74. Exercise the Best Medicine

Currently there are proposals to extend the range of people who will be offered statins on the grounds that this will reduce the risks of developing heart disease. There are serious doubts about the justification of this strategy. Many of the researchers who have evaluated the evidence have concluded that treatment of those who do not have heart disease with statins does not result in any reduction in all-cause mortality. At present the NHS spends about £300 M annually on statins so obviously this figure will increase substantially if there is a big increase in the numbers treated. Furthermore many of those who are on the statin therapy will experience side-effects which can be unpleasant and may actually damage the health of some people.

On the other hand there is now extensive convincing evidence that much of the poor health is directly caused by a lack of physical activity and therefore significant improvements could be achieved by encouraging more people to take regular exercise. The purpose of this blog is to focus on some of the research which demonstrates that those who maintain their physical fitness have a much better standard of health when compared with those who lead a sedentary existence.

In a study in the USA 10,224 men and 3120 women were monitored over a period of about 8 years. During this time 240 men and 43 women died (1).

The results are shown in Table 1.

Table 1 Relationship between fitness level and all-cause mortality in men and women

                  Death rates per 10,000 person   years
  Men Women
Least fit 64 39.5
Most fit 18.6 8.5


The differences in the all-cause mortality rates are absolutely huge. With men those who are unfit are over 3 times more likely to die than those who are sedentary while the difference with women is almost 5. It is important to stress that these differences persisted even when adjustments were made to allow for other factors including smoking habits, blood cholesterol levels, blood pressure, fasting blood glucose and parental history.

In a study conducted in Norway, 1428 men aged 40-60 years at the outset were monitored for their physical fitness on 2 separate occasions between 1972 and 1975 and again between 1980 and 1982 (2). By the end of 1994 there had been 238 deaths of which 120 were attributed to cardiovascular disease, 75 to cancer and 43 to other causes. The results are shown for 4 equal groups which vary according to fitness level with Q1 being the lowest and Q2 the highest (Table 2). It is evident that those who are unfit have almost 3 times the death rate of those who are extremely fit. However it is noteworthy that there is quite a big difference between Q1 and Q2 which suggests that there are significant benefits with a moderate level of fitness. Furthermore there is virtually no difference between Q3 and Q4 indicating that there is little benefit from very high fitness levels.

Table 2. Relationship between physical fitness and all-cause mortality in Norwegian men

Fitness levels Number of deaths
Q1 97
Q2 65
Q3 39
Q4 37


What is even more impressive in this study is the insight gained by considering the impact of changes in fitness levels between the initial assessment and the second one (Table 3).

Table 3 Changes in fitness levels between the 2 assessments and the effect on the mortality ratios.

  Q1 (PF1) Q2 (PF1) Q3 (PF1) Q4 (PF1)
                                Changes in   fitness levels
Q1 (PF2/PF1) 61 62 62 62
Q2(PF2/PF1) 85 84 85 81
Q3 (PF2/PF1) 103 99 98 92
Q4 (PF2/PF1) 136 124 118 110
                               All-cause   mortality ratios
Q1 (PF2/PF1) 1.22 1.19 0.87 0.73
Q2(PF2/PF1) 0.80 0.77 0.62 0.46
Q3 (PF2/PF1) 0.72 0.33 0.60 0.17
Q4 (PF2/PF1) 0.47 0.43 0.40 0.17


At first sight this information may seem rather daunting but it is certainly worthwhile grappling with it. Each column provides information on the fitness level as determined at the first assessment. In the top half of the table the information is broken down in accordance with how the fitness level changed when the second assessment was done. A value below 100 means the fitness level had deteriorated while a value above 100 means there had been an improvement. The values in the lower half show how the death rates for each of the different groups. It is evident a change in fitness level is associated with a corresponding change in relative mortality. When the fitness level drops there is an increase in the death rate and similarly an improvement in fitness level is associated with a reduction in death rate.

The results of this study are in line with those of many other investigations which repeatedly confirm the critical importance of physical fitness in determining a person’s general health and life expectancy. In addition this research demonstrates that raising the level of fitness has a definite impact on life expectancy but also that if the fitness level falls it will be accompanied by an increased risk of death.

The fact that major changes in mortality occur in response to changes in fitness levels comes across very convincingly from this work. This knowledge has enormous implications for public health. If more people can be persuaded of the improvements that can be achieved to their own personal health by taking a moderate amount of exercise then it would follow that they would be less likely to suffer from major diseases and to extend their life span. From a policy perspective, This approach has much to commend it compared with the blanket use of drugs such as statins. First of all, the effect on reducing all-cause mortality is much greater than anything that can be achieved with drugs. Secondly it would be much less expensive. Finally there would be much less undesirable side-effects.


  1. S N Blair et al (1989) Journal of the American Medical Association 262 (17) pp 2395-2401
  2. G E Erikssen et al (1998) The Lancet 352 (9130) pp759-762



73. Epilepsy and the Ketogenic Diet

In the UK about 1 in 100 people suffer from epilepsy. Therefore there is considerable interest in using diet as a means of controlling the condition. Despite the fact that national policy continues to recommend that people should reduce the intake of fat, especially saturated fat (SFA), there are growing doubts about the reliability of this advice. In fact, there is now convincing evidence that many of the individual saturated fatty acids play an important role in the body’s normal functions. On the other hand, excessive consumption of the carbohydrates, particularly those that are rapidly broken down and absorbed such as sugar, is now acknowledged as one of the prime factors which contributes to the development of many of the common chronic diseases/conditions. These include diabetes, kidney disease, hypertension, obesity, heart disease and cancer.

As a consequence there is growing interest in understanding the potential benefits of a ketogenic diet. Essentially this a diet which compared to the typical one consumed in the UK or the USA has a lower content of carbohydrate and a higher content of fat.

With respect to epilepsy it is highly significant to note that as long ago as the 1920s, ketogenic diets were being used to control the condition with a fair degree of success. Unfortunately it fell out of favour because of the development of many drugs and because the dietary guidelines which were devised in the late 1970s/early 1980s included a very strong recommendation to reduce the consumption of SFA.

However in recent years there has been renewed interest in the use of the ketogenic diet as a treatment for epilepsy. For example a research team from Johns Hopkins Medical Institutions in the USA has reported considerable success (1). Over a 4-year period, 23 children with infantile spasms, aged 5 months to 2 years, were started on the ketogenic diet. After 1 year, almost half of the children had improved by>90%. All of them had improved by >50%. It was reported that 57% had their medications reduced or discontinued by 12 months. It was also found that 57% showed improvement in development, which was correlated with seizure control. Independent factors that predicted improvement included age younger than 1 year and previous exposure to 3 or fewer anticonvulsants. No child has died, although 7 children had diet-related adverse reactions.

A few years later Elizabeth Neal and colleagues conducted a randomized controlled trial (RCT) at the Great Ormond Street Hospital in London (2). 145 children aged between 2 and 16 years who had at least daily seizures (or more than 7 per week), had failed to respond to at least 2 antiepileptic drugs and had not previously been treated with a ketogenic diet agreed to take part in the study. 73 were assigned to the ketogenic diet and 72 acted as the control group. Because of drop-outs, only 103 children completed the study, of which 54 were on the diet and 49 were controls. After 3 months it was found that the frequency of seizures in those on the ketogenic diet had been reduced to 62% while there had been an increase to 137% in the control group. In 5 children in the diet group the seizure reduction was >90%. Some side-effects including constipation and vomiting were reported.

