I have now been blogging for 3 years and this is Number 200! Although it has been hard work it has been an amazing experience. In particular, through the medium Twitter I have made contact with many different people from all over the planet. I greatly appreciate the interaction with so many individuals, who are doing excellent work and have fascinating stories to tell. Some like Jen Elliott in Australia and Tim Noakes in South Africa are having to fight battles to defend their professional integrity at considerable personal cost. It is important to understand that they at the forefront of a campaign for a more rational strategy to prevent and treat disease which will mean significant improvements in health and well-being for everyone.

So a great big THANK YOU to all those who responded to my blogs and tweets in any way over the past few years. It is a very special occassion when the opportunity arises to meet you in person for the first time. The usual introductions are superfluous because it is like a re-union with an old friend! The highlight of 2015 for me was the visit to Cape Town for the Low Carb Summit in February. Cape Town is a wonderful city. The event itself was a tremendous occasion and a unique opportunity to meet many of those from all over the world who in their own way are helping to promote a sound approach to nutrition and health. It was striking how many individuals, working away on their own, had reached essentially the same conclusions about the faults in the official dietary guidelines and the steps needed to correct them.

In this post I will tackle one of the original issues which has had a huge influence, namely the cholesterol theory. Despite all the knowledge and information which conclusively demonstrates that blood cholesterol (TC) is not a risk factor for heart disease or anything else, the authorities persist with the myth, spending enormous resources on testing and scaring the living daylights out of many people. (Blog 179 gives a brief run down on how things have gone badly wrong) (1). As an example, the evidence shows that those with the lowest TC and LDL-cholesterol (LDL-C) have the highest all-cause mortality (ACM). For women, those with the highest TC have the greatest life expectancy). The position is rather like when the police arrest the wrong person for a murder which means that the genuine killer remains on the loose. In this context, it is my contention that the focus of attention should be on insulin. Of course insulin plays a number of key roles in the body but if these are disrupted then this can lead to a range of different forms of disease and ill-health.

Essentially what happens is that when the body is subjected to a threat such as an infection, injury or toxic material, there is a response by the immune system to deal with it. Invariably this includes changes which result in insulin resistance (IR). This means that the sensitivity to insulin has been reduced and therefore the amount of insulin required to achieve a given effect has been increased. This can be illustrated by describing how Type 2 Diabetes (T2D) develops. The initial cause is invariably consumption of excessive amounts of sugar and carbohydrates which results in a build-up of glucose in the blood. This triggers an increase in the secretion of insulin by the pancreas in order to direct the glucose to the liver and convert it into fat which is then stored. The effect of this is to ensure that the concentration of glucose in the blood remains under control. However if the high intake of sugar and carbohydrates persists, IR will occur in various organs including the liver and pancreas. As this continues to get worse the pancreas responds with even more insulin. It is possible to maintain control of the blood glucose in this way for up to about 10 years. Eventually a point is reached where the pancreas fails and is no longer able to meet the demand for insulin. This is when the blood glucose starts to rise. If blood glucose measurements are done, then T2D will be diagnosed. Even if T2D does not develop, the IR which is caused by the high level of insulin (hyperinsulinaemia) constitutes a serious risk in its own right, which may result in a range of different chronic diseases/conditions. The relationships have been explained by Gerald Reaven and are shown in a figure which is available at

http://www.cell.com/action/showFullTextImages?pii=S1550-4131%2804%2900007-5

To access this it will be necessary to copy this link and paste into your browser. It is a nuisance but probably worth the trouble if you are interested.

Essentially there are two scenarios. In one the pancreas is damaged to such an extent that it is unable to produce sufficient insulin to maintain control of the blood glucose which means that T2D is the result. Hence it is highly likely that retinopathy, nephropathy and neuropathy will develop. In the other, the pancreas continues to produce sufficient insulin to control the glucose in the blood BUT the high concentration of insulin (compensatory hyperinsulinaemia) causes a different set of diseases. These include hypertension,, stroke, polycystic ovary syndrome (PCOS), non-alcoholic fatty liver disease (NAFLD), cancer sleep apnea. Cardiovascular Disease (CVD) is common to both pathways. From the perspective of the individual, the first warning signs are likely to be when the blood glucose starts to rise. However it is clear that the even without any increase in blood glucose, if the insulin levels are raised this constitutes a genuine increase in the risks of developing many different diseases.

Between 1988 and 1995, 208 healthy volunteers (98 males and 110 females) were monitored for a period of at least 6 years on average (3). During this time, 40 clinical endpoints were identified in 37 of the participants, which consisted of 12 with high blood pressure, 9 with cancer, 7 with CHD, and 5 with T2D, 3 of which also had high blood pressure, and 4 with stroke. There were 6 deaths. Based on the insulin suppression test which is a recognised reliable estimate of IR, the subjects were divided into 3 groups (high, medium and low IR). The male/female ratios and the proportion of smokers were similar in each group. The most impressive finding is that none of the clinical endpoints were recorded in the group with the lowest IR but that there were 28 in the group with the highest IR. This left 12 in the middle range group. There were no deaths in the low IR group, 2 (infection and cancer) in the middle group and 4 (2 CVD and 2 cancer-related) in the high IR group. These results are absolutely remarkable. 

It is important to appreciate that although this is not absolute proof that there is cause and effect, there are sound theoretical reasons why it makes very good sense. These have been elucidated in many papers by Gerald Reaven (See eg 2). Ask yourself which group would you prefer to be in? I know what my answer would be and I would also be much more concerned about an IR that was relatively high than with a high value for my cholesterol! Despite the convincing evidence that IR is almost certainly at the root of many of the common killer diseases, there is little attention paid to it by the medical/health professions or by the policy makers. In the light of the information presented above anyone with a high IR would probably be interested to have that information and would be open to advice on how to lower it. It would make very good sense to switch resources from cholesterol to IR. It is unlikely that this will happen in the short term. Nevertheless for anyone who wishes to act on this information, it would be logical to adjust the habitual diet by reducing the content of sugar and carbohydrates. Effectively this is a sound basis for the Low Carb High Fat (LCHF) which is considered in greater depth in this blog (4).

