Early reports indicated that the disorder was affected by climate and growing conditions. Dry weather before harvest seemed to increase the condition. Light crops, heavy use of fertilizers, large fruit and early harvesting increased the condition. Fruit that were free of bitter pit at harvest were often severely affected after a short period of storage. Bitter pit has been widely reviewed over many decades.

The disorder became a major problem for exports from the Southern Hemisphere to Europe. The breakthrough in control came with the discovery in North America that the mineral calcium was low in affected fruit. This was confirmed elsewhere.

The affected fruit have dark spots, about ½ cm diameter, which occur on the skin and/or in the flesh The cells in the spots are dead (necrotic), and turn brown-black.

Calcium deficiency can sometimes be rectified by adding agricultural lime to acid soils, aiming at a pH of 6.5, unless the subject plants specifically prefer acidic soil. Organic matter should be added to the soil to improve its moisture-retaining capacity. However, because of the nature of the disorder (i.e. poor transport of calcium to low transpiring tissues), the problem cannot generally be cured by the addition of calcium to the roots. In some species, the problem can be reduced by prophylactic spraying with calcium chloride of tissues at risk.

Plant damage is difficult to reverse, so corrective action should be taken immediately, supplemental applications of calcium nitrate at 200 ppm nitrogen, for example. Soil pH should be tested, and corrected if needed, because calcium deficiency is often associated with low pH.

Early fruit will generally have the worst systems, with them typically lessening as the season progresses. Preventative measures, such as irrigating prior to especially high temperatures and stable irrigation will minimize the occurrence.

Calcium deficiency symptoms appear initially as localized tissue necrosis leading to stunted plant growth, necrotic leaf margins on young leaves or curling of the leaves, and eventual death of terminal buds and root tips. Generally, the new growth and rapidly growing tissues of the plant are affected first. The mature leaves are rarely if ever affected because calcium accumulates to high concentrations in older leaves.

Crop-specific symptoms include:

- Apple : 'Bitter pit' – fruit skins develop pits, brown spots appear on skin and/or in flesh and taste of those areas is bitter. This usually occurs when fruit is in storage, and Bramley apples are particularly susceptible. Related to boron deficiency, "water cored" apples seldom display bitter pit effects.

- Cabbage and Brussels sprouts : Internal browning and "tip burn"

- Carrot : 'Cavity spot' – oval spots develop into craters which may be invaded by other disease-causing organisms.

- Celery : Stunted growth, central leaves stunted.

- Tomatoes and peppers: 'Blossom end rot' – Symptoms start as sunken, dry decaying areas at the blossom end of the fruit, furthest away from the stem, not all fruit on a truss is necessarily affected. Sometimes rapid growth from high-nitrogen fertilizers may exacerbate blossom end rot. Water management and preventing water stress is key to minimizing its occurrence.

Little is currently known on brain dysfunction in feather-plucking. However, it may be hypothesized that abnormal brain function is involved, especially in those cases that appear sensitive to treatment with behavioural intervention and/or environmental changes. Psychotropic therapy for birds has been suggested as treatment for feather-plucking although responses seem variable.

Veterinary treatment or an improved and more stimulating environment may help birds suffering from feather-plucking. Organic bitter sprays are sold in pet stores to discourage plucking, especially of newly grown feathers, although this may make general beak-based grooming difficult for the animal. This is not recommended since it does not address the real reason why the bird is picking feathers.

There are numerous steps one has to take to try to manage the disease as best as possible. The aim is at prevention because once the pathogen reaches the cherry trees, disease will surely ensue and there is no cure or remedy to prevent the loss of fruit production as well as the ultimate death of the tree.

Xerostomia, also known as dry mouth syndrome, can precipitate dysgeusia because normal salivary flow and concentration are necessary for taste. Injury to the glossopharyngeal nerve can result in dysgeusia. In addition, damage done to the pons, thalamus, and midbrain, all of which compose the gustatory pathway, can be potential factors. In a case study, 22% of patients who were experiencing a bladder obstruction were also suffering from dysgeusia. Dysgeusia was eliminated in 100% of these patients once the obstruction was removed. Although it is uncertain what the relationship between bladder relief and dysgeusia entails, it has been observed that the areas responsible for urinary system and taste in the pons and cerebral cortex in the brain are close in proximity.

