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Posted: Fri Jul 27th, 2007 01:56 |
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Dr Trevor Marshall
Some Bacteria make you Fat, some Thin
Some of you may have noticed my recent citation of several papers from Jeffrey Gordon's lab canvassing the topic of obesity, and how gut microbiota (bacterial flora) seem to be involved in whether we get fat (or get thin, or stay 'normal').
"Fat people harbour 'fat' microbes"
http://www.bioedonline.org/news/news.cfm?art=3017
and
"An obesity-associated gut microbiome with increased capacity for energy harvest"
http://tinyurl.com/2rfrzp PMID: 17183312
Well, this week I had an abstract accepted for presentation at an upcoming conference, Metagenomics 2007, and as the moderators were browsing through the conference website, Janet noticed that Jeffrey Gordon had spoken at the same conference last year, and that the video of that presentation was still online.
The video "It's So Nice to Have a Few Trillion Friends: Exploring the Structure and Functions of Our Human Gut Microbiota and Microbiome, Jeffrey I. Gordon, Washington University of St. Louis"
is at http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/gordon.rm
This is a "MUST SEE" video. Please put aside 32 minutes of your time to watch it. You will come away with a new appreciation for the bacteria which live in symbiosis with Homo sapiens.
And as an added bonus, there is a video where W. Ford Doolittle, of Dalhousie University (Canada), argues against the concept of Bacterial species altogether. Another 'must see.'
http://rpvss.ucsd.edu:8080/ramgen/calit2/metagenomics/doolittle.rm
Note particularly the "agreement to disagree" during the question and answer session of this latter video. This frank exchange of scientific concepts is something I sorely miss when I am in Clinical Medicine circles, where the instinct is to suppress any thought which conflicts with what one supposes to be 'the consensus'.
So where does Th1 disease come into all this?
Well, as you know, the VDR is blocked by the Th1 pathogens to protect themselves from the beta-Defensin and Cathelicidin anti-microbial peptides. Yet these same Defensins are key to controlling the flora in the small intestine (recall the earlier video about Crohn's disease for more info). I don't think I need to remind anybody that the GI tract seems to be abnormal in just about every member of our cohort
Previously I have noted that, dependent on the infectious history of an individual, the microbiota they are carrying around (the 'pea soup') varies from individual to individual.
Additionally, many of the Th1 co-infections are firmicutes, in any case.
Finally, right at the end of the video, Jeffrey discloses that they were able to take bacterial flora from obese mice, and use them to infect 'normal' mice, turning the normals obese in the process. Oh what a can of worms this opens up...
Note: Mr. Gordon states "the environment inside the uterus is sterile". This is incorrect. The reason the metagenomic teams haven't made a real medical breakthrough is that they are not adequately skilled in a number of clinical areas we stumbled into. We had the necessity to understand Borrelia, for instance, which has been shown to be transmitted during pre-natal gestation. So we have a slightly different view of things to Jeff.
We are told "you are what you eat" but that is not true, because it ignores that the appetite might well be controlled by another factor, eg, Th1 disease. Jeff Gordon's paper showed that obesity was linked to both gut flora and diet. In particular, certain species of bacteria seemed to be encouraged by high fat or high carb diets. In turn, those species all interact with the rest of the flora to determine the efficiency of digestion. I might say "you are what is eating you" but that would be too flippant
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Posted: Fri Jul 27th, 2007 02:02 |
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Probiotics and obesity
The bigger question is how probiotics disturb the balance, not which class they go into. You will note in Jeffrey's presentation that transplanting the Zebra fish bacteria into the mice changed the balance of the bacterial species.
It is not as simple as "popping a pill." IMO that is because the effect of the probiotics will change depending on how your innate immune system is able to respond to the probiotic, and the microbiota already there. And that depends on the state of your Th1 infection....
and:
I am thinking that if innate immunity is functioning correctly then the human body can get by quite well without any flora in the gut. Maybe there will be 20% less conversion of fibre, etc, but I suspect we would just eat more and the undigested fibre would reduce constipation
I am not convinced that any of the microbiota are essential for health. I am still looking for evidence of benefit, I don't see it. The bugs help us grow old, they help us get ill. Maybe there are offsetting positives. I just haven't found any yet
Folk who think they are healthy (but remember everybody is carrying some sort of mix of microbiota) might feel some benefit from using probiotics, but since all they are doing is making their innate immune system work a little harder, I am not sure there is any long-term benefit to be gained from probiotics.
