20 seconds work/20 seconds rest for 6 rounds of each triplet
- Med ball alt. oblique wall thrusts
- Dynamax thrusters
- Knees 2 Elbows
- Bosu push-up w/OH claps
The Diabetes “Crash” Cure & Pancreatic Fat
Of course even if the diet was 50% carbohydrate it would only be 66g/d of carbohydrate per day. Some one should tell these folks they can do as well on this level of carbohydrate restriction without all of that nasty hunger if they ate some decent fat and protein along side their carbohydrate restriction.
It is yet another example of the tragically flawed pseudo-science that damages the health of people with diabetes.
There’s no mystery here, nor is the effect reported a result of “reducing fat in the pancreas” as the doctor who came up with this “cure” suggests. All he has done is craft a “balanced” diet that has so few calories it is also low in carbohydrates.
Hepatic triacylglycerol remained low and unchanged (2.9±0.2 vs 3.0±0.3%; p=0.80), and pancreatic triacylglycerol decreased further to a small extent (6.2±1.1 vs 5.7±1.1%; p=0.005). HbA1c was unchanged (6.0±0.2 vs 6.2±0.1% [42±2 vs 44±1 mmol/mol]; p=0.10) and fasting plasma glucose increased modestly (5.7±0.5 vs 6.1± 0.2 mmol/l; p<0.01), with a 2 h OGTT plasma glucose of 10.3±1.0 mmol/l. Three participants had recurrence of diabetes as judged by a 2 h post-load plasma glucose >11.1 mmol/l. Fasting plasma insulin concentrations were unchanged (57±11 vs 65±15 pmol/l) and fasting plasma NEFA decreased further (0.72±0.06 vs 0.54±0.05 mmol/l;p<0.02).
Again, this is 3 months after returning to a “normal” diet and gaining back around 7 lbs on average. The fasting NEFA — which are elevated in diabetes (although not that much in this group) went predictably up during the dramatic 8 weeks of weight loss, but later went down to lower than the non-diabetic controls.
Jenny also makes a, frankly, ridiculous analogy between this diet — essentially a protein sparing modified fast (PSMF) — and the Minnesota “starvation” diet. C’mon now! I actually find myself in agreement with commenter “blogblog” over at Peter’s on this one. We’ve discussed here before the utterly irrelevancy of that study, and as blogblog pointed out, starving normal weight people on a protein and likely many micro deficient diet for six months is nowhere near the same as putting an overweight/obese person on a PSMF for a couple of months. Yes, as was the case here, a PSMF is best done under medical supervision as there are potential dangers, but apparently none of the participants became suicidal psychotics!
Now they don’t measure such things as pancreatic or hepatic fat on The Biggest Loser, but TBL consultant Dr. Michael Dansinger says that they basically halve the caloric intake of the participants on the show. Couple that with all those hours of exercise and you’re talking a similar very large/sustained caloric deficit. It’s my understanding that one consumes a totally liquid diet — relatively low fat at that as well — for a while following gastric bypass surgery … IOW dramatic/sustained caloric deficit. And guess what? Whether they want to admit it or not, especially the first time around, the spontaneous caloric reduction on a low carb diet is often rather significant. There’s a formerly almost 400 lb guy who used to participate at Jimmy’s who believed all the “high calorie” lore, yet when he averaged his intake on LC he was eating less than 1200 cal/day. That’s a pretty significant deficit!
Yoni Freedhoff weighed in on this over on his Weighty Matters blog with a post entitled Amazing, shocking, unbelievable news about type 2 diabetes and diet! His take, that I agree with, is basically that there’s nothing new about the advice or knowledge that diet/lifestyle change can actually cure diabetes.
I’m guessing if you’ve got type 2 diabetes, you caught that news from your doctor. In fact I’d be shocked to learn if there were a single type 2 diabetic on the planet who wasn’t told at diagnosis that weight loss and/or lifestyle change could reverse the course of their disease, and while they’d need to maintain their losses/changes to maintain the reversal, that lifestyle can have at least as great an impact on disease course as drugs.
