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Dysmetabolic syndrome X
A man with marked central obesity, a hallmark of metabolic syndrome. His weight is 182 kg (400 lbs), height 185 cm (6 ft 1 in), and body mass index (BMI) 53 (normal 18.5 to 25).
Metabolic syndrome is associated with the risk of developing cardiovascular disease and type 2 diabetes. In the U.S., about 25% of the adult population has metabolic syndrome, a proportion increasing with age, particularly among racial and ethnic minorities.
Insulin resistance, metabolic syndrome, and prediabetes are closely related to one another and have overlapping aspects. The syndrome is thought to be caused by an underlying disorder of energy utilization and storage. The cause of the syndrome is an area of ongoing medical research.
The mechanisms of the complex pathways of metabolic syndrome are under investigation. The pathophysiology is very complex and has been only partially elucidated. Most people affected by the condition are older, obese, sedentary, and have a degree of insulin resistance. Stress can also be a contributing factor. The most important risk factors are diet (particularly sugar-sweetened beverage consumption), genetics, aging, sedentary behavior or low physical activity, disrupted chronobiology/sleep, mood disorders/psychotropic medication use, and excessive alcohol use. The pathogenic role played in the syndrome by the excessive expansion of adipose tissue occurring under sustained overeating, and its resulting lipotoxicity was reviewed by Vidal-Puig.
Research shows that Western diet habits are a factor in development of metabolic syndrome, with high consumption of food that is not biochemically suited to humans.[page needed] Weight gain is associated with metabolic syndrome. Rather than total adiposity, the core clinical component of the syndrome is visceral and/or ectopic fat (i.e., fat in organs not designed for fat storage) whereas the principal metabolic abnormality is insulin resistance. The continuous provision of energy via dietary carbohydrate, lipid, and protein fuels, unmatched by physical activity/energy demand, creates a backlog of the products of mitochondrial oxidation, a process associated with progressive mitochondrial dysfunction and insulin resistance.
Central obesity is a key feature of the syndrome, being both a sign and a cause, in that the increasing adiposity often reflected in high waistcircumference may both result from and contribute to insulin resistance. However, despite the importance of obesity, affected people who are of normal weight may also be insulin-resistant and have the syndrome.
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 computers for less than one hour daily, those who carried out these behaviors for greater than four hours daily have a two fold increased risk of metabolic syndrome.
Metabolic syndrome affects 60% 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.
Diabetes mellitus type 2
The metabolic syndrome quintuples the risk of type 2 diabetes mellitus. Type 2 diabetes is considered a complication of metabolic syndrome. In people with impaired glucose tolerance or impaired fasting glucose, presence of metabolic syndrome doubles the risk of developing type 2 diabetes. It is likely that prediabetes and metabolic syndrome denote the same disorder, defining it by the different sets of biological markers.
The presence of metabolic syndrome is associated with a higher prevalence of CVD than found in people with type 2 diabetes or impaired glucose tolerance without the syndrome.Hypoadiponectinemia has been shown to increase insulin resistance and is considered to be a risk factor for developing metabolic syndrome.
Coronary heart disease
The approximate prevalence of the metabolic syndrome in people with coronary artery disease (CAD) is 50%, with a prevalence of 37% in people 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.
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 TNF-? and alter levels of other substances (e.g., adiponectin, resistin, and PAI-1). TNF-? has been shown to cause the production of inflammatory cytokines and also possibly trigger cell signaling by interaction with a TNF-? receptor that may lead to insulin resistance. An experiment with rats fed a diet with 33% 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. The progression from visceral fat to increased TNF-? to insulin resistance has some parallels to human development of metabolic syndrome. The increase in adipose tissue also increases the number of immune cells, which play a role in inflammation. Chronic inflammation contributes to an increased risk of hypertension, atherosclerosis and diabetes.
