Chocolate vs. CFS: flavanols and beyond

There have now been several preliminary studies testing the effects of phytochemical-rich plants in ME/CFS, some of which show benefit (discussed later). Of these, I find the 2010 trial with chocolate particularly intriguing ¹.

This was a very small pilot trial (UK, n=10 CFS, Fukuda criteria + severe fatigue; no mood disorders, no drugs) to test the effect of polyphenol-rich chocolate for 8 weeks on symptoms. It had a double-blind, placebo-controlled, crossover design (8–2–8), with several subjective outcomes; and high methodological quality in a recent systematic review ². The active treatment arm had an improvement in fatigue, anxiety, depression and disability (pre–post effect: –35%, –37%, –45% and +31%, respectively); anecdotally, 2 people with short illness duration even returned to work ¹. For reference, this is a greater reduction in fatigue, depression and anxiety than over a year of CBT or GET in the large PACE trial (UK, n=641 CFS, multiple criteria), which used some of the same outcome measures ³.

Homocysteine on the brain: many paths to many problems

2019 – end edit and update.

Homocysteine might be important in many neurological disorders, especially cognitive decline. I’ve been reading about potential mechanisms—there are a lot! Here’s an attempt to arrange some things of interest as a mini-review.

Homocysteine is a sulfur-containing amino acid, derived from the metabolism of dietary methionine. Homocysteine exists in various forms ¹ and is metabolised via two main pathways: remethylation and transsulfuration. Homocysteine remethylation to methionine maintains levels of SAM, the major methyl-donor, required in over 50 methylation reactions to DNA/RNA, proteins, phospholipids and other metabolites ². Whereas homocysteine catabolism via the transsulfuration pathway yields many other important sulfur metabolites (e.g. cysteine/glutathione, H₂S and taurine). Both of these pathways depend upon B vitamin-derived substrates/cofactors and are regulated by various physiological processes.

Dysbiosis and D-lactate

Lactate (C₃H₆O₃) is an intermediate of carbohydrate metabolism, produced from pyruvate during lactic acid fermentation. Lactate can exist as two enantiomers/stereoisomers, L- and D-lactate, with L-lactate being the main form present in the body. Human cells produce L-lactate from glucose and alanine, while a small amount of D-lactate can be produced via the methylglyoxal pathway ¹. However gut microbes can produce both L- and/or D-lactate as major metabolic by-products ².

Elevated gut and/or blood levels of D-lactate are seen in several conditions and may be harmful ^1–3. An overgrowth of D-lactate-producing gut bacteria has also been implicated in ME/CFS ^4–6; although blood levels and biological interactions/associations have not yet been investigated, making the relevance unclear. Still, I think we can learn something from general research on D-lactate production by the gut microbiota.

Are carbs really that bad?

Low carbohydrate (carb) diets are advocated for all kinds of health conditions (incl. ME/CFS), by Atkins/weight-loss/Paleo movements and some alternative MDs. These movements demonise carbs and oversimplify their role in health and disease. So here is a reappraisal of the humble carb.