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

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
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)


Please take into account that these protocols are taylor made to my particular case, which means that for every patient there are many variants on treatment that each doctor has to determine. Nevertheless these are general lines that gives you a clue of three different approaches to be taken into account because they are very much in the cutting edge of research of this illness.
These approaches are not compatible, either you do one or the other, specially Mhyll and Yasko. Rigau is a more soft approach that does not use heavy orthomolecular prescription that forces detox in the body, as Yasko protocol does for instance.


Treatment of Dr. Rigau:

(Also reflected in Dr. Mhyll below)
1)Omega 3 (up to 6 a day) Eye Q
This is to prevent my propensity for inflammation and cardiovascular problems
2) Probiotics(1-0-0) Ferzym Plus (Specchiasol)
This is to restore folra, vitamins B, Managanesum, zinc, probiotics...

(exclusive from Dr. Rigau based on my genetic profile)
3)SOD from Douglas or Ageloss from Nature Import
This is for the lack of SOD that I show.
4)Milk Thistle (30 drops) or Coenzime Compositum (twice a week)
This is to slow phase I which is too fast, and activate Phase 2 which is too slow, as it shows the study.
5) Naturalith (2-0-2)
6) L Glutamine(1-0-1)
7) Mucosa Compositum
This is to reduce amonia and protect the mucosa from the intestines and colon
8) Homocysteine (Folic Acid and B6)
This is to lower my homocysteine levels
9) Malic Acid (Douglas) or espastrupel (homeopatic) and appe juice in the morning 10) Magnesium
This is to reduce my bilirrubine levels that were high
11) Nivelcol (Tongil) 2 in the morning
This is to help control cholesterol levels
12) Aminoacids: Glicina (2) & Prolina (1) Plus using the vibrating machine of the gym
This is to prevent osteoporosis which will be an issue in my case for the lack of colageno. I can also eat "manitas de cerdo", "codillo"

I can take a break of Labolife in the summer time, because with high temperatures, viruses are not very active.
My metilation pathway is partially bloqued, but the good thing is that the sulfuration pathway is not bloqued, and that offsets part of the problem with metilation.
I do not repair well my DNA, so I should be careful with the sun.
There are three things that are not completely ok in my case: COM (Hormones), MTHFR (metals) and CBS (Homocysteine)

Treatment of Dr. Mhyll

Standard for all Mitochondrial support Extra Anti-oxidants
Morning
1) In ½ to 1 pint of water/ Acetyl L-Carnitine 1 gram
2) 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)

3)Swallow at breakfast with the below 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
-Magnesium 300mg daily orally (more if tolerated – up to 600mgs)

4)-Subcutaneous injection Evans 50% magnesium sulphate ½ ml (0.05ml lignocaine with 0.5ml magnesium)
5)-Subcutaneous injection B12 ½ ml methylcobalamin daily initially for two months and adjust according to clinical response.

______________________________________________________________________________________________
Mid morning
6)D-ribose ½ a teaspoon in tea or coffee
7)Swallow: Co-enzyme Q10 100mg x 1 capsule
_______________________________________________________________________________________________
Midday – lunchtime
8)Dissolve in ½ pint of water D-ribose ½ a teaspoon
9)MMM 1gram 1 scoop
10)Swallow: Co-enzyme Q10 100mg x 1 capsule
Start on 300mg daily split in three dose for 3 months, then a maintenance dose of 100mg daily.
________________________________________________________________________________________________
Mid-afternoon
11)Dissolve D-ribose ½ a teaspoon in tea or coffee
Three teaspoonfuls daily (15gms) should be taken in small doses throughout the day in drinks taking it with green tea, coffee, tea or whatever (hot or cold).
________________________________________________________________________________________________
Evening
12)Dissolve in ½ to 1 pint of water/ Acetyl L-carnitine 1 gram
13)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 of 3 teaspoon per day -15mg)
14)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
_________________________________________________________________________________________
At night
15)Take in water/fruit juice
-D-ribose ½ teaspoon
-Selenium 300mcg 3 drops
-(for 4 months) – GSH-px

