Somatic disorders are very closely related to depression; somatic disorders can lead to depression, and depression can not only cause worsening of the primary somatic disorder, but also increase the risk of suicide. The relationship between the two forms a worsening cycle. In general hospitals, somatic illness with depression is often not taken seriously. There are several cases of depression associated with somatic diseases: 1. central diseases cause depressive symptoms; 2. severe somatic diseases cause patients to fall into a state of extreme mental pain and psychological suffering, resulting in depressive symptoms; 3. somatic diseases cause depression due to a series of biochemical changes; 4. somatic diseases and depression have a common biochemical basis: homo-hemilight amines cause damage to blood vessel walls and increase blood viscosity on the one hand On the other hand, it can cause methylation deficiency, resulting in reduced synthesis of monoamines and depression. Depression due to neurological disorders in epilepsy: Studies have shown that the presence of 5-hydroxytryptamine receptor abnormalities in brain regions far from the abnormal discharge areas in epilepsy patients can cause depression. While antiepileptic drugs such as carbamazepine, lamotrigine, and valproate can increase postsynaptic 5-hydroxytryptamine secretion and improve depressive symptoms, barbiturates cause low folate levels, which in turn aggravate depression. In the use of antidepressants, because tricyclic antidepressants have anticholinergic and antihistamine effects, will aggravate seizures, should not be used cerebrovascular disease: after stroke, the brain frontal lobe, limbic system, thalamus and brainstem, blue spot nucleus and basal ganglia and other parts of the focal effect of destruction of norepinephrine neurons, 5-hydroxytryptamine neurons and their pathways, so that neuronal transmitter synthesis The effect is reduced, causing depressive symptoms. Parkinson’s disease: Parkinson’s disease patients with nigrostriatal degeneration, on the one hand, the reduction of dopamine neurons, on the other hand, the dysfunction of the blood affectin transporter causes depression, many Parkinson’s disease first is depression, at present, the effectiveness and safety of the use of antidepressants in patients with Parkinson’s disease, there is still no clear conclusion. Alzheimer’s disease: Alzheimer’s disease causes neuronal apoptosis leading to monoaminergic neuron deficiency, specifically in the blue spot nucleus noradrenaline and the mid-suture dorsal nucleus 5-hydroxytryptamine and nigrostriatal dopamine deficiency, causing depression. Some studies have shown that the proportion of depressed mood in Alzheimer’s disease patients is as high as 40%. Female patients, early age of onset, widowhood and aggression are risk factors for depressive disorders in Alzheimer’s patients. Depression due to endocrine disorders diabetes mellitus: patients with diabetes mellitus disease have important factors for depressive mood due to abnormal plasma cortisol caused by hyperglycemia. And depressive mood will make B-cell secretion of islet through hypothalamus, pituitary, and target gland axis to decrease, and increase the secretion of glucose rush, resulting in elevated blood glucose. Studies have shown that 15-20% of diabetic patients have major depression, in which the blood glucose is higher and the depressive symptoms are more obvious in patients with chronic complications, and the depressive symptoms are more serious in patients treated with insulin. Hyperthyroidism: Most patients present with a manic-like state, but with occasional anxiety, pessimism, and depressive symptoms. It should be noted that older patients present with apathetic expressions, unresponsiveness, weakness, and drowsiness, clinically referred to as having apathetic hyperthyroidism, which is highly likely to be misdiagnosed as depression. Cardiovascular disease myocardial choke: depression occurs in 15-30%. Cardiac disease causes reduced cardiac output, insufficient blood supply to the brain, manifesting a cluster of symptoms of brain failure, heart failure, angina pectoris attacks, episodes of tachycardia appear anxiety, fear, depression. Studies have shown that increased intima-media thickness, increased platelets and sexuality, reduced nitric oxide synthase levels and altered plasma catecholamine levels in patients with long-term depression can affect coronary heart attacks. The role of psychosocial factors in the development of cancer has been increasingly emphasized. Adverse psychological reactions and coping styles of cancer patients have a serious impact on the progression of their disease and survival. The side effects of cancer diagnosis and treatment are distressing and long-lasting, such as fatigue, pain, social isolation, relationship problems, and fear of recurrence and death. Negative emotions of cancer can also affect the neuroendocrine system, including the hypothalamic-pituitary-adrenergic axis and sympathetic nervous system, which are important factors in depression. Some depression in somatic diseases can be improved and remitted with somatic diseases. In most cases, the physical illness has been healed, but the depression will not get better. In this case, treatment is even more important. However, it is advisable to use antidepressants in small doses, try to use new antidepressants and use tricyclic antidepressants less often, and at the same time, fully consider the relationship between antidepressant side effects and somatic diseases so that drug side effects do not aggravate medical diseases. Medication should be intervened early, and interrupting the vicious circle between somatic diseases and depression is the key to treatment.