Alcohol
Beer vessels dated 3500 years ago
Some people believe it provides Nutritional value, religious ceremonies, socializing
Sustained patterns of drinking
How much they consume
How quickly
Where?
The person’s biology/constitution/physical health
Continuum: physical health issues
Problems as alcohol use increase past 2 drinks daily: heart, liver bone, endocrine, pancreas, brain, gastrointestinal, and immune system
Toxic molecule
What determines who can and can’t drink
Approx 90% do not experience medical harm
10% drink harmful amounts
Risks
Genes
Family history
Age of onset
Stress
Sex
Availability
It’s very available
What is considered one drink?
Beer = malt liquor=table wine= shots of distilled spirits
Whose consuming?
60 mil. People 12 & over reported drinking in the past month
16.2 18 or older reported heavy alcohol use in past month
Heavy drinking
Binge drinking on 5 or more days in the past month
Binge drinking
A pattern of drinking alc that brings blood alcohol concentration to 0.08 percent
A female has 4 or more drinks, or a male has 5 or more drinks within about 2 hrs
Binge drinking and heavy alc use can increase an individual’s risk of AUD
What is alcohol?
Two carbons
Oxygen
6 hydrogens
Water and fat-soluble
First is metabolized in the liver
Metabolism of ethanol into toxic and caloric molecule
Binds to proteins/DNA and can cause mutations. Classified as a group 1 carcinogen by the WHOs internationa; agency for research on cancer
Most of the metabolism happens in liver
Ethanol → aceraldehyde (toxic molecule) → acetate caoloric molecule
The liver is stressed when having to frequently process ethanol
.02-.04: mild intoxication: relaxed
.05-.07: moderate intoxication: euphoria
.08-.10 advanced moderate intoxication: euphoria intensifies
.11-.15: advanced intoxication: “high” is reduced, depressive effects
cog. Function becomes impaired
.16
Stimulant effects are seen at lower doses than the sedation effects
The stimulant effect is not seen in all indiv.
Light drinkers don’t show stim. After 2-3 drinks
Heavy drinkers report stim effect
Light drinkers do not
Heavy drinkers report a reduced sedative response compared to light drinkers
Why the differences?
Alcohol works has dose-dependent responses on different receptors
Diagnosing AUD
Dsm criteria can be used
Aud (alcohol use disorder identification test
Diagnostic criteria checklist
If everyone cut their alc consumption in half, we could save a million lives globally
Associated harm
3 mil deaths from harmful use of alc
90k people die every year
Harmful use
Benerfits to low to moderate abuse
Lower incedencve of heart disease
Reduction in anxoety and stress
Enhanced immune system
Increased bone diverwsity
Heavy use harm
Memory prob.
Stroke
lung/liver/nuro disease
Cancer
Suppression to immune system\
Immune system
Aud associated with significant increase in incidence and severity of bacterial pneumonia, tuberculosis
Gut-Liver-brain axis and AUD
Complex multidirectional interactions between gut (gI tract)
Releasing neurotransmitter and regulating through receptors in brain
If imbalance, effects cog.
Alc creates imbalance and lasts even if they aren’t drunk (days after)
Ethanol kills good bacteria(microbiota) and bad
Imbalances are ass with cog issues mood changes and continued drinking behavior
Inability to stop a habit
Barrier and when someone drinks chronically, microbiota will leak into gut
Causes intestinal inflammation
Inflammatory molecules released (cytokines)
Studies show that transplanting fecal matter from alc mice to nonalc mice transfers the behavioral phenotype of chronic alc use disorder to the recipients
Similar depression
Anxiety
Alcolo seeking behavior
Mice w/ induced immunoinflammatory response colonized
Mice separated in 2 grou[ps
Not lot of time in central area when have aud given intentional fecal matter
Thiamine deficiency
Wernicke korsakoff syndrome
Wernice syndrome
Toxic molecule
Major difference
Associations between alc consumption and gray and white matter volumes in the uk biobank
Neural mechanisms
Research suggests that alc stimulatyes neurons in the ventral tegmental area cauising enhancement in epi
Dopaminergic system
Profound diseases in dopamine release in ventral