RWH could be caused by the release of prostaglandins which some people are not able to metabolize. Prostaglandins are substances that can contribute to pain and swelling. Ibuprofen (Advil), paracetamol (Tylenol) and aspirin are prostaglandin inhibitors. Aspirin and ibuprofen were shown to be effective at blocking both early and late stages of the RWH, and paracetamol (acetaminophen) was effective in blocking the early stage. However, combining paracetamol/acetaminophen and/or NSAIDs (like ibuprofen) with alcohol are not good for the liver, and can be potentially harmful. Some individuals will experience extreme nausea, vomiting, and abdominal pain when combining alcohol with acetaminophen and/or NSAIDs. The combination should never be used.

Tyramine may well be a major player in RWH syndrome. Tyramine is an amine that is produced naturally from the breakdown of protein as food ages. More specifically it is formed by the decarboxylation of the amino acid tyrosine. It is found in aged, fermented, and spoiled foods. Everyday foods we consume including aged cheeses, overripe and dried fruit, sauerkraut, soy, and many processed foods contain high levels of tyramine. Tyramine is suspected of inducing migraine headaches in about 40% of migraine sufferers, according to F.G.Freitag of Diamond Headache Clinic in Chicago.

There is no evidence that any treatment for hangovers is very effective.

- Rehydration: Drinking water before going to bed or during hangover may relieve dehydration-associated symptoms such as thirst, dizziness, dry mouth, and headache.

- Non-steroidal anti-inflammatory drugs such as aspirin or ibuprofen have been proposed as a treatment for the headaches associated with a hangover. There however is no evidence to support a benefit, and there are concerns that taking alcohol and aspirin together may increase the risk of stomach bleeding and liver damage.

- Tolfenamic acid, an inhibitor of prostaglandin synthesis, in a 1983 study reduced headache, nausea, vomiting, irritation but had no effect on tiredness in 30 people.

- Pyritinol: A 1973 study found that large doses (several hundred times the recommended daily intake) of Pyritinol, a synthetic Vitamin B6 analog, can help to reduce hangover symptoms. Possible side effects of pyritinol include hepatitis (liver damage) due to cholestasis and acute pancreatitis.

- Yeast-based extracts: The difference in the change for discomfort, restlessness, and impatience were statistically significant but no significant differences on blood chemistry parameters, blood alcohol or acetaldehyde concentrations have been found, and it did not significantly improve general well-being.

Avoidance of ethanol is the safest, surest, and cheapest treatment. Indeed, surveys find a positive correlation between high incidences of glu487lys ALDH2 allele-related alcohol-induced respiratory reactions as well as other causes of these reactions and low levels of alcohol consumption, alcoholism, and alcohol-related diseases. Evidently, people suffering these reaction self-impose avoidance behavior. There is a proviso here: ethanol, at surprisingly high concentrations, is used as a solvent to dissolve many types of medicines and other ingredients. This pertains particularly to liquid cold medicines and mouthwashes. Ethanol avoidance includes avoiding the ingestion of and, depending on an individual's history, mouth washing with, such agents.

Type H1 antagonists in the histamine antagonist family of drugs were tested in Japanese volunteers with alcohol-induced asthma (who presumably have glu487lys ALDH2 allele-associated asthma) and found to be completely effective in blocking bronchoconstriction responses to alcoholic beverages; these blockers, it is suggested, may be taken 1–2 hours before consumption of alcohol beverages as a preventative of alcohol-induced respiratory reactions. In the absence of specific studies on the prevention of classical alcohol induced rhinitis and asthma due to allergens in alcoholic beverages, see asthma section on Prevention and rhinitis section on Prevention of allergen-induced reactions.

In the absence of specific studies on the treatment of acute alcohol-induced bronchoconstriction and rhinitis, treatment guidelines should probably follow those of their comparable allergen-induced classical allergic reactions (see asthma section on Treatment and rhinitis section on Treatment) but possibly favoring the testing of H1 antagonist anti-histamines as part of the initial protocol.

Hangovers are poorly understood from a medical point of view. Health care professionals prefer to study alcohol abuse from a standpoint of treatment and prevention, and there is a view that the hangover provides a useful, natural and intrinsic disincentive to excessive drinking.

