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Laboratory diagnostics

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for doctors and patients

Laboratory diagnostics,
a prerequisite for a meaningful use of orthomolecular therapy

1. Free radicals and oxidative stress

For higher organisms, it is vital to gain energy by the inhalation and exhalation of oxygen. The radical oxygens formed during this metabolic reaction in small amounts, however, are toxic and therefore responsible for the so-called oxidative stress on the body's own cells. Therefore, an effective and complicated mechanism had to be created in the course of evolution, which prevents the destruction of the cell by radical oxygen species. In addition, the human body has also learned the radical compounds that arise regularly in the cells to use for himself by using it to fight off viruses and bacteria, but also to the destruction of our own over-aged and defective cells. This is known as the cellular immune response.

Only since the 70s was directed scientific publications of view of operations by increasing the number, the reactive oxygen species (ROS) cause in the body. Through increased especially in the US research effort, which also served to uncover these complex protective mechanisms against these destructive compounds, it is now possible to incorporate new knowledge about the oxidative stress in medical diagnostics and therapy.
 

The complex system of formation of oxidative stress should here be explained in order to better assess what investigations are necessary to the level of oxidative stress, the function of the protective mechanisms and the antioxidant capacity of our body that we mobilize against oxidative stress can to be able to measure.

1.1 The development of oxidative stress

Thus, the cells of the human body form by collecting the oxygen necessary for the life energy by staying in this specialized parts of the cell (the mitochondria) to convert oxygen to water (reduction of oxygen). It also comes always to the formation of only partially reduced and thus highly reactive oxygen species, the superoxide radicals (O-2.). With the aid of an enzyme of superoxide dismutase (SOD) is favored to convert this radical compound in the hydrogen peroxide (H2O2), which can then further react with other reactive oxygen species (Fig. 1). These go in the presence of environmental pollutants, with which the human body so constantly in contact, more radical compounds (R.) a.

An accumulation of such radical compounds is responsible for the oxidative stress.

 

Heavy metals are among the most important cellular stress factors not only generate oxidative stress but also inhibit important for the survival of the cell antioxidant defense mechanisms, or even consume.
 

Tab. 1 sources of these so-called reactive O2 species (ROS):

  • Carcinogenic substances
  • smoking
  • Heavy metals (mercury, cadmium, palladium, zinc, lead, etc.)
  • ozone
  • UV light
  • alcohol
  • medication
  • chronic inflammation
  • chronic stress
  • Increased oxygen-sales

The radical formation and thus oxidative stress (eg, cigarette smoke) significantly increased mainly due to the increasing exposure to environmental pollutants, changes in dietary conditions (eg ready meals) and Related consumption.

A wide variety of disorders are now associated with the oxidative stress.

Among them

Atherosclerosis and coronary heart disease, autoimmune diseases and neurodegenerative diseases (Parkinson's, Alzheimer's), damage to the genetic material, tumor formation or general aging processes.

 

Fig.1 development of oxidative stress

 

1.2. Mechanisms of destruction by ROS

Many of these reactive oxygen species can unfortunately large molecules in the human body, such as fats, proteins or nucleic acids - the latter of human genetic information (DNA) is formed - and change other vital substances in the human body adversely. These processes can be thought of as a chain reaction in which more and more radical reactive compounds are formed and react further.

Using the example of polyunsaturated fatty acids, which are among the main components of Zellmem-branes, the destructive effects of free radicals will be described. This as "lipid peroxidation" designated reaction leads to an altered permeability of cell membranes, who are responsible for the exchange of nutrients in and out of the cell and ultimately the collapse of nutrient exchange to the destruction of the cell.

Atherosclerosis, rheumatoid diseases, diabetes, various liver diseases, cancer but also the aging be attributed to this oxidative destruction of the cell membrane.

In the course of peroxidation formed by the destruction of the fatty acid chains malondialdehyde, which is considered as a specific indicator of increased fatty acid degradation by the influence of oxygen radicals.
 

 

Fig.2 mechanism of lipid peroxidation and the generation of detectable breakdown products

 

The radical degradation products of lipid destruction could cause like all other oxygen radicals to damage to the genetic information or amino acids that act as building blocks for proteins change.