All of these results are really very impressive. For anyone who has epilepsy there is everything to gain and very little disadvantage by trying to make changes to the habitual diet. So the question is:

“What exactly is meant by a ketogenic diet?”.

There are plenty of different ideas about how to answer this question but I suggest the best approach is to understand the basic principles and try to find the most suitable ways of applying them to any particular individual. The basics are:

  1. Keep carbohydrate-containing foods to a minimum. The case against sugar is getting stronger every day. The big problem is that nowadays sugar is present in many different types of processed food. Avoid sugar-sweetened soft drinks like the plague. Many low-fat versions of foods such as yoghurts have been formulated by removing the fat and replacing it with sugar. Bread, potatoes, pasta and rice are all sources of starch which breaks down to the simple sugar glucose. Where possible choose the less refined version so that the glucose is only released slowly. With breakfast cereals, those which are high in sugar will break down very quickly resulting in rapid build-up of blood glucose (bad news) whereas with porridge there is slow release (good news).
  2. Forget the official advice and include plenty of fats/oils in the diet. However it is crucial to appreciate the differences between the different types of fat with respect to health. There is virtually universal agreement that the trans/hydrogenated fats, which are present in some processed foods (eg baked goods) are damaging to health and should be kept to a minimum (3). Fortunately the food industry is taking steps to eliminate them. Nevertheless there are many good reasons for consuming as much food as possible which has been prepared in the home.

We are continually bombarded with marketing messages that the polyunsaturated fats (PUFAs) are good for us because they lower cholesterol. However the rationale which underpins this is fundamentally flawed. The whole cholesterol story has been totally discredited. Details can be found here (4). There are 2 main families of PUFAs, namely the omega-3s and the omega-6s. Going back about 100 years ago the ratio of omega-6: omega-3 was about 1. Ideally it should be no higher than 4 but into a typical diet today it is round about 15-30. The omega-3s are present in foods such as oily fish whereas those which lower cholesterol are primarily omega-6s. So these should be avoided (5).

In fact what we really need are the SFAs (6). This means that we can consume full fat milk and other dairy products as well as the fat that is present in various meats. If possible choose foods which have been prepared from animals which have been fed on grass. A particularly good source of SFAs is coconut oil (7). Of the monounsaturated fats, I prefer olive oil, especially when the food is not being cooked. When heating is involved coconut oil is best because it will not break down.

  1. As a general rule try to include plenty of vegetables in the diet but I do not advise excessive fruit consumption because of the sugar content. Nuts, seeds and berries are now readily available in the supermarkets all make a valuable contribution to a balanced diet.

The trick is to introduce changes gradually and to try various strategies. It is important to find out what is best suited for any individual. From the perspective of an epilepsy sufferer, there is very convincing evidence that changes suggested here will not only reduce the frequency of seizures but should also be beneficial in helping to avoid a range of other diseases.


  1. E H Kossoff et al Pediatrics (2002) 109 (5) pp780-783
  2. E Neal et al (2008) The Lancet Neurology, 7 (6)pp 500-506 doi:10.1016/S1474-4422(08)70092-9
  3. http://vernerwheelock.com/?p=354
  4. http://vernerwheelock.com/?p=270
  5. http://vernerwheelock.com/?p=153
  6. http://vernerwheelock.com/?p=155
  7. http://vernerwheelock.com/?p=301
  8. http://authoritynutrition.com/top-10-evidence-based-health-benefits-of-coconut-oil/


72. What The Papers Do Not Tell You About Salt

According to The Guardian to-day (15th April 2014)(1) the reduction in salt in recent years has been a key factor in the large fall in the number of people dying from heart attack or stroke. This is the conclusion of research which has just been published in BMJ Open (2).

The article pointed out that the mortality rate from heart disease in England had fallen from 232/100,000 to 139/100,000 between 2003 and 2011. The corresponding values for stroke were 134/100,000 and 78/100,000. Over the same period the average salt intake in adults fell from 9.5g to 8.1g per day and the average reduction in blood pressure (BP) for adults in England decreased by 3.0/1.4mm Hg.

Based on this reduction in BP the authors conclude strokes would be reduced by approximately 11% and heart attacks by 6%. They go on to state that therefore salt reduction is likely to have played an important role in the decreases in the incidence of strokes and in the mortality from heart attacks. They also claim that this conclusion is supported by evidence from prospective cohort studies and outcome trials, which have demonstrated that a reduction in salt intake is related to a decrease in the risk of cardiovascular disease. However it is important to appreciate the fact that these figures only represent about 25% of the total reductions actually achieved. While the researchers recognise that other factors such as the reduction in smoking and increased consumption of fruit and vegetables also make important contributions, the fact remains that this paper is being used as a justification for the campaign to reduce salt intake. One of the authors, Professor Graham MacGregor, said the results vindicated the action by the Food Standards Agency (FSA) to put pressure on the food industry to reduce the levels of salt in food. A spokesperson for the pressure group, World Action on Salt and Health, said:

It would now be a gross breach of ethical and corporate responsibility for companies not to reduce salt as the benefits of salt reduction are now so clear.”

Before we get carried away with the hype surrounding this article it is important to understand that these results are based on a relatively short period. Furthermore as with so much of the debate on diet and health this work simply presents an association. It certainly does not demonstrate “cause and effect”. In other words it does not prove that if you reduce salt that this will reduce your chances of dying of stroke or a heart attack.

In order to put his into perspective it is worth considering what happened during an earlier period. Data from the National Food Survey (3) show that between 1985 and 2000 in Great Britain the salt intake was virtually constant at about 6.3g per person per day. (This figure is lower than that cited above because a different basis was used to calculate it. Nevertheless the crucial factor is that it did not change.)

The best source of data on deaths from cardiovascular diseases is undoubtedly the British Heart Foundation (4) and so I have used this information to compare the periods 1985 to 2000 when there was no change in salt intake with the period 2000 to 2009 when there was a reduction in the intake of salt. (Note the BMJ Open paper continued until 2011 but the BHF does not go beyond 2009 at present).

It will be evident to anyone who views the BHF publication that for the last 50 years or so there has been a steady decline in the death rates due to the cardiovascular diseases (ie a straight line!). The actual values for the rates of change in death rates are shown in Table 1.

TABLE 1 Comparison in death rates from coronary heart disease and stroke in 1985-2000 and in 2000-2009, expressed as the annual decrease in death rates per 100,000 population

Cause of death Men
  1985-2000 2000-2009
Coronary Heart Disease 12 10
Stroke 3.3 2.7
Coronary Heart Disease 5 5
Stroke 2.7 2.2


These results confirm that there is no difference in the rate of decline between the 2 periods. As there was no change in the intake of salt during the first one it is difficult to understand why anyone can actually reach the conclusion that the reduction in the death rates could be due in any way to a change in the consumption of salt. To have any credence it would be essential to show that there had been a significant increase in the rate at which the deaths were falling. It is absolutely clear that this has not happened. It is difficult to understand why the authors of the recent report have not considered how the death rates have been changing over the much longer time, especially as the data are available.

The reality is that doubts have emerged about the desirability of reducing salt too far (5). These have been spelled out in a recent review published by the prestigious Institute of Medicine (IoM) in the USA. This  considered studies indicating that some sections of the population in the USA may not be consuming adequate quantities of salt, especially those over 51 years, African-Americans, those with hypertension, diabetes, chronic kidney failure or congestive heart failure. The review concluded there was a genuine danger that some people were not consuming enough salt to meet their requirements fully.

