The following is a written response from Prof Tim Noakes regarding a letter published in the Medical Brief.
To the Editor,
I acknowledge Mr Alex Leaf’s recent letter (1) to Medical Brief in response to our recently published peer-reviewed article (2). I particularly appreciate his comment that our study is an “important contribution to the scientific literature”. However I dispute his unproven assumption that persons who have reversed their type 2 diabetes mellitus (T2DM) through dietary means will be able to return to eating any diet they choose, including high carbohydrate diets, provided they keep their body fat content below their “personal fat threshold”. As he writes: “So, diabetes is curable in individuals who do not have too much pancreatic damage, but it requires substantial fat loss. Importantly, cure means that carbohydrate can again be eaten without issue”.
In other words, Mr Leaf believes that T2DM is simply a disease of too much fat accumulation, particularly in the pancreas and liver, and provided this is removed, the disease is cured. With the result that persons can return to eating any diet they choose provided the diet does not cause weight regain.
But this statement is “disingenuous” if, in susceptible individuals with insulin resistance, carbohydrate is the real driver of the weight gain and the fat accumulation in the liver and pancreas which Mr Leaf agrees is the cause of T2DM: “..once we surpass that (personal fat) threshold, we begin to store exponentially more fat in our viscera, especially the liver and pancreas, which causes insulin resistance and metabolic dysfunction (3-6). If you want to actually cure type 2 diabetes, then you need to lose fat”.
My second contention is that Mr Leaf has failed to differentiate between what is established fact rather than an unproven hypothesis, regardless of how attractive that hypothesis may seem.
I will begin by addressing this issue before returning to address Mr Leaf’s contention that persons with “cured” T2DM can eat any amount of carbohydrate that does not cause weight regain.
Mr Leaf’s belief that T2DM is simply a function of the extent of body fatness – “The cause of type-2 diabetes is almost always an issue of surpassing one’s personal fat threshold (1)” is based on an hypothesis developed by Professor R. Taylor from Newcastle University, UK. Professor Taylor is exceptionally highly regarded for his novel, incredibly important and extensive groundbreaking body of work showing that T2DM can be reversed by either a particular diet or by bariatric surgery (7-13). However the fact that Professor Taylor is an absolute doyen in this field does not necessarily guarantee that his favored hypothesis has been proven beyond a reasonable doubt.
Professor Taylor is very careful to acknowledge that the idea advanced by Mr Leaf as an incontrovertible truth, remains an hypothesis: Thus: “We hypothesize (my emphasis) that each individual could have a personal fat threshold (PFT) which determines their susceptibility to developing T2DM, in relation to their degree of B-cell function and insulin sensitivity. Gaining sufficient weight to cross the PFT will trigger the condition, whereas losing their ‘excess weight’ could return them to normal glucose tolerance” (10, p.408).
A key piece of evidence on which Professor Taylor bases his hypothesis is his research team’s finding that 11 persons reversed their T2DM condition within 7 days when they ate an energy-restricted diet that provided 2.5MJ (600 kcal) per day (8). Importantly whilst this diet was low in calories, it was also very low in carbohydrate – 59g/day. Thus subjects received not just a low-calorie diet but also one very much lower in carbohydrate than they would normally have eaten. This raises the obvious question: Was it the reduction in calories or in carbohydrate intake that reversed T2DM already within 7 days in these subjects?
Professor Taylor believes that it is purely the reduction in caloric intake. He further concludes that the dramatic reduction in caloric intake – in effects living on a starvation diet – reverses T2DM by removing intracellular fat (triglyceride) from the liver and pancreas, thereby restoring normal blood glucose control in these formerly T2DM subjects. Thus: “There is now no doubt that this reversal of diabetes depends upon the sudden and profound decrease in food intake” (9, p. 267). So he concludes that T2DM occurs “when the total daily calorie intake exceeds expenditure day after day, and year after year” (5, p. 268).
In other words the nature of the food ingested, particularly its’ carbohydrate, fat and protein composition, is not key to the causation (or reversal) of T2DM. Rather, according to this hypothesis, it’s simply any food eaten in caloric excess. Thus according to his interpretation, reversal of T2DM requires that this caloric excess must be reversed so that subjects lose weight. He believes that a weight loss of about 15% is usually sufficient to “reverse” T2DM.
