Metabolic syndrome

Metabolic syndrome
Dysmetabolic syndrome X
Classification and external resources

An obese male. Weight 146 kg/322 lbs, height 177 cm/5 ft 10 in. The body mass index is 46.
ICD-9 277.7
OMIM 605552
DiseasesDB 31955
MeSH D024821

Metabolic syndrome is a combination of medical disorders that, when occurring together, increase the risk of developing cardiovascular disease and diabetes.[1] It affects one in five people in the United States and prevalence increases with age. Some studies have shown the prevalence in the USA to be an estimated 25% of the population.[2]

Metabolic syndrome is also known as metabolic syndrome X, cardiometabolic syndrome, syndrome X, insulin resistance syndrome, Reaven's syndrome (named for Gerald Reaven), and CHAOS (in Australia).[3] A similar condition in overweight horses is referred to as equine metabolic syndrome; it is unknown if they have the same etiology.


Definitions and diagnosis

Presently there are a couple of sets of defining criteria for metabolic syndrome set out by two different sources -- the International Diabetes Federation[4] and the revised National Cholesterol Education Program. These are very similar and they identify individuals with a given set of symptoms as having metabolic syndrome. There are two differences, however: the IDF state that if BMI > 30 kg/m2, central obesity can be assumed, and waist circumference does not need to be measured. However, this potentially excludes any subject without increased waist circumference if BMI < 30. Conversely, the NCEP definition indicates that metabolic syndrome can be diagnosed based on other criteria. Also, the IDF uses geography-specific cut points for waist circumference while NCEP uses only one set of cut points for waist circumference regardless of geography. These two definitions are much more similar than the original NCEP and WHO definitions.


International Diabetes Federation[4] The IDF consensus worldwide definition of the metabolic syndrome (2006)

Central obesity (defined as waist circumference# with ethnicity specific values)

AND any two of the following:

  • Raised triglycerides: > 150 mg/dL (1.7 mmol/L), or specific treatment for this lipid abnormality.
  • Reduced HDL cholesterol: < 40 mg/dL (1.03 mmol/L) in males, < 50 mg/dL (1.29 mmol/L) in females, or specific treatment for this lipid abnormality
  • Raised blood pressure: systolic BP > 130 or diastolic BP >85 mm Hg, or treatment of previously diagnosed hypertension.
  • Raised fasting plasma glucose :(FPG)>100 mg/dL (5.6 mmol/L), or previously diagnosed type 2 diabetes. If FPG >5.6 mmol/L or 100 mg/dL, OGTT Glucose tolerance test is strongly recommended but is not necessary to define presence of the Syndrome.

# If BMI is >30 kg/m², central obesity can be assumed and waist circumference does not need to be measured


The World Health Organization criteria (1999) require presence of one of:

  • Diabetes mellitus,
  • Impaired glucose tolerance,
  • Impaired fasting glucose or
  • Insulin resistance;

AND two of the following:

  • Blood pressure: ≥ 140/90 mmHg
  • Dyslipidemia: triglycerides (TG): ≥ 1.695 mmol/L and high-density lipoprotein cholesterol (HDL-C) ≤ 0.9 mmol/L (male), ≤ 1.0 mmol/L (female)
  • Central obesity: waist:hip ratio > 0.90 (male); > 0.85 (female), or body mass index > 30 kg/m2
  • Microalbuminuria: urinary albumin excretion ratio ≥ 20 µg/min or albumin:creatinine ratio ≥ 30 mg/g


The European Group for the Study of Insulin Resistance (1999) requires insulin resistance defined as the top 25% of the fasting insulin values among non-diabetic individuals AND two or more of the following:

  • central obesity: waist circumference ≥ 94 cm (male), ≥ 80 cm (female)
  • dyslipidemia: TG ≥ 2.0 mmol/L and/or HDL-C < 1.0 mmol/L or treated for dyslipidemia
  • hypertension: blood pressure ≥ 140/90 mmHg or antihypertensive medication
  • fasting plasma glucose ≥ 6.1 mmol/L


The US National Cholesterol Education Program Adult Treatment Panel III (2001) requires at least three of the following:[5]

  • central obesity: waist circumference ≥ 102 cm or 40 inches (male), ≥ 88 cm or 36 inches(female)
  • dyslipidemia: TG ≥ 1.7 mmol/L (150 mg/dl)
  • dyslipidemia: HDL-C < 40 mg/dL (male), < 50 mg/dL (female)
  • blood pressure ≥ 130/85 mmHg
  • fasting plasma glucose ≥ 6.1 mmol/L (110 mg/dl)

