Coprophagia in humans, the ingestion of feces, is almost always driven by an underlying neurological, psychiatric, or developmental condition. It is rare in the general population, and when it does occur, it typically signals damage or dysfunction in specific parts of the brain rather than a standalone disorder. The causes fall into a few distinct categories, each with different mechanisms and implications.
Brain Damage and Dementia
The most well-documented cause of coprophagia in adults is neurological deterioration, particularly in frontotemporal dementia and Alzheimer’s disease. Brain imaging of dementia patients who develop the behavior consistently shows moderate-to-severe shrinkage of the medial temporal lobe, the region that houses the amygdala and plays a central role in processing disgust, fear, and the ability to distinguish edible from inedible objects. Mild frontal lobe atrophy, which governs impulse control and social behavior, is often present as well.
This pattern closely resembles a condition called Klüver-Bucy syndrome, which was originally described after surgical removal of both temporal lobes in primates. In humans, the syndrome emerges when disease destroys the same tissue gradually. People with Klüver-Bucy symptoms develop “hyperorality,” a compulsive tendency to place objects, including feces, into their mouths. They also lose the normal revulsion response that would prevent this. One case study documented a 70-year-old man with progressive hyperorality, compulsive eating, and loss of visual recognition who died at 77 after choking on a foreign object. Autopsy confirmed Alzheimer’s disease with unusually dense damage concentrated in the amygdala.
Stroke, traumatic brain injury, and brain tumors affecting the same temporal and frontal regions can produce coprophagia through identical mechanisms, even in younger adults. The common thread is always the loss of the brain’s built-in aversion system.
Psychotic and Delusional Disorders
Coprophagia also appears in severe psychiatric illness, most notably chronic schizophrenia. Here the mechanism is different: the behavior is often tied to delusional thinking rather than a loss of disgust. In one documented case, a patient with undifferentiated schizophrenia engaged in coprophagia while expressing the belief that he was “not any ordinary human being but special” and that eating unusual substances would not affect his health. He also held paranoid delusions of being followed and feeling unsafe at home.
In psychotic states, the behavior may be driven by command hallucinations (voices instructing the person to eat feces), grandiose delusions that override normal self-protective instincts, or a general disorganization of thought so severe that the person can no longer categorize objects as harmful. The coprophagia in these cases tends to emerge during acute psychotic episodes or in patients with long-standing, poorly controlled illness.
Developmental and Intellectual Disabilities
Among people with severe intellectual disabilities, coprophagia sometimes develops as a form of self-stimulatory behavior. Research using functional behavior analysis has shown that for some individuals, the behavior is maintained by automatic sensory reinforcement: it produces a sensory experience (taste, texture, or oral stimulation) that the person finds reinforcing, independent of any social attention or external reward.
One well-studied case involved a woman whose coprophagia was treated through a behavioral approach. Therapists provided continuous access to preferred food items that competed with the sensory experience of coprophagia. When these alternative items were freely available, the behavior dropped to zero. Over time, the schedule was thinned so that preferred foods were offered at 30-second intervals rather than continuously, and the behavior remained suppressed. This type of intervention, called noncontingent reinforcement, works specifically because it addresses the sensory function driving the behavior rather than relying on punishment or verbal instruction.
Nutritional Deficiency: Mostly a Myth in Humans
In veterinary medicine, nutritional deficiencies are a recognized trigger for coprophagia. The assumption that the same applies to humans comes up frequently, but the clinical evidence does not support it. A literature review of published case reports found that blood work in coprophagia patients repeatedly came back normal for iron, thiamine, and other nutrients. One patient had a slightly low iron-binding capacity, but an otherwise unremarkable metabolic panel. Multiple other cases specifically tested for and ruled out vitamin and mineral deficiencies.
The one partial exception involves dementia patients who also had mixed anemia (a combination of iron-deficiency and another type), but in those cases, the dementia itself was considered the primary driver rather than the anemia. The review’s authors concluded that psychiatric and neurological presentations explained the behavior far more consistently than any medical comorbidity.
Health Risks of Fecal Ingestion
Regardless of the cause, coprophagia carries serious infectious risks. Human stool contains bacteria, viruses, and parasites that are dangerous when ingested. The CDC notes that even fecal specimens preserved in chemical fixatives can remain infectious, because some parasite cysts and eggs are protected by thick shells that resist standard preservation for days or weeks. Roundworm eggs, for example, can continue developing and stay infectious even in formalin solution.
Bacterial infections from organisms like E. coli, Salmonella, and Shigella are the most immediate concern. Parasitic infections, including giardiasis and amoebiasis, are also possible. Hepatitis A and other enteric viruses transmit through the fecal-oral route. For people who are already medically vulnerable, whether due to dementia, psychiatric illness, or developmental disability, these infections can become life-threatening.
How the Underlying Cause Is Identified
When coprophagia presents in a clinical setting, the evaluation focuses on distinguishing between neurological, psychiatric, and developmental causes because each points toward a different management strategy. A standard workup typically includes brain imaging (MRI or CT scan) to check for temporal and frontal lobe atrophy or lesions, blood work to rule out metabolic abnormalities, and a thorough psychiatric evaluation looking for psychosis, delusions, or cognitive decline.
For individuals with intellectual disabilities, a functional behavior assessment may be the most informative step. This involves observing the behavior under controlled conditions to determine whether it is maintained by sensory stimulation, social attention, escape from demands, or access to preferred items. The results directly inform treatment: a behavior driven by sensory reinforcement calls for a different approach than one driven by delusional beliefs or one caused by progressive brain disease.
In most cases, identifying the cause does not lead to a “cure” for coprophagia itself but rather to better management of the condition producing it. Antipsychotic medications may reduce the behavior when it stems from psychosis. Behavioral interventions can be highly effective for individuals with developmental disabilities. For dementia patients, environmental modifications, such as limiting unsupervised access to feces, often become the most practical strategy as the disease progresses.