U.S. Capitol

An Act of Congress to Treat and Reduce Obesity

Will it take an act of Congress to advance more evidence-based strategies to treat and reduce obesity? Chief Research Officer Ross DeVol of the Milken Institute thinks so. Writing in the Huffington Post this weekend, he says:

The total health and economic cost to treat health conditions related to obesity exceeds $1.4 trillion annually.

If we fail to alter this growing health and economic burden, the cost of obesity truly may cripple America.

Passing the Treat and Reduce Obesity Act, or rolling it into legislation that replaces the ACA, would send an important signal that Washington understands the true health care crisis in America.

Congressional Briefing

DeVol will speak today in a congressional briefing, along with four other experts on obesity, economics, and policy. They will describe the economic and human impact of obesity. It has huge implications for productivity and competitiveness.

A broad coalition of professional, patient, and business organizations, the Obesity Care Advocacy Network, has organized this briefing. Also today, volunteers from all over the country will be speaking with their elected representatives. More than a hundred advocates are bringing unique expertise on the need for better utilization of evidence-based obesity care. They include people from the Obesity Society, the Academy of Nutrition and Dietetics, the Obesity Medicine Association, the Obesity Action Coalition, the American Society for Metabolic and Bariatric Surgery, the Endocrine Society, the American Association of Clinical Endocrinologists, and more.

The common thread is expertise and personal commitment to better use of evidence-based strategies for addressing the chronic disease of obesity. We are indebted to these people and their commitment to the cause.

To read DeVol’s commentary in the Huffington Post, click here.

U.S. Capitol, photograph © Ted Kyle / ConscienHealth

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February 27, 2017

3 Responses to “An Act of Congress to Treat and Reduce Obesity”

  1. February 27, 2017 at 9:17 am, David Brown said:

    Here’s the problem. Medicine is treatment orientated. Treatment involves pharmaceuticals. Drugs make money for companies that develop them. Drugs generally do not cure chronic conditions; they simply manage them. Therefore, the key to reducing medical costs is to reduce demand for drugs by first figuring out what causes obesity and chronic disease and then explaining to the public how to prevent and cure obesity and chronic diseases through proper nutrition. Question is, has Science identified the causes yet? Yes. What’s been learned from endocannabinoid system research over the past 20 years pretty much tells us what the problem is. It’s estimated that upwards of 20,000 papers have been published thus far. Here’s what one of them says.

    Endocannabinoids and their G-protein coupled receptors (GPCR) are a current research focus in the area of obesity due to the system’s role in food intake and glucose and lipid metabolism. Importantly, overweight and obese individuals often have higher circulating levels of the arachidonic acid-derived endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) and an altered pattern of receptor expression. Consequently, this leads to an increase in orexigenic stimuli, changes in fatty acid synthesis, insulin sensitivity, and glucose utilisation, with preferential energy storage in adipose tissue. As endocannabinoids are products of dietary fats, modification of dietary intake may modulate their levels, with eicosapentaenoic and docosahexaenoic acid based endocannabinoids being able to displace arachidonic acid from cell membranes, reducing AEA and 2-AG production. Similarly, oleoyl ethanolamide, a product of oleic acid, induces satiety, decreases circulating fatty acid concentrations, increases the capacity for β-oxidation, and is capable of inhibiting the action of AEA and 2-AG in adipose tissue. Thus, understanding how dietary fats alter endocannabinoid system activity is a pertinent area of research due to public health messages promoting a shift towards plant-derived fats, which are rich sources of AEA and 2-AG precursor fatty acids, possibly encouraging excessive energy intake and weight gain. https://www.hindawi.com/journals/ije/2013/361895/

    Do you see what “a shift towards plant-derived fats” has done to the public health. Both humans and livestock are consuming enormous amounts of omega-6 linoleic acid. In animals, this boosts the omega-6 arachidonic acid content of cell membranes such that even lean meats become problematic. Excerpts:

    “Arachidonic acid (AA) in the diet can be efficiently absorbed and incorporated into tissue membranes, resulting in an increased production of thromboxane A2 by platelets and increased ex vivo platelet aggregability. Results from previous studies have shown that AA is concentrated in the membrane phospholipids of lean meats.” http://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-5-97

    “The highest level of AA in lean meat was in duck (99 mg/100 g), whereas pork fat had the highest concentration for the visible fats (180 mg/100 g). The lean portions of beef and lamb contained the higher levels of n-3 polyunsaturated fatty acids (PUFA) compared with white meats which were high in AA and low in n-3 PUFA. The present data indicate that the visible meat fat can make a contribution to dietary intake of AA, particularly for consumers with high intakes of fat from pork or poultry meat.” https://www.ncbi.nlm.nih.gov/pubmed/9590632

    “Linoleic acid has been found to modulate endocannabinoid synthesis due to its ability to be converted to AA by the human body, although the effect of dietary linoleic acid on human endocannabinoid synthesis has not been investigated. This is a pertinent area of research due to the rapid increase in linoleic acid content in the Western diet as a result of a shift to plant-derived fats and the greater use of soy and corn oils in food production and manufacturing. These dietary changes have resulted in a shift in the n-3 to n-6 FA ratio, as reviewed by Simopoulos, with more than 84% of PUFA fats consumed in the USA being in the form of the AEA precursor linoleic acid. High linoleic acid diets promote obesity in both animals and humans and are correlated with increased fasting blood glucose, fasting insulin, and insulin resistance in humans, making this an important area of further research.” https://www.hindawi.com/journals/ije/2013/361895/

    The problem is essentially this. Our modernized, industrialized food supply contains an imbalance in 18 and 20 carbon chain omega-3s and 6s. This produces an imbalance in the cell membrane content of 20 carbon chain omega-3s and 6s. The ECS uses the 3s and 6s all the time to maintain homeostasis. An imbalance affects endocannabinoid tone producing these sorts of problems.

    “Through direct and indirect actions, endocannabinoids are known to modulate and influence a variety of physiological systems, including appetite, pain, inflammation, thermoregulation, intra-ocular pressure, sensation, muscle control, energy balance, metabolism, sleep health, stress responses, motivation/reward, mood, and memory. https://www.leafly.com/news/science-tech/is-your-endocannabinoid-system-in-balance

    What’s truly disturbing is that there is virtually no reporting on endocannabinoid system research that makes the connection between fatty acid intake and obesity and chronic disease. It’s all about phytocannabinoid research where scientists experiment with cannabis derived compounds and synthetic analogues that can be used to treat obesity and chronic disease.

    • February 27, 2017 at 10:49 am, Ted said:

      Thanks David. Endocannabinoid research is important, fascinating, and enlightening. Unfortunately, it has not yet delivered us a cure for the chronic disease of obesity.

      Until then, people with obesity need good, evidence-based care to manage this condition. Lifestyle, pharmacotherapy, and surgery each play a role. It makes no sense to wait for complications and then spend a fortune on treating those complications.

  2. February 28, 2017 at 5:23 am, Mary-Jo Overwater said:

    Thank you so much for the information on the significance of endocannabinoids, David Brown. Would if be worthwhile to set up a study modifying dietary fats so as to effect in a more optimal ratio of n-3:n-6 fatty acids? If the mechanism of endocannabinoids is so instrumental in affecting glucose, insulin, metabolism, stress, etc., it would be helpful for dietitians if we had clearer evidence to recommend to our clients a group of food sources that could make a clear difference.