This document provides information on alcohol basics including epidemiology, standard drinks, binge drinking, safe drinking levels, where alcohol comes from, cocktails, factors that influence alcohol absorption, the three pathways of ethanol metabolism, genetic variations in alcohol metabolism, metabolic effects of alcohol, possible hepatotoxic effects of acetaldehyde, drug interactions, diagnosis of alcoholism including questionnaires, the typical clinical course, DSM-IV criteria for alcohol abuse and dependence, and methods for collecting blood and breath samples for alcohol analysis.

1. ALCOHOL BASICS
PROF.DR .ELANGOVAN’S UNIT
D.SUBBURAJ

2. EPIDEMIOLOGY
• MC substance abuse in INDIA -ALCOHOL
– NEXT MC- CANNABIS
• South india prevalance -33—55%
• Highest alcohol consumption -- KERALA
– 8 L / CAPITA
• WORLD WIDE—LUXEMBOURG (15.5 L)

3. ALCOHOL
1 unit=10gm=12.5 ml absolute alcohol=1 drink
• Can’t be stored in the body
• Energy -7 kcal gm
• Some amount of other nutrients
– some potassium ; no sodium
– Riboflavin & niacin
– Possible antioxidant benefits from
polyphenols(?)
– sometimes VIT C

4. STANDARD DRINK
• any drink that contains about 14gm
Of absolute alcohol
AUSTRIA 6 gm
U k 8 gm
AUSTRLIA 10 gm
FINLAND 11 gm
CANADA 13.6 gm
U S 14 gm
JAPAN 19.75 gm

5. STANDARD DRINK

6. Beer 4 – 8 %

7. Gin 40.0 - 48.5 Vodkas 40.0 - 50.0 Wines 7– 22 %

8. Rum 40.0 - 95.0 Whiskies 40.0 - 75.0 Brandies 40.0 - 43.0

9. BINGE DRINK
• U S DEFINITION
– Consumption of five or more standard drink by
males , four or more by females in about 2 hrs
• U K DEFINITION
– Drinking more than twice the daily limit (>8 men, >6
women)
• NIAAA DEFINITION
– Any time one reaches a peak BAC of 0.08% or
higher

10. SAFE DRINK
• no uniform guidelines
• UK– 2-3 standard drink daily or 14 per week
• USA– 1 standard drink daily or 7 per week
• Not more than 3 drinks on any one occasion
• Don’t drive or engage in hazardous activities
• Don’t drink if an interacting drug has been
taken

11. Where does Alcohol come from?
Grain  whisky and beer
Potatoes  vodka
Grapes  wine and brandy
Apples  cider
Honey  mead
Sugar  rum

12. COCK TAIL
DRINK KJ
1 glass stout (250 ml) 570
1 glass beer (250 ml) 380
1 Glass white wine (100 ml) 280
1 Glass red wine (280 ml) 280
1 Nip of spirit 40% (30 ml ) 250
1 Glass mixer (440 ml) 440
1 Glass diet mixer (250 ml) 5

13. 13

14. Graph source: National Institue on Alcohol Abuse and Alcoholism
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15. Factors that influence absorption
• Gender
– Women produce less of enzyme needed to breakdown
alcohol
– Women have greater fat content and alcohol is not fat
soluble so it enters the blood stream faster
– Women have less water so alcohol does not become
diluted
– Women absorb more alcohol during the premenstrual
phase

16. • Absorption increased by
– Rapid gastric emptying ( carbonated beverages)
– Absence of meal
– Absence of congener
– Dilution
• Tissue distribution - blood flow & water
content
• Obese persons & women- higher BAC
• Follows zero – order kinetics
• So metabolism doesn’t vary widely in the
population

17. 3-pathways of EtOH metabolism
ADH in stomach (males) ADH & MEOS
in liver (males & females)
Catalase in liver (males & females)
MEOS- microsomal ethanol oxidizing
system -CYP2E1

18. ETHANOL
CATALASE ADH MEOS
ACETALDEHYDE
ALDH
MITOCHONDRIA ACETATE
EXTRA HEPATIC TISSUES

19. Microsomal Ethanol Oxidizing
System (MEOS)
• Alternate pathway used, in addition to ADH,
when alcohol intake is excessive
• End products include:
– Ethanol  acetaldehyde
– NADPH + H+  NADP+
No ATP formation = Energy Wasteful
• Also involved in drug metabolism
– Excess ethanol- less MEOS for drug- drug
overdosage

