Diabetes and Diet

People who are gluten intolerant solve the problem in a straightforward way – by not eating gluten. Likewise for lactose intolerance or any other intolerance or allergy, with one remarkable exception – glucose intolerance. Health professionals still recommend that people who are glucose intolerant continue to eat glucose (carbohydrates), and then prescribe medicines or lifestyle changes to endeavour to manage the consequences.

I’m talking about Type 2 Diabetes (T2D). It is widely understood that T2D arises from a breakdown in insulin regulation of blood glucose as a result of insulin resistance.

When carbohydrate is ingested it is broken down into glucose. Blood glucose rises and triggers insulin secretion from the pancreas. The insulin binds to assemblies called insulin receptors which are found on the surface of various cells of the body – e.g. liver, fat and muscle cells. The action of insulin binding to its receptor is the key that allows glucose to leave the blood and enter the cell. There, it can be burned for energy, used for some other purpose, or stored (as fatty acids in adipose tissue and liver, or glycogen in muscle and liver).

With insulin resistance, some change occurs to the receptor that makes it harder for insulin to bind to it, or makes the receptor less effective if it does. The pancreas releases more insulin to compensate for this resistance and insulin levels rise above normal. The increased insulin availability de-sensitises the receptors and insulin resistance increases. This is the self-reinforcing cycle of spiralling insulin resistance and release that is the signature of T2D progression.

After years of this, something begins to happen in the pancreas and it fails to release as much insulin. This is dangerous because now there is no mechanism for sequestering glucose into cells. Chronically-elevated blood glucose (hyperglycaemia) has dire consequences which, together with abnormal insulin signalling, contributes to advanced symptoms of diabetes including cardiovascular disease (often the fatal end-point), blindness, kidney failure and amputation.

Treatment for T2D

The medical approach to T2D has been to prescribe drugs that target the symptoms (blood glucose and insulin levels) but not the cause (insulin resistance). This turns T2D into a chronic-progressive disease that leaves the sufferer with little hope. There is no choice – medicines are not available to treat the cause.

However, if blood glucose is a problem, then why not just eat less glucose in the first place? Treat T2D with a low-carbohydrate diet as a first resort.

Frederick_Madison_AllenThis is the way diabetes used to be managed before the discovery of insulin and other drugs. The most effective treatment was fasting (as was the case for epilepsy) and/or a low-carbohydrate diet. The ‘Allen Starvation Treatment’ (after Frederick Allen) was highly successful. It was  a calorie-restricted (1000 calories a day), carbohydrate-restricted (<10g a day) diet, which, if necessary, was preceded by a period of hospitalisation during which patients received whiskey and black coffee every 2 hours. Treatment continued until glucose in the urine of the jolly patients had dropped to normal levels.


180px-Fredrick_bantingThe story of insulin started around 1910 when Sir Edward Sharpey-Schafer proposed that diabetes was a hormonal disorder and named the hormone insulin, because diabetes developed in animals after destruction of the Islets of Langerhans in the pancreas. Insulin was later isolated from foetal cow pancreas at the University of Toronto in 1921 by Frederick Banting (not to be confused with William Banting, the 1862 low-carb high-fat celebrity) and Charles Best. The first patient was treated by Banting in 1922. Banting and MacLeod (who provided laboratory facilities) were awarded the Nobel prize in 1923 (a remarkably short time-sequence). The inclusion of MacLeod over Best was controversial and perhaps not one of the Nobel committee’s better decisions (Banting was furious, and gave Best half of his prize money). Banting was an interesting fellow, as well as a Nobel prize, he held a Military Cross for heroism under fire (WWI), and he liked to paint. Only 4 years elapsed between the Military Cross and the Nobel Prize.

The discovery and availability of insulin was pivotal, because now that diabetes was confirmed as a hormonal disorder, medicine could turn to drugs to treat it.

smallpyramidAs with epilepsy, dietary treatment went out of favour. Furthermore, the Dietary Guidelines for Americans became established after the 1960s and carbohydrates were regarded as the healthiest food group (especially glucose-loaded, really digestible, starchy carbohydrates). As well, it was assumed that dietary carbohydrates were essential to supply glucose for the brain (wrong, the brain continues to function with fasting by turning to ketones). This thinking underlies the dietary non-advice for T2D that is recommended today. Diet is no longer part of treatment. It’s part of the problem.

Current Dietary Guidelines for T2D

Current dietary guidelines for diabetes defy belief. They recommend starchy foods that are little more than readily-digestible glucose, or even sweet glucose-laden foods.

The American Diabetes Association (ADA) has this to say: “A healthy meal plan for people with diabetes is generally the same as a healthy diet for anyone”. Which means following a high-carbohydrate low-fat diet. The ADA goes on to confirm this: “Whole grain breads, cereals, pasta, rice and starchy vegetables like potatoes, yams, peas and corn can be included in your meals and snacks.” Incredibly, that’s a list of digestible high-glucose carbohydrates.

