Chapter 43: Obesity and Cancer, Gout, Lower Limb Edema and Gastrointestinal Function
14. Obesity and Cancer
Obesity increases the risk of certain cancers. The relationship between obesity and tumors can be analyzed comprehensively from multiple aspects, including hormone levels, fat distribution, dietary structure, and age. Sustained elevation of estrogen can chronically stimulate abnormal proliferation of the breast and endometrium (especially in postmenopausal women), increasing the incidence of breast and endometrial cancer. Obese individuals have higher estrogen concentrations and lower progesterone concentrations, therefore, the incidence of breast and endometrial cancer in obese women is 3-4 times higher than in non-obese individuals. Furthermore, obese women experience increased estrogen and oxytocin levels due to fat accumulation stimulating the endocrine system. In women sensitive to these two hormones, they may be carcinogenic, increasing the risk of breast and cervical cancer.
Obese men have an increased incidence and mortality rate of anal and rectal cancer and prostate cancer, while obese women have an increased incidence and mortality rate of gallbladder cancer, cervical cancer, endometrial cancer, and breast cancer. Excessive fat accumulation on the abdominal wall and mesentery hinders normal intestinal peristalsis, making it difficult to excrete digested food residue, thus leading to constipation. Once constipation occurs, intestinal contents cannot be expelled in a timely manner, and carcinogens remain in the body for too long, potentially leading to colon and rectal cancer.
The more severe the obesity, the higher the incidence of the aforementioned cancers. Furthermore, abdominal obesity increases the risk of postmenopausal breast cancer.
The main reason why obese people are more prone to cancer is that they often have hyperinsulinemia and hypercholesterolemia, which leads to a decline in the body's immune function.
15. Obesity and Gout
Gout is a metabolic disease caused by long-term purine metabolism disorder. Obese people are prone to developing gout, and gout patients are often obese. Like obesity, gout is increasing year by year as people's nutritional levels improve.
Gout is a disease characterized by long-term purine metabolism disorder, caused by tissue damage due to elevated uric acid levels in the blood. Clinical manifestations include hyperuricemia, recurrent acute arthritis attacks, tophi formation, joint deformities, renal parenchymal damage, and renal uric acid stones.
Purines are products of nucleic acid metabolism in the body and an important component of food. They are mainly derived from protein-rich foods, such as animal organs like the heart, liver, and kidneys; seafood like fish roe, sardines, and oysters; and pharmaceuticals like yeast, all of which contain significant amounts of purines or purine precursors.
Purines are converted into uric acid in the blood and excreted through the kidneys. If uric acid intake exceeds excretion, the level of sodium urate in the blood rises and deposits in tissues, primarily joints and cartilage, causing inflammation and gout. Acute gout attacks can cause redness, swelling, and severe pain in the joints, most commonly the big toe, along with chills and high fever, significantly impacting the patient's quality of life. Uric acid can also deposit in the kidneys, causing chronic nephritis or kidney stones. The prevalence of gout is three times higher in obese individuals than in non-obese individuals, and blood uric acid levels are directly proportional to weight and body mass index.
It is worth noting that women with abdominal obesity are more prone to gout, and the higher the waist-to-hip ratio, the higher the incidence of gout. Obesity can affect blood uric acid levels in the following ways:
(1) Obese people’s diet contains too much high-purine food, such as animal organs, seafood, soybeans, etc., as mentioned above. In addition, their food intake is much larger than that of ordinary people, so the intake of purines is much greater, and the synthesis of uric acid also increases accordingly.
(2) Obese individuals have insulin resistance, which can lead to a decrease in the kidney's clearance of urine and a reduction in uric acid excretion.
(3) During the weight loss process, obese people often consume high-protein, low-fat, and low-sugar foods, which increases the endogenous purine sources. In addition, ketone bodies are easily produced, which reduces the excretion of uric acid in urine.
Several factors combined make it easier for obese individuals to have higher blood uric acid levels than the average person, thus obesity can cause gout. Therefore, obese patients with a history of gout should strictly control their weight, but avoid high-protein foods. While restricting calories, they can appropriately increase the proportion of carbohydrates, adopting a diet that is low in purines, calories, fat, and sugar.
