Tuesday, June 23, 2009
With today's focus the obesity problem, peoples are starting to ask if a little baby
fat showed that infants were getting enough of the right nutrients or maybe there is problem with his/her health.
Is the baby growing properly? Is the baby getting too fat? How do you know between overweight and healthy/normal growth?
One doctor at Children's Hospital of Philadelphia believes that the problem of obesity starts as early as the first few months of our life. He has been combing through records of thousands of babies born in the early 1960s and has found that the amount of weight that children gain in the first four months of life is linked to childhood obesity at age 7, regardless of birth weight or if they were overweight at a year old.
“You can't predict overweight in kids in the first six months," says Frank Greer, professor of pediatrics at the University of Wisconsin and chairman of the American Academy of Pediatrics' committee on nutrition. "We don't want mothers calorie-counting." So if the baby looks fat doesn't mean that he needs to go on a diet. Furthermore, putting a baby on a diet would be dangerous. Because cells, especially those that surround budding brain cells, need fat to support and nurture them. As long as your baby is gaining both height and weight, weight gain shouldn't be a problem.
Until you get a professional opinion about your infant's growth, don't make any changes to his diet. You need the expert to know the difference between normal and overweight.
Be aware about medical consequences for childhood with obesity.
fat showed that infants were getting enough of the right nutrients or maybe there is problem with his/her health.
Is the baby growing properly? Is the baby getting too fat? How do you know between overweight and healthy/normal growth?
One doctor at Children's Hospital of Philadelphia believes that the problem of obesity starts as early as the first few months of our life. He has been combing through records of thousands of babies born in the early 1960s and has found that the amount of weight that children gain in the first four months of life is linked to childhood obesity at age 7, regardless of birth weight or if they were overweight at a year old.
“You can't predict overweight in kids in the first six months," says Frank Greer, professor of pediatrics at the University of Wisconsin and chairman of the American Academy of Pediatrics' committee on nutrition. "We don't want mothers calorie-counting." So if the baby looks fat doesn't mean that he needs to go on a diet. Furthermore, putting a baby on a diet would be dangerous. Because cells, especially those that surround budding brain cells, need fat to support and nurture them. As long as your baby is gaining both height and weight, weight gain shouldn't be a problem.
If your child's weight begins to increase faster than her height, though, you should immediately discuss it with your baby's doctor.
The doctor will compare your child's height and weight with standardized norms for children in the same sex and age. The doctor will also look at your child's weight in relation to his/her height on the growth chart.
Until you get a professional opinion about your infant's growth, don't make any changes to his diet. You need the expert to know the difference between normal and overweight.
Be aware about medical consequences for childhood with obesity.
Monday, June 22, 2009
Because of the dangers associated with childhood obesity, early intervention and family support is critical.
Childhood obesity is associated with a variety of adverse effects on psychosocial function, skeletal growth, and cardiovascular risk factors. Although several periods in childhood appear critical for the development of obesity, it is not yet clear whether these periods are also associated with an increased risk for the complications of obesity in either childhood or adulthood.
PSYCHOLOGICAL CONSEQUENCES
The psychosocial consequences of obesity are among the most widespread adverse effects of the disease. Children in kindergarten have already learned to associate obesity with a variety of less desirable traits, and rank obese children as those they like the least.
College acceptance rates for obese adolescent girls are lower than those for nonoverweight girls of comparable academic background. Adult women who are obese as adolescents or young adults earn less, more frequently remain unmarried, complete fewer years of school, and have higher rates of poverty than their nonobese peers.
Few of these effects occur among obese men. These results persist when controlled for the income and educational level of the young women’s parents, their IQ, or their self-esteem at baseline. The social effects of obesity in young adult women therefore appear related to an extension of the discrimination that begins in early childhood
SKELETAL GROWTH AND MATURATION
Obesity has multiple effects on growth and function in children and adolescents. For example, obese children tend to be taller, their bone ages are advanced, their fat-free mass is increased, and menarche in girls occurs earlier than in the non obese.
