A healthy lifestyle includes:. You're likely to start by seeing your primary care provider. He or she may then refer you to a doctor who specializes in diabetes and other endocrine disorders endocrinologist or one who specializes in heart disease cardiologist.

When you make the appointment, ask if there's anything you need to do in advance, such as fasting for a specific test. Make a list of:. Take a family member or friend with you if possible, to help you remember the information you're given.

On this page. Self care. Preparing for your appointment. Request an appointment. Clinical trials. A healthy lifestyle includes: Regular physical activity.

Health experts recommend getting at least 30 minutes of exercise, such as brisk walking, daily. But you don't have to do that activity all at once. Look for ways to increase activity any chance you get, such as walking instead of driving and using the stairs instead of an elevator.

Weight loss. In fact, any amount of weight loss is beneficial. It's also important to maintain your weight loss. If you're struggling with losing weight and keeping it off, talk to your doctor about what options might be available to help you, such as medications or weight-loss surgery.

Healthy diet. Healthy-eating plans, such as the Dietary Approaches to Stop Hypertension DASH diet and the Mediterranean diet, emphasize eating vegetables, fruits, high-fiber whole grains and lean protein. Healthy-eating plans tend to recommend limiting sugar-sweetened beverages, alcohol, salt, sugar and fat, especially saturated fat and trans fat.

Stopping smoking. Giving up cigarettes greatly improves your overall health. Talk to your doctor if you need help quitting.

Reducing or managing stress. Physical activity, meditation, yoga and other programs can help you handle stress and improve your emotional and physical health. What you can do When you make the appointment, ask if there's anything you need to do in advance, such as fasting for a specific test.

Make a list of: Your symptoms, including any that seem unrelated to the reason for your appointment Key personal information, including major stresses, recent life changes and family medical history All medications, vitamins or other supplements you take, including the doses Questions to ask your doctor Take a family member or friend with you if possible, to help you remember the information you're given.

For metabolic syndrome, basic questions to ask your doctor include: What conditions are causing metabolic syndrome for me? How can I reduce the risk of other health conditions caused by metabolic syndrome? Will losing weight help my condition?

What about exercise? Do I need any additional tests? I have other health conditions. How can I best manage them together? Should I see a specialist? Are there brochures or other printed material I can have?

What websites do you recommend? Don't hesitate to ask other questions. What to expect from your doctor Your doctor is likely to ask about your diet, exercise and other lifestyle habits. By Mayo Clinic Staff. May 06, Show References. Ferri FF. Metabolic syndrome. In: Ferri's Clinical Advisor Elsevier; Accessed March 1, National Heart, Lung, and Blood Institute.

You may be diagnosed with metabolic syndrome if you have three or more of these risk factors: footnote 1. These criteria are from Diabetes Canada. Other organizations may have different criteria for diagnosis. The main goal of treatment is to reduce your risk of coronary artery disease CAD and diabetes.

The first approaches in treating metabolic syndrome are:. Being overweight is a major risk factor for CAD. Weight loss lowers LDL cholesterol and reduces all of the risk factors for metabolic syndrome.

Lack of exercise is a major risk factor for CAD. Regular exercise can help improve cholesterol levels. It can also lower blood pressure, reduce insulin resistance, lower blood sugar levels, and improve heart function.

Then you and your doctor may discuss other treatments to lower LDL, high blood pressure, or high blood sugar. Author: Healthwise Staff Clinical Review Board: E. Gregory Thompson MD - Internal Medicine Kathleen Romito MD - Family Medicine Jennifer Hone MD - Endocrinology, Diabetes and Metabolism.

Author: Healthwise Staff. Medical Review: E. This information does not replace the advice of a doctor. Healthwise, Incorporated, disclaims any warranty or liability for your use of this information. Your use of this information means that you agree to the Terms of Use. Learn how we develop our content.

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Topic Contents Conditions Basics Related Information References Credits. Top of the page. Conditions Basics What is metabolic syndrome?

What causes it? What puts you at risk? The things that make you more likely to develop metabolic syndrome include: Insulin resistance. This means that your body cannot use insulin properly. Abdominal obesity. This means having too much fat around your waist. Your chances of developing metabolic syndrome increase as you get older.

Lack of exercise. If you do not exercise, you are more likely to be obese and develop metabolic syndrome. Hormone imbalance. Family history of type 2 diabetes.

However, recent studies have shown that the IDF and NCEP:ATPIII definitions of MetS predicted DMT2 at least as well as the WHO definition [ 58 , 59 ]. Although the presence of MetS can predict the CVD and DMT2 risk, it cannot estimate the exact risk, as a significant part may be related to other factors such as age, smoking or gender.

Additionally, factors others than those included in the existing definitions of MetS, such as endothelial dysfunction, small dense oxidized LDL, insulin resistance, prothrombotic tendency and a proinflammatory state that are essential components and determinant of future cardiometabolic risk have been left out.

