Patient's question:
What is simple obesityDoctor's answer:
Classification of Obesity:Obesity is generally classified into two categories based on etiology: primary and secondary.
### I. Primary Obesity
#### (1) Simple Obesity
Obesity is the main clinical manifestation, with no obvious morphological or functional changes in the nervous or endocrine systems, but accompanied by disturbances in fat and glucose metabolism. This type is the most common.
1. Constitutional Obesity is caused by adipocyte hyperplasia and is related to excessive nutrition before the age of 25. It often has a familial genetic history. Overweight children usually become overweight adults. Reports indicate that among overweight individuals aged 0–13, 42% of women and 18% of men become obese by the age of 31. During the 30th week of fetal life to the first year after birth, fat cells undergo a highly active proliferation period called the "sensitive period." If excessive nutrition occurs during this period, it can lead to an increase in fat cells. Therefore, maintaining a normal weight during childhood, especially before the age of 10, is crucial.
2. Nutritional Obesity, also known as acquired (exogenous) obesity, is often caused by excessive nutrition after the age of 20–25, with calorie intake exceeding the body's metabolic needs; or by insufficient physical activity or prolonged bed rest due to certain factors or diseases, leading to reduced calorie expenditure and obesity. This type of obesity is primarily due to adipocyte hypertrophy and hyperplasia. Constitutional obesity can also develop into acquired obesity, forming a mixed type.
Both types of obesity are collectively referred to as simple obesity, especially common in women aged 20–30 in urban areas. Middle-aged men and postmenopausal women also tend to develop spontaneous obesity.
#### (2) Water and Sodium Retention Obesity
Also known as idiopathic edema, this type is more common in women during reproductive and menopausal periods. Its occurrence may be related to factors such as increased estrogen leading to higher capillary permeability, increased aldosterone secretion, and slower venous return. Fat distribution is uneven, primarily concentrated in the calves, thighs, buttocks, abdomen, and breasts. Weight gain is rapid and closely related to posture—increasing during exertion or standing and decreasing during rest or lying flat. Normal weight fluctuations in healthy individuals are 0.4 kg, but in patients with this condition, the weight difference between morning and evening exceeds 1 kg. Edema changes often follow a cyclical pattern: morning swelling in the face and eyelids, followed by gradual swelling in the lower limbs and torso after getting up. By dinner time, weight increases by 1.2–4.5 kg compared to breakfast time, averaging 2.4 ± 0.7 kg. Water retention tests in upright and supine positions confirm water and sodium retention in patients.
### II. Secondary Obesity
This is a symptomatic obesity caused by an underlying disease. It is uncommon or rare in clinical practice, accounting for less than 5% of obesity cases.
#### (1) Endocrine Disorders
1. Hypothalamic Obesity includes hypothalamic syndrome and hypothalamic obesity-gonadotropin deficiency syndrome.
(1) Hypothalamic Syndrome can be caused by lesions in the hypothalamus itself, pituitary lesions affecting the hypothalamus, or midbrain or third ventricle lesions. The nature of the lesions may be inflammatory, tumor-related, or traumatic. In some cases, the cause is unknown, primarily presenting with central nervous system symptoms, autonomic nervous system and endocrine-metabolic dysfunction. Damage to the hypothalamic appetite center leads to abnormal appetite, such as hyperphagia, resulting in obesity. Abnormal secretion of hypothalamic releasing hormones disrupts target gland function, such as abnormal sexual function or precocious puberty, thyroid dysfunction, hyperadrenocorticism, amenorrhea with galactorrhea, diabetes insipidus, and other manifestations.
Neurological disorders may include somnolence or insomnia, recurrent hypersomnia, narcolepsy, deep sleep syndrome, or recurrent hypersomnia with hyperphagia; fever or hypothermia; excessive excitement, emotional instability, hallucinations, and irritability; hypothalamic epilepsy; hyperhidrosis or anhidrosis; cyanosis of the extremities;
sphincter dysfunction. Intellectual development may be incomplete or impaired.
