Food reward

[Todd Becker]

Several months ago, Stephan Guyenet started a great discussion about the role of "food reward" in obesity, in a series of articles on his Whole Health Source blog, culminating in thoughtful talk at the Ancestral Health Symposium last month in Los Angeles.  His main argument is that in modern industrialized countries, food has been engineered to be "hyperpalatable" and irresistable by combining flavor, fat, sugar and salt.  Guyenet is not the first to make this claim.  David Kessler laid out a very similar argument in "The End of Overeating", published in 2009, and other versions of the argument pre-date that book.

I just wrote an article about this issue on my blog, "Does tasty food make us fat?"  Guyenet seems to alternate between two contradictory concepts of "food reward". In the first version, food reward is something inherent in certain foods with high fat, sugar or salt.  In his second version, "reward" is a conditioned feature of food, essentially the same as Seth's flavor/calorie association.  But he can't have it both ways -- foods are either inherently rewarding, or their degree of reward can be altered and conditioned.  I think the evidence is pretty strong that what is reward varies a lot between cultures, between individuals, and even during the life of any one individual.

So I think the theory has the causality backwards.  For the most part, we don't get fat because food is too tasty or palatable.  Rather, normal palatability turns into irresistible cravings as a result of the metabolic dysfunctions of obesity, principally leptin resistance and insulin resistance.  This has been shown most elegantly by Robert Lustig's work.  Of course, once palatability has become conditioned, it reinforces the eating habits that promote and maintain obesity.

This question is not merely a theoretical one.  The way you answer it has consequences for what you should do to reverse or prevent obesity.  Guyenet recommends we eat a bland diet to avoid triggering the cravings that may lead us down the road to obesity.  But I think this is a bit like the AA approach to treating alcoholism through abstinence.  It works as long as temptation can be kept at bay, but it does nothing to fundamentally change your response to food.  To do that, I think you have to change your metabolism -- your insulin and leptin sensitivity -- and your psychology, as I've urged in my Deconditioning Diet.

Interested in everyone's thoughts about the food reward theory.

Todd

[shadowfoot]

So again we are back to the ultimate question: what exactly causes that metabolic dysfunction? Consider the case of my family's cats. They are both a tiny bit overweight. They are outdoor cats and roam the world hunting (exercise), they sleep all the time (rest), live in the middle of nowhere which is a very natural environment for them (low-stress). Therefore, the only possible axis is that their store bought food causes them to have a tendency to gain weight. Is it the fact that it is chock full of vegetable oils? Grains? Flavorings? I think it contains enough supplements that nutrient deficiency is not a cause.

I would also like to make a comment on what exactly hyperpalatable food is. If I have homemade food next some something that is "hyperpalatable," the homemade tastes infinitely better. Yet it fills you up instead of giving you that could eat all day feeling. So why does something that tastes worse make you want to eat more? Perhaps someone who has not consumed mostly homemade food their whole life like I have could suggest an explanation. The only thing I can think of is that the "hyperpalatable" food is not satisfying, so you continue eating it in the hopes of being satisfied. This might be because the food is good so that you want to eat it, but not good enough so that it satisfies you. I might be totally off base here, but, in any case, what are your thoughts?

[Todd Becker]

shadowfoot,

Metabolic dysfunction is complex, but it comes down to inefficiency in both storage and utilization of energy compounds like glucose, fatty acids and amino acids.  I like to think of it metaphorically as "plugged pipes". On a biochemical level, this translates to a reduction in the number and sensitivity of receptors, transmembrane transporters and enzymes.  Perhaps paradoxically, it often involves an overcompensation by certain hormones like insulin.  There is increasing evidence that metabolic dysfunction is the product of (a) a pro-inflammatory diet, lacking in protective micronutrients; and (b) insufficient stress (of the good sort).  Your slightly overweight cats sound like they get good exercise from hunting, but otherwise have a low-stress existence.  Perhaps introducing a dog to the scene would up their fight-or-flight hormones and help shed a few pounds! (Read Chapter 2 of The Gabriel Method for just such a story that led Jon Gabriel to lose over 220 pounds). Otherwise, it could be their diet. Your suspicions about vegetable (o-6) oils, grains and artificial flavors may be right.  And just having all the recommended vitamins and minerals is often not enough.  What about essential fatty acids?

Regarding hyperpalatable vs. homemade food, I agree with you that the latter is much more satisfying.  You ask a key question:

If I have homemade food next some something that is "hyperpalatable," the homemade tastes infinitely better. Yet it fills you up instead of giving you that could eat all day feeling. So why does something that tastes worse make you want to eat more? Perhaps someone who has not consumed mostly homemade food their whole life like I have could suggest an explanation. The only thing I can think of is that the "hyperpalatable" food is not satisfying, so you continue eating it in the hopes of being satisfied. This might be because the food is good so that you want to eat it, but not good enough so that it satisfies you.

I think you hit the nail on the head: so-called hyper palatable food generates cravings precisely because it fails to satiate.  This then raises the question: exactly why does it fail to satiate?

The answer, I believe, comes back to metabolic dysfunction, and the theory I first proposed on the Diet page of this blog.  The strong flavors of hyper palatable food activate the vagus nerve, which connects the hypothalamus to both afferent (sensing) circuits in the nose and mouth and efferent (acting) circuits in the digestive tract.  Hyperpalatable foods typically contain readily assimilated carbohydrates and proteins, which spike insulin.  Through experience, the hypothalamus "learns" to secrete insulin and digestive hormones in response to the flavorful stimuli.  These causes a more rapid uptake and storage of the glucose, fatty acids and amino acids that are present, depleting the blood stream of these energy molecules -- a fact that the arcuate nucleus in the brain detects.  So you are left wanting more, and the hypothalamus turns up the drive to eat more.