Besides:
-Eat a Stone Age Diet, Low carbohydrate intake and high dose of "do it yourself" probiotics including Kefir. Some people also need herbal antifungals and some people systemic prescription antifungals to get on top of their yeast problem.
-Sleep between 9.30pm and 6.30am – more in winter, less in summer.
-Avoid chemicals and do a good clean up of the environment to try to reduce the total load and this will also reduce the allergic burden.
-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.
-Run microrespirometry studies which look at oxidative phosphorylation in more detail.
-Far Infra Red saunaing at least two sessions a week. Another method of detoxing is to take high dose essential fatty acids and other oils.Interestingly many people who take VegEPA report much improved sleep.

PROTOCOL Richard A. Van Konynenburg
SIMPLIFIED TREATMENT APPROACH FOR LIFTING THE METHYLATION CYCLE BLOCK

SUPPLEMENTS (www.holisticheal.com)
FolaPro [2]: ¼ tablet (200mcg) daily (5-methyl tetrahydrofolate)
Actifolate [3]: ¼ tablet daily
General Vitamin Neurological Health Formula [4]: start with ¼ tablet and work up dosage as tolerated to 2 tablets daily (multivitamin, multimineral supplement including antioxidants, trimethylglycine, nucleotides, supplements to support the sulfur metabolism, a high ratio of magnesium to calcium, and no iron or copper) starting with ¼ tablet and increasing the dosage as tolerated, to 2 tablets daily
Phosphatidyl Serine Complex [5]: 1 softgel capsule daily (phospholipids and fatty acids)
Activated B12 Guard (hydroxocobalamin)[6]: 1 sublingual lozenge (2,000 micrograms) daily

Here is hard to tell, wether is included in Dr. rigau or Dr Mhyll strategy: Folic Acid is prescribed in Dr.Rigau's protcol to reduce homocisteyn. Multivitamins and Minerals is included in Dr. Mhyll and Dr. Rigau as a general thing. Phospholipids and fatty acids, could be included as the omegas prescribed by Dr. Rigau and Dr. Mhyll. And B12 is included by Dr. Mhyll. The key question is to know which format, and dose is the better advice...

I guess I will discuss the three protocols with Dr. rigau and will come up with something out of it. To be continued...

Martin Pall questions the Richard Konynenburg Protocol

COMENTARIOS DE MARTIN PALL SOBRE EL TEMA DEL CICLO DE METILACION Y PROTOCOLO DE KONYNENBURG

There has been a movement arguing that a deficiency in methylation activity is central to the causation of both autism and chronic fatigue syndrome/myalgic encephalomyelitis. Many have argued that lowered methylation of DNA leads to epigenetic changes that may be responsible for the development of these diseases. While there has been published evidence for lowered DNA methyation, there is no evidence that this has any epigenetic role and an animal model study suggests that is does not. Dr. Richard Van Konynenburg has argued repeatedly that such methylation deficiency leads to lowered levels of reduced glutathione levels which he argues lead, in turn to the symptoms of CFS. My own view is that both of these views are mostly wrong. There is, however, a modest decrease in methylation cycle activity that is a consequence of the NO/ONOO- cycle. Whether this modest decrease in methylation cycle activity has any importance in the pathophysiology of CFS or other NO/ONOO- cycle! diseases is uncertain.

Let me outline my own views on this:

1. 5-methyltetrahydrofolate (5-MTHF) the methyl donor derived from the B vitamin folic acid, has been shown to be a potent scavenger for peroxynitrite. I am aware of some unpublished data that has shown that the levels of 5-MTHF are quite low in the plasma of CFS/ME patients, typically something like 60 to 70% lower than in normal controls. Other folate derivatives are also low, but not as low relative to normals as 5-MTHF. The only interpretation of this that I am aware of is that peroxynitrite, presumably elevated as a consequence of the NO/ONOO- cycle, is leading to the oxidation of 5-MTHF and subsequently some loss of total folate as well. A precursor of 5-MTHF, tetrahydrolate, also has a role as a peroxynitrite scavenger but is considerably less active in this process. The loss of 5-MTHF is opposite what might be expected from the Van Konynenburg model which assumes that lowered methylation is caused by a lowered activity of the enzyme methionine synthase and! lowered vitamin B12 activity. However, both of these mechanisms will produce a lowered utilization of 5-MTHF and should, therefore cause 5-MTHF to accumulate to higher levels. This is the opposite of what is found. So the pattern of changes in folate pools is consistent with the prediction that it is caused by excessive peroxynitrite, reacting with 5-MTHF and to a lesser extent with tetrahydrofolate but is not consistent with the Van Konynenburg model.