A joint interim statement of the International Diabetes Federation Task Force on Epidemiology and Prevention; National Heart, Lung, and Blood Institute; American Heart Association; World Heart Federation; International Atherosclerosis Society; and International Association for the Study of Obesity published a guideline to harmonize the definition of the metabolic syndrome. This definition recognizes that the risk associated with a particular waist measurement will differ in different populations. Whether it is better at this time to set the level at which risk starts to increase or at which there is already substantially increased risk will be up to local decision-making groups. However, for international comparisons and to facilitate the etiology, it is critical that a commonly agreed-upon set of criteria be used worldwide, with agreed-upon cut points for different ethnic groups and sexes. There are many people in the world of mixed ethnicity, and in those cases, pragmatic decisions will have to be made. Therefore, an international criterion of overweight may be more appropriate than ethnic specific criteria of abdominal obesity for an anthropometric component of this syndrome which results from an excess lipid storage in adipose tissue, skeletal muscle and liver.
The previous definitions of the metabolic syndrome by the International Diabetes Federation (IDF) and the revised National Cholesterol Education Program (NCEP) are very similar, and they identify individuals with a given set of symptoms as having metabolic syndrome. There are two differences, however: the IDF definition states that if body mass index (BMI) is greater than 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 is less than 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.
The International Diabetes Federation consensus worldwide definition of metabolic syndrome (2006) is:
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 (BP): 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 is >5.6 mmol/L or 100 mg/dL, an oral 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 (1999) requires the presence of any 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 HDL cholesterol
Central obesity: waist:hip ratio > 0.90 (male); > 0.85 (female), or BMI > 30 kg/m2
Microalbuminuria: urinary albumin excretion ratio >= 20 µg/min or albumin:creatinine ratio >= 30 mg/g
Blood pressure >= 130/85 mmHg (or treated for hypertension)
Fasting plasma glucose >= 5.6 mmol/L (100 mg/dL), or use of medication for hyperglycemia
High-sensitivity C-reactive protein 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 nonalcoholic fatty liver disease (steatohepatitis) in correlation with serum markers that indicated lipid and glucose metabolism. Fatty liver disease and steatohepatitis can be considered manifestations of metabolic syndrome, indicative of abnormal energy storage as fat in ectopic distribution.
Reproductive disorders (such as polycystic ovary syndrome in women of reproductive age), and erectile dysfunction or decreased total testosterone (low testosterone-binding globulin) in men can be attributed to metabolic syndrome.
Various strategies have been proposed to prevent the development of metabolic syndrome. These include increased physical activity (such as walking 30 minutes every day), and a healthy, reduced calorie diet. Many studies support the value of a healthy lifestyle as above. However, one study stated these potentially beneficial measures are effective in only a minority of people, primarily because of a lack of compliance with lifestyle and diet changes. The International Obesity Taskforce states that interventions on a sociopolitical level are required to reduce development of the metabolic syndrome in populations.
The Caerphilly Heart Disease Study followed 2,375 male subjects over 20 years and suggested the daily intake of a pint (~568 mL) of milk or equivalent dairy products more than halved the risk of metabolic syndrome. Some subsequent studies support the authors' findings, while others dispute them. A systematic review of four randomized controlled trials said that, in the short term, a paleolithic nutritional pattern improved three of five measurable components of the metabolic syndrome in participants with at least one of the components.
Generally, the individual disorders that compose the metabolic syndrome are treated separately.Diuretics and ACE inhibitors may be used to treat hypertension. Various cholesterol medications may be useful if LDL cholesterol, triglycerides, and/or HDL cholesterol is abnormal.
Dietary carbohydrate restriction reduces blood glucose levels, contributes to weight loss, and reduces the use of several medications that may be prescribed for metabolic syndrome.
Approximately 20-25 percent of the world's adult population has the cluster of risk factors that is metabolic syndrome. In 2000, approximately 32% of U.S. adults had metabolic syndrome. In more recent years that figure has climbed to 34%.
