We know from qigong meditation that depression is from lung organ damage and alcohol is claimed to cause depression....
0.08% or a blood serum concentration of ~17 mM ethanol [127]. The conversion of ethanol to acetic acid is nearly 1:1, with ~95% of ethanol converted to acetic acid [128]. Thus, for 17 mM of ethanol consumed, the predicted amount of acetic acid produced would be ~16–17 mM. To buffer or neutralize this concentration of protons, roughly 17 mM of bicarbonate would be consumed. The normal concentration of bicarbonate in the serum is ~23–28 mM [129,130]. This bicarbonate consumption creates a high acid load, generating compensatory mechanisms within the kidneys and lungs to maintain pH homeostasis [130,131,132].
Low bicarbonate in the lungs
often means the blood is too acidic (metabolic acidosis), with the lungs trying to compensate by breathing out more carbon dioxide (CO2), leading to deep, fast breaths...kidneys then excrete bicarbonate to compensate, lowering its level....Fast, deep breaths (Kussmaul breathing), headache, confusion, fatigue, rapid heartbeat, nausea, vomiting.https://pmc.ncbi.nlm.nih.gov/articles/PMC10886048/
acetaldehyde that is not converted to acetic acid/acetate and remains in circulation passing to the lungs is exhaled in its gaseous state. Second, in a report published in 1929 by Bowen and Tietz, they noted that acetaldehyde shaken in the presence of oxygen (auto-oxidation) produced a peroxide, identified as peracetic acid [61]. These authors also noted that this type of reaction and similar reactions produced a “long chain mechanism” [61], which would be consistent with what is now a free radical-type mechanism.
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peracetic acid was more cytotoxic than sodium hypochlorite (bleach) [65].
acetic acid/acetate directly fed into the citric acid cycle to generate ATP, it had to be rather benign [1]. Indeed, glucose and L-lactate are both feedstock for the generation of ATP [73] and at face value, would appear benign. Glucose is consumed and L-lactic acid/lactate can be released into circulation and rapidly cleared following exercise [74]. However, both are kept within tight tolerance in humans and drastic deviations from these homeostatic values (glucose 4.0–6.0 mM [75] and L-lactic acid/lactate <2.0 mM) [76] can produce profound effects on physiological function [75,76].
equivalent to a blood alcohol concentration (BAC) of 0.2% the time of metabolism influenced serum acetate concentrations, with peak serum acetate concentrations measured at ~4.2 mM in male rats and ~3.9 mM in female rats (unpublished data
acetate-based hemodialysis solutions increased levels of nitric oxide synthase (NOS) and nitric oxide (NO) [101,102], a powerful radical which stimulates vasodilation [103,104,105]. Several studies have also identified acetate-induced elevations in tumor necrosis factor alpha (TNFa) and cyclic adenosine monophosphate (cAMP), both mediators of NOS [102]. This was seen in dialysis buffers containing as little as 4 mM acetate [102]. A likely mechanism through which ethanol produces vasodilation is through ethanol’s metabolism to acetic acid/acetate, which stimulates production of NOS and NO (Figure 1B).
the major compound driving alcohol-induced cardiomyopathy [122,123] may be acetate rather than ethanol, and as such, future studies of chronic acetate seem warranted.
The acidic hydrogen on acetic acid and the excess carbon dioxide cause activation of (1) peripheral chemoreceptors located in the carotid sinus and aortic arches, and (2) neural control centers in the brain, which control sympathetic outflow and increase sympathetic nerve activity (SNA)
fascinating!
acetic acid increases NOS activity and NO production, which leads to vasodilation [98,101,102]. Arterial baroreceptors located in the carotid sinus and aortic arch [133] would relay the resultant drop in blood pressure to neural control centers, which regulate cardiovascular function [134] (Figure 1C). These neural control centers then increase SNA to constrict the vasculature in an attempt to maintain homeostasis [133]. Third, the acid load generated from the acetic acid and/or excess carbon dioxide would similarly be sensed by the peripheral chemoreceptors, also located in the carotid sinus and aortic arch. And, in the same type of neural feedback loop as the arterial baroreceptor activation, chemoreceptor activation would also increase SNA and constrict the peripheral vasculature [135,136,137,138]. Thus, the complex vasoconstriction and vasodilation effects of ethanol consumption [93] can be explained when looking at the effects being driven by acetic acid and not ethanol per se.
serum acetate is still elevated, typically remaining elevated for 12–24 h post ethanol metabolism [149,150]. As such, reasonable evidence exists that suggests acetate may be a lead compound in driving the ethanol-induced effects on cardiovascular function from a centrally mediated standpoint.
the stark sex difference in acetic acid-induced NMDAR responses may potentially underlie the greater propensity for females to experience accelerated AUD and suffer greater alcohol-induced neurodegeneration compared to males.
Chronic ethanol use, and elevated acetic acid/acetate from its metabolism, would be anticipated to contribute to end organ damage due to increased sympathetic outflow and is potentially further exacerbated by ethanol/acetate-induced dysregulation of NO signaling. Dysregulation of NO signaling is a major finding in essential hypertension [237,238,239,240]. Furthermore, since alcohol and acetic acid/acetate are capable of crossing the blood–brain barrier, the impact of the brain’s metabolism of ethanol on neural control of cardiovascular function also needs to be studied.
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