Professor Taylor’s hypothesis is strongly supported by the finding that the low-calorie (low-carbohydrate) intervention produced a progressive fall in pancreatic and liver fat during the 8-week trial. Thus: “The data are consistent with the hypothesis (my emphasis) that the abnormalities of insulin secretion and insulin resistance that underlie type 2 diabetes have a single, common aetiology, i.e. excess lipid accumulation in liver and pancreas..” (8, p. 2511).
Indeed Professor Taylor has provided a convincing argument that excessive fat accumulation in the pancreas is perhaps the key driver in the development of T2DM with an increased liver fat content amplifying this harmful effect (8,9,11-13).
But what I find less convincing is his explanation of the nature of the physiological processes that cause the rapid reversal of T2DM within 7 days in those subjects considered to be “responders”. Professor Taylor’s hypothesis predicts that his low-calorie diet intervention achieves this by removing fat from the pancreas and liver, thereby restoring normal blood glucose control. Removal of fat from the liver restores the ability of circulating insulin to inhibit the elevated hepatic glucose production (HGP) that is pathognomonic of T2DM (14). Whereas removal of fat from the pancreas normalizes pancreatic insulin secretion in response to an elevated blood glucose concentration.
However his findings are open to a rather different interpretation.
But to be clear and for reasons that will become apparent, I am focusing exclusively on the hyper-acute 7-day response to the diet that reverses T2DM in “responders”. I do not disagree that the long-term effects of returning liver and pancreatic fat contents to normal levels may be critically important in the long-term management of T2DM. But that is not the issue under discussion here.
To repeat, the diet intervention used in these studies includes two components: (i) a reduced calorie content – in truth the diet is a starvation diet; and (ii) a much-reduced carbohydrate content. Since the diet includes (at least) two modifications to the subjects’ usual diets, none of Professor Taylor’s studies can determine which of the two changes is responsible for the beneficial outcome. Or whether, perhaps, it was due to a combination of both.
My interpretation is that the authors’ findings of a hyper-acute reversal of T2DM in “responders” is better explained as a response to the low-carbohydrate content of the intervention diet, and not its’ low-calorie content.
The key point is that these studies show normalization of blood glucose control within 7 days, well before large changes in liver and pancreatic fat content have been achieved.
But the critical metabolic change during the first 7 days of the trial was the normalization of HGP. In contrast, the rate of glucose disappearance, a measure of peripheral tissue insulin sensitivity, remained unchanged throughout the entire 8 weeks of the trial. Reduced HGP in the first 7 days was associated with a sharp increase in hepatic insulin sensitivity. So one possible explanation might be that the removal of (some) fat from the liver already normalizes the (inhibitory) action of insulin on HGP, reducing HGP which returns to the normal range already within the first 7 days of the diet intervention.
However plasma insulin concentrations fell by 52% during the first 7 days of the trial (Table 2 in reference 8) reaching concentrations that were only 63% of values measured in healthy controls. Thus even if hepatic insulin sensitivity had increased somewhat, the marked fall in plasma insulin concentrations would have negated any potentially beneficial effect on HGP of this increased hepatic insulin sensitivity. I, therefore, conclude that increased hepatic insulin sensitivity, due to a removal of some liver fat, cannot be the sole explanation for the spectacular 40% reduction in HGP already within 7 days of commencing the low-calorie low-carbohydrate dietary intervention.
Instead I would argue that the marked reduction in dietary carbohydrate intake is the most likely explanation for both the 52% reduction in plasma insulin concentration AND the 40% reduction in HGP. With a marked fall in exogenous glucose delivery to the liver, HGP would have to fall dramatically (15).
Thereafter, as liver and pancreatic fat content returned to normal values over the next 7 weeks of the trial, the first-phase insulin response normalized completely. This would further improve blood glucose homeostasis. But note that this change would not have a marked effect on blood glucose control in those eating a low carbohydrate diet and who would therefore not benefit greatly from an improved insulin response (to ingested carbohydrate).
Thus a reasonable interpretation of these findings (8,11) would be that a very low-energy (starvation) low-carbohydrate diet can reverse T2DM within seven days, without any change in peripheral insulin sensitivity, some weeks before pancreatic insulin secretion (the first phase insulin response) is normalized, and well before liver and pancreatic fat content are normalized. The effect is due to a reduction in HGP which, in turn, is at least initially, the result simply of a large reduction in exogenous carbohydrate ingestion.
