An alcohol hangover is associated with a variety of symptoms that may include drowsiness, headache, concentration problems, dry mouth, dizziness, gastrointestinal complaints, fatigue, sweating, nausea, hyper-excitability, anxiety, and a feeling of general discomfort that may last more than 24 hours. Alcohol hangover symptoms develop when blood alcohol concentration falls considerably and peak when it returns to almost zero. Hangover symptoms validated in controlled studies include general malaise, thirst, headache, feeling dizzy or faint, tiredness, loss of appetite, nausea, stomach ache, and feeling as though one's heart is racing. Some symptoms such as changes in sleep pattern and gastrointestinal distress are attributed to direct effects of the alcohol intoxication, or withdrawal symptoms. Drowsiness and impaired cognitive function are the two dominant features of alcohol hangover.

A hangover is the experience of various unpleasant physiological and psychological effects following the consumption of ethanol, as found in wine, beer and distilled spirits. Hangovers can last for several hours or for more than 24 hours. Typical symptoms of a hangover may include headache, drowsiness, concentration problems, dry mouth, dizziness, fatigue, gastrointestinal distress (e.g., vomiting), absence of hunger, depression, sweating, nausea, hyper-excitability and anxiety.

While the causes of a hangover are still poorly understood, several factors are known to be involved including acetaldehyde accumulation, changes in the immune system and glucose metabolism, dehydration, metabolic acidosis, disturbed prostaglandin synthesis, increased cardiac output, vasodilation, sleep deprivation and malnutrition. Beverage-specific effects of additives or by-products such as congeners in alcoholic beverages also play an important role. The symptoms occur typically after the intoxicating effect of the alcohol begins to wear off, generally the morning after a night of heavy drinking.

Though many possible remedies and folk cures have been suggested, there is no compelling evidence to suggest that any are effective for preventing or treating alcohol hangover. Avoiding alcohol or drinking in moderation are the most effective ways to avoid a hangover.

The socioeconomic consequences and health risks of alcohol hangover include workplace absenteeism, impaired job performance, reduced productivity and poor academic achievement. A hangover may also compromise potentially dangerous daily activities such as driving a car or operating heavy machinery.

Several symptoms are associated with the sopite syndrome. Typical responses include:

- drowsiness

- yawning

- disinclination for work

- lack of social participation

- mood changes

- apathy

- sleep disturbances

- other fatigue-related symptoms

The sopite syndrome is distinguished from other manifestations of motion sickness (i.e. nausea, dizziness, etc.) in that it may occur before other symptoms of motion sickness or in their absence. The sopite syndrome may persist even after an individual has adapted to the other symptoms associated with motion-induced sickness.

The effects of the sopite syndrome may range from minor physical inconveniences to hazardous conditions. Persons who operate automobiles, airplanes, et cetera, may experience impaired motor function due to the motions of the vehicle. These impairments often result in a decreased attention span; persons who consider themselves well-rested may still succumb to drowsiness at inopportune moments. The sopite syndrome may therefore contribute to motor vehicle accidents in which automobile operators fall asleep at the wheel. However, the sopite syndrome itself does not directly result in death.

A subject experiencing the sopite syndrome on a frequent basis may increase the number of hours spent sleeping by fifty percent. A study of motion sickness occurrences in workers on an offshore oil vessel showed a large majority of participants experienced mild symptoms of fatigue. Many participants also experienced severe sleep disturbances. These symptoms were associated with impaired task performance.

Due to its perception-altering effects, the onset of narcosis may be hard to recognize. At its most benign, narcosis results in relief of anxiety – a feeling of tranquility and mastery of the environment. These effects are essentially identical to various concentrations of nitrous oxide. They also resemble (though not as closely) the effects of alcohol or cannabis and the familiar benzodiazepine drugs such as diazepam and alprazolam. Such effects are not harmful unless they cause some immediate danger to go unrecognized and unaddressed. Once stabilized, the effects generally remain the same at a given depth, only worsening if the diver ventures deeper.

