DiseasesCholesterol and statins — are cardiologists looking at the wrong number?
Sources: 16 · Article: 25 161 characters
Andrzej Frydrychowski and Jerzy Jaśkowski argue that the cholesterol number alone is a misleading target, but Thomas E. Levy considers very high levels risky.
- Andrzej Frydrychowski and Jerzy Jaśkowski give higher values as normal and question the link between cholesterol and atherosclerosis; Nathan S. Bryan also rejects cholesterol as a cause of heart disease.
- Thomas E. Levy links high cholesterol to the buildup of changes in the arteries, but recommends first reducing toxins rather than lowering the number with statins alone.
- Andrzej Frydrychowski, Jerzy Jaśkowski, and Nathan S. Bryan warn about the effects of statins, although Andrzej Frydrychowski allows that they may have a small anti-inflammatory effect.
What the authors write
Andrzej Frydrychowski
Blood cholesterol levels are said to change with the body's needs, and their level is said to have no connection with the severity of atherosclerosis.
„If the body needs more of it (for example, to repair blood vessel walls), its level in the blood increases. If its level rises, this means that the body's need for it is growing. Cholesterol is essential for building the brain, nerve sheaths, hormones (cortisone, testosterone, estrogens, aldosterone), vitamin D3, and so on, so logically, lowering it will have a terrible effect on our health. It must not be lowered carelessly, and certainly not to levels far below physiological values. The physiological range for an adult is 240–280 mg/dl. This value can vary depending on the body's current need for cholesterol or the level 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.”Jeżeli organizm potrzebuje go więcej (np. do naprawy ścian naczyń), to jego poziom we krwi się zwiększa. Jeżeli jego poziom wzrasta, oznacza to, że zapotrzebowanie na niego rośnie. Cholesterol jest niezbędny do budowy mózgu, osłonek nerwowych, hormonów (kortyzon, testosteron, estrogeny, aldosteron), wit. D3 itd., czyli logicznie rzecz biorąc, jego obniżenie wpłynie fatalnie na nasze zdrowie. Nie wolno go lekkomyślnie obniżać, a już na pewno nie do poziomów znacznie poniżej wartości fizjologicznych. 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.
Jerzy Jaśkowski
Cholesterol is a compound the body needs, and Jerzy Jaśkowski links lowering it to ever-lower levels with the interests of pharmaceutical companies.
„It is worth remembering that there is no such thing as bad and good cholesterol. Cholesterol is one chemical compound. It is essential for building the cell framework. From a biochemical point of view, coenzyme Q, a compound responsible in our body for detoxification—that is, removing all toxins—is the end product formed from the same starting substances.”Warto pamiętać, że nie istnieje podział na zły i dobry cholesterol. 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.
Jerzy Jaśkowski
Jerzy Jaśkowski says that in the past, a level of around 200–250 mg was considered normal, and treatment was started at around 400 mg.
„As recently as 30 years ago, academic medicine considered a cholesterol level of 250 mg to be normal. In older people, it may be much higher because of lower sexual activity. Treatment was considered when a patient's cholesterol level was around 400 mg.”Jeszcze 30 lat temu w medycynie akademickiej, uważano że poziom 250 mg cholesterolu jest prawidłowy. U osób starszych, w związku z mniejszą aktywnością płciową, może być nawet znacznie wyższy. Leczeniem zajmowano się gdy poziom cholesterolu u pacjenta wynosił około 400 mg.
Jerzy Jaśkowski
Jerzy Jaśkowski presents the theory that atherosclerotic plaque is linked to cholesterol and claims that statins focus on elevated levels instead of the entire metabolic pathway.
„The makers of these products focused exclusively on an artificial disease which, according to them, was elevated cholesterol, and paid no attention to the so-called cholesterol metabolic pathway.
The theory of atherosclerotic plaque, which was linked to cholesterol, was developed 50 years ago.”Autorzy tych specyfików, skupili się wyłącznie na sztucznej chorobie, jaką według nich był podwyższony poziom cholesterolu, a nie zwracali uwagi na tzw. metaboliczny szlak cholesterolowy.
