The processes which lead to<unk> s are still poorly understood. Several pathophysiological changes may give rise to the alcohol<unk>  including increased levels of acetaldehyde, hormonal alterations of the cytokine pathways and decrease of the availability of glucose. Additional associated phenomena are dehydration, metabolic acidosis, disturbed prostaglandin synthesis, increased cardiac output, vasodilation, sleep deprivation and insufficient eating. Some complex organic molecules found in alcoholic beverages known as congeners may play an important role in producing<unk>  effects because some, such as methanol, are metabolized to the notably toxic substances formaldehyde and formic acid. Pathophysiology Alcohol flush reaction as a result of the accumulation of acetaldehyde, the first metabolite of alcohol After being ingested, the ethanol in alcoholic beverages is first converted to acetaldehyde by the enzyme alcohol dehydrogenase and then to acetic acid by oxidation and egestion process. These reactions also convert nicotinamide adenine dinucleotide (NAD+) to its reduced form NADH in a redox reaction. By causing an imbalance of the NAD+/NADH redox system, alcoholic beverages make normal bodily functions more difficult. Consequences of the alcohol induced redox changes in the human body include increased triglyceride production, increased amino acid catabolism, inhibition of the citric acid cycle, lactic acidosis, ketoacidosis, hyperuricemia, disturbance in cortisol and androgen metabolism and increased fibrogenesis. The metabolism of glucose and insulin are also influenced. However, recent studies showed no significant correlation between<unk>  severity and the concentrations of various hormones, electrolytes, free fatty acids, triglycerides, lactate, ketone bodies, cortisol, and glucose in blood and urine samples. Alcohol also induces the CYP2E1 enzyme, which metabolizes ethanol and other substances into more reactive toxins. In particular, in binge drinking the enzyme is activated and plays a role in creating a harmful condition known as oxidative stress which can lead to cell death. Acetaldehyde Acetaldehyde, the first by-product of ethanol, is between 10 and 30 times more toxic than alcohol itself and can remain at an elevated plateau for many hours after initial ethanol consumption. In addition, certain genetic factors can amplify the negative effects of acetaldehyde. For example, some people (predominantly East Asians) have a mutation in their alcohol dehydrogenase gene that makes this enzyme unusually fast at converting ethanol to acetaldehyde. In addition, about half of all East Asians convert acetaldehyde to acetic acid more slowly (via acetaldehyde dehydrogenase), causing a higher buildup of acetaldehyde than normally seen in other groups. The high concentration of acetaldehyde causes the alcohol flush reaction, colloquially known as the "Asian Flush". Since the alcohol flush reaction is highly uncomfortable and the possibility of<unk> s is immediate and severe, people with this gene variant are less likely to become alcoholics. Finlandia vodka have a lower concentration of congeners Acetaldehyde may also influence glutathione peroxidase, a key antioxidant enzyme, and increases the susceptibility to oxidative stress. Likewise, acetic acid (or the acetate ion) can cause additional problems. One study found that injecting sodium acetate into rats caused them to have nociceptive behavior (headaches). In addition, there is a biochemical explanation for this finding. High acetate levels cause adenosine to accumulate in many parts of the brain. But when the rats were given caffeine, which blocks the action of adenosine, they no longer experienced headaches. Congeners In addition to ethanol and water, most alcoholic drinks also contain congeners, either as flavoring or as a by-product of fermentation and the wine aging process. While ethanol is by itself sufficient to produce most<unk>  effects, congeners may potentially aggravate<unk>  and other residual effects to some extent. Congeners include substances such as amines, amides, acetones, acetaldehydes, polyphenols, methanol, histamines, fusel oil, esters, furfural, and tannins, many but not all of which are toxic. One study in mice indicates that fusel oil may have a mitigating effect on<unk>  symptoms, while some whiskey congeners such as butanol protect the stomach against gastric mucosal damage in the rat. Different types of alcoholic beverages contain different amounts of congeners. In general, dark liquors have a higher concentration while clear liquors have a lower concentration. Whereas vodka has virtually no more congeners than pure ethanol, bourbon has a total congener content 37 times higher than that found in vodka. Several studies have examined whether certain types of alcohol cause worse<unk> s. All four studies concluded that darker liquors, which have higher congeners, produced worse<unk> s. One even showed that<unk> s were worse and more frequent with darker liquors. In a 2006 study, an average of 14 