Of course, the whole population is currently carrying a heavy load of pathogens, so it is not possible to actually test any of this out just yet... but in a few more years..
Dr. Trevor Marshall, Ph.D.
Related FAQ:
What kind of probiotics should I use?
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Posted: Fri Jul 27th, 2007 02:05 |
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Firmicutes and CWD species
I included a link to Prof Doolittle, arguing that species are irrelevant, in the first message of this topic.
'Firmicutes' is a pretty broad brush, certainly inclusive of many of the recognized L-form 'species', but I would emphasize that 94% of the 'species' that Jeff's group found were not able to be identified.
So it's sort of groping around in the dark, at the species level. At the level of "pea soup" it has now been shown that 'transplanting' the pea-soup from ob/ob mice to sterile mice caused those to also become obese.
What was in that pea soup is probably less important at this point; rather the key is that one's infective microbiota can influence one's weight. Which we all sorta knew before, but now our hunch is backed by some science
Dr. Trevor Marshall, Ph.D.
See also Bacteria implicated in obesity
Here is an interesting article which points really well to macrophage-centric immune changes in obesity:
"New method finds networks of genes behind obesity"
http://www.reuters.com/article/healthNews/idUSN1645889420080316
Schadt's team, writing in two studies published in the journal Nature, said the diseases of obesity appear to originate in the immune system. "The network is enriched for genes that are involved in macrophages," Schadt said.
http://www.reuters.com/article/healthNews/idUSN1645889420080316
..Trevor.. Last edited on Mon Mar 17th, 2008 20:50 by Foundation Staff
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Posted: Fri Jul 27th, 2007 02:11 |
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Resolving obesity
I think this will happen automatically as your innate immune system fully recovers. Ultimately you will be making the antimicrobial peptides under control of hormonal feedback from the GI tract, rather than being overwhelmed by the signals from the infected phagocytes. I suspect that the full complement of antimicrobial peptides will allow effective culling of the nasties.
Many folk on the MP are thin, and some go through thinning periods. But weight fluctuates, and I suspect will not totally normalize until the body totally returns to full health.
At that point, 'the world's your oyster'... and we will probably continue to break paradigms as we develop knowledge about 'healthy aging'...
Dr. Trevor Marshall, Ph.D.
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Posted: Fri Jul 27th, 2007 02:12 |
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Diet pills
Xenical (orlistat) works primarily in the intestines but a small amount is absorbed systemically. It is touted to cause weight loss by preventing fat absorption. However, a low-fat diet must be consumed in order to prevent diarrhea and fecal incontinence. Thus, the weight loss could be attributed to diet alone. IMO, a low carb diet would be a safer alternative while you are recovering your health (and a normal weight) on the MP.
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Posted: Fri Jul 27th, 2007 02:14 |
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Members' experiences
I had a weight problem for many years prior to the MP. Here is a 'before and after' picture. ~Meg
Last year I walked at least 2 hours every day and managed to loose a fair bit of weight. Had to give up all that walking on the MP and I was really worried that I would pile the weight back on. Well...first couple of months I lost 4 kg when I changed to a totally low carb diet. Then I slackened on my carbs and quite a few crept back in and I regained the 4 kilos. Now....after a month or so of going back onto the low carb eating I have shed those 4 and 3 others. So...all in all...without any exercise and leading a very sedentary lifestyle...I managed to loose 7 kg in 5 months. ~IngeD
See Will the Marshall Protocol help me lose weight?
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Posted: Fri Jul 27th, 2007 02:16 |
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Do regulatory T Cells Contribute to Th1 Skewness in Obesity?
Svec P, Vásárhelyi B, Pászthy B, Körner A, Kovács L, Tulassay T, Treszl A. Research Group of Pediatrics and Nephrology, Hungarian Academy of Sciences, Budapest, Hungary.
BACKGROUND: Recent data suggest that an increased prevalence of interferon-gamma (IFN-gamma) producing CD4 (+) cells is present in obesity. Regulatory T cells (Tregs) have a strong impact on activation and proliferation of CD4 (+) lymphocytes. Data are not available about Tregs and their possible contribution to chronic mild inflammation in obesity. DESIGN: We investigated the prevalence of Tregs in obese children. We also collected data about dendritic cells and monocytes (so-called antigen presenting cells, APCs), important modulators of Tregs and we determined the cytokine production of CD4 (+) lymphocytes, the main target cells of Tregs.
