Kwashiorkor is mainly caused by inadequate protein intake. The main symptoms are edema, wasting, liver enlargement, hypoalbuminaemia, steatosis, and possibly depigmentation of skin and hair. Kwashiorkor is further identified by swelling of the belly, which is deceiving of actual nutritional status. The term means ‘displaced child’ and is derived from a Ghana language of West Africa, means "the sickness the older one gets when the next baby is born," as this is when the older child is deprived of breast feeding and weaned to a diet composed largely of carbohydrates.

Malnutrition is a condition that results from eating a diet in which nutrients are either not enough or are too much such that the diet causes health problems. It may involve calories, protein, carbohydrates, vitamins or minerals. Not enough nutrients is called undernutrition or undernourishment while too much is called overnutrition. Malnutrition is often used to specifically refer to undernutrition where an individual is not getting enough calories, protein, or micronutrients. If undernutrition occurs during pregnancy, or before two years of age, it may result in permanent problems with physical and mental development. Extreme undernourishment, known as starvation, may have symptoms that include: a short height, thin body, very poor energy levels, and swollen legs and abdomen. People also often get infections and are frequently cold. The symptoms of micronutrient deficiencies depend on the micronutrient that is lacking.

Undernourishment is most often due to not enough high-quality food being available to eat. This is often related to high food prices and poverty. A lack of breastfeeding may contribute, as may a number of infectious diseases such as: gastroenteritis, pneumonia, malaria, and measles, which increase nutrient requirements. There are two main types of undernutrition: protein-energy malnutrition and dietary deficiencies. Protein-energy malnutrition has two severe forms: marasmus (a lack of protein and calories) and kwashiorkor (a lack of just protein). Common micronutrient deficiencies include: a lack of iron, iodine, and vitamin A. During pregnancy, due to the body's increased need, deficiencies may become more common. In some developing countries, overnutrition in the form of obesity is beginning to present within the same communities as undernutrition. Other causes of malnutrition include anorexia nervosa and bariatric surgery.

Efforts to improve nutrition are some of the most effective forms of development aid. Breastfeeding can reduce rates of malnutrition and death in children, and efforts to promote the practice increase the rates of breastfeeding. In young children, providing food (in addition to breastmilk) between six months and two years of age improves outcomes. There is also good evidence supporting the supplementation of a number of micronutrients to women during pregnancy and among young children in the developing world. To get food to people who need it most, both delivering food and providing money so people can buy food within local markets are effective. Simply feeding students at school is insufficient. Management of severe malnutrition within the person's home with ready-to-use therapeutic foods is possible much of the time. In those who have severe malnutrition complicated by other health problems, treatment in a hospital setting is recommended. This often involves managing low blood sugar and body temperature, addressing dehydration, and gradual feeding. Routine antibiotics are usually recommended due to the high risk of infection. Longer-term measures include: improving agricultural practices, reducing poverty, improving sanitation, and the empowerment of women.

There were 793 million undernourished people in the world in 2015 (13% of the total population). This is a reduction of 216 million people since 1990 when 23% were undernourished. In 2012 it was estimated that another billion people had a lack of vitamins and minerals. In 2015, protein-energy malnutrition was estimated to have resulted in 323,000 deaths—down from 510,000 deaths in 1990. Other nutritional deficiencies, which include iodine deficiency and iron deficiency anemia, result in another 83,000 deaths. In 2010, malnutrition was the cause of 1.4% of all disability adjusted life years. About a third of deaths in children are believed to be due to undernutrition, although the deaths are rarely labelled as such. In 2010, it was estimated to have contributed to about 1.5 million deaths in women and children, though some estimate the number may be greater than 3 million. An additional 165 million children were estimated to have stunted growth from malnutrition in 2013. Undernutrition is more common in developing countries. Certain groups have higher rates of undernutrition, including women—in particular while pregnant or breastfeeding—children under five years of age, and the elderly. In the elderly, undernutrition becomes more common due to physical, psychological, and social factors.