Many of the causes for dysgeusia occur due to unknown reasons. A wide range of miscellaneous factors may contribute to this taste disorder, such as gastric reflux, lead poisoning, and diabetes mellitus. A minority of pine nuts can apparently cause taste disturbances, for reasons which are not entirely proven. Certain pesticides can have damaging effects on the taste buds and nerves in the mouth. These pesticides include organochloride compounds and carbamate pesticides. Damage to the peripheral nerves, along with injury to the chorda tympani branch of the facial nerve, also cause dysgeusia. A surgical risk for laryngoscopy and tonsillectomy include dysgeusia. Patients who suffer from the burning mouth syndrome, most likely menopausal women, are often suffering from dysgeusia as well.

Some herbaceous hosts naturally have the Cherry X Disease. Once the spreads to the cherry hosts, with the help of the mountain leafhoppers, the cherry leafhoppers can spread the disease around to other woody hosts. Here are some approaches at management with each host type:

Some fruit juices and fruits can interact with numerous drugs, in many cases causing adverse effects. The effect was first discovered by accident, when a test of drug interactions with alcohol used grapefruit juice to hide the taste of the ethanol.

It is still best-studied with grapefruit and grapefruit juice, but similar effects have more recently been seen with some (not all) other citrus fruits. One medical review advises patients to avoid all citrus juices until further research clarifies the risks. The interacting chemicals are found in many plants, and so many other foods may be affected; effects have been observed with apple juice, but their clinical significance is not yet known.

Normal amounts of food and drink, such as one whole grapefruit or a small glass () of grapefruit juice, can cause drug overdose toxicity. Fruit consumed three days before the medicine can still have an effect. The relative risks of different types of citrus fruit have not been systematically studied. Affected drugs typically have an auxiliary label saying “Do not take with grapefruit” on the container, and the interaction is elaborated on in the package insert. People are also advised to ask their physician or pharmacist about drug interactions.

The effects are caused by furanocoumarins (and, to a lesser extent, flavonoids). These chemicals inhibit key drug metabolizing enzymes, such as cytochrome P450 3A4 (CYP3A4). CYP3A4 is a metabolizing enzyme for almost 50% of drugs, and is found in the liver and small intestinal epithelial cells. As a result, many drugs are affected. Inhibition of enzymes can have two different effects, depending on whether the drug is either

1. metabolized by the enzyme to an inactive metabolite, "or"

2. activated by the enzyme to an active metabolite.

If the active drug is metabolized by the inhibited enzyme, then the fruit will stop the drug being metabolized, leaving elevated concentrations of the medication in the body, which can cause adverse effects. Conversely, if the medication is a prodrug, it needs to be metabolised to be converted to the active drug. Compromising its metabolism lowers concentrations of the active drug, reducing its therapeutic effect, and risking therapeutic failure.

Low drug concentrations can also be caused when the fruit suppresses drug absorption from the intestine.

While it is rare before the age of 3, about 30 percent of children between 7 and 10 years of age and 45 percent of teenagers engage in nail biting. Finally, prevalence decreases in adults. Figures may vary between studies, and could be related to geographic and cultural differences. The proportion of subjects that have ever had the habit (lifetime prevalence) may be much higher than the proportion of current nail-biters (time-point prevalence). Although it does not seem to be more common in either sex, results of epidemiological studies on this issue are not fully consistent. It may be underrecognized since individuals tend to deny or be ignorant of its negative consequences, complicating its diagnosis. Having a parent with a mental disorder is also a risk factor.

The effect of grapefruit juice with regard to drug absorption was originally discovered in 1989. The first published report on grapefruit drug interactions was in 1991 in the Lancet entitled "Interactions of Citrus Juices with Felodipine and Nifedipine," and was the first reported food-drug interaction clinically. However, the effect only became well-publicized after being responsible for a number of bad interactions with medication.

There are also a wide variety of drugs that can trigger dysgeusia, including zopiclone, H-antihistamines, such as azelastine and emedastine. Approximately 250 drugs affect taste. The sodium channels linked to taste receptors can be inhibited by amiloride, and the creation of new taste buds and saliva can be impeded by antiproliferative drugs. Saliva can have traces of the drug, giving rise to a metallic flavor in the mouth; examples include lithium carbonate and tetracyclines. Drugs containing sulfhydryl groups, including penicillamine and captopril, may react with zinc and cause deficiency. Metronidazole and chlorhexidine have been found to interact with metal ions that associate with the cell membrane. Drugs that prevent the production of angiotensin II by inhibiting angiotensin converting enzyme, eprosartan for example, have been linked to dysgeusia. There are few case reports claiming calcium channel blockers like Amlodipine also cause dysguesia by blocking calcium sensitive taste buds.