Unfortunately because of the activities of campaign groups and the response by the Government and health professionals it has become the accepted wisdom that “salt is bad”. While it is probably correct that very high levels of salt are damaging to health, there is certainly no agreement on how much is required. The danger is that some people may not be getting enough and will suffer as a result. Ironically it is probably those who are attempting to eat a healthy diet by acting in accordance with the official advice who will be especially at risk!


  1. http://www.theguardian.com/society/2014/apr/14/research-finds-link-between-drop-in-salt-consumption-and-fall-in-heart-attack-deaths
  2. http://bmjopen.bmj.com/content/4/4/e004549.full
  3. Household Nutrient Data 1940 to 2000 Sourced at:


4.Trends in Coronary Heart Disease, 1961-2011. British Heart Foundation







There is absolutely no doubt that diabetes is one of the major public health issues throughout the world at the present time. Here in Great Britain, the incidence in both men and women has more than doubled in the last 15 years. If current trends continue then it is likely that there will be 5 million cases by the year 2025 in the UK (1). As the condition usually manifests itself later in life this means that a very high proportion of the population is at risk. In fact diabetes is only the tip of the iceberg as those diagnosed with the disease have an increased risk of developing a range of other diseases/conditions including heart disease, kidney disease, hypertension, obesity and various cancers.

The conventional approach is to prescribe various forms of medication in order to control the blood glucose levels and to advise patients to lose weight. The fact that the numbers affected continue to increase demonstrates very clearly that this is not working. With respect to diet, invariably the advice is in line with the official recommendations. Essentially this means people are told that they need to reduce calories, reduce fat, especially saturated fat (SFA) and increase the complex carbohydrates.

It is not in the least surprising that those who follow this advice fail in their attempts to control the disease. The sources of carbohydrates, which are recommended, contain high quantities of starch which is broken down in the alimentary tract to produce glucose which is then absorbed into the blood. So the effect is to increase the concentration of the glucose in the blood, which is the last thing a diabetic would want. Instead of helping to alleviate the problem the dietary carbohydrates are actually causing it to get worse!

To bring this home I will refer to the personal experience of individuals based on their own case histories (2):

  • By the time John had reached the age of 60 years he had been suffering from diabetes for 10 years, during which time it had slowly progressed. He had been prescribed Metformin by his GP and been advised to “eat plenty of starchy carbohydrate”.  At this point he started to monitor his blood glucose. As a consequence he soon learned the effect that different foods had on his blood glucose levels. By using that information and gradually changing his diet over the next two years, he fully overcame his Type 2 diabetes. The main thing he did was to cut out almost all the starchy carbohydrates – e.g. cereals, bread, potatoes, pizza. He was also very careful with rice and pasta. In John’s opinion this was far and away the main reason for the dramatic improvement in his blood glucose levels, which meant that he able to stop taking the Metformin altogether.


  • Kate is a lively 63 year old grandmother who 3 years earlier was diagnosed as pre-diabetic as a routine test showed she had a raised blood sugar level. She was given very little advice and just handed a booklet to read. She followed the advice in the booklet which was to eat plenty of starchy carbohydrate foods, which actually resulted in significant weight gain. Despite this her GP told her to carry on as before. A subsequent test showed that the blood glucose had become even higher and that Kate had developed full blown diabetes. At this point she decided to take control herself. This is the story in her own words:



I decided to take charge of my own disease and destiny, embarking on a read, read and more read programme, it soon made perfect sense that the carbs were the culprit! My newly appointed Diabetes nurse was aghast at my new regime of low carbing, “On your own head be it” were her words! Pretty soon, she had to eat her words as the BG (blood glucose) began to fall without the help of medication and although I wasn’t grossly overweight, my body became toned and healthy at a near perfect 9 stones. The HbA1c result after 8 months was 5.7 and at this juncture, the nurse no longer had an argument, indeed she began to ask me about my regime, taking notes whilst I sang the praises of low carbing,”


Note: HbA1c is glycated haemoglobin which gives a picture of the average blood sugar over a period of several weeks. If it above 6.5% this is considered to be diabetic. A value below 5.9% is regarded as normal.

  • Another John also obtained very good results by reducing his intake of carbohydrates. Here is his story:

In 2003 I weighed 95kg. At 1.83m and large-framed I felt comfortable with myself but knew I was overweight. However, during the period 2006 – 2008 my weight slowly increased to 125kg and I was also exhibiting the familiar symptoms of diabetes – fatigue, frequent urination and thirst. I was diagnosed as a Type 2 diabetic in March 2008. Upon diagnosis, my test results were as follows.

Weight 125kg HbA1c 8.2% BP 167/105 Total/HDL Cholesterol 2.99

In the first three months after diagnosis I read extensively about the effect of carbohydrates on blood glucose levels and decided upon a low carbohydrate dietary approach in an attempt to achieve normal blood glucose levels. I decided to drop rice, pasta, potato, bread and pastry/baked products from my diet and replace them with more meat, fish, vegetables, eggs, dairy foods and nuts. …….Since then all my quarterly HbA1c have all been below 5.5 without the aid of medication and my weight has dropped back down to 95kg with fatigue, frequent urination and thirst gone. My latest annual review results are as follows.

Weight 95kg HbA1c 5.3% BP 120/80 Total/HDL Cholesterol 1.9

I really do believe that the low carb diet is the simplest and most effective method of reducing and stabilising blood glucose levels.”


It is evident that all the numbers have moved in the right direction. John lost about 30 kg and his HbAc1 has come down from the diabetic to normal levels. There was a huge improvement in his blood pressure and values below 4 are considered to be satisfactory for the ratio of Total Cholesterol/HDL Cholesterol.


I find these case histories to be very convincing because it is precisely what would be expected. Diabetes is caused by excess sugar in the blood. This sugar originates in the food so reduce the dietary sugar and the cause is removed! This is not exactly rocket science. It simply beggars belief that so many in the health professions just do not get it. As long as the current attitudes persist it will be impossible to control diabetes and large numbers of people will continue to suffer what is a very nasty and debilitating disease.



  1. https://www.diabetes.org.uk/Documents/Reports/State-of-the-Nation-2012.pdf
  2. http://lowcarbdiabetic.co.uk/My%20Friends%20Stories.htm




“The Truth About Low Fat Food” is the title of a programme broadcast by Channel 4 on 7th April 2014. This confirms that many “low fat” foods contain more sugar than the corresponding full fat version. Furthermore some of them are surprisingly high in fat and in calories. What I found especially fascinating is that any food which is promoted as “low fat” is perceived as “healthy” and so consumers feel free to consume these in relatively large quantities.

On the other hand the programme appeared to accept that the current official dietary recommendations are sound. For example in an interview with Professor Graham MacGregor, the importance of reducing the amount of in the diet was emphasised. The reality is that the case for reducing total fat in the diet does not stand up to examination. Because fat has been demonised, as the programme correctly demonstrated, those who wish to eat a healthy diet often select the products promoted as “low fat”, which are regarded as healthier than the regular version. Consequently there has been an insidious increase in the amount of sugar consumed, in part because many of the low fat products are devised by removing fat and replacing it with sugar.

