“Why do children get metabolic syndrome?”
My son was diagnosed with metabolic syndrome and he's only 13 years old. I feel like he's too young for this disorder. Why do some children get metabolic syndrome? (He's also overweight as well)
6 Answers
It is very hard to make a mother to understand, do not overfeed your child. As mother, she feels obligated to give food to her child in the amount he/she wants to eat. Majority of mothers when told to limit food to their kids, their next question is that you want me to starve my child.
In fact most of the time, this over feeding is the reason for Metabolic Syndrome leading Diabetes and hypertension at younger age. The child when grows up is going to blame the same mother saying I was just a kid why did you not control my food intake.
I hope I answered your question though you may not like it.
In fact most of the time, this over feeding is the reason for Metabolic Syndrome leading Diabetes and hypertension at younger age. The child when grows up is going to blame the same mother saying I was just a kid why did you not control my food intake.
I hope I answered your question though you may not like it.
Metabolic syndrome is a very serious medical condition that affects almost a third of the American adult population. It has high morbidly and mortality rates. It is associated directly and indirectly in a bout 75% of the health care cost of America. That comes to over 2.5 trillion dollars per year out of the 3.5 trillion annual health expense in America. This is bigger than the GNP of many of the advanced countries of Europe. This could have been enough annual budget for free health care system in America. Preventing metabolic syndrome and it grave comorbidities will ease this financial burden. Metabolic syndrome is a constellation of three or more conditions. It is composed of at least 3 of the following 5 conditions:
1) Central obesity
2) Hypertension
3) Hyperglycemia and/or prediabetes
4) Elevated triglycerides
5) Low serum high-density lipoprotein
6) Microalbuminuria
Metabolic syndrome has been defined by at list seven different organizations using any of the above three or more combinations. Definition of Metabolic Syndrome:
1) WHO DEFINITION: Insulin resistance plus any 2 of the above conditions
2) EUROPEAN GROUP FOR STUDY OF INSULIN RESISTANCE DEFINITION:
Insulin resistance and any of the above 2 conditions with the exception of microalbuminuria.
3) NCEP ATP III (national cholesterol education pane lll) DEFINITION:
Any of the three above conditions except microalbuminuria.
4) AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS DEFINITION: No specification of any combination, but considered the following conditions to be included: Elevated triglycerides, reduced HDL-C, high blood pressure, and obesity. The panel also included increase in hypercoagulability, endothelial dysfunction and inflammatory markers.
5) INTERNATIONAL DIABETES FEDERATION GLOBAL CONSENSUS DEFINITION: Increased wait circumference (WC) >94 cm for men and 80cm for women plus 2 of any of the above conditions.
6) AMERICAN DIABETES ASSOCIATION: The panel lowered the criteria for insulin resistance but concur with the definition of NCEP lll definition.
7) AMERICAN HEART ASSOCIATION: Any combination of 3 conditions.
Insulin Resistance is closely related with prediabetes HbA1c >5.7% or impaired fasting glucose >100 mg/dl of glucose or impaired 2 hour postprandial blood glucose (140mg/dl of glucose).
Since many different criteria were used to define metabolic syndrome in adults, defining the metabolic syndrome in children and adolescents has been difficult. So far, there are no consensus or guidelines for the pediatric population, though there are many definitions with sight differences. Currently, the international diabetes federation defines metabolic syndrome in children and adolescents grater than 10 years old as follows. Central obesity plus at least 2 out of 4 criteria ≥3 criteria:
1) Central Obesity: Waist circumference (WC) ≥90th percentile for age and gender.
2) Hypertension: Systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥85 mmHg or treatment with anti-hypertensive medication BP ≥90th percentile for age and gender
3) Hypertriglyceridemia Triglyceride ≥150 mg/dL
4) Low HDL (high Density Lipoprotein cholesterol): HDL <40 mg/dL HDL ≤40 mg/dL
5) Impaired glucose Fasting plasma glucose ≥100 mg/dL or known T2DM
Others define childhood and adolescent metabolic syndrome using 3 or more criteria in a slightly different way. The clinical features seen in metabolic syndrome are as follows:
1) Obesity: Over the last 30 years, the rate of obesity has been speeding up at an alarming rate. During the same period the prevalence of obesity has increased by 3-4 fold both in adults and children. Obesity in children is increasing more in Hispanic and other minorities both in children and adults though every one is getting bigger. Obesity ( weight greater than 95 percentile for age and gender) has a good correlation with the metabolic syndrome in children and adolescents. About 20% (about 15 million children) of children and adolescents are obese ( there are about 85 million children in America). And a much bigger than that are overweight. Almost 30% of Hispanic children, 22% of blacks and 15% of whites are obese. About 80% of them may continue to be obese adults as well. About 90% of obese children have at list one metabolic risk factor. About 30% of obese children have metabolic syndrome. Non-obese over weight children (weight greater than 85 percentile but less than 95 percentile) have 12% prevalence of metabolic syndrome. About 3.5% of the pediatric population have metabolic syndrome. Normal weight children have very low rate of metabolic syndrome (about 0.5%).