Indeed, a substantial amount of knowledge on cardiometabolic risk is provided by markers that define a proinflammatory state, such as hs-CRP, γ-glutamyltransferase γ-GT , uric acid, apoB, apoE, fibrinogen, along with the associated dysfunction of apolipoprotein A-I ApoA-I and HDL [ 62 — 67 ].

In particular, HDL dysfunctionality is closely linked to obesity and low-grade inflammation yet seems to act partly independently of them. Although it is not as yet clear what is the exact contribution of these risk factors to the development of CVD and DMT2, it is probable that along with the mechanisms delineated further below, may account for the residual risk not attributed to the traditional risk factors of these disorders.

A schematic image of the conditions implicated in the pathophysiology of the metabolic syndrome and their potential interactions. IR: Insulin Resistance; HTN: Hypertension; HPA axis : Hypothalamic-Pituitary-Adrenal Axis; DMT2: Diabetes Mellitus type 2; CVD: Cardiovascular disease; CRH: Corticotropin Releasing Hormone; AVP: Arginine Vasopressin.

Despite advances in pathophysiology and delineation of risk factors that predispose to MetS, there are many key aspects that remain unclear. The great variation in susceptibility and age of onset in individuals with a very similar risk profile, suggests a major interaction between genetic and environmental factors [ 68 ].

Although obesity and IR remain at the core of the pathophysiology of MetS, a number of other factors such as chronic stress and dysregulation of the hypothalamic-pituitary-adrenal HPA axis and autonomic nervous system ANS , increases in cellular oxidative stress, renin-angiotensin-aldosterone system activity, and intrinsic tissue glucocorticoid actions, as well as currently discovered molecules such as micro RNAs can also be involved in its pathogenesis Figure 1.

Although not all overweight or obese individuals are metabolically disturbed, the majority are IR [ 69 — 71 ]. Central obesity is thought to be an early step, as visceral adipose tissue secretes a variety of bioactive substances termed adipocytokines, such as leptin, resistin, tumor necrosis factor α TNFα , interleukin-6 IL-6 , and angiotensin II which induce IR, along with plasminogen activator inhibitor 1 PAI-1 , which is related to thrombogenic vascular diseases [ 72 ].

Notably, adiponectin, an important adipocytokine that protects against the development of DMT2, hypertension, inflammation, and atherosclerotic vascular diseases, is decreased in individuals with visceral fat accumulation, and this may be causally related to MetS [ 73 , 74 ].

Moreover, newly recognized adipocytokines such as visfatin, as well as enzymes expressed in adipose tissue, such as neprilysin, and growth factors, like fibroblast growth factor 21, an important regulator of glucose and lipid metabolism, are currently under investigation regarding their role in the pathogenesis of MetS [ 75 — 77 ].

Other compounds produced by adipose tissue possibly implicated in the pathogenesis of MetS, are the non-esterified free fatty acids FFAs. In the presence of IR the process of FFAs mobilization from stored adipose tissue triglycerides is accelerated. In the liver, FFAs result due to hepatic insulin resistance in increased production of glucose and triglycerides and secretion of very low-density lipoprotein VLDL , maintaining a vicious cycle.

FFAs also reduce insulin sensitivity in muscle by inhibiting insulin-mediated glucose uptake and increase fibrinogen and PAI-1 production [ 9 , 79 ].

Chronic hypersecretion of stress mediators, such as cortisol, in individuals with a genetic predisposition exposed to a permissive environment, may lead to visceral fat accumulation as a result of chronic hypercortisolism, low growth hormone secretion and hypogonadism [ 80 , 81 ].

Moreover, hypercortisolism directly causes IR of peripheral target tissues in proportion to glucocorticoid GC levels and a particular target tissue's sensitivity to them as shown by studying polymorphisms of the glucocorticoid receptor gene [ 82 ]. These hormonal alterations may lead to reactive insulin hypersecretion, and increasing visceral obesity and sarcopenia, resulting to dyslipidemia, hypertension and DMT2 [ 83 ].

Stress-related IL-6 hypersecretion plus adipose-tissue-generated inflammatory hypercytokinemia, as well as hypercortisolism, contribute to increased production of acute phase reactants and blood hypercoagulation, which have been recently recognized as components of MetS [ 84 , 85 ].

Moreover, since intracellular GC levels are regulated by 11β-hydroxysteroid dehydrogenase type 1 11β-HSD1 , which converts inactive cortisone to cortisol, a large number of studies have focused on evaluating tissue specific alterations in 11β-HSD1 expression and activity in obesity and IR.

In obesity global 11β-HSD1 activity, as measured by urinary corticosteroid metabolite analysis, is impaired [ 86 , 87 ], while selective 11β-HSD1 inhibitors, are in development with promising results showing improvements in metabolic profile in rodents [ 88 ].

Apart from the stress HPA axis and its end effectors glucocorticoids, another system, the circadian CLOCK system may also be implicated in the pathogenesis of MetS. Interestingly, most of the metabolic phenotypes associated with dysregulation of the CLOCK system and the HPA axis overlap [ 93 ].

