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

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

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

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



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



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


Value Reference Units
Elements in hair:

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

Ratio's

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


Saliva tests
ADRENOCORTEX STRESS PROFILE

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

Organic Acids in urine
CLYCOLYSIS

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

AMINOACID METABOLITES

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

FATTY ACID METABOLITES METABOLITES

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

MISCELLANEOUS

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

YEAST FUNGAL

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

BACTERIAL

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

ANAEROBIC BACTERIAL

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

KREBS CYCLE

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

NEUROTRANSMITTERS

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

PYRIMINIDES

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

MISCELLANEOUS

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

Urine Analysis:

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


Clinical Chemistry:


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

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

Vitamins:

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

Vitamins: mol/l

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


Elements in whole blood:

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

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

Elements in serum:

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

Intracellular concentration:

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

Biological Amines:
CATACHOLAMINES IN PLATELETS

Serotonin 40.8 30-400 ng/10E10

Miscellaneous: (Methylation panel)

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

FOLIC ACID DERIVATIVES

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

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

Aminoacids Urine 24h

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

Klinische Chemie:

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

Inhalent panel IgE

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

MOLDS
Bermuda grass
Jhonson grass
Rye grass
Timothy grass
Ragweed western

WEED POLLEN

Ragweed, western

MISCELLANEOUS
Cockroach german

Food Intolerances IgG

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

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

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


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

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

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

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

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

TRACE ELEMENTS

Manganese (Mn)

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

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

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

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

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

Clinical Associations of Manganese

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Chromium (Cr)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Mercury (Hg)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Of Further Interest…

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

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

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

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

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


Sodium (Na)

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

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

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

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

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

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

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

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

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

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


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

β-Alanine

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

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

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

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

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

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

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








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

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

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

Citrobiotic: Grape Fruit seeds extract every morning

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

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

Probiotics: a lot, changing brands every month

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


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

Ergytaurina: once a day with meals

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

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

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

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

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

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

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

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

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

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

USEFUL TEST LIST FOR CFS (Post 9)

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)

(before this post: 5.536 visits)
Note: You can see the original version of this post with all kind of links to sources cliquing in the title of this post.

CFS-CFIDS-ME, etc, are multi systemic illnesses which have, in most cases, a strong viral and/or toxic component. Several systems are deregulated, or perhaps permanently damaged, including the immune system, the endocrine system and the neurological system.

When we revise all the research trends published they converge in the following theory for CFS:

An external stressor such as toxics, heavy metals, viral infection, trauma, surgery... forces the adrenals, and under this oxidative stress status, glutathione is consumed and exhausted. When this stressor continues and becomes chronic, leads to a blockage of the methylation cycle, which also blocks the Krebs cycle, the immune system, urea cycle, etc... Under this situation, a mitochondrial failure is developed that brings fatigue as a result among many other alterations, like cardiac implications demonstrated by Cheney and Lener... Once the illness has become chronic, with the detox system blocked, a debilitated immune system due to the mitochondrial failure and the lack of genetic material to function properly, opportunistic infections arise and toxics accumulate in the body, aggravating more the condition of patients.

A)Diagnostic Valuable Test Although not generally accepted as a diagnostic test, they have been claimed by researchers to be useful markers for the disease and tend to be present in most of the patients. Nevertheless the value of these is more for diagnosis than for treatment of the condition.In order of importance: RNASe-L, PKR and Elastase levels, Nitric Oxide in serum and oxidation levels, SPECT and xenon SPECT scans of the brain, MRI scans of the brain, PET scans of the brain, Neuropsychological testing, EEG brain maps and QEEG brain maps, Erythrocyte sedimentation rate (ESR), Insulin levels and glucose tolerance tests, 24-Hour Holter monitor, Tilt table examination, Exercise testing and chemical stress tests, Neurological examination and the Romberg or tandem Romberg test.

B)Aditional abnormalities test found in CFS patients should be checked at least once, and based on the criteria of the physician that is treating you, it might be necessary to repeat them periodically to evaluate the evolution of the protocol followed in your case.

-Tests of the immune system: The Th1-Th2 relationship of the immune system, Low NK activity (as opposed to levels), T-Activated Linfocites Count, % Linfocites, Cellular Inversion at CHMI and/or CHMII level, Elevations of circulating cytokines, Immunoglobulin deficiencies
-Serology Test: IgG for viruses such as Epstein-Barr, CMV, HHV6. Additionally we need to get tested for all possible infections that could have caused a reaction in our hormonal stress, and therefore in the serology we should include: mononucleosis, Hepatitis B & C, LES markers, Toxoplasma, antibodies of candida albicans, Babesia, Erchilia, Bartonella, Borrelia etc...
-Levels of amino acids in blood and urine 24h or spot.
-Liver function
-Candida levels, in order to detect subclinical fungi infections like candida albicans, there are special urine test that measure the metabolites that will help us to rule it out it also can be observed the metabolites through an Organic Acids Test.

