Metabolic syndrome

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Overview

Metabolic syndrome is a combination of medical disorders that increase one's risk for cardiovascular disease and diabetes. It affects a large number of people in a clustered fashion. In some studies, the prevalence in the USA is calculated as being up to 25% of the population.

A condition with some similarities to human metabolic syndrome is recognized in horses, see equine metabolic syndrome. It is unknown if they have the same etiology.

It is known under various other names, such as (metabolic) syndrome X, insulin resistance syndrome, Reaven's syndrome or CHAOS (Australia).

Signs and symptoms

Symptoms and features are:

Associated diseases and signs are: fatty liver (especially in concurrent obesity), progressing to non-alcoholic fatty liver disease, polycystic ovarian syndrome, hemochromatosis (iron overload); and acanthosis nigricans (a skin condition featuring dark patches).

Diagnosis

There are currently two major definitions for metabolic syndrome provided by 1) International Diabetes Federation[1] and 2) the revised National Cholesterol Education Program, respectively. The revised NCEP and IDF definitions of metabolic syndrome are very similar and it can be expected that they will identify many of the same individuals as having metabolic syndrome. The two differences are that IDF excludes any subject without increased waist circumference, while in the NCEP definition metabolic syndrome can be diagnosed based on other criteria and 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 closer to each other than the original NCEP and WHO definitions.

WHO

The World Health Organization criteria (1999) require presence of diabetes mellitus, impaired glucose tolerance, impaired fasting glucose or insulin resistance, AND two of the following:

  • blood pressure: ≥ 140/90 mmHg
  • dyslipidaemia: triglycerides (TG): ≥ 1.695 mmol/L and/or 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), and/or body mass index > 30 kg/m2
  • microalbuminuria: urinary albumin excretion ratio ≥ 20 mg/min or albumin:creatinine ratio ≥ 30 mg/g

EGIR

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)
  • dyslipidaemia: TG ≥ 2.0 mmol/L and/or HDL-C < 1.0 mg/dL or treated for dyslipidaemia
  • hypertension: blood pressure ≥ 140/90 mmHg or antihypertensive medication
  • fasting plasma glucose ≥ 6.1 mmol/L

NCEP

The National Cholesterol Education Program Adult Treatment Panel III (2001) requires at least three of the following:[2]

  • central obesity: waist circumference ≥ 102 cm or 40 inches (male), ≥ 88 cm or 36 inches(female)
  • dyslipidaemia: TG ≥ 1.695 mmol/L (150 mg/dl)
  • dyslipidaemia: 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 quite a bit of confusion about whether 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.[3]:

  • Elevated waist circumference: Men — Equal to or greater than 40 inches (102 cm) Women — Equal to or greater than 35 inches (88 cm)
  • Elevated triglycerides: Equal to or greater than 150 mg/dL
  • Reduced HDL (“good”) cholesterol: Men — Less than 40 mg/dL Women — Less than 50 mg/dL
  • 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

Etiology

The cause of the metabolic syndrome is unknown. The pathophysiology is extremely complex and has only been partially elucidated. Most patients are older, obese, sedentary, and have a degree of insulin resistance. The most important factors in order are 1) aging, 2) genetics and 3) lifestyle (i.e., decreased physical activity and excess caloric intake). There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if it is a by-product of a more far-reaching metabolic derangement. Systemic inflammation: a number of inflammatory markers (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 oxidative stress due to a variety of causes including dietary fructose mediated increased uric acid levels.[4][5][6]

Pathophysiology

Commonly, there is development of visceral fat followed by the adipocytes (fat cells) of the visceral fat increasing plasma levels of TNFα and altering levels of a number of other substances (e.g., adiponectin, resistin, PAI-1). TNFα has been shown to not only cause the production of inflammatory cytokines, but may also trigger cell signalling by interaction with a TNFα receptor that may lead to insulin resistance. 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 the metabolic syndrome. The sucrose first elevated blood levels of triglycerides, which induced visceral fat and ultimately resulted in insulin resistance [7]. The progression from visceral fat to increased TNFα to insulin resistance has some parallels to human development of metabolic syndrome.

Therapy

The goal is to get the LDL down to < 100 mg/dl. The first line treatment is change of lifestyle (i.e., caloric restriction and physical activity). However, drug treatment is frequently required. Generally, the individual diseases that comprise the metabolic syndrome are treated separately (e.g. diuretics and ACE inhibitors for 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 and not FDA approved.

