What is the Metabolic Syndrome?

What is the Metabolic Syndrome?

Metabolic syndrome is a medical condition defined by a set of five conditions: abdominal obesity, high blood glucose levels, high triglyceride levels, low high-density lipoprotein (HDL) cholesterol levels, and high blood pressure.1–3 Metabolic syndrome is known to be associated with type 2 diabetes mellitus (T2DM) and other health problems.4,5

 

Diagnostic Criteria for Metabolic Syndrome

The widely used diagnostic criteria by the National Cholesterol Education Program Adult Treatment Panel III (2001) identifies an individual with at least three of the five following conditions as having metabolic syndrome:1–3,6

  • Abdominal obesity: Waist circumference >40 inch in men and >35 inch in women
  • High blood glucose levels: Fasting glucose >100 mg/dL
  • High triglyceride levels: >150 mg/dL
  • Low HDL cholesterol levels: <40 mg/dL in men and <50 mg/dL in women
  • High blood pressure: >130/85 mmHg

 

The Five Components of Metabolic Syndrome

1) Weight – The prevalence of metabolic syndrome often corresponds with the prevalence of obesity, and each component of the metabolic syndrome has been shown to be closely related to weight gain, especially abdominal adiposity and waist circumference.7,8 It is postulated that increased abdominal adiposity may be the primary trigger in the development of metabolic syndrome. Intra-abdominal fat plays an important endocrine role, and an increase in its mass can disrupt the release of hormonal factors that regulate metabolism. Studies have consistently demonstrated abdominal obesity as being a major risk factor for systemic inflammation, insulin resistance, dyslipidemia, and cardiovascular disease (CVD).9,10

2) Blood glucose & insulin resistance – Although a third of individuals with metabolic syndrome have normal insulin sensitivity, it is known that there are links between metabolic syndrome and insulin resistance.8 For instance, individuals with metabolic syndrome have five times greater risk of developing T2DM.1,11 Studies are showing that through complex mechanisms, abdominal obesity increases circulating free fatty acids, which reduces glucose uptake by muscles, resulting in hyperinsulinemia.12,13 This eventually leads to pancreatic b-cell stress and dysfunction, causing insulin resistance. Reducing body weight can confer beneficial effects on insulin resistance among obese individuals with metabolic disturbances.14,15

3) Cholesterol and 4) Triglyceride levels – High levels of triglyceride and low levels of HDL cholesterol are also characteristic of metabolic syndrome.8 The strong association between obesity and dyslipidemia and subsequent CVD risk has been well established.16(p),17 In addition to the significant role obesity plays in the development dyslipidemia, it is hypothesized that through complex mechanisms, insulin resistance can also indirectly cause increases in triglyceride and low-density lipoprotein (LDL) cholesterol levels and decreases in HDL cholesterol levels by increasing circulating free fatty acids and altering lipid metabolism in the liver.7

5) Blood pressure – Various studies have demonstrated that blood pressure and body mass index are correlated, with a linear association between weight and blood pressure.8 Several weight-related factors may contribute to the development of hypertension in metabolic syndrome: elevated circulating volume, activated renin-angiotensin system, increased cardiac output, and vasoconstriction. In addition, insulin resistance may also contribute to the development of hypertension via increased sympathetic activation, sodium reabsorption in the kidneys, vasoconstrictive effects by increased free fatty acids, and changes in various hormone and protein levels that contribute to increased CVD risk.7,8

 

References:
1. Regufe VMG, Pinto CMCB, Perez PMVHC. Metabolic Syndrome in Type 2 Diabetic Patients: A Review of Current Evidence. Porto Biomed J. 2020;5(6):e101. doi:10.1097/j.pbj.0000000000000101
2. Singer GM, Setaro JF. Secondary Hypertension: Obesity and the Metabolic Syndrome. J Clin Hypertens (Greenwich). 2008;10(7):567-574. doi:10.1111/j.1751-7176.2008.08178.x
3. Grundy SM, Cleeman JI, Daniels SR, et al. Diagnosis and Management of the Metabolic Syndrome. Circulation. 2005;112(17):e285-e290. doi:10.1161/CIRCULATIONAHA.105.169405
4. 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
5. About Metabolic Syndrome. www.heart.org. Accessed April 12, 2022. https://www.heart.org/en/health-topics/metabolic-syndrome/about-metabolic-syndrome
6. Huang PL. A Comprehensive Definition for Metabolic Syndrome. Dis Model Mech. 2009;2(5-6):231-237. doi:10.1242/dmm.001180
7. 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
8. Han TS, Lean ME. A Clinical Perspective of Obesity, Metabolic Syndrome and Cardiovascular Disease. JRSM Cardiovasc Dis. 2016;5:2048004016633371. doi:10.1177/2048004016633371
9. 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
10. 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
11. Lee MK, Han K, Kim MK, et al. Changes in Metabolic Syndrome and Its Components and the Risk of Type 2 Diabetes: A Nationwide Cohort Study. Sci Rep. 2020;10(1):2313. doi:10.1038/s41598-020-59203-z
12. 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
13. 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
14. Yuan X, Wang J, Yang S, et al. Effect of the Ketogenic Diet on Glycemic Control, Insulin Resistance, and Lipid Metabolism in Patients With T2DM: a Systematic Review and Meta-analysis. Nutr Diabetes. 2020;10(1):1-8. doi:10.1038/s41387-020-00142-z
15. Westman EC, Tondt J, Maguire E, Yancy WS. Implementing a Low-Carbohydrate, Ketogenic Diet to Manage Type 2 Diabetes Mellitus. Expert Rev Endocrinol Metab. 2018;13(5):263-272. doi:10.1080/17446651.2018.1523713
16. Powell-Wiley TM, Poirier P, Burke LE, et al. Obesity and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2021;143(21):e984-e1010. doi:10.1161/CIR.0000000000000973
17. Feingold KR. Obesity and Dyslipidemia. In: Feingold KR, Anawalt B, Blackman MR, et al., eds. Endotext. MDText.com, Inc.; 2000. Accessed February 8, 2023. http://www.ncbi.nlm.nih.gov/books/NBK305895/

  

(Disclaimer)

The content of this article is intended to provide a general information and knowledge on the subject matter. The views expressed in newsletters, articles, and blogs in the i-SENS USA website are not necessarily those of i-SENS Incorporated, i-SENS USA Incorporated or our publishers. Medical or nutritional information on i-SENS USA website is not intended to replace professional medical advice – you should always consult a specialist with any questions about your specific circumstances.

Add a comment