Reversing Type 2 Diabetes Mellitus - Prof Tim Noakes

Currently there are three proven methods to “reverse” type 2 diabetes mellitus (T2DM) – bariatric surgery in those who are morbidly obese; a low-calorie (low-carbohydrate) diet initiated with the use of a commercially-available meal replacement formula; and a low-carbohydrate ketogenic diet. 


1. Bariatric surgery can “reverse” T2DM in the morbidly obese.


Bariatric surgery appears to be an extremely effective therapy that can “reverse” T2DM in as many as 80% of those with morbid obesity (Body Mass Index >40kg/m2) with similar or better results in those with less marked obesity (Body Mass Index <35kg/m2) (1). Whilst these operations carry significant immediate and long-term risks, the reality is that so too does morbid obesity complicated by T2DM. Keidar (1) has calculated that if 1 000 000 North Americans with morbid obesity and T2DM underwent surgery over a 5-year period, there would be 5000 deaths related to the surgery. However the annual mortality from T2DM during this same 5 year period would be 3 per 1 000, which equals 15 600 deaths.

If the surgery reduced mortality from T2DM by 90% as the data suggest, then in the surgical group there would be only 1404 additional deaths compared to 15 600 in the unoperated group.

As a result, over a 5-year period, there would be 6404 deaths in the operated group and 15 600 in the unoperated group; a saving of 8 296 deaths. (Bariatric surgeon Keidar’s (1) calculations are more optimistic but out by a factor of 42% since he “forgot” to include the 5000 surgical deaths in his final calculations). 

What these calculations properly show is the very high mortality in persons with morbid obesity and T2DM and the urgent need for effective treatments to “reverse” T2DM. 

The proposed mechanisms explaining surgically-induced “hyper-acute” reversal of T2DM include the following, according to Keidar (1): “1) increased postprandial secretion of L cell peptides such as glucagon-like peptide 1 from enhanced distal-intestinal nutrient delivery (hindgut theory); 2) exclusion of the proximal small intestine from nutrient flow, possibly down-regulating unidentified anti-incretin factor(s) (foregut theory); 3) impaired ghrelin secretion; 4) changes in intestinal nutrient-sensing mechanisms regulating insulin sensitivity; 5) bile acid perturbations; and 6) alterations in undiscovered gut factors, especially in the duodenum”. 

He concludes: “Although the precise mechanisms mediating type 2 diabetes remission after certain GI procedures are not yet clear, it is apparent that rearrangements of GI-tract anatomy can exert several discrete antidiabetic effects beyond those related to reduced food intake and body weight” (1, p.S363).

Clearly bariatric surgery can be life-changing for some. 

However I view morbid obesity as evidence for abnormal eating behaviours that might be better managed in some by trying to address the root cause(s). 

I have also seen persons scheduled for bariatric surgery who have reversed their morbid obesity and related medical conditions (2-4) simply by adopting the low-carbohydrate high-fat diet discussed subsequently. There are regular reports on social media of formerly morbidly-obese individuals who have lost in excess of 100kg without requiring bariatric surgery.

In my biased opinion, the first approach to the management of morbid obesity should be the reversal of specific food addictions by replacing a diet of highly processed foods with one emphasizing nutrient-dense “real” foods.


2. Consumption of a very-low calorie low carbohydrate diet initiated with formula feeds – The DIRECT Study.


The Diabetes Remission Clinical Trial (DIRECT) (5) directed by Professors Mike Lean of the University of Glasgow and Professor Roy Taylor of the University of Newcastle, UK, initially screened 1510 persons with T2DM of less than 6 years duration, in 49 UK General Practices for potential inclusion in a 24 month study of a dietary intervention to reverse T2DM. Ultimately 299 patients were randomly allocated to the intervention or control groups and were followed for 24 months. 

Whilst the control group continued to receive their standard care, the intervention group was placed on a “total diet replacement” formula feeding for 12-20 weeks followed by “stepped food reintroduction” (2-8 weeks) leading to “structured support for weight loss maintenance”. The study was funded by Diabetes UK, an organization that is vigorously opposed to the prescription of a low-carbohydrate diet. The meal replacement was Optifast, a commercial Nestle ® product used for the induction of weight loss (6).

