As of November 2013, no identifiable cause for the disease had been found. Pathogenic bacteria did not seem to be present, and though the plague might be caused by a viral or fungal pathogen, no causal agent had been found. Each episode of plague might have a different cause.

Other possible causes of the condition that have been suggested include high sea temperatures, oxygen depletion and low salinity due to freshwater runoff. Research suggests that high water temperatures are indeed linked to the disease, increasing its incidence and virulence. The disease also seems more prevalent in sheltered waters than in open seas with much wave movement. One result of global warming is higher sea temperatures. There is a wave of unusually warm water along the west coast of the United States, which is where all of the sea stars are dying off. These may impact both on starfish and on echinoderm populations in general, and a ciliate protozoan parasite ("Orchitophrya stellarum") of starfish, which eats sperm and effectively emasculates male starfish, thrives at higher temperatures.

Research in 2014 showed that the cause of the disease is transmissible from one starfish to another and that the disease-causing agent is a microorganism in the virus-size range. The most likely candidate causal agent was found to be the sea star-associated densovirus (SSaDV), which was found to be in greater abundance in diseased starfish than in healthy ones.

Sea star wasting disease or starfish wasting syndrome is a disease of starfish and several other echinoderms that appears sporadically, causing mass mortality of affected starfish. There are around 40 different species of sea stars that have been affected by this disease. The disease seems to be associated with raised water temperatures. It starts with the emergence of lesions, followed by body fragmentation and death. In 2014 it was shown that the disease is associated with a densovirus now known as the sea star-associated densovirus (SSaDV).

A study, in community dwelling older adults with an average age of 67 years, found the UK prevalence of sarcopenia to be 4.6% in men and 7.9% in women using the EWGSOP approach. Another study, conducted in the United States among older adults with an average age of 70.1 years, found the prevalence of sarcopenia to be 36.5%. Sarcopenia affects about half of people over 80 in one state in the USA.

Both PMWS and porcine dermatitis and nephropathy syndrome (PDNS) are associated to PCV-2. Many pigs affected by the circovirus also seem to develop secondary bacterial infections, like Glässer disease ("Haemophilus parasuis"), pulmonary pasteurellosis, colibacilosis, salmonellosis and others. Postmortem lesions occur in multiple organs, especially in lymphoid tissues and lung, giving rise to the term "multisystemic". Lesions may also affect the skin, kidney, reproductive tissue, brain, or blood vessels.

Wasting pigs is the most common sign of PMWS infection, increasing the mortality rate significantly.

In an endemic herd, only a minority of the animals develops clinical signs; most animals either eliminate the infection or become asymptomatic carriers. The mortality rate is about 1%, but up to 50% of the animals in the herd can be asymptomatically infected, resulting in losses in production. Once the symptoms appear, paratuberculosis is progressive and affected animals eventually die. The percentage of asymptomatic carriers that develop overt disease is unknown.

François Madec, a French author, has written many recommendations on how reduce PMWS symptoms. They are mostly measures for disinfection, management, and hygiene, referred to as the "20 Madec Points" [Madec & Waddilove, 2002].

These measures have recently been expanded upon by Dr. David Barcellos, a professor at the Veterinary College in the Universidade Federal do Rio Grande do Sul, Rio Grande do Sul, Brazil. He presented these points at "1st Universidade Federal do Rio Grande do Sul Symposium about swine management, reproduction, and hygiene".

He divided his points by pig growth stage, and they can be loosely summarized as:

- keep the gutters clean

- increase feeder space

- use pens or small cages with solid dividers

- avoid mixing pigs from different origins

- improve the quality of air

- decrease maximum capacity, giving each pig more room

- separate sick animals as soon as possible, and treat them in a hospital pen. If they do not respond to antibiotics in three days, they should be culled

- control access of people and other animals

- reduce invironmental stress factors such as gases and air currents

- use immunizations and preventive medications for secondary agents commonly associated with PMWS

MAP is capable of causing Johne's-like symptoms in humans, though difficulty in testing for MAP infection presents a diagnostic hurdle.

Clinical similarities are seen between Johne's disease in ruminants and inflammatory bowel disease in humans, and because of this, some researchers contend the organism is a cause of Crohn's disease. However, epidemiologic studies have provided variable results; in certain studies, the organism (or an immune response directed against it) has been much more frequently found in patients with Crohn's disease than asymptomatic people.

Wasting can be caused by an extremely low energy intake (e.g., caused by famine), nutrient losses due to infection, or a combination of low intake and high loss. Infections and conditions associated with wasting include tuberculosis, chronic diarrhea, AIDS, and superior mesenteric artery syndrome. The mechanism may involve cachectin – also called tumor necrosis factor, a macrophage-secreted cytokine. Caretakers and health providers can sometimes contribute to wasting if the patient is placed on an improper diet. Voluntary weight loss and eating disorders are excluded as causes of wasting.

