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The big fat truth : Nature News & Comment
The big fat truth

More and more studies show that being overweight does not always shorten life — but some public-health researchers would rather not talk about them.
fat  health  obesity  mortality  data 
15 days ago by Quercki
The obesity paradox: Scientists now think that being overweight can protect your health — Quartz
Flegal found the lowest mortality rates among people in the overweight to mildly obese categories. It’s true that these groups are slightly more likely to suffer from heart disease and some other life-threatening conditions in the first place. But many factors influence the likelihood of a person getting heart disease. And a strong link between weight and disease only emerges among people with severe obesity. So taken at face value, the results seemed to be showing that a little extra weight is genuinely beneficial.

Flegal is a meticulous researcher: her most recent analysis incorporated data from almost 100 studies and close to three million people. It was published by the prestigious Journal of the American Medical Association. Yet Flegal’s work has made her a target for those who scoff at the paradox. Walter Willett, a researcher at the Harvard School of Public Health who has taken a high-profile stance against obesity, told NPR that one recent Flegal study was “really a pile of rubbish” and that “no one should waste their time reading it.” (He was later admonished by the editors at Nature. In recent comments to Quartz, he reiterated his view that the study was “rubbish.”)
Being overweight is now believed to help protect patients with an increasingly long list of medical problems.

Willett’s complaints are starting to look less credible, however, because no one has been able to make the paradox go away.
fat  health  obesity  mortality  data 
15 days ago by Quercki
Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms

Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.
Keywords: cravings, evolutionary conflict, host manipulation, microbiome, microbiota, obesity
diet  health  mood  obesity  microbes  gut  brain 
7 weeks ago by Quercki
Weight Science: Evaluating the Evidence for a Paradigm Shift | Nutrition Journal | Full Text
Assumption: The only way for overweight and obese people to improve health is to lose weight
Evidence: That weight loss will improve health over the long-term for obese people is, in fact, an untested hypothesis. One reason the hypothesis is untested is because no methods have proven to reduce weight long-term for a significant number of people. Also, while normal weight people have lower disease incidence than obese individuals, it is unknown if weight loss in individuals already obese reduces disease risk to the same level as that observed in those who were never obese [91, 93].

As indicated by research conducted by one of the authors and many other investigators, most health indicators can be improved through changing health behaviors, regardless of whether weight is lost [11]. For example, lifestyle changes can reduce blood pressure, largely or completely independent of changes in body weight [11, 141, 142, 143]. The same can be said for blood lipids [11, 143, 144, 145]. Improvements in insulin sensitivity and blood lipids as a result of aerobic exercise training have been documented even in individuals who gained body fat during the intervention [145, 146].
fat  obesity  data  facts  lies  truth 
june 2017 by Quercki
“Mindless Eating,” or how to send an entire life of research into question | Ars Technica
Wansink is probably regretting he ever started typing. Tim van der Zee, one of the scientists participating in the ongoing examination into Wansink’s past, keeps a running account of what’s turned up so far. “To the best of my knowledge,” van der Zee writes in a blog post most recently updated on April 6, “there are currently 42 publications from Wansink which are alleged to contain minor to very serious issues, which have been cited over 3,700 times, are published in over 25 different journals, and in eight books, spanning over 20 years of research.”

That’s enough to cause an entire field to rethink what it thought it knew.

