When lovastatin (Mevacor) was approved by the FDA in 1987 there was no hint that it could raise blood sugar. Ditto for many of the popular statins that followed, such as atorvastatin (Lipitor), Rosuvastatin (Crestor), pravastatin (Pravachol) and simvastatin (Zocor). The drug company-sponsored-clinical trials did not detect a metabolic problem. It took the FDA roughly 15 more years to send out a warning that: “Increases in blood sugar levels have been reported with statin use” (FDA Drug Safety Communication, Feb. 28, 2012). Now, seven years later comes confirmation that statins cause diabetes (British Journal of Clinical Pharmacology, March 5, 2019).
When the cholesterol-lowering drug rosuvastatin (Crestor) was associated with type 2 diabetes in the JUPITER trial, many cardiologists were skeptical (New England Journal of Medicine, Nov. 8, 2008). Even the researchers who conducted the trial seemed to downplay the idea that statins cause diabetes. There was no mention in the all-important conclusions that there was a connection between rosuvastatin and diabetes.
Recent findings, which appear in the journal Diabetes Metabolism Research and Reviews, revealed that people who took statins were more than twice as likely to receive a diabetes diagnosis than those who did not take the medication. In this new study, US researchers at the Ohio State University collected data from more than 4,600 men and women who did not have diabetes and were deemed suitable candidates for statins Additionally, people who took statins for longer than 2 years were more than three times as likely to develop diabetes.
Individuals who take cholesterol-lowering statins may be at higher risk for developing high blood sugar levels, insulin resistance, and eventually type 2 diabetes, according to an analysis on more than 9500 adults published in the (British Journal of Clinical Pharmacology, March 5, 2019). Compared with participants who never used statins, those who used statins tended to have higher concentrations of serum fasting insulin and insulin resistance. Participants who ever used statins had a 38 percent higher risk of developing type 2 diabetes during the study. Even in 2014 we knew that statins can lead to weight gain, raised blood sugar levels.
According to results from a study published on 15 May 2020 in the Journal of the Endocrine Society, the use of statin therapy is also associated with elevated levels of insulin resistance in older patients.
In october 2021, a retrospective matched-cohort study published in the journal JAMA Internal Medicine which included 12 years of data (2003 – 2015) from 83 022 statin users and nonusers found that statin use was associated with diabetes progression, including greater likelihood of insulin treatment initiation, significant hyperglycemia, acute glycemic complications, and an increased number of prescriptions for glucose-lowering medication classes.
Shockingly, the Huffington post in 2011 reports that a recent scientific review of 14 studies shows that statins are virtually useless for primary prevention.
It is a pity that mainstream doctors ignore the fact that more 75% of people who suffer heart attacks have normal or low levels of cholesterol. And they downplay the side effects.
One of the most common complaints of people taking statins is muscle pain. One may feel this pain as a soreness, tiredness or weakness in your muscles. statins can cause life-threatening muscle damage called rhabdomyolysis, which can cause severe muscle pain, liver damage, kidney failure and death.
The FDA warns on statin labels that some people have developed memory loss or cognitive impairment while taking statins.
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs.
Now, a new study from 165,411 patients on statins without disease or had suffered a stroke shows that statins don’t even do the one thing they are supposed to do: lower cholesterol. Researchers found that after two years on statins, 51% of the patients failed to reach the standard goal of reducing LDL (bad) cholesterol by 40% or more.
A recent massive study review coordinated by 16 medical scholars and practicing MDs throughout England, Ireland, Italy, Japan, Sweden, and the USA has confirmed the falsity of the lipid theory of heart disease that blames cholesterol, and the disinformation and dangers of cholesterol-lowering statin drugs.
- Statins interfere with the production of coenzyme Q10, which supports the body’s immune and nervous systems, boosts heart and other muscle health, maintains normal blood pressure, and much more. Of all the organs, the heart requires the most energy and CoQ10 to function properly. So why take a medication for heart health that depletes a vital nutrient shown to support the heart—as well as every cell in your body? Low levels of CoQ10 have also been linked to depression and dementia, as well as muscle weakness, fatigue, pain, and nerve damage—all of which are also known side effects of statins.
- Statins weaken the immune system, make it difficult to fight off bacterial infections, and increase the production of cytokines, which trigger and sustain inflammation.
- Statins make some patients unable to concentrate or remember words, and are linked to muscle and neurological problems, including Lou Gehrig’s Disease (Amyotrophic Lateral Sclerosis).