(2) Obesity-Gonadotropin Deficiency Syndrome is caused by pituitary and stalk lesions, with some affecting hypothalamic function. In prepubertal children, obesity is most prominent in the submandibular region, neck, hips, upper thighs, and abdomen; upper limbs are also obese, with long and gradually tapered fingers but full of fat; boys may have gynecomastia, small external genitalia, which may further shrink if buried in fat; bone development is delayed, and diabetes insipidus may occur. If onset occurs after puberty, secondary sexual characteristics may be underdeveloped. In adolescents, genital development is impaired, and intellectual development is delayed. It must be differentiated from constitutional obesity with delayed sexual development in adolescents. The latter has uniform fat distribution, no organic neurological lesions, normal intelligence, and complete final development of sex organs. In adults, this condition may present with loss of sexual function, azoospermia, and amenorrhea.
2. Pituitary Obesity is caused by an ACTH-producing adenoma in the anterior lobe of the pituitary, secreting excessive ACTH, leading to bilateral adrenal cortex hyperplasia and excessive cortisol production, resulting in central obesity, known as Cushing's disease. Pituitary tumors secreting other hormones may compress surrounding tissues, causing secondary hypogonadism and hypothyroidism, leading to obesity. In addition to obesity, patients often have symptoms of pituitary compression, such as headaches, visual impairment, and visual field defects. Imaging studies can reveal sellar changes.
3. Thyroid Obesity occurs in patients with hypothyroidism. Compared to obesity, more prominent symptoms include a bloated appearance, pale skin, fatigue, hair loss, slow reactions, and apathy. Serum T3 and T4 levels are low, while TSH levels are high, and TRH stimulation tests show enhanced responses.
4. Adrenal Obesity is common in adrenal cortex adenomas or carcinomas, with autonomous secretion of excessive cortisol, causing secondary obesity, known as Cushing's syndrome. Characteristics include central obesity, moon face, buffalo hump, plethora, striae, hypertension, and impaired glucose tolerance or diabetes. Blood and urine cortisol levels are elevated, while ACTH levels are low. Imaging studies show adrenal tumors.
5. Pancreatic Obesity is common in early mild type 2 diabetes, pancreatic β-cell tumors, and functional spontaneous hypoglycemia. It is often due to hyperphagia.
Pancreatic β-cell tumors are primarily due to excessive insulin secretion. Recurrent hypoglycemia with fasting blood glucose below 2.8 mmol/L (50 mg/dL), rapidly improving after glucose injection or oral intake.
Spontaneous functional hypoglycemia is reactive (postprandial) hypoglycemia, caused by autonomic nervous system imbalance, particularly high vagal tone, more common in middle-aged women, often occurring after emotional stress, typically 3 hours postprandial, with symptoms such as hunger, palpitations, weakness, sweating, anxiety, pallor, tachycardia, hypertension, tremors, and blurred vision. Brain hypoglycemia symptoms are rare, with occasional fainting. Each episode lasts 15–20 minutes. Symptoms usually resolve spontaneously or with slight food intake. Due to voracious appetite, the only sign is often obesity. Glucose tolerance tests show reactive hypoglycemia at 3–4 hours, normalization at 4–5 hours, while pancreatic β-cell tumors remain hypoglycemic at 4–5 hours. Fasting tests help differentiate the two. This condition can last 10–20 years without worsening.
Diabetic patients have polyuria, polydipsia, and polyphagia, with fasting blood glucose ≥ 7.8 mmol/L (140 mg/dL) or 2-hour post-oral glucose tolerance test blood glucose ≥ 11 mmol/L (200 mg/dL).