If you hide your junk food, you’ve probably heard of Wansink

You’ve probably come across Wansink’s ideas at some point. He researches how subtle changes in the environment can affect people’s eating behavior, and his findings have made a mark on popular diet wisdom. Perhaps you’ve adopted the tip to use smaller plates to trick yourself into eating less, moved your unhealthy snacks into a hard-to-reach place, or placed your fruit bowl prominently on your kitchen counter. Maybe you’ve scoffed at the “health halo” marketing of a decidedly unhealthy food, or chosen 100-calorie snack packs to control your intake.
research  obesity  statistics  lies 
june 2017 by Quercki
Evaluating the Cause of Death in Obese Individuals: A Ten-Year Medical Autopsy Study
Background. Obesity is a growing public health problem associated with increased morbidity and rate of death. Postmortem examination is imperative to determine the cause of death, to detect clinically unsuspected disease entities, and consequently to determine the actual impact of obesity on patient mortality. Methods. A total of 849 adult autopsies were retrospectively reviewed. Obese (BMI ≥ 30 kg/m2) and nonobese patients were separately studied. The primary cause of death in each group was categorized into malignancy, infection, stroke, ischemic and nonischemic heart disease, pulmonary embolism, hemorrhage, and primary nonneoplastic diseases of different organ systems. Results. Of 849 autopsies, 32.3% were obese. The leading causes of death in the obese population were malignancy (31.4%), infection (25.9%), ischemic heart disease (12.8%), and pulmonary embolism (6.2%). Obese individuals were statistically more likely to die from pulmonary embolism and liver disease and less likely to die from neurologic diseases and nonischemic heart disease. Conclusion. Autopsies on obese individuals constitute a third of all adult medical autopsies in our center. Increased death rates in the obese due to pulmonary embolism and liver disease should receive special clinical attention. Autopsy findings in the obese population should contribute to overall premortem disease detection, prevention, and management.
death  autopsy  obesity  correlation  cause  prevention  disease 
june 2016 by Quercki
JAMA Network | JAMA | Increasing Adiposity:  Consequence or Cause of Overeating?
Ninety years ago, an editorial in JAMA questioned the prevailing approach to obesity treatment: “When we read that ‘the fat woman has the remedy in her own hands—or rather between her own teeth’ . . . there is an implication that obesity is usually merely the result of unsatisfactory dietary bookkeeping. . . [Although logic suggests that body fat] may be decreased by altering the balance sheet through diminished intake, or increased output, or both . . . [t]he problem is not really so simple and uncomplicated as it is pictured.”1 Since then, billions of dollars have been spent on research into the biological factors affecting body weight, but the near-universal remedy remains virtually the same, to eat less and move more. According to an alternative view, chronic overeating represents a manifestation rather than the primary cause of increasing adiposity. Attempts to lower body weight without addressing the biological drivers of weight gain, including the quality of the diet, will inevitably fail for most individuals. This Viewpoint summarizes the evidence for this seemingly counterintuitive hypothesis, versions of which have been debated for more than a century.2
obesity  nutrition  weight 
june 2014 by Quercki
PLOS ONE: Perceived Weight Discrimination and Obesity
Weight discrimination is prevalent in American society. Although associated consistently with psychological and economic outcomes, less is known about whether weight discrimination is associated with longitudinal changes in obesity. The objectives of this research are (1) to test whether weight discrimination is associated with risk of becoming obese (Body Mass Index≥30; BMI) by follow-up among those not obese at baseline, and (2) to test whether weight discrimination is associated with risk of remaining obese at follow-up among those already obese at baseline. Participants were drawn from the Health and Retirement Study, a nationally representative longitudinal survey of community-dwelling US residents. A total of 6,157 participants (58.6% female) completed the discrimination measure and had weight and height available from the 2006 and 2010 assessments. Participants who experienced weight discrimination were approximately 2.5 times more likely to become obese by follow-up (OR = 2.54, 95% CI = 1.58–4.08) and participants who were obese at baseline were three times more likely to remain obese at follow up (OR = 3.20, 95% CI = 2.06–4.97) than those who had not experienced such discrimination. These effects held when controlling for demographic factors (age, sex, ethnicity, education) and when baseline BMI was included as a covariate. These effects were also specific to weight discrimination; other forms of discrimination (e.g., sex, race) were unrelated to risk of obesity at follow-up. The present research demonstrates that, in addition to poorer mental health outcomes, weight discrimination has implications for obesity. Rather than motivating individuals to lose weight, weight discrimination increases risk for obesity.