METHODS: Twelve obese children and 10 healthy age-matched controls have been enrolled. For flow cytometric analyses, peripheral blood mononuclear cells were used. We determined the prevalence of Tregs by Foxp3 expression of CD4 (+) cells; prevalence of myeloid and plasmacytoid dendritic cells (DCs); prevalence of tumor necrosis factor (TNF)-alpha and interleukin(IL)-12 producing monocytes; and prevalence of IL-2, IL-4 and IFN-gamma producing CD4 (+) cells. RESULTS: The prevalence of Tregs, DCs, TNF-alpha and IL-12 producing macrophages, IL-2 and IFN-gamma producing CD4 (+) cells was similar in both groups. The prevalence of IL-4 producing CD4 (+) cells was lower in obese children than in healthy controls (p=0.028). The ratio of IFN-gamma (+)/ IL-4 (+) CD4 (+) cells was higher in obese children than in those with normal weight (p=0.046).
CONCLUSIONS: CD4 (+) reactions are polarized toward Th1 direction in obesity. The unaltered number of Treg and APCs suggests that these immune regulator cells do not contribute to altered immune status in obese children.
PMID: 17647141 [PubMed - in process]
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Posted: Mon Jul 30th, 2007 21:44 |
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Social networks and obesity
Your Best Friend Can Make You Fat: Researchers
WASHINGTON (Reuters)
By Maggie Fox, Health and Science Editor
The Spread of Obesity in a Large Social Network over 32 Years
Nicholas A. Christakis, M.D., Ph.D., M.P.H., and James H. Fowler, Ph.D.
New England Journal of Medicine July 26, 2007
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Posted: Wed Sep 5th, 2007 03:34 |
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Childhood obesity
Nature tops nurture in childhood obesity: study
Thu Feb 7, 2008 2:57pm EST
LONDON (Reuters) - Diet and lifestyle play a far smaller role than genetic factors in determining whether a child becomes overweight, according to a British study of twins published on Thursday.
Researchers looking at more than 5,000 pairs of twins wrote in the American Journal of Clinical Nutrition that genes account for about three-quarters of the differences in a child's waistline and weight.
"Contrary to the widespread assumption that family environment is the key factor in determining weight gain, we found this was not the case," said Jane Wardle, director of Cancer Research UK's Health Behavior Centre, who led the study.
Previous studies have pointed to environmental factors as the main cause of obesity, a major problem worldwide that increases the risk later in life of type-2 diabetes, cancer and heart problems.
The World Health Organization classifies around 400 million people worldwide as obese, including 200 million children under the age of five.
The British team looked at pairs of identical twins who share all their genes and compared their measurements with those of non-identical twins who share only half their genes.
A statistical analysis found that the differences in the children's body mass index and waist circumference were 77 percent attributable to genes and 23 percent due to the environment in which the children were growing up.
BMI is calculated by dividing weight by the square of height.
"These results do not mean that a child with a high complement of 'susceptibility genes' will inevitably become overweight, but that their genetic endowment gives them a stronger predisposition," the researchers said.
The results suggest that parents whose children are at the greatest genetic risk may need support to make sure they provide a healthy environment, the researchers said.
"This study shows that it is wrong to place all the blame for a child's excessive weight gain on the parents," the researchers said.
(Reporting by Michael Kahn, Editing by Will Dunham and Tim Pearce)
© Reuters 2007.
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Bacteria Mix in Guts of Babies Predicts Obesity
By Kathleen Doheny
HealthDay ReporterFri Mar 7, 11:47 PM ET
FRIDAY, March 7 (HealthDay News) -- The mix of bacteria in a baby's gut may predict whether that infant will become overweight or obese later in life, a new study suggests.
Babies with high numbers of bifidobacteria and low numbers of Staphylococcus aureus may be protected from excess weight gain, according to a team of researchers from the University of Turku in Finland.
Their study was published in the March issue of The American Journal of Clinical Nutrition.
The researchers suggested their findings may help explain why breast-fed babies are at lower risk for later obesity, since bifidobacteria are prevalent in the guts of breast-fed babies.
