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How Your Gut Feeds Your Fat Addiction


Have you ever wondered why it is almost impossible to only eat one potatoe chip or French fry?

Regular readers may recall a previous post on the discovery that we have specific oral sensory receptors that allow us to sense the ‘fattiness’ of food – a function that makes a lot of sense, given that dietary fat provides the densest source of caloric intake.

Now, Nicholas DiPatrizio and colleagues from the University of California, Irvine, have discovered that these oral dietary fat sensors activate a powerful ‘addiction-type’ mechanism in your gut that serves to promote further fat intake – their study is published in a recent issue of the Proceedings of the US National Academy of Science.

For their studies, the researchers used a well established ‘sham feeding’ model in the rat, where liquid diets eaten by the animal can be drained from the stomach via a chronically implanted gastric cannula, thereby preventing them from reaching the small intestines.

Using this model, the researchers showed that ‘sham feeding’ of a high-fat diet resulted in the potent activation of endocannabinoids in the early part of the small intestine by altering enzymatic activities that control endocannabinoid metabolism. The endocannbinoids (cannabis-like compounds produced in the body) are well known to play an important role in regulating ‘rewarding’ feeding behaviours.

This effect was abolished by surgical transection of the vagus nerve showing that the stimulation of these changes in the gut is driven through a centrally mediated neuronal pathway.

Furthermore, the local application of cannabinoid type 1 receptors blockers (e.g. rimonabant) in the small gut, reduced increased sham fat ingestion.

In other words, this study shows that oral sensing of fat sends a signal to the brain, which in turn sends a signal to the gut leading to formation of endocannabinoids, which in turn re-enforce fat eating.

This is probably why, just eating one piece of fatty food (say one potatoe chip or French fry) is so hard – simply eating one makes you want to continue eating till the whole bag or plate is empty.

Unfortunately, the drug rimonabant, used to effectively block this effect in this study, is no longer available for obesity management (it was withdrawn due to its negative impact on mood), but it may well be that other CB-1 inhibitors that do not enter the brain may prove to be effective to reduce fat intake.

Or, in the words of the authors:

“Our findings identify the gut endocannabinoid system as a critical component of the positive feedback mechanism that drives fat intake and suggest that therapeutic strategies aimed at restraining small intestinal endocannabinoid activity might help to selectively reduce the overeating of fatty foods.”

In the meantime using strategies based on limiting portion size, e.g. asking for a small serving of fries or transferring a small portion of chips into a separate bowl, while leaving the full bag in the pantry, may be the best strategy to thwart this mechanism.

AMS
Duchesnay, Quebec

Dipatrizio NV, Astarita G, Schwartz G, Li X, & Piomelli D (2011). Endocannabinoid signal in the gut controls dietary fat intake. Proceedings of the National Academy of Sciences of the United States of America PMID: 21730161

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7 Comments

  1. This isn’t the only way that dietary fat may affect endocannabinoid production. In those who have high fasting insulin levels, there’s a pathway for dietary linoleic acid (i.e., the omega-6 in veggie oils) to be converted to arachidonic acid and then anandamide, the THC like cannabinoid.

    Emily Deans (a psychiatrist with an evolutionary health perspective) has more here: http://evolutionarypsychiatry.blogspot.com/2011/04/summary-of-endocannabinoids-and-obesity.html

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  2. works in a similar way with carbs …. the more carbs one eats the more cravings for sweets he/she gets as the carbs convert to sugar. It is true for me. As long as I keep a very low carb intake its smooth sailing … (and I always eat whole grains and it still affects me – I can only imagine how it would be with white grains/pasta)

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  3. omega 6, sugar, grains, dense starches are addicting. The only proven treatment for addiction is complete abstinence. Moderation is a suckers game and does not work.

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  4. Speak for yourself, fredt! You sure don’t speak for me, nor my experience.

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  5. Why not create a strain of marijuana that assists in the regulation of rewarding feeding behaviors–the same strain could be tweaked to produce a more positive rather than negative effect on mood. Using a vapo device, the patient could inhale a fine mist rather than risk potentially carcinogenic smoke.

    Actually, such a strain probably already exists and has been in use by some medical marijuana users for several years. Unfortunately, because of current laws (at least in U.S.) mainstream health care providers are unlikely to have access to, or utilize and prescribe such a strain, even if it crosses their pathway.

    A shame.

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  6. Yeah, let’s all smoke more pot. It may give you the munchies but at least it makes you forget to feel guilty for eating when you’re hungry, am I right?

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  7. Very interesting. And so refreshing to read about food intake studies that explore physiological explanations for human food consumption! However, the conclusion that this study has something meaningful to tell us about fat consumption is incomplete.

    From the post: “This is probably why, just eating one piece of fatty food (say one potatoe chip or French fry) is so hard – simply eating one makes you want to continue eating till the whole bag or plate is empty.”

    Would any human really get a rewarding and self reinforcing physiological response from eating pure fat, say a stick of butter or a glass of plain olive oil? One sip of plain oil would almost surely not induce one to continue drinking until the bottle was empty. Almost certainly, this study was measuring something more complex than a neuro-biological response to fat consumption.

    Fatty food may well be addictive, but fat alone isn’t. So is it really the fat that produces this reward response? Or something more complex, like fat in the presence of something else and both of them at a certain concentration? An important question, since thwarting this response is unlikely to be addressed by medication, but it could be eliminated altogether if a person knew what hyper-palatable foods to abstain from completely.

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