In the case of damage to the genetic information in the human organism has indeed developed repair mechanisms, but can counteract only to a certain degree these destructive attacks. Especially with increasing age, the efficiency of the repair options decreases more and more.

The results are:

· Disturbances in the propagation of genetic information through breaks in the chain by mutations, ie, by changes in the composition of the information

· The development of cancers.

As a measure of oxidative stress and the efficiency of the repair system, a substance is used today, resulting in increased oxidative attack on the genetic information and can be detected in urine, 8-hydroxy-deoxyguanosine (8-OHdG). This oxidative modification can also be directly in front of a cellular excretion in the lymphocytes of the peripheral blood measured as 8-oxo-guanine.
 

1.3. Mechanisms of defense against reactive oxygen compounds

Since the human body is constantly exposed to different highly reactive oxygen species, there is a complex defense system in which a lot of so-called. Antioxidants are involved (Figure 3).

In this context, the already previously mentioned enzyme superoxide dismutase plays an important role because it can convert oxygen radicals in the safer hydrogen peroxide, which is then degraded by two enzymes, glutathione peroxidase and catalase into oxygen and water.

The activity of glutathione peroxidase is dependent on the provision of sufficiently high glutathione.

To successfully move the reaction toward glutathione peroxidase are other antioxidants or free radical scavengers necessary that some must be obtained from food. Among them is the vitamin E, which in many cases the degradation of unsaturated fatty acids in the membranes can be prevented by radical oxygen species. By the reaction of the membranes with peroxidized fatty acids, vitamin E is itself a free radical. However, this can be regenerated by vitamin C, b-carotene, ubiquinone or other antioxidants again.

 

Fig.3 defense mechanisms of oxidative stress

 

1.4. Laboratory diagnostic tests for the detection of oxidative stress

Today the laboratory diagnosis is able to determine the extent to which oxidative stress effect on the human organism and the damages have already occurred.

a. Oxidative Destruction:

The combined measurement of various biomarkers accurate information on the level of oxidative stress in the patient can be given. It may thus the risk of oxidative destruction and prevention strategies that can prevent further injury, are presented. So is circumscribed by measuring the degradation products of lipid peroxidation of cellular membranes and the destruction of cardiovascular lipoproteins, while the measurement of 8-Hydrodeoxyguanosin the oxidative destruction within the cells capability, meaning that genetic information displayed.

Malondialdehyde 5 ml EDTA - blood standard value 0.36 - 1,42μmol / l

4-Hydroxynonenal 5 ml EDTA - blood standard value is less than 50 nmol / l

             Both are major degradation products in the oxidation of polyunsaturated fatty acids, which are found mainly in LDL. High concentrations can be increased lipid peroxidation and oxidative stress accept and correlate with an increased risk of diabetes, heart disease and other age-related diseases. There may also be a associated with a reduced antioxidant levels.

8-hydroxy-deoxyguanosine (8-OHdG) 10 ml morning urine

8-oxo-guanine 10 ml sodium heparin whole blood

             This parameter is best shown by the degree of oxidative degradation within the cell, ie in the genetic information to allow possible mutations and thus the risk of developing cancer are presented. 8-OHdG is modified by oxidative stress guanosine, a building block of DNA, which was recognized by the repair mechanism, cut and is excreted in the urine. In general, the repair mechanism works very well, but at permanently increased oxidative stress serious prejudice to the genetic information is not excluded.
           

 

           

b. antioxidant capacity

Total antioxidant status (TAS) 5 ml serum normal range 1.3 to 1.7 mmol / l

The total amount and activity of antioxidants in serum is composed of approximately 57% albumin and uric acid, 9% vitamin C and approximately 34% of vitamin E, bilirubin, ß-carotene and other antioxidants unidentified, but also flavonoids together.

The TAS is dependent oxidative stress bon the current and the sum of the antioxidant defense mechanisms. A low TAS value may be due to an increased production of free radicals and antioxidants to low values, which can be triggered by chronic diseases such as diabetes, poor dietary habits, increased environmental toxins or smoking.