The origin of these effects is unclear. Increased height, advanced bone age, and earlier menarche may reflect the auxotrophic effects of increased food intake, whereas the increase in fat-free mass may result from both the increased muscle mass to support the increased weight and the nuclear mass of adipocytes. Because of their larger size, overweight children are frequently perceived and treated as older than they are, much to their confusion.
Furthermore, the increased stress of weight may cause bowing of the tibia (Blount’s disease) or femur and predispose young children to slipped capital femoral epiphysis.
CARDIOVASCULAR RISK FACTORS
As in adults, obesity affects blood pressure, lipid levels, and glucose tolerance in children and adolescents. Sixty percent of overweight children as young as 5–10 years of age have at least one of these cardiovascular disease risk factors, and more than 20% have two or more.
Obesity appears to be the leading cause of hypertension in children. Lipid profiles are similar to those in adults: low density lipoprotein levels are increased, and high density lipoprotein levels are low.
Increased rates of type 2 diabetes have followed the rapid increases in the prevalence of childhood and adolescent obesity. In some settings, type 2 diabetes now accounts for 30–40% of all new cases of diabetes. Although the prevalence of type 2 diabetes in the general population is low (0.5%), among some Native American groups the prevalence is close to 5%. Pediatric cases of type 2 diabetes generally occur among those 10–19 years of age, with a positive family history of type 2 diabetes, and more frequently among obese females or individuals with acanthosis nigricans.
At presentation, cases of type 2 diabetes in children and adolescents may resemble type 1 diabetes, suggesting that the actual prevalence of type 2 diabetes may be somewhat higher than it currently appears.
The most important factor related to the likelihood of obesity-associated hypertension, hyperlipidemia, and glucose intolerance in adults appears to be visceral fat. The few studies of adolescents that have controlled for total body fat have demonstrated an independent association of visceral fat, with unfavorable levels of systolic blood pressure and low- and high-density lipoprotein cholesterol.
PSEUDOTUMOR CEREBRI, SLEEP APNEA,
HEPATIC STEATOSIS, AND POLYCYSTIC OVARY DISEASE
Two of the most malignant consequences of childhood onset obesity are pseudotumor cerebri and sleep apnea. Obesity accounts for a significant proportion of pseudotumor cerebri, although the mechanism remains unclear.
The diagnosis is established by a history of headaches and the presence of papilledema. The most important sign of sleep apnea is daytime somnolence. Apnea is rarely mentioned spontaneously by parents, despite their apprehension and clear recognition of the difficulty that their child has breathing at night. If the tonsils are enlarged, a tonsillectomy may cure sleep apnea.
However, either unremitting sleep apnea or pseudotumor warrant the aggressive use of a restrictive hypocaloric diet in conjunction with vigorous family therapy.
Recent data from several studies indicate that 5–10% of overweight children and adolescents have modestly elevated liver enzymes. Ultrasound studies of these patients demonstrate increased hepatic fat deposition. Liver biopsies in severe cases have demonstrated steatohepatitis. Alcohol use appears to increase the likelihood of these changes.
Liver enzymes normalize with weight reduction. As in adults, polycystic ovary disease (PCOD) in adolescents is associated with obesity. The pathophysiology of PCOD is complicated; hyperinsulinemia is frequently associated with the syndrome, and hyperandrogenemia may contribute to increased fat-free mass and a male distribution of body fat.
EFFECTS OF CHILDHOOD OBESITY
ON PERSISTENCE INTO ADULTHOOD
The likelihood that obesity present during childhood will persist into adulthood rises with the age of the child, independent of the effect of parental obesity. Several studies have indicated that approximately 70% of overweight adolescents become obese adults. Age-of-onset effects of obesity in childhood or adolescence on either the severity or complications of adult obesity remain uncertain.
Obesity in adolescence appears to entrain a variety of morbid consequences. For example, in a cohort of adults originally studied from the time of their enrollment in elementary school through high school, all-cause and cardiovascular mortality rates were higher among men who were obese in high school, but not among women. The risk of diabetes and subsequent atherosclerosis was greater among both men and women who were obese during high school. Except for diabetes, the risk of death or subsequent morbidity was only modestly attenuated when controlled for the effect of adolescent obesity on adult weight. These results suggested that the effect of adolescent obesity on adult morbidity and mortality was not mediated by the effect of adolescent obesity on adult obesity. Either adolescent obesity had a direct impact on adult morbidity and mortality,or a third factor predisposed individuals to both adolescent obesity and adult disease.
