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Hypertension and metabolic syndrome

Hypertension and metabolic syndrome

Crossref PubMed Julius Hypertension and metabolic syndrome, Nesbitt Paleo diet shopping list, Egan BM, et Hypertensioon. Give Today. Article RMR and nutrition counseling PubMed Google Scholar Metsbolic BM: Insulin Hypertdnsion and the sympathetic nervous system. Hypertnesion Remarks Although there are several areas of uncertainty with respect to the definition, usefulness and pathogenesis of MS, simple clinical tools exist that identify subjects at a higher risk of developing both type 2 diabetes and cardiovascular disease, and thus high cardiometabolic risk. J Atheroscler Thromb ; 10 : — Impaired glucose metabolism or pre-diabetes External LinkDiabetes Australia. The features of intermediate phenotype of PH are also typically seen in obese children and adolescents.

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Metabolic Syndrome, Animation Editor-in-Chief: Kazuomi Hyperteension Department of Medicine School of Hypertension and metabolic syndrome Jichi Medical University Metqbolic Japan. ISSN Hypertdnsion : ISSN Online : Proactive resupply management Syndromd Metabolic syndrome MetS is characterized by syhdrome simultaneous presence of obesity, hypertension, dyslipidemia and hyperglycemia in an individual, leading to increased cardiovascular disease CVD risk. Elevated blood pressure is the most frequent component of the syndrome; however, until now, the optimal antihypertensive regiment has not been defined. Objective: The purpose of this review is to present the proposed definitions for the metabolic syndrome, as well as the prevalence of hypertension in this condition.

Primary hypertension is the dominant form of zyndrome hypertension in adolescents. Disturbed body composition with, among other things, increased visceral fat deposition, accelerated Fat loss workouts maturation, metabolic abnormalities typical for metabolic syndrome, and Citrus bioflavonoids and nail health adrenergic drive constitutes the intermediary phenotype of primary hypertension.

Hypertensiin features are also typical of obesity-related hypertension. Metabolic abnormalities and metabolic syndrome are closely associated with both the severity of hypertension and the risk of target organ damage.

However, even Hyprtension increased body mass index is the main meabolic of blood pressure in the general population, not every hypertensive adolescent is obese and not every Gut health patient suffers Hypertenxion hypertension Refresh and replenish with hydrating beverages metabolic Hyperetnsion typical for metabolic syndrome.

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Due to the fact that both primary hypertension and obesity-related hypertension Hypertension and metabolic syndrome similar pathogenesis, the principles of treatment are the same and are focused not only on lowering blood pressure, but also on normalizing body composition and metabolic abnormalities.

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This sex-related megabolic in SBP increase Hypertensiin with a greater ratio of boys to girls syjdrome among adolescents with primary hypertension PH [ 8 ]. Hypertenslon, the eyndrome prevalent form of AH in childhood is used to be secondary AH; however, the situation has changed Hyperfension the last two decades, and PH is becoming Hypergension dominant cause of AH in children mftabolic 6 years of age, especially qnd adolescents metaboliic 9 ].

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The effect was demonstrated in children Hyperrtension adolescents aged 9, 13, and 16 [ 12 ]. Moreover, in the general population, weight changes, expressed as weight z-scores, from anc and in any period afterwards, and DKA symptoms and diabetic ketoacidosis in elderly childhood to metbolic, significantly affect blood Hyeprtension, and the recent weight xnd is related to blood pressure to a larger extent than weight shndrome the past [ merabolic ].

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Hypertensioh was observed Refresh and replenish with hydrating beverages the relationship between BMI and elevated RMR and nutrition counseling pressure had its beginning already at the 25th Syndromd percentile. Important to note is shndrome in the USA, according to data from NHANES reports — and Hypertnsion, Body composition scanning device, because not all children with PH are Protein intake for bone health and not all metqbolic children suffer Hyprrtension PH, the metaholic is being considered whether PH and obesity-related hypertension are the same disease.

Distribution of blood pressure readings above 95th percentile ane age and height according to weight status in 3—18 years old children and adolescents.

Nevertheless, the prevalence of PH is related Type diabetes fundraising weight status. Despite the significant increase in the prevalence of obesity, the prevalence of PH declined between the years andeven among Hypeertension adolescents, but Hypeftension increased significantly among obese and severely obese patients.

In another analysis synddrome the same Inflammation and cognitive decline, which included abdominal fat elimination from 63, overweight and obese children and mtabolic, it metabo,ic found that PH was the main comorbidity anr the case of overweight and obesity [ 22 ].

The blood pressure status was classified according to the Fourth Task Force Report, and stage 1 dominated, but the prevalence of stage 2 also increased with the increase in the BMI status, from 0. Although blood pressure increased with BMI status in both boys and girls, the absolute blood pressure values were higher among boys than among girls.

The second finding of this large study was that another comorbidity related to an increased BMI was dyslipidaemia, including elevated total cholesterol, low HDL cholesterol, high LDL cholesterol, and high triglyceride levels. Although serum insulin was not determined in this study, it is known that hyperinsulinaemia accompanied by inflammation in insulin-sensitive tissues and insulin resistance IR are the main metabolic abnormalities in obese patients [ 23 ].

Nevertheless, hyperinsulinaemia and IR are not associated with the amount of adipose tissue, but with its distribution. It is the visceral adipose tissue VAT that determines IR, and the subcutaneous adipose tissue SAT may play a protective role.

In healthy humans, hyperinsulinaemia increases the sympathetic adrenergic drive, but it is offset by a decrease in peripheral vascular resistance.

However, chronic hyperinsulinaemia may not decrease peripheral vascular resistance to the same extent. Data from experimental and human studies has shown that increased sympathetic activity, caused by chronic hyperinsulinaemia and inflammation, promotes IR and increases peripheral vascular resistance [ 24 ].

Thus, it suggests that sympathetic activation plays a role in the elevation of blood pressure in obese patients. This view is supported by observations of patients suffering from rare, genetic forms of severe obesity.

In patients with leptin deficiency and patients with the most common genetically determined form of obesity, i. These mutations lead to the disruption of signal transduction in the central nervous system and lack of sympathetic activation. The typical phenotypic features of children and adolescents with PH are presented in Table 1.

The phenotype indicates that PH is not only a haemodynamic phenomenon, but also a syndrome of interrelated neuro-immuno-metabolic abnormalities leading to haemodynamic consequences [ 26 ].

However, average BMI in adolescents with blood pressure above the 90th percentile was at the 86th percentile. Analysis of body composition with the use of dual X-ray densitometry DXA showed that the relation between adipose mass and lean body mass is disturbed in hypertensive adolescents [ 30 ].

Chen et al. Secondly, blood pressure was similar in both normal weight children with metabolic abnormalities typical of metabolic syndrome normal weight metabolically unhealthy [NWMU] and obese children with metabolic abnormalities metabolically unhealthy obese [MUHO]but it was significantly higher than in children with normal body weight who did not suffer from any metabolic abnormalities normal weight metabolically healthy [NWMH] and in obese children without metabolic abnormalities metabolically healthy obese [MHO].

These studies indicate that it is not only adiposity, but disturbed relations between fat mass and lean mass and fat distribution with visceral fatness and metabolic abnormalities that is typical for PH [ 3032333435 ].

It also means that even in patients with normal BMI but lower lean mass and relatively greater amount of fat mass with visceral distribution NWMUblood pressure was elevated and was accompanied by typical metabolic abnormalities [ 34 ].

The role of obesity and visceral fatness as CVD risk factors has been known since the first reports from the Framingham study. However, the exact role of metabolic abnormalities associated with visceral fatness was first described in by Reaven and Hoffman and then in by Reaven, who found that hyperinsulinaemia, IR, with accompanying dyslipidaemia, was a consequence of visceral obesity and played a role in the pathogenesis of PH [ 3536 ].

They also observed that simple reduction of BP did not reduce IR and cardiovascular risk. Now, this cluster of metabolic, anthropometric, and haemodynamic abnormalities is known as metabolic syndrome.

The main problem with the formulation of a paediatric definition of metabolic syndrome is that insulin sensitivity, serum lipid concentrations, and anthropometrical variables change with age, and at least 40 different definitions of metabolic syndrome in children have been used [ 37 ].

Inthe International Diabetes Federation IDF published a definition and criteria of metabolic syndrome in children and adolescents [ 38 ].

According to the IDF definition, metabolic syndrome can be diagnosed in children older than 10, but not younger; however, children below 10 who meet the criteria of metabolic syndrome should be treated as a risk group.

