Porphyrins test - PLEASE HELP- Andy & All

[Guest guest]

Hi all,

I just got back my results of the fractionated urine porphyrin test

and need your input, as I'm not clear how to calculate the proper

ratio. Basically, I need to know whether my levels are high in

relation to the creatinine level. I am 26 years old.

These are the results:

CREATININE

578 mg Ref. level: 500 to 1,500 mg

UROPORPHYRINS

54.07 µg Ref. level: < 33.5 µg

COPROPORPHYRINS

398.78 µg Ref. level: < 183 µg

I would really appreciate your help, as I've been battling a

persistent candida infection for years. I had my amalgams out three

weeks ago and would want to start chelation as soon as possible

(provided it's necessary, of course).

Thank you very much in advance,

Ruth

[Guest guest]

Ruth,

Porphyria can be a sign of severe suphur deficiency.

Just in case it is confusing that the study below reported that these

sulfur-deficient rats were not dumping sulfate into the urine...this is the

place where many of those with autism and those with AIDS seem to be

working with an injured bit of regulation. Your body should be able to

detect the need to retain sulfate when sulfur deficiency has occurred, but

that seems to be broken in many cases of autism.

These rats were also excreting some yucky stuff about the eyes, and that

yucky stuff contained porphyrins as well. (They didn't say yucky, but I

did!)

Unique Identifier

99101090

Authors

Tor-Agbidye J. Palmer VS. Sabri MI. Craig AM. Blythe LL. Spencer PS.

Institution

Center for Research on Occupational and Environmental Toxicology, Oregon

Health Sciences University, Portland 97201, USA.

Title

Dietary deficiency of cystine and methionine in rats alters thiol

homeostasis required for cyanide detoxification.

Source

Journal of Toxicology & Environmental Health. 55(8):583-95, 1998 Dec 25.

Abstract

Nutritional status is an important factor in modulating the metabolic fate

of xenobiotics. Sulfur amino acid (SAA) deficiency has been proposed as a

risk factor for human neurological diseases among protein-poor populations

subsisting on the cyanophoric plant cassava. Female Sprague-Dawley rats

were used to develop and define a model of SAA deficiency for use in

future studies examining cassava-related neurotoxicity. Rats were kept in

metabolic cages for 7-21 d and fed a balanced diet (BD) of known

composition or a comparable diet selectively deficient in methionine and

cystine (SAA-free diet). Animals fed the SAA-free diet failed to thrive,

lost body weight, excreted porphyrinic materials, and showed a steep and

persistent reduction of urinary inorganic sulfate. In contrast, animals on

the BD gained body weight and maintained baseline output of urinary

inorganic sulfate. Urinary thiocyanate excretion did not differ between

groups, but plasma thiocyanate concentrations reached double that in

SAA-deficient rats. Increased plasma thiocyanate suggests mobilization of

sulfur amino acids from endogenous sources. Liver glutathione and blood

cyanide concentrations were similar in animals on the BD and the

SAA-deficient diet. In summary, a diet free of methionine and cystine

results in increased retention of inorganic sulfur as thiocyanate and a

near absence of inorganic sulfur excretion in urine.

At 11:38 AM 12/31/2001 +0000, you wrote:

>Hi all,

>

>I just got back my results of the fractionated urine porphyrin test

>and need your input, as I'm not clear how to calculate the proper

>ratio. Basically, I need to know whether my levels are high in

>relation to the creatinine level. I am 26 years old.

>

>These are the results:

>

>CREATININE

>

>578 mg Ref. level: 500 to 1,500 mg

>

>

>UROPORPHYRINS

>

>

>54.07 µg Ref. level: < 33.5 µg

>

>

>COPROPORPHYRINS

>

>

>398.78 µg Ref. level: < 183 µg

>

>

>

>I would really appreciate your help, as I've been battling a

>persistent candida infection for years. I had my amalgams out three

>weeks ago and would want to start chelation as soon as possible

>(provided it's necessary, of course).

>

>Thank you very much in advance,

>

>

>Ruth

>

>

>

>

>=======================================================

>

[Guest guest]

Thank you for the study . I don't think I suffer from porphyria,

I have checked for symptoms and it's not me at all.

I'm confused about the sulfur issue. I don't tolerate any sulfur-

containing foods, they stop my digestion and I feel terrible for

days. Hence, I have excluded them all from my diet for the time being.

I'm hoping my elevated porphyring levels are due to mercury, but I

need somebody with the right knowledge to interpret my results in

relation to the creatinine level.

Doctors in my country are no use. I'm self-treating/self-diagnosing

because all the doctors do is sending me to the shrink because they

haven't got a clue and prefer to attribute my candidiasis and other

symptoms to my mental state (and I can tell you I'm perfectly normal

in that respect :-)

If you or anybody knows what the results mean in relation to mercury

poisoning, I would appreciate your help very much.

Best wishes,

Ruth

> >Hi all,

> >

> >I just got back my results of the fractionated urine porphyrin test

> >and need your input, as I'm not clear how to calculate the proper

> >ratio. Basically, I need to know whether my levels are high in

> >relation to the creatinine level. I am 26 years old.

