Metabolic syndrome

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The metabolic syndrome is sometimes also called deadly quartet , Reaven's syndrome or Syndrome X refers. It is considered (along with smoking ) to be the decisive risk factor for diseases of the arterial vessels , especially coronary artery disease , and is characterized by the following four factors:

The definition of metabolic syndrome has changed repeatedly in recent years. There is currently no generally accepted definition. The classification is based either on insulin resistance (insulin resistance syndrome, WHO classification 1999) or on clinical parameters ( NCEP-ATP-III ). There is no globally valid ICD-10 code for documenting the disease, but in Germany the DIMDI thesaurus allows coding with the code E88.9 “metabolic disorder, unspecified”. Since there is no specific code for the metabolic syndrome within the ICD-10 classification, the four manifestations must also be encoded in accordance with the German Coding Directive (DKR) D004d. In order to correctly document the syndrome, the codes for obesity (E66.0-), high blood pressure (I10.-), hypertriglyceridemia (E78.1 or E78.2) and impaired glucose tolerance (R73.0) must also be given. This is quite understandable, since the metabolic syndrome is not seen as an independent entity, but also as a “cluster of cardiovascular risk factors” (quoted from the guideline of the German Obesity Society from 2007) .

Treatment is primarily aimed at reducing excess weight . Regardless of this, drug treatment for high blood pressure, sugar and lipid metabolism disorders is necessary.

Pathophysiology

Metabolic syndrome develops due to hypercaloric diet and a lack of physical activity. The resulting obesity leads to insulin resistance . Insulin is mainly responsible for controlling blood sugar levels and ensures that both muscles and adipose tissue can absorb glucose via GLUT -4 transporters. The pancreas can temporarily compensate for excess glucose in the blood by increasing insulin production (hyperinsulinemia) with the aim of maintaining a euglycemic metabolic state. Over time, however, the high insulin levels lead to a loss of effectiveness of the hormone and insulin resistance develops, which can progress to type 2 diabetes . This happens when the pancreas is no longer able to produce enough insulin for the body.

Visceral adipose tissue has a major influence on the development of the metabolic syndrome . It is a tissue rich in adipocytes (fat cells) that is located between the organs of the abdominal cavity (intra-abdominal). These adipocytes are hormonally active and are subject to increased lipolysis , which no longer responds to the inhibiting effect of insulin. Substances that are secreted include TNF-α and interleukin-6 ( inflammation mediators that, among other things, promote insulin resistance). At the same time, the concentration of adiponectin (below 7 to 10 µg / l), a hormone produced by adipocytes, which has an insulin-sensitizing, antiatherogenic (against atherosclerosis ) and anti-inflammatory ( anti-inflammatory ) effect. The increased release of non-esterified fatty acids (= free fatty acids ) by these adipocytes inhibits the effect of insulin on the liver and on the muscles. This promotes glycogenolysis and gluconeogenesis in the liver, and increases the release of glucose from the liver.

At the same time, atherogenic dyslipidemia , a special change in blood lipid levels (low HDL levels and high concentrations of triglycerides and small, dense LDL particles) can often be observed. The VLDL production increases in the liver due to the influence of the free fatty acids. These lipoproteins are characterized by a high concentration of triglycerides, which thus reach the periphery. VLDL particles are metabolized to IDL and LDL within the lipid metabolism with the splitting off of fatty acids by the lipoprotein lipase. These lipoproteins interact with HDL particles and exchange triglycerides for cholesterol esters via the cholesterol ester transfer protein (CETP). This reduces the cholesterol level in the HDL molecules and their concentration drops. The LDL particle composition also changes due to a decrease in the cholesterol content within the lipoproteins. The resulting small, dense LDL molecules are more atherogenic than normal-sized LDL particles. The negative metabolic consequences of the visceral fat tissue can be counteracted by sufficient stress on the muscles using so-called myokines .

According to a theory by Canadian gastroenterologist Ian Spreadbury , the syndrome develops from malnutrition with cell-free flour, sugar, and other refined industrial foods that could promote an inflammatory microbiome in the gut . This mainly affects people who live in industrialized countries. The theory would explain some of the beneficial health effects of the Stone Age diet.

Diagnosis

WHO criteria

According to the 1998 WHO criteria, a metabolic syndrome is present if one

and two of the following parameters:

  • increased arterial blood pressure (≥ 140/90 mmHg),
  • Fat metabolism disorder: triglycerides : ≥ 1.7 mmol / l (150 mg / dl) and / or HDL cholesterol ≤ 0.9 mmol / l (35 mg / dl) (men), ≤ 1.0 mmol / l (39 mg / dl) (women),
  • Trunk weighted obesity: waist-hip ratio > 1.00 (men) or> 0.85 (women), or BMI > 30 kg / m²,
  • Microalbuminuria : urinary albumin excretion ≥ 20 µg / min or albumin-creatinine ratio ≥ 30 mg / g.

