130. A Little Bit of History about LDL Cholesterol

The cholesterol lowering campaign really took off in 1985 with the recommendations of a Consensus Conference sponsored by the National Institutes of Health in the USA (1). I have just come across a commentary written at the time by Gerald Reaven which is absolutely fascinating (2). It is certainly highly relevant to recall the key points which were made almost 30 years ago!

The main conclusion was that raised levels of LDL Cholesterol in the blood plasma are causally related to the development of Cardiovascular Disease (CVD). Therefore steps should be taken to lower the LDL Cholesterol by the use of diet and/or drugs, in order to reduce the incidence CVD. In particular, everyone except children under the age of 2 years should be advised to adopt a diet that reduces the intake of fat from 40% calories as it was then to 30%. Saturated fat (SFA) should be reduced to less than 10% calories while polyunsaturated fat (PUFA) should be increased. In addition, massive education programmes should be launched to ensure that health professionals were aware of the importance of treating hypercholesterolaemia and the food industry was to be encouraged to develop and market products in line with the dietary advice.

First of all, Gerald Reaven pointed out that Implementation of the recommendations would mean there would inevitably be an increase in the carbohydrate content of the national diet in the USA but that there had been no attempt by the Conference to assess the impact of this. In his view, there was enough credible evidence to postulate that a “low fat high carbohydrate (LFHC) diet” would result in metabolic changes in many people, which would be deleterious to health. In particular changes in blood glucose, insulin and HDL Cholesterol would actually increase the risks of developing CVD. This is rather ironic since the justification for the changes was to reduce risks of CVD.

He suggests that the older the individual and /or the more glucose intolerant the greater the chance that LFHC diets would result in significant increases in postprandial blood glucose, which is a risk factor for CVD. Furthermore for those consumers who have impaired glucose tolerance or full blown Type 2 Diabetes (T2D) the recommendation is even more questionable.

He then goes on to consider the role of insulin and states quite bluntly that raising the level of insulin in the blood increases the risk of CVD even in those who do not have T2D. Furthermore there is abundant evidence that increasing the carbohydrate content of the diet will augment the plasma insulin response of normal individuals. Therefore it is predictable that the insulin levels will be raised. While this might not be a major problem in those who are young, slim and physically active, it is almost certainly damaging for those who are getting on in years, well-nourished and sedentary.

A LFHC diet is known to raise the level of triglycerides in the blood, which is associated with an increased risk of CVD. While the importance of this has been questioned, Reaven argues that there is enough evidence to take this seriously. In particular he notes that this may be related to a fall in the level of the HDL Cholesterol, which could be another reason why an LFHC diet would increase the risks of CVD.

Even accepting the “Consensus” position that the LDL Cholesterol should be reduced and that the HDL Cholesterol is beneficial then it follows that the objective should be to increase the HDL:LDL in order to reduce the risks of CVD. Obviously this is what would happen if the LDL Cholesterol is lowered and the HDL Cholesterol is unchanged. Unfortunately because an LFHC diet also reduces the HDL even more than occurs with the LDL Cholesterol, the net effect is to lower the ratio! This is not exactly what the Consensus Conference was trying to achieve.

Finally here is a comment on the organisation of the conference which speaks for itself:

“The most efficient way to reach a consensus concerning a complex issue within a short period is to make sure that controversial views are not represented on the panel. It is clear that the panel assembled by the NIH met this criterion; ie, no one who had published scientific evidence that might have led to the presentation of formidable arguments contrary to conventional wisdom was a member of the panel. I believe it is the responsibility of the organizers of such conferences to make sure that dissenting voices are present, and their absence raises substantial questions concerning the utility of the recommendations that are issued.”

CONCLUSION

Although the information presented here is entirely from the USA, the circumstances in many other countries are virtually the same. Here in the UK, over the past 30 years or so there has been an enormous increase in the use of the lipid lowering drugs (by a factor of about 20) (3). At the same time some of the fat in the diet has been replaced by carbohydrates (4). Although there has been quite an improvement in longevity the impact of this on the quality of life has been tempered by the increase in dementia. The incidence of obesity is evident, while the fact that T2D has doubled in the past 15 years and is expected to continue increasing is clearly a major public health issue. There is absolutely no question that Gerald Reaven has been totally vindicated by events. The fears which he outlined in 1985 have materialised.

It was evident that the doubts which he and others expressed were simply swept aside by those who were determined to implement their own agenda. The current position is now even worse because it is clear that the policy has been a disaster. Yet there is still a complete failure on the part of governments and health professionals to face up to reality. In the meantime huge numbers of people who faithfully comply with the official advice are suffering unnecessarily and many die prematurely. It is difficult to imagine a greater public health policy disaster. It is right up there with those wars which have been started on a false prospectus.

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