The treatment or management of cachexia depends on the underlying causes, the general prognosis and other person related factors. Reversible causes, underlying diseases and contributing factors are treated if possible and acceptable. A growing body of evidence supports the efficacy of (HMB) as a treatment for reducing, or even reversing, the loss of muscle mass, muscle function, and muscle strength that occurs in hypercatabolic disease states such as cachexia; consequently, it is recommended that both the prevention and treatment of muscle wasting conditions include supplementation with HMB, regular resistance exercise, and consumption of a high-protein diet. Progestins such as megestrol acetate are a treatment option in refractory cachexia with anorexia as a major symptom.

Cachexia occurs less frequently now in HIV/AIDS than in the past due to the advent of highly active antiretroviral therapy (HAART). Treatment involving different combinations for cancer cachexia is recommended in Europe, as a combination of nutrition, medication and non-drug-treatment may be more effective than monotherapy. Non-drug therapies which have been shown to be effective in cancer induced cachexia include nutritional counselling, psychotherapeutic interventions, and physical training. Anabolic-androgenic steroids like oxandrolone may be beneficial in cancer cachexia but their use is recommended for maximal 2 weeks since a longer duration of treatment increases the burden from side effects.

Other drugs that have been used or are being investigated in cachexia therapy, but which lack conclusive evidence of efficacy or safety, and are not generally recommended include:

- Thalidomide and cytokine antagonists

- Cannabinoids

- Omega-3 fatty acids, including eicosapentaenoic acid (EPA)

- Non-steroidal anti-inflammatory drugs

- Prokinetics

- Ghrelin and ghrelin receptor agonist

- Anabolic catabolic transforming agents such as MT-102

- Selective androgen receptor modulators

- Cyproheptadine

- Hydrazine

Medical marijuana has been allowed for the treatment of cachexia in some US states, such as Illinois, Maryland, Delaware, Nevada, Michigan, Washington, Oregon, California, Colorado, New Mexico, Arizona, Vermont, New Jersey, Rhode Island, Maine, and New York Hawaii and Connecticut.

There is insufficient evidence to support the use of oral fish oil for the management of cachexia associated with advanced cancer.

Only limited treatment options exist for patients with clinical cancer cachexia. Current strategy is to improve appetite by using appetite stimulants to ensure adequate intake of nutrients. Pharmacological interventions with appetite stimulants, nutrient supplementation, 5-HT antagonists and Cox-2 inhibitor have been used to treat cancer cachexia, but with limited effect.

Studies using a more calorie-dense (1.5 kcals/ml) and higher protein supplementation have suggested at least weight stabilization can be achieved, although improvements in lean body mass have not been observed in these studies.

Therapeutic strategies have been based on either blocking cytokines synthesis or their action. Thalidomide has been demonstrated to suppress TNF-alpha production in monocytes "in vitro" and to normalize elevated TNF-alpha levels "in vivo". A randomized, placebo-controlled trial in patients with cancer cachexia showed the drug was well tolerated and effective at attenuating loss of weight and lean body mass (LBM) in patients with advanced pancreatic cancer. An improvement in the LBM and improved quality of life were also observed in a randomized, double-blind trial using a protein and energy-dense, omega-3 fatty acids-enriched oral supplement, provided its consumption was equal or superior to 2.2 g of eicosapentaenoic acid per day. It is also through decreasing TNF-alpha production. However, data arising from a large, multicenter, double-blind, placebo-controlled trial indicate EPA administration alone is not successful in the treatment of weight loss in patients with advanced gastrointestinal or lung cancer.

Peripheral muscle proteolysis, as it occurs in cancer cachexia, serves to mobilize amino acids required for the synthesis of liver and tumor protein. Therefore, the administration of exogenous amino acids may theoretically serve as a protein-sparing metabolic fuel by providing substrates for both muscle metabolism and gluconeogenesis. Studies have demonstrated dietary supplementation with a specific combination of high protein, leucine and fish oil improves muscle function and daily activity and the immune response in cachectic tumor-bearing mice. In addition, β-hydroxy-β-methyl butirate derived from leucine catabolism used as a supplement in tumor-bearing rats prevents cachexia by modifying NF-κB expression.

