Summary:
Statins do NOT prolong life - Harvard Medical School - 2011
LDL of 140 mg/dL IS OPTIMAL!
The American College of Cardiology wants you to die young of a stroke with their preferred LDL level of 70. (See upcoming blog)
According to Harvard Medical School, treatment with statin drugs does NOT improve outcomes. Proto Magazine is an internal publication for healthcare professionals that are part of the Harvard Medical School healthcare network. In 2011, a feature article was published titled, “Questioning Statins.”[i] The byline was
“WHAT STATINS MIGHT DO FOR YOU:
Lower cholesterol // Reduce risk of cardiovascular disease //
Cause muscle pain and fatigue;
Fail to significantly prolong your life."
[i] https://protomag.com/endocrinology/statins-change-of-heart/, January 15, 2011.
Proto is a national science magazine and website produced by Massachusetts General Hospital.
Other gems in this publication include “Statins don’t seem to confer the ultimate health benefit – longer life. So, is lowering cholesterol as important as everyone has been led to believe?”
Harvard dropped the bombshell in their internal publication, but it remains ignored even at Harvard hospitals.
Also stated in Harvard magazine, “Why did statins appear to protect the hearts of people who didn’t have high cholesterol? It could be that they lower cholesterol and reduce inflammation.”
If you read between the lines, it appears that Harvard Medical School is saying that cholesterol is not the cause of cardiovascular disease, but inflammation is.
We can also infer that statins are anti-inflammatory, but based on their results against cardiovascular disease, they are very poor at the job and have too many side effects.
This Harvard article is not a coincidence. It was published in 2011, when most statin drugs were coming off patent. So, they were going generic, and profits were about to tumble. Harvard was setting up a treatment transition from statins to the new and very expensive on-patent biological drugs. As you saw in a previous blog, they are miserable failures because lowering LDL is harmful. Harvard could not feasibly retract the Proto article, and statins are still heavily prescribed because the new alternative class of drug failed.
What happens if you naturally have either low or high LDL without any treatment? Studies are few and far between. However, one substantial report reveals that an LDL level that is low or very high has close to the same impact on early mortality regardless of treatment. And, having a low LDL is much more hazardous compared to a high LDL.
Again, this is regardless of treatment versus no treatment.
The evaluation included 108,243 individuals aged 20-100, of whom 11,376 (10.5 percent) died during the study, at a median age of 81. The association between LDL levels and the risk of all-cause mortality exhibits a U-shaped curve, as usual.
Low levels of LDL show a dramatic increase in mortality risk, whereas, at high levels, the increase in mortality is much less dramatic, Figure 5.16. These results were consistent in men and women, across age groups, and for cancer and other causes of early death.
Figure 5.16. Early mortality risk with LDL values in people not on LDL-Lowering therapy. The optimal LDL level is 140 mg/dL.
The lowest risk of all-cause mortality is at a concentration for LDL of 140 mg/dL (3.6 mmol/L). The American College of Cardiology sets the standards for LDL normal values and asserts that an LDL below 70 mg/dL is optimal.
As of April 2022, over 100 peer-reviewed publications link low total cholesterol and early death. Searching on the term "LDL" as opposed to "cholesterol" adds another dozen.
More from the article.
One physician looks at a pill and sees a potent defense against the leading cause of death in the United States and much of the world. Another sees an expensive illusion that offers most patients false hope and potential harm. How can that be?
DESPITE ITS SINISTER REPUTATION, CHOLESTEROL IS ESSENTIAL FOR HUMAN HEALTH. The membranes around every cell in the body require cholesterol, as do certain hormones, bile acids and vitamin D.
Between 60% and 80% of the cholesterol in blood travels via LDL. (Meanwhile, high-density lipoprotein, or HDL, carries excess cholesterol to the liver for reuse or removal.)
The drugs have provided enormous benefit to the pharmaceutical industry, which followed Mevacor with a list of other statins, including Zocor (simvastatin), Lipitor (atorvastatin), Baycol (cerivastatin), Crestor (rosuvastatin) and, most recently, Livalo (pitavastatin).
Others, including Beatrice Golomb, a colleague of Steinberg’s at the University of California, San Diego, are less sanguine. Golomb has published several papers linking statins to permanent muscle damage and such cognitive problems as memory loss. Golomb’s data comes from a Website, statineffects.com, that invites statin patients to describe side effects.
