DiseasesCholesterol and statins — are we lowering the wrong number?
Sources: 10 · Article: 16 346 characters
Andrzej Frydrychowski and Jerzy Jaśkowski warn that lowering cholesterol too much may be harmful because the body needs cholesterol.
- Andrzej Frydrychowski gives a physiological reference range of 240–280 mg/dl, while Jerzy Jaśkowski cites an old reference range of 200–250 mg.
- Both describe statins as a way of blocking cholesterol production and point to a decrease in coenzyme Q10.
- They list possible harms, such as muscle weakness, memory problems, and diabetes.
- Jerzy Jaśkowski also links statins to kidney failure and cataracts.
- Andrzej Frydrychowski also mentions reports of improved health and a possible mild anti-inflammatory effect of statins.
What the authors write
Andrzej Frydrychowski
Statins lower cholesterol by blocking the HMG-CoA metabolic pathway.
„First, statins lower cholesterol levels by blocking the HMG-CoA metabolic pathway. This disrupts the synthesis of coenzyme Q10 and squalene. Disruption of Q10 synthesis has serious consequences because it affects the energy production of heart cells.”Po pierwsze, statyny obniżają poziom cholesterolu, blokując szlak metaboliczny HMG CoA. W wyniku tego dochodzi do zaburzeń syntezy koenzymu Q10 i skwalenu. Uszkodzenie syntezy Q10 daje poważne konsekwencje, ponieważ wpływa on na energetykę komórek serca.
Andrzej Frydrychowski
Andrzej Frydrychowski considers lowering cholesterol a bad idea, but also mentions studies reporting improved health and a possible anti-inflammatory effect of statins.
„Some studies report improved health after they are taken. This may be because statins can have a mild anti-inflammatory effect. But is this enough to tip the balance of their benefits against their harmful effects? Please judge for yourself.
1. Hulley S., Walsh J., Newman T.”Niektóre prace donoszą o poprawie stanu zdrowia po ich podawaniu. Może to być związane z tym, że statyny mogą mieć niewielkie działanie przeciwzapalne. Tylko czy to przeważy szalę ich korzyści nad działaniem niekorzystnym? Proszę ocenić samemu.
1. Hulley S., Walsh J., Newman T.
Jerzy Jaśkowski
Cholesterol is needed to build cells, the brain, and other important parts of the body.
„Cholesterol is a single chemical compound. It is essential for building the cell framework. From a biochemical point of view, coenzyme Q is produced as an end product from the same starting substances. This compound is responsible in our body for detoxification, or the removal of all toxins.”Cholesterol to jeden związek chemiczny. Jest on niezbędny do budowy szkieletu komórki. Z biochemicznego punktu widzenia z tych samych substancji pierwotnych jako produkt końcowy powstaje koenzym Q, czyli związek odpowiedzialny w naszym organizmie za detoksykację, czyli usuwanie wszelkich toksyn.
Andrzej Frydrychowski
Andrzej Frydrychowski gives a physiological reference range of 240–280 mg/dl and claims that no link has been demonstrated between cholesterol levels and the severity of atherosclerosis.
„The physiological reference range for an adult is 240–280 mg/dl. This value may vary depending on the body's immediate need for cholesterol or the degree of stress. It tends to fluctuate upward rather than downward. A myth has arisen that elevated cholesterol causes atherosclerotic changes in the arteries. This is a myth because no correlation has been shown between cholesterol levels and the severity of atherosclerotic changes.”Norma fizjologiczna dla osoby dorosłej to wartość 240-280 mg/dl. Wartość ta może się wahać w zależności od chwilowego zapotrzebowania na cholesterol czy stopnia stresu. Waha się raczej w górę, a nie w dół. Powstał mit, że podwyższona wartość cholesterolu jest przyczyną powstawania zmian miażdżycowych naczyń tętniczych. Jest to mit, ponieważ nie wykazano żadnej korelacji między poziomem cholesterolu a nasileniem zmian miażdżycowych.
Andrzej Frydrychowski
Andrzej Frydrychowski links high doses of statins to an increase in diabetes cases due to reduced cell sensitivity to insulin.
