"Too Fat" Part Two!...

The "system" says we ought to "continue on a different" uh "topic" which is the old topic under another name so I do.

What woman congressperson from Florida? A Repub? A Demo?...

dem...Wasserman something?

What about her? Run for prez? I'll look up the Florida congressional delegation and maybe I can find her...

Debbie Wasserman Schultz. She and Grayson make a man think Florida is more than pythons and....

Debbie Wasserman Schultz is her name; she's been the US house rep from Florida's 23rd district (gee in AZ we only got nine!) since 2005. She's a Demo and the district includes Broward county, Fort Lauderdale ("WHERE THE BOYS ARE!" or used to be) and Miami Beach.

She's pro everything I am apparently and though she's Jewish she's for a Palestinian state.

She's blonde and pretty -- more vivacious looking than MY "blonde and pretty" Kyrsten Sinema from AZ's ninth district which is northwest Tempe where I am as well as central-southeast Phoenix.

Where'd you hear about her and what did you hear?...

She's often on the site www.crooksandliars.com saying smart things to reporters.

Well somebody has to -- say "smart things" huh.

By the way it seems we've used this site for our own amusement today; I've enjoyed it but it seems so "quiet" -- late in the day I guess, 4:12 pm here in AZ where we don' need no stinkin' daylight savin's.

Gotta go soon but hey "happy trails"!...

Debbie Wassserman Schultz is the current head of the DNC. She almost came to speak to our Central Committee meeting in Alaska, but Begich's vote on the background search gun bill caused her to cancel.

Robert

Geez, Robert, couldn't you have found a better picture? At least one in which she is still alive?

Methinks "one" does NOT admire Ms W-S???????? Or could I be "wrong"?...

Available to nonsubscribers for a week or so, I think, an article on the science and hype of fructose with regard to obesity:

June 1, 2013; Vol.183 #11
Sweet Confusion: Does high fructose corn syrup deserve such a bad rap?
By Laura Beil
http://www.sciencenews.org/view/feature/id/350460/description/Sweet_Confusion

"The science hasn't settled whether high fructose corn syrup has more damaging overall effects on the human body — or on the ongoing obesity crisis — than table sugar. But there is evidence of the effects that fructose has on various organs and systems."

Citations

L. Tappy and K.A. Le. Does fructose consumption contribute to non-alcoholic fatty liver disease? Clinics and Research in Hepatology and Gastroenterology. Vol. 36, December 2012, pp. 554—560. doi:10.1016/j.clinre.2012.06.005 Abstract available at http://www.ncbi.nlm.nih.gov/pubmed/22795319

K. Stanhope et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. Journal of Clinical Endocrinology and Metabolism. Vol. 96, October 2011, pp. E1596–E1605. See http://chc.ucsf.edu/sew/PDFs/Stanhope_etal_2011.pdf

K.A. Page et al. Effects of fructose vs glucose on regional cerebral blood flow in brain regions involved with appetite and reward pathways. Journal of the American Medical Association. Vol. 309, January 2, 2013, pp. 63-70 Abstract available at http://jama.jamanetwork.com/article.aspx?articleid=1555133

J.L. Sievenpiper et al. Effect of fructose on body weight in controlled feeding trials. Annals of Internal Medicine. Vol. 156, February 21, 2012, pp. 291-304. doi:10.7326/0003-4819-156-4-201202210-00007 Abstract available at http://annals.org/article.aspx?articleid=1132642

S.W. Ng et al. Use of caloric and noncaloric sweeteners in US consumer packaged foods, 2005-2009. Journal of the Academy of Nutrition and Dietetics. Vol. 112, November 2012, pp. 1828-1834. Abstract available at http://www.andjrnl.org/article/S2212-2672%2812%2901201-4/abstract

Suggested Reading

G. Bray and B. Popkin. Calorie-sweetened beverages and fructose: what we have learned 10 years later. Pediatric Obesity. Published online April 29, 2013. 10.1111/j.2047-6310.2013.00171.x . http://onlinelibrary.wiley.com/doi/10.1111/j.2047-6310.2013.00171.x/abstract

R. Ehrenberg. Taste of fructose revs up metabolism. Science News. Vol. 181, April 7, 2012, p. 16. http://www.sciencenews.org/view/generic/id/338193/description/Taste_of_fructose_...

J. Raloff. Simple-sugar effects aren’t necessarily simple, animal study suggests. Science News. Posted online April 13, 2011. http://www.sciencenews.org/view/generic/id/72741/description/Simple-sugar_effect...

Chris Christie IS probably "too fat to be president" and consequently is "on a diet" eh. So am I but then I hardly expect --...

Obese mothers who have weight-loss surgery before giving birth have thinner children, say researchers

"Canadian study found that the children of women who had a gastric band were slimmer than their older siblings born before the procedure"
"Found genetic differences between children born pre and post-operation because babies were 'marinated' in different levels of blood and fat"
"Study shows that it is genes, and not just lifestyle factors such as poor diet and lack of exercise, that are to blame for childhood obesity"

http://www.dailymail.co.uk/health/article-2332088/Should-obese-women-weight-loss...

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To read original study, google "Methylation and expression of immune and inflammatory genes in the
offspring of bariatric surgery patients" by Guénard et al. Bariatric surgery is covered in certain cases by health care in Ontario--and I assume in Quebec, where study was undertaken. It's interesting to read that benefits of surgery extend to subsequent children as well as to moms--a way to "break the cycle", and thus an incentive for universal healthcare at least to continue to cover the surgery.

"The American Medical Association has officially recognized obesity as a disease, a move that could induce physicians to pay more attention to the condition and spur more insurers to pay for treatments. "

http://www.nytimes.com/2013/06/19/business/ama-recognizes-obesity-as-a-disease.h...

"In a frustrating outcome, a long-term weight-loss program aimed at overweight adults with diabetes didn't cut the rate of heart attacks and strokes, a major study showed."

"But losing weight did provide at least one major benefit by cutting the development of chronic kidney disease, a leading cause of premature death in people with Type 2 diabetes. It also showed some ancillary benefits like cutting medicine use, depression and hospitalizations. ..."

http://online.wsj.com/article/SB10001424127887324183204578565531664058760.html
http://www.nejm.org/doi/full/10.1056/NEJMoa1212914?query=featured_home

Overweight? Maybe You Really Can Blame Your Genes
http://www.nytimes.com/2013/07/19/health/overweight-maybe-you-really-can-blame-y...

"...This rare gene-disabling mutation, though, is intriguing because it seems to explain something different, a propensity to pile on pounds even while eating what should be a normal amount of food. Investigators are now searching for other mutations of the same gene in fat people that may have a similar, but less extreme effect. The hope is that in the long term, understanding how this gene affects weight gain might lead to treatments for obesity that alter the rate at which calories are burned..."

" The work fascinates Claude Bouchard, a genetics researcher at the Pennington Biomedical Research Center in Baton Rouge, La., because it might offer insight into an intriguing finding: there are genetic controls not just of how much people want to eat but also how much of what they eat turns into fat or is burned off and not used by the body. Although the common mantra is that a calorie is a calorie and 3,500 extra calories eaten equals a pound of fat on the body, that is not what happens in real life, he found."

"For example, in one of his studies, Dr. Bouchard enlisted 12 pairs of lean identical twins to live in an enclosed area for 120 days so their food and exercise could be monitored while they ate 1,000 calories a day more than needed to maintain their weight. The twins in each pair gained about the same amount of weight, but the amount gained varied threefold among the pairs. Those who gained the most put on as much as 29 pounds while those who gained the least put on 9 ½ pounds."

"“It is not a freak finding,” Dr. Bouchard said, adding that about 20 studies found the same threefold range in weight gain in response to excess calories. But it also is not clear why this occurs. The intriguing possibility, he said, is that the newly discovered gene might be among those involved. The level of its activity might help determine how quickly calories are burned. .."

*************************************

M Asai et al. 2013. Loss of Function of the Melanocortin 2 Receptor Accessory Protein 2 Is Associated with Mammalian Obesity. Science 19 July 2013: 275-278. http://www.sciencemag.org/search?fulltext=Majzoub&issue=6143&submit=yes&...

Editor's Summary: Accessory to Obesity? Melanocortin receptors are a family of cell membrane receptors that control diverse physiological functions. Mutations in the gene encoding melanocortin 4 receptor (MC4R) are a cause of familial early-onset obesity. Asai et al. (p. 275) studied the function of an accessory protein for MC4R signaling, MRAP2, and found that mice genetically deficient in MRAP2 develop severe obesity. Sequencing of MRAP2 in unrelated, severely obese humans revealed one individual with a clearly disruptive genetic variant, suggesting that MRAP2 mutations might also be a rare cause of human obesity. In a zebrafish model, Sebag et al. (p. 278) studied two paralogs of the MRAP2 accessory protein, one of which enhanced MC4R responsiveness to α–melanocyte-stimulating hormone, which regulates feeding and growth.

Abstract: Melanocortin receptor accessory proteins (MRAPs) modulate signaling of melanocortin receptors in vitro. To investigate the physiological role of brain-expressed melanocortin 2 receptor accessory protein 2 (MRAP2), we characterized mice with whole-body and brain-specific targeted deletion of Mrap2, both of which develop severe obesity at a young age. Mrap2 interacts directly with melanocortin 4 receptor (Mc4r), a protein previously implicated in mammalian obesity, and it enhances Mc4r-mediated generation of the second messenger cyclic adenosine monophosphate, suggesting that alterations in Mc4r signaling may be one mechanism underlying the association between Mrap2 disruption and obesity. In a study of humans with severe, early-onset obesity, we found four rare, potentially pathogenic genetic variants in MRAP2, suggesting that the gene may also contribute to body weight regulation in humans.

"Height had a greater impact on (women's) cancer risk than being overweight, according to the results published in the US medical journal Cancer Epidemiology, Biomarkers & Prevention."

http://www.telegraph.co.uk/health/healthnews/10203488/Taller-women-more-likely-t...

Lead scientist: Dr Geoffrey Kabat, Albert Einstein College of Medicine, New York.
Journal: Cancer Epidemiology, Biomarkers & Prevention.

ETA: "Adult height is determined both by genetics and by early life exposures, and environmental circumstances influence the attainment of one’s genetic potential. The influence of environmental exposures on height is evidenced by the secular increase in the height of populations in many countries beginning in the 19th century, probably reflecting improvements in hygiene and nutrition. Height should thus be thought of as a marker for one or more exposures that influence cancer risk rather than a risk factor itself." Read more: http://healthland.time.com/2013/07/26/how-height-is-connected-to-cancer/#ixzz2a9...

Gastric bypass surgery causes sugar-burning gut growth in rats.
Intestinal changes could explain rapid improvements in diabetes.

"After gastric bypass surgery, the intestines of an obese rat (Roux limb indicated by arrow, right) burn more sugar (bright red and yellow) than before the surgery (left). This boost in sugar use could explain why surgery can rapidly improve diabetes....The research helps quash the idea that gastric bypass surgery’s effects stem simply from limiting caloric intake."

http://www.sciencenews.org/view/generic/id/351852/description/Gastric_bypass_sur...

CITATION:

N. Saeidi et al. Reprogramming of intestinal glucose metabolism and glycemic control in rats after gastric bypass. Science. Published online July 25, 2013. doi:10.1126/science.1235103. http://www.sciencemag.org/content/341/6144/406

18> The influence of environmental exposures on height is evidenced by the secular increase in the height of populations in many countries beginning in the 19th century, probably reflecting improvements in hygiene and nutrition.

What does secular mean in that sentence?

Good question. I took it to mean
"of or relating to a long term of indefinite duration", e.g., "secular inflation".
per Merriam-Webster.

I read somewhere that the US used to have the tallest people on average, but now that title goes to the Netherlands.
Nutrition was said to be better there.

"...Rather than acting as a motivating factor to lose weight, discrimination based on a person's BMI may actually increase an obese person's risk of gaining even more of it, a study* published in the journal PLOSE ONE found."

"Conducted by researchers from the Florida State University College of Medicine, the report compared the height and weight of over 6,000 participants in 2006 and 2010. In doing so, they found that those who reported experiencing weight discrimination early on were 2.5 times more likely to become obese by the follow-up assessment four years later..."

http://www.natureworldnews.com/articles/3197/20130727/weight-discrimination-fact...

*Sutin AR, Terracciano A (2013) Perceived Weight Discrimination and Obesity. PLoS ONE 8(7): e70048. doi:10.1371/journal.pone.0070048. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070048

Sugar is toxic to mice in 'safe' doses
New test hints 3 sodas daily hurt lifespan, reproduction

"...Even though the mice didn't become obese and showed few metabolic symptoms, the sensitive test showed "they died more often and tended to have fewer babies," says the study's first author, James Ruff, who recently earned his Ph.D. at the University of Utah. "We have shown that levels of sugar that people typically consume – and that are considered safe by regulatory agencies – impair the health of mice.".."

"...The diet fed to the mice with the 25 percent sugar-added diet is equivalent to the diet of a person who drinks three cans daily of sweetened soda pop "plus a perfectly healthy, no-sugar-added diet," Potts says."

"Ruff notes that sugar consumption in the American diet has increased 50 percent since the 1970s, accompanied by a dramatic increase in metabolic diseases such as diabetes, obesity, fatty liver and cardiovascular disease..."

http://www.eurekalert.org/pub_releases/2013-08/uou-sit080713.php

I tend to stay off this thread since I have no idea where it came from, but I want to thank you two for teaching me a new word use. Who would have thought secular could be used that way?

The thread started as a political question, but there were so many jabs at fat people's willpower and the burden they place on the rest of us that I undertook an education program. Last (wo)man standing wins? :-)

Fat peoples' will power? For one thing that covers a lot of territory. For instance, I was always skinny, but due to lack of exercise I began growing breast fat in my 30s, waist fat in my mid 30s, now stomach fat in my 50s. No health problem is posed so I don't ever do much about it for long. Again this fall I intend to begin long walks every day...
So am i a burden, too? Where is the line drawn?

There is a couple I know well. They're very focused on eating healthily and in restricted amounts, exercising properly and having regular check-ups with various specialists. And they also like to jump off of tall things wearing parachutes. I think it all evens out.

>27 RidgewayGirl:
"There is a couple I know well. They're very focused on eating healthily and in restricted amounts, exercising properly and having regular check-ups with various specialists. And they also like to jump off of tall things wearing parachutes. I think it all evens out."

It appears so !

Parachutes are a placebo anyway. There's no reliable evidence of their effectiveness in preventing injury from falls.

A long look at causes of obesity: The Obesity Era

As the American people got fatter, so did marmosets, vervet monkeys and mice. The problem may be bigger than any of us.

Great overview. Thanks! That's the first I heard of the lab animals...

>30 Amtep:

Interesting article. The comments were even more interesting as they get increasingly shrill and intolerant. The nuanced consideration and discussion that the article advocates is clearly a big challenge to implement.

A gut infection can keep mice lean
Bacteria can invade one rodent from another, preventing both from getting fat

By Meghan Rosen
Web edition: September 5, 2013
http://www.sciencenews.org/view/generic/id/352966/description/A_gut_infection_ca...

"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..." (Bacteroidetes members, apparently)

However, while on a high-fat, low-fiber ("American") diet, "lean-people microbes seemed to protect mice from getting chubby: Mice with these bacteria gained less weight than did mice with obesity microbes. But when researchers caged the two types of mice together, lean microbes were no longer able to invade the guts of mice carrying obesity microbes. And without these invaders, mice couldn’t stave off fat gain."

******************************

V. K. Ridaura. Gut microbiota from twins discordant for obesity modulate metabolism in mice. Science. Published online September 5, 2013. doi: 10.1126/science.1241214.
http://www.sciencemag.org/content/341/6150/1241214

Abstract: The role of specific gut microbes in shaping body composition remains unclear. We transplanted fecal microbiota from adult female twin pairs discordant for obesity into germ-free mice fed low-fat mouse chow, as well as diets representing different levels of saturated fat and fruit and vegetable consumption typical of the U.S. diet. Increased total body and fat mass, as well as obesity-associated metabolic phenotypes, were transmissible with uncultured fecal communities and with their corresponding fecal bacterial culture collections. Cohousing mice harboring an obese twin’s microbiota (Ob) with mice containing the lean co-twin’s microbiota (Ln) prevented the development of increased body mass and obesity-associated metabolic phenotypes in Ob cage mates. Rescue correlated with invasion of specific members of Bacteroidetes from the Ln microbiota into Ob microbiota and was diet-dependent. These findings reveal transmissible, rapid, and modifiable effects of diet-by-microbiota interactions.

******************************

Perspective

Microbiology
Fighting Obesity with Bacteria
Alan W. Walker & Julian Parkhill
http://www.sciencemag.org/content/341/6150/1069

"The human large intestine harbors a complex community of microorganisms (microbiota) that affect many aspects of our physiology and health (1). Numerous lines of evidence, particularly from rodent models, have suggested that the intestinal microbiota may play a role in the development of obesity. On page 1241214 of this issue, Ridaura et al. (2) demonstrate that the microbiota from lean or obese humans induces similar phenotypes in mice and, more remarkably, that the microbiota from lean donors can invade and reduce adiposity gain in the obese-recipient mice if the mice are fed an appropriate diet..."

News in Brief: Fructose may be key to weight gain
Mice that could not make or metabolize the sugar gained less than normal mice

By Nathan Seppa
http://www.sciencenews.org/view/generic/id/353108/description/News_in_Brief_Fruc...

"Mice lacking the ability to metabolize fructose don’t gain nearly as much weight as normal mice do, researchers report September 10 in Nature Communications."

"Fructose, which some people blame for the obesity epidemic and its related health crises, shows up in high-fructose corn syrup and in table sugar, or sucrose. The body also makes home-grown fructose by modifying glucose in a process involving an enzyme called aldose reductase..."

Citations

M. Lanaspa et al. Endogenus fructose production and metabolism in the liver contributes to the development of metabolic syndrome. Nature Communications. In press, released September 10, 2013. doi: 10.1038/ncomms3434. http://www.nature.com/ncomms/2013/130910/ncomms3434/full/ncomms3434.html

"By hijacking connections between neurons deep within the brain, scientists forced full mice to keep eating and hungry mice to shun food. By identifying precise groups of cells that cause eating and others that curb it, the results begin to clarify the intricate web of checks and balances in the brain that control feeding..."

http://www.sciencenews.org/view/generic/id/353537/description/An_on-off_switch_f...

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J.H. Jennings et al. The inhibitory circuit architecture of the lateral hypothalamus orchestrates feeding. Science. Vol. 341, September 27, 2013, p. 1517. doi: 10.1126/science.1241812. http://www.sciencemag.org/content/341/6153/1517

"...maternal high-fat diet (HFD) feeding during lactation* predisposes the offspring for obesity and impaired glucose homeostasis in mice..."

MC Vogt et al. 2014. Neonatal Insulin Action Impairs Hypothalamic Neurocircuit Formation in Response to Maternal High-Fat Feeding. Cell - 23 January 2014. http://www.cell.com/abstract/S0092-8674%2814%2900018-X

*This period thought to be roughly equivalent to last trimester in human pregnancy.

Weight is more than biology; it's also culture. For some people food reflects status and group affinities. My Irish FIL never ate vegetables, for example, but his Italian wife did.

Plus people want to eat what they grew up eating. Unless your mother, like mine, was a terrible cook.

>29 Amtep:
Parachutes are a placebo anyway. There's no reliable evidence of their effectiveness in preventing injury from falls.
========
As a former instructor at the U.S. Army Airborne School, I would like to suggest that parachutes definitely make a difference in how hard you hit the ground.

lqarl

#38: But that's only anecdotal evidence, which is hardly reliable.

lqarl again

So there was a control group that jumped from airplanes aloft without parachutes?

Robert

#38: There has never been a proper double-blind, even single-blind, test of parachutes. In every instance of someone jumping from an airplane sans parachute, the belief that not having a parachute is deadly has started influencing their behavior long before they hit the ground, and thus invalidating any comparison of the with and without parachute jumps.

Perhaps this isn't a proper test, but: In the 70s a Jugoslav Air jet was bombed by Croatian nationalists over Czechoslovakia, exploding at 11,000 meters high; Vesna Vulović, a stewardess, survived without a parachute (broken legs, perhaps more injuries).

Shivering may be as effective as exercise in boosting metabolism and producing calorie-burning brown fat. Sounds like effects are proportional to degree of shivers but cold exposure without shivers is also beneficial.

Paul Lee et al. 2014. Irisin and FGF21 Are Cold-Induced Endocrine Activators of Brown Fat Function in Humans. Cell Metabolism, Volume 19, Issue 2, 302-309, 4 February 2014. http://www.cell.com/cell-metabolism/abstract/S1550-4131%2814%2900006-0

(Funny, though, I thought swimmers tended to carry a bit more fat, because they were in a cool medium?)

I think that the thin layer of water right against the body tends to insulate. I recall a competitive swimmer friend of mine remarking at how hot he got while racing, even though the water felt very cold when he first entered the pool.

"...those in the highest third of genetic risk score who consumed fried foods frequently each week had almost double the increase in BMI than those with the lowest genetic risk score eating the same amount of fried food."

http://www.medpagetoday.com/Endocrinology/GeneralEndocrinology/44820

Qi Qibin, et al. 2014. "Fried food consumption, genetic risk, and body mass index: gene-diet interaction analysis in three US cohort studies" BMJ 2014; 348: g1610. http://www.bmj.com/content/348/bmj.g1610

Gov Christie's gastric surgery appears to be helping him lose weight--below is new finding on mechanism. Interesting that it's bile acids and receptors that appear to regulate weight in mice. A decade or so, it was found that sea lamprey in the Great Lakes are attracted to streams by bile salts excreted by riverine larval lamprey (=pheromone). Bile is a more biologically active substance than I ever suspected!

