Hypothermia can occur. To prevent or treat this, the child can be kept warm with covering including of the head or by direct skin-to-skin contact with the mother or father and then covering both parent and child. Prolonged bathing or prolonged medical exams should be avoided. Warming methods are usually most important at night.

In response to child malnutrition, the Bangladeshi government recommends ten steps for treating severe malnutrition. They are to prevent or treat dehydration, low blood sugar, low body temperature, infection, correct electrolyte imbalances and micronutrient deficiencies, start feeding cautiously, achieve catch-up growth, provide psychological support, and prepare for discharge and follow-up after recovery.

Among those patients who are hospitalized, nutritional support improves protein, colorie intake and weight.

In the United States, biotin supplements are readily available without a prescription in amounts ranging from 1,000 to 10,000 micrograms (30 micrograms is identified as Adequate Intake).

Obesity increases health risks, including diabetes, cancer, cardiovascular disease, high blood pressure, and non-alcoholic fatty liver disease, to name a few. Reduction of obesity lowers those risks.

A 1-kg loss of body weight has been associated with an approximate 1-mm Hg drop in blood pressure.

Social conditions such as poverty, social isolation and inability to get or prepare preferred foods can cause unintentional weight loss, and this may be particularly common in older people. Nutrient intake can also be affected by culture, family and belief systems. Ill-fitting dentures and other dental or oral health problems can also affect adequacy of nutrition.

Loss of hope, status or social contact and spiritual distress can cause depression, which may be associated with reduced nutrition, as can fatigue.

Since biotin is in many foods at low concentrations, deficiency is rare except in locations where malnourishment is very common. Pregnancy, however, alters biotin catabolism and despite a regular biotin intake, half of the pregnant women in the U.S. are marginally biotin deficient.

The following types of diarrhea may indicate further investigation is needed:

- In infants

- Moderate or severe diarrhea in young children

- Associated with blood

- Continues for more than two days

- Associated non-cramping abdominal pain, fever, weight loss, etc.

- In travelers

- In food handlers, because of the potential to infect others;

- In institutions such as hospitals, child care centers, or geriatric and convalescent homes.

A severity score is used to aid diagnosis in children.

Numerous studies have shown that improvements in drinking water and sanitation (WASH) lead to decreased risks of diarrhoea. Such improvements might include for example use of water filters, provision of high-quality piped water and sewer connections.

In institutions, communities, and households, interventions that promote hand washing with soap lead to significant reductions in the incidence of diarrhea. The same applies to preventing open defecation at a community-wide level and providing access to improved sanitation. This includes use of toilets and implementation of the entire sanitation chain connected to the toilets (collection, transport, disposal or reuse of human excreta).

For basic diagnosis, specific helminths can be generally identified from the faeces, and their eggs microscopically examined and enumerated using fecal egg count method. However, there are certain limitations such as the inability to identify mixed infections, and on clinical practice, the technique is inaccurate and unreliable.

A novel effective method for egg analysis is the Kato-Katz technique. It is a highly accurate and rapid method for "A. lumbricoides" and "T. trichiura"; however not so much for hookworm, which could be due to fast degeneration of the rather delicate hookworm eggs.

Prevention and control measures to prevent soil-transmitted helminthiasis are the following: availability of clean water for personal and domestic uses, improved access to sanitation which includes the use of properly functioning and clean toilets by all community members, education on personal hygiene such as hand washing and hygienic and safe food preparation; eliminating the use of untreated human faeces as fertilizer.

Early childhood caries can be prevented through the combination of the following: adhering to a healthy nutritional diet, optimal plaque removal, use of fluoridation on the tooth surface once erupted, care taken by the mother during the pre-natal and peri-natal period and regular dental visits. The following are recommendations to help prevent ECC.