Body fat distribution may represent the mechanism whereby obesity present in adolescence affects morbidity and mortality. Body fat distribution is more strongly centralized in adolescent males than in adolescent females. Therefore, one possibility is that the regionalization of fatness that occurs in obese adolescent males may increase the risk of later complications of obesity.
Based on book : EATING DISORDERS AND OBESITY Edited by Christopher G. Fairburn and Kelly D. Brownell
Childhood obesity is associated with a variety of adverse effects on psychosocial function, skeletal growth, and cardiovascular risk factors. Although several periods in childhood appear critical for the development of obesity, it is not yet clear whether these periods are also associated with an increased risk for the complications of obesity in either childhood or adulthood.
PSYCHOLOGICAL CONSEQUENCES
The psychosocial consequences of obesity are among the most widespread adverse effects of the disease. Children in kindergarten have already learned to associate obesity with a variety of less desirable traits, and rank obese children as those they like the least.
College acceptance rates for obese adolescent girls are lower than those for nonoverweight girls of comparable academic background. Adult women who are obese as adolescents or young adults earn less, more frequently remain unmarried, complete fewer years of school, and have higher rates of poverty than their nonobese peers.
Few of these effects occur among obese men. These results persist when controlled for the income and educational level of the young women’s parents, their IQ, or their self-esteem at baseline. The social effects of obesity in young adult women therefore appear related to an extension of the discrimination that begins in early childhood
SKELETAL GROWTH AND MATURATION
Obesity has multiple effects on growth and function in children and adolescents. For example, obese children tend to be taller, their bone ages are advanced, their fat-free mass is increased, and menarche in girls occurs earlier than in the non obese.
The origin of these effects is unclear. Increased height, advanced bone age, and earlier menarche may reflect the auxotrophic effects of increased food intake, whereas the increase in fat-free mass may result from both the increased muscle mass to support the increased weight and the nuclear mass of adipocytes. Because of their larger size, overweight children are frequently perceived and treated as older than they are, much to their confusion.
Furthermore, the increased stress of weight may cause bowing of the tibia (Blount’s disease) or femur and predispose young children to slipped capital femoral epiphysis.
CARDIOVASCULAR RISK FACTORS
As in adults, obesity affects blood pressure, lipid levels, and glucose tolerance in children and adolescents. Sixty percent of overweight children as young as 5–10 years of age have at least one of these cardiovascular disease risk factors, and more than 20% have two or more.
Obesity appears to be the leading cause of hypertension in children. Lipid profiles are similar to those in adults: low density lipoprotein levels are increased, and high density lipoprotein levels are low.
Increased rates of type 2 diabetes have followed the rapid increases in the prevalence of childhood and adolescent obesity. In some settings, type 2 diabetes now accounts for 30–40% of all new cases of diabetes. Although the prevalence of type 2 diabetes in the general population is low (0.5%), among some Native American groups the prevalence is close to 5%. Pediatric cases of type 2 diabetes generally occur among those 10–19 years of age, with a positive family history of type 2 diabetes, and more frequently among obese females or individuals with acanthosis nigricans.
At presentation, cases of type 2 diabetes in children and adolescents may resemble type 1 diabetes, suggesting that the actual prevalence of type 2 diabetes may be somewhat higher than it currently appears.
The most important factor related to the likelihood of obesity-associated hypertension, hyperlipidemia, and glucose intolerance in adults appears to be visceral fat. The few studies of adolescents that have controlled for total body fat have demonstrated an independent association of visceral fat, with unfavorable levels of systolic blood pressure and low- and high-density lipoprotein cholesterol.