The hall mark of metabolic syndrome is therefore insulin resistance for most definitions. Metabolic syndrome is associated none alcoholic fatty liver, elevated liver enzymes, high uric acid level; nonalcoholic fatty liver disease; vascular inflammation, polycystic ovarian syndrome, acanthosis nigricansin, cardiovascular disease sexual dysfunction and others.
About 30% of adult Americans may have metabolic syndrome with or without obesity. Metabolic syndrome is more common in obese people though none obese people have metabolic syndrome as well. About 80% of obese people have metabolic syndrome (sick obese) in America. In the adult population, about 20% of obese Americans are healthy ( healthy obese). There are over a 100 million Americans with Metabolic syndrome. Out of these 75 million are obese. About 30% of America adult population (100 million) are obese adults as well. About 25 million people have metabolic syndrome but they have normal weight or are slightly over weight (thin sick). The prevalence of metabolic syndrome increases with age and the degree of obesity in both adults and children. The same is also true for obesity.
Obesity may not be a diseases but a metabolic adaption to store excess ingested calories as a body fat. Obesity is an association with metabolic syndrome but not a cause of the disease.
During human evolution the thrifty gene that allowed people to undergo insulin resistance in order to store fat during plenty was selected so that survival will be insured during scarcity. However we live in modern society that we have only plenty and no scarcity. In todays affluent society the same thrifty gene may have become a liability rather than security.
For what ever reason in the majority of obese adults and over 30% obese children the fat cells get sick. Sick fat tissue leads to metabolic syndrome through exporting insulin resistance or other inflammatory or metabolic means. But when fat tissue remain healthy, obesity will not pose a metabolic problem.
When fatty tissue is sick (adiposopathy) it leads to fatty acid leakage which will over load the liver and make fat droplets in the liver leading to fatty liver. This also unleashes inflammatory cytokines that damage the vascular lining leading to inflammation and atherosclerosis. It also exports insulin resistance fueling the metabolic syndrome. Obese people with healthy adipose tissue share non of these metabolic consequence and remain obese healthy. What makes one obese group develop metabolic syndrome but not the other group may be a matter of genetic susceptibility with greater share of environmental factors.
Obesity is not only an important part of the metabolic syndrome but also in the development of cardiovascular disease and type 2 diabetes mellitus. It is quite obvious that there is a strong association between the degree of obesity, insulin resistance and the prevalence of metabolic syndrome.
Obesity is when the body mass index (BMI), is ≥95th percentile for gender and age. Overweight is when the BMI is ≥85th percentile and <95th percentile for age and gender.
Visceral fat has also a strong association with both childhood metabolic syndrome and cardiovascular disease later in life, independent of the degree of obesity. Waist circumference can indicate visceral adiposity. There are no current pediatric reference range for waist circumference, instead waist to hip ratio can be used to determine visceral adiposity. A waist to hip ratio of greater than) 0.6 will be considered a risk for metabolic syndrome.
Metabolic syndrome is therefore an interaction between obesity, insulin and inflammation.
Obesity increases visceral fat that leads to fatty acid leakage that cause decrease glucose uptake by the muscle and increased glucose and triglyceride production by the liver. This increases over production of triglycerides (lipids) by the liver and increased fat synthesis in the adipose tissue. The sick visceral adipose release inflammatory mediators such as Interleukins (IL) 6, tumor necrotic factor alpha, C-reactive proteins and plasminogen. These mediators cause vascular inflammation and hypercoagulable state. These cause insulin resistance and impaired insulin production. Visceral adiposopathy also causes abnormal Adipokines. It cause low adiponectin, an adipokine, (that is important in protecting the body from oxidative stress) and leptin resistance. Leptin is an important hormone made by fat cells and controls satiety in the hypothalamus. Leptin deficiency or leptin resistance leads to continuous hunger as if there is excess ghrelin (a hormone for hunger). Insulin resistance leads to leptin resistance and over eating behavior. Visceral adiposity causes excess release of angiotensin II type receptors leading to activation Reactive oxygen species and increase stimulation of renin angiotensin aldosterone system in the kidneys that will increase salt retention from the kidneys, increased vascular tone. These causes chronic increase in blood pressure and cause chronic tissue oxidative stress.
