CFS / ME

Lab test done before taking Ursobilane treatment

2012-01-24T16:05:00.002+01:00

Total Bilirrubine: *1.6 (0-1.2)
Direct Bilirrubine: *0.5 (0-0.4)
Indirect Bilirrubine: *1.10 (0-1)
Amonio in serum: *60 (11-35)
Total Cholesterol: 215 (<220)
Triglicéridos: 92 (35-200)
HDL: *36 (>45 normalidad <35 Riesgo)
TC/(HDL-TC): *6 (<4.5)
LDL: *161 (<155 normalidad >180 Riesgo)
(LDL-TC)/(HDL-TC) *4.5 (<3.55)
GOT 28 (<45)
GPT 31 (<45)
GGT 12 (8-61)
Fosfotasa Alkaline 54 (25-100)
AC. Antitransglutaminasa IgA 14.9 (>15 Positive) (It is negative, but very close to the limit)

Cryptogenic Chronic Hepatitis ¿Cause or effect of CFS?

2011-12-23T02:48:00.002+01:00

I've seen my results with the hepatologist, no trace of virus B, C or CMV in my liver. But if there is a chronic inflammation that should not be there, and I have been diagnosed with cryptogenic chronic hepatitis (unknown etiology). I was prescribed a non fat diet, ursobilane 300mg (2-2-2) and sports. I see him again in 2 or 3 months.

He tells me that the reference values of GPT and GOT are about to be changed next year to "30" by medical consensus in Spain, instead of 42 as they are now. I have a current value of 41.

He assures me that I have chronic hepatitis, because He has touched my liver and it is confirmed my biopsy and high transaminases, although within range in the current standard reference range. It is also supported by the rest of analisis done before showing apoptosis along these years, such as a high granzyme B, RNase-L, elastase, PKR, free DNA circulating in blood and the FAS ligands.

I keep on wondering if this is cause or consequence of CFS, because cryptogenic does not really solve the puzzle.

One theory that comes to my mind is the following:

- CFS patients with undiagnosed autoimmune hepatitis, might be responding to Rituximab for being an autoimmune disease.
- CFS patients with chronic mutant hepatitis B or hidden hepatitis C, could be responding to Tenofovir (retroviral) for being a chronic viral disease.
- CFS patients with cryptogenic chronic hepatitis might respond to GcMaf if they carry an unknown pathogen.

They are just my theories, but in any case keep them in mind, because these are difficult to diagnose hepatitis cases and often go unnoticed by doctors.

In fact if your GPT and GOT are over 30 you should at least suspect, my hepatologist told me that in 2012 they will lower reference ranges for transaminases at 30 instead of 43 as they are today.

He also mentioned that physical examination of the liver requires a lot of experience and is not easy to detect hepatitis with the hands.

Finally, the 3 hepatitis described will not necessarily yield positive serology or even on PCR. Only a biopsy can rule it out with certainty.

Is CFS an Undiagnosed Liver disease?

2011-12-08T00:17:00.007+01:00

Today, they have started to see my biopsy, they still need to do more tests for the B virus, but they told me that I should not worry about my liver. There is no fibrosis there and is quite "healthy". But there is injury to the hepatocytes, but they still need to know if they are infected with hepatitis B virus, which could cause the injury.

In Pathology, they normally look at 3 parameters, in the first two I have a zero rank, which means I am okay. In the third one, which is the "hepatocyte necrosis" I rank 1 (range 1-3). So there is injury, but the liver is not really damaged as for today, therefore I have no prognosis for cirrhosis at all.

Nevertheless it could potentially explain part of my symptoms, because the liver lesion is present, but that's better to wait for the final report and the interpretation of my liver specialist.

Hepatocyte necrosis is closely linked to apoptosis (programmed cell death), and that is what I have seen in the many analysis that I have done since I fell sick in 2006:

- 2006 RNase-L, elastase and high PKR = programmed cell death -> immunity to fight against something (Redlabs-Belgium)
- 2009 free circulating DNA Very high = programmed cell death -> immunity to fight against something (Acumen-UK)
- 2010, abnormal levels of the ligands FAS = programmed cell death -> immunity to fight against something (Irsi Caixa, Barcelona)
- 2011, elevated Granzyme B = programmed cell death -> immunity to fight against something (Gregorio Marañón, Madrid)

So, apparently it does seem that whatever I have in the liver is related to my CFS history.

It was not easy at all to detect the damage in my liver:

During all these years, no wrong liver function blood standard test (2005-2011):

-All the blood work on liver enzymes came normal
-All liver function came normal (GPT/GOT)
-All B & C serologies came negative
-Even a PCR DNA on B virus came NEGATIVE! But that is because PCR has limitations in the number of copies per ml that they can detect, normally starting from 120 copies.

However, what was present in a more subliminal and less conclusive way, were these traces of other liver malfunction in "not liver exclusive link test": (2005-2011)

-Presence of ammonia in blood
-High levels of nitric oxide in blood
-frequent high levels of bilirubin in blood
-Occasional severe abdominal pain in the right upper quadrant that could last more than 8 hours, 3 times a year that I need to go to the hospital to get a pain killer in vein.
-Occasional mild jaundice
-Frequently elevated fibrinogen
-Protein C active frequently high
-Sleep inverted (cortisol inverted)
-Occasional itching
-Occasional acolia
-Occasional coluria
-Essential amino acid deficiency
-High levels of cholesterol and triglycerides
-HBc antibody-positive on three occasions, intercalated with negative results in many more occasions in the last 3 years.

In November 2011, a very sophisticated PCR technique was used to detect even a single copy of the virus per milliliter, and they found 13 copies in my case, so I was recommended a liver biopsy, which is where they have seen the damage to liver cells.

It is now clear to me that "something" has infected my hepatocytes, and that causes liver inflammation and injury.
The big question is whether it is a mutant version of hepatitis B virus in the pre-core S region, or a hidden hepatitis B virus in the liver, and that will tell me next week.

If this is confirmed, I believe many people with Chronic Fatigue Syndrome may be infected with an undiagnosed B virus that could explain at least part of the clinical symptoms they present. If that was the case, it could also explain why tenofovir therapy works in some patients with CFS.

Another possibility in many patients with CFS is a chronic autoimmune hepatitis is not my case. In autoimmune hepatitis predominantly female (78%) in the absence of virus serological markers, elevated serum levels of IgG, high titers of antibodies (ANA, SMA, anti-LKMI), and 60% have other autoimmune thyroiditis , rheumatoid arthritis, ulcerative colitis. In these cases, immunosuppressive therapy would be effective, so perhaps the work Rituximab in patients with CFS.

Bear in mind that both "autoimmune chronic hepatitis" and "chronic hepatitis by a mutan B virus of the Pre-core region" are not present in common serologies. Autoimmune hepatitis is treated with immunosupression, and chronic Hepatitis B is treated with retrovirals. That could potentially explain why Tenofovir or Rituximab have been effective in different subsets of CFS patients.

Mutant Chronic Hepatitis-B or Hidden Hepatitis-C

2011-11-29T01:07:00.009+01:00

Today I am going to talk about something I think is very important for all that you have a diagnosis of CFS.

As you know I have CFS diagnosed for 6 years now, and despite the fact that my serologies for hepatitis A, B and C were negative during these years, this year Gregorio Marañón Hospital and last year Carlos III detected B viruses in my blood test. This came as a surprise because I was vaccinated against Hepatitis B and I already passed Hepatitis A.

As you can see the evolution of these blood tests, surface antigen HBs came out negative ALWAYS, however HBc core antibody was positive on 2 occasions since 2009. Moreover HBe antigen was detected in blood also on two occasions, and there is as well signs of an infectious component when we observe 2 (IL-2R) in December 2010.

The interpretation of this evolution is NOT easy. Firstly because normally is not standardized to test for HBc nor HBe, and secondly because these results may be interpreted in isolation as a "false positive" because they do not fit together well with a negative HBs Ag.

However Gregorio Marañón Hospital advised me to go for a good Liver specialist to undertake a thorough study, because the B virus that they saw was not from the vaccine. For this reason I went to Vicente Carreño, which is the number 1 in Spain.

Dr. Carreño checked my liver with his hands and it was 2 cm rhomboid (sorry for this translation), which signals inflammation, and because of the abnormalities observed in the blood work, He stated that I could be infected with the Hepatitis B virus, despite of the vaccine. Apparently this is a possibility, although not everybody is aware of it.

There are several types of the B virus, and to some of them the vaccine is not effective. Also it can go unnoticed in a normal hepatitis blood work. So He prescribed some special molecular blood work at NUCLEOTEX laboratory in Spain that performs molecular tests to detect two possible cases:

-Hidden Hepatitis C
-Mutant Hepatitis B in Pre-S region

My Results:

Hepatitis B virus:

PCR DNA (ultracentrifugation): 13 copies / ml
HBV-DNA-PCR PBMC NEGATIVE
Proliferation of CD4 + T lymphocytes specific B virus
S (HBs) NEGATIVE
Core (HBc) NEGATIVE
E (HBe) NEGATIVE

Hepatitis C virus:
HCV RNA-(PCR) in PBMC NEGATIVE
PCR-RNA (ultracentrifugation) NEGATIVE
Proliferation of CD4 + T lymphocytes specific to hepatitis C virus
Core NEGATIVE
NS3 (Helicase) NEGATIVE
NS4 NEGATIVE

Although at first glance it seems all negative, it is not. These tests show there is B virus in my blood (13 copies per ml).
Bear in mind that the standard DNA testing for B & C virus are not as sensible as the one I did here in Spain, normally they have a limitation: (116 to 989,400,000 copies/mL). In my case, I only had 13 copies/ml, therefore I would have come negative in standard DNA testing. This is a very low titer, but still shows is positive. At this point is not contagious, but if it peaks, it could be. Another important factor is that the titer might be very low in blood but not necessarily in the liver. It could also be a "false positive" therefore it needs to be confirmed with a biopsy.

For this reason He recommends a biopsy to confirm the infection and liver status, which not only going to look Hepatitis B and C, but also inflammation, tissue conditions, etc. The sample will frozen just in case more things need to be tested at a later stage (i.e. HGRV) .

In view of these results, the observed abnormalities in previous blood test and my clinical history, it is in the opinion of Dr. Carreño a must to perform a biopsy to confirm the findings.

When confirmed, chronic mutant hepatitis B, is treated with retrovirals (Tenofovir), normally for 6 months, given that this kind of hepatitis is more easily cured than regular chronic Hepatitis B.

I've asked him if it is possible that during these 6 years that I have thought to have CFS, perhaps I simply have had chronic mutant Hepatitis B undiagnosed, and his answer was YES.

It is too early to draw conclusions, however I think it's important enough share this writing, when I know the final results of the biopsy I will let you know. If it turns to be the case, I think everyone with a diagnosis of CFS should go through a good hepatologist who can rule out this possibility.

The standard treatment for this kind of mutant hepatitis is Tenofovir, and it comes to mind to think that people with XMRV treated with Tenofovir, might actually be responding because they might carry an undiagnosed B mutant B virus in the pre core S region.

As I said, it has taken me 6 years of running from one doctor to another to find out, is not an easy diagnosis. And I am not suspect of a wrong CFS diagnosis, De Meirleir, among 6 other specialist diagnosed me in 2006 with my RNASe-L, PKR, Elastase etc. Shara Mhyll also did with my mitochondrial failure. I also met the criteria of Cheney of diastolic disfunction of the left ventricle, Irsi Caixa also observed the same pattern than the CFS group studied with NK & CD8 abnormalities.

I could go on and on...but what I mean with this is that this B virus may be behind many many CFS diagnosed patients, and Tenofovir may be doing the trick for that reason. I also read that GcMAF is a more efficient treatment for Hepatitis B than retrovirals, and that would explain why some patients are responding to this therapy.

Having normal levels of GPT/GPO, and negative serology for hepatitis is not enough to rule it out as you could see. Not that you can do biopsy directly, first make the liver specialist need to run the molecular blood work, and if the virus is found, it is recommended to run the biopsy to confirm it. To be completely honest, in the opinion of my doctor, even if the blood work came negative He would have recommended a biopsy to make sure, given the many years of symptoms of hepatitis like that I had. Bear in mind that you need a very good specialist that is aware of these advances. They are published by the way.

To be continued ...

XMRV Workshop in Barcelona (November 2010)

2010-11-05T23:57:00.002+01:00

A new XMRV Workshop has taken place today in Vall Hebron Hospital in Barcelona. We have had five lectures, all of them full of the history of all the papers that have been published since Dr. Judy Mikovits’s paper came out in September 2009. But each speaker has also given a summary of what are they working on.

Dr. José Alegre opened the session and was the first to speak. He is one of the most well known specialists in CFS, and as soon as the Science paper was published, he immediately tried to involve a group of Biologists from his Hospital in this research. One of the things mentioned by Dr. Alegre was the fact that pregnant women seem to have a remission of their symptoms during their pregnancy and a relapse right after they give birth, which points out a hormonal component in this illness. He also mentioned that it would be interesting to research the genome of post polio patients given that they have similar fatigue symptoms as CFS patients, and in that way it could be understood for both conditions.

Dr. Cecilia Cabrera from IrsiCaixa talked for an hour. Dr. Cabrera discussed that the structure of XMRV was simpler that HIV, and so far, only 3 genes had been identified: gag, pal and M. She mentioned the great importance of Dr. Ila Singh’s study with animals, and all they have learned about XMRV. Then she said that they have tested 11 patients and done 4 controls, that they have identified sequences of XMRV (not polytrophic virus) in B cells of CFS patients and controls, and that they are developing models of infection in human tissues in vitro, and in this way was able to study the viral pathogenicity. In their studies they had observed that XMRV was being restricted by the APO-B system, and also that the lymphoid tissue could act as a reservoir.

Dr. Cabrera also motioned that there is a common effort overseas to find a common assay to allow everybody to detect XMRV in the same way, and this is being developed by the SRWG (Scientific Research Working Group) which is conformed by the Blood Working Group, Retrovirologist teams, CFS researchers and Federal Agencies.

Dr. José Montoya of Stanford University was next. He started explaining that six years ago he met his first CFS patient, and since then he has visited more than 450. He is sure that you can develop CFS after a viral infection, and he believes that 11 % of patients that suffer EBV, Q fever, Ross River virus, etc, can end up with a CFS. About Dr. Judy Mikovit’s paper he remarked that since it was published everybody is turning to CFS with the intention to find out all they can because they have completely changed their opinion.

In a random, double-blind, placebo-controlled study they have found that there was a clinical improvement in patients who were taking valganciclovir for a period of more than six months, compared with placebo. CFS patients met Fukuda’s international criteria and had high antibody data against HHV-6 and EBV. Several immunological markers changed significantly in the treated patients that were not seen in patients taking placebo. This study will be submitted for publication this month, and provides evidence that CFS is a real illness that can be caused by an infectious agent that can be treated with prolonged antiviral intervention. They are also working on the hypothesis that besides the antiviral mechanism there could also be an immune modulator component in the good results.

The dramatic improvement of these patients was both cognitive and physical. Also worth to mention that the medication did not work in every case, and they are working on markers that could help ascertain the suitability of the medication each individual patient. Among the markers monocytes are a good candidate given that in the study they came down significantly and then normalized in the patients where the drug did work. The cytokine profile of the patients also played a role in following the good effects of this medication, specifically:IL5, IL17F, ENA78, EOTAXIN, IP10… Additionally, Dr. Montoya mentioned that HHV6 plays a unique role because it integrated in the chromosome of CFS patients, which is simply not normal in a virus.

Dr. Montoya remarked that the Early Antigen was used to prevent the relapses in naso-pharyngeal cancer, and in CFS patients is very elevated even after 20 years of the acute infection, which is simply not normal. Therefore this is a marker He uses for patients selection in the study.

Dra. Carmen Mendoza from Hospital Carlos III of Madrid did not talked much on XMRV, but instead on HIV. Off the record She mentioned that they have found 0% of XMRV in their lab, and in my view She was a bit lost on the latest advances on XMRV research, as She was still talking about geographical distribution and contamination as potential reasons not to find XMRV in Europe, We had to remind her that XMRV has been found in Spain, Italy, Holland, Norway, UK…It was a bit discouraging to find out that the “extra effort” that Carlos III plans to do is to send to Abbot Labs in the US, the blood of the patients that already they declared “negative” to perform a serological test, that on the other hand has already been criticized of not being accurate out of the animal model, this means in humans. Therefore we do not expect Carlos III to advance on the XMRV research, and postulates to be the Spanish publicly financed entity that slows down the research process with meaningless negative studies.

Dr. Jordi Petriz, of the Vall Hebron Hospital. He told us that the aim of his research with Dr. Alegre was the development of a diagnosis tool for the disease based on the functional response of the cells of CFS patients. It was also mentioned that the interferon response was key to allow XMRV to do damage in the health of CFS patients.

They will use, functional flow cytometry, a very sophisticated technology on the whole blood of people with CFS infected with XMRV, and compare the results with appropriate controls, in the hope of finding a pattern and goal differential characteristic of CFS. These techniques will also allow the analysis of the lymphocytes in the study of CFS patient’s immune system. He has also widely described the study that is focused on neutrophil oxidative metabolism and how this may affect their function. As they plan to study the membrane structure of CFS patients, it was suggested to him in the Q&A to have a look on the paper published on Mitochondrial dysfunction a bacterial translocation by Sarah Mhyll and Kenny De Meirleir.

Our conclusion is that all of them have mentioned the importance of an animal model to study the pathogenesis of XMRV. It’s also very important to have accepted tools to work with, and this means the urgent need of a universal kit. They are all working in the same direction, they are sharing lots of data, samples, etc, and they all agreed with the great complicity between the different groups, which they had not observed so far, for the other diseases they have worked on. Good long term perspectives.

Interesting link for Lab test interpretation on CFS and FM

2010-10-27T12:39:00.001+02:00

http://chronicfatigue.about.com/b/2010/10/26/interpreting-lab-tests-with-fibromyalgia-chronic-fatigue-syndrome.htm

http://labtestinterpreter.about.com/

Friends of the Institute

2010-10-17T01:23:00.000+02:00

Friends of the Institute

For a donation of as little as $60.00 per year, you can become a "Friend of the Institute." You will receive a beautiful WPI Butterfly logo pin, invitations to WPI events, our newsletter and special email updates.

Click here to find out how you can make a donation.

En Español:

Amigos del Instituto

Por una donación de tan sólo $ 60.00 por año, puedes convertirte en un "amigo del Instituto." Recibirás un hermoso pin del WPI con el logotipo de la mariposa, invitaciones a eventos del WPI, el boletín de noticias y actualizaciones especiales por correo electrónico.

Haz clic aquí para saber cómo se puede hacer una donación.

Natural treatments for lowering cholesterol

2010-10-05T01:29:00.001+02:00

Treatments

1. Begin with an exercise program and, if overweight, bring your weight down.

2. In men, especially if you are overweight, have high blood pressure, and have diabetes (or are prediabetic), this may ALL be coming from too low of a testosterone level. If your total testosterone is under 450 on the blood test, I would consider using prescription natural testosterone (Androgel or Testim or compounded) to bring your level up over 700.

3. In women, consider a trial of prescription natural Armour Thyroid—even if the labs are normal. High cholesterol is often caused by low thyroid and the tests are horribly unreliable (they miss the majority of those who need thyroid hormone). Consider an exercise stress test before beginning exercise or thyroid. Both are very healthy for the heart, but could unmask heart disease in those with severe heart blockages.

4. Enjoy eating your eggs and cholesterol. Study after study shows that eating 6 eggs a day for 6 weeks has no effect on cholesterol blood levels. Yet this myth persists. Avoid saturated fats (hard fats) and margarine (butter is much healthier and tastier than margarine).

5. Eat 1-3 cloves of garlic a day. Crushed into olive oil, it makes a yummy treat that may drop your cholesterol. In addition, have a cereal with oats (e.g., Life, Cheerios, Quaker Oats Squares) for breakfast. Simply adding garlic and oats to your diet can lower your cholesterol almost as much as many medications. Artichokes also lower cholesterol.

6. Herbals can be quite effective as well at maintaining a healthy cholesterol level. If you can find one I recommend a product that contains inositol hexaniacinate (flush free niacin), berberine, chromium, artichoke, policosanol and deodorized garlic.

7. If triglycerides are also elevated, especially be sure to avoid sweets and add Acetyl-L-Carnitine 1,000 mg a day to the above for 3 months to see if it lowers the triglycerides.

8. If on cholesterol lowering medications (statins), be sure to take Coenzyme Q10 (200 mg a day).

Source: http://www.healthiertalk.com/8-tips-lower-your-cholesterol-naturally-2532

Published positive XMRV studies

2010-09-15T03:09:00.001+02:00

Published study by FDA in PNAS 2 weeks ago:
http://www.pnas.org/content/early/2010/08/16/1006901107.full.pdf+html

2009 Lombardi study in Science:
http://www.sciencemag.org/cgi/content/abstract/1179052?ijkey=m3wzKT4yJqEyk&keytype=ref&siteid=sci

Press releases of Iris Caixa about their XMRV study in Spain:
http://www.elperiodico.com/es/noticias/sociedad/20100907/detectado-virus-comun-dos-cada-tres-enfermos-fatiga-cronica/469776.shtml

http://www.irsicaixa.org/es/premsa

Regarding the FDA/NIH paper, and its impact of retrovirologist in the world

2010-07-24T04:50:00.007+02:00

I saw Dr. Soriano from Carlos III, 2 weeks ago, because He tested me for XMRV, and He told me that I was NEGATIVE, the same as the rest of CFS patients He tested. He was convinced that the was no link between CFS and XMRV because:

1) He was unable to find it in NONE of the CFS patients He tested, there was no control group, as there was no official study.
2) He was able to detect it in Prostate Cancer patients, and "other" patients, He said... I assume HIV patients, although He did not say. But He is number 1 in HIV in Spain.
3) For CFS patients He used the same primers than in the Science study, He did PCR and serological test from Abbott Labs.