6. Gonadal Hypofunctional Obesity is more common in postmenopausal women and men with testicular dysgenesis. Most cases are due to gonadal hypofunction, such as obesity after castration in men or menopause in women. Male hypogonadal obesity is generally less pronounced than postmenopausal women. Gonadal obesity has more uniform fat accumulation, with prominent fat in the chest, abdomen, thighs, and back. It may be accompanied by hypertension, striae, and impaired glucose tolerance. 24-hour urine 17-hydroxycorticosteroids or 17-ketosteroids are persistently elevated, and dexamethasone suppression tests are often positive. Urinary gonadotropins are elevated. A small portion belongs to Stein-Leventhal (PCO) syndrome, characterized by obesity, amenorrhea, anovulation, infertility, virilization, and polycystic ovaries. Those without virilization are referred to as polycystic ovaries (PCO). The ovaries secrete excessive androgens, with increased urinary 17-ketosteroids, elevated blood testosterone, high LH, and normal or low FSH. LHRH stimulation tests show excessive responses.
#### (2) Congenital Abnormalities
Mostly caused by genetic gene and chromosomal abnormalities. Common conditions include the following.
1. Congenital Hypoplastic Ovarian Dysgenesis presents as females with primary amenorrhea, underdeveloped genital organs, short stature, intellectual impairment, webbed neck, cubitus valgus, and short fourth metacarpals. Estrogen levels are low, while LH and FSH are elevated, with a chromosomal karyotype of XO.
2. Congenital Testicular Dysgenesis is male primary hypogonadism with eunuchoid features (taller stature, long limbs, greater finger span than height, greater distance from pubic symphysis to ground than half of height), underdeveloped secondary sexual characteristics, infantile genitalia, gynecomastia, low blood testosterone, elevated LH and FSH, and a chromosomal karyotype of XXY.
3. Laurence-Moon-Biedl Syndrome has six main features: obesity, intellectual impairment, retinitis pigmentosa, polydactyly, syndactyly, and underdeveloped genital organs. Urinary 17-ketosteroids and blood LH are lower than normal. Chlorpropamide stimulation tests show no response. LHRH stimulation tests show elevated LH responses after one or multiple injections.
4. Glycogen Storage Disease Type I presents as obesity with particularly abundant subcutaneous fat in the face and trunk. Features include delayed development, short stature with dwarfism, hypoglycemia (reaching 0.56 mmol/L), hepatosplenomegaly, muscle weakness, hyperlipidemia, hyperlactacidemia, and ketosis. This is an autosomal recessive disease.
5. Parietal Bone Hyperplasia primarily presents with obesity, headaches, parietal bone hyperplasia, virilization, and mental disorders. Obesity is more prominent in the trunk and proximal limbs. X-rays of the skull show hyperplasia of the frontal bone and/or other parietal bones. Most patients are female, with symptoms typically appearing after menopause.
#### (3) Other
1. Painful Obesity, also known as neurogenic lipomatosis, has an unknown etiology. More common in women, especially after menopause, often with early menopause and reduced sexual function. Clinically, it presents with multiple painful fat nodules or painful fat masses on the basis of obesity. Fat is primarily deposited in the trunk, neck, axillae, waist, and arms. Early fat nodules are soft, becoming hard later. As fat nodules grow, pain intensifies, accompanied by numbness, weakness, and sweating disorders. Pain is sharp or knife-like, intermittent or persistent, with tenderness along nerve trunks. Joint pain may occur. Mental symptoms, such as depression and intellectual impairment, may also be present.
2. Progressive Lipoid Atrophy affects subcutaneous fat in the upper body, with normal or abnormal fat accumulation in the lower body. It may also involve fat atrophy in the lower body with fat deposition in the upper body. It may be accompanied by hyperthyroidism, hepatosplenomegaly, muscle hypertrophy, hyperlipidemia, and diabetes.
Secondary obesity is symptomatic, with obesity being only one manifestation of the underlying disease. It is often not the primary or sole symptom of the disease. Treatment of the primary disease can often resolve obesity.