An Exploration of the Traditional Chinese Medicine Mechanisms of Organ Dysfunction and Obesity Formation

Excessive Heat in the Spleen and Stomach. The spleen and stomach are the foundation of acquired constitution; one is responsible for receiving and digesting food, and the other for transporting and distributing the essence of food. When the spleen and stomach are overactive, leading to excessive hunger and overeating, the essence of food cannot be properly transported and transformed into turbid fat and phlegm, stagnating in the skin and internal organs, resulting in obesity. As Li Dongyuan stated in his *Treatise on the Spleen and Stomach*: "When both the spleen and stomach are strong, one can eat a lot and become fat." Weakness of the Spleen and Stomach. Normal digestive, absorptive, and transport functions of the spleen and stomach ensure that qi and blood are not only generated but also transported and transformed normally. If the spleen and stomach are weak, qi and blood will be deficient, and yin and yang will be imbalanced, leading to obesity. "When both the spleen and stomach are weak, one cannot eat and becomes thin, or eats little and becomes fat, and although fat, the limbs are weak" (Li Dongyuan, *Treatise on the Spleen and Stomach*).

Liver dysfunction. Emotional imbalance disrupts the liver's function of regulating qi, leading to stagnation of liver qi, which then invades the stomach, impairing the spleen and stomach's digestive functions. This can result in impaired water metabolism, or stagnation of liver and gallbladder qi causing abnormal bile secretion and excretion, leading to the accumulation of turbid fats and obesity. Spleen and kidney yang deficiency. Spleen yang deficiency impairs the transformation and transportation of food essence, causing phlegm, dampness, and turbid fats to accumulate, resulting in obesity, as the saying goes, "spleen deficiency leads to excessive phlegm" and "obese people have a lot of phlegm." Kidney yang deficiency impairs the transformation and transportation of qi and water, failing to warm and assist the spleen and stomach's digestive functions, which can also lead to phlegm, dampness, and obesity. Old age and declining qi. As people age, the functions of the internal organs decline, causing the five flavors of food to fail to be transformed into essence, accumulating into phlegm, dampness, and turbid fats, resulting in obesity. Modern medicine believes that the occurrence of simple obesity is mainly related to genetic, dietary, environmental, exercise, mental, and physiological factors.

Obesity is fundamentally caused by an excess of energy intake compared to energy expenditure, with the remaining energy accumulating in the body as fat. The causes of obesity are very complex and not yet fully understood. Several factors need to be considered, such as genetics, the nervous system, dietary and lifestyle habits, metabolic disorders, and endocrine imbalances. It is generally believed to be the result of the combined effects of multiple factors. These factors can be broadly categorized into genetic factors and environmental factors. Environmental factors include dietary habits, lifestyle habits, exercise levels, and socioeconomic status.

Maintaining a normal body weight depends on negative feedback regulation of body weight. In this negative feedback regulatory loop-the loop connecting the weight regulation point (located in the central nervous system) with food intake and tissue metabolism-a problem in any link will lead to an alteration in the regulatory outcome, resulting in obesity. Genetic factors also play a role. Obesity is often related to genetics. In life, we often see that some individuals and families have a higher susceptibility to obesity than others. Statistics show that if both parents have normal weight, the incidence of obesity in their children is 10%; if one parent is obese, the incidence rate in their children is 40%–50%; and if both parents are obese, 60%–70% of their children will be obese.

Identical twins, growing up in the same environment, have similar weights; if one twin is obese, the other will be obese in 90% of cases. Even when growing up in different environments, the weight difference between them is smaller than that between fraternal twins. This familial tendency indicates that obesity has a significant heritability. Obesity in obese patients is hereditary, and the location of fat distribution and bone structure are also hereditary. The hereditary tendency for obesity is also manifested in an increased number and/or volume of fat cells. Of course, in addition to genetic factors, the familial tendency for obesity is also closely related to the similar dietary structure and lifestyle habits within the same family.

As research into the etiology of obesity deepens, the role of genetic factors in its development is receiving increasing attention. Obesity is considered to be caused by an excess of energy intake over expenditure in individuals with a genetic predisposition. This genetic susceptibility results from the abnormal expression and combined effects of multiple genes and related factors, primarily affecting the hypothalamus in the central nervous system and adipocytes in the periphery. The influence of genetic factors on energy and nutrient intake: Studies have shown that energy and nutrient intake exhibit clear familial characteristics; the closer the kinship, the more similar their energy intake and nutrient choices.

For example, twins often have very similar calorie and nutrient intake, and monozygotic twins are even more similar than dizygotic twins. This indicates that genetic factors can influence calorie and nutrient intake. Feeding is regulated by the nervous system, with the center for regulating feeding located in the hypothalamus. The ventromedial hypothalamus (VMN) and lateral hypothalamus (LHA) are the two major nuclei regulating feeding; the LHA and VMN are respectively referred to as the "hunger center" and the "satiety center." Electrical stimulation of the VMN can immediately stop a hungry animal from eating, while disrupting the VMN can increase food intake and lead to obesity.

Conversely, stimulating the LHA with electrodes significantly increases food intake in animals; while destroying the LHA with electrodes significantly reduces food intake, leading to emaciation. The regulatory mechanisms of the "hunger center" and "satiety center" are quite complex, and many peptides can regulate their activity. Differences in the levels of these peptides will lead to differences in appetite among individuals, and genetic factors can influence the levels of these peptides, thereby affecting the intake of energy and nutrients. Peptides that promote appetite include: dynorphin, β-endorphin, growth hormone neuropeptide, growth hormone-releasing hormone, neuropeptide Y, and somatostatin; peptides that inhibit appetite include: anorexia nervosa, bufotoxin, calcitonin, cholecystokinin, corticotropin-releasing hormone, glucagon, insulin, neurotensin, oxytocin, thyrotropin-releasing hormone, and vasopressin.