- Statins inhibit the beneficial effects of omega-3 fatty acids by promoting the metabolism of omega-6 fatty acids, which increases insulin resistance and the risk of developing diabetes.
- There is evidence that statin use blocks the benefits of exercise. Exercise increases the activity and numbers of mitochondria, cells’ “power plants” that process sugars and fat. The study found that with statin use, mitochondrial activity actually decreases with exercise.
- Statins work by reducing the body’s ability to produce cholesterol, which is essential to brain health—the brain is 2% of the body’s weight, but contains 25% of the entire body’s cholesterol.
- Statin users have a higher incidence of nerve degeneration and pain, memory loss, confusion, depression, and a higher risk of ALS and Parkinson’s. Statins also decrease carotenoid levels. Carotenoids, which are found in fresh fruits and vegetables and act as antioxidants, have a number of benefits, including protecting against cell damage, aging, and chronic diseases.
- People taking statins were 14 times more likely to develop peripheral neuropathy than people who were not taking statins, according to the Danish study.
- Statin drugs may also be driving Americans to overeat: a twelve-year study published in JAMA Internal Medicine found that statin users increased their calorie intake by 9%, and fat consumption by 14.4%, over the study period, whereas those who didn’t take statins didn’t significantly change in either measure.
- An animal study linked statin use to muscle damage. Animals that exercised on statins had 226% more muscle damage than those not given statins.
- Statins affect the quality of sleep.
- Statins increase the risk of prostate and breast cancer.
- Statins are known to cause liver damage by increasing the liver’s production of digestive enzymes.
- Statins also speed aging and lower sex drive.
- Statins have been linked to aggressive and violent behavior in women.
Studies reported by TheNNT.com on statins given over a five-year period to people with no known heart disease is a good example of why you need to be aware of the Number Needed to Treat (NNT) and Number Needed to Harm (NNH) for any drug. Over 5 years, the NNT for statins showed that no patients had their lives saved. In addition, only one patient in 104 had a heart attack prevented, and only 1 in 154 had a stroke prevented. However, these same studies showed that 1 in 100 were harmed because they developed diabetes as a direct result of stains, and 1 in 10 developed muscle damage as a direct result!
Conclusion: Statin Drugs seems to be Useless and Dangerous by being one of the greatest failures in modern medicine.
Cholesterol is the source material for all sex hormones including estrogens, progesterone, testosterone, and adrenal hormones such as DHEA, and hydrocortisone. Our brains depend upon the hormones made from cholesterol as much as the rest of our body does. Progesterone and pregnenolone protect the nervous tissue throughout our body. A common explanation for the depletion of DHEA and other hormones (e.g., progesterone, testosterone) due to chronic stress is the phenomenon known as “pregnenolone steal.” Elevated cholesterol may simply be a signal the body is working hard to replenish these hormones in the event hormone levels are low. Cholesterol levels may also increase when thyroid hormone production is inadequate. Correcting sex hormone deficiencies, chronic stress and hypothyroidism may bring cholesterol levels down.
Most people know that statins can cause muscle pain and weakness. Not that many realize that there is now enough data to suggest statins cause diabetes.
P.S
Dietary cholesterol had been labeled “dangerous” by the FDA for decades until it fully reversed that stance in 2018. In fact, the 2015–2020 Dietary Guidelines for Americans removed the recommendations of setting a limit to the maximum intake of 300 mg/day cholesterol.
Could your cholesterol medication cause type-2 diabetes?
A study has found that people taking prescribed cholesterol-lowering statins had at least double the risk of developing type-2 diabetes
This is what researchers from Ohio State University found when they analysed the health records of thousands of patients in a private insurance plan in the Midwest.
Researchers found that those who took statins, a class of drugs that can lower cholesterol and blood pressure, for more than two years had more than three times the risk of diabetes.
The study included 4 683 men and women who did not have diabetes, were candidates for statins based on heart disease risk and had not yet taken the drugs at the start of the study. About 16 per cent of the group – 755 patients – were prescribed statins during the study period, which ran from 2011 until 2014. The participants’ average age was 46.
Cholesterol Does Not Cause Heart Disease – Statin Drugs are Useless
Despite over a half-century of cholesterol causing heart disease dogma, there is an increasing understanding that the mechanisms are more complicated, and that statin treatment, in particular when used as primary prevention, is of doubtful benefit.