Emerging evidence suggests that nitric oxide NO , inflammatory and oxidative stress also play important roles in the pathophysiology of MetS hypertension and DMT2 [ 94 , 95 ]. Increased production of reactive oxygen species ROS in numerous tissues, including skeletal muscle and cardiovascular tissues, has been linked amongst others to activation of the renin-angiotensin-aldosterone system [ 96 , 97 ], which is also implicated in the development of IR [ 98 ].

Elevation of angiotensin II can induce IR via reactive oxygen species ROS production in various tissues, including vascular smooth muscle and skeletal muscle in patients with MetS [ 96 , 98 ]. Furthermore, either use of angiotensin II type 1 receptor antagonists or genetic knockout of angiotensin II type 1 receptor are known to effectively attenuate lipid accumulation in the liver [ 99 — ].

Micro RNAs miRNAs play important regulatory roles in a variety of biological processes including adipocyte differentiation, metabolic integration, IR and appetite regulation [ ]. Although the exact mechanism of action remains to be elucidated, miRNAs may regulate cellular gene expression at the transcriptional or post-transcriptional level, by suppressing translation of protein-coding genes, or cleaving target messenger RNAs mRNAs to induce their degradation, through imperfect pairing with target mRNAs [ , ].

Antagomirs cholesterol conjugated antisense oligonucleotides which target and silence miRNAs, as evidenced by hepatic miR blockade in vivo [ ], have already been successfully tested in a phase I clinical trial.

Further studies are needed to explore the full potential of miRNAs as novel biomarkers and therapeutic agents against MetS. Evidence from both human [ , ] and animal studies [ , ] suggests that the nutritional, hormonal, and metabolic environment of the mother, as well as the early postnatal environment, may permanently reprogram the structure and physiology of the offspring toward the development of metabolic disease, in later life [ 80 , 84 , , ].

Since in vitro fertilization IVF has been widely used, the possible effect of IVF as a result of either intrauterine growth restriction or periconceptual manipulation of the blastocysts per se in the incidence of MetS manifestations has been studied, producing conflicting results [ — ].

More prospective studies on the metabolic profile of children conceived by IVF, with longer follow-up are necessary to draw safe conclusions. Although the role of the all these components as integral parts of MetS has not been evaluated in epidemiological and interventional studies, they may represent the missing link that provides full susceptibility to CVD besides the traditionally accepted components of MetS.

This is particularly relevant for the fetal programming as it may suggest intervention at an earlier stage with lifestyle therapies, since the incidence of MetS in children and adolescents is increasing alarmingly.

The increasing worldwide prevalence of childhood obesity and, in parallel, of DMT2 in the young [ , ], has highlighted the importance of MetS diagnosis in children and adolescents, as a state of high risk for progression to later disease.

Since the first publication of MetS in children, in , [ ], a growing interest emerged investigating MetS prevalence and the potential utility of this diagnosis, as well as therapeutic interventions in adolescents fulfilling it. Later, findings from the Third National Health and Nutrition Examination Survey NHANES , [ ] revealed that 4.

A variety of subsequent studies [ , — ], using three or four criteria and variable definitions, revealed diversity in MetS prevalence in childhood. The NHANES , using the ATPIII definition modified for age, identified a further increase in the prevalence of MetS among US adolescents, from 4.

The prevalence of MetS was almost exclusively found to be high among obese adolescents. Similarly to adults, no general consensus exists regarding the definition of MetS in children and adolescents [ ]. Furthermore, studies published so far have used their own set of variables, number of criteria three or four and different cut-off points to define risk factors associated with MetS.

Obesity has been defined as the 85th to 97th percentile of BMI or waist circumference, while accordingly, a variety of cut-off percentiles have been used for blood pressure, triglycerides, HDL, insulin and glucose [ ].

The rationale of using absolute numbers as cut-offs is based on the heterogeneity of clinical, biochemical and hormonal values during childhood and adolescence, as well as, on the large diversity of proposed percentile cut-offs of different definitions.

The IDF definition is presented in detail in Table 2. The main concern for pediatric clinicians is that all childhood MetS definitions originate from adult definitions and use criteria extrapolated from an adult diagnosis to a younger age group, while, in fact, the utility and predictive value of this diagnosis in young age groups has not been fully established.

Indeed, large longitudinal studies linking pediatric MetS with adult cardiovascular disease are limited, and although it is hypothesized that MetS in childhood is related to MetS in adulthood, this hypothesis has not yet been tested.

A second important issue is the lack of a developmental perspective in MetS definition: MetS as an entity is developing progressively, according to age and pubertal changes, so that the full MetS cannot in general be easily diagnosed in childhood [ ].

Developmentally-appropriate risk or protective factors, such as gestational age, birth weight and breastfeeding, as well as parental obesity and family history, are not typically taken into account [ ]. More importantly, none of the MetS definitions consider the influences of growth and puberty, for instance the 'normal' insulin resistance in puberty [ , ], the changes in fat and fat-free mass and the changes in growth and sex steroid secretion.

Further to these changes, it has been shown that in obese children, insulin resistance as measured by the homeostasis model assessment-insulin resistance HOMA-IR index increases progressively across Tanner stages and is higher in all pubertal stages than in normal weight children [ ].

