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 .
Experimental Weight Gain Increases Ambulatory Blood Pressure in Healthy Subjects: Implications of Visceral Fat Accumulation
Objective : To examine whether experimentally induced weight gain raises ambulatory blood pressure ( BP ) in healthy subjects and identify any relationship between changes in BP and changes in regional fat distribution . Patients and Methods : Twenty‐six normal weight subjects were r and omized to 8 weeks of weight gain through overfeeding ( n=16 ; age , 30.4±6.6 years ) or to weight maintenance ( controls ; n=10 ; age , 27.1±7.7 years ) between July 2004 and August 2010 . Measures of body composition via dual energy X‐ray absorptiometry and computed tomography , circulating biomarkers , and 24‐hour ambulatory BP were obtained at baseline and after the 8‐week experimental phase . Results : Overfeeding result ed in 3.7 kg ( 95 % CI , 2.9‐4.5 ) increase in body weight in weight gainers , with increments in total ( 46.2 cm2 ; 95 % CI , 27.6‐64.9 ) , visceral ( 13.8 cm2 ; 95 % CI , 5.8‐21.9 ) , and subcutaneous fat ( 32.4 cm2 ; 95 % CI , 13.5‐51.3 ) . No changes occurred in the maintenance group . Increases in 24‐hour systolic BP ( 4 mm Hg ; 95 % CI , 1.6‐6.3 ) , mean BP ( 1.7 mm Hg ; 95 % CI , 0.3‐3.3 ) , and pulse pressure ( 2.8 mm Hg ; 95 % CI , 1.1‐4.4 ) were evident after weight gain in the experimental group , whereas BP remained unchanged in controls . Changes in mean BP correlated only with changes in visceral fat ( & rgr;=0.45 ; P=.02 ) , but not with changes in other body composition measures . Conclusion : Modest weight gain causes elevation in 24‐hour BP in healthy subjects . The association between increased BP and abdominal visceral fat accumulation suggests that visceral deposition of adipose tissue may contribute specifically to the enhanced risk of hypertension associated with weight gain
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 .