Antiretrovirals and anabolic steroids have been used to treat HIV wasting syndrome. Additionally, an increase in protein-rich foods such as peanut butter, eggs, and cheese can assist in controlling the loss of muscle mass.

Due to the lessened physical activity and increased longevity of industrialized populations, sarcopenia is emerging as a major health concern. Sarcopenia may progress to the extent that an older person may lose his or her ability to live independently. Furthermore, sarcopenia is an important independent predictor of disability in population-based studies, linked to poor balance, gait speed, falls, and fractures. Sarcopenia can be thought of as a muscular analog of osteoporosis, which is loss of bone, also caused by inactivity and counteracted by exercise. The combination of osteoporosis and sarcopenia results in the significant frailty often seen in the elderly population.

The exact mechanism in which these diseases cause cachexia is poorly understood, but there is probably a role for inflammatory cytokines, such as tumor necrosis factor-alpha (which is also nicknamed 'cachexin' or 'cachectin'), interferon gamma and interleukin 6, as well as the tumor-secreted proteolysis-inducing factor.

Related syndromes include kwashiorkor and marasmus, although these do not always have an underlying causative illness and are most often symptomatic of severe malnutrition.

Those suffering from the eating disorder anorexia nervosa appear to have high plasma levels of ghrelin. Ghrelin levels are also high in patients who have cancer-induced cachexia.

The origin and mode of transmission of the prions causing CWD is unknown, but recent research indicates that prions can be excreted by deer and elk, and are transmitted by eating grass growing in contaminated soil. Animals born in captivity and those born in the wild have been affected with the disease. Based on epidemiology, transmission of CWD is thought to be lateral (from animal to animal). Maternal transmission may occur, although it appears to be relatively unimportant in maintaining epidemics. An infected deer's saliva is able to spread the CWD prions. Exposure between animals is associated with sharing food and water sources contaminated with CWD prions shed by diseased deer.

The disease was first identified in 1967 in a closed herd of captive mule deer in contiguous portions of northeastern Colorado. In 1980, the disease was determined to be a TSE. It was first identified in wild elk and mules in 1981 in Colorado and Wyoming, and in farmed elk in 1997.

In May 2001, CWD was also found in free-ranging deer in the southwestern corner of Nebraska (adjacent to Colorado and Wyoming) and later in additional areas in western Nebraska. The limited area of northern Colorado, southern Wyoming, and western Nebraska in which free-ranging deer, moose, and/or elk positive for CWD have been found is referred to as the endemic area. The area in 2006 has expanded to six states, including parts of eastern Utah, southwestern South Dakota, and northwestern Kansas. Also, areas not contiguous (to the endemic area) areas in central Utah and central Nebraska have been found. The limits of the affected areas are not well defined, since the disease is at a low incidence and the amount of sampling may not be adequate to detect it. In 2002, CWD was detected in wild deer in south-central Wisconsin and northern Illinois and in an isolated area of southern New Mexico. In 2005, it was found in wild white-tailed deer in New York and in Hampshire County, West Virginia. In 2008, the first confirmed case of CWD in Michigan was discovered in an infected deer on an enclosed deer-breeding facility. It is also found in the Canadian provinces of Alberta and Saskatchewan. In February 2011, the Maryland Department of Natural Resources reported the first confirmed case of the disease in that state. The affected animal was a white-tailed deer killed by a hunter.

CWD has also been diagnosed in farmed elk and deer herds in a number of states and in two Canadian provinces. The first positive farmed elk herd in the United States was detected in 1997 in South Dakota.

Since then, additional positive elk herds and farmed white-tailed deer herds have been found in South Dakota (7), Nebraska (4), Colorado (10), Oklahoma (1), Kansas (1), Minnesota (3), Montana (1), Wisconsin (6) and New York (2). As of fall of 2006, four positive elk herds in Colorado and a positive white-tailed deer herd in Wisconsin remain under state quarantine. All of the other herds have been depopulated or have been slaughtered and tested, and the quarantine has been lifted from one herd that underwent rigorous surveillance with no further evidence of disease. CWD also has been found in farmed elk in the Canadian provinces of Saskatchewan and Alberta. A retrospective study also showed mule deer exported from Denver to the Toronto Zoo in the 1980s were affected. In June 2015, the disease was detected in a male white-tailed deer on a breeding ranch in Medina County, Texas. State officials euthanized 34 deer in an effort to contain a possible outbreak.

