BLOG 158. Support for Conventional Dietary Guidelines

Despite the recent report (1) by Zoe Harcombe and her team which demolished one of the main planks used to justify the original advice to reduce the saturated fat (SFA), there are still individuals who are not prepared to accept that the conventional dietary guidelines were fundamentally flawed. One of these is Professor Christine Williams, who holds the Hugh Sinclair Chair in Human Nutrition at the University of Reading. In an article in the New Scientist she states that:
“Claims that dietary fat guidelines in the US and UK were not based on good scientific evidence are misguided” (2).
In her view the use of Randomized Controlled Trials (RCTs) are inappropriate for the development of recommendations which are for the population as a whole.
She then attempts to justify the current recommendations on the basis that it has been demonstrated that SFAs increase the level of cholesterol in the blood (TC) based on animal studies, comparisons of health outcomes between countries with differing diets, and long-term observational studies of large numbers of people.
Professor Williams then goes on to argue that because statins have been shown to lower cholesterol and reduce TC, it must follow that this also works for diet.
This is absolutely bizarre since RCTs have been used to do the studies on statins and it certainly cannot be assumed that the diet will have the same effect as the drugs.
But these factors are of little consequence. The fundamental rationale which she uses in defence of the conventional dietary guidelines is as follows:
• TC is a risk factor for heart disease
• SFA increases TC and hence increases the risk of developing heart disease
• Therefore lowering SFA will reduce the risk of heart disease.
The reality is that this is a load of rubbish! Although much of the research on TC has focussed on heart disease, my view is that the critical indicator must be all-cause mortality. I really cannot get excited if I can reduce my chances of suffering from a heart attack but that comes with a cost of an increase in the risks of dying from cancer. If TC is an accurate reflection of the risks of heart disease then those with low values must have a lower death rate than those with higher values. It so happens this information has been provided in a major study conducted in Norway, in which 52,087 men and women aged 20-74 years were followed over a 10-year period (3). TC levels were measured and details of any deaths which occurred were recorded. In both men and women there was no statistically significant increase in the risk of death at higher TC levels (Table 1). Individuals with a TC of 7.0 mmol/L or higher were no more likely to die of cardiovascular disease than those with levels below 5.0 mmol/L.
In men, there was no increase in the all-cause mortality with raised TC. Those with a TC level between 5.0 and 5.9 mmol/L had the lowest death rate, which was 23% lower than those with a TC below 5.0 mmol/L.
For women the pattern is different. The higher the TC, the lower the risk of dying from all causes. Compared with those with a TC below 5.0 mmol/L, those with the highest TC levels were 28% less likely to die from all causes.

Hazard ratio
TC, mmol/L Men Women
All-cause CVD All-cause CVD
<5.0 1.00 1.00 1.00 1.00
5.0-5.9 0.77 0.80 0.92 0.90
6.0-6.9 0.84 0.87 0.84 0.81
>7.0 0.98 1.05 0.72 0.74

This detailed break-down shows that as expected most deaths occur after the age of 60 years (Tables 2 and 3). Although the optimum TC level for men aged 60-69 is in TC range 5.0 to 5.9 mmol/L, for those over 70 the lowest death rate is in the higher TC level of 6.0 to 6.9 mmol/L. For women it is very clear that the death rate for the over 60s decreases as the TC increases. For this age range it is evident that the highest death rates are for those with a TC level which is below 5.9 mmol/L. The relatively high death rates for those aged 60+ years at low TC values should also be noted (4).

AGES <5.0 5.0-5.9 6.0-6.9 >7.0
20-29 1.10 0.38 0.30 0.00
30-39 0.80 0.57 0.72 0.47
40-49 2.22 1.38 2.27 3.37
50-59 4.54 4.93 6.22 5.74
60-69 20.31 16.20 17.37 18.47
70-74 49.18 40.37 37.93 41.25

AGES <5.0 5.0-5.9 6.0-6.9 >7.0
20-29 0.35 0.30 0.24 0.60
30-39 0.31 0.43 0.82 0.69
40-49 0.89 1.85 1.69 1.12
50-59 2.95 3.59 3.53 3.79
60-69 22.31 10.32 10.47 9.51
70-74 31.46 22.50 21.58 19.23

The authors commented as follows:

‘’If our findings are generalizable, clinical and public health recommendations regarding the ‘dangers’ of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but beneficial.’’

They went on to conclude:

‘’Our results contradict the guidelines’ well-established demarcation line (5 mmol /L) between‘good’ and ‘too high’ levels of cholesterol. They also contradict the popularized idea of a positive, linear relationship between cholesterol and fatal disease. Guideline-based advice regarding CVD prevention may thus be outdated and misleading, particularly regarding many women who have cholesterol levels in the range of 5–7 mmol/Litre and are currently encouraged to take better care of their health’’(4).
In my experience, I have yet to find anyone who is made aware of these results who would wish to lower their TC.
There are lots of other studies which confirm that TC or even the so-called “bad” LDL Cholesterol levels are poor indicators of the risks of developing heart disease (5). It is also highly relevant that in the Lyon Heart Study there was a 74% reduction in the death rates of those on the “healthier diet” but the TC levels were virtually identical in the controls and the treatment groups (6). In a comparison between Belfast and Toulouse, it was found that although the TC levels were the same in both cities, the CVD death rate in Belfast was 4 times that of Toulouse (7).

One final point about statins which is highly relevant. According to NICE, 77 people with heart disease have to be treated with statins for 3 years for one to benefit (8). However for those who did not have previous heart trouble, who are the target for the dietary guidelines
• None were helped (life saved)
• 1 in 104 were helped (preventing heart attack)
• 1 in 154 were helped (preventing stroke).
On the other hand
• 1 in 50 were harmed (develop T2D)
• 1 in 10 were harmed (muscle damage) (9).
If we accept that the statin argument has some merit, the benefits to be expected are negligible. Statins may well do more harm than good.
It will be clear that case presented by Professor Williams lacks any kind of credibility. If we are to make progress then it is vital that these bogus defences of the status quo are exposed so that the authorities are forced to recognize the fundamental flaws in the current official advice. How many more people will have to suffer and die prematurely before reason prevails?