> >

> >These are the results:

> >

> >CREATININE

> >

> >578 mg Ref. level: 500 to 1,500 mg

> >

> >

> >UROPORPHYRINS

> >

> >

> >54.07 µg Ref. level: < 33.5 µg

> >

> >

> >COPROPORPHYRINS

> >

> >

> >398.78 µg Ref. level: < 183 µg

> >

> >

> >

> >I would really appreciate your help, as I've been battling a

> >persistent candida infection for years. I had my amalgams out three

> >weeks ago and would want to start chelation as soon as possible

> >(provided it's necessary, of course).

> >

> >Thank you very much in advance,

> >

> >

> >Ruth

> >

> >

> >

> >

> >=======================================================

> >

[Guest guest]

Hi Ruth,

Since Andy hasn't answered (I think that you asked a few

days ago about this)-- anyway, there is a FILE (from Andy)

about porphyrins. It is here:

/files/porphryins.text

I don't know if this would help you or not.

there is also a section in the file

/files/ANDY_INDEX

which has a heading that looks like this:

DETERMINING MERCURY TOXICITY (fractionated urine porphyrins test)

There are several items there (from Andy).

I don't know if this is any help either.

FWIW.

Moria

At 07:31 PM 1/1/2002 -0000, you wrote:

>Thank you for the study . I don't think I suffer from porphyria,

>I have checked for symptoms and it's not me at all.

>

>I'm confused about the sulfur issue. I don't tolerate any sulfur-

>containing foods, they stop my digestion and I feel terrible for

>days. Hence, I have excluded them all from my diet for the time being.

>

>I'm hoping my elevated porphyring levels are due to mercury, but I

>need somebody with the right knowledge to interpret my results in

>relation to the creatinine level.

>

>Doctors in my country are no use. I'm self-treating/self-diagnosing

>because all the doctors do is sending me to the shrink because they

>haven't got a clue and prefer to attribute my candidiasis and other

>symptoms to my mental state (and I can tell you I'm perfectly normal

>in that respect :-)

>

>If you or anybody knows what the results mean in relation to mercury

>poisoning, I would appreciate your help very much.

>

>Best wishes,

>

>

>Ruth

>

[Guest guest]

Hi Moria,

Thank you for that. I had seen Andy's files but I'm not sure how to

do the porphyrin/creatinine ratio because of the different units. I

need to be sure I'm doing it correctly and that's why I would

appreciate somebody interpreting my results.

In any case, thanks a lot Moria, you're always extremely helpful to

everybody here, it's wonderful of you :-)

Ruth

> >Thank you for the study . I don't think I suffer from

porphyria,

> >I have checked for symptoms and it's not me at all.

> >

> >I'm confused about the sulfur issue. I don't tolerate any sulfur-

> >containing foods, they stop my digestion and I feel terrible for

> >days. Hence, I have excluded them all from my diet for the time

being.

> >

> >I'm hoping my elevated porphyring levels are due to mercury, but I

> >need somebody with the right knowledge to interpret my results in

> >relation to the creatinine level.

> >

> >Doctors in my country are no use. I'm self-treating/self-

diagnosing

> >because all the doctors do is sending me to the shrink because

they

> >haven't got a clue and prefer to attribute my candidiasis and

other

> >symptoms to my mental state (and I can tell you I'm perfectly

normal

> >in that respect :-)

> >

> >If you or anybody knows what the results mean in relation to

mercury

> >poisoning, I would appreciate your help very much.

> >

> >Best wishes,

> >

> >

> >Ruth

> >

[Guest guest]

Ruth and Moria,

I took a look at the page Moria referred to us in the archives where Andy

had calculated this chart:

Upper normal limit versus age for children:

Age uroporphyrin coproporphyrin

mcg/g cr mcg/g cr

birth 92 203

3 mo 111 165

6 mo 50 137

9 mo 43 71

1 yr 39 78

1.5 yr 64 83

2.25 yr 38 85

3 yr 43 78

4 yr 38 61

6 yr 33 60

9 yr 29 47

15 yr 32 48

adult 29 49

What wonderful data. What really is interesting to me is how the level

changes during the first four years. You may have heard that people

reported that Andy Wakefield at the last San Diego Conference presented

data showing that children who became autistic after the MMR failed to grow

normally both after the first and second MMR, and the second MMR was much

later. Deficient growth can be very much a sign of sulfur deficiency, just

like elevated porphyrins. I thought of his finding since the biggest

change in this chart appears at 18 months...which happens to be MMR

time. Were the children in this study immunized and can immunization

affect porphyrin levels? Or if these control children were not immunized,

if the chemistry is going through such a huge shift at this time

developmentally, do we have any idea what the effect of immunization would

be on this chemistry, and how that might affect development?

It may be interesting to listmates to learn that the enzymes of sulfation

are very upregulated in the brain during infancy and early toddlerhood to

accomplish the job of myelinating the brain and building the regulatory

extracellular matrix around neurons. These structures can't form until

glial cells form, and that is because some of the molecules are made and

exported by the glial cells. This process happens almost entirely after

birth and within the same period that these figures on porphyrins are

changing so much. According to Andy's figures, things porphyrinic seem to

ease off at about age four and that is also when most of myelination is

complete. At that point the porphyrins start more of a gentle change from

about four to nine, and then stay about the same from then on.