Recently published studies examined MetS stability in large epidemiological samples of adolescents, using factor analysis. It was found that, though metabolic risk factor clustering was consistent, the categorical diagnosis of MetS was not stable during adolescence [ ], including both gain and loss of diagnosis.

A second, more recent study from the same group, examined the stability of three alternative models of MetS factor structure across three developmental changes [ ]. The researchers suggested that the concepts used to support the utility of MetS in the young do not fit to pediatric populations and may vary by maturation.

In addition to these large epidemiological studies, from US, clinical data also support this idea. Our research group examined the prevalence and stability of MetS diagnosis in children and adolescents aged When examining the effects of puberty, we found that pubertal children had a higher prevalence of full and partial MetS than the prepubertal population.

However, this diagnosis presented a within-person variability when examined at different time points during adolescence [ ].

This new information is further supported by recently published data from the Bogalusa Heart Study and the Cardiovascular Risk in Young Finns [ ]. This study has shown that although children and adolescents with MetS are indeed at an increased risk of adult MetS, subclinical atherosclerosis and diabetes type 2, the BMI alone is an equally accurate measure as MetS in identifying youth at risk for adult MetS and subsequent atherosclerotic disease.

MetS as a concept was originally developed to identify adults at a greatest risk for CVD and DMT2, however, the application of this model has not yet been fully validated in children and adolescents.

Furthermore, the effects of growth and puberty on reference values is a critical issue, because diverse age-dependent cut-off points are needed to define a pathological state, such as MetS.

Longitudinally, the high level of diagnostic inconsistency through adolescence suggests that MetS classification may not be a valuable method for risk identification in the pediatric age group.

These limitations, as well as new data from longitudinal studies in pediatric MetS, suggest that prevention and treatment in childhood and adolescence should better focus on established risk factors rather than the diagnosis of MetS.

Pediatric clinicians may put more emphasis on healthy lifestyle promotion and obesity prevention and treatment rather than targeting specific metabolic alterations. Indeed, advocating weight maintenance rather than weight loss during the years of physical growth, may lead to BMI reduction and cardiovascular risk minimization and may be a more cost-effective approach than pursuing fluctuating biochemical abnormalities.

Due to its impact upon health and financial implications, the mechanisms that contribute to the pathogenesis of MetS remain under intense investigation since their understanding may help design novel therapeutic strategies.

Delineation of the role of these factors along with the established ones and others that are currently being studied may help clarify the exact pathogenesis of the syndrome and may expand the clinical criteria of MetS. This is particularly important as there is still a need to develop uniform criteria that can be used by different clinical and research groups, enabling comparisons between study results, in the hope to better predictor the risk, for CVD and DMT2.

In this direction, further studies exploring the relation of waist circumference thresholds to metabolic risk and cardiovascular outcomes in different populations are encouraged. Adoption of these criteria seem to incorporate the most important aspects of the syndrome, recognizing that the risk associated with a particular waist measurement will differ in different populations, albeit with the limitations that it has when applied to mixed ethnicities.

Finally, the application of the MetS model has not been fully validated in children and adolescents as yet, suggesting that prevention and treatment in childhood and adolescence should better focus on established risk factors rather than the diagnosis of MetS.

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Acta Paediatr. The two most important risk factors are defined by the National Heart, Lung, and Blood Institute as:. If you have high blood sugar, you may notice symptoms of diabetes, including increased thirst, blurred vision, headaches, and fatigue.

If you have one of the five risk factors of metabolic syndrome, talk with a doctor to determine whether you should be tested for the others. To diagnose metabolic syndrome, a doctor will need to perform several different tests. The results of these tests will be used to look for three or more signs of the disorder.

According to best practices , the tests and at-risk levels include:. You may have metabolic syndrome if three or more of these tests come back with a reading within the above ranges.

Having excess weight in your abdominal region can lead to fat accumulating in the liver and muscle cells. Insulin resistance can develop.

This is when your cells stop responding to insulin in the bloodstream. It can lead to higher insulin levels and blood sugar levels. If your blood sugar levels become too high, you can develop type 2 diabetes. The complications that may result from metabolic syndrome are frequently serious and long-term chronic.

They include:. If you are diagnosed with metabolic syndrome, the goal of treatment will be to reduce your risk of developing further health complications. Your doctor may recommend losing around 7 percent of your current weight and getting at least 30 minutes of moderate to intense exercise 5 to 7 days a week.

This may help reverse the syndrome. If symptoms are managed, people with metabolic syndrome can reduce their risks of developing serious health problems such as heart attack or stroke.

The condition may be able to be reversed with weight loss or managed with a combination of diet, exercise, and medication. Although symptom management will reduce health complications, most people with this condition have a long-term risk of cardiovascular disease.

If you develop this condition, you may need to be monitored by your doctor to help prevent serious health problems such as heart attack and stroke. Maintaining a healthy waist circumference and blood pressure and cholesterol levels reduce your risk for metabolic syndrome.

Exercise and weight loss can aid in these efforts and decrease insulin resistance. Talk to a doctor before beginning an exercise program or radically changing your diet. They can help you find an option that is safe for you.

