hereditary obesity
Introduction
Introduction to hereditary obesity Hereditary obesity mainly refers to obesity caused by changes in genetic material (chromosomes, DNA), which is extremely rare and often has a tendency to familial obesity. The incidence of obesity is highlighted in three stages: infancy, puberty, and adulthood over 40 years of age. Most of the infants and adolescents can develop into adult obesity, and the degree of obesity is heavier. basic knowledge The proportion of illness: 10% Susceptible people: no special people Mode of infection: non-infectious Complications: fatty liver, cerebral arteriosclerosis, hypertension
Cause
Causes of hereditary obesity
Obesity caused by changes in genetic material (chromosomes, DNA).
Prevention
Hereditary obesity prevention
Obesity should be based on prevention, and people should be made aware of their risks and keep their weight as normal as possible. Prevention of obesity should begin in childhood. At present, obesity is understood as "the normal physiological process in the pathological environment", and the main reason for the increase in the prevalence of obesity is the environment, not the "pathological" effect of metabolic defects or the mutation of individual genes. Since the factors of the body are immutable, it is necessary to control the rise in body weight by regulating lifestyle, that is, a reasonable diet and appropriate physical activity. Based on this new concept, governments are committed to promoting healthy lifestyles and universal prevention programs.
Complication
Hereditary obesity complications Complications, fatty liver, cerebral arteriosclerosis, hypertension
Skin wrinkles are prone to dermatitis, rubbing, and easy to combine with purulent or fungal infections, obesity chronic dyspepsia, fatty liver, mild to moderate liver dysfunction are also more common, concurrent with atherosclerosis, high blood pressure and so on.
Symptom
Hereditary obesity symptoms Common symptoms Male obesity Concentric obesity Secondary obesity Diabetes Hypertension Atherosclerotic amenorrhea
1. General performance:
Simple obesity can be seen at any age, juvenile type is obese since childhood; adult type is more common in 20 to 25 years old; but clinically, 40 to 50 years old middle-aged women are more, and 60-70 years old or older are also It is not uncommon to see that about 1/2 adult obese people have a history of childhood obesity, generally with a slow increase in body weight (except after women give birth), and the body weight increases rapidly in a short period of time. Secondary obesity should be considered. Male fat distribution is in the neck and trunk. The main part is the head and the head, while the female is mainly the abdomen, lower abdomen, chest breasts and buttocks.
The characteristics of obese people are that they are short and fat, round and round, narrow and wide on the face, double squat, neck short and thick, and the skin folds of the backrest headrest are obviously thickened, chest circumference and intercostal space are not obvious. The milk is thickened by the thickening of the subcutaneous fat. When standing, the abdomen protrudes forward and is higher than the plane of the chest. The umbilicus is deep concave. In a short period of time, the obese person is on both sides of the lower abdomen, and the upper thigh and the upper part of the upper arm and the outer side of the buttock are visible with purple lines or White lines, the child's obese external genitalia is buried in the subcutaneous fat of the perineum and the penis appears small and short, the fingers, toes are short and short, the back of the hand is thickened by the fat and the skin of the metacarpophalangeal joint is sunken, and the bony is not obvious.
Mild to moderate primary obesity may have no symptoms. People with severe obesity are more afraid of heat, have decreased mobility, and even have mild shortness of breath during activities. They may have snoring during sleep, and may have hypertension, diabetes, gout, etc. Clinical manifestations.
2. Other performances:
(1) Obesity and cardiovascular system : obesity patients with coronary heart disease, the risk of hypertension is significantly higher than non-obese, the incidence is generally 5 to 10 times higher than non-obese, especially the central obesity with high waist-to-hip ratio Patients, obesity can cause cardiac hypertrophy, thickening of the posterior wall and interventricular septum, cardiac hypertrophy with blood volume, intracellular and intercellular fluid increase, ventricular end-diastolic pressure, pulmonary artery pressure and pulmonary capillary wedge pressure are increased, some obese people exist Impaired left ventricular function and obesity myocardial disease, the incidence of sudden death in obese patients is significantly increased, may be related to myocardial hypertrophy, arrhythmia caused by fat infiltration of cardiac conduction system and the occurrence of cardiac ischemia, hypertension in obese patients Very common, but also a major risk factor for heart and kidney disease, blood pressure will recover after weight loss.
(2) Respiratory function changes in obesity: obesity patients have reduced lung capacity and decreased lung compliance, which can lead to a variety of pulmonary dysfunction, such as obesity hypoventilation syndrome, clinical sleepiness, obesity, alveolar hypoventilation Characteristics, often accompanied by obstructive sleep apnea, severe cases can cause pulmonary heart syndrome (Pickwickian's syndrome), due to thickening of adipose tissue in the abdominal and chest wall, increased diaphragm muscles and decreased lung capacity, poor lung ventilation, causing post-activity breathing Difficulties, severe cases can lead to hypoxia, cyanosis, hypercapnia, and even pulmonary hypertension leading to heart failure, such heart failure often poor response to cardiotonic agents, diuretics, in addition, severe obesity, can still cause sleep apnea, even See the report of death.
(3) Sugar, fat metabolism of obesity : excessive consumption of calories promotes the synthesis and catabolism of triacylglycerol, lipid metabolism of obesity is more active, and relative glucose metabolism is inhibited. This metabolic change is involved in insulin resistance. Formation, obesity lipid metabolism is accompanied by metabolic disorders, hypertriglyceridemia, hypercholesterolemia and low-density lipoprotein cholesterol, etc., glucose metabolism disorder is abnormal or even impaired glucose tolerance In clinical diabetes, when the body weight exceeds 20% of the normal range, the incidence of diabetes is more than doubled. When BMI>35, the mortality rate is almost 8 times higher than that of normal weight. Central obesity significantly increases the risk of diabetes.
