STUDY - Technical - New Dacian's Medicine
Obesity
(1)
Translation Draft
Obesity is a chronic condition whose prevalence is increasing and which causes the risk for the development of diabetes mellitus, hypertension, heart disease, gallbladder disease and some forms of cancer. Obesity can be seen as a consequence of the interaction between environmental factors and the individual genetic substrate, in particular genetic susceptibility.
These genes increase fat deposits when nutrition is limited, and cause an increase in the risk of obesity when nutrition is abundant and energy consumption is low. The prevalence of obesity has increased slowly since World War II and has increased by 30% over the past decade. In addition to addressing genetic and environmental factors, we will define the problem of obesity, describe the methods of measuring it, and study the impact of different types of obesity in terms of fat disposition, appreciating the prognosis of illness and summarizing the treatment options available.
So let's proceed to specifying the definition and the measurements. Both obesity and the distribution of body fat are useful prognostic factors of excess mortality and the risk of developing diabetes mellitus, heart disease, hypertension and gallbladder disease. Obesity, defined as an increase in the body's total body fat, is commonly known as overweight, as overweight is easily associated with obesity-related risks, and direct measurements of body fat are expensive.
The regional distribution of fat tissue or its topography also has a great influence on the risk of disease. For example, increased visceral or abdominal fat deposits correlate with the risk of developing heart disease, diabetes mellitus, hypertension, gallbladder disease and breast cancer.
The methods/techniques for measuring or estimating the body's body fat and its distribution are quite a lot and are used according to cost, ease of use, accuracy of estimates and measurements of regional adiposity. They are represented by methods: 1. height and weight, 2. skin folds, 3. circumferences, 4. ultrasound (density), 5. immersion, 6. pletismography, 7. heavy water (with a. tritiated and b. deuterium oxide or ozone), 8. isotope of potassium (K40), 9. electrical conductivity of the whole organism, 10. bioelectric impedance, 11. fat-soluble gas, 12. absorption technique (a. dual X-ray absorption and b. dual photon absorption), 13. computed tomography, 14. nuclear magnetic resonance and 15. activation of neutrons.
In addition to techniques for measuring or estimating the body's total body fat, height and weight can also be measured with precision and valuable information can be provided from these measurements. the dual X-ray absorption technique, which has developed to assess bone density, provides the best assessment of the body's total fat. Regional adiposity can be measured exactly by MRI or TC (for practical purposes, measuring waist circumference or sagittal diameter are the most useful parameters). The ratio of waist circumference to hip circumference is widely used to estimate regional fatness, but it is not accurate.
Excess weight can be defined by the tables for height and weight and by assessing the percentages of overweight or relative weight (the ratio between current and ideal weight). However, the most commonly used formula for relation to height with weight is body mass index (BMI), which is the ratio between weight and height square, where weight is expressed in kg and height in meters (about BMI we have presented some elements in previous posts).
A BMI between 20 and 25 kg/ m square is usually considered a good value for most individuals. Overweight is defined by a BMI over 27, and obesity is defined by a BMI above 30. Weight gain can increase the risk of illness, even if BMI does not exceed 25. In women, weight gain of more than 5 kg is associated with increased risk of diabetes and cardiovascular disease, and in men any weight gain after 25 years seems to increase the risk of illness. In practice, the determination of BMI, the estimation of abdominal waist and the assessment of heredo-collateral history of heart disease, diabetes mellitus, biliary disorders or hypertension provide valuable information to assess the obese patient.
On the basis of these considerations, a table was made (to be inserted in the documentation on the www.dorinm.ro at the time) with the ideal weight for men and women. The body's fat tissue and its distribution are determined by sex, age, degree of physical activity and numerous medications. In both men and women, body fat is less than 20 per cent and can increase in older men up to 25 percent. In young women, fat deposits can be below 30% and gradually increase to more than 35% in older women. At all ages after puberty women are fatter than men.
The prevalence of obesity is based on certain diagnostic criteria. In most European countries, obesity is defined by a BMI above 30, and overweight by a BMI between 25-27 and 30. there has been a slow increase in prevalence in both sexes since the beginning of studies more than 40 years ago, and in the 1990s there was an increase of 30%.
