Unfolded Protein Response and A Possible Treatment for CFS

aquariusgirl

Senior Member
Messages
1,734
This is an interesting post taken from Mthfrsupport.com in which a practitioner connects gallbladder issues sulfation & oxolates.


There is a connection between gallbladder function, oxalates and sulfates. I just worked with a Japanese patient in his mid-40's who has suffered from severe depression, fat malabsorption (stool analysis), tachycardia, and severe adrenal fatigue. He currently deals with fatigue, inability to tolerate smells (aldehydes!), headaches, nausea, and irritability with the smallest amount of stress. The patient has a candida and bacteria gut infection, low serotonin, high urinary taurine and very high oxalates, glyceric and glycolic. What is the connection with all these markers?

What we see is that elevated taurine is the body's attempt to produce sulfate via the CDO enzyme. But why would he need sulfate? Well, when oxalates are elevated the body is forced to exchange a sulfate molecule for an oxalate molecule. In other words, the elevated oxalates cause us to pee out our sulfate in very high quantities. As our sulfate levels are lost, the phase II SULT system is slowed. This forces the liver to use other systems like acetylation, methylation and glucoronidation to detox our bodies. The problem is this causes us to use up our methyl groups faster; and it also turns the gallbladder into sludge using too much glucoronidation. This creates the bile sludge we see on ultrasound.

So the gallbladder stops working well, and now fats aren't absorbed well. This causes us to poop out healthy fats and other minerals like calcium, iron, zinc and magnesium. The oxalates are absorbed instead of the fats and minerals. Now the oxalates start going up again, sulfate goes down again, and gallbladder/liver detox and bile gets worse. Around and around like a snowball effect.

As sulfate is lost because of high oxalates, the body cannot keep hormones and neurotransmitters in balance. Loss of sulfate means not only do we not detox, we also don't repair well nor do we keep our hormones in circulation very well. Many hormones and neurotransmitters are "sulfated" and kept in circulation in a turned-off state in case the body needs them in the future. But with low sulfate this doesn't work and we pee out our hormones too fast, leading adrenal fatigue, early menopause, low testosterone, etc. This is one reason why people with gut issues and oxalate issues can be very chronically ill until the oxalate-sulfate situation is addressed.

More to follow in a upcoming video with references and article.

In Health,

Dr. Rostenberg
https://www.facebook.com/mthfrsupport/
redmountainclinic@gmail.com
 
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Flo

Messages
80
This is an interesting post taken from Mthfrsupport.com in which a practitioner connects gallbladder issues sulfation & oxolates.


There is a connection between gallbladder function, oxalates and sulfates. I just worked with a Japanese patient in his mid-40's who has suffered from severe depression, fat malabsorption (stool analysis), tachycardia, and severe adrenal fatigue. He currently deals with fatigue, inability to tolerate smells (aldehydes!), headaches, nausea, and irritability with the smallest amount of stress. The patient has a candida and bacteria gut infection, low serotonin, high urinary taurine and very high oxalates, glyceric and glycolic. What is the connection with all these markers?

What we see is that elevated taurine is the body's attempt to produce sulfate via the CDO enzyme. But why would he need sulfate? Well, when oxalates are elevated the body is forced to exchange a sulfate molecule for an oxalate molecule. In other words, the elevated oxalates cause us to pee out our sulfate in very high quantities. As our sulfate levels are lost, the phase II SULT system is slowed. This forces the liver to use other systems like acetylation, methylation and glucoronidation to detox our bodies. The problem is this causes us to use up our methyl groups faster; and it also turns the gallbladder into sludge using too much glucoronidation. This creates the bile sludge we see on ultrasound.

So the gallbladder stops working well, and now fats aren't absorbed well. This causes us to poop out healthy fats and other minerals like calcium, iron, zinc and magnesium. The oxalates are absorbed instead of the fats and minerals. Now the oxalates start going up again, sulfate goes down again, and gallbladder/liver detox and bile gets worse. Around and around like a snowball effect.

As sulfate is lost because of high oxalates, the body cannot keep hormones and neurotransmitters in balance. Loss of sulfate means not only do we not detox, we also don't repair well nor do we keep our hormones in circulation very well. Many hormones and neurotransmitters are "sulfated" and kept in circulation in a turned-off state in case the body needs them in the future. But with low sulfate this doesn't work and we pee out our hormones too fast, leading adrenal fatigue, early menopause, low testosterone, etc. This is one reason why people with gut issues and oxalate issues can be very chronically ill until the oxalate-sulfate situation is addressed.

More to follow in a upcoming video with references and article.

