Tuesday, February 17, 2009

Axel Konold is a Fraud! Bioressonance Treatment in Munich (Negative critics)

Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)


Basically, since I came back from Munich I feel worse than before. During 2008 I was feeling relatively good, but I had a relapse in October after I got the "treatment" and maybe is coincidental, but is what it is. Recently I am recovering gradually.

Among the things he told me before treatment were:

I do have:
-Fasciola Hepatica
-Fasciola Buski
-Borrelia afdetii
-Borrelia Japonica

And after treatment he said:

-Now, there is no single infecction or inflammation
-Now you are also protected at your immune system, in your cells, for autoimmune diseases (cancer, etc)
-You are fit

Before I got the treatment I did a blood test to verify that I effectively had Fasciola Hepatica in my system, but the test came negative. Fasciola Hepatica is a parasite that you could even see with your eye, so I doubt that it could be an intracellular infection that is not detectable by a blood test as he suggested... If someone knows this detail, I appreciate feedback on this...

After treatment I did check for the things I knew I had in my system, to see how they evolved with the treatment:

My EBV remains high at the IgG level as before 1/80 (Reference value 1/10) when it is above 4 times the reference value, means it is still active in the nucleus of the cell, and therefore your immune system could still try to fight it.

My CMV remains high at the IgG level as before 143 (Reference value 6) when it is above 4 times the reference value, means it is still active in the nucleus of the cell, and therefore your immune system could still try to fight it.

My T8c/T8s is very high 6 (Reference value 5) This reflects a situation of chronic infection against which the immune system is fighting, or an autoimmune situation.

My T-activated Linfocites are too low 7%, which reflects the wasted level of these linfocites that are responsible to fight viruses and bacteria. I can no defend myself propertly against bacteria, because I am too much focus on the virus. (My immunologyst said)

When they performed a colonoscopy, because I was bleeding, they found 2 polips and a white lesion inside that when analized was an espiroquetosis (bacterial infection). Besides, in my stool test they found diminished flora from escherichia coli and enterococus faecium, and a deficiency of the good flora bifidus, lactobacilus, etc... A candida overgrowth was observed, and Tricosporon cutaneum was present. Also an espastic colon was described. Therefore there was infection and inflammation. Next to that in the biopsy of one of the tissues they found HPV 51 and 58, both with high potential to cause cancer, which does not mean that I have cancer of course.

A Tac was performed in my sacro because I fainted after pain, and I was diagnosed with a sacroielitis (inflammation of the articulation), which caused me to have a sincope when the pain arrived and I did not lay. Again, there is inflammation.

All in all, I can confirm, I do not have a fasciola hepatica, never did I guess, nevertheless there are infections in my body, there is inflammation, there is an immune response to this, I am not protected for autoimmune episodes and I do not feel fit.

I know that is a devastating review for the treatment of this doctor, but these are facts, not opinions.

I have confronted the doctor Axel Konold with these facts through my friend, the one that recommended me this doctor. His reaction was very defensive, and He showed a big EGO and lack of recognition of these facts. Of course he did not want to reimburse my money. For me this is a NO NO Doctor, for me he is a FRAUD, and I am talking exclusively about him, not the bioressonance technique as such. So Please avoid coming to this doctor...that is my advice. Waste of money and time in my view.

Friday, February 13, 2009

OZONE Treatment good for intetinal dysbiosis

Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

By: Dr. med. H.G. Eberhardt
The intestine is one of the most important control centers of the human organism, in which capacity it performs three vital functions:
It protects the organism from invasion by intestinal pathogens.
It initiates and regulates the entire humoral and cell-mediated immune response.
It influences the colonization of the intestinal region by bacteria. This regulatory function is of central importance for the body's primary metabolism.
The intestine is an interface organ that plays an active role in defining the symbiontic relationship between the body and the living intestinal contents. Illness is the consequence of a disturbance in this symbiosis. One result of such a disturbance is the intoxication of the host organism by foreign microorganisms that are incapable of human symbiosis. To an increasing extent, these microorganisms include fungi. Owing to an impairment of hematogenic oxygen transport, this systemic intoxication causes a depletion of oxygen potential fixed in the tissue. Correction of this negative oxygen balance is the fundamental prerequisite for the restoration of an intact immunophysiological response. The skillful administration of ozone/oxygen therapy represents the only available therapeutic possibility for regenerating the depleted oxygen reserves. Administered in conjunction with suitable immune modulators, this therapy leads to an active elimination of foreign pathogens and thus to a complete healing of the chronic pathological processes.


Even today, some 5,000 years after the the first attempts of the human species to explore its own biology, the intestine is undisputedly still a great enigma. Professor Ludwig Demling, retired director of Erlangen University Hospital, calls the intestine "an unknown organ that has been criminally neglected by researchers". The time has come, says Demling, for a radical change in medical thinking about the intestinal system.1
The very fact that our intestine is called the "digestive tract" reveals the appalling lack of information about this organ, which peforms five major functions in addition to digestion. The five "cardinal functions" of the intestine are:
(1) The intestine is the central organ of the body's immune system.
(2) In its capacity as a bioreactor, the intestine carries out the process of "primary digestion".
(3) The intestine is responsible for the entire transport of substances from the intestinal lumen into the organism; it organizes the process of reabsorption.
(4) The intestine is the largest "waste removal" organ of the human body.
(5) The intestine plays a major role in regulating theacid-base balance.
These cardinal functions of this extremely important organ, which I also like to call the "root functions", delineate a broad spectrum which I cannot even begin to cover in this paper. For this reason, I have decided to focus on one point which is of crucial importance with respect to the development of therapy-resistant systemic diseases, namely the role played by the intestine as an immune organ. It is in this capacity, in particular, that the intestine not only acts as an interface influencing events around it, but also generates the immunological competence of the entire system.