There’s more: “If eaten as part of a healthy meal plan, or combined with exercise, sweets and desserts can be eaten by people with diabetes. They are no more “off limits” to people with diabetes than they are to people without diabetes.” Sweets – for diabetics?

The ADA offers an example meal. Nearly half the calories in that meal come from carbohydrates. It is as though the ADA is in denial that there is anything wrong with glucose metabolism in T2D.

stopd-iconInspection of the ADA web site reveals that their major sponsors are pharmaceutical companies. The top 5 manufacturers of diabetic drugs are major ADA sponsors (in order: Novo Nordisk, Sanofi, Merck, Eli Lilly and AstraZeneca). It was Eli Lilly that first manufactured insulin. Others include GlaxoSmithKline, Janssen Pharmaceuticals and Pfizer.

Potentially, this is a conflict of interest. An example of a conflict of interest might be if the level of dietary carbohydrate recommended by the ADA was just right for the profitability of their drug company sponsors. From a drug company perspective, a just-right level of dietary carbohydrate might be one that is high enough for the patient to need expensive medication for as long as possible.

Consider the image above-left. If that campaign were to be successful, where would it leave the ADA?

A Sensible Diet for T2D

Fortunately, some pioneering people with T2D are ceasing to be passive participants in the system and are making decisions for themselves (with cooperative physicians). They are reducing their dietary carbohydrates, replacing the missing calories with fats, and seeing improvements in their symptoms (not just T2D symptoms, but also weight, blood pressure and blood lipids). They are on a low-carbohydrate high-fat ketogenic diet. Others have taken the step of fasting, with some spectacularly successful results. Many report complete remission with either approach and cease all medication. Some call this a cure. This is not conceivable in the medical model.

Case studies

There are many case studies to be found on the web. It can be interesting when a medical doctor treats himself this way, and the process can give insights into medical training and thinking. The following 24 min video is an example.

There are other examples at the end of the post. Low-carbohydrate diets can be effective even for late-stage highly-obese diabetics. Blood-pressure and diabetes medications need to be adjusted under professional supervision.

The principles

A low-carbohydrate high-fat (ketogenic) diet for T2D is based on the following principles:

  1. Dietary fat is not a risk factor for heart disease or stroke and does not drive diabetes;
  2. Fat is an essential macronutrient, and a biologically-evolved fuel source;
  3. Carbohydrates are not an essential macronutrient and can be minimised safely;
  4. T2D can be thought of as a form of glucose intolerance that can be treated by restricting dietary carbohydrate intake.

How much plant-based carbohydrate do we need?

It is not commonly known that we do not need any carbohydrate in the diet. There is no such thing as ‘carbohydrate deficiency disease’. We need vitamins, minerals etc that can come with carbohydrates, but we do not need the carbohydrates themselves.

This was famously demonstrated ~1930 by Stefansson and Andersen, who went a year eating nil carbohydrates. The ‘experiment’ was undertaken with medical supervision (Bellevue Hospital, NY). At the end of the year, they were as healthy or healthier. They ate the fatty meat and some of the internal organs (e.g. liver, kidney etc), which gave them extra nutrients (such as vitamin C). The meat and liver they were eating contained glucose (stored as glycogen) and their own livers were able to manufacture glucose (from dietary fats and proteins) if needed.

carbohydrate-glycemic-indexDiet Outline

With T2D, daily carbohydrate consumption probably needs to be below 20g. That’s grams of carbohydrate, not grams of food containing carbohydrate. Online resources, such as this one, give the carbohydrate content of common foods. An alternative, and perhaps easier, approach is to not count carbohydrates at all, but rather to monitor blood ketones (with a finger prick device such as this). If ketones are greater than 0.5 mmol/L, then carbohydrate intake is sufficiently low.

There is no need to count calories, even if weight is an issue. Calorie-restriction is not effective for weight-loss. Replace the energy shortfall from decreased carbohydrates with fat. Good sources of fat are animal fats (including rendered lard or tallow), dairy fat (butter, cream, cheese) and cold-pressed oils (extra virgin olive oil, coconut oil, avocado oil). Eliminate polyunsaturated vegetable oils (canola, sunflower, peanut etc) – this is important for multiple reasons. Maintain adequate protein intake. Eat according to hunger signals. It looks like a dietitian’s nightmare, however it is just a very low-carbohydrate ketogenic diet. As a bonus, ketogenic diets are effective for weight-loss.

I have listed more detailed resources at the end of the post.

Blood glucose

The body can tolerate only a small amount of glucose in the blood. How much? About 1-2 teaspoons (4-8 grams) in the entire blood circulation (of about 5 kilograms). many-grams-teaspoon-sugar_ecbccd3ed258f276Maintaining blood glucose this low in the presence of high dietary glucose is a major challenge for the body. It should be no surprise that if the body is challenged this way hourly and daily for decades, then things can go wrong. What goes wrong is that the body becomes less efficient at getting glucose out of the circulation (because of insulin resistance) and glucose levels become chronically elevated (hyperglycaemia).