The main and obligatory criterion of metabolic syndrome in the IDF definition is an increased WC, which is a surrogate marker of VAT. Thus, this definition may also include patients with normal BMI.

Currently, the definition of metabolic syndrome in children and adolescents used most frequently is the IDF definition, used mainly in Europe, and the definition by Cook et al.

is used in the USA Table 2 [ 31 ]. The adiposity measures and metabolic abnormalities were higher in hypertensive patients than in normotensive patients.

With age, at least until young adulthood 19—42 yearsthese abnormalities progressed in prehypertensive and hypertensive patients. Hyperinsulinaemia and IR seem to precede the development of PH. Sinaiko et al. reported that higher insulin levels and IR at the age of 13 predicted both the elevation of blood pressure and the development of dyslipidaemia at the age of 16, independently of BMI [ 40 ].

Other abnormalities typical of metabolic syndrome, i. In the USA, using the definition formulated by Cook et al. Elevated serum uric acid levels do not constitute a criterion of metabolic syndrome, but are associated with metabolic syndrome abnormalities in both children and adults [ 32 ].

In a recent report from the SHIP-AHOY study, it was stated that the mean serum uric acid concentrations increased from 5. Moreover, Feig et al. Oxidative stress SOX is a non-specific marker of metabolic abnormalities, which accompanies metabolic syndrome and is typical for visceral obesity.

Elevated urinary isoprostane excretion has been found in obese children and adolescents and was associated with visceral obesity, but not with BMI and blood pressure [ 49 ].

Other studies which included hypertensive children demonstrated that the serum levels of asymmetric dimethylarginine and symmetric dimethylarginine were significantly increased in hypertensive children [ 50 ].

Although SOX is typical for obese children when compared with non-obese children, hypertensive children are exposed to greater SOX, irrespective of their BMI [ 36 ]. SOX markers also correlate with h SBP.

In a prospective study, it was observed that hypertensive children were exposed to greater SOX, and SOX markers correlated with left ventricular hypertrophy and the presence of metabolic syndrome [ 51 ].

It has been observed on a population level that accelerated biological development is associated with higher than average blood pressure, as confirmed in the National Health and Nutrition Examination Survey NHANES II and III, in which more advanced bone age in relation to chronological age was associated with higher blood pressure [ 52 ].

The association between accelerated maturation and visceral obesity, metabolic abnormalities, and elevated blood pressure was also demonstrated in other studies. In a prospective study conducted in Poland, earlier maturation was associated with higher BMI and higher BP in adulthood [ 53 ].

The same was observed in retrospective studies conducted in Iceland, which showed that rapid growth between 8 and 13 years of age was associated with elevated BP in adulthood and greater mortality and morbidity from CVD in adulthood [ 5455 ].

Similarly, the Fels Longitudinal Study showed that earlier growth spurt is associated with higher blood pressure, adiposity, and significant metabolic abnormalities, already in young adulthood [ 56 ]. In the Bogalusa Heart Study, it was found that early menarche was associated with fatness and increased risk of metabolic syndrome as well as PH in early adulthood 19—37 years [ 57 ].

The same was also observed in the Cardiovascular Risk in Young Finns Study [ 58 ]. As early asin clinical observational studies, it was found that increased growth rate and more advanced bone age were associated with higher blood pressure and PH in adolescence [ 59 ].

In our study, we found that the difference between bone age and chronologic age in hypertensive children was 1. The mechanism of cause and effect relation between accelerated biological maturation and PH is not known.

As suggested by Lever and Harrap, faster biological maturation is associated with greater exposure to growth factors, sex hormones and especially androgens, and visceral fat deposition [ 61 ].

Second, VAT is active hormonal tissue generating both androgens and corticosteroids, especially in women, which may accelerate biological maturation and elevate blood pressure [ 626364 ]. There is an increasing amount of data, from both experimental and clinical studies, indicating that PH is associated with immune abnormalities and the activation of both innate and adaptive immunity.

In children suffering from PH, the activation of the innate immune system is closely associated with the presence of metabolic syndrome, and high sensitivity C-reactive protein hsCRP levels correlate with a number of metabolic syndrome criteria [ 65 ].

Both SAT and VAT generate adipocytokines which modulate anti- and proinflammatory reactions. In children with PH, peripheral blood leukocytes express adiponectin receptors, and the expression is inversely correlated with the serum adiponectin levels irrespective of BMI; however, it correlates with the severity of hypertension—the more severe the hypertension, the greater the expression of adiponectin receptors and lower adiponectin concentrations [ 66 ].

Matrix metalloproteinases MMPs and their tissue inhibitors TIMPswhich control extracellular matrix remodelling, are secreted by cells of the immune system. It was observed that the pattern of their secretion and gene expression was significantly disturbed in hypertensive children and was associated with VAT [ 6768 ].

Adolescents with PH also show subtle but significant alterations of adaptive immunity, such as alterations in the distribution of T cells, with more mature memory T cells and a lower percentage and number of regulatory T cells [ 6970 ]. According to recent findings, activation of both innate and adaptive immunity in PH leads to arterial wall remodelling and development of hypertensive target organ damage TOD and sustains hypertension [ 71 ].

: Hypertension and metabolic syndrome

What is Metabolic Syndrome?

Metabolic syndrome is a group of five conditions that can lead to heart disease , diabetes , stroke and other health problems. Metabolic syndrome is diagnosed when someone has three or more of these risk factors:.

Although each of these is a risk factor for cardiovascular disease, when a person has three or more and is diagnosed with metabolic syndrome, the chance of developing a serious cardiovascular condition increases. For example, high blood pressure is an important risk factor for cardiovascular disease, but when combined with high fasting blood sugar levels and abdominal obesity large waistline , the chance for developing cardiovascular disease is intensified.

Metabolic syndrome is a serious health condition that puts people at higher risk of heart disease, diabetes, stroke and diseases related to fatty buildups in artery walls atherosclerosis.

Underlying causes of metabolic syndrome include overweight and obesity, insulin resistance, physical inactivity, genetic factors and increasing age. Download our Answers by Heart sheet: What is Metabolic Syndrome?

Distribution of blood pressure readings above 95th percentile for age and height according to weight status in 3—18 years old children and adolescents. Nevertheless, the prevalence of PH is related to weight status. Despite the significant increase in the prevalence of obesity, the prevalence of PH declined between the years and , even among overweight adolescents, but it increased significantly among obese and severely obese patients.

In another analysis of the same group, which included data from 63, overweight and obese children and adolescents, it was found that PH was the main comorbidity in the case of overweight and obesity [ 22 ].

The blood pressure status was classified according to the Fourth Task Force Report, and stage 1 dominated, but the prevalence of stage 2 also increased with the increase in the BMI status, from 0.

Although blood pressure increased with BMI status in both boys and girls, the absolute blood pressure values were higher among boys than among girls. The second finding of this large study was that another comorbidity related to an increased BMI was dyslipidaemia, including elevated total cholesterol, low HDL cholesterol, high LDL cholesterol, and high triglyceride levels.

Although serum insulin was not determined in this study, it is known that hyperinsulinaemia accompanied by inflammation in insulin-sensitive tissues and insulin resistance IR are the main metabolic abnormalities in obese patients [ 23 ]. Nevertheless, hyperinsulinaemia and IR are not associated with the amount of adipose tissue, but with its distribution.

It is the visceral adipose tissue VAT that determines IR, and the subcutaneous adipose tissue SAT may play a protective role. In healthy humans, hyperinsulinaemia increases the sympathetic adrenergic drive, but it is offset by a decrease in peripheral vascular resistance.

However, chronic hyperinsulinaemia may not decrease peripheral vascular resistance to the same extent. Data from experimental and human studies has shown that increased sympathetic activity, caused by chronic hyperinsulinaemia and inflammation, promotes IR and increases peripheral vascular resistance [ 24 ].

Thus, it suggests that sympathetic activation plays a role in the elevation of blood pressure in obese patients. This view is supported by observations of patients suffering from rare, genetic forms of severe obesity.

In patients with leptin deficiency and patients with the most common genetically determined form of obesity, i. These mutations lead to the disruption of signal transduction in the central nervous system and lack of sympathetic activation. The typical phenotypic features of children and adolescents with PH are presented in Table 1.

The phenotype indicates that PH is not only a haemodynamic phenomenon, but also a syndrome of interrelated neuro-immuno-metabolic abnormalities leading to haemodynamic consequences [ 26 ]. However, average BMI in adolescents with blood pressure above the 90th percentile was at the 86th percentile.