Genetic susceptibility/genetic determinism may play a major role in the pathogenesis of obesity or an increase in susceptibility to its occurrence. The dysmorphic types of human obesity in which genetic factors play a major role include Prader-Willi syndrome (a. sporadic heredity, two-thirds have defect, b. small stature, c. generalized to severe obesity with onset at 1-3 years, d. craniofacial aspect with small bifrontal diameter, almond-shaped eyes, strabismus, V-shaped mouth and high palatine vault, e. limbs: small hands and feet, hypotonia, f. reproductive apparatus with hypogonadism, g. other traits: hypoplasia of dental enamel, hyperphagia, choleric temperament and nose speech and h. mild to moderate mental retardation), Ahlstrom syndrome (a. with recessive autosomal heredity, b. normal stature, rarely small, c. obesity on the trunk with early onset at 2-5 years , d. reproductive apparatus with hypogonadism in men, but not in women), Laurence-Moon-Biedl syndrome (a. with recessive autosomal heredity, b. normal stature, rarely small, c. generalized obesity with early onset at 1-2 years, d. in limbs with polydactyly and e. reproductive apparatus with hypogonadism), Cohen syndrome (a. with probable autosomal recessive heredity, b. with small or large stature, c. with obesity on the trunk with onset in childhood at the age of about 5 years, d. craniofacial aspect with high nasal pyramid, arched palate, open mouth, low infranasal depression, e. limbs with hypotonia, narrow hands and feet, f. apparatus reproductive function with normal gonadic function or hypogonadotrophic hypogonadism, g. other features represented by dysplastic ears and delayed puberty and h. with mild retardation) and Carpenter syndrome (a. with recessive autosomal heredity , b. obesity on the trunk and at the gluteal level, c. craniofacial aspect with acrocephaly, low nasal pyramid and high palatal vault, d. limbs with polydactyly, sindactyly and genu valgum, e. reproductive apparatus with hypogonadism and f. very mild mental retardation).
Four genes have been cloned whose mutations cause obesity. the leptin gene has expression only in the fat tissue, and in inherited obesity the two copies of the gene are incomplete, due to the presence of a stop codon that truncates the protein at the level of amino acid 105. Leptin protein is normally secreted by fat cells and circulating leptin levels are elevated in both normal and obese statuses. Treatment with leptin decreases food intake and obesity.
Genetic susceptibility to obesity has been studied a lot, and variability between 30 and 50% in the body's total fat tissue is believed to be genetically determined. In individuals who become obese after a fat diet, at least 12 chromosomal locus play an important role in expressing this susceptibility.
Obesity is a chronic condition whose prevalence is increasing and which causes the risk for the development of diabetes mellitus, hypertension, heart disease, gallbladder disease and some forms of cancer. Obesity can be seen as a consequence of the interaction between environmental factors and the individual genetic substrate, in particular genetic susceptibility.
These genes increase fat deposits when nutrition is limited, and cause an increase in the risk of obesity when nutrition is abundant and energy consumption is low. The prevalence of obesity has increased slowly since World War II and has increased by 30% over the past decade. In addition to addressing genetic and environmental factors, we will define the problem of obesity, describe the methods of measuring it, and study the impact of different types of obesity in terms of fat disposition, appreciating the prognosis of illness and summarizing the treatment options available.
So let's proceed to specifying the definition and the measurements. Both obesity and the distribution of body fat are useful prognostic factors of excess mortality and the risk of developing diabetes mellitus, heart disease, hypertension and gallbladder disease. Obesity, defined as an increase in the body's total body fat, is commonly known as overweight, as overweight is easily associated with obesity-related risks, and direct measurements of body fat are expensive.
The regional distribution of fat tissue or its topography also has a great influence on the risk of disease. For example, increased visceral or abdominal fat deposits correlate with the risk of developing heart disease, diabetes mellitus, hypertension, gallbladder disease and breast cancer.
The methods/techniques for measuring or estimating the body's body fat and its distribution are quite a lot and are used according to cost, ease of use, accuracy of estimates and measurements of regional adiposity. They are represented by methods: 1. height and weight, 2. skin folds, 3. circumferences, 4. ultrasound (density), 5. immersion, 6. pletismography, 7. heavy water (with a. tritiated and b. deuterium oxide or ozone), 8. isotope of potassium (K40), 9. electrical conductivity of the whole organism, 10. bioelectric impedance, 11. fat-soluble gas, 12. absorption technique (a. dual X-ray absorption and b. dual photon absorption), 13. computed tomography, 14. nuclear magnetic resonance and 15. activation of neutrons.
In addition to techniques for measuring or estimating the body's total body fat, height and weight can also be measured with precision and valuable information can be provided from these measurements. the dual X-ray absorption technique, which has developed to assess bone density, provides the best assessment of the body's total fat. Regional adiposity can be measured exactly by MRI or TC (for practical purposes, measuring waist circumference or sagittal diameter are the most useful parameters). The ratio of waist circumference to hip circumference is widely used to estimate regional fatness, but it is not accurate.
