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 .
The effect of metformin and insulin on sympathetic nerve activity, norepinephrine spillover and blood pressure in obese, insulin resistant, normoglycemic, hypertensive men.
To evaluate the effect of metformin on insulin sensitivity and to further examine the relationship between insulin resistance , sympathetic nerve activity and blood pressure , 6 obese insulin resistant , normoglycemic hypertensive men were investigated ( age 49 + /- 2 years , BMI 27.6 + /- 1.2 , mean + /- SEM ) . The study had a placebo controlled , double blind , cross over design with 6 weeks ' metformin treatment ( 850 mg b.i.d ) vs placebo .  Blood pressure was measured weekly . At the end of each treatment period , glucose infusion rate ( GIR ) , muscle sympathetic nerve activity ( MSA ) and renal and total body norepinephrine ( NE ) kinetics ( radioisotope dilution ) were examined during euglycemic hyperinsulinemic clamp . Fasting insulin was 13 + /- 3 and 10 + /- 2 mU/l and fasting glucose 5.3 + /- 0.2 and 5.1 + /- 0.1 mmol/l after placebo and metformin treatment , respectively ( ns ) . GIR during the last hour of the insulin clamp was 3.7 + /- 0.6 vs 3.6 + /- 0.6 mg/kg x min ( ns ) . Resting MSA , total body and right renal NE spillover did not differ significantly after placebo and metformin treatment . Systolic and diastolic blood pressures were 151 + /- 10/95 + /- 5 mmHg after placebo and 146 + /- 5/94 + /- 5 mmHg after metformin treatment ( ns ) . Thus metformin treatment did not have any significant effect on insulin sensitivity , blood pressure or sympathetic activity in this small group of patients . Renal plasma flow and MSA increased significantly during the insulin clamp , whereas renal NE and total body NE spillover remained unchanged , suggesting nonuniform regional sympathetic nerve responses to acute hyperinsulinemia
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 .