According to the results, patients should seek be treated for each one of the abnormalities which show up. There are allopathic treatments (can be problematic for some, as CFS-MEers tend to have also Chemical Sensitivities) or homeopathic treatments (in Germany, they are very commonly used).
Diet is also important regarding dealing with chemical sensitivities, amino acid levels, candida levels.

C) Advance testing on CFS: Besides theses regular, although not standard test mentioned above, there are additional test that can be run, and will deliver relevant input for CFS patients. There is a protocol to regulate these different abnormalities, which might be causing part of the symptoms in CFS, as a few of the latest research published postulates. We will discuss below some of them in here:


-Mitochondrial Profile This is in the latest research the main responsible for CFS. There is a test run in UK by Dr. Myhill. This test measures the enzyme SODase (Superoxide Dismutasa) This enzyme is necessary in the detox process of free radicals of the mitochondria, as well as the CoQ10 levels, Niacinamide and Intracellular Magnesium. And most of all the efficiency of the mitochondria in converting ADP into ATP. It also measures the free ADN which is a nice marker to observe the cellular damage and apoptosis or PKR which is the programmed cellular death due to oxidative stress.

-Adrenal Hormones in Saliva: This test is useful to treat the adrenal failure, because there is a treatment for it. The test is run during a whole day (8:00, 12:00, 16:00, 20:00) Cortisol and DHEA levels are tested. Also is necessary to test for a potential subclinical Thyroids problem (TSH, T3 and T4). Preferably in urine 24h, because subclinical thyroids is not always detectable in serum. Additionally a hair mineral test can be done to observe the unbalance existing in terms of minerals caused by suprarenal malfunction and correct it accordingly. Last but not least,

-HPU Test: This test measures a metabolic disorder, often occuring as a biochemical-enzymatic familiarly during the chemical reaction of formation of the red blood pigment. (Hemosynthesis).
It can be said that Kryptopyrrolurea is not a symptom, but rather the primal cause for different symptoms and disease states, among others hipoglucemia.
In the German-speaking countries, is abbreviated as KPU. In the Netherlands HPU. In England the abbreviation is HPL.

-Hypercoagulation Testing
: As a part of Hemex's research, they have developed a test to determine if a patient has this hypercoagulation disorder. The Immune System Activation of Coagulation (ISAC) tests five substances; abnormal results on any two of the five is considered to be a positive indicator of hypercoagulation. Their results thus far have found 79-92 percent of the CFS and/or FM patients they tested have hypercoagulation. As with many of the more detailed blood tests developed in the past decade, the defects causing hypercoagulation are rarely or not at all detectable by the standard laboratory tests performed at general labs, such as Unilab, Quest Diagnostics, etc. The standard coagulation workup done by these labs assess only the risk of actual clotting, whereas the ISAC panel is 10-20 times more sensitive.

-Metilation Panel (methionine cycle): This blood test is meant to observe the potential blockage of the methylation cycle, and therefore the potential detox treatment and follow up through urine. If after this analysis, you observe a blocked Methylation Cycle, then is wise to do a metal in urine test to have a starting point for the detox treatment. This test will be useful to follow up the metal excretion in the detox protocol or / and adapt the mineral doses intake.

The role of the methylation cycle in the sulfur metabolism is to supply sulfur-containing metabolites to form a variety of important substances, including cysteine, glutathione, taurine and sulfate, via its connection with the transsulfuration pathway.

In autism the methylation cycle was found to be blocked at methionine synthase, which is the step involving methylation of homocysteine to form methionine, resulting in lower plasma levels of cysteine and glutathione and a lowered ratio of reduced to oxidized glutathione. This lowered ratio reflects a state of oxidative stress.

It is known from studies of twins that genetics plays an important predisposing role in autism.The fact that the rate of incidence of autism has increased dramatically in recent years is evidence that there is also an important environmental component in the development of cases of autism, since the population’s genetic inheritance is relatively constant over much longer periods.

Evidence suggests that this same dysfunction is also present in chronic fatigue syndrome: Low methionine levels in serum and urine, below-normal levels of carnitine, coenzyme Q10 and melatonin. All these substances require methylation for their biosynthesis.

RNase-L remains activated in CFS because of the suppression of the cell-mediated immune response and the consequent failure to defeat the viral infection

There is abundant and compelling evidence that the glutathione depletion methylation cycle block mechanism is an important part of the pathogenesis for at least a substantial subset of chronic fatigue syndrome patients.