Other studies repeatedly have found that being breast-fed is associated with a reduced risk of excess weight or obesity in childhood, with the risk lowered from 13 percent to 22 percent.
In the new study, researchers evaluated children who had been part of a long-term study to evaluate the effect of probiotics on allergic disease. Probiotics are potentially beneficial bacteria found in foods such as yogurt and in dietary supplements.
The children had been evaluated at birth, five more times before age 2, and then again at ages 4 and 7. The researchers in the original study had also tested for intestinal microbes in fecal samples collected at 6 months and 12 months.
For this latest study, the Finnish researchers selected 49 participants from the larger study -- 25 of them were overweight or obese at age 7 years, and 24 were normal weight at the same age.
When they looked at the fecal samples, the average bacterial counts of bifidobacteria when taken at 6 months and 12 months were twice as high in those who were a healthy weight as in those who got heavy.
Those who stayed at a healthy weight also had lower fecal S. aureus levels at 6 months and 12 months than did those who got heavy.
The S. aureus may trigger low-grade inflammation, the authors speculated, and that may also contribute to developing obesity.
In other research, gut bacteria in adults have been found to be altered in obese adults who lost weight. Someday, the Finnish researchers speculated, tinkering with gut flora may help prevent or treat obesity.
The latest study doesn't pinpoint exactly why intestinal bacteria are linked with the development of obesity, said Connie Diekman, director of university nutrition at Washington University in St. Louis and president of the American Dietetic Association.
"The exact role that bacteria in the intestine play in development of obesity is still the subject of much research," she said, "but the benefits of breast-feeding are clear. Breast-feeding provides not only the proper nutrition for your infant, but it provides benefits that may impact long-term health and weight issues as well."
However, she added that, "while breast-feeding may play a role in the weight of children, so many other factors influence weight that parents shouldn't ignore good role modeling of healthy food choices, proper portions and regular physical activity. Healthy weight is a combination of factors, and no single issue will be the cause of weight gain or the magic answer to weight loss."
Another expert who has studied how obesity changes microbes in the gut calls the new study unique, because it collected information over several years and could look for differences in gut microflora. "The finding, that the lean children harbored higher levels of bifidobacteria at younger ages, is very intriguing," says Ruth Ley, a research assistant professor at Washington University School of Medicine in St. Louis.
Still, she says, research on the role of gut bacteria in regulating body weight is in the very early stages.
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Vitamin D Status and Response to Vitamin D(3) in Obese vs. Non-obese African American Children
Iron is required for growth of bacteria
Obese U.S. Younsters Suffer Iron deficiency: Study
Blood pressure rising among U.S. children....an alarming trend linked to obesity rates.
Last edited on Wed Mar 19th, 2008 08:11 by Foundation Staff
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Posted: Sun Sep 23rd, 2007 17:22 |
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There is no study proving a causal link between lifestyle and obesity.
Pathways: a school-based, randomized controlled trial for the prevention of obesity in American Indian schoolchildren.
Caballero B, Clay T, Davis SM, Ethelbah B, Rock BH, Lohman T, Norman J, Story M, Stone EJ, Stephenson L, Stevens J; Pathways Study Research Group.Am J Clin Nutr. 2003 Nov;78(5):904-5.
In 2004, researchers published the results of lifestyle modification of 1704 children from American Indian Communities in the Southwest USA. For three years, schoolchildren participated in a massive randomized intervention program, designed to examine the effects of a change in dietary intake, an increase in physical activity, classroom curriculum focused on healthy eating and lifestyle, and a family involvement program.
In the end, there was no difference in the adipose composition of the two groups, there was no causal link found between lifestyle and obesity. "The primary aim of the study was to reduce the rate of body fat gain in intervention schools, documented by a significant difference in the rate for the control schools after 3 years. This goal was not reached, and %BodyFat in both groups was essentially identical at the end of the intervention period"
There is no study proving a causal link between lifestyle and obesity. We are told "you are what you eat" but that is not true, because it ignores that the appetite might well be controlled by another factor, eg, Th1 disease.
..Trevor..
This study in toddlers came to the same conclusion as the Pathways study: Physical activity to prevent obesity in young children: cluster randomized controlled trial
Reilly JJ, Kelly L, Montgomery C, Williamson A, Fisher A, McColl JH, Lo Conte R, Paton JY, Grant S. BMJ. 2006 Nov 18;333(7577):1041.
