More bad info about Statins

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Dansk

Active Member
Americans especially have been led to believe that cholesterol is the end all and be all to heart disease, to think any one thing (in this case cholesterol) is the cause of your heart disease is very narrow minded, sad thing is the MD's have been also been brainwashed into believing this also. Mercola has been alerting about this issue for over 20 years.

Its never any one thing in regards to things like heart disease, its always a hodgepodge of things coming together to create the perfect storm.

Pharma is very good at convincing people otherwise.
 

DragonBits

Well-Known Member
What can I say Statin Drugs crippled me after being saved having heart bypass. Hear is a must read.

e Most Profitable Pill in Medical History Is Based on Flawed Science

e Most Profitable Pill in Medical History Is Based on Flawed Science
pmgamer18

If you analyze the article in MERCOLA, I found at least 1 obvious misstatement. I only looked at the 1 statement, there maybe many more flaws.

Correct me if I am wrong about this.

From the article.
" A Norwegian study5 published in 2012, which assessed the cholesterol levels and rate of ischemic heart disease death among 50,000 people over a period of 10 years, found that as women’s cholesterol levels went up, their risk of death went down.

“Women who had LDL levels of 300 to 400 were 40 percent less likely to die from ischemic heart disease as women who had an LDL level or cholesterol level of 200 or less,” Kendrick says. As noted by the study authors:"

The Norwegian study they quoted NEVER looked at LDL, it only looked at total cholesterol. The author seems to be conflating total cholesterol with LDL cholesterol.

Norwegian study they referenced in the article.

Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study

It probably pretty rare that anyone ever looks at their references.
 

Blackhawk

Member
Has anyone tried turmeric for there pain if so how long did it take to work.

For what kind of pain?

I used curcumin for quite a while until I had to stop due to drug interaction concerns with cancer drugs. For me, it helped take the edge off arthritis inflammation.
 

pmgamer18

Active Member
What caused your clogged arteries?
Hi Vince what I had wrong is called "The Widow Maker" and a birth defect. Along with being secondary low hormones like growth hormone.

I never had high cholesterol in my life the heart Dr. that did my bypass was full of it and saved my life but ruined it.
 

Vince

Super Moderator
Hi Vince what I had wrong is called "The Widow Maker" and a birth defect. Along with being secondary low hormones like growth hormone.

I never had high cholesterol in my life the heart Dr. that did my bypass was full of it and saved my life but ruined it.
Widow Maker is a 100 percent blockage of the left anterior descending artery.

Can you post your lipid panel?
 

Nelson Vergel

Founder, ExcelMale.com
Questioning statin therapy for older patients
Lancet June 12 2020

Single clinical trials have not yet determined whether statin therapy provides more benefit than harm to people older than 75 years with or without a history of vascular disease. The Cholesterol Treatment Tria lists' Collaboration, which alone has access to patient-level data from most trials, is best able to answer these questions. However, we have several concerns about the Article by the Collaboration 1 and the presentation of its results to the media.

First, the collaboration states that rates of use of statin therapy are substantially lower in people older than 75 years,1 but the data in table 2 of one of the two sources cited to support this claim, by Salami and colleagues,2 show just the opposite.

Second, although the collaboration reports that they have data on 14483 trial participants older than 75 years, approximating the total denominator of all such participants from the figures in the 2019 meta-analysis gives only 9473 participants for figure 1A and 10 513 participants for figure 5A (by dividing the number of events by % per annum ÷100 × median number of years per study). Thus, either the collaborations'calculations are missing 27–35% of the available data or a considerable number of trials had short follow-ups. Although short follow-ups would explain this discrepancy through a difference between the median and mean duration of the studies, we find this explanation untenable because of the magnitude of the difference; it is at least worthy of additional explanation.

Third, the collaboration's data show that annually, 1000 people older than 75 years without a history of vascular disease need treatment to prevent a single major vascular event, and cardiovascular or all-cause mortality data are not presented for this population. These results make informed doctor patient decisions impossible, especially when the frequency of side-effects that are meaningful to patients is simply not known.