3. H Petursson et al (2012). Journal of Evaluation in Clinical Practice 18 (1) pp 159-168
4. H Petursson et al (2012). Journal of Evaluation in Clinical Practice 18 (1) pp 170-171

157. Could this be the breakthrough?

A paper entitled:
“Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis” by Zoe Harcombe and colleagues has been picked up by the press in a big way (1). Here are some examples of the headlines:
• Daily Express:
“FAT is the key to living longer: Previous diet advice was WRONG, say experts” (2)
• The Times:
“Saturated fat diet advice not backed by evidence” (3)
• Guardian:
“Fat guidelines lacked any solid scientific evidence, study concludes” (4)
• Irish Times:
“Advice to cut intake of fat and saturated fat ‘wrong’” (5).

The research paper has taken the data from those reliable trials which were available prior to the development of the dietary recommendations to reduce saturated fat (SFA). There were only 6 studies which looked at the relationship between dietary fat, serum cholesterol, and the development of coronary heart disease that were considered to be satisfactory. And all but one focused on secondary rather than primary prevention. The pooled data revealed a total of 740 deaths from all causes, and 423 from coronary heart disease. There was no difference in deaths from all causes between the ‘treatment’ and comparison groups, with 370 deaths in both. And there was no significant difference in deaths from coronary heart disease, with 207 in the ‘treatment’ groups and 216 in the comparison groups. Although there was a reduction in the levels of blood cholesterol (TC) in the treatments groups with reduced intake of SFA this not associated with corresponding reduction in deaths. As all the participants were men, it follows that there was absolutely no information for women.
So the reality is that there was absolutely no justification in 1984 for the official Committee on Medical Aspects of Food Policy (COMA) to recommend that the SFA intake should be reduced from 20% of food energy to 15% as part of a strategy to reduce cardiovascular disease (6). As it happens this target was reached by 2000 (7). 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 (8). What is especially disturbing is that since 1994 the incidence of diabetes has more than doubled for both men and women (9). It is quite obvious that the expected results have not materialised and that the standard of public health have deteriorated.
These results will come as no surprise to anyone who has taken the trouble to review the evidence or to read any of the books written by independent researchers/journalists such as Gary Taubes, Barry Groves, John Briffa, Zoe Harcombe, Malcolm Kendrick or Nina Teicholz.
Publishing this report in a prestigious journal which has open access may prove to be a master stroke as it has clearly been picked up by the press and is certainly having an impact. But what is disturbing, but not surprising, is the response from the establishment. Here are a few examples:
• Dr Rahul Bahl in an editorial in the same issue of BMJ Openheart claims that:
“Epidemiological and ecological evidence suggests a link between fat consumption and heart disease. The seven countries cohort study by Keys referred to by the authors did find that higher serum cholesterol tended to be related to coronary heart disease incidence and that higher saturated fat consumption tended to be related coronary heart disease incidence. These findings were consistent in long-term follow-up” (10).
Nutritional policy has had numerous failures due to the reliance on epidemiological evidence which by itself cannot provide sound evidence on the relationship between diet and health/illness. It is outrageous that anyone can rely on this study by Keys which has been totally discredited (11).
• Dr Alison Tedstone, chief nutritionist at Public Health England, said:
“This paper is not critical of current advice on saturated fats but suggests the advice was introduced prematurely in the 1980s.” (12).
This really is being disingenuous. We just cannot get away from the facts that there was no reliable basis for the introduction of the recommendation to reduce SFA in the first place, that it has not worked and that no studies have provided any justification in the meantime.
• Victoria Taylor, senior dietician at the British Heart Foundation (BHF), said
“Understanding the true relationship between diet and our health is not simple. It would be all but impossible to carry out a research trial where you controlled the diets of thousands of people over many years. We continue to recommend switching saturated fat for unsaturated fat.” (13).
This position is simply untenable. There is very convincing evidence that many of the individual SFAs are actually important nutrients in their own right (14). Furthermore there is simply no case for increasing the intake of the polyunsaturated fats (PUFA) because this will increase the requirements for the omega-3 fatty acids and will probably also have deleterious effects such as increasing the risks of inflammation (15). It is rather ironic that the BHF commissioned research on SFA which concluded 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 (16). Despite this the organisation 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” (17).
Surely the position adopted by the BHF has nothing to do with the support it receives from the manufacturers of Flora which is promoted on the grounds that it will “reduce cholesterol”? (18).
The fundamental problem is that when the dietary guidelines were first devised, the decision to recommend that the fat and the SFA in particular should be reduced was wrong! The focus of attention should have been on sugar and the refined carbohydrates. As a consequence the SFA intake has fallen and there has been a corresponding increase in the intake of sugar and carbohydrates. This is primarily why public health is deteriorating as shown by the rise in obesity and diabetes. The only way to address the issue is to reverse the current trends. Although there is growing recognition of the dangers of sugar, there will be little progress until it is accepted that SFA is a crucial nutrient and that it is actually beneficial to increase it.
Hence it is absolutely appalling that so many of the “great and the good” in the medical and public health professions continue to try to put forward rather pathetic justifications to support the official advice even though it cannot be substantiated. To persist in the light of the evidence is completely irresponsible because it is condemning a huge number of people to a life of misery and early death. It is about time these “deniers” faced up to reality and have the intellectual honesty to admit that they have been wrong. Surely that is the least we can expect?
Finally, congratulations to Zoe and her colleagues for a wonderful initiative. Let’s hope this triggers the breakthrough many of us have been anticipating!

