302. The Conventional Treatment of Type 2 Diabetes (T2D)

I have just been reading a paper published in 1999, which considers data from the UK Prospective Diabetes Control (UKPDS) (1). It is based on the results of patients who have been advised to alter their diet and/or be treated with different drugs. The focus is on the blood glucose (BG) and glycated haemoglobin (HbA1c) levels.

Those who have an HbA1c of 7% or less are regarded as successful. The patients were followed for up to 9 years.


Patients were encouraged by a dietitian to consume a diet that was low in fat, high in carbohydrates and high in fibre.

The results for the different treatments are shown in Table 1.

Table 1. The proportions of patients that achieved HbA1c lower than 7% as the study progressed.

                                                    HBA1c < 7%
3 years6 years9 years
Sulphonyl urea503424


Values are expressed as percentages of those who commenced the treatment.

What comes through here very clearly is that without exception the diet and all the drug treatments were not successful in the long term. It is clear that the proportion that manage to stay below the 7% HbA1c decreased with time. So essentially what this means is the disease deteriorates with time for most of the patients.

As the paper comments:

“The increasing failure of monotherapy with sulphonyl urea, metformin, or insulin to achieve tight glycemic control over the first 9 years following diagnosis of type 2 diabetes is consistent with the progressive decline ?-cell function.”

This means that the capability of the pancreas to produce the necessary quantity of insulin to control the BG is steadily reduced.

If we take a step back, we now know that T2D does not develop overnight. If the pancreas is producing high quantities of insulin on a regular basis, the body develops a condition known as insulin resistance (IR). As a consequence the demand for insulin increases steadily. Ultimately the pancreas is unable to meet the demand so the blood BG is out of control. This explains why the value increases and causes the alarm bells to ring if detected by a routine check. Once this is appreciated, it becomes obvious that the drug treatments do not address the fundamental cause and simply attempt to deal with the symptoms.

It does not take a genius to work out that the demand for insulin is directly related to the total amount of glucose in the blood and this in turn is a reflection of the amount of sugar and starch (that breaks down to glucose) present in the diet. So if you wish to reverse T2D, then the logical approach would be to alter the diet in order to reduce the amount of glucose that enters the body, which would mean that the requirement for insulin is reduced. The way to achieve this is to eat much less sugar and starch, which is present in foods such as wheat, bread, cakes, rice, potatoes and pasta. Advising people to INCREASE the consumption of carbohydrates, which is the conventional approach, just does not make sense. The reality is that it will make things worse. There is ample evidence to demonstrate the truth of this conclusion.

Coping withT2D

It follows from this that the way to combat T2D is to REDUCE the amount of sugar and carbohydrates consumed. There is extensive research, which confirms that this approach is effective (2), not to mention the thousands of individuals who have discovered for themselves that a diet low in carbohydrates and high in healthy fats (LCHF) can overcome T2D successfully. Essentially this means controlling BG thereby reducing the need for drugs. Many have found that they can come off drugs completely.

A complete recovery?

Clearly this is a good result but it also raises the question about the recovery of the underlying damage that has been caused. Recent work at the University of Newcastle under the direction of Professor Roy Taylor provides valuable insight into this issue.

In a study conducted by the Newcastle team, volunteers who had been diagnosed with T2D less than 4 years previously, were requested to consume  a low calorie diet (600Kcal/day) for a period of 8 weeks. It was found that within one week, the fasting BG levels had fallen from 9.2 mmol/L to values comparable to those for non-diabetics. The HbA1c levels had fallen from 7.4% at the outset to 6.0% after 8 weeks, which is also in line with results for non-diabetics. The insulin levels were reduced by over 50%, which indicates a substantially lower demand. The sensitivity of the liver to insulin increased, which indicates that the insulin resistance has been reduced. The production of insulin by the ?-cells increased and was similar to that in the non-diabetic controls. The average weight loss was 15kg.

The authors concluded that:

This study demonstrates that the twin defects of beta cell failure and insulin resistance that underlie type 2 diabetes can be reversed by acute negative energy balance alone.”

 The significance

There is absolutely no doubt that these results are highly significant. Not only has the BG been brought under control, but the fundamental damage has effectively been repaired. Although the strategy has been to reduce the calorie input to a fraction of the requirement, the improved health is undoubtedly caused by the reduction in the quantity of sugars being absorbed into the blood. Hence the demand for insulin has been cut substantially.


This is an important finding. However the serious limitation is that it is not sustainable in the long term. Obviously if the participants revert to their original diet, it is virtually inevitable the T2D will return. It would therefore be essential to adopt a completely different diet. All the evidence points strongly to one that is LCHF (5). Perhaps the Newcastle team could be persuaded to focus on this aspect in a future investigation. I believe it is highly likely that this would approach would produce similar results albeit a bit more slowly. If this is what happens it would provide a solid case for LCHF and totally destroy any possible justification for the official advice to reduce fat and increase carbohydrates.


  1. https://jamanetwork.com/journals/jama/fullarticle/190204
  2. R D Feinman et al (2015). http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/fulltext
  3. F L Lim et al (2011). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/
  4. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3168743/
  5. https://www.sciencedirect.com/science/article/pii/S0899900714003323


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