A phase-2 study involving the administration of antioxidants, pharmaconutritional support, progestin (megestrol acetate and medroxyprogesterone acetate), and anticyclooxygenase-2 drugs, showed efficacy and safety in the treatment of patients with advanced cancer of different sites suffering cachexia. These data reinforce the use of the multitargeted therapies (nutritional supplementation, appetite stimulants, and physical activity regimen) in the treatment of cancer cachexia.

New studies indicate NSAIDS, like Sulindac, were found to significantly decrease cachexia.

Also studies have shown branched-chain amino acids can return the metabolism of a cachectic patient from catabolic-losing weight- to anabolic- increasing muscle, in over 55% of patients. Branched-chain amino acids consist primarily of leucine and valine. In a research paper published by the Indian J of Palliat Care, the effects the findings concluded that bcaa's interfere with brain serotonergic activity and inhibit the overexpression of critical muscular proteolytic pathways. The potential role of branched-chain amino acids as antianorexia and anticachexia agents was proposed many years ago, but experimental studies and clinical trials have since tested their ability to stimulate food intake and counteract muscle wasting in anorectic, weight-losing patients. In experimental models of cancer cachexia, BCAAs were able to induce a significant suppression in the loss of body weight, producing a significant increase in skeletal muscle wet weight[30] as well as in muscle performance and total daily activity.

The conditionally essential amino acid glutamine has been used as a component of oral supplementation to reverse cachexia in patients with advanced cancer or HIV/AIDS.

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.

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

Treatment with antibiotics such as amoxicillin or cefdinir improve the response and survival rate of severely malnourished children to an outpatient treatment plan which provided therapeutic food. This confirms the recommendation, "In addition to the provision of RUTF [ready-to-use therapeutic food], children need to receive a short course of basic oral medication to treat infections." contained in "Community-based management of severe acute malnutrition, A Joint Statement by the World Health Organization, the World Food Programme, the United Nations System Standing Committee on Nutrition and the United Nations Children’s Fund."

Starving patients can be treated, but this must be done cautiously to avoid refeeding syndrome. Rest and warmth must be provided and maintained. Small sips of water mixed with glucose should be given in regular intervals. Fruit juices can also be given. Later, food can be given gradually in small quantities. The quantity of food can be increased over time. Proteins may be administered intravenously to raise the level of serum proteins.

Muscle atrophy can be opposed by the signaling pathways which induce muscle hypertrophy, or an increase in muscle size. Therefore, one way in which not exercise induces an increase in muscle mass is to down regulate the pathways which have the opposite effect.

β-hydroxy β-methylbutyrate (HMB), a metabolite of leucine which is sold as a dietary supplement, has demonstrated efficacy in preventing the loss of muscle mass in several muscle wasting conditions in humans, particularly sarcopenia. A growing body of evidence supports the efficacy of HMB as a treatment for reducing, or even reversing, the loss of muscle mass, muscle function, and muscle strength in hypercatabolic disease states such as cancer cachexia; consequently, it is recommended that both the prevention and treatment of sarcopenia and muscle wasting in general include supplementation with HMB, regular resistance exercise, and consumption of a high-protein diet. Based upon a meta-analysis of seven randomized controlled trials that was published in 2015, HMB supplementation has efficacy as a treatment for preserving lean muscle mass in older adults. More research is needed to determine the precise effects of HMB on muscle strength and function in this age group.

Since the absence of muscle-building amino acids can contribute to muscle wasting (that which is torn down must be rebuilt with like material), amino acid therapy may be helpful for regenerating damaged or atrophied muscle tissue. The branched-chain amino acids or BCAAs (leucine, isoleucine, and valine) are critical to this process, in addition to lysine and other amino acids.

