Last year saw the Japan Society for Lipid Nutrition hold its 20th annual meeting. A panel discussion during the event was held entitled ‘Rethinking Cholesterol Issues’. Recently, the Journal of Lipid Nutrition published an account of that panel discussion [1], and it makes for interesting reading.
The panel was made up of six experts from both sides of the debate: some who believe in the supposed dangers of cholesterol and the need to lower ‘raised levels’, as well as those who doubt the wisdom of and evidence-base for these assertions.
Part of the conventional view came from an expert who quoted data from the so-called ‘Framingham Study’, which found links between higher cholesterol levels and increased risk of heart disease. However, this data revealed that beyond the age of 50, ‘raised’ cholesterol is not associated with an increase in the overall risk of death (the best overall marker of health). Plus, The Framingham data revealed that cholesterol levels falling over time was associated with an increased of dying from cardiovascular disease (such as heart attack and stroke).
The case for the hazardous nature of cholesterol was also supported with evidence in the form of statin trials (statins reduce cholesterol and reduce the risk of cardiovascular disease). However, this evidence is on shaky ground indeed, because statins don’t just reduce cholesterol, but have several mechanisms of action (including anti-inflammatory effects) that might reduce the risk of cardiovascular disease. This means that statins beneficial effects might have nothing to do with their impact on cholesterol.
In fact, there’s some evidence to support this idea in the form of studies which show, for instance, that statins can reduce risk of cardiovascular disease in individuals with normal or low levels of cholesterol, as well as the fact the statins significantly reduce stroke risk despite the fact that cholesterol is a weak risk factor for stroke, if a risk factor at all.
Against this, I think the case against the traditional cholesterol hypothesis was put much more robustly. Experts, for instance, cited evidence which shows that in most Japanese studies, lowest overall risk of death was seen in those with higher levels of total cholesterol or (supposedly unhealthy) LDL-cholesterol.
Those arguing against the cholesterol hypothesis also point out that the impact of statins on overall risk of death is small, if it exists at all. It should be noted, I think, that in individuals with no previous history of cardiovascular disease (a group that makes up the vast majority of people taking statins), statins do not reduce overall risk of death.
The dissenters also draw our attention to the fact that up to the mid-noughties, published literature on statins was overwhelmingly positive, with study after study lauding the ‘benefits’ of these drugs. Since then, the evidence has been overwhelming negative. It is perhaps not a coincidence that in 2005–2006 European legislation came into play which required clinical trial results to be published even if the data were ‘not favorable’. In other words, drug companies could not now so easily bury unfortunate data and selectively publish the stuff that supported their products. The authors of the summary of this paper state: “…the results published before the regulation were questionable and should not be used as the basis for recommendations for treatment with cholesterol-lowering medications.”
It is interesting to note that the Japan Atherosclerosis Society (an organization which takes a conventional view on cholesterol) was invited to send experts to participate in the panel, but declined to do so. I wonder if members of the Society know more that they’re letting on.
References:
1. Rethinking Cholesterol Issues – Summary of the Cholesterol Panel Discussion at the 20th Annual Meeting of the Japan Society for Lipid Nutrition 2011. J Lipid Nutr 2012;21(1):67-75
For me, this is very timely. Yesterday my workplace offered a free cholesterol screening and fasted blood glucose test. I decided to do it because I feel the healthiest I ever have due to eating well (no grains, low carb), intermittent fasting, and really dialing in my workouts–not that I’ve ever really been out of shape. I haven’t been to a doctor in years, so I thought I’d give it a go.
I won’t go into too much detail, but the person who went over my results with me implied that if I didn’t stop eating fatty meat, I’d soon be in the hospital from a heart attack. My triglycerides were low, and my HDL levels were normal, but my LDL was slightly high. He gave me grave warnings and advice. My experience was that they suddenly had transformed me from a very healthy and fit person into someone close to a medical emergency. Amazing.
Thank you for your articles. I’ve been following your newsletter for a while and I appreciate the thought and hard work that you put into them.
This is a very interesting development. Why haven’t other cholesterol-skeptical bloggers picked up on this 2011 event?