Analysis of body composition with the use of dual X-ray densitometry DXA showed that the relation between adipose mass and lean body mass is disturbed in hypertensive adolescents [ 30 ].

Chen et al. Secondly, blood pressure was similar in both normal weight children with metabolic abnormalities typical of metabolic syndrome normal weight metabolically unhealthy [NWMU] and obese children with metabolic abnormalities metabolically unhealthy obese [MUHO] , but it was significantly higher than in children with normal body weight who did not suffer from any metabolic abnormalities normal weight metabolically healthy [NWMH] and in obese children without metabolic abnormalities metabolically healthy obese [MHO].

These studies indicate that it is not only adiposity, but disturbed relations between fat mass and lean mass and fat distribution with visceral fatness and metabolic abnormalities that is typical for PH [ 30 , 32 , 33 , 34 , 35 ].

It also means that even in patients with normal BMI but lower lean mass and relatively greater amount of fat mass with visceral distribution NWMU , blood pressure was elevated and was accompanied by typical metabolic abnormalities [ 34 ].

The role of obesity and visceral fatness as CVD risk factors has been known since the first reports from the Framingham study. However, the exact role of metabolic abnormalities associated with visceral fatness was first described in by Reaven and Hoffman and then in by Reaven, who found that hyperinsulinaemia, IR, with accompanying dyslipidaemia, was a consequence of visceral obesity and played a role in the pathogenesis of PH [ 35 , 36 ].

They also observed that simple reduction of BP did not reduce IR and cardiovascular risk. Now, this cluster of metabolic, anthropometric, and haemodynamic abnormalities is known as metabolic syndrome. The main problem with the formulation of a paediatric definition of metabolic syndrome is that insulin sensitivity, serum lipid concentrations, and anthropometrical variables change with age, and at least 40 different definitions of metabolic syndrome in children have been used [ 37 ].

In , the International Diabetes Federation IDF published a definition and criteria of metabolic syndrome in children and adolescents [ 38 ]. According to the IDF definition, metabolic syndrome can be diagnosed in children older than 10, but not younger; however, children below 10 who meet the criteria of metabolic syndrome should be treated as a risk group.

The main and obligatory criterion of metabolic syndrome in the IDF definition is an increased WC, which is a surrogate marker of VAT. Thus, this definition may also include patients with normal BMI. Currently, the definition of metabolic syndrome in children and adolescents used most frequently is the IDF definition, used mainly in Europe, and the definition by Cook et al.

is used in the USA Table 2 [ 31 ]. The adiposity measures and metabolic abnormalities were higher in hypertensive patients than in normotensive patients.

With age, at least until young adulthood 19—42 years , these abnormalities progressed in prehypertensive and hypertensive patients. Hyperinsulinaemia and IR seem to precede the development of PH. Sinaiko et al. reported that higher insulin levels and IR at the age of 13 predicted both the elevation of blood pressure and the development of dyslipidaemia at the age of 16, independently of BMI [ 40 ].

Other abnormalities typical of metabolic syndrome, i. In the USA, using the definition formulated by Cook et al. Elevated serum uric acid levels do not constitute a criterion of metabolic syndrome, but are associated with metabolic syndrome abnormalities in both children and adults [ 32 ].

In a recent report from the SHIP-AHOY study, it was stated that the mean serum uric acid concentrations increased from 5. Moreover, Feig et al. Oxidative stress SOX is a non-specific marker of metabolic abnormalities, which accompanies metabolic syndrome and is typical for visceral obesity.

Elevated urinary isoprostane excretion has been found in obese children and adolescents and was associated with visceral obesity, but not with BMI and blood pressure [ 49 ]. Other studies which included hypertensive children demonstrated that the serum levels of asymmetric dimethylarginine and symmetric dimethylarginine were significantly increased in hypertensive children [ 50 ].

Although SOX is typical for obese children when compared with non-obese children, hypertensive children are exposed to greater SOX, irrespective of their BMI [ 36 ]. SOX markers also correlate with h SBP.

In a prospective study, it was observed that hypertensive children were exposed to greater SOX, and SOX markers correlated with left ventricular hypertrophy and the presence of metabolic syndrome [ 51 ]. It has been observed on a population level that accelerated biological development is associated with higher than average blood pressure, as confirmed in the National Health and Nutrition Examination Survey NHANES II and III, in which more advanced bone age in relation to chronological age was associated with higher blood pressure [ 52 ].

The association between accelerated maturation and visceral obesity, metabolic abnormalities, and elevated blood pressure was also demonstrated in other studies. In a prospective study conducted in Poland, earlier maturation was associated with higher BMI and higher BP in adulthood [ 53 ].

The same was observed in retrospective studies conducted in Iceland, which showed that rapid growth between 8 and 13 years of age was associated with elevated BP in adulthood and greater mortality and morbidity from CVD in adulthood [ 54 , 55 ]. Similarly, the Fels Longitudinal Study showed that earlier growth spurt is associated with higher blood pressure, adiposity, and significant metabolic abnormalities, already in young adulthood [ 56 ].

In the Bogalusa Heart Study, it was found that early menarche was associated with fatness and increased risk of metabolic syndrome as well as PH in early adulthood 19—37 years [ 57 ]. The same was also observed in the Cardiovascular Risk in Young Finns Study [ 58 ].

As early as , in clinical observational studies, it was found that increased growth rate and more advanced bone age were associated with higher blood pressure and PH in adolescence [ 59 ].

In our study, we found that the difference between bone age and chronologic age in hypertensive children was 1. The mechanism of cause and effect relation between accelerated biological maturation and PH is not known.

As suggested by Lever and Harrap, faster biological maturation is associated with greater exposure to growth factors, sex hormones and especially androgens, and visceral fat deposition [ 61 ].

Second, VAT is active hormonal tissue generating both androgens and corticosteroids, especially in women, which may accelerate biological maturation and elevate blood pressure [ 62 , 63 , 64 ].

There is an increasing amount of data, from both experimental and clinical studies, indicating that PH is associated with immune abnormalities and the activation of both innate and adaptive immunity. In children suffering from PH, the activation of the innate immune system is closely associated with the presence of metabolic syndrome, and high sensitivity C-reactive protein hsCRP levels correlate with a number of metabolic syndrome criteria [ 65 ].

Both SAT and VAT generate adipocytokines which modulate anti- and proinflammatory reactions. In children with PH, peripheral blood leukocytes express adiponectin receptors, and the expression is inversely correlated with the serum adiponectin levels irrespective of BMI; however, it correlates with the severity of hypertension—the more severe the hypertension, the greater the expression of adiponectin receptors and lower adiponectin concentrations [ 66 ].

Matrix metalloproteinases MMPs and their tissue inhibitors TIMPs , which control extracellular matrix remodelling, are secreted by cells of the immune system. It was observed that the pattern of their secretion and gene expression was significantly disturbed in hypertensive children and was associated with VAT [ 67 , 68 ].

Adolescents with PH also show subtle but significant alterations of adaptive immunity, such as alterations in the distribution of T cells, with more mature memory T cells and a lower percentage and number of regulatory T cells [ 69 , 70 ].

According to recent findings, activation of both innate and adaptive immunity in PH leads to arterial wall remodelling and development of hypertensive target organ damage TOD and sustains hypertension [ 71 ]. Although there are no data concerning direct measurements of the activity of sympathetic nerves in children with PH, there is a large amount of data from clinical studies in which the activity of the sympathetic nervous system was assessed on the basis of heart rate, heart rate variability, hyperkinetic circulation, heart rate and blood pressure rhythms, and catecholamine concentrations [ 72 ].

As mentioned, increased sympathetic drive is associated with adiposity. In the Tecumseh study, conducted in the s, it was observed that there was an interrelationship between blood pressure, the adrenergic drive, and adiposity: elevated blood pressure and heart rate at the age of 6 were associated with increased adiposity measures at the age of 22 [ 73 ].

Both blood pressure and adiposity measures were associated with the markers of adrenergic drive. Blood pressure rhythmicity was also significantly disturbed in children suffering from PH, and correlated with metabolic abnormalities typical of metabolic syndrome, especially with amount of VAT [ 74 , 75 ].

It must be noted that in some studies, a significant increase of sympathetic activity, expressed as disturbed heart rate variability, was observed in hypertensive children and the effect was independent of adiposity [ 76 ].

However, in this study, the effect of VAT compartment was not analyzed. The above-described main abnormalities found in children with PH and typical of metabolic syndrome, immune activation, and sympathetic drive, are closely associated with TOD.