Species that have been affected with CWD include elk, mule deer, white-tailed deer, black-tailed deer, and moose. Other ruminant species, including wild ruminants and domestic cattle, sheep, and goats, have been housed in wildlife facilities in direct or indirect contact with CWD-affected deer and elk, with no evidence of disease transmission. However, experimental transmission of CWD into other ruminants by intracranial inoculation does result in disease, suggesting only a weak molecular species barrier exists. Research is ongoing to further explore the possibility of transmission of CWD to other species.

By April 2016 CWD had been found in captive animals in South Korea; the disease arrived there with live elk that were imported for farming in the late 1990s.

Under normal metabolic conditions, the human body relies on free blood glucose as its primary energy source. The level of blood sugar is tightly regulated; as blood glucose is consumed, the pancreas releases glucagon, a hormone that stimulates the liver to convert stored glycogen into glucose. The glycogen stores are ordinarily replenished after every meal, but if the store is depleted before it can be replenished, the body enters hypoglycemia, and begins the starvation response.

After the exhaustion of the glycogen reserve, and for the next 2–3 days, fatty acids become the principal metabolic fuel. At first, the brain continues to use glucose, because, if a non-brain tissue is using fatty acids as its metabolic fuel, the use of glucose in the same tissue is switched off. Thus, when fatty acids are being broken down for energy, all of the remaining glucose is made available for use by the brain. Basically the body will use up stored fat cells first, then move on to muscles.

After 2 or 3 days of fasting, the liver begins to synthesize ketone bodies from precursors obtained from fatty acid breakdown. The brain uses these ketone bodies as fuel, thus cutting its requirement for glucose. After fasting for 3 days, the brain gets 30% of its energy from ketone bodies. After 4 days, this goes up to 75%. Thus, the production of ketone bodies cuts the brain's glucose requirement from 80 g per day to about 30 g per day. Of the remaining 30 g requirement, 20 g per day can be produced by the liver from glycerol (itself a product of fat breakdown). But this still leaves a deficit of about 10 g of glucose per day that must be supplied from some other source. This other source will be the body's own proteins.

After several days of fasting, all cells in the body begin to break down protein. This releases alanine and lactate produced from pyruvate into the bloodstream, which can be converted into glucose by the liver. Since much of human muscle mass is protein, this phenomenon is responsible for the wasting away of muscle mass seen in starvation. However, the body is able to selectively decide which cells will break down protein and which will not. About 2–3 g of protein has to be broken down to synthesize 1 g of glucose; about 20–30 g of protein is broken down each day to make 10 g of glucose to keep the brain alive. However, this number may decrease the longer the fasting period is continued in order to conserve protein.

Starvation ensues when the fat reserves are completely exhausted and protein is the only fuel source available to the body. Thus, after periods of starvation, the loss of body protein affects the function of important organs, and death results, even if there are still fat reserves left unused. (In a leaner person, the fat reserves are depleted earlier, the protein depletion occurs sooner, and therefore death occurs sooner.) The ultimate cause of death is, in general, cardiac arrhythmia or cardiac arrest brought on by tissue degradation and electrolyte imbalances.

For the individual, prevention consists of ensuring they eat plenty of food, varied enough to provide a nutritionally complete diet.

Starvation can be caused by factors, other than illness, outside of the control of the individual. The Rome Declaration on World Food Security outlines several policies aimed at increasing food security and, consequently, preventing starvation. These include:

- Poverty reduction

- Prevention of wars and political instability

- Food aid

- Agricultural sustainability

- Reduction of economic inequality

Supporting farmers in areas of food insecurity through such measures as free or subsidized fertilizers and seeds increases food harvest and reduces food prices.

Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy (TSE) of mule deer, white-tailed deer, elk (or "wapiti"), moose, and reindeer. As of 2016, CWD had only been found in members of the deer family. First recognized as a clinical "wasting" syndrome in 1967 in mule deer in a wildlife research facility in northern Colorado, USA, it was identified as a TSE in 1978 and has spread to free-ranging and captive populations in 23 US states and two Canadian provinces. CWD is typified by chronic weight loss leading to death. No relationship is known between CWD and any other TSE of animals or people.

Although reports in the popular press have been made of humans being affected by CWD, a study by the Centers for Disease Control and Prevention suggests, "[m]ore epidemiologic and laboratory studies are needed to monitor the possibility of such transmissions".

The epidemiological study further concluded, "[a]s a precaution, hunters should avoid eating deer and elk tissues known to harbor the CWD agent (e.g., brain, spinal cord, eyes, spleen, tonsils, lymph nodes) from areas where CWD has been identified".

This disease is often found during the first two months of an infants life, breast-fed infants with a higher chance. Male and female infants are affected equally.

