12/03/2025
Statins Are Mitochondrial Toxins
And CoQ10 isn't enough to fix this.
This is educational in nature and not medical or dietetic advice. See terms in the link for additional and more complete disclaimers.
Blood cholesterol levels, along with LDL particle count, ApoB concentration, LDL particle size, LDL pattern, and the ratio of cholesterol between LDL and HDL are all governed centrally by the LDL receptor.
Genetic mutations in LDLR cause familial hypercholesterolemia by lowering LDL receptor expression. One in a million people are born with homozygous mutations, and this can cause heart attacks as young as 18 months old. One in 300 people are born with heterozygous mutations, which shifts heart disease forward from a phenomenon that primarily kills between the age of 60 to 80 to one that primarily kills between the ages of 35 and 60.
The LDL receptor is the main way you bring cholesterol from outside the cell to inside the cell. While the liver only makes about 16% of the body's cholesterol, it is overwhelmingly responsible for controlling the concentration of cholesterol in the blood by taking it up using the LDL receptor. That cholesterol can then be put to productive use, especially for the synthesis of bile acids to support digestion.
However, there are two primary governors of LDL receptor production:
Thyroid hormone governs it by signaling abundance. This causes the liver to take up more cholesterol than it needs to meet its basic needs, and this is what drives bile acid production to support digestion.
Cholesterol deficiency within the liver cell governs it by signaling scarcity. The liver takes up cholesterol from the blood not to put it to productive use but simply to replenish its own stores.
Statins work by inducing a cholesterol deficiency in the liver. The liver responds to this by taking up more from the blood to bring its stores back up to normal.
In his 1976 book, Solved: The Riddle of Heart Attacks, Broda Barnes reviewed the history of using thyroid hormone to control both cholesterol levels and heart disease risk. It worked extremely well, but it was discontinued due to what Barnes describes as irresponsible dosing that had killed a few people.
It is important to understand here that you do not need to be “hypothyroid” for thyroid hormone to lower your cholesterol. It will work at any dose. Practitioners using it did not realize they were playing with fire by using a hormone to signal a degree of abundance that was not present in the body. Thus, some of them let the dosing get out of hand because it had nothing necessarily to do with correcting a thyroid deficiency.
Nevertheless, their approach was the same as using statins because both thyroid hormone and statins increase the LDL receptor.
On the other hand, it was the opposite, because thyroid signals abundance while statins signal scarcity.
What everyone involved fails to fundamentally understand is that your LDL receptor does not work in a vacuum. It is powered by mitochondrial ATP production.
If your mitochondria are not working well, your LDL receptor simply will not work.
Doctors who use a pharma-first approach have little respect for nature and doctors who use a statin-first, mitochondria-never approach do so because they do not understand the most basic elements of cellular biology.
As covered in What Everyone Should Be Doing For Their Health, everyone must use a food-first, pharma-last approach, which means everyone needs their doctor to follow the same approach. Do your research until you find a good one.
Click through to read my article on how mitochondrial function optimizes your thyroid hormone and LDL receptor activity, how statins act as mitochondrial toxins beyond a simple impairment in CoQ10 synthesis, and what to do about it:
https://chrismasterjohnphd.substack.com/p/statins-are-mitochondrial-toxins