If this argument is correct, the reasonable conclusion then becomes that the reversal of T2DM in these “responders” did not occur because the body fat content of each successful responder had fallen below Professor Taylor’s hypothetical personal fat threshold (PFT) as Mr Leaf presumes.
But rather it occurs because “responders” had reduced their daily dietary carbohydrate intakes to below a personal carbohydrate threshold (PCT) at which HGP was reduced to a rate that their impaired capacity for carbohydrate metabolism could effectively process without a loss of blood glucose homeostasis. This occurred even though “responders” still exhibit severe impairments in peripheral insulin sensitivity, probably in hepatic insulin sensitivity, whilst still showing a grossly abnormal first phase insulin response. However after 8 weeks of the intervention diet all these abnormalities, except for impaired peripheral insulin sensitivity, had reversed, presumably because hepatic and pancreatic fat contents had also normalized (8,11,12).
Why it may be important to identify the role specifically of carbohydrate restriction in the hyper-acute reversal of T2DM in these patients.
Why do I think is it necessary to go into such detail to offer an alternate explanation for why this starvation dietary intervention reversed T2DM within 7 days?
The reason comes from the one piece of novel information that we discovered in our paper (2) and which Mr Leaf fails to grasp. It was that subjects in our study who “reversed” their T2DM, usually on their own, without any input from doctors or dietitians, and often in the face of dire health warnings from these professionals, all reported that the elimination of hunger and food cravings by the low-carbohydrate high-fat (LCHF)/Banting diet was the single most important key to their ultimate success in “reversing” their T2DM.
My personal experience as a person whose T2DM is also in remission following adoption of the LCHF/Banting diet – I am one of the subjects reported in our study (2) – as well as continuing feedback from the huge number, now counting in the millions of South Africans who have adopted the LCHF/Banting diet (16), is that this is the single unique benefit of this particular dietary intervention. This eating plan allows one to regain control of what one eats in a way that other “heart-healthy, prudent, balanced diets in moderation” simply do not.
For the simple reason that this eating plan removes the food cravings produced by highly processed foods that can be highly addictive, in particular because they contain sugar and other addictive components (17,18). Attempting to treat an addiction by allowing the addictive agent to be consumed “in moderation” simply does not work. Rather the addictive agent – in this case, sugar and highly processed foods – must be completely removed from the diet if there is to be any real hope of long term success.
And this, in my opinion, is the key weakness with Mr Leaf’s response and ultimately with Professor Taylor’s diet. Mr Leaf proposes that once subjects have reversed their T2DM and have reduced their body fat content below the hypothetical PFT, they can return to eating essentially whatever they wish since their reduced body fat content has now normalized their blood glucose control. The proviso of course is that the diet must not cause weight regain. But it is part of human folklore that carbohydrates are uniquely fattening and are the basis for the production of fatty liver in birds (7,19).
Crucially the conclusion that “carbohydrates can again be eaten without issue” is not proven by the study that Mr Leaf quotes (11). For the key piece of missing evidence in that study is any report of what those “responders” who avoided both weight regain or any deterioration of their “cured” T2DM, had eaten during the 6-months’ follow-up after the initial 8 weeks exposure to the low-calorie low-carbohydrate diet. My prediction, based on our experience (2,16) and the published literature (20-23) would be that “responders” continued to eat a very low carbohydrate diet during this period. Their low carbohydrate intake then prevented weight regain whilst also maintaining low rates of HGP. The low rates of HGP prevented deterioration in T2DM control.
Indeed Professor Taylor is a strong advocate of the low-carbohydrate diet in the management of T2DM. Thus he writes (13): “UK clinical practice relating to carbohydrate restriction has not kept pace with the evidence base (24). Low carbohydrate diets have been reported to be superior to low-fat diets for short to medium long term use in type 2 diabetes, with comparable longer-term (>12 months) outcomes (25)”.
Perhaps Professor Taylor would have been even more enthusiastic about the low carbohydrate diet for reversal of T2DM had he anticipated the Virta Health studies (20,21) which show “reversal” of T2DM in a large number of subjects (up to 60%) on the low carbohydrate diet. Importantly nowhere in these and other studies (22,23) showing the remarkable effects of the LCHF/Banting diet in “reversing” T2DM do the authors ever suggest that it is safe for their study subjects to return to a high carbohydrate diet once their T2DM is in “remission”. In fact, quite the opposite.