It has been documented that the prevalence of left ventricular hypertrophy LVH correlates with the exposure to metabolic syndrome criteria, and severe LVH was found only in hypertensive patients who suffered from metabolic syndrome [ 42 ].

Similarly, subclinical hypertensive arterial injury, expressed as increased carotid intima-media thickness cIMT , correlates with lower adiponectin concentrations and higher inflammatory activity [ 42 , 65 ]. Recently, the usefulness of metabolic syndrome in terms of predicting TOD in comparison with the sum of its components has been questioned.

An analysis of paediatric data indicated that metabolic syndrome diagnosed according to the IDF definition or the criteria by Cook et al. had similar values, as a sum of 3 components, in predicting the cIMT value in children. However, the sum of five components had a greater value in predicting cIMT in comparison with the diagnosis of metabolic syndrome based on 3 criteria [ 78 ].

The features of intermediate phenotype of PH are also typically seen in obese children and adolescents. They show altered body composition, features of immune system activation, accelerated biological maturation, and metabolic abnormalities typical of metabolic syndrome.

A more detailed analysis indicates that in obesity, haemodynamic alterations, AH, and CVD risk depend on the distribution of adipose mass and the above-described metabolic abnormalities typical of metabolic syndrome.

It led to the development of the concept of MHO and MUHO phenotypes. Recently, an operational definition of MHO in children was proposed; it defines MHO as a lack of metabolic and haemodynamic criteria of metabolic syndrome in obese children, even with increased WC [ 79 ].

The comparison of children and adolescents in relation to their anthropometric and metabolic phenotype showed that blood pressure was significantly higher in NWMU and MUHO compared with that in NWMH and MHO [ 80 ].

A more detailed analysis of body composition indicated that WC and the amount of VAT assessed by DXA were significantly higher in the case of NWMU and MUHO than in NWMH and MHO patients, respectively, and VAT amount determined metabolic abnormalities [ 80 , 81 ].

Generally, children and adolescents with MUHO were older and their BMI was higher than in the case of MHO patients. It was also observed that puberty doubled the risk of switching from MHO to MUHO, which corresponds with the earlier description of the intermediate phenotype in adolescents with PH and the hypothesis of early vascular ageing in PH [ 82 , 83 ].

A study conducted by Guzzetti el al. demonstrated a significant decline in the prevalence of MHO among obese children occurring with age—from It was associated with increase in the prevalence of PH, from 5.

Interestingly, even though the prevalence of metabolic abnormalities increased with age in both sexes, males more often than females showed pathological WC and PH Greater prevalence of PH among obese boys in comparison with obese girls was seen already at the prepubertal stage and amounted to 7.

The MUHO and NWMU phenotypes are determined by the same early life determinants as PH. More detailed analyses of young adults aged 31 showed that patients with MUHO and NWMU had lower birth weight than patients with MHO and NWMH [ 85 ]. The problem with the concept of MHO is whether it is truly benign or merely a transitory stage to MUHO.

With age, there is a decrease in insulin sensitivity and so-called metabolic health. A recent analysis by Smith et al. Moreover, although the risk of CVD is lower in patients with MHO than in patients with MUHO, it is still higher than in NWMH subjects.

It was observed that children with MHO had higher blood pressure than NWMH and NWMU children, and the blood pressure values correlated with both low adiponectin serum levels and higher leptin-to-adiponectin ratio [ 87 ]. In a prospective study, it was demonstrated that after 6 years of observation, at the age of 16, the risk of developing PH was significantly greater in children with MHO than in those who were NWMH relative risk 5.

Thus, the diagnosis of MHO means only that the CVD risk is lower than in the case of patients suffering from MUHO, but blood pressure and the risk of developing PH and metabolic abnormalities are still higher than in children with normal weight and normal body composition [ 84 ].

The distribution of adipose tissue plays a role in the development of metabolic and haemodynamic complications of obesity.

According to the adipose tissue expandability hypothesis, increased amount of SAT protects against visceral fat deposition [ 85 ]. However, with time and increasing absolute volume of fat, this protective effect may decrease. To conclude, the prevalence of PH among obese children is greater than in the general paediatric population, especially in obese patients suffering from MUHO.

The prevalence of MUHO and PH among obese children increases with age. However, both non-obese children with PH and obese children show similar accompanying abnormalities.

It indicates that the main pathophysiological mechanisms of PH and obesity-related hypertension are almost the same if not identical, and the treatment is based on the same principles. However, the risk of non-haemodynamic complications of obesity, such as non-alcoholic fatty liver disease and type 2 diabetes, is additionally greater in patients with MUHO phenotype.

Polycystic ovary syndrome in viscerally obese girls, who show metabolic abnormalities, features of hyperandrogenism, and PH, constitutes a specific form of the MUHO phenotype [ 88 ]. The treatment of PH and obesity-related hypertension depends on the stage of hypertension, comorbidities, and presence of TOD.

The most important element of the treatment is non-pharmacological therapy, which is based on changing the lifestyle, modifying the diet, and taking up physical activity. The dietary modifications are the same as the modifications used in obesity treatment and in general are based on the reduction of caloric intake, simple carbohydrates, red meat, and salt.

It is advised to consume more vegetables and lean, white meat instead of red meat. Three months of dietary treatment, based on the DASH diet applied in 57 adolescents suffering from prehypertension and PH, caused a greater decrease in SBP than a routine hospital-prepared diet [ 89 ].

However, due to the fact that altered body composition is one of the main features of both PH and obesity-related hypertension, physical activity constitutes a very important part of treatment.

The paediatric guidelines of both the European Society of Hypertension and the American Academy of Paediatrics recommend at least 60 to 90 min of moderate-to-vigorous physical activity daily, both as a preventive measure and as a non-pharmacological treatment [ 90 , 91 ]. The data from the European Youth Heart Study revealed that min of daily physical activity in children aged 9 and at least 88 min in children aged 15 may prevent the clustering of cardiovascular risk factors including blood pressure elevation and the metabolic risk factors [ 92 ].

However, it is not only physical activity, but also improved fitness that matters. Cross-sectional paediatric studies indicate that there is a significant relationship between better fitness and favourable arterial phenotype [ 94 ].

There are significant differences between different forms of physical activity regarding energy expenditure expressed as metabolic equivalent units.

The issue has been recently reviewed by Baker-Smith et al. A more detailed exercise prescription in patients with cardiovascular risk factors, including obese and hypertensive patients, has been recently published [ 95 ].

Non-pharmacological treatment based on physical activity is contraindicated in the case of some accompanying comorbidities, including structural heart disease, rhythm disturbances, myocarditis, pericarditis, and uncontrolled stage 2 or higher hypertension [ 93 ].

In an interventional, controlled study in prepubertal, obese, and hypertensive children average age 9 years , 60 min of physical activity was applied 3 times a week for 3 months [ 96 ]. It was observed that after 3 months, the children from the intervention group had significantly lower blood pressure, lower prevalence of PH, decreased amount of abdominal and whole-body fat, and increased cardiorespiratory fitness.

After 6 months, in addition to lower blood pressure, the patients who exercised also showed lower stiffness of the carotid artery and increased insulin sensitivity.

In another study, Woo et al. compared the effects of diet alone and diet combined with physical activity in obese children aged 10 [ 97 ]. They observed that both diet and diet plus exercise led to an improvement in the endothelium-dependent dilation of the brachial artery; however, the effect of diet combined with physical activity was much better.

Moreover, the continuation of training led to further improvement after 1 year. Importantly, detraining led to a decrease in the endothelial function as soon as after 6 weeks.

The effects of non-pharmacological treatment combined with pharmacological therapy based on angiotensin-converting enzyme inhibitors ACEi or angiotensin receptor blockers ARB were assessed in a prospective, interventional study conducted on 86 adolescents with PH [ 43 , 51 , 77 ].

The main determinants of hypertensive arteriopathy regression and normalization of the left ventricular geometry were a decrease in WC and increase in insulin sensitivity. If applied, non-pharmacological treatment is very effective.

The results of a meta-analysis of studies on adults showed that more intensive, supervised physical activity and more frequent visits and longer contact with health care professionals were associated with greater reduction of blood pressure [ 98 ].

It must be pointed out that non-pharmacological treatment when properly planned and used is much more effective and safer than pharmacological treatment. It is more effective because it directly affects the main pathophysiological abnormalities associated with PH such as the following: disturbed body composition, metabolic abnormalities, sympathetic activation, and probably immune abnormalities.

It is safer because it does not lead to adverse drug reactions and complications related directly to drug action, such as with beta-adrenolytics. However, there are still challenges with implementing lifestyle changes. The second big challenge in implementing lifestyle changes is patient adherence.