In severe cases of muscular atrophy, the use of an anabolic steroid such as methandrostenolone may be administered to patients as a potential treatment. A novel class of drugs, called SARM (selective androgen receptor modulators) are being investigated with promising results. They would have fewer side-effects, while still promoting muscle and bone tissue growth and regeneration. These claims are, however, yet to be confirmed in larger clinical trials.

One important rehabilitation tool for muscle atrophy includes the use of functional electrical stimulation to stimulate the muscles. This has seen a large amount of success in the rehabilitation of paraplegic patients.

Measures have been taken to reduce child malnutrition. Studies for the World Bank found that, from 1970 to 2000, the number of malnourished children decreased by 20 percent in developing countries. Iodine supplement trials in pregnant women have been shown to reduce offspring deaths during infancy and early childhood by 29 percent. However, universal salt iodization has largely replaced this intervention.

The Progresa program in Mexico combined conditional cash transfers with nutritional education and micronutrient-fortified food supplements; this resulted in a 10 percent reduction the prevalence of stunting in children 12–36 months old. Milk fortified with zinc and iron reduced the incidence of diarrhea by 18 percent in a study in India.

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.

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.

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.

Treatment is palliative, not curative (as of 2009).

Treatment options for lower limb weakness such as foot drop can be through the use of Ankle Foot Orthoses (AFOs) which can be designed or selected by an Orthotist based upon clinical need of the individual. Sometimes tuning of rigid AFOs can enhance knee stability.

Early high doses of vitamin E in infants and children has shown to be effective.

The drug tafamidis has completed a phase II/III 18-month-long placebo controlled clinical trial

and these results in combination with an 18-month follow-on study demonstrated that Tafamidis or Vyndaqel slowed progression of FAP, particularly when administered to patients early in the course of FAP. This drug is now approved by the European Medicines Agency.

The US Food and Drug Administration's Peripheral and Central Nervous System Drugs Advisory Committee rejected the drug in June 2012, in a 13-4 vote. The committee stated that there was not enough evidence supporting efficacy of the drug, and requested additional clinical trials.

In the absence of a liver transplant, FAP is invariably fatal, usually within a decade. The disadvantage of liver transplantation is that approximately 10% of the subjects die from the procedure or complications resulting from the procedure, which is a form of gene therapy wherein the liver expressing wild type and mutant TTR is replaced by a liver only expressing wild type TTR. Moreover, transplanted patients must take immune suppressants (drugs) for the remainder of their life, which can lead to additional complications. In late 2011, the European Medicines Agency approved the transthyretin kinetic stabilizer Tafamidis or Vyndaqel discovered by Jeffery W. Kelly and developed by FoldRx pharmaceuticals (acquired by Pfizer in 2010) for the treatment of FAP based on clinical trial data. Tafamidis (20 mg once daily) slowed the progression of FAP over a 36-month period and importantly reversed the weight loss and muscle wasting associated with disease progression.

Proper management of diabetes mellitus can prevent proximal diabetic neuropathy from ever occurring.

The incidence of proximal diabetic neuropathy incidence is thought to be correlated to blood glucose control in diabetics, and is likely reversible with better control.

Medication helps reduce the pain involved in proximal diabetic neuropathy. Most patients take oral medication that is prescribed by a doctor. Common types of medication used to treat diabetic amyotrophy include anticonvulsives (e.g. gabapentin, pregabalin) as well as opioid medications, although the latter category is not optimally indicated for neuropathic pain.

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.

Because lack of sialic acid appears to be part of the pathology of IBM caused by GNE mutations, clinical trials with sialic acid supplements, and with a precursor of sialic acid, N-Acetylmannosamine, have been conducted, and as of 2016 further trials were planned.

While CSWS usually appears within the first week after brain injury and spontaneously resolves in 2–4 weeks, it can sometimes last for months or years. In contrast to the use of fluid restriction to treat SIADH, CSWS is treated by replacing the urinary losses of water and sodium with hydration and sodium replacement. The mineralocorticoid medication fludrocortisone can also improve the low sodium level.

