Alcohol Metabolism

Question 1

How is ethanol made?

Answer 1

Starch is converted to simple sugars by alpha and beta amylase. Yeast (micro organisms) convert sugars to ethanol and CO2 in anaerobic conditions at room temp

1 molecule of glucose –> 2 molecules of ethanol and CO2

Fermentation stops when sugar is used up or when the alcohol content is high enough to inactivate the micro-organisms

Question 2

Describe the 3 alcohol metabolism pathways of alcohol from substrate to the end products, mentioning enzymes and by-products

Answer 2

3 pathways for converting ethanol to acetaldehyde

ADH pathway = low-moderate intake (3-7 per week); occurs in gastric cells (20%) and hepatocytes; NAD+ reduced to NADH

MEOS pathway = moderate intake (7-14 per week); occurs in hepatocytes only; mediated by P450; also metabolises drugs and other foreign substances; NADPH oxidises to NADP+; assists in building a tolerance to alcohol over time

Catalase pathway = high intake (>14 per week); occurs in hepatocytes only; oxidation occurs in peroxisomes via peroxisomal catalase; uses hydrogen peroxide to form acetaldehyde and H2O

Acetaldehyde moves to the mitochondria and is metabolised by ALDH2 to acetate. Acetate can bind to CoA to form acetyl-CoA. Acetyl-CoA enters CAC or is used for ketone bodies production or used for lipogenesis depending on metabolic “environment”. Energy status and availability

Question 3

What is the reason for alcohol intolerance?

Answer 3

Some people have low/poor ALDH2 activity

Results in acetaldehyde build up = red flush, dizziness, nausea, headaches, rapid HR and breathing

Question 4

What is the mechanism for increased alcohol tolerance?

Answer 4

Increased MEOS activity

Question 5

What does 5% Alc./Vol. mean?

Answer 5

5% of the volume of the beverage is pure ethanol

Question 6

How much alcohol is in a standard drink? Why this amount?

Answer 6

10g. Based on the assumption that the liver metabolises 10g of ethanol per hour

Question 7

How is the concentration of alcohol in a beverage determined?

Answer 7

(%/100) x mL x 0.789

Question 8

What is the J curve and what does it suggest?

Answer 8

Suggests that the health risks from consuming alcohol are lowest at 1 drink per day and increase rapidly after that

Question 9

What is the latest evidence about the safety of alcohol consumption?

Answer 9

The risk of all-cause mortality dramatically rises with increased alcohol consumption, and the level of consumption that minimises health loss is 0

Question 10

What are the typical acute effects of alcohol abuse?

Answer 10

Relaxation, impaired judgement, reduced inhibitions, slurred speech, impaired balance and coordination, vomiting, sleepiness, memory loss, loss of bladder control, loss of consciousness, coma, death

Question 11

What are the typical outcomes of chronic alcoholism on the liver

Answer 11

Stage 1 - steatosis (alcoholic fatty liver => reversible by abstinence)
Stage 2 - alcoholic hepatitis => reversible with abstinence
Stage 3 - cirrhosis, not reversible. Loss of hepatocyte function as the liver tissue is scarred: cirrhosis; liver failure; hepato-cellular carcinoma

Cirrhosis can be due to:

• Increased concentration of acetaldehyde
• Accumulation of fat in liver resulting in cellular inflammation and damage over time
• Production of free radicals from excessive alcohol metabolism, and reduced activity of antioxidant factors due to poor nutrition that may be the co-habit

Question 12

What are the outcomes of chronic alcoholism on nutritional status?

Answer 12

As food may be replaced by alcohol, most essential nutrients may become scarce, leading to deficiencies
Alcohol beverages are empty of micronutrients, but provide kJ (energy)
=> Protein and moderate energy malnutrition = loss of lean body mass

=> Deficiencies of vitamins and minerals occur because:

	- Decreased intake of nutrition
	- Impaired absorption of nutrients. Alcohol interferes with some nutrient absorption
	- Impaired conversion to the active form of vitamin = less bioactivity
	- Alcohol-related tissue damage. Liver damage = loss of function (e.g. producing bile and carrier proteins to transport fat soluble vitamins, minerals, or cholesterol
	- Increased excretion.  Alcohol inhibits the ADH pathway => increased urination and excretion of water-soluble vitamins and minerals

Question 13

What is Wernicke Korsakoff syndrome? Describe the reasons it develops and the outcomes

Answer 13

A deficiency in thiamine (vitamin B1) can cause Wernicke-Korsakoff syndrome:

	- Decreased thiamine intake due to alcohol reducing expression of thiamine transporters in the enterocytes
	- Decreased thiamine absorption
	- Increased thiamine excretion in urine
	- Signs and symptoms include impaired vision and mental function, poor muscle coordination and shakes

Thiamine deficiency from alcohol abuse was the “reason” for mandatory fortification of thiamine in bread flour, and voluntary fortification of cereal-based foods in Australia

Question 14

What as BAL/BAC? What does a BAL of 0.07 mean?

Answer 14

0.07g (70mg) of ethanol in 100mL of blood

Question 15

How long does it take to return to a BAL of 0.00 for the average weight adult male and female?

Answer 15

Liver breaks down 5-10g/hr