Personal Confusion Regarding Dr. Valter Longo's Proposal of Low-Protein Longevity Diet

I completely agree, which is why I have increased my dosage of Metformin to 500 mg daily (1 g on the day of Rapamycin dosing) and have added 10 mg of Ezetimibe daily.

I tried to add Rosuvastatin, but the side effects were too horrible. If the LDL cholesterol is still an issue, I will consider adding Bempedoic Acid. But, I want to give the Ezetimibe by itself a shot first.

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I was going to ask if you had tried Rosuvastatin. Did you go low dosage? I just started on 5mg every other day about a month ago and zero issues so far. That’s only 15-20 mg per week. Many people are dosing at 20 mg daily which is dramatically larger load at 140 mg in a week.

There is some evidence for Rosuva effectiveness at low levels. I will do a lipid panel in a month or so to check. My LDL was low last test but ApoB and particle count have ranged a bit high in the past and am not only looking for long term particle damage control but for the other less measurable effects of statins as well .
Not on Metformin anymore (no good reason other than muscle studies) nor have I tried Rapa yet. Doing large doses of Omega 3 (3 grams daily) and long term Resveratrol (1 gram daily) user since being “prescribed” for Lyme disease ten years ago by herbalist.

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It seems that the great majority of diet/health/longevity opinion leaders choose managing sarcopenia as a priority over the theoretical dangers of protein as favored by Dr. Longo.
Even those (most!) who greatly respect his fasting centric approach do not seem to concur (in practice) with this aspect of his approach.

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I tried Rosuvastatin 5 mg every other day and it was still horrible. It took me weeks after stopping to get back to normal. The muscle soreness and weakness was unbearable.

It just doesn’t work for some people. I can accept that and move on to other things. At least the ezetimibe also comes with an energy boost.

I also take 2 g of Omega-3 daily and 1 g of Resveratrol 3x a week.

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Ah, ok. I am on the alert myself. I am taking CoQ. It’s interesting how much more that effect seems to happen in real life vs studies.
It seems that you are far more aware and engaged on these fronts than me. I only mentioned the Omega 3 and Res as a reference but I do think that my low triglyceride numbers may be helped by the O-3. I eat a fairly high saturated fat diet and have one APOE4 allele.

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For me, the muscle soreness happened in an instant. It didn’t gradually build up. It was more like getting hit by a truck. I was also taking CoQ10 and that didn’t seem to help.

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Rosuvastatin didn’t work for me too. I was on 5 mg/day. Trying ezetimibe, 10mg, and Pantethine, 500 mg, now.

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Let me interject some ideas in here that I am not so far seeing represented in this discussion,
The first is that Mother Nature (evolution) is not profligate of biologic energy reserves and has conserved the system of cholesterol production for good reason. It is a component of every cell membrane in the body and a precursor of many vital hormones. (All classes of steroid hormones, glucocorticoids, mineralocorticoids, and sex hormones are derivatives of cholesterol.) This system is important enough that it includes a cholesterol making mechanism if we don’t get enough in our diet. To suppose that system in an error is woefully short sighted. Cynics claim the fear of cholesterol is only a result of labs finally having a test to measuire cholesterol.

Gary Taubes book, “Good Calorie Bad Calorie” includes the fact that Dwight Eisenhower’s 1955 heart attack occurred when his cholesterol was 156.

The second. Plaque build up in arteries is a complex process to protect damaged endotheliel cells. The damage is probably just another function of chronic inflammation, but for whatever reason, the damage is repaired with a clotting process (like a scab on the damaged knee) that is essentially an internal scab which eventually incorporates cholesterol. The damage causes the plaque. Cholesterol doesn’t cause the plaque.

But Third–is the kicker. Here is the Summary from The Journal “Annals of Nutrition and Metabolism,” 2015:66 “Cholesterol and Mortality.”

“Overall, an inverse trend is found between all-cause mortality and total (or low density lipoprotein [LDL]) cholesterol levels: mortality is highest in the lowest cholesterol group without exception. If limited to elderly people, this trend is universal. As discussed in Section 2, elderly people with the
highest cholesterol levels have the highest survival rates irrespective of where they live in the world.”

Let us factor in these pieces of information in this discussion of ;longevity and health.

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If nature is good, why aren’t we immortal with an indefinite youth and healthspan?

Cholesterol doesn’t cause the plaque.

