What Is Protein Energy Malnutrition: Types and Causes

Protein energy malnutrition (PEM) is a condition where the body doesn’t get enough protein, calories, or both to maintain normal tissue and organ function. It ranges from mild deficiency, detectable only through blood tests and subtle weight loss, to life-threatening wasting that affects every organ system. Over 150 million children under five were stunted from chronic malnutrition in 2024, with roughly two-thirds of those cases concentrated in South Asia and Sub-Saharan Africa.

The Two Main Types: Marasmus and Kwashiorkor

Healthcare providers classify severe PEM into two distinct forms based on what’s missing from the diet. Marasmus results from a deficiency of all macronutrients: protein, carbohydrates, and fats. People with marasmus are simply not getting enough calories, either because food is scarce, they can’t absorb it, or their body is burning through energy faster than they can replace it. The visible hallmark is severe, generalized wasting with virtually no body fat remaining.

Kwashiorkor, by contrast, is primarily a protein deficiency. A person with kwashiorkor may actually be getting adequate calories, often from starchy foods like rice or corn, but almost no protein-rich foods like meat, eggs, beans, or dairy. The defining feature is swelling (edema), particularly in the feet, legs, and belly. This swelling can mask the underlying muscle loss, making kwashiorkor harder to recognize at first glance than marasmus. Some people develop a combination of both types, sometimes called marasmic kwashiorkor, where calorie deprivation and protein deficiency overlap.

Why the Body Swells Without Enough Protein

The edema in kwashiorkor traces back to a protein made by the liver called albumin. Albumin is a relatively small molecule, but it plays an outsized role in keeping fluid inside blood vessels. It creates what’s known as oncotic pressure, essentially a pull that holds water in the bloodstream rather than letting it seep into surrounding tissues. When protein intake drops severely, the liver can’t produce enough albumin, and that pull weakens. Fluid leaks out of blood vessels and accumulates in tissues, causing the characteristic puffiness.

Children with kwashiorkor also show dramatically low levels of glutathione, the body’s primary internal antioxidant. Researchers initially speculated that the resulting oxidative stress might drive the swelling, but current evidence points to the dangerously low albumin levels as the primary cause, with glutathione depletion being a consequence of the same severe protein shortage rather than an independent trigger.

How the Body Adapts to Starvation

Humans have built-in mechanisms for slowing the progression of PEM, at least up to a point. When calorie intake drops, the body responds by lowering its metabolic rate per unit of active tissue, essentially turning down the thermostat. It also begins breaking down lean tissue, particularly muscle, to conserve fat stores. Muscle protein normally makes up about 80% of lean tissue mass, so it bears the brunt of this sacrifice. Meanwhile, “central” tissues like the liver, kidneys, gut lining, and immune cells are relatively spared in the early stages.

If the calorie and protein deficit isn’t too extreme, this adaptation can actually restore a kind of equilibrium. The now-smaller body needs less energy and less protein, so a meager diet that couldn’t sustain the original body weight becomes just enough to keep essential functions running. But this adaptation has sharp limits. Once involuntary weight loss exceeds about 10%, measurable dysfunction in organs and immunity begins to appear. Beyond 15% weight loss, the impairments become severe and increasingly dangerous.

What PEM Does to the Body

The physical effects of PEM reach well beyond weight loss. Skeletal muscles atrophy and weaken, including the respiratory muscles, making breathing less efficient. Heart muscle mass decreases. The skin thins and becomes fragile, making pressure sores far more likely. Wounds heal poorly. Fatigue and apathy set in, and the body loses the ability to regulate its own temperature, leading to hypothermia even in warm environments. The extracellular fluid compartment expands, sometimes visibly as edema, sometimes less obviously.

The immune system takes a particularly hard hit. PEM causes profound immune deficiency across multiple fronts: the body’s cell-mediated immunity (the branch that fights viruses and certain bacteria directly) weakens significantly, and so do its antibody responses and its nonspecific defenses, the front-line barriers like skin integrity and the protective lining of the gut. This creates a vicious cycle. Weakened immunity leads to infections, which increase the body’s energy and protein demands, which worsens the malnutrition, which further suppresses the immune system. Diarrheal diseases, respiratory infections, and other opportunistic illnesses become common and difficult to recover from.

Causes Beyond Food Scarcity

PEM isn’t always about not having enough to eat. Secondary PEM develops when the body can’t properly absorb nutrients or when a disease dramatically increases energy demands. Inflammatory bowel disease, pancreatic insufficiency (as in cystic fibrosis), and liver cirrhosis can all impair nutrient absorption enough to cause PEM even when food intake seems adequate. Wasting conditions like cancer, tuberculosis, and HIV/AIDS drive the body’s calorie and protein requirements far above normal, sometimes to the point where no realistic amount of food can keep up. Chronic kidney disease is another common driver, both through protein losses and metabolic disruption.

In high-income countries, PEM most often appears in hospital settings. Elderly patients, people recovering from major surgery, individuals with advanced cancer, and those with chronic illnesses that suppress appetite are all at elevated risk. The condition frequently goes unrecognized because clinicians may focus on the primary illness rather than the patient’s nutritional status.

How PEM Is Identified

In children, the World Health Organization defines severe acute malnutrition as a weight-for-height measurement more than three standard deviations below normal, a mid-upper arm circumference below 115 millimeters, or the presence of edema in both feet. The arm measurement is especially useful in field settings because it requires only a simple measuring tape, no scale or height board.

For adults, particularly in hospital and clinical settings, screening tools like the Malnutrition Universal Screening Tool (MUST) help identify people at risk. MUST scores patients on three factors: current BMI (below 18.5 scores highest risk), recent unintentional weight loss (more than 10% scores highest), and whether an acute illness is likely to prevent eating for five or more days. A combined score of two or more points flags someone as high risk, triggering a more detailed nutritional assessment and intervention plan.

How Severe PEM Is Treated

Treating severe PEM, particularly in children, follows a carefully staged approach because a malnourished body can’t handle a sudden flood of calories and protein. The first phase, called stabilization, focuses on correcting life-threatening problems like dehydration, infection, and dangerous electrolyte imbalances. During this phase, patients receive a low-protein, moderate-calorie formula designed to be gentle enough for a body that has adapted to starvation.

Once the patient is medically stable, with appetite returning and edema beginning to resolve, treatment transitions over two to three days into a higher-protein, higher-calorie formula or a ready-to-use therapeutic food. The target during this rehabilitation phase is 100 to 135 calories per kilogram of body weight per day, enough to support catch-up growth without overwhelming the body’s recovering systems. This phase continues until the patient has regained enough weight and strength to return to a normal diet.

The staged approach matters because refeeding a severely malnourished person too quickly can cause dangerous shifts in electrolytes, a complication known as refeeding syndrome, which can be fatal. Recovery takes weeks to months depending on severity, and ongoing nutritional support is typically needed well after the acute phase resolves.

Global Progress and Persistent Challenges

The worldwide prevalence of stunting, which reflects chronic malnutrition during early childhood, dropped from 40% in 1990 to 23.2% in 2024. That’s meaningful progress, but it still leaves over 150 million children under five with impaired growth. Joint estimates from UNICEF, the WHO, and the World Bank published in 2025 highlight that while acute wasting has declined slightly, stunting and childhood overweight remain persistent or worsening in several regions. South Asia and Sub-Saharan Africa continue to carry the heaviest burden, underscoring that the problem is far from solved even as global averages improve.