Because most people older than 75 years do not have vascular disease 3 and the Collaboration does not present mortality data for this population, we believe the Collaboration was irresponsible in relaying to the media that 8000 deaths could be prevented each year if all UK citizens aged 75 years or older took statins. 4 Given these gaps in the data, we believe it is wrong to recommend statin therapy uniformly for people aged 75 or older who do not have cardiovascular disease. A far more beneficial public health message is the strong evidence for the cardiovascular benefit of maintaining a healthy lifestyle, especially including routine exercise.

Finally, doctors and patients need to be reminded that patient-level data held by the Collaboration remain unavailable for independent analysis and therefore have not been verified.

JA has served as an expert for plaintiffs' attorneys in litigation involving Avandia and Crestor, and is writing a book about the pharmaceutical industry. NJ has served as an expert for the defence attorneys in litigation involving Ferrirprox and Aranesp, and for the plaintiffs' attorneys in litigation involving Neratinib, Loestrin 24 Fe, Suboxone, Doryx, Zoloft, Prozac, Lipitor, and Granuflo. All other authors declare no competing interests

ATTACHED ARTICLES
 

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Nelson Vergel

Founder, ExcelMale.com




 

Nelson Vergel

Founder, ExcelMale.com

The impact of rosuvastatin (Crestor) on hypothalamic–pituitary–testicular axis activity in metformin-treated and metformin-naïve men with low testosterone levels: a pilot study​


Background
Intense statin therapy was found to impair testosterone production in men. Metformin administered to subjects with hypergonadotropic hypogonadism decreased gonadotropin production. The current study was aimed at investigating whether metformin treatment modulates the impact of high-dose rosuvastatin therapy on hypothalamic–pituitary–testicular axis activity in men.

Methods
The study included 43 very high cardiovascular risk men with late-onset hypogonadism, 20 of whom had been treated with metformin (1.7–3 g daily) for at least 6 months. In all subjects, unsuccessful initial statin treatment was replaced with rosuvastatin (20–40 mg daily). Plasma lipid levels, glucose homeostasis markers, as well as circulating levels of gonadotropins, testosterone, bioavailable testosterone, dehydroepiandrosterone-sulfate, prolactin, estradiol and creatinine were measured at the beginning of the study and 4 months later in 28 individuals in whom rosuvastatin reduced LDL cholesterol levels to below 70 mg/dL.

Results
There were no differences between treatment-induced changes in plasma lipids. In both study groups, rosuvastatin reduced total and bioavailable testosterone levels. However, only in metformin-naïve men, rosuvastatin increased LH and FSH levels and slightly impaired insulin sensitivity. The impact on gonadotropin concentrations correlated with treatment-induced decrease in testosterone levels. There were no significant differences between baseline and posttreatment values of dehydroepiandrosterone-sulfate, prolactin, estradiol and the glomerular filtration rate.

Conclusion
The obtained results suggest that metformin prevents the compensatory increase in gonadotrope function induced by intense statin therapy.

 

M.J

Well-Known Member
Nelson doctors are putting me on “crestor” as I understood from the above it’s statin ? And it does effect libido ??
my LDL are very high although I am a healthy guy still doing further analysis with my lipidologist.
Should I be on crestor or move to something else like red yest rise ? Does crestor effect libido ?
 

Nelson Vergel

Founder, ExcelMale.com
It’s really the mildest of all statins. Unless you can really bring down your LDL
naturally, I would take it. How high is your LDL? How about triglycerides and HDL?
 

M.J

Well-Known Member
It’s really the mildest of all statins. Unless you can really bring down your LDL
naturally, I would take it. How high is your LDL? How about triglycerides and HDL?
These are my results
34430E4A-B83F-464A-B2BF-E5D4F39609B1.jpeg
C2C0F22A-F9FD-40CC-92ED-0E5EA8EEFD87.jpeg
 

Nelson Vergel

Founder, ExcelMale.com
Those numbers are easy to bring down with a diet low in sweets and high in protein and greens. They are not horrible at all. And your HDL is pretty nice.
 
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