A reader dropped me this question

My Frame Work

One of the problems with ME/CFS is people grasping for solutions, patterns etc.  Usually out of desperation or frustration.  As a statistician, I know that approach is very prone to false positive discoveries. I have been observing the ME/CFS community for over 30 years (sometimes as a active member, other times in remission and interested).

As a result, I keep to gold standard information, i.e. studies on the US National Library of Medicine (PubMed) and in a few cases, ME/CFS Conference Reports (silver standards). Too often, I see turd standards on support groups.

There is a very simple logical measuring stick — if something is easy to measure and there are no studies then one should assume “this hypothesis has been studies many times and there has only been negative results (false hypothesis) — hence no study will be published” That is the norm in publications, finding no results is not worth publishing!

Question #1: Stomach Acid and ME/CFS relationship.

Answer: There is not a single study mentioning “Myalgic encephalomyelitis stomach acid” on PubMed, thus a relationship is very unlikely to exist.

Question #2: What about acidosis

Answer: Acidosis usually means blood acid level, different from stomach acid. Yes, there is some connection between stomach acid and blood acid level, but it appears to be weak. PubMed reports 29 studies.

• The Gut Microbiome in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) [2021] cites D-lactic acidosis as a theory or hypothesis and cites an earlier study “No improvement in fatigue has been seen by targeting the D-lactic acid producing bacteria with antibiotics and probiotics” from Examining Clinical Similarities Between Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and D-Lactic Acidosis: A Systematic Review [2017] Note 2009 study below which instead cites neurocognitive dysfunction and NOT fatigue.
• “This revealed severely affected ME/CFS patients to have higher rates of respiratory acidification ” [2020]
• “Bioenergetic muscle dysfunction is evident in CFS/ME, with a tendency towards an overutilisation of the lactate dehydrogenase pathway following low-level exercise, in addition to slowed acid clearance after exercise” [2016]
• “CFS simulations exhibited an increased acidosis and lactate accumulation consistent with experimental observations.” [2015]
• “However, the CFS group achieving normal PCr depletion values showed increased intramuscular acidosis compared to controls after similar work after each of the three exercise periods with no apparent reduction in acidosis with repeat exercise of the type reported in normal subjects. This CFS group also exhibited significant prolongation (almost 4-fold) of the time taken for pH to recover to baseline.” [2012]
• ” This study suggests a probable link between intestinal colonization of Gram positive facultative anaerobic D-lactic acid bacteria and symptom expressions in a subgroup of patients with CFS. Given this fact. this might explain neurocognitive dysfunction in CFS patients” [2009]
• “Research data on magnetic resonance spectroscopy (MRS) of muscles and brain in CFS patients suggest a cellular metabolic abnormality in some cases. 31P MRS of skeletal muscles in a subset of patients indicate early intracellular acidosis in the exercising muscles. ” [2004]

I believe that every suggestion that works on the hypothesis that stomach acid is significant has been tried multiple times in clinical studies without any results — and thus not published.

Yes, there is acidosis but it is not in the stomach, it is dealing with the ability of the body to remove d-lactic acid from tissue (muscles, brain etc).

The suggestions being tossed around come from simplistic logic. For example:

• If it is Wednesday, then it is raining.
• If it is raining, then we are wet.
• Therefore, if we are wet, it is Wednesday

The suggestions have a positive psychological effect and thus there may be placebo improvement. There is documented evidence saying placebos really help!

No ME/CFS Studies for these searches:

• “Myalgic encephalomyelitis betaine”
• “Myalgic encephalomyelitis HCl”
• “Myalgic encephalomyelitis sodium bicarbonate”

There was an old egroup called: CFSFMExperimental back in the 1990’s. I saw those suggestions tried, become popular and then fade away because of no results.

Bottom Line

It is simple: Use Gold standard research, at least silver standard if it is from a conference report in the last 5 years (older reports should have had published studies by now). This approach was the basis of my recovery from ME/CFS.

Social Comment

Two studies were cited:

Data showed that MRI studies frequently reported structural changes in the white and gray matter. Abnormalities of the functional connectivity within the brainstem and with other brain regions have also been found. The studies have suggested possible mechanisms including astrocyte dysfunction, cerebral perfusion impairment, impaired nerve conduction, and neuroinflammation involving the brainstem, which may at least partially explain a substantial portion of the ME/CFS symptoms and their heterogeneous presentations in individual patients.

Brainstem Abnormalities in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Scoping Review and Evaluation of Magnetic Resonance Imaging Findings [2021]

Brainstem parasympathetic circuits that modulate digestive functions of the stomach are comprised of afferent vagal fibers, neurons of the nucleus tractus solitarius (NTS), and the efferent fibers originating in the dorsal motor nucleus of the vagus (DMV). A large body of evidence has shown that neuronal communications between the NTS and the DMV are plastic and are regulated by the presence of a variety of neurotransmitters and circulating hormones as well as the presence, or absence, of afferent input to the NTS. These data suggest that descending central nervous system inputs as well as hormonal and afferent feedback resulting from the digestive process can powerfully regulate vago-vagal reflex sensitivity. 

Brainstem Circuits Regulating Gastric Function [2011]

To me, this is a case of simplistic logic: The brain stem has abnormalities, the brain stem controls digestive function (stomach acid is NOT mentioned, only “glutamic acid decarboxylase-IR used as a marker”), thus the abnormalities control stomach acid. There are no logic connection, we need to identify which abnormalities impacts stomach acid and have evidence that it actually results in less stomach acid. IMHO, it is an attempt to depend a belief by “tossing a word salad from studies.”