*******************************************************
Bile acids may play lead role in weight-loss surgery
by Ashley Yeager
March 28, 2014
https://www.sciencenews.org/blog/science-ticker/bile-acids-may-play-lead-role-we...

"...The idea is that a person will feel full sooner because they have less room to take in food... However...the value of the stomach-shrinking surgery actually comes from having more gastric juices swirling around a smaller space and a change in the gut microbiome...The finding could lead to less invasive ways to counter obesity, the scientists suggest..."

*******************************************************
Karen K. Ryan et al. 2014 FXR is a molecular target for the effects of vertical sleeve gastrectomy.
Nature. Published online 26 March 2014. http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13135.html

Bariatric surgical procedures, such as vertical sleeve gastrectomy (VSG), are at present the most effective therapy for the treatment of obesity, and are associated with considerable improvements in co-morbidities, including type-2 diabetes mellitus. The underlying molecular mechanisms contributing to these benefits remain largely undetermined, despite offering the potential to reveal new targets for therapeutic intervention. Substantial changes in circulating total bile acids are known to occur after VSG. Moreover, bile acids are known to regulate metabolism by binding to the nuclear receptor FXR (farsenoid-X receptor, also known as NR1H4). We therefore examined the results of VSG surgery applied to mice with diet-induced obesity and targeted genetic disruption of FXR. Here we demonstrate that the therapeutic value of VSG does not result from mechanical restriction imposed by a smaller stomach. Rather, VSG is associated with increased circulating bile acids, and associated changes to gut microbial communities. Moreover, in the absence of FXR, the ability of VSG to reduce body weight and improve glucose tolerance is substantially reduced. These results point to bile acids and FXR signalling as an important molecular underpinning for the beneficial effects of this weight-loss surgery.

>48 margd:

That's really interesting. I had thought the benefits were purely mechanical. Clever study, that. I would never have thought to test it.

Chubby people of European (but not Asian nor African) descent can blame Neandertals?

E.E. Khrameeva et al. Neanderthal ancestry drives evolution of lipid catabolism in contemporary Europeans. Nature Communications. Published online April 1, 2014. doi: 10.1038/ncomms4584.
http://www.nature.com/ncomms/2014/140401/ncomms4584/full/ncomms4584.html

Possible functional implications of changes in LCP (lipid catabolic process):

"...While we find changes at the metabolite concentration and enzyme expression levels, the significance of these changes (in lipid catabolism particular to Europeans) at the organismal level remains to be investigated...Furthermore, genetic variants linked to obesity, hypertriglyceridemia and coronary heart disease, as well as triglycerides and cholesterol levels in genome-wide association studies show a significant enrichment of LCP (lipid catabolic process) genes containing an excess of NLS (Neandertal like sites). Notably, frequencies of these diseases have been shown to differ between individuals of European descent and other human populations. These observations support a contribution of Neanderthal genetic variants to the phenotype of contemporary Europeans."

Exposure to sunlight (especially 7am-9am) is correlated with lower BMI independent of caloric intake. Full spectrum SAD lights in the am might have similar effect? Yellow lenses are sometimes implanted in cararact surgery specifically to block blue light (which can exacerbate macular degeneration as well as influence melatonin production and thus insulin sensitivity)--perhaps melatonin supplementation would also facilitate lower BMI?

"...changes in the timing of light exposure were associated with body weight independent of caloric intake. One possible mechanism linking light directly to BMI, rather than caloric intake may be the influence of light on the expression and secretion of hormones, such as melatonin. In addition to its circadian timing effects, light exposure history during the day can alter nocturnal levels of melatonin and sensitivity of the circadian clock to light . These effects of light may play a role in metabolism and weight regulation. It has been shown, for example, that in middle-aged rats daily nocturnal melatonin administration for 3 weeks reduced weight gain in response to a high-fat diet and decreased nighttime plasma leptin concentrations, independent of total food consumption. Alteration in melatonin level has also been shown to affect insulin sensitivity, and recent studies in humans suggest that a low melatonin level is a risk factor for type 2 diabetes 35."

"Future studies are needed to determine whether the influence of light on BMI is mediated by its effects on melatonin and/or circadian timing and amplitude 34, 35, 36. Other potential mechanisms include the impact of light on sleep quality and autonomic function, 37, 38, 39 which can directly or indirectly affect metabolism and energy balance. For example, light exposure in the blue range (460 nm) in the evening may alter the dynamics of slow wave and rapid eye movement sleep 40, and such changes in sleep have been shown to affect metabolic function."

Reid KJ, Santostasi G, Baron KG, Wilson J, Kang J, et al. (2014) Timing and Intensity of Light Correlate with Body Weight in Adults. PLoS ONE 9(4): e92251. doi:10.1371/journal.pone.0092251.
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0092251

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Bright light - early and often - linked to lower BMI, study finds
By Karen Kaplan
April 2, 2014, 3:25 p.m.
http://www.latimes.com/science/sciencenow/la-sci-sn-early-morning-light-exposure...

"To maximize your chances of fighting flab, new research offers some simple advice: Wake up early and go outside."

"... researchers at Northwestern University’s Feinberg School of Medicine in Chicago persuaded 54 volunteers to wear a wrist monitor that measured their light exposure (including its timing and intensity) as well as their sleep patterns. The volunteers were also asked to keep a detailed log of everything they ate and drank during a seven-day period."

"The volunteers (whose average age was 30) tended to be night owls – on average, they went to sleep at 1:26 a.m. and woke up at 8:49 a.m. Compared to Americans as a whole, they were thin, with 58% reporting a body mass index of 24 or lower."

"When the researchers analyzed the data, they found only one variable that correlated to BMI: MLiT. That stands for “mean light timing above threshold,” and it’s a measurement that takes into account the timing, length and brightness of each volunteer’s light exposure."

"Translating that into practical terms, the researchers said the key was to bask in light of at least 500 lux, and that such basking was most valuable when the exposure came early in the day. For every hour that light exposure was delayed, BMI rose by 1.28 points."

"When the researchers limited their analysis to BMI and light exposure between the hours of 8 a.m. and noon, they found no significant correlation. This suggested that light exposure throughout the day helps regulate body weight, the researchers wrote."

"But there’s clearly something special about morning light. They’re not sure what it is, but one possibility is the fact that morning light contains more wavelengths in the blue portion of the spectrum. “Blue light has been shown to have the strongest effect on the circadian system,” the study authors wrote."

"It shouldn’t be too hard to get yourself exposed to 500 lux. A typical office is about that bright. If you go outside, you’ll get more than 10,000 lux in full daylight, and if it’s overcast you’ll still get more than 1,000 lux...."

"... researchers divided a sample group of 32 female rats into two groups. The first group was fed a diet of relatively unprocessed foods, while the second was given a "junk food" diet of highly processed foods rich in sugar and saturated fat. All of the rats were required to complete a basic task -- pushing a lever -- to receive a food or water reward."

"Three months into the experiment, the researchers observed, unsurprisingly, that the rats on the junk food diet had grown significantly fatter than the others. The more interesting finding, however, was that these obese rats' performance of the lever task had become impaired, as they took much longer breaks than the lean rats between performing the task. The researchers refer to this lack of motivation as "cognitive impairment.""

"At the end of six months, the researchers reversed the rats' diets. But after nine days on the less-processed foods, the obese rats showed little change in weight and no change in their response to the lever task. Similarly, the lean rats remained lean and showed no decrease in motivation after nine days on junk food. According to the researchers, these findings indicate that it is long-term habits, rather than occasional health kicks or junk food binges, that are responsible for our weight and motivation..."

http://www.ctvnews.ca/health/does-junk-food-make-you-lazy-1.1765925#ixzz2yIgrVk6...

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Aaron P. Blaisdell et al. 2014. Food quality and motivation: A refined low-fat diet induces obesity and impairs performance on a progressive ratio schedule of instrumental lever pressing in rats Original Research Article. Physiology & Behavior, Volume 128, 10 April 2014, Pages 220-225
http://www.sciencedirect.com/science/journal/00319384

Abstract

"...Diet-induced obesity produces a substantial deficit in motivated behavior in rats, independent of dietary fat content. This holds implications for an association between obesity and motivation. Specifically, behavioral traits comorbid with obesity, such as depression and fatigue , may be effects of obesity rather than contributing causes. To the degree that refined foods contribute to obesity, as demonstrated in our study, they may play a significant contributing role to other behavioral and cognitive disorders."

That's quite a leap from "not pushing the button as often" to "lack of motivation". I would guess that if you're already well fed then your motivation to get more food would be diminished but I don't see how that would carry over to other activities, or how it would apply to humans who have many more things they could be motivated about.

Most interesting to me: "But after nine days on the less-processed foods, the obese rats showed little change in weight and no change in their response to the lever task. Similarly, the lean rats remained lean and showed no decrease in motivation after nine days on junk food... According to the researchers, these findings indicate that it is long-term habits, rather than occasional health kicks or junk food binges, that are responsible for our weight and motivation..."

Maybe in addition to our Neandertal ancestors, we can blame fast food scientists who design crunch + salt +sugar + fat to be irresistable to us? (A university room-mate of mine went on to do that for a candy bar company!)

"...long-term exposure to bursts of sweet, fatty foods produces animals that appear to seek food not out of hunger, but out of habit. And neural changes associated with habit formation accompany the behavioral changes...control rats and rats given constant access to (sweetened) milk stopped pressing the lever. They were full, thanks, and didn’t want more of what they’d just been pigging out on. But rats that had five weeks with intermittent, binge-like access to the sweetened milk responded differently. They kept pressing for grain, even though they were full of grain, and kept pressing for sugar, even though their sweet tooth should have been satisfied. The rats weren’t pushing the lever because they could use some more grain. Instead, they were pressing the lever out of habit...This lever-pressing routine was associated with increased activity in the dorsolateral striatum, an area of the brain associated with habitual behaviors." Blocking glutamate or dopamine reversed the behavior. "...the results are comparable to other studies with drugs of abuse like cocaine, producing “the same loss of behavioral control”..." https://www.sciencenews.org/blog/scicurious/bingeing-rats-show-power-food-habits

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TM furlong et al. 2014. Binge-Like Consumption of a Palatable Food Accelerates Habitual Control of Behavior and Is Dependent on Activation of the Dorsolateral Striatum. The Journal of Neuroscience, 2 April 2014, 34(14): 5012-5022. http://www.jneurosci.org/content/34/14/5012.short?sid=9dda6fd2-f859-4536-a09a-9d...

Opens next week, 'Fed Up' documentary uncovers the dangers of sugar (01:51)--by producer of Inconvenient Truth.

"...Like the sucrose extracted from sugar cane or beets, HFCS consists of glucose and fructose molecules, which the food industry argues makes it perfectly safe. But there is mounting evidence to suggest otherwise. Unlike sucrose, the glucose and fructose are not bonded in HFCS – which many researchers believe makes a vital difference to the way our bodies react to it."

"In 2010, researchers at Princeton University published a study in which rats fed on a menu that included HFCS gained substantially more weight than those whose diet did not. They also were more inclined to develop metabolic syndrome, a group of conditions including high blood pressure and excessive abdominal fat, both of which are precursors to heart disease, stroke and other serious health issues."

"A 2011 study published in the Journal of Clinical Endocrinology and Metabolism found that people who drank beverages sweetened with HFCS had higher levels of triglycerides, which also can lead to heart disease."

"Many experts believe that HFCS causes problems because the uncoupled fructose is absorbed by the liver and converted into fat that can damage the liver, and lead to cirrhosis and finally organ failure."

"As well, some fat globules can be released into the bloodstream, a risk factor for heart disease. Even if individuals aren’t considered overweight, there is evidence that suggests HFCS could be doing internal damage."

"Fructose also fails to trigger the release of insulin and leptin, which alert the body when someone has eaten enough. This can promote weight gain that leads, in turn, to obesity, metabolic syndrome, diabetes, heart disease and stroke."

"It is difficult to get a clear picture of how much HFCS – or even plain sugar – that Canadians consume. A decade old, Statistics Canada’s most recent figures show that over-all levels of daily added sugar consumption hovered around 10 per cent of total daily calories, the level that the WHO still recommends officially. (The agency says that limiting added sugar to 5 per cent of daily calories is ideal, but difficult for consumers to achieve, given how much is added to food.)"

"Look deeper, though, and it’s apparent that among certain age groups – notably the young – sugar intake is much higher. And the cause seems clear: A Statscan report in 2011 found soft drinks to be the number one source of added sugar in the diet of those between 9 and 18, and the second biggest source for people 19 and older. The vast majority of soft drinks are sweetened with HFCS."

"...Richard Johnson, a professor of medicine at the University of Colorado Denver...says that quibbling over which is worse (sugar or HFCS) is like trying to decide whether cigars do more harm than cigarettes. It also misses the point: that people are simply consuming far too much sweet stuff..."

http://www.theglobeandmail.com/life/health-and-fitness/health/too-much-sweetness...

ETA: Just checked packages and apparently there are 4 gm of added sugar per serving of breaded fish fillets and 7 gms in sweet potato fries I serve my family. And my young men no doubt exceed the portion sze on the package. Dare not look at the salad dressings... I screened the brand of fish a while back to be lowest in carbs... Back to reading labels and to cooking more from scratch! (As time permits.)

"Fiber's ability to curb appetite may come from gut molecules traveling to and acting on the brain, not the gut alone. As mice digest fiber, their guts release a molecule called acetate that appears to influence appetite suppression chemicals sent from the brain... The finding could open up new possibilities for weight management... It's unclear exactly how the gut-made acetate influences the brain chemicals that regulate appetite, and it's unknown whether the amount of fiber given to the mice in the study would be part of a realistic diet."

https://www.sciencenews.org/blog/science-ticker/dietary-fiber-may-curb-appetite-...

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Gary Frost et al. 2014. The short-chain fatty acid acetate reduces appetite via a central homeostatic mechanism. Nature Communications 5, Article number: 3611. Apr 29, 2014. http://www.nature.com/ncomms/2014/140429/ncomms4611/full/ncomms4611.html

Abstract

Increased intake of dietary carbohydrate that is fermented in the colon by the microbiota has been reported to decrease body weight, although the mechanism remains unclear. Here we use in vivo11C-acetate and PET-CT scanning to show that colonic acetate crosses the blood–brain barrier and is taken up by the brain. Intraperitoneal acetate results in appetite suppression and hypothalamic neuronal activation patterning. We also show that acetate administration is associated with activation of acetyl-CoA carboxylase and changes in the expression profiles of regulatory neuropeptides that favour appetite suppression. Furthermore, we demonstrate through 13C high-resolution magic-angle-spinning that 13C acetate from fermentation of 13C-labelled carbohydrate in the colon increases hypothalamic 13C acetate above baseline levels. Hypothalamic 13C acetate regionally increases the 13C labelling of the glutamate–glutamine and GABA neuroglial cycles, with hypothalamic 13C lactate reaching higher levels than the ‘remaining brain’. These observations suggest that acetate has a direct role in central appetite regulation.

Two larger meals early in the day may be better than six small for losing weight and improving insulin sensitivity...

"...The differences were not dramatic, but compared with those eating six meals a day, those who ate just breakfast and lunch reduced their weight and waist circumference. Those eating fewer meals also had improved fasting glucose levels, lower liver fat content and better insulin sensitivity..."

http://well.blogs.nytimes.com/2014/05/15/a-meal-schedule-for-diabetes/?ref=healt...

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Hana Kahleova et al. 2014. Eating two larger meals a day (breakfast and lunch) is more
effective than six smaller meals in a reduced-energy regimen for patients with type 2 diabetes: a randomised crossover study. Diabetologia. 9 p. http://www.diabetologia-journal.org/files/Kahleova.pdf

...After a large meal, fat cells churn out an appetite suppressant called leptin, which hits the brain’s neurons and tickles other kinds of brain cells (in the hypothalamus) called astrocytes. In certain situations, these astrocytes help control hunger, scientists report June 1 in Nature Neuroscience. The results feed into a growing set of studies that elevate the status of astrocytes from mere support cells to regulators of important behavior such as eating....

Astrocytes immune to leptin ... looked different. Compared with normal astrocytes, these cells had fewer tendrils that communicate with other cells, and those tendrils were shorter. The astrocytes themselves weren’t the only cells affected: Neurons that regulate feeding behavior in the hypothalamus, the same cells these astrocytes support, showed signs of listlessness, the researchers found....

Tweaking the behavior of these appetite-regulating astrocytes might be a way to treat obesity, Horvath suggests. But the brain’s leptin machinery is a problematic target, says neuroscientist Jenni Harvey of the University of Dundee in Scotland. Because fat cells produce leptin, obese people generate higher amounts of the hormone in the blood. Faced with a constant barrage of leptin, the brain’s ability to take in the hormone weakens, leading to leptin insensitivity....

https://www.sciencenews.org/article/brain%E2%80%99s-support-cells-play-role-hung...

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J. G. Kim et al. Leptin signaling in astrocytes regulates hypothalamic neuronal circuits and feeding. Nature Neuroscience. June 1, 2013. doi:10.1038/nn.3725. http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.3725.html

"We found that leptin receptors were expressed in hypothalamic astrocytes and that their conditional deletion led to altered glial morphology and synaptic inputs onto hypothalamic neurons involved in feeding control. Leptin-regulated feeding was diminished, whereas feeding after fasting or ghrelin administration was elevated in mice with astrocyte-specific leptin receptor deficiency. These data reveal an active role of glial cells in hypothalamic synaptic remodeling and control of feeding by leptin."

I read that last cited paragraph and didn't understand a word of it. Talk about preaching to the choir! If one wants to lose weight I have a very simple method: eat sushi with a glass of good sauvignon blanc for dinner; eat a cup of yoghurt with a glass of V-8 juice in the morning -NO COFFEE. And nothing in between! Works for me. I've lost 20 pounds with this diet. OK, OK so I was just one step from obesity on that chart all doctors seem to have plastered on their wall, but I feel great and am now only in the middle of "overweight". Do they charge an extra fee when you get to Heaven for your overweight body? They don't in Hell!!!

"...Blaming excess weight on people simply not changing their eating habits goes back thousands of years. Sloth and gluttony are two of the seven deadly sins, after all. But Ludwig and Dr. Mark L. Friedman of the Nutrition Science Initiative in San Diego, argue that this mindset disregards decades of research on the biological factors that control body weight. And they are not just talking about the role genetics play. They say we should stop viewing weight as something separate from other biological functions—like hormones and hunger and the effects of what foods we eat, not just how much of them."

"What, then, is causing the obesity epidemic? The authors say it’s refined carbohydrates. Sugar and processed grains like white bread which have become ubiquitous in our diets, and one of the reasons refined carbs is the prime culprit is that we’ve spent far too long chastising fat. “We have to forget the low-fat paradigm,” says Dr. Ludwig. “Some high fat foods like avocado, nuts and olive oil are among the healthiest foods we could possibly eat.”..."

http://time.com/2809007/eat-less-exercise-more-isnt-the-answer-for-weight-loss/

DS Ludwig and MI Friedman. 2014. Increasing Adiposity:Consequence or Cause of Overeating? (Viewpoint). JAMA. 2014;311(21):2167-2168. http://jama.jamanetwork.com/article.aspx?articleid=1871695

About a quarter of obese people remain healthy, avoiding inflammation and diabetes, etc., apparently because they have less of the enzyme heme oxygenase-1 in their livers and fat tissue. It may be that inhibiting the enzyme might promote better health in obese people.

https://www.sciencenews.org/blog/science-ticker/enzyme-separates-healthy-and-unh...

A Jais et al. 2014. Heme Oxygenase-1 Drives Metaflammation and Insulin Resistance in Mouse and Man. Cell. Volume 158, Issue 1, p25–40, 3 July 2014. http://www.cell.com/cell/abstract/S0092-8674%2814%2900671-0

Too fat to polka!?...

"...Low doses of antibiotics given to pregnant mice and to their newborns led baby mice to become obese as adults, researchers report August 14 in Cell. The effect was not due to the drugs themselves but to the disruption of the rodents’ gut microbiome, the community of microbes living in the mice’s intestines..."

https://www.sciencenews.org/article/antibiotics-infancy-may-cause-obesity-adults
http://www.cell.com/cell/abstract/S0092-8674%2814%2900821-6

Nobody's too fat to polka!...

Bazzano LA, Hu T, Reynolds K, Yao L, Bunol C, Liu Y, et al. Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial. Ann Intern Med. 2014;161:309-318. doi:10.7326/M14-0180.
http://annals.org/article.aspx?articleid=1900694

Conclusion: The low-carbohydrate diet was more effective for weight loss and cardiovascular risk factor reduction than the low-fat diet. Restricting carbohydrate may be an option for persons seeking to lose weight and reduce cardiovascular risk factors.

A Call for a Low Carb Diet
http://www.nytimes.com/2014/09/02/health/low-carb-vs-low-fat-diet.html?_r=0

https://www.sciencenews.org/article/ancient-famine-fighting-genes-cant-explain-o...

Why are some modern humans hefty?

MENU OF OPTIONS Alternative theories to the thrifty gene hypothesis abound. So far, no single hypothesis on the genetic origins of obesity has gained universal acceptance.

