Open Future Health

Prof. Tim Noakes before the Health Professions Council of South Africa

Dr Tim Noakes giving a lecture on nutrition at his "trial."


Edited video of Dr. Noakes' Testimony is available from the Noakes Foundation.

The following is my commentary, a reconstruction, written from my own notes, and may not be entirely as accurate as I (or Dr Noakes) would like.


The Diet - Cholesterol - Heart Hypothesis

The following is my commentary, a reconstruction, written from my own notes, and may not be entirely as accurate as I (or Dr Noakes) would like.

Video eleven, thirteen and fourteen

There are two theories about the cause of heart disease. Today I believe they are both wrong, but support for these ideas remains common.

The Diet Heart Hypothesis: This is a old idea often attributed to Ancel Keys. In 1953 Keys made the assertion that saturated fats caused heart disease and produced "evidence" to support his case in the form of The 6 Country Study. The hypothesis says that what you eat, especially saturated fat, clogs your arteries and causes heart disease. The idea is easy to understand and was widely supported without any scientific effort to see if it's a valid concept.

The Lipid Hypothesis:

This is a separate by related idea, and they are often confused. The idea is that a lipid called cholesterol causes heart disease. This theory came about because in the examination of heart attack victims blood vessels, under an electron microscope, it's easy to see that there is a lot of cholesterol present. Once again this idea was widely accepted. More-so because it was argued that dietary saturated fats would increase blood cholesterol.

And there were paradoxes:
Finland and Israel - have low fat diets and very high heart attack rates.
Sweden, Norway and France - have high fat diets and a low incidence of heart disease.

20 years later it was revealed that there were 22 countries that Keys had data for, and if you included them all, the relationship between dietary fat and heart disease vanished. Using the same data John Yudkin found a better relationship with sugar consumption.

Yudkin was strongly attacked by the sugar industry and his university and professional colleagues abandoned him. This is the power of industry to control the agenda. There's no doubt now that Yudkin was right, but his work was avoided, it became "information we choose not to know."

Dr Noakes believes that this model is wrong

There are five typical types of heart attack.
Sudden death, which is unusual
Myocardial Ischaemia - caused by reduced blood flow and lack of oxygen
Coronary Thrombosis - caused by obstructed blood flow usually from atherosclerosis breakdown
Acute Myocardial Infarction - sudden deprivation of circulating blood damaging heart muscle tissue
and Ventricular Arryhythmias - abnormal rapid heart rhythms starting in the lower chambers of the heart.

Are they all "caused" be the same thing? Your diet, lack of exercise, or high blood cholesterol? Something else?

A prediction of future Heart disease?

There have been many attempts to explore these issues, particularly important is the long running Framingham Heart Study. They began with 5000 participants, in families, and initially they showed that both high cholesterol and high blood pressure were related to cardiovascular disease. They are now working with the third generation of these families.

At first it seemed that total cholesterol would be an excellent predictor of future heart disease. In the diagram there is almost no overlap between those likely to have heart attacks and those who seem to be protected.

Graph

But 30 years later one of the study leaders William Costelli reported: "Most of what we know about the effects of diet factors, particularly the saturation of fat and cholesterol, on blood lipid parameters derives from ward type studies. Alas such findings ... have been disappointing. Indeed the findings have been contradictory."

"For instance in the Framingham Study; the more saturated fat people ate, the more cholesterol they ate, and the more calories they ate, the lower was their serum (blood) cholesterol."

"We discovered that by themselves total cholesterol levels were useless for predicting the risk of heart disease."

"After the age of 50 there is no increased mortality with either high or low serum cholesterol." ... "Between 51 and 65 there is an association between falling cholesterol and the risk of mortality in the next 18 years." .. "But beyond 65 higher cholesterol seem to be protective, reducing both the rate of heart diseases and the rate of cancer."

So he's telling us they have a lot of data about cholesterol and it makes no sense. So the obvious thing is that there is no relationship between cholesterol and heart disease at all. (Maybe a long false trail.)