„Fourth, many studies have shown that high doses of statins increase the incidence of diabetes by reducing cell sensitivity to insulin [3]. This is no joke. Diabetes brings many serious complications, which I will write about in another article.”Po czwarte, w wielu pracach wykazano, że wysokie dawki statyn, powodują wzrost zachorowań na cukrzycę, poprzez zmniejszenie wrażliwości komórek na insulinę [3]. Tutaj żartów nie ma. Cukrzyca przynosi wiele poważnych powikłań, o których napiszę w innym artykule.
Andrzej Frydrychowski
Andrzej Frydrychowski describes pain, weakness, and other muscle problems in people taking statins.
„The clinical spectrum of statin-induced myopathy includes muscle pain, muscle inflammation, an asymptomatic increase in creatine kinase levels, fatigue, muscle tenderness and weakness, night cramps, and tendon pain. It is estimated that about 1,500,000 people worldwide suffer from muscle diseases caused by taking statins.”Spektrum kliniczne miopatii wywołanej przez statyny obejmuje: bóle mięśniowe, zapalenie mięśni, bezobjawowe zwiększenie stężenia kinazy kreatynowej, zmęczenie, tkliwość i osłabienie mięśni, nocne skurcze i ból ścięgien. Szacuje się, że ok. 1 500 000 osób na świecie cierpi z powodu chorób mięśni, spowodowanych zażywaniem statyn.
Andrzej Frydrychowski
Andrzej Frydrychowski cites a study in which a greater risk of death was associated with a drop in cholesterol from a medium to a low level.
„The risk-adjusted all-cause mortality rate was 30% higher (relative risk 1.30; 95% CI, 1.06 to 1.59) among people whose cholesterol levels fell from medium (180 to 239 mg/dl) to low (<180 mg/dl) than among those whose levels remained at a steady, medium level.”Wskaźnik śmiertelności wszystkich przyczyn skorygowany o czynnik ryzyka był o 30% wyższy (ryzyko względne 1,30; 95% CI, 1,06 do 1,59) wśród osób ze spadkiem poziomu cholesterolu ze średniego (180 do 239 mg/dl) do niskiego (<180 mg/dl) niż u osób pozostających na stałym, średnim poziomie.
Jerzy Jaśkowski
Jerzy Jaśkowski describes 200–250 mg as the old reference range and claims that accepted ranges were later lowered.
„Mass measurements of cholesterol levels in human bodies showed in the 1970s that most of the population had a level of about 200–250 mg. This was considered a favorable level, or the so-called normal range. Even 30 years ago, academic medicine considered a cholesterol level of 250 mg to be normal.”Prowadzone na masową skalę pomiary stężenia cholesterolu w organizmach ludzkich wykazały w latach siedemdziesiątych ubiegłego wieku, że większość społeczeństwa posiada poziom ok. 200-250 mg. Był to poziom korzystny, czyli tzw. norma. Jeszcze 30 lat temu w medycynie akademickiej, uważano że poziom 250 mg cholesterolu jest prawidłowy.
Jerzy Jaśkowski
Jerzy Jaśkowski describes statins as HMG-CoA reductase inhibitors and questions whether their long-term effects can be assessed quickly.
„Statins are compounds known as HMG-CoA reductase inhibitors. They were discovered relatively recently, only in 1973. Statins were introduced to the commercial market in 1987. They were introduced by Merck & Co. under the brand name Mevacor. The period from discovery to market launch was relatively short.”Statyny to związki tzw. inhibitorów reduktazy HMG-CoA. Odkryto je stosunkowo niedawno, bo dopiero w 1973 roku. Statyny zostały wprowadzone do obrotu handlowego w 1987 roku. Wprowadziła je firma Merck &Co, pod nazwą handlową Mevacor. Był to stosunkowo bardzo krótki okres czasu, od odkrycia do wprowadzenia na rynek.
Jerzy Jaśkowski
Jerzy Jaśkowski claims that statins reduce the production of coenzyme Q10 and links the blocking of HMG-CoA reductase to muscle weakness and memory problems.
„As I mentioned, by lowering the cholesterol pathway, statins reduce the production of Co Q 10, a natural coenzyme that is absolutely essential to our body. Statistics show that surgery for a “heart attack” results in postoperative mortality of up to 47% within a year.”Statyny, obniżając szlak cholesterolowy, jak wspomniałem, zmniejszają produkcję Co Q 10, absolutnie niezbędnego dla naszego organizmu naturalnego koenzymu. Jak wykazują statystyki, leczenie operacyjne „zawału” powoduje śmiertelność pooperacyjną w okresie roku do 47%.