Thrifty gene hypothesis (James Neel, U.S., 1962). Human history was marked by feast or famine. Humans who had fat reserves — who were exceptionally efficient at storing fat — were more likely to survive.

Drifty gene hypothesis (John Speakman, U.K., 2008). A counter to the thrifty gene theory. Fatness was not a survival advantage. It just stopped being a disadvantage when humans no longer had to run from predators, so obesity drifted into the population.

The thrifty phenotype (Several authors). A handful of hypotheses that revolve around the idea that poor nutrition in the womb encourages the development of diabetes when food is abundant in adulthood.

Genetically unknown foods (Riccardo Baschetti, Italy, 1998). Obesity and diabetes occur when populations are introduced to new foods they have not adapted to.

Aggression control (Prajakta Belsare et al, India, 2010). As humans relied less on fighting and aggression to survive, a propensity for obesity emerged. Over­indulgence becomes less of a problem when being docile is no longer a life-or-death calamity.

Climate adaptations (Dyan Sellayah et al, U.K., 2014). Survival in cold parts of the world favored genes that help preserve body temperature — a higher metabolic rate meant lower obesity and diabetes. In hot spots, lower metabolism meant the opposite.

Sources: E. GennÉ-Bacon/Yale J. Biol. Med. 2014; D. Sellayah et al/Endocrinology 2014

not having looked at the study The drifty gene theory seems unlikely. Gene drift usually requires a small population. Which hardly describes the population of the USA. and it seems also to ignore the fact that most selection is sexual in nature.
It seems to me that the overweight and obese are generally considered as less desirable sexual partners.

Populations were much smaller at various times in human history. As for sexual selection, check out the Venus figurines of the Upper Paleolithic...

I suspect that any genes that control fat storage and body weight regulation would come from far, far before the human lineage.

>66 margd:

I wouldn't really call 30% fat a low-fat diet.

I'd be more convinced by a comparison with the diet that Dr. Dean Ornish found could reverse heart disease, which was a 5-10% fat diet.

ETA - I tend to be suspicious of diets that eliminate entire types of foods be they carbs or fats.

>71 Helcura: I agree. I read an editorial to that effect after posting. In contrast, the 40 g low carb diet is only a bit more than South Beach targets, I think.

I suspect different approaches work for different people, but for most of us, the low glycemic index / low carbohydrate approach works best and is easiest to follow long term.

(New low-GI products and new uses for traditional products help with longterm adherence, e.g., Explore-Asia black bean spaghetti (Costco, Amazon), rosemary onion pancakes made with chickpea flour, (pulse) pappadums in place of corn chips for dips and taco salads, and yellow lentil (in place of potato in Portuguese potato & kale soup)--the last three from Asian Indian grocery. The extra fiber of peas and beans might be a problem for some ailments, though?)

Saccharin is worst, but sucralose and aspartame also changed gut bacteria and facilitated glucose intolerance. ("Please, not Stevia!!", says she, sipping Stevia-sweetened hot cocoa to get through a spot of insomnia..)

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J. Suez et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. Published online September 17, 2014. doi:10.1038/nature13793. http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13793.html

Abstract
Non-caloric artificial sweeteners (NAS) are among the most widely used food additives worldwide, regularly consumed by lean and obese individuals alike. NAS consumption is considered safe and beneficial owing to their low caloric content, yet supporting scientific data remain sparse and controversial. Here we demonstrate that consumption of commonly used NAS formulations drives the development of glucose intolerance through induction of compositional and functional alterations to the intestinal microbiota. These NAS-mediated deleterious metabolic effects are abrogated by antibiotic treatment, and are fully transferrable to germ-free mice upon faecal transplantation of microbiota configurations from NAS-consuming mice, or of microbiota anaerobically incubated in the presence of NAS. We identify NAS-altered microbial metabolic pathways that are linked to host susceptibility to metabolic disease, and demonstrate similar NAS-induced dysbiosis and glucose intolerance in healthy human subjects. Collectively, our results link NAS consumption, dysbiosis and metabolic abnormalities, thereby calling for a reassessment of massive NAS usage.

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T. Feehley and C. Nagler. The weighty costs of non-caloric sweeteners. Nature. Published online September 17, 2014. doi:10.1038/nature13752. http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13752.html

Analyses in mice and humans indicate that non-caloric artificial sweeteners may promote obesity-associated metabolic changes by changing the function of the bacteria that colonize the gut.

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Artificial sweeteners may tip scales toward metabolic problems
In mice and people, saccharin upsets gut microbes, glucose metabolism
by Rachel Ehrenberg
1:00pm, September 17, 2014
https://www.sciencenews.org/article/artificial-sweeteners-may-tip-scales-toward-...

...After 11 weeks of drinking water doped with the sweeteners saccharin, sucralose or aspartame, mice had abnormally high glucose levels in their blood after eating. Digested food gets broken down into glucose, the most common carbohydrate, which then enters the bloodstream to be used as fuel or stored, often as fat. When glucose metabolism is impaired, high blood glucose levels — a hallmark of diabetes — can result.

Since blood glucose levels were most off-kilter in the saccharin-fed mice, the researchers zeroed in on this sweetener, which is found in Sweet N’ Low, jams, salad dressings, vitamins and many other low- and no-calorie foods.The scientists gave saccharin to mice that were fed a high-fat diet or a regular diet. Those mice developed impaired glucose metabolism in as little as five weeks, suggesting the sweetener had the same effect regardless of whether mice were lean or overweight. Meanwhile, mice eating glucose-laced water had normal metabolisms.

Then the scientists gave the saccharin-fed mice antibiotics to wipe out their intestinal bacteria. The mice’s glucose metabolism recovered, suggesting that gut microbes might play an important role in glucose metabolism. So the researchers transplanted fecal microbes from saccharin-fed mice into the guts of mice with microbe-free intestines that then, in turn, developed impaired glucose metabolism.

Genetic analyses of the microbes in the mice’s intestines revealed major differences in the microbial groups present in saccharin-fed mice compared with mice eating a regular diet.

...Why the bacterial community shifts is still unknown. Perhaps some bacteria thrive on saccharin and outcompete their neighbors, or maybe the sweetener kills off other bacteria. The mechanisms that disrupt glucose metabolism also remain mysterious. But it’s clear that saccharin doesn’t pass silently through the mouse intestine with no effect.

It also doesn’t pass through people silently, Segal and Elinav’s team suggests. When the researchers looked at 40 people who reported eating artificial sweeteners and compared them to 236 people who did not, the sweetener-eaters were more likely to have had metabolic problems, including impaired glucose metabolism.

And when seven healthy volunteers ate the Food and Drug Administration’s maximum acceptable daily dose of saccharin for a week, four of them developed off-kilter glucose metabolism . Transferring feces from these four people into mice induced the same problems in the rodents, suggesting that gut microbes were to blame...

‘Fat shaming’ doesn’t encourage weight loss:

"Discrimination against overweight and obese people does not help them to lose weight, finds new UCL research funded by Cancer Research UK."

"In a study of 2,944 UK adults over four years, those who reported experiencing weight discrimination gained more weight than those who did not. On average, after accounting for baseline differences, people who reported weight discrimination GAINED 0.95kg whereas those who did not LOST 0.71kg, a difference of 1.66kg." {emphasis margd's)

"The research, published in the journal Obesity, contradicts the common perception that discrimination or ‘fat shaming’ might encourage weight loss. The study asked people whether they experienced day-to-day discrimination that they attributed to their weight. Examples of discrimination include being treated disrespectfully, receiving poor service in shops, and being harassed..."

http://www.ucl.ac.uk/news/news-articles/0914/110914-Fat-shaming-does-not-encoura...

SE Jackson et al. 2014. Perceived Weight Discrimination and Changes in Weight,
Waist Circumference, and Weight Status. Obesity. Article first published online: 11 SEP 2014
http://onlinelibrary.wiley.com/doi/10.1002/oby.20891/pdf

Thank you for posting these, margd--they're all fascinating (I'd read the one from Science News as I'm a subscriber.) I've personally found the most success in weight loss with a low-carb eating regimen and keeping as much sugar as possible out of my diet.

Weight maintenance is amazingly complex in our culture, that's for sure! I thought it might be interesting to follow the science a bit in one place.

Science News is a great resource, isn't it? Even for non-subscribers, though some restrictions for them--searching archives, some articles--https://www.sciencenews.org/ .

Finding below may lead to remedies for eating disorders such as anorexia, bulimia, but perhaps also give insight to problems of over-eating?

"...A protein made by gut bacteria may trigger a chain of interactions in the body that contribute to eating disorders such as anorexia and bulimia."

"When the protein is produced, the body makes antibodies to bind to it, but the antibodies also attach to a hormone that controls fullness. In tests, mice given bacteria that produce the protein changed how much they ate compared with mice given bacteria that did not make the protein, a new study shows. Researchers also found that the antibodies to the protein were higher in patients with anorexia and bulimia..."

https://www.sciencenews.org/blog/science-ticker/gut-bacteria-protein-linked-anor...

http://www.nature.com/tp/journal/v4/n10/abs/tp201498a.html

"...Over the long term, fast-track and slow-track dieters are equally likely to regain most of the weight they lost...Among the fast-dieting group, more achieved their weight loss target -- 81 per cent compared to half of the other group -- and fewer left the programme..."
http://www.huffingtonpost.ca/2014/10/17/losing-weight-fast_n_6004950.html

Purcell, K, et al. 2014. The effect of rate of weight loss on long-term weight management: a randomised controlled trial. The Lancet Diabetes & Endocrinology, Early Online Publication, 16 October 2014. doi:10.1016/S2213-8587(14)70200-1 . http://www.thelancet.com/journals/landia/article/PIIS2213-8587%2814%2970200-1/ab...

2014: "...A recent study found obese women are more likely than other women to work physically demanding jobs, like the kind that call for hard hats. They're less likely to work in jobs that require a lot of interaction with clients and customers — jobs that, on average, make more money... (Author) Shinall also found that this trend did not apply to obese men..."

http://www.npr.org/2014/11/08/362552448/obese-women-make-less-money-work-more-ph...

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2004: A 65-pound increase in a woman's weight is associated with a 9-percent drop in earnings.

http://www.jstor.org/discover/10.2307/3559022?uid=3739728&uid=2&uid=4&am...

Eating a daily serving of yogurt is associated with an 18% lower risk of type 2 diabetes, says a new study published in the journal BMC Medicine...

The researchers did not find that dairy consumption in general affected diabetes risk, but they did find that yogurt was specifically associated with a lower risk of developing the disease. With further calculations, the researchers concluded that consuming one serving of yogurt per day was associated with an 18% lower risk of type 2 diabetes.

The researchers were not able to determine exactly what was providing the health benefit... More research is needed—but not before making yogurt a dietary staple for health.

https://time.com/3603687/yogurt-lower-diabetes/

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Chen M, Sun Q, Giovannucci E, et al. Dairy consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis. BMC Medicine. 2014. http://www.biomedcentral.com/1741-7015/12/215

Conclusions: Higher intake of yogurt is associated with a reduced risk of T2D, whereas other dairy foods and consumption of total dairy are not appreciably associated with incidence of T2D.

Benefits of time-restricted eating are more profound and forgiving than previously thought--so nix on the night snack! :-(

http://www.salk.edu/news/pressrelease_details.php?press_id=2062

Subjects were mostly men, ~52 years of age, BMI of ~47:

"At the five-year point after (bariatric) surgery, 10.4 percent of the people who did not have surgery had died, while fewer -- 6.4 percent -- of those who got surgery had died. At the 10-year mark, the death rate was 23.9 percent among controls and 13.8 percent in the surgery group."

https://www.sciencenews.org/article/weight-loss-surgery-linked-better-survival

D.E. Arterburn et al. Association between bariatric surgery and long-term survival. JAMA. Vol. 313, January 6, 2015, p. 62. doi: 10.1001/jama.2014.16968. http://jama.jamanetwork.com/article.aspx?articleid=2088854

>81 margd: (on time-restricted eating) contd. Interesting to think that evening lights, i.e., electricity, could be major driver of obesity--by facilitating evening snacks, as well as by messing up our sleep patterns:

A Chaix, A Zarrinpar, P Miu and S Panda. 2014. Time-Restricted Feeding Is a Preventative and Therapeutic Intervention against Diverse Nutritional Challenges. Volume 20, Issue 6, p991–1005, 2 December 2014 .DOI: http://dx.doi.org/10.1016/j.cmet.2014.11.001. http://www.cell.com/cell-metabolism/abstract/S1550-4131%2814%2900498-7

Highlights

•Time-restricted feeding (TRF) confines food access to 9–12 hr during the active phase
•TRF is a therapeutic intervention against obesity without calorie restriction
•TRF protects against metabolic diseases even when briefly interrupted on weekends
•TRF is effective against high-fat, high-fructose, and high-sucrose diets

Summary

Because current therapeutics for obesity are limited and only offer modest improvements, novel interventions are needed. Preventing obesity with time-restricted feeding (TRF; 8–9 hr food access in the active phase) is promising, yet its therapeutic applicability against preexisting obesity, diverse dietary conditions, and less stringent eating patterns is unknown. Here we tested TRF in mice under diverse nutritional challenges. We show that TRF attenuated metabolic diseases arising from a variety of obesogenic diets, and that benefits were proportional to the fasting duration. Furthermore, protective effects were maintained even when TRF was temporarily interrupted by ad libitum access to food during weekends, a regimen particularly relevant to human lifestyle. Finally, TRF stabilized and reversed the progression of metabolic diseases in mice with preexisting obesity and type II diabetes. We establish clinically relevant parameters of TRF for preventing and treating obesity and metabolic disorders, including type II diabetes, hepatic steatosis, and hypercholesterolemia.

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NYT article at
http://well.blogs.nytimes.com/2015/01/15/a-12-hour-window-for-a-healthy-weight/?...

"Manipulating specific sets of brain cells can quash a mouse’s overindulgence of sugar."

"The cells are part of a previously unknown brain circuit that controls compulsive sugar consumption in mice, researchers report in the Jan. 29 Cell. This circuit appears to be distinct from the one that controls normal eating, suggesting that it could be a target for treating obesity caused by overeating in humans..."

Citations

E. Nieh et al. Decoding neural circuits that control compulsive Sucrose seeking. Cell. Vol. 160, January 29, 2015, p. 1. doi: 10.1016/j.cell.2015.01.003.
http://www.cell.com/cell/abstract/S0092-8674%2815%2900004-5

Jennings et al. Visualizing hypothalamic network dynamics for appetitive and consummatory behaviors. Cell. Vol. 160, January 29, 2015, p. 1. doi: 10.1016/j.cell.2014.12.026.
http://www.cell.com/cell/abstract/S0092-8674%2814%2901632-8

https://www.sciencenews.org/article/newly-identified-brain-circuit-could-be-targ...

Could someone please summarize these results: no more aspartame? What about the 2-day-a-week fasting diet?

Here's an evaluation of diets by U.S. News as of December 2014: http://health.usnews.com/best-diet

>85 Doug1943: Could someone please summarize these results: no more aspartame? What about the 2-day-a-week fasting diet?

Re restricted eating, #81 and 83--looks like something to it.

Re artificial sweeteners, #73. Researchers haven't looked at Stevia yet, so fingers crossed that my favorite sugar substitute will pass their test. Sugar's taking a beating (#23, etc.). Can't find posting here on honey, so below are some studies that suggest it isn't that bad EXCEPT that it messed with A1C in diabetics.

My takeaway from the research is that the popular tendency to fat-shame and to prescribe simple remedies like "just stop eating, you spineless slob" aren't supported in the latest literature. We are a product of our genes, microbiome & our environment, and that of our ancestors.

There are no end of mechanisms that drive & govern eating and use of foods consumed and all can be messed up (beginning in the womb). Some mechanisms are difficult/impossible to reset once messed up, which can leave some of us with a particularly big challenge in maintaining a healthy weight.

Modern environmental factors include: refined/processed foods, BPA, electricity (= blue light = insomnia), antibiotics. I think understanding and applying the increasing body of knowledge about those factors--especially with the very young (in the womb, even)--is our best shot as individuals and society for beating the obesity epidemic.

In short, while I wouldn't vote for a thin Governor Christie, I don't think his girth is an impediment to his candidacy any more than Eisenhower's heart (heavy smoker), Roosevelt's polio, Kennedy's pain meds, Reagan's polyps, and McCain's cancer history. Research indicates that his gastric surgery might leave him as healthy as any other candidate--and more than some.

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J Med Food. 2004 Spring;7(1):100-7.
http://www.ncbi.nlm.nih.gov/pubmed/15117561

Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose.

Al-Waili NS.

Abstract
This study included the following experiments: (1) effects of dextrose solution (250 mL of water containing 75 g of dextrose) or honey solution (250 mL of water containing 75 g of natural honey) on plasma glucose level (PGL), plasma insulin, and plasma C-peptide (eight subjects); (2) effects of dextrose, honey, or artificial honey (250 mL of water containing 35 g of dextrose and 40 g of fructose) on cholesterol and triglycerides (TG) (nine subjects); (3) effects of honey solution, administered for 15 days, on PGL, blood lipids, C-reactive protein (CRP), and homocysteine (eight subjects); (4) effects of honey or artificial honey on cholesterol and TG in six patients with hypercholesterolemia and five patients with hypertriglyceridemia; (5) effects of honey for 15 days on blood lipid and CRP in five patients with elevated cholesterol and CRP; (6) effects of 70 g of dextrose or 90 g of honey on PGL in seven patients with type 2 diabetes mellitus; and (7) effects of 30 g of sucrose or 30 g of honey on PGL, plasma insulin, and plasma C-peptide in five diabetic patients. In healthy subjects, dextrose elevated PGL at 1 (53%) and 2 (3%) hours, and decreased PGL after 3 hours (20%). Honey elevated PGL after 1 hour (14%) and decreased it after 3 hours (10%). Elevation of insulin and C-peptide was significantly higher after dextrose than after honey. Dextrose slightly reduced cholesterol and low-density lipoprotein-cholesterol (LDL-C) after 1 hour and significantly after 2 hours, and increased TG after 1, 2, and 3 hours. Artificial honey slightly decreased cholesterol and LDL-C and elevated TG. Honey reduced cholesterol, LDL-C, and TG and slightly elevated high-density lipoprotein-cholesterol (HDL-C). Honey consumed for 15 days decreased cholesterol (7%), LDL-C (1%), TG (2%), CRP (7%), homocysteine (6%), and PGL (6%), and increased HDL-C (2%). In patients with hypertriglyceridemia, artificial honey increased TG, while honey decreased TG. In patients with hyperlipidemia, artificial honey increased LDL-C, while honey decreased LDL-C. Honey decreased cholesterol (8%), LDL-C (11%), and CRP (75%) after 15 days. In diabetic patients, honey compared with dextrose caused a significantly lower rise of PGL. Elevation of PGL was greater after honey than after sucrose at 30 minutes, and was lower after honey than it was after sucrose at 60, 120, and 180 minutes. Honey caused greater elevation of insulin than sucrose did after 30, 120, and 180 minutes. Honey reduces blood lipids, homocysteine, and CRP in normal and hyperlipidemic subjects. Honey compared with dextrose and sucrose caused lower elevation of PGL in diabetics.

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Effects of natural honey consumption in diabetic patients: an 8-week randomized clinical trial
November 2009, Vol. 60, No. 7 , Pages 618-626
http://informahealthcare.com/doi/abs/10.3109/09637480801990389

Mohsen Bahrami, Asal Ataie-Jafari, Saeed Hosseini, Mohammad Hasan Foruzanfar, Mazaher Rahmani, and Mohammad Pajouhi

Endocrinology and Metabolism Research Center, Medical Sciences/University of Tehran, Tehran, Iran

Correspondence: Mohammad Pajouhi, Endocrinology & Metabolism Research Center, 5th Floor, Shariati Hospital, North Kargar Avenue, Tehran 14114, Iran. 982 1 88026902. 982 1 88029399. emrc@sina.tums.ac.ir

Objectives We investigated the effect of natural honey on body weight and some blood biochemical indices of diabetic subjects.

Methods Forty-eight diabetic type 2 patients were randomly assigned into two groups: the honey group received oral natural honey for 8 weeks, and the control group did not take honey. Before the onset of the study (week 0) and after 8 weeks, weight measurements were taken and fasting blood samples were drawn.

Results After adjustment for the baseline values, there were no significant differences in the fasting blood sugars between the two groups. Body weight, total cholesterol, low-density lipoprotein-cholesterol and triglyceride decreased (P = 0.000), and high-density lipoprotein-cholesterol increased significantly (P

" ... is either unhealthy, immoral, or illegal." Even honey? Damn.

Five early-life risk factors are associated with higher risk (4 to 5X!) of early childhood obesity: the mom's obesity, excess weight gain, smoking and low vitamin D levels during pregnancy--and short breastfeeding duration (less than 1 month) after birth:

Modifiable early-life risk factors for childhood adiposity and overweight: an analysis of their combined impact and potential for prevention, Siân M. Robinson, et al., Am J Clin Nutr , doi: 10.3945/​ajcn.114.094268, published online 3 December 2014. http://ajcn.nutrition.org/content/early/2014/12/03/ajcn.114.094268.abstract

Abstract

Background: Early life may be a “critical period” when appetite and regulation of energy balance are programmed, with lifelong consequences for obesity risk. Insight into the potential impact of modifying early-life risk factors on later obesity can be gained by evaluating their combined effects.

Objective: The objective was to examine the relation between the number of early-life risk factors and obesity outcomes among children in a prospective birth cohort (Southampton Women's Survey).