Over-riding all the studies is mankind's total failure to reverse the epidemic of childhood obesity. We can quote as many studies as we like, but until the trend is reversed, there can be no definite statements made about causation, one way or the other.
I am 'calling' the causation early, taking a scientific risk, because I understand what the role of the Th1 bacteria is in obesity, I understand exactly the prevalence of sub-clinical Th1 disease in the community (about 25% in new York residents), and because I have had the opportunity to discuss the latest molecular data from Jeff Gordon's lab with his staff.
..Trevor..
Last edited on Tue Sep 25th, 2007 21:03 by Foundation Staff
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Posted: Thu Nov 1st, 2007 09:59 |
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October 9, 2007
New York Times
Diet and Fat: A Severe Case of Mistaken Consensus
In 1988, the surgeon general, C. Everett Koop, proclaimed ice cream to a be public-health menace right up there with cigarettes. Alluding to his office’s famous 1964 report on the perils of smoking, Dr. Koop announced that the American diet was a problem of “comparable” magnitude, chiefly because of the high-fat foods that were causing coronary heart disease and other deadly ailments.
He introduced his report with these words: “The depth of the science base underlying its findings is even more impressive than that for tobacco and health in 1964.”
That was a ludicrous statement, as Gary Taubes demonstrates in his new book meticulously debunking diet myths, “Good Calories, Bad Calories” (Knopf, 2007). The notion that fatty foods shorten your life began as a hypothesis based on dubious assumptions and data; when scientists tried to confirm it they failed repeatedly. The evidence against Häagen-Dazs was nothing like the evidence against Marlboros.
It may seem bizarre that a surgeon general could go so wrong. After all, wasn’t it his job to express the scientific consensus? But that was the problem. Dr. Koop was expressing the consensus. He, like the architects of the federal “food pyramid” telling Americans what to eat, went wrong by listening to everyone else. He was caught in what social scientists call a cascade.
We like to think that people improve their judgment by putting their minds together, and sometimes they do. The studio audience at “Who Wants to Be a Millionaire” usually votes for the right answer. But suppose, instead of the audience members voting silently in unison, they voted out loud one after another. And suppose the first person gets it wrong.
If the second person isn’t sure of the answer, he’s liable to go along with the first person’s guess. By then, even if the third person suspects another answer is right, she’s more liable to go along just because she assumes the first two together know more than she does. Thus begins an “informational cascade” as one person after another assumes that the rest can’t all be wrong.
Because of this effect, groups are surprisingly prone to reach mistaken conclusions even when most of the people started out knowing better, according to the economists Sushil Bikhchandani, David Hirshleifer and Ivo Welch. If, say, 60 percent of a group’s members have been given information pointing them to the right answer (while the rest have information pointing to the wrong answer), there is still about a one-in-three chance that the group will cascade to a mistaken consensus.
Cascades are especially common in medicine as doctors take their cues from others, leading them to overdiagnose some faddish ailments (called bandwagon diseases) and overprescribe certain treatments (like the tonsillectomies once popular for children). Unable to keep up with the volume of research, doctors look for guidance from an expert — or at least someone who sounds confident.
In the case of fatty foods, that confident voice belonged to Ancel Keys, a prominent diet researcher a half-century ago (the K-rations in World War II were said to be named after him). He became convinced in the 1950s that Americans were suffering from a new epidemic of heart disease because they were eating more fat than their ancestors.
There were two glaring problems with this theory, as Mr. Taubes, a correspondent for Science magazine, explains in his book. First, it wasn’t clear that traditional diets were especially lean. Nineteenth-century Americans consumed huge amounts of meat; the percentage of fat in the diet of ancient hunter-gatherers, according to the best estimate today, was as high or higher than the ratio in the modern Western diet.
Second, there wasn’t really a new epidemic of heart disease. Yes, more cases were being reported, but not because people were in worse health. It was mainly because they were living longer and were more likely to see a doctor who diagnosed the symptoms.
To bolster his theory, Dr. Keys in 1953 compared diets and heart disease rates in the United States, Japan and four other countries. Sure enough, more fat correlated with more disease (America topped the list). But critics at the time noted that if Dr. Keys had analyzed all 22 countries for which data were available, he would not have found a correlation. (And, as Mr. Taubes notes, no one would have puzzled over the so-called French Paradox of foie-gras connoisseurs with healthy hearts.)
