This indicates that even in the absence of metabolic abnormalities , overweight and obesity are not innocuous , perhaps because the traditional cardiovascular risk factors are either not present early or remain undetected using routine clinical assessment .
This raises the concept that early or sub clinical organ damage assessment s may be better at identifying subjects who are more likely to progress to develop cardiovascular disease .
Obesity and Consequences The prevalence of overweight and obesity has reached epidemic proportion , with the recent figures from the World Health Organization indicating that in 2016 39 % of adults aged ≥18 years ( 39 % of men and 40 % of women ) were overweight and 13 % ( 11 % of men and 15 % of women ) obese .
The World Health Organization states that raised body mass index ( BMI ) is a major risk factor for noncommunicable diseases such as cardiovascular diseases ( mainly heart disease and stroke ) , which were the leading causes of death in 2012 , diabetes mellitus , musculoskeletal disorders , and some cancers .
The Framingham Heart Study data have indicated that overweight and obesity are associated with significantly decreased life expectancy .
Nevertheless , and against these strong evidence s , the relationship between BMI and mortality has been challenged by several studies , indicating a survival advantages for those who are overweight and class I obese .
However , the determinants of these observations are poorly understood and continue to be debated because BMI may not be the ideal index of adiposity and fat distribution and fitness and disease prevention may obscure the link between BMI and mortality .
Overweight or obesity is not always accompanied by traditional risk factors .
In fact , a systematic review and meta analysis revealed that about 35 % of obese individuals are metabolically healthy .
There is evidence that an important factor driving at least some of the obesity-associated end-organ damage is overactivity of the sympathetic nervous system ( SNS ) , an observation that suggests that targeting SNS in obesity may help reduce the cardiovascular risk associated with obesity .
In this review , we highlight the current knowledge of the potential role of SNS function in obesity-induced organ damage and examine whether interventions aim ed at reducing cardiovascular risk in obesity may be mediated via alterations in SNS activity .
Antihypertensive effect of alpha- and beta-adrenergic blockade in obese and lean hypertensive subjects.
The purpose of this study was to determine the contribution of the adrenergic system in mediating hypertension in obese and lean patients . Thirteen obese , hypertensive patients with a body mass index ( BMI ) > or = 28 kg/m2 ( obese ) and nine lean patients with a BMI < or = 25 kg/m2 ( lean ) were recruited . After a 1-week washout period , participants underwent daytime ambulatory blood pressure monitoring  ( ABPM ) . Participants were then treated with the alpha-adrenergic antagonist doxazosin , titrating to 4 mg QHS in 1 week . In the next week , the beta-adrenergic antagonist atenolol was added at an initial dose of 25 mg/day and titrated to 50 mg/day within 1 week . One month after the addition of atenolol , all patients underwent a second ABPM session . There were no differences between the obese and lean subjects in baseline systolic ( SBP ) , diastolic ( DBP ) , or mean arterial pressures ( MAP ) measured by office recording or ABPM . However , obese subjects had higher heart rates than lean subjects ( 87.5+/-2.4 v 76.8+/-4.9 beats/min ) . After 1 month of treatment with the adrenergic blockers , obese patients had a significantly lower SBP ( 130.0+/-2.5 v 138.9+/-2.1 mm Hg , P = .02 ) and MAP ( 99.6+/-2.3 v 107.0+/-1.5 mm Hg , P = .02 ) than lean patients . Obese patients also tended to have a lower DBP than lean patients ( 84.3+/-2.5 v 90.9+/-1.6 mm Hg , P = .057 ) , but there was no significant difference in heart rate after 1 month of adrenergic blockade . These results indicate that blood pressure is more sensitive to adrenergic blockade in obese than in lean hypertensive patients and suggest that increased sympathetic activity may be an important factor in the maintenance of hypertension in obesity
This indicates that even in the absence of metabolic abnormalities , overweight and obesity are not innocuous , perhaps because the traditional cardiovascular risk factors are either not present early or remain undetected using routine clinical assessment .
This raises the concept that early or sub clinical organ damage assessment s may be better at identifying subjects who are more likely to progress to develop cardiovascular disease .
Obesity and Consequences The prevalence of overweight and obesity has reached epidemic proportion , with the recent figures from the World Health Organization indicating that in 2016 39 % of adults aged ≥18 years ( 39 % of men and 40 % of women ) were overweight and 13 % ( 11 % of men and 15 % of women ) obese .
The World Health Organization states that raised body mass index ( BMI ) is a major risk factor for noncommunicable diseases such as cardiovascular diseases ( mainly heart disease and stroke ) , which were the leading causes of death in 2012 , diabetes mellitus , musculoskeletal disorders , and some cancers .
The Framingham Heart Study data have indicated that overweight and obesity are associated with significantly decreased life expectancy .
Nevertheless , and against these strong evidence s , the relationship between BMI and mortality has been challenged by several studies , indicating a survival advantages for those who are overweight and class I obese .
However , the determinants of these observations are poorly understood and continue to be debated because BMI may not be the ideal index of adiposity and fat distribution and fitness and disease prevention may obscure the link between BMI and mortality .
Overweight or obesity is not always accompanied by traditional risk factors .
In fact , a systematic review and meta analysis revealed that about 35 % of obese individuals are metabolically healthy .
There is evidence that an important factor driving at least some of the obesity-associated end-organ damage is overactivity of the sympathetic nervous system ( SNS ) , an observation that suggests that targeting SNS in obesity may help reduce the cardiovascular risk associated with obesity .
In this review , we highlight the current knowledge of the potential role of SNS function in obesity-induced organ damage and examine whether interventions aim ed at reducing cardiovascular risk in obesity may be mediated via alterations in SNS activity .