Regular physical exams may also help prevent metabolic syndrome. A doctor can measure your blood pressure and complete blood work. This may help detect the condition in the early stages, and prompt treatment can help reduce health complications over the long term.

Metabolic syndrome refers to a group of five risk factors that together can raise the risk for cardiovascular disease, insulin resistance, diabetes type 2, and stroke. If you have metabolic syndrome, weight loss, regular exercise, a healthy diet, and medications may help reduce your risk for serious health complications.

Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. Hyperglycemic hyperosmolar syndrome HHS is a potentially life threatening condition involving extremely high blood sugar glucose levels.

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An ALD test measures the amount of the hormone aldosterone your blood. Too much aldosterone can be an indicator of a variety of medical conditions. Hormones like estrogen and testosterone are crucial to your health, and a hormonal imbalance can cause symptoms like acne and weight gain.

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Metabolic syndrome is closely linked to overweight or obesity and inactivity. The following factors increase your chances of having metabolic syndrome: Age. Your risk of metabolic syndrome increases with age. In the United States, Hispanics — especially Hispanic women — appear to be at the greatest risk of developing metabolic syndrome.

The reasons for this are not entirely clear. Carrying too much weight, especially in your abdomen, increases your risk of metabolic syndrome.

You're more likely to have metabolic syndrome if you had diabetes during pregnancy gestational diabetes or if you have a family history of type 2 diabetes.

Other diseases. Your risk of metabolic syndrome is higher if you've ever had nonalcoholic fatty liver disease, polycystic ovary syndrome or sleep apnea. Having metabolic syndrome can increase your risk of developing: Type 2 diabetes.

If you don't make lifestyle changes to control your excess weight, you may develop insulin resistance, which can cause your blood sugar levels to rise. Eventually, insulin resistance can lead to type 2 diabetes. Heart and blood vessel disease. High cholesterol and high blood pressure can contribute to the buildup of plaques in your arteries.

These plaques can narrow and harden your arteries, which can lead to a heart attack or stroke. A healthy lifestyle includes: Getting at least 30 minutes of physical activity most days Eating plenty of vegetables, fruits, lean protein and whole grains Limiting saturated fat and salt in your diet Maintaining a healthy weight Not smoking.

By Mayo Clinic Staff. May 06, Show References. Ferri FF. Metabolic syndrome. Demographic transition shift to low fertility, low mortality, and higher life expectancy , and epidemiological transition from widely prevalent infectious diseases to a pattern of a high prevalence of lifestyle related diseases evolved in developing countries as they become economically more resourceful, leading to significant shifts in dietary and physical activity patterns.

These changes cause significant effects on body composition and metabolism, often resulting in an increase in BMI, generalized and abdominal obesity, and an increase in dyslipidemia and DMT2 [ 27 ].

It should be noted however, that even lean individuals may develop features of MetS adding further to the complexity of its pathogenesis [ 28 ].

Thus, the importance of identifying markers for MetS to supplement age-related and obesity-related measures cannot be overstated. Understanding how to use definition criteria in clinical settings will aid physicians in treating the right cohort of at-risk patients. The need to precisely define MetS stems from the need to detect accurately individuals at high risk for CVD and DMT2.

All the components of the various MetS definitions are involved in conferring risk for CVD and DMT2. Central obesity has been shown in several studies to be associated with an increased risk of CVD and DMT2 [ 31 ]. Several epidemiological studies have confirmed the increased risk of CVD in individuals with MetS, independently of the diagnostic criteria used [ 32 — 39 ].

Overall a range of 1. It should be noted however, that several studies amongst which the Casale Monferrato Study and PROSPER conducted in older people, failed to reveal an association between MetS and an increased risk of CVD [ 41 , 42 ].

Due to these inconsistencies several recent studies have aimed to investigate which of the proposed definitions of MetS is particularly related to excessive CVD risk, and thus which one should be implemented in clinical practice.

A recent meta-analysis suggested that the WHO definition was associated with a slightly greater risk than the NCEP:ATPIII definition [ 43 ]. recently reported similar findings for CVD using these definitions [ 45 ].

The assessment of whether the risk of MetS on MI is greater than the risk conferred by the sum of individual component risk factors has also been studied.

A recent report suggested that the MetS-related CVD risk was more than that of the sum of its parts in subjects with MetS, with or without DMT2 [ 46 ]. One major point of note was that the risk of CHD when three components of MetS were present did not appear to be greater than the risk of individual components such as DMT2 and hypertension, and this was in agreement with other reports [ 50 , 51 ].

In this regard, in a recent appraisal of MetS, the American Diabetes Association ADA in conjunction with the European Association for the Study of Diabetes, issued a joint statement raising concerns over the value of using MetS as a CVD risk marker and recommended that clinicians should evaluate and treat all CVD risk factors without considering whether a patient meets the criteria for diagnosis of MetS [ 52 ].

