A paper which has just been published concluded that:
“Recent studies suggest that low carbohydrate diets appear to be safe and effective over the short term, but show no statistical differences from control diets with higher carbohydrate content and cannot be recommended as the default treatment for people with type 2 diabetes.” (1)
This is in direct conflict with a comprehensive review published earlier this year which concluded:
“The benefits of carbohydrate restriction in diabetes are immediate and well documented. Concerns about the efficacy and safety are long term and conjectural rather than data driven. Dietary carbohydrate restriction reliably reduces high blood glucose, does not require weight loss (although is still best for weight loss), and leads to the reduction or elimination of medication. It has never shown side effects comparable with those seen in many drugs. Here we present 12 points of evidence supporting the use of low-carbohydrate diets as the first approach to treating type 2 diabetes and as the most effective adjunct to pharmacology in type 1. They represent the best-documented, least controversial results. The insistence on long-term randomized controlled trials as the only kind of data that will be accepted is without precedent in science.”(2)
In addition there are literally hundreds, if not thousands, of individuals who have successfully coped with type 2 diabetes (T2D) by switching to a diet low in carbohydrates (LC). Many of these people have been able to eliminate medication completely. Similarly those with type 1 diabetes (T1D) have been able to reduce their medication and so avoid the extreme variation in blood glucose levels which can cause hypoglycaemia (3, 4, 5).
I find the totality of evidence which supports the case for diets which are low in carbohydrate convincing. Not only are they superior to drug therapy for T2D but they are also very useful for those who have T1D. Furthermore those who switch to these diets usually also benefit by reducing the level of blood triglycerides and increasing the HDL cholesterol, thereby improving risk factors for heart disease. Many experience weight loss, although this does not always occur.
So why is the latest paper so far out of line? In the introduction it is stated that the carbohydrate debate:
“seems to be based on strong personal opinion and those working in the area tend to cherry-pick the evidence to support their particular view”
“The evidence available is contradictory at best, and leaves both health professionals and people with diabetes alike wondering if low carbohydrate diets do live up to the hype surrounding them, and whether they should be recommended as a suitable treatment”.
There is no question that this scepticism is not justified. It simply dismisses much solid research not to mention all those individuals who have posted details of their success in coping with their disease by choosing an LC diet. There have to be genuine doubts about the objectivity of the author.
As for the study itself, this is a compilation based on 8 different studies which have been conducted in recent years. We can gain some insight into the investigation by considering the individual investigations separately.
- In this study the investigators recognised the value of an LC diet and so the purpose of their research was to focus on compliance (6). In the event they found that:Hence the results can have no bearing on the effect of an LC diet. “Participants in the two groups appeared to consume similar diets, despite the prescription of markedly different intake. Thus, the interventions were not effective in facilitating dietary adherence.”
- In this study the object was to compare an LC Mediterranean diet with a traditional Mediterranean diet and with one which complied with the recommendations of the American Diabetic Association (7). It was found that only the LC Mediterranean diet improved the HDL cholesterol and was superior to the other 2 in improving the glycaemic control as determined by the reduction in HbA1c. This diet also achieved the greatest reduction in blood triglycerides. In any case this LC diet had 35% E as carbohydrates, which is much higher than that normally used.
- The object of the third study was to compare a diet which was high in protein (30% E Protein, 40% E Carbohydrate) with one which was high in carbohydrates (15% E Protein, 55% E Carbohydrate) (8). It was found that there were decreases over time in weight, serum triacylglycerol and total cholesterol, and increases in HDL-cholesterol. So it was concluded that the high protein diet was no better than then the high carbohydrates. As both of these diets had relative high contents of carbohydrate this study makes no contribution to our understanding of the role of LC diets.
- In this study, a comparison was made between a diet which was low in carbohydrates (20% E) and one which was low in fat (55-60% E carbohydrates (9). After 6 months, weight loss was similar but those on the LC diet were able to achieve significant reductions in the doses of insulin required. Although compliance deteriorated subsequently the authors concluded that an LC diet with 20% E from carbohydrates is an effective means of improving glycaemic control in those who have T2D.
- In this study 14 obese patients with T2D were placed on a diet which was low in carbohydrates and high in fat (LCHF) and monitored for body weight, insulin sensitivity, HbA1c, lipids and blood pressure (10). Glycaemic control was significantly improved with resulting reductions in medication. Systolic blood pressure was reduced and the HDL cholesterol increased. The diet was well tolerated and the results fully support the LC approach as an effective means for treating those who have T2D.
- In this study, a comparison was made between participants with T2D who were on either an LC diet or a low fat diet plus the weight loss drug orlistat over a period of 48 weeks (11). It was found that the LC diet resulted in improved glycaemic control and a greater reduction in medication than the low fat diet.
- In this Japanese study, a comparison was made between a conventional calorie-restricted diet and an LC diet which had no calorie restriction for patients with T2D (12). It was found that patients in the LC group had a significant reduction in their HbA1c levels. The patients in the former group also experienced improvements in their triglyceride levels, without experiencing any major adverse effects or a decline in the quality of life. It was concluded that an LC diet is effective in lowering the HbA1c and triglyceride levels in patients with T2D who are unable to adhere to a calorie-restricted diet.