American Heart Association/Updated NCEP

There is confusion as to whether, in 2004, the AHA/NHLBI intended to create another set of guidelines or simply update the NCEP ATP III definition. According to Scott Grundy, University of Texas Southwestern Medical School, Dallas, Texas, the intent was just to update the NCEP ATP III definition and not create a new definition.[6][7]:

  • Elevated waist circumference:
    • Men — greater than 40 inches (102 cm)
    • Women — greater than 35 inches (88 cm)
  • Elevated triglycerides: Equal to or greater than 150 mg/dL (1.7 mmol/L)
  • Reduced HDL (“good”) cholesterol:
    • Men — Less than 40 mg/dL (1.03 mmol/L)
    • Women — Less than 50 mg/dL (1.29 mmol/L)
  • Elevated blood pressure: Equal to or greater than 130/85 mm Hg or use of medication for hypertension
  • Elevated fasting glucose: Equal to or greater than 100 mg/dL (5.6 mmol/L) or use of medication for hyperglycemia


High-sensitivity C-reactive protein (hs-CRP) has been developed and used as a marker to predict coronary vascular diseases in metabolic syndrome and it was recently used as a predictor for non-alcoholic fatty liver disease in correlation with serum markers that indicated lipid and glucose metabolism.[8]


The term "metabolic syndrome" dates back to at least the late 1950s, but came into common usage in the late 1970s to describe various associations of risk factors with diabetes that had been noted as early as the 1920s.[9][10]

  • The Marseilles physician Dr. Jean Vague, in 1947, observed that upper body obesity appeared to predispose to diabetes, atherosclerosis, gout and calculi.[11]
  • Avogadro, Crepaldi and co-workers described six moderately obese patients with diabetes, hypercholesterolemia, and marked hypertriglyceridemia all of which improved when the patients were put on a hypocaloric, low-carbohydrate diet.[12]
  • In 1977, Haller used the term "metabolic syndrome" for associations of obesity, diabetes mellitus, hyperlipoproteinemia, hyperuricemia, and hepatic steatosis when describing the additive effects of risk factors on atherosclerosis.[13]
  • The same year, Singer used the term for associations of obesity, gout, diabetes mellitus, and hypertension with hyperlipoproteinemia.[14]
  • In 1977 and 1978, Gerald B. Phillips developed the concept that risk factors for myocardial infarction concur to form a "constellation of abnormalities" (i.e., glucose intolerance, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and hypertension) that is associated not only with heart disease but also with aging, obesity and other clinical states. He suggested there must be an underlying linking factor, the identification of which could lead to the prevention of cardiovascular disease; he hypothesized that this factor was sex hormones.[15][16]
  • In 1988, in his Banting lecture, Gerald M. Reaven proposed insulin resistance as the underlying factor and named the constellation of abnormalities Syndrome X. Reaven did not include abdominal obesity, which has also been hypothesized as the underlying factor, as part of the condition.[17]

The terms "metabolic syndrome," "insulin resistance syndrome," and "syndrome X" are now used specifically to define a constellation of abnormalities that is associated with increased risk for the development of type 2 diabetes and atherosclerotic vascular disease (e.g., heart disease and stroke).


The exact mechanisms of the complex pathways of metabolic syndrome are not yet completely known. The pathophysiology is extremely complex and has been only partially elucidated. Most patients are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important factors are:

  1. weight
  2. genetics[18][19][20][21]
  3. endocrine disorders, such as polycystic ovary syndrome in women of reproductive age.
  4. aging
  5. sedentary lifestyle, i.e., low physical activity and excess caloric intake.[22]

There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6 (IL–6), Tumor necrosis factor-alpha (TNFα), and others. Some have pointed to a variety of causes including increased uric acid levels caused by dietary fructose.[23][24][25]


It is common for there to be a development of visceral fat, after which the adipocytes (fat cells) of the visceral fat increase plasma levels of TNFα and alter levels of a number of other substances (e.g., adiponectin, resistin, PAI-1). TNFα has been shown not only to cause the production of inflammatory cytokines but possibly to trigger cell signaling by interaction with a TNFα receptor that may lead to insulin resistance[citation needed]. An experiment with rats that were fed a diet one-third of which was sucrose has been proposed as a model for the development of metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance.[26] The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells present within, which play a role in inflammation. Chronic inflammation contribute to an increased risk of hypertension, artherosclerosis and diabetes.[27]

