https://www.statineffects.com/
Have you had any side effects from statin treatment?
If you would like to share your experience on statins with researchers at the University of California in San Diego ,
please email at statinstudy@ucsd.edu
and/or complete an online (paperless) survey at
http://www.statineffects.com
woensdag 29 februari 2012
zondag 26 februari 2012
The hidden cure for viral diseases?
http://www.ceri.com/BHTbook-StevenWmFowkes-100903.pdf
This online book offers a biologically sustainable solution to chronic viral disease (herpes, CMV, ...)
The treatment is about the drug BTH (butylated hydroxytoluene). It will cost you 10$ in bulk or 50$ in capsules. Show it to your doctor.
From what I read, it looks promising. Take your time or have someone take notes for you.
This online book offers a biologically sustainable solution to chronic viral disease (herpes, CMV, ...)
The treatment is about the drug BTH (butylated hydroxytoluene). It will cost you 10$ in bulk or 50$ in capsules. Show it to your doctor.
From what I read, it looks promising. Take your time or have someone take notes for you.
vrijdag 24 februari 2012
Duidelijkheid rond vitamine B12
Naar aanleiding van de ervaringen van een patient met vitamine B12, deel ik hier zijn vaststellingen.
Hij was ernstig beperkt gedurende vele jaren maar is nu bijna volledig hersteld. De moeite waard om het eens door te nemen. Veel mensen prikken of slikken immers vitamine B12.
http://aboutmecfs.org.violet.arvixe.com/Trt/B12Ineffectiveness.aspx
Zelf heb ik geëxperimenteerd met verscheidene injecteerbare producten omdat de vloeistof zo pijnlijk blijkt. Soms kon ik gedurende een dag mijn bed niet meer uit van de pijn. Andere mensen hebben hier ook last van, anderen dan weer niet.
Mogelijk ligt het antwoord in zijn (vertaalde) tekst hieronder.
Niet iedereen blijkt "vitamine B12" te kunnen omzetten. De oorzaken zijn divers:
Hij was ernstig beperkt gedurende vele jaren maar is nu bijna volledig hersteld. De moeite waard om het eens door te nemen. Veel mensen prikken of slikken immers vitamine B12.
Hier vindt u het origineel:
http://aboutmecfs.org.violet.arvixe.com/Trt/B12Ineffectiveness.aspx
Zelf heb ik geëxperimenteerd met verscheidene injecteerbare producten omdat de vloeistof zo pijnlijk blijkt. Soms kon ik gedurende een dag mijn bed niet meer uit van de pijn. Andere mensen hebben hier ook last van, anderen dan weer niet.
Mogelijk ligt het antwoord in zijn (vertaalde) tekst hieronder.
Niet iedereen blijkt "vitamine B12" te kunnen omzetten. De oorzaken zijn divers:
- Onmogelijkheid om vit B12 te absorberen vanwege pernicieuze anemie (genetisch of auto-immuun)
- Men kan vit B12 niet binden voor transport
- Er zijn genetische uitdagingen
- Verlaagde cobalamine niveaus in ruggemerg - hypothetische oorzaak, bevestigd probleem
- Afwezigheid van enzym om methylb12 in adenosylb12 om te zetten - bevestigd, cobalamin letter ziekte
- Afwezigheid van enzym om adenosylb12 in methylb12 om te zetten - bevestigd, cobalamin letter ziekte
- Afwezigheid van enzym om cyanocobalamin in methylb12 of adenosylb12 om te zetten - bevestigd, cobalamin letter ziekte
- Afwezigheid van enzym om hydroxycobalamin in methylb12 of adenosylb12 om te zetten - bevestigd, cobalamin letter ziekte
- Afwezigheid van enzym om glutathionylcobalamin in methylb12 of adenosylb12 om te zetten - hypothetisch, enige aanwijzingen voor probleem
- Te weinig enzymen om foliumzuur om te zetten in de bio-actieve vorm, methylfolaat - bevestigde oorzaak
- Actieve vorm: vit B12 in orale vorm wordt slechts voor 1% opgenomen omdat het door een klein celgaatje moet en omdat de binding verminderd kan zijn door genetische of aangeworven redenen.
- Inactieve vorm = cyanoB12 of hydroxyB12
- voordeel: waarden in bloed stijgen snel boven 300 pg/ml
- nadeel: geneest de schade niet aangericht door tekort aan vit B12
- nadeel: mogelijk blokkeren ze de B12 receptoren op de cellen waardoor de echte B12 niet meer kan werken
- nadeel: beide vormen kunnen maar voor 10 mcg/dag door een celgaatje en dus beperkt omgezet worden
- nadeel: ze doen het niveau van de ongebonden cobalamine niet stijgen (en net deze heb je nodig voor herstel)
- Enzymen: Sommige mensen missen de enzymen om cyanoB12 en hydroxyB12 om te zetten in de actieve vorm
- Verkeerd gebruik: Zuigtabletten blijken alleen te werken als je ze gedurende 45 min tot 2 uur onder de bovenlip of onder de tong laat smelten.
- Verkeerd merk: Slechts enkele merken blijken effectief werkzaam waaronder:
- Enzymatic Therapy 1 mg
- Jarrow Formulas 1 en 5 mg
- Country Life Dibenzodide 1 mg (adenosylB12)
- Solgar Metalfolin (methylfolaat) is beter dan eender welk foliumzuur
- Injecteerbaar product: MethylB12 wordt afgebroken tot hydroxyB12 maar geneest geen mensen met een tekort aan cobalamine. Dat vereist ongebonden methylB12 én adenosylB12. Mensen nemen vaak slechts 1 soort vitamine B12.
- Te lage dosering: mensen nemen te lage doseringen om efficient het ruggemerg te beïnvloeden
- Te weinig methylfolaat: dit is de werkzame vorm van foliumzuur
- Tekort aan essentiële co-factoren
- Suppleren met glutathion of precursors van glutathion: kunnen mogelijk een actieve vit B12 deficiëntie inleiden
Persoonlijk heb ik een vraagteken bij het punt dat het geen schade zou herstellen n.a.v. een tekort. Zelfs indien het geen schade herstelt, merkte ik het eerste jaar toch een mindering van de brainfog en meer stamina zo'n 24 uur na een inspuiting. Hoe meer tijd ik tussen de spuitjes liet, hoe pijnlijker ze telkens weer werden.
