The relationship between obesity and tumors, and its impact on bones and joints, diabetes, and gallstones.

Is there a link between obesity and cancer? Why are obese women more prone to endometrial cancer?

Cancer poses a significant threat to human health, and in recent years, the incidence of cancer has been on the rise in many countries. The relationship between obesity and tumors has been a focus of medical experts since the late 1950s. Numerous studies and animal experiments have shown that obese men who are 40% or more overweight have a significantly higher incidence of colon and rectal cancer; while obese women have a much higher incidence of gallbladder, bile duct, endometrial, cervical, uterine, and ovarian cancers than non-obese women. Furthermore, even among breast cancer patients and other malignant tumor patients, obese individuals show more severe cancerous tissue infiltration, a higher rate of metastasis of undifferentiated cell types, and a higher rate of recurrence after surgery. The survival rate for obese patients to five years after surgery is 56%, compared to 80% for non-obese patients.

The occurrence of tumors is related to abnormal immune function in the human body. People with weakened cellular immunity are more susceptible to various malignant tumors. Whenever a cell in the body becomes cancerous, its cell membrane will display specific antigens, and the body's immune cells will kill these cells carrying tumor antigens. When the body's cellular immune function is low, the body's self-defense mechanism weakens, and tumor cells proliferate.

The exact reasons for the high cancer incidence in obese patients are not fully understood, but excessive fat accumulation in obese women leads to abnormal metabolism of estrogen and androgen secreted by the adrenal glands and ovaries, which may significantly impact the development of breast cancer and endometrial cancer. This could be a carcinogenic factor.

Obese patients often have hyperlipidemia, which can accelerate blood clotting and reduce fibrinolytic activity, making it easier for tumor emboli to form in blood vessels. Cancer cells within these emboli are not easily killed by immune cells in the blood and are more likely to travel throughout the body with the bloodstream, thus increasing the chance of cancer cell metastasis.

In addition, obese individuals often have high cholesterol and hyperinsulinemia, which increases cholesterol levels in immune cells, leading to a decline in the body's immune system's ability to kill tumor cells. On the other hand, insulin inhibits the phagocytic function of immune cells; at the same time, insulin also promotes cell proliferation, so if cells in the body become cancerous, it will also promote the proliferation of cancer cells.

It is evident that obesity impairs the body's immune function and has the adverse effect of promoting the occurrence and development of malignant tumors. Therefore, changing dietary structure, reducing energy intake, controlling weight gain, and avoiding obesity are beneficial for cancer prevention, cancer treatment, and longevity.

It is widely known that obese individuals are prone to cardiovascular diseases such as atherosclerosis, coronary heart disease, and stroke. In women, obesity is also closely related to the development of certain gynecological tumors, particularly endometrial cancer. This is mainly due to hormonal imbalances in women, with estrogen being a major contributing factor. If a woman synthesizes excessive amounts of sex hormones, the excess estrogen is converted into lipids and stored in adipose tissue, increasing the estrogen storage in fat cells. Simultaneously, the estrogen stored in fat cells can be continuously released into the bloodstream, exerting a sustained effect on the endometrium. Under long-term stimulation by estrogen, the endometrium is more susceptible to cancerous transformation.

According to foreign reports, the incidence of endometrial cancer is related to obesity. More than one-third of women with moderate to severe obesity are at risk of developing endometrial cancer. Furthermore, the prognosis of endometrial cancer is closely related to obesity levels; severely obese women have a poor prognosis. In addition to obesity, endometrial cancer patients often experience infertility, diabetes, menstrual irregularities, delayed menopause, and polycystic ovary syndrome. This series of clinical manifestations is medically termed "endometrial cancer syndrome."

Obesity is a high-risk factor for endometrial cancer. To reduce the incidence of endometrial cancer, it is necessary to control obesity and reduce its severity. However, worryingly, the number of overweight children is increasing, and 80% of obese teenage girls develop adult obesity, which is often severe and difficult to treat. Therefore, controlling the weight of young girls and adolescents is beneficial for preventing obesity and is one of the measures to reduce the incidence of endometrial cancer.

Menopausal women experience reduced daily physical activity and energy expenditure, while having more rest time and higher dietary requirements, leading to excess calorie intake. These factors can all contribute to menopausal obesity. Therefore, women entering menopause should engage in regular and appropriate physical exercise to control the occurrence and development of obesity and prevent the development of endometrial cancer.

Currently, the main treatments for endometrial cancer include surgery, radiation, chemotherapy, and integrated traditional Chinese and Western medicine. At the same time, patients should actively treat and control obesity, choose a low-calorie, high-protein, and low-carbohydrate diet, and engage in appropriate physical exercise.

Why are obese people more prone to bone and joint diseases? Is there a relationship between gout and obesity?

Many obese individuals develop osteoarthritis. This is mainly related to mechanical stimulation and metabolic disorders. Mechanical stimulation refers to the increased pressure on joints due to excessive weight, leading to proliferative changes in the joints. Metabolic disorders refer to impaired glucose, lipid, and purine metabolism in obese patients, causing osteoarthritis and related complications. Middle-aged and older obese individuals are highly susceptible to degenerative changes in their joints, resulting in osteoarthritis.

Obese individuals often experience lower back pain, knee pain, and ankle pain, and may develop flat feet. X-rays reveal bone spurs in the lumbar spine, knees, and ankles, a condition known as osteoarthritis. Osteoarthritis, particularly spinal osteoarthritis, is a common complication of obesity, with an alarmingly high incidence rate; this problem was already noted in the 1930s. Clinical observations indicate that over 50% of patients with osteoarthritis are obese middle-aged individuals.