Consideration of the history of the evolution of the dietary guidelines reveals that during the 1970s there was a huge debate in the USA about how the diet should be changed in order to reduce the incidence of heart disease. Essentially the question was: “Excess sugar or excess fat?” In the event it was decided that the problem was too much fat, especially saturated fat (SFA). One of the critical factors influencing the decision was the “Diet Heart Cholesterol” theory which effectively means that the concentration of cholesterol in the blood (TC) is a risk factor for heart disease. Hence these risks  can be altered by raising or lowering the TC. As it was considered that SFA raised the TC, this meant that dietary SFA was undesirable and should therefore be reduced. Similarly the polyunsaturated fatty acids (PUFA) were supposed to lower the TC which was beneficial and therefore there could be some increase in the amount consumed. Subsequently the rationale which underpins these recommendations has been completely discredited (See refs 2, 3, 4). It is rather significant that a recent report prepared by the British Heart Foundation(BHF)has had to conclude that there is not enough evidence to support the current dietary recommendations to reduce SFA and increase PUFA in order to reduce the risk of heart disease(5).

The BHF report is simply reflecting the finding of a major analysis based on many different epidemiological studies which related the SFA intake to the incidence of cardiovascular disease (CVD). It found that there was:

no significant evidence to conclude that dietary saturated fat(SFA) is associated with an increased risk of CHD, stroke or CVD”(6).

But it gets even worse because far from being the hazard implied by the official recommendations, there is actually convincing evidence that many of the individual fatty acids are valuable nutrients in their own right.

Here is a brief selection of some of the functions/benefits of SFA (7):

  • Cell membranes require SFA to be “waterproof” in order to function properly
  • The heart prefers the long chain fatty acids palmitic acid(16 Cs) and stearic acid (18 Cs) to carbohydrates to carbohydrates as a source of energy
  • Bones need SFA in order to assimilate calcium effectively.
  • The short and medium chain length fatty acids, which have up to 12 carbon atoms do not need to be emulsified by bile salts and so are rapidly absorbed into the blood stream from the small intestine. They are especially valuable because they boost the immune system and possess anti-microbial, anti-viral and anti-tumour properties. Lauric acid (C12) is particularly effective
  • It is now known that the LDL cholesterol exists in particles which vary in size. At one end of the extreme they are densely packed and it is now believed that these particular ones initiate the damage which ultimately results in CHD. At the other end are the large fluffy particles which are relatively benign. SFA in the diet favours the formation of the large particles.

The original doubts about the SFA can be traced back to the concerns that arose in relation to the processing of fats which resulted in the production of the trans fatty acids (TFAs). It is now widely accepted that these are damaging to health. For example TFAs alter enzymes that neutralize carcinogens and increase those that potentiate carcinogens. TFAs can depress milk fat production in nursing mothers and cause abnormal sperm to be produced (8). TFAs are quite different from SFA and there was never any justification for tarring them with the same brush. Fortunately genuine efforts are now being made to eliminate them from the human diet.


In order to complete the picture I need to address the issue of the PUFAs. Because these are actively promoted as beneficial (because they lower cholesterol!) they are considered by many consumers as “healthy”. The truth is they are anything but.

We have to understand that there are 2 families of polyunsaturates…the omega-3s and the omega-6s. Up to about 1900 the diet contained approximately equal amounts of each group. However as industrialisation has progressed the intake of the omega 3s has fallen while that of the omega 6s has increased. As a consequence, the ratio of omega-6:omega-3 is now 15-20 in countries such as the USA and the UK. Excessive amounts of omega-6 PUFA and a very high omega-6:omega-3 ratio promote the pathogenesis of many diseases, including cardiovascular disease, cancer, and inflammatory and autoimmune diseases, whereas increased levels of omega-3 PUFA (a lower omega-6:omega-3 ratio),exert suppressive effects

Virtually all those products which claim to lower TC are omega-6. This means that the more of these a person consumes the more the ratio of the two gets out of kilter (9). As I have explained above the cholesterol theory no longer holds water and therefore the case for consuming these products has been destroyed.


When all else fails the advocates for low fat resort to the simple calories in-calories our argument. Essentially this is that because fat is a concentrated source of energy (calories) we must reduce it in order to prevent obesity. So just consider what has happened in Great Britain over the past 50 years or so. National statistics show that amount of fat consumed has fallen from 120gm/day in 1969 to 74gm/day in 2000. When expressed as a proportion of energy consumed the fat intake has decreased from 42.6% in 1980 to 37.7% Calories in 2010.At the same time there has been an increase in the energy as carbohydrate from 44.4 to 47.4%. Consideration of the different types of fats shows that between 1969 and 2000 the intake of saturated fat (SFA) has fallen from 56.7 to 29.2 g/day. In other words it has been reduced by almost half (10). As we are only too well aware, over the same period the incidence of obesity has increased. Since 1994 obesity has doubled in men and increased by 60% in women. Even more worrying is that diabetes has more than doubled in both men and women over the same period. In the light of these results can there be any possible justification for continuing to advocate a reduction in fat? What should be obvious to anyone who looks objectively at the research and the current state of public health is that we must focus on the carbohydrates, especially the sugar.


The big problem is that “the great and the good” in the public health and medical professions are unwilling to admit that they have been wrong about the recommendations on fat. While it is encouraging that the concern about sugar is now being recognized we will not make significant progress until people are provided with accurate advice about fat in general and the different types of fat in particular.


If the Dispatches team on Channel 4 really wishes to get to grips with the key nutrition issues then they should be asking the Government why it continues to advocate a reduction in fat, especially SFA, when there is no reliable evidence to justify this policy. In fact these recommendations are fundamentally flawed and are effectively a major contributor to the current poor standard of public health as shown by the statistics on heart disease, diabetes and cancer.



  1. http://www.channel4.com/programmes/dispatches/episode-guide/series-130/episode-7
  2. http://vernerwheelock.com/?p=82
  3. http://vernerwheelock.com/?p=105
  4. http://vernerwheelock.com/?p=370
  5. http://annals.org/article.aspx?articleid=1846638&atab=7
  6. P. Siri-Tarino (2010) American Journal of Clinical Nutrition 91 (3) pp. 535-546
  7. Mary Enig(2000) “The Skinny on Fats” http://www.westonaprice.org/know-your-fats/skinny-on-fats?
  8. http://vernerwheelock.com/?p=354
  9. http://vernerwheelock.com/?p=153
  10. http://vernerwheelock.com/?p=311





There is no doubt that the results of the study on fruit and vegetables which I discussed in my last blog have made quite an impact. In this blog I have picked out some of the headlines and a selection of the initial paragraphs of each report.


Forget five a day: You need SEVEN portions of fresh fruit and veg per day to live longer, says new research

Chris Green

Eating seven or more portions of fruit and vegetables a day gives people a far greater chance of staving off an early death, according to a study published on Tuesday, which suggests that the Government’s official “five a day” recommendation should be doubled to 10.

Researchers found that eating seven fruit and vegetable helpings a day reduced a person’s risk of dying of cancer by 25 per cent and of heart disease by 31 per cent. But in a surprising finding, eating tinned and frozen fruit appeared to increase the risk.


Are you getting your seven-a-day? Experts say we need more helpings of fruit and veg

Alistair McGeorge

Your usual five portions might not be enough, with a new study suggesting that a magnificent seven could reduce the risk of cancer by 25 per cent

Lead author Dr Oyinlola Oyebode, of UCL’s Department of Epidemiology and Public Health, said: “We all know that eating fruit and vegetables is healthy, but the size of the effect is staggering.