Key Issues Addressed by the Review Authors Analysis of 107 Studies
The hypothesis that high TC or LDL-C causes atherosclerosis and CVD has been shown to be false by numerous observations and experiments.
The fact that high LDL-C is beneficial in terms of overall lifespan has been ignored by researchers who support the lipid hypothesis.
The assertion that statin treatment is beneficial has been kept alive by individuals who have ignored the results from trials with negative outcomes and by using deceptive statistics.
That statin treatment has many serious side effects has been minimized by individuals who have used a misleading trial design and have ignored reports from independent researchers.
That high LDL-C is the cause of CVD in FH [familial hypercholesterolemia] is questionable because LDL-C does not differ between untreated FH individuals with and without CVD.
Millions of people all over the world, including many with no history of heart disease, are taking statins, and PCSK-9 inhibitors to lower LDL-C further are now being promoted, despite unproven benefits and serious side effects.
We suggest that clinicians should abandon the use of statins and PCSK-9 inhibitors, and instead identify and target the actual causes of CVD. (Emphasis added)
Does high total cholesterol cause atherosclerosis?
No association between total cholesterol and degree of atherosclerosis
If high total cholesterol (TC) causes atherosclerosis, people with high TC should have more atherosclerosis than people with low TC. In 1936, Landé and Sperry found that corrected for age, unselected people with low TC were just as atherosclerotic as people with high TC [4 Landé KE, Sperry WM. Human atherosclerosis in relation to the cholesterol content of the blood serum. Arch Pathol. 1936;22:301–312.
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]. Since then, their seminal observation has been confirmed in at least a dozen studies [5 Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM. 2002;95:397–403.
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]. A weak association between TC and degree of atherosclerosis has been found in some studies [5 Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM. 2002;95:397–403.
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], but the authors only studied patients admitted to a hospital and may, therefore, have included patients with familial hypercholesterolemia (FH). As the percentage of such patients in a cardiology department is much higher than in the general population, a bias may have been introduced. In accordance, the positive association between TC and degree of atherosclerosis noted in the study by Solberg et al. disappeared when those with TC above 350 mg/l (9 mmol/l) were excluded
Does high LDL-C cause atherosclerosis?
If LDL-C is atherogenic, people with high LDL-C should have more atherosclerosis than those with low LDL-C. At least four studies have shown a lack of an association between LDL-C and degree of atherosclerosis [5 Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM. 2002;95:397–403.
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], and in a study of 304 women, no association was found between LDL-C and coronary calcification [16 Hecht HS, Superko HR. Electron beam tomography and national cholesterol education program guidelines in asymptomatic women. J Am Coll Cardiol. 2001;37:1506–1511.
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]. One exception is a study of 1779 healthy individuals without conventional risk factors for CVD [17 Fernández-Friera L, Fuster V, López-Melgar B, et al. Normal LDL-cholesterol levels are associated with subclinical atherosclerosis in the absence of risk factors. JACC. 2017;70:2979–2991.
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]. Here, the authors found that LDL-C was significantly higher among those with subclinical atherosclerosis (125.7 vs.117.4 mg/dl). However, association does not prove causation. Mental stress, for instance, is able to raise cholesterol by 10–50% in the course of half an hour [18 Dimsdale JE, Herd A. Variability of plasma lipids in response to emotional arousal. Psychosom Med. 1982;44:413–430.
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,19 Rosenman RH. Relationships of neurogenic and psychological factors to the regulation and variability of serum lipids. Stress Med. 1993;9:133–140.
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], and mental stress may cause atherosclerosis by mechanisms other than an increase in LDL-C; for instance, via hypertension and increased platelet aggregation.
Are Doctors Overprescribing Statins?
There are two kinds of cholesterol, HDL (the “good” kind) and LDL (the “bad” kind). Cholesterol is synthesized by the liver and intestines, and roughly 80% of the cholesterol in your body is produced by it. Only about 20% comes from your diet.
Because high cholesterol, specifically LDL, is associated with cardiovascular disease, it is desirable for people who have a high level of blood cholesterol to lower it. Exercising and eating foods rich in fiber can help. But for some patients, even that is unlikely to be enough. For those unlucky folks who naturally produce a lot of cholesterol, doctors recommend drugs like Lipitor (atorvastatin), a type of drug called a statin that is used to lower cholesterol.
Recently, the CDC assessed the percentage of Americans taking statins. In 2015-16, the CDC found that 50% of men aged 60 years and older were taking a medication to lower cholesterol. Among women, the figure was 38%.