Voor degenen die er meer over willen lezen:
Het verhaal van Fred: http://aboutmecfs.org/Trt/B12Story.aspx
Een intro over B12: http://aboutmecfs.org/Trt/B12Intro.aspx
Het behandelingsplan van Fred: http://aboutmecfs.org/Trt/B12Treatment.aspx
http://www.iherb.com/Jarrow-Formulas-Methyl-B-12-5000-mcg-60-Lozenges/117?at=0
http://www.iherb.com/Country-Life-Gluten-Free-Active-B-12-Dibencozide-3000-mcg-60-Lozenges/1637?at=0
http://www.iherb.com/Solgar-Folate-Metafolin-Folic-Acid-800-mcg-100-Tablets/13961?at=0
http://www.iherb.com/Natural-Factors-Potassium-Citrate-99-mg-90-Tablets/2627?at=0
EXTRA LINK: http://www.diagned.nl/files_content/Diagned38-3.pdf
Een intro over B12: http://aboutmecfs.org/Trt/B12Intro.aspx
Het behandelingsplan van Fred: http://aboutmecfs.org/Trt/B12Treatment.aspx
http://www.iherb.com/Jarrow-Formulas-Methyl-B-12-5000-mcg-60-Lozenges/117?at=0
http://www.iherb.com/Country-Life-Gluten-Free-Active-B-12-Dibencozide-3000-mcg-60-Lozenges/1637?at=0
http://www.iherb.com/Solgar-Folate-Metafolin-Folic-Acid-800-mcg-100-Tablets/13961?at=0
http://www.iherb.com/Natural-Factors-Potassium-Citrate-99-mg-90-Tablets/2627?at=0
EXTRA LINK: http://www.diagned.nl/files_content/Diagned38-3.pdf
maandag 20 februari 2012
Statin Adverse Effects: Evidence for a Mitochondrial Mechanism
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/?tool=pmcentrez
Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
In the case of statins, a potential basis for opposing effects occurring in muscle and in other organs can be identified. Evidence supports the proposition that antioxidant effects of statins underlie (or contribute to) many fundamental statin benefits – including benefits to flow and oxygen delivery46-48 and inflammation.49, 50 These effects may participate in improved walking distance in patients on statins, including benefits to muscle/walking in persons with and without peripheral artery disease.29 Yet a subset of people reproducibly exhibit increases in markers of oxidation on statins,51 and the occurrence of this increase has been tied to muscle pain on statins.52, 53
...
A range of cases have now been reported in which statin use has “uncovered” previously clinically silent or clinically tolerated conditions, ranging from McArdle disease159, 160 to myotonic dystrophy159 to acid maltase deficiency161 to possible Kennedy disease.159 Statins have also exacerbated known muscle conditions, such as myasthenia gravis.78 In the case of mitochondrial myopathies, the relative degree to which statins have unmasked vs induced disease may not always be clear.159, 162
...
Several widely used statins – atorvastatin, simvastatin, and lovastatin (and previously cerivastatin, now off the market) – are metabolized by the cytochrome P450 (CYP)3A4 pathway.318
...
While a medley of potential mechanisms may cause or contribute to statin AEs (and these merit more full review in another venue), mitochondrial mechanisms have been repeatedly implicated in muscle AEs. Mitochondrial defects predispose to problems on statins (as shown in the second to last entry of Table IV, ‘Genetic mutations associated with mitochondrial dysfunction’). Additionally, statins predispose to mitochondrial defects (Table V,22 31, 32, 112, 155, 158, 162, 397, 406-414) – in all users and, to a greater degree, in vulnerable individuals. Dose-dependent reductions in coenzyme Q1020-22 can reduce cell energy, promote oxidation,362, 415 promote apoptosis, and unmask silent mitochondrial defects.23-25, 362, 415-418 The mevalonate pathway, which statins inhibit, also produces heme-A, which has it own central involvement in mitochondrial electron transport.419
...
For instance, mitochondrial encephalomyopathy resulting from heritable coenzyme Q10 deficiency classically produces fatigue, muscle symptoms, and cognitive problems,440 although the cases referred for analysis are often relatively severe.429, 441 Gastrointestinal26 and neurological symptoms,432, 442 psychiatric symptoms,443-446 sleep problems,444, 447 glucose elevations,182 and a range of other symptoms reported on statins also arise in mitochondrial dysfunction.379, 448-457
...
Thus, in an analysis of data, presented in the Australian Adverse Drug Reaction Bulletin, it was noted that “Statin-associated peripheral neuropathy may persist for months or years after withdrawal of the statin… In two ADRAC (Adverse Drug Reactions Advisory Committee) cases of persistent peripheral neuropathy, motor and sensory conduction tests showed minimal recovery 4 and 12 months, respectively, after discontinuation of simvastatin, despite clinical improvement.”561
As reviewed here, AEs on statins may signal a mitochondrial vulnerability, which may alter or perhaps even reverse an otherwise favorable impact of statins on cell energetics. And AEs may signal occurrence of a net prooxidant rather than antioxidant effect of statins53 with possible unfavorable implications for a range of statins' proposed pleiotropic effects.892
Full report here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/?tool=pmcentrez
Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
In the case of statins, a potential basis for opposing effects occurring in muscle and in other organs can be identified. Evidence supports the proposition that antioxidant effects of statins underlie (or contribute to) many fundamental statin benefits – including benefits to flow and oxygen delivery46-48 and inflammation.49, 50 These effects may participate in improved walking distance in patients on statins, including benefits to muscle/walking in persons with and without peripheral artery disease.29 Yet a subset of people reproducibly exhibit increases in markers of oxidation on statins,51 and the occurrence of this increase has been tied to muscle pain on statins.52, 53
...
A range of cases have now been reported in which statin use has “uncovered” previously clinically silent or clinically tolerated conditions, ranging from McArdle disease159, 160 to myotonic dystrophy159 to acid maltase deficiency161 to possible Kennedy disease.159 Statins have also exacerbated known muscle conditions, such as myasthenia gravis.78 In the case of mitochondrial myopathies, the relative degree to which statins have unmasked vs induced disease may not always be clear.159, 162
...
Several widely used statins – atorvastatin, simvastatin, and lovastatin (and previously cerivastatin, now off the market) – are metabolized by the cytochrome P450 (CYP)3A4 pathway.318
...