Within the limited amount of serious study on the subject, there is debate about whether a hangover may be prevented or at least mitigated. There is also a vast body of folk medicine and simple quackery. A four-page literature review in the "British Medical Journal" concludes: "No compelling evidence exists to suggest that any conventional or complementary intervention is effective for preventing or treating alcohol hangover. The most effective way to avoid the symptoms of alcohol induced hangover is to avoid drinking." Most remedies do not significantly reduce overall hangover severity. Some compounds reduce specific symptoms such as vomiting and headache, but are not effective in reducing other common hangover symptoms such as drowsiness and fatigue

In general, any patient who has frequent headaches or migraine attacks should be considered as a potential candidate for preventive medications instead of being encouraged to take more and more painkillers or other rebound-causing medications. Preventive medications are taken on a daily basis. Some patients may require preventive medications for many years; others may require them for only a relatively short period of time such as six months. Effective preventive medications have been found to come from many classes of medications including neuronal stabilizing agents (aka anticonvulsants), antidepressants, antihypertensives, and antihistamines. Some effective preventive medications include Elavil (amitriptyline), Depakote (valproate), Topamax (topiramate), and Inderal (propranolol).

The most common chronic treatment method is the use of medicine. Many people try to seek pain relief from analgesic medicines (commonly termed pain killers), such as aspirin, acetaminophen, aspirin compounds, ibuprofen, and opioids. The long term use of opioids; however, appears to result in greater harm than benefit. Also, abortive medications can be used to "stop a headache once it has begun"; such drugs include ergotamine (Cafergot), triptans (Imitrex), and prednisone (Deltasone). However, medical professionals advise that abuse of analgesics and abortive medications can actually lead to an increase in headaches. The painkiller medicines help headaches temporarily, but as the "quick fix" wears off, headaches become more re-current and grow in intensity. These "rebound headaches" can actually make the body less responsive to preventive medication. The conditions keep worsening if one takes paracetamol, aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) for 15 days a month or more. Therefore, analgesic and abortive medications are often advised for headaches that are not chronic in nature.

MOH is common and can be treated. The overused medications must be stopped for the patient's headache to resolve. Clinical data shows that the treatment of election is abrupt drugs withdrawal, followed by starting prophylactic therapy. However, the discontinuation of overused drugs usually leads to the worsening of headache and the appearance of drug withdrawal symptoms (that greatly depend on the previously overused drugs and typically last from two to ten days and that are relieved by the further intake of the overused medication), which might reinforce the continuation of overuse. Where physical dependence or a rebound effect such as rebound headache is possible, gradual reduction of medication may be necessary. It is important that the patient's physician be consulted before abruptly discontinuing certain medications as such a course of action has the potential to induce medically significant physical withdrawal symptoms. Abruptly discontinuing butalbital, for example, can actually induce seizures in some patients, although simple over the counter analgesics can safely be stopped by the patient without medical supervision. A long-acting analgesic/anti-inflammatory, such as naproxen (500 mg twice a day), can be used to ease headache during the withdrawal period. Two months after the completion of a medication withdrawal, patients suffering from MOH typically notice a marked reduction in headache frequency and intensity.

Drug withdrawal is performed very differently within and across countries. Most physicians prefer inpatients programmes, however effective drug withdrawal may also be achieved in an outpatient setting in uncomplicated MOH patients (i.e. subjects without important co-morbidities, not overusing opioids or ergotaminics and who are at their first detoxification attempt). In the absence of evidence-based indications, in MOH patients the choice of preventive agent should be based on the primary headache type (migraine or TTH), on the drug side-effect profile, on the presence of co-morbid and co-existent conditions, on patient’s preferences, and on previous therapeutic experiences.

Following an initial improvement of headache with the return to an episodic pattern, a relevant proportion (up to 45%) of patients relapse, reverting to the overuse of symptomatic drugs.

Predictors of the relapse, and that could influence treatment strategies, are considered the type of primary headache, from which MOH has evolved, and the type of drug abused (analgesics, and mostly combination of analgesics, but also drugs containing barbiturates or tranquillisers cause significantly higher relapse rates), while gender, age, duration of disease and previous intake of preventative treatment do not seem to predict relapse rate.