Reduced salivary flow rate is associated with increased caries since the buffering capability of saliva is not present to counterbalance the acidic environment created by certain foods. As a result, medical conditions that reduce the amount of saliva produced by salivary glands, in particular the submandibular gland and parotid gland, are likely to lead to dry mouth and thus to widespread tooth decay. Examples include Sjögren's syndrome, diabetes mellitus, diabetes insipidus, and sarcoidosis. Medications, such as antihistamines and antidepressants, can also impair salivary flow. Stimulants, most notoriously methylamphetamine, also occlude the flow of saliva to an extreme degree. This is known as meth mouth. Tetrahydrocannabinol (THC), the active chemical substance in cannabis, also causes a nearly complete occlusion of salivation, known in colloquial terms as "cotton mouth". Moreover, 63% of the most commonly prescribed medications in the United States list dry mouth as a known side-effect. Radiation therapy of the head and neck may also damage the cells in salivary glands, somewhat increasing the likelihood of caries formation.

Susceptibility to caries can be related to altered metabolism in the tooth, in particular to fluid flow in the dentin. Experiments on rats have shown that a high-sucrose, cariogenic diet "significantly suppresses the rate of fluid motion" in dentin.

The use of tobacco may also increase the risk for caries formation. Some brands of smokeless tobacco contain high sugar content, increasing susceptibility to caries. Tobacco use is a significant risk factor for periodontal disease, which can cause the gingiva to recede. As the gingiva loses attachment to the teeth due to gingival recession, the root surface becomes more visible in the mouth. If this occurs, root caries is a concern since the cementum covering the roots of teeth is more easily demineralized by acids than enamel. Currently, there is not enough evidence to support a causal relationship between smoking and coronal caries, but evidence does suggest a relationship between smoking and root-surface caries.

Exposure of children to secondhand tobacco smoke is associated with tooth decay.

Intrauterine and neonatal lead exposure promote tooth decay. Besides lead, all atoms with electrical charge and ionic radius similar to bivalent calcium,

such as cadmium, mimic the calcium ion and therefore exposure to them may promote tooth decay.

Poverty is also a significant social determinant for oral health. Dental caries have been linked with lower socio-economic status and can be considered a disease of poverty.

Forms are available for risk assessment for caries when treating dental cases; this system using the evidence-based Caries Management by Risk Assessment (CAMBRA). It is still unknown if the identification of high-risk individuals can lead to more effective long-term patient management that prevents caries initiation and arrests or reverses the progression of lesions.

Saliva also contains iodine and EGF. EGF results effective in cellular proliferation, differentiation and survival. Salivary EGF, which seems also regulated by dietary inorganic iodine, plays an important physiological role in the maintenance of oral (and gastro-oesophageal) tissue integrity, and, on the other hand, iodine is effective in prevention of dental caries and oral health.

There are certain diseases and disorders affecting teeth that may leave an individual at a greater risk for cavities.

Molar incisor hypomineralization, which seems to be increasingly common. While the cause is unknown it is thought to be a combination of genetic and environmental factors. Possible contributing factors that have been investigated include systemic factors such as high levels of dioxins or polychlorinated biphenyl (PCB) in the mother’s milk, premature birth and oxygen deprivation at birth, and certain disorders during the child’s first 3 years such as such as mumps, diphtheria, scarlet fever, measles, hypoparathyroidism, malnutrition, malabsorption, hypovitaminosis D, chronic respiratory diseases, or undiagnosed and untreated coeliac disease, which usually presents with mild or absent gastrointestinal symptoms.

Amelogenesis imperfecta, which occurs in between 1 in 718 and 1 in 14,000 individuals, is a disease in which the enamel does not fully form or forms in insufficient amounts and can fall off a tooth. In both cases, teeth may be left more vulnerable to decay because the enamel is not able to protect the tooth.

In most people, disorders or diseases affecting teeth are not the primary cause of dental caries. Approximately 96% of tooth enamel is composed of minerals. These minerals, especially hydroxyapatite, will become soluble when exposed to acidic environments. Enamel begins to demineralize at a pH of 5.5. Dentin and cementum are more susceptible to caries than enamel because they have lower mineral content. Thus, when root surfaces of teeth are exposed from gingival recession or periodontal disease, caries can develop more readily. Even in a healthy oral environment, however, the tooth is susceptible to dental caries.

The evidence for linking malocclusion and/or crowding to dental caries is weak; however, the anatomy of teeth may affect the likelihood of caries formation. Where the deep developmental grooves of teeth are more numerous and exaggerated, pit and fissure caries is more likely to develop (see next section). Also, caries is more likely to develop when food is trapped between teeth.

Konzo has been reported in outbreaks mainly among women and children in remote rural populations in DR Congo, Mozambique (where it is known as mantakassa), Tanzania, Central African Republic, Cameroon and Angola.

