This article discusses different aspects of obesity and how to diagnose obesity. Here, learn about the tests, prevention of obesity, and more.
Keywords: Leptin| Ghrelin| Obesity survival paradox | A calorie is a calorie model, satiety center| feeding center| Arcuate nucleus
Table of content
| 1. | Introduction |
| 2. | Physiological Basis of Insomnia |
| 3. | Causes of Insomnia |
| 4. | Prevention Strategies for Insomnia |
| 5. | Conclusion |
| 6. | References |
Definition:
Obesity is abnormal and excessive accumulation of fat in the body. The word obesity originates from the Latin Obesitas’meaning fat, stout or plump. Obesity was known in the early historical period.
The great surgeon of India, Sushruta, had reported about obesity. He related it to heart disease and mentioned that physical activity would cure it.
Obesity is a significant risk to health and increasing globally in developing countries. According to American Medical Association, and American Heart Association, obesity is a chronic disease. Obesity reduces life expectancy on average by 6-7 years.
Incidence: It is more common in females and is prevalent in adults as well as in children. Globally 650 million were obese, which is rising rapidly.
Diagnosis of obesity is based on the Body Mass Index (BMI)
and further evaluated in terms of ‘Waist hip ratio,’ ‘Waist to height ratio,’ and total cardiovascular risk factors.
Category BMI Kg/meter square
Underweight >̲18.5
Normal weight 19.5–24.9
Overweight 25—29.9
Obese class I 30-34.5
Obese class II 35-39.9
Obese class III >40
Some countries use lower values. For example, in Japan, BMI >25 is considered obese, while in China, it is >28.
Causes: Obesity is due to 1. Persistent positive energy balance, and
2. Body weight set point is raised.
Obesity is related to various conditions and syndromes, especially with Diabetic type -2, osteoarthritis, cardiovascular diseases, hypertension, obstructive sleep apnea, asthma, some cancers, etc.
It is associated with rare genetic syndromes like Prader-Willi, Bardet-Bedi, Crohn’s, and MOMO.
Individual causes are -diet habits, physical activity sedentary lifestyle.
Eating disorders like ‘binge eating syndrome ‘and night eating syndrome ‘are also responsible for obesity.
Socioeconomic factors,
Environmental factors
Endocrinal factors: Hypothyroidism, Cushing syndrome, Growth hormone deficiency, etc.
Genetic factors: Alteration is the various genes controlling appetite and metabolism predispose to obesity. Fat mass and obesity-associated genes (FTO gene ) are detected. There are many hypotheses, but none is widely accepted.
1. Thrifty gene hypothesis,
2. Drifty gene hypothesis
3. Thrifty phenotype hypothesis
Obesity shows inheritance. If both parents are obese, 80% of children will be obese. When both parents are normal, children are only 10% likely to be obese.
Carbohydrate insulin model –High glycemic load causes hormonal changes that promote caloric deposits in adipose tissue.
A calorie model-excess food intake and lack of physical activity.
Drugs; Insulin, sulfonylurea, steroids, phenytoin contraceptives, and many more.
Malnutrition in early life causes endocrinal changes, which may promote obesity in a later stage.
Obesity increases the risk of clinical depression, and depression increases the chance of developing obesity.
Gut flora also plays a vital role in the development of obesity.
The complication of obesity:
Directly-Increase in fat mass causes osteoarthritis, non-alcoholic fatty liver, and alters body response to Insulin. Cardiovascular disease, hypertension, lung diseases, mental disorders, gout, low back pain, multiple sclerosis, Carpel tunnel syndrome, etc.
Congenital disabilities, intrauterine fetal death, infertility, and pregnancy and delivery complications.
In certain conditions, obesity is helpful –positive effect, e.g., in heart failure or hemodialysis. This is the ‘Obesity survival paradox.’
Pathophysiology: Leptin, Ghrelin, and other appetite-related hormones act on the hypothalamus. Many pathways describe the development of obesity. However, the melanocortin pathway is widely accepted.
Arcuate nucleus influences 1. The lateral hypothalamus has the feeding center, and 2. The ventromedial nucleus has a satiety center.
One group of neurons in the arcuate nucleus secrete (a) Neuropeptide Y (NPY) and (b)Agouti-related peptide (AgRP). They stimulate the Lateral hypothalamus and inhibit the ventromedial nucleus.
The other group of neurons in the arcuate nucleus secrete (a) Preopiomelanocortin (PoMC) and (b) Cocaine and Amphetamine regulated transcript (CART). They inhibit the Lateral hypothalamus and
stimulate ventromedial nucleus.
Leptin stimulates the second group of the nucleus. Conversely, it inhibits the first group of the nucleus, so leptin deficiency will cause less inhibition to the ist group and less stimulation to another group of the nucleus, increasing overfeeding and obesity.
Prevention:-Change diet, reduce high fat and carbohydrate diet, and increase dietary fiber.
Regular exercise.
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