Cholesterol-lowering statins inhibit substances that protect the cardiovascular system, heart, and brain

Cholesterol is a vital substance found in all cells and involved in many metabolic processes. Our bodies produce most of cholesterol according to its own needs, and the substance only becomes harmful if it oxidizes and gets embedded in the vessel walls. This has nothing to do with cholesterol levels being high or low. There is evidence that cholesterol-lowering statins inhibit the biosynthesis of Q10, vitamin D, vitamin K2, and several selenium-containing proteins. These compounds are important for energy production and serve as essential antioxidants that protect cholesterol from oxidative stress. Because of their reducing impact, statins often lead to fatigue, muscle weakness, oxidative stress, and other side effects that may eventually increase the risk of atherosclerosis, heart failure, and dementia. This is documented in numerous studies published over recent decades.

Although cholesterol is a controversial substance, it does play a crucial role in cell membranes, the brain, the insulating myelin around nerve cells, the immune system, and the synthesis of steroid hormones (sex hormones and cortisol), Q10, vitamin D, vitamin K2, and selenium-containing proteins.
Our liver synthesizes most of our cholesterol. Cholesterol is also found in animal fat, and if we don’t consume cholesterol through our diet, we produce it entirely from carbohydrates.
The reason cholesterol has such a bad reputation is that it also appears in calcified arteries. This, however, has a natural explanation. The cholesterol found in calcified arteries has been damaged by oxidative stress caused by free radicals.
Cholesterol-lowering statins are among the most widely sold drugs. Biochemically, statins work by blocking the enzyme HMG CoA, which is involved in forming an early precursor (mevalonic acid) to cholesterol. Statins have been shown to reduce LDL cholesterol by 30–50%.
Statins also regulate endothelial cell function and inflammation processes that affect circulation. However, since statins also inhibit other functions and substances that depend on mevalonic acid and later precursors to cholesterol, many serious side effects may appear over time, even if the statins initially seem to be well tolerated. Many statin users attribute these side effects to aging, and about one in five discontinues their use after some months or years due to noticeable side effects.

Statins and their inhibition of Q10 and side effects

Q10 is a coenzyme that is crucial for cells to produce energy in the form of ATP. Not surprisingly, the hardworking heart contains particularly high levels of Q10. In addition, Q10 serves as a vital antioxidant that protects the circulatory system, cells, and tissues from oxidative stress.
The body synthesizes most of its Q10, but this production gradually declines from our early 20s - and when using statins. Therefore, statin users often experience abnormal fatigue and poor memory because the brain’s energy metabolism is reduced.
Aching muscles, decreased muscle strength, and other muscle disorders (myopathy) affect nearly 30% of statin users because of the impaired energy production in muscle tissue.
Over time, cholesterol and cells also become more vulnerable to damage from free radicals and oxidative stress, as Q10 also functions as an effective antioxidant.
According to a review article published in Cureus, Q10 supplements can relieve statin-induced myopathy. Q10 supplementation may also counteract oxidative stress and chronic inflammation, which are common threads in aging and most chronic diseases. Q10 can also improve the balance between LDL and HDL cholesterol and enhance the body’s utilization of vitamin C and E, which are part of the body’s antioxidant defense.
When taking supplements, it's worth choosing a pharmaceutical-grade product with documented absorption and bioavailability.

Statins’ inhibition of selenoproteins and their biochemical cooperation with Q10

Selenium is a trace mineral involved in about 25 selenium-containing proteins that are important for energy metabolism, immune function, thyroid function, and heart muscle performance. They also serve as powerful antioxidants. In addition, selenium counteracts several markers of chronic inflammation.
Selenium deficiency is widespread in the Western world due to depleted soils and altered eating habits where less fish and organ meats are consumed. Statins contribute to the selenium deficiency by interfering with the body's complex selenium metabolism, which requires a later precursor of cholesterol (mevalonate). Statins thereby inhibit the body's production of selenocysteine and other selenoproteins such as GPX and thioredoxin reductases that function as powerful antioxidants and are involved in cellular energy metabolism.
It is already known that selenium deficiency is linked to the development of weakened heart muscle (dilated cardiomyopathy). Also, a deadly heart disease (Keshan disease) is caused by severe selenium deficiency.
Nonetheless, sufficient selenium intake from diet and supplements helps reduce the risk of cardiovascular disease, thyroid disorders, viral infections, cancer, and premature death, according to a study published in Frontiers in Nutrition.
Selenium is also needed for Q10 to alternate between its energy-producing form (ubiquinone) and its antioxidant form (ubiquinol).
A groundbreaking randomized controlled trial called KiSel-10 revealed that elderly participants who took 200 micrograms of selenium yeast and 200 milligrams of pharmaceutical-grade Q10 daily for four years had significantly lower cardiovascular mortality and better heart function compared with the placebo group. The group taking the supplements had a 54% lower cardiovascular mortality rate during the study. Follow-up studies showed that the group receiving selenium and Q10 continued to have improved heart function, circulation, quality of life, and longevity.

Statins’ inhibition of vitamin D and side effects

Vitamin D regulates about 10% of our genes and countless biochemical processes, including calcium absorption, muscle function, immune defense, inflammation regulation, insulin sensitivity, and cancer prevention. We form a precursor of vitamin D in the skin with the help of cholesterol and sunlight (UV radiation). But because statins inhibit our cholesterol levels, they can also interfere with our vitamin D synthesis.
According to an Italian study, statin-induced vitamin D deficiency can cause muscle pain and other muscle disorders. A review article published in Nutrients states that low vitamin D levels increase the risk of respiratory infections, high blood pressure, cardiovascular disease, type 2 diabetes, Alzheimer’s disease, cancer, and premature death. Statin users should therefore have their blood vitamin D levels tested (levels should ideally be above 75 nmol/L) and take supplements as needed.