6. Department of Health and Social Security (1984) “Diet and Cardiovascular Disease” London: HMSO
8. Health Survey of England 2010 Adult Trend Tables
9. Health Survey for England 2009

156. Yorkshire Food Revolution

Reducing the risk of heart disease, diabetes and obesity
There is a wide variety of high quality foods produced in Yorkshire, especially meat and meat products as well as butter, cheese, cream and yoghurts which are based on milk from cattle and sheep. Unfortunately many of these are regarded as “unhealthy” because they usually contain saturated fat (SFA). According to the official dietary recommendations SFA is a risk factor for heart disease and so we are advised to limit the amount we eat. The Government has a Responsibility Deal with the food manufacturers and retailers which puts pressure on the industry to reduce the SFA in the food chain. This is encouraging food companies to remove SF from existing products in order to devise “low fat” versions.
During the past few years the rationale used to justify the advice to reduce SFA has come under intensive scrutiny and it is now abundantly clear that it is fundamentally flawed. The reality is that SFA does not represent a threat to health: in fact, certain individual saturated fats are actually important nutrients in their own right! By contrast, it is the sugars and refined carbohydrates which should be the cause for concern. During the past 15 years the incidence of Type 2 Diabetes (T2D) has doubled. Those with T2D have an increased risk of heart disease. Essentially T2D is excess sugar (glucose) in the blood. This is caused by consuming too much sugar and carbohydrate-rich foods like potatoes, rice, bread and pasta which contain starch. These are broken down during digestion to produce glucose which is absorbed into the blood and if there is an overload the result is T2D. Furthermore, soft drinks including fruit juices invariably contain a high content of sugar. In addition, sugar is present in many processed foods. Despite the protests from the vested interests, there is little doubt that current poor standard of public health as shown by the figures for T2D and obesity is primarily because of the high content of sugar and carbohydrates in the typical diet.
It is somewhat ironic that many shoppers choose the “low fat” variants believing them to be healthy. Regrettably this is not the case. By removing the fat a valuable source of nutrients is lost. As the fat is often replaced by sugar the consumer suffers a double whammy!
Although the Government is still pushing a discredited policy, a growing number of consumers recognise that the way forward is to reduce the carbohydrates and increase the amount of fat in the diet. More and more people are finding out for themselves that this actually works and makes them feel better. There is convincing evidence that this type of diet improves health for most people. With respect to weight loss, the effect is noticeable within a matter of weeks. There are literally hundreds of personal case histories on the internet from individuals who have overcome T2D. Many of them have been able to stop using drugs completely
All of this is great news for many Yorkshire food producers. What it means is that foods which have been branded as “unhealthy” should now be regarded as “healthy”. However the most significant development is that even though the Government persists with policies which are doing more harm than good, the message is being picked up by more and more ordinary consumers. This represents a huge opportunity for all those producers of specialised foods here in Yorkshire.
There is no doubt that the time is ripe and things could really explode any time. This has already happened in South Africa. Professor Tim Noakes of the University of Cape Town and colleagues have written a book on this precise issue entitled “The Real Meal Revolution” which has been a phenomenal success. Initially 3,000 copies were printed but it has already sold over 120,000 and has been top of the best seller list for over 20 weeks. Restaurants have devised menus which are in line with the new thinking and are trading extremely well.
Here in Skipton, Malcolm Weaving of The Rendezvous and the Craven Branch of the Federation of Small Businesses have co-operated to organise an event which focused on these exciting concepts. It was held at The Rendezvous on Friday 30th January 2015. The format consisted of:
• A tasting menu of 7 different courses all designed and prepared from ingredients sourced in Yorkshire wherever possible and selected to fit in with the latest thinking on Healthy Eating
• After each course Chris Wildman of the Town End Farm shop described the provenance of the ingredients, the procedures applied to ensure that quality standards are maintained and how the foods can be sourced
• Finally Verner Wheelock, Chairman of Verner Wheelock Associates, specialists in nutrition and food safety training and consultancy to the food industry, discussed the basic principles which underpin these new ideas and how they can be put into practice.
This event was attended by almost 70 people who hopefully now appreciate how it is possible to improve the nutritional quality of the diet by consuming foods that are not only tasty and good to eat but are also produced to the highest ethical standards in the glorious Yorkshire country

155. What Happens to the Cholesterol when the Dietary Fat is Altered?

The official dietary recommendations continue to advise a reduction in saturated fat (SFA) and an increase in the polyunsaturated fat (PUFA). The justification is that the SFA will reduce the Blood cholesterol (TC) and therefore lower the risk of developing heart disease. The same rationale is used to justify the advice to increase the intake of PUFA, which should also reduce the TC. It is therefore relevant to consider the results of some studies which investigate the effects of changes in the dietary fat on the TC.
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 which carried on as normal was used as the control for comparison.
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!
A trial conducted in London under the auspices of the MRC investigated the effect of a cholesterol-lowering diet diet in the prevention of relapse in men aged under 60 years recently recovered from their first myocardial infarction. 199 men recently discharged from hospital were randomly allocated to the experimental group were given a diet low in saturated fats and containing 85 gm of soya-bean oil daily. There was a control group of 194 men who consumed their usual diet. All of them participated for at least 2 years but some continued for over 6 years. Those in the experimental group lowered the TC from a mean initial figure of 272 to 213 mg. per 100 ml. at six months (22% fall). The level in the controls fell from 273 to 259 mg. per 100 ml. (6% fall). Suspected relapses were assessed at regular intervals by a review committee unaware of the patient’s diet group.
Although there were 45 major relapses in the test group and 51 in the controls, those which resulted in death were 25 in each. It was concluded that relapses were not related to initial TC level, to change in cholesterol level during the trial, nor, in any consistent way, to observance of the dietary regimen (2).

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. It is an excellent opportunity to study the impact of increasing the PUFA. 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 (3).
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 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 PUFA resulted in an increase in 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. This investigation must be regarded as highly relevant because the changes are precisely those which are being recommended by the authorities in the UK and in most of the world. It is obvious that the favourable results confidently predicted have not materialized.
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.

Although the TC levels in both groups fell but the decline was much greater in the intervention group than it was in the control group. The cholesterol theory predicts that the death rate attributed to heart disease would be therefore be less than in the control group. In reality it was 70% GREATER than in the control group and only slightly less for all-cause mortality. This is further evidence that the benefits which have been claimed for lowering cholesterol simply do not materialize in the real world.
The case for reducing SFA and increasing PUFA is full of holes as far as the impact on the blood cholesterol levels are concerned. When researchers have attempted to confirm it, they have failed totally. Although the TC has been lowered successfully there certainly has not been the improvement in health so confidently predicted by those who formulate and implement the current policies. Despite this the advice from the NHS and health professionals here in the UK and in most other countries continues to emphasise the importance of limiting the intake of SFA. Furthermore there are many products on the market which are actively promoted on the grounds that that they are high in PUFAs and will therefore “lower cholesterol”!


