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.

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.

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.

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.

The World Health Organization estimates that malnutrition accounts for 54 percent of child mortality worldwide, about 1 million children. Another estimate also by WHO states that childhood underweight is the cause for about 35% of all deaths of children under the age of five years worldwide.

According to a 2008 review an estimated 178 million children under age 5 are stunted, most of whom live in sub-Saharan Africa. A 2008 review of malnutrition found that about 55 million children are wasted, including 19 million who have severe wasting or severe acute malnutrition.

As underweight children are more vulnerable to almost all infectious diseases, the "indirect" disease burden of malnutrition is estimated to be an order of magnitude higher than the disease burden of the "direct" effects of malnutrition. The combination of direct and indirect deaths from malnutrition caused by unsafe water, sanitation and hygiene (WASH) practices is estimated to lead to 860,000 deaths per year in children under five years of age.

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

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.

Not only the causes, but also the complications of the disorder must be treated, including infections, dehydration, and circulation disorders, which are frequently lethal and lead to high mortality if ignored. Initially, the child is given dried skim milk powder mixed with boiled water which is then followed by mixing it with vegetable oils and finally sugar. Once children start to recover, they should have more balanced diets which meet their nutritional needs. Infections are also common in children with marasmus. So, they are also treated with antibiotics. Ultimately, marasmus can progress to the point of no return when the body's ability for protein synthesis is lost. At this point, attempts to correct the disorder by giving food or protein are futile.

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.

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.

Vitamin E supplements have shown to help children with the deficiency.

It can be diagnosed via blood study that identifies fat particles. The patient must fast overnight to prevent interference from fat in the blood due to food intake. The criteria for this (without the involvement of cholesterol-lowering drugs) are total cholesterol levels below 120 mg/dL and LDL cholesterol levels under 50 mg/dL.

Muscular atrophy decreases qualities of life as the sufferer becomes unable to perform certain tasks or worsen the risks of accidents while performing those (like walking). Muscular atrophy increases the risks of falling in conditions such as inclusion body myositis (IBM) . Muscular atrophy affects a high number of the elderly.

In post-menopausal women, the walls of the vagina become thinner (atrophic vaginitis). The mechanism for the age-related condition is not yet clear, though there are theories that the effect is caused by decreases in estrogen levels. This atrophy, and that of the breasts concurrently, is consistent with the homeostatic (normal development) role of atrophy in general, as after menopause the body has no further functional biological need to maintain the reproductive system which it has permanently shut down.

There are many diseases and conditions which cause a decrease in muscle mass, known as atrophy, including activity, as seen when a cast is put on a limb, or upon extended bedrest (which can occur during a prolonged illness); cachexia - which is a syndrome that is a co-morbidity of cancer and congestive heart failure; chronic obstructive pulmonary disease; burns, liver failure, etc., and the wasting Dejerine-Sottas syndrome (HMSN Type III). Glucocorticoids, a class of medications used to treat allergic and other inflammatory conditions can induce muscle atrophy by increasing break-down of muscle proteins. Other syndromes or conditions which can induce skeletal muscle atrophy are liver disease, and starvation.

One drug in test seemed to prevent the type of muscle loss that occurs in immobile, bedridden patients.

Testing on mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy. However, the drug's long-term effect on the heart precludes its routine use in humans, and other drugs are being sought.

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.

Anorexia always precedes liver disease, with the cat refusing to eat enough food for days, or weeks. This may be amplified by frequent vomiting when the cat does choose to eat. A lack of appetite causes the cat to refuse any food, even after it has purged its system of all stomach contents. Severe weight loss proceeds as the liver keeps the cat alive off body fat, causing a yellowing of the skin (jaundice). When the cat runs out of fat to process, severe muscle wasting (cachexia) takes place as the body converts protein into energy. Eventually the body cannot give the brain enough energy to function properly and the cat dies from malnutrition. In addition, an overworked liver can eventually fail causing total system collapse.

Hypobetalipoproteinemia is a disorder consisting of low levels of LDL cholesterol or apolipoprotein B, below the 5th percentile. The patient can have hypobetalipoproteinemia and simultaneously have high levels of HDL cholesterol.

Notably, in people who do not have the genetic disorder hypobetalipoproteinemia, a low cholesterol level may be a marker for poor nutrition, wasting disease, cancer, hyperthyroidism, and liver disease.

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.

The incidence of SIADH rises with increasing age. Residents of nursing homes are at highest risk.

One form is thought to be caused by mutated apolipoprotein B.

Another form is associated with microsomal triglyceride transfer protein which causes abetalipoproteinemia.

A third form, chylomicron retention disease (CRD), is associated with SARA2.

Euthyroid sick syndrome (ESS), sick euthyroid syndrome (SES), thyroid allostasis in critical illness, tumours, uremia and starvation (TACITUS), non-thyroidal illness syndrome (NTIS) or low T low T syndrome is a state of adaptation or dysregulation of thyrotropic feedback control where the levels of T3 and/or T4 are at unusual levels, but the thyroid gland does not appear to be dysfunctional.

This condition is often seen in starvation, critical illness or patients in intensive care unit. Similar endocrine phenotypes are observed in fetal life and in hibernating mammals The most common hormone pattern in sick euthyroid syndrome is a low total and unbound T3 levels with normal T4 and TSH levels.

Causes of euthyroid sick syndrome include a number of acute and chronic conditions, including pneumonia, fasting, starvation, anorexia nervosa, sepsis, trauma, cardiopulmonary bypass, malignancy, stress, heart failure, hypothermia, myocardial infarction, chronic renal failure, cirrhosis, and diabetic ketoacidosis.

Euthyroid sick syndrome (non-thyroidal illness syndrome) has been assumed closely related with a series of diseases, (such as inflammatory bowel disease).

Hospitalization for the diseased person is suggested because of the controlled environment because it may prevent nutritional deficiencies and skin infections. A decrease in severity of symptoms usually happens after a few weeks when treated redness and scaliness usually do not recur. In 10 percent of cases, the result of uncontrolled infections or severe electrolyte loss may be fatal.