Regeneration of of the immunological competence by restoration of the microbal system with support of ozone
In the complex struggle underway between the body and attacking bacteria, the intestinal immune system has been assigned the task of "fighting off" the pathogens in the strictest sense. In addition to this "civil defence" role, however, it has a second task to perform: namely, to regulate the colonization of the intestine by bacteria. Because it has a direct impact on the qualitative composition of the intestinal flora, the immunological integrity of the intestine determines the efficiency with which the intestine carries out its duties as a bioreactor. The results of the stool flora analyses I have been performing in my practice for 20 years demonstrate clearly that the intestinal immune system is able to distinguish between microorganisms that "fit into" the system and are capable of symbiosis and microorganisms that are "outsiders" to the system and incapable of symbiosis. Once it has identified the non-conforming microorganisms, the intact intestinal immune system will respond by secreting them.
On the basis of our current knowledge, we know that the local microflora conforming to the system, i. e. the autochthonous microflora, perform a number of functions of vital importance to the host organism. Since we are not yet able to provide a qualitative description of the enteric microcosmos of the species Homo sapiens, I intend to limit my remarks to a microbe whose role within the complex network of human symbiosis has been relatively well explored, namely non-pathogenic Escherichia coli. We now know that, among the human symbionts, this bacteria plays a dominant role. Moreover, information on the specific characteristics of E.coli with respect to the use of ozone to achieve immunological restoration is of central importance for the clarification of several apparent contradictions in this context.
The normal, i.e. non-pathogenic, form of E. coli can be found both in the lumen and on the wall of the large intestine. An observation of particular importance for the host organism is that this bacteria is capable of attaching itself to the intestinal wall via specific adhesion mechanisms2. This attachment consists of a particular sequence of events presupposing the existence of certain structures on the surface of the microbe as well as specific receptor structures on the epithelial cells or in the superimposed mucinous layer of the colon. The structures involved in this attachment are usually fimbriae on the coli bacteria and membrane-based glycoproteids on the epithelial cells. As a result of this coupling mechanism, a strain of E. coli is able to establish large colonies and thus dominate the micro-ecological terrain for a longer period of time. In this scenario, an important role is played by the affinity of the symbiotic coli strains to the oxygen diffused into the lumen of the intestine via the transepithelial route.
This is of vital importance for the host organism, since the symbiotic bacterial society performs three important functions on the local level:
(1) Coli bacteria pave the way for the further colonization of the intestine by manufacturing colicins, microcins and short-chain fatty acids3. These substances have the effect of counteracting any colonization of the terrain by pathogenic microbes, i.e. microbes alien to the system, and explain the specific antibiotic function of our immune system. In any event, the establishment of this barrier against foreign microbes is one of the most important tasks of the autochthonous intestinal flora.
(2) Owing to their exceptionally high consumption of oxygen4,5, the coli cultures located in the intestinal wall create an anaerobic milieu which constitutes a hospitable climate for anaerobic bifidus and Bacteroides strains. The resulting "bacterial orchestra", which now consists of both aerobic and anaerobic microbes, regulates the energy balance in the intestinal mucosa. In this context, the production of acetic, propionate and butyric acids - as well as the L+ lactic acids produced primarily by the lactobacilli - is of particular importance. These end products of bacterial carbohydrate and protein degradation are easily absorbed by the cells of the mucosa via passive diffusion; according to studies conducted by Roediger, they supply around 40-50ÿ% of the energy requirements of the epithelial cells in the large intestine. The remaining energy required for metabolism is provided by the hexoses and amino acids delivered by the blood stream through the intestinal wall.
(3) The presence of a physiological coli flora is equally indispensable for the induction, via the intestinal immune system, of the humoral and cell-mediated immune response6.