2. The same set of data showed that there was a modest decrease (circa 10-15% lower) in the levels of S-adenosylmethionine (SAM)in CFS/ME patients. SAM is the downstream methyl donor produced in the methylation cycle that is used, in turn, to methylate many compounds in cells. It has been estimated that about 20% of the methyl donors going into the methylation cycle to produce S-adenosylmethionine comes from 5-MTHF with the other 80% coming from betaine (trimethylglycine) and methionine. It is reasonable, therefore, that a 60-70% decrease in 5-MTHF could produce a 10 to 15% lowering of S-adenosylmethionine and thus a modest lowering of methylation cycle activity. The question is whether this modest lowering has any substantial role in the pathophysiology of CFS and other multisystem illnesses? I don't know the answer to that but suspect if it has a role, it is a relatively modest one. In any case, those of you who are taking the whole Allergy Research Gro! up nutritional support protocol including the betaine found within the NAC enhanced antioxidant formula and the hydroxocobalamin form of vitamin B12 found in the MVMA, have probably already normalized methylation activity so I doubt that this is a problem for you.

3. Dr. Neil Nathan and Dr. Van Konynenburg have developed an treatment protocol that they argue should act to increase methylation cycle activity. I believe that this does produce substantial improvements in most CFS/ME patients who have been treated by it and I think this may be an effective treatment approach. However I think that their interpretation of how it works in wrong.

4. Their protocol includes about 300 micrograms per day of 5-MTHF, which they argue is effective because of its role in introducing methyl groups into the methylation cycle. However this amount of 5-MTHF only supplies roughly 1/80,000 of the daily methyl donors in the human diet, almost all of which do go into the methylation cycle. It follows, therefore that the 5-MTHF is probably on the order of 1/10,000th of what is needed to produce anything like a normalization of methylation cycle activity. One can conclude, therefore, that Dr. Van Konynenburg is wrong in ascribing the action of the 5-MTHF in this protocol to acting to introduce methyl groups into the methylation cycle. How can it be acting? It can be acting as a peroxynitrite scavenger, lowering the activity of peroxynitrite and therefore lowering the NO/ONOO- cycle. You may recall that at the heart of the NO/ONOO- cycle is what I call the central couplet, where peroxynitrite oxidized the compound tetrahydrobio! pterin (BH4) and a BH4 deficiency leads to partial uncoupling of the nitric oxide synthases, leading to more peroxynitrite. It has been known for a while that high dose folate supplements lead to increased availability of BH4. It seems likely, now, that the high dose folate acts as a precursor of 5-MTHF, leading to peroxynitrite scavenging and therefore to increased BH4 availability.

5. Dr. Van Konynenburg has told me that if they used doses of 5-MTHF substantially higher than 300 micrograms per day, they have some toxic reactions to it. I have gotten similar information from a physician treating fibromyalgia patients. My guess is that there may be oxidation products produced by the reaction of peroxynitrite with 5-MTHF that may be toxic - this is just a guess, but it makes sense given what we know about the overall mechanism.

6. They have in their protocol both intrinsic factor, a glycoprotein that greatly increases vitamin B12 absorption and also substantial amounts of the hydroxocobalamin form of vitamin B12, which is a potent nitric oxide scavenger. This combination should lead to much higher levels of absorption of hydroxocobalamin than we get just using strait oral hydroxocobalamin in the MVMA component of our protocol, without intrinsic factor. This may be responsible, in part for the clinical response that they see. We have known all along that the amount of hydroxocobalamin absorbed from the Allergy Research Group nutritional support protocol is inadequate to get the full effect of the hydroxocobalamin scavenging of the nitric oxide and many have gone to using hydroxocobalamin IM injections, inhaled nebulized material, nasal spray or other approaches to increase the hydroxocobalamin blood levels. Using intrinsic factor may be another approach that may be useful for this as well, base! d on their observations.