A recent study indicated that cardiovascular exercise was therapeutic in approximately 31% of cases. The most probable benefit was to triglyceride levels, with 43% showing improvement; conversely 91% of test subjects did not exhibit a decrease in fasting plasma glucose or insulin resistance.[8] Many other studies have supported the value of increased physical activity along with restricted calories in metabolic syndrome.

Prevention

Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day),[9] and a healthy, reduced calorie diet.[10] There are many studies that support the value of a healthy lifestyle as above. However, one study stated that these measures are effective in only a minority of people.[8] The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.[11]

A 2007 study of 2,375 male subjects over 20 years suggested that daily intake of a pint of milk or equivalent dairy products more than halved the risk of metabolic syndrome.[12] Other studies both support and dispute the authors' findings.[13]

History

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.[14][15]

  • The Marseilles physician Dr. Jean Vague, in 1947, made the interesting observation that upper body obesity appeared to predispose to diabetes, atherosclerosis, gout, and calculi.[16]
  • Avogaro, 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.[17]
  • In 1977, Haller used the term "metabolic syndrome" for associations of obesity, diabetes mellitus, hyperlipoproteinemia, hyperuricemia and steatosis hepatis when describing the additive effects of risk factors on atherosclerosis.[18]
  • The same year, Singer used the term for associations of obesity, gout, diabetes mellitus, and hypertension with hyperlipoprotenemia.[19]
  • 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, hyperlipidemia [hypercholesterolemia and 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.[20][21]
  • 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.[22]

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).

See also

References

  1. ↑ The IDF consensus worldwide definition of the metabolic syndrome. PDF
  2. ↑ Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. 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 2001;285:2486-97. PMID 11368702.
  3. ↑ 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.
  4. ↑ 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&ndash, F631. PMID 16234313.
  5. ↑ Hallfrisch J (1990). "Metabolic effects of dietary fructose". FASEB J. 4 (9): 2652&ndash, 2660. PMID 2189777.
  6. ↑ 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&ndash, 839. PMID 2497634.
  7. ↑ Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H. (2004). "Role of Fatty Acid Composition in the Development of Metabolic Disorders in Sucrose-Induced Obese Rats". Exp Biol Med. 229 (6): 486&ndash, 493. PMID 15169967.
  8. ↑ 8.0 8.1 Katzmaryk,, Peter T (October 2003). "Targeting the Metabolic Syndrome with Exercise: Evidence from the HERITAGE Family Study". Med. Sci. Sports Exerc. 35 (10): 1703–1709. Retrieved 2007-06-24. Unknown parameter |coauthors= ignored (help); Check date values in: |date= (help)
  9. ↑ 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.
  10. ↑ 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.
  11. ↑ 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. PMID 15167200.
  12. ↑ Elwood, PC (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. PMID 17630368. Unknown parameter |coauthors= ignored (help)
  13. ↑ 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.
  14. ↑ Joslin EP. The prevention of diabetes mellitus. JAMA 1921;76:79–84.
  15. ↑ Kylin E. [Studies of the hypertension-hyperglycemia-hyperuricemia syndrome] (German). Zentralbl Inn Med 1923;44: 105-27.
  16. ↑ Vague J. La diffférenciacion sexuelle, facteur déterminant des formes de l'obésité. Presse Med 1947;30:339-40.
  17. ↑ Avogaro P, Crepaldi G, Enzi G, Tiengo A. Associazione di iperlipidemia, diabete mellito e obesità di medio grado. Acta Diabetol Lat 1967;4:572-590.
  18. ↑ Haller H. [Epidemiology and associated risk factors of hyperlipoproteinemia] (German). Z Gesamte Inn Med 1977;32(8):124-8. PMID 883354.
  19. ↑ Singer P. [Diagnosis of primary hyperlipoproteinemias] (German). Z Gesamte Inn Med 1977;32(9):129-33. PMID 906591.
  20. ↑ Phillips GB. Sex hormones, risk factors and cardiovascular disease. Am J Med 1978;65:7-11. PMID 356599.
  21. ↑ Phillips GB. Relationship between serum sex hormones and glucose, insulin, and lipid abnormalities in men with myocardial infarction. Proc Natl Acad Sci U S A 1977;74:1729-1733. PMID 193114.
  22. ↑ Reaven GM. Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 1988;37:1595-607. PMID 3056758.

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