Re: b12 methyl or hydroxy

[Guest guest]

As far as vitamin b12 goes, anyone know the biological difference between

hydroxycobalamin and methylcobalamin? I'm aware some doctors suggest

hydroxycobalamin, but are the two interchangeable in every way?

all good,

Duncan

>

> Definitely gut dysbiosis issues. Candida, Leaky Gut ,Hypochlorhydria,

> Colitis I.B.S., I.B.D. etc.

> All rooted in the same place.

> For starters she'll probably need B12 injections ( methylocobalamin, NOT

> cyanocobalamin!),

[Guest guest]

Duncan,

I was debating posting this here on coconut oil list, or if it might be a

tad esoteric. But I think it answers your question.

Here is a bunch of snippets from (list owner of Sulfurstories

list) below in italics with comments by me in square brackets.

*in autism that there was very strong evidence of rhodanese dysfunction.

Rhodanese is the mitochondrial enzyme that detoxifies cyanide by forming

thiocyanate from thiosulfate.*

*

When this enzyme isn't working, the burden is put upon methyl or

hydroxycobalamin to detoxify the cyanide by forming cyanocobalamin. This

conversion that becomes necessary with depressed rhodanese activity might

raise serum cyanocobalamin levels, but it would also deplete

methylcobalamin.

This mechanism could furnish a very good reason to explain how methylB12

shots have done so much good in autism. By using up methylcobalamin, large

amounts of cyanide could depress methionine synthase activity because of

shunting its cofactor instead to the formation of cyanocobalamin.

Knowing this vulnerability in autism provides a good reason for avoiding

high cyanide foods and to keep children or others with these issues away

from smoking (which is a huge source of cyanide).

*[i have loathed being around smokers since I was a little child. I never

knew why I hated tobacco smoke so much. Now I know!]

[Here are symptoms of exposure to cyanide, either gas, or from foods (like

Cyano B-12) ]

*Dizziness

Weakness

Nausea and vomiting

Loss of consciousness

*[Those sure seem to me to be what I have been experiencing since I have

been using Cyano B-12 instead of Methyl B-12.]

*Basically, what it says is that cyanide impairs the use of oxygen, so that

the parts of the body most affected are those that use lots of oxygen, like

the heart and brain.

*[For the past several months I have been feeling muzziheaded, been falling

asleep at work, while sitting on the toilet, and while typing at the

computer. Even when I get 9-10 hours of sleep a night.]

Alobar

=========================================

Listmates,

Ten years ago Rosemary Waring found that in autism that there was very

strong evidence of rhodanese dysfunction. Rhodanese is the mitochondrial

enzyme that detoxifies cyanide by forming thiocyanate from thiosulfate.

Here is some data from her paper, " Sulphur metabolism in Autism " from the

Journal of Nutritional and Environmental Medicine (2000) 10, 25-32:

Autism(n=232) Controls (n=68)

Protein 103.2 64.5

Sulphite 106.9 7.1

Thiosulphate 130.8 18.6

Thiocyanate 6.4 44.0

Sulphate 6819.0 3030.8

In the paper, she discusses the role of rhodanese and why it could be

important.

Rhodanese converts thiosulphate to thiocyanate, so the ratio of these two

compounds helps to assess the function of rhodanese. In autism, that ratio

is 20.4. In her control population, the ratio was 0.42. That means the ratio

was 49 times normal in autism....a strong indication that this enzyme was

inhibited in this very large sample population.

When this enzyme isn't working, the burden is put upon methyl or

hydroxycobalamin to detoxify the cyanide by forming cyanocobalamin. This

conversion that becomes necessary with depressed rhodanese activity might

raise serum cyanocobalamin levels, but it would also deplete

methylcobalamin. Those relationships are nicely illustrated in the first

study I've put below which you can read for free at:

http://ndt.oxfordjournals.org/content/12/8/1622.long

..

