STUDY - Technical - New Dacian's Medicine
Obesity
(2)
Translation Draft
I will continue with the presentation of a few "things" about the intake of nutritional factors and the substrate of their oxidation. In order to maintain the body's fat deposits, the nutritional factors in the diet should be oxidized in the body in an amount proportional to that ingested. Since daily carbohydrate intake almost equals the body's glucose deposits, carbohydrate deposits are much more vulnerable to changes in their dietary intake than in their lipid or protein intake.
Oxidation of nutritional factors can be assessed by the respiratory coefficient (CR) which represents the ratio between the carbon dioxide produced and the oxygen used. The appropriate food report shall provide the food coefficient. When the percentage of lipids in the diet increases, the CR must decrease, in order for body weight to remain constant. If CR does not decrease, the body continues to oxidize carbohydrates in storage, which must be replaced by increased nutrition, increased carbohydrate intake or endogenous synthesis from protein deposits.
This adaptation is effective and seems to have a strong genetic determination. Physiologically, adapting to a high-fat diet, such as a Western diet, requires a decrease in carbohydrate oxidation in order to maintain their deposits. If the oxidation of carbohydrates is low, the oxidation of lipids increases and CR decreases.
Measurements using calorimetric chambers or double-marked water show a positive correlation between energy consumption and body mass without lipids or body weight. To maintain body weight, overweight individuals must ingest a large amount of food to ensure energy needs. Obese people tend to significantly underestimate food intake. So a patient who says "Doctor, everything I eat, eat with difficulty" (something like, "I don't eat much" or "I don't eat too much"), means that he either doesn't recognize or doesn't really realize food intake.
Due to the inseriness of patients, anamnesis should be performed to assess energy needs should probably be abandoned. Reasonable assessment of energy consumption (kcal) in obese people is represented "arbitraryly" by multiplying body weight by 10. Another method takes into account the estimation of energy needs according to some equations for assessing the rate of basal metabolism (RMB). These are represented by: 1. in men between 18-30 years RMB = (0.0630 x current weight in kg + 2.8957) x 240 kcal/day, 2. in men between 31-60 years RMB = (0.0484 x current weight in kg + 3.6534) x 240 kcal/day, 3. in women between 18-30 years RMB = (0.0621 x current weight in kg + 2.0357) x 240 kcal/day and 4. in women between 31-60 years RMB = (0.0342 x current weight in kg + 3.5377) x 240 kcal/day.
In these formulas, the total energy requirement should be assessed according to the activity factor according to the energy consumption formula = RMB x activity factor. The activity factor values depend on the activity level and are: a. for the low activity level (sedentarism) the activity factor is 1,3, b. for the intermediate activity level (a few physical exercises) the activity factor is 1,5, and c. for the increased activity level (constant physical activity or job requiring this activity) the activity factor is 1,7.
This leads to the "concretization" of three predictive factors of weight gain: a low metabolic rate, a high CR, which shows carbohydrate oxidation and the need to eat to replace carbohydrates and insulin resistance. Adjusting the intake of nutritional factors can be seen as a feedback system with related and efferent signals. Factors that increase hunger are decreased blood glucose, which is achieved in 60% of cases (or more) before meals and increased gastric contractions and abdominal discomfort. These peripheral signals are integrated through neurotransmitters in the central nervous system and regulate food intake.
In addition, certain neurotransmitters are specific modulators of the ingestion of one or other of the nutritional factors (lipids, carbohydrates or proteins). So an increase or decrease in the intake of lipids, carbohydrates or proteins may occur as the main response to the action of specific neurotransmitters. These peptides and their monoamine substrate provide a powerful system that controls the quantity and quality of food intake.
At least four processes are involved in regulating food intake: 1. olfactory and taste factors (they can stimulate intake when foods are appetizing or inhibit it when they are not), 2. gastrointestinal distension, 3. release of gastrointestinal hormones (such as cholecystokinin and gastrine-releasing peptide) and 4. activation of thermogenesis components of the efferent sympathetic nervous system. These factors act simultaneously after ingestion of food to reduce the feeling of satiety, until a new low blood sugar level or gastric contractions cause the interest in food to increase again.
Let's move now on to more serious things, like obesity and the risk factors associated with it. The increase in mortality associated with obesity comes, in particular, from an increased risk of cardiovascular disease, hypertension, diabetes mellitus and possibly some cancers.
