplements can help alleviate symptoms in patients who fit this profile of late-onset asthma, obesity and decreased exhaled NO,” says Holguin.

Co-authors of the paper include researchers from the University of Pittsburgh School of Medicine, as well as from the Cleveland Clinic, Wake Forest University, University of Wisconsin, University of Texas, Washington University, Emory University, University of Virginia, Harvard University, and Imperial College London.

The National Institutes of Health funded the study.

Source: University of Pittsburgh

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Sleeping teens reveal how brain matures

Sleeping teens reveal how brain matures

Physical exam still key to prostate screening

Physical exam still key to prostate screening

Violence-asthma link for Puerto Rican kids

Violence-asthma link for Puerto Rican kids

Faster MRI finds disease with ‘fingerprints’

Faster MRI finds disease with ‘fingerprints’





The relationship between asthma and obesity is in many ways a conundrum, says the study’s lead author, Fernando Holguin, associate professor in the Division of Pulmonary, Allergy and Critical Care Medicine at University of Pittsburgh School of Medicine, and co-director of the Asthma Institute.

Straight from the Source

Read the original study

DOI: 10.1164/rccm.201207-1270OC

A person who has severe asthma may require frequent steroid treatments and limit his or her activity, resulting in weight gain; in others, obesity seems to aggravate or even initiate asthma symptoms.

“Obese asthma patients tend to have worse symptoms, more frequent episodes of breathing difficulty, and don’t respond as readily to conventional treatments,” says Holguin, whose findings appear in the American Journal of Respiratory and Critical Care Medicine.

“Our study supports the premise that asthma is a multifactorial condition that can be triggered by a variety of underlying problems.” Interventions to improve clinically meaningful outcomes may need to be personalized to the type of asthmatic condition that patient has.

Patients who are obese and develop asthma as adults tend to exhale lower levels of nitric oxide (NO), a compound that relaxes blood vessels and is thought to play a similar role in airways.

The researchers collected blood samples from 155 adults, nearly half of whom had severe asthma and half of whom were obese. The team found that compared to early-onset asthma patients, late-onset obese asthma patients had lower plasma levels of the amino acid arginine and higher levels of an arginine metabolite called ADMA, which interferes with NO production.

“In healthy people, a balance is maintained between arginine and ADMA ensuring normal levels of airway NO,” Holguin says.

“But in obese, adult-onset asthma, the lower arginine and higher ADMA reduces airway NO levels. This finding is promising because it suggests that increasing arginine could restore NO levels and its positive effect on airways.” This might translate into patients having less wheezing and shortness of breath.

Arginine is readily available over the counter as a dietary supplement, but it is rapidly metabolized by the body and reduces its practicality as a treatment, he says. Another supplement called citrulline is known to enhance arginine production, and can be taken in high doses without ill effects.

“We will soon begin a small pilot study to see whether citrulline supplements can help alleviate symptoms in patients who fit this profile of late-onset asthma, obesity and decreased exhaled NO,” says Holguin.

Co-authors of the paper include researchers from the University of Pittsburgh School of Medicine, as well as from the Cleveland Clinic, Wake Forest University, University of Wisconsin, University of Texas, Washington University, Emory University, University of Virginia, Harvard University, and Imperial College London.

The National Institutes of Health funded the study.

Source: University of Pittsburgh

What is cerebral palsy?

Cerebral palsy is defined by a number of neurological conditions, which usually develop in the brain of a baby when it is either very young, newly born or still in the womb. This abnormal development causes damage to the brain, leading to problems with movement, posture and coordination as the child grows up.

What causes it?

Cerebral palsy is caused by damage to a part of the brain called the cerebrum, which controls the body’s muscles. The damage has a negative effect on the muscles and can inhibit their function.

In the past the condition was associated with problems during labour and birth, but now it is generally accepted these cause only around one in ten cases. Most cases occur due to damage to the brain before the child is born. This may occur due to:

  • A child with cerebral palsy being examined

    Periventricular leukomalacia (PVL) – this is damage caused to the white matter of the brain, which in turn may be caused by a reduction in the child’s blood supply. An infection, such as rubella, caught by the mother during pregnancy, the mother having low blood pressure, premature birth or the mother using cocaine during pregnancy could all lead to the child’s brain being damaged.

  • Abnormal brain development – this could be caused by gene alterations that help the brain develop, infections such as Herpes or trauma to the unborn baby’s head.
  • Intracranial haemorrhage – meaning bleeding in the brain. This normally occurs when the unborn baby has a stroke (brought on by pre-existing weakenesses in the baby’s blood vessels, the mother’s high blood pressure, infection during pregnancy).
  • Damage after birth – lack of developed resistance to infections such as Meningitis can sometimes lead to brain damage in very early life.

What are the symptoms?

Cerebral palsy is divided into several different categories due to its varied symptoms. These include:

  • Spastic cerebral palsy – this affects around 70% of cases and is defined by some muscles becoming tight, weak and stiff, making control of movement difficult.
  • Ataxic cerebral palsy – here, problems include difficulty balancing, shaky movements of hands or feet, and speech problems.
  • Athetoid (dyskinetic) cerebral palsy – affects 10% of cases, whereby control of muscles is disrupted by spontaneous and unwanted irregular writhing movements. These may be the result of muscles changing very rapidly from being loose and to tight and tense. The muscles used for speech may also be affected, interfering with communication. Control of posture is also disrupted.
  • Mixed cerebral palsy – a combination of two or more of the above.

[adsense]The cerebrum (the part of the brain that is damaged) also partly controls sight, hearing and communcation ability, so those suffering from cerebral palsy can sometimes also experience:

  • Learning difficulties
  • Problems speaking or understanding others
  • Visual or hearing impairment

It has also been linked with other conditions, which sufferers often experience alongside cerebral palsy, such as Epilepsy, scoliosis and incontinence.

How is it treated?

Unfortunately, there is no cure for cerebral palsy, but there are many treatments and therapies available to manage the condition. The patient and his or her family usually work very closely with health professionals to find the best way to deal with it. Physiotherapy, occupational therapy and speech therapy can also play important roles. Medication is available to relax particularly stiff muscles and surgical procedures have been developed to help combat feeding and drooling problems.

Click here to read about Brad Pitt’s mild viral meningitis and how early meningitis is now detectable through a new test.

Images: Wikipedia and cerebral-palsy.me

Brain tricked into believing false memories, study finds

In a recent attempt to uncover the hidden facts about human memory, a team of scientists have revealed in a study that watching someone else perform a particular action can lead to a distorted impression on the mind resulting in believing that you performed the action yourself.

As reported by www.sciencedaily.com, there have been several studies earlier to know about false memories; however the latest one has left the scientists “stunned”. The study was carried out by researchers at the Jacobs University Bremen. Initially, the researchers set out to uncover more facts about imagination. Little did they know that their endeavour would end up revealing facts about false memories.

As reported by www.physorg.com, during the study, a group of individuals were made to perform small tasks like shuffling a deck of cards and were thereafter shown video clips where a few people were performing such other small tasks. Two weeks later, these individuals were asked as to which of the tasks were performed by them, to which they gave a description that included tasks that were not done by them but were shoen to them being done by others in video clips.

Speaking about the study lead researcher Gerald Echterhoff said: “It’s good to have an informed doubt or informed skepticism about your memory performance, so you don’t just easily trust whatever comes to your mind as true and for granted.”

The study will be be published in the journal ‘Psychological Science‘.

Celebrities who have had brain injuries include Sharon Stone, Bret Michaels and Jackie Chan.

Images: http://www.sxc.hu/photo/1242968, http://www.sxc.hu/photo/880737