AMA Considers Recognizing Obesity as a Disease

June 17th, 2013 No comments »

At their annual meeting this week, the American Medical Association’s governing body, the House of Delegates,  will consider a resolution recognizing obesity as a disease. As they say, we wait with baited breath.

In 2009, the AMA declared that obesity should not be a condition qualifying for disability status. (See post, How the AMA Got It Wrong, Sept. 27, 2009)

In 2012, the American Association for Clinical Endocrinology recognized obesity as a disease. The Obesity Society did so in 2008. This is the white paper of supporting evidence. See also my paper in 2001: Obesity as a disease entity

The Social Security Administration recognized obesity as a disease in 1999. The Internal Revenue Service determined that costs for the treatment of obesity were medical costs eligible for the medical deduction on individual income taxes in 2002. In 2004, the Centers for Medicare and Medicaid Services effectively recognized obesity as a disease by removing language to the contrary from their coverage manual.

 

Snacking is Bad. Right?

June 12th, 2013 No comments »

In this uncertain world, one thing we can be sure of is that adolescent snacking is contributing to the obesity epidemic. Right? Well, er, no. Actually, young snackers (you know who you are) are likely to be less obese.

According to a literature review from 2000 to 2011 by Nicole Larson  and Mary Story at the University of Minnesota, “Although snacks can contribute to intake of key nutrients, frequent snacking has been associated with higher intake of total energy and energy from added and total sugars. Assessments in schools and retail stores have further indicated that energy-dense, nutrient-poor snacks are widely available in settings where youth spend their time. The majority of studies either found no evidence of a relationship between snacking behavior and weight status or found evidence indicating that young people who consumed more snacks were less likely to be obese; however, additional research is needed to address various methodological limitations.”

Picture: Selena Gomez snacking. Source: teennowmagazine.uk

 

Catching Up on Obesity and Neurological Diseases

June 12th, 2013 No comments »

For some time I have been reading papers dealing with the association (or lack thereof) of obesity with neurological disorders, such as Alzheimer’s Disease, autism spectrum disorders, and ADHD. I did not report on them too much, even though I came into the obesity field through my advocacy work in the neurosciences in the 1990s. I just did not ‘get’ the connection.

Now, the veil has been lifted thanks to a talk by Tamas L. Horvath, of Yale University. Dr. Horvath’s talk, at the Research Symposium sponsored by the American Diabetes Association, “Biologic Responses to Weight Loss and Weight Regain,” in Washington DC in April 2013, focused on hunger-producing neurons’ regulation of higher brain functions and longevity.

One slide in particular caught my attention. He was addressing the complexity inherent in satisfying the hunger drive and appetite needs. For example,

-wakefulness is needed. This is controlled by the lateral hypothalamic arousal center. Disorders in wakefulness include narcolepsy and sleep disorders.

- memory of the location of food sources is needed, both long term and short term. This is the role of the brain’s memory and reward systems. Disorders in this realm include dementia, Alzheimer’s disease, mood and addictive disorders.

-decision-making for when and how to acquire and prepare food is required. Related disorders in this sphere include depression and schizophrenia.

-the physical ability to pursue and locate and collect food is needed. Related disorders include Parkinson’s disease and amyotrophic lateral sclerosis (ALS).

-finally, there is food intake itself. Related disorders include obesity, anorexia and diabetes.

This simple schema made a great deal of sense to me. So, with thanks to Dr. Horvath, we will start providing more reports of studies investigating the connections of obesity and these prominent neurological conditions.

For example, Fadel and colleagues are looking at insulin, orexin and leptin, already recognized for regulating food intake, body weight and body composition, for their involvement in addictive behaviors, reproduction and cognitive performance. See, Food for thought: the role of appetitive peptides in age-related cognitive decline.

Vignini et al discuss the association of diabetes mellitus with Alzheimer’s Disease, calling Alzheimer’s Disease “Type 3 Diabetes.” Their paper, “Alzheimer’s disease and diabetes: new insights and unifying therapies” explores common mechanisms and possible remedies for both diseases. Meanwhile, Reitz and colleagues have uncovered variants in the FTO gene (already implicated for obesity) which can be risk factor for Alzheimer’s disease.

 

Economist author of most important unread book on obesity dies

June 12th, 2013 No comments »

The New York Times reports on June 12,  2013 that Robert W. Fogel, Nobel Prize winner in Economics, died at the age of 86. The Time’s obituary notes, “In 2011, Professor Fogel and three co-authors published what the New York Times called the “capstone” of a huge project that had occupied three decades of his later work: The Changing Body: Health, Nutrition and Human Development in the Western World Since 1700.” (Cambridge University Press, New York)

That book (reviewed here in June 2011) established that the human body was increasing in both height and weight for 300 years, not 30 years as many obesity pundits like to allege. Furthermore, the book establishes that the increases in height and weight are due to improved nutrition, which is due, in turn to positive technological improvements in agriculture, food safety, reduction in communicable diseases, improvements in public water and sewer systems, etc. This approach clearly contradicts the mantra of blame attached to food companies, television, computer games, etc. It makes obesity more complicated. It forces people to think. So, of course, people don’t bother with it. Quel dommage!