I tried to explain him about the unpublished study by NIH and FDA, but He would not listen, He only talked about the CDC negative study, and He thinks the Lombardi study is a "bluff"

Both the CDC and the NIH/FDA groups submitted research articles to separate journals for publication, and those journals have completed their respective peer-reviews. However, in the "interest of scientific inquiry and collaboration across HHS", both groups of scientists agreed to conduct further assessments to investigate the discrepancies between their studies prior to publication.

CDC completed their assessment and their paper was published in Retrovirology on July 1, 2010. The NIH/FDA study was further reviewed by the journal editor and currently awaits publication. Its release is controlled by the journal.

The "second look" at both the CDC and the FDA/NIH papers, is kind of dogi, when only one paper is published after "revision".
Now the journal makes the final call, but if they are not satisfied, they can still reject the FDA/NIH paper. This is worrysome.

Scientist do not look at blogs, or articles in newspapers, they only look at published data, and NO positive study is published on CFS patients for XMRV besides the one in Science. If that preveils, they will stop paying attention to XMRV / ME.

I think is dangerous that by September the NIH has not released their study, but I would not know how to force that, other than the media.

Directory of Who is Who in Spain for CFS

2010-07-12T09:37:00.003+02:00

Specialty in alphabetical order:

LAWYERS

Lawyer to help with disability
James Cortes
Collective Ronda
Ronda San Pere, 56 Pral.
93 268 21 99
jcortes@cronda.coop

Enrique Bitchatchi (medical expertise to make in case of CFS, Fibro or SQM) (medical and master's in public health and labor) with a long history in various countries working with these diseases. Collectiu has worked for the Round and the Joan XXIII Hospital. You now have more availability.
If anyone needs to contact their phone and email is 93.4519065 eboccupenviron@gmail.com

Disability attorney in Madrid (This works with Dr. Quintana)
Lourdes: 667 77 79 93 lourdes_mart@yahoo.es

DIGESTIVE

Visit Gascón Lucia by many mutual.
Plaza Dr. I. Barraquer, 6 pral 2 ª Barcelona
tel: 93 439 49 99
email: consulta@luciagascon.com

AUTISM

Dr. Maria Jesus Ortiz Clavera
Col. No. 44 871
General Medicine, Pediatrics, Microbiology, Medicine and Biological Natural
consultoria@medicina-natural.com

Paseo Lluis Companys, 12 5-a
08 018-Barcelona
Tel 934856666
Mobile-670836454

Avenida Almendros, 14
28 529-Rivas-Vaciamadrid
Madrid

CARDIOLOGY

Miguel Campillo
Visit by some mutual
Provence, 74, entlo, 3rd Barcelona
tel: 93 410 85 43

PHYSIOTHERAPY / ACUPUNCTURE / Naturopathy

Juan Mesa (Mesalud) in Madrid but I do not remember the address.
914484424

CENTRO DE CHIEN-KANG ACUPUNCTURE.
Sagasta Street 8, 28004 Madrid
Phone: 91 532 9292

LABORATORIES

CERBAS Laboratories

It is good to start with the realization of lymphocyte typing, ILMI immunity studies and serology tests for Epstein Barr, Cytomegalovirus, Herpes 1,2 and 6, Herpes zoster and Borrelia. If inflammation is necessary to add a protein profile.

Cerb has three points of collection in Madrid:
- Laboratorios Lopez Salcedo, Orense 29, 2 º D-28020m, tel 915 559 605.
- Medical Lab Carpetana Cent, Manuel Alvarez 4 - 28025M, tel 914 662 474.
- Health Analysis Center, Bravo Murillo 81 low - 28003m, tel 915 334 086.

Outside Madrid:
Krumpp 1, rue Kuhn - 67000 Strasbourg, tel 03 88528200 www.laboklumpp.com

METAMETRIX
Stephanie E. Wickham
Consumer / Sales Liaison
sewickham@metametrix.com
www.metametrix.com
Tel: +16786382910

If you want a very good analysis of feces to see is your flora and / or have some type of parasite, I recommend Metametrix test in the U.S., and using PCR with 100% reliability. The only drawback for being in the U.S. is sending you a cooler you can ask cork in a hospital, they tend to overrun them in the laboratories of the samples they receive. It is important that the sample does not freeze, but to be refrigerated all the time. This bubble paper wrapped with the sample, and added four blocks of blue ice (they are like a hard blue plastic bags containing water and you have to put in the freezer until just before shipping is when you include them in the cooler cork without directly touching the sample that will be protected by bubble wrap. So FedEx and it will take to Metametrix. Try it on a Monday so there is no weekend in the middle.

Genova Diagnostics
www.genovadiagnostics.com
Branch Madrid: Holistic Medicine
Sierra Gorda, 18
28031 Madrid
Patricia Martinez +34633393803
smhela@yahoo.es

Data Doctors
Customer Service
Doctor's Data, Inc.
3755 Illinois Avenue
St. Charles, IL 60174-2420
U.S.A
E-mail: inquiries@doctorsdata.com
Phone: 800.323.2784 (USA & Canada)
0871.218.0052 (United Kingdom)
630.377.8139 (Elsewhere)

Sabater Laboratory for genetic profile:
London, 6 tel. 93 444 32 00 (for 7-21 h. 9
Clínica del Pilar c / Balmes, 271 tel. 93 237 57 81 (24 hours)
Pg Bonanova Bonanova Lab, tel 1967-1967. 93 253 January 1949
Gracia-Guinardó Secretary Coloma, 142 tel. 93,285 36 65

European Laboratory of Nutrients
Dr. Voogelar
Regulierenring 9
3981 LA Bunnik
The Netherlands
Phone: +31 30 2871492
Fax: +31 30 2802688
eln@healthdiagnostics.nl

BIOLOGICAL MEDICINE & IMMUNOLOGY

Rigau Josepa
Av Catalunya, 12, 3 º, 1 ª
43002 Tarragona
+34977220358

Dr. Antonio Marco Choven
Pasaje Dr. Serra, 1-3 ª pta 9. - 46004 Valencia
Tel: 96 351 43 83 / 96 352 04 02
Fax: 96 352 41 71
Email: drmarcochover@drmarcochover.com
www.drmarcochover.com

Dr. Kurk
CVS / ME centrum Amsterdam
Waalstraat 25-31
1078 BR Amsterdam
Tel: 020 470 62 90
Fax: 020 470 62 99
info@cvscentrum.nl
afspraak@cvscentrum.nl

INTERNIST

In Belgium
Prof. KENNY DE MEIRLEIR
Protea Biopharma
Z.1 Researchpark 100
B-1731 Belgium Zellik
Email: info@proteabiopharma.com
Phone: +32 2 481 53 10
Fax: +32 2 481 53 11

In Barcelona:
Ana Maria Garcia Quintana col # 25 309
Barcelona Centro Medico Delfos
Military Hospital Avenue, 149-161
08023 Barcelona Spain
Tel: +3493 254 50 78

In Madrid:
UNIT OF FIBROMYALGIA AND CHRONIC FATIGUE
www.novoclinic.com
Prof. KENNY DE MEIRLEIR
Dr. Ana García Quintana
33 21 33 902
91 490 55 69
Centro Medico La Moraleja
@ centromedicolamoraleja.com c.m.moraleja
Phone: 916500612
Phone 2: 916 500 662

Ana María Moreno: Want to replicate the analysis of mitochondrial dysfunction Mac Laren, and validates the level UK study Spanish, because the doctors here do not ignore this study, as well as being in English, do not understand its meaning . This doctor wants to study the FM and CFS at the mitochondrial level.

TRADITIONAL CHINESE MEDICINE

Chinesse Medical Center TASTLY GROUP BV
67-73 Geldersekade
Amsterdam 1011EK
Holland
+3120 623 50 60
info@shenzhou.com
http://www.shenzhou.com/

HOLISTIC DENTISTRY

www.odontologia-holistica.com
Judith Maria Flores Gelfo
Collegiate Odontóloga 3623
C / Alfonso XII, 58
28014 Madrid (Spain)
Tel 91 528 66 14
91 527 17 65

In Barcelona:
Carmen Ros
Corsica, phone 378 934 570 012

ONCOLOGY
Aviano / Umberto Tirelli (specialist in CFS in Italy)
www.umbertotirelli.it
utirelli@cro.it

MULTIPLE CHEMICAL SENSITIVITY

Alborada Foundation
Crtra. M-600 Km 32.400
Brunete (Madrid 28 690)
E-Mail: falborada@orange.es
www.fundacion-alborada.org

SUPPLEMENTS

Maybe You Can try Mutaflor, contains Escherichia coli That, Which is NECESSARY for the rest of flora to grow. If you are deficient On this one, no matter how many strains of lactobacillus or bifidus You Take, They Will Not Grow, and pathogen will.

Here is how to buy MUTAFLOR:

MUTAFLOR
Metropolitan Pharmacy
Apotheke am Flughafen München
Walter M. Verfürth, E.K.
Zentralbereich, Ebene 03
Terminal 2, Ebene 04 und 05
Flughafen München 85 356
Tel: +49 - 89 - 978 802 200
Fax: +49 - 89 - 978 802 206
emails:
fra@metropolitan-pharmacy.de
muc@metropolitan-pharmacy.de
@ metropolitan-pharmacy.de jose.dias
Amtsgericht München HRA 68 267
From day 1 to day 4, one capsule daily Mutaflor, Then 2 capsules daily.
The dose should be complete Taken daily with a meal, if possible with breakfast, and an Appropriate amount of fluid.
Storage: 2 ° C - 8 ° C

You will Benefit from antivirals Labolife Only When your viral load at the IgG level is higher than 4 times the reference value of your lab, if this is not the case, it does not make sense to take Labolife for Epstein Barr or Citomegalovirus:

ANTIVIRAL LABOLIFE

How to get Labolife? www.labolife.com It is for sale in Spain, Italy and Belgium... Try to contact them, maybe there is a way to be sold overseas...

Labo'Life Belgium
Parc scientifique CREALYS
Rue Camille Hubert, 11
5032 Gembloux
BELGIQUE
tel : 00 32 81 40 87 81 - info@labolifebelgium.com

Labo'Life España S.A.
Avenida des Raiguer, 7
07330 Consell - Majorque
SPAIN
tel : 00 34 971 14 20 35 - info@labolifeesp.com

Labo'Life Italia s.r.l
Via Andrea Costa, 2
20131 Milano
ITALY
tel : 00 39 02 763 16 146 - info@labolifeitalia.it

I have something else to add regarding treating EBV with Labolife:

For EBV there are 2 available products

90% of the cases, show an hiporeactivity (that is to say, although some parameter of the lynfocite typology is elevated, some other is diminished CD3 or CD54 etc...) In this case we apply 2LEBV (contains interleukin that activate the immune system + nucleic acids specific for this virus)

The rest 10%, the show immune hiperreactivity (that is to say, some or all parameters of the lynfocite typology are elevated, but none is diminished) In this case we use 2LXFS (Contains interleukins antiinflamatory + nucleic acid secific for EBV+CMV+H.Zoster)
Dose is 1 capsule a day, open it and put in below the tongue, always following the numeration and with an empty stomach, preferably not in the night.

H2S in urine test used as a diagnosis of CFS by KENNY DE MEIRLEIR

In KENNY DE MEIRLEIR Paper explaining the H2S:
http://www.scribd.com/doc/27444865/De-Meirleir-Press-Conference-End-of-a-Medical-Denial

Link to ask the urine test and measure the H2S:
http://www.proteabiopharma.com/page/order-test.php

Article by Dr. Mhyll speaking of treatment with an antibiotic is not absorbed into blood and acts only in the colon on rifaximin H2S-producing bacteria:
http://www.prohealth.com/ME-CFS/library/showArticle.cfm?libid=14757

KINESIOLOGY

The dr. Guxens and dramatic. Rosa Junyent
IGEM c / Marina, 63 bjos. 2nd. (Barcelona)
Tel 932 462 749
www.institut-igem.com

GUESS WHAT?

2010-07-06T12:01:00.003+02:00

XMRV: cause or effect of immunosuppression of Chronic Fatigue Syndrome? A look through the past retroviral link.

2010-07-05T14:37:00.012+02:00

RELEVANT NEWS:

The retrovirus Xenotropic Murine Leukemia Virus Related (XMRV) is a new human pathogen, and possibly the most important scientific discovery since HIV. Has been linked to prostate cancer and Chronic Fatigue Syndrome (CFS).

If confirmed by independent laboratories and the prevalence XMRV association with prostate cancer and CFS according to studies published in the prestigious journal Science, would reach 4% of world population infected, but asymptomatic at this time.

This Retroviruses, in the same family as HIV (AIDS) and HTLV (leukemia), is the third pathogenic retrovirus discovered in humans. Is known to exist for years in mice, but only recently has been discovered in humans, in tissues of patients with prostate cancer. The prostate cancer patients share with Chronic Fatigue Syndrome have altered the antiviral enzyme called RNase-L.

This is the clue that led to Whittermore Peterson Institute (WPI) to connect the two conditions, culminating his studies last October with the publication in Science of a surprising finding, was achieved by isolating the retrovirus XMRV in the nucleus of blood cells 67% of CFS patients and 3.7% of the healthy population. (1-2) After the publication, were improved detection methods and antibodies were found in plasma of 99% of CFS patients, while maintaining the same percentage in the healthy population.

These results have moved scientists around the world to run additional studies that answer the important questions that arise now: modes of transmission of the retrovirus that is present in the blood and body fluids, its pathogenicity and the potential threat to blood banks. Pending to validate the data published by the WPI in Science with other studies, replicated in independent laboratories, the current estimate of carriers gives a figure of 3.7% of the population, which is currently asymptomatic.

Another study just published in Germany, shows a similar percentage XMRV prevalence in the study population: 3.2%. although this percentage rises close to 10% in patients that have suffered transplants and are taking heavy medications. Given that XMRV shows a very little number in titer, this 10% seems more plausible as a population prevalence. In the same direction points an unpublished study by the FDA and NIH that shows up to 7% prevalence of the retrovirus in the general population.

HISTORY OF A MEDICAL SCANDAL:

The association of XMRV with SFC, is a major milestone in the research of the past 20 years in relation to this disease. The SFC was released in 1984, in Incline Village near Lake Tahoe in Nevada in the U.S. Several hundred people developed some kind of flu that ended in neurological and immunological problems, and suffering several viral infections (CMV, EBV, HHV-6) at a time.

Doctors Paul Cheney and Daniel Peterson asked for help from Centers for Disease Control and Prevention (CDC) in Atlanta, which concluded that these patients were not "ordinary Americans." Thus, the entire responsibility of caring and research, these two young men fell to rural doctors. In the early 90s, everyone was talking about the origin of CFS should be a retrovirus and AIDS specialist, Dr. Nancy Klimas, stated that CFS was a form of acquired immunodeficiency.

In early 1990, a virologist from the Wistar Institute, Dr. Elaine DeFreitas, reported that he had found the DNA of a retrovirus in CFS patients. The CDC is not validated their discovery and publicly criticized claims that their blood samples were contaminated by a "rat virus itself, and thus ending the career of this promising young researcher

Now, 20 years later, when scientific studies linking the SFC again with a retrovirus associated with prostate cancer earlier, both the psychiatric lobby and governments, driven by budgetary interests, strive to return to play down the discovery.

There have been three studies in Europe who took to replicate the study of WPI without following his own mythology, claiming not to have detected the XMRV in European patients. The first negative study is published by the team psychiatrist Simon Wessely - head of the SFC in the UK in January 2010 in a magazine on-line payment.

The second study, also in the UK and with the same result, was followed by a third in Holland last February, with the help of researchers from the UMC St. Radboud, who announced the retrovirus had not found XMRV in Dutchmen patients' blood. However, U.S. investigators said they found it XMRV virus in blood samples from the same patients in 3 of the 7 samples exchanged (3-9). This was a scandal in the press in Holland.

Dr. Suzanne Vernon, virologist with extensive experience, has stated that it can be considered the work published by the British as a valid attempt to replicate the discovery of XMRV since has not followed the methodology that led to the three laboratories Americans to discover the relationship between XMRV and the SFC, and denounced the irregular procedures followed in the British case.

Anticipating what was to happen, the associations of British CFS patients (approximately 250,000 cases diagnosed, and as many undiagnosed according to their estimates), with funds raised by donations from the patients themselves, had already commissioned a laboratory in Sweden retrovirology replication of the discovery, because "they had no assurance that the study be done in Britain came to light a single positive result." Individuals and families are counting on going studies will not show a single positive case of infection in Europe, which would serve their governments as justification for cost-cutting research on these diseases.

In Spain, we have better luck. Retrovirology Laboratory of the Hospital de Badalona Germans Trias has been put to work, and has invited itself Mikovits Judy, who published in Science last October XMRV association with CFS, so that they trained in the difficult and laborious technique has been developed. Unfortunately, this laboratory has not received any subsidy, and are themselves sick, and the United Kingdom, who are paying for the research. SFC also Unit of Hospital del Valle d'Hebron in Barcelona is yet to be approved to start a test study.

In this sense, last May in Madrid held a seminar organized by Red Labs laboratories that are working to develop a diagnostic test XMRV will be ready for the summer of 2010. In the U.S. test is now available.

The controversy over negative studies published flared even more when just days ago was published a fourth study in Europe (10), where CFS patients are not involved and where it is found in the respiratory tract XMRV of samples asymptomatic people with a prevalence of 3.2% (similar to 3.7% detected in the American study published in Science), and increasing that percentage nearly 10% in immunocompromised patients who had undergone some type of transplant.

These results give reason to believe that the detection rate increased by two possible reasons: The XMRV could be reactivated if there is an immunodeficiency and / or transplant patients may have contracted the XMRV for a transplant or transfusion. In any case not yet confirmed if the retrovirus is the cause or effect of a weak immune system, and therefore remains a suspect trigger diseases like prostate cancer, and SFC among others.

THE XMRV COULD BE A THREAT TO THE HEALTH OF THE RECIPIENTS OF BLOOD TO A TRANSPLANT CANDIDATES. (HHS Blood Safety Committee USA)

The XMRV transmitted through body fluids and various are the countries that have banned blood donations from patients with Chronic Fatigue Syndrome, regardless of health status of patients, in order to prevent infections in donated blood and transplantation. First it was Canada (11) and has been followed by Australia (12) and New Zealand (13), in the U.S. have banned the carrying XMRV donation and is being studied to generalize to patients diagnosed with CFS, but in Europe there has not risen any prohibition or follow any protocol to protect the blood banks.

Any person regardless of sex, age or sexual orientation can get this debilitating disease, which already affects 17 million people worldwide, and while it is confirmed whether the XMRV is cause or effect of CFS, which is known as XMRV is that poses a risk of infection through transfusion or organ transplant (14-15).

The FDA and NIH have confirmed and are about to publish it independently validated study published last October by the group on the XMRV Lombardi. They confirm that the transmission of blood-XMRV is more than probable, and the clear association with CFS. They also confirm that the XMRV and other leukemia-related virus in rodents are present in blood banks with a prevalence between 3% and 7% (16).

Unfortunately this information was made public by a leak of a journalist Dutchman will not see the light in the short term. The reason that these results of the FDA and NIH are in conflict with a third independent study by a state agency of the U.S. government, the CDC.

Both studies were approved and ready for publication, but the government has decided to push back the publication of positive study of the FDA and the NIH, saying they needed to do more research in the coming weeks to verify "the accuracy" of these results, and yet without changing the study published negative CDC.

It seems that history repeats what has already happened with De Freitas 20 years ago, where he wanted to bury the relationship of a retrovirus with CFS, and now again the government is withdrawing its own study which confirms this relation discovered last Lombardi by the group in October.

The XMRV also be involved in prostate cancer and will hardly be able to bury the truth comes to light, despite wishing to study implicitly censuring the FDA and the NIH as is happening now. But I would welcome the media to take up this history to put pressure on governments and that this study will see the light as soon as possible in their original form as it was when it won approval for publication.

In these videos retrieved from the past thanks to the web www.rescindinc.org, we can observe everything that is happening now, rains, it pours, it's the same story of the past.

Click on Video1:

Primetime from Barborka on Vimeo.

Click on Video2:

DVD Video Recording from Barborka on Vimeo.

Now, many years later, a documentary for release in 2011 is telling exactly the same story, and explaining how this whole story has been covered up for all this years, and seems to be covered again after the positive study from FDA and NIH has also been pulled out from release.

Click on Video 3:

What About Me? US Promo (Spanish Subtitles) from Double D Productions on Vimeo.

The group of patients required written last year by the Ministry of Health in Spain a blood test XMRV within Social Security, to support the clinical diagnosis of Chronic Fatigue Syndrome. However, the Ministry of Health responded that it considered it necessary, and still does not take any measures to protect our blood banks, arguing that only accept samples from people who are in good health.

The problem is that nearly 4% of the asymptomatic population would carry the point XMRV as both the American and German study, published recently. Moreover, some CFS patients have periods of remission can be apparently healthy with the authorities and give blood. In conclusion, not only are not taking any preventive measures in our country to what is a serious potential threat to public health and also to pronounce officially no respect (17).

This issue is not only exceptionally important for all patients with Chronic Fatigue Syndrome Spanish, who spend years journeying through different doctors until a diagnosis, a test XMRV could become a biomarker and save patients and their families suffering as endless as unnecessary. It is society as a whole that should react by the negligence of the Ministry of Health, which is not taking preventive measures - as it did in the 80s with HIV and hepatitis C - the threat of infection by retroviruses transfusion or transplantation

WHY NOT INVEST IN RESEARCH OF CFS?

In view of Professor Kenny Meirlaen, in a recent television interview of the Netherlands, the reason is obvious, the costs would be enormous for governments to bear when the disease and is more economical relegated to prescribe antidepressants and psychiatric field. It happened with other diseases in the past such as HIV or leprosy, and now hides head in the sand by the side of governments, because they fear what may be discovered (18).

Chronic Fatigue Syndrome affects 17 million people worldwide, and 240,000 people in Spain, being able to double that figure with the undiagnosed patients.
Research spending in the U.S. CDC for CFS is a thousand times lower than the $ 3,000 million per year for HIV research, but paradoxically the prevalence of CFS is twice that of HIV or Multiple Sclerosis. CFS is incurable and any of us can get this disease, and you should care because tomorrow could be you.