A key original publication from this group that motivated the DIRECT study, reported that 11 persons “reversed” their T2DM condition within 7 days when they ate the energy-restricted formula diet that provided 2.5MJ (600 kcal) per day (7). Importantly whilst this diet is low in calories, it is 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. The key question is whether it was the reduction in calories or in carbohydrate intake, or both, that explained the dramatic T2DM “reversal” within just 7 days? 

The authors’ conclusion is that it is purely the reduction in caloric intake that produces this effect. Their explanation is that this dramatic reduction in caloric intake – in effect living on a starvation diet – reverses T2DM by removing intracellular fat (triglyceride) from the liver and pancreas and this normalizes their formerly abnormal glucose control. In the words of Professor Taylor: “There is now no doubt that this reversal of diabetes depends upon the sudden and profound decrease in food intake” (8, p. 267).  Thus T2DM develops “when the total daily calorie intake exceeds expenditure day after day, and year after year” (8, p. 268). Progressive fat accumulation causes T2DM when each individual’s “personal fat threshold” (PFT) is exceeded (9). 

According to this explanation, the nature of the food ingested, be it carbohydrate, fat or protein, is not key to the causation (or “reversal”) of T2DM. Rather, any food eaten in caloric excess will cause T2DM once the individual’s “personal fat threshold” is exceeded. According to his interpretation, weight loss is the key to the reversal of T2DM. Professor Taylor believes that a weight loss of about 15% is usually sufficient to “reverse” T2DM. Logically a diet that causes a 15% weight loss will be substantially different from the diet that caused prior weight gain in persons with T2DM. Thus these studies do not establish whether it is the altered dietary composition or the weight loss that reverses T2DM.

Taylor’s hypothesis arose from his finding that the low-calorie (low-carbohydrate) intervention produced a progressive fall in pancreatic and liver fat contents during the 8-week trial (figure 1). 


Legend to figure 1. The Newcastle University study produced a dramatic normalization of blood glucose concentrations (panel A) within 7 days associated with reductions in hepatic glucose production (panel B), in hepatic triglyceride (fat) content (panel C) and with progressive restoration of the first phase hepatic response (panel D) towards a more normal response. Circles indicate normal mean control values; arrows indicate the time point (weeks) at which the greatest change in the measured variable had already happened. Reproduced from reference 7.

Professor Taylor interprets these data as evidence that the low-calorie diet produces an energy deficit that specifically causes fat loss from the liver (panel C) and pancreas with normalization of liver responsiveness to insulin, and of insulin secretion by the pancreas (panel D).

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..” (7, p. 2511). According to this interpretation, removal of fat from the liver restores the ability of circulating insulin to inhibit the elevated hepatic glucose production (HGP) (panel C) that is pathognomonic of T2DM (10).  Whereas removal of fat from the pancreas normalizes pancreatic insulin secretion in response to an elevated blood glucose concentration (panel D) (7-9,11-13).

However Figure 1 reveals that removal of fat from the pancreas and liver cannot be the most important explanation for this hyper-acute reversal of T2DM within the first seven days of eating the low-calorie, low-carbohydrate diet.

The key point is that these studies show normalization of blood glucose control within 7 days (arrow in panel A), which happens well before liver fat content has reached its lowest value (arrow in panel C). Indeed hepatic glucose production had normalized (arrow in panel B) 7 weeks before liver fat content had reached its lowest value. Furthermore, a continuous fall in liver fat content from 1 to 8 weeks was not associated with any further improvements in blood glucose control than had already been achieved after 1 week (arrow in panel A).

So the critical metabolic change during the first 7 days of the trial was the normalization of the abnormal hepatic glucose production (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 (data not shown). 

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 7) 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, and this is critically important, 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 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, since the main determinant of HGP in fed mammals is the rate of exogenous glucose delivery to the liver (14).

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 almost reaching control values (circle in panel D). This would further improve blood glucose homeostasis. But this change would not have much effect on blood glucose control in those eating a low-carbohydrate diet and who would therefore not benefit greatly from any improved insulin response (to ingested carbohydrate). 

Thus a reasonable interpretation of these findings (7,11) would be that a very low-energy (starvation) low-carbohydrate diet can reverse T2DM within seven days, without any change in peripheral insulin sensitivity; this occurs some weeks before pancreatic insulin secretion (the first phase insulin response – panel D) is normalized, and well before liver and pancreatic fat content reach their lowest values, closer to “healthy” values. The effect is due to a reduction in HGP which, in turn in my opinion, is at least initially, the result simply of a large reduction in dietary (exogenous) carbohydrate ingestion with reduced glucose delivery to the liver.