This mechanism could furnish a very good reason to explain how methylB12

shots have done so much good in autism. By using up methylcobalamin, large

amounts of cyanide could depress methionine synthase activity because of

shunting its cofactor instead to the formation of cyanocobalamin. An

evidence that this has happened would be elevated blood cyanocobalamin

levels, or changed ratios of the various cobalamins in serum, as they found

in the study I already referenced, looking at this issue in hemodialysis

patients.

Knowing this vulnerability in autism provides a good reason for avoiding

high cyanide foods and to keep children or others with these issues away

from smoking (which is a huge source of cyanide).

The CDC's agency on toxic compounds has the following limited information:

> Certain bacteria, fungi, and algae can produce cyanide, and cyanide is

found in a number of foods and plants.

> In certain plant foods, including almonds, millet sprouts, lima beans,

soy, spinach, bamboo shoots, and

>cassava roots (which are a major source of food in tropical countries),

cyanides occur naturally as part of

> sugars or other naturally-occurring compounds.

I am in the process of finding if anyone has made a more comprehensive list

of the cyanide content of foods but so far, the information is limited

except to suspect that nuts and seeds tend to be high in cyanide. The

biggest dietary source that has caused obvious problems in large populations

is cassava, from which tapioca is made. Our oxalate project at ARI will try

and get tapioca starch flour tested as soon as possible to see if the

process of extracting the starch is as effective in removing cyanide as it

is effective in removing most of the oxalate.

People should also be aware that this depression of rhodanese could be

brought on by exposures to high levels of oxalate. How is that?

The second article below found that rhodanese messenger RNA levels and

proteins levels were depressed in hemodialysis patients at the same time

that cell reactive oxygen species were increased and superoxide levels were

increased, and this was associated with mortality in these patients.

Reactive oxygen species and elevated superoxide levels both can be CAUSED by

elevated oxalate levels (59 articles in pubmed looking at this!) which makes

sense as being relevant because oxalate levels increase over time in

hemodialysis patients because the dialysis is so inferior to healthy kidneys

in removing oxalate. That is why oxalate is considered to be a major toxin

in uremic patients, as is discussed in the third article below.

What are the symptoms of cyanide poisoning?

Look here:

http://www.bt.cdc.gov/agent/cyanide/basics/facts.asp

Basically, what it says is that cyanide impairs the use of oxygen, so that

the parts of the body most affected are those that use lots of oxygen, like

the heart and brain.

Also, cyanide can cause visual field changes:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1291478/pdf/jrsocmed00165-0053.pdf

The visual field changes in patients with tobacco amblyopia are

characteristic. They consist of a centrocaecal scotoma, usually bilateral

though not necessarily equal on the two sides. The scotoma is horizontally

oval with a sloping edge and is most easily detected by a reduced stimulus

such as a red or small white object. The defect for colour exceeds that for

white and there are usually two definite nuclei within the scotoma on the

horizontal meridian. An impairment of the temporal colour fields exists

within the 300 circle and in more advanced cases a similar defect is also

seen to a small white test object2.

It does concern me that some children with autism are eating large amounts

of products made of almonds, and some are also eating spinach (both whose

high oxalate content might further impair rhodanese furnishing a double

whammy). It equally concerns me that if millet sprouts are high, then

possibly the act of sprouting seeds may increase cyanide when people were

hoping it would decrease oxalate. So far, we haven't been finding that

sprouting is making the oxalate go down, and it might be making the oxalate

level higher, but we still need to test a lot more seeds that way.

I hope this information is of interest and helpful.

Nephrol Dial Transplant. 1997 Aug;12(8):1622-8.

Abnormal cyanide metabolism in uraemic patients.

Koyama K, Yoshida A, Takeda A, Morozumi K, Fujinami T, Tanaka N.

Division of Nephrology, Nagoya Daini Red Cross Hospital, Japan.

Erratum in:

Nephrol Dial Transplant 1998 Mar;13(3):819.