Signed. Carlos Gonzalez

The Chronic Fatigue Syndrome (CFS), a disease classified by WHO with the number G 93.3.en ICD-10 is an organic disease, and multisystem disease. You can progressively affect the immune system, neurological, cardiovascular and endocrine systems and cause characterized by severe fatigue, substantial loss of concentration and memory, spatial disorientation, restless sleep, intolerance to light, sound and temperature changes, intolerance to emotional stress and physical activity, muscle aches and joint pain, multiple chemical sensitivities and a permanent flu-like feeling, among other events.

We have also observed severe alterations in the function of NK cells in blood pressure and orthostatic balance, a significant reduction of blood flow to the brain and a reduced ability of oxygen consumption of cells. At the same time, the external appearance of the patient does not reflect the disease: it looks normal.

Reference: VC Lombardi, Ruscetti FW, Gupta JD, MA Pfost, KS Hagen, Peterson DL, SK Ruscetti, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, and Mikovits JA. Detection of Infectious Retrovirus, XMRV, in Blood Cells of Patients with Chronic Fatigue Syndrome. Online October 8, 2009. Science.

Sources:
1) http://www.sciencemag.org/cgi/content/abstract/1179052
2) http://www.youtube.com/watch?v=RWOWvdiXiSE
3) http://esme-eu.com/news/dutch-press-release-positive-xmrv-study-a-matter-of-time-article340-7.html
4) http://www.euro-me.org/news-Q22010-004.htm
5) http://www.fibromialgia.nom.es/fibromialgia-Síndrome-de-fatiga-Crónica-Síndrome-quimico-mulltiple-Noticias-2010/Síndrome-de-fatiga-Crónica-positivos-en-estudios-XMRV- single-en-question-de-tiempo.html
6) http://www.wpinstitute.org/news/docs/DearDrMcClureaw4.pdf
7) http://www.wpinstitute.org/news/docs/mclure-wpi_ltr_apr10.pdf
8) http://www.wpinstitute.org/news/docs/wpi-mclure_ltr_apr10.pdf
9) http://www.facebook.com/note.php?note_id=424864330914&id=100000436316743&ref=share
10) http://www.cdc.gov/eid/content/16/6/1000.htm # 1
11) http://www.montrealgazette.com/mobile/iphone/story.html?id=2775203
12) http://news.smh.com.au/breaking-news-national/chronic-fatigue-link-prompts-blood-ban-20100428-trsn.html
13) http://www.stuff.co.nz/nelson-mail/news/national-news/3607226/Chronic-fatigue-donors-face-rejection
14) http://online.wsj.com/article/SB10001424052702303450704575160081295988608.html
15) http://ca.news.finance.yahoo.com/s/18052010/34/biz-f-business-wire-whittemore-peterson-institute-cerus-confirm-inactivation-xmrv-intercept.html
16) http://www.mmdnewswire.com/xmrv-9040.html
http://www.facebook.com/ #! / photo.php? pid = 248 617 & id = 100,000,436,316,743
17) http://xmrv.blogspot.com/2009/12/contestacion-al-ministerio-de-sanidad.html
18) http://www.plataformafibromialgia.org/index.php/prensa/409-entrevista-tv-holandesa-prof-de-meirleir-y-sfc.html

Annexes (Links)

Trailer of the British documentary film about to emerge on the scandal surrounding the XMRV and the SFC:
http://www.whataboutme.biz/

In Spanish:

http://www.youtube.com/watch?v=tAzpu6qSKCY
http://www.youtube.com/watch?v=xCT1n_y5kos

Petition to ban U.S. official donation of blood from patients with CFS

http://www.aabb.org/pressroom/Pages/cfsrecommendation.aspx

Introducing Erik A. Klein over the possibility of prostate cancer (and CFS) can be infectious diseases XMRV

http://webcasts.prous.com/netadmin/webcast_viewer/Preview.aspx?type=0&lid=11920&eid=574&pv=2&preview=False&idcl=1

About the oncogenic retrovirus XMRV Whittemore Peterson Institute:
http://www.wpinstitute.org/xmrv/xmrv_qa.html (Official Page WPI)

About the oncogenic retrovirus XMRV National Cancer Institute of the USA:
http://www.cancer.gov/newscenter/pressreleases/XMRV_QandA

Original study published Science magazine:
http://www.sciencemag.org/cgi/data/1179052/DC1/1

Echo of the press in Spain on the news:

La Vanguardia:

http://www.lavanguardia.es/participacion/noticias/20091015/53804083772/hallado-un-vinculo-entre-el-retrovirus-xmrv-y-el-sfc-estados-unidos-cancer-salud.html

El Pais:

http://www.elpais.com/articulo/salud/Eternamente/cansados/elpepusocsal/20100511elpepisal_1/Tes

http://lacomunidad.elpais.com/Síndrome-de-fatiga-Crónica-y/2009/10/15/retrovirus-xmrv-mucho-peor-el-virus-la-gripe-a

http://www.elpais.com/articulo/sociedad/Identificado/virus/relacionado/Síndrome/fatiga/Crónica/elpepusoc/20091009elpepusoc_7/Tes

The World:

http://www.elmundo.es/elmundosalud/2010/06/28/dolor/1277724239.html
http://www.elmundo.es/elmundosalud/2009/09/07/oncologia/1252348915.html

Request of the EMEA (European Alliance ME) to all European countries to ban blood donations from CFS patients proactively to prevent the spread of the retrovirus XMRV in transplantation and transfusion. These measures would follow those taken in Canada, Australia, New Zealand, England, where already banned blood donations from these patients. In the U.S. also has prohibited the donation of the patients who already have confirmed XMRV infection. It only remains to follow Europe:

http://www.mefmaction.net/MECFSFM/MedicalAuthorities/BloodSupply/BloodDonorsESME/tabid/1207/Default.aspx

http://www.euro-me.org/news-Q22010-005.htm

Scandal in the publication of negative studies XMRV in Europe. It seeks to reach a journalist for news: This article, originally in the Netherlands and translated into English and Spanish, is mentioned all the controversy over the 3 negative studies of XMRV made in England and Holland, where information was withheld, despite knowing before publication. Apparently it was detected the presence of XMRV in the patients studied in the samples that were sent to the U.S., but the study authors silenced these data, which planted a lot of controversy and makes clear that to date there has been a study REPLICA American in Science, where XMRV was detected in the vast majority of patients studied and 4% of healthy controls.

http://www.facebook.com/notes/xand-xmrv/se-busca-periodista-noticia-de-alcance/424864330914

Videos explaining the discovery of XMRV and its association with the SFC and prostate cancer.

In English:
http://www.youtube.com/watch?v=RWOWvdiXiSE

In Spanish:
http://www.youtube.com/watch?v=bIE97TwawjA

Whittemore Peterson Institute links with all the news so far on the XMRV and its association with Chronic Fatigue Syndrome

http://www.wpinstitute.org/news/news_current.html
http://www.wpinstitute.org/xmrv/xmrv_qa.html
http://www.wpinstitute.org/

FDA and NIH confirm 'XMRV findings

2010-06-23T12:24:00.000+02:00

Source: http://www.mmdnewswire.com/xmrv-9040.html

Original Press Release from the Netherlands: FDA and NIH confirm 'XMRV findings'

Gendringen, NL (MMD Newswire) June 22, 2010 -- The FDA and the NIH have independently confirmed the XMRV findings as published in Science, October last. This confirmation was issued by Dr. Harvey Alter of the NIH during a closed workshop on blood transfusion held on May 26-27 in Zagreb. Two journalists from the Dutch magazine for health professionals, ORTHO, who have been working on XMRV stories for several months, were able to obtain a copy of the Alter lecture.
In the October 8, 2009 issue of Science Express, the Lombardi-Mikovits group at the Whittemore Peterson Institute (WPI), the Cleveland Clinic and the National Cancer Institute (NCI) reported that 67% of 101 chronic fatigue syndrome (CFS) patients tested positive for infection with xenotropic murine retrovirus (XMRV). Only 3.7% of 218 healthy subjects tested were positive for this gammaretrovirus. Since that time, a number of research groups have proved unable to independently confirm these findings.

On Friday last, the AABB released an Association Bulletin recommending that its member blood collectors actively discourage potential donors who have been diagnosed with CFS from donating blood or blood components. This interim measure was proposed by the AABB Interorganizational Task Force on XMRV. This Task Force includes representatives from several government agencies, including the Center for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA) and the National Institutes of Health (NIH).

The fact that the measure was introduced suggests the presence of information not yet published. The ORTHO journalists were able to obtain a pdf document of the lecture given by Harvey Alter at the IPFA/PEI 17th Workshop on 'Surveillance and screening of Blood Borne Pathogens' in Zagreb. The International Plasma Fractionation Association (IPFA) represents the not-for-profit organizations around the world involved in plasma fractionation. The IPFA is based in Amsterdam, the Netherlands.

The highly-experienced Dr. Harvey Alter is Clinical Studies Chief at the Infectious Diseases and Immunogenetics Section of the Department of Transfusion Medicine at the NIH Clinical Center in Bethesda. "The data in the Lombardi, et al Science manuscript are extremely strong and likely true, despite the controversy", was one comment on the XMRV findings reported by Alter in Zagreb. "Although blood transmission to humans has not been proved, it is probable. The association with CFS is very strong, but causality not proved. XMRV and related MLVs are in the donor supply with an early prevalence estimate of 3%‐7%. We (FDA & NIH) have independently confirmed the Lombardi group findings."

ORTHO contacted Dr. Harvey Alter today for a reaction. He did not want to comment, but confirmed that a paper is soon to be published.

ORTHO is a Dutch magazine for health professionals focusing on nutrition and dietary supplements. ORTHO has been publishing reports on CFS since 1988. Editor-in-chief: Gert E. Schuitemaker (PhD). Tel: + 31 (0) 315 695211 / + 49 (0) 170 808 9484. E-mail: ortho@orthoeurope.com.

what about ME?

2010-06-07T14:34:00.000+02:00

ME Promo 2 from Double D Productions on Vimeo.

26th of May Conference of Daniel Peterson and Kenny de Meirleir

2010-05-28T03:17:00.003+02:00

Yesterday we have gone to Madrid to hear Dr. Dan Peterson’s lecture.
It was an all morning session about XMRV, and the first to talk was Dr. Dan Peterson. He shared with everybody some of the findings in XMRV (nothing new) with many references to Dr. Judy Mikovits and the WPI, and his slides were the same that Dr. Mikovits uses in her lectures. The reasons for leaving the WPI were more a personal decision in order to have more time for himself after 25 years of service. He seems to be having a nice rest and is very happy to have the time to go sailing again.

At some point It was mentioned by Daniel Peterson, that so far the best biomarker for CFS is the Low NKCell function test, and that if your budget was restricted, this would be the test to do, I guess He was referring to the same direction than Dr. Klimas is always talking about as well. http://www.plosone.org/article/info:doi/10.1371/journal.pone.0010817

The second lecture was from Dr. Kenny De Meirleir, very interesting, focused on the fact that the most important thing now is to have a simple and good XMRV Test for all the researchers. He assured that they already have the test and it works, and it is a matter of days that they will make it available, 3 to 4 weeks probably.

De Meirleir also talked about all the work that is being done and possible treatments. Dr. Marc Fremont’s lecture was very technical about this test, and finally, Dr. Chris Roelant talked about the urine test they already have, which indicates intestinal dysbiosis is present in these patients.

Some of the questions posted in the Conference were regarding the recent German study, and the fact that XMRV is 3 times more present in immune compromised patients already tells you that there is an immune problem on CFS patients where most of them have the retrovirus.

There are three pathways affected on CFS which affect muscles and CNS:

2-5A
PKR
NO

There are also 3 pats of the immune system affected:

Th1 Linked to viral reactivation and intracellular infection due to an excessive hypersensitivity
Th2 Linked to pathogens, allergies and inflammation and blood brain barrier dysfunction
Th17 Linked to autoimmunity and inflammation and blood brain barrier dysfunction

De Meirleir elaborated later on that Th2 imbalance that causes diseases such as CFS, Autism, HIV, MCS, Mercury exposure, Allergies, Parasites.
Th1 relates to cell-based immunity Th2 relates to Humoral immunity

You can see a bit on the conference in this link:

Daniel Peterson Q&A
http://www.youtube.com/watch?v=ywLnptBQLeg

Kenny de Meirleir Q&A
http://www.youtube.com/watch?v=5buH30LcTds

When we asked Daniel Peterson to comment on Dr. Hubert lecture of last Monday in London, his answer was that Huber had positives 17 of the 19 samples that were sent to her, but She only spoke of the samples of other doctors who have tested negative. Daniel Peterson has said that once again we face the uncertainty of correctness in the samples tested, but also added that if She would have done a good job, She could not have all negatives, at least 3% would be positive, as we see is happening with the recent German study.

When we asked about the fact that HIV patients that are XMRV positive and have CFS, are not reacting to their current antiretroviral treatment, and that could lead to the possibility that XMRV is just a passenger virus in a depressed immune system, his answer was that actually that would be one possibility, and the other one is that they are taking the wrong drug, because XMRV is a different retrovirus, and they are being treated for HIV.

When we asked about the German study, and the fact that XMRV has been found now in the respiratory tract, and that could lead to new ways to detect XMRV different from the ones used in WPI, He said that is a big possibility. As we know blood is not the reservoir of XMRV, maybe the brain or the liver...

There were some other questions regarding the prevalence of CFS in children, banning blood donations, etc...

I will not add the whole Conference because is very time consuming, but I will review it and if I remember something relevant I will post in written expanding this current facebook note

Detox Plan (lack of GMST1)

2010-02-13T12:37:00.006+01:00

I came across with an article that mentions that GSTM1 is a critical detoxifying enzyme for mercury, and I do not have this gen as you can see in the post where I mentioned my results of my genetic profile.

As you remember through my old posts, I have a problem with mercury of which I became overloaded, probably when they changed my 7 fillings in once without protection back in 2004.

The GST genes are the Glutathione-S-transferases, which provide a major pathway of protection against toxins and carcinogens, as well as reactive oxigen species, and are thought to have evolved as an adaptive response to environmental insult, thus accounting for their wide substrate specifity. There are 4 family members: A, M, T and P. Plymorphisms have been identified in each family. Individuals with polymorphisms in the GST Phase II detoxification genes have a decreased rate of detoxification, with a corresponding increase in levels of carcinogen-DNA adduct formation and also increased level of chromosomal aberrations.Cruciferous vegetables such as brocoli, and members of allium family, such as garlic and onion, have been shown to be potent inducers of these enzymes, which would be expected to increase clearance of potential toxins from the body.

GSTM1- Glutathione-S-transferase M1
Polymorphisms: Gene deletion
-Function: Conjugation of glutathione to hydrophobic compounds.
- Biochemical activity: RX+glutathione= HX+R-S-glutathione
-Structure: Homodimer
- Location: Cytoplasm of the cell, in the liver
- Population frequency: 50% Caucasian

The GSTM1 has the highest activity of the four types of GST, and is located predominately in the liver.Half of caucasian population has a complete deletion of this gene. The effects of diet on activity of the GST enzymes have been demonstrated in several studies. Brassica vegetable diet increases GSTA and GST serum activity in the GSTN1-null individuals. (broccoli, spinach, cabbage, cauliflower, Brussels sprouts, kale, collard greens, pak choi and kohlrabi)

Here are some, but not all, of the factors that can contribute to your total toxic load:

- Exposure to heavy metals like mercury and lead, petrochemicals, residues, pesticides, and fertilizers.
- Internal toxins–things like bacteria, fungus, and yeast inside our gut as well as hormonal and metabolic toxins that we need to eliminate.
- Food allergies, environmental allergies, molds, and toxins from molds.
- Eating a standard American diet.
- Mental, emotional, and spiritual toxins — isolation, loneliness, anger, jealousy, and hostility, all of which translate into toxins in our system.
- Medications can sometimes be toxins. Often we need medications, but the reality is that most of us are overmedicated and use medications to treat problems for which there are better solutions, such as lifestyle and diet.

What they propose in that article in order to detox your body is the following plan:

There are five key steps to optimal detoxification:

1. Identify and Get Rid of Toxins – I listed the primary forms of toxic exposure above. Eliminating them is absolutely essential if you want to rebalance your detox system.

2. Fix Your Gut – Gut imbalances are a key source of toxins for many.

3. Get Moving – This help your blood and lymphatic circulation do its job.

4. Get Your Liver and Detox System Working – If your detoxification system isn’t working properly, this is a serious problem and needs to be addressed. A great place to start is the 10-step approach outlined below. Normal naturopathy approach to detox the liver and reduce Cholesterol levels is the following supplementation:
+ Milk Thistle (500mgr /day with the meals)
+ Artichok (with the meals)
+ Alpha Lipoic Acid (with the meals)
+ Greens Juices (as a breakfast and between meals)
+ Sports
+ Sauna

5. Detox Your Mind, Heart, and Spirit – This is just as important as detoxing your body, and it’s an area few of us ever think about as a source of toxins.

10 Simple Steps to Enhance Detoxification

1. Drink Clean – Drink plenty of clean water, at least eight to ten glasses of filtered water a day.

2. Eliminate Properly – Keep your bowels moving, at least once or twice a day. And if you can’t get going, then you need some help. This can include taking two tablespoons of ground flax seeds and taking acidophilus and extra magnesium citrate capsules. If you have any chronic diseases or problems, you have to be careful about taking supplements and should work with your doctor.

3. Eat Clean – You should also eat organic produce and animal products to eliminate the toxins, hormones, and antibiotics in your food.

4. Eat Detoxifying Food – You should eat 8 to 10 servings of colorful fruits and vegetables a day, particularly family of the cruciferous vegetables (broccoli, collards, kale, cabbage, Brussels sprouts, kohlrabi) and the garlic family (garlic and onions), which help increase sulfur in the body and help detoxification.

5. Minimize Drugs – Avoid stimulants, sedatives, and drugs, such as caffeine and nicotine, and try to reduce alcohol intake.

6. Get Moving – Exercise five days a week with focus on conditioning your cardiovascular system, strengthening exercises, and stretching exercises.

7. Avoid the White Menace – This includes white flour and white sugar.

8. Sweat – Sweat profusely at least three times a week, using a sauna, steam, or a detox bath.

9. Supplement – Take a high-quality multivitamin and mineral supplement.

10. Relax – Relax deeply every day to get your nervous system in a state of calm, rest, and relaxation.

Simply following these steps will help to correct problems caused by toxicity, maximize your body’s own detoxification capacity, and help you safely eliminate toxins stores in your body.

Depending on your symptoms, genetic predispositions and environmental exposures, you may need different levels of nutrients and types of treatment, but this is an excellent way to get started on detoxification today.

2010-01-18T12:04:00.002+01:00

There are a good number of scientific markers of abnormalities in this disease. Here are just some of those:

1- XMRV retrovirus in lab culture test.
Whittemore Petterson Institute-Judy Mikowitz

2- H2S metabolite Urine Test
De Meirleir

3 RNase L enzyme test
Dr. Robert Suhadolnik

4 Mitochondrial Failure
Shara Mhyll

5-Spectroscopic diagnosis of Chronic Fatigue Syndrome by visible and near-infrared spectroscopy in serum samples. Japanese researchers concluded that “Vis-NIR spectroscopy for sera combined with chemometrics analysis could provide a promising tool to objectively diagnose CFS.”
Fatigue Clinical Center in Osaka, Japan

6 Abnormal brain SPECT & PET scans
The Clinical and Scientific Basis of Myalgic Encephalomyelitis/CFS Dr. Byron Hyde

7Mitochondrial encephalopathy
Dr. Paul Cheney using Magnetic Resonance Spectroscopy

8Abnormal capillary flow due to high percentage of flat red blood cells instead of the normal discoid shaped red blood cells
Dr. Les Simpson, rheologist from New Zealand

9 Reduced red blood cell mass (RBC) ...is a critical hematological marker of ME-CIFDS-CFS.
(University of Miami)

10 Low circulating blood volume
Dr. David Bell, Lyndonville, New York

11 Abnormal bicycle ergometry test with gas analysis indicating immediate movement to anaerobic threshold in ME-CFIDS patients
Dr. Paul Cheney, who used this test for his disability reports

12 High percentage of patients with a viral load (HHV-6, EBV, cytomegalovirus) and/or Mycoplasma bacteria
Dr. Ablashi, Dr. Knox, Dr. Carrigan, Dr. Nicholson

13 Cardiac abnormalities due to viral invasion into the heart
Dr. Martin Lerner

14 Disregulated HPA axis
Dr. Mark Demitrack, Dr. Anthony Komaroff

15 Disregulated antiviral pathway
Dr. Suhadolnik

16 Head-up tilt test with haemodynamic instability
Dr. J. E. Naschitz

17 Abnormal T-helper 1/T-helper 2 Function Panel
Dr. Paul Cheney

18 Very low/impaired Natural Killer Cell Function
Dr. Paul Cheney, Dr. Kenny Demeirleir

19 Prolonged vasodilatory effect of acetylcholine on the microvasculature ...in addition to Peripheral Cholinergic illness in ME-CFIDS patients, Gulf War Illness, and illness following Organophosphate Exposure.
(Dr. Vance Spence)

20 Cardiomyopathy, liver failure, pancreatic cancer, brain tumors & renal disease ...reported after 40 years of research in Enteroviral and Toxin Mediated ME-CFIDS and Other Organ Pathologies.
(Dr. John Richardson)

21 Positive testing for Ciguatera Toxin Epitope
Dr. Yoshitsugi Hokama (Research funded by the National CFIDS/M.E. Foundation)

22 Neurally mediated hypotension

23 Abnormal “voyager” RNA (Preliminary studie)
Dr. Paul Cheney

24 5-HIAA, a metabolite of serotonin, may be present in elevated levels in ME-CFIDS patients
Georgetown University

25 Concentrations of a glucose metabolite in red blood cells

26 Differences in gene expression profiles
Dr. William Reeves in the cfids Chronicle

27 Excess nitric oxide activity

28 Blood hypercoagulability

29 Subclinical adrenal insufficiency
(present in about 2/3's of cases)

30 Reduced body temperature (can be caused by hypoadrenal +/- hypothyroid)

31 Magnesium deficiency

Look for "Xand Xmrv" on Facebook...