Disease-related malnutrition can be considered in four categories:

Weight loss issues related to specific diseases include:

- As chronic obstructive pulmonary disease (COPD) advances, about 35% of patients experience severe weight loss called pulmonary cachexia, including diminished muscle mass. Around 25% experience moderate to severe weight loss, and most others have some weight loss. Greater weight loss is associated with poorer prognosis. Theories about contributing factors include appetite loss related to reduced activity, additional energy required for breathing, and the difficulty of eating with dyspnea (labored breathing).

- Cancer, a very common and sometimes fatal cause of unexplained (idiopathic) weight loss. About one-third of unintentional weight loss cases are secondary to malignancy. Cancers to suspect in patients with unexplained weight loss include gastrointestinal, prostate, hepatobilary (hepatocellular carcinoma, pancreatic cancer), ovarian, hematologic or lung malignancies.

- People with HIV often experience weight loss, and it is associated with poorer outcomes. Wasting syndrome is an AIDS-defining condition.

- Gastrointestinal disorders are another common cause of unexplained weight loss – in fact they are the most common non-cancerous cause of idiopathic weight loss. Possible gastrointestinal etiologies of unexplained weight loss include: celiac disease, peptic ulcer disease, inflammatory bowel disease (crohn's disease and ulcerative colitis), pancreatitis, gastritis, diarrhea and many other GI conditions.

- Infection. Some infectious diseases can cause weight loss. Fungal illnesses, endocarditis, many parasitic diseases, AIDS, and some other subacute or occult infections may cause weight loss.

- Renal disease. Patients who have uremia often have poor or absent appetite, vomiting and nausea. This can cause weight loss.

- Cardiac disease. Cardiovascular disease, especially congestive heart failure, may cause unexplained weight loss.

- Connective tissue disease

- Neurologic disease, including dementia

- Oral, taste or dental problems (including infections) can reduce nutrient intake leading to weight loss.

Unintentional weight loss may result from loss of body fats, loss of body fluids, muscle atrophy, or even a combination of these. It is generally regarded as a medical problem when at least 10% of a person's body weight has been lost in six months or 5% in the last month. Another criterion used for assessing weight that is too low is the body mass index (BMI). However, even lesser amounts of weight loss can be a cause for serious concern in a frail elderly person.

Unintentional weight loss can occur because of an inadequately nutritious diet relative to a person's energy needs (generally called malnutrition). Disease processes, changes in metabolism, hormonal changes, medications or other treatments, disease- or treatment-related dietary changes, or reduced appetite associated with a disease or treatment can also cause unintentional weight loss. Poor nutrient utilization can lead to weight loss, and can be caused by fistulae in the gastrointestinal tract, diarrhea, drug-nutrient interaction, enzyme depletion and muscle atrophy.

Continuing weight loss may deteriorate into wasting, a vaguely defined condition called cachexia. Cachexia differs from starvation in part because it involves a systemic inflammatory response. It is associated with poorer outcomes. In the advanced stages of progressive disease, metabolism can change so that they lose weight even when they are getting what is normally regarded as adequate nutrition and the body cannot compensate. This leads to a condition called anorexia cachexia syndrome (ACS) and additional nutrition or supplementation is unlikely to help. Symptoms of weight loss from ACS include severe weight loss from muscle rather than body fat, loss of appetite and feeling full after eating small amounts, nausea, anemia, weakness and fatigue.

Serious weight loss may reduce quality of life, impair treatment effectiveness or recovery, worsen disease processes and be a risk factor for high mortality rates. Malnutrition can affect every function of the human body, from the cells to the most complex body functions, including:

- immune response;

- wound healing;

- muscle strength (including respiratory muscles);

- renal capacity and depletion leading to water and electrolyte disturbances;

- thermoregulation; and

- menstruation.

In addition, malnutrition can lead to vitamin and other deficiencies and to inactivity, which in turn may pre-dispose to other problems, such as pressure sores.

Unintentional weight loss can be the characteristic leading to diagnosis of diseases such as cancer and type 1 diabetes.

In the UK, up to 5% of the general population is underweight, but more than 10% of those with lung or gastrointestinal diseases and who have recently had surgery. According to data in the UK using the Malnutrition Universal Screening Tool ('MUST'), which incorporates unintentional weight loss, more than 10% of the population over the age of 65 is at risk of malnutrition. A high proportion (10-60%) of hospital patients are also at risk, along with a similar proportion in care homes.