20. Genetic Variation
•50% of Asians have inactive ALDH
•Develop flushing reaction
•Acetaldehyde Dehydrogenase (ALDH) varies in
Caucasians, Blacks and Asians.
• poly morphism TNF PROMOTER - susceptible
to alcoholic steatohepatitis
•Alcoholism -inherited ; specific gene not
identified

21. Metabolic effects
• High NADH/NAD RATIO
– Prevents pyruvate entering in to
gluconeogenesis- HYPOGLYCEMIA
– Converts pyruvate to lactate - acidosis-
uricacidaemia- GOUT
– Increase TG - FATTY LIVER
• INDUCES DRUG METABOLISM
• FREE RADICAL FORMATION
• ACCUMALATION OF ACETALDEHYDE

22. POSSIBLE HEPATO TOXIC
EFFECTS OF ACETALDEHYDE
• Increase lipid peroxidation
• Binds plasma membrane
• Interferes with mitochondrial electron
transport chain
• Inhibits nuclear repair
• Interferes with microtubule formation
• Activates complement
• Increases collagen synthesis

23. DRUG INTERACTIONS
• Synergies with anxiolytics, antidepressants,
antihistamines, hypnotics, opioids-- marked CNS
depression with motor impairment -- chances of
accidents increase
• Insulin & sulfonylureas: enhances
hypoglycaemia
• Aspirin & other NSAID –gastric bleeding
• Parcetamol toxicity
• Acute alcohol ingestion inhibits , chronic
alcoholism enhances phenytoin metabolism

24. Disulfiram like reaction
• irreversible ALDH inhibitor- acetaldehyde
accumulates  flushing reaction

25. DIAGNOSIS OF ALCOLISM
• TOLERANCE
– A state of adaptation in which increasing amounts of
alcohol are needed to produce desired effects
• PHYSICAL DEPENDENCE
– A typical withdrawal syn appears on interruption of
drinking , which is relieved by alcohol itself or other
drugs
• IMPAIRED CONTROL
– Total alcohol intake cannot invariably be regulated , once
drinking has begun at any drinking occasion
• CRAVING
– A dysphoria of abstinence that leads to relapse

26. Causes of Alcoholism
• Genetics
– Strong family link
– 50% of fathers, sons, brothers of alcoholics are likely to
become alcoholics
– Children of alcoholics are more then 3-4 times more likely
to become alcoholics
• Personality types
– Low self esteem
– Chronic anxiety
– Antisocial personalities

27. QUESTONNAIRES
• CAGE ( cut down , annoyed ,guilty, eye-
opener)
• MAST (michigan alcoholism screening test)
• AUDIT ( alcohol use disorder identification
test)
• RAPS4 (rapid alcohol problems screen 4)
• QFS ( quantity frequency score)

28. CAGE QUESTIONARE
• Have you ever felt to cut down?
• Have people annoyed you by criticizing ?
• Have you ever felt guilty or bad ?
• Have you ever had a drink first thing in the
morning to steady your nerves or to get ride
of hang over? (eye opener)
One ‘yes’ – suspicion
More than one-alcohol abuse or dependance

29. CLINICAL COURSE
• Age at first drink 13—15 yrs
• Age at first intoxication 15—17 yrs
• Age at first problem 16—22 yrs
• Age at onset of dependence 23---40 yrs
• Age at death 60 yrs
• Spontaneous remission in 20% Same as general
population.

30. DSM-IV CRITERIAS
• ALCOHOL ABUSE
• Recurrent use of alcohol associated with any
one of the following with in 12mns
1. Failure to fulfill major role at work
2. Physically hazardous
3. Related legal problems
4. Despite of having persistent social problems

31. ALCOHOL DEPENDENCE
• Any one of following in 12 mns
• Increased amount of alcohol needed to achieve
desired effect & continued use of same amount
• Withdrawal symptoms
• Persistent desire to cut down
• Important social /recreational activities given up
• Increased time spent to obtain/to use /to recover
from the effects alcohol

32. Collection of blood for alcohol
• Spirit - not used to clean skin
• Preservative –sod fluoride(100mg)+potassium
oxalate(30 mg)
• Refrigerated, should not be freezed
• WIDMARK FORMULA
– Wt of alcohol(gm) in body= BWT X BAC X 0.6
(men) 0.5(women)

33. Breath analysis
• Alcohol absorbs infra red rays
• Amount of infra red rays absorbed is
proportional to alcohol contents
• 60—100ml of air is receieved in a plastic
balloon
• End portion of forced expiration gives correct
results
• Conc in exhaled air is about 0.05% of blood
content

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