Here I am returning to the SLD forums after being away for 2 1/2 years. Returning at the requests of several forum members - Oslo, Heidi555, elenadelphiki -- as well as recent renewed interest on this thread about physiologically grounded explanations as distinct from (but not necessarily in opposition to) to evolutionary or behavioral theories. I now think there is a lot of strong evidence to support a particularly powerful physiological explanation for why the SLD usually works, based upon the actions of the hormone insulin.
Physiological explanations are more readily tested and quantified than behavioral or evolutionary approaches, because they employ empirically measureable quantities, e.g. blood levels of sugars, fatty acids and hormones. By contrast, a "setpoint" is a non-observable, hypothetical quantity, which is only useful to the extent that it is consistent with accurate explanations and predictions. Where do I look inside my body to find this "setpoint" ? Is there a little thermostat in there with the pointer set at 175 lb.? Not trying to be too facetious here, but at least chemicals can be assayed from a blood sample, and biochemical pathways are well proven.
I do believe there is a simpler, more verifiable theory than the setpoint theory that explains why SLD works -- and does so within a broad framework that is meticulously supported by research over the last century and a half. This theory is clearly and forcefully set forth in Gary Taubes "Good Calories, Bad Calories in Chapters 22-24, but especially in the very last (and best!) chapter of book, Chapter 24. In Chapter 24, Taubes deals a real blow to various setpoint theories (there's more than one) including Mayer's glucostat hypothesis (the brain tries to control glucose concentration in the bloodstream) and Kennedy's lipostat hypothesis (the body tries to maintain a fixed reserve of fat in the adipose tissue). Both the glucostat and lipostat hypotheses posit that the setpoint is located in the brain -- specifically, within the hypothalmus. According to the lipostat theory, the difference between lean and obese individuals is the amount of fat stores the hypothalmus is set to defend. According to Seth, the SLD can at least temporarily change this setpoint. I say "temporarily", because presumably if one strays from the SLD diet, the setpoint will go back to its "natural" level. But there is no explanation for what determines this "natural" level.
Taubes offers several criticisms of these setpoint theories, particularly the lipostat hypothesis. First, the lipostat theory does not explain how the brain actually monitors our fat stores and compensates by changing food intake or energy expenditure. No biochemical mechanisms are proposed. Second, it overlooks the far simpler approach employed by physiological psychologists, including Claude Bernard, Walter Cannon and Ivan Pavlov (one of Seth's intellectual forebears, I believe) in the nineteenth century, and Curt Richter and Jacques Le Magnen in the twentieth. The central focus of these researchers was to deduce how the principle of homeostasis (maintenance of a stable internal state against external changes) applied to the control of body weight and appetite on a cellular, biochemical level.
The most revolutionary outcome of Le Magnen's research, including the work of many subsequent researchers, was the proof that both weight regulation and appetite are primarily regulated by a single hormone: insulin. While other hormones like leptin, the sex hormones, and growth hormone modulate the insulin response (e.g. by increasing it or decreasing with age or in specific body tissues such as the abdomen, buttocks, etc.), the fundamental factor that determines whether fats and sugars are moving into storage or moving out of storage is the level of insulin in the blood. Furthermore, insulin also turns on or off enzymes in the cells, such as lipoprotein lipase, which allows cells to "grab" fatty acids on hold onto them tightly.
Now where this gets very interesting is that when insulin levels are elevated, as after a large meal, particularly containing carbohydrates), glucose and fatty acids in the bloodstream are rapidly taken up by the cells, depleting their levels in the blood and inducing hunger. This often causes more eating and more depletion and hunger in several cycles. Whereas when insulin levels are low, as on a low carb diet or the SLD diet (I'll explain why shortly), fat cells cells readily release fatty acids and the liver and muscles release glucose from there glycogen storage, creating the sense of satiety or appetite suppression, which further reduces eating...and leads to weight loss.
So now I'm getting to the punch line. Why does the consumption of flavorless calories lead to weight loss? The answer is quite interesting: flavors induce an insulin response and elevated insulin levels increase appetite; therefore, eliminating flavors and aromas (or blocking them by nose-clipping) suppresses appetite. In fact, research in both animals and humans shows that flavors, aromas, and even the THOUGHT of appetizing food causes a "pre-prandial" or "cephalic phase" (before the meal) secretion of insulin, which is sometimes as much as 1/3 of the total insulin secreted during a meal. This pre-prandial secretion of insulin depletes glucose and fatty acid levels in the blood by driving them into the storage tissues, thereby creating the sensation of hunger and driving us to eat. Once the food is in the stomach, more insulin is secreted, driving further appetite and storage, until an equilibrium is reached. And measurements on obese individuals show that not only are their insulin responses abnormally high, but their pre-prandial insulin secretion responses to the smell, taste or thought of food are especially high! The more you love food, the more quickly your hunger returns and the more tightly your cells store fat and hold on to it...oh, the woes of being a gastronome!