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

154. The Acidity of the Body

These days we are given all sorts of advice on healthy eating. There is much controversy about what actually constitutes a healthy diet. Readers of these blogs will know that there are many criticisms of the current official recommendations. There is a convincing case that complying with these will do more harm than good. Furthermore there is considerable variation in how individuals respond to a particular diet. Therefore it would be very helpful if there was a simple test which would enable people to assess their progress towards achieving good health.
In fact there is evidence which indicates that this can be done by monitoring the pH, which is a measure of the acidity/alkalinity of the body. The pH is a log scale with the range from 0 to 14. Low values are acid and high values are alkaline. A value of 7 is neutral (neither acid nor alkaline). The body pH can be measured using litmus strips on a sample of saliva or urine. The optimum value is about 7.5 which is slightly alkaline. The strips are readily available and inexpensive. It is quite easy for individuals to check their own pH themselves.
Metabolic syndrome (MetS) is defined as a condition characterised by a number of metabolic features including low HDL Cholesterol, raised triglycerides, hypertension, obesity and insulin resistance. These are invariably associated with common chronic diseases such as diabetes, heart disease, various cancers and all-cause mortality. In a recent study with 148 participants it was found that as the number of MetS features increased the pH of the urine decreased progressively. For those with no features the pH was 6.15 but for those with 4 features it had fallen to 5.7 (1).
In a recent European study a total of 66,484 women were followed for 14 years. During this period there were 1,372 cases of type 2 diabetes (T2D). It was found that those with a high acid-forming potential had a much higher incidence of T2D than those with a low value. Interestingly the difference was greater for those with a “normal” Body Mass Index (BMI) than for those who were “overweight“ with a BMI >25 (2). This was the first time that a large prospective study has demonstrated that the dietary acid load was positively associated with T2D risk, independently of other known risk factors,
Other studies have shown that the incidence of T2D is higher in people with a low pH in their urine when compared with those who have a higher urinary pH. The low pH was associated with the uric acid and the presence of stones in the urine. It was found that this condition was prevalent in patients with glucose intolerance and T2D (3).
The famous German Nobel Prize winner, Otto Warburg, discovered that there is only one cause for cancer which is the replacement of the respiration of oxygen in normal body cells by the fermentation of sugar. All normal body cells meet their energy needs by the respiration of oxygen but cancer cells depend on sugar as a source of energy for the fermentation process. Because of this crucial difference between cancer and normal cells, this knowledge can be utilised to devise methods of curing the disease. Protocols which deprive the body of sugar are proving to be effective in this context. Furthermore the fermentation causes the immediate environment of cancer cells to become acidic and therefore reduce the pH below the optimum value of 7.4.
In a highly significant investigation it was noted that the pH range of tumours in mice was between 6.5 and 6.9 (compared with 7.2-7.5 for normal tissue). When the pH was raised by treatment with sodium bicarbonate (baking soda) this resulted in significant reductions in the number and size of metastases to the lungs, intestine and diaphragm (5). The tumours used were models for breast and prostate cancer in humans. This is a practice which has been used successfully for the treatment of various forms of cancer.
Consequently there is considerable interest in understanding the relationship between various foods and their impact on the pH. Various attempts have been made to determine the impact of different foods on the pH of the body.
Chris Woollams has spent years developing his Canceractive website which contains an enormous amount of reliable information which relates to the prevention and curing of cancers. People diagnosed with cancer invariably have an acidic pH and there are strong indications that the consumption of a high proportion on of foods which are known to be alkaline can help to prevent and even cure cancer (6).
These include:
Beetroot, Cabbage, Carrots, Cauliflower, Celery, Cucumber, Fresh green beans, Lettuce
Mushrooms, Parsnips, Potatoes, Spinach, Swede, Watercress
Fresh fruits
Apple, Avocado, Blackberries, Blackcurrants, Cherries, Grapes, Lemons
Olives, Pears, Olives, Raspberries
Fresh ginger, Fresh juices, Green tea, Olive oil, Seeds
By contrast, here are some of the foods which are acidic producers:
Brussel sprouts, Lentils, Peanuts, Rhubarb, Tomatoes
Bananas, Grapefruit, Oranges, Plum, Prunes
All alcohol, Coffee, Fizzy drinks, Sauce, Sugar, Sweets

The above list is certainly not meant to be comprehensive and the degree to which individual foods can exercise their effect on the pH does vary and of course will be influenced by the amount consumed.
For those whose pH levels are in the acidic range it should be possible to raise it into the alkaline range by making adjustments to the diet. The alkaline-producing foods should be reduced at the expense of the acid-producing ones. However it is critical to understand that it is the balance that is important. While there are some acid-producing foods which should be kept to a minimum such as fizzy drinks and sugar, there are others such as Brussel sprouts and tomatoes which should be include in a healthy diet. The above information is simply a guide which hopefully will enable a person to try out different possibilities and discover what actually works and what is feasible.
The significant advantage of the pH is that it provides a means by which anyone can monitor their progress in response to dietary adjustments. As things stand at present we do not have absolute proof that the rationale is sound but it is certainly worth trying. There is no suggestion that attempting to alter the pH by dietary means will cause any possible harm. On the face of it, pH should be a routine check as already applies to body temperature or blood pressure. It would be extremely valuable if the research could be instigated which would explore how this could be achieved.

1. N M Malouf et al (2007) Clinical Journal of the American Society of Nephrology 2 (5) pp883-888
2. G Fagherazzi et al (2013) Diabetologia doi:10.1007/s00125-013-3100-0
3. K Sakhaee et al (2002) Kidney International 62 (3) pp 971-979
5. I F Robey et al (2009) Cancer Research 69 (6) pp 2260-2268


153. Public Accounts Committee Report on Tamiflu and Publication of Drug Evaluation Results

A report from the House of Commons Public Accounts Committee concludes that information is routinely withheld from doctors and researchers about the methods and results of clinical trials on treatments currently prescribed in the United Kingdom (1). Invariably the bodies responsible for the approval of new drugs only have access to the results of studies which present the drug under investigation in a positive light which those which do not as well as those which show no benefit or even undesirable effects may never be revealed. Essentially this means that the regulatory authorities do not have the total picture which is needed if sound decisions regarding approval for usage are to be made. Although this problem has been recognised for many years there has been a failure on the part of government, industry and the professional bodies to take the necessary action to deal with it. It was recommended that the full methods and results are available to doctors and researchers for all trials on all uses of all treatments currently being prescribed.

