Superficiality (or, better said, eminence-based medicine) and laziness (or, better said, lack of patient involvement in improving his or her own health) support pharma’s profit (or, better said, the sale of cholesterol lowering drugs for cardiovascular disease prevention).
Although the decrease in LDL-cholesterol has been Our Holly Father in preventive cardiology for decades, LDL-cholesterol lowering drugs only lower LDL-cholesterol. And that’s all. Nothing more. Nothing less.
If you scratch your brain asking yourself “- What: “And that’s all”?!“ means, it is important to note that lowering LDL-cholesterol does not help most people prevent anything:
- in the case of statins, the absolute clinical benefit is 10% = 90 out of 100 people take the medicine for nothing, paying an average of 20 euros per month only for potential side effects (Collins et al., 2016).
- in the case of evolocumab, the absolute clinical benefit is only 1.5% more than statins = 65 out of 66 people take the medicine for nothing, paying 1,000 euros per month only for potential side effects (Sabatine et al., 2017).
44 randomized controlled trials indicate that lowered LDL-cholesterol does not associate with lowered mortality (DuBroff, 2017), the difference in survival between people with high cardiovascular risk who take statins compared to those who do not take statins being only 4 days (Kristensen, Christensen and Hallas, 2015).
In addition to these findings, some tend to forget or ignore the randomized controlled trial published in 2007 in the New England Jornal of Medicine, a study of 15,067 people at high cardiovascular risk. This study was stopped in progress despite the fact that the drug tested was very effective, combining a 72.1% increase in HDL-cholesterol and a 24.9% decrease in LDL-cholesterol. Only that, despite the improvement of the lipid profile, the actual clinical outcome was increased mortality (Barter et al., 2007).
The hope that lowering LDL-cholesterol lowers cardiovascular mortality is contradicted by the current scientific evidence – evidence that you can read by clicking on the cited links. However, hope dies last, in the meantime helping:
- the researcher in search of sponsors – to be satisfied that he contributes to saving humanity from death by cardiovascular diseases – the purpose being to discover new drugs to lower cholesterol, not to improve patient’s health
- the physician that prescribes statins on autopilot without consulting his own brain – to be satisfied that he has recommended something to the patient – the purpose being to write the prescription, not to improve the patient’s health
- the pharmacist looking for paying customers – to be satisfied that he made his sales plan today – the purpose being to sell drugs, not to improve the patient’s health
- the patient with no willingness to invest nothing but money in his own health – to be satisfied that he kind of contributes to his own health by buying from the pharmacist the prescription recommended by the doctor based on the studies carried out by the researcher – the purpose being to take the pill or the injection administration, not to improve the patient’s condition because he does not identify with the status of “patient”. He is George, Maria or Costel – the person, not “the patient” – and he did everything he was told to do: he went to the doctor, he received a prescription, he took the pills. End of story.
Cardiovascular disease prevention by statins alone works as efficiently as the lovely story of the four people: Everybody, Somebody, Anybody and Nobody:
“There was an important job to be done and Everybody was sure that Somebody would do it. Anybody could have done it, but Nobody did it. And it all ended up with Everybody blaming Somebody when Nobody did what Anybody could have done.”
Everyone is satisfied: we manage to lower LDL-cholesterol. The LDL lowering box is ticked, we’re all good. At least on paper (Diamond and Ravnskov, 2015).
Only that the satisfaction of all these people including George, Maria and Costel cost the health and quality of life of the “patient George, Maria or Costel”, without bringing them any clinical benefit other than the lowering of “bad-bad-bad” LDL-cholesterol (de Lorgeril and Rabaeus, 2015).
Improved blood tests, dead patient. The funeral dinner party and the LDL-cholesterol lowering success congratulations later – each according to the available possibilities. Common menu: burger with fried potatos and a sugar-free cola (to reduce calories) bought on the run from the local Drive Through, eaten also on the run and finished triumphantly with throwing on the window of smoking stumps while driving to the job you hate but have to go to every damn day to pay your bills, lovely place on Earth where you would elegantly sing the entire repertoire of Paraziții (n.a. a Romanian hip-hop group, with dirty language and virulent lyrics).
Cardiovascular risk is multifactorial, lowering LDL is just a single unknown factor in an equation with many other ultra-cognitive things that we DON’T want to, CAN’T, DON’T have time for, DON’T find it EASY to, DON’T feel COMFORTABLE the need to – DON’T LIKE to address them today:
- sedentary normoponderal persons have a higher cardiovascular risk than overweight individuals who regularly practice sports (Pandey, Berry and Lavie, 2015; Mainous III et al., 2019)
- smoking increases cardiovascular risk, but the risk gradually decreases after smoking cessation (Aune et al., 2018; 2019)
- hookah smoking (water pipe smoking) increases cardiovascular risk (Bhatnagar et al., 2019)
- electronic cigarette smoking contributes to increased cardiovascular risk both through the intake of toxic substances and by decreasing the chances of actually ever quitting smoking (Glantz and Bareham, 2018)
- insomnia increases cardiovascular risk (Sofi et al., 2014; Fernandez-Mendoza, 2019)
- depression and anxiety increase cardiovascular risk (Wulsin and Singal, 2003; Suls et al., 2018), completely ignoring the fact that people diagnosed with familial hypercholesterolemia have a higher level of depression and anxiety (Akioyamen et al., 2018). Fortunately, however, psychotherapy can contribute to lower cardiovascular mortality in people with high cardiovascular risk (Richards et al., 2018).