I imported Andy's data into Excel, and graphed the change over time, and it

is just stunning what is happening in the second year particularly. This

is when signs of autism typically show up.

Very interesting.

Ruth, you said:

>I'm confused about the sulfur issue. I don't tolerate any sulfur-

>containing foods, they stop my digestion and I feel terrible for

>days. Hence, I have excluded them all from my diet for the time being.

Ruth, please help me learn about these symptoms, and maybe we can get to

the bottom of this. When you say it stops digestion, what do you think is

happening exactly. Is the food staying in your stomach? Are you getting

heartburn or gas? Do you get constipated or diarrhea? Can you better

describe how you feel? Headachy? Body aches?

Any protein is going to have some sulfur in it, by the way. Some just has

more than others. What are you eating, and what are you excluding? Which

items make you feel the worst?

Have you ever tried the sort of enzymes that are being used in the autism

community, like Serenaid or enzyme-aid, or some other brands? Some of

these are made to help digest foods with a lot cysteine in them like casein

and gluten. A lot of enzymes are dependent on their activity needing to

bind to a sulfated GAG in the environment which protects the enzyme from

degradationf, and also affects the enzyme's shape and function. If lack of

sulfation of intestinal cells is impairing enzyme activity in the gut, then

the more deficient of sulfur you become, the worse the situation with GAG

dependent proteases and peptidases would become. If digestion in the upper

intestines is poor, then more sulfur-containing foods would make it

undigested to the colon where sulfur-loving bacteria can make bad-for-you

things out of them and give you gas. A good measure of the possibility

that this is happening is to measure the level of p-cresol in either urine

or blood, for it is made of leftover tyrosine that comes from underdigested

protein that makes it to the colon.

Do you have exactly the same reaction to " sulfur-foods " as you do to either

MSM or SAMe or NAC? If not, would you mind explaining the

differences? Any other listmate can answer this too, if you'd like.

One thing I wonder about is if the intestinal cells are sulfur deficient,

if that means the levels of some factors inside and out make it where the

transporters don't work the right direction. Scientists talk about

cis-inhibition and trans-inhibition. Some substances inhibit something

crossing a membrane by being on the same side of the membrane as what you

are trying to move across (cis-inhibition). Other substances inhibit it by

being on the opposite side (trans-inhibition). Every transporter which has

been investigated thoroughly has a list of substances that inhibit or

enhance transport from either side.

It may be that higher sulfate is needed on the inside of intestinal cells

to allow transport of some other substances across the apical side. It

looks like most of the sulfate may come from the blood, not from the inside

or from the food side of the intestines. That means that the intestines

are very likely dependent on the liver to provide proper sulfate levels

through the blood after it has used cysteine to make sulfate.

Mercury in the gut may impair sulfate transport there, but I'm not sure how

long that would be a problem after exposure. Intestinal cells turn over

very quickly, so I would expect the problem would move fairly rapidly from

the gut to the kidneys. Mercury does impair the kidney sulfate transporters.

1: J Biol Chem 2001 Aug 24;276(34):32322-9 Role of individual disulfide

bonds in the structural maturation of a low molecular weight glutenin subunit.

Orsi A, Sparvoli F, Ceriotti A.

Istituto Biosintesi Vegetali, Consiglio Nazionale delle Ricerche, via

Bassini 15, 20133 Milano, Italy.

Gliadins and glutenins are the major storage proteins that accumulate

in wheat endosperm cells during seed development. Although gliadins are

mainly monomeric, glutenins consist of very large disulfide-linked polymers

made up of high molecular weight and low molecular weight subunits. These

polymers are among the largest protein molecules known in nature and are

the most important determinants of the viscoelastic properties of gluten.

As a first step toward the elucidation of the folding and assembly pathways

that lead to glutenin polymer formation, we have exploited an in vitro

system composed of wheat germ extract and bean microsomes to examine the

role of disulfide bonds in the structural maturation of a low molecular

weight glutenin subunit. When conditions allowing the formation of

disulfide bonds were established, the in vitro synthesized low molecular

weight glutenin subunit was recovered in monomeric form containing

intrachain disulfide bonds. Conversely, synthesis under conditions that did

not favor the formation of disulfide bonds led to the production of large

aggregates from which the polypeptides could not be rescued by the

post-translational generation of a more oxidizing environment. These

results indicate that disulfide bond formation is essential for the

conformational maturation of the low molecular weight glutenin subunit and

suggest that early folding steps may play an important role in this

process, allowing the timely pairing of critical cysteine residues. To

determine which cysteines were important to maintain the protein in

monomeric form, we prepared a set of mutants containing selected cysteine

to serine substitutions. Our results show that two conserved cysteine

residues form a critical disulfide bond that is essential in preventing the

exposure of adhesive domains and the consequent formation of aberrant

aggregates.

PMID: 11418605 [PubMed - indexed for MEDLINE]