A number of pharmaceuticals may be used in an attempt to bring the polydipsia under control, including:

- Atypical antipsychotics, such as clozapine, olanzapine and risperidone

- Demeclocycline, a tetracycline antibiotic, which is effective due to the side effect of inducing nephrogenic diabetes insipidus. Demeclocycline is used for cases of psychogenic polydipsia, including those with nocturnal enuresis (bed-wetting). Its mechanism of action involves direct inhibition of vasopressin at the DCTs, thus reducing urine concentration.

There are a number of emerging pharmaceutical treatments for psychogenic polydipsia, although these need further investigation:

- ACE Inhibitors, such as enalapril

- Clonidine, an alpha-2 adrenergic agonist

- Irbesartan, an angiotensin II receptor antagonist

- Propranolol, a sympatholytic beta blocker

- Vasopressin receptor antagonists, such as conivaptan

- Acetazolamide, a carbonic anhydrase inhibitor

Lithium was previously used for treatment of PPD as a direct competitive ADH agonist, but is now generally avoided due to its toxic effects on the thyroid and kidneys.

It is important to note that the majority of psychotropic drugs (and a good many of other classes) can cause dry mouth as a side effect, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.

Several trials investigated a possible therapy for ESS. However, they yielded inconsistent and partly contradictory results. This may be caused by the fact that the investigated populations were too heterogeneous in the lack of a consistent definition of "non-thyroid illness syndrome".

Modern theories regard the TACITUS syndrome as an adaptive and therefore possibly beneficial response of thyroid homeostasis. Their proponents are therefore reserved with respect to substitutive treatment.

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.

How to manage SIADH depends on whether symptoms are present, the severity of the hyponatremia, and the duration. Management of SIADH includes:

- Removing the underlying cause when possible.

- Mild and asymptomatic hyponatremia is treated with adequate solute intake (including salt and protein) and fluid restriction starting at 500 ml per day of water with adjustments based on serum sodium levels. Long-term fluid restriction of 1,200–1,800 mL/day may maintain the person in a symptom free state.

- Moderate and symptomatic hyponatremia is treated by raising the serum sodium level by 0.5 to 1 mmol per liter per hour for a total of 8 mmol per liter during the first day with the use of furosemide and replacing sodium and potassium losses with 0.9% saline.

- For people with severe symptoms (severe confusion, convulsions, or coma) hypertonic saline (3%) 1–2 ml/kg IV in 3–4 h should be given.

- Drugs

- Demeclocycline can be used in chronic situations when fluid restrictions are difficult to maintain; demeclocycline is the most potent inhibitor of Vasopressin (ADH/AVP) action. However, demeclocycline has a 2–3 day delay in onset with extensive side effect profile, including skin photosensitivity, and nephrotoxicity.

- Urea: oral daily ingestion has shown favorable long-term results with protective effects in myelinosis and brain damage. Limitations noted to be undesirable taste and is contraindicated in people with cirrhosis to avoid initiation or potentiation of hepatic encephalopathy.

- Conivaptan – an antagonist of both V and V vasopressin receptors.

- Tolvaptan – an antagonist of the V vasopressin receptor.

Raising the serum sodium concentration too rapidly may cause central pontine myelinolysis. Avoid correction by more than 12 mEq/L/day. Initial treatment with hypertonic saline may abruptly lead to a rapid dilute diuresis and fall in ADH.

Congenital dSMA has a relatively stable disease course, with disability mainly attributed to increased contractures rather than loss of muscle strength. Individuals frequently use crutches, knee, ankle, and/or foot orthoses, or wheelchairs. Orthopaedic surgery can be an option for some patients with severely impaired movement. Physical therapy and occupational therapy can help prevent further contractures from occurring, though they do not reverse the effects of preexisting ones. Some literature suggests the use of electrical stimulation or botulinum toxin to halt the progression of contractures.

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.