The evidence that dietary fat correlates with heart disease “does not stand up to critical examination,” the American Heart Association concluded in 1957. But three years later the association changed position — not because of new data, Mr. Taubes writes, but because Dr. Keys and an ally were on the committee issuing the new report. It asserted that “the best scientific evidence of the time” warranted a lower-fat diet for people at high risk of heart disease.
The association’s report was big news and put Dr. Keys, who died in 2004, on the cover of Time magazine. The magazine devoted four pages to the topic — and just one paragraph noting that Dr. Keys’s diet advice was “still questioned by some researchers.” That set the tone for decades of news media coverage. Journalists and their audiences were looking for clear guidance, not scientific ambiguity.
After the fat-is-bad theory became popular wisdom, the cascade accelerated in the 1970s when a committee led by Senator George McGovern issued a report advising Americans to lower their risk of heart disease by eating less fat. “McGovern’s staff were virtually unaware of the existence of any scientific controversy,” Mr. Taubes writes, and the committee’s report was written by a nonscientist “relying almost exclusively on a single Harvard nutritionist, Mark Hegsted.”
That report impressed another nonscientist, Carol Tucker Foreman, an assistant agriculture secretary, who hired Dr. Hegsted to draw up a set of national dietary guidelines. The Department of Agriculture’s advice against eating too much fat was issued in 1980 and would later be incorporated in its “food pyramid.”
Meanwhile, there still wasn’t good evidence to warrant recommending a low-fat diet for all Americans, as the National Academy of Sciences noted in a report shortly after the U.S.D.A. guidelines were issued. But the report’s authors were promptly excoriated on Capitol Hill and in the news media for denying a danger that had already been proclaimed by the American Heart Association, the McGovern committee and the U.S.D.A.
The scientists, despite their impressive credentials, were accused of bias because some of them had done research financed by the food industry. And so the informational cascade morphed into what the economist Timur Kuran calls a reputational cascade, in which it becomes a career risk for dissidents to question the popular wisdom.
With skeptical scientists ostracized, the public debate and research agenda became dominated by the fat-is-bad school. Later the National Institutes of Health would hold a “consensus conference” that concluded there was “no doubt” that low-fat diets “will afford significant protection against coronary heart disease” for every American over the age of 2. The American Cancer Society and the surgeon general recommended a low-fat diet to prevent cancer.
But when the theories were tested in clinical trials, the evidence kept turning up negative. As Mr. Taubes notes, the most rigorous meta-analysis of the clinical trials of low-fat diets, published in 2001 by the Cochrane Collaboration, concluded that they had no significant effect on mortality.
Mr. Taubes argues that the low-fat recommendations, besides being unjustified, may well have harmed Americans by encouraging them to switch to carbohydrates, which he believes cause obesity and disease. He acknowledges that that hypothesis is unproved, and that the low-carb diet fad could turn out to be another mistaken cascade. The problem, he says, is that the low-carb hypothesis hasn’t been seriously studied because it couldn’t be reconciled with the low-fat dogma.
Mr. Taubes told me he especially admired the iconoclasm of Dr. Edward H. Ahrens Jr., a lipids researcher who spoke out against the McGovern committee’s report. Mr. McGovern subsequently asked him at a hearing to reconcile his skepticism with a survey showing that the low-fat recommendations were endorsed by 92 percent of “the world’s leading doctors.”
“Senator McGovern, I recognize the disadvantage of being in the minority,” Dr. Ahrens replied. Then he pointed out that most of the doctors in the survey were relying on secondhand knowledge because they didn’t work in this field themselves.
“This is a matter,” he continued, “of such enormous social, economic and medical importance that it must be evaluated with our eyes completely open. Thus I would hate to see this issue settled by anything that smacks of a Gallup poll.” Or a cascade.
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Posted: Wed Apr 9th, 2008 02:05 |
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Study Ties Belly Fat to Dementia
By SHIRLEY S. WANG March 27, 2008; Page D6 The Wall Street Journal
People who have more belly fat during middle age, even those considered to be of normal weight, have higher rates of dementia when they reach old age, according to a study in the journal Neurology. The link highlights a body of work showing that health is affected by not just overall body weight but how the weight is distributed.