Diarrhea is defined by the World Health Organization as having three or more loose or liquid stools per day, or as having more stools than is normal for that person.

Acute diarrhea is defined as an abnormally frequent discharge of semisolid or fluid fecal matter from the bowel, lasting less than 14 days, by World Gastroenterology Organization.

Diarrhea, also spelled diarrhoea, is the condition of having at least three loose or liquid bowel movements each day. It often lasts for a few days and can result in dehydration due to fluid loss. Signs of dehydration often begin with loss of the normal stretchiness of the skin and irritable behaviour. This can progress to decreased urination, loss of skin color, a fast heart rate, and a decrease in responsiveness as it becomes more severe. Loose but non-watery stools in babies who are breastfed, however, may be normal.

The most common cause is an infection of the intestines due to either a virus, bacteria, or parasite - a condition also known as gastroenteritis. These infections are often acquired from food or water that has been contaminated by feces, or directly from another person who is infected. The three types of diarrhea are: short duration watery diarrhea, short duration bloody diarrhea, and persistent diarrhea (lasting more than two weeks). The short duration watery diarrhea may be due to an infection by cholera, although this is rare in the developed world. If blood is present it is also known as dysentery. A number of non-infectious causes can result in diarrhea. These include lactose intolerance, irritable bowel syndrome, non-celiac gluten sensitivity, celiac disease, inflammatory bowel disease, hyperthyroidism, and a number of medications. In most cases, stool cultures to confirm the exact cause are not required.

Diarrhea can be prevented by improved sanitation, clean drinking water, and hand washing with soap. Breastfeeding for at least six months and vaccination against rotavirus is also recommended. Oral rehydration solution (ORS)--clean water with modest amounts of salts and sugar--is the treatment of choice. Zinc tablets are also recommended. These treatments have been estimated to have saved 50 million children in the past 25 years. When people have diarrhea it is recommended that they continue to eat healthy food and babies continue to be breastfed. If commercial ORS are not available, homemade solutions may be used. In those with severe dehydration, intravenous fluids may be required. Most cases; however, can be managed well with fluids by mouth. Antibiotics, while rarely used, may be recommended in a few cases such as those who have bloody diarrhea and a high fever, those with severe diarrhea following travelling, and those who grow specific bacteria or parasites in their stool. Loperamide may help decrease the number of bowel movements but is not recommended in those with severe disease.

About 1.7 to 5 billion cases of diarrhea occur per year. It is most common in developing countries, where young children get diarrhea on average three times a year. Total deaths from diarrhea are estimated at 1.26 million in 2013 – down from 2.58 million in 1990. In 2012, it was the second most common cause of deaths in children younger than five (0.76 million or 11%). Frequent episodes of diarrhea are also a common cause of malnutrition and the most common cause in those younger than five years of age. Other long term problems that can result include stunted growth and poor intellectual development.

Biotin deficiency is a rare nutritional disorder which can become serious, even fatal, if allowed to progress untreated. It can occur in people of any age, ancestry, or gender. Biotin is part of the B vitamin family.

Biotin deficiency rarely occurs among healthy people because the daily requirement of biotin is low, many foods provide adequate amounts of it, intestinal bacteria synthesize small amounts of it, and the body effectively scavenges and recycles it from bodily waste. However, deficiencies can be caused by consuming raw egg whites over a period of months to years. Egg whites contain high levels of avidin, a protein that binds biotin strongly. When cooked, avidin is partially denatured and binding to biotin is reduced. However one study showed that 30-40% of the avidin activity was still present in the white after frying or boiling. But cooked egg whites are safer to consume. Genetic disorders such as Biotinidase deficiency, Multiple carboxylase deficiency, and Holocarboxylase synthetase deficiency can also lead to inborn or late-onset forms of biotin deficiency. In all cases – dietary, genetic, or otherwise – supplementation with biotin is the primary method of treatment.

The most reliable and commonly used methods for determining biotin status in the body are:

- excretion of 3-hydroxyisovaleric acid and biotin in urine

- activity of propionyl-CoA carboxylase in lymphocytes

Most conditions of STH have a light worm burden and usually have no discernible symptoms. Heavy infections however cause a range of health problems, including abdominal pain, diarrhoea, blood and protein loss, rectal prolapse, and physical and mental retardation.

