In response to my recent post -- Can low carb cause central adiposity? -- James Krieger posted a link to a recent study indicating I may well be on to something. So I thought I would post this study separately (I don't have access to the full text on this one).
Longitudinal adaptations to very low-carbohydrate weight-reduction diet in obese rats: body composition and glucose tolerance.
Longitudinal effects of a very low-carbohydrate (VLC) and a calorie-matched high-carbohydrate (HC) weight reduction diet were compared in dietary obese Sprague-Dawley rats exhibiting impaired glucose tolerance and insulin resistance. Obese rats were divided into weight-matched groups:
(i) VLC rats consumed an energy-restricted 5% carbohydrate, 60% fat diet for 8 weeks,
(ii) HC rats consumed an isocaloric 60% carbohydrate, 15% fat diet, and
(iii) HF rats consumed a high-fat diet ad libitum.
HC and VLC rats showed similar reductions in body fat and hepatic lipid at the midpoint of the weight-reduction program, indicating effects due to energy deficit. At the end point, however, HC rats showed greater reductions in total and percent body fat, hepatic lipid and intramuscular lipid than did VLC rats, suggesting that diet composition induced changes in the relative efficiencies of the HC and VLC diets over time.
Yes ... this is a rat study with all the issues inherent in trying to extrapolate to humans, but let's not forget Dr. Eades' favorite c57bl6-mouse that he says provides evidence for the so-called metabolic advantage of low carb diets. In that study, the growth rate of ketogenic diet fed mice was stunted to that of the calorie restricted diet vs. three other diets. I'll try to remember to update with a citation, but in one longterm study on epileptic children treated with a ketogenic diet, their growth percentiles (height AIR) declined following treatment. But I'll leave a dissembling of this study and the conclusions Eades draws from it for another day.
It is important to note that these were not genetically obese rats, but rather were made obese through diet and then put on weight loss diets. In this study, the VLC and HC rats lost the same for a period of time but the metabolisms of the VLC rats apparently became more efficient indicating an adaptation. Anecdotally, most low carbers seem to plateau out well above their goal weight. The various long term studies of LC diets seem to follow a similar trajectory of rapid initial losses followed by regain that would be consistent with the findings of this study. My own metabolism is in the tank as I do seem to become very efficient during long strings of low carbing. It would be an interesting study to recruit a number of long term weight loss success stories and compare the metabolisms of VLC'ers to LF'ers.
Back to the study:
HC rats showed marked improvement in glucose tolerance at the midpoint and end point, whereas VLC rats showed no improvement.
This ties in with what I've been saying now in many posts regarding "curing" diabetes with low carb diets. Whatever the glycemic issues of the VLC rats before diet and weight loss, the underlying metabolic impairment persists.
Impaired glucose tolerance in VLC rats at the end point was due to insulin resistance and an attenuated insulin secretory response.
So, again, a VLC diet may not only mask symptoms of IR and impaired insulin production, but could potentially sustain the underlying issues and/or further complicate matters by reducing the insulin response.
Glucose tolerance in energy-restricted rats correlated negatively with hepatic and intramuscular lipid levels, but not visceral or total fat mass. These findings demonstrate that adaptations to diet composition eventually enabled HC rats to lose more body fat than VLC rats even though energy intakes were equal, and suggest that the elevated levels of hepatic and intramuscular lipid associated with VLC diets might predispose to insulin resistance and impaired glucose tolerance despite weight loss.
This paragraph reads a little vaguely to me b/c they lump the VLC & HC groups into one when they talk about the energy-restricted rats. It sounds like they are saying that VLC rats had higher hepatic (liver) fat and intramuscular lipid (IMCL) compared to the HC rats and this correlated with impaired glucose tolerance/IR. But visceral and total fat mass was not associated with IGT so it wasn't just the lesser VAT/SCAT fat loss of the VLC group that was responsible for the observed IGT and IR in these rats.
So, yes, this is a rat study. But it is adding to concerns over long term low carbing.