The most dangerous aspects of narcosis are the impairment of judgement, multi-tasking and coordination, and the loss of decision-making ability and focus. Other effects include vertigo and visual or auditory disturbances. The syndrome may cause exhilaration, giddiness, extreme anxiety, depression, or paranoia, depending on the individual diver and the diver's medical or personal history. When more serious, the diver may feel overconfident, disregarding normal safe diving practices. Slowed mental activity, as indicated by increased reaction time and increased errors in cognitive function, are effects which increase the risk of a diver mismanaging an incident. Narcosis reduces both the perception of cold discomfort and shivering and thereby affects the production of body heat and consequently allows a faster drop in the core temperature in cold water, with reduced awareness of the developing problem.

The relation of depth to narcosis is sometimes informally known as "Martini's law", the idea that narcosis results in the feeling of one martini for every below depth. Professional divers use such a calculation only as a rough guide to give new divers a metaphor, comparing a situation they may be more familiar with.

Reported signs and symptoms are summarized against typical depths in meters and feet of sea water in the following table, closely adapted from "Deeper into Diving" by Lippman and Mitchell:

Alcohol (also known as ethanol) has a number of effects on health. Short-term effects of alcohol consumption include intoxication and dehydration. Long-term effects of alcohol consumption include changes in the metabolism of the liver and brain and alcoholism. Alcohol intoxication affects the brain, causing slurred speech, clumsiness, and delayed reflexes. Alcohol stimulates insulin production, which speeds up glucose metabolism and can result in low blood sugar, causing irritability and possibly death for diabetics. A 2014 World Health Organization report found that harmful alcohol consumption caused about 3.3 million deaths annually worldwide.

However, some effects of alcohol consumption are beneficial. Although even moderate alcohol consumption increased the risk of death in younger people, it has been shown to "decrease" the risk of death for individuals ages 55+ (due to decreased risk of ischemic heart disease).

The median lethal dose of alcohol in test animals is a blood alcohol content of 0.45%. This is about six times the level of ordinary intoxication (0.08%), but vomiting or unconsciousness may occur much sooner in people who have a low tolerance for alcohol. The high tolerance of chronic heavy drinkers may allow some of them to remain conscious at levels above 0.40%, although serious health hazards are incurred at this level.

Alcohol also limits the production of vasopressin (ADH) from the hypothalamus and the secretion of this hormone from the posterior pituitary gland. This is what causes severe dehydration when alcohol is consumed in large amounts. It also causes a high concentration of water in the urine and vomit and the intense thirst that goes along with a hangover.

Stress, hangovers, and the oral contraceptive pill may increase the desire for alcohol because these things will lower the level of testosterone and alcohol will acutely elevate it. Tobacco has the same effect of increasing the craving for alcohol.

Warning signs of alcoholism include the consumption of increasing amounts of alcohol and frequent intoxication, preoccupation with drinking to the exclusion of other activities, promises to quit drinking and failure to keep those promises, the inability to remember what was said or done while drinking (colloquially known as "blackouts"), personality changes associated with drinking, denial or the making of excuses for drinking, the refusal to admit excessive drinking, dysfunction or other problems at work or school, the loss of interest in personal appearance or hygiene, marital and economic problems, and the complaint of poor health, with loss of appetite, respiratory infections, or increased anxiety.

Narcosis while diving (also known as nitrogen narcosis, inert gas narcosis, raptures of the deep, Martini effect) is a reversible alteration in consciousness that occurs while diving at depth. It is caused by the anesthetic effect of certain gases at high pressure. The Greek word "ναρκωσις" (narcosis) is derived from "narke", "temporary decline or loss of senses and movement, numbness", a term used by Homer and Hippocrates. Narcosis produces a state similar to drunkenness (alcohol intoxication), or nitrous oxide inhalation. It can occur during shallow dives, but does not usually become noticeable at depths less than .

Except for helium and probably neon, all gases that can be breathed have a narcotic effect, although widely varying in degree. The effect is consistently greater for gases with a higher lipid solubility, and there is good evidence that the two properties are mechanistically related. As depth increases, the mental impairment may become hazardous. Divers can learn to cope with some of the effects of narcosis, but it is impossible to develop a tolerance. Narcosis affects all divers, although susceptibility varies widely from dive to dive, and between individuals.

Narcosis may be completely reversed in a few minutes by ascending to a shallower depth, with no long-term effects. Thus narcosis while diving in open water rarely develops into a serious problem as long as the divers are aware of its symptoms, and are able to ascend to manage it. Diving much beyond is generally considered outside the scope of recreational diving. In order to dive at greater depths, as narcosis and oxygen toxicity become critical risk factors, specialist training is required in the use of various helium-containing gas mixtures such as trimix or heliox. These mixtures prevent narcosis by replacing some or all of the breathing gas with non-narcotic helium.