2009-11-05T00:39:00.002+01:00

That is my Facebook Profile I created for common research and news about XAND and XMRV. It is also an easy way to find other CFS/FM/ME and other neuroimmune disorder patients on the Facebook Community.
You feel free to ask me to be your friend on Facebook, my nick: "XAND XMRV"

Regards

Carlos

XAND substitute CFS now?

2009-10-10T15:09:00.003+02:00

It has been published yesterday in The Wall Street Journal and EL Pais, two main newspapers in USA and Spain. A new virus is apparently linked to prostate cancer and CFS.

This retrovirus is name is XMRV and if this conclusions are taken as a standard it will be the responsible for a change in the name of CFS to XAND (X associated Neuro-Immune Disease).

Now the responsible team of this study increase the % from 67% to 95% of the patients of CFS that do have this retrovirus in their blood. You can read the study in the magazine Science:
http://www.sciencemag.org/cgi/rapidpdf/1179052v1.pdf?ijkey=m3wzKT4yJqEyk&keytype=ref&siteid=sci

It is quite shocking that almost 4% of healthy population also has this virus, because that would mean that if this is contagious it would be a similar thing than HIV and AIDS, some people get sick, some others not, but the ones that are sick, have the virus. With CFS, now XAND, people that has XMRV might get sick or not, but people that do get sick with XAND do have XMRV 95% of the occasions.

Benefits of this disease to be contagious: it will be taken seriously and public funds will be invested in research.
Negative side is the stigmatization for fear, lack of information, etc...

http://online.wsj.com/article/SB125501227713473525.html

Complete GI Test en Metametrix

2009-09-01T13:00:00.006+02:00

N/L ratio evolution on CFS

2009-08-13T20:49:00.007+02:00

H2S The new CFS marker

2009-07-29T04:00:00.009+02:00

Comparision of Protocols: Rigau, Mhyll, Konynenburg (Yasko)

2009-06-13T13:24:00.009+02:00

Summary of Dr. Mhyll recommended Treatment

2009-06-13T12:46:00.004+02:00

Mitocondrial Failure (Acumen and Biolab test)

2009-05-22T02:03:00.007+02:00

Remember that this is just 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 will comment further on this, here goes by now the results obtained which explain my "bad days" and lack of energy...

ATP (adenosine triphosphate), studies on neutrophils
ATP is hydrolysed to ADP and phosphate as the major energy source in muscle and other tissues. It is regenerated by oxidative phosphorylation of ADP in the mitochondria. When aerobic metabolism provides insufficient energy, extra ATP is generated during the anaerobic breakdown of glucose to lactic acid. ATP reactions require magnesium. ADP to ATP conversion can be blocked by environmental contaminants as can the transiocator [TLj in the mitochondrial membrane. [TL] efficiency is also sensitive to pH and other metabolic-factor changes. [TL] defects may demand excessive ADP to AMP conversion (not re-converted to ADP or through to ATP). Defects in Mg-ATP, ADP - ATP conversion and enzyme or [TL] blocking can all result in chronic fatigue - a factor in any disease where biochemical energy availability is reduced.

ATP whole cells:
With excess Mg added 1.37 nmol/106 cells 1.6-2.9
(Standard method of measuring ATP)
Endogenous Mg only 0.74 nmol/106 cells 0.9 - 2.7
(Measured ATP result is lowered during intracellular magnesium deficiency)
Ratio ATP/ATPMg 0.53………………………………….. > 0.6
ADP to ATP conversion efficiency (whole cells):
ATPMg (from above) 1.37 nmol/106 cells (1*) 1.6-2.9
ATPMg (inhibitor present) 0.41 nmol/106 cells (2*) <0.3
AXpMg (inhjbitor removed) 0.78 nmol/106 cells (3*) > 1.4
ADP to ATP efficiency [(3*- 2*)/(l*- 2*)] x 100 = 38.5 % > 60
Blocking of active sites (2*/!*) x 100 = 29.9 % upto 14

ADP-ATP TRANSLOCATOR fTLj (mitochondria, not whole cells):

ATP Ref. range change % ref. range
(pmol/106 cells)
Start 244 290-700

[TL] 'ouf 309 410-950 26.6 over 35% (Increase)
(in-vitro test) reflects ATP supply for cytoplasm
[TL] W 191 140 - 330 21.7 55 to 75% (Decrease)
(in-vitro test) reflects normal use of ATP on energy demand

Comments
Very Low whole-cell ATP. Poor ATP-related Mg availability.
30% blocking of active sites leading to: Very Poor ADP-ATP re-conversion.
Low mt-ATP and poor provision of 'new' mt-ATP. Restricted access to rrit-ATP
secondary to the 3/10 blocking of transiocator function.

Coenzyme 010

ref. range
Serum coenzyme Q10 0.64 jamol/L 0.55 - 2.00

Coenzme Q10 is synthesised naturally in humans and is also found in foods, such as vegetables and fish, it acts as a cofactor in the electron transfer pathway which produces energy (in the form of adenosine triphosphate - ATP) within the mitochondria of human cells. The energy is used for muscie contraction and other vital functions. It is also an antioxidant which may have a sparing effect on vitamins C and E in situations of oxidative stress

SUPEROXIDE DISMUTASE and GLUTATHIONE PEROXIDASE
A functional test looks at the in-vitro efficiency of the patient's red cell superoxide dismutase (SOD) when their neutrophil superoxide production is maximally stimulated. The activity of the individual forms of SOD are explored. General cell protection from damage by superoxide is provided by intracellular zmc:copper-SOD (Zn/Cu-SOD). Mitochondria are protected by manganese-dependent SOD (Mn-SOD). Extracellular SOD (EC-SOD - another Zn/Cu SODase) protects the nitric oxide pathways that relax vascular smooth muscle.
For each form of SODase, genetic variations are known, mutations can occur during excessive oxidative stress on DNA and polymorphisms may be present. DNA adducts can chemically block these genes. Glutathione peroxidase (GSH-PX) activity is measured in red blood cells. It is a selenium-dependent enzyme and selenium deficiency is the commonest cause of poor enzyme activity. As poor glutathione (GSH) availability is easily overlooked as an additional reason for poor GSH-PX activity, we also measure total GSH in red cells.

Blood test results:

Test Result Units Reference range
Functional test 42 % Over 40 (mostly 41 -47)
Zn/Cu-SOD 269 Enzyme activity (u) 240-410
Mn-SOD 158 Enzyme activity (u) 125-208
EC-SOD 31 Enzyme activity (u) 28-70

Gene studies:

Sod form Gene(s) Comments
Zn/Cu-SOD chromosome 21 Normal Normal enzyme activity
Mn-SOD chromosome 6 Normal Normal enzyme activity
EC-SOD chromosome 4 Normal Normal enzyme activity

Result Reference range
Glutathione peroxidase (GSH-PX)
Red cell Glutathione peroxidase (GSH-PX) 48 U/gHb 67-90
Red cell Glutathione (GSH) 1.31mmol/1 1.7-2.6

NIACIN STATUS (vitamin B3)
Red cell nicotinamide adenine dinucleotide (NAD) is a good indicator of B3 status.

Red cell nicotinamide adenine dinucleotide = 12,7 ug/ml 14.0 - 30.0

Interpretation of result:
Reference range (14.0 - 30.0)
Mild B3 deficiency (12.5 - 13.9)
Moderate B3 deficiency (11.0 - 12.4)
Fairly marked B3 deficiency (10.0 - 10.9)
Marked B3 deficiency (8.5 - 9.9)
Severe B3 deficiency (less than 8.5)

References:
1) Fu CS, Swendseid ME, Jacob RA, McKee RW. Biochemical markers for assessment of niacin status in young men: levels of erythrocyte coen2ymes and plasma tryptophan. JNutr 1989: 1949 - 1955.
2) Critical review. Assessment of niacin status in humans. Nutrition Reviews 1990; 48: 318-320

Note:
The amino acid tryptophan is a precursor of niacin. However, protein synthesis has a higher metabolic priority than the conversion of tryptophan to niacin coenzyme and adequate niacin levels cannot always be obtained from tryptophan.

Cell-free DNA in blood plasma

Background. Most of the cell-free DNA present in blood plasma is associated with cell degradation. Very low levels are present in healthy people and increases are associated with serious illnesses such as malignancy, stroke, auto¬immune diseases, severe infections and Chronic Fatigue Syndrome.

Patient's result: Reference range
Cell-free DNA 22.7 ug DNA per litre plasma up to 9.5

Comments:
Mild increase = 9.6 to 12.4
Some increase = 12.5 to 14.9
Definite increase = 15.0 to 20.0
Highiy significant = over 20.0

Method summary* Plasma is incubated with EDTA, a detergent and a proteinase prior to precipitation of the proteins. DNA is then precipitated with alcohol and re-dissolved in a Tris-acetate-EDTA Buffer. The DNA is measured in a Pharmacia GeneQuant™ or Jenway Genova analyser using a micro-cuvette.
*Schmidt B, Weickmann S, Witt C, Fleischhacker M. Improved Method for Isolating Cell-Free DNA. Clin Chem 2005:51(8); 1561-2

Cell-free DNA in chronic fatigue syndrome (CFS) In initial studies on 87 CFS patients, positive results were found in 93% of those with a disease duration of four months to five years (n = 75). In those with a disease duration of five to 14 years (n = 12), 75% had positive results.

Dr Sarah Myhill MB BS, Upper Weston, Llangunllo, Knighton, Powys, Wales, UK LD7 1SL
Tel: 01547550331 Fax: 01547550339 E-mail: office@doctormyhill.co.uk Website: www.drmyhill.co.uk
____________________________________________________________________________
Dictated on 11 May 2009

Dr Josepa Rigau
Av Catalunya 12 3◦ 1a
43002 Tarragona
Spain

Our ref: sm/nw

Dear Dr Rigau,

Re: Carlos Gonzalez Rodriguez
DOB: 29.05.1970

Carlos contacted me for advice about management of his chronic fatigue because I have a particular interest in environmental medicine which is all about looking for causes of illness and treating using micronutrients (for deficiencies), dietary changes (for allergies and intolerances) and identifying and reducing toxic stress. In order to make this style of medicine generally available to patients I have set up a website with information and access to medical tests. The key point to remember about chronic fatigue syndrome is that it is not a diagnosis but a symptom and the name of the game is to identify the underlying causes. Sometimes clues come from the history, sometimes from the tests; the first part of this letter indicates the main and common causes of fatigue, the interpretation of the results refers specifically to your patient and the overall approach to addressing these causes in a logical manner is at the end of this letter.

I have been in the business of treating chronic fatigue syndromes for over 25 years and have now got a very clear idea of the important things that need to be put in place to allow people to recover. I now have a very structured workup and my experience is that with the information that I supply on my website, guidance from biochemical testing, a determined patient, and a supportive GP an awful lot can be achieved. Indeed many patients who have used my website and had access to tests have made good recoveries without having to actually come and see me.

So if Carlos can work through this letter and my standard workup for treating chronic fatigue syndrome in a logical way there is no reason at all why he shouldn’t do well. Carlos tells me he already takes a number of nutritional supplements and so he needs to go through the individual supplement regime I have sent him to make sure he doesn’t double up on any.

Carlos was kind enough to send me a history and account of his symptoms. He requested tests of mitochondrial function and antioxidant status because mitochondrial failure is a very common cause of chronic fatigue syndrome and my standard interpretation of the test results is below. I have to say these tests make a great deal of sense of many of Carlos’s symptoms.

Actually these are extremely poor results with a very high cell free DNA. The lesions we see in Carlos’s case illustrates one of the vicious cycles in fatigue syndromes. When mitochondria go slow there is excessive production of free radicals. These put a strain on the antioxidant system so antioxidants become depleted. Therefore we see more tissue damage thereby impairing mitochondrial function. This self-perpetuating vicious cycle is difficult to get out of but perfectly possible – we have to tackle as many of these biochemical lesions as we can at the same time to allow the system to recover and during this time Carlos needs to carefully pace his activity in order that he doesn’t add to the sum of tissue damage.

Onset of Fatigue
Carlos has a gradual onset of fatigue over two years starting in 2003 and culminating in a nasty virus in September 2005 when he really became much more ill. The tests (see below) show clear evidence of toxic stress – that is to say he has experienced a low grade poisoning. My guess is that there are two issues here. Firstly during his work as a banker, he spent nine years working in very poorly ventilated offices. All soft furnishings these days are treated with insecticides and fire retardants which out-gas during their lifespan. Furthermore there are a great many solvents and other such volatile organic compounds in regular office use. Modern buildings often have air recycling and so the levels of these persistent organic pollutants can build up. They are readily absorbed by the body through inhalation and they bioaccumulate in fatty areas – this includes membranes on which all metabolic activity takes place. Mitochondrial energy production for example is all on the membranes. Another source of exposure could have been from toxic air on aeroplanes and I do recommend you look at www.aerotoxic.com . Cabin air is pulled in over the engines and inevitably gets contaminated with engine fumes including organophosphates used as oil conditioners, namely tricresylphosphate. Carlos flew regularly as part of his job so this would all have compounded his sick building syndrome.

On top of this we have at least two bits of information that show that Carlos is a slow detoxifier. Firstly he has raised levels of bilirubin suggesting Gilbert’s syndrome. This is generally believed to be a benign chemical abnormality; however, in Gilbert’s syndrome people are slow detoxifiers because they are unable to stick a glucuronide group onto endogenous chemicals and xenobiotics. Indeed people with Gilbert’s syndrome are at risk of fatigue. However, they can be improved with high dose micronutrients since these facilitate liver detoxification. My experience is that often these patient do well on B12 injections since this also facilitates detoxification.

Secondly Carlos had tests to look at his methylation cycle which shows low levels of glutathione and high levels of MMA – this means he doesn’t methylate. Carlos can’t use B12 in its usual form so where I recommend B12 below, I would suggest using the methylated form namely, methylcobalamin.

The results that this letter reports pertain to mitochondrial function, but from the history there may be other important clues. The following paragraphs cover the common and important causes of fatigue. Please forgive the obvious standard paragraphs, but it is the only way I can fit in all the necessary information!

Food Allergy
Food allergy – many of my patients are intolerant of a number of foods. Food allergy is a greatly overlooked cause of symptoms, which again masquerade under other diagnoses. For example, the commonest manifestations of food allergy are migraine, irritable bowel syndrome, asthma, skin inflammations (eczema, urticaria etc.), chronic rhinitis and arthritis, all of which are symptoms. None of these constitute a diagnosis since a diagnosis implies a cause. I suspect this is why food allergy has been greatly overlooked as a diagnosis and so the stoneage diet that I recommend to all my patients with CFS may well be an important part of management. The commonest allergens are grains, dairy, yeast and sugar.

The clues from the history that suggest allergies may be a problem are:
• A long history of various and changing problems dating from childhood – A history of tonsillitis as a child is typical of allergy to dairy products. Indeed, a colleague of mine considered it medical negligence to remove a child’s tonsils without first trying a dairy-free diet!
• A shopping list of symptoms - in one study, over 50% of unexplained symptoms were caused by food allergy.
• A particular liking to a food – oddly sufferers often get addicted to the foods which cause them most problems. This is akin to a nicotine or alcohol addiction!
• Irritable bowel syndrome- often caused by wheat allergy.
• Bloating is often induced by wheat, sugar and alcohol and this could also point to yeast allergy. I say this partly because alcohol contains yeast and partly because sugar is often fermented in the gut by yeast and one ends up reacting allergically to endogenous yeast in the gut.
• Rashes and other obvious allergic problems such as asthma or eczema

There aren’t any reliable tests for food allergies and people simply have to do the stoneage diet.

I think that many of Carlos’s symptoms such as his sleep apnoea, vasovagal syncope, headaches, sacroielitis and alternating constipation and diarrhoea could certainly be explained by food allergy. Irritable Bowel Syndrome is not a diagnosis but just a description of gut symptoms which are often caused by food allergy and/or gut dysbiosis. The natural progression of allergy in a patient is for the incitant to remain the same but the target organ to change, which is why we see so many different pathologies throughout a lifetime. I think it is highly likely that for Carlos to do a good stoneage diet is going to be a very important part of getting well. Combined with this I suggest he also try high dose “do it yourself” probiotics and the present flavour of the month is Kefir, which can be easily grown and is very cheap because one sachet can last a lifetime.

Muscle Aching and Pain
I suspect one major overlooked feature of allergy is the allergic muscles. I know this directly from my own experience – in my case dairy products cause acute low back pain. I have to say I’m not sure I would have believed this possible unless I had experienced it myself! Symptoms of muscle stiffness and pain together with tremors and twitching is also typical of magnesium deficiency. The reason for this is that calcium is necessary to contract muscles and magnesium necessary to relax them. Relaxation is an energy-requiring magnesium dependent process, if magnesium is absent then muscle fibres effectively get sticky which means when they are stretched they tear and this results in muscle damage. This explains the symptoms of stiffness and pain and would partly explain the very high cell free DNA that Carlos has (see below).

Yeast/Candida problem.
Respectable doctors nowadays don’t like to call this candida because it has never really been proven that candida is the offending bug. We prefer to call it ‘fungal-type gut dysbiosis’ which may cause problems because a patient is allergic to yeast (and Carlos obviously has allergy problems) or it may cause problems because yeasts ferment food in the gut to produce alcohol, wind and gas which result in bloating. Yeasts interfere with both the absorption of micronutrients and the normal processes of digestion creating leaky gut, which can switch on food allergies. Different people require different levels of treatment to control this problem. The first line of approach is a low carbohydrate diet since this reduces sugars on which yeasts ferment. The second approach is high-dose probiotics and some people also need herbal antifungals and some people systemic prescription antifungals to get on top of their yeast problem.

Poor digestion
Carlos may well be a poor digester of foods – indeed he has already identified lactose intolerance. His urinary organic acids show high levels of arabinose which is suggestive of a yeast overgrowth of the gut – yeasts often get into the gut where there is hypochlorhydria.

Mineral deficiency
Carlos’s symptoms of mitral valve reflux and poor diastolic function is suggestive of magnesium deficiency and indeed this is confirmed in the tests below. Essentially one needs calcium to contract muscles and magnesium to relax them. Poor diastolic function means the heart muscles do not relax properly in order to allow the chambers to fill with blood. Carlos’s symptoms of kidney stones could indicate vitamin D deficiency – it is vitamin D that makes sure that calcium is deposited in bone. Indeed Carlos has low vitamin D at 25.2umol/L – the best source of vitamin D is sunshine but failing that I recommend he take 2,000i.u. daily of vitamin D.

I note Carlos has generally low levels of minerals from the hair analysis but his level of superoxide dismutase is good suggesting adequate mineral status here.

For further information see my website for information on PROBIOTICS and KEFIR, GUT DYSBIOSIS, HYPOCHLORHYDRIA and COMPREHENSIVE DIGESTIVE STOOL ANALYSIS.

Hypochlorhydria
This is an extremely common problem in which insufficient acid is secreted by the stomach for the efficient digestion of proteins. It can have many clinical symptoms including symptoms of GORD (gastro-oesophageal reflux disease) and hyperacidity (I know this sounds rather counter-intuitive but the pyloric sphincter is pH sensitive and unless a certain acidity is achieved then the stomach fails to empty), a tendency to allergies (protein foods are poorly digested and present as large, antigenically interesting molecules, which have a tendency to switch on allergies), failure to sterilise gut contents (this results in bacterial and yeast overgrowth so that food is fermented instead of being digested resulting in wind, gas and bloating and poor absorption of divalent and trivalent cations leading to micronutrient mineral deficiencies).

So, possible symptoms of hypochlorhydria would be:
• Gastro-oesophageal reflux disease and hyperacidity
• Poor digestion of foods with recognisable foods appearing in faeces
• Diarrhoea, malabsorption, irritable bowel and fermentation of foods
• A tendency to allergies
• A tendency to micronutrient deficiencies
• A tendency to get gut infections since acid is normally required to sterilise the contents of the stomach – indeed, I suspect this is part of the mechanism by which CFS sufferers are susceptible to gut viruses like Epstein-Barr.

The treatment is to acidify stomach contents. A traditional remedy is of course cider vinegar but many people will not tolerate the yeast contained in this. Ascorbic acid has a beneficial effect as indeed does betaine hydrochloride 1 – 4 capsules taken with meals depending on the size of the meal.

Carlos’s symptoms are highly suggestive of hypochlorhydria. We now have a test for hypochlorhydria which is to measure salivary vascular endothelial growth factor. It is very common to see hypochlorhydria with allergies and if this test is required then it’s easily arranged.

Carbohydrate intolerance and hypoglycaemia
There are two common ways in which diet can cause fatigue – firstly allergies and secondly carbohydrate intolerance. The carbohydrate intolerance is often a symptom of sugar addiction. Addiction and allergy are closely allied and indeed people get allergic to their addictions and addicted to their allergens.

The clues from the history that suggest this may be a problem are:
• A need for carbohydrate foods
• Missing a meal results in feeling awful – having to snack or graze on foods regularly through the day
• Feeling at one’s worst on waking
• Tendency to gain weight easily (this results from high insulin levels)
• Disturbed sleep / waking in the middle of the night and unable to drop off again – this is because the person is woken by low blood sugar and the adrenalin reaction that accompanies it.
• Anxiety and mood swings.

Because carbohydrates are so addictive, any change in diet should be done gradually – if this is done too quickly symptoms may get much worse. However for many this is an essential and possibly the most important part of treatment. We can test for hypoglycaemic tendency by measuring levels of short chain fatty acids first thing in the morning before breakfast has been taken. This is a blood test and can be arranged on request.

Parasites
Carlos has been tested positive and attempted to eradicate both blastocystis hominis and endolimax nana.