IDF criteria (2005)

The definition of the “International Diabetes Foundation” (IDF) is widely used and internationally recognized.

The prerequisite for the presence of the metabolic syndrome is the presence of a pronounced (so-called central) obesity : in men a waist circumference ≥ 94 cm, in women ≥ 80 cm (people of European origin, other values ​​apply to Asians).

In addition to this key factor, there are at least two of the risk factors

  • Fasting blood sugar values ​​of> 100 mg / dl (> 5.6 mmol / l) measured in the blood plasma or diagnosed diabetes mellitus ,
  • increased triglycerides> 150 mg / dl (> 1.7 mmol / l) or therapy that has already been initiated to lower triglycerides,
  • Low HDL cholesterol: <40 mg / dl (<1.05 mmol / l) in men and <50 mg / dl (<1.25 mmol / l) in women or therapy that has already been initiated to increase HDL
  • High blood pressure (from> 130 mmHg systolic and> 85 mmHg diastolic) or already treated hypertension

in addition, there is a significantly higher risk of suffering cardiovascular disease in the course of life . In this case, the so-called “metabolic syndrome” is present. For this reason, the risk factors obesity, diabetes, lipid metabolism disorders and high blood pressure are also called cardiometabolic risk factors in specialist circles.

Criteria according to NCEP-ATP-III (2002)

According to the "National Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults" (NCEP-ATP-III), the diagnosis of metabolic syndrome is made if at least three of the following five criteria are met:

  • Abdominal fat distribution, determined by a waist circumference of over 102 cm in men or over 88 cm in women,
  • Serum triglycerides of over 150 mg / dl (> 1.7 mmol / l), or therapy that has already been initiated to lower triglycerides
  • HDL cholesterol ≤ 40 mg / dl (<1.05 mmol / l) in men or <50 mg / dl (1.25 mmol / l) in women,
  • Blood pressure of 130/85 mmHg or more, or therapy already initiated to lower hypertension
  • Fasting blood sugar ≥ 110 mg / dl (5.6 mmol / l), or the presence of type 2 diabetes.

Furthermore, the NCEP-ATP-III names a prothrombotic and proinflammatory status as symptoms, but not as diagnostic criteria for the metabolic syndrome.

Waist circumference as a criterion

As already indicated above, an increased waist circumference plays a major role in the definition of the metabolic syndrome. Because for the cardiovascular risk it is less the extent of obesity than the fat distribution pattern that is decisive: fat deposits in the abdominal cavity and on the internal organs have a particularly disadvantageous effect. This inner belly fat - experts call it "intra-abdominal fat" or " visceral fat tissue " - is very metabolically active. It influences the fat and carbohydrate metabolism (sugar metabolism), so that fat metabolism disorders and diabetes can result.

Measuring the circumference of the abdomen at the waist is considered to be a quick and easy way to make an initial risk assessment. According to ATP III, there is an increased risk for women with a waist circumference of more than 88 cm. For men, the risk area starts at 102 cm. In Germany, around 30–40% exceed this risk threshold. By reducing the waist circumference, e.g. B. through exercise, the risk of cardiovascular disease can be significantly reduced.

Significance of the symptoms

Insulin resistance , obesity , high blood pressure and lipid metabolism disorders also occur independently of one another and each represent increased risks for the later occurrence of coronary artery disease and arteriosclerosis .

therapy

Lifestyle changes should be made after diagnosis. The aim is to reduce body weight or waist circumference, lower blood lipids and prevent or postpone the possible occurrence of type 2 diabetes mellitus. Regular physical activity is particularly recommended for this purpose (e.g. 30 minutes a day, at least three times a week, but at least daily noticeable increase in activity).

There are various recommendations for normalizing body weight through diet: the DGE recommends slowly digestible carbohydrates as the largest nutritional component and a reduction in fat (carbohydrates 50 to 60% of total nutrition / fat: 20 to 25% / protein = the rest approx. 15 to 20% ). However, there are also studies that see greater effectiveness in improving the symptoms of metabolic syndrome with a reduction in the amount of carbohydrates in the diet.