In animals kept in a sterile environment, Peyer's patches and the abdominal lymph organs are significantly underdeveloped7. Conversely, the research team headed by Lodinov -Z dnikov in Prague has succeeded in stimulating the development of the intestinal immune system in newborns by implanting a non-pathogenic strain of E. coli at an early stage of the infants' development8. It has thus been demonstrated that the intestinal symbionts are not only of vital importance for the local immune barrier in the mucosa, but also for the entire humoral and cell-mediated immune response of the body.
Illness is the result of a disturbance in the symbiotic relationship between the human being and his or her micro-ecological partner system. Illness is not a state but a dynamic process that is directed at the functions typically performed by the intestine in its capacity as a root organ. Accordingly, illness is always the result of an auto-intoxication, a deficiency of vital substances, and an immune deficit. An observation that is of central importance, especially for the therapist working with oxygen-ozone methods, is that the disturbance of symbiosis described here obviously hinders the diffusion of oxygen in the capillaries. This impairment of gas exchange at oxygen's final metabolic destination results in a negative oxygen balance throughout the entire organism; in turn, this negative balance produces a rigidity of response which initiates and maintains the chronic nature of the illness. The depletion of the oxygen reserves in the tissues results in an over-acidification of the entire system; this explains why chronic illneses always affect the organism as a whole and are by no means limited to single organs or systems.
The objective of this therapy is to restore the micro-ecology of the intestinal tract; this is accomplished by eliminating those microorganisms that are alien to the system and/or incapable of symbiosis and replacing them with an autochthonous flora. The primary prerequisite for the success of the treatment is the regeneration of the oxygen reserves in the tissues by a long-term oxygen-ozone therapy applied rectally and parenterally in order to restore the immunophysiological reaction capability. It is usually urgently necessary to simultaneously correct deficiencies of vital substances such as magnesium, the Vitamin B complex or Vitamin C. These measures give the physiological strains of E. coli a colonization advantage, owing to their affinity to oxygen, and thus permit their implantation in the colon.
This therapeutically induced restoration of the microbial system via the mechanisms described above is invariably associated with an "eviction" of those intestinal residents which had previously colonized the terrain. In patients suffering from disease, these can only be systems incapable of symbiosis, i.e. pathogens in the classic sense of the word; these are now dislodged from the intestinal wall by the activities of the physiological coli flora. The result of this new scenario is the displacement of the pathogens into the intestinal lumen and their elimination with the feces. If bacteria incapable of symbiosis are demonstrated in a patient's stool in the course of treatment, this is considered unmistakable evidence of the restoration of the body's immunological competence and thus of the patient's reconvalescence. This will be illustrated by several examples.


_rzte Zeitung Nr.45 Jhrg.10 M„rz 1991
Abraham, Beachey: Host defences against adhesion of bacteria to mucosal surfaces in: Gallin, Fauci eds. Advances in host defence mechanisms, Vol. 4 Mucosal Immunity. New York: Raven Press 1985 63-88
Baquero,F Moreno,F: The microcins FEMS Microbiol.Lett. 1984, 23 117-24
Sonnenborn,U Greinwald,R: Escherichia coli im menschlichen Darm: Dtsch.Med.Wschr. 1990 115 906-12
Savage DC: Microbiol.ecology of the gastrointestinal tract. Ann.Rev.Microbiol. 1977/31 107-33
Pabst,R: Der Verdauungstrakt als Immunorgan. Med.Klinik und Praxis Jhrg.78, Januar 1983 14-20
Luckey, TD: Gnotobiology and bioisolation Mikro”kologie und Therapie Vol.10 Hrsg.Volker Rusch, Herborn 1980 19-39
Lodinov -Z dnikov ,R: Immunantwort bei neugeborenen und fr_hgeborenen Kindern nach Kolonisierung mit apathogenen E.coli. Vortrg.Medica D_sseldorf am 20.11.1991

Friday, February 06, 2009


Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

I post this information on KRYPTOPYRROLES, because is the second time that I indicate a positive in this therothycally genetic deficiency of B6 and Zinc.

The first time I did, it was in KEAC Laboratories in The Netherlads with a result of:
Hemopyrrollactamcomplex * 0,9 Ref < 0,6 uMol/L (Slightly positive)

The second time I did was last December in ELN Laboratories in The Netherlands, with a result of:
HPL---------------------------------*461 Ref Range 15-250 (Positive)

Both of them measure Kryptopyrrole, and when is positive implies a structural deficiency of B6 and Zinc.

Explanation on HPU:

The HPU test measures the amount of haemopyrrollactam complex in the urine. HPU is a situation in which the body excretes a certain compound called HPL-complex, in the urine.

HPU is an abbreviation of hydroxyhaemopyrrollactumuria. The haemopyrrollactam complex, also called HPL or hydroxyl-HPL, consists of hydroxil-2, 3-dimethylpyrrolidone-5-on and hydroxyhaemopyrrolinon-2-on complexed with pyridoxal-5-phosphate (active vitamin B6) and minerals as zinc and manganese.

The excretion of HPL shows a variety of zero till a few decades of micromoles per litre (uMol/l) and is increased in the case of all kinds of stress. Besides pyrrols also increased concentrations of porphyrins, such as coproporphyrin I, are found in the urine of HPU-patients as well.

HPU can be described as a familiar double deficiency of zinc and vitamin B6 (pyridoxal-5-phosphate). These deficits are linked to the production of a group of chemical compounds that are called pyrrols and porphyrins, and are excreted with the urine. That is why HPU is also called porphyrinuria or toxic induced porphyria.

Because a deficit of vitamin B6 (pyridoxal-5-phosphate), reduces the absorption of zinc, chromium and -to a lesser degree- also manganese and magnesium, one could call it a deficit of only pyridoxal-5-phosphae. Vitamin B6 also plays a role in the production of vitamin B3 from trytophan. This vitamin is often decreased in HPU too. The extent of the deficits are so large that they cannot be counterbalanced by foods that are rich in these vitamins or minerals.

Interpretation of the test:

< 0.4 uMol/L HPU absent
0.4-0.6 uMol/L HPU weak, doubtful
0.6-1.0 uMol/L HPU present, light positive
1.0-2.5 uMol/L HPU positive
2.5-4.0 uMol/L HPU strong positive
>4.0 uMol/L HPU very strong positive

HPL was determined according to GLP-Norms. For children other reference values are used than for adults. Children with HPL values above 0.65 uMol/L that are younger than ten years old, or girls older than ten, but do not menstruate yet, as well as children with values above 0.75 uMol/L that are older than ten years old, or girls younger than ten years old that already menstruate, all are considered POSITIVE. Their value will increase during the onset of puberty. A value above 0.6 uMol/L implies that a treatment should be started for at least 4 months.