Design: Five risk factors were defined: maternal obesity prepregnant body mass index (BMI; in kg/m2) >30 Amtep:, excess gestational weight gain (Institute of Medicine, 2009), smoking during pregnancy, low maternal vitamin D status (less than 64 nmol/L), and short duration of breastfeeding (none or less than 1 mo). Obesity outcomes examined when the children were aged 4 and 6 y were BMI, dual-energy X-ray absorptiometry–assessed fat mass, overweight, or obesity (International Obesity Task Force). Data were available for 991 mother-child pairs, with children born between 1998 and 2003.

Results: Of the children, 148 (15%) had no early-life risk factors, 330 (33%) had 1, 296 (30%) had 2, 160 (16%) had 3, and 57 (6%) had 4 or 5. At both 4 and 6 y, there were positive graded associations between number of early-life risk factors and each obesity outcome (all P less than 0.001). After taking account of confounders, the relative risk of being overweight or obese for children who had 4 or 5 risk factors was 3.99 (95% CI: 1.83, 8.67) at 4 y and 4.65 (95% CI: 2.29, 9.43) at 6 y compared with children who had none (both P less than 0.001).

Conclusions: Having a greater number of early-life risk factors was associated with large differences in adiposity and risk of overweight and obesity in later childhood. These findings suggest that early intervention to change these modifiable risk factors could make a significant contribution to the prevention of childhood obesity.

Teenagers--especially boys--who have a false perception of themselves as being overweight are more likely to become obese as adults.

Body weight misperception in adolescence and incident obesity in young adulthood, Angelina Sutin, et al., Psychological Science, published online 28 January 2015.

Association for Psychological Science news release. http://www.eurekalert.org/pub_releases/2015-01/afps-ssa012715.php

>89 margd: I'd like to see that bumped up against post-tonsillectomy weight gain.

Robert

96 % of us carry bacterium Christensenella minuta in our digestive tracts, but amount is heritable. Slim people tend to have more:

"...When (Cornell grad student) Julia Goodrich ranked the microbes from most to least heritable, she found C. minuta and its close relatives in the Christensenellaceae family were the most heritable bacteria, but C. minuta also appeared in a kind of network with other heritable bacteria and methane-producing microbes called methanogens."

"Goodrich also noticed that C. minuta and this network of microbes were more abundant in lean people. In experiments with mice, Goodrich and colleagues determined that C. minuta alone promoted thinner mice..."

http://www.news.cornell.edu/stories/2014/11/genes-influence-types-microbes-human...

Goodrich, Julia K. et al. 2014. Human Genetics Shape the Gut Microbiome. Cell , Volume 159 , Issue 4 , 789 - 799. Nov 2014

People in the US, with high rates of obesity, have less-diverse gut microbes than people from less developed parts of the world--apparently evident early in life.

Yatsunenko, T., et al. Human gut microbiome viewed across age and geography. Nature 486: 222-227 (2012). PMCID: PMC3376388. http://www.nature.com/nature/journal/v486/n7402/full/nature11053.html

Abstract. Gut microbial communities represent one source of human genetic and metabolic diversity. To examine how gut microbiomes differ among human populations, here we characterize bacterial species in fecal samples from 531 individuals, plus the gene content of 110 of them. The cohort encompassed healthy children and adults from the Amazonas of Venezuela, rural Malawi and US metropolitan areas and included mono- and dizygotic twins. Shared features of the functional maturation of the gut microbiome were identified during the first three years of life in all three populations, including age-associated changes in the genes involved in vitamin biosynthesis and metabolism. Pronounced differences in bacterial assemblages and functional gene repertoires were noted between US residents and those in the other two countries. These distinctive features are evident in early infancy as well as adulthood. Our findings underscore the need to consider the microbiome when evaluating human development, nutritional needs, physiological variations and the impact of westernization.

Helicobacter pylori is associated with stomach ulcers, and it absence is associated with reflux. It also dials back production of hormones ghrelin and leptin--and it is 50% less prevalent in US since 1968, apparently due to better sanitization and widespread use of antibiotics.

"...Evidence points to H. pylori being an ancient and persistent guest in the human gastrointestinal system, rather than an acute infection. But in the past few decades, the prevalence of H. pylori has declined, offering an unprecedented opportunity to track the demise of a member of the normal human flora. In developed countries, the bacteria now affects 20–50% of adults, but studies show that there has been a 50% decline in the prevalence of H. pylori in the USA since 1968 (www.helico.com). At least three factors have a role in its disappearance: cleaner water, less crowding and better hygiene, and the widespread use of antibiotics over the past 60 years...." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479565/

Francois, Fritz et al. “The Effect of H. Pylori Eradication on Meal-Associated Changes in Plasma Ghrelin and Leptin.” BMC Gastroenterology 11 (2011): 37. PMC. Web. 10 Feb. 2015. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089783/

Abstract
Background. Appetite and energy expenditure are regulated in part by ghrelin and leptin produced in the gastric mucosa, which may be modified by H. pylori colonization. We prospectively evaluated the effect of H. pylori eradication on meal-associated changes in serum ghrelin and leptin levels, and body weight.

Methods. Veterans referred for upper GI endoscopy were evaluated at baseline and ≥8 weeks after endoscopy, and H. pylori status and body weight were ascertained. During the first visit in all subjects, and during subsequent visits in the initially H. pylori-positive subjects and controls, blood was collected after an overnight fast and 1 h after a standard high protein meal, and levels of eight hormones determined.

Results. Of 92 enrolled subjects, 38 were H. pylori-negative, 44 H. pylori-positive, and 10 were indeterminate. Among 23 H. pylori-positive subjects who completed evaluation after treatment, 21 were eradicated, and 2 failed eradication. After a median of seven months following eradication, six hormones related to energy homeostasis showed no significant differences, but post-prandial acylated ghrelin levels were nearly six-fold higher than pre-eradication (p = 0.005), and median integrated leptin levels also increased (20%) significantly (p

" The livestock use of antimicrobial agents has sharply increased in the US over the same 20-year period of the obesity epidemic, especially with the expansion of intensified livestock production, such as the concentrated animal feeding operations..."

Riley LW et al. 2013. Obesity in the United States - dysbiosis from exposure to low-dose antibiotics? Front Public Health. 2013 Dec 19;1:69. doi: 10.3389/fpubh.2013.00069. eCollection 2013. http://www.ncbi.nlm.nih.gov/pubmed/24392444

Abstract. The rapid increase in obesity prevalence in the United States in the last 20 years is unprecedented and not well explained. Here, we explore a hypothesis that the obesity epidemic may be driven by population-wide chronic exposures to low-residue antibiotics that have increasingly entered the American food chain over the same time period. We propose this hypothesis based on two recent bodies of published reports - (1) those that provide evidence for the spread of antibiotics into the American food chain, and (2) those that examine the relationship between the gut microbiota and body physiology. Observational and experimental studies support the idea that changes in the intestinal microbiota exert a profound effect on body physiology. We propose that chronic exposures to low-residue antimicrobial drugs in food could disrupt the equilibrium state of intestinal microbiota and cause dysbiosis that can contribute to changes in body physiology. The obesity epidemic in the United States may be partly driven by the mass exposure of Americans to food containing low-residue antimicrobial agents. While this hypothesis cannot discount the impact of diet and other factors associated with obesity, we believe studies are warranted to consider this possible driver of the epidemic.

Fitnessmagazine.com (March 2015) advises:
eat more fiber (20-30 g per day),
choose complex carbohydrates (e.g. apple) over sugars and simple carbs,
pick probiotic foods (e.g. yoghurt, which is associated with weight loss), and
move (= better BMI, more bacteria linked to lower obesity rates*, such as Akkermansiaceae).

I wonder if we will soon have fermented foods that can reseed us with bacteria lost to westernization of ourselves and our ancestors. (I recently noticed that Lifeway kefir contains Lactobacillus reuteri, which apparently reduces the discomfort of colic in babies--and who knows what dis-ease in adults.) Once reseeded, should we avoid animal products raised on antibiotics? (Pharmaceuticals are ubiquitous in surface water, albeit at low levels.)

*S. F. Clarke, E. F. Murphy, O. O'Sullivan, A. J. Lucey, M. Humphreys, A. Hogan, P. Hayes, M. O'Reilly, I. B. Jeffery, R. Wood-Martin, D. M. Kerins, E. Quigley, R. P. Ross, P. W. O'Toole, M. G. Molloy, E. Falvey, F. Shanahan, P. D. Cotter. Exercise and associated dietary extremes impact on gut microbial diversity. Gut, 2014; DOI: 10.1136/gutjnl-2013-306541. http://gut.bmj.com/content/63/12/1913

Abstract
Objective. The commensal microbiota, host immunity and metabolism participate in a signalling network, with diet influencing each component of this triad. In addition to diet, many elements of a modern lifestyle influence the gut microbiota but the degree to which exercise affects this population is unclear. Therefore, we explored exercise and diet for their impact on the gut microbiota.

Design. Since extremes of exercise often accompany extremes of diet, we addressed the issue by studying professional athletes from an international rugby union squad. Two groups were included to control for physical size, age and gender. Compositional analysis of the microbiota was explored by 16S rRNA amplicon sequencing. Each participant completed a detailed food frequency questionnaire.

Results. As expected, athletes and controls differed significantly with respect to plasma creatine kinase (a marker of extreme exercise), and inflammatory and metabolic markers. More importantly, athletes had a higher diversity of gut micro-organisms, representing 22 distinct phyla, which in turn positively correlated with protein consumption and creatine kinase.

Conclusions. The results provide evidence for a beneficial impact of exercise on gut microbiota diversity but also indicate that the relationship is complex and is related to accompanying dietary extremes.

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This paper discusses mechanism by which dairy fat can promote colitis. Not exactly a weight connection but interesting as an indication of how much we have to learn about the effects of foods many of us eat every day...

Suzanne Devkota et al. 2012. Dietary-fat-induced taurocholic acid promotes pathobiont expansion and colitis in Il10−/− mice. Nature 487, 104–108 (05 July 2012) doi:10.1038/nature11225
http://www.nature.com/nature/journal/v487/n7405/abs/nature11225.html

Editor's summary. Milk fat is shown here to potentiate experimental colitis in susceptible mice, in association with increased luminal concentrations of sulphite-reducing bacteria. Mice fed a diet with comparable caloric intake containing unsaturated fatty acids are protected. The inflammation is caused by milk-fat-promoted taurine conjugation with bile acids, which increases the availability of organic sulphur used by the bacteria. This finding supports the suggestion that the recent upwards trend in complex immune disorders such as inflammatory bowel diseases could reflect changes in human microbiomes elicited in genetically susceptible individuals by dietary and other environmental changes.

Abstract. The composite human microbiome of Western populations has probably changed over the past century, brought on by new environmental triggers that often have a negative impact on human health1. Here we show that consumption of a diet high in saturated (milk-derived) fat, but not polyunsaturated (safflower oil) fat, changes the conditions for microbial assemblage and promotes the expansion of a low-abundance, sulphite-reducing pathobiont, Bilophila wadsworthia2. This was associated with a pro-inflammatory T helper type 1 (TH1) immune response and increased incidence of colitis in genetically susceptible Il10−/−, but not wild-type mice. These effects are mediated by milk-derived-fat-promoted taurine conjugation of hepatic bile acids, which increases the availability of organic sulphur used by sulphite-reducing microorganisms like B. wadsworthia. When mice were fed a low-fat diet supplemented with taurocholic acid, but not with glycocholic acid, for example, a bloom of B. wadsworthia and development of colitis were observed in Il10−/− mice. Together these data show that dietary fats, by promoting changes in host bile acid composition, can markedly alter conditions for gut microbial assemblage, resulting in dysbiosis that can perturb immune homeostasis. The data provide a plausible mechanistic basis by which Western-type diets high in certain saturated fats might increase the prevalence of complex immune-mediated diseases like inflammatory bowel disease in genetically susceptible hosts.

Looks like a daily 30 gm of fiber is as effective (statistically) for weight loss as the AHA's more complex diet instructions*. Both groups displayed lower total cholesterol, lower blood pressure, and lower triglyceride levels. Perhaps not statistically significant, a few more people stuck with the high fiber diet than the AHA's, but a few more developed diabetes on high-fiber than AHA's.

*http://www.capitalotc.com/people-trying-to-lose-weight-should-focus-on-fiber-rich-foods-study/29104/

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Yunsheng Ma et al. 2015. Single-Component Versus Multicomponent Dietary Goals for the Metabolic Syndrome: A Randomized Trial. Ann Intern Med. 2015;162(4):248-257. doi:10.7326/M14-0611. http://annals.org/article.aspx?articleid=2118594

Background: Few studies have compared diets to determine whether a program focused on 1 dietary change results in collateral effects on other untargeted healthy diet components.

Objective: To evaluate a diet focused on increased fiber consumption versus the multicomponent American Heart Association (AHA) dietary guidelines.

..Participants: 240 adults with the metabolic syndrome.

...Measurements: Primary outcome was weight change at 12 months.

Results: At 12 months, mean change in weight was −2.1 kg (95% CI, −2.9 to −1.3 kg) in the high-fiber diet group versus −2.7 kg (CI, −3.5 to −2.0 kg) in the AHA diet group. The mean between-group difference was 0.6 kg (CI, −0.5 to 1.7 kg). During the trial, 12 (9.9%) and 15 (12.6%) participants dropped out of the high-fiber and AHA diet groups, respectively (P = 0.55). Eight participants developed diabetes (hemoglobin A1c level ≥6.5%) during the trial: 7 in the high-fiber diet group and 1 in the AHA diet group (P = 0.066).

Limitations: Generalizability is unknown. Maintenance of weight loss after cessation of group sessions at 12 months was not assessed. Definitive conclusions cannot be made about dietary equivalence because the study was powered for superiority.

Conclusion: The more complex AHA diet may result in up to 1.7 kg more weight loss; however, a simplified approach to weight reduction emphasizing only increased fiber intake may be a reasonable alternative for persons with difficulty adhering to more complicated diet regimens.

Emulsifiers that extend shelf life of ice cream, salad dressing, pasta sauce, bread and cookies, e.g., carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type mice and promoted robust colitis in mice predisposed to this disorder.

https://www.sciencenews.org/article/additives-keep-foods-fresh-may-sour-gut

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B. Chassaing et al. Dietary emulsifiers impact the mouse gut microbiota promoting colitis and metabolic syndrome*. Nature. Published online February 25, 2015. doi: 10.1038/nature14232.
http://www.nature.com/nature/journal/vaop/ncurrent/full/nature14232.html

The intestinal tract is inhabited by a large and diverse community of microbes collectively referred to as the gut microbiota. While the gut microbiota provides important benefits to its host, especially in metabolism and immune development, disturbance of the microbiota–host relationship is associated with numerous chronic inflammatory diseases, including inflammatory bowel disease and the group of obesity-associated diseases collectively referred to as metabolic syndrome. A primary means by which the intestine is protected from its microbiota is via multi-layered mucus structures that cover the intestinal surface, thereby allowing the vast majority of gut bacteria to be kept at a safe distance from epithelial cells that line the intestine1. Thus, agents that disrupt mucus–bacterial interactions might have the potential to promote diseases associated with gut inflammation. Consequently, it has been hypothesized that emulsifiers, detergent-like molecules that are a ubiquitous component of processed foods and that can increase bacterial translocation across epithelia in vitro2, might be promoting the increase in inflammatory bowel disease observed since the mid-twentieth century3. Here we report that, in mice, relatively low concentrations of two commonly used emulsifiers, namely carboxymethylcellulose and polysorbate-80, induced low-grade inflammation and obesity/metabolic syndrome in wild-type hosts and promoted robust colitis in mice predisposed to this disorder. Emulsifier-induced metabolic syndrome was associated with microbiota encroachment, altered species composition and increased pro-inflammatory potential. Use of germ-free mice and faecal transplants indicated that such changes in microbiota were necessary and sufficient for both low-grade inflammation and metabolic syndrome. These results support the emerging concept that perturbed host–microbiota interactions resulting in low-grade inflammation can promote adiposity and its associated metabolic effects. Moreover, they suggest that the broad use of emulsifying agents might be contributing to an increased societal incidence of obesity/metabolic syndrome and other chronic inflammatory diseases.

Benefits of time-restricted eating include better heart function, less weight gain, better sleep--in fruit flies at least!

S. Gill et al. Time-restricted feeding attenuates age-related cardiac decline in Drosophila. Science. Vol. 347, March 13, 2015, p. 1265. doi: 0.1126/science.1256682. http://www.sciencemag.org/content/347/6227/1265

Editor Summary: Midnight snacks are bad for the heart
Circadian clocks help animals coordinate their active and rest periods with the daily cycles of light and darkness. As anyone who has suffered jet lag or worked night shifts knows, losing this coordination can have deleterious effects. Gill et al. compared fruit flies that were allowed to eat at any time with flies that were only allowed to eat during the day (when they are active). The flies with restricted feeding times slept better and had a slower decline in heart function as they aged. They also showed less weight gain, even though both groups of flies consumed about the same amount.

Abstract. Circadian clocks orchestrate periods of rest or activity and feeding or fasting over the course of a 24-hour day and maintain homeostasis. To assess whether a consolidated 24-hour cycle of feeding and fasting can sustain health, we explored the effect of time-restricted feeding (TRF; food access limited to daytime 12 hours every day) on neural, peripheral, and cardiovascular physiology in Drosophila melanogaster. We detected improved sleep, prevention of body weight gain, and deceleration of cardiac aging under TRF, even when caloric intake and activity were unchanged. We used temporal gene expression profiling and validation through classical genetics to identify the TCP-1 ring complex (TRiC) chaperonin, the mitochondrial electron transport chain complexes, and the circadian clock as pathways mediating the benefits of TRF.

Volume 10 · August 30th 2012 · Michael Greger, M.D.
Tipping Firmicutes to Bacteroidetes (video 2:34)

Certain phytonutrients may tip the balance of healthy gut bacteria in favor of flora associated with improved weight control. (fruits, green tea, wine vinegar)

http://nutritionfacts.org/video/tipping-the-balance-of-firmicutes-to-bacteroidet...

100 contd. Soluble fiber or resistant starch are not directly digested but fermented in the colon by "good bacteria". One of the many benefits is satiety. Examples of fermentable dietary and chemically modified fibres that are associated with a higher production of SCFAs (short chain fatty acids such as propionate and butyrate) either in vitro or in vivo are oligofructose, inulin, psyllium, germinated barley foodstuff, hydrolysed guar gum.

HAMER, H. M., JONKERS, D., VENEMA, K., VANHOUTVIN, S., TROOST, F. J. and BRUMMER, R.-J. (2008), Review article: the role of butyrate on colonic function. Alimentary Pharmacology & Therapeutics, 27: 104–119. doi: 10.1111/j.1365-2036.2007.03562.x . http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2036.2007.03562.x/full

Short-chain fatty acids (SCFAs), primarily acetate, propionate and butyrate, are organic acids produced within the intestinal lumen by bacterial fermentation of mainly undigested dietary carbohydrates, but also in a minor part by dietary and endogenous proteins, such as mucous, and sloughed epithelial cells....

An important SCFA produced is butyrate that besides being an energy source for the epithelial cells also influences a wide array of cellular functions affecting colonic health. As such, butyrate may have an anticarcinogenic and anti-inflammatory potential, affect the intestinal barrier and play a role in satiety and oxidative stress....

Delivery of butyrate

An important source of butyrate is colonic fermentation of dietary fibre. The rate and amount of butyrate being produced along the colonic lumen during dietary fibre supplementation depends on its chemical structure, such as solubility and degree of polymerization. Insoluble fibres (e.g. cellulose and lignin) have a rather low fermentability, but are associated with increased faecal mass and decreased colonic transit time. Soluble fibres are highly fermentable and hence generate greater quantities of SCFAs in the colon.28 Fibres with a higher degree of polymerization are more resistant to saccharolytic fermentation resulting in prolonged fermentation, expanding towards the distal colon.29 Examples of fermentable dietary and chemically modified fibres that are associated with a higher production of SCFAs either in vitro or in vivo are oligofructose,30 inulin,31 psyllium,32 germinated barley foodstuff,33 hydrolysed guar gum (or acacia,34 oat bran,9, 35 corn starch,12 isomalt,11 gluconic acid36 and butyrylated starch.37 Although the beneficial effects of these fibres are often attributed to the increased butyrate production, these soluble fibres can also affect other intestinal characteristics influencing intestinal health, such as increased faecal bulk, shortened colonic transit time, changes in the composition of the gut microbiota, lowered intraluminal pH and changed bile acid profiles.38...

Butyrate and satiety

It has been hypothesized that SCFAs produced in the large intestine also can influence upper gut motility and satiety.194 Endocrine L-cells present in large concentrations in the colonic mucosa secrete peptides such as glucagon-like peptide 1 (GLP-1), peptide YY (PYY) and oxyntomodulin, which are involved in appetite regulation.195 In several animal studies using fermentable carbohydrates such as inulin,195 lactitol196 and FOS,197, 198 an increased satiety, decreased weight gain and increased endogenous production of GLP-1 and/or PYY were reported. In humans, FOS increased satiety199 and increased plasma GLP-1 concentrations.200 However, lactitol did not affect plasma concentrations of this gut peptide.196

The increased satiety is possibly promoted through the production of SCFAs. This is supported by a number of studies. Butyrate increased the expression of PYY and proglucagon in vitro in rat epithelial cells201 and increased PYY release, but not that of GLP-1, in the isolated colon of rats202, 203 and rabbits.204 In addition, colonic SCFA infusion in rats stimulated PYY release.205 However, colonic infusion with SCFAs in humans did not increase plasma levels of either PYY or GLP-1.206 Activation of the SCFA receptor GPR43 expressed in endocrine L-cells may play a role in this effect on satiety.148

There is increasing evidence that the effect of fermentable dietary fibre on satiety is mediated through the colonic production of SCFAs. However, most evidence originates from rat studies, while again human evidence remains limited....