While a medley of potential mechanisms may cause or contribute to statin AEs (and these merit more full review in another venue), mitochondrial mechanisms have been repeatedly implicated in muscle AEs. Mitochondrial defects predispose to problems on statins (as shown in the second to last entry of Table IV, ‘Genetic mutations associated with mitochondrial dysfunction’). Additionally, statins predispose to mitochondrial defects (Table V,22 31, 32, 112, 155, 158, 162, 397, 406-414) – in all users and, to a greater degree, in vulnerable individuals. Dose-dependent reductions in coenzyme Q1020-22 can reduce cell energy, promote oxidation,362, 415 promote apoptosis, and unmask silent mitochondrial defects.23-25, 362, 415-418 The mevalonate pathway, which statins inhibit, also produces heme-A, which has it own central involvement in mitochondrial electron transport.419
...
For instance, mitochondrial encephalomyopathy resulting from heritable coenzyme Q10 deficiency classically produces fatigue, muscle symptoms, and cognitive problems,440 although the cases referred for analysis are often relatively severe.429, 441 Gastrointestinal26 and neurological symptoms,432, 442 psychiatric symptoms,443-446 sleep problems,444, 447 glucose elevations,182 and a range of other symptoms reported on statins also arise in mitochondrial dysfunction.379, 448-457
...
Thus, in an analysis of data, presented in the Australian Adverse Drug Reaction Bulletin, it was noted that “Statin-associated peripheral neuropathy may persist for months or years after withdrawal of the statin… In two ADRAC (Adverse Drug Reactions Advisory Committee) cases of persistent peripheral neuropathy, motor and sensory conduction tests showed minimal recovery 4 and 12 months, respectively, after discontinuation of simvastatin, despite clinical improvement.”561
As reviewed here, AEs on statins may signal a mitochondrial vulnerability, which may alter or perhaps even reverse an otherwise favorable impact of statins on cell energetics. And AEs may signal occurrence of a net prooxidant rather than antioxidant effect of statins53 with possible unfavorable implications for a range of statins' proposed pleiotropic effects.892
Full report here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/?tool=pmcentrez
Dr. Klinghardt's Treatment of Lyme Disease
http://articles.mercola.com/sites/articles/archive/2009/08/04/Dr-Klinghardts-Treatment-of-Lyme-Disease.aspx
Extract:
Regular lab parameters affected by Lyme:
•Abnormal lipid profile (moderate cholesterol elevation with significant LDL elevation)
•Insulin resistance
•Borderline low white blood cells, normal SED rate and CRP
•Normal thyroid hormone tests but positive Barnes test and excellent response to giving T3
•Type 2 (high cortisol, low DHEA) or type 3 adrenal failure (low cortisol and DHEA)
•Low testosterone and DHEA
•Decreased urine concentration (low specific gravity)
•Complex changes in cytokines, interferones, NK cells, white blood cell indicators, etc.
...
Extract:
Regular lab parameters affected by Lyme:
•Abnormal lipid profile (moderate cholesterol elevation with significant LDL elevation)
•Insulin resistance
•Borderline low white blood cells, normal SED rate and CRP
•Normal thyroid hormone tests but positive Barnes test and excellent response to giving T3
•Type 2 (high cortisol, low DHEA) or type 3 adrenal failure (low cortisol and DHEA)
•Low testosterone and DHEA
•Decreased urine concentration (low specific gravity)
•Complex changes in cytokines, interferones, NK cells, white blood cell indicators, etc.
...
Symptomen van een dopaminestoornis
Symptomen van een dopaminestoornis
zit in pompoenzaden, amandelen, avocado's, bananen, haring, kaas, sesamzaad
Niet geschikt bij migraine, hoge bloeddruk of tegelijkertijd met antidepressiva
Extra:
Vit B = nodig voor aanmaak neurotransmitters
Vit C minimaal 2g
magnesium
Visolie EPA DHA 1 g
Goed supplement bij depressie algemeen:
Nutramin Emotio Balans, 1 x ochtend en 1 x avond
Niet bij zwangerschap of borstvoeding
- besluiteloosheid
- arm aan initiatieven
- depressie
- angst
- uitputting
- chronisch vermoeid, de hele dag kunnen slapen
- tremor
zit in pompoenzaden, amandelen, avocado's, bananen, haring, kaas, sesamzaad
Niet geschikt bij migraine, hoge bloeddruk of tegelijkertijd met antidepressiva
Extra:
Vit B = nodig voor aanmaak neurotransmitters
Vit C minimaal 2g
magnesium
Visolie EPA DHA 1 g
Goed supplement bij depressie algemeen:
Nutramin Emotio Balans, 1 x ochtend en 1 x avond
Niet bij zwangerschap of borstvoeding
zondag 19 februari 2012
Symptomen van een serotoninestoornis
Symptomen van een serotoninestoornis
Supplement: Tryptofaan
= essentieel aminozuur, zit in melk, vlees en chocolade
= even effectief als antidepressivum (SSRI)
verbetert membraanfluiditeit
Vooraleer je aan de slag gaat met SAMe, lees deze link eerst:
http://www.alternativementalhealth.com/articles/walshQZ.htm
A quick way to test for need for methylation therapy is to carry out a cautious trial of SAMe. Within a week or two you should have your answer. If she clearly is improving on the SAMs (which is frightfully expensive)..... you can get usually the same benefits (albeit more slowly) using methionine plus calcium, magnesium, and B-6. This should be side-effect free unless (a) the methylation is begun too abruptly or (b) the patient has a rare genetic enzyme disorder which disrupts the SAM cycle. We've found that direct methylation is usually more successful than tinkering with the SAM cycle. The primary way humans receive most of their methyl groups is from dietary methionine. It's often hard to improve on Mother Nature. (Jan 20, 2003)
SAMe is likely to cause great worsening of symptoms, including mania, if given to an OVER-methylated person. The incidence of overmethylation in our patient database of 1,500 bipolar cases is about 18%. Bipolar disorder is not a single condition, but a collection of very different biochemical disorders under the same umbrella diagnosis. SAMe works great for truly undermethylated patients, but all hell breaks out if given to someone who is overloaded (genetically) with methyl groups. The right way to do this is to (a) first determine the person's innate methylation tendency & then (b) act accordingly. (Jan 31, 2003)
Multiple food & chemical sensitivities are also associated with histapenia (low histamine, overmethylation), the largest of all SZ groups, amounting to about 48% of all cases. For this group, SZ symptoms often worsen if exposed to the offending substances, & nice improvements often occur if they are identified & avoided. However, the food sensitivities usually disappear after about 1 year of aggressive Folate/B-12/B-3 treatment, which is the primary route to a normal life for these patients.
...
Histamine assays for depression were introduced by Dr. Carl Pfeiffer of Princeton, NJ in the 1970' and 1980's. My clinic has found whole blood histamine to be very useful & has used this assay more than 30,000 times.