Present till light positive result:
The excretion of HPL shows a variation between zero and 20 uMol/L, and it increases with all kind of stress: psychological stress, physical stress, such as flu, burns, sun burns, the use of porphyrinogenic pharmaceuticals or the presence of infections will increase the amount of HPL in the urine. The difference between light positive and positive is only arbitrary. A person with a 1.2 value is not necessarily more ill than another one with 0.65. In patients that are chronically ill, much lower values are found, because HPL is not excreted in the morning urine but though out the day, and a 24h urine test is recommended to be certain.

False Positives:
Some illness can influence on the value of HPU excreted on the upside. Mononucleosis, alcoholism, hyperthyroidism, pernicious anaemia, hepatitis, malaria, bartter syndrome, liver cirrhoses, crigler-najjar disease, Gilbert disease, sferocytosis, sickelcell disease, physical stress, psychological stress, short after a heart attack, and short after an operation or accident.
HPU values can also be increased by a chemical load or by foods (a low carbohydrate diet). An extream high value can also indicate another porphyria disease different from HPU.

False Negatives:
The result can give a false negative value if you have taken regularly supplements of vitamin B or biotin, and/or a multivitamin with zinc, manganese or vitamin B for the last few months.
False negative results can also be obtained right after menstruation, or if you have used the toilet during the night previous to the test. Also if you have take diuretics before the test, or after a 3 week relaxed holidays.


a) Complaints caused by deficits of P-5-P, zinc and manganese.

-Reduced muscle building, muscles spams, epileptic like attack, convulsions, cramp attacks.
-Joint problems, hyper-mobility, instability of the pelvis
-Stomach and gut problems (carbohydrate intolerance and faulty protein digestion) allergy.
-Heart and vascular diseases caused by increased homocystein, vascular instability.
-Problems with menstruation, pregnancy and delivery
-Blood sugar problems: reactive hypoglycaemia and diabetes Type II

b) Complaints caused by decreased haem production:

-Fatigue, functional liver problems
-Psychological complains, such as depression, schizophrenia and psychosis.
-Muscle weakness

c) Complaints caused by deviation of the hormonal regulation

-Headache and or migraine
-Allergy and gluten sensitivity
-Low blood pressure
-Auto-immune diseases

d) Complaints caused by deviated liver function

If the haem synthesis id partly blocked, not metabolized porphyrinogens are stored in the tissue. Here they have a toxic effect on the nerve tissue from the central, peripheral or vegetative nervous system. Symptoms can pass from latent to present by the presence of sunburn, infection, stress, pregnancy, porphyrinogenic pharmaceuticals and chemicals. This can overload the faulty enzyme system, completely and definitely.

Further research: When the result is 0.6 or above, further testing is recommended
-HPU blood screening
-Blood test to check the sugar levels by a fructosamine determination.
-IgA Total gluten

Nevertheless, even without this further testing, a treatment can be started.


-Reduce significantly the intake of sugar in your diet.
-Equally divide the food intake during the day. Eat something every 2 hours.
-Reduce the amount of gluten in your diet. If you eat pasta, reduce the amount o grains in other meals, by not eating bread at breakfast or lunch. Eat vegetables and fish.
-Practice daily exercise without exhausting the body (walking, jogging, biking, swimming)
-Do not take high amounts of Vitamin C with high HPL levels. Reduce acid, low amounts of sour milk products, or preserved products with lactate or other acids.
-Do not use food supplements that contain copper in higher dose than 1mgr per day.
-Do not use vitamin B6 in high dose (pyridoxine HCI inactive), however you can use P-5-P.
-Use the following food supplement:
Zinc maximum 30mgr per day (take with dinner)
Manganese maximum 25mgr per day (normally 5mgr per day at dinner)
P-5-P or B6 phosphate 50mgr per day (with breakfast)
The combination of these 3 can be obtained in one single capsule called Depyrrol basis. Take Depyrrol every second day during the first 3 weeks with breakfast. After this periods the amount can be increased if there are no stomach complaints or nausea.

Patients who have or had depression, panic attacks, psychoses or schizophrenia, should start very carefully. Prevent symptoms by starting with one pill every 2 days, or start with the separate ingredients before trying the combination. When you start to feel depressed, stop the treatment and consult with KEAC keac@tip.nl


Pyroluria is a familial disorder which occurs with stress, where an above-average amount of a substance consisting of "kryptopyrroles" circulate in the body. The substance is harmless in itself, but high levels of these pyrrolles systemically bind with B6 and zinc, preventing the use of these essential nutrients in the brain and body.

Pyroluria (originally known as malvaria) is a genetic abnormality in hemoglobin synthesis resulting in a deficiency of zinc and vitamin B6. People with pyroluria produce excess amounts of a byproduct from hemoglobin synthesis, called OHHPL (hydroxyhemoppyrrolin-2-one). In these people an excess amount of pyrrole is found in the urine. Associated changes in fatty acid metabolism lead to low levels of arachidonic acid (an omega-6 fatty acid). The presence of pyroluria can have a profound effect on mental and physical health.