16. Obesity and lower extremity edema
Obesity can easily cause lower limb edema, especially in women. Lower limb edema can occur if a woman's weight exceeds the standard weight by 20%.
The patient's lower limbs not only become thickened, but pressing on the skin with a finger leaves an indentation that takes a long time to heal. In some patients, the edema fluctuates with the menstrual cycle, significantly worsening before menstruation. Some patients even experience edema in other areas, such as the eyelids, abdomen, and breasts.
The reason why lower limb edema occurs in obese individuals is as follows: In normal individuals, there is a pressure balance between the blood inside the blood vessels and the tissue fluid outside the blood vessels, so there is only a certain amount of water in the interstitial spaces, which does not manifest as edema. When the pressure balance of fluid inside and outside the blood vessels is disrupted, too much water flows out of the blood vessels into the interstitial spaces, thus manifesting as edema. In obese individuals, increased adipose tissue in the lower limbs weakens the support for superficial veins, making blood vessels more prone to dilation and increasing water permeability, allowing water to easily seep into the interstitial spaces. Increased adipose tissue in the lower limbs can also weaken the assisting role of muscles in venous return, making blood vessels more prone to dilation and increasing water permeability, allowing water to easily seep into the interstitial spaces. Increased adipose tissue in the lower limbs can also weaken the assisting role of muscles in venous return, increasing venous pressure and forcing water out of the blood vessels into the interstitial spaces. In addition, estrogen is produced in adipose tissue, and obese women often have excessively high estrogen levels, which can also increase capillary permeability, promoting water outflow and aggravating edema. Therefore, edema in female patients can be significantly worse before menstruation. Due to gravity, this type of lower limb edema can worsen with increased upright activity and improve with lying down and rest. In severe cases, excessive fluid loss can lead to insufficient blood volume, requiring significant fluid replenishment. This excessive water retention can cause weight gain, with nighttime weight gain potentially exceeding morning weight by up to 1 kilogram. It should be noted that this type of edema is physiological and can be controlled through weight loss. Exercise can enhance muscle function in assisting venous return, helping to reduce lower limb edema.
17. Obesity and Gastrointestinal Function
It's common to hear obese people lament, "I eat so much because my stomach is much bigger than others, and I'm so fat probably because my stomach's absorption function is better than others." Indeed, the gastrointestinal tracts of obese people differ from those of normal-sized individuals, as manifested in the following ways:
(1) Obese people have a larger stomach capacity than ordinary people and can hold more food.
(2) Obese people also have a faster gastric emptying rate after eating than ordinary people, that is, food passes through the stomach and enters the intestines faster, which makes them more prone to feeling hungry. However, after dieting to lose weight, the above changes can return to normal levels.
(3) Obese individuals have lower gastric juice secretion capacity and lower gastric acid secretion volume after eating than those of normal weight. However, when stimulated by a hormone called gastrin, obese individuals actually secrete more gastric acid than those of normal weight. This indicates that obese individuals have not lost their ability to secrete gastric acid, but rather that it has been inhibited in some way.
(4) Obese individuals exhibit altered insulin and gastrointestinal hormone levels, resulting in poor insulin response, insulin resistance, and consequently hyperinsulinemia. In some obese individuals, the level of glucagon secreted by the pancreas is also elevated. Since glucagon is the primary glucose-raising hormone and has an antagonistic effect on insulin, the elevated glucagon levels in obese individuals may also be a response to insulin resistance and hyperinsulinemia. Some suspect that obese individuals also exhibit glucagon resistance, leading to elevated glucagon levels. Obese individuals have lower levels of pancreatic polypeptides than normal individuals and respond less effectively to food intake. Since the function of pancreatic polypeptides is to induce a feeling of satiety, low pancreatic polypeptide levels may be one of the reasons for the increased appetite in obese individuals.
In short, for various reasons, the stomachs of obese people are often "larger" than those of people with normal weight; and the "large stomach" causes obese people to consume more food than people with normal weight, which in turn creates a vicious cycle.