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 .
Evidence for Pressure‐Independent Sympathetic Modulation of Central Pulse Wave Velocity
Background Whether the sympathetic nervous system can directly alter central aortic stiffness remains controversial , mainly because of the difficulty in experimentally augmenting peripheral vasoconstrictor activity without changing blood pressure . Methods and Results To address this limitation , we utilized low‐level cardiopulmonary baroreflex loading and unloading shown previously to alter sympathetic outflow without evoking parallel hemodynamic modulation . Blood pressure and carotid‐femoral aortic pulse wave velocity ( cf‐PWV ) were measured in 32 healthy participants ( 24±2 years ; women : n=15 ) before and during 12‐minute applications of low‐level lower body negative pressure ;  −7 mm Hg ) and lower body positive pressure ; + 7 mm Hg ) , applied in a r and om order . Fibular nerve microneurography was used to collect muscle sympathetic nerve activity ( MSNA ) in a subset ( n=8 ) to confirm peripheral sympathetic responses . During lower body negative pressure , heart rate , blood pressure , stroke volume , cardiac output , and total peripheral resistance were not statistically different ( all P>0.05 ) ; MSNA burst frequency ( + 15 % ; P=0.007 ) , total MSNA ( + 44 % ; P=0.006 ) , and cf‐PWV ( ∆+0.3±0.2 m/s ; P<0.001 ) increased . In total , 28 ( 88 % ) of participants observed an increase in cf‐PWV greater than the baseline typical error of measurement . During lower body positive pressure , heart rate , stroke volume , cardiac output , and total peripheral resistance were not statistically different ( all P>0.05 ) , though blood pressure increased ( P<0.05 ) and pulse pressure decreased ( P=0.01 ) ; MSNA burst frequency ( −4 % ; P=0.37 ) , total MSNA ( −7 % ; P=0.89 ) , and cf‐PWV ( ∆0.0±0.2 m/s ; P=0.68 ) were not statistically different . Conclusions These findings provide evidence that acute elevations in peripheral sympathetic activity can increase central aortic PWV  in young participants independent of a change in distending or pulsatile blood pressure or heart rate
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 .