7. We have, then, in their protocol, two agents that should be effective in acting to lower peroxynitrite, the most central element in the NO/ONOO- cycle. High dose hydroxocobalamin whose absorption is greatly stimulated by the presence of intrinsic factor and which serves to lower one of the precursors of peroxynitrite, nitric oxide. The other is the 5-MTHF which serves as a potent peroxynitrite scavenger. I think that the roles of both of these are telling us some useful things, which is part of the rationale for this post.

8. They have a number of things in their protocol which I am sure are useful when used as a stand alone approach. These include a number of antioxidants and also a high dose B vitamins. My guess is that the Allergy Research Group nutritional support protocol is at least as good in these areas and probably better.

9. Unfortunately, we do not have any direct comparisons of the two protocols. My guess is that they are roughly similar. I do think that adding 5-MTHF to the Allergy Research Group nutritional support protocol may be quite useful however, based on the reasoning presented above. We already had reason to believe that increasing the hydroxocobalamin levels in the body over that produced by the Allergy Research Group protocol is useful.

I want to add that I am a PhD, not an MD and none of this should be viewed as medical advice.

Martin L. (Marty) Pall

Summary of Dr. Mhyll recommended Treatment

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
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)

SUMMARY OF CARLOS CONDITION

The mitochondrial function score is a measure of how much energy they have got to spend. 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.
The cell free DNA a measure of how well they feel, in other words, cell free DNA is a marker for the symptom of malaise. 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.

Red cell glutathione peroxidase (GSH-PX) 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. Recommended high protein diet (which contains amino acids for endogenous synthesis of glutathione), and take selenium 500mcg daily during 4 months, maintenance dose of 200mcg.


DR. MHYLL TREATMENT SUMMARY:

• PACING,
• MICRONUTRIENTS – multivits (A,B,C, D and E), multimins, EFAs.
• SLEEP – aim for 9 hours between 9.30pm and 6.30am
• STONEAGE DIET (low glycaemic index diet which avoids the major allergens).

(a) Correcting mitochondrial function - D-ribose, Mg injections, NAD (B3), 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.

Standard for all Mitochondrial support Extra Anti-oxidants
Morning
1) In ½ to 1 pint of water/ Acetyl L-Carnitine 1 gram
2) 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)

3)Swallow at breakfast with the below 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
-Magnesium 300mg daily orally (more if tolerated – up to 600mgs)

4)-Subcutaneous injection Evans 50% magnesium sulphate ½ ml (0.05ml lignocaine with 0.5ml magnesium)
5)-Subcutaneous injection B12 ½ ml methylcobalamin daily initially for two months and adjust according to clinical response.

______________________________________________________________________________________________
Mid morning
6)D-ribose ½ a teaspoon in tea or coffee
7)Swallow: Co-enzyme Q10 100mg x 1 capsule
_______________________________________________________________________________________________
Midday – lunchtime
8)Dissolve in ½ pint of water D-ribose ½ a teaspoon
9)MMM 1gram 1 scoop
10)Swallow: Co-enzyme Q10 100mg x 1 capsule
Start on 300mg daily split in three dose for 3 months, then a maintenance dose of 100mg daily.
________________________________________________________________________________________________
Mid-afternoon
11)Dissolve D-ribose ½ a teaspoon in tea or coffee
Three teaspoonfuls daily (15gms) should be taken in small doses throughout the day in drinks taking it with green tea, coffee, tea or whatever (hot or cold).
________________________________________________________________________________________________
Evening
12)Dissolve in ½ to 1 pint of water/ Acetyl L-carnitine 1 gram
13)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 of 3 teaspoon per day -15mg)
14)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
_________________________________________________________________________________________
At night
15)Take in water/fruit juice
-D-ribose ½ teaspoon
-Selenium 300mcg 3 drops
-(for 4 months) – GSH-px

