The risk of chemotherapy-induced nausea and vomiting varies based on the type of treatment received, as well as several outside factors. Some types of chemotherapy are more prone to causing nausea and vomiting than others. Some chemotheraputic agents may not cause nausea and vomiting on their own, but may when used in combination with other agents. Regimens that are linked to a high incidence (90% or higher) of nausea and vomiting are referred to as "highly emetogenic chemotherapy", and those causing a moderate incidence (30–90%) of nausea and vomiting are referred to as "moderately emetogenic chemotherapy".

Some highly emetogenic agents and chemotherapy regimens include:

- Cisplatin

- Dacarbazine

- Cyclophosphamide (>1500 mg/m)

- Carmustine (>250 mg/m)

- Mechlorethamine

- Streptozocin

- ABVD

- MOPP/COPP/BEACOPP

- CBV

- VIP

- BEP

- AC

Some moderately emetogenic agents and regimens include:

- Carboplatin

- Methotrexate

- Doxorubicin/Adriamycin

- Docetaxel

- Paclitaxel

- Etoposide

- Ifosfamide

- Cyclophosphamide (≤1500 mg/m)

- CHOP/CHOP-R

Besides the type of treatment, personal factors may put a patient at greater risk for CINV. Other risk factors include:

- Female sex

- Patient age (under 55 years old)

- History of light alcohol use

- History of previous CINV

- History of nausea and vomiting during pregnancy

- History of motion sickness

- Anxiety or depression

- Anticipation of CINV

There are several subtypes of CINV. The classifications of nausea and vomiting are:

- Acute: occurring within 24 hours of chemotherapy

- Delayed: occurring between 24 hours and 5 days after treatment

- Breakthrough: occurring despite prophylactic treatment

- Anticipatory: triggered by taste, odor, memories, visions, or anxiety related to chemotherapy

- Refractory: occurring during subsequent cycles when antiemetics have failed in earlier cycles

On average the incidence of nausea or vomiting after general anesthesia ranges between 25 and 30% [Cohen 1994]. Nausea and vomiting can be extremely distressing for patients and is therefore one of their major concerns [Macario 1999]. Vomiting has been associated with major complications such as pulmonary aspiration of gastric content and might endanger surgical outcomes after certain procedures, for example after maxillofacial surgery with wired jaws. Nausea and vomiting can delay discharge and about 1% of patients scheduled for day surgery require unanticipated overnight admission because of uncontrolled postoperative nausea and vomiting.

A 2008 study compared 121 Japanese patients who experienced PONV after being given the general anesthetic propofol to 790 people who were free of post-operative nausea after receiving it. Those with a G at both copies of rs1800497 were 1.6 times more likely to experience PONV within six hours of surgery compared to those with the AG or AA genotypes. But they were not significantly more likely to experience PONV more than six hours after surgery.

Postoperative nausea and vomiting results from patient factors, surgical factors, and anesthetic factors. It has been proven that there is a direct like between length of surgery and risk of postoperative nausea and vomiting (PONV). Due to the length of the procedure, abdominal and laparoscopic are at a higher risk for PONV. Procedures in ENT have an increased risk as well due to the involvement of the vestibulocochlear system. In addition to the length of the surgery the dose of the anesthetic also play a large role in the risk of PONV.

Patients that are female or who have a history of postoperative nausea and vomiting are at greater risk. Smokers have a decreased risk, but this would never be recommended by any physician. Older patients suffer less PONV.

Obesity, age less than 16 years, past history of motion sickness and high levels of pre-operative anxiety are also risk factors for PONV.

Fitzpatrick et al. (2007) identified 41 children with CVS. The mean age of the sample was 6 years at the onset of the syndrome, 8 years at first diagnosis, and 13 years at follow-up. As many as 39% of the children had resolution of symptoms immediately or within weeks of the diagnosis. Vomiting had resolved at the time of follow-up in 61% of the sample. Many children, including those in the remitted group, continued to have somatic symptoms such as headaches (in 42%) and abdominal pain (in 37%).

