Those keen to optimise their cardiovascular health and reduce their risk of heart attack and stroke may well, in addition to ‘eating right’, take steps to ‘take exercise’ and be physically fit. Usually, the prescribed exercise here come in the form of ‘cardiovascular’ or ‘aerobic’ forms such as walking, jogging, cycling or rowing. Such activities can increase our ‘fitness’ and capacity for exercise, partly by inducing the production of tiny ‘engines’ in the cells known as mitochondria (my-toe-con-dree-ah). It is in the mitochondria that most of the fuel in our body is converted into energy. The more mitochondria we have (and the more efficiently they work), the fitter and more ‘energised’ we tend to be.
Another quite-common approach to reducing risk of heart attack or stroke is to take a statin. Actually, statins don’t work particularly well for this, and another potential problem is that these drugs deplete levels of the substance coenzyme Q10 (CoQ10) in the body. This is important because CoQ10 performs a vital function in the production of energy in the mitochondria. Low CoQ10 levels could, therefore, stifle energy production and may, theoretically at least, negate some of the benefits one might expect from physical exercise.
Last week, the journal Sports Medicine published a review of the potential impact statins have on effects of regular physical exercise [1]. The authors refer to more than one study in which statins appeared to have no ill-effect on fitness levels (as adjudged by maximum VO2). However, as the authors point out, these studies have generally been done in healthy individuals. This, and other factors such as the short duration of the studies and relatively small sample sizes may mean they do not necessarily tell the whole story.
They refer specifically to one study that provides good evidence, I think, that statins can put a serious brake on the fitness benefits exercise usually offers [2]. In this research, 37 adults underwent 12 weeks of aerobic training. Half of the group just participated in the exercise programme, while the other half took 40 mg of the statin simvastatin (Zocor) each day. Fitness was assessed prior to the study starting, and at the end too.
In those not taking statins, fitness increased by an average of 10 per cent of the 12-week study. However, in those taking simvastatin, fitness increased by only 1.5 per cent.
As part of this study, mitochondrial activity was assessed by measuring activity of the enzyme citrate synthase (a key enzyme involved in energy production in the mitochondria). Citrate synthase activity increased by 13 per cent in those who adopted exercise, but actually fell by 4.5 per cent in those taking the drug.
In the recent review [1], the authors also quote animal research in which statins have been found to reduce endurance and mitochondrial activity.
The evidence suggests, therefore, that statins have the potential to negate at least some of the benefits of exercise. But there is another major problem, too: those who may be fatigued from taking statins or perhaps are suffering from muscle pain (myalgia) as a result of these drugs may be less inclined to take exercise in the first place. The authors of this review cite evidence suggesting that as many as 25 per cent of those taking statins experience muscle symptoms on taking exercise, and that about 40 per cent of people with myalgia avoid even moderate exertion.
Some may say these problems, when they happen, are a small price to pay for the ‘obvious benefits’ of statins. However, it is probably worth bearing in mind that in most people who take statins (those with no history or heart attack or stroke), the research suggests statins have no net health benefit and don’t reduce the risk of death either [3].
References:
1. Murlasits Z, et al. The Effects of Statin Medications on Aerobic Exercise Capacity and Training Adaptations. Sports Medicine epub 11 July 2014
2. Mikus CR, et al. Simvastatin impairs exercise training adaptations. Journal of the American College of Cardiology. Epub 10 April 2013
3. Do statins have a role in primary prevention? An update. Therapeutics Letter Issue 77 Mar-Apr 2010 Therapeutics Initiative University of British Columbia
NSTEMI in June 2009, with 5 stents implanted and lipitor and other drugs prescribed. About three weeks later I experienced hives and pain in my right knee. Was advised to stop lipitor and metoprolol and symptoms abated. Next visit to cardiologist he prescribed crestor, which resulted in return of the knee pain. Walking hurt, squatting near impossible and traversing stairs was difficult. I would not have persisted with daily walking in that state and took the view that that exercise was more important to my long term health than reducing cholesterol from the June level of 5.5mmol/L. Lots of lifestyle tweaking including diet since and today I can walk the dog into the ground, fish in the ocean from a kayak, lift heavier objects than in my youth and have a much better life than ever. F**k ’em
Meanwhile.
