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    why are ketone bodies so prevalent on the breath of a drunk?

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    why are ketone bodies so prevalent on the breath of a person consuming large amounts of alcohol (specifically acetone is detected by breathalizer tests)

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    Re: why are ketone bodies so prevalent on the breath of a drunk?

    Quote Originally Posted by inneedofhumility
    why are ketone bodies so prevalent on the breath of a person consuming large amounts of alcohol (specifically acetone is detected by breathalizer tests)
    Because ...

    Typical Presentation
    This typical situation leading to alcoholic ketoacidosis is a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake. Food intake may be limited because of vomiting. The two key factors are the combination of ethanol and fasting. Presentation is typically a couple of days after the drinking binge has ceased.

    Pathophysiology
    The poor oral intake results in decreased glycogen stores, a decrease in insulin levels and an increase in glucagon levels. Hepatic metabolism of ethanol to acetaldehyde and then to acetate both involve NAD+ as a cofactor. The NADH/NAD+ ratio rises and this:

    inhibits gluconeogenesis
    favours the production of beta-hydroxybutyrate over acetoacetate
    The insulin deficiency results in increased mobilisation of free fatty acids from adipose tissue. The decreased insulin/glucagon ration results in a switch in hepatic metabolism favouring increased beta-oxidation of fatty acids. This results in an increased production of acetylCoA which forms acetoacetate (a keto-acid). (The pathophysiology of the insulin deficiency and the switch in hepatic metabolism is discussed in more detail in DKA section below.)

    Other points to note:

    Volume depletion is common and this can result in increased levels of counter-regulatory hormones (eg glucagon)
    Levels of FFA can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions
    GIT symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena)
    Acidaemia may be severe (eg pH down to 7.0)
    Plasma glucose may be depressed or normal or even elevated
    Magnesium deficiency is not uncommon
    Patients are usually not diabetic

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