Most children who have this disorder miss on average 24 school days a year. The frequency of episodes is higher for some people during times of excitement. Charitable organizations to support sufferers and their families and to promote knowledge of CVS exist in several countries.

The average age at onset is 3–7 years, but CVS has been seen in infants who are as young as 6 days and in adults who are as old as 73 years. Typical delay in diagnosis from onset of symptoms is 2.7 – 3 years. Females show a slight predominance over males; the female-to-male ratio is 57:43.

How common the condition is, is not clear. A prospective study found that 3 in 100,000 five-year-olds are diagnosed with the condition. Two published studies on childhood CVS suggest nearly 2% of school-age children may have CVS. However, diagnosis is problematic and, as knowledge of CVS has increased in recent years, more and more cases are emerging.

The long-term and short-term effects of cannabis use are associated with behavioural effects leading to a wide variety of effects on the body systems and physiologic states.

Sontineni and colleagues in 2009 discussed the cannabinoid hyperemesis syndrome to offer guidelines for the clinical diagnosis.

Individual attacks can lead to complications, such as acute kidney injury.

Cannabinoid hyperemesis was first reported in the Adelaide Hills of South Australia in 2004.

Causes of decreased clearance of saliva include:

- Infections such as tonsillitis, retropharyngeal and peritonsillar abscesses, epiglottitis and mumps.

- Problems with the jaw, e.g., fracture or dislocation

- Radiation therapy

- Neurologic disorders such as myasthenia gravis, Parkinson's disease, multiple system atrophy, rabies, bulbar paralysis, bilateral facial nerve palsy, and hypoglossal nerve palsy

The effects of HG on the fetus are mainly due to electrolyte imbalances caused by HG in the mother. Infants of women with severe hyperemesis who gain less than 7 kg (15.4 lb) during pregnancy tend to be of lower birth weight, small for gestational age, and born before 37 weeks gestation. In contrast, infants of women with hyperemesis who have a pregnancy weight gain of more than 7 kg appear similar to infants from uncomplicated pregnancies. There is no significant difference in the neonatal death rate in infants born to mothers with HG compared to infants born to mothers who do not have HG. Children born to mothers with undertreated Hyperemesis have a fourfold increase in neurobehavioral diagnoses.

Several factors which do not in themselves cause alcohol hangover 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 hangover effects. Existing data shows that drinkers with genotypes known to lead to acetaldehyde accumulation are more susceptible to hangover effects. The fact that about 25% of heavy drinkers claim that they have never had a hangover is also an indication that genetic variation plays a role in individual differences of hangover severity.

- Age: some people experience hangovers 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 hangover symptoms and severity change with age, research shows that drinking patterns change across ages, and heavy drinking episodes that may result in hangover are much less often experienced as age increases.

- Sex: at the same number of drinks, women are more prone to hangover than men, and this is likely explained by sex differences in the pharmacokinetics of alcohol. Women attain a higher blood alcohol concentration (BAC) than men at the same number of drinks. At equivalent BACs, men and women appear to be indistinguishable with respect to most hangover effects.

- Cigarette smoking: acetaldehyde which is absorbed from cigarette smoking during alcohol consumption is regarded as a contributor to alcohol hangover symptoms.

Vomiting is a common condition affecting about 50% of pregnant women, with another 25% having nausea. However, the incidence of HG is only 0.3–1.5%. After preterm labor, hyperemesis gravidarum is the second most common reason for hospital admission during the first half of pregnancy. Factors such as infection with "Helicobacter pylori", a rise in thyroid hormone production, low age, low body mass index prior to pregnancy, multiple pregnancies, molar pregnancies, and a past history of hyperemesis gravidarum have been associated with the development of HG.

Transient gastroparesis may arise in acute illness of any kind, as a consequence of certain cancer treatments or other drugs which affect digestive action, or due to abnormal eating patterns.

It is frequently caused by autonomic neuropathy. This may occur in people with type 1 or type 2 diabetes. In fact, diabetes mellitus has been named as the most common cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. Gastroparesis has also been associated with connective tissue diseases such as scleroderma and Ehlers–Danlos syndrome, and neurological conditions such as Parkinson's disease. It may also occur as part of a mitochondrial disease. Opioids and anticholinergic medications can cause medication-induced gastroparesis.