One of the more interesting things I’ve read recently on cholesterol comes from Thomas Dayspring MD, who posits the view that it is the number of LDL particles and their ability to attach to the arterial wall that causes problems and not the presence of LDL in the blood. There is an interesting video of him with Gary Taubes at http://www.youtube.com/watch?v=hRoxvI1p1Bc.
great quote from the Youtube clip (above): “we must have done the studies (the studies that keep questioning the cholesterol hypothesis) wrong because we know we’re right!” ( this is the response suggested to all the conflicting evidence about cholesterol!). How true!
Whenever it was that living organisms evolved the ability to synthesise cholesterol it marked a notable transition point in the evolution of the tree of life.
Cholesterol is found in the tissues of the eukaryotes. Accordingly cholesterol is found in the tissues of the creatures that populate one sizeable portion of the tree of diversity while being markedly absent from another portion. Cholesterol seems to make possible higher orders of life that include creatures that have some cognitive awareness of their surroundings and some measure of accomplishment in their ability to navigate those surroundings. On the other hand the absence of cholesterol and the presence of simple ‘sterols’ seems to mark species down for a life of being largely immobile (rooted to the spot) and ‘vegetative’.
I’m not so up on these affairs as I would like to be but the absence or presence of cholesterol seems to markedly distinguish one huge aspect of the tree of life from another. Perhaps someone will pass by and put a date upon the emergence of the eukaryotes; it must go some way back and pre-date the now extinct Dr Ancel Keys by some order of magnitude. (Dr Keys was the !**! who fraudulently suggested cholesterol caused atherosclerosis and saturated fats caused high cholesterol – neither of which is authentic and neither of which has been shown to be true.) It seems implausible (to me) that a substance that clearly creates such huge evolutionary opportunities for the emergence of diversity over a long run of time could suddenly become responsible for a modern disease in a species whose alleged intelligence owes something to the presence of cholesterol in the synapses of its’ brain.
Lipoproteins are equally marvellous and intriguing.
The blurring of the distinctions between cholesterol and lipoproteins ought to be recognised by statute as a capital offence. Lipoproteins are not cholesterol and cholesterol is not a lipoprotein. Furthermore the nomenclature we assign to lipoproteins is rather arbitrary when compared to what they are, what they do, and how they operate. How many colours of the rainbow are there? Seven? NO! There are many more because rainbow reflects the full spectrum of light which includes transitional hues between the arbitrary components (R-O-Y-G-B-I-V) we use to describe the sequence of colour.
LDL, HDL, IDL, VLDL, are arbitrary terms that describe sizes of lipoproteins whose sizes really range over a spectrum. Lipoproteins are a slick solution (ingenious) to a natural challenge; how do you transport important fats and fat soluble substances (lipophiles) around a network (the blood) that is lipophobic by natures’ order of design? Lipoproteins are ingenious marco-molecules that offer an aqua-philic exterior to be accepted by the network while retaining a lipophilic interior aspect in which, amongst other things, cholesterol can ride. Lipoproteins shrink in size as convey important constituents around the body. Size may have a bearing upon how and where they might ‘dock’ and discharge measures of their ‘cargo’. Again lipoproteins are such an important and consequential evolutionary advance it ought to be hard to imagine they could be responsible for modern health conditions.
There is an important principle at stake that modern dogma delights in passing over. For an outcome to favour a particular time, place or circumstance so too must it be likely that the cause of the outcome also favours that particular time, place or circumstance. Lipoproteins and cholesterol are more universal in their presence than is the outcome in question.
It is difficult to see how a quantitative concern (the number of LDL particles) could overwhelm a an important qualitative facility (the presence of LDL in the blood) to convert a favourable and functional circumstance into such a contrasting outcome. Don’t get me wrong, I wouldn’t dismiss it out of hand, but the suggestion requires a plausible explanation of a variable (probably qualitative) that can account for a variation in outcome. If Dr Dayspring or anyone, can figure and come up with the authentic explanation that permits intervention at the point of causality they might be on a winner, but the evidence suggests its easier to concoct an inauthentic explanation, pass it off as authentic, then sell cholesterol lowering marvels off the back of that.