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).

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 whole-body carbohydrate metabolism could effectively process, without impaired blood glucose homeostasis. 

This occurred even though “responders” still exhibit severe impairments in peripheral insulin sensitivity, probably also 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 (7,11,15).

Findings from the completed DIRECT study.

Based on these hopeful findings, the DIRECT study was begun in 2015 with two year data reported in February 2019 (5). The study found that 53 of the 149 patients in the intervention group lowered their glycated haemoglobin A1c (HbAIc) content to less than 6.5% without the need for any medication, indicating remission from T2DM. T2DM remission was greatest in those who had lost the most weight (and who subsequently kept it off!). 

Interestingly most of the weight loss was achieved within the first 20 weeks; those who maintained that weight loss were more likely to sustain their T2DM remission.

Lessons from the DIRECT study.

The key finding from the work of Professor Taylor and his team is what happens in the first 1-20 weeks of the intervention. For it is during this period that the “magic” happens (Figure 1). It is critical how we interpret that “magic” in the context of the DIRECT study. 

If the dietary intervention – the prescription of the meal replacement formula – is the magic bullet that can only be achieved through the prescription of the commercially-produced formula – Optifast by Nestle (6) – favoured by the Newcastle team, then it would justify what happens after the patients completed the first 12-20 weeks of the DIRECT study. For during this period subjects must be re-taught how to eat real foods that will not cause their T2DM to return. Surprisingly, the diets followed during this period are not well described which is a major weakness of the DIRECT study.

Principal investigator from the Virta Health study, Sarah Hallberg, weighs in saying: “[It is] absolutely correct that information is missing about what patients were eating for the bulk of the [DIRECT] trial. This is incredibly concerning.  It would be like a study showing antibiotic superiority but never revealing what the antibiotic being tested was.  If participants had a life stressor or “slipped” for other reasons during the trial they were “rescued” with the low carbohydrate meal replacement plan.  It is also important to note the meal replacement plan is not real food.”

Indeed the key piece of missing evidence in the study is any report of what those “responders” who avoided both weight regain or any deterioration of their “cured” T2DM, had eaten during the 19-months’ follow-up after the initial 8-20 weeks exposure to the low-calorie low-carbohydrate formula diet. My prediction, based on our experience (2-4,16,17) and the published literature including the Virta Health Study discussed subsequently, would be that “responders” continued to eat a very low-carbohydrate diet during this period. A low-carbohydrate diet is by its nature also a low(er)-calorie diet (18). Their low-carbohydrate lower-calorie intake then prevents weight regain whilst also maintaining low rates of HGP. The low rates of HGP prevent deterioration in T2DM control.

Indeed Professor Taylor is a strong advocate of the low-carbohydrate diet in the management of T2DM. Thus he writes (19): “UK clinical practice relating to carbohydrate restriction has not kept pace with the evidence base (20). 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 (21)”.


The work of Professor Taylor including the DIRECT study is critically important for a number of reasons. First it shows that recent (less than 6 years) onset T2DM can be “reversed” within as little as 7 days in persons eating a low-calorie low-carbohydrate diet. What is more, T2DM patients who lose significant weight, usually >15kg, and maintain that weight loss are very likely to put their T2DM into permanent remission, maintaining adequate glucose control even without requiring the use of any anti-diabetic medications. In the DIRECT study fully 35% of subjects were able to achieve and maintain their “remission” status for at least 24 months, a remarkable finding.

Thus the DIRECT study disproves the standard medical dogma that T2DM is a chronic progressive disease with an inevitably fatal outcome.

The sole weakness of the study was the failure to determine how the diet of those who were successful in maintaining both their weight loss and their T2DM remission over the 24 months of the study (5), differed from the diets (and behaviours) of those who were unsuccessful. 

Documenting that evidence would have been very helpful in allaying fears that the first author of the final publication, Professor Michael Lean, who has an historic aversion to the low-carbohydrate diet which he equates to a “fashion-cult” (22), might be reluctant to report that a low-carbohydrate diet was a critical component of the long-term successes in the DIRECT trial. 

