Week 3 A Flashcards
Race/ethnic considerations
Asians often lack the enzyme required to metabolize alcohol (alcohol dehydrogenase)
Resulting facial flushing response/headaches/tachycardia/dizziness
Thus lowest levels of consumption
Aboriginal populations
Highest alcohol abuse
1 in 5 people in aboriginal communities are admitted to hospital for alcohol related illness on an annual basis!!
Many reasons (socioeconomic) for this
World’s oldest licensed Distillery
Bushmills (Antrim Coast: Northern Ireland)
Gin: from medicine to mania
1688 the Dutchman, William of Orange, became King of England
He banned the import of French wines
Encouraged the distillation of spirits from home-grown grain
Gin was developed in Holland in 1650 by Francis Sylvius
Produced by distillation of Juniper berries with alcohol derived from fermented barley
Juniper berries as medicine
Folkloric history as a remedy for gout and urinary tract problems such as urine retention
Idea was to produce a diuretic from gin
Gin is composed of 100’s of compounds
One of these, terpinen-4-ol-reduces inflammation
But not enough in gin to have much effect
What is gout??
Joint inflammation and swelling
Caused by uric acid buildup in the blood
Eventually crystals form and cause pain
Most prevalent in people who consume a lot of alcohol and eat a fatty diet
Henry VIII of England had it!
Can be treated with colchicine (an alkaloid)
Gin-soaked raisins for treatment of arthritis
Gin mania in 18th century England
Between 1715 and 1750, more deaths than births in London, with greatest mortality among children
Many of these were due to fetal alcohol syndrome, as unhappy mothers-to-be sought solace in gin
Start of Industrial Revolution meant poor air and water quality
1st Gin Act of 1736
Made sale of gin in quantities under 2 gallons illegal
Taxes on gin were raised
Distillers had to be licenced (50 pound fee!)
Result: riots in the streets!
Black market in gin
2nd Gin Act 1751
Distillers could only sell to licensed retailers
Heavy fines if violated
Eventually “gin mania “ began to fade
Pharmacology of alcohol
Alcohol is a CNS depressant
Releases inhibitions and thus (erroneously) gives the impression that it is a stimulant
Brain is particularly sensitive to depressive effects of alcohol
Strong correlation between BAC (Blood Alcohol Concentration) and behaviour
Alcohol and the Law
Ontario : driving with above above .05 % BAC is an offence : 3 day license suspension for 1st offence; increases with subsequent offences
Range of .05 to .08 is “warning range”
Above .08 % BAC is considered legally drunk in Ontario
Absorption of alcohol
Rapid effects of alcohol are noticed when it is consumed on an empty stomach
Stomach absorbs ~ 25% of the alcohol, with 75% absorbed by the small intestine
Maximum BAC can be reached in 20-30 min.
Effects of alcohol on the liver
Every 4 minutes, the entire blood volume goes thro’ the liver
Alcohol pre-empts fat metabolism in the liver, thus in heavy drinkers, fat deposits accumulate on the liver (cirrhosis)
Ethanol - Breakdown
liver processes blood supply(~6L) every 4 min liver burns up ethanol (=> 7Cal/g) first (apparent stimulant)
excess acetaldehyde ‘ties up’ serotonin in the brain(then acts as a depressant)
cirrhosis = fat deposits/lesions on the liver
Ethanol - the Ups
- moderate use enhances: social interactions, enjoyment of food
- statistical correlation of longer (happier?) life with ~1’drink’ per day • powerful phytochemical antioxidant (resveratrol) in red wine(grape skins?) • almost 60% of NA over 12yr consume alcohol each month