Forgive me if this has already been addressed in one of our Stephan threads. I'm not sure that it has, because it's kind of like a background question for the main issue.
I have an intuitive understanding for why various changes to our way of living can lead to a lower body-fat setpoint. (Note -- I am assuming the setpoint theory, at least for the time being, and so rejecting that calories in and out can give a full explanation of what's going on. Relevant Paleohacks threads here and here.) So, for example, if you do a lot of sprinting, then you're telling your body "Hey, I need to sprint" and your body responds with "OK, I'll give you the kind of body that can sprint -- a leaner one." Sprints can lower the setpoint. I have an intuitive understanding for "metabolic repair" as well. If you screw up your body with fructose and PUFAs then some kind of mechanism goes out of whack (please have mercy on my simplification!) and if we repair that mechanism then we lose body fat, and for good. We bring our body back to the shape that nature intended. Fixing your metabolism can lower the setpoint.
But what kind of intuitive explanation can we come up with for the food reward theory? I just don't see why eating more delicious food would incline my body to carry more fat. Or, put inversely, I don't see why eating less delicious food would incline my body to carry less fat. (Again, warning, we're assuming that it's not just so simple as: delicious food causes me to eat more of it. Because if the theory is right you could be cruising along at a stable body weight, eating delicious food, and then start eating plainer food and then find a new, stable, body weight.)
Does this make sense, what I'm trying to get at? Does anyone have a plausible backstory for plainer food leading to a lower setpoint? Perhaps Stephan himself addresses this somewhere on the blog? Thanks, P.
From this part of the series - http://wholehealthsource.blogspot.com/2011/06/food-reward-dominant-factor-in-obesity_18.html
Reward Centers can Modify the Body Fat Setpoint
Dopamine is a neurotransmitter (chemical that signals between neurons) that is a central mediator of reward and motivation in the brain. It has been known for decades that dopamine injections into the brain suppress food intake, and that this is due primarily to its action in the hypothalamus, which is the main region that regulates body fatness (1). Dopamine-producing neurons from reward centers contact neurons in the hypothalamus that regulate body fatness (2). I recently came across a paper by a researcher named Dr. Hanno Pijl, from Leiden University in the Netherlands (3). The paper is a nice overview of the evidence linking dopamine signaling with body fatness via its effects on the hypothalamus, and I recommend it to any scientists out there who want to read more about the concept.
Increased dopamine signaling, particularly through the dopamine D2 receptor, can attenuate and in some cases reverse obesity in diet-induced obese animals, seasonally obese animals (squirrels, Syrian hamsters, etc.), and overweight/obese humans (4). Not only that, it can increase resting metabolic rate and attenuate the metabolic abnormalities associated with obesity even before the fat is lost, which emphasizes that these circuits control metabolism directly, as well as indirectly by influencing fat mass (5)*. Conversely, people who have genetic or drug-induced reductions in D2 receptor signaling gain fat at an accelerated rate (6, 7).
Together, this supports a hypothesis that I've scarcely seen in the scientific literature: that reward centers, and probably food reward itself, can directly influence body fatness and metabolism. Other people have made parts of this argument, however, I've never seen anyone put together the evidence from psychology, pharmacology and neurobiology into a single coherent hypothesis.
It goes on from there and I won't copy the whole series for you :-)
I would also recommend you read the articles he provided for reference here - http://wholehealthsource.blogspot.com/2011/07/food-reward-dominant-factor-in-obesity.html
BTW - I'm not necessarily endorsing this, just providing an answer to your question.
i think stephan's theory is as simple as saying that more food reward causes you to eat more food, thereby increasing your calories. i think he is positing that a constant hyper-stimulated diet of extremely great-tasting food will move your setpoint because it will mess with reward centers in the brain as it relates to satiety- at least that's what i get from it. i don't know if i'm all the way on board with it but it definitely seems like it could be a factor in obesity- particularly for those on the SAD.
as i believe and others in comments on his posts have mentioned, the distinction has to be made between palatability and reward. i love good food. i cook good, well-seasoned food that is highly palatable. however, it is not rewarding in a way that i felt a half a cheesecake would have been in my past life. the paleo food i cook is tasty but i don't get that drug-like fix.
there's alot of back in forth in his comments section about dopamine and its receptors and other things that are above my head but seem very relevant and interesting.
I think food reward does influence overall weight. If you have tasty foods around, you eat more, a little bit more. Steak is delicious so you might eat a bit more. But delicious by itself does not throw your whole body set point of drastically over the long haul. It doesn't trash your metabolism and cause you to be undernourished even when fat. That's why eating top quality meat and top quality delicious paleo may make you a few pounds heavier than if you at grisly tough low quality half burned meat all the time, but it's not going to make a huge health difference overall. No matter how delicious the food, taste alone does not move the setpoint greatly. You can only eat so much of even the best tasting steak in the whole world.
What screws up the set point are some foods that are unnatural and that the body does not know how to safely and properly process on a regular basis. What also may screw up the set point is chronic lack of nutrition. You can eat tons of calories and be overweight, but if what you are eating has no nutrition, you can still be in a sense very starved. Many of the low nutrition unnatural foods do trigger addictive responses and some of them even taste good.
But I think you will find, on careful examination, that many of these unnatural foods do not actually taste all that great. Instead, what you respond to is satiation of an addiction, which has a high value in itself, but is not actually related much to taste. Many cakes, breads, noodles, crackers, etc have very little taste. From a taste perspective, they have very little value. Yet they still give a satiated feeling from relief of an addiction craving. And they do often lead to movement of the body weight set point.
I also have no idea how set point alteration works, but Stephen's food reward theory reminds me a lot of the Shangri-La diet, where one introduces flavorless calories into the diet, which have zero food reward.
I'm not sure that the method works by lowering set point, or whether the weight loss results from keeping the body in a semi-fasted state for longer by suppressing appetite without stimulating taste cravings.
IMO physically eating processed crap and sugars can induce a high setpoint as the body's biochemistry is messed up. However, the reward theory (which i believe is effective) seems to simply lower your own intake rather than DIRECTLY influencing setpoint (which is leptin). As a former obese guy, when I eat "tasty" foods I get this little high in my head and I start chomping WAY more than satiety. I start confusing satiety with whether my stomach is full. This short-term overfeeding leads to inflammation (excess calories) and reinforcing leptin resistance, leading to my inability to lose the last 15lbs. However, I think if you're fit and lean, a little overfeeding can be compensated without gaining weight. But for those who are still fat and wish to decrease weight, overeating is very hindering as the body's adipose tissue is already causing excess baseline inflammation.
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