International Journal of Global Health
ISSN: 2693-1176
Current Issue
Volume No: 1 Issue No: 1
share this page

Mini Review | Open Access
  • Available online freely | Peer Reviewed
  • The Hazards of Abdominal Obesity

    Seyedeh Nasim Habibzadeh 1      

    1School of Health and Life Since, Teesside University, United Kingdom.

    Abstract

    Abdominal obesitywith a big belly is one of the worse type of morbid obesity that is associated with different health failure outcomes. Central obesity leads to an increased risk of health complications such as metabolic syndrome, hypertension, insulin resistance,type 2 diabetes, heart disease and various cancers. Abdominal obesity also can specifically cause to spinal nerve pain and backache. Depression and disability are other subsequent hazards of central fatness. More importantly ,excessive central body fat ultimately contributes in all-causes of early mortality. In regards to this, individuals with abdominal obesity is urgently needed to reduce central obesity using behavior modifications. Changes in diet and performing some exercise in everyday living are essential steps.

     

    Received 13 Mar 2020; Accepted 10 Apr 2020; Published 13 Apr 2020;

    Academic Editor:Qianqian Song, Wake Forest School of Medicine, Wake Forest Baptist Comprehensive Cancer Center, Medical Center Boulevard, Winston-Salem, NC 27157, USA

    Checked for plagiarism: Yes

    Review by:Single-blind

    Copyright©  2020 Seyedeh Nasim Habibzadeh

    License
    Creative Commons License    This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

    Competing interests

    The authors have declared that no competing interests exist.

    Citation:

    Seyedeh Nasim Habibzadeh (2020) The Hazards of Abdominal Obesity . International Journal of Global Health - 1(1):11-13.
    Download as RIS, BibTeX, Text (Include abstract )
    DOI10.14302/issn.2693-1176.ijgh-20-3269

    Introduction

    Abdominal or central obesity are characterized with excessive body fat in waist circumference1. The prevalence of visceral fat that accumulates around abdominal organs is increasing worldwide2, 3. Visceral fat cells have an crucial impact on overall health and well-being.

    Gene-based association studies suggest a strong correlation between genes and abdominal fat4. Heredity and genetic variants and hormones abnormalities can affect abdominal fat5.

    Inappropriate diets such as high-calorie foods are other main influential risk factors for increasing abdominal obesity. High-sugar foods such as sweets, cakes, biscuits, pizza and chips can dramatically enhance intra-abdominal fat cells6. Cigarette smoking habits and alcohol intakes also seem to increase central adiposity with an adverse health consequences7.

    Moreover, sedentary life - style such as sitting for long hours (i.e. low physical job demand) develops the abdominal adipose that intensifies central obesity over time. Sedentary individuals burn fewer calories than active individuals per day in terms of daily energy expenditure which leads to the belly fat accumulation in long-terms. Overall central body fat owing to prolong inactive life–style pattern can cause sitting diseases8.

    In accordance to this, abdominal adiposity alters normal lipid metabolism at which reduces the low-density-lipoprotein (LDL) cholesterol (or good cholesterol) levels and raises the high-density lipoprotein (HDL) cholesterol (or bad cholesterol) levels  in body. Abdominal obesity also increases blood sugar, triglycerides that is assumed to be the predominant risk factors for metabolic syndrome9. Indeed , visceral adiposity is closely linked to the insulin resistance, which can lead to the glucose intolerance and type 2 diabetes in obese individuals10, 11. Excessive central body fat has an important role in coronary artery disease such as hypertension (high-blood pressure) and atherosclerosis12, 13. Furthermore, central body fatness is a strong predictors for different cancers incidence among obese and overweight populations14. With regards to this, growing evidence shows that prenominal abdominal obesity is associated with an increased risk of lifetime disability and greater reduction in life expectancy in part for male individuals15, 16.

    Therefore, the prevention and treatment of abdominal obesity is urgently required. The key health strategies for preventing and managing the abdominal obesity are minimizing over-eating and increasing physical activity levels in daily life17. In regards to this, behavioural consultation to promote a healthy diet and physical activity account for very useful therapeutic strategy to reduce the abdominal obesity for individual with central obesity.

