All ethnic groups and income levels are susceptible to the illness. The CDC states that CFS is "at least as common" in African Americans and Hispanics as Caucasians. A 2009 meta-analysis, however, showed that compared with the White American majority, African Americans and Native Americans have a higher risk of CFS, though it acknowledged that studies and data were limited. More women than men get CFS — between 60 and 85% of cases are women; however, there is some indication that the prevalence among men is underreported. The illness is reported to occur more frequently in persons between the ages of 40 and 59. CFS is less prevalent among children and adolescents than among adults.

Blood relatives of those who have CFS appear to be more predisposed. There is no direct evidence that CFS is contagious.

Psychological stress, childhood trauma, perfectionist personalities, old age, lower middle education, low physical fitness, preexisting psychological illness, and allergies may be risk factors for developing chronic fatigue syndrome. This has led some to believe that stress-related visceral responses underlie CFS. Pre-existing depressive and anxiety disorders, as well as high expectation of parents and family history were predisposing factors identified in another review.

People with CFS and their relatives tend to attribute their illness to physical causes (such as a virus or pollution) rather than to psychological causes. Such attributions are associated with increased symptoms and impairment, and worse outcomes over time.

A systematic review described improvement and occupational outcomes of people with CFS found that "the median full recovery rate was 5% (range 0–31%) and the median proportion of patients who improved during follow-up was 39.5% (range 8–63%). Return to work at follow-up ranged from 8 to 30% in the three studies that considered this outcome." ... "In five studies, a worsening of symptoms during the period of follow-up was reported in between 5 and 20% of patients." A good outcome was associated with less fatigue severity at baseline. Other factors were occasionally, but not consistently, related to outcome, including age at onset (5 of 16 studies), and attributing illness to a psychological cause and/or having a sense of control over symptoms (4 of 16 studies). Another review found that children have a better prognosis than adults, with 54–94% having recovered by follow-up compared to less than 10% of adults returning to pre-illness levels of functioning.

A functional disorder is a medical condition that impairs the normal function of a bodily process, but where every part of the body looks completely normal under examination, dissection or even under a microscope. This stands in contrast to a structural disorder (in which some part of the body can be seen to be abnormal) or a psychosomatic disorder (in which symptoms are caused by psychological or psychiatric illness). Definitions vary somewhat between fields of medicine.

Generally, the mechanism that causes a functional disorder is unknown, poorly understood, or occasionally unimportant for treatment purposes. The brain or nerves are often believed to be involved. It is common that a person with one functional disorder will have others.

Whether a given medical condition is termed a "functional disorder" depends in part on the state of knowledge. Some diseases, including epilepsy, schizophrenia, and migraine headaches were once considered functional disorders, but are no longer generally classified that way.

The ambient temperature appears to play a role as cold is frequently reported as causing symptom aggravation and heat is often reported to be ameliorating. It appears that cold is one of the factors that can trigger a process resulting in CP/CPPS. Cold also causes aggravation of symptoms and can initiate a relapse. A survey showed that the occurrence of prostatitis symptoms in men living in northern Finland —a cold climate—is higher than that reported in other parts of the world. This could be partly caused by the cold climate.

The annual prevalence in the general population of chronic pelvic pain syndrome is 0.5%. 38% of primary care providers, when presented with a vignette of a man with CPPS, indicate that they have never seen such a patient. However, the overall prevalence of symptoms suggestive of CP/CPPS is 6.3%. The role of the prostate was questioned in the cause of CP/CPPS when both men and women in the general population were tested using the (1) National Institutes of Health Chronic Prostatitis Symptom Index (NIH-CPSI) —with the female homolog of each male anatomical term use on questionnaires for female participants— (2) the International Prostate Symptom Score (IPSS), and (3) additional questions on pelvic pain. The prevalence of symptoms suggestive of CPPS in this selected population was 5.7% in women and 2.7% in men, placing in doubt the role of the prostate gland. New evidence suggests that the prevalence of CP/CPPS is much higher in teenage males than once suspected.

Symptoms of OI are triggered by the following:

- An upright posture for long periods of time (e.g. standing in line, standing in a shower, or even sitting at a desk).

- A warm environment (such as in hot summer weather, a hot crowded room, a hot shower or bath, after exercise).

- Emotionally stressful events (seeing blood or gory scenes, being scared or anxious).

- Astronauts returning from space not yet re-adapted to gravity.

- Extended bedrest

- Inadequate fluid and salt intake.