Anytime we see half of an entire population (in this case, men aged 60+) being prescribed a drug, it might be time to ask if we’re overdoing it. It’s possible that we aren’t. Prevention, after all, is the best medicine. So if statins are saving thousands or millions of lives, perhaps it’s worth it.
But there is something of a public war going on over the use of statins. Indeed, there is tremendous confusion over which patients should receive prescriptions. Professional organizations provide widely varying recommendations on statin use, and researchers clash on their costs and benefits.
Yes, statins do save lives, and some people really need to take them. From that perspective, they are good and necessary drugs. But they also have side effects, such as muscle pain and fatigue. In other words, they can lower a patient’s quality of life and/or prevent him from exercising, which is counterproductive.
The biomedical community and public health agencies would be well advised to investigate the pros and cons of such high statin prescription rates. If we can achieve the same health outcomes with fewer meds, we should probably aim for that.
Statins stimulate atherosclerosis and heart failure
In contrast to the current belief that cholesterol reduction with statins decreases atherosclerosis, we present a perspective that statins may be causative in coronary artery calcification and can function as mitochondrial toxins that impair muscle function in the heart and blood vessels through the depletion of coenzyme Q10 and ‘heme A’, and thereby ATP generation. Statins inhibit the synthesis of vitamin K2, the cofactor for matrix Gla-protein activation, which in turn protects arteries from calcification. Statins inhibit the biosynthesis of selenium containing proteins, one of which is glutathione peroxidase serving to suppress peroxidative stress. An impairment of selenoprotein biosynthesis may be a factor in congestive heart failure, reminiscent of the dilated cardiomyopathies seen with selenium deficiency. Thus, the epidemic of heart failure and atherosclerosis that plagues the modern world may paradoxically be aggravated by the pervasive use of statin drugs. We propose that current statin treatment guidelines be critically reevaluated.
Can statin drug trials lead to deceptive and misleading media reporting?
I just read a fantastic article by Dr. Malcolm Kendrick about how deceptive and misleading media reporting on statin drug trials can be.
Dr. Kendrick uses the Heart Protection Study (HPS) as an example. From the press release for the study:
“In this trial, 10 thousand people were on a statin. If now, an extra 10 million high-risk people worldwide go onto statin treatment, this would save about 50,000 lives each year—that’s a thousand a week.”
That sounds pretty compelling, doesn’t it? It’s hard to argue against saving 50,000 lives a year.
But that’s not what the study showed at all. In fact, the following would be a more accurate report on the results of this study, couched in the context of what we know from other statin drug trials:
Out of 100 high-risk people taking a statin for five years, 98.2 will not see any benefit to their heart health at all—but they will be exposed to significant side effects and complications, including muscle damage and diabetes.
The 1.8 people that do benefit will live an average of 6 months (and a maximum of one year) longer than those that didn’t take the statin.
These results only apply to the people at highest risk for a future heart attack: middle-aged men who’ve already had a heart attack (aka “secondary prevention”). There is no compelling evidence that statins extend lifespan at all in men without pre-existing heart disease, or women with or without heart disease.
It’s misleading to claim that the HPS study showed that statins “save lives.” According to the HPS data, even in the highest risk populations, the best that statins can do is extend lifespan for a few months for <2 out of 100 people who take them.
For the 2 people that did get the benefit, are the possible side effects (some of which can be debilitating, like muscle fatigue, cognitive decline, and diabetes) worth the additional 6 months of life?
And since there’s no way of knowing in advance whether you’ll be one of the 2 people that benefit, or more likely, one of the 98 that don’t, is the very small chance that you’ll gain an extra 6 months of life by taking a statin for five years worth the considerably higher risk of experiencing significant side effects that could impair the quality of your life during that period?
When you think of it this way, statins start to seem somewhat less like the “wonder drugs” they’ve been made out to be, no?
Why Statins Might Raise Diabetes Risk
Taking statins can lead to weight gain, raised blood sugar levels, and it can increase the chances of getting type 2 diabetes, say scientists who have been trying to explain why.
But the team of international researchers acknowledges the cholesterol-lowering medication taken by millions of people can help prevent heart attacks and strokes and should continue to be prescribed.
Heart specialists agree, saying the health benefits outweigh the “small” effect on the risk of getting diabetes.