(4) Obesity and musculoskeletal disorders :
1 arthritis: the most common is osteoarthritis, due to long-term weight bearing, the articular cartilage surface structure changes, knee joint lesions are most common.
2 Gout: About 10% of obese patients have hyperuricemia and are prone to gout.
3 Osteoporosis: Because adipose tissue can synthesize and secrete estrogen, the main source of estrogen in postmenopausal women is secreted by adipose tissue. Many studies have found that obese women after menopause have higher bone density than normal weight. Osteoporosis is rare in obese patients.
(5) Endocrine system changes in obesity :
1 Growth hormone: The release of growth hormone in obese people is reduced, especially insensitive to factors that stimulate the release of growth hormone.
2 Pituitary-adrenal axis: The secretion of adrenal cortex hormone is increased in obese people, the secretion rhythm is normal, but the peak value is increased, and the ACTH concentration is also slightly increased.
3 hypothalamic-pituitary-gonadal axis: obesity is associated with hypogonadism, pituitary gonadotropin reduction, testosterone response to gonadotropin is reduced, male obese, blood total testosterone (T) level is reduced, but light In obesity, free testosterone (FT) is still normal, probably due to the decrease of sex hormone binding globulin (SHBG), while FT can also be decreased in severely obese people. In addition, adipose tissue can secrete estrogen, so obese people are often accompanied by Increased blood estrogen levels, obese girls, early menarche, adult women with obesity often have menstrual disorders, increased ovarian transparency, emergence of egg-free follicles, decreased blood SHBG levels, hairy, anovulatory menstruation or amenorrhea, adolescents Obesity, the incidence of infertility increased, often accompanied by polycystic ovary and surgery, obesity in the mid-menstrual period, the peak of FSH is low and the level of progesterone (P) in the luteal phase is low, ovarian function decline and FSH level Elevation occurs early, men are accompanied by decreased sexual desire and feminization, and the incidence of estrogen-related tumors is significantly increased.
4 Hypothalamic-pituitary-thyroid axis: Obesity thyroid responsiveness to TSH decreased, and pituitary responsiveness to TRH decreased.
(6) Obesity and insulin resistance : Body fat accumulation can cause insulin resistance, hyperinsulinemia, and research on related factors are mainly concentrated in the following aspects.
1 Free fatty acid (FFA): When obese, increased sugar-fatty acid uptake and oxidation can cause defects in glucose metabolism and non-oxidation pathways, and decreased utilization of sugar. Increased plasma FFA levels increase hepatic gluconeogenesis and The ability of the liver to clear insulin decreases, causing hyperinsulinemia. When the function of B cells can still be compensated, normal blood sugar can be maintained. After a long period of time, it leads to B cell failure, and hyperglycemia develops into diabetes.
2 Tumor necrosis factor (TNF-): It has been found that the expression of TNF- is significantly increased in adipose tissue of insulin-resistant obese patients and obese type 2 diabetic patients. The mechanisms by which TNF- enhances insulin resistance include: Accelerated fat breakdown leads to elevated FFA levels; TNF- produced by fat cells of obese people can inhibit insulin receptors in muscle tissue and reduce insulin; TNF- inhibits glucose transporter 4 (GLUT4) expression and inhibits insulin stimulation Glucose transport.
3 Peroxisome-activated proliferators (PPAR2): PPAR2 is involved in the regulation of adipose tissue differentiation and energy storage, and PPAR2 activity is decreased in severely obese individuals, which is involved in the formation of insulin resistance.
(7) Others : obesity metabolic abnormalities, increased plasma uric acid, so that the incidence of gout is significantly higher than normal people, with coronary heart disease have a history of angina pectoris, obesity serum total cholesterol, triglyceride, low-density lipoprotein cholesterol Often elevated, high-density lipoprotein cholesterol decreased, easily lead to atherosclerosis, due to venous circulation disorders, prone to varicose veins of the lower extremities, embolic phlebitis, venous thrombosis, the patient's skin may have pale purple or white lines, Distributed in the lateral side of the buttocks, the inner thighs, knee joints, lower abdomen, etc., wrinkles are prone to wear, causing dermatitis, skin sputum, and even rubbing, usually sweating more heat, low resistance and easy to infect.
Examine
Hereditary obesity check
Examination and diagnosis of hereditary obesity
The incidence of obesity is highlighted in three stages: infancy, puberty, and adulthood over 40 years of age. Most of the infants and adolescents can develop into adult obesity, and the degree of obesity is heavier.
Diagnosis
Diagnosis and diagnosis of hereditary obesity
After obesity is determined, it can be combined with medical history, body film and laboratory data to identify simple secondary depression. If you have high blood pressure, central obesity, purple streak, amenorrhea, etc. with 24-hour urine 17-hydroxysteroids, you should consider hypercortisolism. Those with low metabolic rate should further check T3, T4 and TSH. test. In addition, it is often necessary to pay attention to the presence of diabetes, coronary heart disease, atherosclerosis, gout, cholelithiasis and other concomitant diseases.
The incidence of obesity is highlighted in three stages: infancy, puberty, and adulthood over 40 years of age. Most of the infants and adolescents can develop into adult obesity, and the degree of obesity is heavier.
