In the UK and Europe generally, it is recommended that levels of cholesterol in the blood should not be above 5.0 mmol/l (= about 190 mg/dl). We are given the impression that having levels above this puts us at increased risk of heart disease – a major ‘killer’. However, if this is true, it does not tell the whole story. Because while having a ‘raised’ cholesterol may be associated with an increased risk of heart disease, it might also be associated with a reduced risk of other conditions.
It is known, for instance, that higher levels of cholesterol are associated with a reduced risk of cancer. And even last week I wrote about some research which suggests that putting downward pressure on cholesterol levels increases the risk of death due to suicide, accidents and violence.
For these reasons, when assessing the relationship between any lifestyle factor and health, it pays to take as wider a view as possible. This is best done by focusing on the relationship the factor has with overall risk of death.
Such a study published recently in the Scandinavian Journal of Health Care makes for some interesting reading, I think [1]. Here, researchers assessed the levels of cholesterol and risk of death in almost 120,000 adults living in Denmark.
The researchers found that having higher than recommended levels of total cholesterol was associated with a reduced risk of death. For instance, in men aged 60-70, compared with those of total cholesterol levels of less than 5.0 mmol/l, those with total cholesterol levels of 5.00-5.99 had a 32 per cent reduced risk of death. For those with levels 6.0-7.99 mmol/l, risk of death was 33 per cent lower. Even in individuals with levels with 8.00 mmol/l and above, risk of death was no higher than it was for those with levels less than 5.0 mmol/l.
The results were similar for women too. In women aged 60-70, levels of 5.0-5.99 and 6.0-7.99 were associated with a 43 and 41 per cent reduced risk of death respectively.
In individuals aged 70 and over, the results were similar, except here, levels of total cholesterol of 8.00 mmol/l or more were associated with a reduced risk of death too (in both men and women).
Cholesterol in the blood stream is made up of two main types: LDL-cholesterol and HDL-cholesterol, dubbed ‘bad’ and ‘good’ cholesterol respectively. In this study, higher levels of LDL-cholesterol (above 2.5 mmol/l) were consistently associated with a reduced risk of death, irrespective or age or sex.
Together, these findings suggest that the current total cholesterol and LDL recommendations advised by doctors and other health professionals are way off beam. The authors of this study concluded that: “These associations indicate that high lipoprotein levels do not seem to be definitely harmful in the general population.”
Some have suggested that low cholesterol is a marker for ‘frailty’ in the elderly. However, this concept is contradicted by evidence finding that the association between low cholesterol levels and enhanced risk of mortality occurs in younger individuals too [2].
It has also been suggested the relationship between low cholesterol and enhanced risk of mortality is the result of ‘reverse causality’ i.e. that chronic conditions such as cancer can cause lowered cholesterol, rather than the other way round (sometimes referred to as ‘Iribarren’s hypothesis’).
However, evidence refuting this concept comes in the form of a long-term study which found that individuals with a low serum cholesterol maintained over a 20-year period had the worst outlook in terms of overall risk of death [3]. The authors of this study write: “Our present analysis suggests that this [Iribarren’s] hypothesis is implausible and is unlikely to account for the adverse effects of low cholesterol levels over twenty years.”
In the Danish study, the relationship between blood fats known as triglycerides and risk of death was also assessed. In women aged 50-60, higher triglyceride levels were consistently found to be associated with increased risk of death. This was somewhat true for women aged 60-70.
This does not mean that higher triglyceride levels cause heart disease – only that these two things are associated with each other. However, the major driver of triglyceride levels is dietary carbohydrate. And previous studies have found that swapping certain carbohydrates for fat in the diet is associated with an increased risk of cardiovascular disease [4,5].
All-in-all, I’d say this research should cause us to pause before recommending individuals aspire to current cholesterol recommendations. And, I think, we should be particularly wary about recommending that people adopt a lower-fat diet richer in carbohydrate to achieve these goals. There is at least some evidence which suggests that this is likely to do more harm than good.
References:
1. Association of lipoprotein levels with mortality in subjects aged 50 + without previous diabetes or cardiovascular disease: A population-based register study. Scandinavian Journal of Primary Health Care 2013;31(3):172-180
2. Ulmer H, et al. Why Eve is not Adam: prospective follow-up in 149650 women and men of cholesterol and other risk factors related to cardiovascular and all-cause mortality. J Womens Health 2004;13(1):41-53
3. Schatz IJ, et al. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program: a cohort study. Lancet 2001;358(9279):351-5
4. Jakobsen MU, et al. Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. Am J Clin Nutr 2010;91(6):1764-8
5. Jakobsen MU, et al. Major types of dietary fat and risk of coronary heart disease: a pooled analysis of 11 cohort studies. Am J Clin Nutr 2009;89(5):1425-32
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Interesting point from the study “However, cholesterol-lowering treatment in the form of statins provides a survival benefit without correlation to cholesterol level.”
The dictinction between good and bad cholesterol should be revised. LDL is part of the immune system. That’s why it is found in arteries, where it tries to heal inflammation.