Study Details
The latest research was led by a team from University College London and the University of Glasgow and was published in The Lancet. It looked at genetic data from 223,463 people, and from 129,170 people who had taken part in clinical trials that tested the effect of statins on heart disease and stroke.
The new study shows that people prescribed statins rather than placebo medication had about a 12% greater risk of getting type 2 diabetes over a 4-year period, and also gained about half a pound in weight on average.
Do Statins Save Lives in Healthy People without Heart Disease?
while statins do moderately reduce cardiovascular events such as heart attack in people without heart disease, they’ve never been shown to extend lifespan in this population. This is true even when the risk of heart disease is high. In a large meta-analysis of 11 randomized controlled trials by Kausik Ray, MD, and colleagues published in the Archives of Internal Medicine, statins were not associated with a significant reduction in the risk of death from all causes. (6)
This trial included 65,000 people without pre-existing heart disease but with intermediate to high risk of heart disease. It was important because it was the first review that only included participants without known heart disease. Previous studies suggesting that statins are effective in reducing death in people without pre-existing heart disease included some people that did have heart disease, which would have skewed the results.
The lack of significant effect on mortality is even more interesting in light of the fact that LDL cholesterol levels did decrease significantly in the statin group; the average LDL level in those taking placebo was 134 mg/dL and the average in the statin-treated patients was 94 mg/dL—roughly 30 percent lower. Yet in spite of this marked reduction in LDL cholesterol in the statin group, there was no difference in lifespan between the two groups. This is yet another line of evidence suggesting that the amount of cholesterol in LDL particles is not the driving factor in heart disease.
What are The Adverse Effects of Statins?
If statins were harmless and free, then it wouldn’t matter how many people need to be treated to prevent a heart attack or extend someone’s lifespan. But statins are not free, nor are they harmless. Statin use has been associated with a wide range of side effects, including:
Myopathy (muscle pain)
Liver damage
Cataracts
Kidney failure
Cognitive impairment
Impotence
Diabetes
Unfortunately, studies show that physicians are more likely to deny than affirm the possibility of statin side effects, even for symptoms with strong evidence in the scientific literature. (9) Assuming that physicians would likely not report the adverse reaction in these circumstances, it’s probable that the incidence of statin side effects is much higher than the reported rates.
One of the most troubling side effects of statins is their potential to increase the risk of diabetes, especially in women. A study by Dr. Naveed Sattar and colleagues published in The Lancet in 2010 examined 13 randomized clinical trials involving over 90,000 patients taking statins. They found that statin use was associated with a 9 percent increased risk in developing diabetes. Note that this is a relative risk, so the absolute risk of developing diabetes while taking a statin is very low. That said, observational data from the Women’s Health Initiative found a 48 percent increased risk of diabetes in healthy women taking statins after adjusting for other risk factors. (10)
What’s more, a 2019 study found a 38 percent increased risk of type 2 diabetes in patients who took statins over a 15-year period. (11) The study also showed:
Even people on low doses of statins were at increased risk of developing diabetes
The increase in risk was significantly higher in those who were overweight or obese
Patients’ risk of diabetes climbed higher the longer they took statins
Lowering Cholesterol with Statin Drugs – Big Pharma’s Queen of Deception
People and medical professionals seriously underestimate human physiology and mental states. They also don’t understand the relationship between physiological states and nutrition, where cholesterol is essential to our bodies’ physiology.
In fact, now that scientists know the intricacies of cholesterol’s role in our trillions of cell membrane functions including the universe of nutrient transportation across membranes, they are starting to realize what a bad idea all this statin thing is. The target of statin therapy –cholesterol – just happened to be vital to all membranes for their proper functioning and structure. Processes and mechanisms such as “vesicle formation, migrations and membrane functions throughout the cellular apparatus” whose implications we are just starting to comprehend.
We are making highly unstable and dysfunctional cell membranes with our restriction of animal fats, which then has a toll on our cell membrane’s function.
The past decade of research has exposed the importance of cholesterol rich membranes with fundamental implications for our brains and nervous tissues, immune system and all areas where lipoproteins are created, secreted, delivered and utilized.[1]
Cholesterol is vital to the formation and correct operation of neurons to such an extent that neurons require additional sources of cholesterol to be secreted by brain cells. No wonder people lose their memories and brains with statin therapy!
Statin drugs also impair the secretion of new myelin. A connection between cholesterol and its fundamental role in the immune system and in the cell membrane’s function and structure and its role should not be forgotten when it comes to autoimmune diseases such as multiple sclerosis.