- In this study conducted in Australia, the effects of a diet very low in carbohydrates which was high in unsaturated fat and low in saturated fat was compared with one which was low in fat and high in unrefined carbohydrates (13). The subjects were obese patients with T2D. Although both diets were effective in reducing body weight, blood pressure and fasting blood glucose, the LC diet achieved greater reductions in HbA1c, glucose variability and in medication. The LC diet also raised the HDL cholesterol. The authors concluded:“…the LC diet induced greater improvements in glycemic control, blood glucose profiles, and reductions in diabetes medication requirements compared with the HC diet. The LC diet also promoted a more favorable CVD risk profile by elevating HDL-C and reducing TG levels, with comparable reductions in LDL-C compared with the HC diet. These effects were most evident in participants with greater metabolic derangements, suggesting that an LC diet with high–unsaturated/low–saturated fat content can improve primary clinical diabetes management targets beyond conventional lifestyle management strategies and weight loss.”In a further paper on this research project, the authors commented as follows:This is one of the groups to have included glucose variability in the values monitored. These results emphasise that one of the important factors is the reduction in the use of drugs, which has been substantial in this case. “In the current study, although no apparent diet differences in HbA1c were evident, greater reductions in diabetes medications occurred with the LC diet. Compared with the HC diet, the LC diet achieved comparable HbA1c reductions with a significantly greater reduction in diabetes medication requirements, suggesting the achievement of better glycemic control. Because of the progressive nature of T2D, a reduced reliance on pharmacotherapy to achieve glycemic control presents important advantages for long-term diabetes management. These advantages include potential reductions in treatment costs and a reduced likelihood of drug-related side effects including hypoglycemia risk and weight gain with implications for long-term weight-loss maintenance.” (14)
Getting back to the original papers cited in this report has proved to be an enlightening experience. I cannot find any evidence to support the conclusion of the author that there are no statistical differences between diets wish are LC and HC with respect to the treatment of T2D. This is simply a misrepresentation of the information.
In Study no. 5 there was a significant improvement in glycaemic control as determined by a reduction in HbA1c. Similar results were obtained in Study no. 6 which also recorded a big drop in the use of medication by the LC group. Further confirmation that the LC improves glycaemic control was provided by the Japanese study (no. 7). In this one, the triglycerides declined from 141.7 to 83.5 mg/Dl while in the control the reduction was from 155.2 to 148.4 which is a huge difference as this is one of the critical risk factors for heart disease. In the Australian work (Study no.8) there were statistically significant improvements in HDL cholesterol and in triglycerides for those with an LC diet.
It turns out that discounting those studies which are not applicable because the amount of carbohydrate in the diet was too high or because of non-compliance, these results confirm the fact that a diet which is LC does benefit a person with T2D. This is precisely what would be expected since T2D is caused by excessive glucose in the blood, which means the pancreas has to increase insulin production. The excess insulin causes insulin resistance in many organs including the pancreas. Ultimately the pancreas is damaged and is no longer able to produce enough insulin to cope with the glucose in the blood. This is full blown T2D. The most effective way to deal with the disease is to eliminate the cause, which means altering the diet to reduce the amount of glucose entering the blood. In other words, just eat less sugar and other foods which contain carbohydrates.
This paper badly misrepresents and distorts the research which has been considered. It is certainly not an objective evaluation. It is somewhat ironic that the author alleges that those who advocate LC diets as a form of treatment for T2D of “cherry-picking” without any evidence to justify her charge, does exactly that herself! She has conveniently ignored any evidence which supports the case for using the LC approach in an attempt to cast doubt on the validity of such diets. In particular there is a failure to recognise the value of LC diets in reducing the amount of medication needed.
It is extremely unfortunate that this paper has been published. It is seriously misleading. I strongly recommend that it should be retracted.
Anyone interested in those studies which contribute to our understanding of the benefits of a diet which is LC (and high in fats) will find many of them here (15)
- P Dyson (2015) http://link.springer.com/article/10.1007/s13300-015-0136-9/fulltext.html#copyrightInformation
- R D Feinman (2015) http://www.nutritionjrnl.com/article/S0899-9007(14)00332-3/pdf
- N Iqbal et al(2012) http://onlinelibrary.wiley.com/doi/10.1038/oby.2009.460/abstract
- A Elhayany et al (2010) http://onlinelibrary.wiley.com/doi/10.1111/j.1463-1326.2009.01151.x/abstract
- R N Larsen et al (2011) http://link.springer.com/article/10.1007%2Fs00125-010-2027-y
- H Guldbrand et al (2012) http://link.springer.com/article/10.1007%2Fs00125-012-2567-4
- J D Krebs et al (2013) http://www.tandfonline.com/doi/full/10.1080/07315724.2013.767630
- S B Mayer et al (2014) http://onlinelibrary.wiley.com/doi/10.1111/dom.12191/abstract
- Y Yamada et al (2014) https://www.jstage.jst.go.jp/article/internalmedicine/53/1/53_53.0861/_pdf
- J Tay et al (2014) http://care.diabetesjournals.org/content/37/11/2909.full
- J Tay et al (2015) http://ajcn.nutrition.org/content/102/4/780.full.pdf