A couple of weeks back one of my blog posts highlighted a study from England in the UK which found that total cholesterol levels had no relationship with risk of death from heart disease. Moreover, higher cholesterol levels were associated with a reduced risk of stroke. Such findings obviously ask serious questions about the concept that cholesterol causes things like heart attacks and strokes. It also casts considerable doubt on the idea that we should be attempting to drive our cholesterol down.
Currently in the UK, as in some other countries, we are advised to ensure our total cholesterol levels are less than 5.0 mmol/l (193 mg/dl). I’ve lost count of the number of fit, healthy individuals with no hint of illness who have told me they have a ‘raised’ cholesterol. Average cholesterol levels in adults in the UK are about 6.0 mmol/l. This means that significantly more than half adults have ‘raised’ cholesterol.
Remember, cholesterol is an essential body constituent: it is a component in the membranes of all cells, and a constituent of key hormones (e.g. testosterone, oestrogen and cortisol) and vitamin D. It is also an important component of the brain and nervous system. Does it seem right that an essential body constituent present a normal levels in the body somehow poses dire risks to health?
Well, not according to the study I wrote about a couple of week’s back, and not according to another study I am going to highlight here.
This particular study was conducted in Norway. It assessed more than 52,000 Norwegians over a 10-year period [1]. Part of the study was to assess the relationship between total cholesterol levels and risk of death from cardiovascular disease (mainly heart attacks and strokes) and death from heart disease alone. Norway also uses 5.0 as their cholesterol cut-off. Risk of death in different cholesterol bands was assessed, the lowest band being levels of less than 5.0 mmol/l, while the highest band was levels of 7.0 mmol or more.
In both men and women, there was simply no relationship between cholesterol levels and risk of death from these things. Individuals with cholesterol levels of 7.0 mmol/or more were no more likely to die from cardiovascular disease than those with cholesterol levels less than 5.0 mmol/l.
These results are interesting, but the researchers went further by assessing the relationship between cholesterol levels and overall risk of death (overall mortality). This is important here because low cholesterol levels are actually associated with an increased risk of certain conditions including cancer and a type of stroke known as ‘haemorrhagic stroke’.
In the Norwegian study, overall risk of death was not any higher in men with cholesterol levels of 7.0 mmol/l or higher than in individuals with levels of less than 5.0 mmol/. Actually, the lowest risk of death in men was seen in individuals with cholesterol levels in the 5.0 – 5.9 mmol/l. In this group, overall risk of death was actually 23 per cent lower than in men with the lowest cholesterol levels.
In women, the results were somewhat different: the higher the cholesterol level was, the lower the overall risk of death. However, this finding only became statistically significant in the category of cholesterol levels of 7.0 mmol or higher. Compared to women with cholesterol levels less than 5.0 mmol/l, the women with the highest cholesterol levels were 28 per cent less likely to die overall.
One thing this study reminds us is that, generally speaking, it makes sense to assess the relationship between cholesterol (or any other factor) and overall risk of death rather than individual conditions. It should also remind us that having a cholesterol level above 5.0 mmol/l is not a cause for concern, and may in fact be a cause of celebration.
References:
1. Petursson H, et al. Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study. J Eval Clin Pract. 25 Sept 2011 [Epub ahead of print]
The word needs spreading that the reference ranges for cholesterol and other NHS tests are created by those with a vested interest in selling drugs.
I shall go and fry my breakfast now – All power to the sausage!
G Bottomley
“All power to the sausage”
Yes, and may the sauce be with you 😉
I have been studying all sorts of reports coming out all the time about these kind of results. I have familial Cholesterolemia and at the moment my levels are approacing 10. I have had to make the decision to not take lowering cholesterol drugs. My Lipid specialist is not happy, but I have weighed it all up and becasue of ill effects from drugs, have decided to not take them. There are numerous books on the subject incl Malcom Kendricks The Great Cholesterol Con and Uffe Ravnskovs Ignore the Obvious. It seems that these men were pioneers in the subject, and now studies such as this Norwegion one are catching up. Its Good!
Eggsactly!
Why, why, why, given this overwhelming research on cholesterol levels and mortality, has the Danish government recently brought in a tax on saturated fat? And now, I understand that the UK government wants to follow suit.
I READ A REPORT SOMETIME AGO THAT STATED OVER 50% OF PEOPLE ADMITTED TO HOSPITAlS FOR HEART PROBLEMS OR HEART ATTACKS HAD NORMAL CHOLESTEROL READINGS OR LEVELS.
Two questions, John. Firstly, since these results are so clear-cut, how come we’ve been led to believe for so long that the opposite was true ?
Secondly, I’m surprised no mention was made of levels of so-called “good” and “bad” cholesterol. Are they not relevant ?