First of all, the analysis must be done for whole blood (not plasma, serum, etc), strictly adhering to the sampling protocol. We presently use LabCorp but in the past Quest also had proficiency for this assay.
The reference "normal" range for mental health is 40 to 70 ng/dL. Levels above 70 indicate undermethylation, whereas levels below 40 suggest overmethylation.
Undermethylated depressives thrive on l-methionine, calcium, magnesium, B-6, Zinc, and Vitamin C. In severe cases, up to 3,000 mg/day of methionine and 2,000 mg/day of Ca may be needed. However, we also like to routinely run a homocysteine test to assure the safety of the methylation protocol. This population is believed to result in low serotonin activity. This methylation therapy is quite slow in taking effect.... and often 6-8 weeks pass before progress is obvious.
Overmethylated (low-histamine) depressives thrive on folic acid, B-12, niacin (or niacinamide), B-6, Zinc, Manganese, DMAE, and Vitamins, C and E. In severe cases, up to 5,000 mcg/day of FA may be needed. Response is more rapid with this phenotype, with clear progress usually by week 4. This population is believed to have an innate tendency for elevated serotonin, dopamine, and norepinephrine levels.
This test can also help guide psychiatrists in selection of psychiatric medications. For example high histamine persons may do quite well on SSRI's, but low-histamine persons usually reactly very badly to SSRI's and are better candidates for benzodiazapines.
We like to augment the histamine blood test with an "absolute basophil" test offered by Direct Healthcare, Inc. The histamine assay can be affected by antihistamines and other medications with AH properties. The reference range for ABC's is 30-50.
- slaapproblemen
- spijsverteringsproblemen
- te weinig serotonine geeft obstipatie
- teveel serotonine geeft diarrhee
- angst met diepe triestheid
- depressie
- verhoogde pijngevoeligheid
- hoofdpijn
- niet lekker in je vel zitten
- uitputting
Supplement: Tryptofaan
= essentieel aminozuur, zit in melk, vlees en chocolade
- L-tryptofaan: lichaam kan het omzetten naar believen en wat het nodig heeft
- 5 hydroxitryptofaan: kan alleen omgezet worden in serotonine en geeft soms bijwerkingen
Supplement: SAMe butaandisulfonaat
= lichaamseigen stof = even effectief als antidepressivum (SSRI)
verbetert membraanfluiditeit
Vooraleer je aan de slag gaat met SAMe, lees deze link eerst:
http://www.alternativementalhealth.com/articles/walshQZ.htm
A quick way to test for need for methylation therapy is to carry out a cautious trial of SAMe. Within a week or two you should have your answer. If she clearly is improving on the SAMs (which is frightfully expensive)..... you can get usually the same benefits (albeit more slowly) using methionine plus calcium, magnesium, and B-6. This should be side-effect free unless (a) the methylation is begun too abruptly or (b) the patient has a rare genetic enzyme disorder which disrupts the SAM cycle. We've found that direct methylation is usually more successful than tinkering with the SAM cycle. The primary way humans receive most of their methyl groups is from dietary methionine. It's often hard to improve on Mother Nature. (Jan 20, 2003)
SAMe is likely to cause great worsening of symptoms, including mania, if given to an OVER-methylated person. The incidence of overmethylation in our patient database of 1,500 bipolar cases is about 18%. Bipolar disorder is not a single condition, but a collection of very different biochemical disorders under the same umbrella diagnosis. SAMe works great for truly undermethylated patients, but all hell breaks out if given to someone who is overloaded (genetically) with methyl groups. The right way to do this is to (a) first determine the person's innate methylation tendency & then (b) act accordingly. (Jan 31, 2003)
Multiple food & chemical sensitivities are also associated with histapenia (low histamine, overmethylation), the largest of all SZ groups, amounting to about 48% of all cases. For this group, SZ symptoms often worsen if exposed to the offending substances, & nice improvements often occur if they are identified & avoided. However, the food sensitivities usually disappear after about 1 year of aggressive Folate/B-12/B-3 treatment, which is the primary route to a normal life for these patients.
...
Histamine assays for depression were introduced by Dr. Carl Pfeiffer of Princeton, NJ in the 1970' and 1980's. My clinic has found whole blood histamine to be very useful & has used this assay more than 30,000 times.
First of all, the analysis must be done for whole blood (not plasma, serum, etc), strictly adhering to the sampling protocol. We presently use LabCorp but in the past Quest also had proficiency for this assay.
The reference "normal" range for mental health is 40 to 70 ng/dL. Levels above 70 indicate undermethylation, whereas levels below 40 suggest overmethylation.
Undermethylated depressives thrive on l-methionine, calcium, magnesium, B-6, Zinc, and Vitamin C. In severe cases, up to 3,000 mg/day of methionine and 2,000 mg/day of Ca may be needed. However, we also like to routinely run a homocysteine test to assure the safety of the methylation protocol. This population is believed to result in low serotonin activity. This methylation therapy is quite slow in taking effect.... and often 6-8 weeks pass before progress is obvious.
Overmethylated (low-histamine) depressives thrive on folic acid, B-12, niacin (or niacinamide), B-6, Zinc, Manganese, DMAE, and Vitamins, C and E. In severe cases, up to 5,000 mcg/day of FA may be needed. Response is more rapid with this phenotype, with clear progress usually by week 4. This population is believed to have an innate tendency for elevated serotonin, dopamine, and norepinephrine levels.
This test can also help guide psychiatrists in selection of psychiatric medications. For example high histamine persons may do quite well on SSRI's, but low-histamine persons usually reactly very badly to SSRI's and are better candidates for benzodiazapines.
We like to augment the histamine blood test with an "absolute basophil" test offered by Direct Healthcare, Inc. The histamine assay can be affected by antihistamines and other medications with AH properties. The reference range for ABC's is 30-50.
vrijdag 17 februari 2012
Herprogrammeer uw hond
http://www.gva.be/nieuws/wetenschap/aid1120069/hond-aan-de-rilatine.aspx
Honden zijn het volgende slachtoffer van de farma-industrie. Ze worden nu ook aan de Rilatine en antidepressiva gezet. De farma-industrie heeft reeds alle koeien, varkens en kippen volgepropt met antibiotica. Dat volstond blijkbaar niet.