Severe ascariasis is typically a pneumonia, as the larvae invades lungs, producing fever, cough and dyspnoea during early stage of infection.

Hookworm infections insinuate a skin reaction (dermatitis), increased white blood cells (eosinophils), a pulmonary reaction (pneumonitis), and skin rash (urticarial).

Iron deficiency anaemia due to blood loss is a common symptom.

STH is often associated with malnutrition in children as it worsens their nutritional status in multiple ways. The worms can induce intestinal bleeding, competition for nutrients (malabsorption of nutrients), frequent anaemia and diarrhoea. Soil-transmitted helminths can also cause loss of appetite. These nutritional "knock on" effects of STH can have a significant impact on the mental and physical development of children. In endemic countries, communities remain suppressed due to malnourishment, cognitive disability and physical weaknesses as a result of heavy infections.

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.

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.

Early Childhood Caries (ECC), formerly known as nursing bottle caries, baby bottle tooth decay, night bottle mouth and night bottle caries, is a disease that affects teeth in children aged between birth and 71 months. ECC is characterized by the presence of 1 or more decayed (noncavitated or cavitated lesions), missing (due to caries), or filled tooth surfaces in any primary tooth. ECC has been shown to be a very common, transmissible bacterial infection, usually passed from the primary caregiver to the child. The main bacteria responsible for dental caries is Streptococcus mutans (S. Mutans) and Lactobacillus. There is also evidence that supports that those who are in lower socioeconomic populations are at greater risk of developing ECC.

Early childhood caries (ECC) is a multi-factorial disease, referring to various risk factors that inter-relate to increase risk of developing the disease. These risk factors include but not limited to, cariogenic bacteria, diet practices and socioeconomic factors. Normally after 6 months, deciduous teeth begin to erupt means, they are susceptible to tooth decay or dental caries. In some unfortunate cases, infants and young children have experienced severe tooth decay called ECC. This can result in the child experiencing severe pain, extensive dental restorations or extractions. The good news is that ECC is preventable, however, still remains a large burden particularly towards health care expenditure.

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.

Patients with Zollinger–Ellison syndrome may experience abdominal pain and diarrhea. The diagnosis is also suspected in patients who have severe ulceration of the stomach and small bowel, especially if they fail to respond to treatment.

- Chronic diarrhea, including steatorrhea (fatty stools)

- Pain in the esophagus, especially between and after meals at night

- Nausea

- Wheezing

- Vomiting blood

- Malnourishment

- Loss of appetite

Gastrinomas may occur as single tumors or as multiple small tumors. About one-half to two-thirds of single gastrinomas are malignant tumors that most commonly spread to the liver and to lymph nodes near the pancreas and small bowel.

Nearly 25 percent of patients with gastrinomas have multiple tumors as part of a condition called multiple endocrine neoplasia type 1 (MEN 1). MEN I patients have tumors in their pituitary gland and parathyroid glands, in addition to tumors of the pancreas.

Zollinger–Ellison syndrome (ZES) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.

The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. The tumor causes excessive production of gastric acid, which leads to the growth of gastric mucosa and proliferation of parietal and ECL cells.

ZES may occur on its own or as part of an autosomal dominant syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum or abdominal lymph nodes, but ectopic locations (e.g., heart, ovary, gallbladder, liver, and kidney) have also been described.

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.

As of 2007, fewer than 500 Yakut individuals have been infected with VE. Viliuisk Encephalomyelitis is classified as a progressive neurological disorder that ultimately ends in the death of the infected individual. The disease has three distinguishable phases: The acute form, the progressive form, and the chronic form.

The acute form is the most rapid and most violent of all the stages. It begins with the characteristic rigidity of the muscles, accompanied by slurred speech, severe headaches, and exaggeration of cold-like symptoms. Patients usually die within weeks of the initial symptoms. Routine post-mortem examinations yield: severe inflammation of the brain lining, clusters of dead cells and tissue, and largely increased amounts of macrophages and lymphocytes.