Dietary habits and the presence of cariogenic bacteria within the oral cavity are an important factor in the risk of ECC. ECC is commonly caused by bottle feeding, frequent snacking and a high sugar diet

In regards to preventing ECC through bottle feeding, it is fundamental not to allow the child to sleep using ‘sippy cups’ or bottles as this is a large factor contributing to baby bottle decay/caries. This is highly encouraged as it prevents continuous exposure to non-milk extrinsic sugars and therefore the potential progression of caries – this means the oral cavity can return to a neutral pH and therefore decreased acidity. These researches also suggest trying to introduce cups to children as they approach their first birthday and to reduce the use of a bottle.

A low-sugar and high nutritional diet is recommended for both the mother and the child especially during breastfeeding, and it is also recommended to avoid frequent snacking

One of the main effects of cadmium poisoning is weak and brittle bones. Spinal and leg pain is common, and a waddling gait often develops due to bone deformities caused by the cadmium. The pain eventually becomes debilitating, with fractures becoming more common as the bone weakens. Other complications include coughing, anemia, and kidney failure, leading to death.

A marked prevalence in older, postmenopausal women has been observed. The cause of this phenomenon is not fully understood, and is currently under investigation. Current research has pointed to general malnourishment, as well as poor calcium metabolism relating to the women's age.

Recent animal studies have shown that cadmium poisoning alone is not enough to elicit all of the symptoms of itai-itai disease. These studies are pointing to damage of the mitochondria of kidney cells by cadmium as a key factor of the disease.

Zollinger–Ellison syndrome may be suspected when the above symptoms prove resistant to treatment, when the symptoms are especially suggestive of the syndrome, or when endoscopy is suggestive. The diagnosis is made through several laboratory tests and imaging studies:

- Secretin stimulation test, which measures evoked gastrin levels

- Fasting gastrin levels on at least three separate occasions

- Gastric acid secretion and pH (normal basal gastric acid secretion is less than 10 mEq/hour; in Zollinger–Ellison patients, it is usually more than 15 mEq/hour)

- An increased level of chromogranin A is a common marker of neuroendocrine tumors.

In addition, the source of the increased gastrin production must be determined using MRI or somatostatin receptor scintigraphy.

Itai-itai disease was caused by cadmium poisoning due to mining in Toyama Prefecture. The earliest records of mining for gold in the area date back to 1710. Regular mining for silver started in 1589, and soon thereafter, mining for lead, copper, and zinc began. Increased demand for raw materials during the Russo-Japanese War and World War I, as well as new mining technologies from Europe, increased the output of the mines, putting the Kamioka Mines in Toyama among the world's top mines. Production increased even more before World War II. Starting in 1910 and continuing through 1945, cadmium was released in significant quantities by mining operations, and the disease first appeared around 1912. Prior to World War II, the mining, controlled by the Mitsui Mining & Smelting Co., Ltd., increased to satisfy the wartime demand. This subsequently increased the pollution of the Jinzū River and its tributaries. The river was used mainly for irrigation of rice fields, but also for drinking water, washing, fishing, and other uses by downstream populations.

Due to the cadmium poisoning, the fish in the river started to die, and the rice irrigated with river water did not grow well. The cadmium and other heavy metals accumulated at the bottom of the river and in the water of the river. This water was then used to irrigate the rice fields. The rice absorbed heavy metals, especially the cadmium. The cadmium accumulated in the people eating contaminated rice.

When the population complained to Mitsui Mining & Smelting Co. about this pollution, the company built a basin to store the mining waste water before leading it into the river. This proved ineffective, and many had already been sickened. The causes of the poisoning were not well understood and, up to 1946, it was thought to be simply a regional disease or a type of bacterial infection.

Medical tests started in the 1940s and 1950s, searching for the cause of the disease. Initially, it was expected to be lead poisoning due to the lead mining upstream. Only in 1955 did Dr. Hagino and his colleagues suspect cadmium as the cause of the disease. Toyama Prefecture also started an investigation in 1961, determining that the Mitsui Mining and Smelting's Kamioka Mining Station caused the cadmium pollution and that the worst-affected areas were 30 km downstream of the mine. In 1968, the Ministry of Health and Welfare issued a statement about the symptoms of "itai-itai" disease caused by the cadmium poisoning.