Visceral adiposity can lead to neurohumoral activation, chronic inflammation and insulin resistance. The interaction of these entities leads to metabolic syndrome.
2) Dyslipidemias; Abnormal lipids mainly triglyceride abnormalities are essential in the metabolic syndrome. Insulin resistance leads to fatty acid leakage (adiposopathy). There is activation of protein kinases that control over production of liver glucose and synthesis of lipids in the liver and adipose tissue (lipogenesis) The liver over produces triglycerides (VLDL) and sugars. The muscle glucose uptake decreases. The excess production of triglycerides in the liver are transported to the muscle and adipose tissue for energy use and storage. Since lipids are not soluble in plasma they are transported in lipoproteins called Apoliporoteins. Apolipoprotein B transports triglycerides from the liver to tissue as VLDL(very low density lipoproteins). The VLDL binds to it receptor in the tissue to deliver the triglyceride for energy and/or storage in adipose tissue. Once it sheds most of it triglycerides it be come smaller but cholesterol richer particle known as IDL (intermediate lipoprotein lipase) This IDL continues to give up more of its Triglycerides to the tissues with the help of an enzyme called lipoprotein lipase with the help of another apolipoprotein call Apo C2. Once it gives up most of it triglycerides it becomes cholesterol enriched species called LDL low density lipoprotein. LDL gives its cholesterol to all the cells for the repair of their extensive cell membrane and those tissues that need to make androgens estrogen vitamin D and others from cholesterol. The rest of the LDL traffics back to the liver to be dismantled by the liver and repackaged with triglycerides in the liver. This cycle goes on and on in life. During its trafficking LDL can give some of it cholesterol or triglycerides to HDL (high density lipoprotein) a lipoprotein called good cholesterol that scavenges any cholesterol in the body so that un used cholesterol does not precipitate to form atherosclerosis in the vasculature when LDL is trafficking.
However in the metabolic syndrome or insulin resistance, an enzyme that controllers triglyceride hydrolysis in the tissue called ApoC3 is over produced. This this blocks the hydrolysis of triglycerides by the tissue causing elevated triglyceride level (VLDL) before and after a meals. There is also an overproduction of Triglycerides (elevated VLDL) from the liver since there is fatty acid leakage from sick adipose tissue and the liver is over producing triglycerides from fatty acids and package them as VLDL for trafficking. The triglycerides can only be trafficked from liver as VLDL in the blood since they are not soluble in plasma. So VLDL which is Apo B particle, also called LDL(p) particle increases though the LDL cholesterol LDLc may not increase. In insulin resistance or metabolic syndrome there is over production of triglycerides in the liver and trafficked as VLDL out of the liver in the plasma. The excess triglycerides (VLDL) atherogenic particles called LDLp that are small dense easily oxidized particles that cause atherosclerosis by breaching the vascular endothelium. The overproduced VLDL (triglycerides out side the liver) donate their triglycerides to HDL (the good cholesterol) depleting it cholesterol content and making it small and susceptible to renal elimination. This makes the HDL cholesterol low in metabolic syndrome.
Some of the triglycerides overproduced in the liver become oil droplets and sequester in the liver causing non alcoholic fatty liver which can lead to fatty liver disease and cirrhosis. None alcoholic fatty liver also exports insulin resistance independent of visceral obesity.
3) Insulin resistance can lead to glucose impaired fasting glucose or impaired 2 hour post prandial after 75 grams of glucola or heavy carbohydrate meal and may progress to Type 2 diabetes when of β-cell function deteriorates as a result of diminished insulin secretion. Impaired fasting glucose is defined as fasting blood glucose of ≥100mg/dL and impaired glucose tolerance is diagnosed if blood glucose is ≥140 at the 2-h mark of the oral glucose tolerance test. Routine monitoring of the progression from insulin resistance to type 2 diabetes is important since the progression is variable
4) None alcoholic fatty liver disease (NAFLD): This is becoming the most common cause of liver disease in children due to the rise obesity. Obesity strongly correlates with fatty liver disease in children.
Diet such as high fructose consumption may also lead to NAFD independent of obesity. Excess ingestion of high fructose, branched chain aminoacides and lactate are converted into triglycerides. Excess triglycerides lead to fat droplets is the liver, and excess VLDL when triglycerides are trafficked out side the liver. This can lead to cirrhosis. Monitoring of liver with US or other non invasive modalities are required. Liver biopsy may be indicated in some cases.