The observation of the presence of MetS predicting the risk for DMT2 has also been examined by numerous studies; according to these reports, it is well accepted that the presence of MetS not only increases this risk, but is also highly predictive of new-onset DMT2 [ 6 , 42 , 53 — 55 ].

Indeed, MetS is associated with an approximately five times higher risk for incident DMT2 [ 56 ]. The presence of MetS predicting the incidence of DMT2 also varies depending on how MetS is defined. IFG and IGT can predict the development of DMT2, independently of other components of MetS [ 56 ].

However, recent studies have shown that the IDF and NCEP:ATPIII definitions of MetS predicted DMT2 at least as well as the WHO definition [ 58 , 59 ]. Although the presence of MetS can predict the CVD and DMT2 risk, it cannot estimate the exact risk, as a significant part may be related to other factors such as age, smoking or gender.

Additionally, factors others than those included in the existing definitions of MetS, such as endothelial dysfunction, small dense oxidized LDL, insulin resistance, prothrombotic tendency and a proinflammatory state that are essential components and determinant of future cardiometabolic risk have been left out.

Indeed, a substantial amount of knowledge on cardiometabolic risk is provided by markers that define a proinflammatory state, such as hs-CRP, γ-glutamyltransferase γ-GT , uric acid, apoB, apoE, fibrinogen, along with the associated dysfunction of apolipoprotein A-I ApoA-I and HDL [ 62 — 67 ].

In particular, HDL dysfunctionality is closely linked to obesity and low-grade inflammation yet seems to act partly independently of them. Although it is not as yet clear what is the exact contribution of these risk factors to the development of CVD and DMT2, it is probable that along with the mechanisms delineated further below, may account for the residual risk not attributed to the traditional risk factors of these disorders.

A schematic image of the conditions implicated in the pathophysiology of the metabolic syndrome and their potential interactions. IR: Insulin Resistance; HTN: Hypertension; HPA axis : Hypothalamic-Pituitary-Adrenal Axis; DMT2: Diabetes Mellitus type 2; CVD: Cardiovascular disease; CRH: Corticotropin Releasing Hormone; AVP: Arginine Vasopressin.

Despite advances in pathophysiology and delineation of risk factors that predispose to MetS, there are many key aspects that remain unclear. The great variation in susceptibility and age of onset in individuals with a very similar risk profile, suggests a major interaction between genetic and environmental factors [ 68 ].

Although obesity and IR remain at the core of the pathophysiology of MetS, a number of other factors such as chronic stress and dysregulation of the hypothalamic-pituitary-adrenal HPA axis and autonomic nervous system ANS , increases in cellular oxidative stress, renin-angiotensin-aldosterone system activity, and intrinsic tissue glucocorticoid actions, as well as currently discovered molecules such as micro RNAs can also be involved in its pathogenesis Figure 1.

Although not all overweight or obese individuals are metabolically disturbed, the majority are IR [ 69 — 71 ]. Central obesity is thought to be an early step, as visceral adipose tissue secretes a variety of bioactive substances termed adipocytokines, such as leptin, resistin, tumor necrosis factor α TNFα , interleukin-6 IL-6 , and angiotensin II which induce IR, along with plasminogen activator inhibitor 1 PAI-1 , which is related to thrombogenic vascular diseases [ 72 ].

Notably, adiponectin, an important adipocytokine that protects against the development of DMT2, hypertension, inflammation, and atherosclerotic vascular diseases, is decreased in individuals with visceral fat accumulation, and this may be causally related to MetS [ 73 , 74 ].

Moreover, newly recognized adipocytokines such as visfatin, as well as enzymes expressed in adipose tissue, such as neprilysin, and growth factors, like fibroblast growth factor 21, an important regulator of glucose and lipid metabolism, are currently under investigation regarding their role in the pathogenesis of MetS [ 75 — 77 ].

Other compounds produced by adipose tissue possibly implicated in the pathogenesis of MetS, are the non-esterified free fatty acids FFAs. In the presence of IR the process of FFAs mobilization from stored adipose tissue triglycerides is accelerated.

In the liver, FFAs result due to hepatic insulin resistance in increased production of glucose and triglycerides and secretion of very low-density lipoprotein VLDL , maintaining a vicious cycle. FFAs also reduce insulin sensitivity in muscle by inhibiting insulin-mediated glucose uptake and increase fibrinogen and PAI-1 production [ 9 , 79 ].

Chronic hypersecretion of stress mediators, such as cortisol, in individuals with a genetic predisposition exposed to a permissive environment, may lead to visceral fat accumulation as a result of chronic hypercortisolism, low growth hormone secretion and hypogonadism [ 80 , 81 ].

Moreover, hypercortisolism directly causes IR of peripheral target tissues in proportion to glucocorticoid GC levels and a particular target tissue's sensitivity to them as shown by studying polymorphisms of the glucocorticoid receptor gene [ 82 ].

These hormonal alterations may lead to reactive insulin hypersecretion, and increasing visceral obesity and sarcopenia, resulting to dyslipidemia, hypertension and DMT2 [ 83 ].