Conclusions

Short-chain fatty acids are important end-products of microbial fermentation. Among the SCFAs produced in the human intestine, butyrate has been widely studied and has been shown to play an important role in the maintenance of colonic health. Increased butyrate production in the large intestine seems to be responsible for at least some of the protective effects of fermentable dietary fibre. However, it should be taken into account that the effects of increased butyrate production may be accompanied by other effects of dietary fibres and its fermentation, such as changes in the composition of the intestinal microbiota and increased faecal bulking.

The effects of butyrate are diverse and complex and involve several distinct mechanisms that go beyond the classical impact as an energy source for the intestinal epithelial cells. Frequently described are the effect on gene expression because of the inhibition of histone deacetylase and the suppression of NF-κB activation. Hence, butyrate exerts multiple effects such as the inhibition of colonic carcinogenesis, inflammation and oxidative stress, the improvement of the colonic defence barrier function and the promotion of satiety.

It should, however, be noted that also some equivocal results have been reported, which partly can be explained by the different butyrate concentrations and models used. In addition, a few animal and in vitro studies demonstrate negative effects at higher butyrate concentrations on permeability and visceral sensitivity of the large intestine.

In conclusion, in the last decade, several new insights into possible mechanisms and effects revealed that butyrate is a pivotal metabolite produced within the large intestine. However, these new insights are mainly based on in vitro data, animal models and some clinical intervention studies. More emphasis should be placed on human in vivo studies to elucidate the role of butyrate in health and disease.

Extract of thunder god vine extract appears to sensitize mice to leptin, reducing appetite:

Junli Liu and Jaemin Lee et al. 2015. Treatment of Obesity with Celastrol. Cell. Volume 161, Issue 5, p999–1011, 21 May 2015. DOI: http://dx.doi.org/10.1016/j.cell.2015.05.011.

http://www.cell.com/cell/abstract/S0092-8674%2815%2900559-0?_returnURL=http%3A%2...

Highlights

•Celastrol is a natural compound extracted from thunder god vine
•Celastrol creates similar expression profile to those of reduced ER stress conditions
•Celastrol is a powerful leptin sensitizer
•Celastrol has potential as an anti-obesity therapeutic agent

Summary

Despite all modern advances in medicine, an effective drug treatment of obesity has not been found yet. Discovery of leptin two decades ago created hopes for treatment of obesity. However, development of leptin resistance has been a big obstacle, mitigating a leptin-centric treatment of obesity. Here, by using in silico drug-screening methods, we discovered that Celastrol, a pentacyclic triterpene extracted from the roots of Tripterygium Wilfordi (thunder god vine) plant, is a powerful anti-obesity agent. Celastrol suppresses food intake, blocks reduction of energy expenditure, and leads to up to 45% weight loss in hyperleptinemic diet-induced obese (DIO) mice by increasing leptin sensitivity, but it is ineffective in leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mouse models. These results indicate that Celastrol is a leptin sensitizer and a promising agent for the pharmacological treatment of obesity.

Sebastian Brandhorst. 2105. A Periodic Diet that Mimics Fasting Promotes Multi-System Regeneration, Enhanced Cognitive Performance, and Healthspan. Publication stage: In Press Corrected Proof. DOI: http://dx.doi.org/10.1016/j.cmet.2015.05.012 . http://www.cell.com/cell-metabolism/abstract/S1550-4131%2815%2900224-7

Highlights

•FMD rejuvenates the immune system and reduces cancer incidence in C57BL/6 mice
•FMD promotes hippocampal neurogenesis and improves cognitive performance in mice
•FMD causes beneficial changes in risk factors of age-related diseases in humans

Summary

Prolonged fasting (PF) promotes stress resistance, but its effects on longevity are poorly understood. We show that alternating PF and nutrient-rich medium extended yeast lifespan independently of established pro-longevity genes. In mice, 4 days of a diet that mimics fasting (FMD), developed to minimize the burden of PF, decreased the size of multiple organs/systems, an effect followed upon re-feeding by an elevated number of progenitor and stem cells and regeneration. Bi-monthly FMD cycles started at middle age extended longevity, lowered visceral fat, reduced cancer incidence and skin lesions, rejuvenated the immune system, and retarded bone mineral density loss. In old mice, FMD cycles promoted hippocampal neurogenesis, lowered IGF-1 levels and PKA activity, elevated NeuroD1, and improved cognitive performance. In a pilot clinical trial, three FMD cycles decreased risk factors/biomarkers for aging, diabetes, cardiovascular disease, and cancer without major adverse effects, providing support for the use of FMDs to promote healthspan.

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http://www.nzherald.co.nz/lifestyle/news/article.cfm?c_id=6&objectid=1146908...

Day One

FMD permitted calories: 1,090 max
Breakfast: Black or Green Tea; one boiled egg (78 calories) + one slice whole wheat toast (68 calories)
Lunch: black coffee or tea; small green salad with avocado, dressed with olive oil (300 calories)
Snack: two almonds (28 calories)
Dinner: Large helping of mixed green vegetable soup with borlotti beans, and slice of whole wheat bread (616 calories)

Day Two

FMD permitted calories: 725 calories max
Breakfast: Black or green tea; one poached egg with a grilled tomato (100 calories)
Lunch: Miso soup (21 cals)
Snack: 7 walnut halves (90 cals)
Dinner: Vegetable chilli with kidney beans and two tsp sour cream (514 cals)

Day Three

FMD permitted calories: 725 calories max
Breakfast: Black or Green tea: one slice whole wheat toast with two tsp of cashew butter (150 calories)
Lunch: Espresso; Smoked Salmon (100g) with watercress (200 cals)
Snack: Blueberries (100g) (57 cals)
Dinner: Large portion vegetable soup (318 cals)

Day Four

FMD permitted calories: 725 calories max
Breakfast: Black or Green tea; half an avocado on one slice of whole wheat toast (220 cals)
Lunch: Espresso; 250ml glass of almond milk (60 cals)
Snack: two squares 70 per cent dark chocolate (110 cals)
Dinner: Large green salad with 100g prawns, dressed with olive oil and lemon juice (335 cals)

Day Five

FMD permitted calories: 725 calories max
Breakfast: black or green tea; two boiled eggs (156 cals)
Lunch: Half an avocado on toast; miso soup (210 cals)
Snack: An apple (60 cals)
Dinner: Large portion of vegetable soup with 10g toasted pine nuts (299 cals)

Firstborns more likely to be overweight/obese:

"...It’s possible that in later pregnancies, changes occur that increase the amount of blood supply to the placenta, Cutfield said. That means that during the first pregnancy, the blood vessels may be comparatively narrower, limiting blood flow, he said.

"This reduces nutrient supply, thus reprogramming the regulation of fat and glucose, so that in later life, the individual is at risk of storing more fat and having insulin that works less effectively," he said. Insulin resistance, a condition in which a person's body cells do not use insulin effectively, is a risk factor for Type 2 diabetes...."

http://www.huffingtonpost.com/entry/first-born-women-at-higher-risk-of-overweigh...

I've been looking for a book that pulls together recent science on pro- and prebiotics to manage beneficial microbes in the gut--weed, seed, and feed as one blogger puts it. Not sure that this book quite does it, but, maybe?

From review of The Diet Myth; the Real Science Behind What We Eat by Tim Spector, Kings College Professor of Genetic Epidemiology and architect of British twins registry:

For 10 days, Tom Spector lived off McDonald’s. He had chicken nuggets or Big Macs for meals and McFlurries for dessert. Tom, a 22-year-old student, was re-creating a version of the diet made famous in the film Supersize Me. But Tom’s plan had a twist: Before and after the diet, he gave his dad some poop.

Tom’s father, Tim, wanted to see how the bacteria in Tom’s intestines dealt with junk food. Tim Spector, a genetic epidemiologist at Kings College London, thinks that the billions of bacteria in our guts may help explain health problems including obesity and allergies.

In The Diet Myth, Spector makes a convincing case. His son’s McDonald’s diet whittled down microbial diversity, which has been linked to health. The diet also swapped out friendly, diarrhea-preventing bacteria for ones that trigger inflammation. ...

Dairy products...high-fat milk, yogurt and cheese...actually seem to be good for you, Spector argues. But stick to cheddar, Gouda and other aged cheeses, he advises, or blue-veined varieties such as Roquefort. These cheeses are microbe metropolises and may keep people healthy, studies in humans have shown...

...To take care of your body, Spector suggests, take care of your microbes. That means mixing up your diet, he says.

Variety is key. Try to avoid antibiotics. And one thing most diet books can agree on: Lay off the McDonald’s.

https://www.sciencenews.org/article/microbes-make-meal-new-diet-book-proposes?tg...

From my superficial read, sounds like quantification of how we can use (soluble) fiber, legumes, yoghurt, fruits and vegetables work to influence BMI and cardiovascular health by influencing community of bacteria in the gut. Faecal transplants are no doubt best left to the experts. ;-)

J Fu et al, 2015. The Gut Microbiome Contributes to a Substantial Proportion of the Variation in Blood Lipids. Circulation Research. Published online before print September 10, 2015, doi: 10.1161/CIRCRESAHA.115.306807. http://circres.ahajournals.org/content/early/2015/09/09/CIRCRESAHA.115.306807.fu...

ABSTRACT

Rationale:
Evidence suggests the gut microbiome is involved in the development of cardiovascular disease (CVD), with the host-microbe interaction regulating immune and metabolic pathways. However, there was no firm evidence for associations between microbiota and metabolic risk factors for CVD from large-scale studies in humans. In particular, there was no strong evidence for association between CVD and aberrant blood lipid levels.

Objectives:
To identify intestinal bacteria taxa, whose proportions correlate with body mass index (BMI) and lipid levels, and to determine whether lipid variance can be explained by microbiota relative to age, gender and host genetics.

Methods and Results:
We studied 893 subjects from the LifeLines-DEEP population cohort. After
correcting for age and gender, we identified 34 bacterial taxa associated to BMI and blood lipids; most are novel associations. Cross-validation analysis revealed that microbiota explain 4.5% of the variance in BMI, 6% in triglycerides, and 4% in high-density lipoproteins (HDL), independent of age, gender and genetic
risk factors. A novel risk model including the gut microbiome explained up to 25.9% of HDL variance, significantly outperforming the risk model without microbiome. Strikingly, the microbiome had little effect on low-density lipoproteins or total cholesterol.

Conclusions:
Our studies suggest that the gut microbiome may play an important role in the variation in BMI and blood lipid levels, independent of age, gender and host genetics. Our findings support the potential of therapies altering the gut microbiome to control body mass, triglycerides and HDL.

... Discussion...Our results for the microbiota associated to BMI are in line with a recent study of 416 twin-pairs from the TwinsUK population; in particular, we confirmed that lower abundances of families Christensenellaceae, Rikenellaceae, class Mollicutes, genus Dehalobacterium and kingdom Archaea were associated to a high BMI. Of 22 independent taxa associated with BMI by our study, 16 were also accessed in the TwinsUK study: 11 (68.8%) showed significant association to BMI ... with the same direction of effect as we found (Online Table V). We also identified a correlation of decreased bacterial diversity with increased BMI, which is in line with previous observations.

However, many of the taxonomies we identified are novel findings. Several of the identified bacteria are known to be involved in the bile acid metabolic pathway. In particular, order Bacteroidales (phylum Bacteroidetes) and family Clostridiaceae
(phylum Firmicutes) are both negatively correlated with BMI and TG, and known to be involved in bile acid metabolism.

Bile acid activity of commensal bacteria are involved in a complex interplay with host hepatic enzymes, and together they promote digestion and absorption of dietary lipids.

Interestingly, several small-scale studies reported lowered cholesterol upon
using probiotics with bile salt hydrolytic activity.*

Our study found support for the role of bacterial bile acids in lipid metabolism. Another pathway enriched in several associated bacteria is short chain fatty acids
(SCFA) metabolism. Both orders Bacteroidales and Clostridiales, identified in our study, are involved in SCFA metabolism.

SCFA are produced by microbiota from dietary fibers, effect host body energy
homeostasis, and are protective against metabolic syndrome, type 2 diabetes, and atherosclerosis.

...In contrast to genetics, gender and age (all fixed characteristics), an individual’s microbiota composition can be modified by diet, pre- and probiotics, and fecal transplantation. Studies have shown that diet can alter the gut microbiome...

...*Hepner G, Fried R, St Jeor S, Fusetti L, Morin R. Hypocholesterolemic effect of yogurt and milk. Am J Clin Nutr. 1979;32:19–24.

*Hlivak P, Odraska J, Ferencik M, Ebringer L, Jahnova E, Mikes Z. One-year application of probiotic strain Enterococcus faecium M-74 decreases serum cholesterol levels. Bratisl Lek Listy. 2005;106:67–72...

Index approach used to interpret adults' risk has been adapted/proven for use in predicting younger people's risk, so they can see future and act to change lifestyle if needed. Accounts for gender and race, which is good since I understand non-obese SE Asians can develop type 2 diabetes, etc.

Metabolic Syndrome Severity Calculator:
http://publichealth.hsc.wvu.edu/biostatistics/metabolic-syndrome-severity-calcul...

...The new diagnostic test...relies on an evaluation of metabolic syndrome, a conglomeration of conditions including increased blood pressure, high levels of blood sugar, excessive body fat around the abdomen and waist and abnormal cholesterol levels that together increase the risk of cardiovascular disease. It takes into account variables specific both to race and gender.

...In creating the test, DeBoer and Gurka examined metabolic severity scores from children in the 1970s that assessed body mass index (BMI), systolic blood pressure, fasting triglycerides, HDL cholesterol and fasting glucose. The children were followed up as recently as 2014, at an average age of 49.6 years. “The current study was targeted at using that metabolic syndrome severity score on data from individuals who were children in the ‘70s to see if it correlated with their risk on developing CVD and type 2 diabetes later in life. We found that there was a high correlation between the metabolic severity score for those children and for their later development of cardiovascular disease and diabetes,” DeBoer explained.

...The test is innovative in that it is able to assess changes in metabolic syndrome severity in a person over time and creates a specific number predicting risk. Previous diagnostic tests have been merely positive or negative, stating that a person either has or does not have metabolic syndrome, but the new test is able to create a scale, delineating the precise degree to which a youth is at risk.

“We are hopeful that this score can be used to assess the baseline risk for adolescents regarding metabolic syndrome and their risk for future disease and use it as a motivator for individuals to try to change their risk so that they may have a healthier diet, engage in more physical activity or get medication to reduce their metabolic syndrome severity and their future risk for disease,” DeBoer said...

http://newsroom.uvahealth.com/about/news-room/archives/new-test-predicts-teens-f...

The Future of Dieting Is Personalized Algorithms Based on Your Gut Bacteria

http://nymag.com/scienceofus/2015/10/future-of-dieting-is-personalized-algorithm...

Study: added sugar linked to obesity and metabolic syndrome in children with these conditions--more specifically, fructose, i.e., a calorie is not a calorie.

RH Lustig et aI. 2015. Isocaloric Fructose Restriction and Metabolic Improvement in Children with Obesity and Metabolic Syndrome. Obesity (2015) 00, 00–00. doi:10.1002/oby.21371. https://s3.amazonaws.com/objects.readcube.com/articles/downloaded/wile/8268151c6...

Conclusion
Concerns surrounding the role of sugar consumption in chronic disease have previously focused on its caloric equivalence and its role in fomenting increases in weight. Furthermore, previous clinical studies have relied upon excessive sugar administration, which introduces experimental artifact. This study mitigates all three of these concerns by intervening in children who are already sick with metabolic syndrome and by adjusting for effects of calories, weight gain, and adiposity. This study argues that the health detriments of sugar, and fructose specifically, are independent of its caloric value or effects on weight. Further studies will be required to determine whether sugar restriction alone can impact metabolic syndrome in adults and whether such effects are short-lived or long-term.

Infodump. Information overload. I've found over the years that when I post something relating to outside sources, I'm satisfied with providing a link or two to help prove my point or to document the source of my point. A glut of information won't persuade. On the contrary, it encourages people to shut down.

Sign of the times.

You are right, of course, but you may wish to skip this topic, as I intend to continue. There seems to be so much misinformation on obesity, etc., and people willing to argue against all evidence that "a calorie is a calorie", etc., that a little science is warranted!!

I for one am glad every time I see that @margd has added to this topic.

Robert

Me, too.

Relieved that others also find this stuff interesting!

Some presentations from American Heart Association conference, not yet published but covered in Science News article (https://www.sciencenews.org/article/simple-steps-can-offer-health-benefits):

B. Kingwell et al. Interrupting Prolonged Sitting Reduces Resting Blood Pressure and Plasma Norepinephrine in Adults with Type 2 Diabetes. American Heart Association Scientific Sessions, Orlando, Florida, November 9, 2015.

M. Chui et al. Moving to a Highly Walkable Neighborhood and Incidence of Hypertension: A Propensity-score Matched Cohort Study. American Heart Association Scientific Sessions, Orlando, Florida, November 8, 2015.

H. Tsuji et al. Commuting by Public Transportation is Associated with Lower Prevalence of Excess Body Weight, Hypertension, and Diabetes. American Heart Association Scientific Sessions, Orlando, Florida, November 8, 2015.

G. Zong et al. Frequent Consumption of Meals Prepared at Home and Risk of Type 2 Diabetes among American Men and Women. American Heart Association Scientific Sessions, Orlando, Florida, November 8, 2015.

Amazing--some people's blood sugar spike more after low GI foods (tomatoes!) than high (cookies, ice cream). Researchers find our person-to-person responses to various foods highly variable:

The Algorithm That Creates Diets That Work for You
It crunches hundreds of factors to make personalized plans for controlling blood sugar. Some people even get cake and cookies.
http://www.theatlantic.com/science/archive/2015/11/algorithm-creates-diets-that-...

*****************************************

D Zeevi et al. 2015. Personalized Nutrition by Prediction of Glycemic Responses. Volume 163, Issue 5, p1079–1094, 19 November 2015. http://dx.doi.org/10.1016/j.cell.2015.11.001 .
http://www.cell.com/abstract/S0092-8674%2815%2901481-6

...our results suggest that personalized diets may successfully modify elevated postprandial blood glucose and its metabolic consequences...

My bacteria made me do it!

Gut microbes signal to the brain when they are full (or not!)
http://medicalxpress.com/news/2015-11-gut-microbes-brain-full.html

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Breton et al. 2015. "Gut Commensal E.coli Proteins Activate Host Satiety Pathways Following Nutrient-Induced Bacterial Growth",Cell Metabolism. dx.doi.org/10.1016/j.cmet.2015.10.017
http://www.cell.com/cell-metabolism/abstract/S1550-4131%2815%2900566-5

Summary

The composition of gut microbiota has been associated with host metabolic phenotypes, but it is not known if gut bacteria may influence host appetite. Here we show that regular nutrient provision stabilizes exponential growth of E. coli, with the stationary phase occurring 20 min after nutrient supply accompanied by bacterial proteome changes, suggesting involvement of bacterial proteins in host satiety. Indeed, intestinal infusions of E. coli stationary phase proteins increased plasma PYY and their intraperitoneal injections suppressed acutely food intake and activated c-Fos in hypothalamic POMC neurons, while their repeated administrations reduced meal size. ClpB, a bacterial protein mimetic of α-MSH, was upregulated in the E. coli stationary phase, was detected in plasma proportional to ClpB DNA in feces, and stimulated firing rate of hypothalamic POMC neurons. Thus, these data show that bacterial proteins produced after nutrient-induced E. coli growth may signal meal termination. Furthermore, continuous exposure to E. coli proteins may influence long-term meal pattern.

Stored fat produces protein (sLR11) that fights body’s attempts to lose weight

Press Release: http://www.cam.ac.uk/research/news/stored-fat-fights-against-the-bodys-attempts-...

**************************************************

Whittle, AJ, Jiang, M, et al. Soluble LR11/SorLA represses thermogenesis in adipose tissue and correlates with BMI in humans. Nature Communications; 20 November 2015. http://www.nature.com/ncomms/2015/151120/ncomms9951/full/ncomms9951.html

Abstract. Thermogenesis in brown adipose tissue (BAT) is an important component of energy expenditure in mammals. Recent studies have confirmed its presence and metabolic role in humans. Defining the physiological regulation of BAT is therefore of great importance for developing strategies to treat metabolic diseases. Here we show that the soluble form of the low-density lipoprotein receptor relative, LR11/SorLA (sLR11), suppresses thermogenesis in adipose tissue in a cell-autonomous manner. Mice lacking LR11 are protected from diet-induced obesity associated with an increased browning of white adipose tissue and hypermetabolism. Treatment of adipocytes with sLR11 inhibits thermogenesis via the bone morphogenetic protein/TGFβ signalling pathway and reduces Smad phosphorylation. In addition, sLR11 levels in humans are shown to positively correlate with body mass index and adiposity. Given the need for tight regulation of a tissue with a high capacity for energy wastage, we propose that LR11 plays an energy conserving role that is exaggerated in states of obesity.