    Conclusion

    Abdominal obesity (or abdominal adiposity) is increasing worldwide . Visceral fat cells affect the overall health and well-being and is associated with all-causes of morbidity. Genetic , unhealthy diets and an inactive lifestyle are main risk factors of central obesity. In regards to this, behavior modifications such as increasing the physical activity levels and controlling the food intakes using an appropriate healthy diet can be very good approach to prevent and to reduce the visceral obesity over time.

    References

    1.PaleyCA JohnsonMI. (2018) Abdominal obesity and metabolic syndrome: exercise as medicine?BMC Sports Sci MedRehabil. 10, 7.
    2.MTO Olinto, Theodoro H, Canuto R. (2017) . Epidemiology of Abdominal Obesity, Adiposity - Epidemiology and Treatment Modalities, Jan Oxholm Gordeladze, IntechOpen .
    3.Pi-Sunyer F X. (2004) The epidemiology of central fat distribution in relation to disease. Nutr Rev . 62(7), 120-126.
    4.EmdinCA KheraAV, KathiresanS.Genetic Predisposition to Abdominal Obesity and Cardiometabolic Risk-Reply.JAMA.2017;317(22):. 2334-2335.
    5.Been L F, Hatfield J L.Shankar A,Aston CE,Ralhan S,Wander GS,MehraNK,Singh JR,Mulvihill JJ,Sanghera DK. A low frequency variant within the GWAS locus of MTNR1B affects fasting glucose concentrations: genetic risk is modulated by obesity. Nutr Metab Cardiovasc Dis 2012;22:. 944-951.
    6.Ross R, Dagnone D, PJH Jones. (2000) Diet-induced weight loss or exercise-induced weight loss in men. , Ann Intern Med 133, 92-103.
    7.Canoy D, Wareham N, Luben R, Welch A. (2005) Bingham S,Day N,KhawKT. Cigarette smoking and fat distribution in 21,828 British men and women: a population-based study. Obes Res. 13, 1466-1475.
    8.Owen N, Sparling P B, Healy G N, Dunstan D W, Matthews C E. (2010) Sedentary behavior: emerging evidence for a new health risk.Mayo Clin Proc. 85(12), 1138-41.
    9.Habibzadeh N. (2015) The Effect of Sedentary Life Style on "Good" and "Bad" Cholesterols in Young Adults. , WJMS 12(1), 62-66.
    10.Cefalu W T, Wang Z Q, Werbel S, Crouse JR Bell-Farrow, Hinson W H et al. (1995) Contribution of visceral fat mass to the insulin resistance of aging. Metabolism. 44, 954-959.
    11.Miyazaki Y, Glass L, Triplitt C, Wajcberg E, Mandarino L J et al. (2002) Abdominal fat distribution and peripheral and hepatic insulin resistance in type 2 diabetes mellitus. , Am J Physiol Endocrinol Metab 283, 1135-1143.
    12.Wright AP OhmanMK, Wickenheiser K J, Luo W, EitzmanDT. (2009) Visceral adipose tissue and atherosclerosis.CurrVascPharmacol. 7(2), 169-79.
    13.Guo X, Xu Y, He H. (2019) Visceral fat reduction is positively associated with blood pressure reduction in overweight or obese males but not females: an observational study. , Nutr Metab (Lond) 16(44).
    14.Barberio A M, Alareeki A, Viner B. (2019) Central body fatness is a stronger predictor of cancer risk than overall body size. , Nat Commun 10(383).
    15.Pi-SunyerX. (2019) The medical risks of obesity.Postgrad Med.121(6):. 21-33.
    16.AbdelaalM le Roux CW, Docherty N G. (2017) Morbidity and mortality associated with obesity.AnnTranslMed. 5(7), 161.
    17.Erhardt J KesztyüsD, SchönsteinerD KesztyüsT. (2018) Therapeutic Treatment for Abdominal Obesity in Adults.DtschArzteblInt.115(29-30):. 487-493.