The funder of the DIRECT study, DiabetesUK, is also avowedly anti-low carbohydrate diets, preferring to promote high-carbohydrate “balanced”, largely plant-based diets, for diabetes management. Nestle, the manufacturers of the product used to initiate the weight-loss in the DIRECT trial, are also biased towards a commercial solution, not a diet of real foods, for the treatment of T2DM. 

It would be extremely difficult for any of these role players to admit that a low-carbohydrate diet might be the key to the successful outcomes in the DIRECT study.

Dr Sarah Hallberg, the principal investigator of the Virta Health study, explains that she supports the value of the DIRECT trial despite her personal and research preference for a low carbohydrate approach to diabetes reversal: “…the information generated from it is critical as patients who wish to reverse their diabetes should decide which option to do so is best for them as an individual.” 


3. The Virta Health studies of low-carbohydrate ketogenic diets for reversal of T2DM.


In 2014 Stephen Phinney MD and Jeff Volek PhD, two of the three authors of the book that changed and indeed saved my life, The New Atkins for a New You (23), approached a young Finnish IT entrepreneur Sami Inkinen with a proposal. They had a vision of using a ketogenic version of the LCHF diet to reverse T2DM. But they needed a CEO who could make their vision a reality. Inkinen, a world-class Ironman triathlete, had consulted Phinney for advice about the management of his own insulin resistant state. 

Phinney was also in the process of preparing Inkinen and his future wife, Meredith, to become ‘fat adapted’ for a 4500km row across the Pacific from California to Hawaii in the summer of 2014. The goal of their Fat Chance Row was to raise awareness about the dangers of sugar and its connection to T2DM. Once the fat-adapted Inkinens had safely reached Hawaii without needing any carbohydrates, Sami, Phinney and Volek agreed to found a new company, Virta Health, with the goal of reversing diabetes in 100 million persons by 2025. 

By the end of 2017, the company reported the findings from their first studies of the use of the LCHF diet to reverse diabetes in ~260 subjects (24,25). They found that at the end of the first year of their trial, 60% of subjects had “reversed” their T2DM by lowering their HbA1c values to below 6.5%, the same criterion used for diabetes “remission” in the DIRECT study. This represented an average 1.3% reduction in HbA1c values (despite reduced medication use) (25). Furthermore 94% of subjects had either reduced or eliminated their need for insulin.  Subjects also lost an average of 12% of body weight, equivalent to 14kg. 

An important difference between the Virta Health and DIRECT studies was that the Virta Health study included patients with T2DM regardless of duration.

Changes in conventional metabolic risk factors for coronary heart disease were also dramatic. When compared to subjects receiving conventional management for T2DM, those receiving the Virta intervention showed significantly greater beneficial improvements in increased ApoA1 and HDL-C concentrations; in reduced high sensitivity CRP values (a measure of inflammation); in reduced triglyceride/HDL-C ratios; in reduced ApoB/ApoA1 ratios; in reduced total LDL particle numbers and especially reduced in small, dense LDL particle numbers; in reduced large VLDL particle numbers; in reduced blood pressure and in reduced anti-hypertensive medication use; and in reduced white blood cell counts (26).

As a result 10-year atherosclerotic cardiovascular disease (ASCVD) risk decreased 12%. 

Subsequent publication of the 2-year data (27) confirm the continuing benefits of the intervention with 54% of subjects in T2DM reversal and 18% in remission at 2 years. Medication use, other than metformin, decreased from 56% to 27%; 62% terminated insulin use and 100% ceased use of sulfonlyureas. The control group showed no such improvements. There were also encouraging improvements in markers of non-alcoholic fatty liver disease (NAFLD) (28).

The 31/2-year data (29) found that these benefits were maintained. Forty-six percent of subjects maintained “remission” levels of HbA1c (<6.5%) with either no medications or with the use of metformin alone whilst maintaining weight loss, lower blood triglyceride concentrations and elevated blood HDL-cholesterol concentrations. 