The report considered what happened with Tamiflu, which had been stockpiled between 2006-07 and 2012-13, on the basis that it would be needed in the event of a pandemic of influenza. During this time the Department of Health spent £560 on antiviral medicines, of which £424 was for Tamiflu and £136 for Relenza. Valuable insight into the background to this policy can be gained from some of the evidence presented to the Committee by Ben Goldacre author of “Bad Pharma” and Fiona Godlee, editor-in-chief of the British Medical Journal.

With respect to Tamiflu, Fiona referred to the work of a team at the Cochrane Commission led by Tom Jefferson who discovered that there had been about 123 trials conducted on Tamiflu and that the pharmaceutical company Roche was aware of 74 completed trials. Of those, it appears that the European Medicines Agency (EMA) had access to only 15 incomplete accounts. In the UK, the National Institute for Health and Care Excellence (NICE) had received 4incomplete accounts of trials.

She described those involved in Cochrane Commission reviews as

“slightly obsessive and very scientifically determined people”

While it might be expected that the regulatory bodies would require all the evidence to be provided for evaluation in practice according to Fiona they do not ask for it even though they are entitled to have it. Because they are under-resourced and stretched they tend to take the manufacturer’s word for it. By contrast, in Germany, manufacturers have a legal obligation to provide the Institute for Quality and Efficiency in Healthcare (IQWIG), which performs a similar role to NICE, with a full list of clinical trials and supporting clinical study reports.
In a letter to the Chair of NICE, Sir Michael Rawlins, Fiona described the response from IQWIG when it discovered that had not been provided with all the relevant data on reboxitine, a drug produced by Pfizer(2). The company was told it would only approve the drug for reimbursement if all the results were made available to the Institute. The full dataset showed that the drug was ineffective and possibly harmful. This illustrates very effectively how the regulatory bodies can actually be misled and in reality manipulated by the drug companies.
The report implied that those responsible for the expenditure involved in stockpiling the Tamiflu did not have the evidence which clearly demonstrated the efficacy of the drug, especially in the light of the Cochrane report cited above. Hence it is particularly relevant that when the Chief Medical Officer, Dame Sally Davies, was presenting evidence to the Committee she attempted to cast doubts on the credibility of the Cochrane conclusions. In particular she claimed that the Cochrane group

“extracted data from 25 studies but excluded 43 and took no data from published studies.”

The reply to this comment included the following points:
• Not all the trials on conducted on Tamiflu, produced by Roche had been published in the scientific literature
• Not all of those published have been totally accurate. The original results are contained in “Clinical Study Reports” which are extremely detailed and comprehensive. The experience of the Cochrane group has provided examples of discrepancies between the information in these Clinical reports and what appeared in the scientific paper. The group cited 2 examples which stated that:
“there were no drug related serious adverse events”
“No serious adverse events were noted in the major trials and no significant changes were noted in laboratory parameters”

However, the equivalent clinical study reports for these two trials describe 10 serious adverse events (in nine participants), some of which were classified as “possibly” related to Tamiflu. They also discovered many of the authors of the scientific papers had not actually seen the raw data. At least one paper had been ghost written.
As a consequence the team decided that there were serious doubts about the reliability of the scientific papers from Roche and that they should restrict their analyses to the original Clinical Study Reports, a strategy which seems entirely reasonable
• There was one study, which was the largest treatment trial of Tamiflu, where the only published information was a 300-word abstract of a conference presentation. The author, Professor Treanor did not participate in the original study and admitted on Channel 4 News that he could not even remember presenting it at a conference in 2000
• Hence it was not correct for Dame Sally to conclude that 42 studies had been excluded. The position was that for 42 studies it was possible to obtain sufficient information to determine their suitability for further assessment and analysis in the review… a very different context

The work of the Cochrane team was fraught with difficulties and in some cases the information was only released in response to Freedom of Information requests and even then there was great reluctance to provide it. The claims of the regulators that they had all the information needed to make sound decisions just do not stand up to rigorous examination.
There is absolutely no reason to doubt the Cochrane conclusion its review has had access to the most extensive data set ever used in these particular drug types and therefore provides a transparent assessment. Consequently it has not been possible to draw conclusions about its effect on complications or transmission. Accepting that it is incomplete at this stage, it is certainly the best that has been produced so far and must carry mush more weight than anything from the regulators who have not had access to such comprehensive evidence.
The Government and the officials in the Department of Health would do well to take note of the Public Accounts Committee Report.


152. You Must Be Nuts!

I have just been watching the video entitled “You must be nuts!” which has been made by Obhi Chatterjee and colleagues. It can be viewed on You Tube here:

