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A man can fail many times, but he isn't a failure until he begins to blame somebody else.


how is formaldehyde a by-product of alcohol consumption?

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Many people who have livers that don't have enough resources to break down aldehydes can have resulting inflammation, brain fog, muscle aches and blood pressure problems.

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It was interesting to know that aldehydes gets into the body through the inhalation or consumption of formaldehyde containing products. I always get to learn something every time I visit your blog.

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Check your blood pressure from time to time. It`s important to start doing it now.

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Thanks for your comments, Stephen! Yeah, I've considered all these things,
and did try to talk to him about it. But he shied away from telling me any
good reasons soooo..... I'll really never know! But it's entertaining now
(not back then!) to ruminate on reasons why. Thanks for your added thoughts!

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In spontaneously hypertensive rats (SHRs), excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing cytosolic free calcium and blood pressure. The thiol compound, N-acetyl cysteine, normalizes elevated blood pressure in SHRs by binding excess endogenous aldehydes and normalizing membrane Ca2+ channels and cytosolic free calcium.

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Guanethidine (G) is currently used in the treatment of essential hypertension. Acetaldehyde (A), acrolein (AR), formaldehyde (F) and propionaldehyde (P) are constituents of cigarette smoke and (A) is also an intermediate oxidative metabolite of ethanol. These aldehydes are known to produce sympathomimetic effects by the release of NE from adrenergic neurons and to exert cardioinhibitory effects. The type of predominant effect is dose-dependent. This study was undertaken to determine if these aldehydes result in sympathomimetic effects in the presence of G (15 mg/kg iv) in anesthetized rats. G enhanced the pressor responses to A and P in dose ranges of 5-20 and 5-10 mg/kg respectively. However, AR and F at dose ranges of 0.05-5 and 0.1-10 mg/kg, respectively, elicited only depressor responses after G. Thus, A and P exerted greater sympathomimetic effects through the release of intraneuronal NE in the presence of G. The adrenergic neuronal blocking action of G changes the blood pressure effects of AR and F. When these two compounds are administered in the absence of G, they cause predominant pressor effects, whereas in the presence of G a depressor response is noted. This depressor response is possibly by vagal stimulation and/or direct vasodilation.

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