Dr. Davis, of course, contends that all those other doctors, who advise patients to go on a traditional weight loss diet and increase their activity to lose weight are just doing that to hook them on medications. Surely they don’t have their patients’ well-being in mind. I’m guessing most aren’t ratcheting up the hyperbole because they’re coming out with their own line of gluten free products to hawk, but I digress … Back to Yoni for one more excerpt:
Wanna know what else disappeared for the participants?
Weight. In the first week they lost nearly 10lbs, or 5% of their presenting body weights. By the end of 8 weeks, they lost nearly 30lbs or 13% of their presenting body weights.
So is it surprising that a recently diagnosed type 2 diabetic who loses 30lbs living off an extremely low calorie, low carb diet, can come off of their oral hypoglycemics?
What would be interesting, to me at least, is for this group to repeat the study (measuring pancreatic fat and insulin response) in another group of subjects put on a 1200 cal/day diet for however long it takes for them to lose the same average 30 lbs and compare the results to these. Is it just the weight loss after all? After all, in long term intervention studies such as Shai, the average weight losses weren’t all that impressive – about 10 lbs at 1yr to 2yrs in both the Mediterranean and LC groups, and even the max loss around 4 months for LC was only avg of around 15 lbs. (See graphic here).
But maybe there’s something to this aside from the weight, or maybe the speed of the weight loss matters? After all, what do SAD-to-VLC-or-Paleo converters, 600 cal/day dieters (which includes such plans as KK, Medifast, HCG injections, and a caloric intake Gary Taubes’ Diet Doctor friend would be delighted to see), TBL contestants, and many many “crash” diets have in common? The establishment of a substantial and sustained caloric deficit. This of course leads to rapid weight loss. Does the rate of the loss, however, impact the fat content of the pancreas? I’ll speculate on that in my closing comments.
Getting back to Jenny’s contention that lowering pancreatic fat had nothing to do with it, and the paper that was open in my browser when this story landed in my Inbox, let’s talk pancreatic fat content for a bit. It is not controversial that the pancreas requires fatty acids for the secretion of insulin. It’s often not known by most because we focus on what elicits an acute insulin response — that being glucose (and the oft forgotten amino acids) — but we’ve discussed this here before (and I’ll have more to come). The long story short of it is that fatty acids fuel the ß-cell for glucose-stimulated insulin secretion, but they also stimulate basal insulin secretion, e.g. in the fasted state. When exposure to fatty acids is excessive, lipid accumulates in the ß-cell and causes lipotoxicity and/or cell death (apoptosis). The direct relationship between circulating free fatty acid (NEFA) levels and lipid accumulation in the pancreas (or any organ for that matter) is somewhat complicated. It appears to me that when our bodies are in a state of negative energy balance or increased usage of fatty acids as fuel, the elevated levels do not contribute to such accumulation and/or the accumulation is not detrimental but acts more as a local storage depot for the cells. But in the context of chronic energy surplus and/or the failure of adipose tissue to adequately trap and store NEFA, elevated NEFA lead to detrimental accumulation of lipid in the cells. And it appears one such cell type most affected are the ß-cells.
The paper I had open in my browser was this one: (A more detailed analysis is forthcoming in a separate post)
Pancreatic Fat Content and ?-Cell Function in Men With and Without Type 2 Diabetes
This group used an analytical method to assess the pancreatic lipid content in diabetic men and non-diabetic controls. Here’s what they found:
Median pancreatic fat content was significantly higher in diabetic compared with nondiabetic men: 20.4% (13.4–43.6 [interquartile range]) vs. 9.7% (7.0–20.2)
Note: Interquartile range (IQR) is the range of levels for the middle half of the sample. One quarter of each group had levels less than the minimum of the IQR, and one quarter of them had levels exceeding the maximum. Clearly there’s no absolute relationship between fat content (25% of the non-diabetics had fat content greater than roughly half of the diabetics), but …
This is the first report to show that, in addition to liver fat, pancreatic fat content is increased in men with type 2 diabetes, relative to nondiabetic men. In nondiabetic men, the pancreatic fat content was inversely associated with various features of ?-cell function.
Although pancreatic fat was associated with all but one model/parameter of ?-cell function, ?-cell glucose sensitivity correlated most strongly with pancreatic fat. This parameter of ?-cell function has been demonstrated to be most reproducible (14) and a good predictor of progression to type 2 diabetes in nondiabetic subjects (18).