“The clear message here is that the more fruit and vegetables you eat, the less likely you are to die at any age. Vegetables have a larger effect than fruit, but fruit still makes a real difference.

“If you’re happy to snack on carrots or other vegetables, then that is a great choice but if you fancy something sweeter, a banana or any fruit will also do you good.”

“Another possibility is that there are confounding factors that we could not control for, such as poor access to fresh groceries among people who have pre-existing health conditions, hectic lifestyles or who live in deprived areas.”


Forget five a day, we should eat SEVEN a day for a long life: Eating more portions of fruit and veg can cut risk of dying prematurely by 42%

  • Study shows eating more cuts chance of dying from      cancer by a quarter
  • Experts now want guidelines advising people to eat      5-a-day changed
  • But others believe advising on 7-a-day will deter      people from even trying

Jenny Hope

Eating seven portions of fruit and vegetables a day – two more than currently recommended – helps you live longer, claim researchers.

A new study shows that more fruit and veg slashes the risk of premature death by 42 per cent, compared with less than one helping a day.

Boosting consumption cuts the chances of dying from cancer by a quarter and heart-related deaths by one third.


Diet that adds years to life: Seven fruit and veg a day halves risk of an early death

A DIET rich in vegetables, salads and fruit can cut the risk of death from heart attacks and strokes by almost half, a study said yesterday.

 Jo Willey

Seven portions a day slashes the chance of an early death – and it is never too late to increase the amount.

Experts say the more fruit and vegetables you eat the better, with some suggesting up to 10 helpings a day.

NHS guidelines recommend five 80g portions of fruit and vegetables daily to help lower the risk of serious conditions such as heart disease, stroke, Type 2 diabetes and obesity.

But there is increasing evidence this is not enough to keep fit and healthy for the longterm.

Research shows seven or more helpings could reduce the risk by 42 per cent compared to someone who has just one portion daily.

It can reduce the risk of dying of cancer by 25 per cent and of heart disease by 31 per cent.


Eating More Fruits And Veggies Daily May Reduce Risk Of Death

Alice G. Walton

Adding to the overwhelming evidence that the road to health is paved with plants, a new study in BMJ today finds that consuming seven servings of fruits and vegetables per day reduces one’s death risk considerably. Researchers followed a nationally representiave sample of over 65,000 people in Britain, and found that those who ate more fruits and veggies were much less likely to die of any cause. In particular, they were less likely to die of heart disease, stroke, and cancer. And, happily, the more fruits and veggies the people consumed, the more their death risk fell.



Eating More Vegetables Can Almost Halve Your Risk of Dying

Fruit makes a difference too, but fresh veggies have a larger effect

Alexandra Sifferlin@acsifferlin

We’ve all been told to eat our vegetables, and even if we don’t like it, we know they’re good for us. But a new study shows just how good for our longevity they may be.

Seven or more portions of fruit and vegetables a day can lower your risk of dying by an astonishing 42%, according to a new study published in the Journal of Epidemiology & Community Health. The more fruits and vegetables the participants ate, the less likely they were to die at any age, and the protective benefit increased with consumption.


It is very clear that the message which comes across is that there will be very significant benefits to health for the majority of the population if they increase the amount of fruit and vegetables they consume. While some of the reports do go on to express caveats and quote from those who are less than enthusiastic about all the hype, this does not really detract from the view that most of us should be eating more fruit and vegetables and that the current advice on ‘5-a-day’ needs to be altered.

As I explained in Part 1 (7) those people who eat lots of fruit and vegetables are quite different from those who eat virtually none because they smoke less cigarettes, take more exercise, abuse alcohol less, are better educated and almost certainly have much higher incomes. All of these factors contribute to the improved life expectancy. While there may be some marginal benefit from increasing the consumption of fruit and vegetables, the fact remains that to achieve the huge improvements in life expectancy observed in this research it will require very substantial changes in lifestyle. To imply otherwise is not helpful. It is particularly regrettable that the various contributors of the articles referred to here just accepted the line taken by the official press release. It is a very sad reflection on the quality of journalism dealing with health issues. Unfortunately this criticism extends to reputable newspapers and magazines. If these articles were the subject of an old-fashioned school report my comments would have to include “very poor work” and “must try harder”!



  1. http://www.independent.co.uk/news/science/forget-five-a-day-new-research-suggests-that-you-need-seven-portions-of-fresh-fruit-and-veg-per-day-to-live-longer-9226653.html
  2. http://www.mirror.co.uk/news/uk-news/seven-fruit-veg-day-five-a-day-3320754
  3. http://www.dailymail.co.uk/health/article-2593791/Forget-five-day-eat-SEVEN-day-long-life-Eating-portions-fruit-veg-cut-risk-dying-prematurely-42.html
  4. http://www.express.co.uk/news/health/467994/Diet-that-adds-years-to-life-Seven-fruit-and-veg-a-day-halves-risk-of-an-early-death?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed:+daily-express-news-showbiz+(Daily+Express+::+News+/+Showbiz+Feed)
  5. http://www.forbes.com/sites/alicegwalton/2014/04/01/7-servings-of-vegetables-a-day-may-keep-death-away/
  6. http://time.com/#45790/eating-more-vegetables-can-almost-halve-your-risk-of-dying/
  7. http://vernerwheelock.com/?p=390



“Fruit and vegetable intake: five a day may not be enough, scientists say” is one of the headlines in the Guardian to-day 1st April 2014(1). In the article it is stated that:

“The clear finding was that eating more fresh fruit and vegetables, including salads, was linked to living a longer life generally and in particular, to a lower chance of death from heart disease, stroke and cancer.”

This is based on the results of research conducted at University College London in which data collected for the Health Survey of England (HSE) have been analysed. The report of the work has just been published in the Journal of Epidemiology and Community Health and is freely available to all (2).

The big problem with any research of this type is that although it can be demonstrated that those who consume plenty of fruit and vegetables, on average, live longer than those who consume a small amount, this is not proof that if you eat plenty of fruit and vegetables then this in itself will increase your life span. It may well be that a high intake of fruit and vegetables is simply an indicator of a generally healthy lifestyle. If this is the case then the impact of increasing consumption of fruit and vegetables on its own will be relatively small.

As it happens the research paper actually provides comprehensive information on the characteristics of those involved in the HSE. Table 1 shows how these vary with the consumption of fruit and vegetables.

Table 1. Variation in personal characteristics with consumption of fruit and vegetables

Portions per day, F&V 0-1 1-3 3-5 5-7 7+
Fruit 0.2 1.2 2.5 3.8 6.1
Vegetables 0.3 1.1 1.6 2.2 3.1
Male,% 49.5 46.1 42.6 41.4 41.3
Non-manual,% 33.5 43.9 51.2 56.3 60.8
Degree or equivalent,% 7.4 12.1 16.9 22.0 28.5
Current smoker,% 39.0 24.3 15.4 11.1 10.4
Inactive,% 6.1 4.7 3.7 2.5 1.4
Vigorous activity,% 5.9 7.1 9.0 11.4 13.8
Alcohol, over double daily recommendation,% 18.7 14.6 11.1 10.1 9.6
BMI, 27.7 27.7 27.7 27.6 27.6
Deaths,% 8.2 7.9 6.4 5.3 4.1


The picture which emerges from these data is somewhat different from that presented in the media to the public. While it is evident that over the time of the investigation, those who consumed over 7 portions of fruit and vegetables had a death rate which was only 50% of those who consumed very little, there were also very big differences with respect to other factors. Those with the highest death rate were also much heavier smokers, took less exercise and were much more likely to be manual workers who did not have a degree qualification. They were also more likely to abuse alcohol. The fact that women, who have a life expectancy which is about 5 years greater than men, are more strongly represented in the low death rate group is not in the least surprising.