In young children, there is no consensus on how to measure metabolic syndrome since age-specific cut points and reference values that would indicate "high risk" have not been well established. A continuous cardiometabolic risk summary score is often used for children instead of a dichotomous measure of metabolic syndrome.
In the late 1950s, the term metabolic syndrome was first used
In 1967, Avogadro, Crepaldi and coworkers described six moderately obese people with diabetes, hypercholesterolemia, and marked hypertriglyceridemia, all of which improved when the affected people were put on a hypocaloric, low-carbohydrate diet.
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.
^ abKatzmarzyk PT, Leon AS, Wilmore JH, Skinner JS, Rao DC, Rankinen T, Bouchard C (October 2003). "Targeting the metabolic syndrome with exercise: evidence from the HERITAGE Family Study". Medicine and Science in Sports and Exercise. 35 (10): 1703-09. doi:10.1249/01.MSS.0000089337.73244.9B. PMID14523308.
^Xi B, He D, Zhang M, Xue J, Zhou D (August 2014). "Short sleep duration predicts risk of metabolic syndrome: a systematic review and meta-analysis". Sleep Medicine Reviews. 18 (4): 293-97. doi:10.1016/j.smrv.2013.06.001. PMID23890470.
^Vancampfort D, Vansteelandt K, Correll CU, Mitchell AJ, De Herdt A, Sienaert P, Probst M, De Hert M (March 2013). "Metabolic syndrome and metabolic abnormalities in bipolar disorder: a meta-analysis of prevalence rates and moderators". The American Journal of Psychiatry. 170 (3): 265-74. doi:10.1176/appi.ajp.2012.12050620. PMID23361837.
^Sun K, Ren M, Liu D, Wang C, Yang C, Yan L (August 2014). "Alcohol consumption and risk of metabolic syndrome: a meta-analysis of prospective studies". Clinical Nutrition. 33 (4): 596-602. doi:10.1016/j.clnu.2013.10.003. PMID24315622.
^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 (March 2006). "A causal role for uric acid in fructose-induced metabolic syndrome". American Journal of Physiology. Renal Physiology. 290 (3): F625-31. doi:10.1152/ajprenal.00140.2005. PMID16234313.
^ abGatta-Cherifi, Blandine; Cota, Daniela (2015). "Endocannabinoids and Metabolic Disorders". Endocannabinoids. Handbook of Experimental Pharmacology. 231. pp. 367-91. doi:10.1007/978-3-319-20825-1_13. ISBN978-3-319-20824-4. PMID26408168. The endocannabinoid system (ECS) is known to exert regulatory control on essentially every aspect related to the search for, and the intake, metabolism and storage of calories, and consequently it represents a potential pharmacotherapeutic target for obesity, diabetes and eating disorders. ... recent research in animals and humans has provided new knowledge on the mechanisms of actions of the ECS in the regulation of eating behavior, energy balance, and metabolism. In this review, we discuss these recent advances and how they may allow targeting the ECS in a more specific and selective manner for the future development of therapies against obesity, metabolic syndrome, and eating disorders.
^ abcVemuri VK, Janero DR, Makriyannis A (March 2008). "Pharmacotherapeutic targeting of the endocannabinoid signaling system: drugs for obesity and the metabolic syndrome". Physiology & Behavior. 93 (4-5): 671-86. doi:10.1016/j.physbeh.2007.11.012. PMC3681125. PMID18155257. The etiology of many appetitive disorders is characterized by a pathogenic component of reward-supported craving, be it for substances of abuse (including alcohol and nicotine) or food. Such maladies affect large numbers of people as prevalent socioeconomic and healthcare burdens. Yet in most instances drugs for their safe and effective pharmacotherapeutic management are lacking despite the attendant medical needs, collateral adverse physical and psychological effects, and enormous global market potential. The endocannabinoid signaling system plays a critical role in motivational homeostasis as a conduit for reward stimuli and a positive modulator of brain reward circuits. Endocannabinoid-system hyperactivity through CB1 receptor transmission is considered contributory to a range of appetitive disorders and, hence, is a major focus of contemporary pharmaceutical research.