The first reported outbreak occurred in Bandundu Province in present-day DR Congo in 1936-1937 and the second in Nampula Province of Northern Mozambique in 1981. Each of these outbreaks numbered more than 1000 cases. Familial clustering is common. Outbreaks typically occur in the dry season in households living in absolute poverty that have sustained themselves for weeks or months on insufficiently processed bitter cassava. Both smaller outbreaks and sporadic cases have been reported from all the countries above.

Konzo can be prevented by use of the “wetting method,” which is used to remove residual cyanogens from cassava flour, as an additional processing method. Cassava flour is placed in a bowl and the level marked on the inside of the bowl. Water is added with mixing until the height of the wet flour comes up to the mark. The wet flour is placed in a thin layer on a mat for 2 hours in the sun or 5 hours in the shade to allow the escape of hydrogen cyanide produced by the breakdown of linamarin by the enzyme linamarase. The damp flour is then cooked in boiling water in the traditional way to produce a thick porridge called “fufu” or “ugali”, which is flavoured by some means such as a sauce. The wetting method is accepted by rural women because it requires little extra work or equipment and produces fufu which is not bitter, because the bitter tasting linamarin has gone.

In 2010 the wetting method was taught to the women in Kay Kalenge village, Popokabaka Health Zone, Bandundu Province, DRC, where there were 34 konzo cases. The women used the method and during the intervention there were no new konzo cases and the urinary thiocyanate content of the school children fell to safe levels. Konzo had been prevented for the first time ever in the same health zone in which it had first been discovered by Dr Trolli in 1938. Fourteen months after the intervention ceased the village was visited again. It was found that there were no new cases of konzo, the school children had low urinary thiocyanate levels, the wetting method was still being used and it had spread by word of mouth to three nearby villages. It is important to teach the women that konzo is due to a poison present in their food, to get them to regularly use the wetting method and posters are available in 13 different languages as a teaching aid as an additional method to remove residual cyanogens.

The wetting method has now been used in 13 villages in DRC with nearly 10000 people. The time of the intervention has been reduced from 18 months in the first intervention, to 12 months in the second intervention, to 9 months in the third and fourth interventions. This has reduced the cost per person of the intervention to prevent konzo by removing cyanogens from cassava flour, to $16 per person. This targeted method to reduce cyanide intake is much cheaper and more effective in preventing konzo than broad based interventions.

It can be caused by any of the following:

- Nutritional factors.

- Some diseases (such as undiagnosed and untreated celiac disease, chicken pox, congenital syphilis).

- Hypocalcemia.

- Fluoride ingestion (dental fluorosis).

- Birth injury.

- Preterm birth.

- Infection.

- Trauma from a deciduous tooth.

Estimates vary from 1.2 to 5.5 million snakebites, 421,000 to 2.5 million envenomings, and 20,000 to 125,000 deaths. Since reporting is not mandatory in much of the world, the data on the frequency of snakebites is not precise. Many people who survive bites have permanent tissue damage caused by venom, leading to disability. Most snake envenomings and fatalities occur in South Asia, Southeast Asia, and sub-Saharan Africa, with India reporting the most snakebite deaths of any country.

Most snakebites are caused by non-venomous snakes. Of the roughly 3,000 known species of snake found worldwide, only 15% are considered dangerous to humans. Snakes are found on every continent except Antarctica. The most diverse and widely distributed snake family, the colubrids, has approximately 700 venomous species, but only five genera—boomslangs, twig snakes, keelback snakes, green snakes, and slender snakes—have caused human fatalities.

Worldwide, snakebites occur most frequently in the summer season when snakes are active and humans are outdoors. Agricultural and tropical regions report more snakebites than anywhere else. In the United States, those bitten are typically male and between 17 and 27 years of age. Children and the elderly are the most likely to die.

Other body-focused repetitive behaviors include excoriation disorder (skin picking), dermatophagia (skin biting), and trichotillomania (the urge to pull out hair), and all of them tend to coexist with nail biting. As an oral parafunctional activity, it is also associated with bruxism (tooth clenching and grinding), and other habits such as pen chewing and cheek biting.

In children nail biting most typically co-occurs with attention deficit hyperactivity disorder (75% of nail biting cases in a study), and other psychiatric disorders including oppositional defiant disorder (36%) and separation anxiety disorder (21%). It is also more common among children and adolescents with obsessive–compulsive disorder. Nail biting appeared in a study to be more common in men with eating disorders than in those without them.