50 lat temu stworzono teorię blaszki miażdżycowej, którą powiązano z cholesterolem.
Jerzy Jaśkowski
Jerzy Jaśkowski rejects the hypothesis that cholesterol is the main cause of atherosclerosis and heart attacks.
„“The hypothesis that cholesterol is harmful as the main cause of atherosclerosis and heart attacks is not only without any scientific basis but, as distinguished experts have summed it up, is complete nonsense” — Prof. Walter Hartenbach, MD, PhD (“Myths About Cholesterol,” Oficyna Wydawnicza “Interspar,” 2007, translated by …).”„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.
Jerzy Jaśkowski
Jerzy Jaśkowski describes cholesterol as necessary for the body and presents the link between cholesterol and hard atherosclerotic plaque as one that does not fit.
„There is no bad and good cholesterol. This distinction was introduced by advertising specialists. Cholesterol is one 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.”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.
Nathan S. Bryan
Nathan S. Bryan says that most patients admitted to hospital with a heart attack had normal cholesterol, and claims that statins do not prevent heart attacks or strokes.
„Well today we know that 75 percent of patients hospitalized for a heart attack have normal cholesterol levels. Whereas the deaths from sudden cardiac arrest have declined over the past 25 years, the absolute number of heart attacks and strokes have continued to increase, despite almost 75% of patients with known cardiovascular disease are on statins and almost 50% of all patients over the age of 75 regardless of diagnosis or risk of cardiovascular disease.”Well today we know that 75 percent of patients hospitalized for a heart attack have normal cholesterol levels. Whereas the deaths from sudden cardiac arrest have declined over the past 25 years, the absolute number of heart attacks and strokes have continued to increase, despite almost 75% of patients with known cardiovascular disease are on statins and almost 50% of all patients over the age of 75 regardless of diagnosis or risk of cardiovascular disease.
Thomas E. Levy
Thomas E. Levy links very high cholesterol levels with a greater risk of heart attack and faster buildup of plaques in the arteries.
„Very elevated cholesterol levels clearly increase the chances of having a heart attack as long as they are up, with the highest levels having the highest risks. So, extremely elevated cholesterol levels (280 mg% or greater) need to be avoided at all costs.”Very elevated cholesterol levels clearly increase the chances of having a heart attack as long as they are up, with the highest levels having the highest risks. So, extremely elevated cholesterol levels (280 mg% or greater) need to be avoided at all costs.
Thomas E. Levy
Thomas E. Levy says cholesterol may rise as a defensive response to toxins and recommends reducing their sources rather than lowering cholesterol without addressing them.
„But... you don't want to lower the cholesterol levels without lowering the toxin presence as well. Otherwise, you'll just have more un-neutralized toxins in the blood and in the body, causing increased oxidative stress and damage wherever they go.
Then what do I do when my cholesterol is elevated?”But... you don't want to lower the cholesterol levels without lowering the toxin presence as well. Otherwise, you'll just have more un-neutralized toxins in the blood and in the body, causing increased oxidative stress and damage wherever they go.
Then what do I do when my cholesterol is elevated?
Thomas E. Levy
Thomas E. Levy gives a range of 160–220 mg% as a general guideline after reducing toxins and warns against levels that stay below 150 mg% over time.
„As a general guideline, when new toxin exposures have been properly addressed, and normal daily toxin exposures are all that remain, most adults will end up with a "normal" cholesterol level between 160 and 220 mg%. You never want a cholesterol level to chronically stay below 150 mg%.”As a general guideline, when new toxin exposures have been properly addressed, and normal daily toxin exposures are all that remain, most adults will end up with a "normal" cholesterol level between 160 and 220 mg%. You never want a cholesterol level to chronically stay below 150 mg%.
Andrzej Frydrychowski
Andrzej Frydrychowski considers 200 mg/dl too low a normal level and gives a range of 240–280 mg/dl as normal.
