The Shangri-La diet depends on two theories:
The Set-Point Theory, that claims the brain - in particular the hypothalamus - has a target weight, and it adjusts the body's resting metabolic rate (RMR) to ensure that the target weight is achieved.
The brain's target weight is set by one parameter that can be adjusted lower through the use of bland foods.
Set-Point Theory is controversial, in that it is popular, but lacks scientific evidence.
Bruce Jancin of International Medical News writes:
It's high time to toss out the long-popular set point theory of obesity, according to speakers at an international conference of the Academy for Eating Disorders.
The set point theory holds that obesity entails a metabolic defect that functions as a homeostatic mechanism. This defect is supposed to result in a slowdown of resting metabolic rate in an overweight or obese individual who has lost weight. The resultant reduction in energy expenditure is said to be responsible for the often-observed scenario in which the individual regains the weight that was lost and thereby returns to his or her set point.
The set point theory enjoys widespread popularity among the overweight public, in whom it fosters a fatalism regarding the condition of obesity. The theory also holds sway among many physicians who work with obese patients and/or those with eating disorders.
But scientific support for the set point theory is limited to old data derived from outdated methods of physiologic measurement.
A 1990 study published in FASEB, Role of set-point theory in regulation of body weight, is an example of research contradicting set-point theory:
Current working hypotheses include roles for nutrients, dietary composition and organoleptic properties, hormones, neural pathways, various brain nuclei, and many neurotransmitters in the regulation of food intake. It is concluded that regulation of body weight in relation to one specific parameter related to energy balance is unrealistic. It seems appropriate to assume that the level at which body weight and body fat content are maintained represents the equilibria achieved by regulation of many parameters.
So, it isn't one point in your brain deciding on your target weight, but lots of different factors throughout the body.
What about the research that supports it?
Well, the article quoted in the question is this one:
While this looks like a journal article, in fact, it is just a few paragraphs (less than a page) explaining what the diet is and nothing else. There is no evidence here to support it.
There do seem to be legitimate researchers out there who take the complicated version of set-point theory seriously.
In a 2007 article published in Diabetes Spectrum, The Physiology of Body Weight Regulation: Are We Too Efficient for Our Own Good?:
This so-called set-point theory of body weight regulation has been slowly developed over a number of years and backed by a plethora of experimental approaches.
They go on to cite at least five studies they claim support the set-point theory hypothesis. One of which was the first one I listed above. Some of which are rodent studies, which may not apply to humans.
They make the case that the best evidence for the set-point theory is that it is ubiquitous among weight-loss studies that the participants regain the weight, going back to their original point. They claim the main mechanism here is a change in the resting metabolic rate (RMR):
With the body being more metabolically efficient than before, a return to the original feeding level after a period of weight loss through decreased caloric intake would regain the lost weight. For individuals who are particularly efficient, it may even lead to net weight gain.
However, one of their cited papers, Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory (2000, AJCN) refutes this:
The results also suggest that adaptive down-regulation of RMR is not a characteristic of weight-reduced individuals and does not explain their weight-regain tendency. The weight-gain tendency of obesity-prone persons appears to be caused by factors other than variations in metabolic rate.
Other factors, not RMR, explains why dieters tend to return to their original weight.
In conclusion: There are some complex versions of set-point theory that researchers are still working on, involving many (rather than a single) biological feedback loops.
Roberts vastly oversimplifies the theory by reducing it to a single parameter. His version of set-point theory is not supported by the scientific research.