standard drinks (330 ml each) of beer was needed to produce a<unk> , but only 7 to 8 drinks was required for wine or liquor (note that one standard drink has the same amount of alcohol regardless of type). Another study ranked several drinks by their ability to cause a<unk>  as follows (from low to high): distilled ethanol diluted with fruit juice, beer, vodka, gin, white wine, whisky, rum, red wine and brandy. One potent congener is methanol. It is naturally formed in small quantities during fermentation and it can be accidentally concentrated by improper distillation techniques. Metabolism of methanol produces some extremely toxic compounds, such as formaldehyde and formic acid, which may play a role in the severity of<unk> . Ethanol slows the conversion of methanol into its toxic metabolites so that most of the methanol can be excreted harmlessly in the breath and urine without forming its toxic metabolites. This may explain the temporary postponement of symptoms reported in the common remedy of drinking more alcohol to relieve<unk>  symptoms. Since methanol metabolism is effectively inhibited by consumption of alcohol, methanol accumulates during drinking and only begins to be metabolized once ethanol has been cleared. This delayed action makes it an attractive candidate explanation for delayed post-intoxication symptoms and correlations between methanol concentrations and the presence of<unk>  symptoms that have been found in studies. Vitamin and electrolyte loss The metabolic processes required for alcohol elimination deplete essential vitamins and electrolytes. Furthermore, alcohol is a diuretic, causing excretion of electrolytes through urination. After a night of drinking, the resulting lack of key B and C vitamins, as well as potassium, magnesium, and zinc may cause fatigue, aching and other<unk> -like symptoms. Dehydration Ethanol has a dehydrating effect by causing increased urine production (diuresis), which could cause thirst, dry mouth, dizziness and may lead to an electrolyte imbalance. Studies suggest that electrolyte changes play only a minor role in the genesis of the alcohol<unk>  and are caused by dehydration effects. Drinking water may help relieve symptoms as a result of dehydration but it is unlikely that rehydration significantly reduces the presence and severity of alcohol<unk> . Alcohol's effect on the stomach lining can account for nausea because alcohol stimulates the production of hydrochloric acid in the stomach. Low blood sugar Studies show that alcohol<unk>  is associated with a decrease in blood glucose concentration (less than 70 ml/dl), but the relationship between blood glucose concentration and<unk>  severity is unclear. Also known as insulin shock, hypoglycemia can lead to coma or even death. Immune system In current research, the significant relationship between immune factors and<unk>  severity is the most convincing among all factors so far studied. An imbalance of the immune system, in particular of cytokine metabolism has been identified as playing a role in the pathophysiology of the<unk>  state. Especially the<unk>  symptoms nausea, headache, and fatigue have been suggested to be mediated by changes in the immune system. The concentration of several cytokines have been found to be significantly increased in the blood after alcohol consumption. These include interleukin 12 (IL-12), interferon gamma (IFNγ) and interleukin 10 (IL-10). Some pharmacological studies such as on tolfenamic acid and Opuntia ficus-indica (OFI) have also indicated an involvement of the immune system. These studies suggest that the presence and severity of<unk>  symptoms can probably be reduced by administration of a cyclooxygenase inhibitor such as aspirin or ibuprofen. Person-related factors Several factors which do not in themselves cause alcohol<unk>  are known to influence its severity. These factors include personality, genetics, health status, age, sex, associated activities during drinking such as smoking, the use of other drugs, physical activity such as dancing, as well as sleep quality and duration. * Genetics: alleles associated with aldehyde dehydrogenase (ALDH) and flushing phenotypes (alcohol flush reaction) in Asians are known genetic factors that influence alcohol tolerance and the development of<unk>  effects. Existing data shows that drinkers with genotypes known to lead to acetaldehyde accumulation are more susceptible to<unk>  effects. The fact that about 25% of heavy drinkers claim that they have never had a<unk>  is also an indication that genetic variation plays a role in individual differences of<unk>  severity. * Age: some people experience<unk> s as getting worse as one ages. This is thought to be caused by declining supplies of alcohol dehydrogenase, the enzyme involved in metabolizing alcohol. Although it is actually unknown whether<unk>  symptoms and severity change with age, research shows that drinking patterns change across ages, and heavy drinking episodes that may result in
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