Spotlight Now on Dad

December 4th, 2015 No comments »

It always feels as if mothers take the rap for their children’s overweight status. (See The Putative 104 Causes of Obesity post.) Now, in a provocative study, the attention is turning to Dad, particularly Dad’s sperm, according to a New York Times  story. For more information, see the recent study in Science Daily.

Look AHEAD provides insights on the role of genes in weight loss

September 3rd, 2015 No comments »

While the Look AHEAD Clinical Trial was discontinued some time ago, and while some the interpretations of the study remain controversial, continuing studies are showing some interesting interactions between behavior and genes. Jeanne Mc Caffery and colleagues have published one study showing that variations in the FTO and BDNF genes predicted weight regain across treatment arms.  Another study from a number of over-lapping researchers shows that variations in genes can affect the frequency of eating episodes and their composition as well. Click here for Dr. Arya Sharma’s recent post on a landmark study establishing how the FTO gene works.

 

New Insights on the Intergenerational Transmission of Metabolic Disease

July 31st, 2015 No comments »

Dr. Arya Sharma has a very useful post on the transgenerational transmission of metabolic disease, including obesity. As Dr. Sharma points out, if anyone says that obesity is not genetic, they don’t know what they are talking about. The article cited by Dr. Sharma recalls an earlier post on a three-generation transmission of the memory of starvation. Just goes to show that there much to be learned.

 

How Obesity is Changing the Environment

January 5th, 2015 No comments »

The association of overweight and obesity with type 2 diabetes is one of the strongest in the scientific literature. Well known to many is that the drug, metformin, is a front-line treatment for type 2 diabetes. But now come researchers with something unexpected: high levels of metformin in the Great Lakes is affecting the fish population and may be changing the expression of genes in some fish. According to a report in MedScape Today, researchers at the School of Freshwater Sciences at the University of Wiscon-Milwaukee found such high levels of metformin in the waters of Lake Michigan. There are some 180 million prescriptions written for diabetes drugs in 2013, a $213 billion market. Metformin has about 70 million prescriptions written in 2013.

The level of metformin, measured in fathead minnows in the lab, were enough to disrupt gene expression in the endocrine system of male fish but not females. The males were producing biochemical that are associated with female minnows. It has been assumed that the volume of water in the Great Lakes would dilute such a drug. The new study casts doubt on that assumption.

 

New Insight on the Effect of Time on Genetic Expression

January 5th, 2015 No comments »

A New Year’s Eve story in the New York Times reported on a new study about a well-studied gene, FTO, which is strongly correlated with the development of obesity.  Previous research had established that, on average, one copy of a variant of FTO tended to have an extra 3.5 pounds. Persons with two copies of the gene have an extra 7 pounds, significantly increasing the risk of becoming obese.

The new study, published in the Proceedings of the National Academy of Sciences, indicates that this effect did not exist before World War II. Using the longitudinal data from the Framingham Heart Study the researchers led by James Niels Rosenquist of Massachusetts General Hospital found a “robust” relationship between birth cohort and the genotype-phenotype correlation between the FTO risk allele and Body Mass Index (BMI) with an observed inflection point for those born after 1942. The authors observe that “genetic influences on complex traits like obesity can vary over time, presumably because of global environmental changes that modify allelic penetrance.”

 

The Memory of Starvation

November 13th, 2014 No comments »

Movie buffs may remember the 1999 movie A Bridge Too Far and the book by Cornelius Ryan of the same title on which it was based. The book and movie told the tale of an Allied operation to liberate Holland and achieve a bridgehead over the Rhine and into Germany. It failed. The book and movie only dealt with the military aspects of Operation Market-Garden, as it was called. Left out was what happened afterward.