Besides:
-Eat a Stone Age Diet, Low carbohydrate intake and high dose of "do it yourself" probiotics including Kefir. Some people also need herbal antifungals and some people systemic prescription antifungals to get on top of their yeast problem.
-Sleep between 9.30pm and 6.30am – more in winter, less in summer.
-Avoid chemicals and do a good clean up of the environment to try to reduce the total load and this will also reduce the allergic burden.
-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.
-Run microrespirometry studies which look at oxidative phosphorylation in more detail.
-Far Infra Red saunaing at least two sessions a week. Another method of detoxing is to take high dose essential fatty acids and other oils.Interestingly many people who take VegEPA report much improved sleep.

Mitocondrial Failure (Acumen and Biolab test)

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

I 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?

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
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)

As you can see below on the chart, I have registered my daily evolution of Symptoms. From 1 to 10, meaning 1= 10% of my capabilities, and 10=100% of my capabilities. When I fell sick in 2005 I was 1 most of the time... laid in a bed or a coach.



In this chart, there is not a daily evolution, it is an average 10 day chart, and that explains the lower volatility.As you can see the most clear improvement shows in 2007 when I start the treatment of Dr. Rigau, and later on at the end of 2008 I have a relapse, that is recovering since March 2009, so far so good, and the things that I introduced that can explain this recovery are:

a) Mutaflor i is a probiotic that contains Escherichia Coli, which is necessary to allow bifidus and lactobacillus to grow in the colon. This is only for sale in Germany, but you can buy via internet.

Besides MUTAFLOR, it is advisable to supplement her with more probiotics of good quality such as VSL-3, Natreen Healthy Trinity, Ferzym Plus, or others that contains lactobacillus and Bifidus. But as a complement of MUTAFLOR.

b)Homeopathic drops for candida overgrowth made out of a MORA TEST. Dr. Guxens in Catalunya made it for me. I find it a bit surrealistic, but I mention it because together with Mutaflor is what I did introduced.

c)Homocysteine pills containing Folic Acid and B6 and B12 to decrease my homocysteine levels that were very high

CDo you know MUTAFLOR? Should you take it to increase Escherichia coli and balance your flora? http://www.ardeypharm.de/pdfs/en/mutaflor_drugforlife_e.pdf

How to take it?:
In adults:

First 4 days, 1 capsule of Mutaflor daily, later, increase the dose at 2 per day.

Preferaably in the breakfast with a glass of Juice or so.
Keep it at: 2°C - 8°C

Where to buy it?:

Metropolitan Pharmacy
Apotheke am Flughafen München
Walter M. Verfürth, e.K.
Zentralbereich, Ebene 03
Terminal 2, Ebenen 04 und 05
85356 München Flughafen
Tel: +49 - 89 - 978 802 200
Fax: +49 - 89 - 978 802 206
email: MUC@metropolitan-pharmacy.de
Amtsgericht München HRA 68267

This second chart has more volatility because is not an averge, is daily data. It contains data since 2006, I fell sick in 2005. I am close to recovery as you can see.



A usefull address:

Laboratorio Sabater for making a genetic profile:
Londres, 6 tel. 93 444 32 00 (de 7 a 21 h. 9
Clínica del Pilar c/ Balmes, 271 tel. 93 237 57 81 ( 24 horas)
Lab. Bonanova Pg. Bonanova, 67-67 tel. 93 253 01 49
Gràcia-Guinardó Secretari Coloma, 142 tel. 93 285 36 65

New tretament based on Genetic Profile

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
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)

Click on he image to see a bigger detailed picture.

Click on he image to see a bigger detailed picture.

Click on he image to see a bigger detailed picture.



I just came back from my visit with Dr. Josepa Rigau in Tarragona, and I got a new treatment based on my gene map which I did recently. Among other things I have to be careful with obesity, cholesterol, homocysteine, cardiovascular diseases, lipid metabolism, lack of colageno, and propensity to colon cancer... all these are predispositions, not necessarily will happen, although cholesterol and homocystein is already happening.

