Thread by @holmanm

1/7 Statins are fungal secondary metabolites which selectively inhibit (HMG-CoA) reductase, the first enzyme in cholesterol biosynthesis.
’Secondary metabolite” is the euphemism that agenda-driven scientists and drug companies use for toxic Statins.

2/7 There are many ways to lower cholesterol. There are a few poisonous food mold toxins that will do the trick if you’re willing to take the risk:

To name but two

Ochratoxin-A (lactone/UV-flourescent)
Citrinin (inverted lactone/UV-fluorescent

3/7 A friend suffering from MND/ALS after using 80mg Lipitor took the drug to an INDEPENDENT lab to get the drug tested.
Two tests on 80 mg of Atorvastatin (Lipitor) came back with Ochratoxin A and Citrinin with 39 ug/g

4/7 The MAXIMUM TOLERANCE to humans of these toxins as set by international grain boards are
15 ug/g. !!!!

Considering the molecular structure of mycotoxins such as aflatoxin B1 and G1, produced by certain species of Aspergillus flavus, and cholesterol,

5/7 the mechanistic associations of the functional groups, there seemed a possibility of interactions through the breaking and remaking of bonds. Already, it is known that the rate-limiting step of cholesterol biosynthesis is catalyzed by HMG-CoA reductase that is responsible for

6/7 most of the complex regulatory controls. Mycotoxins are capable of disrupting the action of this rate-limiting HMG-CoA enzyme because, the reactions of mycotoxins fit into,

7/7 have affinity for, and are very similar to those of cholesterol biosynthesis.
So there we have it in a nutshell. Mycotoxins in Statin drugs lower cholesterol.

@QuickFang (does this answer your question ?)