(Meanwhile, I thrive on two eggs a day, and intend to continue doing so.)
I have been having statins for the past 10 yrs with dieting with no effect at all .My range was 7 but in the past 6 months I read that chillis lower cholesterol and blood pressure .I have just done my tests,where 2 days before I ate a buffet of mussels,shrimps and sweets and an icecream everyday since it is summer and my cholesterol went down to 6 and my HDL rose so CHILLI really works if you manage to shred it fresh better than the prcessed one,GOOD LUCK By the way it is also good for metabolism to put down your weight.
I remember marching into see the GP (can’t say “my doctor” – just the one available) and opened with the phrase “don’t ever try prescribing me statins. I’ve read the research.” He was quite taken aback and mumbled something like “so have I”. Couldn’t quote me anything, though.
Everybody I know who’s been prescribed them has found the side-effects daunting.
Good article, DB, though jokes pretty dire. :o)
I know two women in their mid eighties who have cholesterol levels of over 7 and 10. They both look 20 years younger and are fit and healthy. One was on statins but found it was badly affecting her memory and caused muscle pains, as it did with me-Tony
may I re-ask the key question: In good faith, how is it that for so long the opposite view of the relationship between Cholesterol and CHD has been the guiding principle? Surely this was led by credible studies? I am cautious about defaulting to drug company conspiracy theories. There are simply too many credible medical professionals out there to counter a deceit of this extent. Please help me with this confusion.
“…the women with the highest cholesterol levels were 28 per cent less likely to die overall.”
Surely “less likely to die of CVD overall…” – as far as I know death is inevitable 🙂
my cholesterol readings were always about 6.3, but having had a stroke two years ago, the doc put me on statins – which didnt agree with me, nasty side effects. So now I take an older remedy, Lipantil. It has brought my level down to 4.3, but now Im wondering if I really need to take it? It would be one less tablet to remember!
Emma
“as far as I know death is inevitable”
Err, no Emma, not over a finite period of time as made clear in the blog post here “It assessed more than 52,000 Norwegians over a 10-year period…”
Andre
This is a complex issue. A lot of the problem has been down to selective quoting or misquoting of the evidence, and a lack of desire to embrace the stack of evidence that does not support the cholesterol hypothesis.
Some of this is unwitting (arising from, say, cognitive dissonance), and some of it appears to be a concerted effort by industry (drug and food companies, mainly), to establish and maintain the theory. We even have doctors being remunerated by their governments for getting cholesterol levels down.
Many of the key opinion leaders in the area are conflicted in terms of professional reputation and/or income which depends on support for the cholesterol hypothesis. My sense is that, in this area, true objectivity is hard to find.
I’m always heartened by these sorts of studies, but I have yet to encounter one that calms my concern over my own high total cholesterol level, which is 355 (U.S.) or 9.2 mmol. All other markers (trigyceride, etc) are considered good by my doctor. I’ve followed a low carb diet for many years so I believe I my eating habits are what they should be. Can you point me to such a study or to any research material that addresses level this high?
The information in this blog is misleading and poorly written. I am a cardiologist and know the effects of cholesterol on diet. This blog and the study both look at total cholesterol and not at whether the individuals had high HDL or LDL. The ratio of HDL and LDL cholesterol is important as this is what causes heart disease and CAD.
For example:
If someone had a measurement of 2 for HDL and 5 for LDL that gives their total to 7. But this is healthy because their HDL is ‘good cholesterol’ an d their LDL is 5 which is low enough to be considered healthy.
Similarly if someone had 2 HDL but 3 LDL they have a total cholesterol of 5. They are still as healthy as the previous example (the one with 7) as they both have high HDL and average or low LDL.
This study does not look at either HDL or LDL content which means its a false study that is not informing the public of the real problems associated with cholesterol.
On another note to reply to some of the comments, statins are scientifically proven to help lower LDL by increasing HDL content, but they do have side affects. A better way would be to increase your omega oils intake and change your diet. By increasing your HDL content you will automatically lower your LDL content. Simple.
Fiona
I make it clear in the blog that many health professionals and official guidelines encourage getting total cholesterol levels down to below 5.0 mmol/l, and the point of the blog was to provide evidence that this is not necessarily scientifically tenable. I’m sorry if this point was lost on you.
But if this is the case, then just as invalid are the official recommendations regarding total cholesterol (which was the point of the blog). As a cardiologist are you happy to go on record to say we’ve got our recommendations of total cholesterol wrong, and would you like to include declare your full name?
Your calculations re total/LDL/HDL cholesterol are wrong, but the way.