-Glutathione and Selenium Test: The best complement to Methylation Panel, would be to check Reduced Glutathione RBC GSH, Oxidated Glutathione (RBC GSSG) and Total Glutathione (RBC). The important one is RBC GSH, and also the ratio of this one versus RBC GSSG. This is relevant given that the low levels of glutathione due to the blocked methylation cycle, is the main responsible for the symptoms of CFS. In the initial states of oxidative stress in this illness Total Glutathione could be miss leading and be normal or even high, that is why we test for the other two as well. Besides, even if Glutathione comes normal, if Selenium level is low, the enzymes could not work properly.

Depletion of reduced glutathione likewise causes a shift to Th2. Depletion of reduced glutathione is the trigger for the reactivation of latent viral and intracellular bacteria in CFS. In general, intracellular glutathione depletion is associated with the activation of several types of viruses. It is likely that glutathione depletion is responsible for reactivation of Epstein-Barr virus, cytomegalovirus and HHV-6 in CFS. Populations more deficient in selenium would be expected to be more vulnerable to Coxsackie B3 infection.

-LITOCROMO P450 (Genetic Profile of the Urine Cycle) This is a genetic study that can be done later, and it reflects the pharma genetic of the liver taking into account 15 genes and 92 polyforms. This study will give us information of what foods or medications are not assimilated by our liver and therefore should be skipped. The problem again is that insurance only covers you this study when you have cancer or aids… This test is particularly useful in the case that Glutathione and Selenium comes out normal, but what is not working are the enzymes that regulate it due to their genetic polyforms.

-DETOXIFICATION TEST: Our bodies must be able to detoxify, or neutralize, toxins from the external environment as well as those produced within our own bodies. This process takes place mostly in the liver, and consists of two phases. In Phase I toxins are activated, which means that they are altered in such a way that carrier molecules (Phase II) are able to transport them out of the body. A handy analogy is the bagging of our trash (Phase I), so that the garbage man can pick it up and cart it away (Phase II). Phase I is accomplished by a family of enzymes called "cytochrome P450", and Phase II takes place via a number of important mechanisms, four of which we measure in this test, with the help of the challenge substances, caffeine, acetaminophen and aspirin. Both Phase I and Phase II of detoxification must function adequately so that toxins are able to be neutralized, and the two phases must be in balance with each other so that the activated compounds from Phase I cannot accumulate in the body and cause damage. Laboratory: Genova Diagnostics

-Porphyrine Test is different of methylation panel, in the sense that is useful to corroborate that toxicity comes from mercury or lead. Metals would not normally show up in the urine unless you are following a detox protocol, the reason for this is that they are accumulated in the organs. Elevations of the individual porphyrin species can have a number of causes, including heredity and environmental contact. Chronic exposure to toxic metals, including lead, mercury, arsenic, aluminum, and cadmium often results in organ-specific accumulation that compromises target organ physiological function. Heavy metals impair many aspects of metabolism, while chronic exposure to organic chemicals, such as pesticides, can have deleterious effects on the body’s biochemistry and adversely affect cellular function.

-Complete Stool Analysis including parasites: Stools are teeming with bacteria, some beneficial, some neutral, and some that can be harmful. It is important to know what you have, especially if you have health problems. Health-enhancing intestinal bacteria serve to prevent the overgrowth of potentially harmful bacteria in the gut. Stool testing can also assess your body’s ability to digest food, the pH, and the amount of mucus present. A Triple Faeces Test is recommended for parasite testing, given that specificity drops when a single sample is taken. Three days in a row is recommended and scraped in the external annus is also necessary, given that is where parasites eggs are normally displayed.

-Metabolic Analysis Profile or Organic Acids Test: This profile measures 39 organic acids that play a role in four critical areas: gastrointestinal function and dysbiosis, cellular and mitochondrial energy metabolism, neurotransmitter metabolism, and nutritional assessment of vitamins and minerals that serve as critical enzyme cofactors. Test results allow practitioners to design comprehensive, customized therapies to restore optimal metabolic health. This test can be done at Genova Diagnostics USA

Urinary organic acid analysis for metabolic profiling has traditionally been used for detection of neonatal inborn errors of metabolism. Since the reporting of isovaleric acidemia in 1966, there has been a rapidly growing list of disorders resulting in elevated excretion of metabolic intermediates. The application of the testing to assess special nutrient requirements of individuals is discussed in a variety of sources. Organic acid profiling has also been useful in identification of the source of toxicants from the environment and the gut.