Stress-related IL-6 hypersecretion plus adipose-tissue-generated inflammatory hypercytokinemia, as well as hypercortisolism, contribute to increased production of acute phase reactants and blood hypercoagulation, which have been recently recognized as components of MetS [ 84 , 85 ].

Moreover, since intracellular GC levels are regulated by 11β-hydroxysteroid dehydrogenase type 1 11β-HSD1 , which converts inactive cortisone to cortisol, a large number of studies have focused on evaluating tissue specific alterations in 11β-HSD1 expression and activity in obesity and IR.

In obesity global 11β-HSD1 activity, as measured by urinary corticosteroid metabolite analysis, is impaired [ 86 , 87 ], while selective 11β-HSD1 inhibitors, are in development with promising results showing improvements in metabolic profile in rodents [ 88 ]. Apart from the stress HPA axis and its end effectors glucocorticoids, another system, the circadian CLOCK system may also be implicated in the pathogenesis of MetS.

Interestingly, most of the metabolic phenotypes associated with dysregulation of the CLOCK system and the HPA axis overlap [ 93 ]. Emerging evidence suggests that nitric oxide NO , inflammatory and oxidative stress also play important roles in the pathophysiology of MetS hypertension and DMT2 [ 94 , 95 ].

Increased production of reactive oxygen species ROS in numerous tissues, including skeletal muscle and cardiovascular tissues, has been linked amongst others to activation of the renin-angiotensin-aldosterone system [ 96 , 97 ], which is also implicated in the development of IR [ 98 ].

Elevation of angiotensin II can induce IR via reactive oxygen species ROS production in various tissues, including vascular smooth muscle and skeletal muscle in patients with MetS [ 96 , 98 ].

Furthermore, either use of angiotensin II type 1 receptor antagonists or genetic knockout of angiotensin II type 1 receptor are known to effectively attenuate lipid accumulation in the liver [ 99 — ].

Micro RNAs miRNAs play important regulatory roles in a variety of biological processes including adipocyte differentiation, metabolic integration, IR and appetite regulation [ ].

Although the exact mechanism of action remains to be elucidated, miRNAs may regulate cellular gene expression at the transcriptional or post-transcriptional level, by suppressing translation of protein-coding genes, or cleaving target messenger RNAs mRNAs to induce their degradation, through imperfect pairing with target mRNAs [ , ].

Antagomirs cholesterol conjugated antisense oligonucleotides which target and silence miRNAs, as evidenced by hepatic miR blockade in vivo [ ], have already been successfully tested in a phase I clinical trial. Further studies are needed to explore the full potential of miRNAs as novel biomarkers and therapeutic agents against MetS.

Evidence from both human [ , ] and animal studies [ , ] suggests that the nutritional, hormonal, and metabolic environment of the mother, as well as the early postnatal environment, may permanently reprogram the structure and physiology of the offspring toward the development of metabolic disease, in later life [ 80 , 84 , , ].

Since in vitro fertilization IVF has been widely used, the possible effect of IVF as a result of either intrauterine growth restriction or periconceptual manipulation of the blastocysts per se in the incidence of MetS manifestations has been studied, producing conflicting results [ — ].

More prospective studies on the metabolic profile of children conceived by IVF, with longer follow-up are necessary to draw safe conclusions. Although the role of the all these components as integral parts of MetS has not been evaluated in epidemiological and interventional studies, they may represent the missing link that provides full susceptibility to CVD besides the traditionally accepted components of MetS.

This is particularly relevant for the fetal programming as it may suggest intervention at an earlier stage with lifestyle therapies, since the incidence of MetS in children and adolescents is increasing alarmingly.

The increasing worldwide prevalence of childhood obesity and, in parallel, of DMT2 in the young [ , ], has highlighted the importance of MetS diagnosis in children and adolescents, as a state of high risk for progression to later disease.

Since the first publication of MetS in children, in , [ ], a growing interest emerged investigating MetS prevalence and the potential utility of this diagnosis, as well as therapeutic interventions in adolescents fulfilling it.

Later, findings from the Third National Health and Nutrition Examination Survey NHANES , [ ] revealed that 4. A variety of subsequent studies [ , — ], using three or four criteria and variable definitions, revealed diversity in MetS prevalence in childhood.

The NHANES , using the ATPIII definition modified for age, identified a further increase in the prevalence of MetS among US adolescents, from 4. The prevalence of MetS was almost exclusively found to be high among obese adolescents.

Similarly to adults, no general consensus exists regarding the definition of MetS in children and adolescents [ ]. Furthermore, studies published so far have used their own set of variables, number of criteria three or four and different cut-off points to define risk factors associated with MetS.

Obesity has been defined as the 85th to 97th percentile of BMI or waist circumference, while accordingly, a variety of cut-off percentiles have been used for blood pressure, triglycerides, HDL, insulin and glucose [ ]. The rationale of using absolute numbers as cut-offs is based on the heterogeneity of clinical, biochemical and hormonal values during childhood and adolescence, as well as, on the large diversity of proposed percentile cut-offs of different definitions.