Here’s the conventional wisdom on this:
total cholesterol = HDL + LDL + (triglycerides/5)
So, total cholesterol is not simply the sum of HDL and LDL as you state.
I’ve found that a lot of people who read this site know better than to concern themselves with the effect of statins on cholesterol. They realise that the only really important thing is the impact of statins (and other drugs) on health. Though I appreciate this crucial distinction can be lost on some people.
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I agree with the cardio doctor—it is NOT TOTAL cholesterol that matters but the HDL. When I increased my HDL above 60 with exercise, more fish and fish oil & walnuts–I saw big improvements in my memory—senior moments ceased. What is good for the heart is good for the brain.
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Thoughts on the importance of being able to distinguish a lipoprotein from cholesterol
Hello Roy, hi Fiona,
I am not out to dispute your experience, Roy, that the alterations to diet and lifestyle may have raised the quality of your life experience – I would tend to endorse them (in a non-qualified way). And in agreement .. ..
Improved HDL counts may well associate with the benefits you describe. But ..
The benefits you describe could be/also-be the result of other changes (in the business they call these ‘confounding factors’) and not just the HDL. Plus .. ..
In mentioning HDL and cholesterol in the same breath you are confusing ‘high-density lipoprotein’ (HDL) with cholesterol. This is a bit like referring to a ‘passenger’ as a ‘taxi.’ Cholesterol is not a lipoprotein; and lipoproteins are not cholesterol. Cholesterol (and other fatty substances that dislike water) can be found riding in lipoproteins – cos lipoproteins are tasked with ferrying aqua-phobes around the body in the blood. Cholesterol is a passenger in HDL. So everybody, – and Fiona .. ..
Cholesterol is invariable, so far as we know, it only comes in one formula and one physical form. Lipoproteins are composite bodies whose ‘shell’ includes proteins, phospholipids, and triglicerides, and whose ‘passengers’ include cholesterol and fat soluble vitamins. The sizes, or densities, of lipoproteins can vary and no doubt they do so as a result of subtle alterations to their composition. Therefore .. ..
If cholesterol is present in lipoproteins of different densities the cholesterol is the same cholesterol in each: The lipoprotein is the variable and not the cholesterol. Hence .. ..
What has come to be regarded as the diet-heart hypothesis’s greatest asset is additional evidence that the cholesterol component (cholesterol hypothesis) of the diet-heart ‘made up phenomena’ is utter bunkum. (My instinct suggested a courser term!) This HDL / LDL ratio may well have substance that could tell us something, but unless Fiona can bring some highly pivotal explanation to bear, what the HDL-LDL analysis tells me is that cholesterol cannot be the active or pertinent variable in heart disease because the same cholesterol sits in LDL as sits in HDL. Furthermore .. ..
The HDL/LDL ratio was a late refinement to a hypothesis that was not stacking up very well because total cholesterol is a poor surrogate to use in the prediction of heart disease. 75% or persons admitted following a heart attack have ‘normal’ cholesterol. Whether the revision is helpful or otherwise is not in dispute, but the revision to the cholesterol hypothesis actually constitutes a transition to a lipoprotein hypothesis that GPs and cardiologists seem to have failed to have noticed and continue blithely on. The lipoprotein hypothesis casts the greatest aspersions yet upon the cholesterol hypothesis because the lipoprotein (or something about its’ composition), and not the cholesterol, is demonstrably the variable that may associate with increased risk of heart disease.
The cholesterol hypothesis only ever determined cholesterol was present at the scene of the crime, and finding evidence to prove involvement in the crime has remained elusive for 150 years. 100 years ago a re-enactment of the alleged crime involving the feeding of cholesterol to rabbits was misleading, because the cholesterol may not have been ‘pure’, and therefore consequences of feeding ‘oxy-cholesterols’ to rabbits were falsely attributed to ‘cholesterol’ – an understandable and forgiveable mistake 100 or so years ago. In the post-war era Ancel Keys delivered evidence to the ‘cholesterol court and contributed highly selective and misleading evidence upon saturated fats. The diet-heart hypothesis and bandwagon connecting saturated fat consumption with cholesterol and thence to heart disease, was born. Simple, elegant, comprehensible, and its’ only failing so far as I can see is that it is wrong. Its’ greatest virtue is that it has become highly lucrative.
To fail to acknowledge that the cholesterol hypothesis has made the significant transition to lipoprotein hypothesis is nothing short of criminal. The sad part is that so many persons are accessories to this crime. If the transition and its’ implications were adopted it would remove the wheels from the cholesterol bandwagon. People who owe their living to this bandwagon would be reluctant to do that.