When you do the Organic Acids Test plus Figlue (Formiminoglutamic acid), then is not necessary a MAP.
MAP is a variation of organic acids test, but besides looks at FIGLU, which is necessary to know the state of methylation cycle. FIGLU will be high if there is a deficiency of Tetrahidrofolate (THF), a type of B9, and this occurs when there is a blocked methylation cycle. If you run a Methylation Panel, they already look at THF level, and therefore FIGLU is not necessary. In conclusion, when you run a methylation panel plus an organic Acids Test, a MAP won’t be necessary, neither the FIGLU.

For further interpretation of additional test results, visit: http://www.metametrix.com/content/Home

D) Ruling out test: Numerous CFS specialists have reported that a subgroup of those diagnosed with CFS, especially those whose CFS was gradual-onset as opposed to sudden-onset, have been misdiagnosed and actually have another chronic medical condition. The following medical conditions should be ruled out before a diagnosis of CFS can be made:

•Multiple Sclerosis (MS). ~5% of cases are missed MS according to Dr. Byron Hyde.
•Systemic Lupus Erythematosus (SLE). ~5% of cases are missed SLE according to Dr. Chris Reading.
•Myocardial infarcts. At least 5-10% of cases according to Dr. Byron Hyde. (1)
•Cerebral-Arterial Obstructions.
•Primary adrenal insufficiency (Addison's Disease). (2)
•Primary hypothyroidism (3)
•Liver disease.
•Renal (kidney) disease.
•Haemochromatosis.
•Parathyroidism.
•Rheumatoid arthritis.
•Reiter's disease.
•Sjogren's syndrome.
•Diabetes mellitus.
•Inflammatory bowel disease.
•Hepatitis B/C & HIV.
•Scleroderma.
•Malignancy.
•Cancer Screening test Ca 125 (Ovarian Cancer)
•Espirometry and full functional study including effort test (Neumologyst)
•Ross River Vius (Australian mosquito, in case you have travelled in the area)
•Colonoscopy for Celiac Disease
•Lyme Test: This is something that need to be ruled out, and the Elisa test that checks for IgG and IgM for Borrelia has a very low specificity, and therefore is not enough. Also need to test for potential coinfections: Babesia, Erchilia, Bartonella... Preferably a Western Blot test and CD57 count should be run to rule out this disease. Igenex and Labcorp in the US are the best labs to get tested. In Europe you can try Melisa labs in Germany. Lyme disease is as controversial as CFS. Some say that is simply part of SCF, because normally Lyme should be cure with a short time set of antibiotics, and some other say is a different illness with an specific long term antibiotic protocol. Either case, it will help you to know if you have an active tick bite toxicity in your body. Note that infectious pathogens are included among the possible biological stressors that can contribute to the onset of CFS. In particular, Borrelia burgdorferi, the bacterium responsible for Lyme disease, has been found to deplete glutathione in its host. This may explain the very similar pathophysiologies of chronic Lyme disease and CFS. This may also explain the epidemic clusters of CFS, which seem to have been produced by a virulent infectious pathogen (or pathogens). Perhaps the genetic factors are less important in producing the onset if a very virulent pathogen is present.
•Notes:
(1)Electrocardiogram & Ecocardiogram - Doppler (Cardiologyst)
(2)Not to be confused with sub-clinical adrenal insufficiency secondary to pituitary dysfunction, which is a common feature of CFS.
(3)Not to be confused with sub-clinical thyroid dysfunction, which is a common feature of CFS.


Note: Obviously the vast majority o these tests are not covered by the insurance companies, given the unfair status that this medical condition has at the moment. All this testing can contribute to a significant improvement on the quality of life of patients. It could also help researchers to find better protocols and treatment if the size of the CFS patients sample was bigger, while being covered by insurers. This eventually could lead to a cure.

Also you can check this laboratory in europe for many of the test described in C) Advance Testing:

EUROPEAN LABORATORY OF NUTRIENTS
REGULIERENRING 9, 3981 LA BUNNIK
POSTBUS 10, 3980 CA BUNNIK

Dr E. F. Vogelaar (This laboratory is the only one in Europe that they do the methylation panel)
Prof Clinitian Nutrition
Benadir University, Mogadishu
Tel: +31 30 287 14 92
Fax: +31 30 280 26 88
Work Mail: e.vogelaar@healthdiagnostics.nl
Website: http://www.europeanlaboratory.com/

Besides there is also another good choice in The Netherlands which is a subsidiary of Genova Diagnostics (www.genovadiagnostics.com):