An interesting finding which seems to have been ignored so far is that the BMI for all the groups is virtually the same. So here we have a big difference in death rate despite the fact that there is no change in BMI, which seems to fly in the face of all the hype about obesity.

Although there is no information on incomes shown it is almost certain that there is a relationship between death rates and income levels, which may well be n important contributory factor. Nevertheless it is clear that the cohort of people who consume lots of fruit and vegetables is very different from those who consume hardly any. It is not in the least surprising that those smoke the most cigarettes, exercise least, abuse alcohol the most as well as having a low consumption of fruit and vegetables have a reduced life expectancy. This is not exactly rocket science. In fact it is only what is to be expected. We know that there are big differences in life expectancy between different parts of the country and even between different areas within cities.

Unfortunately the authors of the paper fall into the trap of reading too much into their results. They claim that:

With increasing evidence of their health benefits, policy-makers may need to consider broader initiatives to promote fruit and vegetable consumption, particularly vegetables and salad”

The press release which accompanied publication states that:

Eating at least 7 daily portions (of fruit and vegetables) was linked to a 42% lower risk of death from all causes and from cancer and heart disease/stroke of 25% and 31% respectively    They conclude that the current dietary guidelines…..might need to be revised

The press release concludes that:

The study findings imply that even those who do get their recommended quota, need to eat more, they say. “Is it perhaps time to update the ‘5-a-day’ message to ‘10-a-day’?they ask”.

It may well be that increasing consumption will result in some improvement in general health and possibly a small increase in life expectancy. But the message that is being presented is very different. There is a very clear implication that there will be very substantial benefits. This is quite misleading. If people increase their fruit and vegetable consumption from the lowest to the highest in this study there is absolutely no possibility they will halve their death rate, unless they also make other fundamental changes to their lifestyle. This means increasing exercise, reducing smoking and avoiding excessive alcohol consumption.

The harsh reality is that many people simply do not have the opportunity or the inclination to make the changes because they are restricted by their income, where they live and their general background.

My fundamental criticism is not with the research but with the way in which the results have been portrayed and the response from journalists, who have accepted the line presented to them. This is particularly regrettable as in this case the original research paper is freely available and it would have been very easy for any individual to do what I have done here.


  1. http://www.theguardian.com/uk-news/2014/apr/01/fruit-and-vegetables-seven-portions-ucl-study
  2. http://jech.bmj.com/content/early/2014/03/03/jech-2013-203500.full.pdf+html



Statins are certainly in the news these days. NICE has put forward proposals that all those with a 10% risk of developing heart disease should be treated with statins. Effectively this means that everyone over the age of 50 years, including those who are fit and healthy, would be expected to have the treatment. On the other hand this strategy is being questioned by many within the medical profession. In this blog I will try to tease out the information which individuals need in order to make a sound judgment on whether or not to go on statins.

Essentially people need to know if they will derive any benefit from the statins which will have to be balanced against the type, frequency and severity of any side-effects.

According to Professor Sir Rory Collins, from Oxford University, GPs and the public are being made unjustifiably suspicious of the drug, creating a situation that has echoes of the MMR vaccine controversy(1). Collins is the leader of the Cholesterol Treatment Trialists’ (CTT) Collaboration which has been analysing data on the effects of statins which has been supplied to them by the drug companies. In their latest report it was claimed that statins significantly reduced major cardiovascular events and all-cause mortality in people at low risk (2). The results of this trial were a critical factor influencing the position taken by NICE.

This is somewhat surprising because other studies have concluded that statins are not beneficial to people at low risk. It is also highly relevant that the CTT study has been subject to severe criticisms.

In an exercise of this kind one would expect the investigators to compare the results of those who had been treated with statins with those of a control, consisting of a similar group of people who had not been treated. When this approach has been used, others have not been able to find that there were any appreciable benefits in the statin group. For example, Ray and co-workers analysed the results of 11 clinical trials involving 65,229 participants with approximately 244,000 person-years of follow-up and 2793 deaths (3). All of these individuals were high risk but without previous cardiovascular disease. Over an average treatment period of 3.7 years the use of statin therapy did not result in any reduction in all-cause mortality.

By contrast the CTT group has adopted a totally different approach which has been explained by Dr David Newman in an article on his blog (4). Instead of comparing those who were treated with statins with the controls, they selected those individuals in which the statin treatment reduced the LDL Cholesterol 1 mmol/L or 40 points in US terms. As Dr Newman describes it:

“…they shifted the data so that their numbers corresponded precisely to patients whose cholesterol responded perfectly.”

He goes on:

“Patients whose cholesterol drops 40 points are different than others, and not just because their body had an ideal response to the drug. They may also be taking the drug more regularly, and more motivated. Or they may be exercising more, or eating right, and more health conscious than other patients. So it should be no surprise that this analysis comes up with different numbers than a simple comparison of statins versus placebo pills. Ultimately, then, this new information tells us little or nothing about the benefits someone might expect if they take a statin. Instead it tells us the average benefits among those who had a 40-point drop in LDL.”

Furthermore the LDL Cholesterol drop cannot be predicted because the effect of the statins is unknown. This means that the conclusions of this analysis have absolutely no relevance to patients and doctors who have to decide if statins should be prescribed.

Here is a final quote from Dr Newman:

“Perhaps never has a statistical deception been so cleverly buried, in plain sight. The study answers this question: how much did the people who responded well to the drug benefit? This is, by definition, a circular and retrospective question: revisiting old data and re-tailoring the question to arrive at a conclusion. And to be fair they may have answered an interesting, and in some ways contributory, question. However the authors’ conclusions imply that they answered a different, much bigger question. And that is not a true story.”

But it does not stop here because the CTT also argued that the side-effects of the statin treatments are relatively small. Rhabdomolysis, which is the catastrophic breakdown of muscle tissue, has an excess incidence of about 0.1 per 1000 over 5 years according to CTT calculations. However Dr Malcolm Kendrick, author of “The Great Cholesterol Con” refers to a study conducted in the USA, which analysed data on statin side-effects recorded on the FDA’s Medwatch. Between July 2005 and March 2011 there were 186,796 case reports of which 8,111 were due to rhabdomolysis. This equates to 811 deaths over this period. As it is accepted that reporting rates are extremely low, this figure can be multiplied by a factor of 10 or even 100 to obtain the true value (5). If precedents were followed up this evidence should be more than enough to have the drugs withdrawn.

The CTT authors reported a 10% increase in the relative risk of developing diabetes while on statins. This equates to 5 new cases per 1000 people treated for 5 years. However other studies have reported values of up to 50% more (6).