Dr Sarah Hallberg, principal investigator of the Virta Health Study, explains the continuation of metformin in those who ‘reversed’ their T2DM in their study: “Our criteria for reversal was slightly different from DIRECT.  We allowed patients to choose to stay on metformin if they wanted after they brought their HbA1c below 6.5% and were off all other diabetes medications.  This was a decision made by me as the PI of the study.  I find it very concerning that any trial would require patients to come off a medication such as metformin which has other indications outside of diabetes, and has been found to be helpful in preventing diabetes progression.  It also takes away individual control which is critical. There is no group more at risk for progressing to diabetes then a group who has already struggled with the disease.  I discussed metformin with patients and allowed them to choose if they wanted to continue taking it as I felt that was the best medical care for individual patients.”  

The most recent study (30) found that the low-carbohydrate ketogenic diet has major effects on a range of inflammatory mediators linked to the NLRP3 inflammasome. 

The authors conclude that the low-carbohydrate ketogenic diet “has broad-spectrum anti-inflammatory and immune modulatory effects” in patients with T2DM and pre-diabetes. 

Summary of effects of different dietary interventions on blood HbA1c values in persons with T2DM.

Figure 2 provides a summary of a range of studies that have reported the effects of different dietary interventions on blood HbA1c levels in persons with T2DM .

 Legend to figure 2: The reported effects of 6 different interventions (25,27,31-34) on blood HbA1c values in persons with T2DM. 

Figure 2 shows that the only dietary interventions that have been shown to lower HbA1c values below the T2DM threshold of <6.5mmol/L are those promoting low-carbohydrate ketogenic diets (25,27,33,34) including the original low-carbohydrate study of Yancy et al in 2005 (33). (Data from the DIRECT study are not included as it is unclear what was the exact diet followed by the majority in that study).

Importantly, the original vegetarian (high fibre) diet of Simpson et al. (31) and the vegan diet of Barnard et al. (32) failed to produce any meaningful changes in HbA1c values. Nor did the control diet in the Barnard vegan study; a diet modelled on the 2003 American Diabetes Association Guidelines.

Importantly the study of Simpson et al (31) and related studies from the same group (35,36) all of which failed to show any metabolic benefits of a high-carbohydrate high-fibre vegetarian-type diet on HbA1c values in persons with T2DM – producing identical post-trial HbA1c values of 11% (35) and 8.3% (36) in both control and high-carbohydrate diet groups – were used in the 1970s and beyond (36) as definitive evidence, rated Grade A, that high-carbohydrate diets are the diet of choice for persons with T2DM. Thus (37, p.379): 

  • “Carbohydrate intake may range between 45% to 60% of total energy. Grade C (evidence)”. 
  • “Metabolic characteristics suggest the most appropriate intakes within this range for individuals with T1DM and T2DM. Grade A (evidence)”.
  • “Vegetables, legumes, fruits and wholegrain cereals should be incorporated into the diet of persons with T1DM and T2DM. When carbohydrate intake is at the upper end of the recommended range it is particularly important to emphasize foods rich in dietary fibre and with a low glycaemic index.. Grade A (evidence). 
  • “There is no justification for the recommendation of very low carbohydrate diets in persons with diabetes….Grade B (evidence)”.   

The ex-South African lipophobe Professor Jim I. Mann who coordinated this review, has maintained a life-long distrust of low-carbohydrate diets with a permanent devotion to his belief in the still-unproven Burkitt-Truswell Dietary Fibre depletion theory for chronic disease (38).


4. Our study of patients who reversed their T2DM without the support of medical practitioners or dietitians. 


My colleagues and I (16) evaluated 28 persons with T2DM who had self-administered the low-carbohydrate diet described in The Real Meal Revolution (3). In 24 subjects available for follow-up between 26-53 months after adopting the low-carbohydrate diet, HbA1c had decreased from 7.5% to 5.9%. Of the 24 participants assessed at follow-up after an average of 35 months on the diet, 7 were in “complete” remission with HbA1c <5.7% and using no medications; 10 were in partial remission (HbA1c<6.5% and taking no medications other than metformin) whilst 7 were not in remission as the still required to take medication and their HbA1c values were >6.5%. 

Thus 17 of 24 subjects (71%) with clinically-diagnosed T2DM were able to put their condition into “remission” simply by following the advice in a popular book, much as I had done the same for myself after reading The New Atkins for a New You (23). 

Perhaps the novel finding from this study was that participants who were successful reported that the most important aspect of the diet was its ability to reduce their hunger. 

Of concern, was that many participants felt unsupported by their doctors.