It is my argument that Mr. Leaf’s unquestioning acceptance of the still hypothetical PFT theory as an absolute truth explains why he may have overlooked the real reasons for Professor Taylor’s successful reversal of T2DM. Specifically the adoption and continued use of low carbohydrate diets by the successful “responders”.
What does this mean for those wishing to put T2DM into “remission” in large numbers of patients?
Our study (2) suggests that the key event determining whether or not subjects in our report reversed their T2DM was their choice of a low carbohydrate diet that allowed each to regain control of their eating, specifically by removing food cravings; that is to master the addictive eating pattern that led to the biological changes causing their T2DM.
The net effect of this specific diet change would be to reduce the subjects’ dietary energy intakes, producing the negative energy balance necessary for the weight loss. Importantly this was achieved without hunger as so well described by Dr Robert Atkins (26) and others (27). Progressive weight loss would ultimately return pancreatic and liver fat contents to normal.
Thus the ultimate goal of T2DM management is to allow subjects to regain control of their hunger and to avoid food cravings. To achieve this does not require persons first to lose weight so that they are again below their PFTs.
Instead it requires the prescription of a low carbohydrate diet comprising non-addictive “real” foods of the kind we have described in The Real Meal Revolution (28). The recently released Banting 7 Day Meal Plans (29) which includes recipes chosen from the experiences of the 2 million members of the Banting 7 Day Meal Plan Facebook page (16) – is another very valuable resource in this regard.
The point of course is that this low carbohydrate dietary intervention should be initiated immediately the diagnosis is made and not delayed by 8 weeks with the prescription of a liquid diet that is high in sugar as is the Optifast (Nestle â) diet. It is my contention that since the “magic” of the liquid diet is its’ low carbohydrate content, then any diet low in carbohydrate will have the same effects. But this should indeed be a diet of “real”, not processed foods.
In summary, our study is important because we asked subjects who had reversed their T2DM through their own efforts and without medical support, why they had been successful. Their answers were similar and unequivocal. They had regained control of their eating behaviours by ridding themselves of food cravings. They had done this by replacing highly addictive processed foods in their diets with real food options from our and other books. They had learned that eating addictive foods “in moderation” cannot control the addiction.
Thus whilst the biology may indeed show that T2DM occurs when liver and fat content exceed each individual’s PFT, this really explains only the HOW of T2DM. It does not explain the WHY.
Our study uncovers one possible WHY.
It suggest that T2DM is a disease of behavior, driven today by sugar and other forms of food addiction.
The reason why the LCHF/Banting eating plan works so effectively is quite simply because it removes the addictive foods from the diet.
In time this allows a return to a normal human physiology as so elegantly described by Professor Taylor’s exceptional work.
- Our study (2) suggests that the key to “reversal” of T2DM is the individual’s mastery of those food cravings which are driven by highly addictive food choices.
- The clear evidence is that this is achieved most effectively by a diet low in carbohydrate and in refined foods and with a complete absence of any sugar.
- There is currently no published evidence showing that persons who have “reversed” the T2DM or who are in T2DM “remission” can revert to any diet other than the one that produced that “reversal” or “remission”, without again returning to their former diabetic state.
- The (anecdotal) experience of clinicians treating patients with T2DM who have “reversed” their T2DM is that their blood glucose control remains extremely brittle even in their “cured” state. Any increase in carbohydrate intake greater than about 25g/day is associated in the majority, within hours or days, with a deterioration in blood glucose control, well before there can be any increase in the fat content of the liver or pancreas.
- This alone is strong evidence against the PFT hypothesis.
- Suggesting that persons who are in T2DM “remission” or “reversal” can return to eating a high carbohydrate diet, provided they do not gain weight, is simply not supported either by the published evidence or by the clinical experience of those working with such patients.
- This statement of Mr Leaf is therefore “disingenuous”. It is most certainly not evidence-based. Nor does it match the experience of clinicians using the LCHF/Banting diet in working with T2DM patients (21,22,26,27).
Professor Timothy Noakes OMS, MBChB, MD, DSc, PhD (hc), FACSM, (hc) FFSEM (UK), (hc) FFSEM (Ire).
22nd January 2020
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