Why are obese people prone to osteoarthritis? The reasons are not yet fully understood, but in terms of obesity itself and osteoarthritis, it is clearly related to long-term excessive weight load. Joints such as the waist, knees, and ankles are the main support points for the body's weight. In obese patients, because their weight exceeds the supporting capacity of bones and tendons, the load on the articular cartilage is increased, causing it to wear and tear more severely. This leads to changes in the structure within the joint, thus resulting in osteoarthritis.

When obese individuals suffer from osteoarthritis, their joints become swollen or deformed, forcing them to reduce their activity levels. If their activity levels decrease while their diet remains the same, their weight will increase further, putting even more pressure on their joints and worsening the osteoarthritis. Therefore, obese patients with osteoarthritis should start by losing weight. As their weight decreases, the pressure on their joints also decreases, their symptoms will gradually lessen, and they will be able to move more freely.

In addition, obese individuals with diabetes may develop diabetic osteoarthritis. 85% of diabetic patients were obese before the onset of the disease. This type of osteoarthritis is a neurogenic arthropathy, primarily affecting unilateral lower limbs and distal joints, with a relatively high incidence in the metatarsophalangeal joints. It rarely involves the spine. The main characteristics of this disease are local ulceration and gangrene. X-rays may show signs of bone destruction in the joints. Treatment for this type of patient should focus on both weight loss and diabetes management, timely control of the primary disease, improvement of local symptoms, and prevention of new lesions.

Gout is a group of diseases caused by purine metabolism disorders. Its clinical features include hyperuricemia accompanied by recurrent attacks of acute gouty arthritis, tophi deposition, chronic tophaceous arthritis, and joint deformities. It often affects the kidneys, causing chronic interstitial nephritis and uric acid kidney stones. Normal serum uric acid levels range from 119 to 237.9 μmol/L; levels above 237.6 μmol/L are considered hyperuricemia. The incidence of gout is 1.1% for individuals with serum uric acid levels between 237.9 and 359.1 μmol/L, and 83.3% for those with levels above 359.1 μmol/L. Gout is also a complication of obesity. Obese individuals have a three times higher prevalence of hyperuricemia than non-obese individuals; the higher the degree of obesity, the higher the serum uric acid level, and the higher the prevalence of gout. Some reports indicate that among those who are less than 20% overweight, approximately 9.2% have hyperuricemia; those who are 20-40% overweight account for approximately 9.4%; and those who are more than 40% overweight account for up to 20%.

Gout is common in obese patients with excessively rich diets because high-protein foods contain purines. Long-term excessive intake leads to an increase in purines in the body. The final product of purine metabolism is uric acid. When uric acid levels exceed the kidneys' excretion capacity, it causes hyperuricemia. Uric acid deposits as urate crystals in joints and cartilage, causing inflammation and a foreign body reaction at the affected sites, resulting in bone and joint damage-a condition known as gouty arthritis.

To prevent gout in obese individuals, it's advisable to reduce the intake of purine-rich foods, such as animal organs like liver, kidneys, intestines, and brain, which are high in protein. A low-fat, low-calorie, and bland diet is preferable. Drinking plenty of water is also important, maintaining a daily urine output of over 2000 ml to facilitate uric acid excretion. During acute attacks, medications such as nitroglycerin and indomethacin can be used to relieve the symptoms.

Does obesity cause diabetes and gallstones?

The link between obesity and diabetes is well-known. Diabetes is a metabolic disorder complication in obese patients. Long-term, persistent obesity significantly increases the incidence of diabetes. Some statistics show that the incidence of diabetes in the normal population is 0.7%; the incidence is 2% for those over 20% of their ideal weight; and the incidence reaches as high as 10% if the weight exceeds the ideal weight by 50%.

Insulin is the only hormone in the human body that lowers blood sugar, and absolute or relative insulin deficiency is the main cause of diabetes. Tests on plasma insulin levels in obese patients have revealed that obese patients with diabetes have significantly higher plasma insulin levels than diabetic patients of normal weight, and even higher than normal individuals; obese patients with normal blood sugar levels have even higher plasma insulin levels, approximately four times that of normal individuals. Pathological examinations have also confirmed hypertrophy and proliferation of insulin-secreting β-cells in obese individuals, suggesting reduced insulin activity and insulin resistance. Further research has found that the main reason for this reduced activity is the enlargement of fat cells in obese patients, which significantly reduces the number of insulin receptors on the cell surface or weakens their binding capacity to insulin. Therefore, it can be inferred that in the early stages of obesity, enlarged fat cells reduce insulin activity. To maintain normal blood sugar levels, pancreatic β-cells proliferate and hypertrophy, increasing insulin secretion. Long-term obesity damages pancreatic β-cells due to overload, resulting in insufficient insulin secretion and inducing diabetes. Thus, obesity itself is one of the causes of diabetes, and in clinical observation, obesity is often a precursor to diabetes. If weight is lost as early as possible, the above situation can be significantly improved, and plasma insulin levels can also decrease.

Cholelithiasis is a disease characterized by the formation of stones in any part of the gallbladder and bile ducts. The main chemical components of gallstones are cholesterol stones and pigment stones. In obese individuals, the incidence of gallstones increases with the degree of obesity; the incidence is higher in obese people than in those of normal weight, with men being twice as likely and women nearly three times as likely. The stones associated with obesity are primarily cholesterol stones. Why are obese patients prone to gallstones? This is because obese individuals often have hypercholesterolemia, leading to increased cholesterol secretion from the liver and a corresponding increase in cholesterol content in bile. Due to abnormal cholesterol metabolism, coupled with reduced physical activity in obese individuals, cholesterol stones are easily formed. The presence of stones in the gallbladder or bile ducts obstructs bile flow; if infected by bacteria, cholecystitis (cholecystitis) can occur.