5) Polycystic ovarian syndrome (PCOS): PCOS is another very important risk factor for metabolic syndrome. It is a constellation such as Amenorrhea, high androgen levels or phenotypic manifestations of hyper androgenemia such as hirsutism, severe acne, voice changes etc. with or with out cysts in the ovaries. PCOS is strongly associated with obesity and insulin resistance. It is an independent risk factor for metabolic syndrome regardless of obesity or presence of insulin resistance.
Women with PCOS should be screened for metabolic syndrome regularly.
Children and adolescents should be screened for overweight and obesity , fatty liver disease dyslipidemias, diabetes, PCOS, metabolic syndrome and hypertension annually and when indicated. Risk factors should be identified on individual bases. Fasting lipid profile should be obtained specially in overweight children. The triglyceride and HDL need to be look at carefully. The triglyceride should not be more than 3 times than HDL (good cholesterol) ratio of TG/HDL <3. If it is >3.0 there is a risk metabolic syndrome should be considered.
Prevention should be directed towards maintaining healthy weight though regular structured physical activity and healthy diet. Soft drinks, sports drinks including diet drinks should be avoided if possible. Avoiding salty foods and processed foods will be very important. Children should be encouraged to eat plenty of vegetables and reasonable amount of fresh fruits. Unlike vegetables excess fruits have a lot of sugar though they contain fibers to slow glucose absorption. So, the amount of fruits should be limited to a reasonable portion a day.
Metabolic syndrome should be managed initially, with healthy balanced diet and regular structured physical activity. For insulin resistance, insulin sensitizers such as metformin and actos should be considered. For patients with fatty liver actos (pioglitazone) could be tried both in children and adults.
Lipids and high blood pressure should be treated aggressively if life style change, diet and exercise are not enough. A good dietician is of at most importance in this case. Behavioral modification and psychological counseling may help in some cases. It is also important to work with your doctor closely for a good outcome.
Going back to your son: Metabolic syndrome is getting common with the emergence of overweight/obesity. There are almost 15 million children (20%)with obesity in the USA. About 30% of obese children have metabolic syndrome. There also 12% children with metabolic syndrome who are not obese but they are over weight. About 0.5% of normal weight children have metabolic syndrome. The degree of overweight correlates with metabolic syndrome though it is hard to make a causal relationship. Most overweight kids will end up overweight as adults and will have all the metabolic syndrome and its associates, such as type 2 diabetes, cardiovascular disease, high blood pressure, abnormal lipids, fatty liver, PCOS, and other diseases.
Most of metabolic syndrome and diabetes are associated with overweight/obesity. Visceral fat can lead to insulin resistance, release of inflammatory chemicals, fatty liver and abnormal lipids. Genetic interaction may have weak association with obesity and metabolic syndrome. Most of it is environmental exposures such as high sugar intake specially high fructose syrups added to almost 80% our processed foods and drinks. We are consuming more sugar now than 30 years ago. We started consuming high sugars since cheaper highly sweet corn syrup emerged in the late 70's. Metabolic diseases take time to emerge after the time of exposure. And the metabolic consequences have now expressing at a younger age. The average sugar consumption should be 5 teaspoon per day. Currently we consume about 20 teaspoon per day. We are consuming about 170 pounds of sugar per year per person. This adds about 300 extra calories a day. These sugars are cheap and very sweet. Mostly they are high fructose corn syrup added to our processed food and drinks. Fructose does not burn in the body. It is converted at a cost of energy to glucose and fat only in the liver. Excess fat will cause weight gain and insulin resistance leading to metabolic syndrome. It can also lead to metabolic syndrome without causing obesity. There are other causes of metabolic syndrome as discussed above. Children as young as 2 years old are getting type 2 diabetes. Metabolic syndrome is also happening at this early age. The reason is there is something in the environment (such as fructose) that we have created or are exposed that is causing these epidemic of metabolic diseases including metabolic syndrome. Diseases that are supposed to be of adulthood are starting early in childhood now.
You should make sure you son is getting good care. With proper diet structured physical activity and reasonable weight loss you should try to reverse the situation. If diet and physical activity are not enough and if indicated use of insulin sensitizer such as metformin and actos will be helpful. Pioglitazones (actos) are options in fatty liver well. You should see a good nutritionist to help you about the direction of over all diet plan. Counseling may be necessary indicated as well. It is very important that you work closely with your son's doctor.
Good luck.
1) Central obesity
2) Hypertension
3) Hyperglycemia and/or prediabetes
4) Elevated triglycerides
5) Low serum high-density lipoprotein
6) Microalbuminuria
Metabolic syndrome has been defined by at list seven different organizations using any of the above three or more combinations. Definition of Metabolic Syndrome:
1) WHO DEFINITION: Insulin resistance plus any 2 of the above conditions
2) EUROPEAN GROUP FOR STUDY OF INSULIN RESISTANCE DEFINITION:
Insulin resistance and any of the above 2 conditions with the exception of microalbuminuria.