The list of complaints of HPU is very wide: chronic fatigue, menstruation problems, hypoglycemy, migraines, flatulence, irritable bowel, diarrhea, constipation, pregnancy complaints, anaemia, low blood pressure, returning infections, muscle weakness, overweight, hypermobility, muscle spams, cramp attacks, sleep impairments, allergies, food intolerances, cardiovascular problems, depression...

Of course, having some symptoms does not guaranty that you have HPU, but the more symptoms you recognize as yours, the higher the chance will be to get a positive urine test on HPU.

Some external factors can contribute to a deficiency of Vitamin B6, zinc and manganese, and the risk for health is high. The most important charging factors are stress, the contraceptive pill, medicines, a vegetarian feeding pattern and other sicknesses (for example the sickness of mononucelosis).

Many patients with HPU are tired. Fatigue at HPU can be the consequence of hypoglycemy, a reduced liver capacity, a low histamine quality and/or low activity of the adrenal gland. HPU patients become tired.

Conversations between the two laboratories, regarding the confict of results: a positive HPU (Keac) and a hight P-5-P (ELN)

My HPU test that came out slightly positive 0,9, indicating a deficiency of P5P, magnesium and zinc, in which you recommended taking Depyrrol. But at the same time I did took some other tests in ELN which showed high levels of P5P, and therefore posted the doubt if I should take any supplement at all regarding B6.


Your HPU came positive, With values above 0.6 a treatment is helpfull. The best to use is Depyrrol basic, If not available you cane use at least P5P 50 mg and zinc 30 mg daily for long time.

In the ELN, they do not measure P5P, nor pyridoxin, but PLP, which is much easier to measure.I don't think that ELN has determined P5P. Most laboratory's determine PLP, which is incorrectly presented as P5P. It could also be the fact that you took supplements of B6 before what could be interferring with results.

In the case that it is realy P5P you should take folinic acid with vitamin B12 the lower the P5P levels in you blood. In this case you can take taurine 500 mg each morning in combination with zinc 30 mg with the warm meal.




“Kryptopyrrole” is the name given to a pyrrole-zinc-vitamin B6 complex that may be excreted in the urine of affected individuals [1]. Kryptopyrroluria, which may be associated with abdominal pain or a haemolytic crisis, can result in zinc and vitamin B6 deficiency and also schizophrenia. The condition has similarities to acute intermittent porphyria in that coproporphyrins are also excreted. In the scientific literature kryptopyrroles are also referred to as the “Mauve Factor” [2].

The assay procedure described depends on the extraction of the kryptopyrrole (KP) containing fraction from the urine with chloroform and its subsequent reaction with Ehrlich’s acid aldehyde reagent (p-dimethylaminobenzaldehyde in hydrochloric acid). This reaction is non-specific since most indoles, simple pyrroles or more complex pyrrole derivatives such as bilanes, which may be chloroform soluble, will also give a colour. Urobilinogen (UBG), which is a product of bilirubin metabolism, formed as a result of bacterial action in the gut and a normal component of many urine samples, also gives a magenta-red colour with Ehrlich’s reagent which can be extracted into chloroform. Porphobilinogen (PBG), which is an intermediate in the biosynthesis of haem but not a normal component of urine, gives a red colour with Ehrlich’s reagent, but will not extract into chloroform [3]. On the other hand, indican gives a red colour with Ehrlich’s reagent which can be extracted into alkali, but not into organic solvents.

In the situation we are considering,

a) Kryptopyrroles appear in the urine when the patient is suffering from combined zinc and vitamin B6 deficiency.

b) Failure to incorporate these pyrrole rings fully into Hb synthesis results in their appearance in the urine.

c) Such patients may suffer from eg autism or schizophrenia.

It is also possible that a toxin (e.g. a food additive absorbed through the GIT wall) could cause an idiosyncratic disturbance of haemoglobin metabolism and accumulation of pyrroles in the blood and urine, with consequent excessive loss of zinc and vitamin B6. Treatment involves identification and removal of the toxin from the diet, as well as replacement of zinc and vitamin B6. Hence kryptopyrroluria is a secondary coproporphyrinuria (i.e. a porphyrinuria which develops on the basis of a disease other than a primary disturbance of haemoglobin synthesis). The presence of porphyrins in the blood due to an inherited metabolic defect can also cause psychiatric disturbances. However, patients with kryptopyrroluria are not thought to suffer from other recognised porphyrin defects.

Thursday, February 05, 2009

Vitamin D Tips yaken from Carol's Blog

Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

Time for more vitamin D

September brings the end of summer in the northern hemisphere and, for many of us, that means less time in the sun. The sun’s rays provide ultraviolet B (UVB) energy, and the skin uses it to start making vitamin D. (The skin actually produces a precursor that is converted into the active form of the vitamin by the liver and kidneys.) Vitamin D is best known for its vital role in bone health. Without this "sunshine vitamin," the body can’t absorb the calcium it ingests, so it steals calcium from bones, increasing the risk of osteoporosis and fractures. Vitamin D also helps maintain normal blood levels of phosphorus, another bone-building mineral.

Vitamin D would be essential if it did nothing else. But researchers have discovered that it’s active in many tissues and cells besides bone and controls an enormous number of genes, including some associated with cancers, autoimmune disease, and infection. Hardly a month goes by without news about the risks of vitamin D deficiency or about a potential role for the vitamin in warding off diseases, including breast cancer, multiple sclerosis, and even schizophrenia. In June 2008, a study published in the Archives of Internal Medicine found that low blood levels of vitamin D were associated with a doubled risk of death overall and from cardiovascular causes in women and men (average age 62) referred to a cardiac center for coronary angiography. At a scientific meeting in May 2008, Canadian researchers reported that vitamin D deficiency was linked to poorer outcomes in women with breast cancer. And a large study of aging in the Netherlands published in the May 2008 issue of Archives of General Psychiatry found a relationship between vitamin D deficiency and depression in women and men ages 65 to 95.