The progressive form is the most common case. Patients initially experience acute-like symptoms which are not as severe, and subside within a few weeks. Following the sub-acute phase, the patients experience a few mild symptoms including some behavioral changes, incoordination, and difficulty in speech. Eventually the disease developed fully and those infected were stricken with the characteristic symptoms of rigidity, slurred speech, and deterioration of cognitive functions. Ultimately, brain function depreciates rapidly resulting in death.

Many patients who undergo the chronic form claim never to have had an acute attack. These patients endure varying measures of impairment and suffer mental deterioration for the remainder of their lives. Usually they live to be very old and succumb to other diseases.

In almost all cases there are changes characteristic of VE. Early onset shows an increased number of lymphocytes and increased protein concentration — which reduces over many years. These factors help neurologists determine the form of VE based on progression. The trademark changes in the brain include: thickened inflamed meninges, necrotic cortical lesions, increased number of lymphocytes, and neuronal death.

Animal hoarding is keeping a higher-than-usual number of animals as domestic pets without ability to properly house or care for them, while at the same time denying this inability. Compulsive hoarding can be characterized as a symptom of mental disorder rather than deliberate cruelty towards animals. Hoarders are deeply attached to their pets and find it extremely difficult to let the pets go. They typically cannot comprehend that they are harming their pets by failing to provide them with proper care. Hoarders tend to believe that they provide the right amount of care for them. The American Society for the Prevention of Cruelty to Animals provides a "Hoarding Prevention Team", which works with hoarders to help them attain a manageable and healthy number of pets.

Lymphangiomatosis has been reported in every region of the abdomen, though the most reported sites involve the intestines and peritoneum; spleen, kidneys, and liver. Often there are no symptoms until late in the progression of the disease. When they do occur, symptoms include abdominal pain and/or distension; nausea, vomiting, diarrhea; decreased appetite and malnourishment. When the disease affects the kidneys the symptoms include flank pain, abdominal distension, blood in the urine, and, possibly, elevated blood pressure, which may result in it being confused with other cystic renal disease. When lymphangiomatosis occurs in the liver and/or spleen it may be confused with polycystic liver disease. Symptoms may include abdominal fullness and distension; anemia, disseminated intravascular coagulopathy (DIC), fluid accumulation in the abdomen(ascites), decreased appetite, weight loss, fatigue; late findings include liver failure.

Lymphangiomatosis is a multi-system disorder. Symptoms depend on the organ system involved and, to varying degrees, the extent of the disease. Early in the course of the disease patients are usually asymptomatic, but over time the abnormally proliferating lymphatic channels that constitute lymphangiomatosis are capable of massive expansion and infiltration into surrounding tissues, bone, and organs. Because of its slow course and often vague symptoms, the condition is frequently under-recognized or misdiagnosed.

Early signs of disease in the chest include wheezing, cough, and feeling short of breath, which is often misdiagnosed as asthma. The pain that accompanies bone involvement may be attributed to "growing pains" in younger children. With bone involvement the first indication for disease may be a pathological fracture. Symptoms may not raise concern, or even be noted, until the disease process has advanced to a point where it causes restrictive compression of vital structures. Further, the occurrence of chylous effusions seems to be unrelated to the pathologic "burden" of the disease, the extent of involvement in any particular tissue or organ, or the age of the patient. This offers one explanation as to why, unfortunately, the appearance of chylous effusions in the chest or abdomen may be the first evidence of the disease.

Following are some of the commonly reported symptoms of lymphangiomatosis, divided into the regions/systems in which the disease occurs:

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.

Perhaps the strongest psychological model put forward to explain animal hoarding is obsessive–compulsive disorder (OCD). An overwhelming sense of responsibility for something is characteristic of people with OCD, who then take unrealistic measures to fulfill their perceived duty. Animal hoarders often feel a strong sense of responsibility to take care of and protect animals, and their solution—that of acquiring as many animals as they possibly can—is unrealistic. Further, the hoarding of inanimate objects, practiced by a majority of animal hoarders, is a fairly common occurrence in people with OCD. These connections between animal hoarding and obsessive–compulsive disorder suggest that OCD may be a useful model in explaining animal hoarding behavior. However, this theory has also been refuted by some; Dr. Akimitsu Yokoyama theorizes that animal hoarding could be explained using Asperger syndrome.