Chronic gastroparesis can be caused by other types of damage to the vagus nerve, such as abdominal surgery. Heavy cigarette smoking is also a plausible cause since smoking causes damage to the stomach lining.

Idiopathic gastroparesis (gastroparesis with no known cause) accounts for a third of all chronic cases; it is thought that many of these cases are due to an autoimmune response triggered by an acute viral infection. Gastroenteritis, mononucleosis, and other ailments have been anecdotally linked to the onset of the condition, but no systematic study has proven a link.

Gastroparesis sufferers are disproportionately female. One possible explanation for this finding is that women have an inherently slower stomach emptying time than men. A hormonal link has been suggested, as gastroparesis symptoms tend to worsen the week before menstruation when progesterone levels are highest. Neither theory has been proven definitively.

Gastroparesis can also be connected to hypochlorhydria and be caused by chloride, sodium and/or zinc deficiency, as these minerals are needed for the stomach to produce adequate levels of gastric acid (HCl) in order to properly empty itself of a meal.

Hangovers occur commonly.

- A study in college students found that 25% had experienced a hangover in the previous week and 29% reported losing school time for hangover recovery.

- 15% of men and women who have consumed alcohol experience hangovers at least monthly and ten percent of British men reported hangover-related problems at work at least monthly.

- An estimated 9.23% (11.6 million workers) of the U.S. labor force work with a hangover.

- About 23% of drinkers do not report any hangover after drinking to intoxication.

Conditions that can cause saliva overproduction include:

- Rabies

- Pellagra (niacin or Vitamin B3 deficiency)

- Gastroesophageal reflux disease, in such cases specifically called a water brash, and is characterized by a sour fluid or almost tasteless saliva in the mouth

- Gastroparesis (main symptoms are nausea, vomiting, and reflux)

- Pregnancy

- Excessive starch intake

- Anxiety (common sign of separation anxiety in dogs)

- Pancreatitis

- Liver disease

- Serotonin syndrome

- Mouth ulcers

- Oral infections

Medications that can cause overproduction of saliva include:

- aripiprazole

- clozapine

- pilocarpine

- ketamine

- potassium chlorate

- risperidone

- rabeprazole sodium (Aciphex)

Toxins that can cause hypersalivation include:

- mercury

- copper

- organophosphates (insecticide)

- arsenic

Morning sickness may be an evolved trait that protects the baby against toxins ingested by the mother. Evidence in support of this theory includes:

- Morning sickness is very common among pregnant women, which argues in favor of its being a functional adaptation and against the idea that it is a pathology.

- Fetal vulnerability to toxins peaks at around 3 months, which is also the time of peak susceptibility to morning sickness.

- There is a good correlation between toxin concentrations in foods, and the tastes and odors that cause revulsion.

Women who have "no" morning sickness are more likely to miscarry. This may be because such women are more likely to ingest substances that are harmful to the fetus.

In addition to protecting the fetus, morning sickness may also protect the mother. A pregnant woman's immune system is suppressed during pregnancy, presumably to reduce the chances of rejecting tissues of her own offspring. Because of this, animal products containing parasites and harmful bacteria can be especially dangerous to pregnant women. There is evidence that morning sickness is often triggered by animal products including meat and fish.

If morning sickness is a defense mechanism against the ingestion of toxins, the prescribing of anti-nausea medication to pregnant women may have the undesired side effect of causing birth defects or miscarriages by encouraging harmful dietary choices.

There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. Heightened mast cell activation has been proposed to be a common factor among FGIDs, contributing to visceral hypersensitivity as well as epithelial, neuromuscular, and motility dysfunction.

The distinction between complications of hepatitis X and symptoms of hepatitis X is often obscure. While jaundice (yellow discoloration of the skin or whites of the eyes due to an increase of bile pigments in the blood), is a symptom of hepatitis, it is also a complication. Further complications that may arise include hyperpigmentation, renal (kidney) failure, and CSF xanthochromia. Liver disease is another fatal complication of hepatitis X. This could potentially lead to abdominal pain, hepatomegaly, splenomegaly, chest pain, and an altered bowel habit.