Cholesterol can have no more than a passive role in the crime of causing death by heart disease. Yet enthusiasm for down-managing cholesterol is rife. What’s being overlooked is that managing cholesterol is doing nothing positive for total mortality, while the mass prescription of statins must do inevitable harm because statins interfere with the biosynthesis of several vital biochemicals and not just the vital cholesterol.
Fiona, I am sure, is pleasant and personable, and she would remain pleasant and personable if she were to take a ride in a taxi. For the sake of character assassination I am going to suggest Fiona the cardiologist, trained and tutored to save lives, becomes a crazed killer when she steps out of a taxi and into a minibus. That’s preposterous !! Yes it is preposterous, and it is as preposterous as the idea that cholesterol transported in HDL can be ‘good’, while the same and identical cholesterol being conveyed in LDL can be ‘bad’: The character assassination of cholesterol is just as unjust. Fiona, are you, or have you ever been, a crazed killer? I thought not.
Muammar Gaddafi’s dead body resides in a commercial freezer after an uprising triggered by his tyrannical elitist and oppressive rule that was not promotional of, and did not preserve, satisfactory levels of ‘economic democracy’. His actions and directions are said to have resulted not just in misery but also directly in many deaths. [I’ll risk sounding more radical than I intend to be earnest and pragmatic. ..] The false diet-heart hypothesis and the misguided war on cholesterol, plus the markets that trade off it, does for ‘economic democracy’ in the west what a deranged dictator did for ‘economic democracy’ in an Arab land. When considered in the harshest of lights the fallacious diet heart hypothesis may have resulted in the premature deaths of more persons than did the rule of Gaddafi. Certainly the misguided war on cholesterol is deleterious to the quality of life of persons directed to an unjustified regime of cholesterol control by statin prescription. The primary difference is Libyan nationals came to realise they were being ripped off, but equipped with the right conceptual tools the similarities between different but nonetheless oppressive regimes are striking. Proponents of the diet-heart hypothesis, and those that make a living from it, get to live, not in palaces, but in the bigger houses placed in the better neighbourhoods.
Fiona, if you became vocally cholesterol sceptic overnight, what would it do for your career prospects as a cardiologist?
Dr Briffa sets out to inform, not mislead, and he attains high standards. Sometimes those standards are a leap that others find difficult, or inexpedient, to make.
A cardiologist ought to know cholesterol has no impact upon diet. It has been said diet has no impact upon cholesterol although this seems counter intuitive because cholesterol can be dynamic and can respond to dietary changes, moreover cholesterol is a constituent in bile, so if demand for bile increases in response say, to alterations to diet (more fat, perhaps) then one may anticipate the body may ramp up bio-synthesis of cholesterol in response to increased demand.
Do we count barrow-boys and barrows to compute the stock of bananas thus?:
Bananas = (barrow-boys * 3) + (barrows * 17) – (pears /4)
Cholesterol in the diet ought not to impact much upon serum cholesterol because dietary cholesterol meets only a portion of that which the body requires for healthy and normal function. We may typically synthesise three to four times more cholesterol than that which a typical diet may supply. And if the body can self-regulate synthesis and serum levels in line with demand then variations in dietary cholesterol will be taken into account by the bodies marvellous self regulating systems.
John, if the medical profession cannot be objective about cholesterol, and if that lack of objectivity propagates harm, perhaps the cholesterol issue should be reviewed by the judiciary?
Nobody should take my opinions as established ‘fact’, cos my only qualification is a vocational driving licence, (I work in distribution – which may contribute to understand the task of a lipoprotein 🙂 ) but (PLEASE!,) am I missing something momentous that would make this apparent bunkum hold water?
I would like to comment on the enthusiasm for sausages. I agree the fat content is good. However, most sausages contain about 40% wheat which is not good and are preserved with nitrates which are even worse. Nitrates do their damage through a massive increase in exogenous AGEs. I recently found wheat free, nitrate free sausages on the internet and they are delicious. The nitrate free bacon was good too.
.. ..Then only permit yourself to devolve power to sausages of satisfactory quality by electing not to buy inferior ones !!
Jessh Chris, you leave me breathless! BUT! Suddenly I feel I understand the difference between a lipoprotein and cholesterol and reckon the difference is important. How did you figure it?
Can someone explain this for me, please. I am a vegetarian and my Husband is a meat eater.
On a resent health check my cholesterol was found to be high 6.9 – HDL =1.0 Glucose = 5.0 – What has glucose got to do with it? No mention of LDL! Everything else was normal and I was given a green light.
On the other hand my husband’s level was 5.2 – HDL =1.6 Glucose = 4.4! He is over weight so was given an orange light for BMI.
This time we didn’t have to fast and the blood was taken by a prick in the finger then measured by computer so the nurse received the results straight away. I had eaten lunch my husband hadn’t!