When the article entitled “Saturated fat is not the major issue” by cardiology specialist DR Aseem Malhotra appeared in the BMJ there were over 30 responses. These give us a valuable insight into the debate.
Dr Malhotra concludes that the advice to reduce saturated fat (SFA) has increased the risks of cardiovascular disease (CVD) rather than lowered them. In particular he refers to the evidence that SFA reduces the large buoyant LDL particles (Type A) which are protective when it is the small dense LDL particles (Type B) that are implicated in CVD. He also notes that a number of prospective cohort studies have indicated that SFA are actually protective for CVD.
The article has received substantial press coverage but it is especially useful to consider the points raised by those who made responses. At the time of writing there had been 33 responses of which 14 were generally supportive, 7 were opposed and effectively supported the status quo and the remaining 12 did not take a position.
Here is a selection of the points raised by the respondents:
• Mark Burkitt was critical of both supporters and critics of Dr Malhotra because many of them argued their case solely from the position of statistical ‘risk factors’ without any attempt to consider the underlying mechanisms. Nevertheless he agreed with the main thrust of the article. There is strong evidence that the key factor is the oxidation of the LDL Cholesterol and therefore the focus should be on understanding what causes this and how it can be prevented. Unfortunately diets which are high in polyunsaturates and low in SFA can logically be expected to promote the oxidation of the LDL Cholesterol (2). Essentially the same point was made by Richard Hoffman who advocated a diet rich in antioxidants in order to reduce/prevent the oxidation of the LDL Cholesterol
• Alison Tedstone and Vicki Pyne of Public Health England presented the current UK government position that SFA should be no more than 11% of total food energy. This was based on the advice of the Scientific Advisory Committee on Nutrition. They refer to a Cochrane Collaboration systematic review which concluded that reducing saturated fat by reducing and/or modifying dietary fat intakes lowered the risk of cardiovascular events by 14% (3). However they failed to mention that there were no clear effects of modified fat diets on total or cardiovascular mortality, despite the inclusion of over 13,000 participants in studies of over six months which presents a rather different picture. A few days earlier I had pointed out that the intake of SFA had fallen from 56.7 g/day in 1969 to 29.2 g/day in 2000. Furthermore the target set in 1984 to reduce SFA from 20% to 15% of food energy had been reached in 2003. Over this period the incidence of obesity had continued to increase. In men it had doubled since 1993. Furthermore since 1994 the incidence of diabetes has more than doubled for both men and women. Regrettably these contributors made no attempt to answer my question that if reducing SFA in the past had obviously not produced the predicted results, how can we justify that it will succeed in the future.
• Peter Clifton claimed that the article had done a disservice to the public debate on nutrition. He cited one paper in which hundreds of experiments had showed that SFA elevates LDL cholesterol (4). It is difficult to understand the significance of this statement as the main focus of this paper was the ratio of Total Cholesterol: HDL Cholesterol. In fact the authors emphasised the dubiousness of relying on cholesterol alone as a marker of the risk of coronary artery disease. Although many studies predict the effects of the various fats on the fats in the blood, this cannot determine whether a fat will cause the disease. It is all too true that many people simply ignore this important proviso and assume that changes in the blood fats automatically reflect the impact on the incidence of heart disease.
• Malcolm Kendrick, a GP in Cheshire and author of “The Great Cholesterol Con” was particularly enthusiastic about the article. He commented that for those who look at the evidence rather than accept the dogma, the facts are clear. SFA is healthy, trans fats are not. The recent epidemic of obesity has been driven by the lunacy of replacing fat with sugars.

The above contribution just about sums up the current position. Those critical of Dr Malhotra are either nit-picking or have to rely on sources which have been discredited time and time again. How often do people have to be told that an association does not demonstrate “cause and effect”? On the other it is very encouraging that so many of the respondents have come to the same conclusion as Dr Malhotra. When the recommendations on fat and SFA were initially devised it was accepted that final proof did not exist but it was confidently predicted that it would emerge from major investigations which were planned or were already in progress. As it happens, these studies failed to deliver the expected results. There has been enormous success in reducing the intake of SFA in the UK and in many other countries with a similar type of food supply. Despite this, obesity is now prevalent and diabetes continues to increase. There is now convincing evidence that it is the increase in sugars and refined carbohydrates which is responsible for the deterioration of public health. The emphasis on SFA has been a great mistake. Unfortunately there are still many people, especially those in a position to implement a totally re-vamped healthy eating policy, who fail to recognise reality. The tragedy is that until this is put into place large numbers will continue to suffer poor health and premature death. Hopefully the positive response to the Malhotra paper will increase the pressure needed to bring about change.

1. http://www.bmj.com/content/347/bmj.f6340
2. http://www.bmj.com/content/347/bmj.f6340?tab=responses
3. L Hooper et al (2012) Cochrane Database of Systematic Reviews 5 Art. No.: CD002137. DOI: 10.1002/14651858.CD002137.pub3
4. R P Mensink et al (2003) American Journal of Clinical Nutrition 77 (5) pp111