„The normal cholesterol range is not 200 mg/dl, as pharmaceutical companies would have it, but 240 to 280 mg/dl. When doctors recommend that people over 70 use statins, I consider it practically a crime. We often measure a cholesterol level that makes no sense and has no health-related correlation with cardiovascular diseases.”Norma cholesterolu wynosi bowiem nie 200 mg/dl, jak chcą koncerny farmaceutyczne, ale od 240 do 280 mg/ dl. Gdy lekarze zalecają osobom powyżej 70. roku życia używanie statyn, to uważam, że jest to wręcz zbrodnia. Często oznaczamy poziom cholesterolu, który nie ma żadnego sensu ani korelacji zdrowotnych ze schorzeniami naczyniowo-sercowymi.
Andrzej Frydrychowski
Andrzej Frydrychowski links statins to the disruption of processes that produce coenzyme Q10 and squalene, and to possible harm to health.
„First, statins lower cholesterol 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 warns about the effects of statins, such as muscle pain and memory problems, and also claims that lowering cholesterol itself brings no benefit.
„Serious complications of this approach have emerged (muscle pain, memory problems or loss, decreased libido, general weakness, difficulty moving, etc.). The most commonly used pseudo-drugs to lower cholesterol include statins sold under the names atorvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin.”Pojawiły się ciężkie powikłania takiego postępowania (bóle mięśni, zaburzenia lub utrata pamięci, spadek libido, ogólne osłabienie, trudności w poruszaniu się itd.). Do najczęściej stosowanych pseudoleków na obniżenie poziomu cholesterolu możemy zaliczyć statyny, występujące pod nazwami: atorwastatyny, lovastatyny, pravastatyny, rosuvastatyny i simvastatyny.
Andrzej Frydrychowski
Andrzej Frydrychowski links long-term statin use to a higher risk of breast cancer and low cholesterol in older people to a higher risk of death.
„Ninth, studies published in 2001 (lasting 20 years) showed that low cholesterol was associated with an increased risk of death in older people. The earlier patients had their cholesterol lowered, the greater their risk of dying sooner [7].”Po dziewiąte, badania opublikowane w 2001 r. (czas trwania 20 lat) wykazały, że niski poziom cholesterolu był związany ze zwiększeniem ryzyka zgonu u osób starszych. Im wcześniej pacjenci mieli obniżany poziom cholesterolu, tym większe było ryzyko wcześniejszej śmierci [7].
Andrzej Frydrychowski
Andrzej Frydrychowski allows that statins may have a small anti-inflammatory effect, but leaves it to readers to decide whether this outweighs the harms.
„This may be related to the fact that statins may have a small anti-inflammatory effect. But will that tip the balance of their benefits against their harmful effects? Please judge for yourself.
1. Hulley S., Walsh J., Newman T. Health Policy in Blood Cholesterol Time to Change Direction.”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. Health Policy in Blood Cholesterol Time to Change Direction.
Jerzy Jaśkowski
Jerzy Jaśkowski links statins to cataracts and worsening vision and claims that cholesterol is an important component of the eye's lens.
„The use of drugs called statins has also been linked to cataracts in older people. The first reports on this subject appeared as early as 1990 in Exp. Eye. Res. 50, but they did not reach the relevant information sources in Poland. They could have a negative effect on the statin trade.”Przyjmowanie leków zwanych statynami wiązane jest także z występowaniem zaćmy u osób starszych. Pierwsze doniesienia na ten temat były już w 1990 roku, w Exp.Eye. Res.50, jednak nie trafiły do odpowiednich informatorów w Polsce. Mogłyby bowiem wpłynąć negatywnie na handel statynami.
Jerzy Jaśkowski
Jerzy Jaśkowski links statins to kidney failure, diabetes, and other harms, and accuses cardiologists of creating more people with chronic illnesses.
„The Canadian Network of 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 lists the risk of prostate and breast cancer and an increase in atherosclerotic changes as possible effects of taking statins.
„Further studies have shown that statin use causes an increase in the formation of atherosclerotic plaques in the coronary arteries and an increase in aortic atherosclerosis.
Other studies show that taking statins not only increases the risk of type 2 diabetes but also speeds up the onset of cardiovascular complications associated with diabetes.”Kolejne badania udowodniły, że stosowanie statyn powoduje wzrost tworzenia się blaszek miażdżycowych w tętnicach wieńcowych i wzrost miażdżycy aorty.