Dierengedragstherapeut Dany Grosemans zegt in een artikel spijtige trend". "In mijn praktijk zie ik iets helemaal anders. Ik heb de indruk dat de farmaceutische firma's de dierenartsen het hoofd gek maken. Het is zelfs zo ver gekomen dat ik in een krant een advertentie zag verschijnen van een farmaceutisch bedrijf met de slogan "Herprogrammeer uw hond".
Tiens, dat zei die biopsychosociale arts in het CVS-centrum ook tegen mij tijdens mijn eerste gesprek: "U moet geherprogrammeerd worden."
Het zal wel toeval zijn zeker ...
Bron: http://www.gva.be/nieuws/wetenschap/aid1120069/hond-aan-de-rilatine.aspx
Honden zijn het volgende slachtoffer van de farma-industrie. Ze worden nu ook aan de Rilatine en antidepressiva gezet. De farma-industrie heeft reeds alle koeien, varkens en kippen volgepropt met antibiotica. Dat volstond blijkbaar niet.
Dierengedragstherapeut Dany Grosemans zegt in een artikel spijtige trend". "In mijn praktijk zie ik iets helemaal anders. Ik heb de indruk dat de farmaceutische firma's de dierenartsen het hoofd gek maken. Het is zelfs zo ver gekomen dat ik in een krant een advertentie zag verschijnen van een farmaceutisch bedrijf met de slogan "Herprogrammeer uw hond".
Tiens, dat zei die biopsychosociale arts in het CVS-centrum ook tegen mij tijdens mijn eerste gesprek: "U moet geherprogrammeerd worden."
Het zal wel toeval zijn zeker ...
Bron: http://www.gva.be/nieuws/wetenschap/aid1120069/hond-aan-de-rilatine.aspx
donderdag 16 februari 2012
Panax Ginseng
I wanted to try a new supplement to stimulate the bloodcirculation as well as my brain. A therapist in plants and herbs had recommended me asian panax ginseng. The siberian ginseng was a no go.
Two days later I was blessed with an acute attack of rheumatoid arthritis in my hand. First, a miserable night in which every cell of my body ached as if I was lying in barbed wire. The next morning my fingers were swollen with thick veins, a few hours later I was bedridden with a flu attack. Then my fingers were very painful and stiff for some days. It feels better now. .
So, for those who want to stimulate their immune system, go for panax ginseng.
But if you're sure that you suffer from Crohn's disease or lupus, stay away from it!
Two days later I was blessed with an acute attack of rheumatoid arthritis in my hand. First, a miserable night in which every cell of my body ached as if I was lying in barbed wire. The next morning my fingers were swollen with thick veins, a few hours later I was bedridden with a flu attack. Then my fingers were very painful and stiff for some days. It feels better now. .
So, for those who want to stimulate their immune system, go for panax ginseng.
But if you're sure that you suffer from Crohn's disease or lupus, stay away from it!
Panax ginseng
Ik dacht eens een nieuw supplement uit te proberen om de bloedsomloop te stimuleren en mijn brein wat aan de praat te houden. Het plantje dat een fytotherapeut had aangeraden was panax ginseng, de aziatische. De siberische, die mocht ik zeker niet nemen. Zo gezegd, zo gedaan.
Twee dagen later ben ik gezegend met een acute aanval van reumatoide artritis aan mijn hand blijkt nu. Eerst een mega-ellendige nacht waarbij elke cel van mijn lijf pijn deed alsof ik in de prikkeldraad lag. De volgende ochtend dikke vingers met gezwollen aders, enkele uren laten een griepaanval van jewelste. Dan een paar dagen zeer pijnlijke en stijve vingers. Vandaag is het voor het eerst weer wat beter.
Zo, voor diegenen die hun immuunsystem willen stimuleren: neem panax ginseng
En als je zeker bent dat je aan Crohn of lupus lijdt, a.f.b.l.i.j.v.e.n.
Twee dagen later ben ik gezegend met een acute aanval van reumatoide artritis aan mijn hand blijkt nu. Eerst een mega-ellendige nacht waarbij elke cel van mijn lijf pijn deed alsof ik in de prikkeldraad lag. De volgende ochtend dikke vingers met gezwollen aders, enkele uren laten een griepaanval van jewelste. Dan een paar dagen zeer pijnlijke en stijve vingers. Vandaag is het voor het eerst weer wat beter.
Zo, voor diegenen die hun immuunsystem willen stimuleren: neem panax ginseng
En als je zeker bent dat je aan Crohn of lupus lijdt, a.f.b.l.i.j.v.e.n.
Neuron memory key to taming chronic pain
http://www.mcgill.ca/newsroom/news/item/?item_id=214078
Neuron memory key to taming chronic pain
Feb. 13, 2012
Study suggests erasing neuronal memories may help control persistent pain
For some, the pain is so great that they can’t even bear to have clothes touch their skin. For others, it means that every step is a deliberate and agonizing choice. Whether the pain is caused by arthritic joints, an injury to a nerve or a disease like fibromyalgia, research now suggests there are new solutions for those who suffer from chronic pain.
A team of researchers led by McGill neuroscientist Terence Coderre, who is also affiliated with the Research Institute of the McGill University Health Centre, has found the key to understanding how memories of pain are stored in the brain. More importantly, the researchers are also able to suggest how these memories can be erased, making it possible to ease chronic pain.
It has long been known that the central nervous system “remembers” painful experiences, that they leave a memory trace of pain. And when there is new sensory input, the pain memory trace in the brain magnifies the feeling so that even a gentle touch can be excruciating.
“Perhaps the best example of a pain memory trace is found with phantom limb pain,” suggests Coderre. “Patients may have a limb amputated because of gangrene, and because the limb was painful before it was amputated, even though the limb is gone, the patients continue to feel they are suffering from pain in the absent limb. That’s because the brain remembers the pain. In fact, there’s evidence that any pain that lasts more than a few minutes will leave a trace in the nervous system.” It’s this memory of pain, which exists at the neuronal level, that is critical to the development of chronic pain. But until now, it was not known how these pain memories were stored at the level of the neurons.
Recent work has shown that the protein kinase PKMzeta plays a crucial role in building and maintaining memory by strengthening the connections between neurons. Now Coderre and his colleagues have discovered that PKMzeta is also the key to understanding how the memory of pain is stored in the neurons. They were able to show that after painful stimulation, the level of PKMzeta increases persistently in the central nervous system (CNS).
Even more importantly, the researchers found that by blocking the activity of PKMzeta at the neuronal level, they could reverse the hypersensitivity to pain that neurons developed after irritating the skin by applying capsaicin – the active ingredient in hot peppers. Moreover, erasing this pain memory trace was found to reduce both persistent pain and heightened sensitivity to touch.