Too much abdominal fat, which extends into the body cavity around major organs, is known to be a risk factor for cardiovascular disease and diabetes. These new findings, published Wednesday, show that large amounts of belly fat are associated with declining cognitive function as well. "There is something very potent about collecting fat in your belly," said Rachel Whitmer, lead study author and a scientist at the research division of Kaiser Permanente in Oakland, Calif.
It is possible the link between belly fat and dementia is better explained by some other factor, such as poor diet, that wasn't measured in this study, said P. Murali Doraiswamy, an Alzheimer's researcher and chief of biological psychiatry at Duke University who wasn't involved with the study. Using medical records, researchers examined the belly size of 6,583 middle-age people between 1964 and 1973 and then looked to see whether those same individuals were diagnosed with dementia an average of 36 years later.
They found that just being overweight or obese nearly doubles one's risk of dementia in old age, even after taking into account other risk factors such as diabetes and heart disease. But having high levels of central-body fat increases the risk more, boosting an obese person's risk 3.6 times higher than a normal-weight individual with low belly fat. And, as a group, normal-weight individuals with high levels of belly fat showed an elevated risk of dementia.
"It's really a red flag for all of us boomers," said Duke's Dr. Doraiswamy. "Waist size may not be reflective of just your heart health, but your brain function decades later." However, Dr. Doraiswamy said there was more variability in the normal-weight group compared with heavier subjects, suggesting that some normal-weight people may be more vulnerable to dementia than others, perhaps due to a genetic predisposition.
This study didn't look at genetic risk, he said. Why belly fat appears to wreak such havoc on the body isn't completely understood. Fat is known to produce a variety of potentially harmful substances that cause inflammation, disrupting blood flow to the heart and possibly the brain, which could be one reason for its link to dementia, said Jean-Pierre Despres, director of research at the Quebec Heart Institute at Laval University in Quebec City, who wasn't involved in the study.
More research is needed to figure out the exact mechanisms of action, he and other experts said. The study wasn't able to examine whether people who lost weight during the 30-year time period decreased their risk of developing dementia, but it is an area of research interest, said study author Dr. Whitmer. Much of where an individual accumulates fat is genetically determined, but abdominal fat is easier to lose than fat stored elsewhere. "This is not a stubborn fat," Dr. Whitmer said. "It is a toxic fat."
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Posted: Sun Oct 19th, 2008 05:50 |
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[filelink]
New twist in brain obesity riddle
The discovery of another way in which the body appears to control how much it eats could shed fresh light on obesity.
US researchers said poor diets may trigger a signalling system which prompts the body to consume even more.
When the signals - involving a protein linked to inflammation - were blocked in mice, they maintained normal weight.
A UK expert warned that the finding, in the journal Cell, may not lead to an effective anti-obesity drug because it could interfere with the immune system.
The complexity of the controls governing the human metabolism, appetite and the laying down of fat has become clear over recent years.
Despite some promising experiments in animals, none has yet produced a breakthrough in the battle against obesity.
The latest "pathway" under investigation, by scientists at the University of Wisconsin-Madison, is normally associated with the immune system, and inflammation, one of the body's defence systems.
Mouse diet
The link to obesity was made when scientists investigated "metabolic inflammation", a chronic, low-level condition often seen in obesity-related diseases.
In mice, a protein connected to inflammatory reactions appeared to be switched on when the animals were given a high fat, high sugar diet.
Not only this, but once the protein was switched on, the mice started eating more, suggesting that it was part of a pathway involving the regulation of food intake.
Closer examination of the a part of the brain called the hypothalamus, which is known to be involved in energy regulation, revealed the protein present there too.
In mice genetically altered to block the pathway, even with a high fat diet available, they were able to maintain a healthy weight.
Dr Dongsheng Cai, who led the research, said that that the pathway could possibly be used in anti-obesity drugs.
He said: "The ultimate goal will certainly be to identify a selective and effective suppressor of the pathway to target related neurons."
However, Professor Fran Ebling, from the University of Nottingham, said that other potential targets might prove more fruitful.
He said: "It's certainly interesting, but if we have some drugs that target this pathway, they may well interfere with some other part of the immune system."
Story from BBC NEWS:
http://news.bbc.co.uk/go/pr/fr/-/2/hi/health/7649261.stm
Published: 2008/10/03 00:19:17 GMT
© BBC MMVIII
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