Treatment is similar to treatment for benign fasciculation syndrome.

Carbamazepine therapy has been found to provide moderate reductions in symptoms.

Cramp fasciculation syndrome (CFS) is a rare peripheral nerve hyperexcitability disorder. It is more severe than the related (and common) disorder known as benign fasciculation syndrome; it causes fasciculations, cramps, pain, fatigue, and muscle stiffness similar to those seen in neuromyotonia (another related condition). Patients with CFS, like those with neuromyotonia, may also experience paresthesias.

Most cases of cramp fasciculation syndrome are idiopathic.

Cramp fasciculation syndrome is diagnosed by clinical examination and electromyography (EMG). Fasciculation is the only abnormality (if any) seen with EMG.

Cramp fasciculation syndrome is a chronic condition. Treatment options include anti-seizure medications such as carbamazepine, immunosuppressive drugs and plasmapheresis.

Orthostatic intolerance is divided, roughly based on patient history, in two variants: acute and chronic.

The prevalence of POTS is unknown. One study estimated a minimal rate of 170 POTS cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. Another study estimated that there were between 500,000 and 3,000,000 cases in the United States. POTS is more common in women, with a female-to-male ratio of 5:1. Most people with POTS are aged between 20 and 40, with an average onset of 30. Diagnoses of POTS beyond age 40 are rare, perhaps because symptoms improve with age.

POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. About 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens during a period of rapid growth will most likely see complete symptom resolution in two to five years. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.

A Low FODMAP diet now has an evidence base sufficiently strong to recommend its widespread application in conditions such as IBS and IBD. Restriction of Fermentable Oligo-, Di- and Mono-

saccharides and Polyols globally, rather than individually, controls the symptoms of functional gut disorders (e.g. IBS), and the majority of IBD patients respond just as well. It is more successful than restricting only Fructose and Fructans, which are also FODMAPs, as is recommended for those with Fructose malabsorption. Longer term compliance with the diet was high.

A randomised controlled trial on IBS patients found relaxing an IgG-mediated food intolerance diet led to a 24% greater deterioration in symptoms compared to those on the elimination diet and concluded food elimination based on IgG antibodies may be effective in reducing IBS symptoms and is worthy of further biomedical research.

Intestinal or bowel hyperpermeability, so called leaky gut, has been linked to food allergies and some food intolerances. Research is currently focussing on specific conditions and effects of certain food constituents. At present there are a number of ways to limit the increased permeability, but additional studies are required to assess if this approach reduces the prevalence and severity of specific conditions.

The prognosis of children diagnosed with intolerance to milk is good: patients respond to diet which excludes cow's milk protein and the majority of patients succeed in forming tolerance. Children with non-IgE-mediated cows milk intolerance have a good prognosis, whereas children with IgE-mediated cows milk allergy in early childhood have a significantly increased risk for persistent allergy, development of other food allergies, asthma and rhinoconjunctivitis.

A study has demonstrated that identifying and appropriately addressing food sensitivity in IBS patients not previously responding to standard therapy results in a sustained clinical improvement and increased overall well being and quality of life.

The cause of AHC is unknown. It was initially thought to be a form of complicated migraine because of strong family histories of migraine reported in AHC cases. AHC has also been considered to be a movement disorder or a form of epilepsy. Suggested causes have included channelopathy, mitochondrial dysfunction, and cerebrovascular dysfunction. The disorder most closely related to AHC is familial hemiplegic migraine, and this was recently discovered to be caused by a mutation in a gene for calcium channel receptors. It is suspected that AHC may be caused by a similar channelopathy, and this is a current area of investigation into the cause of AHC. An association with "ATP1A2" mutation has been found in some patients, but other studies have found no mutations and thus a lack of evidence that mutations which cause AHC are in the same genes as mutations which cause familial hemiplegic migraine.

Because alternating hemiplegia of childhood is so rare, there is no increased risk of AHC for the children of siblings of someone with AHC, but it is believed to be autosomal dominant, by which a person with AHC has a 50% change of passing the disorder on to their children. AHC is questionably a progressive disease, because cognitive abilities do appear to decline over time. This cannot be completely determined however, because the mechanism of AHC's progression is unknown. It is likely that it is caused by a generalized cellular dysfunction caused by a mitochondrial disorder. However, studies involving mechanisms of AHC have been inconclusive. Experts currently researching this disorder believe that the cause of AHC is a mutated ion channel. This would make the cause difficult to find because one disrupted channel may be represented differently in different tissues. This mutation is suspected because the most closely related disease, FHM, is also caused by a mutated ion channel. A small number of genes which were suspected to carry a mutation for AHC have been screened for sodium channel protein mutations, ATP pump mutations, and excitatory amino acid transmitter mutations. None of these have yet been successful in determining the underlying cause of AHC.