Jerzy Jaśkowski
Jerzy Jaśkowski links taking statins to kidney failure and a higher incidence of diabetes.
„The Canadian Network for Observational Drug Effect Studies (CNODES) published a report clearly indicating a link between kidney failure and statin use. The study examined 2,067,639 patients over the age of 40 who were treated with statins and hospitalized for kidney failure.”Kanadyjska sieć Badań Obserwacyjnych Działań Leków CNODES opublikowała raport wskazujący jednoznacznie na istnienie związku niewydolności nerek z przyjmowaniem statyn. Po przebadaniu 2 067 639 chorych, w wieku powyżej 40 lat, leczonych statynami, hospitalizowanych z powodu niewydolności nerek.
Jerzy Jaśkowski
Jerzy Jaśkowski links statins to cataracts and claims that lowering cholesterol worsens eyesight.
„Every drug that lowers blood cholesterol worsens eyesight. So far, statins have been shown to have more than 300 negative health effects, including cardiotoxicity. It is worth noting that a cardiologist, a specialist in heart disease, prescribes drugs that cause heart disease so that pharmaceutical companies can profit from selling drugs for cataracts.”Każdy lek obniżający poziom cholesterolu we krwi pogarsza widzenie. Do tej pory udowodniono, że statyny mają ponad 300 negatywnych skutków zdrowotnych, w tym kardiotoksyczność. Warto zauważyć, że lekarz kardiolog, czyli specjalista od chorób serca przepisuje leki powodujące choroby serca, aby koncerny zarabiały na sprzedaży leków na zaćmę.
Jerzy Jaśkowski
Jerzy Jaśkowski claims that cholesterol is needed to build cells and to produce coenzyme Q and hormones.
„There is no bad or good cholesterol. This division was introduced by advertising specialists. Cholesterol is a single chemical compound. It is always the same. It is essential for building the cell framework. It is also a precursor in the so-called cholesterol pathway. In other words, cholesterol is used to make not only vitamin D but also coenzyme Q, which is responsible for detoxifying the body, and sex hormones.”Nie ma złego i dobrego cholesterolu. Ten podział został wprowadzony przez specjalistów od reklamy. Cholesterol to jeden związek chemiczny. Zawsze taki sam. Jest on niezbędny do budowy szkieletu komórki. Jest także prekursorem tzw. szlaku cholesterolowego. Czyli, innymi słowy, z cholesterolu powstaje nie tylko witamina D, ale także koenzym Q odpowiedzialny za detoksykację organizmu czy hormony płciowe.
Jerzy Jaśkowski
Jerzy Jaśkowski cites a claim that long-term statin use was associated with a higher risk of breast cancer.
„Thus, women who took statins for 10 years or longer had a 1.83-fold greater risk of invasive ductal cancer and a 1.97-fold increase in the risk of lobular cancer. Further studies proved that statin use increases the formation of atherosclerotic plaques in the coronary arteries and increases atherosclerosis of the aorta.”I tak, kobiety, które przyjmowały statyny 10 lat lub dłużej, mają 1.83-krotnie większe ryzyko zachorowania na inwazyjnego raka przewodowego i 1.97-krotne zwiększenie ryzyka raka zrazikowego. Kolejne badania udowodniły, że stosowanie statyn powoduje wzrost tworzenia się blaszek miażdżycowych w tętnicach wieńcowych i wzrost miażdżycy aorty.
Andrzej Frydrychowski
Andrzej Frydrychowski considers measuring cholesterol levels alone to be of little use and points to homocysteine as an important amino acid.
„We often measure cholesterol levels, which makes no sense and has no health-related correlation with cardiovascular diseases. Only about 3% of doctors, however, measure homocysteine levels. Homocysteine is an important sulfur-containing amino acid that starts inflammatory processes in the blood vessel lining, from which an atherosclerotic plaque will then develop.”Często oznaczamy poziom cholesterolu, który nie ma żadnego sensu ani korelacji zdrowotnych ze schorzeniami naczyniowo-sercowymi. Jedynie około 3% lekarzy oznacza natomiast poziom homocysteiny – ważnego aminokwasu siarkowego, który rozpoczyna procesy zapalne w śródbłonku naczyń, od którego dalej będzie się tworzyła blacha miażdżycowa.