Glutathione peroxidase 5 ml EDTA blood

Glutathione peroxidase is an important for the detoxification of reactive oxygen species selenium-dependent enzyme. It builds V. A. Hydroperoxides, including hydrogen peroxide, as well as lipid hydroperoxides from the Menbranen are starting to harmless compounds. Since the activity of glutathione peroxidase by the presence of oxygen radicals is cranked, high values can be an indication of oxidative stress.

5 ml of serum glutathione reductase

Glutathione reductase is an enzyme that regenerates the oxidized in the degradation of reactive oxygen species and glutathione again provides the active glutathione for detoxification so again. At high Glutathionverbrauch and turnover of glutathione reductase increases.

Glutathione 2 ml of blood plasma or 5 ml EDTA whole blood

Glutathione is the main reducing substance in the cells. Glutathione plays an important role in the detoxification of mycotoxins (eg, aflatoxins), aldehydes, aromatic hydrocarbons and pesticides. In the oxidation of glutathione results in a sulfur-sulfur compound of two Glutathionmolekülen, which is re-reduced by glutathione reductase again. Glutathione is, inter alia, used as an important factor that binds the toxins to better detoxify.

Glutathiondefizite occur when the precursors for the production of glutathione (glycine, glutamine or cysteine) are present in too small amounts, if a B12 vitamin deficiency, heavy metals or enhanced detoxification reaction with consumption of glutathione is present.

Superoxide dismutase 5 ml EDTA blood

Superoxide dismutase is essential for the elimination of superoxide radical anions, the main oxygen radical compound responsible. There are various subgroups of superoxide dismutases, which are found in different parts of the body and differ in that they require different metal ions for their activity. Some are dependent on the presence of copper and zinc, while others of manganese.

Vitamin E 2ml serum

Vitamin E is one of the most important fat-soluble antioxidants, which are not produced in the body and must be supplied. Vitamin E shows the fatty acid radical from a hydrogen atom and so terminates the lipid peroxidation of unsaturated fatty acids in many cases. The so radicalized Vitamin E is in turn is regenerated by Vitamin C Vitamin E .. therefore more precautionary against heart disease, also discussed a possible positive impact on cancer prevention.



carotenoids

Normal values in blood



carotenoids

normal range

 

carotenoids

normal range

ß-carotene

150 – 1250 µg/l

a-carotene

54 – 489 µg/l

Lutein/Zeaxanthin

159 – 660 µg/l

ß-Cryptoxanthine

33 – 509 µg/l

Lycopene

75 – 880 µg/l

Canthaxanthin

0 – 68 µg/l

The carotenoids can in oxygen-free (a-carotene, beta-carotene, lycopene) and oxygenated carotenoids (lutein, zeaxanthin, beta-cryptoxanthin), the so-called. Xanthophylls are divided. The difference lies mainly in the heat stability, the former are relatively heat stable, while xanthophylls are destroyed during the cooking process to 60-100%. Epidemiological studies show that unheated vegetable has a stronger anti-cancer Wikung, indicating the special function of heat-sensitive xanthophylls in cancer prevention.

Carotenoids act as antioxidants in part stronger than vitamin E. The antioxidant effect takes place as follows:

Lycopene> ß-Cryproxanthin / ß-carotene> lutein / zeaxanthin> a-carotene

There is evidence that the combination of different carotenoids enhances the antioxidant benefits.

Ubiquinone / coenzyme Q

Ubiquinone is also a potent antioxidant that is found in all cell membranes and as intermediaries for energy education acts through the breathing process. It neutralizes reactive oxygen species and inhibits lipid peroxidation. Coenzyme Q is partially synthesized by the body, but also must be obtained from food.

Next important antioxidants are vitamin C, selenium, zinc, cysteine / methionine, niacin, etc, which are dealt with in the context of vitamin and mineral research.

 

c. pro-oxidants

Iron status and copper status

             Iron may act pro-oxidative especially in connection with vitamin C in higher doses

             It is reduced by vitamin C in divalent iron and, in this value, as well

as the divalent copper hydrogen peroxide into highly reactive hydroxyl radicals implement.