Coderre and his colleagues believe that building on this study to devise ways to target PKMzeta in pain pathways could have a significant effect for patients with chronic pain. “Many pain medications target pain at the peripheral level, by reducing inflammation, or by activating analgesia systems in the brain to reduce the feeling of pain,” says Coderre. “This is the first time that we can foresee medications that will target an established pain memory trace as a way of reducing pain hypersensitivity. We believe it’s an avenue that may offer new hope to those suffering from chronic pain.”
The full article can be found at: http://www.molecularpain.com/content/7/1/99
Other contributing researchers on this study include Andre Laferrière, Mark H Pitcher, Anne Haldane, Yue Huang, Virginia Cornea, Naresh Kumar, Fernando Cervero (all from the Alan Edwards Centre for Research on Pain at McGill) and co-author Todd C Sacktor (State University of New York Downstate Medical Center).
This research was supported by grants from Canadian Institutes of Health Research (CIHR), the Louise and Alan Edwards Foundation, National Institutes of Health (NIH) and an Astra-Zeneca/AECRP fellowship.
Source : http://www.mcgill.ca/newsroom/news/item/?item_id=214078
Neuron memory key to taming chronic pain
Feb. 13, 2012
Study suggests erasing neuronal memories may help control persistent pain
For some, the pain is so great that they can’t even bear to have clothes touch their skin. For others, it means that every step is a deliberate and agonizing choice. Whether the pain is caused by arthritic joints, an injury to a nerve or a disease like fibromyalgia, research now suggests there are new solutions for those who suffer from chronic pain.
A team of researchers led by McGill neuroscientist Terence Coderre, who is also affiliated with the Research Institute of the McGill University Health Centre, has found the key to understanding how memories of pain are stored in the brain. More importantly, the researchers are also able to suggest how these memories can be erased, making it possible to ease chronic pain.
It has long been known that the central nervous system “remembers” painful experiences, that they leave a memory trace of pain. And when there is new sensory input, the pain memory trace in the brain magnifies the feeling so that even a gentle touch can be excruciating.
“Perhaps the best example of a pain memory trace is found with phantom limb pain,” suggests Coderre. “Patients may have a limb amputated because of gangrene, and because the limb was painful before it was amputated, even though the limb is gone, the patients continue to feel they are suffering from pain in the absent limb. That’s because the brain remembers the pain. In fact, there’s evidence that any pain that lasts more than a few minutes will leave a trace in the nervous system.” It’s this memory of pain, which exists at the neuronal level, that is critical to the development of chronic pain. But until now, it was not known how these pain memories were stored at the level of the neurons.
Recent work has shown that the protein kinase PKMzeta plays a crucial role in building and maintaining memory by strengthening the connections between neurons. Now Coderre and his colleagues have discovered that PKMzeta is also the key to understanding how the memory of pain is stored in the neurons. They were able to show that after painful stimulation, the level of PKMzeta increases persistently in the central nervous system (CNS).
Even more importantly, the researchers found that by blocking the activity of PKMzeta at the neuronal level, they could reverse the hypersensitivity to pain that neurons developed after irritating the skin by applying capsaicin – the active ingredient in hot peppers. Moreover, erasing this pain memory trace was found to reduce both persistent pain and heightened sensitivity to touch.
Coderre and his colleagues believe that building on this study to devise ways to target PKMzeta in pain pathways could have a significant effect for patients with chronic pain. “Many pain medications target pain at the peripheral level, by reducing inflammation, or by activating analgesia systems in the brain to reduce the feeling of pain,” says Coderre. “This is the first time that we can foresee medications that will target an established pain memory trace as a way of reducing pain hypersensitivity. We believe it’s an avenue that may offer new hope to those suffering from chronic pain.”
The full article can be found at: http://www.molecularpain.com/content/7/1/99
Other contributing researchers on this study include Andre Laferrière, Mark H Pitcher, Anne Haldane, Yue Huang, Virginia Cornea, Naresh Kumar, Fernando Cervero (all from the Alan Edwards Centre for Research on Pain at McGill) and co-author Todd C Sacktor (State University of New York Downstate Medical Center).
This research was supported by grants from Canadian Institutes of Health Research (CIHR), the Louise and Alan Edwards Foundation, National Institutes of Health (NIH) and an Astra-Zeneca/AECRP fellowship.
Source : http://www.mcgill.ca/newsroom/news/item/?item_id=214078
zondag 12 februari 2012
donderdag 9 februari 2012
Increased ventricular lactate in chronic fatigue syndrome.
http://onlinelibrary.wiley.com/doi/10.1002/nbm.2772/abstract
Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology
Dikoma C. Shungu1,*, Nora Weiduschat1, James W. Murrough2, Xiangling Mao1, Sarah Pillemer2, Jonathan P. Dyke1, Marvin S. Medow3, Benjamin H. Natelson4, Julian M. Stewart3, Sanjay J. Mathew2,5Article first published online: 27 JAN 2012
DOI: 10.1002/nbm.2772
Copyright © 2012 John Wiley & Sons, Ltd.
Pathophysiological model of chronic fatigue syndrome (CFS) which attempts to explain the consistent observation of cross-sectional elevations of ventricular lactate in the disorder. Highlighted are the experimentally measurable items, with the red arrows showing the model-predicted outcomes. This series of neuroimaging studies aimed to validate this model by measuring each key item and comparing the results with the model-predicted outcomes.
Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness. In two previous reports, using 1H MRSI, we found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in patients with CFS relative to those with generalized anxiety disorder and healthy volunteers (HV), but not relative to those with major depressive disorder (MDD).
In this third independent cross-sectional neuroimaging study, we investigated a pathophysiological model which postulated that elevations of CSF lactate in patients with CFS might be caused by increased oxidative stress, cerebral hypoperfusion and/or secondary mitochondrial dysfunction.
Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the following modalities: (i) 1H MRSI to measure CSF lactate; (ii) single-voxel 1H MRS to measure levels of cortical glutathione (GSH) as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL) MRI to measure regional cerebral blood flow (rCBF); and (iv) 31P MRSI to measure brain high-energy phosphates as objective indices of mitochondrial dysfunction.
We found elevated ventricular lactate and decreased GSH (glutathion) in patients with CFS and MDD relative to HVs. GSH did not differ significantly between the two patient groups. In addition, we found lower rCBF in the left anterior cingulate cortex and the right lingual gyrus in patients with CFS relative to HVs, but rCBF did not differ between those with CFS and MDD.
