The Metabolic Syndrome
Thirty to forty percent of Austrians are affected by the Metabolic Syndrome and live with a higher health risk. The Metabolic Syndrome is classified by meeting three of the following five range limits:
When the belly width for women is over 88cm, or, for men, over 102cm. Another way to measure is to compare the width of belly to the widths of the hips. For men, this ratio should be smaller than 1.0 and with women smaller than 0.85.
When the Triglycerid levels lie above 150mg/dl in a fasting subject; if the HDL Cholesterol is under 40mg/dl for women and/or under 35mg/dl for men; if the blood pressure is over 135/85mmHg; if the blood sugar level lies over 100mg/dl for a fasting patient or if diabetes is diagnosed as mellitus. An excess in an individual value indicates an increased health risk, but several simultaneous increases in these limit factors can raise the risk for diabetes, cardiac infarct or apoplexy up to twenty-three times the norm ak.a. the " Metabolic Syndrome".
The main cause of the metabolic syndrome lies, apart from the genetic factors, in the lifestyle choices made by the individual. As the quality of life increases for most humans the amount of physical action decreases, while the diet sees a rise of overall fat consumption.
With a permanent increase in the fat and nutrient content of one's food, an individuals' metabolism changes. Cells become less reactive to the hormone insulin, which transports glucose into the cells.
As a result the body produces more insulin, in order to be able to supply the cells sufficiently. Furthermore, many foods lead to the creation of adipose tissue and thus to heavy physical damages. Adipose tissue is a type of fat that can cover the major organs, is absorbed by the liver and taken into the bloodstream. The consequences of fat metabolic disturbances also raise Cholesterol, lower HDL, cause hypertension (hypertonia) and increased blood sugar levels. The Metabolic Syndrome can be treated and/or prevented by a balanced diet (with less and healthier fats) and increased exercise. However, the genetic factors leading to an increased risk of the Metabolic Syndrome cannot be influenced.
The Metabolic Syndrome is regarded today as a crucial factor in the risk of a heart coronary and cardiovascular disease. This factor is also connected with various metabolic disturbances and other standard health imbalances such as obesity.
One of the most common metabolic disturbances that affects humans world-wide is Diabetes (see Wikipedia). Epidemiological studies show that arterioscleroses and cardiac infarcts, which in a healthy human are rare, are the most frequent causes of death in the Western world. Cardiovascular diseases are all based on disturbances in the levels and make up of an individuals' blood fats. (see Lit. 2)
The cause of the Metabolic Syndrome lies in a poor diet and/or hypernutrion caused by frequent consumption of saturated fats (those contained in animal products such as meat, sausage, butter, cheese and other fat containing dairy products as well as hardened vegetable oils) and carbohydrates, which can be taken up rapidly by the body. Such a diet leads, with appropriate genetic predisposition, (genetically caused disposition or susceptibility for certain diseases) to an accumulation of fat in stomach, insulin resistance and/or too high a concentration of insulin.
belly-stressed (viszerales) predominance
Hypertonia ( increased blood pressure or a tension beyond the standard levels, ie high blood pressure)
Hyper- /Dyslipidimia (disturbance of the synthesis of lipoproteins)
Hampered glucose tolerance/diabetes mellitus type 2
possibly Steatosis hepatis (fatty liver)
Hyperuricemia (increase of the uric acid level in the blood)
The danger of the Metabolic Syndrome is that it does not cause long term pain: one does not feel the increased cholesterol and blood sugar levels. However by the time one lands in the hospital with a heart attack many of the blood vessels are damaged beyond repair.
All factors of the Metabolic Syndrome are positively influenced by losing weight. However, not only better nutrition, but also regular exercise are potent means to provide a healthy future.
http://www.akh-consilium.at /daten/ me...syndrom. htm#D1
http://de.wikipedia.org /wiki/ Metabolisches_ Syndrom
http://de.wikipedia.org /wiki/ Diabete...tus# Diagnostik
Lit. 2 Lehrbuch der biologischen Medizin H. Heine Hippokrates
http://www.stern.de/ gesundheit/ ernae...15788.html?p=6
Distribution in the human body:
Copper is present in the human body and food in a bound form and not as an ion. Adult humans have approx. 50-120mg copper in their bodies. In principle only the forms Cu+ and the oxidized form Cu2+ play a role in the human body, and the greater physiological importance is attributed to the oxidized form. The highest concentrations of copper are found in the liver, brain, heart, bone, hair and the nails.
Copper is essential for the creation of most enzymes and proteins. Furthermore, copper plays a physiological role with growth, defense, bone density, brain development, the building of connective tissue, the defense against free radicals and much more. In addition copper affects the metabolism and transport of iron. Important cuprous proteins and enzymes:
Is a trans-membrane protein, which is essential for oxidation and reduction reactions. It is also an important component of the mitochondria.
Is a connection and transportation protein, and is responsible for the distribution of iron and copper. In addition it prevents the build-up of free radicals by hindering the binding of free copper and iron ions.
Is an important part of building connective tissue and bone formation.
Is an enzyme, which reduces free radicals and prevents the oxidation of sensitive molecules.
Metabolism of copper:
The copper absorption mostly takes place in the small intestine. The absorption rate varies between 35% and 70%, since it depends strongly on the composition of the food.
The copper content in the human body is regulated by its absorption or exclusion in the small intestine: With a deficit of copper the copper absorption is increased, and prevented when there is a surplus of copper.
In the case of low concentrations copper is brought by active transportation mechanisms into the cells of the intestine.
An active transportation mechanism is one that transfers a material against a concentration gradient through the consumption of energy. With high concentrations it is transported through passive transportation; ie the copper is transported through the cell membrane to the side with the smaller concentration without consuming any energy.