Risk Factors


Recent research indicates that prolonged stress can be an underlying cause of metabolic syndrome by upsetting the hormonal balance of the hypothalamic-pituitary-adrenal axis (HPA-axis).[28] A dysfunctional HPA-axis causes high cortisol levels to circulate which results in raising glucose and insulin levels which cause insulin-mediated effects on adipose tissue, ultimately promoting visceral adiposity, insulin resistance, dyslipidemia and hypertension with direct effects on the bone, causing “low turnover” osteoporosis.[29] HPA-axis dysfunction may explain the reported risk indication of abdominal obesity to cardiovascular disease, type 2 diabetes and stroke.[30] Psychosocial stress is also linked to heart disease.[31]

Overweight and obesity

Central adiposity is a key feature of the syndrome, reflecting the fact that the syndrome's prevalence is driven by the strong relationship between waist circumference and increasing adiposity. However, despite the importance of obesity, patients that are of normal weight may also be insulin-resistant and have the syndrome.[32]

Sedentary lifestyle

Physical inactivity is a predictor of CVD events and related mortality. Many components of metabolic syndrome are associated with a sedentary lifestyle, including increased adipose tissue (predominantly central); reduced HDL cholesterol; and a trend toward increased triglycerides, blood pressure, and glucose in the genetically susceptible. Compared with individuals who watched television or videos or used their computer for less than one hour daily, those that carried out these behaviors for greater than four hours daily have a twofold increased risk of metabolic syndrome.[32]


Metabolic syndrome affects 44% of the U.S. population older than age 50. With respect to that demographic, the percentage of women having the syndrome is higher than that of men. The age dependency of the syndrome's prevalence is seen in most populations around the world.[32]

Diabetes mellitus

It is estimated that the large majority (~75%, or just above 40 million[33]) of patients with type 2 diabetes or impaired glucose tolerance (IGT) have metabolic syndrome - . The presence of metabolic syndrome in these populations is associated with a higher prevalence of CVD than found in patients with type 2 diabetes or IGT without the syndrome.[32] Hypoadiponectinemia has been shown to increase insulin resistance,[34] and is considered to be a risk factor for developing metabolic syndrome.[35]

Coronary heart disease

The approximate prevalence of the metabolic syndrome in patients with coronary heart disease (CHD) is 50%, with a prevalence of 37% in patients with premature coronary artery disease ( age 45), particularly in women. With appropriate cardiac rehabilitation and changes in lifestyle (e.g., nutrition, physical activity, weight reduction, and, in some cases, drugs), the prevalence of the syndrome can be reduced.[32]


Lipodystrophic disorders in general are associated with metabolic syndrome. Both genetic (e.g., Berardinelli-Seip congenital lipodystrophy, Dunnigan familial partial lipodystrophy) and acquired (e.g., HIV-related lipodystrophy in patients treated with highly active antiretroviral therapy) forms of lipodystrophy may give rise to severe insulin resistance and many of metabolic syndrome's components.[32]

Schizophrenia and other psychiatric illnesses

Patients with schizophrenia, schizoaffective disorder or bipolar disorder may have a predisposition to metabolic syndrome that is exacerbated by sedentary lifestyle, poor dietary habits, possible limited access to care, and antipsychotic drug-induced adverse effects. It has been found that 32% and 51%[36] of individuals with schizophrenia meet criteria for metabolic syndrome; the prevalence is higher in women than in men.[37]

Rheumatic diseases

There are new findings regarding the comorbidity associated with rheumatic diseases. Both psoriasis and psoriatic arthritis have been found to be associated with metabolic syndrome.[38]

Signs and symptoms

Symptoms and features are:

Associated diseases and signs are: hyperuricemia, fatty liver (especially in concurrent obesity) progressing to non-alcoholic fatty liver disease, polycystic ovarian syndrome (in women), and acanthosis nigricans.


Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day),[39] and a healthy, reduced calorie diet.[40] There are many studies that support the value of a healthy lifestyle as above. However, one study stated that these potentially beneficial measures are effective in only a minority of people, primarily due to a lack of compliance with lifestyle and diet changes.[22] The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.[41]

A 2007 study of 2,375 male subjects over 20 years suggested that daily intake of a pint (~568 ml) of milk or equivalent dairy products more than halved the risk of metabolic syndrome.[42] Some subsequent studies support the authors' findings, while others dispute them.[43]


The first line treatment is change of lifestyle (e.g., Dietary Guidelines for Americans and physical activity). However, if in three to six months of efforts at remedying risk factors prove insufficient, then drug treatment is frequently required. Generally, the individual disorders that comprise the metabolic syndrome are treated separately. Diuretics and ACE inhibitors may be used to treat hypertension. Cholesterol drugs may be used to lower LDL cholesterol and triglyceride levels, if they are elevated, and to raise HDL levels if they are low. Use of drugs that decrease insulin resistance, e.g., metformin and thiazolidinediones, is controversial; this treatment is not approved by the U.S. Food and Drug Administration.

A 2003 study indicated that cardiovascular exercise was therapeutic in approximately 31% of cases. The most probable benefit was to triglyceride levels, with 43% showing improvement; but fasting plasma glucose and insulin resistance of 91% of test subjects did not improve.[22] Many other studies have supported the value of increased physical activity and restricted caloric intake (exercise and diet) to treat metabolic syndrome.

Restricting the overall dietary carbohydrate intake is more effective in reducing the most common symptoms of metabolic syndrome than the more commonly prescribed reduction in dietary fat intake.[44]


The clinical value of using "metabolic syndrome" as a diagnosis has recently come under fire. It is asserted that different sets of conflicting and incomplete diagnostic criteria are in existence, and that when confounding factors such as obesity are accounted for, diagnosis of the metabolic syndrome has a negligible association with the risk of heart disease.[45]

These concerns have led to the American Diabetes Association and the European Association for the Study of Diabetes to issue a joint statement identifying eight major concerns on the clinical utility of the metabolic syndrome.[46]

It is not contested that cardiovascular risk factors tend to cluster together, but what is contested is the assertion that the metabolic syndrome is anything more than the sum of its constituent parts.