3) NCEP ATP III (national cholesterol education pane lll) DEFINITION:
Any of the three above conditions except microalbuminuria.
4) AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS DEFINITION: No specification of any combination, but considered the following conditions to be included: Elevated triglycerides, reduced HDL-C, high blood pressure, and obesity. The panel also included increase in hypercoagulability, endothelial dysfunction and inflammatory markers.
5) INTERNATIONAL DIABETES FEDERATION GLOBAL CONSENSUS DEFINITION: Increased wait circumference (WC) >94 cm for men and 80cm for women plus 2 of any of the above conditions.
6) AMERICAN DIABETES ASSOCIATION: The panel lowered the criteria for insulin resistance but concur with the definition of NCEP lll definition.
7) AMERICAN HEART ASSOCIATION: Any combination of 3 conditions.
Insulin Resistance is closely related with prediabetes HbA1c >5.7% or impaired fasting glucose >100 mg/dl of glucose or impaired 2 hour postprandial blood glucose (140mg/dl of glucose).
Since many different criteria were used to define metabolic syndrome in adults, defining the metabolic syndrome in children and adolescents has been difficult. So far, there are no consensus or guidelines for the pediatric population, though there are many definitions with sight differences. Currently, the international diabetes federation defines metabolic syndrome in children and adolescents grater than 10 years old as follows. Central obesity plus at least 2 out of 4 criteria ≥3 criteria:
1) Central Obesity: Waist circumference (WC) ≥90th percentile for age and gender.
2) Hypertension: Systolic blood pressure ≥130 mmHg or diastolic blood pressure ≥85 mmHg or treatment with anti-hypertensive medication BP ≥90th percentile for age and gender
3) Hypertriglyceridemia Triglyceride ≥150 mg/dL
4) Low HDL (high Density Lipoprotein cholesterol): HDL <40 mg/dL HDL ≤40 mg/dL
5) Impaired glucose Fasting plasma glucose ≥100 mg/dL or known T2DM
Others define childhood and adolescent metabolic syndrome using 3 or more criteria in a slightly different way. The clinical features seen in metabolic syndrome are as follows:
1) Obesity: Over the last 30 years, the rate of obesity has been speeding up at an alarming rate. During the same period the prevalence of obesity has increased by 3-4 fold both in adults and children. Obesity in children is increasing more in Hispanic and other minorities both in children and adults though every one is getting bigger. Obesity ( weight greater than 95 percentile for age and gender) has a good correlation with the metabolic syndrome in children and adolescents. About 20% (about 15 million children) of children and adolescents are obese ( there are about 85 million children in America). And a much bigger than that are overweight. Almost 30% of Hispanic children, 22% of blacks and 15% of whites are obese. About 80% of them may continue to be obese adults as well. About 90% of obese children have at list one metabolic risk factor. About 30% of obese children have metabolic syndrome. Non-obese over weight children (weight greater than 85 percentile but less than 95 percentile) have 12% prevalence of metabolic syndrome. About 3.5% of the pediatric population have metabolic syndrome. Normal weight children have very low rate of metabolic syndrome (about 0.5%).
The hall mark of metabolic syndrome is therefore insulin resistance for most definitions. Metabolic syndrome is associated none alcoholic fatty liver, elevated liver enzymes, high uric acid level; nonalcoholic fatty liver disease; vascular inflammation, polycystic ovarian syndrome, acanthosis nigricansin, cardiovascular disease sexual dysfunction and others.
About 30% of adult Americans may have metabolic syndrome with or without obesity. Metabolic syndrome is more common in obese people though none obese people have metabolic syndrome as well. About 80% of obese people have metabolic syndrome (sick obese) in America. In the adult population, about 20% of obese Americans are healthy ( healthy obese). There are over a 100 million Americans with Metabolic syndrome. Out of these 75 million are obese. About 30% of America adult population (100 million) are obese adults as well. About 25 million people have metabolic syndrome but they have normal weight or are slightly over weight (thin sick). The prevalence of metabolic syndrome increases with age and the degree of obesity in both adults and children. The same is also true for obesity.
Obesity may not be a diseases but a metabolic adaption to store excess ingested calories as a body fat. Obesity is an association with metabolic syndrome but not a cause of the disease.
During human evolution the thrifty gene that allowed people to undergo insulin resistance in order to store fat during plenty was selected so that survival will be insured during scarcity. However we live in modern society that we have only plenty and no scarcity. In todays affluent society the same thrifty gene may have become a liability rather than security.