PSEUDOTUMOR CEREBRI, SLEEP APNEA,
HEPATIC STEATOSIS, AND POLYCYSTIC OVARY DISEASE
Two of the most malignant consequences of childhood onset obesity are pseudotumor cerebri and sleep apnea. Obesity accounts for a significant proportion of pseudotumor cerebri, although the mechanism remains unclear.
The diagnosis is established by a history of headaches and the presence of papilledema. The most important sign of sleep apnea is daytime somnolence. Apnea is rarely mentioned spontaneously by parents, despite their apprehension and clear recognition of the difficulty that their child has breathing at night. If the tonsils are enlarged, a tonsillectomy may cure sleep apnea.
However, either unremitting sleep apnea or pseudotumor warrant the aggressive use of a restrictive hypocaloric diet in conjunction with vigorous family therapy.
Recent data from several studies indicate that 5–10% of overweight children and adolescents have modestly elevated liver enzymes. Ultrasound studies of these patients demonstrate increased hepatic fat deposition. Liver biopsies in severe cases have demonstrated steatohepatitis. Alcohol use appears to increase the likelihood of these changes.
Liver enzymes normalize with weight reduction. As in adults, polycystic ovary disease (PCOD) in adolescents is associated with obesity. The pathophysiology of PCOD is complicated; hyperinsulinemia is frequently associated with the syndrome, and hyperandrogenemia may contribute to increased fat-free mass and a male distribution of body fat.
EFFECTS OF CHILDHOOD OBESITY
ON PERSISTENCE INTO ADULTHOOD
The likelihood that obesity present during childhood will persist into adulthood rises with the age of the child, independent of the effect of parental obesity. Several studies have indicated that approximately 70% of overweight adolescents become obese adults. Age-of-onset effects of obesity in childhood or adolescence on either the severity or complications of adult obesity remain uncertain.
Obesity in adolescence appears to entrain a variety of morbid consequences. For example, in a cohort of adults originally studied from the time of their enrollment in elementary school through high school, all-cause and cardiovascular mortality rates were higher among men who were obese in high school, but not among women. The risk of diabetes and subsequent atherosclerosis was greater among both men and women who were obese during high school. Except for diabetes, the risk of death or subsequent morbidity was only modestly attenuated when controlled for the effect of adolescent obesity on adult weight. These results suggested that the effect of adolescent obesity on adult morbidity and mortality was not mediated by the effect of adolescent obesity on adult obesity. Either adolescent obesity had a direct impact on adult morbidity and mortality,or a third factor predisposed individuals to both adolescent obesity and adult disease.
Body fat distribution may represent the mechanism whereby obesity present in adolescence affects morbidity and mortality. Body fat distribution is more strongly centralized in adolescent males than in adolescent females. Therefore, one possibility is that the regionalization of fatness that occurs in obese adolescent males may increase the risk of later complications of obesity.
Based on book : EATING DISORDERS AND OBESITY Edited by Christopher G. Fairburn and Kelly D. Brownell
Monday, June 22, 2009
Obesity is of public health concern because of its association with serious medical complications that lead to increased morbidity and mortality. Being overweight is a problem in the United States. A third of all adult Americans are overweight.
If you are overweight, you are at high risk for obesity. And even if you don’t become obese, you are at a higher risk than a person with a healthy weight.
The most common complications associated with obesity are insulin resistance, diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, gallstones and cholecystitis, respiratory dysfunction, and increased incidence of certain cancers.
DIABETES MELLITUS
There is a strong positive correlation between the average weight in a population and the presence of type 2 (non-insulin-dependent) diabetes mellitus. In a male population divided into groups with BMIs of 25.0 to 26.9, 29 to 30, and greater than 35, the risk for diabetes (compared to a population with BMIs less than 21) increases 2.2-, 6.7-, and 42- fold, respectively.
The severity of the obesity is a determinant, as is the length of time obesity has been present. The pathogenesis of the diabetes is related to the insulin resistance caused by the obesity, which tends to increase in severity as BMI rises.
HYPERTENSION
About one-third of all obese persons are hypertensive. Epidemiological studies have demonstrated that for every 10-kilogram rise in body weight over normal, there is an average increase of 3 mm Hg in systolic and 2 mm Hg in diastolic pressure.
