Governments in many parts of the world devote enormous resources to the measurement of cholesterol because this is supposed to be a very good indicator of the risks of developing heart disease.
If you have a blood test and the results show that you have a high reading for total cholesterol in the blood (TC), this would be regarded as very bad news. You would be advised on what steps to take to reduce the risks of having a heart attack.
You may be encouraged to reduce the intake of saturated fat (SFA) and increase that of polyunsaturated fat (PUFA). These changes would both be expected to reduce TC and therefore lower the risks of heart disease.
Almost certainly you will be recommended strongly to start taking statins, which are justified on the same grounds. It is likely you will be told that that statins will be effective in reducing the risks of heart disease.
A critical examination of the rationale that underpins the cholesterol programme raises very serious doubts about the validity of using cholesterol as a risk factor for heart disease.
#There is convincing evidence that those with low cholesterol have an increased risk of dying from other causes including cancer and, somewhat bizarrely, deaths due to violence such as suicide, murders and accidents.
There are also high death rates caused by liver disease and mental conditions in those who have low TC values.
So even if there is some reduction in deaths from heart disease if the all-cause mortality rates show a significant increase, the total impact is not exactly desirable. This means your time of death will not be altered but the information on your death certificate may be altered.
In the Finnish city of Kuopio, 490 men and women aged over 75 were monitored for six years. None was on cholesterol-lowering medication.
Those who complied with the current TC guidelines (below 5.0 mmol/L) had a death rate that was more than double that of those with a value of 6.00mmol/L and higher.
A study in Norway in which over 50,000 men and women were monitored for 10 years provides more convincing evidence. The deaths rates were related to the TC values that had been collected while the participants were still alive.
This is the ultimate test because it provides definitive information on the probability of dying as shown by the TC values.
Surprise, surprise, those in their sixties and seventies who comply with the official guidelines for TC have the highest death rates. This result has been confirmed by another major research project in Japan.
Furthermore, for women in these age groups, the higher the TC, the greater the life expectancy. In the light of this knowledge, it simply does not make sense to attempt to lower cholesterol.
Hence, we are left with the very definite conclusion that there is no case for reducing SFA, increasing PUFA or using statins.
There is a very real possibility that your life will be shortened as a result.
In fact, cholesterol is a vital constituent that has a many important functions in the body. We probably need all we can get.
It is highly relevant that 25 per cent of our body cholesterol is present in our brains and therefore lowering TC may affect behaviour which might perhaps explain the increased incidence of violent deaths mentioned above.
Cholesterol may have an important healing role. The high values sometimes noted in heart disease may reflect the fact that the cholesterol is being mobilised in response to the trauma. Unfortunately, many researchers have failed to understand this and wrongly concluded it is a cause rather than an effect.
There are genuine doubts about the way these trials are conducted and how the results are handled.
First, the regulations that apply to the conduct of clinical trials were tightened up in 2005/2006 because of the Vioxx scandal. Vioxx was used to treat rheumatoid arthritis. It caused at least 60,000 deaths, possibly as many as 250,000. Many of the victims died of heart attacks. Since then, there has not been a single trial that demonstrates the effectiveness of statins.
Second, the trials to determine the effectiveness of drugs do not make any attempt to collect detailed information about the adverse side effects. In practice these are less likely to appear in the trials because during the selection process anyone who reacts badly to the drug will not be allowed to participate in the trial.
Third, the results are presented to ensure that the drug will appear in the best possible light. Here is a quote from one paper, which has taken a very critical look at the trials on statins. It refers to one of the most notorious trails, JUPITER:
“Your chance to avoid a non-fatal heart attack in the next two years is about 97% without treatment, but you can increase to 98% by taking Crestor (a statin) every day. However, you will not prolong your life and there is a risk that you will develop diabetes, not to mention other serious adverse effects.”
Looked at the other way, this means your risk of getting a heart attack is reduced from 3% to 2%. The promotion will use the relative risk, which is 33%!!!
Another take on the JUPITER trial is:
“Ultimately, cardiovascular mortality was not judged different in the placebo and rosuvastatin groups, and the small difference in overall mortality was not validated by the statisticians of the FDA.”
Fourth, the raw data is not usually open to independent scrutiny and evaluation. This is a serious limitation. Sometimes this information has had to be released because of court orders that have revealed how the data has been twisted to emphasise the benefits of the drug.
Even if all of this is discounted, the best possible spin from NICE is that among those with heart disease 77 people must take statins for three years for a single person to benefit. This may only be a few extra months of life.
Against this you should consider all the possible side effects, which vary from aches and pains in muscles and joints to mental conditions such as memory loss.