Inne badania dowodzą, że przyjmowanie statyn nie tylko powoduje wzrost ryzyka wystąpienia cukrzycy typu 2, ale także przyspieszenie występowania powikłań sercowo-naczyniowych związanych z cukrzycą.
Jerzy Jaśkowski
Jerzy Jaśkowski links statins to reduced production of cholesterol, hormones, and memory proteins, and to muscle weakness.
„The body uses this enzyme to produce cholesterol, adrenal cortex hormones, sex hormones, and memory proteins. Thus, a reduction in memory proteins is directly linked to dementia. HMG-CoA reductases are also responsible for maintaining energy in the cell.”Enzym ten jest wykorzystywany przez organizm do produkcji cholesterolu, hormonów kory nadnerczy, hormonów płciowych i białek pamięci. Tak więc obniżenie poziomu białek pamięci bezpośrednio związane jest z demencją. Reduktazy HMG-CoA są odpowiedzialne także za utrzymanie energii w komórce.
Nathan S. Bryan
Nathan S. Bryan links statins to diabetes, memory problems, Alzheimer's disease, and muscle pain.
„Statins have been shown to increase incidence of diabetes, dementia and Alzheimers’ disease, they are mitochondrial toxicants that interfere with cellular energy production and cause muscle aches and pains.
We have an epidemic of patients with low Vitamin D levels which lead to decreased immune function and increased susceptibility to infections and changes in calcium metabolism, osteoporosis.”Statins have been shown to increase incidence of diabetes, dementia and Alzheimers’ disease, they are mitochondrial toxicants that interfere with cellular energy production and cause muscle aches and pains.
We have an epidemic of patients with low Vitamin D levels which lead to decreased immune function and increased susceptibility to infections and changes in calcium metabolism, osteoporosis.
Nathan S. Bryan
Nathan S. Bryan presents statins as cholesterol-lowering drugs whose effectiveness and safety he assesses based on the available data on health outcomes.
„Now 35 years later, we have an abundance of data on the safety and efficacy of these drugs but more importantly we have outcome data on their effects related to cardiovascular disease, heart attacks and strokes.
There are always many unwanted side effects of these drugs.”Now 35 years later, we have an abundance of data on the safety and efficacy of these drugs but more importantly we have outcome data on their effects related to cardiovascular disease, heart attacks and strokes.
There are always many unwanted side effects of these drugs.
Research from PubMed · Europe PMC
We selected 7 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: 5 503.
A review found that apoB indicates atherosclerotic disease risk better than LDL-C and generally better than non-HDL-C.
Aim of the study: Conventional statistical approaches are not designed to compare highly correlated variables such as low-density lipoprotein cholesterol (LDL-C), non-high density lipoprotein cholesterol (non-HDL-C), and apolipoprotein B (apoB). Discordance analysis was designed to overcome this limitation by creating groups in which the predictions of 2 markers differ.
Results: ApoB outperformed LDL-C in 9 of 9 studies whereas LDL P was superior to LDL-C in 2 of 3 comparisons. In 1 study, non-HDL-C was superior to apoB, in 1 study apoB and non-HDL-C were equivalent, whereas in 7 studies, apoB, overall, was a significantly more accurate marker of atherosclerotic cardiovascular disease risk than non-HDL-C. Discordance analysis provides robust evidence that apoB is a more accurate marker of cardiovascular risk than either LDL-C or non-HDL-C, notwithstanding these variables are highly intercorrelated. Thus, neither LDL-C nor non-HDL-C are adequate clinical surrogates for apoB. Accordingly, apoB should be the primary measure in clinical care to estimate the cardiovascular risk attributable to the apoB lipoproteins and the adequacy of lipid-lowering therapy to reduce this risk.
Money for the studycompany together with others · McGill University Health Centre, Servier
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?YES
Type of studyreview of many studies
Participants593 354
“Not stated” does not mean nobody paid — the database does not always record it.
The statement indicates that hsCRP predicts the risk of cardiovascular events even in people treated with statins, and that statins reduce risk in people with elevated hsCRP despite normal LDL-C.