Over in la-la alterno-land, where white is black and down is up, Professor Mark Baker strongly defends NICE’s position that millions more in the UK should be offered a statin.
The facts seem of no consequence to Prof. Baker, like the fact that it is impossible for someone like myself (male 160lb 5’11” age 63) to get the QRISK®2 calculator to give me a score of less than 10% risk – however I manipulate the variables.
Like the fact that the drug companies have been ‘economical with the actualitee’ over statins in respect of the necessity of including CoQ10 in the drug package for over 24 years and counting http://www.functionalmedicineuniversity.com/statin-CoQ10.pdf
If Prof Baker would like to pop round I am sure I could stamp out the fire blazing in his trousers.
What is of most concern though is that by this action Prof Baker has made it inevitable that Jeremy Hunt will use the failure to prescribe statins to an increasingly aware public as a stick to beat GPs with.
Sad really.
And the argument that many statins are now off patent won’t wash since the majority of the costs in mass statination arise from measuring, cajoling, and then checking adverse effects on the liver (as the drug advice notes all state should be done but aren’t in my limited experience), and subsequent to statin damage treating patients for the side-effects that the experts on and advising NICE continue to say don’t exist to any significant degree.
The NICE experts sound a little like the British Journalist in Humbert Wolfe’s epigram;
You cannot hope
to bribe or twist,
thank God! the
British journalist.
But, seeing what
the man will do
unbribed, there’s
no occasion to.
My brother had a heart attack at the age of 43, had a stent fitted, has type 2 diabetes, is overweight, on Statins and BP medication. Has been a smoker and fairly heavy drinker. Also has had a stressful working life, long unsocial hours, with financial stress.
I recently had my “age 60 health check ” and my total cholesterol was 7.7 . I’ve been told because of my brothers history that I may need to be prescribed Statins!!! ( over my dead body)
I was given a print out by the Dr of the dietary changes I should make ( which said a 3 rd of my diet should consist of starchy carbs!! I nearly choked on my full fat yogurt and nuts) I don’t eat grains of any sort, or potatoes, cakes biscuits etc, and to go back in 3 months time for another blood test, with a view of being ‘ prescribed the dreaded Statins’
Am I being foolhardy in scoffing at this advice? Am I more at risk of a CV event even though I’m not overweight, low BP, active and healthy, never smoked, enjoy a glass or two of wine a day ( but no more) honestly! It’s so hard to put your point across to a GP who obviously has this in mind to get me on the tablets! I know I don’t have to take them, but do feel like I’m being blinded with science and feel vulnerable sitting on the other side of the desk! Advice please!
Jennie,
Your remarks reveal your intuition is far more astute than the supposed ‘knowledge’ of many a conventionally minded GP. And in your three paragraphs you highlight the great dilemma faced by astute, interested, and informed patients. Despite your comments reveal sound familiarity with pertinent risk factors how can you become confident and assured your own analysis and judgement is more correct than is your GPs? It is easy to be self-doubting isn’t it?
“Am I being foolhardy in scoffing at this advice? Am I more at risk of a CV event even though I’m not overweight, low BP, active and healthy, never smoked, enjoy a glass or two of wine a day ( but no more) honestly! It’s so hard to put your point across to a GP who obviously has this in mind to get me on the tablets! I know I don’t have to take them, but do feel like I’m being blinded with science and feel vulnerable sitting on the other side of the desk! Advice please!”
I regret it is inappropriate to give advice but it is acceptable to talk around the issues. The best issue to begin with is the notion of biological age compared with chronological age.
