Metabolism of alcohol and alex went on to ramble about biochem effects.

Metabolism of alcohol and NAD
Alcohol -> acetaldehyde -> acetate -> acetyl CoA -> goes into citric cycle.

2NADH is produced by the reduction. (Increase in NADH)
Most of the acetaldehyde is rapidly turned into acetate, but a small percentage escapes to the blood and produces effects elsewhere in the body. Acetaldehyde can damage cells, causes the hangover effects. In the liver, acetaldehyde disturbs the protein metabolism, resulting in protein accumulation and extra expansion of the liver.

Most of the acetaldehyde is rapidly turned into acetate, but a small percentage escapes to the blood and produces effects elsewhere in the body. Acetaldehyde can damage cells, thereby slowing down the rate at which the acetaldehyde is metabolized. In the liver, acetaldehyde disturbs the protein metabolism, resulting in protein accumulation and extra expansion of the liver.

Metabolism of alcohol by MEOS
MEOS (microsomal ethanol-oxidizing system)
- occurs only during heavy alcohol intake.
- produces free radicals (hydroxide and so on)
- these free radicals will cause damage to the vital components of cells.
- normally, antioxidants can counter effect these free radicals, but after MEOS, the amount of free radicals build up and upsets the balance.
- free radicals are made from oxygen atoms and this causes the amount of oxygen atoms in the blood to decrease. this leads to oxidative stress.


Lactate acidosis
As mentioned earlier, when excessive alcohol is introduced to the body, the alcohol is then metabolized to produce NADH and acetate.
lactate + NAD <-> pyruvate + NADH
This means that the amount of NADH in the body increases drastically. In turn, this will cause a shift and the amount of lactate and NAD increases. The increase in lactate acid will result in lactate acidosis.

Hypoxia
As mentioned earlier, the main pathway of alcohol metabolism, which involves ADH and ALDH, results in the generation of NADH. The NADH then is oxidized by a series of chemical reactions in the mitochondria (i.e., the mitochondrial electron transport system, or respiratory chain), eventually resulting in the transfer of electrons to molecular oxygen (O2), which then binds protons (H+) to generate water (H2O). To have enough oxygen available to accept the electrons, the hepatocytes must take up more oxygen than normal from the blood.

Liver
The liver is most commonly affected by alcohol-induced damage. The first stage of liver damage following chronic alcohol consumption is the appearance of fatty liver, which is followed by inflammation, apoptosis, fibrosis, and finally cirrhosis. The development of fatty liver is induced by the shift in the redox state of the hepatocytes that results from ethanol metabolism by ADH. This shift in the redox state favors the accumulation of fatty acids, rather than their oxidation. In addition to these metabolic effects, chronic ethanol consumption contributes to the development of fatty liver by influencing the activities of several proteins that help regulate fatty acid synthesis and oxidation

Neurodegeneration
Occurs because of the hypoglycemia. The proliferation of neural stem cells and the survival of neurons produced from the stem cells during alcohol exposure are decreased (Nixon and Crews 2002). The prefrontal cortex is involved in high-level cognitive and executive functions, such as planning complex cognitive behaviors, decisionmaking, and moderating correct social behavior.) have central roles in executive functions, such as decisionmaking.

Hypoglycemia
1) Lactate + NAD <-> pyruvate + NADH
2) Pyruvate <-> glucose

As mentioned earlier, when excessive alcohol is introduced to the body, the alcohol is then metabolized to produce NADH and acetate.
This means that the amount of NADH in the body increases drastically. In turn, this will cause a shift in the first equation to the left, and the amount of lactate and NAD increases.
This also means that the amount of pyruvate will decrease. When the amount of pyruvate decreases, the second reaction will then shift to the left as well, resulting in a decrease in blood glucose.
Alcohol-induced hypoglycemia occurs in the fasted state, when the diabetic's blood sugar levels are already low and the body depends on the production of new glucose molecules (i.e., gluconeogenesis) to maintain sufficient blood glucose levels. Gluconeogenesis, which occurs in the liver, requires certain compounds whose levels are regulated by a substance called reduced nicotinamide adenine dinucleotide (NADH). Alcohol metabolism in the liver generates excessive NADH levels and thus reduces the levels of the compounds needed for gluconeogenesis, thereby contributing to a further drop in blood sugar levels.

Hepatitis C
Hepatitis C is the inflammation of the liver caused by the hepatitis C virus. High alcohol intake causes the depression of the immune system, which in turn causes the susceptibility of the human to virus attacks. Another theory is that there is increased replication of HCV in the liver.

Hyperlipidemia
The increase in NADH also affects the ratio of NAD to NADH. NAD is needed to accept the hydrogen ions for the continuity of the citric cycle and the conversion of fatty acids to acetyl CoA. This results in a build up of acetyl CoA and fatty acids. The build up of fatty acids results in hyperlipidemia.
In people with hyperlipidemia, the levels of fat molecules in the blood - particularly molecules called triglycerides - are higher than normal. This condition can be associated with an increased risk of various health problems, the most serious of which is cardiovascular disease. Alcohol consumption may exacerbate hyperlipidemia, because the same metabolic alcohol effects that inhibit gluconeogenesis also inhibit fat metabolism. As a result, the production of certain molecules called very low density lipoprotein (VLDL) particles is increased.

Damage to the heart
Moderate drinking:
Reduced plaques leading to less risk of artherosclerosis.
Reduced blood clots.

Heavy drinking:
Heart muscle inflamed and thinning leading to cardiomyopathy.
Increased risk of arrhythmia (irregular heart beating)
Increased risk of hypertension (heart needs to pump faster to compensate for nutrient defiency, hypoxia, hypoglycemia.)



http://pubs.niaaa.nih.gov/publications/arh313/185-195.htm
http://www.nlm.nih.gov/medlineplus/ency/article/000174.htm
http://pubs.niaaa.nih.gov/publications/arh294/245-255.htm
http://health.howstuffworks.com/alcohol12.htm
http://www.enotalone.com/article/11222.html
http://findarticles.com/p/articles/mi_m0CXH/is_1_23/ai_57050109