IFG
Biltstraat 152
3572 BN Utrecht
Nederland
info@ivfg.nl
www.ivfg.nl
www.ivfg.nl/Spain.htm
Tel.: +31 (0) 24 3572545
Fax: +31 (0) 24 6452899

In the US, this is the laboratory that runs the methylation panel:

Vitamin Diagnostics
Industrial Drive & Route 35
Cliffwood Beach, N.J. 07735 USA
(732) 583-7773
Email: vitamindia@aol.com
Phone: 1 (732) 583-7773
Fax: 1 (732) 583-7774)

THIS WORKS! Immunology and the treatment of CFS (Post 8)

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 in the chart, I have been registering the "status" of my days scoring days from 1 to 10 based on my symptoms and intensity. Since I am following the protocol of my immunologist Josepa Rigau, I am experiencing a clear average score improvement.

For those of you that follow my blog and want to leave a comment, be aware that most of the time i can't respond to you. So if you want me to respond, is better to send me an email or to leave an email in your comment. My email is carlitos.gonzalez@gmail.com, and yes Catalunya is in Spain :-)

In this post I will talk about my new approach to CFS through an immunologist that I just visited in Tarragona (Catalunya). It changes the whole approach for treatments, and on top of making a lot of sense, it is working big time, or at least to me.

The latest studies of CFS points to a chronic infection in the stomach of enterovirus. The theory for this illness is that they always appear after a viral insult to the body that leaves the intestine affected and exposed to the leak of all kind of toxins and heavy metals. Besides the flora gets unbalanced and that is why we develop so many intolerances such as gluten, etc.

After trying a lot of treatments with antiviral, antibiotics, supplements… and after having several doctors: Dr. Quintana, Dr. De Meirleir, Dr. Kurk… I can’t say that they have solved the problem. I think that they have done their best, and they have achieved some progress, but the underlying condition remains there: recurrent infections, intestinal parasites, fungi, faringitis, extreme fatigue depending on the day or the moment… Also I did not like the fact that these doctors sometimes prescribed antibiotics, without really confirming the presence of a pathogen, only assuming it... I prefer to use antibiotics, ONLY when is necessary and the pathogen has been identified...

The new protocol that I am trying does not contain a single medication, and is working the best so far up until now. Dra. Josepa Rigau is an immunologist specialized in treating cancer patients, but she started to treat some people with CFS by azar, when a cousin of her came to her with the problem. She realized that it was an immune problem from the very beginning. She treated her with autovaccum for cytomegalovirus and other supplements, and she is doing quite well now. The same I can say for myself. She gave a presentation in Barcelona recently: (in spanish, but soon to be translated)
http://www.ligasfc.org/index.php?name=News&file=article&sid=167


In her opinion, with viruses, and pathogens in general, the best strategy is not the use of antiviral, antibiotics, etc… because that helps to kill them, but also kills the whole immune system. The way to go in her opinion is to create a hostile environment in our body for this viruses and parasites, so that they do not feel comfortable anymore in there and they tend to leave. Just as an example, if we fill our colon with the gas oz Ozone which will nourish the lining of the colon with oxygen, that will make that parasites that live in the intestine wall do not feel well there anymore, as they can’t live in the oxygen, and they will go with the food trying to look for another place to live.

Here is my meeting with Dr. Rigau and the results of Analysis performed and treatment proposed:

SUMMARY OF MY VISIT TO IMMUNOLOGIST DR. JOSEPA RIGAU


IMMUNITY ANALYSIS

In Madrid I run some blood test called IMI in Labs CERBA in order to check for amino acids and serology and the functioning of my white cells. Depending on that we would decide to go for the autovaccum or the homeopathic antiviral.

The autovaccum consists on extracting some blood, treat it with alcohol and eater, covert it into powder, and inject it under the skin, where the lymphocytes T act, and not the Lymphocytes B that acts in the blood stream.

Al alternative to the autovaccum is the homeopathic antiviral from Labo Life, there are versions for EBV, CMV, HHV6, etc… This acts as an immune activator and as a blocker of cellular division that avoids the mutation of active viruses.

The Transfer Factor that I used to take, acts as an immune modulator, but stays in the intestine, and therefore is not comparable to the autovaccum or the homeopathic antiviral of Labo Life. Finally after receiving my results, the doctor opted for Labo Life in my case, given that my immune system responds properly to viruses.