 

2. DIAGNOSIS of the performance of the human detoxification systems

The most important own defense mechanism of the human body are the alteration and removal of waste products from the metabolism as well as of toxic substances (toxins) from the environment, which are ingested by humans.

When recording systems of the body, namely skin or gastrointestinal tract, are not intact, toxic chemicals, environmental toxins, endotoxins (poisonous substances that are formed in the gastrointestinal tract by bacteria) increasingly penetrate and other substances on food, skin and intestine in the body and thus the detoxification machinery set in motion and strain. This leads to increased production of free radicals, that is, a higher oxidative stress and an increased risk of systematic destruction of the body.

The liver is the main detoxifying organ in our body. This is where two from interrelated detoxification processes that are as Phase I and Phase II - called detoxification.

In Phase I substances over a complex enzyme system (cytochrome P-450 complex) can be modified in its structure so that the solubility of the substances and the reactivity is increased with polar compounds. This reaction is important for the further smooth adjustment, but itself produces an increased amount of reactive oxygen compounds that are toxic to our organism. Of course, where the cells in which these reactions take place, even before these destructive compounds by antioxidants (vitamin E, vitamin C, glutathione, etc.) to protect.

In Phase II, these reactive substances were only soluble in fat and very slow to react until then are converted into water-soluble forms that can then be easily eliminated or be divorced. For the various detoxification reactions as a carrier glutathione, sulfate, glycine, acetic acid, cysteine and glucuronic acid are necessary on the transport of pollutants to the outside and is removed via the urine or bile.

 

Figure 4. Principle of pollutant detoxification

 


When a man is long enough exposed to an elevated amount of toxic substances, detoxification systems are constantly stressed. This inevitably leads to increased oxidative stress, constantly high levels of cytochrome P-450 enzymes and a more limited Phase II - detoxification capacity. The result is then the accumulation of highly reactive radikalischenToxinzwischenproduten in the body, first initiate the destruction of essential fatty acids, lipid peroxidation, and ultimately reduced energy production.

It is now believed that this mechanism is causally associated with the chronic fatigue syndrome (CMS). This is a chronic disease that is often triggered by a viral infection, vaccination or surgery and is characterized by an inexplicable persistent or relapsing fatigue. Today we bring this disease with both an impaired function of organs for energy, detoxify the mitochondria, further oxidative stress and reduced ability in communication. According to new research, it is apparently possible that CMS arises when one is exposed to an increased extent debt and toxins.

There are now in a modern laboratory diagnostics to determine the possibility that the detoxification in the liver is functioning satisfactorily, which can be viewed from several sides. On the one hand, a functional verification of the individual phases detoxification is possible, on the other hand, the activity of the individual enzymes that are active in the detoxification mechanism to be tested. Finally offer genetic testing the possibility to study genetic components of sensitivity to environmental conditions.

Today it is known that environmental chemicals and impurities are not equally fast and well metabolized and detoxified by everyone and that the susceptibility to tumor formation is individual. This is due to small changes in the genetic heredity, the genes, which are also responsible for the formation and activity of detoxification enzymes. Such changes at the molecular level can be analyzed in routine diagnosis and are appropriately involved in the treatment of a disorder in the detoxification system today.

2.1. functional assays

The advantage of this function tests is that no blood sample is needed and they are easy to handle.

DETOX-test: urine sample collected in special tube for 5 hours after caffeine ingestion

after a 24-hour caffeine-free diet, avoiding certain foods is Caffeine and metabolized by cytochromes and the N-acetyltransferase 2. The amounts of certain urinary metabolites provide a measure for the activity of four represents Detoxifikationsenzymen Phase I and II.

Caffeine - Clearance: 2 saliva samples 2 and 14 hours after caffeine ingestion

Via this assay, the detoxification function of the system I, that is, the oxidation of foreign substances and toxins from food ingredients and additives, drugs, environmental toxins, among others checked in the liver. For heavier loads, the activity of the corresponding enzymes is very high.