The stimulus for this video was to try to understand why Obhi’s father had developed dementia and to identify ways in which the condition could be alleviated. It is absolutely staggering to learn that that the incidence of Alzheimer’s Disease (AD) has increased from about 2% in those over 85 years old about 40 years ago to over 50% to-day. So it cannot be shrugged off on the grounds that it is just because people are getting older. In any case much of the increased life expectancy is the result of reduced infant mortality. In addition, AD is now being detected in young people, which is a new phenomenon.
This is an excellent compilation of information which conveys a prime facie case that changes to our diet, food production methods and medical treatments have combined to produce what is in effect a toxic environment. A number of individuals who can speak with authority on the different aspects have been interviewed and some of the relevant research has been cited. For anyone who is unaware of how bad things have become, the conclusions will come as a great shock. The big advantage of this form of presentation is that the messages come across very clearly and therefore should have a big impact on those who actually take the time to sit down and watch it.
The so-called “Lipid hypothesis”, which is based on the level of cholesterol in the blood (TC) as a risk factor for heart disease, underpins the conventional advice on healthy eating and is the justification for the use of statins. This leads to the conclusion that if we can lower our TC, then we will reduce the risk of heart disease. It is argued that because saturated fat (SFA) in the diet increases TC, it should be reduced and by the same reasoning the polyunsaturates (PUFA) should be increased. As statins lower TC so the story goes, they should be prescribed for virtually all men and women when they reach their 60s. The original work by Ancel Keys which led directly to the Lipid hypothesis has now been totally discredited.
Unfortunately those who have been diligent in following the advice, like the Chatterjee family, are now probably suffering the consequences. There is very convincing evidence that many of the individual fatty acids are actually important nutrients in their own right and play a critical role in supplying energy to the vital organs like the heart and brain. On the other hand, the PUFAs are highly reactive and can be converted to trans fats by various processes including heat, which are damaging to health. As the PUFAs in in “cholesterol lowering” foods such as margarine/spreads are mainly omega-6s the effect has been to increase the omega-6:omega-3 ratio from about 1-4 to 15 or even as much as 50, which is bad news!
But it gets worse. As shoppers try to avoid the fat, they invariably opt for the “low fat” variants. This is absolutely disastrous because not only are they missing out on the fat but also increasing their intake of sugar and/or sweeteners. In fact anyone who chooses processed foods will inevitably increase their intake of sugar because it is added to many of them. There can be no doubt that the increased consumption of sugar and refined carbohydrates is the prime reason why Type 2 diabetes (T2D) has doubled in the last 15 years. Those with T2D have a much increased risk of developing AD, not to mention heart disease, obesity and cancer. AD is often referred to as Type 3 Diabetes.
On top of all this we have the drugs which are being prescribed more and more. The video explains how crucial cholesterol is for brain function and why restricting the supply may have disastrous consequences. This of course is exactly what the statins would do. Despite all the hype, any benefits resulting from the use of statins is very small and is restricted to men who have suffered from heart disease in the past. Then there are other drugs which are also widely prescribed such as aspirin and omeprazole, which is supposed to protect the stomach from the damaging effect of the aspirin. Last May the FDA in the USA, warned against the general use of aspirin for the primary prevention of a heart attack or stroke.
Another concern is the widespread and extensive use of pesticides which may reduce the availability of the minerals in the foods which are being produced. A specific example is Vitamin B12 which is depleted by glyphosate or “Round up”.
To sum up, the case is made that the following factors have combined to cause this serious deterioration in our health as shown by the increased incidence of AD and T2D:
• The unscientific advice, especially to reduce SFA
• Routine use of drugs for the elderly
• High carbohydrate diet/processed foods
• Use of chemical fertilisers and pesticides in horticulture and agriculture.
I strongly recommend that everyone watch this video. It presents a very powerful series of arguments that things have gone badly wrong in the past 40-50 years. The case presented may not be correct in every aspect, but that is not the point. It is vital that these issues are addressed and that the resources are made available to get to the fundamental causes. Despite the comments at the end from Paul Burstow MP, I believe that politicians are reluctant to face up to what is undoubtedly a systemic failure with respect to policy formulation and regulatory controls. This will only change with pressure from the grassroots. Viewing this video should help to generate this pressure.

151. Praluent: New Cholesterol Drugs Get Riskier By The Day

This is a re-post of the article by Francois Lubbe of The Cholesterol Truth. I am most grateful to him for permission to post here.
The original is available at

Big Pharma seems intent in sticking to its backward way of thinking when it comes to cholesterol. So far their efforts, to create a drug that can prevent heart disease failed miserably.

Fortunately, many people have cottoned onto the fact that lowering cholesterol to ridiculously low levels with drugs is a bad idea because it can seriously put your health at risk. In the last few years, even some mainstream experts are beginning to agree that the Big Pharma has got it all wrong and that cholesterol is not the villain it is made out to be.

As a result, fewer people are taking cholesterol-lowering statin drugs and there is no doubt Big Pharma will feel this in their pockets — these drugs are among the top-selling of all time raking in billions of pounds each year.

However, instead of trying a different approach, Big Pharma and its cronies have their minds set on developing new cholesterol-lowering drugs, which are proving to be even more dangerous.

Cholesterol drugs: Going one step too far

Recently, the pharmaceutical giant Sanofi submitted its application to the European Medicines Agency (EMA) for the approval of a new cholesterol-lowering drug, Praluent (alirocumab).

Praluent is in a class of drug known as PCSK9 inhibitors. It is intended for the treatment of patients with hypercholesterolemia — people with hereditary high cholesterol. PCSK9 promises to reduce LDL cholesterol levels to previously unheard of lows… dangerously low levels!

The bigwigs at Sanofi are probably rubbing their hands together as they wait for the EMA’s approval, because as far as they are concerned they have struck gold.

Statin drugs reduce your cholesterol by blocking an enzyme in your liver that is responsible for making cholesterol. When taking a statin drug, people are usually able to reduce their cholesterol to between 70 and 100 mg/dL. However, patients with hypercholesterolemia usually cannot reach the ridiculously low targets set by the mainstream and that’s where PCSK9 inhibitors come into the picture.

According to Dr. Elliott Antman, president-elect of the American Heart Association and a dean at Harvard Medical School, PCSK9 inhibitors can reduce cholesterol levels to below 50 mg/dL.

That’s just madness! Too low cholesterol levels — even for those with hypercholesterolemia — will make patients vulnerable to a host of health problems. For example, research published in the journal Arteriosclerosis, Thrombosis, and Vascular Biology, showed that low cholesterol levels are associated with poor memory and even memory loss in middle-aged adults. That’s because cholesterol helps your brain form memories and it is vital to your neurological function.

Here’s where the prospect of Praluent hitting the market gets a bit more disturbing: When the company submitted its approval for Praluent to the American Food and Drug Administration (FDA), the first thing the agency said was that it was concerned about the neurocognitive side effects these drugs have shown.

That’s right, PCSK9 inhibitors damage your brain.

In fact, the FDA is so concerned about the detrimental effect these drugs can have on your brain that it asked Sanofi to show neurocognitive testing in outcomes trials. In other words, the drug maker needs to show that Praluent won’t fry your brain.

Furthermore, studies have also shown that if your cholesterol levels are too low, and if these low levels begin to affect your brain, you increase your risk of dementia, violent and aggressive behaviour, depression, suicide, cancer, Parkinson’s disease — and likely heart disease, as a result of cholesterol sulphate deficiency.