The picture of vitamin D’s health benefits beyond bones has been drawn mainly from epidemiologic and observational investigations. The findings of such studies can suggest correlations between disease risk and certain factors - sun exposure or blood levels of vitamin D, for example - but they don’t prove cause and effect. Promising findings from observational studies don’t always pan out when put to the test in clinical trials. However, in one of the few randomized trials testing the effect of vitamin D supplements on cancer outcomes, postmenopausal women who took 1,100 international units (IU) of vitamin D plus 1,400 to 1,500 milligrams of calcium per day reduced their risk of developing non-skin cancers by 77% after four years, compared with a placebo and the same dose of calcium. The 1,100 IU dose - nearly three times the 400 IU per day recommended in federal and other expert guidelines - was correlated with a 35% higher blood level of vitamin D, on average. In the only other randomized trial of vitamin D and cancer - part of the Women’s Health Initiative - researchers found no effect on colorectal cancer. Critics say that the dose, 400 IU per day, was too small to make a difference.

More trials are needed to elucidate vitamin D’s benefits and risks at different doses and in different populations. In fact, a large-scale randomized trial that would include 20,000 U.S. women and men has been proposed by Harvard researchers and will be considered for funding by the National Institutes of Health. In the meantime, the evidence is so compelling that some experts already recommend at least 800 to 1,000 IU of vitamin D per day for adults.

Latitude and vitamin D production in the skin

Except during the summer months, the skin makes little if any vitamin D from the sun at latitudes above 37 degrees north (in the United States, the shaded region in the map) or below 37 degrees south of the equator. People who live in these areas are at relatively greater risk for vitamin D deficiency.

In search of vitamin D

Under the right circumstances, 10 to 15 minutes of sun on the arms and legs a few times a week can generate nearly all the vitamin D we need. Unfortunately, the "right circumstances" are elusive: the season, the time of day, where you live, cloud cover, and even pollution affect the amount of UVB that reaches your skin. What’s more, your skin’s production of vitamin D is influenced by age (people ages 65 and over generate only one-fourth as much as people in their 20s do), skin color (African Americans have, on average, about half as much vitamin D in their blood as white Americans), and sunscreen use (though experts don’t all agree on the extent to which sunscreen interferes with sun-related vitamin D production).

Lack of sun exposure would be less of a problem if diet provided adequate vitamin D. But there aren’t many vitamin D-rich foods (see chart, below), and you need to eat a lot of them to get 800 to 1,000 IU per day. People who have trouble absorbing dietary fat - such as those with Crohn’s disease or celiac disease - can’t get enough vitamin D from diet no matter how much they eat (vitamin D requires some dietary fat in the gut for absorption). And people with liver and kidney disease are often deficient in vitamin D, because these organs are required to make the active form of the vitamin, whether it comes from the sun or from food.

Selected food sources of vitamin D


Vitamin D (IU*)

Salmon, 3.5 ounces


Mackerel, 3.5 ounces


Tuna, canned, 3.5 ounces


Orange juice, fortified, 8 ounces


Milk, fortified, 8 ounces


Breakfast cereals, fortified, 1 serving


*IU = international units

Source: Office of Dietary Supplements, National Institutes of Health

For these and other reasons, a surprising number of Americans - more than 50% of women and men ages 65 and older in North America - are vitamin D-deficient, according to a consensus workshop held in 2006. Growing awareness of vitamin D’s benefits coupled with the risk of vitamin D deficiency has led some experts to recommend a blood test that assesses the amount of vitamin D in the body. The test measures the concentration of 25-hydroxyvitamin D3, or 25(OH)D, the precursor produced by the skin and converted in the body to vitamin D. If you’re over age 70, have darker skin, or live at a northern latitude, you might want to ask your clinician about the test. People who have malabsorption problems or take medications that interfere with vitamin D activity (for example, glucocorticoids) should consider it as well. However, some experts think testing is unnecessary as long as you get 800 to 1,000 IU of vitamin D a day.

Although there’s no agreement on an optimal level of 25(OH)D, deficiency is generally defined as a blood level less than 20 nanograms per milliliter, or 20 ng/mL (see chart). Levels that low have been linked to poor bone density, falls, fractures, cancer, immune dysfunction, cardiovascular disease, and hypertension. Many experts recommend a level of at least 32 and suggest that 800 to 1,000 IU of vitamin D per day is required to maintain that level.

Vitamin D status by blood levels of 25(OH)D*

Vitamin D status

25(OH)D in nanograms per milliliter (ng/mL)


Less than 20 ng/mL


20 to 29 ng/mL


30 ng/mL or more

Potentially harmful

More than 150 ng/mL

*25-hydroxyvitamin D3 (vitamin D precursor)

Source: Holick MF. "Vitamin D Deficiency," New England Journal of Medicine (July 19, 2007), Vol. 357, No. 3, pp. 266-80.