Treatment:

SOD from Douglas or Ageloss from Nature Import
This is for the lack of SOD that I show.
Omega 3 (up to 6 a day) Eye Q
This is to prevent my propensity for inflammation and cardiovascular problems
Milk Thistle (30 drops) or Coenzime Compositum (twice a week)
This is to slow phase I which is too fast, and activate Phase 2 which is too slow, as it shows the study.
Licopen (Douglas) or 3 tomato juices
This is for the gene GSTM
Naturalith (2-0-2), L Glutamine(1-0-1), Probiotics(1-0-0), and Mucosa Compositum
This is to reduce amonia and protect the mucosa from the intestines and colon
Homocysteine (Folic Acid and B6)
This is to lower my homocysteine levels
Malic Acid (Douglas) or espastrupel (homeopatic) and appe juice in the morning & Magnesium
This is to reduce my bilirrubine levels that were high
Nivelcol (Tongil) 2 in the morning
This is to help control cholesterol levels
Ferzym Plus (Specchiasol)
This is to restore folra, vitamins B, Managanesum, zinc, probiotics...
Aminoacids: Glicina (2) & Prolina (1) Plus using the vibrating machine of the gym
This is to prevent osteoporosis which will be an issue in my case for the lack of colageno. I can also eat "manitas de cerdo", "codillo"
I can take a break of Labolife in the summer time, because with high temperatures, viruses are not very active.
My metilation pathway is partially bloqued, but the good thing is that the sulfuration pathway is not bloqued, and that offsets part of the problem with metilation.
I do not repair well my ADN, so I should be careful with the sun.
There are three things that are not completely ok in my case: COM (Hormones), MTHFR (metals) and CBS (Homocysteine)

Homocysteine, cholesterol and ammonia

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
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)

In My latest blood test I seem to have a problem with LDL cholesterol 199, which means that if I do not solve it with diet in 3 months, I will have to take medication for life to prevent arteriosclerosis. This was also confirmed with my genetic study that I will eventualy translate into englesh, which said that I had familiar hipercolesteremia in my genes, and I need to do diet for life the same as sports.

Together with this, I also showed amonia in my blood, high bilirrubine, and high homocysteine.

The findings some studies on homocysteine show several biological conditions that can contribute to conditions such as CFS. In the elderly, some natural processes of aging exist and environmental factors such malnutrition may produce similar patterns to CFS. Inflammatory processes have been implicated in a number of diseases including diabetes and atherosclerosis. The results of these studies also show that CFS has an important inflammatory component as well that could very well lead to those illnesses and others.

Notes:

-Homocysteinemia can be caused by a genetic defect of methionine.
-Homocysteine can accumulate in blood due to dietary deficiencies of folate and vitamins B12 and B6 or through excessive intake of the amino acid methionine. Homocysteinemia is assumes to occur through different pathways. (Troen)
-Homocysteine impairs the nitric oxide pathway which contributes to endothelial dysfunction. (Stuhlinger)

Regland, B., Andersson, M., Abrahamsson, L., Bagby, J., Dyrehag, L. E., and Gottfries, C. G. (1997). Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome. Scandinavian journal of rheumatology, 26(4):301-307. http://www.citeulike.org/user/HEIRS/article/4180014
Insciences. (2008). Study shows inflammation from chronic fatigue syndrome may be risk factor for other illnesses. http://www.citeulike.org/user/HEIRS/article/4180039
Ventura, E., Durant, R., Jaussent, A., Picot, M. C., Morena, M., Badiou, S., Dupuy, A. M., Jeandel, C., and Cristol, J. P. (2009). Homocysteine and inflammation as main determinants of oxidative stress in the elderly. Free radical biology & medicine, 46(6):737-744. http://www.citeulike.org/user/HEIRS/article/4180037
Stuhlinger, M. C., Tsao, P. S., Her, J.-H., Kimoto, M., Balint, R. F., and Cooke, J. P. (2001). Homocysteine impairs the nitric oxide synthase pathway: Role of asymmetric dimethylarginine. Circulation, 104(21):2569-2575. http://www.citeulike.org/user/HEIRS/article/4180066