BLOOD TEST

SEROLOGY

HHV-6 IgG 1/80 >1/40 POSITIVE
HHV-6 IgM NEGATIVE <1/10 NEGATIVE
Borrelia Burgdorferi IgG 0,58 <1 NEGATIVE
AC Borrelia Burgdorferi IgM 0,07 <1 NEGATIVE
AC Herpes Simplex1 IgG 0,48 <0,9 NEGATIVE
AC Herpes Simplex1 IgM 0,24 <0,9 NEGATIVE
AC Herpes Simplex2 IgG 0,15 <0,9 NEGATIVE
AC Herpes Simplex2 IgM 0,36 <0,9 NEGATIVE
AC Varicela Zorster IgG 1,77 >0,9 POSITIVE
AC Varicela Zoster IgM 0,32 <0,9 NEGATIVE
AC EBV IgM V.C.A. 1/10 >1/10 POSITIVE (greater or equal to)
AC EBV IgG V.C.A. 1/640 >1/10 POSITIVE
AC EBV IgG ANTI E.B.N.A. 1/320 >1/10 POSITIVE
AC EBV IgG ANTI E.A. 1/5 <1/10 NEGATIVE
AC CMV IgM 0,19 <0,4 NEGATIVE
AC CMV IgG 233,2 >15 POSITIVE

CONCLUSIONS:

The results of the analysis, showed a high level of cholesterol and LDL. As well there was presence of antibodies of IgG HHV6. The proteic profile did not show inflammatory signs.

The results of the virology test reveal the presence of Herpes Zoster under normal limits. Nevertheless there is a clear chronic mononucleosis infection by Epstein Barr Virus. There is evidence of the existence of antibodies of anti-EBNA (Epstein Barr Nuclear Antigens), together with presence of antibodies IgG anti-VCA (Anti viral capside ). This is the typical case of a constant state of infection where there has not been reached any immunity. There is also clear activity of Cytomegalovirus, where we should see an IgG below 100 in order to consider that immunity has been reached.
EBV and CMV act many times together, therefore we will try to reduce both through homeopathic antiviral of Labo Life.

The lymphocyte count reveals a situation of normal activity from the immune system point of view. There is a good response of the CHM I, nevertheless important to mention that there is a cellular inversion in the CHM II and a dip below normal limits in the tactive cells (precursors for T8cit).

In theory, this let us observe a deficiency of the immune system against intestinal parasites, fungi and pathogens, probably due to the extra effort that the immune system is doing in the viral part.


BIOLOGIC STUDY OF CARLOS GONZALEZ

AMINOACIDS AND PROTEINS

ESENTIAL AMINOACIDS

Arginina 61 40-102
Fenilalanina 51 37-61
Histidina 56 45-61
Isoleucina 62 37-87
Leucina 126 82-153
Lisina 124 123-237
Metionina * 35,5 19-31
Treonina * 52,7 87-124
Triptofano * 38,2 44-55
Valina 230,8 177-298

NON ESENTIALS

Alanita 285 240-405
Asparragina 63 45-65
Aspartico 3,6 2-4,65
Cisterna 16,2 8,5-24
Glicina 177 166-300
Glutámico 41,1 30-57
Glutamina * 435 490-600
Prolina 152 130-220
Serina 93 72-119
Tirosina 62 42-70

THE REST

Metilhistidina 0 <10
Alfa amino adipico 0 <5
Alfa amino butirico 15,4 11-25
Anserina 0
Beta Alanita 0 4,5-8
Carnitina 0
Cistationina-1 0
Cistationina-2 0
Beta amino isobutirico 0
Citrulina 25 25-40
Fosfoetanolamina 0,7 3,3-8,3
Fosfoserina 2,9 5,3-10,5
Gamma Aminobutirico 4,2 0,8-8,1
Hidroxilisina-1y2 0
Hidroxiprolina 9,1 4,3-23
Ornitina 88,5 60-129
Taurina* 68,8 80-152


COMMENTS:

A) Amino acids that contain sulfur

Taurina Low Level: Indicates digestive problems with fat, deficit of lipolitic proteins. They are associated with high cholesterol levels, cardiovascular alterations and beta adrenergic dysfunctions.

Metionina high level, is associated with hepatic detox function, ileocecal and gastric resection or unbalanced intestinal flora.

B) Amino acids for polypeptides and sources of energy. They are used to sensitize peptides and proteins. Represent 50% of ingestion.


Treonina Low Levels are associated with hypoglycemia manifested with fatigue, headaches and anxiety.


Neurotransmitters and precursors

Triptofano Precursor of serotonin (stabilizer of mood ) and melatonin (controller of sleep/insomnia). Low level implies tendency to depression.

Amino acids related with the cycle of UREA. This is a critical metabolic process.

Glutamine: Is the source of energy of enterocites and neurons. Is a natural balance. Reflects problems of desintoxication from the ammonia and / or a diet poor in essential amino acids.

Amino acids related with Glicina and Serina

Fosfoetanolamina Competes in the brain with GABA and controls its inhibitory action.
Fosfoserina, in neurodegeneration.