Date of birth is the give-away to chronological age. Nature has scripted a maximum life-expectancy into all living things, and even non-living features of the Universe have a finite life-spans. Stars live for billions of years, but one day each must die. Finality is an inescapable universal rule, especially for living things.
Let’s say your maximum expectancy possible is 110 years. Nature has programmed something within you that says Jennie B’s life-expectancy fuse should last no more than 110 years, then her spark of life must extinguish itself. I don’t think one single aspect represents that fuse but aspects of your genes and telomeres suffer attrition each day of your life. The shortening of telomeres and alterations to the coding of genes are changes, ‘wear and tear’, ‘attrition’, that record how fast your ageing. It is ‘oxidative stress’ that causes ‘wear and tear’.
Oxidation and oxidative stress are unavoidable, for it is the burning of metabolites that keeps your cells alive, and just as with petrol in car burning fuel produces ‘exhausts’ and wastes. Accumulated oxidation and oxidative stress is the wear and tear of life. If you keep oxidative stress to a bear minimum nature would allow to attain your maximum life-expectancy, whereas if you permit or tolerate exposure to increased levels of oxidation and oxidative stress then the attrition rate of the natural time-delay fuse will be greater, and you will become old before your time.
Biological age describes how much you have aged over and above what nature dictates is your best prospect. So, if your brother suffered heart attack at (chronological) age 43 his biological age might rank, say, as around 65 at that time.
Your brother has all the hallmarks of an emotional stressful life and physiologically stressful one. he had been hyperinsulinemic (overweight and insulin resistant) smoked, drank, and suffered work-related and economic lifestyle stresses. Some stresses arise outside the body and some arise within. Key thing of note is that lifestyle and emotional stresses alter the way certain hormones go about their business. Next key thing of note is that the production and turnover of certain hormones can consume antioxidant resources. Through the action of certain hormones, being ‘stressed’ consumes a lot of antioxidants, and this results in physiological stress. There are too few antioxidants available to detoxify normal metabolic by-products, and the level of oxidative stress always there in the background rises. This, it increasingly seems, contributes to attrition rate of telomeres and aberrant of genetic coding.
Smoking and alcohol misuse each add to oxidative stress, and added more to the work and socio-economic stresses your brother faced. Hence the attrition rate of oxidative stress your brother faced was high. But how does this bring about a heart attack?
In this it is hard to be certain, medical science is often imprecise. As a self-taught health scientist I would say competition for antioxidants brought on elevation of something called homocysteine and other reactive oxygen species. Homocysteine is a better marker for risk of many a disease, including CVD and heart attack, than is ‘cholesterol’ for CVD and heart attack. Homocysteine levels report levels of oxidative stress, and quite reliably. Homocysteine has been proven to be highly atherogenic in several species including humans. High homocysteine promotes growth in those atheromas, or ‘plaques’, that narrow, harden, and weaken, arteries. Homocysteine can be highly atherogenic and toxic to certain cell types.
Other identified atherogens and cytotoxins implicated in promoting growth of atheromas and arterial disease are certain oxides of cholesterol. Much the same body of work says cholesterol is not an atherogen. Egro cholesterol is not a cuase of heart disease. The big question is; does homocysteine cause cholesterol to become oxidised to its cytotoxic and atherogenic oxidised variants? If so when, where, and under what circumstances? I don’t think anybody knows the answer for sure, but when cholesterol becomes oxidised its properties change and certain of the possible oxides of cholesterol are highly deleterious to cell viability. It is possible, even if still conjecture, that cholesterol oxides are involved in biological attrition.
You are doing many of the right things. There is no reason to exclude fat from diet, though I think it a good thing not to over-consume veg oil and marg and I eat next to none. Soluble fibre from medium and low GI/GL plant foods is good. Contrary to dogma low carb is better than low fat. Keep physically active, that is good for NO. Never take a statin for they are cytoxic and genetically damaging. And enjoy red wine. Live a little, enjoy your time of life, and do not be browbeaten.