Citation: Sutin AR, Terracciano A (2013) Perceived Weight Discrimination and Obesity. PLoS ONE 8(7): e70048. doi:10.1371/journal.pone.0070048
obesity  research  fat  discrimination 
october 2013 by Quercki
A gut infection can keep mice lean | Nutrition | Science News
Skinniness could be contagious. Gut bacteria from thin people can invade the intestines of mice carrying microbes from obese people. And these invaders can keep mice from getting tubby, researchers report in the Sept. 6 Science.

“It’s very surprising,” says molecular microbiologist Andreas Schwiertz of the University of Giessen in Germany, who was not involved in the work. “It’s like a beneficial infection.”

But the benefits come with a catch. The invading microbes drop in and get to work only when mice eat healthy food. Even fat-blocking bacteria can’t fight a bad diet, suggests study leader Jeffrey Gordon, a microbiologist at Washington University in St. Louis.

In recent years, researchers have collected clues that suggest that gut microbes can tweak people’s metabolism. Fat and thin people have different microbes teeming in their intestines, for example. And normal-weight mice given microbes from obese mice pack on extra fat, says coauthor Vanessa Ridaura, also of Washington University.

These and other hints have led researchers to experiment with fecal transplants to flush out bad gut microbes and dump in good ones. The transplants can clear up diarrhea and may even help some obese people regain insulin sensitivity. But feces can house dangerous microbes as well as friendly ones.
diet  obesity  microbes  research 
september 2013 by Quercki
Long-term weight-loss maintenance: a meta-ana... [Am J Clin Nutr. 2001] - PubMed - NCBI
Am J Clin Nutr. 2001 Nov;74(5):579-84.
Long-term weight-loss maintenance: a meta-analysis of US studies.
Anderson JW, Konz EC, Frederich RC, Wood CL.
VA Medical Center, Graduate Center for Nutritional Sciences, University of Kentucky Health Management Resources Weight Management Program, Lexington, KY, USA.
Current perception is that participants of a structured weight-loss program regain all of their weight loss within 5 y.
The objective was to examine the long-term weight-loss maintenance of individuals completing a structured weight-loss program.
Studies were required to 1) have been conducted in the United States, 2) have included participants in a structured weight-loss program, 3) have provided follow-up data with variance estimates for > or =2 y. Primary outcome variables were weight-loss maintenance in kilograms, weight-loss maintenance as a percentage of initial weight loss, and weight loss as a percentage of initial body weight (reduced weight).
Twenty-nine studies met the inclusion criteria. Successful very-low-energy diets (VLEDs) were associated with significantly greater weight-loss maintenance than were successful hypoenergetic balanced diets (HBDs) at all years of follow-up. The percentage of individuals at 4 or 5 y of follow-up for VLEDs and HBDs were 55.4% and 79.7%, respectively. The results for VLEDs and HBDs, respectively, were as follows: weight-loss maintenance, 7.1 kg (95% CI: 6.1, 8.1 kg) and 2.0 (1.5, 2.5) kg; percentage weight-loss maintenance, 29% (25%, 33%) and 17% (13%, 22%); and reduced weight, 6.6% (5.7%, 7.5%) and 2.1% (1.6%, 2.7%). Weight-loss maintenance did not differ significantly between women and men. Six studies reported that groups who exercised more had significantly greater weight-loss maintenance than did those who exercised less.
Five years after completing structured weight-loss programs, the average individual maintained a weight loss of >3 kg and a reduced weight of >3% of initial body weight. After VLEDs or weight loss of > or =20 kg, individuals maintained significantly more weight loss than after HBDs or weight losses of <10 kg.
diet  weight  fat  obesity  **** 
june 2013 by Quercki
Long-term weight loss maintenance. [Am J Clin Nutr. 2005] - PubMed - NCBI
Am J Clin Nutr. 2005 Jul;82(1 Suppl):222S-225S.
Long-term weight loss maintenance.
Wing RR, Phelan S.
Brown Medical School, The Miriam Hospital, Department of Psychiatry, Providence, RI, USA.
There is a general perception that almost no one succeeds in long-term maintenance of weight loss. However, research has shown that approximately 20% of overweight individuals are successful at long-term weight loss when defined as losing at least 10% of initial body weight and maintaining the loss for at least 1 y. The National Weight Control Registry provides information about the strategies used by successful weight loss maintainers to achieve and maintain long-term weight loss. National Weight Control Registry members have lost an average of 33 kg and maintained the loss for more than 5 y. To maintain their weight loss, members report engaging in high levels of physical activity ( approximately 1 h/d), eating a low-calorie, low-fat diet, eating breakfast regularly, self-monitoring weight, and maintaining a consistent eating pattern across weekdays and weekends. Moreover, weight loss maintenance may get easier over time; after individuals have successfully maintained their weight loss for 2-5 y, the chance of longer-term success greatly increases. Continued adherence to diet and exercise strategies, low levels of depression and disinhibition, and medical triggers for weight loss are also associated with long-term success. National Weight Control Registry members provide evidence that long-term weight loss maintenance is possible and help identify the specific approaches associated with long-term success.
PMID: 16002825 [PubMed - indexed for MEDLINE] Free full text
fat  weight  diet  obesity  **** 
june 2013 by Quercki
JAMA Network | JAMA | Association of All-Cause Mortality With Overweight and Obesity Using Standard Body Mass Index CategoriesA Systematic Review and Meta-analysisAll-Cause Mortality Using BMI Categories
Results  Random-effects summary all-cause mortality HRs for overweight (BMI of 25-<30), obesity (BMI of ≥30), grade 1 obesity (BMI of 30-<35), and grades 2 and 3 obesity (BMI of ≥35) were calculated relative to normal weight (BMI of 18.5-<25). The summary HRs were 0.94 (95% CI, 0.91-0.96) for overweight, 1.18 (95% CI, 1.12-1.25) for obesity (all grades combined), 0.95 (95% CI, 0.88-1.01) for grade 1 obesity, and 1.29 (95% CI, 1.18-1.41) for grades 2 and 3 obesity. These findings persisted when limited to studies with measured weight and height that were considered to be adequately adjusted. The HRs tended to be higher when weight and height were self-reported rather than measured.

