Cholesterolmaxxing - How to fix your lipids

This is too complicated. I lowered my cholesterol by eating less junk and drinking more water
 
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mirin high quality post i need PCSK-9 inhibitors and reta
 
Cholesterolmaxxing - How to fix your lipids

What even is "cholesterol"?

For the sake of this thread, I want you to forget everything you’ve ever heard about cholesterol.

Cholesterol is a fatty substance that is part of every animal cell. I can't stress this enough: you need to manage your lipids. Take a look at this chart JFL.

View attachment 3788463


The Role of cholesterol in the body

Unlike with DHT after puberty, you should think twice before nuking your cholesterol to the ground. Cholesterol is required to build and maintain membranes, whilst regulating their fluidity. It also affects substrate presentation, plays a major rule in the epidermis, and has its own signalling pathways.

I am sure you have seen the image below before: it shows the importance of cholesterol for the steroidogenesis, the process by which many sex hormones including testsoterone are synthesised.

View attachment 3788507

There are a few studies claiming that there is a weak correlation between dietary cholesterol and total testosterone levels. This study suggests that HDL levels are correlated with androgen levels. And this one suggests the opposite.

View attachment 3788631

It is only logical that cholesterol affects hormone levels via the steroidogenesis pathway. Though additional dietary cholesterol intake may not result in increased testosterone levels. Additionally, the body compensates for dietary cholesterol intake by reducing its own cholesterol production. Unlike what many believe, dietary cholesterol doesn't cross the blood-brain barrier. The brain produces its own supply via astrocytes.

What does this even tell us?

Cholesterol isn't bad at all. The dose makes the poison. The thing is, you can't know if it is the poison without getting a blood test. Stay better safe than sorry. Use the table below as a general guide.

View attachment 3788530

Additionally you can use Apob/ApoA as guidance, since all those values correlate with eachother.

View attachment 3788557


Atherosclerosis

Atherosclerosis is a progressive disease marked by the accumulation of lipids and fibrous elements in the large arteries in response to oxidative stress. Let me make it more clear: there are multiple factors contributing to atherosclerosis. Gene polymorphisms heavily influence whether your body can effectively clear LDL cholesterol. I checked my genome and found a mutation in the LDL-receptor. :feelskek:

View attachment 3788672

Apart from that, obviously LDL and HDL levels directly influence the risk of developing atherosclerosis. Oxidative stress is a heavily underestimated factor too. The best way to mitigate the risks would be managing all of those factors. This is where the real thread starts.


Effective ways to reduce your risk of developing atherosclerosis
  • Low bodyfat%: it may not look healthy to normies, but being at a low bodyfat% in general is extremely healthy, whilst being the biggest Looksmax simultaneously. It can improve your lipids naturally without pharmacological intervention.
  • Exercise: be it aerobic exercise or strength training, just stay the fuck in shape and move around. This will also reduce your blood pressure.
  • Antioxidants: to mitigate the oxidative stress aspect of atherosclerosis you should eat a balanced, non-processed diet. It is fucking simple. Extremely beneficial antioxidants are coQ10, OPC and NAC just to name a few.
  • Quit smoking: smoking is one of the worst things you could do for your lipids and health in general. There are three primary ways in how smoking affects coronary heart disease:
  1. Carbon monoxide promotes atherogenesis by damaging the endothelium and reducing oxygen delivery.
  2. Nicotine stimulates the adrenergic system, leading to increased blood pressure and myocardial oxygen demand.
  3. Smoking disrupts the lipid metabolism resulting in higher LDL and lower HDL cholesterol levels. Also, keep in mind smokers usually maintain a lower bf%, meaning smoking completely negates the benefits of being at a low bf% in the first place. There are countless other risks associated with smoking. If you insist on continuing, don’t call yourself a Looksmaxxer.
Pharmacology

Now that we covered the water topics, let's discuss the real shit. This is for you if you want to take your longevity protocol to the next level.

Statins
General info

Let’s cover this first. It’s the primary normie method for lowering cholesterol and LDL levels. They’re also the best-selling pharmaceuticals ever in history so if you’re skeptical about biased/manipulated studies, this is one of the first compounds you should question. Statins are generally less effective in treating individuals with genetic disorders such as familial hypercholesterolemia.

Mechanisms of action (MOA)

Statins work by inhibiting HMG-CoA reductase, an enzyme involved in a key step of the cholesterol synthesis pathway. They also increase LDL receptors in the liver, meaning more LDL can be removed from the bloodstream.

Benefits

Reduction in C-Reactive protein, tumornecrosis factor alpha and interleukins. Statins also slightly activate PPARα via overexpression of COX-2.

Side effects

We can differentiate between two groups of statins: Hydrophilic and lipophilic statins.