A way to minimise oxidative stress is to relax, enjoy, love, and eat a varied diet rich in minerals and antioxidants, and may be a daily tab of the same is prudent. You would never wish to be short of methyl donating antioxidants or sources of sulphur. Green leafy veg and broccoli are recommended along with garlic and onions. I take garlic caps and turmeric to supplement my sulphur. These all help combat oxidative stress and the kind of attrition that hastens ageing.
Things that arise outside the body, and that we subject it to, can commute to a specific kind of physiological stress within the body, and it is the ongoing prevalence of these physiological stresses that hastens ageing or invites departure from wellness. If you, or anybody else, can grasp that simple premise it represents a significant, if incremental, advance for the good of health science. Biological ageing needn’t arise faster than chronological ageing. I do not think statins put the brakes upon ageing at all, rather they hasten it.
Try to inquire what your GP knows about homocysteine, methylation, and certain oxides of cholesterol. Already I suspect you now know more.
Is it not just a tab ironic that COQ10 is prescribed for heart failure? As adequate COQ10 levels are necessary for the smooth running of the body’s most important muscle, the heart, it can only be counter productive to prescribe stains, which deplete the body’s supply of COQ10!
I haven’t seen the esteemed Professor Sir Rory Collins’ answer to this conundrum.
Not only do you not have to take the tablets, you also do not have to go back to the GP. What, exactly, is the point?
Jennie B
Ask your GP how much longer will your life be extended by taking a statin.
Answer: it won’t.
Ask your GP why, if higher cholesterol levels are protective for women of any age, he would wish you to lower yours?
Print out and show him the graph: “Total Cholesterol Levels vs Mortality Data from 164 Countries” and ask your GP why you would want to reduce your cholesterol?
http://renegadewellness.files.wordpress.com/2011/02/cholesterol-mortality-chart.pdf
Jennie, just say no, I did. And if the doctor you normally see is adamant, see another! Mine has capitulated recently. I think he probably still believes in them, but he can see all the hoo ha about them and so isn’t as insistent this last time. He knows I read all about it, that I’m lo carb, high fat and I have given him permission to tut and say I told you so if I die early. I saw another doctor at our surgery about something else, he mentioned statins and I said I didn’t/wouldn’t take them and he was surpisingly ok with that.
And there is proof that older women are better off with a bit higher cholesterol! (I’m 65)
There are studies that show that in athletes there can be a high incidence of muscle pain in very active, muscular individuals. This is logical as statins disrupt the production of ubiquinon, as essential intra-cellular, and natural anti-oxidant for the protection of mtDNA. This was known about by Merck in 1990 when they took out US patents to combine CoQ10 (ubiquinon) with their two statins.. and then “forgot” about it.
There are studies that show statins can cause cardiomyopathy. This is not surprising as the heart is a very hardworking muscle with lots of mitochondria.
Around 2002-2004, both the US CDC and NHBLI came out with a warning about an increasing epidemic of congestive heart failure. I took one look at the graph and saw an obvious association with the increasing sales of cholesterol lowering drugs. Others obviously saw it too and very rapidly this epidemic disappeared from both web sites. I am assured by an American cardiologist that the epidemic is still there and going strong.
Missing data again even from tax payer funded organisations.
One just accepts the prescription, collects the medication from the pharmacy, and on getting home, disposes of the statins. Less than honest I suppose, and a tad expensive for the NHS, if everyone did this. But what’s the alternative? If I give my GP a plain ‘NO!’ there’s a half hour of ‘conventional wisdom’ to suffer. I think we are losing the battle, thanks to programmes like ‘Embarrassing Bodies’, and other ‘medically aware’ programmes and commentators on British TV. I have decided to just care for myself and my family; and let the others stew in their own misguided fervour.