There has been no specific drug therapy developed for hepatitis, with the exception of hepatitis C. Patients are advised to rest in the early stages of the illness, and to eat small, high-calorie, high-protein meals in order to battle anorexia. Larger meals are more easily tolerated in the morning, for patients often experience nausea later in the day. Although high-protein meals are recommended, protein intake should be reduced if signs of precoma — lethargy, confusion, and mental changes — develop.

In acute viral hepatitis, hospitalization is usually required only for patients with severe symptoms (severe nausea, vomiting, change in mental status, and PT greater than 3 seconds above normal) or complications. If the patient experiences continuous vomiting and is unable to maintain oral intake, parenteral nutrition may be required.

In order to relieve nausea and also prevent vomiting, antiemetics (diphenhydramine or prochlorperazine) may be given 30 minutes before meals. However, phenothiazines have a cholestatic effect and should be avoided. The resin cholestyramine may be given only for severe pruritus.

Primary complications of gastroparesis include:

- Fluctuations in blood glucose due to unpredictable digestion times (in diabetic patients)

- General malnutrition due to the symptoms of the disease (which frequently include vomiting and reduced appetite) as well as the dietary changes necessary to manage it

- Severe fatigue and weight loss due to calorie deficit

- Intestinal obstruction due to the formation of bezoars (solid masses of undigested food)

- Bacterial infection due to overgrowth in undigested food

An increasing number of people are now surviving cancer, with improved treatments producing cure of the malignancy (cancer survivors). There are now over 14 million such people in the US, and this figure is expected to increase to 18 million by 2022. More than half are survivors of abdominal or pelvic cancers, with about 300,000 people receiving abdominal and pelvic radiation each year. It has been estimated there are 1.6 million people in the US with post-radiation intestinal dysfunction, a greater number than those with inflammatory bowel disease such as Crohn's disease or ulcerative colitis.

There is a lack of good evidence to support the use of any particular intervention for morning sickness.

Symptoms of mild cinchonism (which may occur from standard therapeutic doses of quinine) include flushed and sweaty skin, ringing of the ears (tinnitus), blurred vision, impaired hearing, confusion, reversible high-frequency hearing loss, headache, abdominal pain, rashes, drug-induced lichenoid reaction (lichenoid photosensitivity), vertigo, dizziness, dysphoria, nausea, vomiting and diarrhea.

Large doses of quinine may lead to severe (but reversible) symptoms of cinchonism: skin rashes, deafness, somnolence, diminished visual acuity or blindness, anaphylactic shock, and disturbances in heart rhythm or conduction, and death from cardiotoxicity (damage to the heart). Quinine may also trigger a rare form of hypersensitivity reaction in malaria patients, termed blackwater fever, that results in massive hemolysis, hemoglobinemia, hemoglobinuria, and kidney failure. Most symptoms of cinchonism (except in severe cases) are reversible and disappear once quinine is withdrawn. Attempted suicide by intake of a large dose of quinine has caused irreversible tunnel vision and very severe visual impairment.

Patients treated with quinine may also suffer from low blood sugar, especially if it is administered intravenously, and hypotension (low blood pressure).

Quinine, like chloroquine, inactivates enzymes in the lysosomes of cells and has an anti-inflammatory effect, hence its use in the treatment of rheumatoid arthritis. However, inactivation of these enzymes can also cause abnormal accumulation of glycogen and phospholipids in lysosomes, causing toxic myopathy. It is possible this action is the root cause of cinchonism.

Alimentary toxic aleukia, or Aleukia, is a mycotoxin-induced condition characterized by nausea, vomiting, diarrhea, leukopenia (aleukia), hemorrhaging, skin inflammation, and sometimes death. Alimentary Toxic Alekia almost always refers to the human condition associated with presence of T2 Toxin.

Functional gastrointestinal disorders (FGID) include a number of separate idiopathic disorders which affect different parts of the gastrointestinal tract and involve visceral hypersensitivity and impaired gastrointestinal motility.