The reduction of the levels of cadmium in the water supply reduced the number of new disease victims; no new victim has been recorded since 1946. While the victims with the worst symptoms came from Toyama prefecture, the government found victims in five other prefectures.

The mines are still in operation and cadmium pollution levels remain high, although improved nutrition and medical care has reduced the occurrence of itai-itai disease.

Sick cell syndrome or cell sickness syndrome is a medical condition characterised by reduced functioning of the cellular Na+/K+ pump, which is responsible for maintaining the internal ion homeostasis. The clinical result is a rise in blood K+ level and drop of blood Na+ levels

There are a wide range of possible pathological conditions that can cause sick cell syndrome, including:

- hypoxia

- sepsis

- hypovolaemia

- malnourishment

This syndrome is well known in the field of palliative medicine as many terminal patients develop this condition.

Another human health issue caused by animal hoarding is the risk of zoonotic diseases. Defined as "human diseases acquired from or transmitted to any other vertebrate animal", zoonotic diseases can often be lethal and in all cases constitute a serious public health concern. Examples of well-known zoonotic diseases include bubonic plague, influenza, and rabies. Common domesticated animals constitute a large portion of animals carrying zoonoses, and as a result, humans involved in animal hoarding situations are at particular risk of contracting disease. Zoonoses that may arise in hoarding situations—through vectors such as dog, cat, or rat bites—include rabies, salmonellosis, catscratch fever, hookworm, and ringworm. One zoonosis of special concern is toxoplasmosis, which can be transmitted to humans through cat feces or badly-prepared meat, and is known to cause severe birth defects or stillbirth in the case of infected pregnant women. The risk of zoonotic diseases is amplified by the possibility of community epidemics.

Because it is rare and has a wide spectrum of clinical, histological, and imaging features, diagnosing lymphangiomatosis can be challenging. Plain x-rays reveal the presence of lytic lesions in bones, pathological fractures, interstitial infiltrates in the lungs, and chylous effusions that may be present even when there are no outward symptoms.

The most common locations of lymphangiomatosis are the lungs and bones and one important diagnostic clue is the coexistence of lytic bone lesions and chylous effusion. An isolated presentation usually carries a better prognosis than does multi-organ involvement; the combination of pleural and peritoneal involvement with chylous effusions and lytic bone lesions carries the least favorable prognosis.

When lung involvement is suspected, high resolution computed tomography (HRCT) scans may reveal a diffuse liquid-like infiltration in the mediastinal and hilar soft tissue, resulting from diffuse proliferation of lymphatic channels and accumulation of lymphatic fluid; diffuse peribronchovascular and interlobular septal thickening; ground-glass opacities; and pleural effusion. Pulmonary function testing reveals either restrictive pattern or a mixed obstructive/restrictive pattern. While x-rays, HRCT scan, MRI, ultrasound, lymphangiography, bone scan, and bronchoscopy all can have a role in identifying lymphangiomatosis, biopsy remains the definitive diagnostic tool.

Microscopic examination of biopsy specimens reveals an increase in both the size and number of thin walled lymphatic channels along with lymphatic spaces that are interconnecting and dilated, lined by a single attenuated layer of endothelial cells involving the dermis, subcutis, and possibly underlying fascia and skeletal muscle. Additionally, Tazelaar, et al., described a pattern of histological features of lung specimens from nine patients in whom no extrathoracic lesions were identified, which they termed "diffuse pulmonary lymphangiomatosis" (DPL).

Recognition of the disease requires a high index of suspicion and an extensive workup. Because of its serious morbidity, lymphangiomatosis must always be considered in the differential diagnosis of lytic bone lesions accompanied by chylous effusions, in cases of primary chylopericardium, and as part of the differential diagnosis in pediatric patients presenting with signs of interstitial lung disease.