Excess weight can be defined by the tables for height and weight and by assessing the percentages of overweight or relative weight (the ratio between current and ideal weight). However, the most commonly used formula for relation to height with weight is body mass index (BMI), which is the ratio between weight and height square, where weight is expressed in kg and height in meters (about BMI we have presented some elements in previous posts).
A BMI between 20 and 25 kg/ m square is usually considered a good value for most individuals. Overweight is defined by a BMI over 27, and obesity is defined by a BMI above 30. Weight gain can increase the risk of illness, even if BMI does not exceed 25. In women, weight gain of more than 5 kg is associated with increased risk of diabetes and cardiovascular disease, and in men any weight gain after 25 years seems to increase the risk of illness. In practice, the determination of BMI, the estimation of abdominal waist and the assessment of heredo-collateral history of heart disease, diabetes mellitus, biliary disorders or hypertension provide valuable information to assess the obese patient.
On the basis of these considerations, a table was made (to be inserted in the documentation on the www.dorinm.ro at the time) with the ideal weight for men and women. The body's fat tissue and its distribution are determined by sex, age, degree of physical activity and numerous medications. In both men and women, body fat is less than 20 per cent and can increase in older men up to 25 percent. In young women, fat deposits can be below 30% and gradually increase to more than 35% in older women. At all ages after puberty women are fatter than men.
The prevalence of obesity is based on certain diagnostic criteria. In most European countries, obesity is defined by a BMI above 30, and overweight by a BMI between 25-27 and 30. there has been a slow increase in prevalence in both sexes since the beginning of studies more than 40 years ago, and in the 1990s there was an increase of 30%.
Genetic susceptibility/genetic determinism may play a major role in the pathogenesis of obesity or an increase in susceptibility to its occurrence. The dysmorphic types of human obesity in which genetic factors play a major role include Prader-Willi syndrome (a. sporadic heredity, two-thirds have defect, b. small stature, c. generalized to severe obesity with onset at 1-3 years, d. craniofacial aspect with small bifrontal diameter, almond-shaped eyes, strabismus, V-shaped mouth and high palatine vault, e. limbs: small hands and feet, hypotonia, f. reproductive apparatus with hypogonadism, g. other traits: hypoplasia of dental enamel, hyperphagia, choleric temperament and nose speech and h. mild to moderate mental retardation), Ahlstrom syndrome (a. with recessive autosomal heredity, b. normal stature, rarely small, c. obesity on the trunk with early onset at 2-5 years , d. reproductive apparatus with hypogonadism in men, but not in women), Laurence-Moon-Biedl syndrome (a. with recessive autosomal heredity, b. normal stature, rarely small, c. generalized obesity with early onset at 1-2 years, d. in limbs with polydactyly and e. reproductive apparatus with hypogonadism), Cohen syndrome (a. with probable autosomal recessive heredity, b. with small or large stature, c. with obesity on the trunk with onset in childhood at the age of about 5 years, d. craniofacial aspect with high nasal pyramid, arched palate, open mouth, low infranasal depression, e. limbs with hypotonia, narrow hands and feet, f. apparatus reproductive function with normal gonadic function or hypogonadotrophic hypogonadism, g. other features represented by dysplastic ears and delayed puberty and h. with mild retardation) and Carpenter syndrome (a. with recessive autosomal heredity , b. obesity on the trunk and at the gluteal level, c. craniofacial aspect with acrocephaly, low nasal pyramid and high palatal vault, d. limbs with polydactyly, sindactyly and genu valgum, e. reproductive apparatus with hypogonadism and f. very mild mental retardation).
Four genes have been cloned whose mutations cause obesity. the leptin gene has expression only in the fat tissue, and in inherited obesity the two copies of the gene are incomplete, due to the presence of a stop codon that truncates the protein at the level of amino acid 105. Leptin protein is normally secreted by fat cells and circulating leptin levels are elevated in both normal and obese statuses. Treatment with leptin decreases food intake and obesity.
Genetic susceptibility to obesity has been studied a lot, and variability between 30 and 50% in the body's total fat tissue is believed to be genetically determined. In individuals who become obese after a fat diet, at least 12 chromosomal locus play an important role in expressing this susceptibility.