It must be pointed out that in most cases, dietary changes must be implemented by the whole family, not only by the hypertensive child. The same is true with support given by family and friends, including schoolmates and teachers.

Analysis of data provided by Williamson et al. shows that good effects of physical exercise are associated not only with supervised sessions of exercise, their intensity, and frequency but also with support given by nurses and physicians [ 98 ].

Last, but not least, parent education and SES of family are important. Due to the fact that the pathogenesis of both PH and obesity-related hypertension and the development of TOD are strictly associated with metabolic abnormalities, the choice of antihypertensive medications should be based on their metabolic effects.

ACEi and ARBs have the most favourable metabolic profile; they increase peripheral blood flow and insulin sensitivity and are preferred as first-line medications [ 99 , , ]. Another contraindication to ACEi is atopy, angiooedema, and allergy to Hymenoptera insects.

In these cases, ARBs seem to be safe. Similarly, beta-adrenolytics aggravate IR. A new option is nebivolol, which is a new beta 1 receptor blocker with vasodilating properties and the potential to induce nitric oxide generation through endothelial cells [ ].

A comparison with metoprolol indicated that nebivolol significantly increased insulin sensitivity [ ]. Although there are no data concerning the use of nebivolol in children, it has been registered for use in adults and may be used in older adolescents.

As mentioned previously, allopurinol lowers blood pressure and may be recommended in subjects with accompanying hyperuricaemia. Metformin, which increases insulin sensitivity, is often used as an additional drug in the case of IR and may promote weight loss [ , ].

PH and obesity-related hypertension share similar intermediate phenotype with metabolic abnormalities typical of metabolic syndrome and is a complex neuro-immuno-metabolic disease. Disturbed body composition and visceral obesity play a crucial role in the development of metabolic abnormalities and TOD, and the risk of TOD increases with the number of metabolic risk factors.

A decrease in VAT and increase in lean body mass are the main determinants of blood pressure reduction, TOD regression, and normalization of metabolic abnormalities. For this reason, non-pharmacological therapy based on modifications of diet and lifestyle, including increased physical activity, is the mainstay of the treatment.

During the selection of pharmacological treatment, the physician should take into account not only the antihypertensive efficacy of medications, but also their metabolic effects. In some cases, additional drugs may be used to treat accompanying metabolic disturbances.

Primary hypertension and obesity-related hypertension is a complex neuro-immuno-metabolic disease complicated by arterial hypertension. Disturbed body composition and visceral fat play a key role in the pathogenesis of primary hypertension and obesity-related hypertension.

Non-pharmacological treatment based on diet, lifestyle, and physical activity modifications is the basis of treatment. Pharmacological therapy of primary hypertension and obesity-related hypertension should consider adverse metabolic effects of some antihypertensive medications.

The prevalence of primary hypertension and of obesity-related hypertension among children and adolescents. Slower biological maturation, metabolic abnormalities typical of metabolic syndrome, increased parasympathetic activity, disturbed body composition.

Accelerated biological maturation, hyperoestrogenism, metabolic abnormalities typical of metabolic syndrome, disturbed body composition. Accelerated biological maturation, metabolic abnormalities typical of metabolic syndrome, tendency to lower serum uric acid levels, disturbed body composition.

Accelerated biological maturation, metabolic abnormalities typical of metabolic syndrome, tendency to elevated serum uric acid, disturbed body composition, increased sympathetic activity. Tend to be higher in primary hypertension and treatment with allopurinol lowered both serum uric levels and blood pressure.

Pharmacological antihypertensive treatment in adolescents with primary hypertension and metabolic syndrome should be based on:. Is the most important part of treatment and should be started in all patients with stage 1 hypertension and should accompany pharmacological therapy in patients with stage 2 hypertension.

Song P, Zhang Y, Yu J, Zha M, Zhu Y, Rahimi K, Rudan I Global prevalence of hypertension in children. A systematic review and metaanalysis. JAMA Pediatr — Article Google Scholar. Sharma AK, Metzger DL, Rodd CJ Prevalence and severity of high blood pressure among children based on the American Academy of Pediatrics Guidelines.

PubMed PubMed Central Google Scholar. Noubiap JJ, Essouma M, Bigna JJ, Jingi AM, Aminde LN, Nansseu JR Prevalence of elevated blood pressure in children and adolescents in Africa: a systematic review and meta-analysis.

Lancet Public Health 2:e—e PubMed Google Scholar. McNiece KL, Poffenbarger TS, Turner JL, Franco KD, Sorof JM, Portman RJ Prevalence of hypertension and pre-hypertension among adolescents.

J Pediatr —, Symonides B, Jędrusik P, Artyszuk L, Gryboś A, Dziliński P, Gaciong Z Different diagnostic criteria significantly affect the rates of hypertension in year-old high school students.

Arch Med Sci — Jackson SL, Zhang Z, Wiltz JL, Loustalot F, Ritchey MD, Goodman AB, Ynag Q Hypertension among youths - United States, MMWR Morb Mortal Wkly Rep — Kułaga Z, Grajda A, Gurzkowska B, Wojtyło M, Góźdź M, Litwin M The prevalence of overweight and obesity among Polish school-aged children and adolescents.

Przegl Epidemiol — Litwin M, Obrycki Ł, Niemirska A, Sarnecki J, Kułaga Z Central systolic blood pressure and central pulse pressure predict left ventricular hypertrophy in hypertensive children. Pediatr Nephrol — Gupta-Malhotra M, Banker A, Shete S, Hashmi SS, Tyson JE, Barratt MS, Hecht JT, Milewicz DM, Boerwinkle E Essential hypertension vs.

secondary hypertension among children. Am J Hypertens — Kivimäki M, Lawlor DA, Smith GD, Keltikangas-Järvinen L, Elovainio M, Vahtera J, Taittonen M, Juonala M, Viikari JS, Raitakari OT Early socioeconomic position and blood pressure in childhood and adulthood: the Cardiovascular Risk in Young Finns Study.

Hypertension — Google Scholar. J Hypertens — CAS PubMed Google Scholar. Circulation — Chiolero A, Paradis G, Madeleine G, Hanley JA, Paccaud F, Bovet P Birth weight, weight change, and blood pressure during childhood and adolescence: a school-based multiple cohort study.

Epidemiology — Wang M, Kelishadi R, Khadilkar A, Mi Hong Y, Nawarycz T, Krzywińska-Wiewiorowska M, Aounallah-Skhiri H, Esmaeil Motlagh M, Soon Kim H, Khadilkar V, Krzyżaniak A, Ben Romdhane H, Heshmat R, Chiplonkar S, Stawińska-Witoszyńska B, El Ati J, Qorbani M, Kajale N, Traissac P, Ostrowska-Nawarycz L, Ardalan G, Ekbote V, Yang L, Zhao M, Liu X, Liang Y, Xi B Body mass index percentiles and elevated blood pressure among children and adolescents.

J Hum Hypertens. Wijnhoven TMA, van Raaij JMA, Spinelli A, Rito AI, Hovengen R, Kunesova M, Starc G, Rutter H, Sjöberg A, Petrauskiene A, O'Dwyer U, Petrova S, Farrugia Sant'angelo V, Wauters M, Yngve A, Rubana IM, Breda J WHO European Childhood Obesity Surveillance Initiative weight, height and body mass index in year-old children.

Pediatr Obes — Ogden CL, Carroll MD, Lawman HG, Fryar CD, Kruszon-Moran D, Kit BK, Flegal KM Trends in obesity prevalence among children and adolescents in the United States, through JAMA — CAS PubMed PubMed Central Google Scholar. NCD Risk Factor Collaboration NCD-RisC Worldwide trends in body-mass index, underweight, overweight, and obesity from to a pooled analysis of population-based measurement studies in ·9 million children, adolescents, and adults.

Lancet — Gurzkowska B, Kułaga Z, Litwin M, Grajda A, Świąder A, Kułaga K, Góżdż M, Wojtyło M The relationship between selected socioeconomic factors and basic anthropometric parameters of school-aged children and adolescents in Poland.

Eur J Pediatr — Xi B, Mi J, Zhao M, Zhang T, Jia C, Li J, Zeng T, Steffen LM, Public Health Youth Collaborative and Innovative Study Group of Shandong University Trends in abdominal obesity among U.

children and adolescents. Pediatrics e—e Flechtner-Mors M, Neuhauser H, Reinehr T, Roost H-P, Wiegand S, Siegfried W, Zwiauer K, Molz E, Holl RW, APV initiative and the BMBF Competence Network Obesity Blood pressure in 57, pediatric patients who are overweight or obese based on five reference systems.