In the case of the cardiovascular system, in addition to increased pre and post-pregnancy, obesity is also associated with an increased risk of sudden death, probably through cardiac arrhythmias, as well as an increased risk of atherosclerosis, as a result of an abnormal lipid profile, which includes decreased levels of high-density lipoproteins (HDL) and increased levels of low-density lipoproteins, and , in particular, those with very low VLDL density (form B). The prevalence of hypertension is also very high, although the mechanism is unclear. One hypothesis suggests that hyperinsulinemia and insulin resistance increase sodium reabsorption in the renal tube and increase sympathetic control that causes arterial vasoconstriction.
Then it's the turn of diabetes. Type 2 diabetes mellitus - non-insulin dependent diabetes mellitus (DZNID) is almost non-existent in individuals with a BMI below 22. In "closed" social groups, the increased risk of diabetes in obese people has a strong family tinge (if one or both parents are diabetic, all children will develop diabetes if they become obese enough). If none of the parents is diabetic, less than 20% of children will develop diabetes. But in general, obesity precedes the onset of diabetes by a few months or years. Among the most early prognostic factors of diabetes is the development of insulin resistance. In conclusion, obesity prevention prevents, in most cases, diabetes.
Now, about cancer. The incidence of endometrial and postmenopausal breast cancer in women, prostate cancer in men and colorectal cancer in both women and men is related to the degree of obesity. Visceral obesity increases the risk of breast cancer in the postclimax period, independent of the degree of obesity. One explanation for susceptibility to endometrial and breast cancer in obese women lies in increasing estrogen production by flavouring circulating androstendionin in fat tissue.
Gallbladder disorders increase with obesity and age, possibly by increasing the excretion of bile cholesterol. The amount of cholesterol synthesized by the body each day increases by almost 20 mg per kilogram of fat tissue, so at a 10 kg increase in fat tissue the daily production and excretion of cholesterol increases by an amount comparable to the amount of cholesterol in an egg. Disturbances of nesting factors in the bile and alterations in the levels of bile acids and phospholipids can precipitate the appearance of gallstones.
For lung function, moderate obesity, in the absence of an underlying lung condition, has a weak effect on respiratory function. Sleep apnea, however, occurs in individuals with severe obesity and poses serious problems. Obstructive sleep apnea is believed to occur due to a local accumulation of fat in the tracheoopharynx area. Obstructive episodes of sleep apnea cause sleep disruption, as well as hypoxia and hypercapnia. If not corrected, this condition can lead to right heart failure. Continuous positive airway pressure can be administered at night to reduce or eliminate sleep apnea episodes. Weight loss has a particular value in remedying this condition.
In terms of joint and skin damage, the increase in the incidence of osteoarthritis is undoubtedly due on the one hand to trauma suffered by joints within obesity, but on the other hand, osteoarthritis also occurs without a direct link to weight gain, which suggests the involvement of other factors, the prevalence of gout is also increased and may reflect a decrease in the clearance of the ugly. Ketone bodies act competitively in the renal tube with the reabsorption of urates, and an increase in ketone production from lipid metabolism can increase urate levels.
Among the skin disorders in obesity are acanthosis nigricans, manifested by hyperpigmentation of skin folds in the neck, elbows and interphalangeal spaces associated with insulin resistance and DZNID. Skin turgor and friability can be increased in obesity, thus increasing the risk of fungal infections in the skin folds. Finally, venous stasis is increased in obese people.
Let's move on to the endocrine system. Insulin resistance, which leads to hyperinsulinemia, is a characteristic feature and is directly related to the degree of obesity. Growth hormone secretion is low, but insulin-like growth factor I levels are normal, suggesting that growth hormone is sufficient to stimulate the production of this important hormone. Testosterone levels are low in men, but free testosterone levels decrease only in conditions of massive obesity.
Obesity causes an early onset of menarche, a higher frequency of irregular and anovulatory cycles and an early menopause. The distribution of adiposity influences steroid metabolism in women. Women with predominantly central or visceral adiposity have a higher production of androgen hormones, such as testosterone, and women with gluteofemural obesity have increased emrone levels due to peripheral aromatization of circulating androgens. Changes in thyroid hormones and their metabolism occur with quantitative changes in nutritional factors. Triiodothyronine (T3) can be increased by overeating and decreased by starvation.
T3 levels are also elevated through a high carbohydrate diet and low through a low-carbohydrate diet. In contrast, levels of thyroxine and thyrotropin (TSH) are not influenced by diet. Obesity can sometimes be mistaken for Cushing's syndrome. The normal pattern of diurnal variations of plasma cortisol and urinary concentration of free cortisol are normal in obesity, but abnormal in Cushing's disease. if these patterns are equivocal, dynamic tests of the adrenal function are indicated.