Sleep problems
It is a sine qua non that poor sleep will result in chronic fatigue. The average sleep requirement is for 9 hours sleep between 9.30pm and 6.30am – more in winter, less in summer and the most restorative hours of sleep come before midnight when melatonin is produced. Sleep doesn’t creep up on us during the course of the evening, it comes in waves and there is a sleep wave roughly every 90 minutes. So I would like Carlos to catch the relative sleep wave and use whatever herbs or medications necessary to help him achieve this. If combined with a sleep dream, this produces a Pavlovian conditioned reflex and this prevents problems of tachyphylaxis and dependency. See SLEEP section in my CFS book.

Thyroid Problems
Hypothyroidism is both a clinical and a biochemical diagnosis and can certainly present with fatigue. Anybody suffering CFS could well be hypothyroid! So I would very much like to see the results of a recent or new free T4, free T3 and TSH.

The clues from the history that suggest this may be a problem are:
• A gradual descent into fatigue often attributed to ageing
• Feeling cold, cold hands and feet, low basal body temperature
• Slow pulse and inability to get fit (relative to current ability), shortness of breath
• Dry hair, skin, loss of hair, loss of eyebrows
• Headache
• Other members of the family also affected by thyroid problems.

Adrenal stress problems
If one thinks of oneself as a car, the mitochondria represent the engine of that car, the thyroid gland the accelerator pedal and the adrenal gland is the gearbox. It allows one to move up into fourth gear or fifth gear when one is stressed and this allows individuals to achieve extraordinary feats! However it is not sustainable long term. If there is unremitting stress (and this may be financial, physical, mental, emotional, nutritional, infectious stress or whatever) then the adrenal glands fail, output of stress hormones falls dramatically and effectively one is left stuck in first gear. With prolonged rest the adrenal glands do eventually recover but in the interim adrenal supplements can be helpful. Adrenal tests show that Carlos has low cortisol and high DHEA levels.

Depression
There is a clear clinical difference between fatigue and depression. In depression there is no volition, but often when people are made to do things they feel better as a result. In fatigue the desire is there but the patient does not have the energy to undertake the task, and indeed, quickly discovers that if they do push themselves to do something it makes them feel very much worse. This is an important difference to make clinically and failure to do so has resulted in many wrong diagnoses. It is not unusual for patients to become frustrated by their inability to do things and, indeed, are possibly secondarily depressed because nobody is addressing the root cause of their problems. There is a difference between depression and being “pissed off”! This can usually be discerned from careful history taking. However this has major implications for choice of medication. This is because the stimulating antidepressants such as the SSRIs increase the desire to do things but do very little for the performance and thereby increase the frustration factor. The important point is that SSRIs may be making some patients with fatigue worse.

Actually my preference is to use the tricyclic antidepressants at night in order to improve the quality of sleep and the length of sleep and this may have a very beneficial effect on the fatigue. If there is secondary depression then this may help address that side as well but at worst one can do little harm with low dose tricyclics. Most patients with fatigue syndromes are intolerant of normal doses of medication and should a tricyclic be tried then it needs to be in much smaller doses than generally considered to be therapeutic. For example with amitriptyline I usually start patients off on 5 to 10 mg at night and it is unusual for them to tolerate more than 25mg. And with Trimiprimine (Surmontil) I suggest 10mgs at night because sometimes this also has a beneficial effect on muscle pain. Having said all that a few patients are improved by small doses of SSRI and I suspect this is because SSRIs also have mild anti-inflammatory actions and downgrade the nitric oxide/peroxynitrite pro-inflammatory cycle and, if relevant, Carlos may feel he would like to discuss these options with you.

Multiple chemical sensitivity
One problem Carlos has identified is a multiple chemical sensitivity – he has to avoid chemicals paints and other chemicals or toxins. Again this is extremely common in patients with fatigue syndromes, especially those who already know they are food allergic. Really MCS is an extension of allergy to drugs and indeed prescription drugs can certainly trigger multiple chemical sensitivity. However sufferers sensitise so they start to react to tiny amounts of chemicals. Treating chemical sensitivity is an absolute nightmare – the single most important thing to do is to avoid chemicals. With chemical sensitivity it is all about total load – this means the total load of chemicals in the diet, prescription medications, hormones, cleaning chemicals, cosmetics and so on may all be a problem. It is essential to do a good clean up of the environment to try to reduce the total load and this will also reduce the allergic burden.

Toxic Stress
Sometimes there are obvious clues from the history such as being present at the Gulf War, farmers with sheep dip ‘flu, aerotoxic pilots, firemen with 9/11 syndrome, women with silicone implants and so on. In practice, the commonest problems are from mercury dental amalgam, nickel toxicity, fire retardants (dichlorobenzenes from soft furnishings) and wood preservatives (lindane and other organochlorines).

As you can see from the results below we have a very significant problem with toxic stress with Carlos which is most likely to be the cause of his severely impaired translocator protein function (see below). In 2003 Carlos had 7 mercury fillings removed, but this had to be carried out a second time because of errors during the original procedure and so if there was some leakage of mercury, this could be all or part of the problem here.

Medication
It is a feature of CFS that standard prescription medications often make patients/sufferers worse. Many sufferers know they are intolerant of alcohol and caffeine which may reflect slow ability to detoxify – this may also be a reason for intolerance of prescription medication. The commonest problems I see are:

• Standard doses of medication are not tolerated and the sufferer sees many side effects – this may reflect slow detox or poor micronutrient status.
• Intolerance of medications – may reflect a tendency to allergies and multiple chemical sensitivity
• Antibiotics causing thrush/yeast problems
• Statins making symptoms much worse - possibly because statins inhibit endogenous production of co Q 10 (see below)
• Beta blockers making fatigue much worse – this is because in severe CFS the patient is in a low cardiac output state (secondary to mitochondrial failure) and beta blockers exacerbate this.

Chest Pain
People with fatigue syndromes commonly complain of chest pain. The heart is the most physically active organ in the body, but when mitochondrial function in the heart is impaired there is a tendency to switch into anaerobic metabolism with the production of lactic acid. It is this lactic acid build up in the heart which, I believe, causes the chest pain. It can be very persistent because metabolising lactic acid back into glucose (via the Cori cycle) is highly energy requiring. So whilst the chest pain is arguably angina, it is rather atypical because it is more persistent than the angina of blood supply which clears rapidly as soon as the patient rests. My experience is that as the mitochondrial function improves this symptom goes away.

Mitochondrial Failure
I am increasingly coming to the view that chronic fatigue syndrome is a symptom of mitochondrial failure and I find that mitochondrial function tests are extremely helpful in sorting out what is going wrong, why and where.

Whilst all cells are different, the way in which energy is supplied to cells is the same – all mitochondria are identical and when there is mitochondrial pathology we see widespread symptoms as a result because all cells, metabolically speaking, go slow. The function of mitochondria is to produce ATP and we now have a test, namely ATP profiles, which measures the rate at which ATP is recycled – this I believe will turn out to be the most useful test for diagnosing and managing chronic fatigue syndrome.

When mitochondrial function is impaired, all muscle function is impaired and this includes cardiac muscle. Indeed low cardiac output has already been demonstrated in fatigue syndromes and elegantly explains the symptoms these patients suffer from. For example, they have low blood pressure, marked postural hypotension, low blood volume and perfusion defects. Poor circulation of skin would explain cold hands, cold feet and difficulty with temperature regulation, poor circulation of the brain explains the cerebral symptoms and so on. I have also become interested in the views of a cardiologist in America who believes that many of the cardiomyopathies and congestive cardiac failures are not just due to poor blood supply, but again a mitochondrial induced cardiomyopathy. What is so fascinating is that this cardiologist has come up with a cocktail of micronutrients which reverses the cardiac damage namely, magnesium, co-enzyme Q10, acetyl L-carnitine and D-ribose, to which I would add vitamin B3. By identifying and correcting deficiencies, mitochondrial function can be restored and symptoms such as Carlos’s post exertional malaise improved. This established treatment protocol can be applied directly to patients with fatigue. Thanks to a brilliant biochemist, Dr John McLaren Howard, we now have a test to demonstrate mitochondrial lesions.

Carlos’s symptoms of postural orthostatic tachycardia syndrome and vasovagal syncope is suggestive of poor cardiac output secondary to poor mitochondrial function – we have certainly confirmed this in the tests below.

I am also a co-author of an article that the International Journal of Clinical and Experimental Medicine has published online (Jan 2009) with details of this biochemical test which measures energy supply to cells and therefore fatigue levels in people with chronic fatigues syndrome/myalgicencephalomyelitis (CFS/ME). Ref: www.ijcem.com/files/KJCEM812001 Int J Clin Exp Med (2009) 2, 1-16. What this study shows is that the mitochondrial function test is an accurate and objective way to measure energy levels and the mitochondrial function score is a helpful measure of the level of disability.

So this test can be used to confirm the clinical picture of CFS, to assess the level of disability objectively, to identify where the biochemical lesion lies and give pointers as to how to further elucidate and correct that biochemical lesion. Even if the results are not too bad mitochondrial function could be further improved by taking the supplements suggested. There are three parts to the test: 1. Levels of ATP 2. Oxidative phosphorylation Kreb’s Citric Acid Cycle and ADP to ATP conversion, and 3. Movement of ATP and ADP across mitochondrial membranes.

Interpretation of Mitochondrial Function Test
1. Levels of ATP
The level of ATP in cells is shown by ATP with excess Mg added and with endogenous magnesium only. With excess Mg added the result is 1.37 (1.6-2.9nmol/106). This shows very low levels of ATP, so I recommend supplementing with D-ribose (the body uses this to make brand new ATP – as opposed to recycled ATP) building up to three teaspoonfuls daily (15gms) and adjusting according to response. Indeed, and see below, Carlos has a very high cell free DNA, which may be caused by an inappropriate switch from efficient aerobic mitochondrial metabolism into inefficient anaerobic glycolosis with excessive production of lactic acid which causes secondary cell damage. Indeed this often causes a symptom of fibromyalgia. D-ribose has already been trialled in the treatment of fibromyalgia with excellent results. D-ribose has a very short half life and should be taken in small doses throughout the day in drinks (hot or cold). Interestingly caffeine enhances the effects of D-ribose so I recommend taking it with green tea, coffee, tea or whatever. It is worth supplementing with D-ribose even with low normal results because I have so much happy feedback from patients taking this supplement.

With endogenous Mg only the result is 0.74 (0.9-2.7nmol/106) with a ratio of 0.54 (>0.65). This result shows a low magnesium status. Magnesium is a difficult mineral to replete and some people have to have it by injection. So I recommend taking at least 300mg magnesium daily orally (more if tolerated – up to 600mgs) present in my physiological mix of minerals (MMMs), together with magnesium by subcutaneous injection. I usually use Evans 50% magnesium sulphate. One can give 2mls on a weekly basis, but large volume injections like this can be uncomfortable. I have to say my preference nowadays is to use ½ ml insulin syringes and for patients to inject themselves every day for two months then adjust the frequency of dose according to clinical response Many people end up injecting 2-3 times a week until they are much better. These small volume injections are far better tolerated and less inclined to leave injection lumps. Adding lignocaine often improves matters (0.05ml lignocaine with 0.5ml magnesium). I would be grateful if you could prescribe and demonstrate how to do these injections. Magnesium is a real problem in patients with fatigue syndromes – it is necessary for ATP to release its energy, it is necessary for oxidative phosphorylation and much of resting energy goes to maintain calcium magnesium ion pumps. That is to say low intracellular magnesium is both a cause and a symptom of mitochondrial failure. So there is a very clear indication here to give magnesium by injection.

The main problem can be injection lumps. To avoid these, wait for 2 minutes after the injection to allow capillary bleeding to stop. Then feel the injection site and a small “puddle” of magnesium can easily be felt – then massage the area gently until this “puddle” disperses completely. However if you are still bruising using this technique, try a few injections when you do not massage the site at all.

Epsom salts in the bath (a double handful) will improve magnesium status since magnesium is absorbed through the skin. The bath needs to be as warm as can be tolerated for at least 15 minutes – really the longer the better. Epsom salts can be purchased by the 20kg sack from garden centres or farm supply shops or try www.justasoap.co.uk. who will deliver.

2. Oxidative phosphorylation – Kreb’s Citric Acid Cycle and ADP to ATP conversion
This is going very slow at 38.5% (normal range >60%). In order to assess the efficiency with which ADP is converted to ATP, an inhibitor is added and then removed to see how quickly ATP is reformed. Having added the inhibitor one expects levels of ATP and magnesium to drop below 0.3 – if this does not happen this suggests there is blocking of the active sites. The acceptable percentage is up to 14% and Carlos’s result is 29.9% (up to 14%). This suggests that there is significant blockage of the active sites (i.e. complexes I,II,III,IV and V on inner mitochondrial membranes). The likeliest reason for this is toxic stress and we could explore further by doing microrespirometry studies which look at oxidative phosphorylation in more detail.

We need to explore this result further by looking at:
a) Vitamin B3 levels. The red cell NAD shows a mild B3 deficiency at 12.7µg/ml (14 – 30). This is an interesting result because NAD is a functional test. Whilst it reflects B3 status, it also reflects function of Kreb’s citric acid cycle. The job of KCA is to take energy from acetyl groups and convert it into NADH, which is then of course converted to NAD in the process of driving oxidative phosphorylation. Therefore to see normal levels of NAD needs not only an adequate supply of B3, but also a functioning Kreb’s citric acid cycle. So a low NAD may (amongst other things) also imply poor acetyl L carnitine levels. Whilst most people can obtain all the NAD they need from a combination of diet and a good B complex vitamin preparation, some people seem to need much higher levels to correct blood levels. I usually start off with 500mgs of niacinamide daily (this is the form of vitamin B3 that is free from side effects - do not use niacin or nicotinamide, which cause unpleasant flushing). Acetyl L carnitine is normally present in mutton, lamb, beef and pork. If these foods are not consumed then I recommend taking acetyl L carnitine 2 grams daily. Lamb contains about 5grams per kilo of acetyl L carnitine so one needs to eat quite a lot! A small supplement, geared to meat intake, may be necessary. Indeed acetyl L carnitine has been trialled in the treatment of CFS with positive results.

b) The Co-enzyme Q10 result is back within the normal range but lower than I like it to be at 0.64umol/l (0.55 – 2.0). This is the most important antioxidant inside mitochondria and also a vital molecule in oxidative phosphorylation. Co-Q10 deficiency may also cause oxidative phosphorylation to go slow, but interestingly not invariably. The best results clinically are achieved if levels get up to 2.5 or above. This seems to be necessary to kick start the mitochondria, at which point the dose can probably be reduced according to clinical response. This regime has been worked out by an American cardiologist, Dr Sinatra, who uses Co-Q10 to treat patients with congestive heart failure secondary to mitochondrial failure, which effectively results in a mitochondrial myopathy. The underlying pathology in these cardiomyopathies is the same as that in fatigue syndromes. The problem in heart failure is primarily in the heart muscles, in fatigue syndromes, probably all cells are affected. Co-Q10 is also called ubiquinone, which reflects its presence in all tissues because it is present in all mitochondria. Therefore I suggest starting on 300mg daily of Co-Q10 (the dose should be split into 100mg three times daily) for three months then a maintenance dose of 100mg daily. It is possible for Co-Q10 to be prescribed on an NHS prescription. This is prescribable in capsule form and should you feel able to do this then you would need to prescribe ubidecarenone 100mg capsules.

c) When oxidative phosphorylation goes slow it is often because of free radicals which are produced, in particular nitric oxide and superoxides which combine to form peroxynitrite. These are potentially very damaging but efficiently mopped up by vitamin B12. So often there is very poor antioxidant status in CFS and B12 takes on many of the functions of other antioxidants so effectively giving “instant cover”. So there is a good indication to try B12 subcutaneous injections. Indeed B12 has been shown to be effective in CFS, but in much higher doses than is required to treat pernicious anaemia. Therefore measuring blood levels is irrelevant. Giving B12 with an insulin syringe renders the injection virtually painless so these tiny doses are an excellent way of administering B12. I suggest ½ ml methylcobalamin daily initially for two months and adjust according to clinical response. B12 is a joy to use with no known toxicity. Please would you consider supplying the necessary?

d) Magnesium is also required for oxidative phosphorylation so the magnesium injections will also assist this side of things.

This result simply shows how well oxidative phosphorylation is working at the time the test was taken – it does not predict what will happen if the patient increases exercise levels! So it is important to continue pacing carefully! Indeed as mitochondrial function improves, the first task is for healing and repair of damaged tissues (see cell free DNA result), not to increase activity levels. So it is vital to continue pacing until feeling completely well at rest – only then may a very gentle graded activity programme be considered, and only allowed to continue so long as the patient feels fine – i.e. not at the expense of tissue damage.

3. Movement of ATP and ADP across mitochondrial membranes.
This looks at ability to move ATP and ADP across mitochondrial membranes and this is dependant on translocator protein. Translocator protein ‘out’ is a poor result of 26.6% (normal range >35%). Translocator protein ‘in’ is also a poor result of 21.7% (normal range 55 - 75%). Translocator proteins can be blocked in many different ways. The commonest is toxic stress, which can be chemical or viral or possibly free radical in origin. By chemicals I mean pollutants such as pesticides, volatile organic compounds and heavy metals. One day we may have specific antidotes for specific toxins, but at the present, sweating regimes probably get rid of most toxins. The most physiological way to sweat is to exercise but this is not possible for many sick patients. Therefore I recommend Far Infra Red saunaing at least two sessions a week – more if possible using FIR blanket or sit-in sauna (see enclosed FIR sauna h/o). Using this technique it is only the subcutaneous fat which is warmed, with the idea being to mobilise the chemicals from the subcutaneous fat onto the lipid layer on the surface of the skin, they can then be washed off. Inevitably some chemicals will be mobilised into the bloodstream with the potential to make that person feel ill, but this would be much less than if a traditional sauna was used and the core temperature of the patient raised. So Far Infra Red is as effective as, but less likely to produce initial worsening, as traditional saunas.

There are three key points about saunaing and sweating. The first one is that not only are toxins excreted in sweat, but so are the beneficial minerals. So after a sweat it is vital to re-hydrate with a physiological mix of minerals (such as my mix of MMMs – 1g in a glass of water) containing all essential minerals and take a small supplement of salt (say an eighth of a teaspoon salt on food). Secondly, it is important to shower immediately after a sweat in order to wash away chemicals which may otherwise be reabsorbed back through skin. Thirdly the most excretion of toxins occurs in the first few minutes of sweating as they move onto the surface of the skin – so the best results come from many short sessions (eg one daily just to the point of sweating) rather than protracted sweating which may make the patient feel ill.

Another method of detoxing is to take high dose essential fatty acids and other oils. The idea here is to replace contaminated fats in cell membranes and fatty organs with clean fats. The particular group of oils which are pertinent to fatigue syndromes are made up in the preparation VegEPA and I enclose my handout on this. Interestingly many people who take VegEPA report much improved sleep.

TL protein function is an area where more research is being done, but another possible reason for TL protein blockage is intracellular acidosis. This can occur with hyperventilation, which, I suspect, is much more common in CFS than realised. Hyperventilation causes a respiratory extracellular alkalosis, and intracellular acidosis – these changes can occur within a few abnormal breaths (see hyperventilation in CFS book).

If we are not making progress on this front then we could do more specialised tests of translocator protein function to see exactly what is blocking it. John McLaren Howard has now developed this test that we could do if we wanted to explore this area further.

Mitochondrial Function Score
I am now able to score mitochondrial function tests in order to give an energy score. I have now done several hundred of these tests, and the mitochondrial energy score accords closely with the level of disability. This score takes into account the levels of ATP, how well it releases energy (a magnesium dependent process), how efficiently oxidative phosphorylation works as well as translocator protein function. Carlos’s score is just 0.04 which equates to about 5/100 on my enclosed CFS disability scale (also see CFS book), so it is no wonder that there is a major problem with fatigue.

If the score does not fit clinically, then this may well be because of tissue damage. Many CFS sufferers push themselves to do things at the expense of damaging their tissues. So they can choose between feeling better and doing very little, or having a life and feeling terrible. Most do the latter. So the mitochondrial function score is a measure of how much energy they have got to spend and the cell free DNA a measure of how well they feel.

Note: DNA and ATP disability score do not match my present physical ability.The only thing I could suggest is that the mitochondria in my neutrophils, which are evaluated in the ATP profiles test, are in worse condition than those in my muscle cells. I don't know why this would occur.

Cell free DNA result
When cells are damaged or die, they spill their contents into the blood stream. All DNA should be contained within cell membranes. However, DNA from damaged cells is not – thus this is a good measure of cellular damage. This result shows a highly significant increase in cell degradation at 22.7ug DNA per litre (up to 9.5). To give an idea of the level of severity of this result, people with severe flu or who are on cancer chemotherapy produce cell free DNA levels of 30-40 ug DNA per litre. A high cell free DNA can result from any of the following, all of which need tackling as a separate problem:

a) There is poor antioxidant status (see Co Q 10, SODase, glutathione peroxidase),
b) There is ongoing toxic stress (such as from pesticides, volatile organic compounds, heavy metals etc),
c) There is immune activation (as, for example, in acute infection),
d) There is very poor mitochondrial function (see mitochondrial function) score but the patient is forced to do some muscular activity just in order to live.
e) The patient is not pacing well – i.e. pushing too hard and this is resulting in cell damage. However some people who are very disabled have no choice – just the energy required to exist will cause tissue damage. So people with the worst mitochondrial function score often have high cell free DNAs even though they are doing almost nothing.

People who come and see me with chronic fatigue syndrome often complain of the symptom of malaise - that is to say they just feel ill all the time. I suspect this is a symptom that arises from the immune reaction from damaged tissue, in other words a cell free DNA is a marker for this symptom of malaise.

Antioxidant status: Superoxide dismutase
The SODase result is fine at 42% (>40%). The normal level is above 40% inhibition, but the normal range is very narrow and a small deviation from this represents a clinically significant deficiency. Further analysis of this enzyme shows that the Zn/Cu form is 269 (240-410 enzyme units), the Mn form is 158 (125-208) and the EC (extra-cellular) form (another Zn/Cu SODase but not part of the functional SODase test) is 31 (28 – 70).

The gene studies show that the genes for Zn/Cu-SODase, Mn-SODase and EC-SODase are all normal.

