susan owens, low zinc wastes taurine and sulphate

[Guest guest]

you can see why ala chelation is so uneven with its spilling of zinc.

anyway susan has not posted this here so i am taking the liberty of

doing so

" From: Owens <lwo@i...>

Date: Wed Dec 31, 2003 2:07 am

Subject: The relationship between zinc deficiency and sulfur

excretion

Listmates,

I've been analyzing the data from a paper which looked at rats, but

compared two groups: one that had adequate zinc in its diet, and

another

group where zinc was restricted. This restriction continued for three

weeks, but every week, the authors looked at their excretion of

labelled

sulfate and labelled taurine that was derived from a dose of labelled

cystine..

What the study found is that by the third week of zinc restriction,

the

rats were excreting five times the normal amount of taurine, and

three and

a half times the normal amount of sulfate that was derived from that

cystine. It was amazing how the differences in just one more week of

zinc

being low made the curve for the amount of this sulfur loss go up

dramatically, and since they stopped at three weeks, we don't know

how much

more restriction for even longer would have affected the loss of

sulfur in

urine.

They did another test in a different group of rats and measured things

after two weeks of zinc restriction, but this time they compared the

total

sulfur or the sulfate excreted when it was derived (was metabolized

from)

various different sulfur compounds. In this time frame, the labelled

sulfur excreted was about one and a half times normal if the source

of the

sulfur was thiamine or thiourea and just a bit higher than that if the

source were cystine. If the original source of the label were

sulfate, it

was just a bit lower than one and a half times normal, but if the

source of

the label were methionine, the loss was about double.

When they only looked at labelled sulfate alone that was being

excreted

under these conditions, the excretion rate in zinc deficiency was a

bit

higher proportionately than had been the labelled sulfur, but the real

difference occurred when methionine was the source of the labelled

sulfur,

for then the zinc deficient rats excreted three and three/quarters the

amount of sulfate as the rats who had been on a diet restricting zinc

for

two weeks. The study suggested that this difference derived from the

difficulty the rats would have had trying to use methionine to form

proteins under the zinc deficient condition, so they suggested that

the

methionine, instead of being incorporated into proteins, was instead

being

broken down to sulfate. Another study had actually already shown that

zinc

deficiency made it more difficult to use methionine for building

proteins.

Of course this study was in rats, and we humans might be a bit

differerent,

but the study does need to make us think how terrifically important

zinc is

to sulfur homeostasis. If you lose sulfur in the urine, as happens in

HIV,

you might develop problems maintaining body stores of sulfur with

unfortunate consequences.

Curiously, zinc deficiency occurs in HIV, and the degree of

deficiency is

somewhat predictive of survival. However, those with HIV are known to

dump

sulfate in high quantities in the urine from the first days of

infection

and long before the symptoms of AIDS shows up. This has been

quantified to

represent a loss equivalent to 4.4 pounds of excess sulfate loss in

urine

every year. This is such a high proportion of the body's sulfur stores

that it is not surprising this disease becomes fatal.

Doe this connection with AIDS maybe hint at how activation of the

immune

system may deplete zinc? Last night I took a look at the literature

to see

if I could find information about what depletes zinc or causes us to

lose

zinc, and I wasn't very successful finding a lot of discussion of this

area, so I hope perhaps some other listmates may have had more

success in

the past.

By the way, predictably, zinc deficiency retards growth, which is

quite

logical if it depletes sulfur and keeps cells from using their

methionine

to make protein.

One of the things this perhaps should make us think about is how a

lot of

doctors and parents have been beefing up zinc before initiating

chelation

and during chelation in children they were treating with DMSA or other

chelating agents. If this extra zinc actually helped these children

retain

sulfur, then that (even if it were not followed by chelation) would

have

improved their sulfur chemistry and their ability to deal with heavy

metals, especially since if you improve their sulfur status, then

they can

make more metallothionein whose main amino acid component is cysteine.

Those who find they are excreting high levels of taurine or sulfate

may

need to take a closer look at zinc status.

Does this information jibe with the personal experience of listmates

who

have found their children improved with zinc supplementation? I'm

thinking

of you, mainly, !

Be sure and read the abstracts below if this is an area of interest

to you.

J Nutr. 1970 Oct;100(10):1189-95. Related Articles, Links

Zinc deficiency and urinary excretion of taurine-35S and inorganic

sulfate-35S following cystine-35S injecion in rats.

Hsu JM, WL.

PMID: 5471053 [PubMed - indexed for MEDLINE]

Clin Infect Dis. 2003;37 Suppl 2:S117-23. Related Articles, Links

[Click here to read]

Zinc status in human immunodeficiency virus type 1 infection and

illicit drug use.

