I got a press release today from the consumer advocacy group Which? informing me that “Misleading health claims to be banned at last”.
Apparently, European Union Member States today voted to adopt a list of scientifically proven health claims that can be made about food and drink products. Claims for green tea and glucosamine (regarding benefits for blood pressure and joint health) are examples of a couple of things that did not make the cut. On the other hand, it seems the following claims will be allowed to be made:
- reduced consumption of saturated fat contributes to the maintenance of normal blood cholesterol levels
- plant sterols and plant stanols contribute to the maintenance of normal blood cholesterol
Cholesterol levels are widely recognised as a marker for heart disease, and so the logic goes that reducing cholesterol levels will help prevent this condition. In this case, cholesterol is being used as what is known as a ‘surrogate marker’. The assumption is that a positive change in surrogate marker levels will translate into benefits for health.
However, is this actually true?
Taking dietary steps to reduce cholesterol has not been convincingly shown to reduce the risk of heart disease or overall risk of death. If this practice does not have benefits for health or extend life, why bother? Eating less saturated fat and swallowing stanols and sterols can reduce cholesterol all they like, but none of it has proven benefits for health.
It is perhaps worthy of note that a PR representative of the Unilever-made Flora Proactiv products commented here that:
“We absolutely agree that simply lowering cholesterol without making wider positive changes to one’s diet and lifestyle will not make a significant positive health impact.”
I take this as admission of the general uselessness of cholesterol reduction in terms of its impact on health.
It can be hard for some to make sense that taking dietary steps to reduce cholesterol is not broadly beneficial to health. However, we should perhaps not be too surprised, when we consider that we have plenty of similar experiences regarding pharmaceutical drugs.
For example:
- drugs called resins reduce cholesterol but do not reduce overall risk of death
- the drug ezetimibe reduces cholesterol but has never been shown to benefit health
- drugs called fibrates improve the ratio of ‘good’ and ‘bad’ cholesterol but don’t reduce overall mortality
- hormone replacement therapy improves the ratio of ‘good’ and ‘bad’ cholesterol but doesn’t reduce overall mortality and increases the risk of cardiovascular disease
The situation with statin drugs is somewhat nuanced. In primary prevention (in essentially healthy individuals) statins do not reduce risk of death. In secondary prevention (those who have already had, say, a heart attack or stroke), they do, but the fact remains that even in high risk individuals, the great majority of people who take statins do not stand to benefit from them at all. There is reason to believe, by the way, that the little benefit statins have is not as a result of their cholesterol-reducing action, but due to other effects including anti-inflammatory blood-thinning actions.
In short, the fact that foods low in saturated fat and/or rich in sterols/stanols may contribute to lowered cholesterol levels is irrelevant. The idea that this translates into benefits for health is simply unproven. My advice? Don’t swallow it.
A few years ago a British doctor emphasized that the most important factor in cardio-vascular disease is the homocysteine level – if that is normal, high cholesterol and/or high blood pressure will not be as dangerous and v.v.
He went on to say that testing for homocysteine and the treatment thereof are not very expensive, as opposed to the treatment of cholesterol and blood pressure.
Just food for thought …
Raised triglycerides are the real issue. They are also an indicator of Syndrome X or Metabolic Syndrome. Recent research done by Prof. C. Von Shacky has shown how EPA from Omega 3 can reduce Triglycerides by 30%. Again it is dose dependent 2-4 grams per day. Exercise is possibly the single best way to increase your HDL. I totally agree with you that exercising on an empty tummy first thing in the morning is the most effective way to loose weight. Fat cells otherwise known as Adipocytes have powerful chemical machinery within them which has the ability to wreak havoc on other cells, tissues and organs. Get moving!
… Thank you Dr. Briffa. I wanted to ask about the saturated fat/cholesterol link. In all the studies that you have seen, is the fat raw (coconut oil, raw butter, etc) or cooked? I think this may make a difference.