Aim of the study: The crucial role of inflammation in the pathogenesis and clinical outcomes of cardiovascular disease (CVD) has recently gained increased attention. In particular, residual inflammation, measured with high-sensitivity C-reactive protein (hsCRP) remains strongly predictive of recurrent events, even in statin-treated patients.
Results: Additionally, in successful trials, the interplay between inflammation and key physiological systems often remains incompletely examined. Another promising area of research is the role that novel special pro-resolving bioactive lipid molecules play in promoting the resolution of inflammation and CVD risk reduction. In aggregate, the evidence linking inflammation with atherosclerotic CVD is no longer exploratory but is compelling and clinically actionable. The time for taking action has now arrived.
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
The review indicates that, in addition to LDL-C, factors such as lipoprotein(a), apolipoprotein B, and coronary artery calcification should be considered, while statins remain a mainstay of treatment.
Aim of the study: Prevention of atherosclerotic cardiovascular disease (ASCVD) is fundamental for both cardiologists and primary care physicians. From risk estimation to medical therapy for primary and secondary prevention, management is evolving with increasing evidence.
Results: Lipoprotein(a) and apolipoprotein B measurement and coronary artery calcification (CAC) scoring have emerged as tools for identifying residual risk and making decisions in cases of borderline risk. While statins remain foundational to management, newer treatment paradigms emphasize early intensification of therapy and addition of non-statin agents. These trends are reflected in recent guideline updates from the American College of Cardiology/American Heart Association (ACC/AHA) and European Society of Cardiology/European Atherosclerosis Society (ESC/EAS). In the future, polygenic risk scoring and RNA-based therapies may offer opportunities to identify and treat those at highest residual risk.
Money for the studynot stated
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studydiscussion of other studies
“Not stated” does not mean nobody paid — the database does not always record it.
In a laboratory study, atorvastatin metabolites limited lipoprotein oxidation, which may reduce the atherogenicity of Lp(a).
Aim of the study: Lipoprotein(a) [Lp(a)] levels are associated with increased cardiovascular risk, possibly linked to its oxidized phospholipid content that may accelerate lipoprotein oxidation. Attenuating this process could reduce Lp(a) atherogenicity.
Results: Lp(a) oxidized more rapidly than other apolipoprotein B particles and accelerated in a nonlinear fashion at levels associated with cardiovascular risk. The metabolites inhibited oxidation of each fraction in contrast to other statins and consistent with cholesterol-enriched membranes. The metabolites' unique phenoxy group facilitated membrane partitioning, leading to free radical scavenging activity as compared with other statins. The antioxidant actions of atorvastatin metabolites may reduce the atherogenicity of Lp(a) in patients independent of their levels.
Money for the studycompany or manufacturer
Do the authors have ties to companies?yes — the authors reported it
Did a manufacturer help with the study?YES
Type of studylaboratory study (on cells)
“Not stated” does not mean nobody paid — the database does not always record it.
In this study, adding atorvastatin to standard treatment was associated with a better clinical response and more favorable lipid results.
Aim of the study: To evaluate the clinical efficacy of combining cardiovascular agents with statins in the treatment of coronary heart disease(CHD).
Results: The overall response rate was 95% in the treatment group and 80% in the control group, with a statistically significant difference(p= 0.02). Post-treatment levels of total cholesterol, triglycerides, and low-density lipoprotein cholesterol were significantly lower in the treatment group than in the control group, while high-density lipoprotein cholesterol levels were significantly higher (p= 0.00, respectively). Inflammatory markers, including interleukin-6, C-reactive protein, and tumor necrosis factor-alpha, were also significantly reduced in the treatment group compared with the control group (p= 0.00). The adverse reaction rate was 13% in the treatment group and 15% in the control group, showing no statistically significant difference(p= 0.76). The combination of cardiovascular agents with statins, particularly atorvastatin, demonstrates significant clinical benefits in the management of CHD.
Money for the studynot stated
Do the authors have ties to companies?no — the authors say so
Did a manufacturer help with the study?NO
Type of studyobservation of people
Participants110
“Not stated” does not mean nobody paid — the database does not always record it.