Obese dads can pass on obesity tendency to children they father (epigenetics):

http://www.newsweek.com/fathers-can-pass-down-traits-through-sperm-400902

http://www.cell.com/pb-assets/journals/research/cell-metabolism/on/cmet1935_r.pd...

In several ways, 5 c of beans a week is health-equivalent to calorie restriction (500 calories?)!

(IMHO, balela is tasty way to get those beans: http://allrecipes.com/recipe/218648/balela-salad/ )

***************************************************************

R C Mollard, B L Luhovyy, S Panahi, M Nunez, A Hanley, G H Anderson. Regular consumption of pulses for 8 weeks reduces metabolic syndrome risk factors in overweight and obese adults. Br J Nutr 2012 108 - Suppl - 1:S111 – 22. http://www.ncbi.nlm.nih.gov/pubmed/22916807 . http://journals.cambridge.org/download.php?file=%2FBJN%2FBJN108_S1%2FS0007114512... .

...In conclusion, five cups of pulses/week incorporated into
the participants’ habitual diet spontaneously led to health ben-
efits without dietary counselling and these benefits were simi-
lar to those seen with energy restriction dietary counselling.
Also, there were further benefits to pulse consumption com-
pared with an energy-restricted diet, including greater
improvements in glycaemic control and increased HDL.
From these findings, it can be speculated that the continuation
of the pulse diet beyond 8 weeks would have led to a further
reduction in waist circumference and improvements in post-
prandial blood glucose and HDL, and eventual weight loss
(based on 24 h food recalls), which would reduce the risk of
the MetSyn and related chronic diseases. Thus, these results
support the recommendation of regularly consuming pulses
for the prevention or management of risk factors of the
MetSyn

A hormone found in the liver has the ability to reduce sweet and alcohol cravings in mammals (mice and monkeys), a recent study found...fibroblast growth factor 21 (FGF21), works through the brain's reward system to weaken cravings. It is induced in the body by extreme cold temperatures, sudden changes in diet and in carbohydrate consumption...http://www.upi.com/Health_News/2015/12/26/Study-Liver-hormone-regulates-sweet-alcohol-preferences/8271451143498/

S Talukda et al. 2015. FGF21 Regulates Sweet and Alcohol Preference. Cell Metabolism. Published online Dec. 24, 2015. DOI: http://dx.doi.org/10.1016/j.cmet.2015.12.008 . http://www.cell.com/cell-metabolism/abstract/S1550-4131%2815%2900623-3

Ironic, given the Flint debacle in the news, but, small, significant reduction in childhood obesity in NY schools which installed water jets--chilled, oxygenated water dispensed into cups:

AE Schwartz et al. 2016. Effect of a School-Based Water Intervention on Child Body Mass Index and Obesity. JAMA Pediatrics. Jan 16, 2016.
http://archpedi.jamanetwork.com/article.aspx?articleid=2480887

Conclusion: Decreasing the amount of caloric beverages consumed and simultaneously increasing water consumption is important to promoting child health and decreasing the prevalence of childhood obesity. Moreover, schools are a natural setting for such interventions, and many policy makers are turning attention to promoting water drinking among students. Results from this study show an association between a relatively low-cost water availability intervention and decreased student weight. Additional research is needed to examine potential mechanisms for decreased student weight, including reduced milk taking, as well as assessing impacts on longer-term outcomes. Water jets could be an important part of the toolkit for obesity reduction techniques at the school setting.

>125 margd: That's interesting. My children's school's lunchroom has dispensers offering still or sparkling water. Germans tend to prefer sparkling water to tap and drink far less soda. I wonder if we just respond to having something "special" to drink?

Avoid middle age spread with high flavonoid fruits and vegetables, e.g., apples, pears, berries esp blue, prunes, grapes, peppers, celery, onions...tea? OJ? TJ? (See Figure 1 in paper.)

M. Bertoia et al. 2016. Dietary flavonoid intake and weight maintenance: three prospective cohorts of 124,086 US men and women followed for up to 24 years. BMJ 2016;352:i17:http://dx.doi.org/10.1136/bmj.i17 . http://www.bmj.com/content/352/bmj.i17

Conclusions and policy implications
These data may help to refine previous dietary recommendations for the prevention of obesity and its potential consequences. Our results suggest that choosing high flavonoid fruits and vegetables, such as apples, pears, berries, and peppers, may help with weight control. Most Americans consume less than one cup (less than two servings) of fruits and less than two cups of vegetables daily, and juice and potatoes are major contributors to intake. Beyond increasing intake to current recommendations of two cups of fruit and 2.5 cups of vegetables per day,39 people may be able to maximize their health benefit by including optimal fruits and vegetables in their daily diets.

A study of 40,000 shows limitations of using BMI as indicator for cardiovascular and metabolic health:

A J Tomiyama, J M Hunger, J Nguyen-Cuu and C Wells. 2016. Misclassification of cardiometabolic health when using body mass index categories in NHANES 2005–2012. Short Communication.
International Journal of Obesity accepted article preview 4 February 2016; doi: 0.1038/ijo.2016.17 . http://www.nature.com/ijo/journal/vaop/naam/abs/ijo201617a.html

Abstract .... Nearly half of overweight individuals, 29% of obese individuals, and even 16% of obesity type II/III individuals were metabolically healthy. Moreover, over 30% of normal weight individuals were cardiometabolically unhealthy. ... Using BMI categories as the main indicator of health, an estimated 74 936 678 US adults are misclassified as cardiometabolically unhealthy or cardiometabolically healthy. Policymakers should consider the unintended consequences of relying solely on BMI, and researchers should seek to improve diagnostic tools related to weight and cardiometabolic health.

**********************************************************
Authors say:

data show there are tens of millions of people who are overweight and obese and are perfectly healthy

(such people would be) unlikely incur higher medical expenses, and it would be unfair to charge them more for health care premiums

people (should) focus on eating a healthy diet and exercising regularly, rather than obsessing about their weight

strongly oppose(d to) stigmatizing people who are overweight.

http://newsroom.ucla.edu/releases/dont-use-body-mass-index-to-determine-whether-...

Soon to be published in PNAS, research by Shuai Liu (U Calgary) links consumption of fatty, sweetened food to over-eating--changing mouse synapses at least. The effect is quick and lasts about a week. (Means that paczki is just now wearing off??)

http://www.calgarysun.com/2016/02/15/u-of-c-study-links-junk-food-to-overeating

Vegan MD Michael Greger argues the importance of fiber in combating obesity. (He's sometimes accused of cherry-picking, and I think I see it sometimes, but he sure has me eating more plants!):

Paleopoo: What We Can Learn from Fossilized Feces (5:05)
Ancient dietary practices based on analyzing the fiber content of fossilized human waste can give us insights for combating the modern obesity epidemic.
http://nutritionfacts.org/video/paleopoo-what-we-can-learn-from-fossilized-feces...

Video Sources

J H Cummings. Topics in Dietary Fiber Research. Gut. 1978 Nov; 19(11): 1087.

K K Ryan, R J Seeley. Food as a Hormone. Science. 2013 Feb 22; 339(6122): 918–919.

K M Tuohy, C Gougoulias, Q Shen, G Walton, F Fava, P Ramnani. Studying the human gut microbiota in the trans-omics era--focus on metagenomics and metabonomics. Curr Pharm Des. 2009;15(13):1415-27.

NA. Who are we? Nature 453, 563 (29 May 2008).

G S Frost, G E Walton, J R Swann, A Psichas, A Costabile, L P Johnson, M Sponheimer, G R Gibson, T G Barraclough. Impacts of plant-based foods in ancestral hominin diets on the metabolism and function of gut microbiota in vitro. MBio. 2014 May 20;5(3):e00853-14.

C M Hladik, P Pasquet. The human adaptations to meat eating: a reappraisal. Human Evolution, Springer Verlag, 2002, 17, pp.199-206.

P S Ungar, M Sponheimer. The Diets of Early Hominins. Science 14 Oct 2011: Vol. 334, Issue 6053, pp. 190-193.

C M Hladik, P Pasquet. The human adaptations to meat eating: a reappraisal. Human Evolution, Springer Verlag, 2002, 17, pp.199-206.

M L Sleeth, E L Thompson, H E Ford, S E Zac-Varghese, G Frost. Free fatty acid receptor 2 and nutrient sensing: a proposed role for fibre, fermentable carbohydrates and short-chain fatty acids in appetite regulation. Nutr Res Rev. 2010 Jun;23(1):135-45.

T Ulven. Short-chain free fatty acid receptors FFA2/GPR43 and FFA3/GPR41 as new potential therapeutic targets. Front Endocrinol (Lausanne). 2012 Oct 2;3:111.

New study shows food sound (of chewing, crunching) is an important sensory cue in the eating experience. New doctor’s orders: No earbuds, no music, and no watching TV while eating.

https://news.byu.edu/news/sounds-eating-may-reduce-how-much-you-eat#sthash.jxCPp...

http://www.ibnlive.com/news/lifestyle-2/listening-to-yourself-chew-could-help-yo...

Enzyme in mouse brain appears to govern amount eaten:

Olof Lagerlöf et al.. 2016. The nutrient sensor OGT in PVN neurons regulates feeding.
Science 18 Mar 2016: Vol. 351, Issue 6279, pp. 1293-1296
DOI: 10.1126/science.aad5494
http://science.sciencemag.org/content/351/6279/1293

When enough isn't enough
Overeating and obesity are rapidly becoming worldwide problems. Normally, mice do not overeat—they balance their caloric intake with their caloric needs. Lagerlöf et al. deleted an enzyme called O-GlcNAc transferase (OGT) from a subset of neurons in the mouse hypothalamus (see the Perspective by Schwartz). After the loss of OGT, the animals began to overeat and rapidly gained weight. The animals ate more at meal times, rather than eating more often. Thus, OGT seems to regulate satiety and helps to couple caloric intake to caloric need.

Eating beans, peas, chickpeas or lentils may help lose weight and keep it off
http://www.stmichaelshospital.com/media/detail.php?source=hospital_news/2016/033...

Eating one serving a day of beans, peas, chickpeas or lentils could contribute to modest weight loss, a new study suggests.

Eating about 3/4 cup (130 grams) each day of these foods known as pulses led to a weight loss of 0.34 kilograms (just over half a pound), in a systematic review and meta-analysis of all available clinical trials on the effects of eating pulses.

The paper, by lead author Dr. Russell de Souza, a researcher with the Li Ka Shing Knowledge Institute of St. Michael’s Hospital, was published today in The American Journal of Clinical Nutrition.

The research builds on previous work by the hospital’s Clinical Nutrition and Risk Factor Modification Centre, that a daily serving of pulses makes people feel fuller than if they ate a control diet, and that eating pulses can significantly reduce “bad cholesterol.”

“Despite their known health benefits, only 13 per cent of Canadians eat pulses on any given day and most do not eat the full serving,” Dr. de Souza said. “So there is room for most of us to incorporate dietary pulses in our diet and realize potential weight management benefits.” ...

*********************************************

Effects of dietary pulse consumption on body weight: a systematic review and meta-analysis of randomized controlled trials Am J Clin Nutr ajcn124677; First published online March 30, 2016. http://ajcn.nutrition.org/content/early/2016/03/30/ajcn.115.124677.full.pdf+html

BPA

Despite the push to remove bisphenol A from food packaging, the industrial chemical linked to obesity and insulin resistance is still present in an “alarming” number of food can linings and lids collected in Ontario and 19 states. http://www.ctvnews.ca/health/health-headlines/alarming-number-of-canned-foods-st...

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The Report:

Buyer Beware: BPA and regrettable substitutes found in linings of canned food. A report by Breast Cancer Fund, Campaign for Healthier Solutions, and the Environmental Defence in Canada. et al. 2016. (76p) http://www.toxicfoodcans.org/wp-content/uploads/2016/03/BPA-BuyerBeware.pdf

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Six Tips for Avoiding BPA in Food:

http://www.ctvnews.ca/health/health-headlines/infographic-6-tips-for-avoiding-bp...

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FDA’s current perspective, based on its most recent safety assessment, is that BPA is safe at the current levels occurring in foods. Based on FDA’s ongoing safety review of scientific evidence, the available information continues to support the safety of BPA for the currently approved uses in food containers and packaging. http://www.fda.gov/NewsEvents/PublicHealthFocus/ucm064437.htm#summary

Health Canada's Food Directorate has concluded that the current dietary exposure to BPA through food packaging uses is not expected to pose a health risk to the general population, including newborns and infants. http://www.hc-sc.gc.ca/fn-an/securit/packag-emball/bpa/index-eng.php

2 servings per day for 24 weeks of Lactobacillus rhamnosus typically found in a single serving of yogurt almost doubled weight loss in WOMEN during 12 weeks of diet, kept it off (actually lost a bit more), with less fat mass and leptin, "a key player in regulating appetite and metabolism".

http://www.npr.org/sections/thesalt/2014/02/05/271153568/ladies-good-bacteria-in...

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Sanchez M et al. 2014. Effect of Lactobacillus rhamnosus CGMCC1.3724 supplementation on weight loss and maintenance in obese men and women.
Br J Nutr. 2014 Apr 28;111(8):1507-19. doi: 10.1017/S0007114513003875. Epub 2013 Dec 3.

Abstract

The present study investigated the impact of a Lactobacillus rhamnosus CGMCC1.3724 (LPR) supplementation on weight loss and maintenance in obese men and women over 24 weeks. In a double-blind, placebo-controlled, randomised trial, each subject consumed two capsules per d of either a placebo or a LPR formulation (1.6 × 10(8) colony-forming units of LPR/capsule with oligofructose and inulin). Each group was submitted to moderate energy restriction for the first 12 weeks followed by 12 weeks of weight maintenance. Body weight and composition were measured at baseline, at week 12 and at week 24. The intention-to-treat analysis showed that after the first 12 weeks and after 24 weeks, mean weight loss was not significantly different between the LPR and placebo groups when all the subjects were considered. However, a significant treatment × sex interaction was observed. The mean weight loss in women in the LPR group was significantly higher than that in women in the placebo group (P = 0.02) after the first 12 weeks, whereas it was similar in men in the two groups (P= 0.53). Women in the LPR group continued to lose body weight and fat mass during the weight-maintenance period, whereas opposite changes were observed in the placebo group. Changes in body weight and fat mass during the weight-maintenance period were similar in men in both the groups. LPR-induced weight loss in women was associated not only with significant reductions in fat mass and circulating leptin concentrations but also with the relative abundance of bacteria of the Lachnospiraceae family in faeces. The present study shows that the Lactobacillus rhamnosus CGMCC1.3724 formulation helps obese women to achieve sustainable weight loss.

Japanese study shows weight loss of 5 lbs over 12 weeks with daily consumption of 2 T vinegar. Visceral fat, especially.

T Kondo, M Kishi, T Fushimi, S Ugajin, T Kaga. 2009. Vinegar intake reduces body weight, body fat mass, and serum triglyceride levels in obese Japanese subjects. Biosci Biotechnol Biochem. 2009 Aug;73(8):1837-43. http://www.ncbi.nlm.nih.gov/pubmed/19661687

http://nutritionfacts.org/video/apple-cider-vinegar-help-weight-loss/?utm_source...

After ‘The Biggest Loser,’ Their Bodies Fought to Regain Weight

...resting metabolism, which determines how many calories a person burns when at rest. When the show began, the contestants, though hugely overweight, had normal metabolisms for their size, meaning they were burning a normal number of calories for people of their weight. When it ended, their metabolisms had slowed radically and their bodies were not burning enough calories to maintain their thinner sizes.

...What shocked the researchers was what happened next: As the years went by and the numbers on the scale climbed, the contestants’ metabolisms did not recover. They became even slower, and the pounds kept piling on. It was as if their bodies were intensifying their effort to pull the contestants back to their original weight.

Mr. Cahill was one of the worst off. As he regained more than 100 pounds, his metabolism slowed so much that, just to maintain his current weight of 295 pounds, he now has to eat 800 calories a day less than a typical man his size. Anything more turns to fat.

...“The key point is that you can be on TV, you can lose enormous amounts of weight, you can go on for six years, but you can’t get away from a basic biological reality,” said Dr. Schwartz, who was not involved in the study. “As long as you are below your initial weight, your body is going to try to get you back.”

http://www.nytimes.com/2016/05/02/health/biggest-loser-weight-loss.html?_r=0

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Fothergill, E., Guo, J., Howard, L., Kerns, J. C., Knuth, N. D., Brychta, R., Chen, K. Y., Skarulis, M. C., Walter, M., Walter, P. J. and Hall, K. D. (2016), Persistent metabolic adaptation 6 years after “The Biggest Loser” competition. Obesity. doi: 10.1002/oby.21538. http://onlinelibrary.wiley.com/doi/10.1002/oby.21538/full

Healthiest weight just might be ‘overweight’

...As a group, overweight people are living the longest nowadays, suggests an almost four-decade study in Denmark published May 10 in JAMA. And obese people seem to be at no higher risk of dying than those of normal weight. The new analysis fuels ongoing debate about what’s a healthy body mass index — especially in light of rising obesity rates, improved heart health treatments and other factors influencing health and longevity.

...A new study of more than 100,000 adults from Copenhagen shows that, since the 1970s, the healthiest BMI has shifted from 23.7 to 27...

https://www.sciencenews.org/article/healthy-weight-bmi-overweight?tgt=nr

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S. Afzal et al. Change in body mass index associated with lowest mortality in Denmark, 1976-2013. JAMA. Vol. 315, May 10, 2016, p. 1989. doi:10.1001/jama.2016.4666. http://jama.jamanetwork.com/article.aspx?articleid=2520627

Importance Research has shown a U-shaped pattern in the association of body mass index (BMI) with mortality. Although average BMI has increased over time in most countries, the prevalence of cardiovascular risk factors may also be decreasing among obese individuals over time. Thus, the BMI associated with lowest all-cause mortality may have changed.

...Conclusions and Relevance Among 3 Danish cohorts, the BMI associated with the lowest all-cause mortality increased by 3.3 from cohorts enrolled from 1976-1978 through 2003-2013. Further investigation is needed to understand the reason for this change and its implications.

Brain cells that aid appetite control identified
http://publications.mcgill.ca/medenews/2016/05/12/brain-cells-that-aid-appetite-...

...The McGill research team has now discovered that without a particular group of cells (known as NG2-glia cells) in place in the median eminence, the leptin receptors in the brain never receive the messages from the body telling it that it is sated.

“Most of the brain is a well-protected fortress, designed to shelter delicate nerve cells,” says Kokoeva. “The median eminence is outside these protections, and so can be a dangerous environment for the nerve cells that detect leptin. We think that the NG2-glia cells act to support and shelter the leptin receptor neurons, enabling them to instruct the body when to stop eating.”...

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Tina Djogo et al. 2016. Adult NG2-Glia Are Required for Median Eminence-Mediated Leptin Sensing and Body Weight Control. Cell Metabolism. Volume 23, Issue 5, p797–810, 10 May 2016
http://www.cell.com/cell-metabolism/abstract/S1550-4131%2816%2930164-4
http://www.cell.com/cell-metabolism/abstract/S1550-4131%2816%2930164-4

Highlights

•Pharmacological and genetic ablation of NG2-glia, but not microglia, leads to obesity
•NG2-glial ablation causes LepR processes in the median eminence to degenerate
•Arcuate nucleus LepR neurons lose responsiveness to leptin after NG2-glia ablation
•X-irradiation aimed at the median eminence is sufficient for weight gain induction

Summary

While leptin is a well-known regulator of body fat mass, it remains unclear how circulating leptin is sensed centrally to maintain energy homeostasis. Here we show that genetic and pharmacological ablation of adult NG2-glia (also known as oligodendrocyte precursors), but not microglia, leads to primary leptin resistance and obesity in mice. We reveal that NG2-glia contact the dendritic processes of arcuate nucleus leptin receptor (LepR) neurons in the median eminence (ME) and that these processes degenerate upon NG2-glia elimination, which explains the consequential attenuation of these neurons’ molecular and electrical responses to leptin. Our data therefore indicate that LepR dendrites in the ME represent the principal conduits of leptin’s anorexigenic action and that NG2-glia are essential for their maintenance. Given that ME-directed X-irradiation confirmed the pharmacological and genetically mediated ablation effects on body weight, our findings provide a rationale for the known obesity risk associated with cranial radiation therapy.

...The study showed blue-enriched light exposure acutely altered metabolic function in both the morning and the evening compared to dim light. While morning and evening blue-enriched light exposure both resulted in higher insulin resistance, evening blue-enriched light led to higher peak glucose. This suggests a greater inability of insulin to adequately compensate for the increase in glucose in the evening.

http://www.sleepreviewmag.com/2016/05/bright-light-exposure-meals-increases-insu...

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Ivy N Cheunget al. 2016. Morning and Evening Blue-Enriched Light Exposure Alters Metabolic Function in Normal Weight Adults. PLOS. May 18, 2016.
http://dx.doi.org/10.1371/journal.pone.0155601 . http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0155601 .