For what ever reason in the majority of obese adults and over 30% obese children the fat cells get sick. Sick fat tissue leads to metabolic syndrome through exporting insulin resistance or other inflammatory or metabolic means. But when fat tissue remain healthy, obesity will not pose a metabolic problem.
When fatty tissue is sick (adiposopathy) it leads to fatty acid leakage which will over load the liver and make fat droplets in the liver leading to fatty liver. This also unleashes inflammatory cytokines that damage the vascular lining leading to inflammation and atherosclerosis. It also exports insulin resistance fueling the metabolic syndrome. Obese people with healthy adipose tissue share non of these metabolic consequence and remain obese healthy. What makes one obese group develop metabolic syndrome but not the other group may be a matter of genetic susceptibility with greater share of environmental factors.
Obesity is not only an important part of the metabolic syndrome but also in the development of cardiovascular disease and type 2 diabetes mellitus. It is quite obvious that there is a strong association between the degree of obesity, insulin resistance and the prevalence of metabolic syndrome.
Obesity is when the body mass index (BMI), is ≥95th percentile for gender and age. Overweight is when the BMI is ≥85th percentile and <95th percentile for age and gender.
Visceral fat has also a strong association with both childhood metabolic syndrome and cardiovascular disease later in life, independent of the degree of obesity. Waist circumference can indicate visceral adiposity. There are no current pediatric reference range for waist circumference, instead waist to hip ratio can be used to determine visceral adiposity. A waist to hip ratio of greater than) 0.6 will be considered a risk for metabolic syndrome.
Metabolic syndrome is therefore an interaction between obesity, insulin and inflammation.
Obesity increases visceral fat that leads to fatty acid leakage that cause decrease glucose uptake by the muscle and increased glucose and triglyceride production by the liver. This increases over production of triglycerides (lipids) by the liver and increased fat synthesis in the adipose tissue. The sick visceral adipose release inflammatory mediators such as Interleukins (IL) 6, tumor necrotic factor alpha, C-reactive proteins and plasminogen. These mediators cause vascular inflammation and hypercoagulable state. These cause insulin resistance and impaired insulin production. Visceral adiposopathy also causes abnormal Adipokines. It cause low adiponectin, an adipokine, (that is important in protecting the body from oxidative stress) and leptin resistance. Leptin is an important hormone made by fat cells and controls satiety in the hypothalamus. Leptin deficiency or leptin resistance leads to continuous hunger as if there is excess ghrelin (a hormone for hunger). Insulin resistance leads to leptin resistance and over eating behavior. Visceral adiposity causes excess release of angiotensin II type receptors leading to activation Reactive oxygen species and increase stimulation of renin angiotensin aldosterone system in the kidneys that will increase salt retention from the kidneys, increased vascular tone. These causes chronic increase in blood pressure and cause chronic tissue oxidative stress.
Visceral adiposity can lead to neurohumoral activation, chronic inflammation and insulin resistance. The interaction of these entities leads to metabolic syndrome.
2) Dyslipidemias; Abnormal lipids mainly triglyceride abnormalities are essential in the metabolic syndrome. Insulin resistance leads to fatty acid leakage (adiposopathy). There is activation of protein kinases that control over production of liver glucose and synthesis of lipids in the liver and adipose tissue (lipogenesis) The liver over produces triglycerides (VLDL) and sugars. The muscle glucose uptake decreases. The excess production of triglycerides in the liver are transported to the muscle and adipose tissue for energy use and storage. Since lipids are not soluble in plasma they are transported in lipoproteins called Apoliporoteins. Apolipoprotein B transports triglycerides from the liver to tissue as VLDL(very low density lipoproteins). The VLDL binds to it receptor in the tissue to deliver the triglyceride for energy and/or storage in adipose tissue. Once it sheds most of it triglycerides it be come smaller but cholesterol richer particle known as IDL (intermediate lipoprotein lipase) This IDL continues to give up more of its Triglycerides to the tissues with the help of an enzyme called lipoprotein lipase with the help of another apolipoprotein call Apo C2. Once it gives up most of it triglycerides it becomes cholesterol enriched species called LDL low density lipoprotein. LDL gives its cholesterol to all the cells for the repair of their extensive cell membrane and those tissues that need to make androgens estrogen vitamin D and others from cholesterol. The rest of the LDL traffics back to the liver to be dismantled by the liver and repackaged with triglycerides in the liver. This cycle goes on and on in life. During its trafficking LDL can give some of it cholesterol or triglycerides to HDL (high density lipoprotein) a lipoprotein called good cholesterol that scavenges any cholesterol in the body so that un used cholesterol does not precipitate to form atherosclerosis in the vasculature when LDL is trafficking.