MOH is clearly a cause of disability and, if not adequately treated, it represents a condition of risk of possible co-morbidities associated to the excessive intake of drugs that are not devoid of side-effect. MOH can be treated through withdrawal of the overused drug(s) and by means of specific approaches that focus on the development of a close doctor-patient relationship in the post-withdrawal period.

The most common medicines used to treat chronic (daily) headaches are called prophylactic medicines, which are used to prevent headaches. Such preventative medication is taken on a daily basis, even when a person may not have a headache. Prophylactic medicines are recommended for chronic headache patients because varied experiments prove that the medications "reduce the frequency, severity, and disability associated with daily headaches". A majority of the prophylactic medications work by inhibiting or increasing neurotransmissions in the brain, often preventing the brain from interpreting pain signals.

Preventative medicines include gabapentin (Neurontin), tizanidine (Zanaflex), fluoxetine (Prozac), amitriptyline (Elavil), and topiramate (Topamax). In testing, gabapentin was found to reduce the number of headache days a month by 9.1%. Tizanidine was found to decrease the average frequency of headaches per week, the headache intensity, and the mean headache duration. Through studies, Fluoxetine resulted in better mood ratings and "significant increases in headache-free days". Despite being associated with depression, antidepressants, such as amitriptyline, have been found to effectively treat "near-daily headaches" and numerous chronic pain conditions as well as improving mood and sleep—two possible triggers for chronic headache sufferers. One study found that the headache frequency over a 28-day period lowered for chronic headache patients on topiramate. Another medication to prevent headaches is botulinum toxin type A (BoNTA or BOTOX), which is given by injection instead of being taken orally. In a clinical study of botulinum toxin type A, patients participating in the 9-month treatment period with three treatments experienced headache frequency decreases up to 50%. As with all medications, the preventative medications may have side effects. Since different people respond to drugs differently, chronic headache sufferers may have to go through a "trial-and-error" period to find the right medications. The previously mentioned medicines can improve headaches, but physicians recommend multiple forms of treatments.

The mainstays of treatment are removal from the source of lead and, for people who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy. Treatment of iron, calcium, and zinc deficiencies, which are associated with increased lead absorption, is another part of treatment for lead poisoning. When lead-containing materials are present in the gastrointestinal tract (as evidenced by abdominal X-rays), whole bowel irrigation, cathartics, endoscopy, or even surgical removal may be used to eliminate it from the gut and prevent further exposure. Lead-containing bullets and shrapnel may also present a threat of further exposure and may need to be surgically removed if they are in or near fluid-filled or synovial spaces. If lead encephalopathy is present, anticonvulsants may be given to control seizures, and treatments to control swelling of the brain include corticosteroids and mannitol. Treatment of organic lead poisoning involves removing the lead compound from the skin, preventing further exposure, treating seizures, and possibly chelation therapy for people with high blood lead concentrations.

A chelating agent is a molecule with at least two negatively charged groups that allow it to form complexes with metal ions with multiple positive charges, such as lead. The chelate that is thus formed is nontoxic and can be excreted in the urine, initially at up to 50 times the normal rate. The chelating agents used for treatment of lead poisoning are edetate disodium calcium (CaNaEDTA), dimercaprol (BAL), which are injected, and succimer and d-penicillamine, which are administered orally.

Chelation therapy is used in cases of acute lead poisoning, severe poisoning, and encephalopathy, and is considered for people with blood lead levels above 25 µg/dL. While the use of chelation for people with symptoms of lead poisoning is widely supported, use in asymptomatic people with high blood lead levels is more controversial. Chelation therapy is of limited value for cases of chronic exposure to low levels of lead. Chelation therapy is usually stopped when symptoms resolve or when blood lead levels return to premorbid levels. When lead exposure has taken place over a long period, blood lead levels may rise after chelation is stopped because lead is leached into blood from stores in the bone; thus repeated treatments are often necessary.

People receiving dimercaprol need to be assessed for peanut allergies since the commercial formulation contains peanut oil. Calcium EDTA is also effective if administered four hours after the administration of dimercaprol. Administering dimercaprol, DMSA (Succimer), or DMPS prior to calcium EDTA is necessary to prevent the redistribution of lead into the central nervous system. Dimercaprol used alone may also redistribute lead to the brain and testes. An adverse side effect of calcium EDTA is renal toxicity. Succimer (DMSA) is the preferred agent in mild to moderate lead poisoning cases. This may be the case in instances where children have a blood lead level >25μg/dL. The most reported adverse side effect for succimer is gastrointestinal disturbances. It is also important to note that chelation therapy only lowers blood lead levels and may not prevent the lead-induced cognitive problems associated with lower lead levels in tissue. This may be because of the inability of these agents to remove sufficient amounts of lead from tissue or inability to reverse preexisting damage.