We found no differences between the three groups in terms of any high-energy phosphate metabolites. In exploratory correlation analyses, we found that levels of ventricular lactate and cortical GSH were inversely correlated, and significantly associated with several key indices of physical health and disability. Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS etiopathophysiology.
Copyright © 2012 John Wiley & Sons, Ltd.
http://onlinelibrary.wiley.com/doi/10.1002/nbm.2772/abstract
Increased ventricular lactate in chronic fatigue syndrome. III. Relationships to cortical glutathione and clinical symptoms implicate oxidative stress in disorder pathophysiology
Dikoma C. Shungu1,*, Nora Weiduschat1, James W. Murrough2, Xiangling Mao1, Sarah Pillemer2, Jonathan P. Dyke1, Marvin S. Medow3, Benjamin H. Natelson4, Julian M. Stewart3, Sanjay J. Mathew2,5Article first published online: 27 JAN 2012
DOI: 10.1002/nbm.2772
Copyright © 2012 John Wiley & Sons, Ltd.
Pathophysiological model of chronic fatigue syndrome (CFS) which attempts to explain the consistent observation of cross-sectional elevations of ventricular lactate in the disorder. Highlighted are the experimentally measurable items, with the red arrows showing the model-predicted outcomes. This series of neuroimaging studies aimed to validate this model by measuring each key item and comparing the results with the model-predicted outcomes.
Chronic fatigue syndrome (CFS) is a complex illness, which is often misdiagnosed as a psychiatric illness. In two previous reports, using 1H MRSI, we found significantly higher levels of ventricular cerebrospinal fluid (CSF) lactate in patients with CFS relative to those with generalized anxiety disorder and healthy volunteers (HV), but not relative to those with major depressive disorder (MDD).
In this third independent cross-sectional neuroimaging study, we investigated a pathophysiological model which postulated that elevations of CSF lactate in patients with CFS might be caused by increased oxidative stress, cerebral hypoperfusion and/or secondary mitochondrial dysfunction.
Fifteen patients with CFS, 15 with MDD and 13 HVs were studied using the following modalities: (i) 1H MRSI to measure CSF lactate; (ii) single-voxel 1H MRS to measure levels of cortical glutathione (GSH) as a marker of antioxidant capacity; (iii) arterial spin labeling (ASL) MRI to measure regional cerebral blood flow (rCBF); and (iv) 31P MRSI to measure brain high-energy phosphates as objective indices of mitochondrial dysfunction.
We found elevated ventricular lactate and decreased GSH (glutathion) in patients with CFS and MDD relative to HVs. GSH did not differ significantly between the two patient groups. In addition, we found lower rCBF in the left anterior cingulate cortex and the right lingual gyrus in patients with CFS relative to HVs, but rCBF did not differ between those with CFS and MDD.
We found no differences between the three groups in terms of any high-energy phosphate metabolites. In exploratory correlation analyses, we found that levels of ventricular lactate and cortical GSH were inversely correlated, and significantly associated with several key indices of physical health and disability. Collectively, the results of this third independent study support a pathophysiological model of CFS in which increased oxidative stress may play a key role in CFS etiopathophysiology.
Copyright © 2012 John Wiley & Sons, Ltd.
http://onlinelibrary.wiley.com/doi/10.1002/nbm.2772/abstract
Heart failure explained and proven
http://www.cfids-cab.org/MESA/DrMyhill-373.pdf
Heart failure in ME is caused by poor muscle function.
Traditional tests like ECG, ECHO's, angiograms, ... will be normal.
Impedence cardiography however accurately measure cardiac output by measuring the electrical impedence across the chest wall.
Do the test in upright position and then again supine.
Disability can be proven with this test. It is completely independent and reliable.
Heart failure in ME is caused by poor muscle function.
Traditional tests like ECG, ECHO's, angiograms, ... will be normal.
Impedence cardiography however accurately measure cardiac output by measuring the electrical impedence across the chest wall.
Do the test in upright position and then again supine.
Disability can be proven with this test. It is completely independent and reliable.
dinsdag 7 februari 2012
The relationship between the liver, exercise and candida
The relationship between the liver, exercise and candida
The liver is a ingenious detox factory. Through two steps, Phase I and II, toxins, pesticides, heavy metals, additives are dismantled and disarmed and removed from the body via the urine e.g.
Phase I
During this process toxic substances undergo a treatment which converts them into bio-active substances. This makes them much more toxic but it is necessary to be able to bind to water in stage II. The cytochrome P 450 enzymes get in action during this phase.
Phase II
The bio-active substances are converted into bio-inactive substances. For example, they can bind to water and avoids toxic loads that are stacked in the liver. During this phase the toxins lose their fragrance.
The enzymes responsible for the conversion of glutathione, glutathione transferase, in particular, are also active during the second phase of detoxification. They need a co-enzyme to function, in particular: selenium, zinc, magnesium, vitamin B (3, 6, 8, 11, 12), and alpha-lipoic acid.
Phase II proceeds via glutathione transferases but on one condition only. It needs (daily) exercise to be useful. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid.
Cysteine is a troublemaker if there is no exercise. How come? Cysteine can always be present into the cell. Outside the cell, only if there is sufficient cysteine to be converted via exercise.
If the person moves insufficiently, then the cell imports cystine. The cell is equipped with cystine channels. Only 1 cystine can pass at a time. This in turn gives a glutathione.
A cystine => a cysteine => 1 glutathione
Suppose the person exercises enough, no need to import cystine. Cysteine passes via specific channels, 10 cysteine enter at the same time the cell. Thus, it produces 10 times more glutathione.
Someone who has little chance to move or exercise, will detox 10x less than a active person. This is not without consequences.
Another stumbling block for Phase II of the detoxification is Candida or fungus. This causes leaky gut and too little recognized by mainstream medicine. Fungus produces acetyldehyde via the enzyme pyruvate decarboxylase. Acetyldehyde is dismantled by cysteine. The more candida, the greater the use of cysteine. Moreover, it compeeds with vitamine B6 and affects normal detox processes.
The effects of candida are far-reaching. The chemical by-products react with serotonin and dopamine. Acetaldehyde is then transformed into opiate substances that affect the functioning of the brains. The neurons are able to communicate less well and influences the red blood cells negatively. They have more trouble to transport oxygen. Thus, you are tired of candida.
Interesting to know is that everyday substances can limit stage II. These are coffee and tea, sugar and lactose (milk and cheese), smoking and alcohol, stress, paracetamol and too little exercise as previously cited.