See also


  1. ^ MedlinePlus: Metabolic Syndrome
  2. ^ Ford ES, Giles WH, Dietz WH (2002). "Prevalence of metabolic syndrome among US adults: findings from the third National Health and Nutrition Examination Survey". JAMA 287 (3): 356–359. doi:10.1001/jama.287.3.356. PMID 11790215. 
  3. ^ In his case studies poster presented at the Chronic Fatigue Syndrome Conference in Sydney, Australia (February 12–13, 1998), Dr Allen E. Gale, Consultant Physician (Allergy), identifies the acronym CHAOS as an abbreviation for Coronary artery disease, Hypertension, Atherosclerosis, Obesity, and Stroke.
  4. ^ a b The IDF consensus worldwide definition of the metabolic syndrome. PDF
  5. ^ Expert Panel On Detection, Evaluation, And Treatment Of High Blood Cholesterol In Adults (May 2001). "Executive Summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III)". JAMA: the Journal of the American Medical Association 285 (19): 2486–97. doi:10.1001/jama.285.19.2486. PMID 11368702. 
  6. ^ Grundy SM, Brewer HB, Cleeman JI, Smith SC, Lenfant D, for the Conference Participants. Definition of metabolic syndrome: report of the National, Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition. Circulation. 2004;109:433-438.
  7. ^ [Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Jr, Spertus JA Costa F. Diagnosis and Management of the Metabolic Syndrome: An American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement. Circulation 2005, 112:2735-2752: originally published online September 12, 2005; doi: 10.1161/CIRCULATIONAHA.105.169404]
  8. ^ Kogiso T, Moriyoshi Y, Shimizu S, Nagahara H, Shiratori K (March 2009). "High-sensitivity C-reactive protein as a serum predictor of nonalcoholic fatty liver disease based on the Akaike Information Criterion scoring system in the general Japanese population". J. Gastroenterol. 44 (4): 313–21. doi:10.1007/s00535-009-0002-5. PMID 19271113. 
  9. ^ Joslin EP. The prevention of diabetes mellitus. JAMA 1921;76:79–84.
  10. ^ Kylin E. [Studies of the hypertension-hyperglycemia-hyperuricemia syndrome] (German). Zentralbl Inn Med 1923;44: 105-27.
  11. ^ Vague J. La diffférenciacion sexuelle, facteur déterminant des formes de l'obésité. Presse Med 1947;30:339-40.
  12. ^ Avogadro A, Crepaldi G, Enzi G, Tiengo A. Associazione di iperlipidemia, diabete mellito e obesità di medio grado. Acta Diabetol Lat 1967;4:572-590.
  13. ^ Haller H (April 1977). "Epidermiology and associated risk factors of hyperlipoproteinemia.". Zeitschrift fur die gesamte innere Medizin und ihre Grenzgebiete 32 (8): 124–8. PMID 883354. 
  14. ^ Singer P (May 1977). "Diagnosis of primary hyperlipoproteinemias.". Zeitschrift fur die gesamte innere Medizin und ihre Grenzgebiete 32 (9): 129–33 concl. PMID 906591. 
  15. ^ Phillips GB (July 1978). "Sex hormones, risk factors and cardiovascular disease.". The American journal of medicine 65 (1): 7–11. doi:10.1016/0002-9343(78)90685-X. PMID 356599. 
  16. ^ Phillips GB (April 1977). "Relationship between serum sex hormones and glucose, insulin and lipid abnormalities in men with myocardial infarction". Proceedings of the National Academy of Sciences of the United States of America 74 (4): 1729–33. doi:10.1073/pnas.74.4.1729. PMC 430867. PMID 193114. 
  17. ^ Reaven (1988). "Role of insulin resistance in human disease". Diabetes 37 (12): 1595–607. doi:10.2337/diabetes.37.12.1595. PMID 3056758. 
  18. ^ Pollex, R.L.; Hegele, R.A. (2006). "Genetic determinants of the metabolic syndrome". Nat Clin Pract Cardiovasc Med 3 (9): 482–9. doi:10.1038/ncpcardio0638. PMID 16932765. 
  19. ^ Poulsen, P.; Vaag, A.; Kyvik, K.; Beck-nielsen, H. (2001). "Genetic versus environmental aetiology of the metabolic syndrome among male and female twins". Diabetologia 44 (5): 537–543. doi:10.1007/s001250051659. PMID 11380071. Retrieved 2009-04-29. 
  20. ^ Groop, Leif (2000). "Genetics of the metabolic syndrome". British Journal of Nutrition 83 (83): S39–S48. doi:10.1017/S0007114500000945. Retrieved 2009-04-29. 
  21. ^ Bouchard, G. (1995). "Genetics and the metabolic syndrome". International journal of obesity 19: 52–59. Retrieved 2009-04-29. 
  22. ^ a b c Katzmaryk,, Peter T; Leon, Arthur S.; Wilmore, Jack H.; Skinner, James S.; Rao, D. C.; Rankinen, Tuomo; Bouchard, Claude (October 2003). "Targeting the Metabolic Syndrome with Exercise: Evidence from the HERITAGE Family Study". Med. Sci. Sports Exerc 35 (10): 1703–1709. doi:10.1249/01.MSS.0000089337.73244.9B. PMID 14523308. Retrieved 2007-06-24. 
  23. ^ Nakagawa T, Hu H, Zharikov S, Tuttle KR, Short RA, Glushakova O, Ouyang X, Feig DI, Block ER, Herrera-Acosta J, Patel JM, Johnson RJ (2006). "A causal role for uric acid in fructose-induced metabolic syndrome". Am J Phys Renal Phys 290 (3): F625–F631. doi:10.1152/ajprenal.00140.2005. PMID 16234313. 