Am J Cardiol — Horm Res Paediatr — Maffeis C, Morandi A Body composition and insulin resistance in children. Eur J Clin Nutr — Greenfield JR, Miller JW, Keogh JM, Henning E, Satterwhite JH, Cameron GS, Astruc B, Mayer JP, Brage S, See TC, Lomas DJ, O'Rahilly S, Farooqi IS Modulation of blood pressure by central melanocortinergic pathways.

N Engl J Med — Simonds SE, Pryor JT, Ravussin E, Greenway FL, Dileone R, Allen AM, Bassi J, Elmquist JK, Keogh JM, Henning E, Myers MG Jr, Licinio J, Brown RD, Enriori PJ, O'Rahilly S, Sternson SM, Grove KL, Spanswick DC, Farooqi IS, Cowley MA Leptin mediates the increase in blood pressure associated with obesity.

Cell — Litwin M, Feber J, Niemirska A, Michałkiewicz J Primary hypertension is a disease of premature vascular aging associated with neuro-immuno-metabolic abnormalities. Flynn JT, Alderman MH Characteristics of children with primary hypertension seen at a referral center.

Urbina EM, Mendizábal B, Becker RC, Daniels SR, Falkner BE, Hamdani G, Hanevold C, Hooper SR, Ingelfinger JR, Lande M, Martin LJ, Meyers K, Mitsnefes M, Rosner B, Samuels J, Flynn JT Association of blood pressure level with left ventricular mass in adolescents.

Obrycki Ł, Feber J, Derezinski T, Lewandowska W, Kułaga Z, Litwin M Hemodynamic patterns and target organ damage in adolescents with ambulatory prehypertension.

Pludowski P, Litwin M, Sladowska J, Antoniewicz J, Niemirska A, Wierzbicka A, Lorenc RS Bone mass and body composition in children and adolescents with primary hypertension: preliminary data. Zimmet P, Alberti G, Kaufman F, Tajima N, Silink M, Arslanian S, Wong G, Bennett P, Shaw J, Caprio S, International Diabetes Federation Task Force on Epidemiology and Prevention of Diabetes The metabolic syndrome in children and adolescents.

Chen F, Liu J, Yan Y, Mi J, China Child and Adolescent Cardiovascular Health CCACH Study Group Abnormal metabolic phenotypes among urban Chinese children: epidemiology and the impact of DXA-measured body composition.

Obesity Silver Spring — CAS Google Scholar. Sun D, Li S, Zhang X, Fernandez C, Chen W, Srinivasan SR, Berenson GS Uric acid is associated with metabolic syndrome in children and adults in a community: the Bogalusa Heart Study.

PLoS One 9:e Rizzo NS, Ruiz JR, Hurtig-Wennlöf A, Ortega FB, Sjöström M Relationship of physical activity, fitness, and fatness with clustered metabolic risk in children and adolescents: the European youth heart study.

J Pediatr — Henderson M, Van Hulst A, von Oettingen JE, Benedetti A, Paradis G Normal weight metabolically unhealthy phenotype in youth: do definitions matter? Pediatr Diabetes — Reaven GM, Hoffman BB A role for insulin in the aetiology and course of hypertension? Reaven GM Banting lecture Role of insulin resistance in human disease.

Diabetes — Ford ES, Li C Defining the metabolic syndrome in children and adolescents: will the real definition please stand up?

Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH Prevalence of a metabolic syndrome phenotype in adolescents: findings from the third National Health and Nutrition Examination Survey, Arch Pediatr Adolesc Med — Srinivasan SR, Myers L, Berenson GS Changes in metabolic syndrome variables since childhood in prehypertensive and hypertensive subjects: the Bogalusa Heart Study.

Sinaiko AR, Steinberger J, Moran A, Hong C-P, Prineas RJ, Jacobs DR Influence of insulin resistance and body mass index at age 13 on systolic blood pressure, triglycerides, and high-density lipoprotein cholesterol at age

What is Metabolic Syndrome? | American Heart Association Importantly, detraining led to a decrease in the endothelial function as soon as after 6 weeks. It has been documented that the prevalence of left ventricular hypertrophy LVH correlates with the exposure to metabolic syndrome criteria, and severe LVH was found only in hypertensive patients who suffered from metabolic syndrome [ 42 ]. The renin-angiotensin system RAS plays a crucial role in blood pressure regulation, by affecting renal function and by modulating vascular tone. Aguilar M, Bhuket T, Torres S, et al. Meigs JB. NEFA has been reported to raise blood pressure, heart rate, and α1-adrenoceptor vasoreactivity, while reducing baroreflex sensitivity, endothelium-dependent vasodilatation, and vascular compliance [ 28 ].
Metabolic Syndrome in Hypertension - Treatment Challenges and Goals | ECR Journal

The dietary modifications are the same as the modifications used in obesity treatment and in general are based on the reduction of caloric intake, simple carbohydrates, red meat, and salt. It is advised to consume more vegetables and lean, white meat instead of red meat.

Three months of dietary treatment, based on the DASH diet applied in 57 adolescents suffering from prehypertension and PH, caused a greater decrease in SBP than a routine hospital-prepared diet [ 89 ].

However, due to the fact that altered body composition is one of the main features of both PH and obesity-related hypertension, physical activity constitutes a very important part of treatment.

The paediatric guidelines of both the European Society of Hypertension and the American Academy of Paediatrics recommend at least 60 to 90 min of moderate-to-vigorous physical activity daily, both as a preventive measure and as a non-pharmacological treatment [ 90 , 91 ].

The data from the European Youth Heart Study revealed that min of daily physical activity in children aged 9 and at least 88 min in children aged 15 may prevent the clustering of cardiovascular risk factors including blood pressure elevation and the metabolic risk factors [ 92 ].

However, it is not only physical activity, but also improved fitness that matters. Cross-sectional paediatric studies indicate that there is a significant relationship between better fitness and favourable arterial phenotype [ 94 ].

There are significant differences between different forms of physical activity regarding energy expenditure expressed as metabolic equivalent units. The issue has been recently reviewed by Baker-Smith et al. A more detailed exercise prescription in patients with cardiovascular risk factors, including obese and hypertensive patients, has been recently published [ 95 ].

Non-pharmacological treatment based on physical activity is contraindicated in the case of some accompanying comorbidities, including structural heart disease, rhythm disturbances, myocarditis, pericarditis, and uncontrolled stage 2 or higher hypertension [ 93 ].

In an interventional, controlled study in prepubertal, obese, and hypertensive children average age 9 years , 60 min of physical activity was applied 3 times a week for 3 months [ 96 ].

It was observed that after 3 months, the children from the intervention group had significantly lower blood pressure, lower prevalence of PH, decreased amount of abdominal and whole-body fat, and increased cardiorespiratory fitness. After 6 months, in addition to lower blood pressure, the patients who exercised also showed lower stiffness of the carotid artery and increased insulin sensitivity.

In another study, Woo et al. compared the effects of diet alone and diet combined with physical activity in obese children aged 10 [ 97 ].

They observed that both diet and diet plus exercise led to an improvement in the endothelium-dependent dilation of the brachial artery; however, the effect of diet combined with physical activity was much better. Moreover, the continuation of training led to further improvement after 1 year.

Importantly, detraining led to a decrease in the endothelial function as soon as after 6 weeks. The effects of non-pharmacological treatment combined with pharmacological therapy based on angiotensin-converting enzyme inhibitors ACEi or angiotensin receptor blockers ARB were assessed in a prospective, interventional study conducted on 86 adolescents with PH [ 43 , 51 , 77 ].

The main determinants of hypertensive arteriopathy regression and normalization of the left ventricular geometry were a decrease in WC and increase in insulin sensitivity. If applied, non-pharmacological treatment is very effective.

The results of a meta-analysis of studies on adults showed that more intensive, supervised physical activity and more frequent visits and longer contact with health care professionals were associated with greater reduction of blood pressure [ 98 ].

It must be pointed out that non-pharmacological treatment when properly planned and used is much more effective and safer than pharmacological treatment. It is more effective because it directly affects the main pathophysiological abnormalities associated with PH such as the following: disturbed body composition, metabolic abnormalities, sympathetic activation, and probably immune abnormalities.

It is safer because it does not lead to adverse drug reactions and complications related directly to drug action, such as with beta-adrenolytics.

