Causes Of Eating Disorders – Biological Factors

Eating disorders, encompassing conditions such as anorexia nervosa, bulimia nervosa, and binge-eating disorder, are complex mental health issues characterized by severe disturbances in eating behaviors and related thoughts and emotions. These disorders can have profound physical, psychological, and social consequences. While the exact cause of eating disorders remains intricate and multifaceted, involving a blend of biological, environmental, and psychological factors, this article focuses specifically on the biological underpinnings. The exploration into the biological causes aims to shed light on the genetic, neurochemical, and physiological aspects that may predispose individuals to developing eating disorders. Understanding these factors is crucial in devising more effective treatments and interventions for those afflicted.

Genetic Predisposition and Heritability

Research provides strong evidence for an inherited predisposition (tendency) toward developing an eating disorder. In other words, eating disorders are often biologically inherited and tend to run in families. Recent research suggests that inherited biological and genetic factors contribute approximately 56% of the risk for developing an eating disorder. Individuals who have a mother or a sister with anorexia nervosa are approximately twelve times more likely to develop anorexia and four times more likely to develop bulimia than other individuals without a family history of these disorders. Studies of twins have shown a higher rate of eating disorders when they are identical (compared to fraternal twins or other siblings). Samples of DNA, the substance inside cells that carries genetic information, from pairs of siblings with eating disorders are now being analyzed to determine if they share genetic characteristics that are different from pairs of siblings without these disorders.

Neurobiological Mechanisms

Research has also focused on abnormalities in the structure or activity of the hypothalamus, a brain structure responsible for regulating eating behaviors. Studies suggest that the hypothalamus of bulimics may not trigger a normal satiation (feeling full or finished) response. So, even after a meal, these individuals do not feel full. A wealth of research suggests that several different neurotransmitters are involved in eating disorders. Before discussing the contributions of specific neurotransmitters to different disorders, it is important to provide a bit of background about the functioning of these chemicals.

Neurotransmitters carry messages from cell to cell throughout the brain and nervous system. Neurotransmitters released from one cell travel across a cellular space (called a synapse) and attach to another cell’s receptors. These receptors are specifically designed to receive certain neurotransmitters. In our brain and nervous system, multiple neurotransmitters are working simultaneously to control all sorts of functions such as mood, appetite, energy level, memory, etc. The effect of the neurotransmitter depends on the type of receptor being stimulated (i.e., whether it slows down or speeds up the receiving cell) as well as the part of the brain or nervous system that receives it. For example, serotonin (discussed below) can affect sleep, eating, temperature regulation, muscle movement, memory, and host of other behaviors depending on the specific receptors stimulated, and where in the body or brain those receptors are located. Be proactive about your health. Gauge your food habits with our Eating Disorder Quiz.

The neurotransmitter serotonin affects binging behavior in bulimics. These individuals often crave (and gorge) on foods rich in carbohydrates. The body converts sugars from carbohydrates, through a multi-step process, into tryptophan. Tryptophan is then used to create serotonin, which is partially responsible for the regulation of appetite, creating a sense of satiation, and regulating emotions and judgment. Thus, the binge behavior of bulimics may also be a response to low serotonin levels in the brain. A research team at the University of Pittsburgh found that individuals successfully treated for bulimia still had abnormally low serotonin levels, although other brain chemicals, such as dopamine and norephinephrine, were normal in comparison to individuals with no history of eating disorders. The successful treatment of bulimia with Prozac (a medication typically used for depression), which acts to increase the amount of serotonin in the brain, is additional evidence of the importance of this brain chemical.

Metabolic Factors and Eating Disorders

The intricate link between metabolism and psychiatric health has led to the recognition of “metabo-psychiatric disorders,” a term that underscores the intertwined nature of metabolic and psychological processes in conditions like eating disorders. Metabolic changes, whether as cause or consequence, play a significant role in the manifestation and outcome of eating disorders. These changes can influence eating behaviors, affect the success of recovery efforts, and even predispose individuals to the development of such disorders.

Central to the discussion of metabolic factors are hormones like leptin and ghrelin, which are pivotal in hunger and satiety signals within the brain. Leptin, a hormone produced by fat cells, signals the brain to reduce appetite when fat stores are sufficient, whereas ghrelin, secreted by the stomach, triggers feelings of hunger. Discrepancies in the levels or functioning of these hormones have been implicated in the abnormal eating behaviors seen in disorders such as anorexia nervosa and bulimia nervosa. For instance, individuals with anorexia may have higher than normal levels of leptin due to their body’s attempt to signal satiety and prevent further weight loss, even when fat stores are critically low.

The exploration of obesity genetics has revealed a surprising link to eating disorder risk. Certain genetic variants associated with obesity may also predispose individuals to binge-eating disorders, suggesting a shared genetic pathway that influences both conditions. This connection underscores the complex relationship between genetic factors related to body weight regulation and the development of eating disorders.

Understanding these metabolic factors sheds light on the multifaceted nature of eating disorders and holds the promise of developing more nuanced treatment and recovery strategies that address these underlying metabolic dysfunctions.

Additional Biological Factors

In the quest to understand the complex interplay of factors contributing to eating disorders, two additional biological aspects warrant close examination: sleep and circadian rhythms, and the influence of early life stress on the hypothalamic-pituitary-adrenal (HPA) axis. Additionally, the biological effects of exercise on eating behaviors and disorder recovery offer promising insights.

Sleep, Circadian Rhythms, and Eating Behaviors

Research has increasingly highlighted the intricate links between sleep patterns, circadian rhythms, and eating disorders. Circadian rhythms, the natural cycles of physical, mental, and behavioral changes that follow a 24-hour cycle largely influenced by light and darkness in an organism’s environment, play a crucial role in regulating hunger and satiety. Disruptions in these rhythms, such as those caused by inadequate or irregular sleep, can lead to altered eating behaviors, potentially exacerbating or triggering disordered eating patterns. Individuals with disrupted sleep patterns may experience hormonal imbalances affecting ghrelin and leptin, the hormones responsible for hunger and fullness, hence influencing their eating behaviors.

Early Life Stress and the HPA Axis

Early life stress, including trauma or persistent stress during childhood, can have a profound impact on the development and function of the hypothalamic-pituitary-adrenal (HPA) axis, a major part of the neuroendocrine system that controls reactions to stress and regulates many body processes, including digestion, the immune system, mood and emotions, and energy storage and expenditure. Dysregulation of the HPA axis has been associated with eating disorders, suggesting that early stressors can predispose individuals to these conditions. This dysregulation can lead to alterations in cortisol levels and other stress-related hormones, affecting appetite and stress-related eating behaviors.

The Role of Exercise in Recovery and Eating Behaviors

Exercise, while generally beneficial for mental and physical health, presents a nuanced picture in the context of eating disorders. On one hand, appropriate and moderate exercise can improve mood, reduce anxiety, and enhance the overall recovery process through its positive effects on the brain and body. On the other hand, excessive or compulsive exercise can serve as a symptom or exacerbating factor in eating disorders, particularly those characterized by a preoccupation with body image and weight control. Understanding the biological effects of exercise, including its impact on neurotransmitters, mood regulation, and body image perception, is crucial for incorporating physical activity into treatment plans effectively and safely.