The real bad cholesterol is the small dense variety. This type comes from the fat that the liver makes from too much bloodsugar.
To improve the cholesterol status, cut down on carbs. Lowering all cholesterol with statines will impair the immunesystem and hence increase cancer risk.
The best way to improve cholesterol is to eat lots of fat; the saturated kind.
Although the benefit from statins is small, and the risk under-appreciated, there is some truth to that Reijo. Serum cholesterol tells you nothing about what cholesterol is doing in cells. If you eat lots of linoleic acid from recommended oils and spreads, your liver makes extra LDL receptors and your liver takes in more cholesterol; this promotes NAFLD and NASH. And these are associated with an increased risk of heart attacks. So taking statins to damp down hepatic cholesterol might make sense (were it not for the side effects). But why are people using these omega 6 PUFA oils and spreads, and eating too much carbohydrate, in the first place? Bad dietary advice given at the same time as the statins ensures that they continue to seem a little useful.
Reijo, I would like to know what these benefits are, as I expect you would too.
My mother died 20 years ago, in her late 70s, having coronary artery disease, presumably due to years of smoking from her teens to her sixties.
12 years ago my sister and brother, both in their late 50s were put on statins, and are still on them, and now in their 70s, despite discussions with their GPs. Neither have ever smoked, ever been overweight or had a cardiac event of any description. Both were prescribed statins after attending their GPs “Well Clinics”, and answering ticky-box questionaires.
10 years ago I was put on statins, following my ticky-box experience, and purely because:-
1)Mother suffered fatal cardiac event.
2) sister was already prescribed statins.
3) brother was already prescribed statins.
I protested at this revolving door approach, being cardiac-fit and post-menopausal in my mid fifties. I was not Type 2 diabetic at that time.( oh, ho! Fancy that!)
But no! Must take stains, it is imperative!
Brother forgot his statins when away from home for a weekend recently. He phoned his GP for advice, and was told he must attend A & E, or get home for his supplies.
Now then…….
Am I missing something here?
Are our GPs scaring the living daylights out of us, and just who is fuelling the over use of A & E?
I am off them for good. At 65, being literate and numerate, ( yes, docs, we can read and write, just like you), as well as fit and healthy, I am not playing their game any longer!
I agree that the studies do seem to be contradictory and it is hard sometimes to sort out what’s good and what’s bad for you. Generally, however, studies do show that higher HDL levels are associated with a lower risk of death from cardiovascular disease as you have pointed out.
Also, there are plenty of studies showing the benefits of Statins on lowering morbidity and mortality. That is. . if you can get past the side effects. About 20 – 25% have significant side effects.
I have never seen anyone who feels better on statins. People tend to be breathless and tired, if they do not develop gut and muscle problems. I’m opposed to taking any drug that doesn’t make you happier and healthier than you were before you started. Diarrhea and ulcerative colitis are statin side effects that are under-reported because attributed to other causes, whereas myositis is unusual in other contexts so easier to diagnose. And then there are the neurological syndromes.
In theory one could get the same benefits by supplementing taurine, magnesium and fish oil, or by restricting dietary cholesterol, refined carbohydrate and omega-6 oils.
John
Would it not be better to make a distinction between LDL type A (good) and LDL type B (bad)?
Yossi, I quite agree with the need to distinguish the types of LDL. as it is of great importance in our understanding of the cholesterol/statin con we have been subjected to for far too long. BUT…..Have you ever asked your GP for this info? Crickey….I did a few years back…..and it landed me in the dog house.
I suppose I ought to go ‘private’ if I desire the info. In the mean time, I will just continue as I am– eating superb, fresh foods in moderation, with mimimal CHO, and staying away from the surgery, lest I get brow beaten into returning to my bad old ways.
Jennifer
The point you raise about asking for info about LDL particle size (or number) is very relevant, and so is your point about your dietary approach and desire to stay away from bad advice.
You’re a great example of self-empowerment, to my mind.
John you mention the link of triglycerides to carbs. Can you please say a bit more?
tnx Elena
@
Dr Briffa has written about this here
High cholesterol does not cause stroke (but carbohydrate might)
Dr Briffa is also a major contributor to Jimmy Moore’s new book Cholesterol Clarity: What The HDL Is Wrong With My Numbers? [Kindle Edition] £7.50
The kindle edition has the advantage of being able to search for the terms like “Triglyceride” “carbohydrate” so you can quickly track down the experts views on their relationship.
I haven’t finished reading the book (housepainting) yet but it is very much aimed at providing a basic understanding of the cholesterol issue.