Chelating agents can have adverse effects; for example, chelation therapy can lower the body's levels of necessary nutrients like zinc. Chelating agents taken orally can increase the body's absorption of lead through the intestine.

Chelation challenge, also known as provocation testing, is used to indicate an elevated and mobilizable body burden of heavy metals including lead. This testing involves collecting urine before and after administering a one-off dose of chelating agent to mobilize heavy metals into the urine. Then urine is analyzed by a laboratory for levels of heavy metals; from this analysis overall body burden is inferred. Chelation challenge mainly measures the burden of lead in soft tissues, though whether it accurately reflects long-term exposure or the amount of lead stored in bone remains controversial. Although the technique has been used to determine whether chelation therapy is indicated and to diagnose heavy metal exposure, some evidence does not support these uses as blood levels after chelation are not comparable to the reference range typically used to diagnose heavy metal poisoning. The single chelation dose could also redistribute the heavy metals to more sensitive areas such as central nervous system tissue.

There are no permanent cures for urticaria pigmentosa. However, treatments are possible. Most treatments for mastocytosis can be used to treat urticaria pigmentosa. Many common anti-allergy medications are useful because they reduce the mast cell's ability to react to histamine.

At least one clinical study suggested that nifedipine, a calcium channel blocker used to treat high blood pressure, may reduce mast cell degranulation in patients with urticaria pigmentosa. A 1984 study by Fairly et al. included a patient with symptomatic urticaria pigmentosa who responded to nifedipine at dose of 10 mg po tid. However, nifedipine has never been approved by the FDA for treatment of urticaria pigmentosa.

Another mast cell stabilizer Gastrocrom, a form of cromoglicic acid has also been used to reduce mast cell degranulation.

Effect on the body is weakness and mild to moderate dehydration from the severe anxiety and both blood and sweat loss.

The condition is very rare but there are reports in medical literature of successful treatment with beta blockers (propranolol 10 mg) with significant reduction in the frequency of spontaneous blood oozing. The successful use of beta blockers supports the theory that the condition is induced by stress and anxiety yet this etiology is not established yet as the high prevalence of stress and anxiety in the modern era did not change the incidence of this extremely rare disease, suggesting that other co-abnormality also play a key role in this disease. Atropine sulfate transdermal patches have also been used successfully.

Favorable results with psychiatric counselling to reduce stress highlight the relationship between psychogenic causes and hematohidrosis.

The condition usually resolves on its own, and treatment is not required. Oral antihistamines or topical steroids may be used to decrease itching. Steroids do provide relief from itching, and improve the appearance of the rash, but they also cause the new skin that forms (after the rash subsides) to take longer to match the surrounding skin color. While no scarring has been found to be associated with the rash, scratching should be avoided. It's possible that scratching can make itching worse and an itch-scratch cycle may develop with regular scratching (that is, you itch more because you scratch, so you scratch more because you itch, and so on). Irritants such as soaps with fragrances, hot water, wool, and synthetic fabrics should be avoided. Lotions that help stop or prevent itching may also be helpful.

Direct sunlight makes the lesions resolve more quickly. According to this principle, medical treatment with ultraviolet light has been used to hasten resolution, though studies disagree whether it decreases itching or not. UV therapy is most beneficial in the first week of the eruption.

Oral erythromycin was effective in treating patients in one early trial, but a later study could not confirm these results. Since Human Herpes Virus 6 or Human Herpes Virus 7 has been hypothesized to be the cause, the antiviral drug Acyclovir may reduce length of duration and severity.

Preventive and management strategies include the following:

- Avoid sweet and acid foods. Even low sugar contained in fruit is bad for the teeth since it is the sugar/acid exposure time which erodes the teeth, not the amount of sugar.

- Modifying the pH of the food or beverage contributing to the problem, or changing lifestyle to avoid the food or beverage.