The Nazi regime was going to punish the Dutch for their support to the combined English-American invasion of Holland. So they cut off food supplies to Holland in the winter of 1944-5. Thousands starved. Subsequently, researchers found that women who were pregnant during this period had offspring who were more prone to obesity, diabetes and cardiovascular disease and who were also smaller than those who were not exposed to the “Hunger Winter.” But, they also found that the grandchildren of those women had similar health problems. This helped establish the field of epi-genetics, i.e., that there were inheritance factors other than genes which might respond to early environmental stimulus, or the lack thereof. Now, in perhaps a groundbreaking paper, Dr. Oded Rechavi and colleagues may have found the mechanism. By studying worms exposed to starvation conditions, they observed a mechanism they call, ‘small RNA inheritance’ that enables worms to pass on the memory of starvation to at least three generations, perhaps more. At the very least, the study demonstrates that we still have a lot to learn about the gene-environment interaction as it affects the development of obesity and that those who say obesity is not genetic  only show they don’t know much about genetics or obesity.

 

Genetic Breakthrough?

July 19th, 2013 No comments »

The New York Times’ Gina Kolata reports today on a study in Science that researchers at Boston Children’s Hospital have made an important finding in the obesity genetic puzzle. Scientists have known for a long time that a person’s genetic inheritance influences their body weight. Studies of twins in controlled laboratory settings showed a significant range in how much weight a twin gained. Now comes a possible explanation. The team led by Dr. Joseph Majzoub found a gene, MRAP2, acts as a helper gene to signal another gene which controls appetite. When they removed the gene, animals doubled their weight. The only way these mice could remain slim was to be fed about 10-15% less than their siblings with the gene. In mouse-adolescence, they were ok. But as adults, they developed great appetites.

 

Reflections on the AMA Decision – Part 2

July 4th, 2013 No comments »

Sugarpova

One of the more curious comments on the AMA decision came from Hank Cardello of the Hudson Institute. Hank (with whom I have broken bread a couple of times) is a former food industry executive who believes that the food industry can basically down-shift the calories in the marketplace, resulting in lower obesity rates. Writing in Forbes Magazine, Why the AMA’s Obesity Ruling is Bad Medicine, Hank appears offended that doctors went off to decide what is a disease without checking first with the food industry. If they had, Hank would have told them how declaring obesity a disease gives health activists and policymaker a “new blunt instrument to use against the food industry.” Those crazy folks will now revive calls for Twinkie taxes, soda cup size bans and restrictions on full-fat pizza. Writes Hank,“These newly ignited brushfires, fanned and fed by social media and zealous lawmakers, could cost the food and restaurant industries enormous time and money to fight. If the activists were to claim that the industries are selling products that worsen a disease called obesity, they would have no choice but to lawyer up and defend themselves. As the decades-long tobacco wars proved, this would only greatly delay getting both parties to come to an equitable agreement.”

Whoa! Hank! Take a breath! Walk around the block.

First, numerous authorities have recognized obesity as a disease. It has been in the International Classification of Diseases for at least 20 years. The Social Security Administration, Food and Drug Administration, National Institutes of Health, Internal Revenue Service have described obesity as a disease for about 10 years or so. So, it isn’t new. If the ‘health activists’ will now ‘use’ it, where have they been? Do you really want to draw a parallel between the food industry and the tobacco industry? I don’t think it is apt and I would think you wouldn’t either.

But Hank presses on predicting (threatening?) that the food industry will now back off creating more healthy foods because they are being demonized “as purveyors of disease.” Well, it didn’t take any time to throw in the towel on the food industry meeting consumer demands for healthier alternatives! That was quick. Was the industry looking for a way out? It certainly feels that way since there is nothing really new in the AMA policy.

But it is next part of Hank’s paper that is embarrassing. It is like being at a party with a friend who starts to say something really unfortunate. You know it is too late to stop them. So, Hank goes on,

“Labeling obesity as a disease also ignores the almost taboo subject of personal responsibility. Describing obesity as purely a disease overlooks the complex role of a person’s psychological profile and attitudes. A study led by Angela Sutin of the National Institutes of Health highlighted that the most disciplined consumers had lower rates of obesity while larger weight gains were linked to personality factors such as impulsiveness, low conscientiousness, and a willingness to take risks. The authors concluded that any obesity solution must address these psychological factors, which general practitioners cannot.”

Well, I guess ‘personal responsibility’ isn’t so taboo after all. Never too late to call obese people damaged in the head. Persons with obesity have been called worse but trying to rope in a researcher from NIH for support was novel.

