A Long Covid hypothesis: acids and bases.

Frontiers In Immunology has published a hypothesis – which is basically a call for more research – put out by two Long Covid sufferers who noticed something interesting about their own bodies that seems like it might explain all the 200-plus symptoms linked to the condition. What they first found, using a home blood-lactate meter, was abnormally high levels of lactate, as if their muscles were constantly producing the level of lactic acid they would during a heavy workout. The “unifying mechanism” this points to is an acid-base balance that’s been knocked out of whack by inflammation:

The mechanism of Long Covid (Post-Acute Sequelae of COVID-19; PASC) is currently unknown, with no validated diagnostics or therapeutics. SARS-CoV-2 can cause disseminated infections that result in multi-system tissue damage, dysregulated inflammation, and cellular metabolic disruptions. The tissue damage and inflammation has been shown to impair microvascular circulation, resulting in hypoxia, which coupled with virally-induced metabolic reprogramming, increases cellular anaerobic respiration. Both acute and PASC patients show systemic dysregulation of multiple markers of the acid-base balance. Based on these data, we hypothesize that the shift to anaerobic respiration causes an acid-base disruption that can affect every organ system and underpins the symptoms of PASC. This hypothesis can be tested by longitudinally evaluating acid-base markers in PASC patients and controls over the course of a month. If our hypothesis is correct, this could have significant implications for our understanding of PASC and our ability to develop effective diagnostic and therapeutic approaches.

We propose the testable hypothesis that PASC is underpinned by an inflammatory acid-base disruption. If the proposed evaluations confirm the hypothesis, this offers both a diagnostic pathway for PASC and suggestions for treatment. As PASC may be a reinforcing cycle of tissue damage, blood flow and oxygenation impairment, dysregulated inflammation, and acid-base disruption, then a treatment protocol could be designed to simultaneously address each disease component through pharmaceutical and/or non-pharmaceutical interventions. It is possible that PASC is not the only pathogen-induced inflammatory acid-base disorder, as several other pathogens cause persistent disease. ME, in particular, shares many features with PASC and the symptom profile of both diseases overlaps with that of acute and chronic acidosis (9, 33). Thus, the proposed hypothesis may be of broader relevance. Additionally, it is possible that even people without persistent symptoms following SARS-CoV-2 infection harbor residual tissue damage and viral proteins, increasing their risk of new health conditions in the future (34). There are still many unanswered questions and the data from this hypothesis testing is urgently needed.

Maybe they’re wrong, maybe they’re right… but it’s an interesting avenue to investigate.

[via Vicky Van Der Togt’s Mastodon]