The Two-Way Link Between Mood Disorders and Obesity: Pathogenesis, Clinical Manifestations, and Intervention Strategies

I. Overview A dysthymic disorder, also known as an affective disorder or mood disorder, refers to an exaggeration, confusion, or reduction of normal emotional responses. Determining whether an emotional response is normal or pathological requires considering three conditions: the intensity of the emotional response, its duration, and whether it is consistent with the surrounding environment. Dysthymic disorders are a group of mental illnesses that occur in childhood and adolescence, characterized primarily by anxiety, phobias, and depression. Even minor triggers can induce illness, sometimes leading to irreversible destructive situations and losses. Due to the physiological and psychological development and age characteristics of children, their clinical manifestations differ significantly from adult neuroses, and are currently generally referred to as dysthymic disorders. Epidemiological data shows that the incidence of childhood mental and behavioral disorders is as high as 10%–20%, with dysthymic disorders being one of the important mental disorders. Research results indicate that dysthymic disorders are more likely to occur in adolescence, and girls are more prone to them, although the gender difference remains controversial. Anxiety disorders are the most common type of dysthymic disorder in children. Studies have shown that dysthymic disorders can increase the risk of obesity; chronic stress, anxiety, and depression can lead to obesity. Obese individuals have a higher risk of developing anxiety disorders than the general population, demonstrating that obesity and mood problems can be mutually causal. Scholars studying the relationship between obesity and mental disorders believe that a major reason is the abnormal eating behavior caused by mental disorders. Under stress, people tend to relieve their emotions through food, especially choosing high-sugar and high-fat foods. Coupled with a lack of physical activity, this excessive energy intake further exacerbates obesity. II. Pathophysiological Changes 1. Pathogenesis of Mood Disorders From a biological perspective, neurotransmitters and genetics have significant influences on depression, especially neurotransmitters. For example, a deficiency in neurotransmitters like serotonin is often associated with depression and is considered one of the main causes. Serotonin's precursor, tryptophan (Trp), is an essential amino acid that the body cannot synthesize and must obtain from food. A lack of tryptophan alters brain chemistry and mood. Like serotonin, a decrease in norepinephrine is also a cause of depression. 2. Possible Pathogenesis of Obesity and Mood Disorders Multiple mechanisms, including hypothalamic-pituitary-adrenal (HPA) axis dysregulation, the role of anti-inflammatory factors, antidepressants, and sociopsychological factors, have confirmed that obesity is related to depression. (1) HPA Axis Dysregulation: The HPA axis is a complex system that regulates the secretion of corticosteroids. Stress stimulates the hypothalamus to secrete corticotropin-releasing hormone (CRH), which in turn stimulates the anterior pituitary to release adrenocorticotropic hormone (ACTH). ACTH then stimulates the adrenal glands to secrete cortisol. Cortisol flows through the bloodstream and affects the release of CRH through a negative feedback mechanism, which in turn activates the HPA axis. Chronic stress leads to a long-term activated state of the HPA axis, resulting in HPA axis dysfunction. HPA axis dysfunction is associated with both obesity and depression. Various neurons, hormones, and anti-inflammatory factors play important roles in the development of obesity and depression by regulating the HPA axis. Elevated cortisol levels lead to increased carbohydrate and fat intake while reducing energy expenditure. Sustained elevated cortisol levels also promote the accumulation of abdominal fat, leading to obesity. Elevated cortisol levels affect systemic obesity by influencing leptin secretion. Leptin stimulates the activation of the HPA axis by influencing cortisol production. Obese patients have elevated leptin levels, which makes the HPA axis insensitive to leptin, thus leading to depression. (2) Anti-inflammatory factors: Anti-inflammatory factors are also closely related to the function of the HPA axis. Many anti-inflammatory factors have a stimulating effect on the activation of the HPA axis. Tumor stimulating factor, interleukin-1E, interleukin-6, and C-reactive protein are all associated with obesity and depression. Elevated anti-inflammatory factors in obese individuals are associated with depressive symptoms such as anhedonia and increased sleep. (3) Psychosocial factors: Social factors have the same psychological and physical stress on overweight children, including social isolation and peer relationship disorders. Overweight and obese individuals frequently face direct discrimination, negative judgment, and social isolation, enduring physical inconvenience or hardship. Obese children often develop depression due to isolation. Eating is the most common coping mechanism for this discrimination, thus exacerbating obesity. III. Clinical Manifestations: Common mood disorders include emotional blunting, elevated mood, depressed mood, mood inversion, emotional outbursts, pathological passion, and anxiety/pharmacology, among others. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) of the American Psychiatric Association, depression is classified as a mood disorder, including major depressive disorder and dysthymic disorder. Major depressive disorder is characterized by one or more major depressive episodes, i.e., a period of at least two weeks of depressed mood or loss of interest and joy, accompanied by at least four of the following depressive symptoms: ① Mood is often described by the individual as depressed, sad, hopeless, frustrating, or a general loss of interest or joy; appetite is usually reduced, but may also increase appetite and cravings for specific foods; insomnia or excessive sleep (hypnotics); ② Psychomotor changes including agitation or retardation; ③ Decreased volume, intonation, amount of speech, and variability of content of speech, even muteness; loss of energy and fatigue; feelings of worthlessness or guilt. Mild depressive disorder is characterized by at least two years of depressed mood, during which there are more days of depressed mood than non-depressed days, accompanied by multiple depressive symptoms. IV. Treatment and Prognosis Currently, treatment for mood disorders includes psychotherapy, pharmacology, physical therapy, and traditional Chinese medicine. Psychotherapy is an essential treatment for mood disorders; mild mood disorders can be significantly improved with psychotherapy alone. For obese patients with concurrent mood disorders, in addition to routine dietary control, exercise therapy, and medication, emphasis should be placed on cognitive behavioral interventions and mental and psychological support. Appropriate health education for obese patients can improve their understanding of obesity, enabling them to control and intervene in their own behavior, thus more effectively maintaining weight loss. Treatment for obese patients should not only focus on changing weight and other numerical values, but also on the underlying causes of obesity. They need to be treated with utmost respect, requiring more patient listening and the establishment of trust between doctor and patient, along with more praise and encouragement.