How to reach 1,000 IU

Unless you live in the South and spend a fair amount of time outdoors, or you like eating lots of fatty fish and vitamin D-fortified foods, supplements are the best way to make sure you’re getting 800 to 1,000 IU per day. (Higher doses may be prescribed if you’ve been diagnosed with vitamin D deficiency.) Most multivitamins contain only 400 IU. But don’t just take two, because getting double doses of other vitamins and minerals can be unsafe (for example, too much vitamin A as retinol can cause hair loss and diarrhea and is associated with hip and other bone fractures, possibly due to an adverse interaction with vitamin D). Many calcium pills contain about 200 IU of vitamin D, so one multivitamin and two or three calcium pills should suffice. Or you can take a vitamin D pill to round out your daily needs. Until we know more, make sure your intake from supplemental sources doesn’t exceed 2,000 IU per day, the current upper limit set by the National Academy of Sciences.

Monday, February 02, 2009

Latest aminoacid test December 2008

Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

Interpretation of Lab test December 2008

Free Homocysteine 24h. ---------------------------> (Dec 2008) *5 (0-4)

Moderately elevated levels of homocystine are associated with a significantly increased risk of atherosclerosis. High levels in body fluids of this amino acid have been associated with increased risk of cardiovascular disease as well as ocular, neurological, musculoskeletal and joint abnormalities.

A commoncause of this metabolic disorder is impaired function of the enzyme cystathionine β-synthetase for conversion to cystathionine. This enzyme is vitamin B 6-dependent and supplementation of the vitamin has been used to treat elevated homocysteine. A second route in metabolism of homocysteine is remethylation to methionine using vitamin B 12, folic acid and betaine (trimethylglycine).

Supplementation of betaine has proven useful for people with high homocysteine who do not respond to vitamin B 6. Adequate intake of vitamins B 6 and B 12, folic acid and magnesium is necessary for insuring proper methionine metabolism to prevent the accumulation of homocysteine. Homocystine (HCys) Cystathionine.

For lowering of elevated homocysteine, in addition to the supplementation of folate, B 12 and B6, some have advocated the use of betaine to support the betaine-methyl transfer reaction in reformation of methionine. Recent evidence demonstrates that plasma betaine concentration is, indeed, inversely related to homocysteine levels. Because betaine levels are raised by folic acid supplementation, additional betaine supplementation is less likely to be effective when the B vitamins are used at appropriate doses.

Treatment: B6, 100 mg; Folate, 800 µg; B12, 1,000 µg; Betaine, 1,000 mg
The supplement from Health Aid that I am taking contains: (up to 4 tablets a day)
-Trimetiglicina 500mg
- Colina, cloruro 100mg
- Inositol 100mg
- B6 (Pyridoxine Hydrochloride) 3mg(PN)
- B12 1mcg
- Folacina 200mcg
-Zinc, oxido 8mcg
I alternate it with Depyrrol Basis plus B12 & Folic acid that contains:
- B6 (Pyridoxine Hydrochloride) 10mg(PN)
- Mangaangluconaat 41,7mg
- Pyridoxal-5-fosfaat 50mg (PLP)
- Zincgluconaat 210 mg
- B12 10000 mcg
- Folic Acid 200 mcg

History of Lab test regarding Homocysteine-Metionine 2007 y 2008

December 2008

Free Homocysteine 24h. ---------------------------------> (Dec 2008) *5 (0-4) HIGH=> Risk for cardiovascular disease or renal insufficiency=> Current treatment B12+B6+Folic Acid+Zinc

May 2008

Total homocysteine ----------------------------------------> (May 2008) 5.8 (4.5-12.4) umol/l (NORMAL)
Homocystine (free) -----------------------------------------> (May 2008) 3 0-4 umol/24h (NORMAL)
S-Adenosylhomocisteine (plasma)------------------------------> (May 2008) *39.7 21-35 nmol/l (HIGH)
S-Adenosylhomocisteine (RBC)--------------------------------> (May 2008) *52.3 38-49 umol/dl (HIGH)
10-FORMIL-THF -------------------------------------------> (May 2008) *1 1.5-8.2 nmol/l (HIGH)
5-FORMIL-THF --------------------------------------------> (May 2008)*0.83 1.2-11.7 nmol/l (HIGH)
Folinic Acid (WB)--------------------------------------------> (May 2008) *1.4 9-35.5 nmol/l (HIGH)
Folic Acid (RBC) --------------------------------------------> (May 2008)*305 400-1500 nmol/l (HIGH)
Adenosine ------------------------------------------------> (May 2008)*37.5 16.8-21.4 10^-8M (HIGH)

S-adenosylhomocysteine is a more sensitive indicator of renal insufficiency than homocysteine; also appears to be a more sensitive indicator of the risk for cardiovascular disease than is homocysteine.

December 2007

Metionina------------------------------------------------------> (Dic 2007) * 35,5 19-31 (HIGH)
Homocystein was not checked at this time...
Cystine (Jun 2008) 30 (21-83)----------------- -------->(Dec 2008) *7

Low cystine levels may impair cellular synthesis of taurine, in which case plasma and urinary taurine will
also be low. Low plasma cyst(e)ine may reflect a dietary deficiency of methionine and/or cysteine in which case N-acetylcysteine (NAC) would be an appropriate intervention. High dietary intake of condensed tannins as in heavy users of tea can lower plasma cystine.