In insulin-sensitive individuals, the elevated insulin crosses the blood-brain barrier, where it is detected in the hypothalamus, leading before too long to satiation.  In insulin-resistant, leptin-resistant individuals, however, insulin does not readily cross the blood brain barrier, so satiation does not occur.  This makes the cravings worse, and the vagus nerve "learns" to secrete even more insulin to compensate, leading to a vicious cycle.  Even worse, many of these hyper palatable foods are pro-inflammatory, further reducing the sensitivity of glucose transporters and reducing the permeability of the blood-brain barrier to insulin.

By contrast, home made foods are typically lower in fast-release carbohydrates, blunting the insulin response.  And even if they do contain starches and sugars, they generally are non-inflammatory, so the efficiency of insulin and transmembrane transport are improved.  The appetite centers in the brain can thus be more readily accessed, leaving you satisfied.

Subjectively, all you know is that the hyper palatable food is generating a stronger craving.  But underlying all of this is a biochemical set of events that train the hypothalamus to treat the flavors, aromas (and other sensory stimuli) from these particular foods as more salient by a conditioned release of dopamine -- a neurotransmitter that can lead to addictive behavior when over secreted. 

At base, however, this response to flavor is learned.  As Seth Roberts discovered in his Shangri-la Diet, breaking the association between the flavor and the calories removes the drive to eat and restores healthy appetite suppression.  The flavor by itself -- devoid of calories -- is impotent.  There are no "hyper palatable" calorie-free foods.

[shadowfoot]

One of the things I like so much about the hormesis approach is the idea what while it is true that many people have too much "bad" stress, getting enough "good" stress is just as essential as reducing the "bad" kind for optimal health. During the summer, as an experiment I removed almost all stress from my life. The result? I became lethargic and bored.

I am a little bit confused by your explanation of the initiation of metabolic dysfunction here. In your "Is Tasty Food Making Us Fat?" post, you said that you did not think that hyper-palatable food was the primary cause of weight gain, but rather that metabolically challenged individuals become sensitized to hyper-palatable food which then becomes addictive. But now you are saying that though vagal nerve stimulation the hypothalamus learns to respond a certain way to hyper-palatable food, namely, by depleting the bloodstream of glucose, amino acids, etc more than is necessary, which leaves you "wanting more." Are you trying to say that the combination of hyper-palatable food and high GI carbohydrates causes an imbalance blood glucose through the action of the hypothalamus that leads to metabolic damage? Please explain.

By the way, my spell check doesn't think that hormesis is a real word

Edit: Oh, and double by the way, I have three stars and an avatar now.

[Rudy]

I'm with gnolls.org on that one...

[Todd Becker]

shadowfoot,

Somehow I missed this earlier post of yours.  So that explains the delayed response here:

The essence of my point has to do with the order of causality of craving.  Is it the flavor of certain foods that initially causes us to crave them?  Or do those very foods (and similar foods) eaten frequently have other attributes besides flavor that alter our metabolisms and brain circuitry to increase their perceived palatability to the point of irresistability?  I think the evidence supports the latter scenario.  

Suppose you had never eaten any Western foods and were raised in the jungles of Borneo, and had a lean, insulin-sensitive metabolism.  Then you were exposed to Coke and natchos.  At first, you might find these foods odd tasting.  Their ready availabity of glucose, fructose and starch would also cause you to feel full quite readily.  Your well functioning pancreas would quickly deliver glucose, amino acids and fatty acids to the cells. Your insulin would cross the blood brain barrier quickly and provide a satiety signal to your hypothalamus.  So you would feel full and not inclined to overconsume these new foods. They might even make you feel a bit wired or sick.  But if you began to eat such foods regularly, your liver would start increasing triglyceride levels (from the fructose and carbs) and non-esterified fatty acids which in combination would begin to cause some degree of insulin resistance, first in the muscles and liver, and then even in the brain.  Insulin and leptin transport across the blood brain barrier would become impaired, so the satiety signal would be delayed and impaired.  The insulin resistance would also lead to hyperinsulinemia, which would tend to drive down the concentration of glucose, fatty acids and amino acids in the bloodstream and inhibit their release from glycogen, adipose tissue and muscle tissue.  The net effect of reduced availabilty of nutrients in the bloodstream, and impaired appetite satiation in the hypothalamus, would increase general hunger and cause you to eat larger meals before reaching fullness.  The pscychological correlate would be a desire to eat more of the specific foods that quickly raise insulin levels, since high insulin levels are now needed to turn off the appetite signal in the brain.

This process plays out over years, not instantly.  So it is more difficult to prove the causal sequence.  But I think that work by Lustig and others is starting to make this clear.

I have a new article that will be posted soon that builds on the idea above and adds some new twists.

Hope that helps resolve the confusion.  Let me know.  And congrats on reaching 3 stars.  You are in the upper echelon of contributors here!


Rudy,

I like what I read so far on gnolls.com.  I'm interested in what parts of his discussion of satiety is most convincing to you.  I was particularly intrigued by the mouse study showing that food reward (behaviorally defined) can exist even in animals that are genetically unable to taste flavor!  I take this as evidence for my own view, which is that "reward" is initiated as response to metabolism, not the other way around.  Of course, once "reward" behavior is learned and becomes associated with the flavor, appearance, etc. of a food, it because self-reinforcing so long as it continues to deliver reinforcing nutrients and so long as the metabolism remains hyper-responsive to the effects of these nutrients on hormone signalling and the hypothalamus.

Todd