If type 2 diabetes mellitus is present, it should be treated with medication if the nutritional and exercise therapy is inadequate. The same applies to the setting of high blood pressure. The best way to correct hypertriglyceridemia is through lifestyle measures. Unsaturated fatty acids have a particularly positive influence. Omega-3 fatty acids are considered to be particularly effective ; they can be consumed in the form of a diet rich in sea fish , in the form of vegetable oils such as linseed oil , as medication or food additives. Alcohol increases triglycerides and blood pressure and should also be avoided to reduce body weight. Low HDL cholesterol is a risk factor for cardiovascular disease and diabetes. However, there is currently no evidence of the benefit of increasing the HDL cholesterol level with drugs. Only patients with a combination of low HDL cholesterol and high triglycerides benefit from fenofibrate.

Raising vitamin D levels may help. A meta-analysis of 100,000 patients showed that the metabolic syndrome was only half as common in subjects with high vitamin D levels as in subjects with little vitamin D in the blood.

See also

literature

  • H. Toplak: The Metabolic Syndrome - Beginning of the “Deadly Quartet”? In: Journal of Cardiology. 2005; 12 (Supplementum C), pp. 6-7.
  • F. Hoppichler: The metabolic syndrome: epidemiology and diagnosis. In: Acta Medica Austriaca. 2004; 31/4, pp. 130-132.
  • M. Hanefeld: The metabolic syndrome: definitions, common soil for diabetes and cardiovascular diseases, consequences for therapy. In: ObesitySpectrum. 03/2006, pp. 7-10.
  • R. Eckel: The Metabolic Syndrome. edit OE Janssen u. OH Jannsen, Chapter 236 In: Harrison's Internal Medicine. 17th edition. 2009.
  • D. Effertz: The metabolic syndrome: Physical activity as a drug, principles and recommendations for patients and relatives (Radikal Gesund, Volume 1). 1st edition. 2018.

Web links

Individual evidence

  1. ^ Roche Lexicon Medicine . 5th edition. Elsevier, Urban & Fischer Verlag, Munich 2003, ISBN 3-437-15072-3 (keyword: Syndrom X ).
  2. ↑ Frank Hermann, Peter Müller, Tobias Lohmann: endocrinology practice: diagnosis and treatment of A-Z . 6th edition. Thieme Verlag, Leipzig 2010, ISBN 978-3-13-131016-3 , p. 37 .
  3. ↑ Guideline of the German Obesity Society from 2007, p. 8, pdf , last viewed on May 4, 2019
  4. ↑ Eckel, Grundy, Zimmet: The metabolic syndrome. In: Lancet. (2005); 365 (9468), pp. 1415-1428.
  5. ^ Inflammation during Obesity - Pathophysiological Concepts and Effects of Physical Activity. Retrieved January 26, 2019 .
  6. ↑ I. Spreadbury: Comparison with ancestral diets Suggests dense acellular carbohydrates promote to inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. In: Diabetes, metabolic syndrome and obesity: targets and therapy. Volume 5, 2012, pp. 175-189, doi: 10.2147 / DMSO.S33473 , PMID 22826636 , PMC 3402009 (free full text).
  7. ^ KG Alberti, PZ Zimmet: Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification of diabetes mellitus provisional report of a WHO consultation. In: Diabetic medicine: a journal of the British Diabetic Association. Volume 15, Number 7, July 1998, pp. 539-553, ISSN  0742-3071 . doi : 10.1002 / (SICI) 1096-9136 (199807) 15: 7 <539 :: AID-DIA668> 3.0.CO; 2-S . PMID 9686693 . Full text ( Memento of August 21, 2014 in the Internet Archive ) (PDF) p. 32 f.
  8. ^ Institute for Preventive Medicine at the University of Erlangen-Nürnberg: Definition (PDF; 30 kB) of the International Diabetes Federation
  9. ↑ National Cholesterol Education Program (NCEP): Third Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (ATP III Final Report), NIH Publication No. 02-5215, September 2002 ( Memento of the original dated May 24, 2005 in the Internet Archive ) Info: The archive link was inserted automatically and has not yet been checked. Please check the original and archive link according to the instructions and then remove this notice. @1@ 2Template: Webachiv / IABot / www.nhlbi.nih.gov
  10. ↑ JS Volek, RD Feinman: Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction . In: Nutr Metab (Lond) . tape 2 , no. 1 , 2005, p. 31 , doi : 10.1186 / 1743-7075-2-31 , PMID 16288655 , PMC 1323303 (free full text) - (English).
  11. ↑ Eric C Westman, Richard D Feinman, et al. a .: Low-carbohydrate nutrition and metabolism. In: Am J Clin Nutr August 2007 vol. 86 no. 2. ajcn.org, August 1, 2007, pp. 276–284 , accessed on June 20, 2012 (English).
  12. ↑ Maturitas 65, 2010, 225, cited by doctors newspaper. February 24, 2010, p. 4.