The association of pancreatic fat and ?-cell function was found in nondiabetic but not in diabetic men. This may be explained by both methodological (relatively small number of diabetic men and low numerical values for the ?-cell parameters assessed with too little variation to allow detection of any association) and pathophysiological factors, which are more likely to account for the findings. In diabetes, the presence of pancreatic fat may be permissive to the deleterious action of hyperglycemia on the ?-cell (glucolipotoxicity) (2). Thus, because of the simultaneous activation of many deleterious cascades, including oxidative stress, inflammation, and apoptosis but also hypoperfusion of the islets, ?-cell function deterioration may develop at a rate disproportional to that of pancreatic fat accumulation. Conversely, hyperglycemia via malonyl-CoA inhibits carnitine palmitoyltransferase-1, leading to a decrease in mitochondrial ?-oxidation and further stimulation of intracellular triglyceride accumulation. As stated above, this mechanism may, among others, contribute to the higher pancreatic fat content observed in diabetic relative to nondiabetic men.
Translation: When some degree of normal function exists, pancreatic fat content correlates with the extent of that function in an inverse manner. In non-diabetics, higher pancreatic fat content is associated with reduced ß-cell function. But once some threshold has been exceeded — e.g. we now have ß-cell impairment and frank diabetes — further accumulations of fat don’t seem to exacerbate things much. That kind of makes sense to me. If someone adds dirt to a wheelbarrow, the speed with which I can move it declines as the amount of dirt increases. But once it’s filled with a certain weight I can no longer push it at all. My inability to push the wheelbarrow is not impacted further by adding even more dirt. The amount of dirt that renders a wheelbarrow immovable varies with the person trying to push it.
One other note:
Interestingly, no correlation was found between hepatic and pancreatic fat content … [and] we found no association between pancreatic and visceral fat.
I’ll leave that for another day except to say that essentially any intervention that has been demonstrated to alter body composition, or reduce hepatic (liver) or visceral (around abdominal organs) fat will not necessarily impact pancreatic fat.
Type 2 diabetes has long been regarded as a chronic progressive condition, capable of amelioration but not cure. A steady rise in plasma glucose occurs irrespective of the degree of control or type of treatment . Beta cell function declines linearly with time, and after 10 years more than 50% of individuals require insulin therapy . The underlying changes in beta cell function have been well described [3, 4], and beta-cell mass decreases steadily during the course of type 2 diabetes [5, 6]. Overall, there is strong evidence that type 2 diabetes is inexorably progressive, with a high likelihood of insulin therapy being eventually required to maintain good glycaemic control. However, type 2 diabetes is clearly reversible following bariatric surgery . The normalisation of plasma glucose concentration follows within days of surgery, long before major weight loss has occurred, and it has become widely assumed that the protective effects of gastrointestinal surgery are mediated by altered secretion of incretin hormones [8, 9]. Improved control of blood glucose in type 2 diabetes by moderate energy restriction has been demonstrated by others . We have hypothesised that the profound effect of a sudden negative energy balance on the metabolism could explain the post-bariatric surgery effect  and, specifically, that the decrease in the intracellular fatty acid concentrations in the liver would lead to a lower export of lipoprotein triacylglycerol to the pancreas, with the release of beta cells from the chronic inhibitory effects of excess fatty acid exposure.
This study was designed to test the hypothesis that acute negative energy balance alone reverses type 2 diabetes by normalising both beta cell function and insulin sensitivity.
Yoni Freedhoff seems to take umbrage a bit with the reference to diabetes being seen as progressive and uncurable. Perhaps the LC crowd has so distorted the “misguidedness” of mainstream recommendations to lose weight and exercise more so as to have had an impact? I don’t think so, rather the darned recidivism rate of maintaining lifestyle changes is at play here. However, I’ve seen enough diabetics on low carb forums — many who firmly believe that LC is the only right way to treat the disease — make similar statements. Jenny herself discusses BG control with moderate carb restriction (I would take issue with 30g/day being anything but extreme) but has discussed the limitations for such an approach to “cure” diabetes. The insurance establishment in this country certainly considers it an incurable disease — once a diabetic, always a diabetic. Perhaps studies of this nature can open the door for a new dialog here, and I’m glad to see doctors such as Yoni — who specializes in treating the obese BTW — express this. Wheat Belly Davis, on the other hand, is resigned to putting diabetes in remission but remains anything but cured as do so many VLC low carbers who manage their hyperglycemia but cannot eat a small potato without sending their blood glucose levels spiraling out of control.