As for fat cells and
obesity, in addition to the role in fat storage, the fat cell is
also an important secretory
organ. It produces protein-lipase, which is involved in hydrolysis of triglycerides, very low density lipoproteins (VLDL), chilomicrons and complement factors D (adipsin) and C3b. Adipocyte also produces cytokines such as the alpha factor of tumor necrosis, angiotensin and leptin.
Fat cells produce large amounts of lactate and metabolize glucose to provide glycerol-3-phosphate for triglyceride synthesis. Under the conditions of an excessive diet, fat cells synthesize long-chain fatty acids. Most forms of obesity are associated with increased fat cell counts and increased basal lipolysis rate. Fat cells serve as a reservoir for the deposit of fatty acids released from chilomicrons and may instead release these fatty acids through a lipaco-sensitive intracellular hormone. In many forms of severe obesity with onset in childhood, the total number of fat cells is increased.
organ. It produces protein-lipase, which is involved in hydrolysis of triglycerides, very low density lipoproteins (VLDL), chilomicrons and complement factors D (adipsin) and C3b. Adipocyte also produces cytokines such as the alpha factor of tumor necrosis, angiotensin and leptin.
Fat cells produce large amounts of lactate and metabolize glucose to provide glycerol-3-phosphate for triglyceride synthesis. Under the conditions of an excessive diet, fat cells synthesize long-chain fatty acids. Most forms of obesity are associated with increased fat cell counts and increased basal lipolysis rate. Fat cells serve as a reservoir for the deposit of fatty acids released from chilomicrons and may instead release these fatty acids through a lipaco-sensitive intracellular hormone. In many forms of severe obesity with onset in childhood, the total number of fat cells is increased.
Environmental factors
interact with genetic susceptibility within the pathogenicity of
obesity.
For example, damage to the
hypothalamus through trauma or surgery and destructive damage in
the region of the ventromedial or paraventricular nuclei of the
hypothalamus may cause obesity. The two major factors of
hypothalamic obesity are hyperphagia and damage to the
vegetative nervous system, in the sense of increasing the
activity of the parasympathetic nervous system and decreasing
the activity of the sympathetic one.
An explanation for this sequence of events may be given by impairment of neuropeptide Secretion Y (NPY). NPY is produced in the arcuat nucleus and acts at the level of the hypothalamus, stimulating hunger (may also affect reproductive function, decrease sympathetic activity and increase parasympathetic activity - other characteristic traits of hypothalamic obesity). Hypothalamic obesity syndrome is the end of a combination of genetic and environmental factors.
Also at this end are some endocrine diseases associated with obesity, including Cushing's disease and polycystic ovary syndrome, as well as drug-induced obesity. medicines associated with increased body weight are represented by: phenothiazide (in descending order of "force of effect": chlorpromazine, thioritazine, trifluoperazine, mesoridazine, promazine, mepazine, perfhesine, prochlorperazine, haloperidol and loxapine), antidepressants (in the same "order": amitriptilin, imipramine, doxepin, phenelzine, amoxapine, desipramine, trazodon and troilcipromine), antiepileptics (valproate and carbamazepine), steroids (glucocorticoids and megestrol acetate) and antihypertensives (trazosin). Some of the drugs, such as megestrol acetate, have been used to increase appetite for anorexia within neoplastic cheesexia.
All right, that's enough for today!
An explanation for this sequence of events may be given by impairment of neuropeptide Secretion Y (NPY). NPY is produced in the arcuat nucleus and acts at the level of the hypothalamus, stimulating hunger (may also affect reproductive function, decrease sympathetic activity and increase parasympathetic activity - other characteristic traits of hypothalamic obesity). Hypothalamic obesity syndrome is the end of a combination of genetic and environmental factors.
Also at this end are some endocrine diseases associated with obesity, including Cushing's disease and polycystic ovary syndrome, as well as drug-induced obesity. medicines associated with increased body weight are represented by: phenothiazide (in descending order of "force of effect": chlorpromazine, thioritazine, trifluoperazine, mesoridazine, promazine, mepazine, perfhesine, prochlorperazine, haloperidol and loxapine), antidepressants (in the same "order": amitriptilin, imipramine, doxepin, phenelzine, amoxapine, desipramine, trazodon and troilcipromine), antiepileptics (valproate and carbamazepine), steroids (glucocorticoids and megestrol acetate) and antihypertensives (trazosin). Some of the drugs, such as megestrol acetate, have been used to increase appetite for anorexia within neoplastic cheesexia.
All right, that's enough for today!
Let us have understanding,
love and gratitude!
Dorin, Merticaru