Uffe Ravnskov is an independent researcher in Sweden who has suggested that if you are a healthy person who is being advised to go on statins then this is what you should be told before going ahead (7):

Your chance not to get a non-fatal heart event during the next five years ……is 97.1 per cent. You can increase your chance to 98.1 per cent if you take a statin every day. But then your risk of suffering muscle problems is about 25 per cent unless you never exercise (1); your risk of becoming sexually impotent is about 20 per cent (2); your risk of suffering from diabetes is about 4 per cent (3), and you also run a risk of memory loss, liver damage, peripheral neuropathy, cataract, and cancer, but we do not yet know how large these risks are. And don´t forget that many non-fatal heart events may heal with minor health consequences or none at all.”

The picture now becomes very clear. The positive results which have been claimed for the CTT study have only been obtained by manipulating the data. Unfortunately this is typical of how the modern pharmaceutical industry functions. It hypes up the benefits and plays down the undesirable side-effects. This is a particularly bad example because the leader of the CTT is a knighted professor from the prestigious University of Oxford. Nevertheless the case which they present should be subject to rigorous examination. It is extremely regrettable that NICE has allowed itself to be taken in by what can only be described as rubbish!

There is no doubt that there is growing awareness that the case in support of statins is full of holes. To-day in The Daily Telegraph there is an article by Haroun Gajraj, a vascular surgeon, no less, who decided to stop his treatment with statins. After looking more closely at the research, he concluded that statins were not going to prevent a heart attack and that his cholesterol levels were all but irrelevant. He also draws attention to a recent survey by Pulse magazine, which found that six out of 10 GPs opposed the draft proposal to lower the risk level at which patients are prescribed statins. As many as  55% said they would not take statins themselves or recommend them to a relative, based on the proposed new guidelines(8).


  1. http://www.theguardian.com/society/2014/mar/21/-sp-doctors-fears-over-statins-may-cost-lives-says-top-medical-researcher
  2. CTT (2012) Lancet 380 pp 581-590.
  3. http://archinte.jamanetwork.com/article.aspx?articleid=416105
  4. http://cardiobrief.org/2012/05/27/guest-post-data-drugs-and-deception-a-true-story/
  5. http://drmalcolmkendrick.org/tag/rhabdomyolysis/
  6. http://www.abc.net.au/catalyst/heartofthematter/download/StatinsshouldNOTbebroadedtowiderpopulation.pdf
  7. http://www.bmj.com/content/348/bmj.g280?tab=responses
  8. http://www.telegraph.co.uk/health/10717431/Why-Ive-ditched-statins-for-good.html



According to the latest report prepared for the British Heart Foundation there is not enough evidence to support the current dietary recommendations to reduce saturated fat(SFA) and increase polyunsaturated fats (PUFA) in order to reduce the risk of heart disease(1).

This finding should come as no surprise to anyone who has bothered to keep up to date with the existing scientific literature.

For example, in 2010, the results of another analysis found that there was:

“no significant evidence to conclude that dietary saturated fat(SFA) is associated with an increased risk of CHD, stroke or CVD”

There is also extensive evidence that many of the individual fatty acids play a vital role in the body. Further support is provided by the finding in the study that margaric acid, a saturated fat in milk and dairy products, was associated with lower cardiovascular risk.

Further details on my blog (2).

With respect to the PUFAs the evidence that they are beneficial does not stand up to examination. Products containing PUFAs are rich in omega-6 fatty acids and therefore increasing consumption increases the ratio of omega-6:omega-3 (the type found in fish oils) fatty acids. Up to about 1900 the diet contained approximately equal amounts of each group. However as industrialisation has progressed the intake of the omega 3s has fallen while that of the omega 6s has increased with the result that the ratio of omega 6:omega 3 is now 15-40 in countries such as the USA and the UK. This high ratio can be damaging to health. Ideally this ratio should be about unity and certainly no higher than 4 (3).

In fact, a number of the omega-6 polyunsaturated fatty acids, commonly found in vegetable oils and processed foods, may actually pose risks according to the study.

Furthermore the researchers did find a link between trans fats, the now widely maligned partially hydrogenated oils(trans fats) that had long been added to processed foods, and heart disease. One of the reasons why SFAs have been vilified in the past is due to the failure to distinguish between the trans fats and the SFAs. As a consequence the ill-effects of the trans fats have been wrongly attributed to the SFAs.

In an interview the lead researcher Dr Rajiv Chowdhury pointed out the need to appreciate that there are different types of LDL-Cholesterol (the so-called “bad” one). It is the small dense particles which are dangerous because they are easily oxidised and are more likely to cause inflammation and so contribute to the build-up of plaque inside the arteries. Crucially, these particles are not increased by SFA but by sugary foods and excess carbohydrates. In his view:

It’s the high carbohydrate or sugary diet that should be the focus of dietary guidelines. If anything is driving your low-density lipoproteins in a more adverse way, it’s carbohydrates.”(4).

Despite this comment, which appeared in the New York Times the BHF could not resist putting their own spin on the research by making this statement on their website:

“We know there are good biological reasons for encouraging a Mediterranean-style diet, where we eat more unsaturated than saturated fat, that lower our levels of ‘bad’ LDL cholesterol” (5)

This conveniently ignores the important fact that not all LDL-Cholesterol is the same and that the small dense ones which cause the damage are not increased by the SFA.

The justification for recommending that SFA should be reduced and that PUFAs should be increased quite simply does not exist. The cholesterol theory has been totally discredited yet the public health bodies, the medical profession and governments continue to rely on it (6,7). The reality is the fundamental issue is the increasing consumption of sugar and refined carbohydrates, which explains why obesity, diabetes and related diseases/conditions are increasing. To his credit Dr Chowdhury recognizes that it is the carbohydrates, not the SFA which are a critical factor in the development of heart disease.

While there is nothing new about these findings it will definitely have been worthwhile if it forces the medical and public health to re-assess their position on the dietary recommendations, especially in regard to the different types of fat.

Finally this report completely demolishes the rationale which underpins the Government Responsibility Deal with respect to SFA. According to the official website:

Recognising the role of over-consumption of saturated fat in the risk of premature avoidable mortality from cardiovascular and coronary heart disease, and public health recommendations to reduce saturated fat consumption (to less than 11% of food energy for everyone over 5yrs of age, compared to current levels of 12.7%):

We will support and enable people to consume less saturated fat through actions such as product/menu reformulation, reviewing portion sizes, education and information and incentivising consumers to choose healthier options. We will monitor and report on our actions on an annual basis. Progress in reducing people’s saturated fat intakes will be measured via the National Diet and Nutrition Survey.”(8).

In the light of recent developments it is essential that this responsibility Deal is thoroughly re-evaluated as it is no longer credible. Ministers might usefully consider what has happened over the past 40 or so years. The National Food Survey shows that the intake of SFA had fallen from 56.7 g/day in 1969 to 29.2 g/day in 2000(9).

In 1984 the official Committee on Medical Aspects of Food Policy (COMA) recommended that the SFA intake should be reduced from 20% of food energy to 15% as part of a strategy to reduce cardiovascular disease (10). This target was reached by 2000(11). Currently the amount of SFA in the British diet is 12.7% of energy. Over this period the incidence of obesity has continued to increase. In men it has doubled since 1993, which is when detailed information was first collected (12). What is especially disturbing is that since 1994 the incidence of diabetes has more than doubled for both men and women (13).

The Responsibility Deal with the food industry aims to reduce the SFA level even more to 11% of energy in the hope and expectation that there will be a reduction in “ the risk of premature avoidable mortality from cardiovascular and coronary heart disease”(14). As it is evident that reducing SFA has not delivered the expected results in the past, why on earth should anyone believe that the same strategy will work in the future?