The authors of this study pointed out what I’ve found amazing, the incredible CURE rate for diabetes with gastric bypass, as I discussed here. I still lean heavily towards the incretin hypothesis on this one playing at least a significant role in all this, but these researchers wanted to know if, perhaps, it’s just the “shock value” of a dramatic calorie restriction.
In closing, some speculation on my part:
It seems very possible that the dramatic imposition of a large caloric deficit may well establish a metabolic milieu that results in rather rapid and substantial release of fatty accumulation in the pancreas. In doing so, provided the permanent damage to ß-cells (as in reduction in ß-cell mass) is not extensive, the cells themselves regain their regular ability to produce and secrete insulin. The fatty accumulation was merely suppressing this ability. It’s like someone came and shoveled dirt out of my wheelbarrow until I could move it again provided there wasn’t so much dirt put in there in the first place such as to bend or break the axle. Indeed the degree of recovery for the GBP patients is related to how long they’ve been diabetic. The longer the diabetes, the less likely the recovery or degree of recovery.
I tend to believe there’s merit to some sort of individualized critical fat mass threshold. This marries well with the observations that, although obesity exacerbates diabetes, the vast majority of the obese remain non-diabetic. And it also marries well with the observation that even small reductions in body fat (as little as 5% even in the severely obese population) can reverse the diabetic state. If someone has been being tested all along and is only recently diagnosed recently with diabetes, chances are they have only just exceeded that threshold. This is one area I generally support screenings but have reservations on this as well (e.g. the conversion rate from prediabetes to diabetes is in the single digit percents for like 5 years out, so I would hate for a diagnostic label to negatively impact a person’s ability to obtain life insurance and such).
So what of all those LC and Paleos who have cured their diabetes? Well, if they’re indeed cured, as in they can handle eating a potato, this is usually accompanied by a rather rapid and substantial initial weight loss. And perhaps these are the ones who eat a higher carb version of Paleo and haven’t subscribed to the buttered prime rib version of low carb. Or, perhaps, rather than engaging in an idiotically dangerous PSMF-type diet for a couple of months, they’ve rather consumed nothing (IOW fasted) for periods of 24 hours or more. But by far, we see more folks who’ve driven their hyperglycemia into remission but cannot handle eating said potato. Perhaps the reason these folks do not enjoy an actual cure, despite maintained significant weight loss for many, is because they are still now bathing their ß-cells in ketones and fatty acids. Let’s not forget that two years out, the group of diabetic subjects in Shai that fared best was the Mediterranean group (ate the most carbs).
Now I have to add a personal note here. Nothing can mess with one’s head and trigger disordered eating behavior more than a hunger-inducing extreme low calorie diet. But even given my history with that, if I were diagnosed with diabetes tomorrow, I would give serious consideration to this program. And if I couldn’t do it alone, I might just consider the expense of doing so in a supervised facility a worthwhile one. Going in, however, I would have to commit to maintenance. Expect some rebound (that did not elicit a return of diabetes in 7 of the 11 here) but implement some sort of regime to maintain. Perhaps take a page from the IF’ers? Perhaps revisit the diet for three or four days every month or so? This seems far less “idiotic” than the legions of diabetics who cannot sustain the extreme carbohydrate restriction to “control” their hyperglycemia while remaining obese. Or, for that matter, even those who obtain and maintain a slimmer body but live in fear of a sliver of birthday cake.
The authors of the study, E. L. Lim, K. G. Hollingsworth, B. S. Aribisala, M. J. Chen, J. C. Mathers, and R. Taylor, might just be on to something here. I know this much. They do not deserve the derision aimed at them! I also don’t rule out that there’s an overweight lipophile out there who is at this moment seeking a pharmaceutical means to allow consumption of tons of fat while preventing its accumulation in the pancreas … or better yet, to prevent fatty pancreas continuing to eat the way they are.