Anorexia Nervosa (AN) is a serious eating disorder characterized by persistent restriction of energy intake, leading to an abnormally low body weight, and an intense fear of gaining weight. This condition subjects the body to a state of chronic, severe malnutrition, which can have profound effects on virtually every physiological system. The question of whether this chronic state of starvation and its related behaviors increase the risk of developing cancer requires a careful examination of the relationship between long-term nutritional deprivation and oncology.
Addressing the Causal Link
Based on current large-scale epidemiological studies, Anorexia Nervosa itself is not associated with an increased risk of cancer overall compared to the general population. In fact, some research has suggested that women with a history of AN may have a reduced risk of developing certain common cancers, such as breast cancer, with one meta-analysis reporting a relative risk of 0.60. This decreased risk may be due to the low body fat and chronic suppression of reproductive hormones like estrogen, which is a known risk factor for hormone-sensitive cancers.
The relationship between AN and cancer is not a straightforward causal link but is instead site-specific and complex. While the overall cancer risk may not be elevated, specific types of cancer have shown increased incidence in people with AN. For instance, studies have reported an increased risk for cancers of the lung and esophagus, suggesting that risk may be concentrated in specific organs affected by either the malnutrition or associated behaviors. It is important to consider confounding factors, such as the co-occurrence of smoking or alcohol use in individuals with severe mental health issues, which can significantly influence the risk of lung and esophageal cancers.
How Anorexia Affects Cellular Defense
Chronic severe malnutrition, a defining feature of AN, creates systemic changes that can compromise the body’s cellular defense mechanisms. The immune system is highly dependent on a steady supply of micronutrients and macronutrients to function correctly, and a lack of these can compromise surveillance against abnormal cell growth. Although patients with AN do not typically suffer from frequent infections, their immune cell populations are often altered.
Malnutrition can lead to changes in T-cell populations, which are a part of the immune system responsible for identifying and destroying cancer cells. Studies have shown that the number of certain T-cell subsets, such as CD4+ and CD8+ cells, can be decreased or dysregulated in patients with AN. This potentially impairs the body’s ability to monitor for and eliminate precancerous cells. Furthermore, severe nutritional deprivation can impact bone marrow, which is the factory for all blood cells, including the white blood cells that make up the immune system.
Anorexia Nervosa also causes endocrine disruption, which plays a role in cellular regulation. The chronic energy-deprived state results in elevated levels of the stress hormone cortisol, which can have immunosuppressive effects. Additionally, the body develops a state of growth hormone resistance, leading to low levels of Insulin-like Growth Factor 1 (IGF-1). Since IGF-1 promotes cell proliferation, its suppression may contribute to the reduced risk of certain cancers, but this hormonal imbalance still represents a deviation from healthy cellular regulation.
Risks Related to Compensatory Behaviors
Beyond the systemic effects of starvation, the compensatory behaviors such as purging create localized damage. Self-induced vomiting repeatedly exposes the esophagus and throat to caustic stomach acid. This chronic irritation can lead to inflammation and damage to the lining of the upper gastrointestinal tract.
The long-term reflux of acid into the esophagus can cause a condition known as esophagitis, which is the inflammation of the esophageal lining. In rare cases, this chronic acid exposure can lead to a cellular change called Barrett’s esophagus. Barrett’s esophagus is a precancerous condition where the normal cells of the esophagus are replaced by cells similar to those found in the intestine. This cellular transformation significantly increases the risk of developing esophageal adenocarcinoma.
Laxative abuse, another compensatory behavior, can also contribute to localized health problems, particularly in the colon. While evidence linking laxative abuse directly to colon cancer is not definitive, the chronic misuse of these products can irritate the bowel lining and cause significant gastrointestinal distress. The long-term impact of this constant irritation and the resulting nutritional malabsorption on the colon’s cellular environment remains a concern for overall digestive tract health. The increased risk of esophageal and lung cancer found in some studies on AN patients is thought to be tied to these behaviors and to shared co-occurring risk factors like smoking, rather than to the low body weight itself.