- Rinsing immediately after drinking or eating.

- Drinking through a straw

- Avoid abrasive forces. Use a soft bristled toothbrush and brush gently. Avoid brushing immediately after consuming acidic food and drink as teeth will be softened. Leave at least half an hour of time in between. Rinsing with water is better than brushing after consuming acidic foods and drinks.

- Using a remineralizing agent, such as sodium fluoride solution in the form of a fluoride mouthrinse, tablet, or lozenge, immediately before brushing teeth.

- Applying fluoride gels or varnishes to the teeth.

- Drinking milk or using other dairy products.

- Dentine bonding agents applied to areas of exposed dentin

- Use a neutralizing agent such as antacid tablets only as a last-resort. They have negative long-run effects.

- Treating the underlying medical disorder or disease.

The other primarily recommended treatment of acute attacks is subcutaneous or intranasal sumatriptan. Sumatriptan and zolmitriptan have both been shown to improve symptoms during an attack with sumatriptan being superior. Because of the vasoconstrictive side-effect of triptans, they may be contraindicated in people with ischemic heart disease.

Over-the-counter drugs, like acetaminophen, aspirin, or ibuprofen, can be effective but tend to only be helpful as a treatment for a few times in a week at most. Analgesic/sedative combinations are widely used (e.g., analgesic/antihistamine combinations like Syndol, Mersyndol and Percogesic, analgesic/barbiturate combinations such as Fiorinal). Frequent use of analgesics may, however, lead to medication overuse headache.

Botulinum toxin does not appear to be helpful.

People who have 15 or more headaches in a month may be treated with certain types of daily antidepressants which act to prevent continued tension headaches from occurring. In those who are predisposed to tension type headaches the first-line preventative treatment is amitriptyline, whereas mirtazapine and venlafaxine are second-line treatment options. Tricyclic antidepressants appear to be useful for prevention. Tricyclic antidepressants have been found to be more effective than SSRIs but have greater side effects. Evidence is poor for the use of SSRIs, propranolol, and muscle relaxants for prevention of tension headaches.

Oxygen therapy may help people with CH, but it does not help prevent future episodes. Typically it is given via a non-rebreather mask at 12–15 liters per minute for 15–20 minutes. One review found about 70% improve within 15 minutes. The evidence for effectiveness of 100% oxygen however is weak. Hyperbaric oxygen at pressures of ~2 times greater than atmospheric pressure may relieve cluster headache.

Tension-type headaches can usually be managed with NSAIDs (ibuprofen, naproxen), acetaminophen or aspirin. Triptans are not helpful in tension-type headaches unless the person also has migraines. For chronic tension type headaches, amitriptyline is the only medication proven to help. Amitriptyline is a medication which treats depression and also independently treats pain. It works by blocking the reuptake of serotonin and norepinephrine, and also reduces muscle tenderness by a separate mechanism. Studies evaluating acupuncture for tension-type headaches have been mixed. Overall, they show that acupuncture is probably not helpful for tension-type headaches.

Abortive therapy for cluster headaches includes subcutaneous sumatriptan (injected under the skin) and triptan nasal sprays. High flow oxygen therapy also helps with relief.

For people with extended periods of cluster headaches, preventive therapy can be necessary. Verapamil is recommended as first line treatment. Lithium can also be useful. For people with shorter bouts, a short course of prednisone (10 days) can be helpful. Ergotamine is useful if given 1–2 hours before an attack. See cluster headaches for more detailed information.

Treatment of atrophic rhinitis can be either medical or surgical.

Medical measures include:

- Nasal irrigation using normal saline

- Nasal irrigation and removal of crusts using alkaline nasal solutions prepared by dissolving a spoonful of powder containing one part sodium bicarbonate, one part sodium biborate and two part sodium chloride.

- 25% glucose in glycerine can be applied to the nasal mucosa to inhibit the growth of proteolytic organisms which produce foul smell.

- Local antibiotics, such as chloromycetine.

- Vitamin D (Kemicetine).

- Estradiol spray for regeneration of seromucinous glands and vascularization of mucosa.

- Systemic streptomycin (1g/day) against Klebsiella organisms.

- Oral potassium iodide for liquefaction of secretion.

- Placental extract injected in the submucosa.

Surgical interventions include:

- Young's operation.