Caffeine is absorbed and metabolized by the detoxification system I. The concentration of caffeine in saliva and its degradation rate can then be measured. Faster degradation indicates greater exposure to environmental toxins or drugs, while slower degradation indicates damage to the liver cells, which can also be done by environmental toxins.

Benzoate - Clearance: urine sample collected over 4 hours after Benzoateinnahme

Due to the detoxification step II fat-soluble environmental toxins, and other foreign substances by various enzymes in the liver are rendered water-soluble by, among others, substances such as glutathione, sulfate, glycine, acetic acid are bound and excreted by the kidney.

Benzoic acid, taken with caffeine is bound to glycine, thus forming a new substance, hippuric acid, which is then determined in the urine. Decreased hippuric acid on the one hand to environmental stress, on the other hand, the absence of binding partners glycine, glutathione above point. However, increased excretion of hippuric acid may indicate an increased exposure to environmental pollutants.

2.2. genetic testing

Currently, the genetic analysis of various pollutant degradation pathways in the liver is possible with the cytochrome P450 system, glutathione S-transferases and Acetyltansferase are best studied.

For the investigation of genetic predisposing factors for a limited detoxification function 2 ml EDTA blood is required per test. Meanwhile, it is also already possible to carry out the tests with a special Rachenspüllösung, or swab.

Cytochrome P-450 polymorphism for the variants CYP 1A1, CYP1A2, CYP2A6, CYP2D6, CYP2E1, CYP2C9, CYP2C19 and CYP2E1

In the genetic analysis of various cytochrome P450 variants can be determined if the patient is already carries a limited detoxification capacity of Phase I in his possession. Cytochrome P450 1A1, for example, has an important role in the detoxification of dioxin, PCB or Benzapyrene who highly toxic or even carcinogenic properties.

Glutathione S-transferase genetic tests for Varanten GST-M1 and GST GST-P1-T1

The glutathione-S-transferase is involved in the detoxification reaction phase II in the liver (and other organs), and helps to dispose of many chemicals, as well as heavy metals such as cadmium or mercury by the attachment of glutathione to the toxin. In addition, the glutathione-S-transferase plays an important role in the reduction of oxidative stress in the cells. A decreased activity by genetic predisposition, one can imagine that this is also an increased risk of developing diseases such as liver cirrhosis, chronic. Bronchitis or various cancers is caused.

N-acetyltransferase II gene test

N-Acetyltansferase is an enzyme that in phase II detoxification eg acetic acid transmits on aromatic amines and other pollutants, and thus this degrades. This can impact in the event of reduced activity of this enzyme by demonstrating genetic variation in an increased risk of cancer formation.

1.3. Tests for the enzymatic activity

Glutathione S-transferase type alpha (2 ml serum), theta (2 ml EDTA), pi (2 ml EDTA)

The glutathione S-transferase is crucially involved in the detoxification of raised external and toxins in Phase II. The glutathione S-transferase glutathione transmits the pollutant, which can then be excreted in the urine and bile without problems. The glutathione-S-transferase consists of a number of different shapes that can eliminate pollutants in each case different. Low GST values can be made longer lasting high levels of pollutants either by a genetic defect (see above), lack of pollution or. Elevated levels usually go hand in hand an increased volume of pollutants.
 

 

3. How to recognize vitamin deficiencies?

Vitamin analyzes are becoming increasingly important as vitamins (gg example. Oxidative stress) play an important role in defense mechanisms and functions of the body play.

In the assessment of micronutrient status of the population very controversial beach points are often represented. While some assume that there is virtually no vitamin deficiencies in our current living conditions, authors have increasingly towards more or less severe supply shortages already on larger population units.

Possible factors influencing these different reviews on the one hand, the orientation at different stages of deficiency, divergent threshold determinations and analytical methods differences.

Due to a reduced supply of many vitamins vitamin use is made of the body depots in the case. To counter the increasing availability decreased vitamin, vitamin concentration is initially decreased in the blood and reduces the vitamin excretion in the urine. Then, the formation is reduced by metabolically active vitamin levels, which is also reflected in declining blood and urine values. In the further course this leads to the decrease in activity of the enzymes and hormones, which are dependent on vitamins. Only now finds early signs of changes in metabolism and externally visible changes, but they are very often nonspecific. Only in severe deficiency caused pathological changes that are attributable to a particular enzyme deficiency. If no vitamin supplementation is started at this time, this damage may be irreparable.