Abstract

BACKGROUND: We previously investigated the factors involved in uraemic

neuropathy in patients undergoing regular haemodialysis and found a

significant relationship between the severity of vibration sensation

impairment and the patients' smoking habits. The administration of

methylcobalamin markedly improved the severity of uraemic neuropathy in

terms of vibration perception thresholds. We presumed that abnormal cyanide

metabolism is involved in the development of uraemic neuropathy.

METHODS: Serum levels of thiocyanate (SCN-), the detoxication product of

cyanide, were determined in 12 patients with preterminal chronic renal

failure (PCRF), 30 patients undergoing regular haemodialysis (HD patients),

and 13 healthy volunteers as a control group. Nine of the 30 HD patients

were smokers. In addition, in 10 HD patients without smoking habits and 10

non-smoking healthy volunteers, the proportion of each vitamin B12 analogue

in total vitamin B12 was estimated.

RESULTS: The mean serum SCN- level of the 12 PCRF patients (5.1 +/- 1.5

micrograms/ml) was significantly higher than that of the control (2.8 +/-

0.9 micrograms/ml) (P < 0.01). The mean SCN- level before haemodialysis in

the 21 non-smoking HD patients was identical to that in the PCRF group,

whereas the level in the nine smoking HD patients (7.2 +/- 1.8

micrograms/ml) significantly higher than that in the non-smoking subgroup (P

< 0.01). In 16 HD patients with methylcobalamin treatment, serum SCN- levels

were lower than in those without methylcobalamin treatment (4.5 +/- 0.5

micrograms/ml in non-smoking subgroup, P < 0.05). And in the

methylcobalamin-treated subgroup (n = 5), the proportion of each vitamin B12

analogue in total vitamin B12 was normal. In the untreated subgroup (n = 5),

the proportion of cyanocobalamin fraction (10.5 +/- 2.6%) was as high as the

level in Leber's disease patients, while the proportion of methylcobalamin

fraction was low. And the serum cyanocobalamin level was higher in the

treated subgroup.

CONCLUSION: In uraemic patients, cyanide detoxication capability is impaired

because of a reduced SCN- clearance, and increased cyanocobalamin synthesis

indicates elevation of cyanide pool, which would be related to the

development of uraemic neuropathy. Methylcobalamin was considered to be

utilized in cyanide detoxication process via cyanocobalamin synthesis.

PMID: 9269639

Clin Biochem. 2010 Jan;43(1-2):95-101. Epub 2009 Aug 18.

Low expression of thiosulfate sulfurtransferase (rhodanese) predicts

mortality in hemodialysis patients.

Krueger K, Koch K, Jühling A, Tepel M, Scholze A.

Medizinische Klinik, Nephrologie, Charité Campus lin,

Hindenburgdamm 30, 12200 Berlin, Germany.

Abstract

OBJECTIVES: To test the hypothesis that impaired expression of the

thiosulfate sulfurtransferase rhodanese is associated with oxidative stress

and may predict mortality in hemodialysis patients.

DESIGN AND METHODS: Sixty-two hemodialysis patients were investigated to

determine protein and mRNA expression of rhodanese in monocytes. Whole cell

reactive oxygen species and mitochondrial superoxide production were

measured by fluorescence spectrophotometry.

RESULTS: Compared to healthy subjects, hemodialysis patients showed

significantly lower rhodanese mRNA and protein expression and significantly

increased reactive oxygen species. Lower rhodanese protein expression was

significantly associated with higher mitochondrial superoxide production.

The hazard ratio for mortality in hemodialysis patients with rhodanese mRNA

below compared to patients above the median was 2.22. Survival was shorter

with rhodanese mRNA below compared to patients above the median.

CONCLUSION: Impaired rhodanese expression is associated with increased whole

cell reactive oxygen species as well as higher mitochondrial superoxide

production and predicts mortality in hemodialysis patients. Copyright 2009

Vnitr Lek. 2010 Jul;56(7):695-701.