  24. ^ Hallfrisch J (1990). "Metabolic effects of dietary fructose". FASEB J 4 (9): 2652–2660. PMID 2189777. 
  25. ^ Reiser S, Powell AS, Scholfield DJ, Panda P, Ellwood KC, Canary JJ (1989). "Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch". Am J Clin Nutr 49 (5): 832–839. PMID 2497634. 
  26. ^ Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H. (1 June 2004). "Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats". Exp Biol Med 229 (6): 486–493. PMID 15169967. 
  27. ^ Whitney, Ellie and Ralfes, R. Sharon. 2011. Understanding Nutrition. Wadsworth Cengage Learning: Belmont, CA
  28. ^ Gohill, BC; Rosenblum, LA; Coplan, JD; Kral, JG; (July 2001). "Hypothalamic-pituitary-adrenal axis function and the metabolic syndrome X of obesity". CNS Spectr. 6 (7): 581–6, 589. PMID 15573024. 
  29. ^ Tsigos, C; Chrousos, GP; (October 2002). "Hypothalamic-pituitary-adrenal axis, neuroendocrine factors and stress". J Psychosom Res. 53 (4): 865–71. doi:10.1016/S0022-3999(02)00429-4. PMID 12377295. 
  30. ^ Rosmond, R; Björntorp, P; (February 2000). "The hypothalamic-pituitary-adrenal axis activity as a predictor of cardiovascular disease, type 2 diabetes and stroke". J Intern Med. 247 (2): 188–97. doi:10.1046/j.1365-2796.2000.00603.x. PMID 10692081. 
  31. ^ Brunner, EJ; Hemingway, H; Walker, BR; Page, M; Clarke, P; Juneja, M; Shipley, MJ; Kumari, M; Andrew, R; Seckl, JR; Papadopoulos, A; Checkley, S; Rumley, A; Lowe, GD; Stansfeld, SA; Marmot, MG; (November 2002). "Adrenocortical, autonomic, and inflammatory causes of the metabolic syndrome: nested case-control study". Circulation. 106 (21): 2634–6. PMID 12438290. 
  32. ^ a b c d e f Fauci, Anthony S. (2008). Harrison's principles of internal medicine. McGraw-Hill Medical. ISBN 0-07-147692-X. 
  33. ^ Diabetes and Metabolics
  34. ^ Lara-Castro C, Fu Y, Chung BH, Garvey WT (June 2007). "Adiponectin and the metabolic syndrome: mechanisms mediating risk for metabolic and cardiovascular disease". Curr. Opin. Lipidol. 18 (3): 263–70. doi:10.1097/MOL.0b013e32814a645f. PMID 17495599. 
  35. ^ Renaldi O, Pramono B, Sinorita H, Purnomo LB, Asdie RH, Asdie AH (January 2009). "Hypoadiponectinemia: a risk factor for metabolic syndrome". Acta Med Indones 41 (1): 20–4. PMID 19258676. 
  36. ^ John, A. P.; Koloth, R.; Dragovic, M.; Lim, S. C. (2009). "Prevalence of metabolic syndrome among Australians with severe mental illness". The Medical journal of Australia 190 (4): 176–179. PMID 19220180.  edit
  37. ^ Narasimhan M, Raynor JD. Evidence-based perspective on metabolic syndrome and use of antipsychotics. Drug Benefit Trends. 2010;22:77-88.
  38. ^ Quilon A III, Brent L. The primary care physician's guide to inflammatory arthritis: diagnosis. J Musculoskel Med. 2010;27:223-231.
  39. ^ Lakka TA, Laaksonen DE (2007). "Physical activity in prevention and treatment of the metabolic syndrome". Applied physiology, nutrition, and metabolism = Physiologie appliquée, nutrition et métabolisme 32 (1): 76–88. doi:10.1139/h06-113. PMID 17332786. 
  40. ^ Feldeisen SE, Tucker KL (2007). "Nutritional strategies in the prevention and treatment of metabolic syndrome". Appl Physiol Nutr Metab 32 (1): 46–60. doi:10.1139/h06-101. PMID 17332784. 
  41. ^ James PT, Rigby N, Leach R (2004). "The obesity epidemic, metabolic syndrome and future prevention strategies". Eur J Cardiovasc Prev Rehabil 11 (1): 3–8. doi:10.1097/01.hjr.0000114707.27531.48. PMID 15167200. 
  42. ^ Elwood, PC; Pickering JE, Fehily AM (2007). "Milk and dairy consumption, diabetes and the metabolic syndrome: the Caerphilly prospective study". J Epidemiol Community Health 61 (8): 695–698. doi:10.1136/jech.2006.053157. PMC 2652996. PMID 17630368. 
  43. ^ Snijder MB, van der Heijden AA, van Dam RM, et al. (2007). "Is higher dairy consumption associated with lower body weight and fewer metabolic disturbances? The Hoorn Study". Am. J. Clin. Nutr. 85 (4): 989–95. PMID 17413097. 
  44. ^ Volek JS, Feinman RD (2005). "Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction". Nutr Metab (Lond) 2 (1): 31. doi:10.1186/1743-7075-2-31. PMC 1323303. PMID 16288655. 
  45. ^ Richard Kahn (2008). "Metabolic syndrome—what is the clinical usefulness?". Lancet 371 (9628): 1892–1893. doi:10.1016/S0140-6736(08)60731-X. 
  46. ^ Kahn R, Buse J, Ferrannini E, Stern M (2005). "The metabolic syndrome: time for a critical appraisal. Joint statement from the American Diabetes Association and the European Association for the Study of Diabetes". Diabetes Care 28 (9): 2289–2304. doi:10.2337/diacare.28.9.2289. PMID 16123508. 

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