For the determination of vitamin deficiency - phenomena we have various analytical methods are available:

- The concentration of vitamins or metabolites is measured in biological material such as whole blood, serum, red blood cells, the erythrocytes, urine, cerebrospinal fluid and tissue

- Indirect tests take into account features such as enzyme activity, which are directly related to the status of various vitamins

To obtain actual evidence about the vitamin status, various vitamins must be determined in various biological materials. So are the vitamins B6, biotin, nicotinamide, pantothenic acid and vitamin C in blood serum and erythrocytes, red blood cells, distributed largely the same, while thiamine, riboflavin and folic acid are mainly represented in the erythrocytes. Vitamin B12 and fat-soluble vitamins A and E are mainly found in certain organs and tissues, but are related to the blood serum in equilibrium, so that any provision in this is preferred.

In principle, the determination in urine would reflect the vitamin balance, however, cause food-related influences but also urine collection errors to significant errors.

3.1. Vitamin status in serum / whole blood

DieProbennahme them every morning before breakfast and before any medication

occur and the blood are taken from the ungestauten vein. Hemolysis is to be avoided. In the following list you can see the individual vitamins necessary Maßnahmenfür. The material for urine determination should be shipped in principle protected from light!
 

 

vitamin

material

standard valuesv

Vitamin A

serum

200 - 1000 µg/l

beta-carotine

serum

150 - 1250 µg/l

vitamin B1

thoroughbred

 

thiamine

 

< 5,0          µg/l

thiamine pyrophosphate

 

30 - 90       µg/l

vitamin B2

thoroughbred

 

  FAD

 

125 – 200   µg/l

riboflavin

 

2 - 15         µg/l

vitamine B6

thoroughbred

 

  pyridoxal phosphate

 

5 - 30         µg/l

vitamin B12

 

serum

200 - 950   pg/ml

vitamin C/ascorbic acid

 

Li-Heparin blood, l

2 - 14         µg/ml

folic acid

serum

3,6 - 16,9   µg/ml

vitamin E/Tocopherol

 

serum

5 - 16         mg/l

Biotin

serum

>200          ng/l

 

3.2. Functional tests for vitamins

  • Homocysteine produced in the conversion of the amino acid methionine in cysteine. The enzymatic conversion is dependent on Vitamin B6, Vitamin B12 and folic acid. An elevated homocysteine level is found in lack of these enzymes and elevated homocysteine level is a risk factor for atherosclerosis.
     
  • Kryptopyrrol n is a possible by-product that can occur erratically in the Synthes of hemoglobin. It has the characteristic of vitamin B6 and zinc to complex, the complex is excreted in the urine, and so there is a constant withdrawal of vitamin B6 and zinc, which should be addressed therapeutically to eliminate deficiencies
     
  • Vitamin B12:
    In a functional test, the so-called. Schilling test, 1 mg of vitamin B12 is taken, after which the blood of the vitamin levels must rise. If there is no increase in this test with additional intake of intrinsic factor, which supports the absorption of vitamin B12 from the gastrointestinal tract repeated. In this way, a possible inclusion disorder can be analyzed.
    In vitamin B12 serum levels below 100 pg / ml, in the addition to a measurably increased excretion of urinary methylmalonic acid
     
  • Folic acid:
    To assess the folate status is also the sigenannte FIGLU is - excretion after Histidinbelastung. Since the degradation of histidine is folic acid-dependent, the FIGLU excretion in urine increased folate deficiency.
     
  • Transketolase activity in red blood cells is an indicator for a lack of vitamin B1, vitamin B1 is because the coenzyme of the transketolase, an enzyme which is involved in sugar degradation of the body.
     
  • Vitamin B2:
    Malfunctions can be detected with the measurement of the glutathione reductase (GR), whose coenzyme is riboflavin or vitamin B2. The GR is involved in the regeneration of spent glutathione, which is involved in defense against reactive oxygen species in the body.
     