With low enough cholesterol levels, plaque never even forms and we have evidence of soft plaque decreasing with low levels of LDL cholesterol.

“Overall, an inverse trend is found between all-cause mortality and total

This is an observational study that doesn’t take cofounding factors into account, like all the others. Why do you ignore the intervention studies where statins do indeed decrease all cause mortality?

“The risk of all-cause mortality was significantly reduced in statin users (hazard ratio: 0.72, 95% confidence interval: 0.66−0.76). The reduction in mortality risk was similar in CVD studies (0.73, 0.66−0.76) and non-CVD studies (0.70, 0.67−0.79).”

Effect of Statins on All-Cause Mortality in Adults: A Systematic Review and Meta-Analysis of Propensity Score-Matched Studies - PubMed (nih.gov)

Systematic reviews trump observational trials by the way, as indicated by this picture below.

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My mother, 91, has high cholesterol for at least 30 years (before it was not measured). She refuses to take any statins. Amazingly, her heart is very healthy, she has normal BP, etc. She’s pretty active and lives independently. Her doctor, who’s at least 30 years younger, said he envies her bloodwork results. And I do too :grinning:

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For me, the muscle soreness happened in an instant. It didn’t gradually build up. It was more like getting hit by a truck. I was also taking CoQ10 and that didn’t seem to help.

I really wish we could know why statins do this with some people and not others. I feel like I’m notorious for getting side effects but somehow taking 20mg rosuvastatin is like eating m&ms. No issues even in the sluggtes.

But then I try to take finasteride for hair loss and it makes me feel like complete garbage.

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Finasteride also negatively affects me as well, but I guess not as bad as you. But I am glad you can handle Rosuvastatin. I wish I could.

Smoking is good for you.
‘World’s Oldest Man’ Is 114 Years Old, Smokes Every Day (newsweek.com)

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For me it’s the opposite. I can take finasteride without any issues whatsoever but anything above 10mg of rosuvastatin makes me feel miserable even when supplementing with ubiquinol.

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You’re making the assumption that Mother Nature intended humans to live for 80-100 years. I doubt that is the case.

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Please show me how that assumption follows from the biology. It may be obvious but I’m not seeing how. Thanks.

To suppose that system in an error is woefully short sighted.

According to you, nature is perfect and does not make any errors. So why are humans not immortal? Why does reducing apoB via statins reduce all cause mortality in intervention trials while being very safe and tolerable?

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I assume you’re responding to @KarlT immediately up-thread? If so, I can’t speak for him, but I agree with the overall sentiment in this case, and I’ll explain why.

90 years old is old. It’s old for humans today, and modern low-tech and hunter-gatherer societies have similar (slightly shorter) maximal lifespans, with overall higher mortality at all ages. So any evolutionary benefit of adaptations that specifically impact 90 year olds is very low. Now, that phrasing “specifically impact” is important: aging causes morbidity and mortality in mid-life where there’s still quite a large population in any society, so this argument certainly doesn’t hold for aging in general. (Notably, this holds across most animal species!) But in the case of ASCVD, I’m not convinced, since at least in terms of mortality it’s not really a problem in the lifestyle of modern hunter-gatherers. IMO it’s perfectly plausible that the problems of normal endogenous cholesterol just don’t appear in “wild” populations.

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I certainly did not say nature is perfect. I’m presenting ideas that have not been mentioned that I and a lot of other people think are worth looking at. I said “Mother Nature (evolution) is not profligate of biologic energy reserves” At least. I’d ask not to be misrepresented!

The whole cholesterol system has been conserved in all higher animals. If that does not speak to the importance (positively) of the whole thing, I’d be very surprised. You can argue that it’s purpose is less important in old age, I guess, if you do not think cell membranes and all those hormones (also spinal cord and brain, etc) are also not important in old age But no one I’ve read has claimed that. So it seems pretty self evident the stuff is important for life not just growth or reproduction.

Every cell in the human body produces its own cholesterol which is crucial for life. The issue is that the liver produces additional cholesterol which causes ASCVD to develop in humans. The use of statins inhibits some of that extra cholesterol production and thereby decreases all cause mortality (which wouldn’t be the case if it was needed in the body).

If we want to go down the rabbit hole of appeal to nature, every organism has mTOR activity so clearly it must be crucial for life and no one should be using rapamycin to inhibit it because it goes against nature.

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