Hydrophilic statins: Won't cross the blood-brain barrier, more inflammation. Examples: Rosuvastatin and pravastatin.

Lipophilic statins: Crosses the blood-brain barrier, less inflammation. Examples: Pitavastatin, atorvastatin and simvastatin.

Besides that statins have a ±10% risk of causing diabetes in men.

Recommendation

The best statins by far are pitavastatin and rosuvastatin as they have the best side effect profile.

Pitavastatin

A study shows that pitavastatin reduces total cholesterol by 21%, LDL-C by 31% and increases HDL-C by 14% and 25% at 12 and 104 weeks. Dose: Take 1-4mg daily.

Rosuvastatin

This is by far one of the best statins besides pitavastatin in terms of side effect profile and effectiveness.

View attachment 3788822

Dose: You can take anything from 5 to 40mg. Even a low dosage of 5mg seems to be quite effective.(10)

Ezetimibe
Ezetimibe inhibits the absorption of dietary cholesterol. You can expect a reduction of around 30% in total cholesterol. It can improve nonalcoholic fatty liver disease. Besides that ezetimibe reduces c-reactive protein. It doesn't affect fat-soluble vitamins unlike popular belief.

View attachment 3788827

Ezetimibe monotherapy isn't as effective as combining it with another compound like statins. Dose: 5-10mg once daily.

Obicetrapip
Obicetrapip is the first CETP inhibitor that effectively manages lipids without being utter garbage. It is significantly better than torcetrapib, dalcetrapib and evacetrapib combined. The compound is quite new and already showed promising results. Besides that it improves alzheimer's disease.

"LDL-C decreased from baseline to week 12 by 63.4%, 43.5%, and 6.35% in combination, monotherapy, and placebo groups, respectively (p<0.0001 vs. Placebo).

Obicetrapip and ezetimibe together significantly reduced concentrations of non-HDL-C, apolipoprotein B, and total and small LDL particles. It was well tolerated and no safety issues were mentioned. Dose: 5-10mg daily.

PCSK-9 inhibitors
This is one of the best pathways to improve your lipids drastically. PCSK-9 inhibitors are fully humanized monoclonal antibodies that prevent the enzyme PCSK-9 from binding to LDL receptors in the liver. This leads to an upregulation in receptors leading to a reduction in LDL. The apolipoprotein B autoantibody and anti-PCSK9 antibody reduced the level of LDL and plaques in animal studies. Dose: Alirocumab and evolocumab are injected subcutaneously every 2 to 4 weeks. Sourcing is extremely hard and you are better off trying to get a prescription.

Here is my personal alirocumab. :what:

View attachment 3788838

It is extremely expensive, so try to have the cost covered by your health insurance.

SR9009
SR9009 (Stenabolic) is an agonist of Rev-Erbα/ß along with SR9011 and other synthetic Rev-Erbα/ß ligands. It is being used to boost mitochondrial activity and fat metabolism. It can also have a positive impact on your circadian rhythm, endurance and inflammation.

View attachment 3788846

You can see a few benefits of agonizing this pathway below.

View attachment 3788847

You should use this compound ideally for the lipid aspect, in conjunction with the tons of other benefits. If you're trying to negate some side effects of PEDs, you should look into SR9009/SR9011 as well. Dose: 10-40mg.

Retatrutide
Retatrutide is a godsent molecule. It is a triple agonist of GLP-1, GIP and the glucagon receptor. You can expect an inprovement in insulin sensitivity, increased energy expenditure, and appetite supression with barely any side effects. It also can support lipids drastically according to this study.

"apoB was reduced by up to 19.6% and 24.2% at 24 and 48 weeks"

"At 48 weeks, the drug reduced triglycerides and apoC-III levels by up to 40.6% and 38.0%"

"Retatrutide also reduced the number of total and highly atherogenic small LDL particles (LDLP)"


Retatrutide is by far one of the best compounds for literally anything, be it Looksmaxxing or just general health. Dose: Anything between 4-8mg weekly is a good effective dose. Doses above 8mg have extreme diminishing returns in terms of effectiveness. You can split the dosage to twice a week.

Bempedoic acid
Bempedoic acid is an oral prodrug that inhibits ATP citrate lyase, which is involved in the liver's biosynthesis of cholesterol upstream of HMG-CoA reductase, the enzyme that is blocked by statins. It mogs according to this study. Dose: 180mg daily.

"At week 12, bempedoic acid reduced the mean LDL cholesterol level by 19.2 mg per deciliter (0.50 mmol per liter)."
Statins are toxic to your mitochondria, they literally damage your cells and such they become frail and beg for low-density lipoprotein, thus increasing their receptor count for low-density lipoprotein. It also is known to harm your capacity to use to create your own coenzyme Q10, which is basically playing with fire, in my opinion.
 

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