Cholesterol drugs: It’s time to dig deeper

Yes, that’s right, too low cholesterol levels may cause heart disease. A well-respected researcher at the Massachusetts Institute of Technology, Dr. Stephanie Seneff, recently said in an interview: “Heart disease, is a cholesterol deficiency problem, and in particular a cholesterol sulphate deficiency problem…”

Dr. Seneff points out that all of the information is available in research literature, to support her statement. By carefully dissecting all the research available on heart disease, she has come to the conclusion that the mechanism we call “cardiovascular disease,” of which arterial plaque is a hallmark, is actually your body’s way to compensate for not having enough cholesterol sulphate.

Now there’s a surprise, especially since conventional medicine has been telling us for years that heart disease is due to elevated cholesterol levels and it has been recommending that we lower our cholesterol to extremely low levels… levels that clearly harm our overall health…

Perhaps it’s time for Big Pharma to throw in the towel. Their drugs seem to be becoming more vicious and more damaging and they still have not figured out what really lies at the root of the problem.

And if you pay attention to what Dr. Seneff says, then these snake oil salesmen definitely have been pulling the wool over our eyes for much longer than we know.

As a sufferer of with hypercholesterolemia, one thing is certain, you won’t see me taking a statin drug and you certainly won’t ever see me anywhere near PCSK9 inhibitors.

Heart to a healthy and happy heart,

Francois Lubbe
The Cholesterol Truth


Arteriosclerosis, Thrombosis, and Vascular Biology June 30, 2008

New Cholesterol Drug PCSK9 Is Likely to Prematurely Kill You, published online 03.06.13,

Could THIS Be the Hidden Factor Behind Obesity, Heart Disease, and Chronic Fatigue?, published online 17.09.11

Praluent (anti-PCSK9), published online,

150. “Pure, White and Deadly”: What Sugar Does to You

Following on from the previous blog (1) based on the epidemiological evidence in John Yudkins’ book “Pure, White and Deadly: How Sugar Is Killing Us and What We Can Do to Stop It” this will focus on results from the experiments conducted with sugar. Here is a selection:
• One way of assessing the capability of the liver to produce fat is to measure the activity of some of the enzymes which are involved in the synthesis of fat. Using young rats it was found that those given sugar had 5 times the activity of one of these enzymes when compared with those not given any sugar. In another study, when sugar replaced starch in the diet of the rats. The activity another enzyme was doubled. With starch it is only glucose that is produced but sucrose is broken down to release both glucose and fructose. This particular result is consistent with other studies which confirm that the role of fructose is different from that of glucose and may possibly be even more damaging. It was also found that the sugar-fed rats show an increase in blood pressure, a deterioration in the ability to cope with high levels of blood glucose, an alteration in the properties of blood platelets and a change in the level of insulin in the blood. These are all observed in people with heart disease. When sugar was included in the diet of pigs, there was an increase in the level of triglycerides, which gives a much better indication of risk of heart disease than total blood cholesterol or LDL cholesterol. There was also an increase in the level of insulin in the blood.
• Studies with young men by Professor Ian MacDonald at Guy’s Hospital in London that consuming sugar for a few days caused a rise in blood triglycerides. With women it was observed in those after the menopause but not before. In Yudkins’ research team, it was found that in a group of 19 young men, they all had raised triglyceride levels after 2 weeks on a high sugar diet. In addition, 6 of them also gained about 2 kgs in body weight, there was an increase in insulin in the blood and the stickiness of the blood platelets increased. All of these changes reverted to the original values when they resumed their usual diet. These results raised a number of interesting issues:
1. The possibility that some individuals are susceptible to a heart attack specifically because of sugar.
2. The increased level of insulin in these men was in agreement with other researchers who had suggested insulin could be a critical factor in the development of atherosclerosis.
3. The rapid gain in weight which provided a clue about the relationship between excess weight and the risks of developing heart disease.
• Further studies with those who showed an increase in insulin concentration, confirmed that after a period on a high sugar diet, the platelets behaved like those of people with atherosclerosis, which returned to normal after cessation of the experimental diet.
• When Dr Robert Ahrens from the USA spent a period with Yudkins in London he studied the effect of sugar in the diet on blood pressure in young men. He observed a rise blood pressure, which was proportional to the amount of sugar added to the diet. In a review on sugar and heart disease he wrote that coronary heart disease:
“continues to increase on a world-wide scale in rough proportion to the increase in sugar consumption but not in proportion with saturated-fat intake”
• In another experiment with those who produced high insulin levels it was found that a 40% rise in insulin after 2 weeks on the high-sugar diet was accompanied by a rise of 300 to 400% in the level of the adrenal hormone. A further study in which volunteers reduced their intake of sugar from150 gms to 55 gms per day showed that this was associated with a reduction of about 30% in the oestrogen level. These findings confirm that the sugar is causing a disturbance in the hormone balance.
• Discussing the significance of these results, Yudkin emphasises that because of the effects of sugar on the liver. kidney and the hormone balance, sugar is a food which does have a considerable impact on the body and the way in which it functions. In particular the disturbance of hormones would explain why sugar may be responsible for a number of different forms of ill-health as well as the differences between individuals. It is known that many people who have definite atherosclerosis have a high level of insulin in the blood. The risk of coronary disease is increased by other factors including cigarette smoking, being overweight , peripheral vascular disease and Type 2 Diabetes (T2D) and all of these are associated with increased insulin in the blood. Similarly, a reduction in excess weight and/or increased physical activity both reduce the risk of heart disease, result in a fall in insulin levels.
However the most compelling reason for believing that insulin, or possibly some other hormone, plays a central role in the development of heart disease is multiplicity of changes that accompany the disease. It is difficult to see how these could occur unless there has been some disturbance of the hormone levels. He considers that insulin is the most likely hormone to be involved. Yudkin suggests that a continuing high-sugar diet means that there is a persistent high demand for the pancreas to produce insulin. Because insulin has many different functions the excess may well be deleterious in other ways, such as upsetting the established hormone balance. It might be expected that the insulin would increase the deposition of fat resulting in obesity. It could also increase the accumulation of fatty material inside the arteries and alter the properties of the platelets thereby leading to atherosclerosis.
All of these comments are extremely perceptive. There is now little doubt about the role of insulin not only in heart disease but in a range of other diseases and conditions. There can no question that even if all his ideas do not prove to be absolutely accurate, he has been totally vindicated by the subsequent events. In fact, the incidence of obesity and T2D continued to increase enormously since the second edition of his book. This would have been entirely predictable on the basis of his work. Furthermore, it is self-evident that current policies are failing and failing badly.
It is a great pity that there was no-one in a position to influence policy who recognised the significance of the work of Yudkin and those who had taken a similar stance. The time has come when his ideas must be applied. Unfortunately there is still powerful opposition as politicians and their acolytes continue to defend the indefensible.