Physiologically, the insulin response is governed by the vagus nerve, which induces pancreatic and gastric secretions in response to flavors, aromas and appetizing thoughts. The vagus nerve extends from the hypothalmus to many of the tissues involved in nutrient metabolism, such as the stomach, intestine, pancreas, and liver. This is all set out nicely in a 1996 article by Karen L. Teff: "Physiological effects of flavor perception" (Trends in Food Science & Technology, Volume 7, Issue 12, December 1996, Pages 448-452). Many studies have shown that cutting this nerve or blocking it chemically results in significant and rapid weight loss.
The insulin response to flavors and foods is gradually adjusted over time. This is true both with respect to meal volume and nutrient content AND with respect to induction by flavors, aromas, visual cues -- even other psychological factors such as stress and mood. It is a learned response, and as such, does not turn on a dime but changes gradually. Which is why your appetite suppression doesn't go away immediately when you stop SLD for a few days. Seth has argued that this slow adjustment is evidence that the "setpoint' takes time to readjust. I think a better explanation is that the insulin response is at least in part a conditioned response -- biochemically realized in the vagal nerve response -- takes time to adjust the amount of insulin that is secreted in response to a meal or a pre-meal trigger. It also slowly changes due to other variables such as exercise, aging, and other factors.
In short: The net outcome of the SLD is to reduce insulin levels, inducing satiety and allowing the release and oxidation of fatty acids stored in fat cells -- thereby resulting in weight loss. It is particularly powerful because it gets the satiety inducing nutrients -- fatty acids and glucose -- into to the bloodstream in a "stealth" manner -- with no or little insulin secretion, so instead of being whisked away to storage in the cells, these satiety inducing nutrients are allowed to remain there, shut down appetite and provide a supply of energy! Even better, the body is now in a mode where it can pull additional fatty acid and gluose energy from storage to provide further energy. Great deal!
The insulin hypothesis is also attractive because it explains much, much more than just the SLD diet. For example, it explains why it is so hard for obese individuals, or people with certain genetic backgrounds, e.g. the Puma indians, to lose weight -- it is because their genes in combination with their diets have caused them to become hyperinsulimic -- their basal level of insulin is so high that even the tiniest amount of food is scavenged by their cells. These high insulin levels are REAL -- unlike a "setpoint" they can be measured from blood samples! And it takes a lot to quiet this insulin response, but it can be done -- by a very low carb diet, by the SLD diet, or even by meditation and stress reduction as proven by Jon Gabriel (See his amazing diet, The Gabriel Method which, I believe, facilitates weight loss by using visualization and mediation to quiet the insulin response). This also explains why dieting and excercise so often fail, because elevated insulin levels leave the blood depleted of glucose and fatty acids, and cause intense cravings even when calories are cut back. On the other hand, it should be encouraging to those who have the patience and persistence to know that, as they lose weight and reduce insulin levels, their basal insulin levels will slowly decrease, and maintaining their low weight will become easier with time. Setpoint theories, by themselves., would not predict this fact.
(Another interesting aside relevant to the SLD: fructose, the sugar in Kool-Aid and other flavored sodas mentioned in SLD, has no ability by itself to induce an insulin response. So that could explain the appetite suppressing effect of some of Seth's French sodas. However, if any glucose is combined with fructose, as is the case with sucrose (table sugar) or high fructose corn syrup, the insulin response is induced and in fact fructose is more easily converted to triglycerides in the liver as long as there is insulin around).
To summarize: The key to weight loss is ingesting calories without inducing insulin. Flavorless calories just happen to be one cleverly stealth way of doing this, but it is certainly not the only technique available.
In any case, I'd be interested to hear what others think of the the insulin hypothesis as an alternative to the pure behavioral and evolutionary explanations. (Notice that in all of the above discusion, there was no need to refer to evolutionary theories of feast or famine by our ancestors!)
Todd
P.S. In a recent post by Shovelqueen, I see that she and others in the forums are on to Taubes, whose book I first read when it came out. It is really a masterpiece of synthesizing research from many fields into a coherent whole. I also see that Seth interviewed him, but for some reason there was no real discussion of the setpoint theory vs. the insulin hypothesis.
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Topic: Appetite Suppression vs. Setpoint Adjustment (Read 54443 times)