[Oxalic acid--important uremic toxin]

[Article in Czech]

Mydlík M, Derzsiová K.

IV. interná klinika Lekárskej fakulty UPJS a FN L, Pasteura, Kosice,

Slovenská republika.

Abstract

INTRODUCTION: Oxalic acid is thought to be a significant uremic toxin that

participates in the pathogenesis of uremic syndrome. AIM OF THE STUDY was to

summarise results which we obtained during the study ofoxalic acid in

biological fluids (plasma, saliva, urine and dialysate) in patients

suffering from chronic kidney diseases (CKD), stage 3-5 and after renal

transplantation.

PATIENTS AND METHODS: In the retrospective study were investigated 28

healthy subjects, 112 CKD stage 1-4 patients, 39 haemodialysis patients and

27 CAPD patients. Besides 21 patients were investigated after renal

transplantation. We used the following therapeutic methods: maximal water

diuresis, diet with low (2g/day) and high (15g/day) sodium chloride intake,

administration intravenous furosemide (20mg) and renal replacement therapy

[CAPD, haemodialysis (HD), haemofiltration (HF) and postdilution

haemodiafiltration (HDF)] and renal transplantation. Oxalic acid was

determined by spectrophotometric method using oxalate oxidase which is free

from vitamin C interference. Vitamin C was determined by spectrophotometric

method.

RESULTS: In CKD patients and those after renal transplantation direct

relationships between plasma oxalic acid and serum creatinine were found (r

= 0.904 and 0.943, respectively, P < 0.001). Despite of high plasma oxalic

acid in uremic patients (23.1 +/- 10 micromol/l), there was no significant

difference in salivary oxalic acid between control subjects (126.5 +/- 18

micromol/l) and CKD stage 3-4 patients (133.9 +/- 23.7 micromol/I). The

urinary excretion of oxalic acid during maximal water diuresis in healthy

subjects (n = 15) (from 37.5 +/- 17.4 to 110.2 +/- 49.3 micromol/4 hours)

and after intravenous furosemide (CKD stage 3-4, n = 15) (from 34.5 +/- 5.5

to 66.7 +/- 8.1 micromol/3 hours) increased significantly, but was not

affected by high intake of NaCI in diet (CKD stage 3-4, n = 12). One tablet

of Sorbifer Durules containing 100 mg Fe2+ and 60 mg vitamin C did not lead

to further increase of uremic hyperoxalemia in haemodialysis patients.

Four-hour HD, H F and HDF led to the significant decrease of plasma oxalic

acid, but the most significant decrease was observed during HDF (63.3%).

CONCLUSION: The results of this study indicate, that renal replacement

therapy is not effective for permanent reduction of elevated plasma levels

of oxalic acid--important uremic toxin.

PMID: 20842915

Biosens Bioelectron. 2010 Mar 15;25(7):1729-34. Epub 2009 Dec 22.

Effect of calcium oxalate on renal cells as revealed by real-time

measurement of extracellular oxidative burst.

Gáspár S, Niculi e C, Cucu D, Marcu I.

International Centre of Biodynamics, 1B Intrarea Portocalelor Street, 060101

Bucharest, Romania. sgaspar@...

Abstract

Calcium oxalate is one of the main constituents of kidney stones and has a

proved deleterious effect on renal cells that is mediated by oxidative

stress. However, the subcellular source of this oxidative stress, and

whether it is extending to the extracellular space or not, is still

disputed. Therefore, an electrochemical superoxide biosensor was

constructed, positioned above A6 renal cells, and used to measure in

real-time the extracellular oxidative burst following addition of calcium

oxalate crystals. It was observed that A6 cells do secrete superoxide into

their extracellular space in few minutes after encountering calcium oxalate

crystals. The amount of released superoxide peaks at about 20 min.