Conclusions and Relevance  Relative to normal weight, both obesity (all grades) and grades 2 and 3 obesity were associated with significantly higher all-cause mortality. Grade 1 obesity overall was not associated with higher mortality, and overweight was associated with significantly lower all-cause mortality.
weigth  obesity  death  mortality  health  diet 
january 2013 by Quercki
Weight loss does not lower heart disease risk from type 2 diabetes, October 19, 2012 News Release - National Institutes of Health (NIH)
Although the intervention did not reduce cardiovascular events, Look AHEAD has shown other important health benefits of the lifestyle intervention, including decreasing sleep apnea, reducing the need for diabetes medications, helping to maintain physical mobility, and improving quality of life. Previous Look AHEAD findings are available at

"Look AHEAD found that people who are obese and have type 2 diabetes can lose weight and maintain their weight loss with a lifestyle intervention," said Dr. Rena Wing, chair of the Look AHEAD study and professor of psychiatry and human behavior at Brown University. "Although the study found weight loss had many positive health benefits for people with type 2 diabetes, the weight loss did not reduce the number of cardiovascular events."

Data are currently being analyzed to fully understand the cardiovascular disease results. Investigators are preparing a report of the findings for a peer-reviewed publication.
diabetes  cardiovascular  heart  obesity  research  Look_AHEAD 
october 2012 by Quercki
NIH stops treatment arm in the Look AHEAD Trial: Interpretation and Implications
At the 4-year follow-up, lifestyle intervention participants had an average weight loss of 6.2% of their start weight (vs. 0.9% among the diabetes support and education group). They also had greater improvements in diabetes control (and reduced diabetes medications), blood pressure, HDL cholesterol, triglycerides, and fitness and functional mobility. Reports from their earlier follow-ups found greater improvements in quality of life and in sleep apnea. Such benefits are very important for a healthier, more fulfilling life.