Jerzy Jaśkowski
Jerzy Jaśkowski rejects the view that cholesterol is the main cause of atherosclerosis and heart attacks.
„“The hypothesis that cholesterol is harmful and is the main cause of atherosclerosis and heart attacks not only lacks any scientific basis but, as eminent experts have concluded, is one great nonsense” — Prof. Walter Hartenbach, MD, PhD (“Myths About Cholesterol,” Interspar Publishing House, 2007, trans.”„Hipoteza o szkodliwości cholesterolu jako głównego sprawcy rozwoju miażdżycy i zawału serca nie tylko pozbawiona jest jakichkolwiek podstaw naukowych, lecz, jak podsumowali ją wybitni eksperci, jest jednym wielkim nonsensem” – prof. dr hab. med. Walter Hartenbach („Mity o cholesterolu”, Oficyna Wydawnicza „Interspar” 2007, tłum.
Research from PubMed · Europe PMC
We selected 3 studies with the best, positive results. This is a selection, not a full review of all research.
Total number of studies on this topic in PubMed: 27 490.
A meta-analysis found that more intensive LDL lowering with statins reduces the number of major vascular events.
Aim of the study: Lowering of LDL cholesterol with standard statin regimens reduces the risk of occlusive vascular events in a wide range of individuals. We aimed to assess the safety and efficacy of more intensive lowering of LDL cholesterol with statin therapy.
Results: In the trials of more versus less intensive statin therapy, the weighted mean further reduction in LDL cholesterol at 1 year was 0·51 mmol/L. Compared with less intensive regimens, more intensive regimens produced a highly significant 15% (95% CI 11-18; p<0·0001) further reduction in major vascular events, consisting of separately significant reductions in coronary death or non-fatal myocardial infarction of 13% (95% CI 7-19; p<0·0001), in coronary revascularisation of 19% (95% CI 15-24; p<0·0001), and in ischaemic stroke of 16% (95% CI 5-26; p=0·005). Per 1·0 mmol/L reduction in LDL cholesterol, these further reductions in risk were similar to the proportional reductions in the trials of statin versus control.
Money for the studygovernment, public institutions · Medical Research Council, British Heart Foundation, European Community Biomed Programme
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)
“Not stated” does not mean nobody paid — the database does not always record it.
A meta-analysis found that lowering LDL with statins was associated with lower mortality and fewer major vascular events.
Aim of the study: Results of previous randomised trials have shown that interventions that lower LDL cholesterol concentrations can significantly reduce the incidence of coronary heart disease (CHD) and other major vascular events in a wide range of individuals. But each separate trial has limited power to assess particular outcomes or particular categories of participant.
Results: During a mean of 5 years, there were 8186 deaths, 14,348 individuals had major vascular events, and 5103 developed cancer. Mean LDL cholesterol differences at 1 year ranged from 0.35 mmol/L to 1.77 mmol/L (mean 1.09) in these trials. There was a 12% proportional reduction in all-cause mortality per mmol/L reduction in LDL cholesterol (rate ratio [RR] 0.88, 95% CI 0.84-0.91; p<0.0001). This reflected a 19% reduction in coronary mortality (0.81, 0.76-0.85; p<0.0001), and non-significant reductions in non-coronary vascular mortality (0.93, 0.83-1.03; p=0.2) and non-vascular mortality (0.95, 0.90-1.01; p=0.1). There were corresponding reductions in myocardial infarction or coronary death (0.77, 0.74-0.80; p<0.0001), in the need for coronary revascularisation (0.76, 0.73-0.80; p<0.0001), in fatal or non-fatal stroke (0.83, 0.78-0.88; p<0.0001), and, combining these, of 21% in any such major vascular event (0.79, 0.77-0.81; p<0.0001).
Money for the studyuniversity or foundation · Wellcome Trust
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)
“Not stated” does not mean nobody paid — the database does not always record it.
A meta-analysis found similar reductions in the risk of major vascular events in women and men when LDL was lowered with statins.