Critics question this methodology—“she doesn’t have a control group,” Steinberg notes—but Golomb counters that randomized controlled trials often exclude people most likely to suffer adverse events from taking a drug, including those who are sick or who take other medications.
And she challenges the conventional wisdom that statin-induced muscle aches and fatigue always go away when a patient stops taking the drugs, citing a “reasonably high fraction” of patients who are left with residual discomfort and weakness. Statin defenders dispute Golomb’s assertion that the drugs cause cognitive problems, noting that memory complaints are widespread among the predominantly middle-aged and older population who take the pills. “Then why would memory loss reverse itself when the patients go off statins?” Golomb asks.
Considering that statins don’t seem to confer the ultimate health benefit—longer life—some clinicians question whether lowering cholesterol is as important as everyone has been led to believe. “If you decrease your chance of having heart attacks, you’d think you would live longer,” Redberg says. “But that doesn’t turn out to be true. So what is the benefit of taking this pill for the rest of your life?”
“I like to practice evidence-based medicine,” says Rita Redberg, the journal’s editor. “The evidence is not strong enough to support statins for primary prevention.”
Kira Endo is credited with discovering and applying the first statins. The paragraph below documents his first presentation of the findings.
KIRA ENDO SCANNED THE ROOM, WAITING FOR HIS TURN TO SPEAK. The turnout was impressive—some 200 physicians and scientists. Endo had traveled from Tokyo to the sixth International Symposium on Drugs Affecting Lipid Metabolism in Philadelphia on this day in 1977 to elaborate on his discovery of a molecule called compactin in blue-green mold.
In college Endo had been impressed by the biography of Alexander Fleming, the Scottish scientist who discovered penicillin in a moldy culture plate. Endo knew that penicillin and other antibiotics can inhibit many enzymes, and he hoped that studying molds might yield a substance that would block HMG-CoA reductase, an enzyme that raises cholesterol levels. After testing more than 6,000 fungal extracts, he finally found one that safely inhibited the enzyme. He thought compactin might hold the key to treating elevated cholesterol, which had recently been linked to heart attacks and strokes.
Lewis comment: This is the first clue that statins are antibiotics (see previous blog)
In a twist worthy of O. Henry, the man who discovered the first statin learned during a medical checkup in 2000 that his own LDL was rising. “Don’t worry,” the doctor told Endo, “I know some very good drugs to lower your cholesterol.”
But here’s the real twist: Endo refused the statin prescription. His LDL was only modestly elevated, so Endo decided to try bringing his cholesterol under control by exercising more. Eventually, though, Endo chose to take his own medicine. “The exercise did not work well,” he wrote in an e-mail. “I am now taking a statin. However, I shouldn’t specify which one.”
Lewis comment: Why didn't exercise NOT improve his cholesterol?
BECAUSE IT WAS ALREADY OPTIMAL!
Index & Upcoming (short) blogs on cholesterol and statins
Number 1: Cholesterol fun (true) facts - completed
Number 2: Is the actual cholesterol molecule important? c - completed
Number 3: What is an optimal TC value? Remember, no one knows their actual cholesterol molecule value. - completed
Number 4: Surprising fact about cholesterol as an antibiotic - completed
Number 5: TC simple math - dumb doctors - completed
Number 6: What is LDL really? - completed
Number 7: Statins - do they lower the cholesterol molecule? - completed
Number 8: What did we learn from the new "biologics" to lower "cholesterol" - completed
Number 9: Niacin and other "cholesterol" management treatments - completed
Number 10: What did Natasha Campbell-McBride say about cholesterol/lipids? - completed
Number 11: What is a QALY, and how does it relate to "cholesterol"? - completed
Number 12: Idiot doctor from Johns Hopkins, Roger Blumenthal - completed
Number 13: Statins cause Alzheimer's and ALS - THEHIGHWIRE - completed
Number 14: Statin drugs CAUSE diabetes - completed
Number 15: The statin merry-go-round to poor cardiovascular outcomes - completed
Number 16: How statins CAUSE heart disease - completed
Number 17: How statins CAUSE heart disease - part 2 - completed
Number 18: Women and statin drugs - completed
Number 19: If not "cholesterol," then what? - completed
Number 20: If not "cholesterol," then what? - part 2 - completed
Number 21: Statins and erectile dysfunction - completed
Number 22: Who says statins do NOT extend life? - completed
Number 23: Statins cause strokes.
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