Therefore, a distinction should be made about the Look AHEAD study. The study has found that among individuals who are already diabetic, a lifestyle intervention producing moderate weight loss does provide significant health benefits; however, the intervention did not reduce the occurrence of heart attacks or strokes below what was seen in the study's diabetes education and support group. Since the study's primary question had been answered, it was decided to stop the intervention and inform the study participants of the results. It should also be noted that a not dissimilar trial performed among prediabetic patients (Diabetes Prevention Program demonstrated that weight loss and lifestyle modification reduced the incidence of diabetes during the 10 year follow-up period thus affirming that life style intervention provides a host of other health benefits.
diabetes  obesity  research 
october 2012 by Quercki
Adenovirus serotype 36 - Wikipedia, the free encyclopedia
Human adenovirus 36 (HAdV-36) or Ad-36 or Adv36 is one of 52 types of adenoviruses known to infect humans. AD-36 was first isolated in 1978 from the feces of a girl suffering from diabetes and enteritis,[1] and has long been recognized as a cause of respiratory and eye infections in humans.[2] It was first shown to be associated with obesity in chickens by Dr. Nikhil Dhurandhar.[3][4]
There has been a positive correlation between body fat and the presence of AD-36 antibodies in the blood.[5] Previous research showed that chicken or mice injected with similar types of viruses show a statistically significant weight gain.[3]
To date, AD-36 is the only human adenovirus that has been linked with human obesity, present in 30% of obese humans and 11% of nonobese humans.[6] In addition, a study of obese Americans indicates that about 30% of the obese individuals and only 5% of non-obese individuals have antibodies to Ad-36.[3] Another study determined that children with the virus averaged 52 pounds heavier than those with no signs of it and obese children with the virus averaged 35 pounds heavier than obese children with no trace of the virus.[7] AD-36 also causes obesity in chickens, mice, rats, and monkeys.[6]
AD-36 infection can induce cellular differentiation of 3T3-L1 preadipocytes and stem cells derived from human adipose tissue.[8]
Contents  [hide] 
1 Public awareness
2 See also
3 References
4 External links
[edit]Public awareness

On March 18, 2006 the research of Richard Atkinson (University of Wisconsin) was posted on some websites. In those studies, blood tests conducted on over 2000 Australians showed that more than 20% of the study participants had contracted Ad-36 viral infection.
On January 26, 2009, many popular internet news portals ran reports of the pending release of scientific research by Professor Nikhil Dhurandhar (Pennington Biomedical Research Centre, Louisiana) implicating AD-36 as a potential cause for Britain's relatively high rate of adult obesity.[9]
fat  virus  cold  flu  obesity 
august 2012 by Quercki
Weight Science: Evaluating the Evidence for a Paradigm Shift
Current guidelines recommend that "overweight" and "obese" individuals lose weight through engaging in lifestyle modification involving diet, exercise and other behavior change. This approach reliably induces short term weight loss, but the majority of individuals are unable to maintain weight loss over the long term and do not achieve the putative benefits of improved morbidity and mortality. Concern has arisen that this weight focus is not only ineffective at producing thinner, healthier bodies, but may also have unintended consequences, contributing to food and body preoccupation, repeated cycles of weight loss and regain, distraction from other personal health goals and wider health determinants, reduced self-esteem, eating disorders, other health decrement, and weight stigmatization and discrimination. This concern has drawn increased attention to the ethical implications of recommending treatment that may be ineffective or damaging. A growing trans-disciplinary movement called Health at Every Size (HAES) challenges the value of promoting weight loss and dieting behavior and argues for a shift in focus to weight-neutral outcomes. Randomized controlled clinical trials indicate that a HAES approach is associated with statistically and clinically relevant improvements in physiological measures (e.g., blood pressure, blood lipids), health behaviors (e.g., eating and activity habits, dietary quality), and psychosocial outcomes (such as self-esteem and body image), and that HAES achieves these health outcomes more successfully than weight loss treatment and without the contraindications associated with a weight focus. This paper evaluates the evidence and rationale that justifies shifting the health care paradigm from a conventional weight focus to HAES.
diet  HAES  fat  research  PubMed  obesity  hypertension  diabetes 
july 2012 by Quercki
Overeating and Obesity: Should we really call it food addiction? | Neurotic Physiology
First off, it's important to separate food addiction from obesity. Binge eating does not necessarily mean you are overweight, and being overweight does not necessarily mean that you binge eat. Ranking by BMI is not going to work.

