re: Lipitor side effects

K

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It’s sounds like trying to convince some of these guys is like having a discussion with anti-vaxxers, it doesn’t matter what good information you present you just can’t win

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Absolutely untrue and a completely false equivalence

In fact, I'd go so far as to say that those who cling to bad science (outdated and corrupted cholesterol and sat fat hypotheses for e.g.) are more like the anti-vaxxers than those who actually follow the science (and not "Dr. Google").

I haven't read through all the posts here. But what I have read, studied and analyzed are the studies and continued well-informed hypotheses (teed up for further research) related to cholesterol (off all types), relative risk reduction schemes used to totally distort actual mortality and disease statistics re statins, cholesterol as a response to inflammation, the causes of inflammation and what inflammation actually is, how to fight inflammation without drugs, the effects of certain genotypes on our response to lipids (e.g., the APOE4 allele), lipid hyper-responders, the neuroprotective attributes of cholesterol (yes including LDL), LDL particle count and size as decent proxies for certain potential cvd risk factors but still not shown to be a direct cause of cvd, etc.

Has anyone discussed CAC tests? I would want one of those before moving forward also.

Bookmark this and come back in a decade. This will be much more common knowledge then. Cholesterol, a necessary protective lipoprotein. LOTS of cholesterol? Why? well we have to look at various factors--are the levels there due to increased inflammation or are they in good proportion given other factors and markers? What does this LDL look like (particle size and count). VLDL? triglycerides? What's the patient/subject's CRP level? So much more involved than "LDL is high, high fiber, low fat diet didn't work (duh), stick em on sum drugs.

And also seriously read up on relative risk reduction and how it applies to statins and cvd (NOT just all-cause mortality).

There may be a small subset of people who already have heart disease and can't or won't improve their risk profile with diet and exercise who see some benefit from statins. Beyond that, nope.

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Niacin? It can raise your HDL by 30% in high enough doses

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I haven't looked into this much. I may have to n=1 it before my next lipod panel.

BTW, you can do a full LDL-P test that includes the normal lipid panel + particle number and size and other breakdowns, through Walk-In Labs. You just order online and go to Quest or LabCorp. It's usually under $100.

I like to experiment on myself to see what effects my profile. I haven't gone above 1:1 trig:hdl since cutting carbs and raising good fats. LDL count is high side of "normal" (whatever that means) and particle size and count are super healthy.

The NMR LipoProfile gives you some decent population stats and a patholigic insulin resistance score.

A plant-based diet is not best. Period. Enjoy your propaganda though.

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Good god man, you're a fricking pill pusher. Thank god you're not my fricking doctor.

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You don't need a doctor, you are smarter than doctors.

Also, I can see why you were depressed, you're a fricking nut job.

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I said it CAN be. Many high fat diet proponents do not discriminate the types of fats they are eating. Trans-fats and saturated fats are bad and very-proinflammatory. The most inflammatory thing humans eat is red meat.

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I bet that you didn't know that beef fat is roughly ~48% monounsaturated fat, ~48% saturated fat, ~4% PUFA. I have a hard time believing beef is inflammatory when there is so much MUFA in it, which is considered a great fat by nearly everyone. One will argue that the high amount of SFA is cause for concern, but I would argue SFA is benign at worst.

In fact, their O3:O6 profile does change slightly from grass to grain fed, but not near the amount as compared to chicken or farm/fresh caught salmon.

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Why don't you go prove I am wrong.

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Because even if I did you wouldn't believe it. Youve made your mind up, there's no reason to engage with you.

And I'm not even saying that I disagree with you

Try Food grade diatomaceous earth, it keeps my cholesterol in check.

I just grabbed the first LIPITOR study from the FDA database

Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT)

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In the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), the effect of LIPITOR on fatal and non-fatal coronary heart disease was assessed in 10,305 hypertensive patients 40–80 years of age (mean of 63 years), without a previous myocardial infarction and with TC levels =251 mg/dL (6.5 mmol/L)........ In this double-blind, placebo-controlled study..........and allocated to
either LIPITOR 10 mg daily (n=5168) or placebo (n=5137)

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LIPITOR significantly reduced the rate of coronary events [either fatal coronary heart disease (46 events in the placebo group vs. 40 events in the LIPITOR group) or non-fatal MI (108 events in the placebo group vs. 60 events in the LIPITOR group) with a relative risk reduction of 36% [(based on incidences of 1.9% for LIPITOR vs. 3.0% for placebo), p=0.0005 (see Figure 1). The risk reduction was consistent regardless of age, smoking status, obesity, or presence of renal dysfunction. The effect of LIPITOR was seen regardless of baseline LDL levels. Due to the small number of events, results for women were inconclusive.

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Great, now let’s look at Lipitor.

Out of 10,305 patients, 5,168 had Lipitor and 5137 a placebo. Of these, (fatal CHD – 46 in the placebo group vs 40 that took Lipitor) (Non-Fatal MI – 108 for placebo vs 60 in lipitor). Let's dive into some numbers to look at this another way.

AR (absolute risk) = the number of events (good or bad) in treated or control groups, divided by the number of people in that group

What about the absolute risk (AR)? How much did that decline? Let’s take a look. Fatal CHD of the placebo group , 46/5137=0.00895 or .895%. Fatal CHD of the LIPITOR group, 40/5168=0.00774 or .774%. We’ve reduced the AR by 0.00121….0.121%, or by 6 people…out of a 10,305 total. The Relative Risk (RR) was 1.1569 (1.16) with the equation (46/5137)/(40/5168)=1.1569 In RR, anything less the 2 is very weak, and anything less than 3 should be scrutinized. I run a relative risk of 1.16 if I do not take Lipitor if I meet the qualifications taken in the study.

What about non-fatal MI? the number are better but not much. 108 events for placebo vs 60 events in LIPITOR. So AR for non-fatal MI: Placebo 108/5137=0.0210, or 2.1% vs Lipitor 60/5168=0.0116, or 1.16%. We’ve reduced the AR 0.0094 or 0.94%.....by 48 people out of a 10,305 total. The RR gets better, (108/5137)/(60/5168)= 1.8 which gets us nearer the scrutinized, but still weak. The relative risk reduction

Of all events included. Placebo had 154/5137=0.02998, or 2.998% risk while LIPITOR had 100/5168=0.01935, or 1.935% risk. Those numbers are good, until we take into account the 5,000 other people who didn’t have anything happen on either side. AR was reduced by .01063 or 1.063%. (154/5137)/(100/5168)=1.5493 or RR=1.55. Out of 10,305 patients in the study, 54 more had an event happen by not taking LIPITOR. They have increased their AR by 1.063%

These numbers tell a different tale.

In the second study listed, 2838 subjects either LIPITOR 10 mg daily (1429) or placebo (1411), LIPITOR decreases their AR by 3.2% in the cardiovascular events group, 1.3% for the stroke group, 1.85% for the MI group, and decreased death by 1.54%

*there is rounding involved

** 3:50 update. One could argue that the change of % (.895% to .774% represents a ~13.5% reduction) or (2.1% to 1.16% for a ~45% reduction), which would be significant and they would be correct. But look at the actual numbers that change, or AR, (46-40, 108-60) and compare that to the numbers involved (5168, 5137). Those 54 subjects and the % off of the 10,305 gets a lot smaller. Congratulations everyone, we saved 1.04% of the subjects involved 54/5168 as the placebo group did not have LIPITOR.

Liver failure is a side effect, I was on it for 3 months, it took a year for my liver levels to return to normal