Red cell glutathione peroxidase (GSH-PX)
Red cell glutathione (GSH) – 1.31mmol/l (1.7 – 2.6) - normal result
Red cell glutathione peroxidase (GSH-PX) - 48U/gHb (67 – 90) – very poor result

Glutathione peroxidase is made up of glutathione, combined with selenium. There is a particular demand in the body for glutathione. Not only is it required for GSH-Px, which is an important frontline antioxidant, it is also required for the process of detoxification. Glutathione conjugation is a major route for excreting xenobiotics. This means that if there are demands in one department, then there may be depletions in another, so if there is excessive free radical stress, glutathione will be used up and therefore less will be available for detoxification and vice versa. Of course in patients with chemical poisoning or other such xenobiotic stress, there will be problems in both departments, so it is very common to find deficiencies in glutathione.

I recommend that Carlos eat a high protein diet (which contains amino acids for endogenous synthesis of glutathione), and take selenium 200mcg daily (which is present in my physiological mix of minerals MMMs).
For this really poor result I would add in extra selenium, say another 300mcgms at night for four months (total daily dose 500mcgms) to bring Se levels up, then reduce to a maintenance dose of 200mcgms

A summary of the important antioxidants to consider are:
Superoxide dismutase (see above)
Glutathione peroxidase (see above) – this requires selenium 200mcgms daily (present in my physiological mix of minerals MMMs) and amino acids for its synthesis (high protein diet).
Co-enzyme Q 10 - is the most important antioxidant inside mitochondria (see above)
B12 – this is an excellent scavenger of the free radical peroxynitrite and may take over some of the function of SODase if this is very deficient
Other antioxidants also important as mentioned above – acetyl L carnitine, NAD (especially in the brain). Also vitamins A, C and E are essential antioxidants.
Natural antioxidants are also present in vegetables, nuts and seeds.

To Summarise
Although the regimes seem complicated, it is simply like getting a car engine to work. It is no good just filling the tank with fuel, or just unblocking the fuel pipe, or doing any one of the necessary jobs such as cleaning the spark plugs, unblocking the air filter, filling the engine with oil, unblocking the exhaust pipe etc on its own – one has to do all these bits in order to make it run. I have to say I have had such happy feedback from patients able to complete the regime that it is really well worth working hard at. The above recommendations have to be done in conjunction with my basic work up of all CFS sufferers with respect to:

• PACING,
• MICRONUTRIENTS – multivits, multimins, EFAs, vit C and D (‘Standard for all’ column on enclosed nutritional supplement sheet)
• SLEEP – aim for 9 hours between 9.30pm and 6.30am
• STONEAGE DIET (low glycaemic index diet which avoids the major allergens).

These “cornerstones” of recovery are described in detail in my CFS book. Once they are in place, Carlos should then introduce the other elements of the overall regime i.e.

(a) Correcting mitochondrial function - D-ribose, Mg injections, NAD, acetyl L carnitine, meat, Co Q 10.
(b) Addressing poor antioxidant status - B12, Co Q 10, glutathione peroxidase
(c) Detox regimes where appropriate – i.e. sweating techniques
(d) Identifying chronic infections
(e) Correcting any secondary hormonal lesions in particular secondary hypothyroidism, secondary hypoadrenalism and poor melatonin levels.

I know I am asking for much to be done and it maybe there is insufficient energy to put in place all the interventions required at once. Furthermore some of my very tender flowers do not tolerate all the interventions at once and so one has to progress slowly. I like to see patients get the regime in place and get the regime as tight as possible with respect to all the problems identified. Then I like them to be feeling well at rest. Then, and only then, may they risk trying to do a little more, but this must be on the proviso that any loss of stamina or delayed fatigue and they must pull back again. What many people are tempted to do is to cherry pick – that is to say just put in place the things they can do easily. However often the most difficult lifestyle changes are the most important – especially diet and sleep – and my experience is that the best results are achieved when all these issues are tackled simultaneously.

Carlos has chosen to receive this correspondence from me via email but if he wishes to receive my CFS book (which is too large an attachment to send) which goes into some of the above issues in more detail and contains many of the information sheets alluded to in the text, it is now available as a PDF file to download directly from my website, or a hard copy can be ordered by him postal charge only through my office.

I hope the above is helpful for management, please contact me directly if you have any queries.

Yours sincerely,

Dr Sarah Myhill

Encs: Magnesium by injection, B12 paper, Test results, CFS disability scale, FIR Sauna h/o, Feedback from mito tests h/o, Hypochlorhydria h/o, Supplement h/o, Stoneage Diet h/o, VegEPA h/o, Individual supplement regime, SF h/o, Cc.

Further details available on line at www.drmyhill.co.uk - my CFS book is now available as a PDF file for anybody to download directly from the website. Alternatively a copy of my CFS can be emailed to anyone requesting it from office@doctormyhill.co.uk.

Unfortunately we are unable to supply supplements to non-UK patients. To help you to source the supplements recommended above you can try the following websites.

www.biocare.co.uk , www.puritan.com , www.igennus.com , www.vrp.com .

Dr Sarah Myhill MB BS, Upper Weston, Llangunllo, Knighton, Powys, Wales, UK LD7 1SL
Tel: 01547550331 Fax: 01547550339 E-mail: office@doctormyhill.co.uk Website: www.drmyhill.co.uk
______________________________________________________________________________
CARLOS RODRIGUEZ INDIVIDUAL SUPPLEMENT REGIME MAY 2009
This regime of nutritional supplements comprises my standard supplements that all patients should have regardless of their problems, with the mitochondrial support as a bolt-on extra and the antioxidant support also as an extra as dictated by the tests that have been done. Some supplements have more than one function e.g. Co-Q 10 is essential for mitochondrial function and also an important antioxidant. Supplements in italics go into drinks. Introduce each supplement one at a time and it’s a good idea to keep a supplement diary so that you can pinpoint any that you are intolerant of. These amounts are what you should aim for, but start with tiny amounts and build up gradually.

Standard for all Mitochondrial support Extra Anti-oxidants
Morning
In ½ to 1 pint of water/ Acetyl L-Carnitine 1 gram
some fruit juice dissolve: (1 small scoop)
Ascorbic acid 1 g (1 small scoop)
(Or BioCare Vit C 1 g = 2x 500mg caps)
MMM 2 grams (2 small scoops) D-ribose 2.5 grams (½ teaspoon)

Swallow at breakfast with
the above solution:
BioCare Adult multivitamins x 1 capsule
Igennus VegEPA x 4 capsules
Vitamin Research Vit D3 x 2 caps Co-Enzyme Q10 100mg x 2 capsules
Niacinamide 500mg x 1 capsule

By injection Magnesium sulphate ½ ml B12 ½ ml
______________________________________________________________________________________________
Mid morning
D-ribose ½ a teaspoon in tea or coffee
_______________________________________________________________________________________________
Midday – lunchtime
Dissolve in ½ pint of water D-ribose ½ a teaspoon
MMM 1gram 1 scoop

Swallow: Co-enzyme Q10 100mg x 1 capsule
________________________________________________________________________________________________
Mid-afternoon
Dissolve D-ribose ½ a teaspoon in tea or coffee
________________________________________________________________________________________________
Evening
Dissolve in ½ to 1 pint of water/ Acetyl L-carnitine 1 gram
some fruit juice:
Ascorbic acid 1 gram
(Or BioCare Vit C 1 g = 2x 500mg caps)
MMM 2 grams D-ribose ½ a teaspoon
(or adjust to complete your daily dose)
With the above solution swallow
the following caps with food: Co-enzyme Q10 100mg 1 capsule - (after 3 months reduce dose to 100mg daily)
Igennus VegEPA x 4 capsules
After 3 months VegEPA can be reduced to 2-4 capsules daily
_________________________________________________________________________________________
Last thing at night in water/fruit juice D-ribose ½ teaspoon
Selenium 300mcg 3 drops
(for 4 months) – GSH-px

Recovery from the relapse... Mutaflor? Homeopathic drops?

2009-04-30T17:06:00.005+02:00

New tretament based on Genetic Profile

2009-04-18T03:57:00.008+02:00

Homocysteine, cholesterol and ammonia

2009-03-16T12:36:00.006+01:00

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

2009-02-17T02:09:00.005+01:00

OZONE Treatment good for intetinal dysbiosis

2009-02-13T11:20:00.004+01:00

KRYPTOPYRROLE / HPU / HPL / PORPHYRIA / B6 & Zinc

2009-02-06T16:49:00.005+01:00

Vitamin D Tips yaken from Carol's Blog

2009-02-05T12:58:00.003+01:00

Latest aminoacid test December 2008

2009-02-02T18:33:00.006+01:00

starting well 2009...

2008-12-31T16:24:00.004+01:00

Bioresonance Treatment in Munich (Not recommended)

2008-12-17T13:56:00.013+01:00

How to read an EBV blood test (Post 13)

2008-09-03T20:33:00.010+02:00

WINNING THE BATTLE TO EBV AND CMV!!! (LABOLIFE ANTIVIRALS) (Post 12)

2008-07-09T04:49:00.010+02:00

Comprehensive Stool Test (Post 11)

2008-06-11T18:20:00.012+02:00

NUTRITIONAL PROFILE: Glutathione Depletion and Blocked Methylation Cycle (Post 10)

2008-05-21T08:56:00.020+02:00

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)

These are my preliminary results on the lab test I did in European Laboratory of Nutrients. What is noticeable is the lack of Vitamin D, the glutathione depletion and the blockage of the methylation cycle. Nevertheless a more descriptive interpretation of these results will follow...

I will update this post with the conclusion in the coming days...

HPU Test Keac Laboratories
Carlos Gonzalez
Date 29/04/08
Value Reference Value
Hemopyrrollactamcomplex 0,9 < 1 uMol/L
Slightly Positive in Urine=> (Deficiency of P5P, manganese and Zinc)

ELN European Laboratory of Nutrients
Lab results 6/5/2008
Carlos Gonzalez

Value Reference Units
Elements in hair:

Calcium 1330 200-2000 mg/l
Magnesium 47 25-150 mg/l
Zinc 181 140-240 mg/l
Copper 17 12-60 mg/l
Manganese *0.10 0.15-2.30 mg/l
Selenium 0.66 0.40-2 mg/l
Chromium *0.10 0.15-1.40 mg/l
Cadmiun 0.10 0-0.5 mg/l
Lead 2.90 0-7 mg/l
Mercury *5.2 0-2 mg/l
Nickel 0.4 0-2.1 mg/l
Selenium 0.66 0.40-2 mg/l
Silver 1.57 1-1.9 mg/l
Aluminium 1 0-10 mg/l
Sulphur 49700 40000-60000 mg/l
Phosfor 148 90-180 mg/l
Iron *4.9 5-15 mg/l
Silicium *75.6 4-20 mg/l
Sodium *2 18-90 mg/l
Vanadium 31 9-80 mg/l

Ratio's

Calcium / Magnesium *28.3 5-18
Zinc / Copper *10.6 4-10
Zinc / Cadmium 1810 >400

Saliva tests
ADRENOCORTEX STRESS PROFILE

Morning cortisol *7 13-24 n/mol
Noon Cortisol *11 5-10 n/mol
Afternon Cortisol 8 3-8 n/mol
Midnight Cortisol 4 1-4 n/mol
DEHA-S *17 3-10 ug/l
Cortisol burden 30 23-42 (in a later analisys fell to 22)

Organic Acids in urine
CLYCOLYSIS

Lactic acid 42.65 0-10 mmol/mcr
Pyruvic acid 1.24 0-50 mmol/mcr
2-hydroxybutyric acid 0.83 0-2 mmol/mcr
Glyceric acid 1.42 0-10 mmol/mcr

AMINOACID METABOLITES

2-hydroxysovaleric acid 0.61 0-2 mmol/mcr
2- Oxoisovaleric acid 0 0-2 mmol/mcr
3-methyl 2- Oxoisovaleric acid 1.96 0-2 mmol/mcr
Hydroxyisovaleric acid 1.07 0-2 mmol/mcr
2- Oxoisocaproic acid 0 0-2 mmol/mcr
2-Oxo 4-Methybutyric acid 0 0-2 mmol/mcr
Mandelic acid 0 0-5 mmol/mcr
Phenyllactic acid 0.20 0-2 mmol/mcr
Phenypyruvic acid 0.42 0-5 mmol/mcr
Homogentisic acid 0.06 0-2 mmol/mcr
4-Hydroxyphenyllactic acid 0.47 0-50 mmol/mcr
Pyroglutamic acid *13.19 20-115 mmol/mcr
3-Indoleacetic acid 3.83 0-10 mmol/mcr
Kynurenic acid 0.46 0-2 mmol/mcr

FATTY ACID METABOLITES METABOLITES

3-Hydroxybutyric acid 1.21 0-10 mmol/mcr
Acetoacetic acid 0 0-10 mmol/mcr
Ethylmalonic acid 0.92 0-10 mmol/mcr
Methylsuccinic acid 0.96 0-5 mmol/mcr
Adipic acid 0.52 0-12 mmol/mcr
Suberic acid *3.22 0-2 mmol/mcr
Sebacic acid 0.09 0-2 mmol/mcr

MISCELLANEOUS

Glutaric acid 0.26 0-2 mmol/mcr
Methylmalonic acid *5.49 0-5 mmol/mcr
N-Acetyl-Aspartic acid 0.43 0-3.5 mmol/mcr
Orotic acid 1.64 0-36 mmol/mcr
3-hydroxy-3-methyglutaric acid 1.82 0-20 mmol/mcr
Hydroxyhippuric acid

YEAST FUNGAL

Cittramalic acid 0.84 0-2 mmol/mcr
5-Hydroxymethyl-2-furoic acid 17.25 0-80 mmol/mcr
3-Oxoglutaric acid 0 0-0.5 mmol/mcr
Furan-2,5-dicarboxylic acid 9.57 0-50 mmol/mcr
Furancarbocinglycine 0 0-60 mmol/mcr
Tartaric acid *30.56 0-16 mmol/mcr
Arabinose 17.65 0-47 mmol/mcr
Carboxycitric acid 0 0-46 mmol/mcr

BACTERIAL

2-hydroxyphenylacetic acid 0.55 0-10 mmol/mcr
4-hidroxyphenylacetic acid 9.28 0-50 mmol/mcr

ANAEROBIC BACTERIAL

DHPPA-analog 19.10 0-150
VMA-analog 2.45 0.31

KREBS CYCLE

Succinic acid 3.29 0-20 mmol/mcr
Fumaric acid 0.07 0-10 mmol/mcr
2-oxo-glutaric acid *11.68 15-200 mmol/mcr
Anconitic acid 14.70 0-25 mmol/mcr
Citric acid 518.05 180-560 mmol/mcr

NEUROTRANSMITTERS

HVA acid 2.12 0-3.5 mmol/mcr
VMA acid *3.69 0-3.5 mmol/mcr
5-hydroxindoleacetic acid 1.04 0-20 mmol/mcr

PYRIMINIDES

Uracil 5.89 0-22 mmol/mcr
Thymine 0.31 0-2

MISCELLANEOUS

Glycolic acid 14.35 0-100 mmol/mcr
Oxalic acid 2.90 0-100 mmol/mcr
Malonic acid 5.67 0-10 mmol/mcr
Methylglutaric acid 0.63 0-10 mmol/mcr
Hyppuric acid 360.89 10-400 mmol/mcr
4-hydroxybutyric acid 1.58 0-5 mmol/mcr
Phenylcarboxylic acid 0.50 0-15 mmol/mcr
Indol-like-compound 0.24 0-60 mmol/mcr

Urine Analysis:

Volume 1850 600-2500 ml
T3 *669 800-1800 pmol/24h
T4 *1664 1800-3000 pmol/24h
T3%mean ref. value 51.5
T3%mean ref. value 69.3
T3/T4 ratio *0.40 0.63-1
Reversed T3 *131 46-130 pmol/24h
T3/RT3 ratio *5.1 10-20
17-ketoSteroid 8.9 7-20 mg/24h
17-OH Steroid 10.4 6-21 mg/24h

Clinical Chemistry:

Malondialdehyde 0.71 <1.75 umol/l
Total homocysteine 5.8 4.5-12.4 umol/l
Lipoprotein A 99 0-300 mg/dl
DHEA Sulphate 3.96 0.94-11.7 umol/l

Glutathione Oxidized 0.49 0.16-0.50 nmol/l
Glutathione reduced 4.2 3.8-5.5 umol/l
Ratio Reducido/Oxidado 6.57 = (4,2-2x(0,49))/0,49

Vitamins:

Viatmin A 95 63-115 ug/100ml
Pantotenic Acid (B5) 1056 592-1842 ug/l
Vitamin B6 act (P-5-P) *33.8 13-30 ug/l
Vitamin C 1.36 0.9-2.1 mg%
Viatmin E 1.4 1.3-3.7 mg%
Vitamin D *25.2 32.8-86.8 ug/l

Vitamins: mol/l

Viatmin A 3.3 2.2-4 umol/l
Pantotenic Acid (B5) 4.8 2.7-8.4 umol/l
Vitamin B6 act (P-5-P) *137 48.6-121.4 umol/l
Vitamin C 77 50-120 umol/l
Viatmin E 33 30-87 umol/l
Vitamin D *63 82-217 umol/l

Elements in whole blood:

Sodium 1820 1820-2050 mg/l
Potassium 1860 1670-1970 mg/l
Calcium 51 48-61 mg/l
Magnesium 40.9 34-48 mg/l
Zinc 6 5.3-6.5 mg/l
Copper 0.9 0.8-1.3 mg/l
Selenium 0.139 0.12-0.41 mg/l
Manganese 17.2 14-37 ug/l

Sodium levels are quite low... sodium is involved in carrying nutrients across the cell membrane, neurological signalling and is controlled by adrenal hormones. Low sodium to potassium will create depression, paranoia and other nuerological issues. Low sodium is generally the result of an adrenal situation

Elements in serum:

Magnesium 21.3 19-24 mg.l
Zinc 0.9 0.8-1.4 mg/l
Copper 1 0.7-1.4 mg/l

Intracellular concentration:

Zinc 12 10.5-13.7 mg/l
Magnesium 63.9 52-80 mg/l
Copper 0.8 0.7-1.3 mg/l
Zinc/Copper ratio 15 9-16

Biological Amines:
CATACHOLAMINES IN PLATELETS

Serotonin 40.8 30-400 ng/10E10

Miscellaneous: (Methylation panel)

S-Adenosylmethionine (plasma) 93.4 82.7-156 nmol/l
S-Adenosylmethionine (RBC) 241 221-256 umol/dl
S-Adenosylmethionine (WBC) *3.7 3.9-8 cells
S-Adenosylhomocisteine (plasma) *39.7 21-35 nmol/l
S-Adenosylhomocisteine (RBC) *52.3 38-49 umol/dl

FOLIC ACID DERIVATIVES

5-CH3-THF 8.7 8.4-72.6 nmol/l
10-FORMIL-THF *1 1.5-8.2 nmol/l
5-FORMIL-THF *0.83 1.2-11.7 nmol/l
THF 0.76 0.6-6.8 nmol/l
Folic Acid 10.2 8.9-24.6 nmol/l
Folinic Acid (WB) *1.4 9-35.5 nmol/l
Folic Acid (RBC) *305 400-1500 nmol/l

Plasma Nucleoside
Adenosine *37.5 16.8-21.4 10^-8M

Aminoacids Urine 24h

Phosphoserine 55 28-91 umol/24h
Taurine 905 220-1292 umol/24h
Phosphoethanolamine 40 19-55 umol/24h
Aspartic Acid *153 29-149 umol/24h
Hydroxyproline 32 0-54 umol/24h
Threonine 153 83-321 umol/24h
Serine 382 132-580 umol/24h
Asparagine 130 66-306 umol/24h
Glutamic Acid 29 10-58 umol/24h
Glutamine 455 109-551 umol/24h
Sarcosine <1 0-2 umol/24h
α amino adipic Acid *57 9-51 umol/24h
Proline 14 0-35 umol/24h
Glycine 1429 380-2432 umol/24h
Alanine 355 141-491 umol/24h
Citrulline 5 0-28 umol/24h
α aminobutyric acid 19 11-35 umol/24h
Valine 46 10-54 umol/24h
Cystine 30 21-83 umol/24h
Methionine 51 16-62 umol/24h
Cystathione 19 15-75 umol/24h
Isoleucine 14 5-33 umol/24h
Leucine 39 11-51 umol/24h
Tyrosine 95 40-168 umol/24h
B Alanine *61 0-51 umol/24h
Phenylalanine 37 31-95 umol/24h
Beta Aminoisobutyric Acid 63 0-208 umol/24h
Homocystine (free) 3 0-4 umol/24h
Gamma-Aminobutyric Acid 11 7-35 umol/24h
Ethanolamine 277 146-352 umol/24h
Hydroxylisine 18 0-22 umol/24h
Ornithine 19 6-38 umol/24h
Lysine 99 76-336 umol/24h
1 Methylhistidine *504 128-392 umol/24h
Histidine 805 103-1207 umol/24h
Tryptophane 55 31-101 umol/24h
3 Methylhistidine 253 73-301 umol/24h
Anserine *48 0-46 umol/24h
Carnosine 70 0-98 umol/24h
Arginine 22 7-39 umol/24h
Volume 1850 600-2500 ml

Klinische Chemie:

DHEA Sulphate 3.99 0.94-11.7 umol/L
Cortisol 0.28 0.14-0.69 umol/L

Inhalent panel IgE

TREE / SHRUB (*Out of reference range)
Alder White
Penicillin
American Beech
American Hazel Nut
CottonWood
Elm mix
Mesquite
Oak Black
Sycamore Eastern

MOLDS
Bermuda grass
Jhonson grass
Rye grass
Timothy grass
Ragweed western

WEED POLLEN

Ragweed, western

MISCELLANEOUS
Cockroach german

Food Intolerances IgG

No apparent food intolerances on the test! In the past I had many... probably because I killed all the parasites: Giardia, Entamoeba hystolitica, etc... I only have blastocystis Hominis at the moment.

Notes:
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.