- Modified Young's operation.

- Narrowing of nasal cavities, submucosal injection of Teflon paste, section and medial displacement of the lateral wall of the nose.

- Transposition of parotid duct to maxillary sinus or nasal mucosa.

The anti-bacterial nature of alcohol has long been associated with soothing stomach irritations and ailments like traveler's diarrhea where it was a preferred treatment to the less palatable bismuth treatments. The risk of infection from the bacterium "Helicobacter pylori", strongly associated with causing gastritis and peptic ulcers as well as being closely linked to stomach cancer, appears to lessen with moderate alcohol consumption. A German study conducted in the late 1990s showed that non-drinkers had slightly higher infection rates of "Helicobacter pylori" than moderate wine and beer drinkers.

Wine's positive effects on the metabolism of cholesterol has been suggested as a link to lower occurrences of gallstones among moderate drinkers since cholesterol is a major component of gallstones.

Acute alcohol poisoning is a medical emergency due to the risk of death from respiratory depression and/or inhalation of vomit if emesis occurs while the patient is unconscious and unresponsive. Emergency treatment for acute alcohol poisoning strives to stabilize the patient and maintain a patent airway and respiration, while waiting for the alcohol to metabolize. This can be done by removal of any vomitus or, if patient is unconscious or has impaired gag reflex, intubation of the trachea using an endotracheal tube to maintain adequate airway:

Also:

- Treat hypoglycaemia (low blood sugar) with 50 ml of 50% dextrose solution and saline flush, as ethanol induced hypoglycaemia is unresponsive to glucagon.

- Administer the vitamin thiamine to prevent Wernicke-Korsakoff syndrome, which can cause a seizure (more usually a treatment for chronic alcoholism, but in the acute context usually co-administered to ensure maximal benefit).

- Apply hemodialysis if the blood concentration is dangerously high (>400 mg/dL), and especially if there is metabolic acidosis.

- Provide oxygen therapy as needed via nasal cannula or non-rebreather mask.

- Provide parenteral Metadoxine.

Additional medication may be indicated for treatment of nausea, tremor, and anxiety.

Poisonous mushrooms contain a variety of different toxins that can differ markedly in toxicity. Symptoms of mushroom poisoning may vary from gastric upset to life-threatening organ failure resulting in death. Serious symptoms do not always occur immediately after eating, often not until the toxin attacks the kidney or liver, sometimes days or weeks later.

The most common consequence of mushroom poisoning is simply gastrointestinal upset. Most "poisonous" mushrooms contain gastrointestinal irritants that cause vomiting and diarrhea (sometimes requiring hospitalization), but usually no long-term damage. However, there are a number of recognized mushroom toxins with specific, and sometimes deadly, effects:

The period of time between ingestion and the onset of symptoms varies dramatically between toxins, some taking days to show symptoms identifiable as mushroom poisoning.

- Alpha-amanitin: For 6–12 hours, there are no symptoms. This is followed by a period of gastrointestinal upset (vomiting and profuse, watery diarrhea). This stage is caused primarily by the phallotoxins and typically lasts 24 hours. At the end of this second stage is when severe liver damage begins. The damage may continue for another 2–3 days. Kidney damage can also occur. Some patients will require a liver transplant. Amatoxins are found in some mushrooms in the genus "Amanita", but are also found in some species of "Galerina" and "Lepiota". Overall, mortality is between 10 and 15 percent. Recently, "Silybum marianum" or blessed milk thistle has been shown to protect the liver from amanita toxins and promote regrowth of damaged cells.

- Orellanine: This toxin causes no symptoms for 3–20 days after ingestion. Typically around day 11, the process of kidney failure begins, and is usually symptomatic by day 20. These symptoms can include pain in the area of the kidneys, thirst, vomiting, headache, and fatigue. A few species in the very large genus "Cortinarius" contain this toxin. People having eaten mushrooms containing orellanine may experience early symptoms as well, because the mushrooms often contain other toxins in addition to orellanine. A related toxin that causes similar symptoms but within 3–6 days has been isolated from "Amanita smithiana" and some other related toxic "Amanita"s.