Secondly, it's important to differentiate food addiction from substance abuse criteria, as so many of the clinical criteria for substance abuse don't really translate to food addiction. The authors call for a set of measurable behaviors which can be clearly defined, and which demonstrate a change from normal food intake to compulsive eating. I would make the criteria here similar to those of binge eating disorder (or even merge the two).

Finally, things will have to change in how we study "food addiction" in humans. Getting a bunch of people with BMIs over 40 and popping them in a scanner isn't going to cut it. In order to get a picture of what food addiction really is, we need to use the measures that we could come up with that apply specifically to food addiction, and study only those who meet those measures. Again, just categorizing by BMI does not mean you get the correct subset of people.

All this doesn't mean we should throw the food addiction model out with the bathwater. The animal literature and binge eating in humans show indications that the food addiction model may be a good one. What this perspective suggests instead is that we need to take a more careful approach in adopting the model, to make sure that we are, in fact, modeling the right things. By modeling the right things and coming up with a useful definition of food addiction, we may be able to create a consistent picture of what changes are taking place.
obesity  addiction  research 
march 2012 by Quercki
Obesity among poor children tied to diet | The Times Leader, Wilkes-Barre, Scranton PA - News
Researchers have long blamed childhood obesity and diabetes, especially in poor neighborhoods, on too much food and too little exercise.

But new findings from a San Antonio study point to another explanation: children living in poverty are obese in part because they don’t eat enough to meet the daily nutritional requirements needed for cell function and metabolism.

A 9-year-old should consume 1,400 to 2,200 calories daily to sustain growth, said Dr. Roberto Trevino, director of the nonprofit Social and Health Research Center. But in the study of 1,400 inner-city children, 44 percent were consuming less than 1,400 calories, and 33 percent were obese.

“They were not overeating,” Trevino said. “This study shows these kids were not eating enough, and when they did eat it was all the wrong things.”

Missing from the children’s diets were four key nutrients: calcium, magnesium, potassium and phosphorus. All play important roles, but magnesium is involved in more than 300 enzymatic reactions in the body that help to spur metabolism and cell function.

When magnesium — found in cooked spinach, black beans, bran cereal and other foods — is missing from the diet, it can predispose an individual to diabetes, Trevino said.

Nearly 7 percent of children in the study screened positive for type II diabetes, typically an adult disease, Trevino said.
poverty  children  obesity  diabetes  nutrition 
november 2011 by Quercki
Refusing the default: More research on weight
Mortality rates

The results - not surprisingly, by now - confirm the previous US, German and Canadian population studies. There is no statistically significant correlation between mortality and BMI - a person with a BMI of 19 and a person with a BMI over 40 have virtually identical chances of dying in any year. (Chapter 6)

There does seem to be some difference in causes of death - respiratory conditions are less common causes of death in "obese" people, and endocrine and metabolic conditions are more common - but as the German study pointed out - that just means we have a better idea of what statistically kills fat people. It doesn't make thin people any less dead.
fat  obesity  weight 
october 2011 by Quercki
Impact of diet in shaping gut microbiota revealed by a comparative study in children from Europe and rural Africa
Gut microbial composition depends on different dietary habits just as health depends on microbial metabolism, but the association of microbiota with different diets in human populations has not yet been shown. In this work, we compared the fecal microbiota of European children (EU) and that of children from a rural African village of Burkina Faso (BF), where the diet, high in fiber content, is similar to that of early human settlements at the time of the birth of agriculture. By using high-throughput 16S rDNA sequenc- ing and biochemical analyses, we found significant differences in gut microbiota between the two groups. BF children showed a significant enrichment in Bacteroidetes and depletion in Firmi- cutes (P < 0.001), with a unique abundance of bacteria from the genus Prevotella and Xylanibacter, known to contain a set of bacterial genes for cellulose and xylan hydrolysis, completely lack- ing in the EU children. In addition, we found significantly more short-chain fatty acids (P < 0.001) in BF than in EU children. Also, Enterobacteriaceae (Shigella and Escherichia) were significantly underrepresented in BF than in EU children (P < 0.05). We hypoth- esize that gut microbiota coevolved with the polysaccharide-rich diet of BF individuals, allowing them to maximize energy intake from fibers while also protecting them from inflammations and noninfectious colonic diseases. This study investigates and com- pares human intestinal microbiota from children characterized by a modern western diet and a rural diet, indicating the impor- tance of preserving this treasure of microbial diversity from an- cient rural communities worldwide.