To summarize: This study is important because my colleagues asked subjects who had reversed their T2DM through their own efforts and without medical support, why they believed they had been successful. Their answers were similar and unequivocal. Respondents told us that 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 ever control the addiction in the long term.

Thus whilst the biology may indeed show that T2DM occurs when liver and pancreas fat contents 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 behaviour, 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.  


5. Other recent studies of relevance.


Another very recent relevant study (39) is from the Johns Hopkins University School of Medicine in Baltimore, Maryland. The study involved a retrospective analysis of 49 T2DM patients treated by physicians and endocrinologists attached to the Johns Hopkins Medical School. Subjects were included in the study if they had followed a low-carbohydrate high-fat diet (LCHF) (<20g carbohydrate/day) for at least 3 months. Their outcomes were compared to those of 75 similar patients who received conventional T2DM care but without the LCHF dietary intervention. The results of the study are shown in figure 3.

Legend to figure 3. Changes in HbA1c (top panel), weight (middle panel) and daily insulin dosage (bottom panel) in T2DM patients following a low-carbohydrate high-fat diet for at least 3 months. Control data are from subjects who received standard medical care for T2DM at the same institutions. Reproduced from figures 1 and 2 in reference 39. 

Figure 3 shows that the LCHF diet produced changes in HbA1c compatible with T2DM “remission”, with progressive weight loss and a marked reduction in daily insulin use.

The second relevant recent study was a 90-day dietary intervention trial (34) in which 11 obese women recently diagnosed with T2DM were placed on a low-carbohydrate ketogenic diet that restricted carbohydrate to <30 grams per day. Subjects lost an average of 9kg body weight, lowered their diastolic and systolic blood pressures, and serum triglyceride concentrations whilst raising blood HDL-cholesterol concentrations. Importantly blood HbA1c levels dropped from 8.9% to 5.6% indicating “reversal” to T2DM in 90 days (Figure 2).

What does this mean for those wishing to put T2DM into “remission” in large numbers of patients?

All these studies cited here confirm what I had written in The Real Meal Revolution (3) in 2013. T2DM is a reversible medical condition.

By implication all of the other components of the insulin resistance syndrome should also be reversible with the prescription of the LCHF diet. Indeed we have reported that the low-carbohydrate diet was able to “reverse” the metabolic syndrome in 60% of subjects in a Canadian study (40).

Our more recent study (16) suggests that the key event determining whether or not subjects with T2DM will go into remission on the low-carbohydrate diet is their commitment to food choices that will allow each to regain control of their eating, specifically by removing food cravings. We conclude that it was this ability to master their previously addictive eating behaviours that led ultimately to the biological changes that put their T2DM into “remission”. 

The net effect of this specific low-carbohydrate diet of “real foods” (3) 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 (41) and many others (18,23).  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 the weight loss is the result of controlling the food cravings; all else follows from this. 

Thus we argue that the initiation of the weight loss that will assist in putting T2DM into “remission” requires the prescription of a low-carbohydrate diet comprising non-addictive “real” foods of the kind we have described in The Real Meal Revolution (3). The recently released Banting 7 Day Meal Plans Recipe Book (4) which includes recipes chosen from the experiences of the 2 million members of the Banting 7 Day Meal Plan Facebook page (17) – 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 of T2DM is made – and preferably many years early when the HbA1c value starts to creep above 5.5% – and not delayed by 8 weeks with the prescription of a liquid diet that is high in sugar as is the Optifast (Nestle ®) diet used in the DIRECT study. 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 highly-addictive processed foods from which the subjects will have to be weaned if they are to achieve long-term T2DM remission.

Take home messages.

  1. The key to “reversal” of T2DM is the individual’s mastery of those food cravings which are driven by highly addictive food choices.
  2. 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 and minimal amounts of industrially-produced “vegetable oils”, margarines and shortenings.
  3. There is currently no published evidence showing that persons who have “reversed” their T2DM or who are in T2DM “remission” can revert to any diet other than the one that induced that “reversal” or “remission”, without again returning to their former diabetic state.
  4. 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. 
  5. This alone is strong evidence against Professor Taylor’s PFT hypothesis.
  6. The postulate 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 any published evidence or by the clinical experience of those working with such patients. 
  7. The clear evidence is that carbohydrate restriction plays a unique role in managing insulin resistance and in reversing the metabolic syndrome (40,42-48) and this effect is independent of weight-loss (48).



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