From Seth Roberts, 6:01 a.m. today as Reply #1:The proof is in the pudding -- that is you've lost weight easily -- but can we really trust the recipe from which the pudding was made? yes, it would be odd indeed if I used wrong ideas to come up with a really good diet.
here is what your alternative explanation doesn't explain:
1. there is lots of evidence for a set point apart from my particular version of setpoint theory . It is a 50-year-old idea.
2. Whatever your dosage of SLD calories -- say 2 T of oil/day -- eventually your appetite will return and you will stop losing weight. My theory predicts this: you have reached a new equilibrium. Your alternative does not.
3. my theory doesn't say that any flavors stimulate appetite, only flavors associated with calories. Unfamiliar flavors should have no effect. This is a prediction that conventional ideas about weight control do not make -- that familiarity matters. In particular familiar foods are more fattening than the same foods when they are new.
I believe my theory because it has repeatedly suggested new ways of losing weight that, when tried, actually work. This has now happened about six times.My reply:
1. It would not be odd that a wrong or less adequate theory generates a good invention or predictions. This has happened often in the history of science and technology, e.g., the phlogiston theory of combustion helped provide a coherent explanation of phenomena as various as combustion, metabolism, and formation of rust, but eventually was replaced by Lavoisier's caloric theory of combustion based on his experiments with oxygen.
2. The 50-year age of the setpoint theory is not in itself an argument in its favor. And even if there are such things as setpoints, they may not be the BEST explanation of how the SLD diet works.
3. From reading the forums, it appears that consistent intake of a set amount of oil or sugar doesn't always produce the classical asymptotic approach to a new fixed equilibrium weight that one would expect if weight setpoints were like thermometer setpoints. Often the weight drops, plateaus, moves up a little; in other individuals there is a long, linear decline; and other times there is flattening and sudden drops. This doesn't sound to me like an approach to "equilibrium". But suppose in fact that after daily doses of 2T/day oil, my appetite eventally "returns" and I stop losing weight. That can also be explained by pointing out that, while the oil exerts a fixed contribution as an appetite suppression, appetite is a function not just of the suppressant dosage, but of other factors such as adaptation of tissues and receptors, blood concentrations of various metabolites, etc., that could in fact be a function of the individual's weight. Levels of obesity hormones such as leptin and ghrelin may vary as individuals become leaner.
4. The fact that only familiar flavors stimulate appetite may be explained by an alternative physiological mechanism. Apparently, ghrelin -- a peptide hormone proven to be a potent appetite stimulator -- is secreted into the stomach by "anticipation" of a meal, apparently after flavors are detected by the vagus nerve via acetylcholine synapses:http://nielsolson.us/archives/2006/05/ghrelin_leptin.php
Couldn't it be that the vagus nerve and acetylcholine synapses respond better to familiar flavors than unfamiliar ones? One could posit that neural pathways become more established upon repeated exposure to a stimulus.
Similarly, the presence or absence of calories might be detected by other hormones like insulin. So appetite changes may results by a complex physiological calculation resulting from these hormone levels. Further, it is well know that levels of insulin, ghrelin, leptin, etc. are influenced by adiposity and overall body composition. So one can explain why the effectiveness of an appetite suppressant or stimulant might change as we gain or lose weight.
I would think that a physiological approach based on multiple biochemical inducers and inhibitors is more likely than a simple setpoint model to explain the wide variety of responses seen by people following the SLD diet.
My main point is not that the setpoint theory is wrong, but that there may be more useful and adequate theories which not only explain a greater variety of individualized response to the SLD diet, but more importantly, which are more scientifically productive because they are based on empirically measureable entities such as peptide hormones, rather than theoretical "constructs" like "setpoint" which can't really be observed directly. And empirical theories are better suited to being tested, refined, and used to generate more specific predictions.
Here's an example of a specific prediction: Flavors that will not increase appetite are those which do not stimulate the vagus nerve. One recent article provides data that of five flavors tested, only sucrose did not induce a vagus nerve response as measured by an increase in heartrate! Take a look:http://chemse.oxfordjournals.org/cgi/content/full/25/2/149
That would explain the oft-raised puzzle as to why sucrose is not a "flavor". A secondary prediction is that SLD-friendly calories do not cause an increase in heartrate. And presumably all the above would have some connection to ghrelin or other appetite hormones. So measure your pulse next time you try taking your oil or sugar! In short:
Sometimes a very nice theory generates a large number of very useful observations and results. But then one must be willing to follow the observations wherever they go, and modify, revise, or even overthrow the theory in favor of one that is more adequate to the data -- when this becomes necessary or more productive.