In Health,

Dr. Rostenberg

redmountainclinic@gmail.com

Soprry, wrong. Too much wrong to point out. Sorry.

Anyone who uses the word "detox" in their talks should be ignored completely.
 

Flo

Messages
80
@Flo

Could you help (if you know of course) finding the rs# for AKR1D1 ? See the positions below :

I will but it is useless to look at these genes. They are secondary if not tertiary to the issue of disease.

rs6945659 G or T
rs6467734 G or T
rs6943498 C or T
rs10263802 A or G
rs2120846 G or T
rs10257928 A or G
rs6943935 C or T
rs8180809 C or T
rs6467735 C or T
rs3805362 A or G
rs11982192 G or T
rs17169518 A or G
rs17169521 C or T
rs1872929 A or C
rs1872930 C or T
rs17169522 C or T
rs17169523 C or T
 

mariovitali

Senior Member
Messages
1,214
I will but it is useless to look at these genes. They are secondary if not tertiary to the issue of disease.

rs6945659 G or T
rs6467734 G or T
rs6943498 C or T
rs10263802 A or G
rs2120846 G or T
rs10257928 A or G
rs6943935 C or T
rs8180809 C or T
rs6467735 C or T
rs3805362 A or G
rs11982192 G or T
rs17169518 A or G
rs17169521 C or T
rs1872929 A or C
rs1872930 C or T
rs17169522 C or T
rs17169523 C or T


Thanks. So when the paper states "homozygous for a missense mutation (662 C>T" which rs# from the above does this refer to?


This may be highly relevant to a subset of sufferers..
 

Flo

Messages
80
Thanks. So when the paper states "homozygous for a missense mutation (662 C>T" which rs# from the above does this refer to?


This may be highly relevant to a subset of sufferers..

The only reason I think it is not relevant is that there is nothing that can be done about it. There are no cofactors for that enzyme.

I do not know which SNP they are referring too. It takes a lot of effort to find it and to me it is not worth the energy.
 

Flo

Messages
80
Now *there's* a statement. :rolleyes::rolleyes::rolleyes::rolleyes: IMO anyone who makes statements like that should be ignored completely. :lol: :lol: :rofl: Except I'm not dumb enough to ignore anyone completely just because they say one or two things I don't agree with. Would that everyone felt the same way.


If you can explain the metabolic action of "gallbladder/liver detox", scientifically, I would be glad to hear it.

Plus he does not use a single footnote.

But by all means, listen to him. I was just expressing my opinion and did not want to spend MY time refuting what he claims in text.

If someone is not producing enough sulfates all they need is molybdenum to up regulate their SUOX enzyme.
 

whodathunkit

Senior Member
Messages
1,160
Go to MTHFR support.com facebook page ..,it's there or ill post link later
I don't do FB. If you could post a link it would be appreciated. If not, that's okay, too.

If someone is not producing enough sulfates all they need is molybdenum to up regulate their SUOX enzyme.
This is useful. Thanks. Glad I didn't throw the baby out with the bathwater and ignore you completely, despite my initial knee-jerk inclination.

See how that can work? :)
 

Flo

Messages
80
I don't do FB. If you could post a link it would be appreciated. If not, that's okay, too.


This is useful. Thanks. Glad I didn't throw the baby out with the bathwater and ignore you completely, despite my initial knee-jerk inclination.

See how that can work? :)

The more you know the more accurate your knee jerks. :)
 

Valentijn

Senior Member
Messages
15,786
So with a faulty HSD3B7, CYP8B1, FXR ....
Why do you believe that the SNPs you listed means that those genes are faulty? Two of those SNPs have no known impact, and are extremely unlikely to have any impact. The third SNP potentially has a very tiny impact and even that has not been replicated. All versions of the SNPs are extremely common.
 
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Flo

Messages
80
Why do you believe that the SNPs you listed means that those genes are faulty? Two of those SNPs have no known impact, and are extremely unlikely to have any impact. The third SNP potentially has a very tiny impact and even that has not been replicated. All versions of the SNPs are extremely common.

Even common SNPs can influence risk, yes?
 
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mariovitali

Senior Member
Messages
1,214
@Valentijn


I will not get into this conversation again, i am putting this for others. The statements that you are making may have serious implications (I talk about hypotheses here, remember?) and i hope that all people that read what you say are aware of the dangers.

I asked you how it is possible that NAT2PRED (http://nat2pred.rit.albany.edu/) is possible to PREDICT fast vs slow acetylators from a COMBINATION of SNPs of the same group NAT2.

I still wait for your "scientific" explanation.

I mean i do realize that -in my point of view-, you THINK that you know and so i accept that. I really do not know what others will do in the unlikely event that the hypothesis discussed in this Thread is true.