  • Vitamin B6:
    A functional test, where you have to take 5 g of tryptophan, is its degradation via enzymes transketolase activity in red blood cells is an indicator of vitamin B1 deficiency, because vitamin B1 is the coenzyme of transketolase, an enzyme that is involved in the breakdown of sugar in the body.
     
  • Vitamin B2:
    Cellular dysfunction can be detected with the measurement of erythrocyte glutathione reductase (GR), the coenzyme is riboflavin or vitamin B2. The GR is involved in the regeneration of spent glutathione, which is involved in the defense of Sauerstoffradukalen in the body.

4. mineral and trace element profile

By conscious or unconscious Malnutrition disease development is affected that are now leading cause of death in industrialized and highly developed areas of the world. Our current eating habits and the advanced food technologies have increasingly a discrepancy between demand and actual recording of vital substances are formed.

In this context, in addition to the vitamins, the composition of minerals and the so-called. Trace elements in the body of great importance. Although they account for, and receive enable trace elements together with minerals life is only about 0.01% of body weight. Of nine elements we know that they are absolutely vital for humans, iron, zinc, copper, manganese, iodine, molybdenum, chromium, selenium, at least another three, fluorine, vanadium, silicon, are also vital. Others again are already harmful in trace amounts. They include lead, mercury, cadmium and arsenic.

Since the so-called. Essential minerals can not be synthesized by the human body itself, it is dependent on an adequate and continuous supply of food. A deficiency may be responsible for malfunctions and diseases - an abundance can often have toxic effects. Was largely unknown until now in many cases the mutual influence of trace elements.

Modern methods of analytical chemistry, such as flameless atomic absorption spectroscopy or analysis by neutron activation are capable of distinguishing trace elements at concentrations below 0.1 millionths. In order to obtain a meaningful picture of the Elemetstatus, must also be decided which part of the body that should be analyzed.

In the living patient usually is only a rather small range of options available for sampling. Lead should actually be best determined in the bones, cadmium in the liver or the kidneys. In daily practice, however, there are only very limited possibility to specifically refer to body tissue, although the bulk of the minerals can be found inside the cells.

Therefore, other less invasive methods of analysis are preferred in the daily routine, requiring a less complex sampling. Among them are blood tests in plasma and whole blood and urine. Each of these studies shows us different states of the mineral composition in the body.

The blood analyzes reflect the current mineral status in and outside the cells, while only the minerals are found in the urine that are being eliminated, making the urine more limited use.

Minerals, and their main determinants materials
 

  • Aluminum plasma / urine
  • Lead whole blood / urine
  • Urine cadmium / whole blood
  • Chrome urine / serum
  • cobalt urine
  • Iron serum (serum ferritin, iron binding capacity, free iron porphyrins)
  • Gold nails / hair / urine / (plasma)
  • Copper plasma / hair / (urine)
  • Manganese plasma / S.urin / chair / hair
  • Molybdenum plasma / urine / hair
  • Nickel urine / plasma / (hair)
  • Palladium urine / hair / whole blood
  • Platinum urine / plasma / hair
  • Mercury Whole Blood / prox.Haare / urine
  • Selenium plasma / urine / hair / Glutathionp.
  • Strontium urine / hair
  • Thallium urine / feces / hair
  • Titan urine
  • Zinc urine, hair

 

4.1. The blood analysis

Depending on the diagnostic problem, representative samples of the organism can be studied. Usually the blood is therefore a suitable specimen because it represents a transport medium between all parts of the body and a beacon for this biochemical change may also have difficulty in inaccessible organs. Nevertheless pushes the significance of mineral provisions in the blood of frontiers, since the blood is just a limited compensation and balance indicator for the current exchange of trace elements between the various organs.

Thus, a zinc deficiency manifest initially for a long time, no changes in the blood because muscle and bone tissue accumulate abundant reserves, even if they have no real storage organs. On the other hand, by surgery, larger wounds or burns lead to quick but short-term changes in blood zinc.

A mineral investigation in the blood so primarily shows the average power status and consumption rate of trace elements and minerals, and not so much the exact proportions of each institution.

