Re: Hi Everyone I was diagnosed with PSC, and I am new here. Is thee any progress ?

[Guest guest]

Thanks a lot.

I read most of the PDF file attached, you sent me.

Since I am not a doctor, I am not sure I understood all the

terminology.

About DHA: Is it possible to take it not as a supplement but somehow

get this same 800mg in your diet?

And about that HP deficiency, is it a result of the disease (like the

deficiency of vitamin A) or might it be the cause? And what is

exactly?

Thanks for your help.

> >

> > Is there any progress in finding some better treatment for PSC?

> > Thanks.

> >

>

[Guest guest]

Thanks a lot.

I read most of the PDF file attached, you sent me.

Since I am not a doctor, I am not sure I understood all the

terminology.

About DHA: Is it possible to take it not as a supplement but somehow

get this same 800mg in your diet?

And about that HP deficiency, is it a result of the disease (like the

deficiency of vitamin A) or might it be the cause? And what is

exactly?

Thanks for your help.

> >

> > Is there any progress in finding some better treatment for PSC?

> > Thanks.

> >

>

[Guest guest]

Hi " mishapog20 " ;

Sorry for not replying to your questions sooner. I'll try to answer

as best as I can.

You could potentially get all of that DHA from dietary sources by

eating fish:

http://www.health.gov/dietaryguidelines/dga2005/report/

Look under Section 4: Fats, and the Tables showing EPA and DHA levels

of various fish.

I don't fully uunderstand the significance of the haptoglobin

polymorphism described by the Hungarian group. It appears to be a

genetic link, meaning that it may be a possible cause of PSC? I am

still reading about what haptoglobins do in the body, and so I don't

know all the details yet. But haptoglobins seems to be involved in

regulation of iron levels, particularly removal of heme from

hemoglobin:

GJ, Frazer DM 2005 Hepatic iron metabolism. Semin. Liver

Dis. 25: 420-432.

http://www.ncbi.nlm.nih.gov/pubmed/16315136

Bamm VV, Tsemakhovich VA, Shaklai M, Shaklai N 2004 Haptoglobin

phenotypes differ in their ability to inhibit heme transfer from

hemoglobin to LDL. Biochemistry 43: 3899-3906.

http://www.ncbi.nlm.nih.gov/pubmed/15049697

Suppose that PSCers had impaired heme metabolism (as a result of this

haptoglobin polymorphism). This could lead to " oxidative stress " , and

depletion of reduced glutathione. This could then result in impaired

ability to conjugate bile with glutathione, therefore impaired

clearance of bile acids from the liver, as another member of the

group has been pointing out lately.

Heme accumulation could lead to impaired retinoid X receptor (RXR-

alpha) activity, and therefore impaired activity of all other nuclear

receptors in the liver, resulting in further disturbances of bile

transport and metabolism.

Gotoh S, Ohgari Y, Nakamura T, Osumi T, Taketani S (2008) Heme-

binding to the nuclear receptor retinoid X receptor alpha (RXRalpha)

leads to the inhibition of the transcriptional activity. Gene 423

(2):207-14.

http://www.ncbi.nlm.nih.gov/pubmed/18675890

DHA (and the vitamin A derivative, 9 cis-retinoic acid) could

possibly reverse this heme impairment of RXR because they bind to

RXRalpha.

Fan YY, Spencer TE, Wang N, Moyer MP, Chapkin RS 2003 Chemopreventive

n-3 fatty acids activate RXRalpha in colonocytes. Carcinogenesis.

2003 Sep;24(9):1541-8.

http://www.ncbi.nlm.nih.gov/pubmed/12844485

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)

>

> Thanks a lot.

> I read most of the PDF file attached, you sent me.

> Since I am not a doctor, I am not sure I understood all the

> terminology.

> About DHA: Is it possible to take it not as a supplement but

somehow

> get this same 800mg in your diet?

> And about that HP deficiency, is it a result of the disease (like

the

> deficiency of vitamin A) or might it be the cause? And what is

> exactly?

> Thanks for your help.

>

[Guest guest]

Hi " mishapog20 " ;

Sorry for not replying to your questions sooner. I'll try to answer

as best as I can.

You could potentially get all of that DHA from dietary sources by

eating fish:

http://www.health.gov/dietaryguidelines/dga2005/report/

Look under Section 4: Fats, and the Tables showing EPA and DHA levels

of various fish.

I don't fully uunderstand the significance of the haptoglobin

polymorphism described by the Hungarian group. It appears to be a

genetic link, meaning that it may be a possible cause of PSC? I am

still reading about what haptoglobins do in the body, and so I don't

know all the details yet. But haptoglobins seems to be involved in

regulation of iron levels, particularly removal of heme from

hemoglobin:

GJ, Frazer DM 2005 Hepatic iron metabolism. Semin. Liver

Dis. 25: 420-432.

http://www.ncbi.nlm.nih.gov/pubmed/16315136

Bamm VV, Tsemakhovich VA, Shaklai M, Shaklai N 2004 Haptoglobin

phenotypes differ in their ability to inhibit heme transfer from

hemoglobin to LDL. Biochemistry 43: 3899-3906.

http://www.ncbi.nlm.nih.gov/pubmed/15049697

Suppose that PSCers had impaired heme metabolism (as a result of this

haptoglobin polymorphism). This could lead to " oxidative stress " , and

depletion of reduced glutathione. This could then result in impaired

ability to conjugate bile with glutathione, therefore impaired

clearance of bile acids from the liver, as another member of the

group has been pointing out lately.