  1. http://annals.org/article.aspx?articleid=1846638&atab=7
  2. http://vernerwheelock.com/?p=155
  3. http://vernerwheelock.com/?p=153
  4. http://well.blogs.nytimes.com/2014/03/17/study-questions-fat-and-heart-disease-link/
  5. https://www.bhf.org.uk/media/news-from-the-bhf/fats-in-your-diet.aspx
  6. http://vernerwheelock.com/?p=370
  7. http://vernerwheelock.com/?p=105
  8. https://responsibilitydeal.dh.gov.uk/pledges/pledge/?pl=41
  9. http://webarchive.nationalarchives.gov.uk/20130103014432/http://www.defra.gov.uk
  10. Department of Health and Social Security (1984) “Diet and Cardiovascular Disease” London: HMSO
  11. http://webarchive.nationalarchives.gov.uk/20130103014432/http://www.defra.gov.uk
  12. Health Survey of England 2010 Adult Trend Tables
  13. Health Survey for England 2009
  14. https://responsibilitydeal.dh.gov.uk/new-saturated-fat-pledge/



65. Do you really want to lower your Cholesterol?

The so-called “cholesterol/diet/heart disease” theory is based on the belief that the risks of death due to heart disease are associated with the concentration of cholesterol in the blood (TC). In other words if you have a high TC you can lower your chances of developing heart disease by reducing the TC level. It is claimed that the saturated fat (SFA) in the diet will raise the TC and that the polyunsaturated fat (PUFA) will lower it. Hence it follows that consumers are advised to reduce their intake of SFA and increase that of the PUFA.

Therefore it is highly relevant to examine the results of investigations where these changes have been made to see what actually happens.

Way back in the 1960s members of the Anti-Coronary Club in New York volunteered to participate in a trial (1). A total of 814 men aged between 40 and 59 years old were placed on the “Prudent Diet” which involved a very substantial reduction in their intake of animal fat, which is rich in SFA, and a corresponding increase in that of PUFA. A separate group of 463 men carried on as normal was used as the control for comparison.

The results are shown in Table 1’

Table 1 Death rates and Total Cholesterol (TC) levels in the Anti-Coronary Club Study

Prudent Diet Control
TC level mmol/L 5.8 6.7
Coronary death rate /100 1.1 0
All-cause death rate /100 3.4 1.3


In this investigation there is no question that the TC was lowered. However there were 9 deaths due to heart disease in those on the Prudent Diet but not a single death in the control group. Even more worrying was the fact that the total mortality was about 2.5 times greater in those consuming the “healthier” diet!

The Sydney Diet Heart Study (SDHS), conducted between 1966 and 1973 was a randomized control trial in which the intervention group was advised to replace the SFA with safflower oil. This is a concentrated source of the omega 6 PUFA Linoleic Acid (LA) and does not contain any omega-3. Hence it is an excellent opportunity to study the impact of increasing the omega-6. In the original report, deaths due to cardiovascular disease and coronary heart disease were not shown. In an analysis of the data conducted recently by Chris Ramsden and colleagues it has been possible to gain insight into the effects of the different types of fats (2).

The participants were 458 men aged 30-59 years at the outset who had experienced a coronary event shortly before the commencement of the trial.

The intervention group received instructions to increase their PUFA intake to about 15% of food energy, and to reduce their intake of SFA to less than 10% of food energy. To achieve this target, intervention participants were provided with liquid safflower oil and safflower oil polyunsaturated margarine. The control group received no specific dietary instruction. However, some participants began replacing butter with margarine if they had suffered a coronary event.

The results in Table 2 show that the PUFA content of the diet in the intervention group more than doubled and the SFA content was reduced to below 10% of total energy. Compared with the control group, the intervention group had an increased risk of all cause mortality (17.6% v 11.8%; hazard ratio 1.62). The corresponding values for cardiovascular mortality (17.2% v 11.0%; 1.70) and for coronary heart disease), and mortality from coronary heart disease (16.3% v10.1%; 1.74) were similar. This study demonstrates that selectively increasing omega-6 PUFA LA from safflower oil and safflower polyunsaturated margarine increased rates of death from cardiovascular disease, coronary heart disease, and all cause mortality compared with a control diet rich in SFA from animal fats and common margarines. When this result is taken in conjunction with other investigations it is highly probable the raised level of LA is the critical factor responsible for the increased mortality rates which have been observed.

It is also important to note that although there was a decline in the TC levels of both groups it was much greater in the intervention group. This provides further confirmation that lowering TC does not result in a corresponding reduction in the coronary death rate.

Table 2 Changes in the Composition of Dietary Fatty Acids

PUFA,%E 6.2 6.1 8.4 15.4
SFA,%E 15.6 16.2 13.5 9.3
PUFA:SFA 0.41 0.38 0.63 1.72

The Lyon Heart Study is one of the most successful investigations which demonstrate that a change in diet results in a significant improvement in the survival rates of men and women aged <70 years old who have experienced a heart attack.

Volunteers who had survived a heart attack were allocated to either a control group (n=303) or an experimental group(n=302). Those in the experimental group were advised to consume a Mediterranean type diet which involved a reduction in the consumption of total fat, saturated fat and linoleic acid (omega-6s) and an increase in the consumption of oleic acid (mainly olive oil) and alpha-linolenic acid (omega-3s). The participants were seen 8 weeks after the beginning of the trial and then again every year for up to 5 years.

At the first follow-up (minimum period 1 year) it was found that those on the Mediterranean diet had a much better chance of survival than those in the control group. As a consequence the decision was taken to stop the trial so that those in the control group were free to make changes to their diet and follow the advice given to the experimental group if they so wished. Nevertheless the research team continued with the original plan and a final assessment of all existing participants was done after about 4 years.

It was found that the death rate attributed to heart disease has been reduced by 65% in those consuming the Mediterranean diet while the all-cause death rate has been reduced by over a half. Because of the decision to effectively halt the trial after the first year this means that almost certainly these values are an under estimate. It cannot be over-emphasised that this is an enormous reduction which is even more impressive when the short time frame is recognised. It is also very much greater than anything that has been achieved using drugs.

It is highly significant that the values for TC were virtually the same for both groups demonstrating the futility of the current focus on reducing TC as a means of controlling heart disease. The values for the “bad” LDL cholesterol were also the same for the controls and experimental groups.

It is absolutely essential that anyone who is being advised to reduce their TC should be made aware of this information.

  • On the one hand, it is obvious that those who successfully reduced their TC by altering the fat content of their diet INCREASED their risk of heart disease, despite the fact that the justification for making change would decrease the risk.
  • On the other hand, an unprecedented reduction in deaths due to heart disease and to all causes was achieved even though the cholesterol in the blood remained unchanged.

So if you think increasing your consumption of PUFA will be beneficial because it will lower you cholesterol, then you should think again. In reality it may be damaging to your health. Similarly the case for not eating butter is demolished by these results. There is plenty of evidence to show that many of the individual fatty acids are important nutrients, not to mention the presence of key fat-soluble vitamins including vitamins A,D and K2.


  1. G Christakis et al (1966) Journal of the American Medical Association 198 (6) pp 597-604
  1. C E Ramsden et      al(2013) British Medical Journal 346:e8707


  1. M de Lorgeril et al(1996) Journal of the American College of Cardiology 28 (5) pp 1103-1108