A few things are wrong with Hank’s description of this paper. First, it appears the study sample had many more ‘normal’ weight participants than the general population (45% to 31%) which might affect the outcomes. Second, Sutin and her co-authors acknowledge the possibility of reverse causation, i.e. that excess weight and the health and stigma attendant thereto can affect personality development. Hank ignores this. Third, while Hank is trying to say these overweight/obese customers can’t control themselves, Sutin points out, “Individuals high on Neuroticism, in particular the impulsiveness facet, and low on Conscientiousness have elevated triglycerides, hypertension, and clinically elevated levels of inflammation, even after controlling for differences in adiposity. Abnormal weight may be one mechanism that partially mediates the relationship between personality and these health outcomes.” (Emphasis added.) Sutin’s paper concludes, “The cognitive, emotional, and behavioral patterns associated with personality traits likely contribute to unhealthy weight and difficulties in weight management. Identifying the personality traits associated with obesity may help to elucidate the role of personality traits in disease progression.” Whoops! Did she just call obesity a disease?

This paper was published in 2011. To pull it out, Hank had to skip over 2 of her papers published earlier this year which have produced some dramatic and unexpected findings.

In the first 2013 paper, she and her colleagues found that individuals who rated high on impulsiveness and lacked discipline or low conscientiousness had high circulating levels of leptin, which plays a critical role in regulating body weight, even after controlling for body mass index, waist circumference or inflammatory markers.

Sutin’s second 2013 paper, “I Know Not To, but I Can’t Help It: Weight Gain and Changes In Impulsivity Related Personality Traits,” has much greater implications. In this study, Sutin and colleagues picked up where the 2011 study left off. They looked to see whether weight gain or loss of 10% or more led to personality changes, specifically impulsiveness and deliberation. They found that, compared to participants to stayed weight-stable, those who gained weight became more impulsive. Those who did not gain weight showed a predicted loss in impulsiveness. Then came the surprise. Contrary to their hypothesis, weight gain was also associated with increases in deliberation. That is, with gaining weight, subjects became more thoughtful before acting. This was especially strong among younger participants. The authors considered that, as participants gained weight, they bought into the American stereotypes about persons with obesity. So they saw themselves as more impulsive even as they were increasing in deliberativeness. They had no change in self-discipline. The authors speculate further, “A second possibility is that physiological mechanisms associated with weight gain could contribute to the relation between weight gain and changes in personality. For example, overweight and obese individuals tend to have higher levels of inflammation and chronic inflammation may reduce the ability to effectively regulate emotions and control behavior.”

Sutin et al suggest more research to help identify how considerations of personality traits can enhance interventions. For example, information on healthy lifestyles may be less useful for some than information on emotional aspects of impulsivity.

Finally, Hank concludes that the ‘disease’ label will be a crutch and cause people to stop making lifestyle changes and probably backslide. Why do these pundits make such negative generalizations about 2/3 of the population? Has the food industry decided just to insult its customers? You may want to see what happened with Michael Jefferies, the head of the head of Abercrombie & Fitch who said he did not want fat customers in his store. Donny Deutsch, advertising executive and TV personality, recently called him “disgusting” and “vile.” or University of New Mexico professor Geoffrey Miller who said he did not want students with obesity to apply to his Ph.D. program. He is being investigated by his university.

Oh, if only we would just leave obesity in the hands of the benevolent food industry!

Remember, those are the folks who are re-introducing Twinkie’s to America’s stores.

Twinkies

The same folks who have brought us  tennis superstar Maria Sharapova whole line of candy called, Sugarpova. (Get it?) See picture above.

 

And let’s not forget Sonic’s new 1,700 calorie peanut butter and bacon milk shake.

Sonic" peanut butter and bacon milk shake

Oh, and then there is Safeway’s leadership to shift the costs of health insurance onto overweight and obese employees based on dubious representation of their program and Kroger’s and Safeway’s efforts to derail front of package calorie labeling in supermarkets. Yeah, let’s all follow those guys.