So much for today...
I will continue with the presentation of a few "things" about the intake of nutritional factors and the substrate of their oxidation. In order to maintain the body's fat deposits, the nutritional factors in the diet should be oxidized in the body in an amount proportional to that ingested. Since daily carbohydrate intake almost equals the body's glucose deposits, carbohydrate deposits are much more vulnerable to changes in their dietary intake than in their lipid or protein intake.
Oxidation of nutritional factors can be assessed by the respiratory coefficient (CR) which represents the ratio between the carbon dioxide produced and the oxygen used. The appropriate food report shall provide the food coefficient. When the percentage of lipids in the diet increases, the CR must decrease, in order for body weight to remain constant. If CR does not decrease, the body continues to oxidize carbohydrates in storage, which must be replaced by increased nutrition, increased carbohydrate intake or endogenous synthesis from protein deposits.
This adaptation is effective and seems to have a strong genetic determination. Physiologically, adapting to a high-fat diet, such as a Western diet, requires a decrease in carbohydrate oxidation in order to maintain their deposits. If the oxidation of carbohydrates is low, the oxidation of lipids increases and CR decreases.
Measurements using calorimetric chambers or double-marked water show a positive correlation between energy consumption and body mass without lipids or body weight. To maintain body weight, overweight individuals must ingest a large amount of food to ensure energy needs. Obese people tend to significantly underestimate food intake. So a patient who says "Doctor, everything I eat, eat with difficulty" (something like, "I don't eat much" or "I don't eat too much"), means that he either doesn't recognize or doesn't really realize food intake.
Due to the inseriness of patients, anamnesis should be performed to assess energy needs should probably be abandoned. Reasonable assessment of energy consumption (kcal) in obese people is represented "arbitraryly" by multiplying body weight by 10. Another method takes into account the estimation of energy needs according to some equations for assessing the rate of basal metabolism (RMB). These are represented by: 1. in men between 18-30 years RMB = (0.0630 x current weight in kg + 2.8957) x 240 kcal/day, 2. in men between 31-60 years RMB = (0.0484 x current weight in kg + 3.6534) x 240 kcal/day, 3. in women between 18-30 years RMB = (0.0621 x current weight in kg + 2.0357) x 240 kcal/day and 4. in women between 31-60 years RMB = (0.0342 x current weight in kg + 3.5377) x 240 kcal/day.
In these formulas, the total energy requirement should be assessed according to the activity factor according to the energy consumption formula = RMB x activity factor. The activity factor values depend on the activity level and are: a. for the low activity level (sedentarism) the activity factor is 1,3, b. for the intermediate activity level (a few physical exercises) the activity factor is 1,5, and c. for the increased activity level (constant physical activity or job requiring this activity) the activity factor is 1,7.
This leads to the "concretization" of three predictive factors of weight gain: a low metabolic rate, a high CR, which shows carbohydrate oxidation and the need to eat to replace carbohydrates and insulin resistance. Adjusting the intake of nutritional factors can be seen as a feedback system with related and efferent signals. Factors that increase hunger are decreased blood glucose, which is achieved in 60% of cases (or more) before meals and increased gastric contractions and abdominal discomfort. These peripheral signals are integrated through neurotransmitters in the central nervous system and regulate food intake.
In addition, certain neurotransmitters are specific modulators of the ingestion of one or other of the nutritional factors (lipids, carbohydrates or proteins). So an increase or decrease in the intake of lipids, carbohydrates or proteins may occur as the main response to the action of specific neurotransmitters. These peptides and their monoamine substrate provide a powerful system that controls the quantity and quality of food intake.
At least four processes are involved in regulating food intake: 1. olfactory and taste factors (they can stimulate intake when foods are appetizing or inhibit it when they are not), 2. gastrointestinal distension, 3. release of gastrointestinal hormones (such as cholecystokinin and gastrine-releasing peptide) and 4. activation of thermogenesis components of the efferent sympathetic nervous system. These factors act simultaneously after ingestion of food to reduce the feeling of satiety, until a new low blood sugar level or gastric contractions cause the interest in food to increase again.
Let's move now on to more serious things, like obesity and the risk factors associated with it. The increase in mortality associated with obesity comes, in particular, from an increased risk of cardiovascular disease, hypertension, diabetes mellitus and possibly some cancers.