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

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
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)

UPDATE ON MY REVIEW: NEGATIVE ONE



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

Among the things he told me before treatment were:

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

And after treatment he said:

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

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

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

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

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

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

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

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

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

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

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

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

OZONE Treatment good for intetinal dysbiosis

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

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

--------------------------------------------------------------------------------

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

--------------------------------------------------------------------------------

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

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

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REFERENCES
_rzte Zeitung Nr.45 Jhrg.10 M„rz 1991
Abraham, Beachey: Host defences against adhesion of bacteria to mucosal surfaces in: Gallin, Fauci eds. Advances in host defence mechanisms, Vol. 4 Mucosal Immunity. New York: Raven Press 1985 63-88
Baquero,F Moreno,F: The microcins FEMS Microbiol.Lett. 1984, 23 117-24
Sonnenborn,U Greinwald,R: Escherichia coli im menschlichen Darm: Dtsch.Med.Wschr. 1990 115 906-12
Savage DC: Microbiol.ecology of the gastrointestinal tract. Ann.Rev.Microbiol. 1977/31 107-33
Pabst,R: Der Verdauungstrakt als Immunorgan. Med.Klinik und Praxis Jhrg.78, Januar 1983 14-20
Luckey, TD: Gnotobiology and bioisolation Mikro”kologie und Therapie Vol.10 Hrsg.Volker Rusch, Herborn 1980 19-39
Lodinov -Z dnikov ,R: Immunantwort bei neugeborenen und fr_hgeborenen Kindern nach Kolonisierung mit apathogenen E.coli. Vortrg.Medica D_sseldorf am 20.11.1991
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KRYPTOPYRROLE / HPU / HPL / PORPHYRIA / B6 & Zinc

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

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

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

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

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

Explanation on HPU:

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

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

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

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

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

Interpretation of the test:

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

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

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

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

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

Symptoms

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

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

b) Complaints caused by decreased haem production:

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

c) Complaints caused by deviation of the hormonal regulation

-Fatigue
-Headache and or migraine
-Allergy and gluten sensitivity
-Infections
-Low blood pressure
-Infertility
-Overweight
-Auto-immune diseases

d) Complaints caused by deviated liver function

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


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

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

Treatment:

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

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

http://www.hputest.nl/ewhat.htm


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

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

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

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

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

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

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

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

Keac:

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

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

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



DETERMINATION OF URINARY KRYPTPYRROLES

(COLORIMETRIC METHOD)

PRINCIPLE

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

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

In the situation we are considering,

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

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

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

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

Vitamin D Tips yaken from Carol's Blog

You can always contact me at carlitos.gonzalez@gmail.com
Please, do not leave anonymous comments because I can't respond to you then...
Remember that this is juat a post of my blog, and it evolves, so to see the full story go to: www.pochoams.blogspot.com (English) or www.sfc-tratamiento.blogspot.com (Spanish)
My current doc: Josepa Rigau Av Catalunya, 12, 3º, 1ª 43002 Tarragona Spain +34977220358 (I do recommend! hoeopathy and biological medicine, significant improvement)
My previous docs: De Meirleir (www.redlabs.be), Dra Quintana (CMD), (Lots of medication, antibiotics etc... no significant improvement)

Time for more vitamin D

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

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

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

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

Latitude and vitamin D production in the skin



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

In search of vitamin D

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

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

Selected food sources of vitamin D

Food

Vitamin D (IU*)

Salmon, 3.5 ounces

360

Mackerel, 3.5 ounces

345

Tuna, canned, 3.5 ounces

200

Orange juice, fortified, 8 ounces

100

Milk, fortified, 8 ounces

98

Breakfast cereals, fortified, 1 serving

40-100

*IU = international units

Source: Office of Dietary Supplements, National Institutes of Health

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

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

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

Vitamin D status

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

Deficient

Less than 20 ng/mL

Insufficient

20 to 29 ng/mL

Sufficient

30 ng/mL or more

Potentially harmful

More than 150 ng/mL

*25-hydroxyvitamin D3 (vitamin D precursor)

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

How to reach 1,000 IU

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