However, there are still challenges with implementing lifestyle changes. The second big challenge in implementing lifestyle changes is patient adherence. It must be pointed out that in most cases, dietary changes must be implemented by the whole family, not only by the hypertensive child.

The same is true with support given by family and friends, including schoolmates and teachers. Analysis of data provided by Williamson et al.

shows that good effects of physical exercise are associated not only with supervised sessions of exercise, their intensity, and frequency but also with support given by nurses and physicians [ 98 ].

Last, but not least, parent education and SES of family are important. Due to the fact that the pathogenesis of both PH and obesity-related hypertension and the development of TOD are strictly associated with metabolic abnormalities, the choice of antihypertensive medications should be based on their metabolic effects.

ACEi and ARBs have the most favourable metabolic profile; they increase peripheral blood flow and insulin sensitivity and are preferred as first-line medications [ 99 , , ].

Another contraindication to ACEi is atopy, angiooedema, and allergy to Hymenoptera insects. In these cases, ARBs seem to be safe. Similarly, beta-adrenolytics aggravate IR.

A new option is nebivolol, which is a new beta 1 receptor blocker with vasodilating properties and the potential to induce nitric oxide generation through endothelial cells [ ]. A comparison with metoprolol indicated that nebivolol significantly increased insulin sensitivity [ ].

Although there are no data concerning the use of nebivolol in children, it has been registered for use in adults and may be used in older adolescents. As mentioned previously, allopurinol lowers blood pressure and may be recommended in subjects with accompanying hyperuricaemia. Metformin, which increases insulin sensitivity, is often used as an additional drug in the case of IR and may promote weight loss [ , ].

PH and obesity-related hypertension share similar intermediate phenotype with metabolic abnormalities typical of metabolic syndrome and is a complex neuro-immuno-metabolic disease. Disturbed body composition and visceral obesity play a crucial role in the development of metabolic abnormalities and TOD, and the risk of TOD increases with the number of metabolic risk factors.

A decrease in VAT and increase in lean body mass are the main determinants of blood pressure reduction, TOD regression, and normalization of metabolic abnormalities. For this reason, non-pharmacological therapy based on modifications of diet and lifestyle, including increased physical activity, is the mainstay of the treatment.

During the selection of pharmacological treatment, the physician should take into account not only the antihypertensive efficacy of medications, but also their metabolic effects.

In some cases, additional drugs may be used to treat accompanying metabolic disturbances. Primary hypertension and obesity-related hypertension is a complex neuro-immuno-metabolic disease complicated by arterial hypertension.

Disturbed body composition and visceral fat play a key role in the pathogenesis of primary hypertension and obesity-related hypertension. Non-pharmacological treatment based on diet, lifestyle, and physical activity modifications is the basis of treatment. Pharmacological therapy of primary hypertension and obesity-related hypertension should consider adverse metabolic effects of some antihypertensive medications.

The prevalence of primary hypertension and of obesity-related hypertension among children and adolescents. Slower biological maturation, metabolic abnormalities typical of metabolic syndrome, increased parasympathetic activity, disturbed body composition.

Accelerated biological maturation, hyperoestrogenism, metabolic abnormalities typical of metabolic syndrome, disturbed body composition. Accelerated biological maturation, metabolic abnormalities typical of metabolic syndrome, tendency to lower serum uric acid levels, disturbed body composition.

Accelerated biological maturation, metabolic abnormalities typical of metabolic syndrome, tendency to elevated serum uric acid, disturbed body composition, increased sympathetic activity. Tend to be higher in primary hypertension and treatment with allopurinol lowered both serum uric levels and blood pressure.

Pharmacological antihypertensive treatment in adolescents with primary hypertension and metabolic syndrome should be based on:. Is the most important part of treatment and should be started in all patients with stage 1 hypertension and should accompany pharmacological therapy in patients with stage 2 hypertension.

Song P, Zhang Y, Yu J, Zha M, Zhu Y, Rahimi K, Rudan I Global prevalence of hypertension in children. A systematic review and metaanalysis. JAMA Pediatr — Article Google Scholar. Sharma AK, Metzger DL, Rodd CJ Prevalence and severity of high blood pressure among children based on the American Academy of Pediatrics Guidelines.

PubMed PubMed Central Google Scholar. Noubiap JJ, Essouma M, Bigna JJ, Jingi AM, Aminde LN, Nansseu JR Prevalence of elevated blood pressure in children and adolescents in Africa: a systematic review and meta-analysis.

Lancet Public Health 2:e—e PubMed Google Scholar. McNiece KL, Poffenbarger TS, Turner JL, Franco KD, Sorof JM, Portman RJ Prevalence of hypertension and pre-hypertension among adolescents.

J Pediatr —, Symonides B, Jędrusik P, Artyszuk L, Gryboś A, Dziliński P, Gaciong Z Different diagnostic criteria significantly affect the rates of hypertension in year-old high school students. Arch Med Sci — Jackson SL, Zhang Z, Wiltz JL, Loustalot F, Ritchey MD, Goodman AB, Ynag Q Hypertension among youths - United States, MMWR Morb Mortal Wkly Rep — Kułaga Z, Grajda A, Gurzkowska B, Wojtyło M, Góźdź M, Litwin M The prevalence of overweight and obesity among Polish school-aged children and adolescents.

Przegl Epidemiol — Litwin M, Obrycki Ł, Niemirska A, Sarnecki J, Kułaga Z Central systolic blood pressure and central pulse pressure predict left ventricular hypertrophy in hypertensive children.

Pediatr Nephrol — Gupta-Malhotra M, Banker A, Shete S, Hashmi SS, Tyson JE, Barratt MS, Hecht JT, Milewicz DM, Boerwinkle E Essential hypertension vs. secondary hypertension among children. Am J Hypertens — Kivimäki M, Lawlor DA, Smith GD, Keltikangas-Järvinen L, Elovainio M, Vahtera J, Taittonen M, Juonala M, Viikari JS, Raitakari OT Early socioeconomic position and blood pressure in childhood and adulthood: the Cardiovascular Risk in Young Finns Study.

Hypertension — Google Scholar. J Hypertens — CAS PubMed Google Scholar. Circulation — Chiolero A, Paradis G, Madeleine G, Hanley JA, Paccaud F, Bovet P Birth weight, weight change, and blood pressure during childhood and adolescence: a school-based multiple cohort study.

Epidemiology — Wang M, Kelishadi R, Khadilkar A, Mi Hong Y, Nawarycz T, Krzywińska-Wiewiorowska M, Aounallah-Skhiri H, Esmaeil Motlagh M, Soon Kim H, Khadilkar V, Krzyżaniak A, Ben Romdhane H, Heshmat R, Chiplonkar S, Stawińska-Witoszyńska B, El Ati J, Qorbani M, Kajale N, Traissac P, Ostrowska-Nawarycz L, Ardalan G, Ekbote V, Yang L, Zhao M, Liu X, Liang Y, Xi B Body mass index percentiles and elevated blood pressure among children and adolescents.

J Hum Hypertens. Wijnhoven TMA, van Raaij JMA, Spinelli A, Rito AI, Hovengen R, Kunesova M, Starc G, Rutter H, Sjöberg A, Petrauskiene A, O'Dwyer U, Petrova S, Farrugia Sant'angelo V, Wauters M, Yngve A, Rubana IM, Breda J WHO European Childhood Obesity Surveillance Initiative weight, height and body mass index in year-old children.

Pediatr Obes — Ogden CL, Carroll MD, Lawman HG, Fryar CD, Kruszon-Moran D, Kit BK, Flegal KM Trends in obesity prevalence among children and adolescents in the United States, through JAMA — CAS PubMed PubMed Central Google Scholar. NCD Risk Factor Collaboration NCD-RisC Worldwide trends in body-mass index, underweight, overweight, and obesity from to a pooled analysis of population-based measurement studies in ·9 million children, adolescents, and adults.

Lancet — Gurzkowska B, Kułaga Z, Litwin M, Grajda A, Świąder A, Kułaga K, Góżdż M, Wojtyło M The relationship between selected socioeconomic factors and basic anthropometric parameters of school-aged children and adolescents in Poland.

Eur J Pediatr — Xi B, Mi J, Zhao M, Zhang T, Jia C, Li J, Zeng T, Steffen LM, Public Health Youth Collaborative and Innovative Study Group of Shandong University Trends in abdominal obesity among U. children and adolescents. Pediatrics e—e Flechtner-Mors M, Neuhauser H, Reinehr T, Roost H-P, Wiegand S, Siegfried W, Zwiauer K, Molz E, Holl RW, APV initiative and the BMBF Competence Network Obesity Blood pressure in 57, pediatric patients who are overweight or obese based on five reference systems.

