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 .
Autonomic Blockade Reverses Endothelial Dysfunction in Obesity-Associated Hypertension
Impaired nitric oxide ( NO ) vasodilation ( endothelial dysfunction ) is associated with obesity and thought to be a factor in the development of hypertension . We previously found that NO synthesis inhibition had similar pressor effects in obese hypertensives compared with healthy control during autonomic blockade , suggesting that impaired NO vasodilation is secondary to sympathetic activation . We tested this hypothesis by determining the effect of autonomic blockade ( trimethaphan 4 mg/min IV ) on NO-mediated vasodilation ( increase in forearm blood flow to intrabrachial acetylcholine ) compared with endothelial-independent vasodilation ( intrabrachial sodium nitroprusside ) in obese hypertensive subjects ( 30<body mass index<40 kg/m2 ) .  Acetylcholine and sodium nitroprusside were given at equipotent doses ( 10 , 30 , and 50 & mgr;g/min and 1 , 2 , and 3 & mgr;g/min , respectively ) to 14 obese subjects ( 49±3.6 years , 34±1 kg/m2 , 165/94±7/6 mm Hg ) , on separate occasions 1 month apart , r and omly assigned . Autonomic blockade increased basal forearm blood flow ( from 3.9±0.7 to 5.2±1.2 mL/100 mL per minute , P=0.078 ) . As expected , NO-mediated vasodilation was blunted on the intact day compared with NO-independent vasodilation ; forearm blood flow increased from 3.6±0.6 to 10.1±1.1 with the highest dose of nitroprusside , but only from 3.7±0.4 to 7.2±0.8 mL/100 mL per minute with the highest dose of acetylcholine , P<0.05 . In contrast , forearm blood flow responses to acetylcholine  were restored by autonomic blockade and were no longer different to nitroprusside ( from 6.2±1.1 to 11.4±1.6 mL/100 mL per minute and from 5.2±0.9 to 12.5±0.9 , respectively , P=0.58 ) . Our results support the concept that sympathetic activation contributes to the impairment in NO-mediated vasodilation seen in obesity-associated hypertension and provides further rationale to explore it as a therapeutic target
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 .