Treatment: NAC, 500 mg BID

Anserine *48 0-46-----------------------------------> (Dec 2008)*120

Zinc is the cofactor for carnosinase and elevations of carnosine or anserine may be one effect of zinc deficiency. A patient with zinc deficiency who consumes a high-poultry diet would tend to show increased anserine excretion because of low carnosinase activity. Anserine have the capacity to modulate the immune response.

1-Methylhistedine *504 128-392-----------------------> (Dec 2008) *863

1-Methylhistidine is derived mainly from hydrolysis of the anserine of dietary meat, especially poultry.Carnosinase splits anserine into β-alanine and 1-methylhistidine (Figure 4.27) and since 1-methylhistidine is not normally metabolized in human tissues, most of it rapidly appears in urine. Urinary excretion of 1-methylhistidine has been used as a marker to distinguish meat-eating individuals from vegetarians.Vitamin E deficiency can lead to 1-methylhistidinuria from increased oxidative effects in skeletal muscle509mass (SM) in healthy adults on a meat-free diet. Excessive muscle tissue breakdown can be associated with inadequate antioxidant protection in the muscle.

Supplementation of the natural antioxidants—vitamins A, C, E and B2 and selenium, β-carotene, lipoic acid and coenzyme Q 10 (CoQ10)—may be useful in preventing excessive free radical pathology associated with this problem. BCAAs have also been indicated to lower plasma levels of 3-MHis by preventing muscle proteolysis.

Treatment:Vitamin E, 400 IU

Gamma-aminobutyric Acid 11 (7-35)--------------> *4 (Dec 2008)

Low levels in plasma are characteristic of one subset of patients with depression.368 The neurodegenerative condition, Huntington’s disease, also manifests as lowered levels of GABA as neuron loss proceeds.Vitamin B6 deficiency impairs GABA formation, offering one option to help assist patients with inadequate GABA production. In animal models of seizure, lysine has dose-dependent anticonvulsant effects that appear to be
due to GABA receptor modulation.

Alpha-Aminadipic Acid *57 (9-51)-------------------> *60 (Dec 2008)

Elevated alpha-aminoadipic acid is a clue that a patient is consuming large amounts of lysine. Elevation of a-aminoadipic acid could result from vitamin B 6 deficiency. The high positive correlation between homocysteine and a-amino adipic acid suggests that they share metabolic marker status in the etiology of atherosclerosis and myocardial infarction. Elevated alpha-aminoadipic acid is a risk factor for heart disease. Unlike homocysteine, a-aminoadipic acid is not vitamin B 12 dependent and thus its elevation may indicate a specific need for vitamin B 6

Treatment: B 6, 100 mg; alpha-KG, 300 mg TID

Suberic acid *3.22 0-2 mmol/mcr---------------------> *2,23 (Dec 2008)

suberic acids are by-products of an alternative fatty acid oxidation pathway that is utilized when mitochondrial oxidation is limited. A secondary cause of elevated adipate and suberate is riboflavin insufficiency.52 Once they are inside the mitochondria, fatty acids cannot undergo oxidative metabolism without riboflavin coenzymes. Functional carnitine deficiency is revealed by elevated urinary excretion of adipic, suberic and ethylmalonic acid. The action of carnitine may be described as a key that opens the gate of energy flow in most cells

Treatment: Carnitine

Hippuric Acid-----------------------------------> *511,59 (10-400)

Implies high rate of intestinal bacteria

Arabinose 17,65 0-47----------------------------> *135 (Dec 2008)

Implies Yeast infection (Candida tenius)
D-Arabinitol is the only urinary biomarker of invasive Candida sp. overgrowth that has reliable scientific support.

- General Encourage high fiber diet, remove mucosal irritants such as allergenic or IgG-positive foods, alcohol, and NSAIDs
- Antibacterial Pharmaceutical: Amoxycillin/Clavulanic Acid. Natural: Goldenseal or other berberine- containing herbs, citrus seed extract, garlic, uva ursi, aloe vera, glycyrrhiza, olive leaf extract, garlic.
- Anti-fungal Pharmaceutical: Nystatin. Natural: See natural antibacterials plus oil of oregano, undecylenic acid and caprylic acid
- Anti-protozoal Pharmaceutical: Flagyl Natural: Goldenseal or other berberine- containing herbs, citrus seed extract, garlic, uva ursi, aloe vera, glycyrrhiza, olive leaf extract, garlic.
- Probiotic: L. acidophilus, L. sporogenes, Bifidobacteria sp., S. boulardii, soil organisms.
- Prebiotic Fructo-oligosaccharide (FOS), increase use of raw and cooked vegetables
- Mucosal Regeneration: Glutamine, pantothenic acid, deglycyrrhizinated licorice, slippery elm, oligopeptide preparations.

Citramalic 0,84 0-2-----------------------------> *2,52 (Dec 2008)

Also indicative of invasive candida, although less scientific.

3-Oxoglutaric acid 0 0-0,5--------------------------> *1,20 (Dec 2008)


2-oxo-glutaric acid *11.68 15-200 mmol/mcr--------> *2,59 (Dec 2008)

Citric Acid 518 180-560 nmol/mcr------------------> *718 (Dec 2008)

Arginine insufficiency quickly leads to hyperammonemia due to failure of ammonia removal. Citric acid, cisaconitic acid, isocitric acid and orotic acid appearance in urine are other biochemical markers of this condition.
Elevated Citric acid is also a sign of mitochondrial failure and toxicity or B-Complex deficiencies.