The longer the duration of obesity, the greater the risk of developing hypertension. Using data from the U.S. National Health Examination II Survey (in which obesity was defined as a weight for height above the 85th percentile of that of men and women in the third decade of life), the prevalence of hypertension in persons 20% or more overweight was twice that of persons of normal weight.
STROKE
Directly linked to the increased prevalence of hypertension in obese persons is an increased risk of stroke. In the Framingham Heart Study, for instance, there was a steeply rising curve of stroke with increasing weight.
For example, in the male group under 50 years of age, the risk of stroke rose from 22 to 30 to 49 per thousand as relative weights rose from 110% to 129% to higher than 130%, respectively.
DYSLIPIDEMIA
Obesity is associated with three particular abnormalities of circulating lipids:
1. Elevation of triglyceride levels,
2, Depression of high-density lipoprotein cholesterol (HDL-C) levels, and
3. Increased presence of small, dense low-density lipoprotein (LDL) particles.
CARDIOVASCULAR DISEASE
Coronary heart disease is usually described epidemiologically as cardiovascular disease (CVD), which includes angina pectoris, nonfatal myocardial infarction, and sudden death. These conditions occur more frequently in obese persons.
GALLBLADDER DISEASE
A number of changes that occur with obesity predispose an individual to gallstone formation. As cholesterol excretion from the liver increases, the bile becomes supersaturated with cholesterol.
Also, the motility of the gallbladder decreases, so that the sac is emptied much less efficiently. Whether this condition is due to a decreased sensitivity to the cholecystokinin released with each meal is unclear. The net effect is to increase the formation of predominantly cholesterol-containing stones.
These stones enhance the propensity to gallbladder inflammation, so that acute and chronic cholecystitis is much more common in obese persons. The incidence of this condition is higher in women than in men, partly because the prevalence of obesity is higher in women, but there may be other, as yet undiscovered reasons.
The need for surgery to remove diseased gallbladders is much more common in obese persons, and more so in women than in men.
RESPIRATORY DISEASE
The increased weight of the chest in obese persons leads to poor respiratory motion and also decreased compliance of the respiratory system, so that both vital capacity and total lung capacity are often low.
As the overweight becomes more severe, ventilation–perfusion abnormalities impair adequate oxygenation of the blood, even though carbon dioxide escape is adequate. With continued and persistent obesity, sleep apnea, either peripheral or central, may occur. Peripheral apnea is manifested by obstruction of the airway, caused by excess fatty tissue and the relaxation of the pharyngeal and glossal muscles. Central apnea is the result of a cessation of the signals that initiate inspiration.
The mechanism for this cessation of signals is unclear but apneic episodes may occur many times during the night, causing significant hyperventilation. The severity of all these abnormalities may lead to progressively more severe hypoxemia and hypercapnia, which in turn may lead to pulmonary hypertension, right heart failure, and cor pulmonale.
CANCER
The relationships of obesity to various forms of cancer are somewhat unclear, and more data are required. However, there is an association between some cancers and overweight.
It is not known whether the association may be due to other relationships, such
as a high-fat diet, elevated total calories, or other specific dietary components. However, the associations, leaving causality unclear, have been well described.
In women, higher rates have been described for endometrial, gallbladder, cervical, and ovarian cancers. For breast cancer, premenopausal women who are obese are less at risk, while postmenopausal women are at greater risk. It is possible that some of this postmenopausal effect on breast cancer is related to the increasing estrogenicity that occurs with increasing obesity as women age. This increased estrogenicity is the result of estrogen production in adipose tissue from sex hormone precursors that are soluble in fat and converted there to active estrogen. This combined estrogenicity might affect breast cancer incidence. An increased incidence of colorectal and prostate cancers has been found in obese men. The mechanisms of this effect are unknown, although recent evidence suggests that the increased insulin levels resulting from the insulin resistance of
obesity may have mitogenic effects.
ARTHRITIS AND GOUT
Because of the increased stress on the weight-bearing joints caused by increased weight, degenerative disease of these joints is quite common in obese persons, particularly as the duration and severity of the obesity increases.