However in the metabolic syndrome or insulin resistance, an enzyme that controllers triglyceride hydrolysis in the tissue called ApoC3 is over produced. This this blocks the hydrolysis of triglycerides by the tissue causing elevated triglyceride level (VLDL) before and after a meals. There is also an overproduction of Triglycerides (elevated VLDL) from the liver since there is fatty acid leakage from sick adipose tissue and the liver is over producing triglycerides from fatty acids and package them as VLDL for trafficking. The triglycerides can only be trafficked from liver as VLDL in the blood since they are not soluble in plasma. So VLDL which is Apo B particle, also called LDL(p) particle increases though the LDL cholesterol LDLc may not increase. In insulin resistance or metabolic syndrome there is over production of triglycerides in the liver and trafficked as VLDL out of the liver in the plasma. The excess triglycerides (VLDL) atherogenic particles called LDLp that are small dense easily oxidized particles that cause atherosclerosis by breaching the vascular endothelium. The overproduced VLDL (triglycerides out side the liver) donate their triglycerides to HDL (the good cholesterol) depleting it cholesterol content and making it small and susceptible to renal elimination. This makes the HDL cholesterol low in metabolic syndrome.
Some of the triglycerides overproduced in the liver become oil droplets and sequester in the liver causing non alcoholic fatty liver which can lead to fatty liver disease and cirrhosis. None alcoholic fatty liver also exports insulin resistance independent of visceral obesity.
3) Insulin resistance can lead to glucose impaired fasting glucose or impaired 2 hour post prandial after 75 grams of glucola or heavy carbohydrate meal and may progress to Type 2 diabetes when of β-cell function deteriorates as a result of diminished insulin secretion. Impaired fasting glucose is defined as fasting blood glucose of ≥100mg/dL and impaired glucose tolerance is diagnosed if blood glucose is ≥140 at the 2-h mark of the oral glucose tolerance test. Routine monitoring of the progression from insulin resistance to type 2 diabetes is important since the progression is variable
4) None alcoholic fatty liver disease (NAFLD): This is becoming the most common cause of liver disease in children due to the rise obesity. Obesity strongly correlates with fatty liver disease in children.
Diet such as high fructose consumption may also lead to NAFD independent of obesity. Excess ingestion of high fructose, branched chain aminoacides and lactate are converted into triglycerides. Excess triglycerides lead to fat droplets is the liver, and excess VLDL when triglycerides are trafficked out side the liver. This can lead to cirrhosis. Monitoring of liver with US or other non invasive modalities are required. Liver biopsy may be indicated in some cases.
5) Polycystic ovarian syndrome (PCOS): PCOS is another very important risk factor for metabolic syndrome. It is a constellation such as Amenorrhea, high androgen levels or phenotypic manifestations of hyper androgenemia such as hirsutism, severe acne, voice changes etc. with or with out cysts in the ovaries. PCOS is strongly associated with obesity and insulin resistance. It is an independent risk factor for metabolic syndrome regardless of obesity or presence of insulin resistance.
Women with PCOS should be screened for metabolic syndrome regularly.
Children and adolescents should be screened for overweight and obesity , fatty liver disease dyslipidemias, diabetes, PCOS, metabolic syndrome and hypertension annually and when indicated. Risk factors should be identified on individual bases. Fasting lipid profile should be obtained specially in overweight children. The triglyceride and HDL need to be look at carefully. The triglyceride should not be more than 3 times than HDL (good cholesterol) ratio of TG/HDL <3. If it is >3.0 there is a risk metabolic syndrome should be considered.
Prevention should be directed towards maintaining healthy weight though regular structured physical activity and healthy diet. Soft drinks, sports drinks including diet drinks should be avoided if possible. Avoiding salty foods and processed foods will be very important. Children should be encouraged to eat plenty of vegetables and reasonable amount of fresh fruits. Unlike vegetables excess fruits have a lot of sugar though they contain fibers to slow glucose absorption. So, the amount of fruits should be limited to a reasonable portion a day.
Metabolic syndrome should be managed initially, with healthy balanced diet and regular structured physical activity. For insulin resistance, insulin sensitizers such as metformin and actos should be considered. For patients with fatty liver actos (pioglitazone) could be tried both in children and adults.
Lipids and high blood pressure should be treated aggressively if life style change, diet and exercise are not enough. A good dietician is of at most importance in this case. Behavioral modification and psychological counseling may help in some cases. It is also important to work with your doctor closely for a good outcome.