The IDF definition is presented in detail in Table 2. The main concern for pediatric clinicians is that all childhood MetS definitions originate from adult definitions and use criteria extrapolated from an adult diagnosis to a younger age group, while, in fact, the utility and predictive value of this diagnosis in young age groups has not been fully established.

Indeed, large longitudinal studies linking pediatric MetS with adult cardiovascular disease are limited, and although it is hypothesized that MetS in childhood is related to MetS in adulthood, this hypothesis has not yet been tested. A second important issue is the lack of a developmental perspective in MetS definition: MetS as an entity is developing progressively, according to age and pubertal changes, so that the full MetS cannot in general be easily diagnosed in childhood [ ].

Developmentally-appropriate risk or protective factors, such as gestational age, birth weight and breastfeeding, as well as parental obesity and family history, are not typically taken into account [ ]. More importantly, none of the MetS definitions consider the influences of growth and puberty, for instance the 'normal' insulin resistance in puberty [ , ], the changes in fat and fat-free mass and the changes in growth and sex steroid secretion.

Further to these changes, it has been shown that in obese children, insulin resistance as measured by the homeostasis model assessment-insulin resistance HOMA-IR index increases progressively across Tanner stages and is higher in all pubertal stages than in normal weight children [ ]. Recently published studies examined MetS stability in large epidemiological samples of adolescents, using factor analysis.

It was found that, though metabolic risk factor clustering was consistent, the categorical diagnosis of MetS was not stable during adolescence [ ], including both gain and loss of diagnosis. A second, more recent study from the same group, examined the stability of three alternative models of MetS factor structure across three developmental changes [ ].

The researchers suggested that the concepts used to support the utility of MetS in the young do not fit to pediatric populations and may vary by maturation.

In addition to these large epidemiological studies, from US, clinical data also support this idea. Our research group examined the prevalence and stability of MetS diagnosis in children and adolescents aged When examining the effects of puberty, we found that pubertal children had a higher prevalence of full and partial MetS than the prepubertal population.

However, this diagnosis presented a within-person variability when examined at different time points during adolescence [ ]. This new information is further supported by recently published data from the Bogalusa Heart Study and the Cardiovascular Risk in Young Finns [ ].

This study has shown that although children and adolescents with MetS are indeed at an increased risk of adult MetS, subclinical atherosclerosis and diabetes type 2, the BMI alone is an equally accurate measure as MetS in identifying youth at risk for adult MetS and subsequent atherosclerotic disease.

MetS as a concept was originally developed to identify adults at a greatest risk for CVD and DMT2, however, the application of this model has not yet been fully validated in children and adolescents. Furthermore, the effects of growth and puberty on reference values is a critical issue, because diverse age-dependent cut-off points are needed to define a pathological state, such as MetS.

Longitudinally, the high level of diagnostic inconsistency through adolescence suggests that MetS classification may not be a valuable method for risk identification in the pediatric age group.

These limitations, as well as new data from longitudinal studies in pediatric MetS, suggest that prevention and treatment in childhood and adolescence should better focus on established risk factors rather than the diagnosis of MetS.

Pediatric clinicians may put more emphasis on healthy lifestyle promotion and obesity prevention and treatment rather than targeting specific metabolic alterations. Indeed, advocating weight maintenance rather than weight loss during the years of physical growth, may lead to BMI reduction and cardiovascular risk minimization and may be a more cost-effective approach than pursuing fluctuating biochemical abnormalities.

Due to its impact upon health and financial implications, the mechanisms that contribute to the pathogenesis of MetS remain under intense investigation since their understanding may help design novel therapeutic strategies.

Delineation of the role of these factors along with the established ones and others that are currently being studied may help clarify the exact pathogenesis of the syndrome and may expand the clinical criteria of MetS. This is particularly important as there is still a need to develop uniform criteria that can be used by different clinical and research groups, enabling comparisons between study results, in the hope to better predictor the risk, for CVD and DMT2.

In this direction, further studies exploring the relation of waist circumference thresholds to metabolic risk and cardiovascular outcomes in different populations are encouraged. Adoption of these criteria seem to incorporate the most important aspects of the syndrome, recognizing that the risk associated with a particular waist measurement will differ in different populations, albeit with the limitations that it has when applied to mixed ethnicities.

Finally, the application of the MetS model has not been fully validated in children and adolescents as yet, suggesting that prevention and treatment in childhood and adolescence should better focus on established risk factors rather than the diagnosis of MetS. For ethnic South and Central Americans, South Asian data are used, and for sub-Saharan Africans and Eastern Mediterranean and Middle East Arab populations, European data are used.

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Treatment for metabolic syndrome usually involves making changes to your lifestyle. The best way to prevent metabolic syndrome, to treat it and prevent complications is through a healthy lifestyle.

eat less saturated fat and meat and dairy products and have more fruit, vegetables and whole grains. do at least minutes of moderate to intense exercise a week, spread over at least 4 or 5 days. try to cut down or quit smoking if you smoke.

Metabolic syndrome increases your chances of having cardiovascular disease and type 2 diabetes. Page last reviewed: 16 November Next review due: 16 November Home Health A to Z Back to Health A to Z.