Last Thursday, President Bill Clinton appeared on CNN’s Piers Morgan show.
The former President’s Clinton Foundation has become increasingly involved in health issues … especially childhood obesity.
Among other topics, the guest host – film producer Harvey Weinstein – asked him about his remarkable success in losing weight and eating more healthfully.
President Clinton highlighted the issue and his own battle of the bulge in a blurb he wrote for Dr. Hyman’s recent bestseller, The Blood Sugar Solution:
“In the last decade, the rise of obesity and diabetes has emerged as a crisis that threatens our families, the global economy, and the success of our next generation. I’ve made drastic changes to my own diet and exercise routine since my heart troubles surfaced in 2004 and I hope Dr. Hyman’s new book will inspire you as he has inspired me.”
Obviously, President Clinton’s battle involved much more than replacing junk food with fish … but that move may have played a part in his success, judging by the known metabolic benefits of the omega-3s in seafood.
Based on cell, animal, and human studies, those apparent benefits seem to include increased burning of body fat and resistance to metabolic syndrome … a cluster of signs that raises the risk of obesity, diabetes, and cardiovascular disease.
(For example, see “Omega-3s Seen to Fight Metabolic Syndrome” and other reports in the Omega-3s & Metabolic Health section of our news archive.)
Coincidentally, a paper presented at a conference we just attended underscores one possible reason why the former President’s weekly salmon habit may have aided and enhanced his weight-loss efforts.
The paper concerned a mouse study led by clinical psychiatrist Capt. Joe Hibbeln, M.D., of the National Institute on Alcohol Abuse and Alcoholism (NIAAA) … a division of the National Institutes of Health.
He and his NIAAA colleagues presented this intriguing paper at last week’s Congress of the International Society for the Study of Fatty Acids and Lipids (ISSFAL) in Vancouver, Canada … just an hour north of our Bellingham, Washington home base.
(Over the coming weeks, we’ll cover more research presented at the conference.)
The results of Dr. Hibbeln’s research affirm the role that America’s “omega imbalance” plays in the current epidemic of overweight and obesity … and its possible role in promoting and/or sustaining excessive alcohol intake.
The role of omega-6 fats in appetite, via that body’s own cannabis
Before getting into the study and its implications, we need to explain something called the “endocannabinoid system”.
This term refers to a group of fats (lipids) that modulate activities of the nervous system affecting a variety of physiological processes … including appetite, pain sensation, mood, and memory.
The suffix “cannabinoid” in endocannabinoid derives from the Latin term for marijuana, which is cannabis.
This is because marijuana contains cannabinoid compounds similar or identical to the endocannabinoids found in the human nervous system.
(The prefix “endo” means “internal”, or natural to the body, as opposed to “exo” or external to the body. The body’s endocannabinoid system mediates the psychoactive effects of the exocannibinoids in marijuana, some of which are structurally identical.)
Endocannabinoids that promote appetite are derived from a long-chain omega-6 fatty acid called arachidonic acid (AA), which is essential to human immune and brain functions.
The main appetite-driving endocannabinoids are called 2-AG and anandamide … with “ananda” meaning “bliss” in yoga’s ancient Sanskrit texts.
As you might expect, the exocannabinoids in marijuana activate the cell receptors for their hunger-stimulating endocannabinoid cousins.
This explains why marijuana produces “the munchies” and can help people suffering disease- or chemotherapy-driven appetite loss and related wasting syndrome.
Unfortunately, it appears that America’s excessive intake of omega-6 fatty acids also stimulates appetite, thanks to the fact that they body uses them to make the appetite-driving endocannabinoids.
As we said, the body makes appetite-enhancing endocannabinoids from omega-6 AA, which abounds in beef, pork, and poultry.
But the body also makes omega-6 AA from the short-chain omega-6 fat called linoleic acid (LA), which predominates in the most commonly consumed vegetable oils (corn, soy, safflower, sunflower, cottonseed).
This sets the stage for the exciting results of Dr. Hibbeln’s animal study, which affirms the idea that America’s “omega imbalance” promotes overeating and obesity.
Study finds omega-6s promote overeating; omega-3s oppose the effect
Dr. Hibbeln’s team wanted to test the idea that excessive dietary intake of omega-6 LA – the precursor to omega-6 AA, from which the body makes appetite-driving endocannabinoids – would promote obesity in mice.
They designed their experiment to mimic the rise in American’s intake of omega-6 LA during the 20th century, from one percent of calories to eight percent (Hibbeln JR et al. 2012).
As they wrote, “These animal diets modeled 20th century increases of human [omega-6] LA consumption, changes that closely correlate with increasing prevalence rates of obesity. Similar patterns of increasing [omega-6] LA consumption and alcohol consumption are evident in the 20th century.”
They divided mice into two major groups for a study that lasted for 14 weeks from weaning:
Medium-fat diet (35 percent of calories as fat)
High-fat diet (60 percent of calories as fat)
Within each of those two groups, they further divided the mice into three subgroups:
One percent of calories from omega-6 LA
Eight percent of calories from omega-6 LA
Eight percent of calories from omega-6 LA and one percent of calories from omega-3s (EPA + DHA)
Compared with mice in the one percent omega-6 LA subgroups, the levels of appetite-driving endocannabinoids in blood and liver cell were three times higher in the eight percent omega-6 LA subgroups.
But the mice in the eight percent omega-6 LA subgroups that also got one percent of calories as omega-3s showed metabolic patterns similar to the mice in the one percent omega-6 LA subgroups.
In addition, the mice in the high-fat diet group that received only one percent of calories as omega-6 LA did not suffer the “obesogenic” metabolic properties of the high-fat diet that included eight percent of calories from omega-6 LA.
As the team wrote, “In summary, dietary [omega-6] LA increased tissue [levels of omega-6] AA, and subsequently elevated [tissue levels of the appetite-driving endocannabinoids] … resulting in the development of diet-induced obesity.” (Hibbeln JR et al. 2012)
Their conclusion has pretty dramatic implications for American’s diets and health:
“The adipogenic [body-fat promoting] effect of [omega-6] LA can be prevented by consuming sufficient [omega-3] EPA and DHA to reduce the [omega-6] AA … pool and normalize endocannabinoid tone.”
Put more simply, if Americans were to cut back on omega-6-rich vegetables oils – and the many processed and takeout foods filled with them – that change could make a huge difference to their risk of obesity and related diseases.
Hibbeln JR. Hong Lin Y, Alvheim AR. A century of change in linoleic acid: Endocannabinoids, obesity and addiction. National Institute on Alcohol Abuse and Alcoholism, USA.