Beta Aminoácids. Does not make part of the proteins. Is a precursor of biliar acids, antioxidants of neurotransmitters and metabolic control.


Beta Alanita low, status of exhaustation..

ANTI FREE RADICALS

In general is recommended to eat antioxidants in a natural way: 5 pieces of fruits or vegetables a day, mixing 4 different colors: white, green, red and yellow. What counts is the color of what you eat. In that way you will have daily all the minerals that you need.


PROPOSED TREATMENT IN MI CASE

With the meals:

- Eye-Q (Vitae): 2 pills in each meal. Is an Omega 3 that alleviates the dry eyes and lowers the cholesterol..
- L’equilibrium Vital (Minerals -2 in each meal ), take it only when the PH in the urine is unbalanced. Its rol is to balance the acids and the alkaline among the things we eat. We need to measure the PH in the urine 3 times a day, once every 10 days.
- Microfloriana: probiotic to restore the flora in the intestine. Preferably take at the same time we do the cleansing with Puricorp.
Semana1: 5cc with breakfast
Week 2: 5cc with breakfast and 5cc with dinner
Week 3: 10cc with breakfast y 10cc with dinner
Week 4: 10cc with breakfast, 10cc with lunch y 10cc with dinner
From the 5th week onwards, take 10cc in the morning until you finish the product., and then switch to another probiotic: Darmocare, Acydophilus, Lactobacilus, VSL-3...
- Milk thistle, artichoke and chlorophyll in pills or solution diluted in juice. This will help the liver to detox, take with the main meals, especially when there is fat or proteins. Cat’s Claw in an activator of the immune system, but I do not need it at this time
- Chlorella & espirulina, one cleans you from minerals, and the other one does them, and although seems like a contradiction to take both at the same time, both of them have chlorophyll, and therefore oxygenates the intestinal tract and prevent bacteria to remain there.

Out of the Meals:


(Morning and night cocktail)

- Envozyme (Papaya Enzyme Complex) doses of 6 pills, to be taken out of meals, and only when there is muscle pain and illness sensation.
- Puricorp (Suravitasan-Antiparasites treatment of 21 days- 5 in the morning and 5 in the night – not with the meals
- Citrobiotic/Citriplus: Extract of grape frut seeds to fight fungical infections. Take daily during 3 months, and then one week out of 4. Always dilute 15 drops in water in the morning and the night without mixing it with probiotics. Also can be used as an antiseptic in the skin, but not directly, but mixed with water.
- Glutamine: Twice a day, in the morning and the night. It is a source of energy for the intestinal mucosa and the brain.
- Ergytaurina (Nutergia) twice a day with the meals.

(Only in the mornings : Can still take what I used to)

- NAC + Vitamin C in ascorbat form
- Multivitamin supplement

(Sublinguals- only in the morning)

- 2LEBV (Labolife) once a day with no food in the stomach. (Continue until June to check again the blood)
- 2LCMV (Labolife) once a day with no food in the stomach, not in the night because it could alter the quality of sleep. (Continue until June, but only the first 10 days of each month, and the in June check again the blood)
- Magnesium+Vitamin B6 (PHO) Discoflash one tablet
- Mucosa Compositum (Heel) Is an activator of the intestinal mucosa. Box1 (one a day with empty stomach), Box 2 (3 per week with empty stomach), Box 3 and 4 (2 per week with empty stomach)
- Coenzyme Compositum (Heel) Is the same principal, but for the liver. Take once you are done with the previous one. Box1 (one a day with empty stomach), Box 2 (3 per week with empty stomach), Box 3 and 4 (2 per week with empty stomach)

(Only in the night)

- 5 http/Solgar (one a day) This one enhances the mood and offsets the low level of triptofano which is the precursor of serotonin.

Additional Treatments Recommended:

Colon cleansing with oxygen (ozone treatment) Institute of Biological Medicine (Dr. Domingo Garcia de Leon)
Blood cleansing with ozone treatment (like a dialysis) This one is less recommendable, given that the anticoagulant can cause allergies, and therefore is an effective but invasive method.

These treatments, oxygen our blood and our colon, and both viruses and parasites feel quite uncomfortable in a place where there is oxygen. Therefore we will become more resistant to these pathogens, and our immune systems is stronger. This is the objective actually, to save work to the immune system creating an alkaline environment and oxygenated that does not allow the virus to divide and creates an unfriendly ambience for pathogens.

