To the Editor
Dr Tim Noakes’ recent study is an important contribution to the scientific literature, as one of the primary issues with any diet is that people cannot adhere to them over the long-term, writes nutritionist Alex Leaf. But his statement that type 2 diabetes is a reversible condition “if patients will simply restrict their daily carbohydrate intake to less than 25g/day” is disingenuous for several reasons.
Therefore, looking at the dietary habits of those who have adhered to a particular diet for long periods of time can give insight into what people are doing in the real world (i.e., not in a lab). In Noakes’ study, the focus was on adults with type 2 diabetes who reported deliberately avoiding carbohydrate-rich foods for the previous six months.
The participants had their diet assessed from a food frequency questionnaire, 3-day diet log, and 1-day diet recall when they enrolled in the study. Total carbohydrate intake was 20–50 g/d for 10 participants, 50–115 g/d for 17 participants, and was 142 g/day for one participant. Protein intake averaged 92 g/d (20% of calories) and fat intake averaged 121 g/d (66% of calories). Average intakes of folate, vitamin D, vitamin E, and calcium were below 50% of recommended daily allowances (RDAs), while intakes of thiamin, vitamin B6, vitamin C, magnesium, manganese, and potassium intakes were between 50% and 100% of RDAs.
These are important findings, as they indicate that (1) individual definitions of a “low-carbohydrate diet” differ widely, and (2) individuals may not be meeting their needs for several vitamins and minerals. Importantly, of the 25 most frequently eaten foods, 7 (28%) were isolated sources of fat like cream, butter, and coconut oil, which do not provide much if any nutritional value outside of being a source of fat calories. For individuals embarking on a low-carbohydrate diet, it is important to select more nutrient-dense low-carbohydrate foods, such as non-starchy vegetables, nuts and fatty fruits, eggs, and whole-fat dairy with the protein component retained (cheese and yogurt).
Noakes’ also looked at the participants’ HbA1c, a marker of average blood glucose concentrations over the previous three months, and diabetes medication use when the participants were diagnosis with type 2 diabetes, when they started eating a low-carbohydrate diet, and at the assessments alongside dietary analysis. Most participants reported greatly reducing their medication use after starting a low-carbohydrate diet, including 8 of 11 who completely discontinued exogenous insulin and 2 of 11 that reduced their dose by 20% and 70%. Additionally, of 24 participants taking an average of 1850 mg/d of metformin, 8 discontinued use and the average dose dropped to 1000 mg/d for the remaining 16 after starting a low-carbohydrate diet. Even with less medication, the average HbA1c was reduced from 7.5% before starting a low-carbohydrate diet to 5.8% afterwards. Body weight was also substantially reduced by an average of 17%, ranging from 7% to 25%, after adopting a low-carbohydrate diet.
Given what this study investigated and reported, I believe that Noakes’ statement that type 2 diabetes is a reversible condition “if patients will simply restrict their daily carbohydrate intake to less than 25g/day” is disingenuous for several reasons: (1) most of the participants did not consume less than 25 g/d of carbohydrates, (2) the study was observational and could not establish cause and effect, (3) diabetes reversal cannot be determined on the basis of average blood glucose concentrations, and (4) there is no way to disentangle the effects of eating a low-carbohydrate diet from the effects of substantial weight loss.
I want to focus on points 3 and 4. Type 2 diabetes is ultimately a condition of fat cell dysfunction and insulin resistance. It is expected that reducing the amount of carbohydrates you eat will lower markers of glycemia since dietary carbohydrate are the primary driver of glycaemic changes. Accordingly, HbA1c is not a useful marker for whether diabetes has been reversed. This point was demonstrated in Noakes’ study by the fact that 2 of the participants diagnosed with diabetes from an oral glucose tolerance test (a test to assess insulin resistance) had normal HbA1c and fasting glucose levels. Accordingly, a low-carbohydrate diet does not intrinsically address the underlying causes of type 2 diabetes.
As an analogy, consider the autoimmune Celiac disease. If you take someone with Celiac disease and remove the gluten from the diet, then is their disease gone or simply being managed by the dietary changes? In order to cure Celiac disease, you can’t just remove the insulting component of the diet, you have to address the disease processes, which in this case would be preventing the autoimmune attack against the intestinal cells when gluten is consumed. Eating a low-carbohydrate diet is just symptom management for diabetes unless you simultaneously address the cause of the diabetes.
The cause of type-2 diabetes is almost always an issue with surpassing one’s personal fat threshold . Basically, we all have an amount of fat we can store safely (due to genetic, environmental, and lifestyle factors), and once we surpass that threshold, we begin to store exponentially more fat in our viscera, especially the liver and pancreas, which causes insulin resistance and metabolic dysfunction [2–5]. If you want to actually cure type 2 diabetes, then you need to lose fat. This has been unequivocally demonstrated by the Counterpoint and Counterbalance studies out of Newcastle University .
In Counterpoint , individuals with type 2 diabetes were placed on a meal-replacement diet providing about 600 kcal per day (60 g of carbs) for 8 weeks. They lost 15% of their body weight, reduced their liver fat content from 13% to 3%, and reduced their pancreatic fat content from 8% to 6%. This extensive fat loss occurred alongside notable reductions in HbA1c, fasting glucose, fasting insulin, fasting triglycerides, as well as normalization of hepatic insulin sensitivity, the pancreatic response to glucose, and peripheral insulin sensitivity.
The Counterbalance Study built on these findings . The same intervention was used for 8-weeks, which was then followed by 6 months of eating normally and maintaining any weight loss. Not only did glycaemic control and insulin sensitivity improve as a result of substantial fat loss, but these improvements were maintained even when the participants started eating a normal amount of carbohydrate. When the participants looked at the participants who responded well to treatment and those who did not, the non-responders simply didn’t achieve the same level of pancreatic fat reduction. In particular, non-responders were characterized by evidence of insulin deficiency at baseline and lack of ability to regenerate insulin secretion capacity.
So, diabetes is curable in individuals who do not have too much pancreatic damage, but it requires substantial fat loss. Importantly, cure means that carbohydrates can again be eaten without issue. Certainly, a low-carbohydrate diet can help with fat loss through reducing hunger and increasing satiety. It is also excellent for managing the signs of type 2 diabetes (elevated blood glucose and insulin levels), but it needs to be coupled with fat loss to address the disease itself.
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Alex Leaf, MS, CISSN
Lecturer at Western States University and researcher for Examine.com