I've spent the past four days doing a lot of research (medline, mostly, but at the U, too) on this issue (because of my own stunningly low metabolic rate) and wanted to share some of the results here.

From what I can find, VLCD (very low calorie diets) have been proven several times to lower metabolic rate. However what we've been saying here, that this phenomenon is due to the loss of LBM, may well not be true. At least there is no study that supports this assertion.

Does metabolic rate (RMR) lower with hypocaloric diets? Several studies say yes. Some say that upon ceasing the diet, the RMR goes back up--but those studies tend to have kept the subjects on the VLCD for something like 3-7 days. (like, sure--that's all we need to drop 50 or 150 pounds! lol) The problem is, they really don't entirely know why it drops.

Yes, LBM is lost during VLCD. only 75% of weight loss on diets of <900 calories is fat. (another irritating issue--the literature examines everything from 1350 calorie diets to 330 calorie diets and calls them all "VLCDs" which may not help in unraveling this mystery)

BUT! According to the abstract of an article by a Dr. Burgess of Northwestern U, "it appears that the decrease in resting metabolic rate that occurs during treatment with VLCD does not correlate with changes in lean body mass." That is, some of the subjects who lost the most LBM had the least effect on their RMR and vice versa.

Then what's the mechanism for reduction of RMR during and after lowering caloric intake? All the following may be part of the true answer:

Possibility one--most research supports the finding that T3 levels are lowered in VLCD dieters. "It was concluded that fat-free mass loss, combined with periferic thyroxin (T4) reduced monodeiodination in its more active form mainly due to low calorie intake T3 could be responsible for the important reduction observed in the resting metabolic rate." (now where'd I put that physiology degree? )

Another possibility somehow (either it didn't explain well enough or I didn't comprehend well enough) connects clear changes in IGF-I and IGFBP-3 (insulin-like Growth Factor-I and insulin-like Growth Factor binding protein) that result from VLCDs to the lowering of RMR.

Possibility number 3--Related is that DHEA levels may drop during and after a VLCD in perimenopausal and menopausal women. Another researcher says the change in DHEA is age-dependent (but doesn't speculate if it's related to levels of sex hormones). However, according to the Eades, those of us who weightlift should be producing more DHEA and HGH...I'll have to go back and see if they footnote that claim.

Possility 4 is of course "they don't have a clue yet," which may be the most likely. Irrespective, RMR clearly does lower in women (not much research on men). 23-25% drop in RMR is what most of the research shows.

That means if, like me, you've done years of VLCDs, and fitday.com says that for a woman of your age and weight and job, you should be burning off 1600 calories before exercise, you're probably only burning 1200 as your basal metabolic rate.

Thus, the only way to lose additional weight for me (and anyone like me) may well be to lower calories to more like 1200...but then the cost of that may be lowering RMR further. Option 3 of course would be to say "phooey on concepts of 'ideal thinness' and let me just accept my current weight as perfect."

There's no research at all on whether a period of time of re-feeding with high-calories and low carbs can re-set metabolism, but it'd sure be a useful thing to know. Anecdotally, I've heard of it working, but when I tried it, my weight crept up for a month, and I was afraid to keep up the trial.

Anyway, since we tell people here that it's the LBM decrease that lowers metabolism, and there really doesn't seem to be any support for that which I can find in the literature, thought I'd share this. (hi nat--knew you'd be interested! )

Hi Razzle, I find this interesting too.

My immediate gut reaction to it is that I have seen this kind of response before - in hibernating and semi-torpid animals. Is it possibly some kind of defence mechanism in the human body, triggered by what it recognises as a starvation message, to try and induce a kind of torpor, rather than allow the body to starve by letting it continue to burn calories at the normal rate?

I would also be interested to know what sort of reaction you get from increasing your calorie intake to, say, double the usual quantity (provided the additional calories come from fat and protein, of course).

Andy

THere is also a nice study posted on the atkinscenter site about leptin levels and low-carb/high carb dieting. Leptin levels fall short term more on a low-carb diet, but long term sustains higher levels. Remember set-point is also in play. In my opinion, the caloric observations tend to be linked more greatly with being below/above ones set-point then the caloric consumption of the individual. This is also observed in leptin experiments. But, is Leptin the master that a lot of us think it is? Thats another question.

thanks, tec, for your addition. Leptins is another issue.

Yeah, there's always that problem, isn't there...you find some correlation but...what does that really say? As I repeat to my students several times every term...correlation is not causation. And even if it is...what's the precise causal chain? And even if we know THAT, can any of the problems be corrected by administering a drug or procedure? (Makes me realize that LCing working for most people at least in the short term is really something of a miracle.)