 

New Insights into how sleep deprivation leads to obesity

February 28th, 2013 No comments »

New research, published in the Proceedings of the National Academy of Science, is shedding light on the interaction of sleep and genes. Researchers at Surrey University took a small group of 26 subjects. Half slept for less than six hours a night; the other for 10. The sleep-deprived group was found to have altered functions in 711 genes, including some involved in metabolism, inflammation, and stress. The body’s normal circadian rhythms were also affected.

Getting fewer than six hours’ sleep per night deactivates genes which play a key role in the body’s constant process of self-repair and replenishment, according to a new study.

Genes produce proteins which are used to replace or repair damaged tissue, but after a week of sleep deprivation some of these ceased functioning.

The subjects’ bodies returned to normal after a period of regular sleep but prolonged deprivation could lead to major problems. The Center for Disease Control reports that 25% of Americans have occasional sleep problems and 10% have chronic sleep disorders.

 

 

Myths, Presumptions and Facts About Obesity

January 31st, 2013 No comments »

David Allison and 19 prestigious researchers have published an article in the New England Journal of Medicine on the Myths, Presumptions and Facts About Obesity. The myths they identify as being widely held are:

  1. Small, sustained changes in energy intake or expenditure will produce large, long-term weight changes.

  2. Setting realistic goals for weight loss is important, because otherwise patients will become frustrated and lose less weight.

  3. Large, rapid weight loss is associated with poorer long-term weight-loss outcomes, as compared with slow, gradual weight loss.

  4. It is important to assess the stage of change or diet in order to help patients who request weight-loss treatments.

  5. Physical education classes, in their current form, play an important role in reducing or preventing childhood obesity.

  6. Breast-feeding is protective against obesity.  (See my recent post on breastfeeding and obesity.)

  7. A bout of sexual activity burns 100 to 300 kcal for each participant.

They go on to identify six presumptions, which are widely accepted beliefs that have neither been proved nor disproved, so that we may move forward to collect solid data to support or refute them.

  1. Regularly eating (versus skipping) breakfast is protective against obesity.

  2. Early childhood is the period in which we learn exercise and eating habits that influence our weight throughout life.

  3. Eating more fruits and vegetables will result in weight loss or less weight gain, regardless of whether any other changes to one’s behavior or environment are made.

  4. Weight cycling (i.e. yo-yo dieting is associated with increased mortality.

  5. Snacking contributes to weight gain and obesity.

  6. The built environment, in terms of sidewalk and park availability, influences the incidence or prevalence of obesity.

They authors posit nine facts that we do know about obesity. The first two are:

  1. Although genetics plays a role, heritability is not destiny.

  2. Diets reduce weight but trying to go on a diet o recommending someone go on a diet generally does not work well in the long-term.

The remaining facts address specific tools: physical activity, maintenance, parent-child interventions, meal replacements, pharmacology and bariatric surgery.

An excellent discussion of the myth around how many calories does it take to make one overweight is the blog from Arya Sharma.

The article does not discuss a couple of observations. First, the media is a powerful tool in perpetuating many of these myths and presumptions. Second, policy-makers, especially at the federal level, repeat these myths when they know, or should know better. Third, it may be that our brains do not do a good job in analyzing data to overcome assumptions and stereotypical views.

We will have more on the myths and presumptions and role in policy-making in the days ahead.

 

Clarifying the Obesity Genetics Picture

December 13th, 2012 No comments »

Obesity has always been known to carry a strong genetic component. At first, there was hope of finding “the gene.” This turned out to be a flawed strategy as many genes were identified which affected body weight and body weight distribution. In a new study, a team using genome-wide association studies (GWAS) studied extreme obesity cases and never-overweight controls as well as families segregating extreme obesity and thinness. They found 16 genome-wide significant signals with the FTO gene being the strongest signal. The second most powerful signal was the MC4R gene. Adding total body weight, waist circumference and waist to hip ration, they found a strong signal for the NRXN3 gene. The researchers state, “The results therefore strongly suggest that FTO and MC4R might be the only two major-effect genes for obesity with common variants in population of European ancestry.” PLOS ONE: Genome-Wide Association Study on Obesity

 

Novel Gene-Policy Research

December 13th, 2012 No comments »

In a novel study, Jason Fletcher of Yale School of Public Heath, looked at the response to increases in cigarette taxes according to a genetic variation in the nicotinic acetylcholine receptor (CHRNA6). Using NHANES data, he found that one variation in the receptor responded to the taxation while another variation did not respond. Fletcher: Why Have Tobacco Control Policies Stalled?

The research needs to be confirmed of course. However, if it holds up, it may provide a new avenue to evaluate variations in response to anti-obesity public policies.