^ abcdTurcotte C, Chouinard F, Lefebvre JS, Flamand N (June 2015). "Regulation of inflammation by cannabinoids, the endocannabinoids 2-arachidonoyl-glycerol and arachidonoyl-ethanolamide, and their metabolites". Journal of Leukocyte Biology. 97 (6): 1049-70. doi:10.1189/jlb.3RU0115-021R. PMID25877930. S2CID206999921.
^Fukuchi S, Hamaguchi K, Seike M, Himeno K, Sakata T, Yoshimatsu H (June 2004). "Role of fatty acid composition in the development of metabolic disorders in sucrose-induced obese rats". Experimental Biology and Medicine. 229 (6): 486-93. doi:10.1177/153537020422900606. PMID15169967. S2CID20966659.
^Expert Panel On Detection, Evaluation (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. 285 (19): 2486-97. doi:10.1001/jama.285.19.2486. PMID11368702.
^Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F (October 2005). "Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement". Circulation. 112 (17): 2735-52. doi:10.1161/CIRCULATIONAHA.105.169404. PMID16157765. S2CID7571079.
^Kogiso T, Moriyoshi Y, Shimizu S, Nagahara H, Shiratori K (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". Journal of Gastroenterology. 44 (4): 313-21. doi:10.1007/s00535-009-0002-5. PMID19271113. S2CID1193178.
^Brand JS, van der Tweel I, Grobbee DE, Emmelot-Vonk MH, van der Schouw YT (February 2011). "Testosterone, sex hormone-binding globulin and the metabolic syndrome: a systematic review and meta-analysis of observational studies". International Journal of Epidemiology. 40 (1): 189-207. doi:10.1093/ije/dyq158. PMID20870782.
^Lakka TA, Laaksonen DE (February 2007). "Physical activity in prevention and treatment of the metabolic syndrome". Applied Physiology, Nutrition, and Metabolism. 32 (1): 76-88. doi:10.1139/h06-113. PMID17332786.
^Feldeisen SE, Tucker KL (February 2007). "Nutritional strategies in the prevention and treatment of metabolic syndrome". Applied Physiology, Nutrition, and Metabolism. 32 (1): 46-60. doi:10.1139/h06-101. PMID17332784.
^Snijder MB, van der Heijden AA, van Dam RM, Stehouwer CD, Hiddink GJ, Nijpels G, Heine RJ, Bouter LM, Dekker JM (April 2007). "Is higher dairy consumption associated with lower body weight and fewer metabolic disturbances? The Hoorn Study". The American Journal of Clinical Nutrition. 85 (4): 989-95. doi:10.1093/ajcn/85.4.989. PMID17413097.
^Kylin E. [Studies of the hypertension-hyperglycemia-hyperuricemia syndrome] (German). Zentralbl Inn Med 1923; 44: 105-27.
^Vague J. La diffférenciacion sexuelle, facteur déterminant des formes de l'obésité. Presse Med 1947;30:339-40.
^Avogaro, Piero; Crepaldi, Gaetano; Enzi, Giuliano; Tiengo, Antonio (1967). "Associazione di iperlipemia, diabete mellito e obesita' di medio grado" [Association of hyperlipemia, diabetes mellitus and middle-degree obesity]. Acta Diabetologica Latina (in Italian). 4 (4): 572-90. doi:10.1007/BF01544100. S2CID25839940.
^Haller H (April 1977). "[Epidermiology and associated risk factors of hyperlipoproteinemia]". Zeitschrift für Sie Gesamte Innere Medizin und Ihre Grenzgebiete. 32 (8): 124-28. PMID883354.
^Singer P (May 1977). "[Diagnosis of primary hyperlipoproteinemias]". Zeitschrift für die Gesamte Innere Medizin und Ihre Grenzgebiete. 32 (9): 129-33. PMID906591.