Statins’ inhibition of vitamin K2 and side effects

Vitamin K2 is important for both bones and the circulatory system, as it regulates calcium distribution in the body. It helps produce a protein named MGP (matrix Gla protein), which removes calcium from the bloodstream. Vitamin K2 is also needed for producing osteocalcin, which embeds calcium into bone tissue.
Vitamin K2 works with vitamin D to regulate inflammation, which is common in aging and most chronic diseases.
K2 is mainly found in fermented products like butter, cheese, and sauerkraut, as well as in fatty cuts from grass-fed animals. People’s fear of fat combined with things like unnatural animal diets contribute to these deficiencies.
Humans are also able to convert vitamin K1 (found in dark green vegetables) into K2, although this requires a well-functioning gut flora. Statins also inhibit the body’s own production of vitamin K2.
Over time, vitamin K2 deficiency can increase the risk of atherosclerosis and osteoporosis as a result of calcium ending up in the wrong tissues. According to a study published by the Alzheimer’s Association, vitamin K2 deficiency can raise the risk of dementia and Alzheimer’s disease. This is mainly because vitamin K2 counteracts calcifications and the accumulation of harmful proteins and inflammation in the brain.

Statins increase the risk of a wide range of side effects, including:

• Fatigue and poor memory
• Muscle pain or muscle weakness (myalgia)
• Liver damage
• Diabetes (which itself increases cardiovascular risk)
• Impotence
• Sleep disturbances
• Atherosclerosis
• Weakened heart and heart failure (dilated cardiomyopathy)
• Other indirect side effects due to inhibited production of Q10, selenoproteins, vitamin D, and vitamin K2

It is not cholesterol that causes atherosclerosis, it’s oxidative stress

Oxidative stress is a condition where potentially harmful free radicals outnumber the protective antioxidants. We all produce free radicals as a natural waste product of various metabolic processes. The free radical load rises significantly in response to factors such as tobacco smoke, toxins, aging, excess weight, and chronic diseases like diabetes, which is also associated with chronic inflammation. Free radicals are highly reactive molecules. During oxidative stress, they can attack cholesterol that is transported in the blood to cells in the form of LDL cholesterol. When LDL cholesterol oxidizes, it turns rancid and can no longer be used for its numerous functions. As a result, the oxidized cholesterol is consumed by white blood cells (monocytes) that then turn into foam cells. These foam cells migrate to areas in the vessel wall where inflammation already exists due to ruptures, bacteria, or other irritants. After entering the vessel wall, the foam cells die and leave behind the oxidized cholesterol. This increases local inflammation and attracts more foam cells, thereby creating a vicious cycle.
Atherosclerosis is a complex process that in its later stages also involves a fibrin layer and a calcium matrix around the embedded foam cells in the vessel wall.
As shown, it’s oxidative stress, chronic inflammation, and the accumulation of cholesterol-rich foam cells and calcium in the vessel walls that set the stage for atherosclerosis, and this has nothing to do with cholesterol levels being high or low.

• Always consult your doctor before you discontinue your statin use.

Good advice for the natural prevention of atherosclerosis

Atherosclerosis is typically a lifestyle-related condition characterized by oxidative stress and chronic inflammation. Therefore, it is important to address underlying causes such as an unhealthy diet high in refined carbohydrates, overweight, smoking, alcohol abuse, and exposure to toxins. It is also essential to maintain an adequate supply of antioxidants such as Q10, selenium, zinc, and vitamins A, C, E, D plus magnesium and omega-3 fatty acids to help regulate inflammation. In addition, make sure to get enough vitamin K2, which helps remove calcium from the bloodstream and deposits it in the bones. Physical activity, regular breaks, and high-quality sleep also play a crucial role.

References:

Khoula Ahmad et al. Effectiveness of Coenzyme Q10 Supplementation in Statin-Induced Myopathy: A Systematic Review. 2024

Urban Alehagen et al. Improved cardiovascular health by supplementation with selenium and coenzyme Q10: applying structural equation modeling (SEM) to clinical outcomes and biomarkers to explore underlying mechanisms in a prospective randomized double-blind placebo-controlled intervention project in Sweden. European Journal of Nutrition. 2022

Yuchen Zhang et al. Association of dietary selenium intake with the risk of chronic diseases and mortality in US Adults. Frontiers in Nutrition 2024

Manuella Pennisi et al. Vitamin D Serum Levels in Patients with Statin-Induced Musculoskeletal Pain. Disease Markers 2019

William B. Grant. A Narrative Review of the Evidence for Variations in Serum 25-Hydroxyvitamin D Concentration Thresholds for Optimal Health. Nutrients 2022

Sarah L. Booth. Association of vitamin K with cognitive decline and neuropathology in community-dwelling older persons. Alzheimer’s Association. 2022

Harumi Okuyama et al. Statins stimulate atherosclerosis and heart failure: Pharmacological mechanism, Expert Review of Clinical Pharmacology. 2015

Uffe Ravnskov. Hvorfor et højt kolesterol er nyttigt. Hovedland. 2010