Baum MK, Campa A, Lai S, Lai H, Page JB.

Florida International University, College of Health and Urban Affairs,

University Park, Rm. HLS 337, Miami, FL 33199, USA. baumm@f...

Zinc deficiency is the most prevalent micronutrient abnormality seen

in human immunodeficiency virus (HIV) infection. Low levels of plasma

zinc

predict a 3-fold increase in HIV-related mortality, whereas

normalization

has been associated with significantly slower disease progression and

a

decrease in the rate of opportunistic infections. Studies in Miami,

Florida, indicated that HIV-positive users of illicit drugs are at

risk for

developing zinc deficiency, at least partially because of their poor

dietary intake. Zinc deficiency characterized by low plasma zinc

levels

over time enhances HIV-associated disease progression, and low

dietary zinc

intake is an independent predictor of mortality in HIV-infected drug

users.

The amount of zinc supplementation in HIV infection appears to be

critical,

because deficiency, as well as excessive dietary intake of zinc, has

been

linked with declining CD4 cell counts and reduced survival. More

research

is needed to determine the optimal zinc supplementation level in

HIV-infected patients, to prevent further burden on an already

compromised

immune system.

PMID: 12942385 [PubMed - indexed for MEDLINE]

AIDS Res Hum Retroviruses. 2000 Feb 10;16(3):203-9. Related Articles,

Links

[Click here to read]

Massive loss of sulfur in HIV infection.

Breitkreutz R, Holm S, Pittack N, Beichert M, Babylon A, Yodoi J,

Droge W.

Division of Immunochemistry, Deutsches Krebsforschungszentrum,

Heidelberg, Germany.

Skeletal muscle tissue from SIV-infected macaques was previously found

to contain abnormally high sulfate and low glutathione levels

indicative of

an excessive cysteine catabolism. We now confirm the peripheral

tissue as a

site of massive cysteine catabolism in HIV infection and have

determined

the urinary loss of sulfur per time unit. The comparison of the

sulfate

concentrations of the arterial and venous blood from the lower

extremities

of 16 symptomatic HIV+ patients and 18 HIV- control subjects (study 1)

revealed (1) that the peripheral tissue of HIV+ patients with or

without

highly active antiretroviral therapy (HAART) releases large amounts of

sulfate and (2) that plasma sulfate, thioredoxin, and interleukin-6

levels

are elevated in these patients. A complementary investigation of 64

asymptomatic HIV+ patients and 65 HIV- subjects (study 2) revealed

increased plasma sulfate levels in the asymptomatic patients. The

analysis

of the daily urinary excretion of sulfate and urea of another group

of 19

HIV+ patients and 22 healthy HIV- subjects (study 3) confirmed (1)

that

HIV+ patients experience a massive loss of sulfur and (2) that this

loss is

not ameliorated by HAART. The sulfur loss of asymptomatic patients was

equivalent to a mean loss of about 10 g of cysteine per day. If

extrapolated, this would correspond to an alarming negative balance of

approximately 2 kg of cysteine per year under the assumption that the

normal sulfate excretion equivalent to approximately 3 g of cysteine

per

day is balanced by a standard Western diet. The abnormally high

sulfate/urea ratio suggests that this process drains largely the

glutathione pool.

PMID: 10710208 [PubMed - indexed for MEDLINE]

J Trop Pediatr. 2003 Jun;49(3):187-8. Related Articles, Links

Zinc deficiency: a contributing factor of short stature in growth

hormone deficient children.

Siklar Z, Tuna C, Dallar Y, Tanyer G.

Ministry of Health Ankara Hospital, Department of Pediatrics, Turkey.

zeynepsklr@h...

Zinc is an essential trace element which affects growth by promoting

DNA and RNA synthesis and cell division. Zinc deficiency causes growth

retardation and its frequency is high in developing countries. It

could

contribute to the effect of growth hormone (GH) treatment in GH

deficient

children. In this study, we investigated zinc deficiency in GH

children.

Twenty-four GH deficient children (treated with GH for 2.2 +/- 1.6

years)

were recruited for the study. Intracellular erythrocyte zinc levels

were

measured. Eleven (45.9 per cent) were found to be zinc deficient

(Group 1),

while 13 patients (54.1 per cent) had normal zinc levels (Group 2).

The

mean growth velocity was 5.98 +/- 0.8 cm/year in Group 1 and 6.9 +/-

1.4

cm/year in Group 2. Group 2 was given oral zinc supplementation with a

resultant growth velocity of 7.51 +/- 0.5 cm/year. During GH

treatment in

GH deficient children, zinc status should be evaluated as severe zinc

deficiency could affect the response to GH treatment.

PMID: 12848213 [PubMed - indexed for MEDLINE]