Easier said than done, this statin-avoidance 😛 My total cholesterol is high, my HDL is high and my LDL is high. I asked for the VAP test to determine whether I was truly at risk of anything…conveniently, they “didn’t do the test properly” so could not give me the results. My Triglyercides to HDL ratio was um…perfect. I also provided my doctor a copy of Dr. Malcolm Kendrick’s book, The Great Cholesterol Con. What I got in return was a demand for having my bloodwork done every 6 weeks until I was brow-beaten into taking a statin. I refused until I could not longer…he was actually holding my other medications “hostage” to my bad behavior. Now faced with incredibly high costs, since I refused to take Crestor from previous muscle problems, he gave me the choice of continuing on the high-dollar statin or to “simply change my diet to vegetarian.” What kind of choice is that. He knew I lost nearly 100 pounds on Atkins…he knew that since he demanded that I cut my fat intake that I had gained almost 30 pounds in a year. He told me to increase my exercise and when walking wasn’t doing anything (he told me to start jogging…um…at 60 years old)…
Okay…new doctor is in order, right? How do you find one that is going to be any different or better? I am so confused with what I read, what I believe and what I can accomplish. I could use a little advice here. Anybody?
Dr. Briffa…wanna start a practice in Dallas, Texas?
JUST TO SEE THE AMOUNT OF DRUG COMPANIES THAT FINANCIALLY BACKED THIS STUDY, SHOULD BE SUFFICIENT NOT TO ACCEPT RIDKER’S FINDINGS!
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein
Paul M Ridker, M.D., Eleanor Danielson, M.I.A., Francisco A.H. Fonseca, M.D., Jacques Genest, M.D., Antonio M. Gotto, Jr., M.D., John J.P. Kastelein, M.D., Wolfgang Koenig, M.D., Peter Libby, M.D., Alberto J. Lorenzatti, M.D., Jean G. MacFadyen, B.A., Børge G. Nordestgaard, M.D., James Shepherd, M.D., James T. Willerson, M.D., and Robert J. Glynn, Sc.D. for the JUPITER Study Group
N Engl J Med 2008; 359:2195-2207November 20, 2008DOI: 10.1056/NEJMoa0807646
Supported by AstraZeneca.
Dr. Ridker reports receiving grant support from AstraZeneca, Novartis, Merck, Abbott, Roche, and Sanofi-Aventis; consulting fees or lecture fees or both from AstraZeneca, Novartis, Merck, Merck–Schering-Plough, Sanofi-Aventis, Isis, Dade Behring, and Vascular Biogenics; and is listed as a coinventor on patents held by Brigham and Women’s Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease, including the use of high-sensitivity C-reactive protein in the evaluation of patients’ risk of cardiovascular disease. These patents have been licensed to Dade Behring and AstraZeneca. Dr. Fonseca reports receiving research grants, lecture fees, and consulting fees from AstraZeneca, Pfizer, Schering-Plough, Sanofi-Aventis, and Merck; and Dr. Genest, lecture fees from AstraZeneca, Schering-Plough, Merck–Schering-Plough, Pfizer, Novartis, and Sanofi-Aventis and consulting fees from AstraZeneca, Merck, Merck Frosst, Schering-Plough, Pfizer, Novartis, Resverlogix, and Sanofi-Aventis. Dr. Gotto reports receiving consulting fees from Dupont, Novartis, Aegerion, Arisaph, Kowa, Merck, Merck–Schering-Plough, Pfizer, Genentech, Martek, and Reliant; serving as an expert witness; and receiving publication royalties. Dr. Kastelein reports receiving grant support from AstraZeneca, Pfizer, Roche, Novartis, Merck, Merck–Schering-Plough, Isis, Genzyme, and Sanofi-Aventis; lecture fees from AstraZeneca, GlaxoSmithKline, Pfizer, Novartis, Merck–Schering-Plough, Roche, Isis, and Boehringer Ingelheim; and consulting fees from AstraZeneca, Abbott, Pfizer, Isis, Genzyme, Roche, Novartis, Merck, Merck–Schering-Plough, and Sanofi-Aventis. Dr. Koenig reports receiving grant support from AstraZeneca, Roche, Anthera, Dade Behring and GlaxoSmithKline; lecture fees from AstraZeneca, Pfizer, Novartis, GlaxoSmithKline, DiaDexus, Roche, and Boehringer Ingelheim; and consulting fees from GlaxoSmithKline, Medlogix, Anthera, and Roche. Dr. Libby reports receiving lecture fees from Pfizer and lecture or consulting fees from AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Merck, Pfizer, Sanofi-Aventis, VIA Pharmaceuticals, Interleukin Genetics, Kowa Research Institute, Novartis, and Merck–Schering-Plough. Dr. Lorenzatti reports receiving grant support, lecture fees, and consulting fees from AstraZeneca, Takeda, and Novartis; Dr. Nordestgaard, lecture fees from AstraZeneca, Sanofi-Aventis, Pfizer, Boehringer Ingelheim, and Merck and consulting fees from AstraZeneca and BG Medicine; Dr. Shepherd, lecture fees from AstraZeneca, Pfizer, and Merck and consulting fees from AstraZeneca, Merck, Roche, GlaxoSmithKline, Pfizer, Nicox, and Oxford Biosciences; and Dr. Glynn, grant support from AstraZeneca and Bristol-Myers Squibb. No other potential conflict of interest relevant to this article was reported.
LOL, Pip…favorite line of the whole post has got to be, “No other potential conflict of interest relevant to this article was reported.” Um…as if that wasn’t enough? Thanks for the laugh!