- Muscarine: Muscarine stimulates the muscarinic receptors of the nerves and muscles. Symptoms include sweating, salivation, tears, blurred vision, palpitations, and, in high doses, respiratory failure. Muscarine is found in mushrooms of the genus "Omphalotus", notably the Jack o' Lantern mushrooms. It is also found in "A. muscaria", although it is now known that the main effect of this mushroom is caused by ibotenic acid. Muscarine can also be found in some "Inocybe" species and "Clitocybe" species, in particular "Clitocybe dealbata", and some red-pored "Boletes."

- Gyromitrin: Stomach acids convert gyromitrin to monomethylhydrazine (MMH), a compound employed in rocket fuel. It affects multiple body systems. It blocks the important neurotransmitter GABA, leading to stupor, delirium, muscle cramps, loss of coordination, tremors, and/or seizures. It causes severe gastrointestinal irritation, leading to vomiting and diarrhea. In some cases, liver failure has been reported. It can also cause red blood cells to break down, leading to jaundice, kidney failure, and signs of anemia. It is found in mushrooms of the genus "Gyromitra". A gyromitrin-like compound has also been identified in mushrooms of the genus "Verpa".

- Coprine: Coprine is metabolized to a chemical that resembles disulfiram. It inhibits aldehyde dehydrogenase (ALDH), which, in general, causes no harm, unless the person has alcohol in their bloodstream while ALDH is inhibited. This can happen if alcohol is ingested shortly before or up to a few days after eating the mushrooms. In that case the alcohol cannot be completely metabolized, and the person will experience flushed skin, vomiting, headache, dizziness, weakness, apprehension, confusion, palpitations, and sometimes trouble breathing. Coprine is found mainly in mushrooms of the genus "Coprinus", although similar effects have been noted after ingestion of "Clitocybe clavipes".

- Ibotenic acid: Decarboxylates into muscimol upon ingestion. The effects of muscimol vary, but nausea and vomiting are common. Confusion, euphoria, or sleepiness are possible. Loss of muscular coordination, sweating, and chills are likely. Some people experience visual distortions, a feeling of strength, or delusions. Symptoms normally appear after 30 minutes to 2 hours and last for several hours. "A. muscaria", the "Alice in Wonderland" mushroom, is known for the hallucinatory experiences caused by muscimol, but "A. pantherina" and "A. gemmata" also contain the same compound. While normally self-limiting, fatalities have been associated with "A. pantherina", and consumption of a large number of any of these mushrooms is likely to be dangerous.

- Psilocybin: Dephosphorylates into the psychoactive psilocin upon ingestion, which acts as a psychedelic drug. Symptoms begin shortly after ingestion. The effects can include euphoria, visual and religious hallucinations, and heightened perception. However, some persons experience fear, agitation, confusion, and schizophrenia-like symptoms. All symptoms generally pass after several hours. Some (though not all) members of the genus "Psilocybe" contain psilocybin, as do some "Panaeolus", "Copelandia", "Conocybe", "Gymnopilus", and others. Some of these mushrooms also contain baeocystin, which has effects similar to psilocin.

- Arabitol: A sugar alcohol, similar to mannitol, which causes no harm in most people but causes gastrointestinal irritation in some. It is found in small amounts in oyster mushrooms, and considerable amounts in "Suillus" species and "Hygrophoropsis aurantiaca" (the "false chanterelle").

Some mushrooms contain less toxic compounds and, therefore, are not severely poisonous. Poisonings by these mushrooms may respond well to treatment. However, certain types of mushrooms, such as the Amanitas, contain very potent toxins and are very poisonous; so even if symptoms are treated promptly mortality is high. With some toxins, death can occur in a week or a few days. Although a liver or kidney transplant may save some patients with complete organ failure, in many cases there are no organs available. Patients hospitalized and given aggressive support therapy almost immediately after ingestion of amanitin-containing mushrooms have a mortality rate of only 10%, whereas those admitted 60 or more hours after ingestion have a 50–90% mortality rate.

Alcohol-induced respiratory reactions, also termed alcohol-induced asthma and alcohol-induced respiratory symptoms, are increasingly recognized as a pathological bronchoconstriction response to the consumption of alcohol that afflicts many people with a "classical" form of asthma, the airway constriction disease evoked by the inhalation of allergens. Alcohol-induced respiratory reactions reflect the operation of different and often racially related mechanisms that differ from those of classical, allergen-induced asthma.