There is also an increased incidence of gout in persons who are overweight. Such an association has been found repeatedly in cross-sectional studies. This association of gout and overweight is manifested to a much greater degree in men than in women, in whom higher levels of excess fat are needed for the disease to develop.
EFFECTS OF FAT DISTRIBUTION
Epidemiological data from many countries have established fat distribution as an important determinant of disease risk. As a result, not only the degree of obesity but also the location of deposited fat are important. Results of available studies suggest that intra-abdominal, or visceral, fat is crucial in this regard. The pathophysiology may be related to the increased lipolytic activity of fat cells in this region, which release large amounts of FFA to the liver and the periphery. The combination of hyperlipacidemia and hyperinsulinemia leads to increased VLDL production, with resultant hypertriglyceridemia. The lipacidemia also inhibits glucose transport and oxidation in muscle, increasing the insulin resistance and the propensity for diabetes. The hyperinsulinemia leads to increased sodium absorption and increases the risk of hypertension.
The medical complications of obesity are considerable. It must be realized that diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, and stroke—aside from cancer, AIDS, and violence—are the leading causes of morbidity and mortality in the developed world. If cancer, a condition in which obesity often plays a part, is added, obesity is a large contributor to the burden of disease affecting industrialized countries.
Whether the effect of these diseases is direct and independent or indirect, through enhancing other risk factors, is essentially irrelevant from a public health perspective. If obesity could be prevented, a very significant and positive impact on chronic disease and mortality would occur.
Based on book : EATING DISORDERS AND OBESITY Edited by Christopher G. Fairburn and Kelly D. Brownell
This posting about medical consequences for childhood with obesity
If you are overweight, you are at high risk for obesity. And even if you don’t become obese, you are at a higher risk than a person with a healthy weight.
The most common complications associated with obesity are insulin resistance, diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, gallstones and cholecystitis, respiratory dysfunction, and increased incidence of certain cancers.
DIABETES MELLITUS
There is a strong positive correlation between the average weight in a population and the presence of type 2 (non-insulin-dependent) diabetes mellitus. In a male population divided into groups with BMIs of 25.0 to 26.9, 29 to 30, and greater than 35, the risk for diabetes (compared to a population with BMIs less than 21) increases 2.2-, 6.7-, and 42- fold, respectively.
The severity of the obesity is a determinant, as is the length of time obesity has been present. The pathogenesis of the diabetes is related to the insulin resistance caused by the obesity, which tends to increase in severity as BMI rises.
HYPERTENSION
About one-third of all obese persons are hypertensive. Epidemiological studies have demonstrated that for every 10-kilogram rise in body weight over normal, there is an average increase of 3 mm Hg in systolic and 2 mm Hg in diastolic pressure.
The longer the duration of obesity, the greater the risk of developing hypertension. Using data from the U.S. National Health Examination II Survey (in which obesity was defined as a weight for height above the 85th percentile of that of men and women in the third decade of life), the prevalence of hypertension in persons 20% or more overweight was twice that of persons of normal weight.
STROKE
Directly linked to the increased prevalence of hypertension in obese persons is an increased risk of stroke. In the Framingham Heart Study, for instance, there was a steeply rising curve of stroke with increasing weight.
For example, in the male group under 50 years of age, the risk of stroke rose from 22 to 30 to 49 per thousand as relative weights rose from 110% to 129% to higher than 130%, respectively.
DYSLIPIDEMIA
Obesity is associated with three particular abnormalities of circulating lipids:
1. Elevation of triglyceride levels,
2, Depression of high-density lipoprotein cholesterol (HDL-C) levels, and
3. Increased presence of small, dense low-density lipoprotein (LDL) particles.
CARDIOVASCULAR DISEASE
Coronary heart disease is usually described epidemiologically as cardiovascular disease (CVD), which includes angina pectoris, nonfatal myocardial infarction, and sudden death. These conditions occur more frequently in obese persons.
GALLBLADDER DISEASE
A number of changes that occur with obesity predispose an individual to gallstone formation. As cholesterol excretion from the liver increases, the bile becomes supersaturated with cholesterol.