Diarrhea and other infections can cause malnutrition through decreased nutrient absorption, decreased intake of food, increased metabolic requirements, and direct nutrient loss. Parasite infections, in particular intestinal worm infections (helminthiasis), can also lead to malnutrition. A leading cause of diarrhea and intestinal worm infections in children in developing countries is lack of sanitation and hygiene. Other diseases that cause chronic intestinal inflammation may lead to malnutrition, such as some cases of untreated celiac disease and inflammatory bowel disease.

Children with chronic diseases like HIV have a higher risk of malnutrition, since their bodies cannot absorb nutrients as well. Diseases such as measles are a major cause of malnutrition in children; thus immunizations present a way to relieve the burden.

In almost all countries, the poorest quintile of children has the highest rate of malnutrition. However, inequalities in malnutrition between children of poor and rich families vary from country to country, with studies finding large gaps in Peru and very small gaps in Egypt. In 2000, rates of child malnutrition were much higher in low income countries (36 percent) compared to middle income countries (12 percent) and the United States (1 percent).

Studies in Bangladesh in 2009 found that the mother’s literacy, low household income, higher number of siblings, less access to mass media, less supplementation of diets, unhygienic water and sanitation are associated with chronic and severe malnutrition in children.

This disease is endemic in Portuguese locations Póvoa de Varzim and Vila do Conde (Caxinas), with more than 1000 affected people, coming from about 500 families, where 70% of the people develop the illness. ll the analysed Portuguese families presented the same haplotype (haplotype I) associated with the Met 30 mutation. In northern Sweden, more specifically Piteå, Skellefteå and Umeå, 1.5% of the population has the mutated gene. There are many other populations in the world who exhibit the illness after having developed it independently.

Proventricular dilatation disease (PDD) is a disease affecting psittacines (parrots). It was first recognized and described in 1978 by Dr. Hannis L. Stoddard. Since the first reported cases were involving species of macaw, the condition was termed macaw wasting syndrome.

The cause of this disease is unknown; some infants may have a severe case, others may have immunodeficiency.

In July 2008, a team of researchers at the University of California, San Francisco was able to identify a virus that may cause PDD, which they have named avian bornavirus. A member of the Bornaviridae family, avian bornavirus was isolated in 71 percent of samples from infected birds, but in none of the healthy birds. The researchers were able to clone a full-length genome of the virus from avian tissue. Later analyses revealed that numerous distinct avian bornaviruses exist - not all of them cause PDD. Gancz "et al." succeeded in inducing PDD in cockatiels by inoculation of brain tissue from avian bornavirus-positive birds while Gray "et al." caused PDD in Patagonian conures by inoculation of a tissue-culture derived isolate of avian bornavirus.

Despite many reports, avian bornaviruses should not be stated as the cause of PDD.

Untreated, the disease has a mortality rate upwards of 90%. Cats treated in the early stages can have a recovery rate of 80–90%. Left untreated, the cats usually die from severe malnutrition or complications from liver failure. Treatment usually involves aggressive feeding through one of several methods.

Cats can have a feeding tube inserted by a veterinarian so that the owner can feed the cat a liquid diet several times a day. They can also be force-fed through the mouth with a syringe. If the cat stops vomiting and regains its appetite, it can be fed in a food dish normally. The key is aggressive feeding so the body stops converting fat in the liver. The cat liver has a high regeneration rate and the disease will eventually reverse assuming that irreparable damage has not been done to the liver.

The best method to combat feline hepatic lipidosis is prevention and early detection. Obesity increases the chances of onset. In addition, if a cat stops eating for 1–2 days, it should be taken to a vet immediately. The longer the disease goes untreated, the higher the mortality rate.

Persons in prisons, concentration camps, and refugee camps tend to suffer from marasmus, due to poor nutrition.

About 50% of all cancer patients suffer from cachexia. Those with upper gastrointestinal and pancreatic cancers have the highest frequency of developing a cachexic symptom. This figure rises to 80% in terminal cancer patients. In addition to increasing morbidity and mortality, aggravating the side effects of chemotherapy, and reducing quality of life, cachexia is considered the immediate cause of death of a large proportion of cancer patients, ranging from 22% to 40% of the patients.

Symptoms of cancer cachexia include progressive weight loss and depletion of host reserves of adipose tissue and skeletal muscle. Cachexia should be suspected if involuntary weight loss of greater than 5% of premorbid weight occurs within a six-month period. Traditional treatment approaches, such as appetite stimulants, 5-HT antagonists, nutrient supplementation, and COX-2 inhibitor, have failed to demonstrate success in reversing the metabolic abnormalities seen in cancer cachexia.