Based on the results of this Nutritional Profile, the supplements recommended are the following:

Suprasquash 2-3 capsules/day
Glutathion 150 mg or increase NAC dose 1-2 capsules/day
Magnesium taurate Plus (incl.B6) 2-3 capsules/day
Vitamin B2 - active 1 capsule/day
GTF chromium 50mcg 2 tables/day
Multivitamin 2 capsules/day
Manganese 1 tablet/day
Folinic/Folic acid 0.8-2 mg/day
B6/12/folic acid formula 1 capsule/day
Maybe also TMG/Bataine/Choline or lecithine: omnicholine 2-3 capsules/day

Apply with meals divided over the day. Start each product in lowest dose. Gradually increase on daily basis until the above mentioned rage has been reached. Consider testing vitamins and minerals 4-6 months after start supplements.

Supplements available at vital cell life, ask for 25% price reduction
Phone +31302871008
www.vital-cell-life.com
vcl@healthdiagnostics.nl

This supplements still have to be approved by my immunologist Josepa Rigau.

BIBLIOGRAPHY REGARDING THE TOPICS THAT CAME ABNORMAL IN THIS TEST (Source Metametrics)

TRACE ELEMENTS

Manganese (Mn)

Adequacy assessment: RBC Mn; BUN, urinary ammonia markers, arginine/ornithine ratio
Optimal forms: Sulfate, lactate, succinate, gluconate and citrate salts
Clinical indications: Deficiency: increased oxidative activity, Toxicity: neurotoxicity, including parkinsonism
Food sources: Tea, whole grains, legumes, nuts, green vegetables

The average adult contains 10 to 12 mg total-body manganese (Mn),32 primarily concentrated in tissues requiring high energy, including brain, and also found in liver, pancreas and kidney.432 Manganese is a group VII transition metal, existing in a number of different oxidation states, but in biological systems, the most prevalent are +2 and +3.

Chemically, manganese is similar to iron, so an imbalance in one may induce imbalance in the other. For example, iron deficiency may increase manganese transport, both in the GI and CNS, creating the potential for a toxic manganese burden.

Manganese is a cofactor for enzymes involved in metabolism of amino acids, lipids and carbohydrates. Manganese-dependent enzyme families include oxido-reductases, transferases, hydrolases, lyases, isomerases and ligases. Examples of manganese-containing enzymes are arginase, glutamine synthase and mitochondrial superoxide dismutase (referred to as SOD2 or MnSOD).

Physiological activities include immune function, regulation of blood sugar and cellular energy, reproduction, digestion, bone growth, and protection from oxidative challenge. Manganese with vitamin K supports blood clotting and hemostasis.

Clinical Associations of Manganese

Change in CNS manganese tissue concentration may be accompanied by convulsions. Both high and low blood manganese has been associated with seizure disorders. In one reported case, a 3-year-old child presented with idiopathic seizure disorder.

The only abnormal findings were elevated blood manganese and encephalopathy on EEG. The patient, who was non-responsive to antiepileptic medication, deteriorated to status epilepticus. Immediate resolution was attained upon administration of IV Ca-EDTA therapy. Exposure to welding done by her father over 1 month was the reason for the child’s manganese burden.

Increased activity in MnSOD with concurrent reduction in cytosolic SOD (which is copper and zinc dependent) was demonstrated in vitro after cellular gamma ray irradiation exposure, demonstrating that MnSOD assessment may be a biomarker of radiation sensitivity, as well as illustrating the import of MnSOD in radiation-induced tissue damage.
Iron overload disorders such as Friedreich’s ataxia (FA), sideroblastic anemia (SA) and hemochromatosis demonstrate reduced activity of MnSOD.

Both FA and SA present with increased iron deposition in mitochondria. FA, a neurodegenerative and myocardial disease, is caused by decreased expression of the iron-regulating mitochondrial protein, frataxin. Low frataxin causes iron overload and manganese depletion, greatly reducing MnSOD activity. In a frataxin-deficient yeast model, manganese was shown to increase MnSOD, whereas a MnSOD mimetic showed little effect. These iron-overload conditions require increased antioxidative support as afforded by MnSOD.437-441 Manganese may be a worthy treatment consideration in such disorders.

High doses of N-acetylcysteine was shown to induce formation of manganese superoxide dismutase in vitro, thereby preserving its activity. Women demonstrate increased absorption of manganese and increased MnSOD activity mediated by estrogen, which may exert antioxidant effects by this mechanism.

All forms of SOD are down-regulated in estrogen deficient mice that also show increased vascular free radical activity. Progesterone has been shown to reduce SOD activity, and thus antagonize the vasoprotection induced by estrogen. These findings may in part explain why hormone replacement therapy with estrogen plus progesterone displayed no beneficial effect on cardiovascular event rates in prospective clinical
trials.

Frank manganese deficiency in humans to date has been studied only by chemically induced manganese depletion. However, individuals with low manganese intake have impaired growth, poor bone formation and skeletal defects, reduced fertility and birth defects, abnormal glucose tolerance, and altered lipid and carbohydrate metabolism. Men experimentally placed on manganese-depleted diets developed a rash on their torsos, and women consuming < 1 mg manganese/d in
their diet developed altered mood and increased pain during premenstruation.

Arginine converts to either ornithine or citrulline, producing urea or nitric oxide (NO), respectively. Inhibition of arginase reduces conversion of arginine to ornithine and promotes conversion into citrulline, thereby increasing NO production (and decreasing urea production). Because manganese is the cofactor for arginase, lowered plasma manganese correlated with lower arginase activity and corresponding increased nitric oxide production in patients with childhood asthma.

Similarly, manganese deficiency in rats enhances endothelium-dependent vasorelaxation of aorta. Arginase inhibitors are being considered as potential interventions for increasing nitric oxide.

Toxic effects of inhaled manganese in dust or aerosols have been reported from occupational exposure in welding or steel alloy production. Toxicity via ingestion, primarily from water sources, has also been reported.

Total parenteral nutrition is a potential iatrogenic route of toxic exposure to manganese. Manganese is being considered as an additive for gasoline, as a lead replacement. Although it has been shown to greatly improve oil combustion, attention must be given to the potential for increased exposure.

Vegetarianism may increase manganese body burden via increased dietary consumption and/or iron deficiency-induced increased manganese absorption. Soy beverages, including infant formula, have been shown to contain 100-fold greater amounts of manganese than human milk, and 10-fold greater amounts than bovine sources. Studies using soybased formulas in primates show increased incidence of behavioral disorders. However, soy is rich in phytates that inhibit absorption of manganese as well as other elements. Thus, vegetarians eating large amounts of soy may, paradoxically, develop manganese deficiency. Since bile is the main route of manganese elimination, individuals with liver disease frequently present with higher levels of manganese, and therefore are at greater risk of toxicity.

The organ most vulnerable to manganese toxicity is the brain. Manganese concentrates in areas with high iron, including the caudate-putamen, globus pallidus (GP), substantia nigra and subthalamic nuclei. The neurotoxicity of manganese appears to be mediated by the oxidation of divalent to highly oxidative trivalent manganese via superoxide, inducing a cascade of oxida-
tive mediators damaging cellular components, primarily in the mitochondria. Chronic, low-level exposure to manganese has been implicated in neurologic changes, decreased learning ability in school-aged children, and increased propensity for violence in adults.

Frank manganese toxicity, “manganese madness,” presents similarly to schizophrenia. Symptoms include compulsive or violent behavior, emotional instability, hallucinations, fatigue and sexual dysfunction.Mechanistically, this initial presentation is likely due to lesions in the GABAergic neurons of the globus pallidus.

As the condition progresses, damage to the dopaminergic neurons in the substantia nigra causes a clinical presentation similar to parkinsonism, but differentiable by the presense of dystonia induced by GP lesions. Furthermore, manganese-induced dopaminergic neuronal oxidation caused general derangements in the hypothalamic-pituitary-adrenal (HPA) axis, including abnormal serum prolactin, TRH, FSH and LH. Additionally, excess manganese can inhibit astrocyte glutamate reuptake, thereby increasing glutamate’s excitotoxic potential, and its time in the synapse.

Clinical efficacy has been demonstrated for EDTA chelating therapy in a case of occupational parkinsonism due to manganese exposure. Improved clinical pattern due to reduction of heavy metal deposition in basal ganglia was confirmed by MRI.

Occupational exposure to manganese compounds in this case resulted in high blood and urinary levels of the metal.
Manganese enters the CNS and is absorbed along the length of the small intestine through the divalent metal transporter 1 Maximal GI absorption is about 3%. Since iron shares the same transporter, increased manganese GI absorption and CNS delivery has been shown to occur in iron deficiency states, contributing to increased manganese burden.

Conversely, manganese absorption is decreased in the presence of iron. Excretion is primarily via bile to feces, with minimal elimination in urine. Phytates may inhibit absorption, and reducing dietary manganese and increasing biliary elimination further decrease manganese in the body.32, 100 Given the similarity manganese has with iron, it may be that similar counter-ions would increase GI bioavailability, including sulfate, gluconate and citrate.

Manganese is rapidly cleared from blood and stored in liver and other organs.32 In plasma, manganese is largely bound to gamma-globulin and albumin, with a small fraction of trivalent manganese bound to the iron-carrying protein, transferrin.
Assessing Manganese Status Some review articles have concluded that there is no reliable index or biomarker for evaluating manganese insufficiency. Others have concluded that of the direct biomarkers used, RBCs are best associated with long-term levels and are considered to be a good index of manganese status. Manganese is frequently measured in profiles of trace elements in RBCs or whole blood where low levels are found in manganese-depleted individuals.

A number of studies examining normal or deficient manganese in a variety of human populations have relied on erythrocyte measurements. Such findings may be combined with other functional markers known to appear abnormal when manganese insufficiency is affecting metabolic activity. Altered plasma concentrations of ammonia and urea are found in association with decreased hepatic manganese concentration in young growing rats.465 Thus, serum BUN and sensitive urinary markers of urea cycle activity may be helpful along with demonstration of an elevated plasma arginine-ornithine ratio to achieve an assessment of low manganese effects.

Hair manganese is a valid indicator of toxicity in cases of manganese excess, but there is controversy over its use for deficiency states.Inconsistent results have been reported from studies using plasma, serum or urine to evaluate manganese status.Because of its strong paramagnetic quality and primary site of toxicity in the CNS, manganese toxic burden is readily assessed using T1-weighted MRI. RBC manganese demonstrates a high correlation with MRI (r = 0.55, p = 0.02) in manganese-exposed workers prior to onset clinical symptoms. Additionally, RBC manganese was shown to correlate specifically with CNS globus pallidus burden. RBC and MRI manganese assessment also correlated in liver cirrhosis patients.

Manganese Repletion Dosing Bioavailable forms of managnese include sulfate, lactate, succinate, gluconate and citrate. Dosing range is 5 to 13 mg/d for adults residues on thyroglobulin and is responsible for phenoxy-ester bond formation between the rings of monoiodo-L- tyrosine (MIT) and diiodo-L-tyrosine (DIT) to form T3 and T4 on Tgb. Afterwards, lysozome-mediated hydrolysis liberates the iodinated compounds from Tgb. MIT and DIT are recycled and T3 and T4 are released into the bloodstream. Peripheral conversion of T4 to the metabolically active T3, and subsequent breakdown of T3, requires the selenoproteins476 iodothyronine deiodinases (D1 and D2).32 Similarly, the deiodinases work inside the follicular cell to recycle tyrosine and iodine.

Chromium (Cr)

Adequacy assessment: RBC, whole blood, urine, hair; Insulin, blood glucose
Optimal forms: Nicotinate, chloride, histidine or picolinate salts
Clinical indications of deficiency: Blood sugar dysregulatory conditions
Food sources: Whole grains, legumes, nuts, yeast, meats

Unlike most essential elements that have multiple metabolic functions, the only known role for chromium
(Cr) is in potentiating insulin receptor tyrosine kinase This autoamplification allows chromium to exert broad influence on carbohydrate, lipid and protein metabolism. Total-body chromium concentration is only about 4 to 6 mg, and decreases with age.

There are small chromium storage pools in the testes, kidneys and spleen. Trivalent chromium is the only oxidation state required in biological systems. Hexavalent chromium is a well-known carcinogen that is particularly associated with lung tumor induction.

Clinical Associations of Chromium
Chromium and insulin work in tandem. When insulin is released into circulation, chromium transport to insulin-sensitive cells is increased. Once inside the cell, chromium acts as an autoamplifier of the insulin receptor tyrosine kinase. However, chromium is a nutritional double jeopardy. It is known to be removed from some carbohydrates during the refinement process,
making it less available during the insulin rise. It has also been demonstrated that increased urinary wasting of chromium occurs in conditions of elevated blood glucose and insulin. Thus, consuming refined carbohydrates exacerbates losses of chromium and induces insulin resistance.

In the 1950s, rats on a chromium-deficient diet were found to have reduced ability to remove glucose from blood. Subsequent research demonstrated that chromium transport and cellular uptake is stimulated by the presence of insulin. Chromium is delivered to insulin-sensitive cells on the iron-binding transport protein transferrin. In the cytosol, it is theorized that chromium complexes with apochromodulin, inducing a conformational change, which creates active chromodulin.

Chromodulin is a protein that is rich in cysteine, glycine, glutamate and aspartate residues and tightly binds four ions of trivalent chromium. It is also referred to as low-molecular-weight chromium-binding substance (LMWCr), and is similar in structure to yeast glucose tolerance factor (GTF). Chromodulin dramatically increases the tyrosine kinase activity of the insulin
receptor, thereby inducing downstream events stimulated by insulin. For example, chromium supplementation enhanced translocation to the plasma membrane of glucose transporter 4 protein in insulin-resistant animals. Once blood insulin levels drop, the insulin receptors undergo a conformational change that allows for the release of chromodulin, which is then apparently expelled from the cell and eliminated in urine. However, in cases of insulin resistance, with increased concentra-
tion of blood glucose and insulin, there is a paradoxical urinary wasting of chromium, most likely in the form of chromodulin.
Since chromium is integral to insulin signaling, all insulin-mediated metabolic events improve with identification and correction of chromium insufficiency.

Chromium-induced improvements have been demonstrated in type 2 diabetes, including improved lipid and carbohydrate metabolism, reduced blood insulin and glucose, and reduced body weight.607 Chromium supplementation has shown efficacy with atypical depression, illustrating a link between blood sugar, insulin and mood. Both gestational and steroid-induced diabetics have demonstrated positive response to chromium supplementation. Chromium use in individuals exhib-
iting no blood sugar irregularities has no demonstrated beneficial effect.Hexavalent chromium (Cr VI) is 1,000 times more
toxic than trivalent chromium (Cr III). In addition to its carcinogenicity, topically, hexavalent chromium is an irritant, causing severe dermatitis. Cr VI is still widely used in industry, and is present in cigarette smoke, paint pigment, chrome plating, leather tanning, metal pros-theses and copy-machine toner.609 Microflora appear to participate in the reduction of hexavalent chromium to trivalent chromium, minimizing the effects of toxic exposure.

Contamination of ground water with hexavalent chromium, and the associated morbidity and mortality to residents of the area resulted in the largest settlement paid in a direct action lawsuit in US history and was the subject of the film Erin Brockovich.
Jejunal absorption is inversely related to dietary intake, but is generally quite low, ranging from 0.5 to 2%. Similar to iron, chromium absorption is inhibited by phytates and enhanced by ascorbic acid. There appears to be competition by other elements, including iron, zinc, manganese and vanadium. Excretion is via both renal and fecal routes.

Chromium appears in urine primarily as chromodulin. There is a lag time between oral ingestion of chromium and appearance in urine, indicating incorporation into chromodulin prior to excretion. Elevation of glucose and insulin lead to increased excretion of chromium, as chromodulin. The Fe-transport protein, transferrin, appears to maintain Cr3+ levels in the blood plasma and to transport Cr to tissues in an insulin-responsive manner.

Assessing Chromium Status
Total-body chromium is so low that analytical issues have limited accurate direct measures of the element. However, instrumentation advances such as the addition of the dynamic reaction cell (DRC) filters for inductively coupled plasma mass spectrographic (ICP-MS) methods allow accurate detection of chromium in urine, serum and whole blood. The DRC adaptation removes interfering argon carrier gas atomic species, largely eliminating interferences that have compromised chromium
measurements in the past. While methodology has improved, chromium levels in states of insufficiency differ depending on matrix and physiological conditions, resulting in inconsistencies that appear to greatly complicate interpretation.

Erythrocyte chromium has been used to assess excessive levels of exposure in workers exposed to chromate. When exogenous chromium contaminationis limited, hair continues to be a viable specimen option for establishing long-term chromium status.
Given the difficulties with interpretation of direct chromium concentration measurements, functional evidence for dysglycemia, such as elevated blood glucose and insulin levels, or an abnormal glucose-insulin tolerance test can provide a functional assessment of chromium insufficiency. Thus far, the reversal of symptoms with chromium supplementation is currently
the only generally accepted indicator of chromium deficiency.

Since chromium is excreted as the insulin-stimulated metalloprotein chromodulin, urinary chromium presents a special situation, where levels may provide a type of functional assessment because of the high percentage that is excreted in the form of chromodulin.

Further research into the interpretation of fasting and non-fasting urinary chromium levels is warranted. When exogenous chromium contamination is limited, hair continues to be a viable specimen option for establishing long-term chromium exposure. An abnormal glucose-insulin tolerance test may provide a functional assessment of chromium insufficiency.

Chromium Repletion Dosing
Chromium picolinate (200–100 µg) is an effective supplementation for treating diabetes and weight gain from insulin insensitivity. Chromium picolinate may function similarly to chromodulin. The form derived from yeast called chromium-glucose tolerance factor (GTF), the glutathione-dinicontinate complex similar to the chromodulin complex, is not effectively
absorbed. The chromium-histidine complex appears to be highly bioavailable.

Mercury (Hg)

Toxicity symptoms: Mental symptoms (erethism, insomnia, fatigue, poor short-term memory), tremor, stomatitis, gingivitis, GI and renal disturbances, decreased immunity Body burden assessment: Whole blood, erythrocyte, serum, hair, urine, urinary porphyrins
Protective measures: Selenium (protects against cellular toxic effects)
Chelating agent: DMSA, DMPS
Common sources: Dental amalgams, fish consumption, preservatives (esp. thimerosal), industrial relaease

Mercury (Hg) as a neurotoxin has an intriguing history. The phrase “mad as a hatter” has its origins with the seventeenth and eighteenth century hat makers who suffered from mercurialism due to their use of liquid mercury in the manufacture of the popular felt-brimmed hats. Sir Issac Newton, the famous seventeenth century physicist, experienced a year of dark moods and marked personality change that puzzled friends and close associates.

Posthumous analysis of archived samples of Newton’s hair revealed highly elevated concentrations of mercury, which is evidence that supports the historical hypothesis that Issac Newton’s “madness” was a result of his exposure to the toxic metal while he was conducting experiments to study its properties. The human population is exposed daily to naturally occurring mercury. The earth’s crust releases approximately 30,000 tons of mercury per year as a product of natural outgassing from rock. Mining, smelting and combustion of fossil fuels, particularly coal, are a primary source of anthropomorphic mercury exposure.

Approximately 6,000 tons/year of mercury are used in the manufacture of electrical switches, for electrolysis, and as a fungicide. Ninety tons of mercury are used each year for making dental amalgams. According to the CDC, mercury released from amalgams may comprise up to 75% of an individual’s mercury exposure.

The amount of mercury released from amalgams ranges between 1.2 to greater than 27 µg/d. Toxicity associ- ated with mercury amalgams continues to be a serious concern, particularly in regard to pregnant women, as mercury is a known neuroteratogen.

In its elemental form, mercury (Hg0) is non-toxic. However, once chemically or enzymatically altered to the ionized, inorganic form (Hg2+), it becomes toxic. Thus, bioconversion of mercury to its organic alkyl forms renders some forms such as methyl mercury highly toxic with great avidity for the nervous system.

Another commonly encountered organomercury compounds is ethylmercury that is released from thimerosal. Microorganisms in the environment and in the human intestinal tract can bioconvert non-toxic elemental mercury to inorganic Hg2+ and organic mercurous alkyl compounds.

Methylmercury is highly water soluble and readily enters aquatic food chains, accumulating at higher concentrations in the tissue as it moves up the food chain of marine organisms. Bioaccumulation of methylmercury in organisms at the top of the aquatic food chain is on the order of 10,000 to 100,000 times greater than concentration in the ambient waters.Indeed, methylmercury from seafood is considered to be the most important source of non-occupational human mercury exposure.

Analysis of commercial fish in New Jersey markets found bioaccumulation to be the highest (in descending order of magnitude) in yellow fin tuna, Chilean sea bass, bluefish and snapper.

Thimerosal has been widely used to preserve vaccines used for immunizations. The mercury thioether structure of thimerosal can be metabolized or chemically degraded to release the much more toxic ethylmercury.

Although lack of data makes precise comparisons of safe levels of exposures to different forms of mercury difficult, we may gain insight about the potential for toxic effects from the available data on mercuric chloride, ethylmercury and methlmercury. Thimerosal, a mercury-containing preservative used in vaccines, has been a common source of mercury exposure for children.

In the human body, thimerosal releases ethylmercury. In 2002, it was demonstrated that the mean total mercury dose in vaccines received by 6-month-olds was 111.3 µg (range 87–175 µg).In a 6.2 kg infant, 111.3 µg translates to 18 µg/kg/d or about 2.6 times the adult minimal risk level (MRL) of 7 µg/kg/d for acute mercuric chloride exposure.

The US Environmental Protection Agency (EPA) sets a reference dose (RfD) of 0.1 µg/kg body weight/d for chronic exposure to methylmercury, at which there are no recognized effects. Using the EPA’s RfD, a vaccination containing 111.3 µg mercury would expose a 6.2 kg infant to 29 times the safe level for chronic methylmercury exposure. Based on such inferences, governmental health authorities now advocate removal of thimerosal-containing childhood vaccines.

Clinical Associations of Mercury Toxicity
There are three known ways by which toxic effects are produced by mercury: (1) It reacts with sulfhydryl groups impairing the activity of enzymes, (2) it generates protein adducts that are immunogenic, and (3) its highly lipophilic alkyl forms alter nerve membrane function.Autoimmune glomerulonephritis in mercury-exposed individuals has suggested an association between exposure and autoimmunity in humans.

