Any Japanese or Koreans here ever tried those Hovenia raisin hangover supplements for reducing PEM symptoms?
I woke up this morning with PEM feeling like I had a really bad hangover, almost identical in feeling except additional physical symptoms.
I also remembered that alcohol intolerance is often reported early on in mitochondrial dysfunction related conditions (MECFS, long COVID, MCAS).
It got me wondering, has anyone ever tried those Hovenia dulcis raisin hangover supplements? I don't believe it would be a cure, but something relatively accessible to see some mild reduction in PEM symptoms might be useful. And this is widely available and consumed in Japan and Korea.
TLDR for below:
Acetaldehyde and other stuff like inflammatory mediators, and anti-inflammatory pathways are involved in hangovers. Holvenis has 9 or more compounds that can target these things by upregulating useful stuff and downregulating harmful stuff. There's also some stuff that happens with fibrosis inhibition, stabilization of mitochondria via modulation of reactive oxidation species and antioxidants, cell death and phagy, etc.
Details
I found this: Heightened innate immunity may trigger chronic inflammation, fatigue and post-exertional malaise in ME/CFS | npj Metabolic Health and Disease - https://www.nature.com/articles/s44324-025-00079-w
After exercise, levels of retina-specific copper amine oxidase (AOC2) and copper homeostasis protein cutC homolog (CUTC) were higher in ME/CFS (Fig. 2F). AOC2 is a copper-dependent enzyme that catalyzes oxidation of primary amines, including neurotransmitters such as dopamine and serotonin, into aldehydes, H2O2, and ammonia. CUTC facilitates intracellular copper transport and regulates copper homeostasis. Copper is a cofactor for the oxidant defense system, which includes superoxide dismutase (SOD), catalase (CAT) and glutathione (Supplementary Text 1.3.10 and 1.3.11 for peroxisomal dys
And also this:
Molecular mechanism underlying alcohol's residual effects: The role of acetaldehyde in mitochondrial dysfunction at synapses in mouse brain cortex - ScienceDirect - https://www.sciencedirect.com/science/article/abs/pii/S074183292500117X
"Acetaldehyde drives mitochondrial dysfunction in ethanol hangover."
And this (though idk about this journal's reputability):
Long COVID, POTS, and ME/CFS: Lifting the Fog - https://www.iomcworld.org/open-access/long-covid-pots-and-mecfs-lifting-the-fog-98646.html
Without P5P glutathione cannot be synthesized from Hcy (Figure 1). A gut microbiome that lacks an abundance of histamine degrading Bifidobacteria leaves allergic features unopposed [42]. This may be contributory to MCAS. GABA secreted by histaminergic neurons also downregulates histamine signaling. The endogenous pathways for the degradation of histamine require either methylation (SAMe, Mg2+, and ATP) or mitochondrial ALDH. Alcohol intolerance is a primary complaint in LC, CFS, and MCAS with their dysfunctional mitochondria. Hepatic metabolism of alcohol in such individuals stops at acetaldehyde and a giant hangover.
https://pmc.ncbi.nlm.nih.gov/articles/PMC11033337/table/T1/
https://pmc.ncbi.nlm.nih.gov/articles/PMC11033337/
"nine chemical constituents such as beta-sitosterol, DHM, quercetin naringenin, lutein, myricetin, kaempferol, emodin, and apigenin, were verified to be related to [alcohol-associated liver disease]"
Quercetin is often taken by people with MCAS. These other molecules seem to target stuff I've seen mentioned with MECFS.