Immune system manipulates cholesterol to weaken virus – implications for ME/CFS?

Researchers at Edinburgh University have published two reports on their findings regarding the role of cholesterol production in the body’s virus-suppression response; and fatigue expert Jacob Teitelbaum has a theory as to how this new understanding may play into therapies for ‘chronic fatigue syndrome’ (ME/CFS) and fibromyalgia.

Study #1: Mar 2011

In March 2011, researchers at Edinburgh University led by Steven Watterson and Prof. Peter Ghazal reported finding that the body fights viral infection by suppressing cholesterol production.(1)

That is, they found that “a key immune hormone stimulated upon infection can lower cholesterol levels and thereby deprive viral infections of the sustenance they need to grow.”

A finding suggesting that, with further research, it might be possible to mimic or encourage these immune signals so as to:

• Bolster the body’s response to viral infection as an alternative to antiviral therapies that attack the virus itself.

• And/or lower cholesterol naturally, as an alternative to use of statin drugs, and potentially without the statin drugs’ often harmful collateral damage to muscle and other cells.

See the EU press release, “Curbing Cholesterol Could Combat Infections,” Mar 22. 2011.

At that time, fatigue and nutrition specialist Jacob Teitelbaum, MD, proposed a theory regarding how this discovery might offer some answers for treatment of ‘chronic fatigue syndrome’ (ME/CFS).

A long-time critic of statin drug over-use, Dr. Teitelbaum begins: “New research suggests that statins might have a very helpful antiviral effect at high dose, and they may even hold promise as an effective new therapy for CFS and fibromyalgia if special (and simple) precautions are added in. The new theory I will present today also offers new possibilities for helpful and easy testing and therapy, while offering an understanding of a large new piece of the CFS/FMS puzzle.” See “Statins, Coenzyme Q10, and Pregnenolone for Addressing CFS” at

Study #2: Sep 2012

Now the Edinburgh team has published a second study that explains the body’s cholesterol-related viral response more specifically – suggesting even more promising therapeutic possibilities for cholesterol controlling and anti-viral therapies.(2)

What they find is that this innate viral response mechanism appears to avoid the collateral damage of statin drugs. As they point out, “high levels of cholesterol increase the risk of heart disease but, because cholesterol is vital to ensure the body’s normal function, managing levels in the blood can be difficult.”

• Statin drugs curb cholesterol production – a complex series of chemical reactions that take place in the liver – by blocking the entire process at one specific point upstream.

• However, because statin drugs do block this entire cascade of reactions, they prevent the production of other molecules that play crucial roles in the body, such as making cell & mitochondrial membranes, and production of hormones, vitamin D, etc.

• By comparison, rather than blocking all these chemical reactions at one point in the cascade, the body’s natural means of suppressing cholesterol to defend against viruses simply slows every step, enabling the other essential functions to continue.

See EU Press Release, “Cholesterol Study Points to New Drugs,” Sep 17, 2012.

Dr. Teitelbaum, any further thoughts?


1. Open access. Host Defense against viral infection involves Interferon mediated down-regulation of sterol biosynthesis,”PloS Biology, March 2011.

2. Open access. “A model of flux regulation in the cholesterol biosynthesis pathway: Immune mediated graduated flux reduction versus statin-like led stepped flux reduction,” Biochimie, Sep, 2012.

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