Carlotta De Filippoa, Duccio Cavalieria, Monica Di Paolab, Matteo Ramazzottic, Jean Baptiste Poulletd, Sebastien Massartd, Silvia Collinib, Giuseppe Pieraccinie, and Paolo Lionettib,1
bacteria  science  obesity 
april 2011 by Quercki
Religion and obesity: Study links church and being fat - Chicago Sun-Times
A new study has found that young adults who frequently attend religious activities are 50 percent more likely to become obese by middle age compared with those who don’t take part in any religious events.
Christian  obesity  religion 
march 2011 by Quercki
Too much light at night at night may lead to obesity, study finds
"Although there were no differences in activity levels or daily consumption of food, the mice that lived with light at night were getting fatter than the others," said Laura Fonken, lead author of the study and a doctoral student in neuroscience at Ohio State University.

Proceedings of the National Academy of Sciences.

...Results suggest that mice living with light at night eat at times they normally wouldn't.

In one study, mice exposed to light at night – but that had food availability restricted to normal eating times – gained no more weight than did mice in a normal light-dark cycle.

"Something about light at night was making the mice in our study want to eat at the wrong times to properly metabolize their food," said Randy Nelson, co-author of the study and professor of neuroscience and psychology at Ohio State.

If these results are confirmed in humans, it would suggest that late-night eating might be a particular risk factor for obesity, Nelson said.
obesity  mice  lighting 
october 2010 by Quercki
Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity -- Bray et al. 79 (4): 537 -- American Journal of Clinical Nutrition
The increased use of HFCS in the United States mirrors the rapid increase in obesity. The digestion, absorption, and metabolism of fructose differ from those of glucose. Hepatic metabolism of fructose favors de novo lipogenesis. In addition, unlike glucose, fructose does not stimulate insulin secretion or enhance leptin production. Because insulin and leptin act as key afferent signals in the regulation of food intake and body weight, this suggests that dietary fructose may contribute to increased energy intake and weight gain. Furthermore, calorically sweetened beverages may enhance caloric overconsumption. Thus, the increase in consumption of HFCS has a temporal relation to the epidemic of obesity, and the overconsumption of HFCS in calorically sweetened beverages may play a role in the epidemic of obesity.
obesity  research  high_fructose_corn_syrup  diabetes  insulin 
april 2010 by Quercki
Fat Factors - New York Times
bacteria associated with obesity. Virus causes obesity.
fat  obesity  firmicutes 
march 2010 by Quercki
An obesity-associated gut microbiome with increased capacity for energy harvest
The worldwide obesity epidemic is stimulating efforts to identify host and environmental factors that affect energy balance.
Comparisons of the distal gut microbiota of genetically obese mice and their lean littermates, as well as those of obese and
lean human volunteers have revealed that obesity is associated with changes in the relative abundance of the two dominant
bacterial divisions, the Bacteroidetes and the Firmicutes. Here we demonstrate through metagenomic and biochemical
analyses that these changes affect the metabolic potential of the mouse gut microbiota. Our results indicate that the obese
microbiome has an increased capacity to harvest energy from the diet. Furthermore, this trait is transmissible: colonization of
germ-free mice with an ‘obesemicrobiota’ results in a significantly greater increase in total body fat than colonization with a
‘lean microbiota’. These results identify the gut microbiota as an additional contributing factor to the pathophysiology of
obesity  health  fat  bacteria 
june 2009 by Quercki

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