Proton pump inhibitors (such as omeprazole and lansoprazole) and histamine H2-receptor antagonists (such as famotidine and ranitidine) are used to slow acid secretion. Once gastric acid is suppressed, symptoms normally improve.

Animal hoarding also causes many health problems for the people involved. Hoarders, by definition, fail to correct the deteriorating sanitary conditions of their living spaces, and this gives rise to several health risks for those living in and around hoarding residences. Animal hoarding is at the root of a string of human health problems including poor sanitation, fire hazards, zoonotic diseases, envenomation, and neglect of oneself and dependents.

Satoyoshi syndrome, also known as Komura-Guerri syndrome, is a rare progressive disorder of presumed autoimmune cause, characterized by painful muscle spasms, alopecia, diarrhea, endocrinopathy with amenorrhoea and secondary skeletal abnormalities. The syndrome was first reported in 1967 by Eijiro Satoyoshi and Kaneo Yamada in Tokyo, Japan. To this date, fewer than 50 cases worldwide have been reported for the Satoyoshi syndrome.

People with the syndrome typically develop symptoms of the illness at a young age, usually between the age of six and fifteen years old. The initial symptoms are muscle spasms in the legs and alopecia, also known as baldness. The spasms are painful and progressive and their frequency varies from 1 or 2 to 100 per day, each lasting a few minutes. It can be sufficiently severe to produce abnormal posturing of the affected limbs, particularly the thumbs. With progression the illness involves the pectoral girdle and trunk muscles and finally the masseters and temporal muscles. The spasms usually spare the facial muscles. Severe spasms can interfere with respiration and speech. During an attack-free period, non-stimulus-sensitive myoclonus can occur in the arms, legs and neck. Diarrhea occurs in the first 2–3 years with intolerance to carbohydrate and high glucose diets. Endocrinopathy manifests as amenorrhea and hypoplasia of the uterus. Affected children fail to attain height after 10–12 years of age.

The syndrome is not known to be a primary cause of mortality, but some patients have died as a result of secondary complications, such as respiratory failure and malnourishment.

In one 6-year-old patient antibodies to GABA-producing enzyme glutamate decarboxylase were detected.

Thoracocentesis, pericardiocentesis, pleurodesis, ligation of thoracic duct, pleuroperitoneal shunt, radiation therapy, pleurectomy, pericardial window, pericardiectomy, thalidomide, interferon alpha 2b, Total Parenteral Nutrition (TPN), medium chain triglyceride (MCT) and high protein diet, chemotherapy, sclerotherapy, transplant;

Currently the mechanism of spread and infection is unknown despite the tedious epidemiological, clinical, and neurological studies that have been conducted. Recent Studies show Horizontal Disease Transmission, or the transmission of a disease from one individual to another of the same generation. It appears that VE is an infectious disease; however, the incubation period would have to be very extensive (in excess of 5 years). Many infected individuals attribute the initial symptoms as a result of a plunge in frigid waters. So far, no causative agent has been found in blood, spinal fluid, or brain tissue.

Viliuisk Encephalomyelitis (VE) is a fatal progressive neurological disorder found only in the Sakha (Iakut/Yakut) population of central Siberia. About 15 new cases are reported each year. VE is a very rare disease and little research has been conducted. The causative agents, origin of the disease, and involved candidate genes are currently unknown, but much research has been done in pursuit of the answers.

Those inflicted with the disease survive for a period of only a few months to several years. VE follows three main courses of infection: an acute form, a sub-acute form subsiding into a progressive form, and a chronic form. Initially, the infected patients experience symptoms such as: severe headaches, delirium, lethargy, meningism, bradykinesia, and incoordination. A small percentage of patients die during the acute phase as result of a severe coma. In all cases the disease is fatal.