Also, the motility of the gallbladder decreases, so that the sac is emptied much less efficiently. Whether this condition is due to a decreased sensitivity to the cholecystokinin released with each meal is unclear. The net effect is to increase the formation of predominantly cholesterol-containing stones.
These stones enhance the propensity to gallbladder inflammation, so that acute and chronic cholecystitis is much more common in obese persons. The incidence of this condition is higher in women than in men, partly because the prevalence of obesity is higher in women, but there may be other, as yet undiscovered reasons.
The need for surgery to remove diseased gallbladders is much more common in obese persons, and more so in women than in men.
RESPIRATORY DISEASE
The increased weight of the chest in obese persons leads to poor respiratory motion and also decreased compliance of the respiratory system, so that both vital capacity and total lung capacity are often low.
As the overweight becomes more severe, ventilation–perfusion abnormalities impair adequate oxygenation of the blood, even though carbon dioxide escape is adequate. With continued and persistent obesity, sleep apnea, either peripheral or central, may occur. Peripheral apnea is manifested by obstruction of the airway, caused by excess fatty tissue and the relaxation of the pharyngeal and glossal muscles. Central apnea is the result of a cessation of the signals that initiate inspiration.
The mechanism for this cessation of signals is unclear but apneic episodes may occur many times during the night, causing significant hyperventilation. The severity of all these abnormalities may lead to progressively more severe hypoxemia and hypercapnia, which in turn may lead to pulmonary hypertension, right heart failure, and cor pulmonale.
CANCER
The relationships of obesity to various forms of cancer are somewhat unclear, and more data are required. However, there is an association between some cancers and overweight.
It is not known whether the association may be due to other relationships, such
as a high-fat diet, elevated total calories, or other specific dietary components. However, the associations, leaving causality unclear, have been well described.
In women, higher rates have been described for endometrial, gallbladder, cervical, and ovarian cancers. For breast cancer, premenopausal women who are obese are less at risk, while postmenopausal women are at greater risk. It is possible that some of this postmenopausal effect on breast cancer is related to the increasing estrogenicity that occurs with increasing obesity as women age. This increased estrogenicity is the result of estrogen production in adipose tissue from sex hormone precursors that are soluble in fat and converted there to active estrogen. This combined estrogenicity might affect breast cancer incidence. An increased incidence of colorectal and prostate cancers has been found in obese men. The mechanisms of this effect are unknown, although recent evidence suggests that the increased insulin levels resulting from the insulin resistance of
obesity may have mitogenic effects.
ARTHRITIS AND GOUT
Because of the increased stress on the weight-bearing joints caused by increased weight, degenerative disease of these joints is quite common in obese persons, particularly as the duration and severity of the obesity increases.
There is also an increased incidence of gout in persons who are overweight. Such an association has been found repeatedly in cross-sectional studies. This association of gout and overweight is manifested to a much greater degree in men than in women, in whom higher levels of excess fat are needed for the disease to develop.
EFFECTS OF FAT DISTRIBUTION
Epidemiological data from many countries have established fat distribution as an important determinant of disease risk. As a result, not only the degree of obesity but also the location of deposited fat are important. Results of available studies suggest that intra-abdominal, or visceral, fat is crucial in this regard. The pathophysiology may be related to the increased lipolytic activity of fat cells in this region, which release large amounts of FFA to the liver and the periphery. The combination of hyperlipacidemia and hyperinsulinemia leads to increased VLDL production, with resultant hypertriglyceridemia. The lipacidemia also inhibits glucose transport and oxidation in muscle, increasing the insulin resistance and the propensity for diabetes. The hyperinsulinemia leads to increased sodium absorption and increases the risk of hypertension.
The medical complications of obesity are considerable. It must be realized that diabetes mellitus, hypertension, dyslipidemia, cardiovascular disease, and stroke—aside from cancer, AIDS, and violence—are the leading causes of morbidity and mortality in the developed world. If cancer, a condition in which obesity often plays a part, is added, obesity is a large contributor to the burden of disease affecting industrialized countries.