Superoxide is cleared away from the extracellular space after approximately

3h. Superoxide secretion depends on the presence of superoxide-scavenging

enzyme superoxide dismutase, the age of the cells, the amount of calcium

oxalate crystals, and the temperature. Moreover, the effect of calcium

oxalate crystals was mimicked by phorbol 12-myristate 13-acetate. The

developed sensing system can be a useful tool for biologists investigating

nephrolithiasis at cellular level.

© 2009 Elsevier B.V. All rights reserved.

PMID: 20047824

On Mon, Mar 28, 2011 at 11:03 AM, Duncan Crow <duncancrow@...> wrote:

> As far as vitamin b12 goes, anyone know the biological difference between

hydroxycobalamin and methylcobalamin? I'm aware some doctors suggest

hydroxycobalamin, but are the two interchangeable in every way?

>

> all good,

>

> Duncan

>

[Guest guest]

Thanks for the info Alobar. So, it follows that methylcobalamin may reduce any

cyanide and also increase methionine creation by recirculating homocysteine more

effectively, which means I think reduced oxidative stress too

all good,

Duncan

>

>

[Guest guest]

One observation: If I take one sublingual dot of methyl-cobalamine then I feel

hungry IMMEDIATELY, as if it opens some blocked path.

The same was reported to me by my relation who had lost appetite. It seems this

type of B12 is replenishing methyl group to liver.

Duncan there are two if not more paths to make glutathione. One you already know

(via the precursors that you know too much of). The second is by methylation

cycle of homocysteine. I know the intermediary steps in this if you need.

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

Ratan Singh, Phone: 91 141 2652561, mail: ratanpsych@...

- Certificate in Food & Nutrition; Diploma in Nutrition and Health Education;

Life Member, Nutrion Soc. India.

- Member ISOM;

Author of " Nutrition & Supplements in Major Mental Illnesses " ;

- M.A. (Psychol), Postgraduate Diploma in Medical & Social Psychology, Ph.D.;

- Certified Behavior Therapist (from late Prof. J. Wolpe's Unit, Temple Univ Med

School, USA);- www.RegainMentalHealth.com/  www.ejcbs.com

From: Duncan Crow <duncancrow@...>

Subject: Re: b12 methyl or hydroxy

Coconut Oil

Date: Tuesday, March 29, 2011, 4:27 AM

 

Thanks for the info Alobar. So, it follows that methylcobalamin may reduce

any cyanide and also increase methionine creation by recirculating homocysteine

more effectively, which means I think reduced oxidative stress too

all good,

Duncan

>

>

[Guest guest]

Hi Ratan, I agree that it seems that both halfs of the methylcobalamin, the

vitamin B half and the methyl half, seem to be useful. Whether the methyl half

was actually used by the body had escaped me previously; now I can see also that

TMG trimethylglycine for example could also be a major methyl source because it

contains three methyls per amino acid and the body probably does not squander

methyl molecules from that either.

One of the booklets and tapes called Methylate or Die was very popular about 12

years ago. The most common approach given was b-6, b-12 and folic acid

supplementation, which today is well known.

Methylating does not create new glutathione precursors out of thin air, it

simply recycles existing homocysteine. As glutathione is depleted, even

efficient homocysteine recycling fails to replenish it. That depletion is why

one needs fresh precursors. I know about homocysteine recycling, and also

glutathione recycling with alpha-lipoic acid, but the rate-limiting feature of

glutathione production is still dietary bonded cysteine intake, so I use whey as

well as b-vitamins.

all good,

Duncan

>

> One observation: If I take one sublingual dot of methyl-cobalamine then I feel

hungry IMMEDIATELY, as if it opens some blocked path.

> The same was reported to me by my relation who had lost appetite. It seems

this type of B12 is replenishing methyl group to liver.

>

> Duncan there are two if not more paths to make glutathione. One you already

know (via the precursors that you know too much of). The second is by

methylation cycle of homocysteine. I know the intermediary steps in this if you

need.