Going back to your son: Metabolic syndrome is getting common with the emergence of overweight/obesity. There are almost 15 million children (20%)with obesity in the USA. About 30% of obese children have metabolic syndrome. There also 12% children with metabolic syndrome who are not obese but they are over weight. About 0.5% of normal weight children have metabolic syndrome. The degree of overweight correlates with metabolic syndrome though it is hard to make a causal relationship. Most overweight kids will end up overweight as adults and will have all the metabolic syndrome and its associates, such as type 2 diabetes, cardiovascular disease, high blood pressure, abnormal lipids, fatty liver, PCOS, and other diseases.
Most of metabolic syndrome and diabetes are associated with overweight/obesity. Visceral fat can lead to insulin resistance, release of inflammatory chemicals, fatty liver and abnormal lipids. Genetic interaction may have weak association with obesity and metabolic syndrome. Most of it is environmental exposures such as high sugar intake specially high fructose syrups added to almost 80% our processed foods and drinks. We are consuming more sugar now than 30 years ago. We started consuming high sugars since cheaper highly sweet corn syrup emerged in the late 70's. Metabolic diseases take time to emerge after the time of exposure. And the metabolic consequences have now expressing at a younger age. The average sugar consumption should be 5 teaspoon per day. Currently we consume about 20 teaspoon per day. We are consuming about 170 pounds of sugar per year per person. This adds about 300 extra calories a day. These sugars are cheap and very sweet. Mostly they are high fructose corn syrup added to our processed food and drinks. Fructose does not burn in the body. It is converted at a cost of energy to glucose and fat only in the liver. Excess fat will cause weight gain and insulin resistance leading to metabolic syndrome. It can also lead to metabolic syndrome without causing obesity. There are other causes of metabolic syndrome as discussed above. Children as young as 2 years old are getting type 2 diabetes. Metabolic syndrome is also happening at this early age. The reason is there is something in the environment (such as fructose) that we have created or are exposed that is causing these epidemic of metabolic diseases including metabolic syndrome. Diseases that are supposed to be of adulthood are starting early in childhood now.
You should make sure you son is getting good care. With proper diet structured physical activity and reasonable weight loss you should try to reverse the situation. If diet and physical activity are not enough and if indicated use of insulin sensitizer such as metformin and actos will be helpful. Pioglitazones (actos) are options in fatty liver well. You should see a good nutritionist to help you about the direction of over all diet plan. Counseling may be necessary indicated as well. It is very important that you work closely with your son's doctor.
Good luck.
Hello. Unfortunately we are seeing metabolic syndrome and obesity in children in scary numbers. Yes it is possible for your son to have metabolic syndrome. There are certain criteria that needs to be present to make the diagnosis of metabolic syndrome in children. Such as waist circumference, elevated lipid levels, elevated blood pressure. The criteria from adult metabolic syndrome is about different than in children. My recommendation is to see a pediatric endocrinologist or a obesity medicine specialist.
Being overweight (i.e., TOO FAT) IS THE USUAL ASSOCIATION (OR CAUSE) of the "metabolic syndrome." There is a HUGE and GROWING epidemic of this in the USA (in KIDS as well as ADULTS) due to lack of exercise, too much junk food, too much computer games/use with the associated sedentary lifestyle, etc.
Overweight and obesity are the causes of metabolic syndrome in children and adolescents. It is the first step towards diabetes mellitus.
Metabolic syndrome (MS) is caused by 2 factors. 1) inheritance of diabetic genes. This of course we cannot change. 2) environmental or life style problems (overwt). This we can & must attack. We used to not see MS in children but times have changed. Now over 30% of children are overweight & MS is increasing rapidly in children. If not treated this can wear out the insulin production & Type2 diabetes is the consequence even in children. I have had a 4 yr. old child in my practice with "full blown" type 2 diabetes after 1-2 yrs of overwt. You must attack the environmental life style problem & get the wt. down. The overwt. problem causes resistance to the action of insulin and the pancreas has to secrete more insulin to keep the blood sugar down. This wears out the pancreas too early & insulin goes down & blood sugar goes up (Type 2 diabetes). So there are several things you can do. 1) he should be taking a drug called metformin that reduces blood sugar & thus takes some of the strain off the pancreas ( it also depresses appetite some). 2) limit his screen time so he can exercise 3) see a dietician & get a good wt. loss or stabilization as he grows, diet plan. 4) start a well controlled exercise plan & make him stick to it. 5) if you the parents are overwt. then all of you need the wt. loss. If you don't do it, he won't. If you have access the YMCA is a good place to do this. It is cheap, they have dieticians & exercise supervisors to help. Please do this to slow or prevent him going on to diabetes. Good Luck!