REMEMBER : I discuss a Hypothesis (count how many times "hypothesis" exists in this Thread), you are making statements.

How are you so confident that the Hypothesis discussed here is False?


In the unlikely event that this Hypothesis is true, You may be in serious trouble to be honest...
 

Bdeep86

Senior Member
Messages
278
@Sam7777 @Violeta @Bdeep86 @Flo @whodathunkit @ahmo
@jump44



We are getting very close ...






Please check the following SNPs :


HSD3B7 (rs9938550) Variant Allele : G
GPBAR1 (rs3731859) Variant Allele : A




Why Choline helps (My Hypothesis)



The role of dietary choline in the beneficial effects of lecithin on the secretion of biliary lipids in rats.
LeBlanc MJ1, Gavino V, Pérea A, Yousef IM, Lévy E, Tuchweber B.
Author information

Abstract
Earlier studies showed that dietary soybean lecithin increases biliary lipid secretion, which mainly comes from the contribution of high density lipoprotein (HDL) and hepatic microsomal pools of phosphatidylcholine and cholesterol. In addition, a lecithin diet enhances bile secretion and prevents bile acid-induced cholestasis. This study evaluated the contribution of choline, a component of lecithin, to the observed effect of lecithin on biliary secretory function. Rats were fed either a control diet (CD), a choline diet (ChD) or a lecithin-enriched diet (LD) for 2 weeks. Results showed that like LD, ChD induced an increase in bile flow and bile acid secretion rate when compared with the control diet. However, unlike LD, ChD did not significantly increase biliary phospholipids and cholesterol output. An increase of hydrophilic bile acids (i.e. ursodeoxycholic and muricholic acids) in bile of rats fed choline could explain why the biliary phospholipid and cholesterol secretion was not increased. During taurocholic acid infusion, both experimental diets increased bile flow and the bile acid secretion rate maximum (BASRm). The cholestasis usually observed after the BASRm is reached was inhibited by ChD and LD. Both diets induced a decrease in plasma cholesterol (total and HDL), however, only LD induced statistically significant changes. Analysis of total cholesterol and phospholipid content of microsomes and canalicular membranes indicated no statistically significant difference between control and experimental groups either under basal conditions or after bile acid infusion. Similarly, the phospholipid classes and fatty acid composition of biliary phosphatidylcholine were not altered by feeding ChD and LD. We conclude that choline contributes to the beneficial effect of a lecithin diet on bile secretion. It is postulated that this effect may be attributed to modulation of HDL and an enhancement of the cholesterol and phospholipid pools destined for biliary secretion.


This is a really really nice find, nicely done!
 

ahmo

Senior Member
Messages
4,805
Location
Northcoast NSW, Australia
Please check the following SNPs :


HSD3B7 (rs9938550) Variant Allele : G
GPBAR1 (rs3731859) Variant Allele : A
I'm AA for both of these.

Anyone who uses the word "detox" in their talks should be ignored completely.
bandeau-lol.gif

You might not like the word. You might prefer words like chelation or anti-bacterial, anti-viral, anti-parasite therapies. What about organophosphates? Detox is common parlance. Detoxifying all of the above radically improved my health.
 
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mariovitali

Senior Member
Messages
1,214
@ahmo

Sorry for not being very accurate at what i say, could you check also the following (apart from HSD3B7, GPBAR1) :

rs3808607 CYP7A1 G
rs3824260 CYP7A1 A
rs3732860 CYP8B1 T
rs35724 NR1H4 G
rs10808739 CYP7B1 A
rs72554620 CYP7B1 A
rs7083869 AKR1C4 A
AKR1D1 should be here also but need to find the rs# involved...

(rs3731859 GPBAR1 A)
(rs9938550 HSD3B7 G)
 

ahmo

Senior Member
Messages
4,805
Location
Northcoast NSW, Australia
@ahmo

Sorry for not being very accurate at what i say, could you check also the following (apart from HSD3B7, GPBAR1) :

rs3808607 CYP7A1 G TT
rs3824260 CYP7A1 A GG
rs3732860 CYP8B1 T TT
rs35724 NR1H4 G CC
rs10808739 CYP7B1 A GG
rs72554620 CYP7B1 A GG
rs7083869 AKR1C4 A GG

(rs3731859 GPBAR1 A) AA
(rs9938550 HSD3B7 G) AA
I use snptips on Firefox, which lights up those rs numbers when I have them, and I can then mouse over them for my specifics. I didn't do all of them because my working memory is non-existent, I have to keep scrolling back and forth to get results and record them. :rolleyes:
 
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