During periods of continual high copper levels, copper is bound in the mucous membrane cells of the small intestine to the protein metallothionein and preserved to be delivered when necessary.
In the intestine, absorbed copper is bound in the blood, to the plasma proteins albumin and transcuprein and to various amino acids. With the blood it arrives at the liver, where it is stored. There it is built into the enzyme ceruloplasm, which Fe2+ oxidizes into Fe3+. Here one can see the connections between iron and copper:
80% of the extra copper is transported through the gall bladder, approx. 15% is delivered through the small intestine wall into the intestine and from there separated, only 2-4% is removed through urination.
Distribution in the human body:
Adults have about 3-4g iron in the body (45-55mg/kg of body mass). These lie in different oxidation states such as (Fe22+, Fe3+, and rare Fe4+).
60-70% of the iron is in hemoglobin (red blood coloring material). A further 10% is in myoglobin (an enzyme, responsibly for oxygen transport within the cell from the cell membrane to the mitochondria), in cytochromen (an enzyme, that is responsible for the cell's breathing and serves as a catalyst for redox reactions) and other ferrus enzymes. A further 20-30% occurs in hemosiderin (iron storing protein) and ferritin (the most important iron storing protein).
As a component of hemoglobin iron plays an important role in oxygen transport. Furthermore, it is essential for the synthesis of DNA, RNA, proteins and enzymes, which are involved in various cellular processes. As factor for the development of nerve cells iron is essential for the normal function of the brain.
The human organism separates 1-2mg iron per day approx. For this reason, each day the same quantity must be taken up again. Three possibilities exist for the bodies' regularization of its iron levels, i.e. by avoidance of, lack of, or building an iron surplus.
The first mechanism is to re-use the preexisting hemoglobin iron. Iron is set free and bound by the dismantling of red blood corpuscles to the enzyme transferrin. Thus it is available afterwards again for other cells. A further method is storage of iron in the memory protein ferritin. Depending upon the need of the body, iron is bound to the enzyme and/or set free again.
A further method is storage of iron in the memory protein ferritin. Depending upon the need of the body, iron is bound to the enzyme and/or set free again. The third method is the absorption of the iron from food into the intestine. In the upper small intestine are cells, which are responsible for the resorption of iron (called enterocytes). By the enzyme DMT-1 (also DCT-1 and NRAMP2) Fe2+ is transferred into the cells. Fe3+ is reduced before, by reducing agents, to Fe2+. Subsequently, the iron is bound either at ferritin or transported by the enzyme Ferroportin 1 (also called IREG 1) in the blood. The regularization of iron use takes place on the other one hand via the restriction of the absorption rate of the enterocytes.
These take up smaller quantities of iron after a strong iron consumption of several days. On the molecular level the regularization takes place via increased and/or decreased production of the iron transportation proteins DMT-1 or Ferroportin 1.
The iron is stored in the liver, surplus iron is removed with the stool.
Important proteins of the iron metabolism:
In most cells of the body and particularly in the liver, non-functional iron is stored in the form of ferritin. A ferritin molecule can bind 4500 iron atoms. Thus it prevents the free iron, which promotes the emergence of free radicals. During the release of iron from Ferritin the iron is oxidized by the copper binding enzyme ceroloplasmin into Fe3+ . This is the cross connection between the copper and iron metabolisms.
In the case of transport for iron within the body - between intestines,
places of storage and points of usage - iron is bound to the protein transferrin, since
Fe3+ has a limited solubility by the pH values predominating in the blood.
In addition, with the connection, the increased elimination of iron is prevented and the tissue is protected from the oxidative effects of iron.
Thus the iron complex in cells require that the transferrin receptors 1 (TfR1) be present in order to penetrate into them. The transferrin commits itself to the receptor and the iron is delivered into the cell. There it is then available for the cell to use. The transferrin bound at the receptor is channeled lastly into the cell.
Transferrin is normally about 30% satisfied, i.e. the iron storage capacity is working at full capacity only 30% of the time.
Distribution in the human body:
Zinc occurs in the human body in all tissues. 85% of it is in skeletal musculature and bone, 11% in the skin and the liver, and the remainder in the other building materials of the body. The zinc content in the body of an adult human is with approx. 10-15μmol/l.
Zinc has an essential function in the human body and is responsible for the activity of more than 200 different enzymes. One can find enzymes, which are dependent on zinc, in almost all groups of enzymes. Zinc is also important for maintaining the protein and cell membrane structures, for the promotion of growth, for protein synthesis and the stimulation of the immune system.
It is currently unclear, how the absorption of zinc functions exactly. Zinc is taken up over the food. Problematic is however the so-called bio-availability. How well zinc is taken up can vary depending on which source it comes from. Zinc, which originates from plants, is less well accepted into the human body than zinc from animal products.
blood laboratory/blood values
We started by going in teams of two to the Oberndorf Hospital, and with the help of their MTAs (Medical Technical Assistants) more closely examined our 325 blood samples. Karin, Carmen, and Elizabeth graciously accepted us into their team and showed us the daily workings of a hospital laboratory. The laboratory in Obendorf is small but very modern. The devices there can break blood down into its component parts and measure blood lipids, sugars, insulin, urea, pH value, oxygen saturation, trace minerals and elements, and many other blood components. We will now discuss what constitutes a deviation from normal, in regards to the parameters we were using, before continuing a discussion of the illness. A day in the life of a MTA starts with the adjustment and calibration of the lab equipment. This is very important in order to be able to accurately perform tests, and get back meaningful results.
We were allowed to help differentiate leukocytes under the microscope. And we worked on investigations into immunology, diabetes, blood sedimentation and an investigation of blood serum with an examination of blood clotting and blood cell count.