Cholesterol is a lipid - a fat - and it's not water soluble so in the blood it's contained in a lipo-protein. We should not speak of the two types of cholesterol, HDL-C and LDL-C as good and bad cholesterol. We think HDL-C is protective and LDL-C is probably harmless. It's possible that small dense particles in LDL-C are damaging, we can't be sure.

Norway has a very healthy population. Norwegian data shows no relationship between cholesterol and cardiovascular disease.

South African insurance companies have good reasons for keeping their own data on heart attack risk. They did a study of 165,000 people, and their data also shows no relationship to cholesterol. If you just look at the statistics for the 46-55 group there appears to be a relationship indication that higher cholesterol is a risk factor, but in the 56+ group that apparent trend is gone. Cholesterol is meaningless as a risk factor.

There are three significant risk factors for heart disease; diabetes, age and smoking. Blood pressure comes in a poor fourth.

Diabetes is a generalised vascular disease caused by damaged glucose metabolism. The problem is excess insulin in the blood stream for long periods, causing inflammation. Insulin resistance develops, but it's hard to test for that. I believe the Framingham study points to two reliable indicators of insulin resistance, low HDL-C and high triglyceride's. High fat diets produce high HDL-C and low triglyceride's, and that's desirable.

Ongoing Controversy

The title for this 2012 debate at the University of Cape Town, is That Cholesterol is not an important risk factor for heart disease, and the current dietary recommendations do more harm than good. This is the university trying to get important public health messages into the public mind. It's been known for 20 years that cholesterol is not an important risk factor for heart disease, although some question mark remains over small dense particles in LDL cholesterol. People should know that. People only need to look at the statistics for obesity and diabetes, to understand that there is a problem with the dietary recommendations too. Public interest should be in what way those recommendations are misleading.

Genetic Adaptation

Video Ten

Generally genetic adaptations occur randomly and change is slow. We still have the same basic digestive system we developed 150,000 ago. That's why some people can't eat gluten. And why some people are intolerant of wheat. Natural selection acts on random genetic variation to "choose" the ones best adapted. But this basic human metabolism was lactose intolerant after weaning.

Today 90% of people of European extraction, can digest lactose without difficulty. That was not always so. In Europe some 5000 years ago there was severe famine, or warfare, the food supply was severely constrained. The milk from cows became essential food. Those who were by some good fortune better able to digest lactose were advantaged. This caused a rapid change in the genetic pool towards people who were able to drink milk.

People of African, Asian or Mediterranean descent, may not be able to digest lactose at all.

"Epigenetic" effects on the mother, change the gene expression of the child by creating heritable changes in gene expression that are not mediated by alterations in the DNA sequence. A mother who is starving might alter the gene expression in her child to expect and cope with a lack of food. But also to fatten very quickly when good food is available.

It's known that the diet of mothers to be influences the child. It's thought that the experience of the mother to be might also affect the child. We know that the child of a type 2 diabetic women, is more likely to develop type 2 diabetes.

Observational Studies and Associations

Video Twelve

It's very difficult to study nutrition in a scientific way. Nutrition is slow acting. People always know what they are eating, so you can't do blind studies on diet. You can't force people to eat a special diet, certainly not for long periods of time. In some cases we're interested in what happens over 20 or 30 years like in the development of my diabetes. A clinical study like that is not possible

So most or what we claim to know about nutrition science is based on observational studies. Records of the dietary habits of a group of people are kept. These are usually self reported, reconstructions of "what I ate today" or yesterday. Often this might be a "recorded diet" for a week, plus a self report on work, exercise and general health; taken once a year, or once every two years, and kept for a long time.

When these records are evaluated for patterns one might observe how diets have changed, and how diet, exercise of work, might be connected to health outcomes.

If patterns can be revealed, these are "associations" in the data; they don't demonstrate a cause and effect relationship. Associations need to be tested in a clinical way to make that sort of finding. Usually that's not possible.

In the case of smoking there is a very clear association between smoking rates and heart disease, but it took a long time for that relationship to reveal itself. And then it still had to be clinically tested to prove that the association did in fact reveal something important.

So with diets, smoking, drug use, and other lifestyle influences, it's not possible to do the sort of clinical testing that routine when evaluation a pharmaceutical product.

Red Divider Line

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