The above two rules are the only dietary rules you need to maintain ideal weight for the rest of your life, assuming you apply common sense and avoid extremes. The diet works by building in regular periods of insulin relief, keeping your body from becoming resistant to insulin. Following these two rules, you will maintain your weight and health by never entering the vicious cycle of increasing insulin resistance.
The extent of weight loss required to reverse type 2 diabetes is much greater than conventionally advised. A clear distinction must be made between weight loss that improves glucose control but leaves blood glucose levels abnormal and weight loss of sufficient degree to normalize pancreatic function. The Belfast diet study provides an example of moderate weight loss leading to reasonably controlled, yet persistent diabetes. This study showed that a mean weight loss of 11 kg decreased fasting blood glucose levels from 10.4 to 7.0 mmol/L but that this abnormal level presaged the all-too-familiar deterioration of control (87).
Magnesium deficiency is not uncommon in people with diabetes, and it can worsen high blood sugar and insulin resistance. Some studies suggest that supplementing with magnesium may improve insulin function and lower blood sugar levels, but other studies have shown no benefit. Have your doctor check you for deficiency before supplementing with magnesium. These are signs that you’re not getting enough magnesium.
Foods high in chromium: Chromium is a nutrient that’s involved in normal carbohydrate and lipid metabolism. Foods high in chromium can improve the glucose tolerance factor in your body and naturally balance out blood glucose levels. It plays a role in insulin pathways, helping bring glucose into our cells so it can be used for bodily energy. Broccoli has the highest amounts of chromium, but you can also find it in raw cheese, green beans, brewer’s yeast and grass-fed beef. (10)
The twin cycle hypothesis of the etiology of type 2 diabetes. During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis, which particularly promotes fat accumulation in the liver. Because insulin stimulates de novo lipogenesis, individuals with a degree of insulin resistance (determined by family or lifestyle factors) will accumulate liver fat more readily than others because of higher plasma insulin levels. In turn, the increased liver fat will cause relative resistance to insulin suppression of hepatic glucose production. Over many years, a modest increase in fasting plasma glucose level will stimulate increased basal insulin secretion rates to maintain euglycemia. The consequent hyperinsulinemia will further increase the conversion of excess calories to liver fat. A cycle of hyperinsulinemia and blunted suppression of hepatic glucose production becomes established. Fatty liver leads to increased export of VLDL triacylglycerol (85), which will increase fat delivery to all tissues, including the islets. This process is further stimulated by elevated plasma glucose levels (85). Excess fatty acid availability in the pancreatic islet would be expected to impair the acute insulin secretion in response to ingested food, and at a certain level of fatty acid exposure, postprandial hyperglycemia will supervene. The hyperglycemia will further increase insulin secretion rates, with consequent enhancement of hepatic lipogenesis, spinning the liver cycle faster and driving the pancreas cycle. Eventually, the fatty acid and glucose inhibitory effects on the islets reach a trigger level that leads to a relatively sudden onset of clinical diabetes. Figure adapted with permission from Taylor (98).
Formal recommendations on how to reverse type 2 diabetes in clinical practice must await further studies. In the meantime, it will be helpful for all individuals with newly diagnosed type 2 diabetes to know that they have a metabolic syndrome that is reversible. They should know that if it is not reversed, the consequences for future health and cost of life insurance are dire, although these serious adverse effects must be balanced against the difficulties and privations associated with a substantial and sustained change in eating patterns. For many people, this may prove to be too high a price to pay, but for those who are strongly motivated to escape from type 2 diabetes, the new understanding gives clear direction. Physicians need to accept that long-term weight loss is achievable for a worthwhile proportion of patients (96). In the United States, diabetes costs $174 billion annually (97), and in the United Kingdom, it accounts for 10% of National Health Service expenditure. Even if only a small proportion of patients with type 2 diabetes return to normal glucose control, the savings in disease burden and economic cost will be enormous.
However, the observation that normalization of glucose in type 2 diabetes occurred within days after bariatric surgery, before substantial weight loss (15), led to the widespread belief that surgery itself brought about specific changes mediated through incretin hormone secretion (16,17). This reasoning overlooked the major change that follows bariatric surgery: an acute, profound decrease in calorie intake. Typically, those undergoing bariatric surgery have a mean body weight of ∼150 kg (15) and would therefore require a daily calorie intake of ∼13.4 MJ/day (3,200 kcal/day) for weight maintenance (18). This intake decreases precipitously at the time of surgery. The sudden reversal of traffic into fat stores brings about a profound change in intracellular concentration of fat metabolites. It is known that under hypocaloric conditions, fat is mobilized first from the liver and other ectopic sites rather than from visceral or subcutaneous fat stores (19). This process has been studied in detail during more moderate calorie restriction in type 2 diabetes over 8 weeks (20). Fasting plasma glucose was shown to be improved because of an 81% decrease in liver fat content and normalization of hepatic insulin sensitivity with no change in the insulin resistance of muscle.