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 (mg/100ml) Men Women
  All-cause CVD All-cause CVD
<5.0          (<194) 1.00 1.00 1.00 1.00
5.0-5.9     (194-228) 0.77 0.80 0.92 0.90
6.0-6.9     (232-267) 0.84 0.87 0.84 0.81
>7.0          (>270) 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).


                               (TC LEVELS, mmol/L(mg/100ml)
MEN, ages <5.0(<194) 5.0-5.9(194-228) 6.0-6.9(232-267) >7.0(>270)
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



(TC LEVELS, mmol/L(mg/100ml)

Women, ages        
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
69-74 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