149. “Pure, White and Deadly”: The Epidemiological Evidence

“Pure, White and Deadly: How Sugar Is Killing Us and What We Can Do To Stop It” is the title of a book written by Professor John Yudkin, who was in the Department of Nutrition at Queen Elizabeth College, London for many years (1). The first edition was published in 1972 and a revised edition appeared in 1986. Professor Yudkin died in 1995 and for many years the book was out of print. However in 2012 Penguin decided to publish it again with an introduction by Robert Lustig, Professor of Pediatrics at the University of California, San Francisco and an ardent campaigner for reducing sugar consumption.
We have now reached a point where there is overwhelming evidence that the official advice to reduce total fat/ saturated fat (SFA) formulated over 30 years was fundamentally flawed. In fact, it is virtually certain this recommendation has been one of the crucial factors contributing to the increased incidence of obesity, Type 2 Diabetes (T2D) and related conditions/diseases. It is arguably the most disastrous policy failures in the field of public health which has ever occurred. The inevitable consequence is that millions of people have suffered and died prematurely.
In order to understand how and why this happened we have to look at the developments in research in the period after the war, when there was a concerted effort, particularly in the USA, to tackle heart disease because it was one of the leading causes of death. It was accepted that the habitual diet was one of the factors involved but 2 different theories emerged. In the USA, Ancel Keys put forward the proposition that excess fat/SFA was a primary cause and therefore the amounts of these constituents in the diet should be reduced. By contrast, John Yudkin argued that the key issue was excessive sugar in the diet. It was of course Keys who prevailed and his views were effectively endorsed by publication of “Dietary Goals for the United States” for the McGovern Committee of Congress in February 1977 (2). An excellent account of the politics and other relevant issues is given by Nina Teicholz in “The Big Fat Surprise” (3).
Once the Americans decided that fat was the key problem, the same approach was adopted by the WHO and so many other countries devised nutrition/public health policies using similar “principles”. It is also meant that anyone who did not follow the party line, including John Yudkin, was effectively marginalised. He must have been extremely frustrated at the time of his death although he has been totally vindicated by the recent developments which I am convinced will inevitably force the politicians to re-shape policies on nutrition and public health.
In the meantime it is fascinating to re-visit “Pure, White and Deadly” to discover what exactly the views and conclusions of John Yudkin about 30 years ago. Here is a selection:
• The view that everything that increases cholesterol in the blood is likely to cause heart disease and vice versa is simplistic and naïve. It has hindered a proper understanding of the disease and its causes, which is why more progress has not been made on prevention. The reality is that there are more extensive disturbances than just a rise in in the blood cholesterol. These a rise in the blood triglycerides, a fall in the HDL cholesterol, changes in the blood glucose similar to those which occur with diabetes, including an increase in the insulin level in the blood. The activity of many enzymes is altered and the behaviour of the blood platelets is changed. As many as 20 different indicators are changed in people with severe atherosclerosis and so it does not make sense to focus specifically on cholesterol, which any case is not a specially reliable indicator of heart disease. All of this has been confirmed by subsequent research and events.
• With reference to the role of fat in heart disease, he notes that few people were not happy about the original work of Ancel Keys which was based on analyses of data which related the amount of fat consumed to the incidence heart disease in 6 different countries to produce a straight line. Although this showed an association it certainly did not confirm cause and effect. However Yudkin commented that the straight line disappeared when data from other countries, were incorporated into the study. More recently Zoe Harcombe has done a detailed critique of the Keys work, which completely destroyed any credibility which still existed (4).
• Epidemiological studies with sugar and heart disease for many countries showed that the there was a closer relationship than with fat. Accepting the limitations of this approach it at least makes the point that the case against sugar is at least as strong as that against fat. In addition the information for Great Britain demonstrated that the rise in sugar consumption preceded very closely the rise in deaths from heart disease. Data from South Africa showed that black population, which consumed little sugar, had a low incidence of heart disease. By contrast, the whites and the Indians who consumed much the same as the British, Americans or Australians, had comparable rates of heart disease. Furthermore, as sugar consumption by the blacks increased there was also an increase in heart disease. A similar picture was observed in Yemenis who moved to Israel. When they arrived, the incidence of heart disease was relatively low but it increase as they adapted to the typical diet in Israel, which has a high sugar content. Coronary disease is common on the island of St Helena where the residents consume less fat than in the USA or Great Britain, are very active because there is little mechanical transport and cigarette smoking is limited. However their consumption of sugar is about 40 kg per year which is high. It is clear that the totality of the epidemiological evidence is undoubtedly consistent with the case that sugar is a prime (but not the only) factor causing heart disease.
• In order to go beyond the study of populations, Yudkin and colleagues decided to investigate the sugar consumption of individuals to see if there was any differences between those with heart disease and those without. In one study, patients who had just suffered their first heart attack were compared with a control group. The sugar intake of the coronary patients was 113 gms per day but in the controls it was 58 gms per day. This study was criticised on the grounds that it had not been blinded (those obtaining the data knew which people had suffered a heart attack). In a second study, blinding was done but the results were essentially similar. The coronary patients were consuming 74 gms per day. This time there were 2 control groups: one had 67 gms and the other 74 gms per day. This type of study had NEVER been done for fat. Once again, the results were consistent! Although Yudkin goes to great pains to emphasise that this evidence does not constitute absolute proof and even if sugar is shown to be a cause of heart disease it will not be the only one.

1. John Yudkin (2012) “Pure, White and Deadly” Penguin London ISBN: 978-0-241-96528-3
3. Nina Teicholz. (2014)“The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet” Simon & Shuster: New York
4. Zoe Harcombe (2010) “The Obesity Epidemic” Columbus