The effect of mercury took some time – the latent period between ingestion and the first symptoms (typically paresthesia – numbness in the extremities) was between 16 and 38 days. Paresthesia was the predominant symptom in less serious cases. Worse cases included ataxia (typically loss of balance), blindness or reduced vision, and death resulting from central nervous system failure. Anywhere between 20 and 40 mg of mercury has been suggested as sufficient for paresthesia (between 0.5 and 0.8 mg/kg of body weight). On average, individuals affected consumed 20 kg or so of bread; the 73,000 tonnes provided would have been sufficient for over 3 million cases.

The hospital in Kirkuk received large numbers of patients with symptoms that doctors recognised from the 1960 outbreak. The first case of alkylmercury poisoning was admitted to hospital on 21 December. By 26 December, the hospital had issued a specific warning to the government. By January 1972, the government had started to strongly warn the populace about eating the grain, although dispatches did not mention the large numbers already ill. The Iraqi Army soon ordered disposal of the grain and eventually declared the death penalty for anyone found selling it. Farmers dumped their supplies wherever possible, and it soon got into the water supply (particularly the River Tigris), causing further problems. The government issued a news blackout and released little information about the outbreak.

The World Health Organization assisted the Iraqi government through the supply of drugs, analytical equipment and expertise. Many new treatments were tried, since existing methods for heavy metal poisoning were not particularly effective. Dimercaprol was administered to several patients, but caused rapid deterioration of their condition. It was ruled out as a treatment for this sort of poisoning following the outbreak. Polythiol resins, penicillamine and dimercaprol sulfonate all helped, but are believed to have been largely insignificant in overall recovery and outcomes. Dialysis was tested on a few patients late in the treatment period, but they showed no clinical improvement. The result of all treatments was varied, with some patients' blood mercury level being dramatically reduced, but a negligible effect in others. All patients received periods of treatment interspersed with lay periods; continuous treatment was suggested in future cases. Later treatment was less effective in reducing blood toxicity.

Turner's hypoplasia is an abnormality found in teeth. Its appearance is variable, though usually is manifested as a portion of missing or diminished enamel on permanent teeth. Unlike other abnormalities which affect a vast number of teeth, Turner's hypoplasia usually affects only one tooth in the mouth and, it is referred to as a Turner's tooth.

Once kidney failure has developed in dogs and cats, the outcome is poor.

Some of grain (73,201 tonnes of wheat grain and 22,262 tonnes of barley), coloured a pink-orange hue, were shipped to Iraq from the United States and Mexico. The wheat arrived in Basra on SS "Trade Carrier" between 16 September and 15 October, barley between 22 October and 24 November 1971. Iraq's government chose Mexipak, a high-yield wheat seed developed in Mexico by Norman Borlaug. The seeds contained an average of 7.9 μg/g of mercury, with some samples containing up to nearly twice that. The decision to use mercury-coated grain has been reported as made by the Iraqi government, rather than the supplier, Cargill. The three Northern governorates of Ninawa, Kirkuk and Erbil together received more than half the shipments. Contributing factors to the epidemic included the fact that distribution started late, and much grain arrived after the October–November planting season.

Farmers holding grain ingested it instead, since their own planting had been completed. Distribution was hurried and open, with grain being distributed free of charge or with payment in kind. Some farmers sold their own grain lest this new grain devalue what they had. This left them dependent on tainted grain for the winter. Many Iraqis were either unaware of the significant health risk posed, or chose to ignore the warnings. Initially, farmers were to certify with a thumbprint or signature that they understood the grain was poison, but according to some sources, distributors did not ask for such an indication. Warnings on the sacks were in Spanish and English, not at all understood, or included the black-and-white skull and crossbones design, which meant nothing to Iraqis. The long latent period may have granted farmers a false sense of security, when animals fed the grain appeared to be fine. The red dye washed off the grain; the mercury did not. Hence, washing may have given only the appearance of removing the poison.

Mercury was ingested through the consumption of homemade bread, meat and other animal products obtained from livestock given treated barley, vegetation grown from soil contaminated with mercury, game birds that had fed on the grain and fish caught in rivers, canals, and lakes into which treated grain had been dumped by the farmers. Ground seed dust inhalation was a contributing factor in farmers during sowing and grinding. Consumption of ground flour through homemade bread is thought to have been the major cause, since no cases were reported in urban areas, where government flour supplies were commercially regulated.

BMS is fairly common worldwide, (however, other sources describe it as rare), and affects up to five individuals per 100,000 general population. People with BMS are more likely to be middle aged or elderly, and females are three to seven times more likely to have BMS than males. Some report a female to male ratio of as much as 33 to 1. BMS is reported in about 10-40% of women seeking medical treatment for menopausal symptoms, and BMS occurs in about 14% of postmenopausal women. Males and younger individuals of both sexes are sometimes affected.

Asian and Native American people have considerably higher risk of BMS.