By restricting cholesterol we change the form and function of every single membrane from head to toe. This harmful effect has indeed far reaching consequences.
Why statin drugs is actually linked with microalbuminuria?
The use of statin drugs is actually linked with microalbuminuria which is known to double the risk for a heart attack or stroke in patients with type 2 diabetes; it is also a marker of poor endothelial function which determines cardiovascular disease risk.[4] Moreover, more frequent statin drug use is associated with accelerated coronary artery and aortic artery calcification, both of which greatly contribute to cardiovascular and all-cause mortality.[5] So doctors are prescribing a medicine which causes the very thing they are trying to prevent. Congratulations! We’ve been had! People are getting increasingly high levels of calcified hearts, and typically during heart surgery “bone eaters” end up being used to replace valves that should had remained silky and smooth. I know where I speak of!
The decades of massive anti-fat propaganda has brainwashed all of us. Upon questioned about their dietary habits, a patient might recall only the fats they ate and think that those are to blame. Never mind that they eat mostly carbs, that is, sugar based foods. Then they remove fat and get frustrated when their cholesterol levels remain high or get even higher. Here is when the statin drug comes. The beginning of the end, since once you start a pill, then comes the other one to counteract the side effects of the first one. And on and on it goes.
It is then when enough levels of cholesterol aren’t available for the body’s repair system, for the uptake of our feel good serotonin brain chemical, for the full initiation of Vitamin D and hormone production and their regulation of blood sugar and inflammation.
Yes, there is a teensy percentage of people out there who genuinely have a true genetic high blood cholesterol that could be dangerous, familial hypercholesterolemia, which is a condition where there is an impaired or even lack of ability to metabolize cholesterol. This doesn’t mean this can be juxtaposed to families with “elevated” (that is, normal) cholesterol.
Sound and reliable medical research hasn’t proved that lowering (or low) cholesterol in and of itself reduces risk of death from heart disease across a population. Moreover, the consumption of animal fats has no link whatsoever with heart disease[6].
Men with very low cholesterol levels are prone to premature death. Below 160 milligrams per deciliter (mg/dl), the lower the cholesterol level, the shorter the life due to cancer, respiratory and digestive diseases, and trauma. As for women, if anything, the higher their cholesterol, the longer they seem to live.
Big Pharma and Big Agra systemically destroyed our health in order to fulfill its business customer potential with its cheap and toxic substitutes that have nothing to do with a fulfilling life. It is a crime to give a statin drug to an elderly person, full end of story.
Does atorvastatin cause muscle pain?
Yes, muscle pain and weakness is one of the most common complaints with statins. The muscle pain can occur in several different ways.
Mild to moderate muscle pain (myalgia) is the most commonly reported side effect with statins, and 1% to 10% (1 to 10 out of every 100 people) may report this effect.
Myositis is a less common inflammation of your muscles that may be accompanied by an elevation in your creatine kinase (CK) which can be determined from a blood test.
Rhabdomyolysis is a very rare but serious form of muscle pain, occurring in less than 0.1% of people. Severe effect leads to a rapid breakdown of muscle tissue, high elevation of creatine kinase (over 10 times higher), and possible kidney damage or kidney failure.
Severe muscle breakdown and kidney damage occurs more often in women, in older patients, or those with ongoing kidney disease or an underactive thyroid (hypothyroidism).
Drug interactions can also lead to muscle pain. Use of higher doses of atorvastatin with certain medications, such as cyclosporine, clarithromycin, itraconazole, and some HIV and hepatitis drugs can increase the risk of muscle pain. Always have your pharmacist run a drug interaction screen any time to start or stop a new medication.
If you notice symptoms of muscle toxicity or rhabdomyolysis such as fatigue, malaise, pain, tenderness, stiffness, cramping, weakness, bruising, low urine output, fever, or brown-colored urine you should call your doctor immediately. Your medication may need to be stopped, your dose adjusted or your medication changed completely.
How does atorvastatin cause type 2 diabetes?
The use of statins may lead to a small increased risk of higher blood sugar (glucose) levels and type 2 diabetes. In general, most doctors agree that the benefits of statins in lowering your heart risk clearly outweigh any risk from the development of diabetes.
A large review of 13 studies (called a meta-analysis) with over 90,000 patients found that use of statins does lead to a small but statistically significant increased risk of developing diabetes (9%). Statins appear to elevate diabetes risk by impairing insulin sensitivity and insulin secretion, although the exact causes are not fully known. One study suggested an immune response may stop insulin from doing its job properly.