Heme accumulation could lead to impaired retinoid X receptor (RXR-

alpha) activity, and therefore impaired activity of all other nuclear

receptors in the liver, resulting in further disturbances of bile

transport and metabolism.

Gotoh S, Ohgari Y, Nakamura T, Osumi T, Taketani S (2008) Heme-

binding to the nuclear receptor retinoid X receptor alpha (RXRalpha)

leads to the inhibition of the transcriptional activity. Gene 423

(2):207-14.

http://www.ncbi.nlm.nih.gov/pubmed/18675890

DHA (and the vitamin A derivative, 9 cis-retinoic acid) could

possibly reverse this heme impairment of RXR because they bind to

RXRalpha.

Fan YY, Spencer TE, Wang N, Moyer MP, Chapkin RS 2003 Chemopreventive

n-3 fatty acids activate RXRalpha in colonocytes. Carcinogenesis.

2003 Sep;24(9):1541-8.

http://www.ncbi.nlm.nih.gov/pubmed/12844485

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)

>

> Thanks a lot.

> I read most of the PDF file attached, you sent me.

> Since I am not a doctor, I am not sure I understood all the

> terminology.

> About DHA: Is it possible to take it not as a supplement but

somehow

> get this same 800mg in your diet?

> And about that HP deficiency, is it a result of the disease (like

the

> deficiency of vitamin A) or might it be the cause? And what is

> exactly?

> Thanks for your help.

>

[Guest guest]

Hi " mishapog20 " ;

Sorry for not replying to your questions sooner. I'll try to answer

as best as I can.

You could potentially get all of that DHA from dietary sources by

eating fish:

http://www.health.gov/dietaryguidelines/dga2005/report/

Look under Section 4: Fats, and the Tables showing EPA and DHA levels

of various fish.

I don't fully uunderstand the significance of the haptoglobin

polymorphism described by the Hungarian group. It appears to be a

genetic link, meaning that it may be a possible cause of PSC? I am

still reading about what haptoglobins do in the body, and so I don't

know all the details yet. But haptoglobins seems to be involved in

regulation of iron levels, particularly removal of heme from

hemoglobin:

GJ, Frazer DM 2005 Hepatic iron metabolism. Semin. Liver

Dis. 25: 420-432.

http://www.ncbi.nlm.nih.gov/pubmed/16315136

Bamm VV, Tsemakhovich VA, Shaklai M, Shaklai N 2004 Haptoglobin

phenotypes differ in their ability to inhibit heme transfer from

hemoglobin to LDL. Biochemistry 43: 3899-3906.

http://www.ncbi.nlm.nih.gov/pubmed/15049697

Suppose that PSCers had impaired heme metabolism (as a result of this

haptoglobin polymorphism). This could lead to " oxidative stress " , and

depletion of reduced glutathione. This could then result in impaired

ability to conjugate bile with glutathione, therefore impaired

clearance of bile acids from the liver, as another member of the

group has been pointing out lately.

Heme accumulation could lead to impaired retinoid X receptor (RXR-

alpha) activity, and therefore impaired activity of all other nuclear

receptors in the liver, resulting in further disturbances of bile

transport and metabolism.

Gotoh S, Ohgari Y, Nakamura T, Osumi T, Taketani S (2008) Heme-

binding to the nuclear receptor retinoid X receptor alpha (RXRalpha)

leads to the inhibition of the transcriptional activity. Gene 423

(2):207-14.

http://www.ncbi.nlm.nih.gov/pubmed/18675890

DHA (and the vitamin A derivative, 9 cis-retinoic acid) could

possibly reverse this heme impairment of RXR because they bind to

RXRalpha.

Fan YY, Spencer TE, Wang N, Moyer MP, Chapkin RS 2003 Chemopreventive

n-3 fatty acids activate RXRalpha in colonocytes. Carcinogenesis.

2003 Sep;24(9):1541-8.

http://www.ncbi.nlm.nih.gov/pubmed/12844485

Best regards,

Dave

(father of (23); PSC 07/03; UC 08/03)

>

> Thanks a lot.

> I read most of the PDF file attached, you sent me.

> Since I am not a doctor, I am not sure I understood all the

> terminology.

> About DHA: Is it possible to take it not as a supplement but

somehow

> get this same 800mg in your diet?

> And about that HP deficiency, is it a result of the disease (like

the

> deficiency of vitamin A) or might it be the cause? And what is

> exactly?

> Thanks for your help.

>