In the case of the cardiovascular system, in addition to increased pre and post-pregnancy, obesity is also associated with an increased risk of sudden death, probably through cardiac arrhythmias, as well as an increased risk of atherosclerosis, as a result of an abnormal lipid profile, which includes decreased levels of high-density lipoproteins (HDL) and increased levels of low-density lipoproteins, and , in particular, those with very low VLDL density (form B). The prevalence of hypertension is also very high, although the mechanism is unclear. One hypothesis suggests that hyperinsulinemia and insulin resistance increase sodium reabsorption in the renal tube and increase sympathetic control that causes arterial vasoconstriction.
Then it's the turn of diabetes. Type 2 diabetes mellitus - non-insulin dependent diabetes mellitus (DZNID) is almost non-existent in individuals with a BMI below 22. In "closed" social groups, the increased risk of diabetes in obese people has a strong family tinge (if one or both parents are diabetic, all children will develop diabetes if they become obese enough). If none of the parents is diabetic, less than 20% of children will develop diabetes. But in general, obesity precedes the onset of diabetes by a few months or years. Among the most early prognostic factors of diabetes is the development of insulin resistance. In conclusion, obesity prevention prevents, in most cases, diabetes.
Now, about cancer. The incidence of endometrial and postmenopausal breast cancer in women, prostate cancer in men and colorectal cancer in both women and men is related to the degree of obesity. Visceral obesity increases the risk of breast cancer in the postclimax period, independent of the degree of obesity. One explanation for susceptibility to endometrial and breast cancer in obese women lies in increasing estrogen production by flavouring circulating androstendionin in fat tissue.
Gallbladder disorders increase with obesity and age, possibly by increasing the excretion of bile cholesterol. The amount of cholesterol synthesized by the body each day increases by almost 20 mg per kilogram of fat tissue, so at a 10 kg increase in fat tissue the daily production and excretion of cholesterol increases by an amount comparable to the amount of cholesterol in an egg. Disturbances of nesting factors in the bile and alterations in the levels of bile acids and phospholipids can precipitate the appearance of gallstones.
For lung function, moderate obesity, in the absence of an underlying lung condition, has a weak effect on respiratory function. Sleep apnea, however, occurs in individuals with severe obesity and poses serious problems. Obstructive sleep apnea is believed to occur due to a local accumulation of fat in the tracheoopharynx area. Obstructive episodes of sleep apnea cause sleep disruption, as well as hypoxia and hypercapnia. If not corrected, this condition can lead to right heart failure. Continuous positive airway pressure can be administered at night to reduce or eliminate sleep apnea episodes. Weight loss has a particular value in remedying this condition.
In terms of joint and skin damage, the increase in the incidence of osteoarthritis is undoubtedly due on the one hand to trauma suffered by joints within obesity, but on the other hand, osteoarthritis also occurs without a direct link to weight gain, which suggests the involvement of other factors, the prevalence of gout is also increased and may reflect a decrease in the clearance of the ugly. Ketone bodies act competitively in the renal tube with the reabsorption of urates, and an increase in ketone production from lipid metabolism can increase urate levels.
Among the skin disorders in obesity are acanthosis nigricans, manifested by hyperpigmentation of skin folds in the neck, elbows and interphalangeal spaces associated with insulin resistance and DZNID. Skin turgor and friability can be increased in obesity, thus increasing the risk of fungal infections in the skin folds. Finally, venous stasis is increased in obese people.
Let's move on to the endocrine system. Insulin resistance, which leads to hyperinsulinemia, is a characteristic feature and is directly related to the degree of obesity. Growth hormone secretion is low, but insulin-like growth factor I levels are normal, suggesting that growth hormone is sufficient to stimulate the production of this important hormone. Testosterone levels are low in men, but free testosterone levels decrease only in conditions of massive obesity.
Obesity causes an early onset of menarche, a higher frequency of irregular and anovulatory cycles and an early menopause. The distribution of adiposity influences steroid metabolism in women. Women with predominantly central or visceral adiposity have a higher production of androgen hormones, such as testosterone, and women with gluteofemural obesity have increased emrone levels due to peripheral aromatization of circulating androgens. Changes in thyroid hormones and their metabolism occur with quantitative changes in nutritional factors. Triiodothyronine (T3) can be increased by overeating and decreased by starvation.
T3 levels are also elevated through a high carbohydrate diet and low through a low-carbohydrate diet. In contrast, levels of thyroxine and thyrotropin (TSH) are not influenced by diet. Obesity can sometimes be mistaken for Cushing's syndrome. The normal pattern of diurnal variations of plasma cortisol and urinary concentration of free cortisol are normal in obesity, but abnormal in Cushing's disease. if these patterns are equivocal, dynamic tests of the adrenal function are indicated.
So much for today...
Days full of
understanding, love and gratitude!!!
Dorin, Merticaru