The analysis is carried out either in the blood plasma, ie, in the colorless portion of the blood, whole blood or red blood cells the red blood cells and plasma serum are adapted to represent a current state or short-term changes.

In the literature there are most measurements for mineral concentrations in serum and plasma before, so that the measurements can be based on relatively precise standard values

A relatively significant parameter is the determination of minerals in the erythrocytes, the könnem reflect chronic losses and deficiencies due to their average life of about 120 days.

Sampling:

In medical studies in biological material, it also depends on proper sampling. In spite of the low concentration of minerals in the human body should impurities, as far as possible, especially be on substances which are ubiquitous in nature, are excluded. They include zinc or copper, but also manganese and chromium. The decrease in this parameter, there are special metal analysis sampling sets that exclude contamination during sampling almost.

 

Calcium, copper, fluorine, selenium low risk of contamination
Aluminum, chromium, cobalt, manganese, zinc contamination risk by high air, dust, blood collection, processing, storage, shipment
Iron, magnesium, manganese, potassium, molybdenum, zinc hemolytic effects
Iron, zinc fluctuations during the day
Zink ingestion (Fasting blood collection!)

Are already in the blood taking so precautions are taken, an emphasis on freedom from contamination of the acceptance device (teflon-coated needles, plastic tubes) are placed and hemolysis be avoided.

Individual predictors

The mineral profile may vary due to physiological factors such as age, sex, diet, pregnancy. All of these factors should therefore be included in the form of a detailed medical history in the assessment.

Predictors description
Biorhythm daily and seasonal rhythm, menstrual cycle
Constitution physical activity, body position, fluid distribution in the body, pregnancy, lactation, growth
Disease Disease stage of this disease, therapy, narcotics, alcohol consumption
nutrition Fasting diet, dieting, utilization disorders
Age / Gender

Stages of development of the child, ages of geschelchtsabh. Metabolic functions (eg, puberty, menopause)

medication Diuretika

 

Standard ranges of whole blood analysis

From a lithium heparin blood analysis is to trace elements and toxic metals through and to create a detailed special findings.

element

Normal values in plasma

Standard levels in erythrocytes

sodium

135 - 144   mmol/l

<5           mmol/l

potassium

3,7 - 5,7     mmol/l

126 – 144     mmol/l

Calcium

2,15 - 2,6   mmol/l

0,3 – 0,81     mmol/l

Magnesium

0,73 - 1,05 mmol/l

1,80 – 2,60   mmol/l

Zinc

70 – 127    µg/dl

1000 – 1500 µg/dl

iron

35 – 168    µg/dl

131 – 144     mg/dl

copper

80 – 160    µg/dl

87 – 128       µg/dl

Strontium

10 - 70       µg/l

<10               µg/l

Chrome

0,15 - 0,41 µg/l

0,2 – 0,5       µg/l

Cobalt

0 – 1,         µg/l

0 - 1,4           µg/l

Nickel

0- 1,1         µg/l

2,7 – 5,7       µg/l

Selenium

74 – 139    µg/l

85 – 140       µg/l

Manganese

0,3 – 1,3    µg/l

18 - 53         µg/l

Molybdenum

0 - 1,3        µg/l

0 - 2             µg/l

Cadmium

0-0,4          µg/l

0 - 1,6          µg/l

lead

0-300         µg/l

47 - 85         µg/l

Aluminium

2 - 15         µg/l

3 - 15           µg/l

mercury

0,1 - 7,2     µg/l

0,1-7,2         µg/l

Thallium

0 – 0,3       µg/l

0 – 1            µg/l

Platinum

0 – 0,1       µg/l

0 – 0,1         µg/l

Silver

0 – 0,3       µg/l

0 – 0,3         µg/l

Titanium

0 - 7,7        µg/l

0 - 7,7          µg/l

Gold

0 – 0,3       µg/l

0 – 0,3         µg/l

Palladium

0 – 0,2       µg/l

0 – 0,2         µg/l

Arsenic

0 - 10         µg/l

0 – 10          µg/l

 

Publications

by

Dr. Peter H. Lauda

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