One large study has identified the gene ATP1A3 as the likely genetic cause of this disorder. This gene is located on the long arm of chromosome 19 (19q13.31).

Hemiplegic attacks can be brought on by particular triggers, and management of AHC often centers around avoiding common or known triggers. While triggers vary greatly from person to person, there are also some common ones which are prevalent in many patients. Common triggers include temperature changes, water exposure, bright lights, certain foods, emotional stress, and physical activity. While avoiding triggers may help, it cannot prevent all hemiplegic episodes because many occur without being triggered. Because attacks and other associated symptoms end with sleep, various sedatives can be used to help patients sleep.

There is no specific treatment for infectious mononucleosis, other than treating the symptoms. In severe cases, steroids such as corticosteroids may be used to control the swelling of the throat and tonsils. Currently, there are no antiviral drugs or vaccines available.

It is important to note that symptoms related to infectious mononucleosis caused by EBV infection seldom last for more than 4 months. When such an illness lasts more than 6 months, it is frequently called chronic EBV infection. However, valid laboratory evidence for continued active EBV infection is seldom found in these patients. The illness should be investigated further to determine if it meets the criteria for chronic fatigue syndrome, or CFS. This process includes ruling out other causes of chronic illness or fatigue.

Symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person's life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. Reactivated and post-latent virus may pass the placental barrier in (also seropositive) pregnant women via macrophages and therefore can infect the fetus. Also re-infection of prior seropositive individuals may occur. In contrast, reactivation in adults usually occurs without symptoms of illness.

EBV also establishes a lifelong dormant infection in some cells of the body's immune system. A late event in a very few carriers of this virus is the emergence of Burkitt's lymphoma and nasopharyngeal carcinoma, two rare cancers. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease.

Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent.

The clinical diagnosis of infectious mononucleosis is suggested on the basis of the symptoms of fever, sore throat, swollen lymph glands, and the age of the patient. Usually, laboratory tests are needed for confirmation. Serologic results for persons with infectious mononucleosis include an elevated white blood cell count, an increased percentage of certain atypical white blood cells, and a positive reaction to a "mono spot" test.

Fragile sites are associated with numerous disorders and diseases, both heritable and not. The FRAXA site is perhaps most famous for its role in Fragile X syndrome, but fragile sites are clinically implicated in many other important diseases, such as cancer.

These are much more common in premature babies, particularly those under 1500 g at birth. Premature birth can be associated with problems that result in sensorineural hearing loss such as anoxia or hypoxia(poor oxygen levels), jaundice, intracranial haemorrhages, meningitis. Fetal alcohol syndrome is reported to cause hearing loss in up to 64% of infants born to alcoholic mothers, from the ototoxic effect on the developing fetus, plus malnutrition during pregnancy from the excess alcohol intake.

There can be damage either to the ear itself or to the central auditory pathways that process the information conveyed by the ears. People who sustain head injury are susceptible to hearing loss or tinnitus, either temporary or permanent. Contact sports like football (U.S. NFL), hockey and cricket have a notable incidence of head injuries (concussions). In one survey of retired NFL players, all of whom reported one or more concussions during their playing careers, 25% had hearing loss and 50% had tinnitus.

A chromosomal fragile site is a specific heritable point on a chromosome that tends to form a gap or constriction and may tend to break when the cell is exposed to partial replication stress. Based on their frequency, fragile sites are classified as "common" or "rare". To date, more than 120 fragile sites have been identified in the human genome.

Common fragile sites are considered part of normal chromosome structure and are present in all (or nearly all) individuals in a population. Under normal conditions, most common fragile sites are not prone to spontaneous breaks. Common fragile sites are of interest in cancer studies because they are frequently affected in cancer and they can be found in healthy individuals. Sites FRA3B (harboring the "FHIT" gene) and FRA16D (harboring the "WWOX" gene) are two well known examples and have been a major focus of research.

Rare fragile sites are found in less than 5% of the population, and are often composed of two- or three-nucleotide repeats. They are often susceptible to spontaneous breakage during replication, frequently affecting neighboring genes. Clinically, the most important rare fragile site is FRAXA, which is associated with the fragile X syndrome, the most common cause of hereditary mental retardation.