Abstract

Increasing evidence points to associations between light-dark exposure patterns, feeding behavior, and metabolism. This study aimed to determine the acute effects of 3 hours of morning versus evening blue-enriched light exposure compared to dim light on hunger, metabolic function, and physiological arousal. Nineteen healthy adults completed this 4-day inpatient protocol under dim light conditions: less than 20lux. Participants were randomized to 3 hours of blue-enriched light exposure on Day 3 starting either 0.5 hours after wake...n = 9; morning group...or 10.5 hours after wake...n = 10; evening group. All participants remained in dim light on Day 2 to serve as their baseline. Subjective hunger and sleepiness scales were collected hourly. Blood was sampled at 30-minute intervals for 4 hours in association with the light exposure period for glucose, insulin, cortisol, leptin, and ghrelin. Homeostatic model assessment of insulin resistance...HOMA-IR...and area under the curve...AUC...for insulin, glucose, HOMA-IR and cortisol were calculated. Comparisons relative to baseline were done using t-tests and repeated measures ANOVAs. In both the morning and evening groups, insulin total area, HOMA-IR, and HOMA-IR AUC were increased and subjective sleepiness was reduced with blue-enriched light compared to dim light. The evening group, but not the morning group, had significantly higher glucose peak value during blue-enriched light exposure compared to dim light. There were no other significant differences between the morning or the evening groups in response to blue-enriched light exposure. Blue-enriched light exposure acutely alters glucose metabolism and sleepiness, however the mechanisms behind this relationship and its impacts on hunger and appetite regulation remain unclear. These results provide further support for a role of environmental light exposure in the regulation of metabolism.

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margd: Opthalmologists have been offering yellow tinted replacement lenses in cataract surgery to filter blue light, and thus protect against age-related degeneration of the macula. Hopefully, tradeoffs for individual patients will be weighed as more is learned about the role of blue light in regulating sleep and metabolism.

Contain BMI and avoid insomnia: two good reasons to wear yellow glasses if one must use computer screens in the evening? Also, don't wear blue-screening sunglasses on one's morning walk?

Ramon Estruch et al. 2016. Effect of a high-fat Mediterranean diet on bodyweight and waist circumference: a prespecified secondary outcomes analysis of the PREDIMED randomised controlled trial> Lancet Diabetes & Endocrinology: June 6, 2106. http://dx.doi.org/10.1016/S2213-8587(16)30085-7 | http://www.thelancet.com/journals/landia/article/PIIS2213-8587%2816%2930085-7/ab...

Summary
...Interpretation

A long-term intervention with an unrestricted-calorie, high-vegetable-fat Mediterranean diet was associated with decreases in bodyweight and less gain in central adiposity compared with a control diet. These results lend support to advice not restricting intake of healthy fats (olive oil, nuts in Mediterranean Diet) for bodyweight maintenance.

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Counting calories IS a waste of time: Mediterranean diet rich in 'good' fats 'is the BEST way to lose weight'

http://www.dailymail.co.uk/health/article-3628227/Counting-calories-waste-time-M...

Interesting, unconventional theory that associates a chicken virus with obesity in humans. (Chickens are raised in close proximity to one another, facilitating spread of virus, and producers probably favor fast growth, so if virus plumps up chickens, it might be selected for... Many pathogens that we take for granted have origins in domestic animals...)

Virus in Chicken Could Be Linked to Obesity
Michael Greger M.D., June 7th, 2016
http://nutritionfacts.org/2016/06/07/virus-in-chicken-could-be-linked-to-obesity...

...Most studies done to date on adults have found a connection between exposure to Ad-36 and obesity, and all studies done so far on childhood obesity show an increase in prevalence of infection in obese children compared to non-obese children. We’re now up to more than a thousand children studied with similar findings. Obese children who tested positive for the virus weighed 35 pounds more than children who tested negative.

The virus appears to both increase the number of fat cells by mobilizing precursor stem cells and increase the accumulation of fat within the cells. If we take liposuction samples of fat from people, the fat cell precursors turn into fat cells at about five times the rate in people who came to the liposuction clinic already infected. Fat taken from non-infected people that was then exposed to the virus start sucking up fat at a faster rate, potentially inducing obesity without increasing food intake.

Just as Ad-36 can be transmitted horizontally from one infected chicken to another in the same cage, subsequently causing obesity in each chicken, this same virus is also easily transmitted among humans, raising the question as to whether at least some cases of childhood obesity can be considered an infectious disease. Researchers publishing in the International Journal of Pediatric Obesity speculate that this animal adenovirus may have mutated to become a human adenovirus capable of infecting humans and causing obesity.

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One of the articles cited by Greger:

Lin WY et al. 2013. Long-term changes in adiposity and glycemic control are associated with past adenovirus infection. Diabetes Care. 2013 Mar;36(3):701-7. doi: 10.2337/dc12-1089. Epub 2012 Nov 16. http://www.ncbi.nlm.nih.gov/pubmed/23160725

CONCLUSIONS:

This study strengthens the plausibility that in humans, Ad36 increases adiposity and attenuates deterioration of glycemic control. Panoptically, the study raises the possibility that certain infections may modulate obesity or diabetes risk. A comprehensive understanding of these under-recognized factors is needed to effectively combat such metabolic disorders.

Soluble fiber (and exercise) is associated with less visceral fat accumulation over five years. Soluble fiber is found in foods such as steel cut oatmeal, beans/legumes, cruciferous vegetables and fruit, onions, and in powder-supplements such as inulin and acacia senegal.

Kristen G Hairston et al. 2012. Lifestyle Factors and 5-Year Abdominal Fat Accumulation in a Minority Cohort: The IRAS Family Study. Obesity (Silver Spring). 2012 Feb; 20(2): 10.1038/oby.2011.171. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3856431/

...Soluble fiber intake and participation in vigorous activity were inversely related to change in VAT (Visceral Adipose Tissue), independent of change in BMI. For each 10 g increase in soluble fiber, rate of VAT accumulation decreased by 3.7% .... Soluble fiber was not associated with change in SAT (Subcutaneous Adipose Tissue)... Moderately active participants had a 7.4% decrease in rate of VAT accumulation and a 3.6% decrease in rate of SAT accumulation versus less active participants .... Total energy expenditure was also inversely associated with accumulation of VAT. Soluble fiber intake and increased physical activity were related to decreased VAT accumulation over 5 years.

The decline in smoking can explain as much as 4 percent of the increase in obesity in the U.S. over 30 years, the biggest driving factor that the researchers analyzed.

Baum and Chou. 2016.
Why has the prevalence of obesity doubled? Review of Economics of the Household. June 2016, Volume 14, Issue 2, pp 251-267. http://link.springer.com/journal/11150

I wonder how reverse feeding tube compares with bariatric surgery and rubber bands with respect to diabetes development and changes in gastro-intestinal microbiome. Weird at first blush, but seems to have worked for fellow interviewed in article?

Reverse feeding tube developed in St. Louis is approved to treat obesity

http://www.stltoday.com/lifestyles/health-med-fit/health/reverse-feeding-tube-de...

K Obayeshi et al. 2016. Ambient Light Exposure and Changes in Obesity Parameters: A Longitudinal Study of the HEIJO-KYO Cohort. J of Clinical Endocrinology and Metabolism. First Published Online: July 06, 2016. http://press.endocrine.org/doi/10.1210/jc.2015-4123

CONCLUSIONS:

Ambient light exposure, such as increased nighttime or evening light exposure and decreased morning light exposure, was independently associated with subsequent increases in obesity parameters. Further interventional studies are warranted to establish an optimal controlled lighting environment as a preventive option against obesity.

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...Younger people are more sensitive to ambient light than the elderly, (the author) noted, so it may have even more of an effect for them...Trying to get more sunlight in daytime and less artificial light from TVs, smartphones and bedroom lights at night may be best for obesity prevention, he said.

http://www.huffingtonpost.com/entry/the-amount-of-light-in-your-bedroom-could-up...

J.A. Gonzáles et al. Inhibitory interplay between orexin neurons and eating. Current Biology. Published online August 18, 2016. doi: 10.1016/j.cub.2016.07.013. (Can't access at the moment.)

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Fractions of a second after food hits the mouth, a specialized group of energizing nerve cells in mice shuts down. After the eating stops, the nerve cells spring back into action, scientists report August 18 in Current Biology. This quick response to eating offers researchers new clues about how the brain drives appetite and may also provide insight into narcolepsy.

...The results suggest that giving orexin to people who lack it may reduce obesity. But that might not be a good idea. An overactive orexin system has been tied to stress and anxiety, Burdakov says. Orexin’s link to stress raises a different possibility —that anxiety can be reduced by curbing orexin nerve cell activity. “And our study suggests that the act of eating can do just that,” Burdakov says. “This provides a candidate explanation for why people turn to eating at times of anxiety.”

https://www.sciencenews.org/article/eating-shuts-down-nerve-cells-counter-obesit...

Zap to the head leads to fat loss
Stimulating vestibular nerve to reduce obesity shows promise in small study

A nerve-zapping headset caused people to shed fat in a small preliminary study.

Six people who had received the stimulation lost on average about 8 percent of the fat on their trunks in four months, scientists reported November 12 at the annual meeting of the Society for Neuroscience.

The headset stimulated the vestibular nerve, which runs just behind the ears. That nerve sends signals to the hypothalamus, a brain structure thought to control the body’s fat storage. By stimulating the nerve with an electrical current, the technique shifts the body away from storing fat toward burning it, scientists propose...

...Earlier studies had found that vestibular nerve stimulation causes mice to drop fat and pack on muscle, resulting in what McKeown called Schwarzenegger mice. Though small, the current study suggests that the approach has promise in people. McKeown and colleagues have started a company based on the technology and plan to test it further, he said.

https://www.sciencenews.org/article/zap-head-leads-fat-loss

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J. McKeown et al. Modulation of body mass composition using galvanic vestibular stimulation. Neuroscience 2016, San Diego, November 12, 2016. http://www.abstractsonline.com/pp8/index.html#!/4071/presentation/20259

Abstract
In a series of experiments participants consumed high calorie diets for prolonged periods, in some cases up to 10,000 calories a day, while at the same time refraining from physical exercise. In most cases the subjects gained a surprisingly modest amount of weight. This observation supports the concept that there is a "set-point" for body mass composition as modulated by the hypothalamus. Deviation too far in either direction from this set-point is restricted by ill-understood mechanisms.

It has been known for some time that animals living in a state of chronic centrifugation show a marked change in their body mass composition. In particular, they go through a process of "de-fatting", with their total body fat dropping from in excess of 20% to around 5%. Experiments using a type of mutant mouse that is missing the otolith organs from its inner ear have shown that, rather than being a non-specific effect of hypergravity, this change in body mass composition appears to be mediated by a specific vestibulo-hypothalamic pathway.

We attempted to replicate its effect by stimulating the otolith organs using galvanic vestibular stimulation (GVS). This technology involves passing a small electric current into the skin overlying the mastoid process, and has been shown at currents less than 3mA to preferentially activate the otolith organs.

In a pilot study we recruited 10 overweight (BMI 25-30) or obese (BMI >30 Amtep:) subjects. Three were randomly selected as blinded control subjects and 7 were given between 20 and 40 hours of binaural GVS in a 0.5 Hz sinusoid as tolerated up to 2mA. All the participants had their body mass composition measured at the start and end of the study period using dual energy X-ray absorptiometry. We found that in contrast to the control group, the GVS group had up to a 16% reduction in their total body fat. This observation was supported by an analysis of secretion of leptin, the "satiety hormone", in the saliva of subjects undergoing GVS.

We postulate that prolonged vestibular stimulation most likely acts via the parabrachial nucleus in the pons which is known to integrate vestibular, sympathetic and parasympathetic afferent activity. Via this pathway GVS modulates the function of the dorsomedial hypothalamus. We suggest that repeated GVS acts to alter the set-point for body mass to lower the proportion of body fat.

Not to be neglected--the triple dog sandwich:

http://www.chipublib.org/blogs/post/the-health-king-of-chicago/

Yikes--all those nitrites (and simple carbs)! Hopefully, the cantaloupe and grapes on the table were also consumed!

In case of interest, TED talks on "The Food We Eat"review how our diets have and are changing: http://www.npr.org/programs/ted-radio-hour/493930098
(Something like 73% of items in typical US grocery store contain added sugar!)

One Weight-Loss Approach Fits All? No, Not Even Close

Dr. Frank Sacks, a professor of nutrition at Harvard, likes to challenge his audience when he gives lectures on obesity.

“If you want to make a great discovery,” he tells them, figure out this: Why do some people lose 50 pounds on a diet while others on the same diet gain a few pounds?...

Dr. Sacks’s challenge is a question at the center of obesity research today. Two people can have the same amount of excess weight, they can be the same age, the same socioeconomic class, the same race, the same gender. And yet a treatment that works for one will do nothing for the other.

The problem, researchers say, is that obesity and its precursor — being overweight — are not one disease but instead, like cancer, they are many. “You can look at two people with the same amount of excess body weight and they put on the weight for very different reasons,” said Dr. Arya Sharma, medical director of the obesity program at the University of Alberta....

http://www.nytimes.com/2016/12/12/health/weight-loss-obesity.html?src=me

"...A new study offers evidence that diet-induced obesity alters the brain’s functioning in ways that suppress the natural impulse to move around...

When researchers fattened mice up on high-fat chow, they saw the activity of a specific class of dopamine receptor in the brain’s striatum (a center of movement control and reward-seeking behavior) fall. Along with that change, they observed that the obese mice adopted more sedentary habits than their lean peers.

When researchers experimentally turned down or knocked out that brain receptor’s activity in lean mice who were fed normal chow, those mice too lost the impulse to run on their running wheels or zip around their cages. They did not, however, become obese.

And when researchers took obese mice and experimentally “turned up” the receptor’s faulty signaling, they saw the chubby mice step up the frequency of their physical activity.

The new research, published Thursday in the journal Cell Metabolism, suggests that inactivity is not a natural cause of obesity. The activity of the affected dopamine receptor varies considerably among mice and presumably in humans, and it’s clearly not the case that the lazy among us all get fat.

Rather, inactivity appears to be a downstream consequence of excess weight, the new findings suggest. As such, it may not only encourage further weight gain. Since we know that regular exercise can prevent or mitigate the effects of obesity-related diseases, lack of exercise may foster the development of such conditions as Type 2 diabetes, hypertension and worrisome cholesterol.

The research also suggests that carrying excess weight may subtly interfere with the rewards we are meant to get from physical activity..."

http://www.latimes.com/science/sciencenow/la-sci-sn-obesity-inactivity-20161229-...

Danielle Friend et al. 2016. Basal Ganglia Dysfunction Contributes to Physical Inactivity in Obesity. Cell Metabolism. Corrected proof. http://dx.doi.org/10.1016/j.cmet.2016.12.001. http://www.cell.com/cell-metabolism/fulltext/S1550-4131(16)30596-4

"...We conclude that deficits in striatal D2R signaling contribute to physical inactivity in obesity, but inactivity is more a consequence than a cause of obesity."

Another reason to turn down the thermostat?

Why global warming could lead to a rise of 100,000 diabetes cases a year in the U.S.

..Even when the researchers adjusted for the prevalence of obesity in each state, they found that each 1-degree (C) temperature increase was associated with 2.9 additional cases of diabetes per 10,000 people.

...beyond the United States to examine the connection between temperature and conditions related to Type 2 diabetes. Sure enough, they found that as the temperature rose by 1 degree C, the prevalence of high fasting blood sugar (a marker for diabetes) rose by nearly 0.2% and the prevalence of obesity rose by just under 0.3%...

http://www.latimes.com/science/sciencenow/la-sci-sn-global-warming-diabetes-2017...

(Don't see article yet at http://drc.bmj.com/ Maybe later?)

The weirder side of obesity: genetic forms of obesity are rare yet numerous
By Susan Scutti, March 27, 2017

...The...researchers have identified and cataloged 79 rare genetic syndromes where obesity is a key symptom.

"For the study, we focused on monogenic forms of obesity," said (David Meyre, senior author of the study and an associate professor at McMaster University's School of Medicine in Ontario, Canada). He explained that monogenic or "Mendelian" forms mean that if you have one mutation, you develop the disease. "It's not that it increases your risk, it's 100% sure you develop the disease"

...In the monogenic obesity syndromes, not only does the genetic defect result in obesity but it also causes additional abnormal features, including mental disability, characteristic facial features, kidney disease and heart malformation.

..."We also hope that our study will help clinicians to recognize these syndromes"

...Additionally, the results will help scientists better understand the genes and molecules important to obesity among members of the general population.

..."Most of the obesity in the United States is NOT syndromic, said (Mary Freivogel, president of the National Society of Genetic Counselors). She explained that the overwhelming majority of cases are "polygenic and multifactorial," meaning it has resulted from a combination of multiple genetic factors, as well as environmental and lifestyle factors.

http://www.cnn.com/2017/03/27/health/obesity-rare-genetic-syndromes-study/

Food odors are more enticing to sleep-deprived brains
Activity boost seen in areas linked to olfaction
By Laurel Hamers | April 2, 2017

...Adults operating on only four hours of sleep inhaled food odors such as those from potato chips and cinnamon rolls, and nonfood smells like fir trees while undergoing functional MRI scans. (The scientists carefully controlled participants’ food intake throughout the day.) A few weeks later, the same participants repeated the experiment — this time with a full eight hours of sleep.

When tired, participants showed greater brain activity in two areas involved in olfaction — the piriform cortex and the orbitofrontal cortex — in response to food smells than they did when well rested. That spike wasn’t seen in response to nonfood odors, says study coauthor Surabhi Bhutani, of the Northwestern University Feinberg School of Medicine in Chicago....

https://www.sciencenews.org/article/food-odors-are-more-enticing-sleep-deprived-...

S. Bhutani, J. Gottfried and T. Kahnt. Central olfactory mechanisms underlying sleep-dependent changes in food processing. Cognitive Neuroscience Society annual meeting, San Francisco, March 27, 2017.

L. Sanders. One sleepless night weakens resolve in the face of doughnuts. Science News. Vol. 184, August 24, 2013, p. 18.

>155 margd: As a frequent insomniac, I can attest that this is true.

>156 sturlington: I was pleased to learn from my Fitbit that most nights I sleep 7+ hrs with 85-90% efficiency. Unfortunately there are some nights when that is not the case. Right now, leftover moussaka is calling to me from the fridge... ;-)

From article, below, sounds like my parents acquired Tinker and Dusty in time to help my younger sibs, at least... My adopted kids would have spent first six months in hospital before moving on to less hygenic orphanages, so hope their biological moms had lots of exposure to correcting microbes. Once with us, one son required long course of antibiotics and the other anti-parasite meds, which hopefully didn't undo benefits of any maternal microbe exposure!

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Study suggests pet exposure might help protect babies from allergies, obesity
Having fur babies may help your human baby build immunity
John Cotter | Apr 07, 2017

...Research at the University of Alberta shows infants from families with furry pets, especially dogs, showed higher levels of two types of gut microbes associated with lower risks of obesity and allergic disease.

"The abundance of these bacteria were increased twofold when there was a pet in the house," said Anita Kozyrskyj, a pediatric epidemiologist who is one of the world's leading researchers on gut microbes.

...The study theory suggests that babies exposed to dirt and bacteria from a pet's fur or paws can create early immunity. The exposure can happen from pet-to-mother-to-unborn baby as well as during the first three months of the infant's life.

..."The microbes are training the immune system to react to harmful entities like pathogenic microbes and not react to beneficial microbes and food nutrients."

...Higher levels of one of the microbes are associated with leanness and protect against obesity....

http://www.cbc.ca/news/canada/edmonton/university-alberta-edmonton-research-dogs...

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Hein M. Tun et al. 2017. Exposure to household furry pets influences the gut microbiota of infant at 3–4 months following various birth scenarios. Microbiome20175:40. DOI: 10.1186/s40168-017-0254-x . https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-017-0254-x

Abstract

Background
Early-life exposure to household pets has the capacity to reduce risk for overweight and allergic disease, especially following caesarean delivery. Since there is some evidence that pets also alter the gut microbial composition of infants, changes to the gut microbiome are putative pathways by which pet exposure can reduce these risks to health. To investigate the impact of pre- and postnatal pet exposure on infant gut microbiota following various birth scenarios, this study employed a large subsample of 746 infants from the Canadian Healthy Infant Longitudinal Development Study (CHILD) cohort, whose mothers were enrolled during pregnancy between 2009 and 2012. Participating mothers were asked to report on household pet ownership at recruitment during the second or third trimester and 3 months postpartum. Infant gut microbiota were profiled with 16S rRNA sequencing from faecal samples collected at the mean age of 3.3 months. Two categories of pet exposure (i) only during pregnancy and (ii) pre- and postnatally were compared to no pet exposure under different birth scenarios.

Results
Over half of studied infants were exposed to at least one furry pet in the prenatal and/or postnatal periods, of which 8% were exposed in pregnancy alone and 46.8% had exposure during both time periods. As a common effect in all birth scenarios, pre- and postnatal pet exposure enriched the abundance of Oscillospira and/or Ruminococcus (P 

N A Rybnikova, A Haim, B A Portnov. 2016. Does artificial light-at-night exposure contribute to the worldwide obesity pandemic? International Journal of Obesity (22 January 2016) | doi:10.1038/ijo.2015.255

Abstract
Background:

Worldwide overweight and obesity rates are on the rise, with about 1 900 billion adults being defined as overweight and about 600 million adults being defined as obese by the World Health Organization (WHO). Increasing exposure to artificial light-at-night (ALAN) may influence body mass, by suppression of melatonin production and disruption of daily rhythms, resulting in physiological or behavioral changes in the human body, and may thus become a driving force behind worldwide overweight and obesity pandemic.

Methods:

We analyzed most recent satellite images of night time illumination, available from the US Defense Meteorological Satellite Program (DMSP), combining them with country-level data on female and male overweight and obesity prevalence rates, reported by the WHO. The study aims to identify and measure the strength of association between ALAN and country-wide overweight and obesity rates, controlling for per capita GDP, level of urbanization, birth rate, food consumption and regional differences.

