Abdominal Obesity

Abdominal Obesity

 What Is Abdominal Obesity? 

Obesity is a chronic disease defined as a body mass index (BMI) greater than 30 kg/m2 and is one of the leading causes of morbidity and mortality worldwide.1,2 However, perhaps even more detrimental than overall obesity is abdominal obesity. Abdominal obesity is characterized by increased adipose (ie, fat) tissues around the intra-abdominal organs.3 It is also referred to as visceral obesity or central obesity. Abdominal obesity is measured independent of BMI and is typically defined as increased waist circumference of >88 cm or >35 inch in nonpregnant women and >102 cm or >40 inch in men.4

 

How Does Abdominal Obesity Affect Health? 

Abdominal obesity is linked with an array of health issues, including increased risk of metabolic syndrome, type 2 diabetes mellitus (T2DM), and cardiovascular diseases (CVD). For instance, abdominal obesity is one of the defining characteristics of metabolic syndrome, a medical condition associated with T2DM as well as a host of other health problems.5,6 It is defined by high blood pressure, high blood glucose levels, high triglyceride levels, low high-density-lipoprotein cholesterol levels, and abdominal obesity. It is hypothesized that increased abdominal adiposity may be the primary trigger in the development of metabolic syndrome.

 

Additionally, there is strong evidence suggesting that obesity is the greatest risk factor for developing prediabetes and T2DM, with estimates that nearly 90% of T2DM can be attributed to obesity.7 Excess visceral and abdominal adiposity are associated with metabolic abnormalities linked with the development of T2DM such as insulin resistance, pancreatic b-cell dysfunction, and dyslipidemia.8,9

 

Intra-abdominal fat plays an important endocrine role, and an increase in its mass can disrupt the release of hormonal factors that regulate metabolism.7,10–12 It is thought that increases in plasma free fatty acid (FFA) levels (from increased adiposity and dietary intake) encourage cellular uptake and utilization of lipids instead of glucose, leading to a persistent hyperglycemic (ie, high blood sugar) state and insulin resistance. Additionally, abdominal adiposity is associated with greater insulin resistance than peripheral adiposity as abdominal fat is more metabolically active and lipolytic, actively releasing FFAs into the bloodstream. In accordance, studies have consistently demonstrated that abdominal obesity is a major risk factor for insulin resistance, dyslipidemia, systemic inflammation, and CVD.13,14

 

References:
1. Purnell JQ. Definitions, Classification, and Epidemiology of Obesity. In: Feingold KR, Anawalt B, Blackman MR, et al., eds. Endotext. MDText.com, Inc.; 2000. Accessed February 16, 2023. http://www.ncbi.nlm.nih.gov/books/NBK279167/
2. Health Effects of Overweight and Obesity in 195 Countries over 25 Years. N Engl J Med. 2017;377(1):13-27. doi:10.1056/NEJMoa1614362
3. Shuster A, Patlas M, Pinthus JH, Mourtzakis M. The Clinical Importance of Visceral Adiposity: A Critical Review of Methods for Visceral Adipose Tissue Analysis. Br J Radiol. 2012;85(1009):1-10. doi:10.1259/bjr/38447238
4. Ross R, Neeland IJ, Yamashita S, et al. Waist Circumference as a Vital Sign in Clinical Practice: A Consensus Statement from the Ias and Iccr Working Group on Visceral Obesity. Nat Rev Endocrinol. 2020;16(3):177-189. doi:10.1038/s41574-019-0310-7
5. Shin J, Lee J, Lim S, et al. Metabolic Syndrome as a Predictor of Type 2 Diabetes, and Its Clinical Interpretations and Usefulness. J Diabetes Investig. 2013;4(4):334-343. doi:10.1111/jdi.12075
6. About Metabolic Syndrome. www.heart.org. Accessed April 12, 2022. https://www.heart.org/en/health-topics/metabolic-syndrome/about-metabolic-syndrome
7. Verma S, Hussain ME. Obesity and Diabetes: An Update. Diabetes Metab Syndr. 2017;11(1):73-79. doi:10.1016/j.dsx.2016.06.017
8. Magkos F, Fraterrigo G, Yoshino J, et al. Effects of Moderate and Subsequent Progressive Weight Loss on Metabolic Function and Adipose Tissue Biology in Humans With Obesity. Cell Metab. 2016;23(4):591-601. doi:10.1016/j.cmet.2016.02.005 
9. Zheng Y, Ley SH, Hu FB. Global Aetiology and Epidemiology of Type 2 Diabetes Mellitus and Its Complications. Nat Rev Endocrinol. 2018;14(2):88-99. doi:10.1038/nrendo.2017.151
10. Kahn SE, Hull RL, Utzschneider KM. Mechanisms Linking Obesity to Insulin Resistance and Type 2 Diabetes. Nature. 2006;444(7121):840-846. doi:10.1038/nature05482
11. Rochlani Y, Pothineni NV, Kovelamudi S, Mehta JL. Metabolic Syndrome: Pathophysiology, Management, and Modulation by Natural Compounds. Ther Adv Cardiovasc Dis. 2017;11(8):215-225. doi:10.1177/1753944717711379
12. Han TS, Lean ME. A Clinical Perspective of Obesity, Metabolic Syndrome and Cardiovascular Disease. JRSM Cardiovasc Dis. 2016;5:2048004016633371. doi:10.1177/2048004016633371
13. Paley CA, Johnson MI. Abdominal Obesity and Metabolic Syndrome: Exercise as Medicine? BMC Sports Sci Med Rehabilitation. 2018;10(1):7. doi:10.1186/s13102-018-0097-1
14. Pedersen BK, Saltin B. Exercise as Medicine - Evidence for Prescribing Exercise as Therapy in 26 Different Chronic Diseases. Scand J Med Sci Sports. 2015;25(S3):1-72. doi:10.1111/sms.12581

  

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