Genetic Profile of the urine:

This is a genetic study that can be done later, and it reflects the farmacogenetic of the liver taking into account 15 genes and 92 poliformisms. This is called LITOCROMO P450, and it also is done out of Spain. This study will give us information of what foods or medications are not assimilated by our liver and therefore should be skipped. The problem is that insurance only covers you this study when you have cancer or aids…

Advice for the comments I received: (Please better send me an email, I can't otherwise answer an anonymous comment)

Is definitely worth to pay a visit to Dr. Josepa Rigau, since I started her protocol i feel a clear improvement, not yet 100%, but my average day is 60%, when it used to be 40%, so is only 4 months since i started, and i already feel a difference. Josepa Rigau: +34977220358

It would be very revealing to check your flora, when you have a disbiosys (altered balance of good and bad bacteria) your whole immune system can be depressed and could explain why you are not able to fight viruses or other infections. To check your flora, you need to pass a TFT (Triple Faeces Test - 3 samples, 3 days in a row). If they find a pathogen like entamoeba Histolitica, Giardia Lambia, etc you will be treated with antibiotics, if so, take a lot of probiotics to restore your flora. In any case, even if you only show comensals such as blastocystis hominis, endollimax nana, entamoeba coli, etc... still it is a good idea to use probiotics regularly. Witch brands so that you put inside a variety of good bacterias: acydophilus, lactobacilus, etc... Also very highly recomended to search for a doctor that puts ozone in your colon with gas, it is a natural antibiotic and wont harm you at al, and will make your colon an unfriendly place for parasites, bacteria and viruses...all that will boost your immune system.

Only if HHV6, EBV or CMV were an issue in your case, then labolife will help you to reduce the viral load.

This antivirals are supposed to lower the viral load through some months you should get tested again to see if it helped you. I do not know if there are other medications for HHV6, but before trying heavy stuff that Dr. Montoya is using for a clinical trial, I would try better the omeopatic antiviral I told you, it contains very mall dosis of interferon, and it will help you to reduce the virus.

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

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

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

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



Hope this helps you, and wish you the best....

Gut problems...the next step Post 7

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)


Well, here I come to continue this blog with an update of my current medical condition.

Because I had parasitosis, rectal bleeding, food intolerances and celiac markers in my serum, the gastroenterologist decided to run a colonoscopy and endoscopy with biopsy to rule out celiac disease or other diseases. The results of the biopsy were good, I am not celiac, but they diagnosed a espastic colon, which is no news to me, because I suffer from IBS for a long time already.

The thing is that during one month I have been eating gluten, lactose, and all the things that I am supposed to be intolerant to, due to this colonoscopy that had to be done. Probably because of this I have been feeling worse with my IBS. Besides I have experienced gastritis once or twice a month since June 2007, and unfortunatelly my EBV IgM became positive in my last blood test.

The 31st of October I obtained my last stool test, after 20 days treatment of my Entamoeba Hystolitica with yodoxin and metronidazol, and these were the results:

- Cysts of Endolimax nana (POSITIVE)
- Cysts of Iodamoeba butschlii (POSITIVE)
- Cysts of Blastocystis Hominis (POSITIVE)
- ELISA de Helicobacter Pylori (POSITIVE)

The good news is that there is no trace of Entamoeba Hystolitica, and the bad news is that Blastocystis Hominis is still present, as well as other commensals that point for an umbalanced flora in my gut.

In January I repeated the stool test, after taking a natural treatment with Puri-corp (roots to clean parasites), and the results were slightly better (one less):

- Cysts of Endolimax nana (POSITIVE)
- Cysts of Blastocystis Hominis (POSITIVE)
- ELISA de Helicobacter Pylori (POSITIVE)

Besides this, I am going to see an inmmunologist in Tarragona the 5th of November (Spain) that someone reccomended me, her name is:

Josepa Rigau
Av. Catalunya 12, 3º 1ª
43002 Tarragona
tel: 977220358

As well, I spoke with Jose Jimeno from ZELTIA (Cancer biotechnology company that just launched Yondelis in the market), and he tells me that a good friend of him, that is an oncologist, has specialized in CFS and is one of the best practicioners in Europe, his name is Humberto Tirelli, and is located in Aviano, close to Venice. I will get his address from Jose Jimeno soon, and I will also pay him a visit. (utirelli@cro.it / 0434 41416)

The reason for keep on seeking specialized medical help, is simply because I am still not recoverd, I have improved, yes I have, but I still suffer crisis, and the underlying condition is still there. So I hope that my experience keeps on bringing light to those of you that play in this team.

I consider myself lucky in many respects, my personality helps, I am a positive person, my economical situation helps as well, I had access to good professionals, my progression has been slow, but positive. I am full of hope, and confident that I will recover, and I beleive on that from my heart.