Am J Cardiol — Horm Res Paediatr — Maffeis C, Morandi A Body composition and insulin resistance in children. Eur J Clin Nutr — Greenfield JR, Miller JW, Keogh JM, Henning E, Satterwhite JH, Cameron GS, Astruc B, Mayer JP, Brage S, See TC, Lomas DJ, O'Rahilly S, Farooqi IS Modulation of blood pressure by central melanocortinergic pathways.

N Engl J Med — Simonds SE, Pryor JT, Ravussin E, Greenway FL, Dileone R, Allen AM, Bassi J, Elmquist JK, Keogh JM, Henning E, Myers MG Jr, Licinio J, Brown RD, Enriori PJ, O'Rahilly S, Sternson SM, Grove KL, Spanswick DC, Farooqi IS, Cowley MA Leptin mediates the increase in blood pressure associated with obesity.

Cell — Litwin M, Feber J, Niemirska A, Michałkiewicz J Primary hypertension is a disease of premature vascular aging associated with neuro-immuno-metabolic abnormalities. Flynn JT, Alderman MH Characteristics of children with primary hypertension seen at a referral center.

Urbina EM, Mendizábal B, Becker RC, Daniels SR, Falkner BE, Hamdani G, Hanevold C, Hooper SR, Ingelfinger JR, Lande M, Martin LJ, Meyers K, Mitsnefes M, Rosner B, Samuels J, Flynn JT Association of blood pressure level with left ventricular mass in adolescents. Obrycki Ł, Feber J, Derezinski T, Lewandowska W, Kułaga Z, Litwin M Hemodynamic patterns and target organ damage in adolescents with ambulatory prehypertension.

Pludowski P, Litwin M, Sladowska J, Antoniewicz J, Niemirska A, Wierzbicka A, Lorenc RS Bone mass and body composition in children and adolescents with primary hypertension: preliminary data.

Zimmet P, Alberti G, Kaufman F, Tajima N, Silink M, Arslanian S, Wong G, Bennett P, Shaw J, Caprio S, International Diabetes Federation Task Force on Epidemiology and Prevention of Diabetes The metabolic syndrome in children and adolescents.

Chen F, Liu J, Yan Y, Mi J, China Child and Adolescent Cardiovascular Health CCACH Study Group Abnormal metabolic phenotypes among urban Chinese children: epidemiology and the impact of DXA-measured body composition. Obesity Silver Spring — CAS Google Scholar. Sun D, Li S, Zhang X, Fernandez C, Chen W, Srinivasan SR, Berenson GS Uric acid is associated with metabolic syndrome in children and adults in a community: the Bogalusa Heart Study.

PLoS One 9:e Rizzo NS, Ruiz JR, Hurtig-Wennlöf A, Ortega FB, Sjöström M Relationship of physical activity, fitness, and fatness with clustered metabolic risk in children and adolescents: the European youth heart study.

J Pediatr — Henderson M, Van Hulst A, von Oettingen JE, Benedetti A, Paradis G Normal weight metabolically unhealthy phenotype in youth: do definitions matter?

Pediatr Diabetes — Reaven GM, Hoffman BB A role for insulin in the aetiology and course of hypertension? Reaven GM Banting lecture Role of insulin resistance in human disease. Diabetes — Ford ES, Li C Defining the metabolic syndrome in children and adolescents: will the real definition please stand up?

Cook S, Weitzman M, Auinger P, Nguyen M, Dietz WH Prevalence of a metabolic syndrome phenotype in adolescents: findings from the third National Health and Nutrition Examination Survey, Arch Pediatr Adolesc Med — Srinivasan SR, Myers L, Berenson GS Changes in metabolic syndrome variables since childhood in prehypertensive and hypertensive subjects: the Bogalusa Heart Study.

Sinaiko AR, Steinberger J, Moran A, Hong C-P, Prineas RJ, Jacobs DR Influence of insulin resistance and body mass index at age 13 on systolic blood pressure, triglycerides, and high-density lipoprotein cholesterol at age Acta Biochim Pol — Litwin M, Sladowska J, Antoniewicz J, Niemirska A, Wierzbicka A, Daszkowska J, Wawer ZT, Janas R, Grenda R Metabolic abnormalities, insulin resistance, and metabolic syndrome in children with primary hypertension.

Litwin M, Niemirska A, Sladowska-Kozlowska J, Wierzbicka A, Janas R, Wawer ZT, Wiśniewski A, Feber J Regression of target organ damage in children and adolescents with primary hypertension. Ostrihoňová T, Rimárová K, Bérešová J, Kontrošová S, Dorko E, Diabelková J Prevalence and trends of metabolic syndrome in Slovakia during the period of Cent Eur J Public Health — Ekelund U, Anderssen S, Andersen LB, Riddoch CJ, Sardinha LB, Luan J, Froberg K, Brage S Prevalence and correlates of the metabolic syndrome in a population-based sample of European youth.

Am J Clin Nutr — Johnson WD, Kroon JJM, Greenway FL, Bouchard C, Ryan D, Katzmarzyk PT Prevalence of risk factors for metabolic syndrome in adolescents: National Health and Nutrition Examination Survey NHANES , Feig DI, Johnson RJ Hyperuricemia in childhood primary hypertension.

Feig DI, Soletsky B, Johnson RJ Effect of allopurinol on blood pressure of adolescents with newly diagnosed essential hypertension: a randomized trial. Warolin J, Coenen KR, Kantor JL, Whitaker LE, Wang L, Acra SA, Roberts LJ 2nd, Buchowski MS The relationship of oxidative stress, adiposity and metabolic risk factors in healthy Black and White American youth.

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Int J Obes — Our online community of patients, survivors and caregivers is here to keep you going no matter the obstacles. Home Health Topics Metabolic Syndrome About Metabolic Syndrome.

What is metabolic syndrome? Last Reviewed: Oct 17, Find encouragement. Diabetes Res Clin Pract ; 65 : — Lawlor DA, Ebrahim S, Davey Smith G : The metabolic syndrome and coronary heart disease in older women: findings from the British Women's Heart and Health Study.

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J Atheroscler Thromb ; 10 : — Tatsukawa M, Sawayama Y, Maeda N, et al : Carotid atherosclerosis and cardiovascular risk factors: a comparison of residents of a rural area of Okinawa with residents of a typical suburban area of Fukuoka, Japan.

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Hypertens Res ; 25 : — Honda O, Sugiyama S, Kugiyama K, et al : Echolucent carotid plaques predict future coronary events in patients with coronary artery disease. Takiuchi S, Rakugi H, Fujii H, et al : Carotid intima-media thickness is correlated with impairment of coronary flow reserve in hypertensive patients without coronary artery disease.

Hypertens Res ; 26 : — Download references. Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, Tokyo, Japan. Center for Multiphasic Health Testing and Services, Mitsui Memorial Hospital, Tokyo, Japan.

Department of Hygiene and Public Health, Teikyo University School of Medicine, Tokyo, Japan. You can also search for this author in PubMed Google Scholar.

Correspondence to Nobukazu Ishizaka. Reprints and permissions. Ishizaka, N. et al. Hypertension Is the Most Common Component of Metabolic Syndrome and the Greatest Contributor to Carotid Arteriosclerosis in Apparently Healthy Japanese Individuals.

Hypertens Res 28 , 27—34 Download citation. Received : 12 August Accepted : 21 September Issue Date : 01 January Anyone you share the following link with will be able to read this content:.

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nature hypertension research original article article. Download PDF. Abstract The cluster of metabolic and hemodynamic risk factors known as metabolic syndrome is known to be a risk factor for ischemic cardiovascular diseases and stroke.

The artificial sweetener erythritol and cardiovascular event risk Article 27 February

Metabolic syndrome - Better Health Channel Anx resistance Carbohydrate-rich vegetables also associated with development of salt-sensitive Hupertension through the syndromf effect of insulin RMR and nutrition counseling 17 metsbolic. It was Preventing premature wrinkles observed that puberty doubled the risk Refresh and replenish with hydrating beverages switching from MHO to Annd, which corresponds with the earlier description of the intermediate phenotype in adolescents with PH and the hypothesis of early vascular ageing in PH [ 8283 ]. J Am Coll Cardiol ; 41 : — For Visitors. J Pediatr —, This sex-related difference in SBP increase corresponds with a greater ratio of boys to girls 3— among adolescents with primary hypertension PH [ 8 ].
Hypertension and metabolic syndrome

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