Interesting as always Dr. B. I wrote an article for a friend’s site the other day in which I mentioned blood sugar balance – insulin being the key factor here. Many people believe the ‘reducing foods rich in saturated fat & cholesterol for heart health’ hype, but as we all know, most cholesterol is made in the liver. The enzyme involved in the making of cholesterol (HMG-CoA reductase) is stimulated by insulin. So would you agree that for ‘healthy’ cholesterol levels, a reducing of processed carbohydrates and sugars (and thereby ensuring healthy blood sugar balance) would be a lot more beneficial than reducing saturated fats and cholesterol rich foods? As part of a healthy diet of course 🙂
What do you mean, “benefit health”? Western medicine defines health in negative terms i.e. a person is healthy if they are NOT sick, so Western medicine doesn’t know what health is. Apparently ezetimibe is a drug that does not make you sick.
There is no such thing as bad cholesterol just bad medicine. The liver produces most of the bodies cholesterol in response to stress. I have cited more than 30 well done studies that show a very positive association between sugar and cholesterol. Lower the sugar and you lower the cholesterol, but cholesterol is not the criminal it is just the bodies band aid for treating internal injuries like damaged arteries. Lower the sugar (high GI foods and fructose) and you eliminate most of the problem.
Dr Kilmer McCully is ‘le grand fromage’ of the homocysteine theory, Barbara, and his theory implicates protein toxicity (really toxicity arising from a specific amino acid) in the absence or shortage of B class vitamins, esp. Vit. B6. His book, ‘The Homocysteine Revolution’, makes for interesting reading, both for his explanation upon homocysteine and for his knowledge upon history and events that contributed to the rise of the cholesterol hypothesis.
I am in no doubt that events that lead to the damnation of cholesterol culminating in the 1950s involved those that were not founded upon sound pretences, but I find further study of the topic frustrating and downright annoying. Common and colloquial reference that refers to lipoproteins as ‘HDL-cholesterol’ and ‘LDL-cholesterol’ is infuriating because it blurs the distinction between entirely different entities. Neither HDL nor LDL are cholesterol, albeit cholesterol may be found riding in the lipophilic core of these, and other, lipoproteins.
Then the widespread practice of referring to very-low-density lipoprotein (VLDL) and IDL as ‘triglycerides’ is just as shoddy and just as annoying.
And there are contradictions on points that ought to be clear. Some sources indicate synthesis of VLDL is exclusive to the liver, while others indicate VLDL can originate from the guts and the liver. This distinction could be important because the provenance of lipoproteins could have a bearing upon the substances being conveyed, be they endogenous or exogenous (dietary in origin), and be they influenced as a factor of cyclical staging or certain conditions.
A triglycride is an amalgam of three fatty acid molecules bound by a molecule of glycerol at one end, and the triglcerides then go on to form an alliance with phospholipids and proteins to become the basis of the shell of a lipoprotein. The lipoprotein is outwardly hydrophilic while being inwardly lipophilic, providing a haven for hydrophobes, like cholesterol and fat soluble vitamins and a suitable vehicle for transportation. So calling VLDL and IDL ‘triglycerides’ gets my goat. In addition to performing other functions lipoproteins, esp. VLDL, could be acting as a short-term buffer managing reserves of things, fatty acids for eg., not needed for immediate use. Getting hung up on the numbers associated with VLDL, aka ‘triglycerides’, may not be impertinent, but pertinence could be limited.
Then, Gaye, appealing as it may seem dosing up on omega-3 may not be so wise as it is often suggested. Chris Masterjohn (link to site) discusses the view that quantitative regard for lipoproteins may be unhelpful, as there are qualitative distinctions that may arise that could be causative. Size of LDL can vary in response to conditions, apparently, and the ‘reactivity’ of lipoproteins, and their ability to contribute to inflammation, can alter if the lipoprotein suffers oxidative stress. Chris Masterjohn comes down on surplus PUFAs, omega-6 and omega-3 EFAs, as placing the lipoproteins under oxidative stress. He advocates that supply of EFAs should not greatly exceed the threshold that satisfies minimum requirements. He has a detailed paper on the subject, available upon payment of a fee.
Dr Briffa, with so much contradictory information about it is hard to know where the truth lies. Causation could arise in association with a number of factors but there are some clues that causative variables connected with lipoproteins are qualitative by nature and not just a factor of lipoprotein, or LDL, counts. One big clue, I think is that when monkeys and rabbits were fed ‘pure’ cholesterol added to their chow the results were largely innocuous, but when monkeys and rabbits were fed oxy-cholesterols the researchers found atheromas and arteriosclerosis had been promoted. I think regard for the numbers has been overcooked.