Studies seems to suggest that pravastatin is the statin with the lowest risk of causing diabetes, and high-intensity therapy, such as atorvastatin, rosuvastatin or simvastatin may lead to a greater risk. A review from Lancet estimated that if 10,000 patients were treated for 5 years with atorvastatin 40 mg per day (high-intensity therapy), 50 to 100 new cases of type 2 diabetes might occur.
Will atorvastatin make me drowsy?
While atorvastatin won’t cause you to be drowsy or sleepy right after you take it, some people do experience a level of lower energy and tiredness (fatigue) throughout the day. Higher doses may worsen this effect, and women seem to be especially at risk. Fatigue or weakness may also be a sign of more serious effects, such as muscle problems or liver toxicity.
Research published in the journal Archives of Internal Medicine evaluated the side effect of fatigue with statins. Researchers looked at the effect of two other statins, pravastatin and simvastatin, compared to a placebo (sugar pill) in 1016 people. Forty percent, or about 4 out of 10 women reported fatigue and loss of energy after exertion. Older people between 70 and 75 years of age also experienced this effect.
Does atorvastatin cause liver problems?
Atorvastatin can cause liver damage. In clinical trials, liver toxicity was reported in less than 1% (1 out of 100) of patients overall, but was more common with higher doses. Statins are extensively metabolized (broken down) by the liver. Your doctor will check your liver enzymes with a simple blood test before you start treatment with statins.
Liver problems might first be noticed on a blood test ordered by your doctor or you might have symptoms of liver disease. Enzyme blood levels (known as transaminases, or AST and ALT) may be high in your lab report. If these levels get to be about 3 times higher than normal, your doctor may decide to stop your medication, lower your dose, or change your medication to a different class.
If you notice symptoms of liver disease, such as severe fatigue or weakness along with loss of appetite, stomach pain, dark-colored urine or yellowing of skin or eyes, contact your doctor for medical advice immediately.
Can I drink alcohol while taking atorvastatin?
There is no specific drug interaction between alcohol and atorvastatin; however, you may consider limiting your alcohol intake because statins plus excessive alcohol may raise your triglyceride levels and possibly lead to liver toxicity. If you drink more than 2 glasses of alcohol per day, discuss this with your doctor. High cholesterol and alcohol use can be linked if alcohol is consumed chronically and excessively.
Why does atorvastatin have a drug interaction with grapefruit juice?
Drinking grapefruit juice or eating grapefruit while taking atorvastatin (Lipitor) can increase the risk of some side effects, such as liver disease or muscle damage. Blood levels of the drug may increase leading to side effects.
Drug levels rise because grapefruit compounds block enzymes involved in the breakdown of atorvastatin (known as cytochrome P450 3A4 [CYP3A4] enzymes). These enzymes are involved in the metabolism of more than 50% of all drugs, and are needed to help eliminate drugs from the body.
Lovastatin and simvastatin also have drug interactions with grapefruit juice, and you should not drink grapefruit juice at all with these medications.
The drug maker of atorvastatin suggests that people taking this drug avoid large quantities of grapefruit juice (more than 1 quart per day). Always follow the directions on your prescription label.
If you drink grapefruit juice on a daily basis, tell your doctor. He or she may decide to change your statin to one that does not interact with grapefruit juice (such as pravastatin, fluvastatin, rosuvastatin, or pitavastatin). Some interactions are theoretical, based on their CYP3A4 enzymes, but a warning is still important.
Statin therapy and risk of polyneuropathy in type 2 diabetes: A Danish cohort study
Researchers investigated if the risk of diabetic polyneuropathy (DPN) is impacted by statin therapy. For this purpose, they selected all Danish patients with incident type 2 diabetes during 2002–2016. New users were those who started taking statins between 180 days prior to and 180 days following their first diabetes record; prevalent users were defined as those who started statins prior to that time. In this study, 59,255 (23%) new users, 75,528 (29%) prevalent users, and 124,842 (48%) nonusers were analyzed. A median follow-up of 6.2 years was performed. Based on the findings, it was concluded that an increase or mitigation of the risk of DPN in correlation with statin therapy was unlikely in patients suffering from type 2 diabetes, although that could not exclude a small acute risk of harm. There was a slightly increased DPN risk during the first year among new users, but it was gone following >2 years of follow-up.