Nature is generous, and also provides ways to stimulate phase II. Daily exercise is an obvious move with the knowledge what the lack of exercise can do. Vegetables and plants have to offer: onion, garlic, leeks, chicory, endive, artichoke, broccoli, radish, spinach, olive oil, fatty fish, avocado, turmeric, milk thistle, dandelion, Swedish herb, liver herb.
The liver is a ingenious detox factory. Through two steps, Phase I and II, toxins, pesticides, heavy metals, additives are dismantled and disarmed and removed from the body via the urine e.g.
Phase I
During this process toxic substances undergo a treatment which converts them into bio-active substances. This makes them much more toxic but it is necessary to be able to bind to water in stage II. The cytochrome P 450 enzymes get in action during this phase.
Phase II
The bio-active substances are converted into bio-inactive substances. For example, they can bind to water and avoids toxic loads that are stacked in the liver. During this phase the toxins lose their fragrance.
The enzymes responsible for the conversion of glutathione, glutathione transferase, in particular, are also active during the second phase of detoxification. They need a co-enzyme to function, in particular: selenium, zinc, magnesium, vitamin B (3, 6, 8, 11, 12), and alpha-lipoic acid.
Phase II proceeds via glutathione transferases but on one condition only. It needs (daily) exercise to be useful. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid. Glutathione is as we know, composed of three amino acids: cysteine, glycine and glutamic acid.
Cysteine is a troublemaker if there is no exercise. How come? Cysteine can always be present into the cell. Outside the cell, only if there is sufficient cysteine to be converted via exercise.
If the person moves insufficiently, then the cell imports cystine. The cell is equipped with cystine channels. Only 1 cystine can pass at a time. This in turn gives a glutathione.
A cystine => a cysteine => 1 glutathione
Suppose the person exercises enough, no need to import cystine. Cysteine passes via specific channels, 10 cysteine enter at the same time the cell. Thus, it produces 10 times more glutathione.
Someone who has little chance to move or exercise, will detox 10x less than a active person. This is not without consequences.
Another stumbling block for Phase II of the detoxification is Candida or fungus. This causes leaky gut and too little recognized by mainstream medicine. Fungus produces acetyldehyde via the enzyme pyruvate decarboxylase. Acetyldehyde is dismantled by cysteine. The more candida, the greater the use of cysteine. Moreover, it compeeds with vitamine B6 and affects normal detox processes.
The effects of candida are far-reaching. The chemical by-products react with serotonin and dopamine. Acetaldehyde is then transformed into opiate substances that affect the functioning of the brains. The neurons are able to communicate less well and influences the red blood cells negatively. They have more trouble to transport oxygen. Thus, you are tired of candida.
Interesting to know is that everyday substances can limit stage II. These are coffee and tea, sugar and lactose (milk and cheese), smoking and alcohol, stress, paracetamol and too little exercise as previously cited.
Nature is generous, and also provides ways to stimulate phase II. Daily exercise is an obvious move with the knowledge what the lack of exercise can do. Vegetables and plants have to offer: onion, garlic, leeks, chicory, endive, artichoke, broccoli, radish, spinach, olive oil, fatty fish, avocado, turmeric, milk thistle, dandelion, Swedish herb, liver herb.
maandag 6 februari 2012
Kill the virus with
Viri Balance
https://www.gezondheidaanhuis.nl/nl/product/10195/Viri-Balance-Pervital-30-ml
Lymfo Balance
https://www.gezondheidaanhuis.nl/nl/product/13749/Lymfo-Balance-Pervital-30-ml
Detox Balance
https://www.gezondheidaanhuis.nl/nl/product/11801/Detox-Balance-Pervital-30-ml
Brand: Pervital
http://www.nutramin.nl/
If results are not satisfying, add Elaps Balance.
https://www.gezondheidaanhuis.nl/nl/product/13747/Elaps-Balance-Pervital-30-ml
Also helpful against HPV (human papilloma virus responsible for cervix cancer).
https://www.gezondheidaanhuis.nl/nl/product/10195/Viri-Balance-Pervital-30-ml
Lymfo Balance
https://www.gezondheidaanhuis.nl/nl/product/13749/Lymfo-Balance-Pervital-30-ml
Detox Balance
https://www.gezondheidaanhuis.nl/nl/product/11801/Detox-Balance-Pervital-30-ml
Brand: Pervital
http://www.nutramin.nl/
If results are not satisfying, add Elaps Balance.
https://www.gezondheidaanhuis.nl/nl/product/13747/Elaps-Balance-Pervital-30-ml
Also helpful against HPV (human papilloma virus responsible for cervix cancer).
zondag 5 februari 2012
Living is ...
"Perhaps it is true that we do not really exist until there is someone there to see us existing;
that we cannot properly speak until there is someone there who can understand what we are saying;
that, in essence, we are not wholly alive until we are loved."
Alain de Botton: On Love
that we cannot properly speak until there is someone there who can understand what we are saying;
that, in essence, we are not wholly alive until we are loved."
Alain de Botton: On Love
woensdag 1 februari 2012
Mitochondrial changes associated with glutathione deficiency
http://www.sciencedirect.com/science/article/pii/092544399500007Q
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with Ks of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species = damaging free radicals) ; this is opposed by reactions involving glutathione.
Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate (= vitamin C). Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.
Abstract
Glutathione deficiency produced by giving buthionine sulfoximine (an inhibitor of γ-glutamylcysteine synthetase) to animals, leads to biphasic decline in cellular glutathione levels associated with sequestration of glutathione in mitochondria. Liver mitochondria lack the enzymes needed for glutathione synthesis. Mitochondrial glutathione arises from the cytosol. Rat liver mitochondria have a multicomponent system (with Ks of approx. 60 μM and 5.4 mM) that underlies their remarkable ability to transport and retain glutathione. Mitochondria produce substantial quantities of reactive oxygen species = damaging free radicals) ; this is opposed by reactions involving glutathione.
Glutathione deficiency leads to widespread mitochondrial damage which is lethal in newborn rats and guinea pigs, animals that do not synthesize ascorbate (= vitamin C). Glutathione esters and ascorbate protect against the lethal and other effects of glutathione deficiency. Ascorbate spares glutathione; it increases mitochondrial glutathione in glutathione-deficient animals. Glutathione esters delay onset of scurvy in ascorbate-deficient guinea pigs; thus, glutathione spares ascorbate. Glutathione and ascorbate function together in protecting mitochondria from oxidative damage.
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