Drinking enough to cause a blood alcohol concentration (BAC) of 0.03–0.12% typically causes an overall improvement in mood and possible euphoria (a "happy" feeling), increased self-confidence and sociability, decreased anxiety, a flushed, red appearance in the face and impaired judgment and fine muscle coordination. A BAC of 0.09% to 0.25% causes lethargy, sedation, balance problems and blurred vision. A BAC of 0.18% to 0.30% causes profound confusion, impaired speech (e.g. slurred speech), staggering, dizziness and vomiting. A BAC from 0.25% to 0.40% causes stupor, unconsciousness, anterograde amnesia, vomiting (death may occur due to inhalation of vomit (pulmonary aspiration) while unconscious and respiratory depression (potentially life-threatening). A BAC from 0.35% to 0.80% causes a coma (unconsciousness), life-threatening respiratory depression and possibly fatal alcohol poisoning. With all alcoholic beverages, drinking while driving, operating an aircraft or heavy machinery increases the risk of an accident; many countries have penalties for drunk driving.

Alcohol intolerance is due to a genetic deficiency of the enzyme alcohol dehydrogenase, the enzyme that metabolises ingested alcohol. It can also be an effect or side effect associated with certain drugs such as disulfiram, metronidazole, or nilutamide. It is characterized as intolerance of and unpleasant symptoms upon the ingestion of alcohol, causing hangover symptoms similar to the "disulfiram-like reaction" of aldehyde dehydrogenase deficiency or chronic fatigue syndrome.

If people are intolerant, some nearly non-alcoholic beverages may be a problem, similar to alcohol-containing medications, vinegar, inhalation of alcohol or the vapour of alcohol-containing cleaning agents.

Drinking alcohol first or afterwards together with Calcium cyanamide, an inorganic compound used as a fertilizer, can cause permanent or long lasting intolerance (nitrolime disease), contributing together with other substances to the accumulation of harmful Acetaldehyde by inhibiting the enzyme acetaldehyde dehydrogenase.

Headaches due to environmental causes are usually diagnosed by taking an exposure history.

Symptoms vary according to individuals' hydration level and sensitivity to the rate and/or magnitude of decline of their blood glucose concentration.

A crash is usually felt within four hours or less of heavy carbohydrate consumption. Symptoms of reactive hypoglycemia include:

- double vision or blurry vision

- unclear thinking

- insomnia

- heart palpitation or fibrillation

- fatigue

- dizziness

- light-headedness

- sweating

- headaches

- depression

- nervousness

- muscle twitches

- irritability

- tremors

- flushing

- craving sweets

- increased appetite

- rhinitis

- nausea, vomiting

- panic attack

- numbness/coldness in the extremities

- confusion

- irrationality

- bad temper

- paleness

- cold hands

- disorientation

- the need to sleep or 'crash'

- coma can be a result in severe untreated episodes

The majority of these symptoms, often correlated with feelings of hunger, mimic the effect of inadequate sugar intake as the biology of a crash is similar in itself to the body’s response to low blood sugar levels following periods of glucose deficiency.

Reactive hypoglycemia, postprandial hypoglycemia, or sugar crash is a term describing recurrent episodes of symptomatic hypoglycemia occurring within 4 hours after a high carbohydrate meal in people who do not have diabetes.

The condition is related to homeostatic systems utilised by the body to control blood sugar levels. It is variously described as a sense of tiredness, lethargy, irritation, or hangover, although the effects can be less if one has undertaken a lot of physical activity within the next few hours after consumption.

The alleged mechanism for the feeling of a crash is correlated with an abnormally rapid rise in blood glucose after eating. This normally leads to insulin secretion (known as an "insulin spike"), which in turn initiates rapid glucose uptake by tissues either accumulating it as glycogen or utilizing it for energy production. The consequent fall in blood glucose is indicated as the reason for the "sugar crash".. A deeper cause might be hysteresis effect of insulin action, i.e., the effect of insulin is still prominent even if both plasma glucose and insulin levels were already low, causing a plasma glucose level eventually much lower than the baseline level.