Aim of the study: Whether statin therapy is as effective in women as in men is debated, especially for primary prevention. We undertook a meta-analysis of statin trials in the Cholesterol Treatment Trialists' (CTT) Collaboration database to compare the effects of statin therapy between women and men.
Results: 46,675 (27%) of 174,149 randomly assigned participants were women. Allocation to a statin had similar absolute effects on 1 year lipid concentrations in both men and women (LDL cholesterol reduced by about 1.1 mmol/L in statin vs control trials and roughly 0.5 mmol/L for more-intensive vs less-intensive therapy). Women were generally at lower cardiovascular risk than were men in these trials. The proportional reductions per 1.0 mmol/L reduction in LDL cholesterol in major vascular events were similar overall for women (rate ratio [RR] 0.84, 99% CI 0.78-0.91) and men (RR 0.78, 99% CI 0.75-0.81, adjusted p value for heterogeneity by sex=0.33) and also for those women and men at less than 10% predicted 5 year absolute cardiovascular risk (adjusted heterogeneity p=0.11). Likewise, the proportional reductions in major coronary events, coronary revascularisation, and stroke did not differ significantly by sex.
Money for the studygovernment, public institutions · Australian National Health and Medical Research Council, National Institute for Health Research (NIHR), Cancer Research UK
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)
“Not stated” does not mean nobody paid — the database does not always record it.
Perspectives and opinion materials
The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.
Orthomolecular Medicine News Service Opinion material
„Introduction Statins are a class of drugs commonly prescribed to lower cholesterol levels, particularly low-density lipoprotein (LDL) cholesterol, which has traditionally been linked to an increased risk of cardiovascular diseases (CVD) such as heart attacks, strokes, and atherosclerosis. Statins work by inhibiting HMG-CoA reductase, an enzyme in the liver responsible for producing cholesterol. By reducing cholesterol production, statins aim to prevent plaque buildup in the arteries, which can lead to blockages and cardiovascular events.”Introduction Statins are a class of drugs commonly prescribed to lower cholesterol levels, particularly low-density lipoprotein (LDL) cholesterol, which has traditionally been linked to an increased risk of cardiovascular diseases (CVD) such as heart attacks, strokes, and atherosclerosis. Statins work by inhibiting HMG-CoA reductase, an enzyme in the liver responsible for producing cholesterol. By reducing cholesterol production, statins aim to prevent plaque buildup in the arteries, which can lead to blockages and cardiovascular events.
Orthomolecular Medicine News Service Opinion material
„Niacin vs Statins Simple, inexpensive immediate-release niacin works on its own and has been shown to reduce carotid intima thickness, while statins have repeatedly failed to achieve this endpoint. [7] Niacin raises HDL more than any pharmaceutical, while lowering triglycerides, excessive cholesterol, LDL, Lp(a), ApoB, and VLDL. Statins do not achieve any of these endpoints as well, and in fact they raise Lp(a), which is a bad thing because Lp(a) is one of the most important lipid markers of all.”Niacin vs Statins Simple inexpensive immediate release niacin works on its own demonstrably reducing carotid intima thickness, while statins have repeatedly failed to achieve this endpoint. [7] Niacin raises HDL more than any pharmaceutical, while lowering triglycerides, excessive cholesterol, LDL, Lp(a), ApoB, and VLDL. Statins do not achieve any of these endpoints as well and statins in fact raise Lp(a), which is actually a bad thing as Lp(a) happens to be one of the most important lipid markers of all.
Orthomolecular Medicine News Service Opinion material
„The AHA’s Symptom-Focused Paradigm The AHA and its endorsed guidelines exemplify a symptom-focused approach to ASCVD management, prioritizing LDL cholesterol reduction through statins while neglecting the root causes of the disease (9). This strategy oversimplifies the complexity of cardiovascular disease and does not adequately address foundational contributors such as poor diet, chronic inflammation, environmental toxins, and nutritional deficiencies.”The AHA’s Symptom-Focused Paradigm The AHA and its endorsed guidelines exemplify a symptom-focused approach to ASCVD management, prioritizing LDL cholesterol reduction through statins while neglecting the root causes of the disease(9). This strategy oversimplifies the complexity of cardiovascular disease and does not adequately address foundational contributors such as poor diet, chronic inflammation, environmental toxins and nutritional deficiencies.
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