Murphy’s Law

Unfortunately the news just gets worse. There are other factors which contribute to the IR so this is probably one of the best examples of Murphy’s Law (where everything possible goes wrong) that I have encountered.

  • Insufficient Vitamin D. There is convincing evidence that Vitamin D plays a critical role in many of the steps which contribute to the development of IR (5). These include the efficient functioning of the immune system and the production of insulin by the pancreas. There are several studies which show that IR is reduced by supplementation with Vitamin D. However in order to achieve a positive result it is necessary to use much higher amounts that recommended in official guidelines.
  • Omega-6 and omega-3 polyunsaturated fatty acids (PUFAs). The emphasis in the recommendations to increase the intake of PUFAs in order to reduce TC levels has resulted in an increase in the ratio of omega-6:omega-3 in many countries to the range of 15-30 or possibly even more. Ideally the ratio should be 1 and no more than 4. Omega-6s are pro-inflammatory while omega-3s are anti-inflammatory. It has been shown that increasing the intake of omega-3s in middle-aged men was associated with greater insulin sensitivity and a more favourable metabolic profile (6). The tertile (third) with highest omega-3 index had insulin sensitivity that was 43% greater than the two lower tertiles. It was also found that this group had improved ?-cell function which meant that the ability of the pancreas to secrete insulin had been increased. Because of the pro-inflammatory characteristics of the omega-6s it follows that a relatively high intake in the diet will increase the IR (7).
  • Reduction in salt intake. There is growing concern that those who attempt to follow the current recommendations on sodium intake may actually cause some damage to their health. Experimental investigations have shown that volunteers on a low sodium intake (20 mmol/day) had an IR which was considerably higher than those who had a much higher intake (200 mmol/day) (8). There was a 4–5 fold increase in serum aldosterone and also an increase in plasma noradrenaline concentration in those in the low salt group compared with the high-salt one. It was suggested that this may have contributed to the differences in insulin sensitivity following the adjustment in dietary sodium intake. These results were effectively conformed in a study involving much larger numbers a few years later (9).
  • It has been established that statins increase the risks of developing T2D. Recent studies have shown that certain statins trigger a series of steps which result in increased IR (10). A recent evaluation of statins concluded that the benefits were limited to a few extra days of life (11). Based on this information, it is difficult to understand why anyone would agree to using these drugs. However I do accept that a rather different case is presented by the pharmaceutical industry and its supporters.

Conclusion

We now have a very convincing and comprehensive case to focus on the role of insulin as a crucial factor in avoiding many of the common chronic disease which are prevalent and having a reasonably healthy existence. The occasional need to increase the amount of insulin secreted is a perfectly normal response to cope with variations in the quality and quantity of food which is consumed. However when the habitual diet persistently contains excessive amounts of sugar and other carbohydrates, the system is overloaded and eventually breaks down. In reality the system is extremely robust because it can cope with abuse for several years before serious problems arise. It could be argued that protocols should be introduced so there is a programme to test for high levels of insulin. But the procedures are relatively complex and expensive to deliver. On the other hand if the population generally could be advised and persuaded to reduce the consumption of sugar and carbohydrates, there would be widespread improvement in public health and the effects would be evident relatively quickly. Although I have not really touched on the subject of obesity here, there is overwhelming evidence that it is the consumption of so much sugar and carbohydrates which is the primary cause of the so-called obesity crisis. A diet based on low carbohydrate intake is therefore the way to tackle this issue. The big problem is the inertia and even hostility to any policy initiative along these lines. In fact it is ironic that several of the other aspects of official advice are also contributing to the present appalling standards of public health. On a more positive note, it is a “no-brainer” for individuals and their families to take the initiative themselves. It is not all that difficult and the benefits will become apparent in a very short time. For more information on the practicalities just follow the lead given by progressive doctors like Dr David Unwin in Stockport or Dr Rangan Chatterjee who made the excellent TV programmes “Doctor in the House” broadcast recently on BBC TV. Details are shown in these 2 blogs (12, 13).

  1. http://vernerwheelock.com/179-cholesterol-and-all-cause-mortality/
  2. G M Reaven (2005) Cell Metabolism 1 (1) pp 9-14
  3. F S Facchini et al (2001) The Journal of Clinical Endocrinology & Metabolism 86 (8) pp 3574-3578
  4. http://vernerwheelock.com/192-assessing-diets-which-have-low-carbohydrates/
  5. C-C Sung et al (2012) Journal of Biomedicine and Biotechnology Article 634195, 11 pages http://dx.doi.org/10.1155/2012/634195
  6. B B Albert et al (2014) Scientific Reports 4 Article number: 6697 doi:10.1038/srep06697
  7. E Patterson et al (2012) Journal of Nutrition and Metabolism Article ID 53946, 16 pages http://dx.doi.org/10.1155/2012/539426
  8. R R Townsend et (2007) Clinical Science 113 (2) pp 141-148
  9. R Garg et al (2011) Metabolism 60 (7) pp 965-968
  10. B D Henriksbo et al (2014) Diabetes 63 (11) pp3742-3747
  11. M L Kristensen et (2015) BMJ Open 9 (5) pp1-5
  12. http://vernerwheelock.com/198-more-good-work-from-dr-david-unwin/
  13. http://vernerwheelock.com/197-the-exploits-of-dr-rangan-chatterjee/