Sugar crashes are not to be confused with the after-effects of consuming large amounts of "protein", which produces fatigue akin to a sugar crash, but are instead the result of the body prioritising the digestion of ingested food.

The prevalence of this condition is difficult to ascertain because a number of stricter or looser definitions have been used. It is recommended that the term reactive hypoglycemia be reserved for the pattern of postprandial hypoglycemia which meets the Whipple criteria (symptoms correspond to measurably low glucose and are relieved by raising the glucose), and that the term idiopathic postprandial syndrome be used for similar patterns of symptoms where abnormally low glucose levels at the time of symptoms cannot be documented.

To assist diagnosis, a doctor can order an HbA1c test, which measures the blood sugar average over the two or three months before the test. The more specific 6-hour glucose tolerance test can be used to chart changes in the patient's blood sugar levels before ingestion of a special glucose drink and at regular intervals during the six hours following to see if an unusual rise or drop in blood glucose levels occurs.

According to the U.S. National Institute of Health (NIH), a blood glucose level below 70 mg/dL (3.9 mmol/L) at the time of symptoms followed by relief after eating confirms a diagnosis for reactive hypoglycemia.

These headaches have been further sub classified by the ICHD2 into

- Headaches induced by acute substance use or exposure

- Medication overuse headaches (MOH)

- Headaches attributed to chronic medication use

- Headaches attributed to substance withdrawal

The short-term effects of alcohol consumption range from a decrease in anxiety and motor skills at lower doses to unconsciousness, anterograde amnesia, and central nervous system depression at higher doses. Cell membranes are highly permeable to alcohol, so once alcohol is in the bloodstream it can diffuse into nearly every cell in the body.

The concentration of alcohol in blood is measured via blood alcohol content (BAC). The amount and circumstances of consumption play a large part in determining the extent of intoxication; for example, eating a heavy meal before alcohol consumption causes alcohol to absorb more slowly. Hydration also plays a role, especially in determining the extent of hangovers. After excessive drinking, unconsciousness can occur and extreme levels of consumption can lead to alcohol poisoning and death (a concentration in the blood stream of 0.40% will kill half of those affected). Alcohol may also cause death indirectly, by asphyxiation from vomit.

Alcohol can greatly exacerbate sleep problems. During abstinence, residual disruptions in sleep regularity and sleep patterns are the greatest predictors of relapse.

A drug-related blackout is a phenomenon caused by the intake of any substance or medication in which short term and long term memory creation is impaired, therefore causing a complete inability to recall the past. Blackouts are most frequently associated with GABAergic drugs. Blackouts are frequently described as having effects similar to that of anterograde amnesia, in which the subject cannot recall any events after the event that caused amnesia. Research on alcohol blackouts was begun by E. M. Jellinek in the 1940s. Using data from a survey of Alcoholics Anonymous (AA) members, he came to believe that blackouts would be a good determinant of alcoholism. However, there are conflicting views whether this is true. The negative psychological effects of an alcohol-related blackout are often worsened by those who suffer from anxiety disorders. Impairment of the liver will also allow more alcohol to reach the brain and hasten the individual's blackout.

The term "blackout" can also refer to a complete loss of consciousness, or syncope.

Altitude sickness, also known as acute mountain sickness (AMS), is a negative health effect of high altitude, caused by acute exposure to low amounts of oxygen at high altitude.

Although minor symptoms such as breathlessness may occur at altitudes of , AMS commonly occurs above .

It presents as a collection of nonspecific symptoms, acquired at high altitude or in low air pressure, resembling a case of "flu, carbon monoxide poisoning, or a hangover". It is hard to determine who will be affected by altitude sickness, as there are no specific factors that correlate with a susceptibility to altitude sickness. However, most people can ascend to without difficulty.

Acute mountain sickness can progress to high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE), both of which are potentially fatal, and can only be cured by immediate descent to lower altitude or oxygen administration.

Chronic mountain sickness is a different condition that only occurs after long term exposure to high altitude.

People have different susceptibilities to altitude sickness; for some otherwise healthy people, acute altitude sickness can begin to appear at around above sea level, such as at many mountain ski resorts, equivalent to a pressure of . This is the most frequent type of altitude sickness encountered. Symptoms often manifest themselves six to ten hours after ascent and generally subside in one to two days, but they occasionally develop into the more serious conditions. Symptoms include headache, fatigue, stomach illness, dizziness, and sleep disturbance. Exertion aggravates the symptoms.