Results:

ALAN emerged as a statistically significant and positive predictor of overweight and obesity (t>1 Michael_Welch:.97; P

OT, but just a bit (arthritis of the knee):

High-Fiber Diet Tied to Less Knee Arthritis
NICHOLAS BAKALAR | MAY 24, 2017

...As fiber intake increased, the prevalence of arthritis decreased. In the larger study, those who ate the most fiber were 30 percent less likely to have knee osteoarthritis than those who ate the least, and in the smaller study, they were 61 percent less likely. The associations persisted even after controlling for age, sex, race, education, smoking, total calorie intake, physical activity, the intake of polyunsaturated fat and other dietary factors.

The mechanism is unclear, but fiber may reduce inflammation and help control weight. The average intake of fiber in the study was 15 grams a day, but the recommended level is 25 to 30 grams a day for most people...

https://www.nytimes.com/2017/05/24/well/eat/high-fiber-diet-tied-to-less-knee-ar...
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Zhaoli Dai et al. 2016 Dietary intake of fibre and risk of knee osteoarthritis in two US prospective cohorts. BMJ Annals of the Rheumatic Diseases May 23, 2017.
http://ard.bmj.com/content/early/2017/05/04/annrheumdis-2016-210810

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Also, of course, tart cherries help many with knee pain:

...Joint Defense

Experts estimate that one out of every two Americans will develop symptomatic osteoarthritis at some point in their lifetime.36 Osteoarthritis is a chronic condition characterized by a breakdown of joint cartilage that leads to pain and injury.37

The Arthritis Foundation reports that the risk of developing osteoarthritis is greater among those of increased age, those who are athletic or regularly engage in repetitive-motion work, and those who are obese.38

Osteoarthritis has a strong inflammatory component.39 Acetaminophen is the most commonly used osteoarthritis pain medication.40 However, this pain-reliever does not help lower inflammation,40 and its side effects can include kidney or liver damage.41

In a 2007 pilot study, researchers at Baylor Research Institute gave tart cherries in pill form to patients with osteoarthritis of the knee. They documented that, after 8 weeks, more than half the subjects experienced a significant improvement in pain and function.42

Then, in 2012, a double-blind, randomized, placebo-controlled trial was presented at the annual meeting of the American College of Sports Medicine, ahead of publication. Scientists measured the impacts of tart cherry on serum inflammatory biomarkers among inflammatory osteoarthritis patients. (Patients with inflammatory or erosive osteoarthritis are those who suffer from sudden signs of inflammation, such as redness, pain, and swelling.)

The trial included 20 female participants between 40 and 70 years old who experienced at least moderate pain from osteoarthritis. The participants consumed two 10.5-ounce bottles of either tart cherry juice or a control beverage for 3 weeks.

Among those patients consuming the tart cherry juice, there was a statistically significant decrease in inflammation, indicated by reduced levels of C-reactive protein (CRP). The impact was greatest for those women who had shown the highest inflammation levels at the start of the investigation.43

This research demonstrates that tart cherry juice provides osteoarthritis patients with anti-inflammatory activity without the adverse effects and risks of traditional arthritis medications.

Gout is another type of inflammatory arthritis, and it is associated with higher risks of cardiovascular disease and mortality.44 High blood concentration of uric acid is considered its main pathway.45

Typically, drugs such as allopurinol and probenecid are used to help lower uric acid levels. But the side effects of these drugs can include difficulty breathing, unusual bleeding, vomiting, nausea, or severe skin rash.46,47 They may even interfere with other medications.48,49

Fortunately, research has spotlighted a safe alternative. For decades, gout sufferers have consumed tart cherry juice for symptomatic relief, on the basis of anecdotal evidence. Now, rigid science has begun to support this tradition.

A study conducted by scientists at Boston University found that intake of cherry extract reduced the risk of gout attacks in those who suffered recurrent gout attacks by 45%.50 Additionally, the researchers discovered that when cherry intake was combined with allopurinol use, the risk for gout attacks was reduced by 75% versus no intervention. What’s more, these results persisted even across subgroups stratified for sex, obesity status, purine intake, and alcohol use.50 Tart cherries appear to be a natural—and safe—way to inhibit the key gout pathway.

Quelling the Chronic Inflammation of Obesity

Chronic inflammation significantly boosts the risk of a number of conditions, including cancer and heart disease.51 But few people realize that obesity can be both a cause—and a consequence—of chronic low-level inflammation.52,53

Adipose cells are not simply fat stores—they are chemically active cells.52 In obese individuals, belly fat deposits generate a torrent of pro-inflammatory cell-signaling molecules known as cytokines.54 Left unchecked, these cytokines trigger a cascade of destruction that can lead to a number of degenerative diseases.55,56

Researchers demonstrated that obese or overweight human adults who consumed 8 ounces daily of tart cherry juice for 4 weeks exhibited significantly lowered inflammation. This was evidenced by marked decreases in erythrocyte sedimentation rate, tumor necrosis factor levels, and monocyte chemotactic protein—all key indicators of inflammation.44

Tart cherries are clearly a potent tool for inhibiting the chronic, often obesity-related, low-level inflammation that can lead to many disorders—and they could even inhibit obesity itself!...

http://www.lifeextension.com/Magazine/2013/6/Anti-Inflammatory-Properties-of-Tar...

Does my sense of smell make me ... fat? In mice, the answer seems to be yes

...Mice stripped of their sense of smell burn fat differently — more intensively — than do mice whose olfaction is normal, the new study found. They typically have higher levels of adrenaline — the “go” signal in the body’s fight-or-flight system — than do mice with an intact sense of smell. And even when all they eat is high-fat chow, they don’t appear as likely as capable smellers to develop such afflictions as fatty liver or the kind of dangerous fat deposits that settle around the midsection.

...while mice probably rely on their sense of smell more than humans, they can tell us a lot about human obesity, (UC Berkeley stem cell biologist and geneticist Andrew) Dillin said. And these findings do suggest an intriguing way to help those with obesity lose some weight and improve their metabolic function without having to change what, or how much, they eat, he added.

Researchers know that when people lose their sense of smell — an effect seen in certain strokes, brain injuries and neurodegenerative diseases — their appetites wane, they eat less, and (no surprise) they lose weight. It’s also well known that the acuity of our sense of smell rises and falls depending on circumstance: It’s at its zenith when we haven’t eaten in several hours, and plummets just after we’ve had a meal.

The first observation suggests that smell piques or sustains interest in eating directly. The second suggests that smell may set off a host of signals about the body’s energy needs that work indirectly to affect metabolic function. That side of the equation is a lot less obvious, and has been studied far less.

The new research suggests that reducing olfactory cues might do more than help overweight people shed pounds. It may also right some of the metabolic and hormonal signals that get pushed out of whack as a person accumulates too much fat...

http://www.latimes.com/science/sciencenow/la-sci-sn-sense-smell-weight-20170705-...

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Celine E. Riera et al. 2017. The Sense of Smell Impacts Metabolic Health and Obesity. Cell Metabolism. Volume 26, Issue 1, p198–211.e5, 5 July 2017. DOI: http://dx.doi.org/10.1016/j.cmet.2017.06.015 . http://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30357-1

Highlights

•Loss of adult olfactory neurons protects against diet-induced obesity
•Loss of smell after obesity also reduces fat mass and insulin resistance
•Loss of IGF1 receptors in olfactory sensory neurons (OSNs) improves olfaction
•Loss of IGF1R in OSNs increases adiposity and insulin resistance

Summary

Olfactory inputs help coordinate food appreciation and selection, but their role in systemic physiology and energy balance is poorly understood. Here we demonstrate that mice upon conditional ablation of mature olfactory sensory neurons (OSNs) are resistant to diet-induced obesity accompanied by increased thermogenesis in brown and inguinal fat depots. Acute loss of smell perception after obesity onset not only abrogated further weight gain but also improved fat mass and insulin resistance. Reduced olfactory input stimulates sympathetic nerve activity, resulting in activation of β-adrenergic receptors on white and brown adipocytes to promote lipolysis. Conversely, conditional ablation of the IGF1 receptor in OSNs enhances olfactory performance in mice and leads to increased adiposity and insulin resistance. These findings unravel a new bidirectional function for the olfactory system in controlling energy homeostasis in response to sensory and hormonal signals.

NAFTA! (HFCS, High Fructose Corn Syrup)

NAFTA is making Canadians fat, new study suggests
Erica Alini | July 5, 2017

...Scientists disagree about whether the human body assimilated HFCS differently than other types of sugars but agree that excessive consumption of sugars of any kind is linked to weigh gain, type 2 diabetes and a higher risk of heart disease, among other health issues.

...The CMAJ study, which looked at the period from 1985 to 2000, found that lower tariffs on HFCS likely resulted in an increase of 41.6 kilocalories in the daily supply of caloric sweeteners (which include HFCS, fructose and maltose, maple sugar and syrup, glucose, dextrose, lactose and molasses).

Soaring Canadian imports of HFCS were correlated with a sharp rise in obesity rates, from 5.6 per cent in 1985 to 14.8 per cent in 1998, the authors noted.

The period after the implementation of NAFTA (in 1994) also saw diabetes rates balloon, from 3.3 per cent to 5.6 per cent, between 1998-99 and 2008-09.

With NAFTA in place, tariffs on food and drinks containing HFCS were gradually removed between 1994 and 1998. However, tariffs on cane and beet sugar remained due to a long-standing trade dispute between Canada and the U.S.

The researchers found that Canada’s supply of caloric sweeteners kept rising with every gradual lowering of the tariffs on HFCS and held steady after the final reduction in 1998.

The country’s overall supply of sugars and sweeteners also stopped declining, as it had been for some time before the introduction of NAFTA, they noted.

Countries that are not parties to NAFTA, including Australia and the U.K., didn’t see a similar increase over the same time period, the authors said.

NAFTA also coincided with HFCS gaining a larger share of the Canadian market for sugar and sweeteners.

Caloric sweeteners including HFCS accounted for only 4.8 per cent of total sweetener use in Canada before NAFTA, but a whopping 13.5 per cent after the implementation of the free trade agreement.

The findings raise concerns about the public health implications of free trade deals with the U.S. that would use NAFTA as a blueprint, according to the authors.

These include a potential new deal between the U.S. and the U.K. after the latter decided to leave the European Union, and the Trans-Pacific Partnership, which would create a free-trade zone among the U.S., Canada, Mexico and nine other Pacific Rim countries.

Such “new trade deals could harm population health should lower tariffs lead to increased supply and potential consumption of unhealthy food items, particularly those containing HFCS,” the study concluded.

http://globalnews.ca/news/3577044/nafta-obesity-canada/

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Pepita Barlow et al. 2017. Impact of the North American Free Trade Agreement on high-fructose corn syrup supply in Canada: a natural experiment using synthetic control methods. CMAJ July 4, 2017 vol. 189 no. 26 doi: 10.1503/cmaj.161152. http://www.cmaj.ca/content/189/26/E881.full

Abstract

BACKGROUND: Critics of free trade agreements have argued that they threaten public health, as they eliminate barriers to trade in potentially harmful products, such as sugar. Here we analyze the North American Free Trade Agreement (NAFTA), testing the hypothesis that lowering tariffs on food and beverage syrups that contain high-fructose corn syrup (HFCS) increased its use in foods consumed in Canada.

METHODS: We used supply data from the Food and Agriculture Organization of the United Nations to assess changes in supply of caloric sweeteners including HFCS after NAFTA. We estimate the impact of NAFTA on supply of HFCS in Canada using an innovative, quasi-experimental methodology — synthetic control methods — that creates a control group with which to compare Canada’s outcomes. Additional robustness tests were performed for sample, control groups and model specification.

RESULTS: Tariff reductions in NAFTA coincided with a 41.6 (95% confidence interval 25.1 to 58.2) kilocalorie per capita daily increase in the supply of caloric sweeteners including HFCS. This change was not observed in the control groups, including Australia and the United Kingdom, as well as a composite control of 16 countries. Results were robust to placebo tests and additional sensitivity analyses.

INTERPRETATION: NAFTA was strongly associated with a marked rise in HFCS supply and likely consumption in Canada. Our study provides evidence that even a seemingly modest change to product tariffs in free trade agreements can substantially alter population-wide dietary behaviour and exposure to risk factors.

Bones make hormones that communicate with the brain and other organs
Mouse studies reveal bone-body connection in appetite, metabolism and more
Cassie Martin | June 21, 2017

....Of the hormones on the list of bones’ messengers — osteocalcin, sclerostin, fibroblast growth factor 23 and lipocalin 2 — the last is the latest to attract attention. Lipocalin 2, which bones unleash to stem bacterial infections, also works in the brain to control appetite, physiologist Stavroula Kousteni of Columbia University Medical Center and colleagues reported in the March 16 Nature.

After mice eat, their bone-forming cells absorb nutrients and release a hormone called lipocalin 2 (LCN2) into the blood. LCN2 travels to the brain, where it gloms on to appetite-regulating nerve cells, which tell the brain to stop eating, a recent study suggests.

Researchers previously thought that fat cells were mostly responsible for making lipocalin 2, or LCN2. But in mice, bones produce up to 10 times as much of the hormone as fat cells do, Kousteni and colleagues showed. And after a meal, mice’s bones pumped out enough LCN2 to boost blood levels three times as high as premeal levels. “It’s a new role for bone as an endocrine organ,” Kousteni says.

...More recent mouse data indicate that osteocalcin may play a role in energy metabolism. After an injection of the hormone, old mice could run as far as younger mice. Old mice that didn’t receive an osteocalcin boost ran about half as far, Karsenty and colleagues reported last year in Cell Metabolism. As the hormone increases endurance, it helps muscles absorb more nutrients. In return, muscles talk back to bones, telling them to churn out more osteocalcin.

...Another emerging bone messenger is sclerostin. Its day job is to keep bone growth in check by telling bone-forming osteoblasts to slow down or stop. But bones may dispatch the hormone to manage an important fuel source — fat. In mice, the hormone helps convert white (or “bad”) fat into more useful energy-burning beige fat...

...In the study recently published in Nature, Kousteni’s team found that boosting LCN2 levels in mice missing the LCN2 gene tamed their voracious feeding habits. Even in mice with working LCN2 genes, infusions of the hormone reduced food intake, improved blood sugar levels and increased insulin sensitivity.

...In a small group of people with type 2 diabetes, those who weighed more had less LCN2 in their blood, the researchers found. And a few people whose brains had defective LCN2 docking stations had higher blood levels of the hormone...

Citations

Mosialou et al. MC4R-dependent suppression of appetite by bone-derived lipocalin 2. Nature. Vol. 543, March 16, 2017, p. 385. doi: 10.1038/nature21697.

K. Fulzele et al. Osteocyte-secreted Wnt signaling inhibitor sclerostin contributes to beige adipogenesis in peripheral fat depots. Journal of Bone and Mineral Research. Vol. 32, February 3, 2017, p. 373. doi: 10.1002/jbmr.3001.

P. Mera et al. Osteocalcin signaling in myofibers is necessary and sufficient for optimum adaptation to exercise. Cell Metabolism. Vol. 23, June 14, 2016, p. 1078. doi: 10.1016/j.cmet.2016.05.004.

F. Oury et al. Maternal and offspring pools of osteocalcin influence brain development and functions. Cell. Vol. 155, September 26, 2013, p. 228. doi: 10.1016/j.cell.2013.08.042.

F. Oury et al. Osteocalcin regulates murine and human fertility through a pancreas-bone-testis axis. Journal of Clinical Investigation. Vol. 123, June 3, 2013, p. 2421. doi: 10.1172/JCI65952.

N.K. Lee et al. Endocrine Regulation of Energy Metabolism by the Skeleton. Cell. Vol. 130, August 10, 2007, p. 456. doi: 10.1016/j.cell.2007.05.047.

Study of KRN23 in Adults with X-linked Hypophosphatemia (XLH). Center for X-Linked Hypophosphatemia, Yale University.

Study of the safety, pharmacodynamics and efficancy of KRN23 in children from 1 to 4 years old with X-linked Hypophosphatemia (XLH). Center for X-Linked Hypophosphatemia, Yale University.

https://www.sciencenews.org/article/bones-make-hormones-communicate-brain-and-ot...

Sugary drinks in pregnancy tied to heavier kids later
Gia Miller | July 10, 2017

...Eight-year-olds who drank at least a half of a sugar-sweetened beverage each week were about 2 pounds heavier if their moms consumed more than two sugar-sweetened beverages a day during the second trimester of pregnancy, according to the researchers.

The study authors said it appears that mom's consumption of sugary beverages made the difference in the child's weight, not the child's diet...

Read more at: https://medicalxpress.com/news/2017-07-sugary-pregnancy-tied-heavier-kids.html#j...

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Matthew W. Gillman et al. 2017. Beverage Intake During Pregnancy and Childhood Adiposity. Pediatrics. July 2017.
http://pediatrics.aappublications.org/content/pediatrics/early/2017/07/06/peds.2...

What’s Known on This Subject:

Maternal diet during pregnancy may entrain offspring obesity. One potential dietary factor is sugar-sweetened beverages, intake of which appears to cause obesity in children and adults.

What This Study Adds:

In this prospective prebirth cohort study, school-aged children of mothers who consumed more sugary beverages in midpregnancy had higher levels of adiposity, measured by BMI, skinfold thicknesses, and dual-energy radiograph absorptiometry.

Olivia M Farr et al. 2017. Walnut consumption increases activation of the insula to highly desirable food cues: A randomized, double-blind, placebo-controlled, cross-over fMRI study. Diabetes, Obesity, and Metabolism. 17 August 2017. DOI: 10.1111/dom.13060 . http://onlinelibrary.wiley.com/doi/10.1111/dom.13060/abstract
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Walnuts for Weight Loss?
NICHOLAS BAKALAR | AUG. 18, 2017

A handful of walnuts may be an effective weight loss tool.

Researchers...had nine hospitalized obese patients drink, on five consecutive days, either a smoothie containing 48 grams of walnuts (1.7 ounces, or about 14 walnut halves and 315 calories) or a placebo smoothie identical in taste and calorie content. Then, after a month on their regular diet, the patients returned for a second five-day trial, with placebo drinkers on the first trial receiving a walnut smoothie, and vice versa.

The participants underwent M.R.I. brain exams while looking at pictures of high-fat food (cake, for example), low-fat food (vegetables) or neutral pictures of rocks and trees.

The study, published in Diabetes, Obesity and Metabolism, found that when people looked at pictures of high-fat food, activation in the insula, a part of the brain involved in appetite and impulse control, increased among those who drank the walnut smoothie, but not among placebo drinkers. The study was funded in part by the California Walnut Commission...

https://www.nytimes.com/2017/08/18/well/eat/walnuts-for-weight-loss.html

Skin Patch Dissolves “Love Handles” in Mice
Microneedle skin patch that delivers fat-shrinking drug locally could be used to treat obesity and diabetes
September 15, 2017

Researchers have devised a medicated skin patch that can turn energy-storing white fat into energy-burning brown fat locally while raising the body’s overall metabolism. The patch could be used to burn off pockets of unwanted fat such as “love handles” and treat metabolic disorders, such as obesity and diabetes, according to researchers at Columbia University Medical Center (CUMC) and the University of North Carolina.

...transform an adult’s white fat into brown fat—a process named browning—which can happen naturally when the body is exposed to cold temperatures—as a treatment for obesity and diabetes.

“There are several clinically available drugs that promote browning, but all must be given as pills or injections,” said study co-leader Li Qiang, PhD, assistant professor of pathology & cell biology at Columbia. “This exposes the whole body to the drugs, which can lead to side effects such as stomach upset, weight gain, and bone fractures. Our skin patch appears to alleviate these complications by delivering most drugs directly to fat tissue.”

...Mice treated with either of the two drugs (rosiglitazone (Avandia) or CL316243) had a 20 percent reduction in fat on the treated side compared with the untreated side. They also had significantly lower fasting blood glucose levels than untreated mice.

Tests in normal, lean mice revealed that treatment with either of the two drugs increased the animals’ oxygen consumption (a measure of overall metabolic activity) by about 20 percent compared with untreated controls.

Genetic analyses revealed that the treated side contained more genes associated with brown fat than on the untreated side, suggesting that the observed metabolic changes and fat reduction were due to an increase in browning in the treated mice...

http://newsroom.cumc.columbia.edu/blog/2017/09/15/skin-patch-dissolves-love-hand...

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Yuqi Zhang et al. 2017. Locally-Induced Adipose Tissue Browning by Microneedle Patch for Obesity Treatment. American Chemical Society ACS Nano, Article ASAP. DOI: 10.1021/acsnano.7b04348 . http://pubs.acs.org/doi/10.1021/acsnano.7b04348

Abstract. Obesity is one of the most serious public health problems in the 21st century that may lead to many comorbidities such as type-2 diabetes, cardiovascular diseases, and cancer. Current treatments toward obesity including diet, physical exercise, pharmacological therapy, as well as surgeries are always associated with low effectiveness or undesired systematical side effects. In order to enhance treatment efficiency with minimized side effects, we developed a transcutaneous browning agent patch to locally induce adipose tissue transformation. This microneedle-based patch can effectively deliver browning agents to the subcutaneous adipocytes in a sustained manner and switch on the “browning” at the targeted region. It is demonstrated that this patch reduces treated fat pad size, increases whole body energy expenditure, and improves type-2 diabetes in vivo in a diet-induced obesity mouse model.