Type 2 diabetes and nutrition

The relationship between diabetes and nutrition is often oversimplified and equated with an excess of ‘sugar’ or glucose in the diet, by clinicians and laypeople alike.Unfortunately, this widely held belief and the resulting dietary choices are contributing to the current epidemic of type 2 diabetes and poor outcomes for patients with diabetes. Certainly, both types of diabetes are defined by an excess of glucose in the blood. However, the amount of glucose in our blood depends mostly on our body’s ability to use the glucose we consume, with availability and sensitivity to insulin being the critical factor. Excitingly, by revising our own and our patients’ nutritional approach to diabetes,we can ‘reverse’ most cases of type 2 diabetes, and help those with type 1 diabetes dramatically reduce their insulin use and risk of complications and chronic disease.


It is now well known that body mass index and type 2 diabetes are closely related.

This diet is characterised by high fat consumption, high protein consumption (both largely from animal sources), and a moderate intake of carbohydrate (largely from refined sources, especially sugar and flour). For example, the average diet in Australia and New Zealand is approximately 32% energy from fat, 17% protein, and 46% carbohydrate1,2. As we see populations that have traditionally consumed a diet considerably higher in carbohydrate, but lower in fat and protein move towards the Western dietary pattern, a dramatic corresponding increase in type 2 diabetes occurs.

In China in 1980 less than 1% of the population had type 2 diabetes3. At this stage, the Chinese diet had just begun to shift towards Westernisation. In 1970 for example, the Chinese diet was approximately 8% energy from fat, 10% protein, and 83% carbohydrate4. By 2011, this had ‘Westernised’ to 32% fat, 13% protein, and 54% carbohydrate5. It has been estimated that 11.6% of the Chinese population now have diabetes and 50.1% have prediabetes6.

Across the Pacific in the United States, the Native American Pima people of Arizona are thought to have perhaps the highest prevalence of type 2 diabetes in the world: about 50% of all Pima over the age of 35 are affected7. Their diet is similar in both total energy and macronutrient composition to that of the general population in the US, with approximately 35% energy from fat, 15% protein, and 47% carbohydrate8. Intriguingly, the Pima of Mexico, who are very closely related genetically, have a substantially lower prevalence of type 2 diabetes at 13.4%. Their diet is more traditional and ‘…remarkable for the low percentage of calories derived from fat…’ at approximately 26% fat, 11% protein, and 62% carbohydrate9.

While Westernisation of diet is also accompanied by increased food availability and substantially reduced physical activity, increases in rates of type 2 diabetes trend with increased fat intake, not an increased carbohydrate intake. Even refined sugar, often blamed for the diabetes epidemic, seems to have little role in its aetiology besides as a source of additional energy10. Furthermore, the idea that refined sugar is hazardous for glycemic control in people with type 2 diabetes is not supported by research. In one study, glucose control actually improved on a higher sugar diet, where participants were supplemented with 60g of fructose per day in place of complex carbohydrates, despite no changes in body weight10! Of course, there are plenty of other reasons why we should all minimise or avoid refined sugar, but at the very least from the above examples we can conclude it is possible to eat a diet that is very high in carbohydrate, perhaps even refined carbohydrate, compared to current diets in Australia and New Zealand without developing type 2 diabetes. If the high fat intake of the Western diet is instead implicated, why might this be the case?

It is now well known that body mass index and type 2 diabetes are closely related.

The risk essentially increases linearly as BMI increases, and weight gain after age 18 is a major determinant of risk11. While it is often assumed that refined sugar and carbohydrate are the major contributors to excess energy intake in Western society, again this idea is not supported by research. A recent UK study found that compared to those with normal BMI, obese participants had a 14.6%, 13.8%, 9.5% and 4.7% higher intake from fat, protein, starch and sugar, respectively12. In fact, it was concluded that because the proportion of fat in the diet, rather than sugar, was higher among overweight and obese individuals, focusing public health messages on sugar may mislead on the need to reduce fat and overall energy consumption.


Unsurprisingly then, type 2 diabetes can be effectively treated by weight loss.

A recent and exciting finding was that intensive weight management in a primary care setting resulted in remission of diabetes in 46% of participants13. Remission varied with the weight loss achieved, increasing from 7% of participants who maintained 0-5kg of weight loss to 86% of those who lost 15kg or more. Unfortunately, the intervention was indeed ‘intensive’, replacing all food with a mere 825-853kcal a day of a high carbohydrate, low fat formula for between 3-5 months. Just under 20% of participants who began treatment withdrew prematurely, the majority for social reasons. Almost half of participants reported the side effect of constipation, and well over a third reported sensitivity to cold, headaches, and dizziness. Given the intensive energy restriction it is also unsurprising that 32.4% reported fatigue. However, in fairness, the majority of these cases were mild, and the vast majority of them resolved during the food reintroduction and maintenance phases.