- metabolic syndrome increases cardiovascular risk (Mottillo et al., 2010)
- liver steatosis increases cardiovascular risk (Targher, Day and Bonora, 2010)
- obesity increases cardiovascular risk (Eckel et al., 2016)
- in the case of normal-weight persons with high cardiovascular risk, excess fat stored on the abdomen increases the cardiovascular risk (Coutinho et al., 2011)
- weight loss for the sake of weight loss through brain-dead but popular diets leads to long-term metabolism disorders and increases cardiovascular risk (Chaston and Dixon, 2008; Lavie et al., 2016)
- people who are too slim, with too little fat, also have an increased cardiovascular risk (Chehab, 2008)
We will address these issues on Monday. Next Monday. Or the next.
Sedentarism, smoking, insomnia, depression, anxiety, metabolic syndrome, hepatic steatosis, abdominal fat storage, underweight or obesity of the patient George, Maria or Costel are frequently ignored by both George, Maria or Costel, as well as most autopilot-recipes-writers calling themselves physicians (Daniels, Pratt and Hayman, 2011; Vancheri et al., 2016).
And I highlight the automatism of the autopilot-recipes-writers because the international medical community is divided: some doctors consider statins a damn crap, while others consider statins the golden egg that will save anyone over the age of 50 (Rabaeus et al., 2017; McCartney, 2012).
The patient with primary or secondary cardiovascular risk who is taking their medication + properly improves their nutrition + gives up smoking + works on assertiveness (and possibly practice some for of meditation instead of swallowing his frustration while passive-agressivingly cursing his boss or his wife in his mind) and who also practices regular sports = gets LDL-cholesterol lowering + cardiovascular risk lowering ± side effects. All three consequences of disciplined and improved eating beahavior and life style but only as long as he administers his medication and practices his healthy lifestyle and nutrition.
The patient who only takes her 20 euro pills or who only administers his 1,000 euro injection but who does not improve his quality of life and nutrition = only gets LDL-cholesterol lowering ± side effects. Both only as long as he administers his medication.
The lowering of the LDL-cholesterol trumpeted out loud by different eminences at various congresses and conferences – where we charm the audience with relative values, while hiding absolute values – is the way in which statins are pushed forward in the working mind of the autopilot-recipes written by those doctors who do not bother with improving patient’s health. Especially if the patient does not bother himself with improving patient’s health. Why would the doctor care more about the patient than the patient cares about the patient?
The patient wants a quick fix. You got it!
Decreasing LDL-cholesterol helps the researcher to have something to present at the congresses, it helps the doctor to have what to recommend and it helps the pharmacist to have what to sell. Only that without sports, without giving up smoking, without fat loss (not water and muscles loss), without developing mental strategies to counteract stress conditions, and without assuming responsibility by George, Maria and Costel it has zero benefits for the patient. And the even harder part is that to work, these behaviors must be practiced daily FOR THE ENTIRE DAMN LIFE.
Cardiovascular mortality is increasing worldwide because most aren’t practicing the healthy eating and lifestyle behaviors.
But although it sounds like the hard work no one is actually willing to do, in the actual world we all live into not practicing these behaviors cannot be compensated by the administration of drugs.
Akioyamen, Leo E., et al. Anxiety, depression, and health-related quality of life in heterozygous familial hypercholesterolemia: A systematic review and meta-analysis. Journal of psychosomatic research 109 (2018): 32-43.
Aune, Dagfinn, et al. Tobacco smoking and the risk of atrial fibrillation: A systematic review and meta-analysis of prospective studies. European journal of preventive cardiology 25.13 (2018): 1437-1451.
Chaston, T. B., & Dixon, J. B. (2008). Factors associated with percent change in visceral versus subcutaneous abdominal fat during weight loss: findings from a systematic review. International journal of obesity, 32(4), 619.
Collins, R., Reith, C., Emberson, J., Armitage, J., Baigent, C., Blackwell, L., … & Evans, S. (2016). Interpretation of the evidence for the efficacy and safety of statin therapy. The Lancet, 388(10059), 2532-2561.
Coutinho, Thais, et al. Central obesity and survival in subjects with coronary artery disease: a systematic review of the literature and collaborative analysis with individual subject data. Journal of the American College of Cardiology 57.19 (2011): 1877-1886.
de Lorgeril, M., & Rabaeus, M. (2015). Beyond Confusion and Controversy, Can We Evaluate the Real Efficacy and Safety of Cholesterol-Lowering with Statins?. Journal of Controversies in Biomedical Research, 1(1), 67-92.
Diamond, D. M., & Ravnskov, U. (2015). How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert review of clinical pharmacology, 8(2), 201-210.
Mainous III, Arch G., et al. Effect of Sedentary Lifestyle on Cardiovascular Disease Risk Among Healthy Adults With Body Mass Indexes 18.5 to 29.9 kg/m2. The American journal of cardiology 123.5 (2019): 764-768.
Rabaeus, Mikael, Paul V. Nguyen, and Michel de Lorgeril. Recent flaws in Evidence Based Medicine: statin effects in primary prevention and consequences of suspending the treatment. Journal of Controversies in Biomedical Research3.1 (2017): 1-10.