Those individuals with the lowest initial partial pressure of end-tidal pCO (the lowest concentration of carbon dioxide at the end of the respiratory cycle, a measure of a higher alveolar ventilation) and corresponding high oxygen saturation levels tend to have a lower incidence of acute mountain sickness than those with high end-tidal pCO and low oxygen saturation levels.

Blackouts can generally be divided into 2 categories, "en bloc" blackouts and "fragmentary" blackouts. En bloc blackouts are classified by the inability to later recall any memories from the intoxication period, even when prompted. These blackouts are characterized also by the ability to easily recall things that have occurred within the last 2 minutes, yet being unable to recall anything prior to this period. As such, a person experiencing an en bloc blackout may not appear to be doing so, as they can carry on conversations or even manage to accomplish difficult feats. It is difficult to determine the end of this type of blackout as sleep typically occurs before they end, although it is possible for an en bloc blackout to end if the sufferer has stopped drinking in the meantime. Fragmentary blackouts are characterized by a person having the ability to recall certain events from an intoxicated period, and yet being unaware that other memories are missing until reminded of the existence of those 'gaps' in memory. Research indicates that such fragmentary blackouts, also known as brownouts, are far more common than en bloc blackouts. Memory impairment during acute intoxication involves dysfunction of episodic memory, a type of memory encoded with spatial and social context. Recent studies have shown that there are multiple memory systems supported by discrete brain regions, and the acute effects of alcohol and learning and memory may result from alteration of the hippocampus and related structures on a cellular level. A rapid increase in blood alcohol concentration (BAC) is most consistently associated with the likelihood of a blackout. However, not all subjects experience blackouts which implies that genetic factors play a role in determining central nervous system (CNS) vulnerability to the effects of alcohol. The former may predispose an individual to alcoholism, as altered memory function during intoxication may affect an individual’s alcohol expectancy, one may perceive positive aspects of intoxication while unintentionally ignoring the negative aspects.

The overstimulation of the semicircular canals during PAN I and PAN II is associated with the unsteadiness, nausea, and vertigo felt by intoxicated people. PAN I is more associated with postural problems (e.g. standing and walking) while PAN II has been more associated with the feelings of a hangover.

There is a brief period between PAN I and PAN II when the alcohol concentrations in the canal membrane and extracellular fluid are in equilibrium. During this time, neither PAN I nor PAN II is present.

As soon as a person starts drinking, the body begins to process and eliminate the alcohol. The rate of elimination is fairly constant. Initially, the rate of absorption exceeds the rate of elimination, which results in a rising BAC. Some time after a person stops drinking, the rate of absorption drops below the rate of elimination, and the BAC begins falling. As alcohol is eliminated from the body, it is removed from the membrane of the semicircular canal faster than the surrounding fluid. This creates the reverse situation of PAN I, as the specific gravity of the fluid is now lower than that of the membrane. This results in PAN II.

PAN II is characterized by a nystagmus to the right when the left side of the head is down.

Ethanol is the type of alcohol found in alcoholic beverages. It is a volatile, flammable, colorless liquid that acts as a central nervous system depressant. Ethanol can impair different types of memory.

"Prospective memory" involves remembering to carry out an intended action in the future without an explicit reminder. Alcohol has been found to impair this ability. Chronic heavy alcohol users report significantly more prospective forgetting compared to low-dose and alcohol-free controls. The Prospective Memory Questionnaire assesses short-term habitual prospective memory, long-term episodic prospective memory, and internally cued prospective memory. Chronic heavy alcohol users reported significantly greater deficits for all three aspects of prospective memory. Individuals that report heavy alcohol use report 24% more difficulties with prospective memory than those who report that they are light drinkers and 30% more difficulties than those who report that they never drink. The effects of alcohol on prospective memory can also be assessed in the laboratory by simulating prospective memory tasks that individuals face in everyday life. Individuals who are given 0.6 g/kg alcohol prior to performing prospective memory tasks do significantly poorer than a placebo group. Alcohol can damage the prefrontal and frontal areas of the brain, and this may be responsible for prospective memory impairments since prospective memory performance is highly correlated with frontal executive functions.