The benefits of a diet which restricts the amount of carbohydrates consumed have had further confirmation in a recent paper by Dr David Unwin and colleagues (1). This is a continuation of the work reported in an earlier blog (2). The primary objective is to treat and control Type 2 Diabetes (T2D) while keeping the use of drugs to a minimum. It is accepted that non-alcoholic fatty lever disease (NAFLD) plays an important role in the development of T2D and of obesity. NAFLD is now found in 20% of the population of the developed world, so it was decided to monitor the activity of the enzyme gamma-glutamyl transferase (GGT) which is a reliable marker for NAFLD.
A total of 36 women and 33 men (average age 58 years) agreed to participate. In order to adjust to a low carbohydrate (LC) diet they were advised to reduce sugar and foods with a high starch content such as bread, pasta and rice. This could be replaced by increasing consumption of green vegetables, whole-fruits, such as blueberries, strawberries, raspberries and the “healthy fats” found in olive oil, butter, eggs, nuts and full-fat plain yoghurt were advocated. There was no need to do any calorie counting. Progress was reviewed every month with a GP or practice nurse. All but 2 of the participants completed at least 3 months. The average follow-up period was 13 months so compliance was excellent.
The participants reported that they felt healthier and more energetic on the LC diet. They also appreciated that the diet did not involve any weighing of food or calorie counting.
The results were all very positive. There was an average reduction in the HbA1c from 52.4, to 42.4 mmol/mol which is regarded as “normal”. These results were only for the 27 people who had raised levels at the start of the investigation The GGT activity also showed a marked and significant reduction and, on average, the weight loss was almost 9kg.
The case history of one patient is particularly impressive.
This was a 55-year old woman who started out with an HbA1c of 84 mmol/mol (9.8%) which is effectively out of control and a GGT of 103 iu/L which showed that the liver function was deranged. Essentially this is a bad case of T2D. She had been prescribed metformin. After 3 months on the LC diet the GGT was down to 12 iu/L (a reduction of almost 90%!!) and an ultrasound scan confirmed the liver was functioning normally. She also lost 7.9 kg. In the longer term she has lost a bit more weight, the liver function is fine, her HbA1c is just about OK but she has come off the metformin. She has lost 17 cm from her waist and says she feels “10 years younger”.
This is all great news. This study shows that with the right kind of support and advice very high compliance can be achieved. This is absolutely crucial and contrasts with the conventional calorie reduction strategy which invariably has very high drop-out rates. Even more important is that the results for the important biomarkers like HbA1c are in the right direction. In addition this work also has the information on NAFLD which is extremely valuable.
It was highly significant that there was no clear relationship between weight loss and the reduction in GGT. In fact in most cases, it was found that most of the improvements in GGT were observed in the first month which was well before the majority of weight loss was achieved. If this is confirmed in subsequent investigations then it has enormous implications for the treatment of T2D. This is because it means that the reduction in the NAFLD which is a key element of T2D is independent of weight loss per se.
This result complements the work of Gannon & Nuttall who found that by reducing the carbohydrate content of the diet in T2D patients they could achieve a substantial reduction in the HbA1C within 5 weeks without any concomitant weigh loss (3). However there is extensive evidence that LC diets which also have a high fat content can achieve weight loss in the long term (4).
In the conventional approach to T2D there is much emphasis on weight loss and the usual advice by the NHS is to reduce calories, in which the emphasis is on reducing fat because it is a concentrated form of calories(5). Furthermore in a healthy diet carbohydrates should be the body’s main source of energy (6).
It is not in the least surprising that those who follow this advice rarely succeed.
The implications are really quite profound. T2D is caused by excessive glucose in the body. The logical and obvious way to overcome this is to reduce the supply which means reducing the amount of sugar and other carbohydrates in the diet. When this is done as demonstrated here and in many other investigations the pressure is off and the body can start to recover. One aspect of the recovery is that the fat which has accumulated in the liver starts to be dispersed quite quickly.
Dr Unwin and colleagues are to be congratulated on the work they are doing. His patients are receiving sound advice which is enabling them to improve their health. The use of drugs has been reduced which means less risks of exposure to undesirable side effects not to mention the cost savings to the NHS.
All of this pales into insignificance when compared with the value of the insight and knowledge gained which has the potential to transform the national and international strategies for the treatment of T2D and related conditions. The tragedy is that this is not happening. There is absolutely no recognition of the contribution this kind of information can make in the development of the Diabetes Prevention Programme (7).
It is staggering what has been achieved by this team since it was effectively working with a shoestring budget. Bear in mind too that as well as directing this project, Dr Unwin had to carry on his duties as a GP.
Would it not make much better sense to encourage more projects like this rather than continuing to spend zillions of $/£/€ on so-called high powered research which is making little contribution to overcoming the common contemporary forms of ill-health??
- D Unwin et al (2015)http://www.diabesityinpractice.co.uk/media/content/_master/4311/files/pdf/dip4-3-102-8.pdf
- M C Gannon & F Q Nuttall (2006) Nutrition and Metabolism (London) 3 pp16-24
- R D Feinman et al (2015) Nutrition 31 (1) pp 1-13