Mercury intoxication, in turn, can produce a triad of symptoms: (1) mental changes, (2) spontaneous tremor and deficits in psychomotor performance, and (3) stomatitis and gingivitis. The mental effects include erethism (excessive irritability, excitability or sensitivity to stimulation), depression, short-term memory loss, difficulty concentrating, insomnia and fatigue. Additional signs of neurotoxicity include loss of vision, hyperreflexia, sensory disturbances, imparement of speech and hearing, hyperhidrosis and muscular rigidity. Signs and symptoms of mercury intoxication involving other organ systems include renal and gastrointestinal disturbances, pain in joints and limbs, weight loss, metallic taste in the mouth and increased susceptibility to infections.

Mercury released from dental amalgams, which are composed of as much as 50% mercury, can have a negative impact on an individual’s health. Although mercury-containing amalgams have been in use for over 100 years, their use was intensely debated at the turn of the century and again in the 1930s. Small yet measurable amounts of mercury are continuously released from the amalgam surface; the rate of release is accelerated by hot liquids and chewing. Normal bacterial flora converts a fraction of the released elemental mercury to its toxic forms, Hg2+ and alkyl mercury. A portion of the elemental mercury released from amalgams is unavoidably inhaled into the lungs, where it can be biotransformed to its toxic forms. Studies have suggested that chronic mercury exposure in amounts released by amalgams provokes an increase in both mercury- and antibioticresistant strains of bacteria in the oral and intestinal flora.

Such mercury-induced aquired resistance to antibiotics has been found worldwide in fish and soil bacteria. Epidemiologic data from the US EPA and CDC have led to estimates that more than 300,000 newborns each year may have increased risk of learning disabilities associated with in utero exposure to methylmercury.

Chinese children with both inattentive and combined attention deficit hyperactivity disorder (ADHD) have blood mercury levels higher than controls. Risk of ADHD was found to be nearly 10 times higher when blood mercury was above 29 nmol/L. With the pronounced rise in the incidence of autism over the last decades, much debate continues regarding mercury’s role in the pathogenesis of this neurodevelopmental condition. Although research does point to the eitiology of autism being multifactorial, numerous reports demonstrate that aspects of mercury toxicity appear similar to autism symptomatology.

In 2002, thimerosal was phased out of some vaccines, as recommended by the US Public Health Service and the American Academy of Pediatrics. Data from the Vaccine Adverse Event Reporting System (VAERS) reported a significant reduction in the proportion of neurodevelopmental disorders, including autism, mental retardation and speech disorders, as thimerosal was removed from childhood vaccines in the United States from mid-1999 onward. As of the date of this writing, since regulations do not govern all sources, vaccines must still be verified as thimerosal free.

In addition to the previously discussed nutritional factors, gender and age can also influence mercury status and toxic consequences. In an Austrian population with generally low levels of mercury, values in males were influenced by fish intake, amalgam fillings, age and education level, whereas those for females varied only with dietary fish intake, indicating gender-specific effects. In older Americans, visual memory ability declines as blood mercury levels rise, although other neurological tests such as finger tapping were uaffected.867

Assessing Mercury Body Burden and Toxic Effects
A primary function of the clinical laboratory is to assist clinicians in making decisions about when to treat a patient for heavy metal toxicity. However, there is considerable debate over how to establish reference limits for mercury (and other toxic metals) on clinical laboratory reports. The US EPA RfD for chronic mercury exposure of 0.1 µg/kg/d is equivalent to a total exposure of 7 µg/d in a 70 kg adult. If the amount of mercury absorbed from dental amalgams is combined with all other sources of mercury (e.g., fish, environmental, occupational and medicinal), the daily exposure to mercury is expected to exceed the RfD for some individuals.In populations such as occupationally exposed workers and the elderly, the percentage of mercury-threatened individuals can be much higher.

Based on a study of normal, presumably healthy populations, mean wholeblood mercury concentration was found to be < 5 µg/L. About 1% of this population had whole-blood levels of mercury greater than 5 µg/L. Individuals with occupational exposure to mercury, such as dentists and dental technicians, may routinely have whole-blood mercury up to 15 µg/L. Significant exposure is evident when whole-blood alkyl mercury is greater than 50 µg/L, or when Hg2+ exposure is greater than 200 µg/L. Based on the first German Environmental Survey on Children, lowering of reference values for whole-blood mercury from 1.5 to 1.0 µg/L has been proposed.

Consumption of large amounts of fish by pregnant women in Hong Kong results in prenatal exposure to moderately high levels of mercury shown by finding cord-blood mercury levels above 29 nmol/L (5.8 µg/L) in newborn infants. A separate study found that, compared with the national average, women who ate fish were 3 times more likely to have elevated cord-blood levels. Of the 275 women who completed the study, 28.3% had cord-blood mercury above the 5.8 µg/L reference level set by the EPA. In a random sample of 474 subjects in Baltimore, Maryland, 9% had blood mercury levels above the 5.8 µg/L limit. However, elevated levels (> 5.8 µg/L) are found in 16.5 % of women in populations with high fish consumption.

Blood mercury has revealed low level chronic and acute exposure from work environments, whereas elevations of mercury have been reported as high as 16,000 µg/L in blood and 11,000 µg/L in urine. At massive elevation levels, interpretation is straightforward, allowing assessment of patient exposure factors and clinical consequences. As with most tests performed on a broadly varying outpatient population, interpretation of results from measurements of mercury in blood or urine become more difficult as concentrations approach the population norms of 10 to 20 µg/L.

Concurrent or follow-up testing of biomarkers that show toxic consequences, such as elevated porphyrins, beta-2-microglobulin or N-acetyl-beta-D-glucosamine can be very helpful.

The level of mercury in urine is a reliable way to assess exposure to inorganic mercury. Daily urinary levels greater than 50 µg indicate a Hg2+ overload. Hair levels of mercury greater than 1 µg/g also indicate mercury toxicity. The quantity of mercury assayed in blood and hair, but not urine, correlates with the severity of toxicity symptoms.

Erythrocyte mercury shows a strong relationship with erythrocyte selenium, suggesting a chemical linkage between the two elements. Erythrocyte mercury was strongly correlated with plasma mercury, and both mercury and selenium levels were strongly correlated with fish intake.Hair has been a frequently used specimen by CDC and EPA for accurately assessing mercury exposure in selected populations.A number of studies have shown positive associations between mercury concentrations in blood and hair. Hair to blood ratios ranging from 200 for maternal hair-cord blood to 360 for hair-blood values in 7-year-old children have been reported. Populations of Brazilian communities showed a positive correlation of blood pressure with levels of hair mercury. At levels above 10 µg/g, the odds ratio for elevated systolic blood pressure was 2.9.

Both blood and hair mercury levels drop between the second and third trimesters of pregnancy. Maternal hair correlates with cord blood, both levels being related to fish intake. Measurement of mercury concentrations in body tissues or fluids provides evidence of exposure, but it does not answer the question of toxic effects that are dependent on many other factors. Variations in status of thiols such as glutathione, cysteine or lipoic acid shift the dynamics of mercury’s effects, as do the levels of metallothionein, zinc and selenium, or even glutamine. Specific patterns of urinary porphyrin abnormalities have been clearly associated with mercury, providing a convenient and sensitive biochemical marker of metabolic toxicity.

Management of the Mercury-Toxic Patient
Removing the source and optimizing routes of mercury elimination should be the first treatment for mercury toxicity. Antioxidant intervention may be helpful for mitigating the oxidative damage caused by mercury toxicity. Some antioxidants such as N-acetyl- cysteine, alpha-lipoic acid and glutathione may posess chelative effects. Selenium has been demonstrated to effectively bind mercury, rendering the mercury ineffective (see the section “Selenium” above). More aggressive treatment for mercury toxicity calls for chelation therapy.

Administration of BAL, penicillamine, EDTA, DMSA or DMPS will mobilize mercury and cause a rise in the daily urinary mercury excretion rate. The preferred chelation agents, based on their affinity for mercury and low toxicity, are DMSA or DMPS.2 All of these agents should be used with monitoring of mercury metabolic toxicity, since they can mobilize relatively inert bound forms of mercury. If porphyrin profile signs start to worsen, treatment may need to be suspended until newly mobilized mercury reaches equilibration with metallothionein and other routes of binding for excretion.

Removing brain accumulations of mercury is a challenge. DMSA and DMPS may not be effective agents for removing toxic metals found in the CNS, as they are very unlikely to cross the blood-brain barrier. It has been suggested that alpha-lipoic acid may cross the blood-brain barrier, and combinations of ascorbic acid and glutathione may help to allow mercury transport away from tissues by altering the ionic form. However, when combinations of these interventions were tested in mercury-exposed rats, no reduction in brain mercury was found.

Of Further Interest…

Toxic element accumulation is dependent on route and duration of exposure, form of toxic element and presence of protective measures. For example, rats maintained for 18 months on low-selenium diets and consuming drinking water containing 5.0 ppm of mercury as methylmercury had 10-fold higher mercury in brain compared with those given water with 0.5 ppm mercury. However, brain mercury increased only slightly in similarly exposed rats fed diets with high selenium content (0.6 vs. 0.06 ppm), and no increase was seen at lower levels of exposure, showing the protective effect of dietary selenium.

Another important observation from these experiments was that mercury was higher in neonatal rats that also had lower retention of selenium, and blood and brain mercury levels fell with age as selenium levels stabilized. Such results raise timing issues and possible protective measures. Administration of vitamin C, glutathione or lipoic acid in combination with DMPS or DMSA to young rats for 7 days following a 7-day exposure to elemental mercury vapor had no effect on brain mercury.

Here, the toxic element form was elemental versus methyl mercury, and administration was by inhalation for 7 days rather than ingestion for 18 months. The protective measures were administered for only 7 days and only after exposure had occurred. Longer-term administration of the protective nutrients might produce quite different results, especially if tissue levels are raised before exposure. Kidney mercury in the rats exposed to mercury vapor was lowered by DMPS and DMSA, but no combination was found to affect levels in brain.

These results provide insight about differences in tissue distribution and ligand character. In metallothionein-rich kidney tissue, bound mercury is more dissociable than that bound to enzymes in the brain. Such differences among tissues in their sequestration tendencies leads to concern about potential redistribution induced by therapies that cause mobilization of toxic metals. Thus mercury released from extrahepatic tissues might transfer to brain as a result of chelation therapies. Very little is known about how much such redistribution actually occurs for any given chelator. Such effects may account for the suggestions that treatments of past mercury exposures with N-acetylcysteine or reduced glutathione may be counterproductive.

For toxic elements other than mercury, the constant redistribution over time produces an accrual in bone, where they are bound in the hydroxyappetite matrix. These forms are of lower concern (and low contribution to laboratory element testing) until they are remobilized during bone resorption. Such issues complicate the evaluation and treatment of patients with toxic element effects.

Sodium (Na)

Sodium (Na) along with chloride comprise the major electrolytes of the body’s extracellular fluid (ECF). Sodium deficiency is rarely considered outside of unusual circumstances of losses due to vomiting and diarrhea or sweating. In such cases, the imbalance in ECF and intracellular fluid (ICF) allow water to pass into the cells in excess, leading to symptoms of water toxicity, including apathy, muscle twitching and loss of appetite. When both sodium and water are lost, total blood volume decreases, causing hypotension, tachycardia and other heart disturbances. Prolonged imbalances in ECF and ICF can become serious emergencies.

Excessive sodium intake is widely considered to be a risk factor in certain cases of hypertension, and frequent monitoring with 24-hour urinary sodium measurements is recommended to help educate patients who need to lower sodium intake. Magnesium deficiency has been demonstrated to impact electrolytes, including sodium, potassium and calcium.

Iron (Fe)
Adequacy assessment: Ferritin, hemoglobin, hematocrit, total iron binding capacity, transferrin saturation
Iron excess: Transferrin saturation
Optimal forms: Ferrous gluconate, fumarate, and citrate salts; combine with ascorbate
Clinical indications of deficiency: Fatigue, delay in growth or cognitive development, weakness, arthralgias, organ damage
Food sources: Organ meats, brewer’s yeast, wheat germ, egg yolk, oyster, dried beans, and some fruits

It has been estimated that 6 of 100 Americans are in negative iron balance, whereas 1 of 100 have iron (Fe) overload. Iron overload can be caused by a common genetic disorder in the United States. There are only about 2.5 to 4 grams of iron in the healthy human body, yet this element has critical functions, and the human body has an intricate system of maintaining homeostasis.

Human understanding of iron and anemia has a long history, and therefore a wealth of information is available on its absorption, transport, storage and biochemical roles, as well as appropriate laboratory evaluation.

Hemoglobin contains 70% of total-body iron. Another 3.9% is found in myoglobin and in mitochondrial proteins involved in energy metabolism and respiration such as cytochromes, catalase, peroxidase and metallo-flavoprotein enzymes. Plasma iron is largely bound to transport proteins (mainly ferritin, transferrin and albumin), leaving only 0.1% of total-body iron as free
iron in plasma.

Dietary sources of iron include heme iron (meat) or non-heme iron (iron-rich plants), which is less bioavailable. Homeostasis of iron is carried out by up- or down-regulation of transferrin and ferritin receptors on cell surfaces to balance absorption, storage, circulation and excretion of iron. Absorption of non-heme iron is mediated by the divalent metal transporter 1 DMT1, among others. This transporter is up-regulated in iron deficiency.

Toxic elements such as cadmium and lead share the same transporter, and it may be the reason that iron deficiency predisposes humans to cadmium and lead toxicity. By the same token, an iron-replete diet may protect from other element toxicities. There is no mechanism to excrete excess iron by the body, though small amounts of iron are lost through urine, bile and sloughing of intestinal mucosal cells in the feces. This loss amounts to less than 1 mg/d, so the daily need of iron is about 1 to 1.5 mg for healthy adults. The RDA is much higher, reflecting low GI absorption of iron in healthy individuals. Premenopausal women are subject to a much greater loss of iron during menstruation.

Toxic elements can “piggy back” on the homeostatic mechanisms for iron regulation and can pose a second adverse consequence for the patient with either extremely high iron stores or for the patient with iron deficiency.

DMT1 mediates absorption of iron, manganese, cadmium, and lead,98 and some toxic elements use transferrin as their carrier protein (e.g., aluminum). Iron Deficiency Anemia Iron deficiency anemia (IDA) has effects on tissue and cardiac health, physiological growth, productivity, maternal and fetal mortality, cognitive development, and attention span. Although hemoglobin (Hb) is routinely measured to monitor the critical stages of anemia, Hb is not the most sensitive marker of iron deficiency which advances in stages, starting with decreased iron stores (ferritin) and ultimately ending in effects on erythrocytes.

β-Amino Acids
β-Amino acids are so named because their amino groups are attached to the beta carbon. These com- pounds are not found in proteins. They serve physiological functions ranging from bile acid precursor and antioxidant to neurotransmitter and metabolic control.
They can be acquired from the diet or synthesized de novo. Taurine is a β-amino acid, but was also discussed under the sulfur amino acids. Taurine and the other β-amino acids use the same carrier-mediated active transport into cells.

β-Alanine

β-Alanine is released from skeletal muscle during strenuous exercise and it occurs in food mainly as carnosine in red meats or anserine in poultry. The pyrimidines cytosine and uracil from DNA and RNA are degraded to β-alanine.

β-Alanine can become elevated in plasma or urine due to enzyme deficiency, dietary intake, intestinal microbial overgrowth, or high turnover of muscle tissue

β-Alanine has been used as an index of carnosine catabolism. Deficient activity of the enzyme β-alanyl-a-ketoglutarate transaminase in a 4-year-old girl was corrected by oral pyridoxine therapy in one reported case. Intermittent seizures and lethargy were reduced. The biochemical pathway involved in this case is the conversion of β-alanine to a-ketoglutarate
Vitamin B deficiency generally causes lowered activity of the enzymes that degrade β-alanine, resulting in high urinary excretion. High β-alanine is frequently associated with generalized β-aminoaciduria and concomitant loss of other amino acids such as taurine, due to impairment of renal tubular resorption. Low taurine levels may indicate taurine depletion by this
mechanism. High levels of β-alanine are frequently accompanied by increases in 1- and 3-methyl-histidine, carnosine and anserine.

Uptake of taurine occurs by a carrier-mediated active transport process specific for β-amino acids. Because there is transporter competition for β-amino acid entry into cells, excessive taurine administration may cause elevated carnosine (resulting in muscle weakness) or elevated β-alanine.486 Therefore, monitoring β-alanine levels can help the clinician appropriately adjust taurine supplementation. Use of taurine should be decreased when β-alanine is elevated. Excess excretion of taurine may indicate β-aminoaciduria. β-Alanine impairs renal tubular resorption of a variety of amino acids, including taurine, thus propagating amino acid deficiencies

The origins and dispositions for β-alanine are quite different from those for alanine discussed previously. At cell death, DNA
catabolism releases β-alanine from breakdown of cytosine. Dietary carnosine and anserine are normally hydrolyzed rapidly
with release of β-alanine. β-Alanine is used for synthesis of muscle carnosine and for ubiquitously distributed coenzyme A that is required for multiple central energy pathways. Excess β-alanine is oxidized via conversion to acetate.

Epileptic patient treatment with the GABA transaminase inhibitor, vigabatrin, produces elevated β-alanine because the drug also blocks its breakdown.I did take Gabapentine in high dose 3 years ago, I wonder if that matters.

Intestinal bacteria and/or Candida albicans can also make β-alanine, which can raise plasma levels of β-alanine. With high β-alanine, check urinary indican or other dysbiosis markers as a measure of bowel dysbiosis. A bowel detoxification program may be appropriate with supplementation of a high-potency Lactobacillus acidophilus and L. bifidus products along with prebiotics and a high-fiber diet to support growth of the favorable organisms. Because of the competition of β-alanine for the taurine transporter, a bowel detoxification program to remove a major source (microbial overgrowth) of β-alanine can help to raise the kidney threshold to taurine spill and, therefore, help raise plasma taurine levels.

Suplements taken during the last 4 months (not the week previous to blood and urine test)

2LCMV (Antiviral Homeopatico para el CMV) daily only first 10 days of the month
2LEBV (Antiviral homeopatico para el EBV) daily

Glutamine: Every Morning
L-Glutamine 5,000 mg **
N-Acetyl D Glucosamine 200 mg **
Gamma Oryzanol 125 mg **
Proprietary Herbal Blend 75 mg **
Cranesbill Root (Geranium maculatum) **
Ginger Root (Zingiber officinale) **
Marigold Flower (Calendula officinalis) **
Marshmallow Root (Althaea officinalis) **

Citrobiotic: Grape Fruit seeds extract every morning

B6+Magnesio (Oral Flash): daily in the morning
B6 1,5mgr
Magnesio 250mgr

Body Bio Balance Oil: with meals
Linoleic omega 6 8,3gr
Linoleic omega 3 2,1gr
Linoleic omega 9 1,9gr

Probiotics: a lot, changing brands every month

Antibiotics: in the last 4 months before this test was done, only once cefalosporina for a Haemofilus Parainfluenza infection.

5-HTP: just occasionally
Magnesium 50mg
5HTP (L-5 Hydrotryptophan from griffonia simplicifolia seed extract) 100mgr
Valerian Root podwer extract 100mgr
Vitamin B6 (as Pyridoxine hydrochloride P-5-P) 10mgr

Ergytaurina: once a day with meals

Taurina 120mgr
Glutation 3mgr
Metionina 30mgr
Zinc 3,5mgr
Sulforafano 150 ug
B6 800 ug
B9 100 ug
Selenio 25 ug

MVM-A: twice a week a multivitaminic ( Dr. Pall supplements)

Vitamin C 67 mgr
Vitamin D3 267 IU
Vitamin K1 25 mcg
Thiamin 8mgr
Riboflavin 10 mgr
Niacin 18 mgr
B6 8 mgr
Folic Acid 400 mcg
B12 30 mcg
Biotin 100 mcg
Panthotenic Acid 20 mg
Calcium 83 mg
Iodine 50 mg
Zinc 40 mg
Selenium 67 mcg
Copper 0,4 mg
Manganese 1,5 mg
Chromium 50 mcg
Glycine 8 mg
Strontium 7 mg
Taurine 83 mg
Aceyil L Carnitine 100 mg
Lipoic Acid 40 mg

CoQ Gamma E: Daily ( Dr. Pall supplements)
Vitamin A 6980 IU
Vitamin C 34 mg
Vitamin E 47 IU
Mixed Tocotrienols and Tocopherols 20mg
DeltaGold Tocotrienols 80mg
Gamma Tocopherol 200mg
Mixed Carotenoids 6mg
Lycopene 6mg
Lutein 6mg
Coenzyme Q10 150 mg
Alph Lipoic Acid 18mg

NAC: Daily ( Dr. Pall supplements)
N-Acetyl L-Cyseine 200mg
Trimethylglycine 300mg
Ribonucleic Acid 120mg
Alpha Lipoic Acid 100mg

FlaviNox: Daily ( Dr. Pall supplements)
Milk Thistle 80mg
Bilberry 100mg
Ginko 40mg
Grape Seed Extract 100mg
Green tea extract 80mg
Cranberry Juice 100mg
Hawthorn extract 100mg

Carnitine 1gr daily, before the test, and currently 3 gr daily after seeing Dr. Kurk and getting prescription.

L'equilibre Vital: only when my PH is unbalance
Citrato de potasio 65mg
Citrato de sodio 40mg
Citrati de Calcio 23,3mg
Citrato de hierro 1,16 mg
Citrato de manganeso 0,16 mg

Candi Bactrin: Only 21 days durin March to try to get rid of Blastocystis Hominis (did not work)
Coptis Root (Containing berberine) & Rhizome 30mg
Oregon Grape Root 4:1 Extract (Berberis aquifolium) 70mg
Berberine Sulfate 400mg

For digestions:
Artichoke extract 400gr
Cardo Mariano (Milk Thistle)
Enzymes: amilasa, lipasa, lactasa, etc...

USEFUL TEST LIST FOR CFS (Post 9)

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