Consistent with the strong association between type 2 diabetes and obesity, it has been proposed that a very important contributor to insulin resistance is fat (lipid) droplets in tissues such as the heart, liver, and especially skeletal muscle. Skeletal muscle is particularly important in keeping glucose levels in the circulation normal as it can account for up to 80-90% of insulin-stimulated glucose disposal14. The ability of our fat cells to store excess energy as fat is limited. Once this limit is exceeded, fat is stored in the aforementioned tissues and lipid intermediates reduce their sensitivity to insulin. The number of fat cells we have is limited too, and is set during childhood and adolescence15, which may well explain the importance of weight gain after age 18 as noted earlier. A recent systematic review has noted that while diets with an increased proportion of carbohydrate decrease these fat stores in muscle, high fat diets increase them16.


However, to attempt to reduce the relationship between diabetes and nutrition to single macronutrients is a gross oversimplification.

After all, we eat foods, not fat, protein, and carbohydrate. So what can be learned when we look at specific types of foods? In the second Adventist Health Study, lower consumption of animal products was associated with reduced risk of type 2 diabetes. Compared with non-vegetarians, risk of type 2 diabetes was 79% for pesco-vegetarians, 64% for lacto-ovo vegetarians, 45% for semi-vegetarians (consume dairy and eggs, but red meat and poultry less than once a week), and 38% for vegans17. In China, significant increases in animal product consumption have occurred, with consumption almost tripling between 1970 and 19924, and continuing to rise thereafter5. Both processed and unprocessed red meat are associated with a 51% and 19% increased risk of type 2 diabetes, along with haeme iron (found in all meat), which is associated with a 31% increased risk3. In contrast, fruit and vegetable consumption, particularly green leafy vegetable consumption, appears protective18. Likewise, wholegrain consumption is protective, decreasing risk by 32% for every 3 servings consumed3.

This implies that a return to a more traditional dietary pattern based around whole, unrefined foods of plant origin could provide an effective treatment for type 2 diabetes.

Whole food plant-based diets have demonstrated impressive efficacy for weight loss, and because such diets reduce energy density of food, they can be very effective even with ‘ad libitum’ eating patterns19,20. In fact, our smaller Gisborne study achieved greater average weight loss at 12 months than the DiRECT trial, with 11kg of weight loss on average at 12 months vs 10kg despite our participants having a slightly lower average weight, with no energy restriction whatsoever20. Furthermore, although only a handful of our participants had been diagnosed with diabetes, and we started with an average A1c of just 42, an average reduction of 5mmol/mol was observed in the group, which compares quite favourably to the 9.6mmol/mol drop in the DiRECT participants who started with an average A1c of 60.2. Participants in our research found the lack of requirement for energy restriction a major advantage and this is something that made the intervention more palatable and sustainable despite the considerable shift in dietary pattern that was required: at 6 months, just one participant who began the intervention was discontinued due to non-attendance/adherence.

Recently, analysis of three large prospective cohort studies in the US (the Nurses’ Health Study; the Nurses’ Health Study 2; and the Health Professionals Follow Up Study) has suggested that plant-based dietary patterns are associated with a substantially lower risk of developing type 2 diabetes21. Another analysis looked at a prospective cohort in the Netherlands, and similarly concluded that a more plant-based and less animal-based dietary pattern may lower risk of insulin resistance, prediabetes, and type 2 diabetes22. As an intervention for type 2 diabetes, low-fat exclusively plant-based diets have demonstrated greater medication reductions23 and improvements in glycemic control23,24 than conventional diets for type 2 diabetes, along with similar acceptability to patients25.

It is very important to consider, in the cases of both type 1 and type 2 diabetes, that cardiovascular complications are the leading cause of morbidity and mortality6. A plant-based eating pattern is the only dietary intervention that has demonstrated regression of atherosclerosis26,27. It is perhaps not an unreasonable assumption that the qualities of a plant-based diet that have proven so beneficial for macrovascular disease might also help prevent microvascular complications. A recent pilot study also suggested that such an eating pattern had potential value in the treatment of painful diabetic neuropathy28. Finally, being a (comparatively) low-protein and high nutrient diet a more plant-based eating pattern is likely to be beneficial in protecting kidney function29.


Although there are other diets that have been proposed as treatments for diabetes, it is clear from the epidemiological literature that more traditional plant-based ‘high carbohydrate’ diets are associated with very low rates of type 2 diabetes. Such eating patterns are associated with substantial and sustainable weight loss, and greater improvements in glycemic control and reduction in medications than standard diets for diabetes. Most importantly, plant-based diets are proven to be ‘heart healthy’ and for people with type 2 diabetes who do not achieve substantial enough glycemic control to be considered non-diabetic, and people with type 1 diabetes, plant-based diets provide the best chance of avoiding longterm complications, and significantly extending life expectancy. In fact, the longest living people in the world are the Okinawans of Japan, whose diet is almost entirely plant-based and 85% carbohydrate (most of which is from sweet potato)30. When it comes to nutrition, those wanting to avoid type 2 diabetes or those with type 1 or type 2 diabetes would do well to attempt to emulate this more traditional dietary pattern rather than the current Western pattern which appears to be a major factor driving the current epidemic.

Dr Luke Wilson is a New Zealand-based General Practitioner and co-founder of Two Zesty Bananas.

More articles from Luke:

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This article has been written for the Australasian Society of Lifestyle Medicine (ASLM) by the documented original author. The views and opinions expressed in this article are solely those of the original author and do not necessarily represent the views and opinions of the ASLM or its Board.