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 .
Effects of glucagon-like peptide-1, yohimbine, and nitrergic modulation on sympathetic and parasympathetic activity in humans.
Glucagon-like peptide-1 ( GLP-1 ) , an incretin , which is used to treat diabetes mellitus in humans , inhibited vagal activity and activated nitrergic pathways . In rats , GLP-1 also increased sympathetic activity , heart rate , and blood pressure ( BP ) . However , the effects of GLP-1 on sympathetic activity in humans are unknown . Our aims were to assess the effects of a GLP-1 agonist with or without alpha(2)-adrenergic or -nitrergic blockade on autonomic nervous functions in humans . In this double-blind study , 48 healthy volunteers were r and omized to GLP-1-(7 - 36 ) amide , the nitric oxide synthase ( NOS ) inhibitor N(G)-monomethyl-l-arginine acetate ( l-NMMA ) , the alpha(2)-adrenergic antagonist yohimbine , or placebo ( i.e. , saline ) , alone or in combination . Hemodynamic parameters , plasma catecholamines , and cardiac sympathetic and parasympathetic modulation were measured by spectral analysis of heart rate . Thereafter , the effects of GLP-1-(7 - 36 ) amide on muscle sympathetic nerve activity ( MSNA ) were assessed by microneurography in seven subjects . GLP-1 increased ( P = 0.02 ) MSNA but did not affect cardiac sympathetic or parasympathetic indices , as assessed by spectral analysis . Yohimbine increased plasma catecholamines and the low-frequency ( LF ) component of heart rate power spectrum , suggesting increased cardiac sympathetic activity . l-NMMA increased the BP and reduced the heart rate but did not affect the balance between sympathetic and parasympathetic activity .  GLP-1 increases skeletal muscle sympathetic nerve activity but does not appear to affect cardiac sympathetic or parasympathetic activity in humans
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 .