A consequence of chronic hyperglycaemia is an increase in a process called glycation. With glycation, a glucose molecule randomly attaches itself to a passing protein molecule and irreversibly disables the function of the protein. This is why high blood glucose is so damaging. A useful measure of average blood glucose is the percentage of haemoglobin that has been glycated (it goes under the abbreviation HbA1c). Because red blood cells have about a 3 month lifespan, this gives a measure of average glucose levels over that period, and is an important index for monitoring long-term changes in blood-glucose. A less-elevated HbA1c is used to diagnose pre-diabetes.

As an aside, glycation is the chemical process that occurs at the onset when browning meat in a pan – it is the reaction between proteins in the meat and glucose in muscle glycogen stores. Under high heat, the process is accelerated, becomes more complex and produces many flavourable end products. You just don’t want anything like it happening in your body.

Insulin resistance and obesity

Insulin resistance is not binary (yes/no) – it is best thought of as a continuum. Low levels of insulin resistance and hyperglycaemia (below a diagnosis for pre-diabetes) can occur in otherwise healthy individuals and be associated with weight-gain. 75598cbb-206e-4ad0-9e3e-f90e90f0eabcThis is because insulin resistance causes the pancreas to release extra insulin, and insulin is a fat-storing hormone. One of its actions is to remove glucose from the blood by triggering the liver to convert glucose into fatty acids that are transported (by very low-density lipoproteins) to adipose tissue for storage, or stored in the liver resulting in non-alcoholic fatty liver. Insulin then locks the fat into storage (fat doesn’t get released and burned for energy if there is insulin around). This is why lowering dietary carbohydrate (and therefore blood glucose and insulin level) is so effective for reducing weight in nearly everyone. It is also why T2D is so strongly associated with obesity. So strongly, that obesity is often thought to be a cause of diabetes, whereas it is mostly a symptom of insulin resistance.

Diet as a first resort in T2D

Recently (2015), a group of 26 scientists published a critical review of diabetes in the journal Nutrition. They made the case that dietary carbohydrate restriction should be the first approach in diabetes management. They discuss 12 reasons to support or expand on that statement. I quote them here:

1. ‘Hyperglycaemia is the most salient feature of diabetes. Dietary carbohydrate restriction has the greatest effect on decreasing blood glucose levels.’

2. ‘During the epidemics of obesity and type 2 diabetes, caloric increases have been due almost entirely to increased carbohydrates.

3. ‘Benefits of dietary carbohydrate restriction do not require weight loss.’

4. ‘Although weight loss is not required for benefit, no dietary intervention is better than carbohydrate restriction for weight loss.’

5. ‘Adherence to low-carbohydrate diets in people with type 2 diabetes is at least as good as adherence to any other dietary interventions and is frequently significantly better.

6. ‘Replacement of carbohydrate with protein is generally beneficial.

7. ‘Dietary total and saturated fat do not correlate with risk for cardiovascular disease.’

8. ‘Plasma saturated fatty acids are controlled by dietary carbohydrate more than by dietary fats.’

9. ‘The best predictor of microvascular and, to a lesser extent, macrovascular complications in patients with type 2 diabetes, is glycemic control (HbA1c).

10. ‘Dietary carbohydrate restriction is the most effective method (other than starvation) of reducing serum triglycerides and increasing high-density lipoprotein.’

11. ‘Patients with type 2 diabetes on carbohydrate-restricted diets reduce and frequently eliminate medication. People with type 1 usually require lower insulin.’

12. ‘Intensive glucose lowering by dietary carbohydrate restriction has no side effects comparable to the effects of intensive pharmacologic treatment.’

They review the literature to support each of these statements. They also address common concerns about low-carbohydrate diets in people with diabetes. I draw your attention to points 1, 4, 7 and 11. To clarify point 8 – they don’t mean that dietary carbohydrates lower circulating saturated fatty acids, they mean the opposite (carbohydrates raise blood saturated fats whereas dietary fats lower them).

The full article can be read here. It is possible that a very low carbohydrate ketogenic diet might be poised to go mainstream for diabetes treatment.

Then again – T2D is not just a disease, it’s an industry.

Meanwhile, people with T2D are making their own decisions, reducing dietary carbohydrates, and finding out for themselves that T2D is a reversible disease and not a chronic-progressive disease associated with a lifetime of ill-health.

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Note: The content of this post is intended to be educational and informative. It should not be taken as medical advice.

Further resources:

I have done an update on how insulin resistance develops here.

There is more on low-carbohydrate diets on my ketogenic diet page.

If you are living with diabetes and need more detailed information on low-carbohydrates and diabetes, I recommend the diet doctor diabetes page. Also information on low-carb eating and carbohydrate guide. Read some of the success stories here.

For information on fasting as a treatment option, see Jason Fung’s site or Facebook page.

Some videos,including interviews with people who have treated their diabetes this way: