In daily clinical practice, doctors tend to give less consideration to less important substances (such as vitamins) or phenomena (such as poisoning); while precisely these seemingly less important substances or phenomena may play an important role in some cases and even affect the patient’s regression (secondary contradictions can rise to become primary contradictions, which is the transformation of contradictions in the law of unity of opposites). I. Wernicke encephalopathy Wernicke encephalopathy ( Wernicke encephalopathy) was first discovered by Carl Wernicke in 1881, it is an encephalopathy caused by vitamin B1 (thiamine) deficiency, is an acute life-threatening neurological syndrome, composed of symptoms such as impaired consciousness (such as delirium), emotional indifference, retardation, delirium, oculomotor paresis and gaze (the third III and IV pairs of cranial nerve nuclei damage), nystagmus and balance disturbances (vestibular nuclei damage), ataxia (cerebellar cortical damage), and severe cis- and retrograde amnesia, sometimes fictitious. One of the common causes is thiamine deficiency associated with chronic alcoholism, and without immediate replacement therapy, patients are likely to progress to Korsakoff’s psychosis. Wernicke’s encephalopathy is often considered clinically when chronic alcoholism and some other causes of eating disorders exist, causing a triad of oculomotor abnormalities, ataxia, and impaired consciousness. Clinicians should have sufficient understanding of Wernicke’s encephalopathy, which is mainly due to vitamin B1 deficiency caused by long-term alcoholism, malnutrition, improper feeding and chronic gastrointestinal diseases. Vitamin B1 should be given promptly for treatment, and the condition often improves rapidly as a result. Note that glucose and corticosteroids are prohibited before vitamin B1 supplementation, because the latter two can slow down the oxidative decarboxylation of pyruvate, leading to thiamine deficiency and rapid deterioration of the disease. 1. The possibility of this disease should be considered when brain symptoms appear in susceptible individuals; Wernicke’s encephalopathy is often considered clinically when chronic alcoholism and other causes of eating disorders exist, causing the triad of abnormal eye movements, ataxia, and impaired consciousness. 2.The disease can be clearly diagnosed based on typical medical history, symptoms and signs combined with laboratory and MRI examinations; when the above symptoms and examination results are not typical, experimental treatment with drugs including vitamin B1 can be given, and if the symptoms are quickly relieved, the diagnosis can be clearly made and most of them do not leave sequelae. 3, pay attention to Wernicke encephalopathy treatment before the supplementation of vitamin B1 glucose and corticosteroids are prohibited, because the latter two can slow down the oxidative decarboxylation of pyruvate, leading to thiamine deficiency state, so that the condition deteriorates sharply. Although Wernicke’s encephalopathy is a fairly common diagnosis, it is often underdiagnosed or delayed, with unfortunate consequences, so clinicians should be aware of Wernicke’s encephalopathy. In conclusion, vitamin deficiency can cause major problems, while eating disorders and fasting are common clinical phenomena, and the connection between the two deserves our attention and consideration.