After a heart attack, around 60% of patients reached the target LDL-C below 70 mg/dL, and this proportion was maintained for a year.
Aim of the study: There are limited data on contemporary lipid management practices after acute myocardial infarction (AMI) in Japan and on factors associated with achieving the low-density lipoprotein cholesterol (LDL-C) target recommended by current Japanese guidelines (<70 mg/dL).
Results: The mean age was 69.5 years, and approximately three-quarters of the patients were male. At discharge, only 3.6% of patients were prescribed high-intensity statin therapy according to the American College of Cardiology and the American Heart Association definition, whereas 41.5% were categorized as high-intensity according to the Japan Atherosclerosis Society definition. At 3 months, the mean LDL-C level decreased to 67.3 mg/dL, and approximately 60% of patients achieved LDL-C < 70 mg/dL; this proportion was maintained through 1 year. Factors independently associated with achieving LDL-C < 70 mg/dL at 1 year included absence of baseline dyslipidemia (OR, 1.31; 95% CI, 1.05-1.65), baseline LDL-C levels (OR, 0.99; 95% CI, 0.99-1.00), ST-segment elevation myocardial infarction (OR, 1.53; 95% CI, 1.19-1.96), use of moderate- or high-intensity statins (OR, 2.37; 95% CI, 1.79-3.15), and ezetimibe prescription (OR, 1.95; 95% CI, 1.51-2.52).
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studyobservation of people
Participants2 984
“Not stated” does not mean nobody paid — the database does not always record it.
The review indicates that pitavastatin, including when combined with ezetimibe, may help lower LDL-C and achieve treatment targets.
Aim of the study: Pitavastatin, indicated for lowering low-density lipoprotein cholesterol (LDL-C), is particularly beneficial for patients who experience side effects with other statins. When used in combination with other cholesterol-lowering medications, such as ezetimibe, pitavastatin can enhance LDL-C reduction, improving patient outcomes and facilitating achievement of LDL-C targets.
Results: It highlights pitavastatin's effectiveness in managing dyslipidemia and its potential to mitigate CV complications, particularly in patients with atherosclerotic cardiovascular disease (ASCVD). Feedback from practicing healthcare providers across several countries in the Middle East, including Kuwait, Saudi Arabia, the United Arab Emirates, Lebanon, and Jordan, emphasizes the importance of early intervention and achieving optimal LDL-C levels to reduce CV risk. It also underscores the relevance of adhering to international guidelines for dyslipidemia management in regional clinical practice. This paper offers practical recommendations to address challenges and improve the management of dyslipidemia in the Middle East through the use of pitavastatin, with the aim of achieving LDL-C targets and reducing CV events.
Money for the studycompany or manufacturer · Algorithm
Do the authors have ties to companies?yes — the authors reported it
Did a manufacturer help with the study?YES
Type of studydiscussion of other studies
“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
„[31] Statins increase Lp(a) by as much as 30% to raise the risk of major cardiovascular events (MACE) [32,33]. Statin patients with statin elevated Lp(a) is known to increase progression of calcific aortic stenosis. [34] Multiple studies have proven no benefit for statins for this indication. Niacin lowers Lp(a) to reduce MACE risk and are known to reduce carotid intimal calcifications (CIMT), while have failed to demonstrate benefits for CIMT.”[31] Statins increase Lp(a) by as much as 30% to raise the risk of major cardiovascular events (MACE) [32,33]. Statin patients with statin elevated Lp(a) is known to increase progression of calcific aortic stenosis. [34] Multiple studies have proven no benefit for statins for this indication. Niacin lowers Lp(a) to reduce MACE risk and are known to reduce carotid intimal calcifications (CIMT), while have failed to demonstrate benefits for CIMT.
Orthomolecular Medicine News Service Opinion material
„While statins have demonstrated efficacy in reducing certain cardiovascular events, a singular focus on LDL cholesterol fails to incorporate a more holistic understanding of ASCVD pathophysiology.”While statins have demonstrated efficacy in reducing certain cardiovascular events, a singular focus on LDL cholesterol fails to incorporate a more holistic understanding of ASCVD pathophysiology.
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