Whether the effect of these diseases is direct and independent or indirect, through enhancing other risk factors, is essentially irrelevant from a public health perspective. If obesity could be prevented, a very significant and positive impact on chronic disease and mortality would occur.
Based on book : EATING DISORDERS AND OBESITY Edited by Christopher G. Fairburn and Kelly D. Brownell
This posting about medical consequences for childhood with obesity
Sunday, June 21, 2009
Here’s a few practical tips for you as a parents if you have an obese children. It’s good to keep in mind that obesity is a medical problem. Just as people shouldn’t be judged if they have high blood pressure or are blind. Obesity is related to certain health risks, but the good news is that obesity is treatable.
Remember this two points when you think about helping children with obese.
First of all is try to involve the whole family to building healthy eating habits.
This benefits for everyone, does not only for child who is overweight. Balance the calories in the foods — provide adequate nutrition and an appropriate number of calories. Include plenty of vegetables, fruits, low-fat or non-fat milk, and whole-grain products. You can also encourage your family to drink lots of water, limit sugar-sweetened beverages, add more fiber, and make their favorite dishes healthier.
Try to always eat meals together as a family. Eating together at meal times helps children learn to enjoy a variety of foods. Don’t force your kids, but don’t give up and try again, and again. Some kids will need to have a new food served to them 10 times or more before they will eat it.
Be aware that some high-fat or high-sugar foods and beverages may be strongly marketed to kids. Stay away your kids from this kind of foods.
The next step is increase the physical activity.
You must help your kids to stay active. Regular physical activity has many health benefits. Do it with the whole families and make it a fun time. Family bike ride, or a walk through a local park on Sunday is a good idea.
Encourage your child to join a sports team or class, such as soccer, dance, basketball, or gymnastics at school. Help him or her find which one physical activities that are fun and comfortable.
Do not put your child on a weight-loss diet unless your health care provider tells you to. If children do not eat enough, they may not grow and learn as well as they should.
Think about a treatment program only if changed your family’s eating and physical activity not reached a healthy weight or your child’s health or emotional is at risk because of their weight.
Children cannot lose weight on their own. They need a parent who can help them make smart food choices and who will encourage them to exercise. Childhood obesity associated with serious medical consequences, so do your best to help your children.
Remember this two points when you think about helping children with obese.
1. General purpose for overweight and obese children or teens is to reduce the rate of weight gain while allowing normal growth.
2. Healthy eating and physical activity habits are key to achieve that goals. Eating too much and exercising too little ( the general prime factor ) may lead your child to obesity
First of all is try to involve the whole family to building healthy eating habits.
This benefits for everyone, does not only for child who is overweight. Balance the calories in the foods — provide adequate nutrition and an appropriate number of calories. Include plenty of vegetables, fruits, low-fat or non-fat milk, and whole-grain products. You can also encourage your family to drink lots of water, limit sugar-sweetened beverages, add more fiber, and make their favorite dishes healthier.
Try to always eat meals together as a family. Eating together at meal times helps children learn to enjoy a variety of foods. Don’t force your kids, but don’t give up and try again, and again. Some kids will need to have a new food served to them 10 times or more before they will eat it.
Be aware that some high-fat or high-sugar foods and beverages may be strongly marketed to kids. Stay away your kids from this kind of foods.
The next step is increase the physical activity.
You must help your kids to stay active. Regular physical activity has many health benefits. Do it with the whole families and make it a fun time. Family bike ride, or a walk through a local park on Sunday is a good idea.
Encourage your child to join a sports team or class, such as soccer, dance, basketball, or gymnastics at school. Help him or her find which one physical activities that are fun and comfortable.
Do not put your child on a weight-loss diet unless your health care provider tells you to. If children do not eat enough, they may not grow and learn as well as they should.
Think about a treatment program only if changed your family’s eating and physical activity not reached a healthy weight or your child’s health or emotional is at risk because of their weight.
Children cannot lose weight on their own. They need a parent who can help them make smart food choices and who will encourage them to exercise. Childhood obesity associated with serious medical consequences, so do your best to help your children.
