2nd TEI Hair Analysis (after 2 months of avoiding calcium)

Helen

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5,415
SAMe being a pecursor to cysteine is good. Zinc, cysteine and histidine are all important parts of alcohol dehydrogenase, needed to remove accutane(retinoic acid).

ADH makes retinal and then retinoic acid.

ADH is a limiting step of making retinoic acid, it cant remove any accutane. accutane is 5 steps above/

ADH makes retonoic acid.

Accutane actually can influence ADH enzyme heavily. since it is rate limiting enzyme, and after you stop accutane, the whole pathway might not work.

since cysteine is not available.

but SAME does not make cysteine directly, cysteine is made from SERINE. and homocysteine.

and homocysteine is high in those tests that we saw from PFS people.


that is why it is important to see if cysteine is normal or not, if cysteine is not normal but homocysteine is high then the thing that is stopping methylation and SAME is the build up of homocysteine and inability to covert into cysteine

and since cysteine is low. you lose zinc into the urine. and this raises cortisol, since it is not working. since zinc finger is out.

and this causes alkalosis thus SAME is prohibited since adrenaline is not allowed it would ventilate your faster, causing lower CO2. and in alkalosis you need higher CO2. body tries to retain Co2.

So it would be interesting to see the cysteine levels in Accutane people and serine levels.





Some retinol dehydrogenases are in extra-ocular tissues, such as human retinol dehydrogenase-4 (RoDH-4), which converts retinol and 1-cis-retinol to different aldehydes in liver and skin. It was also found that 13-cis-retinoic acid (isotretinoin), 3,4-didehydroretinoic acid, and 3,4-didehydroretinol can act as competitive inhibitor of the 3α-hydroxysteroid dehydrogenase oxidative activity of the enzyme. This can potentially explain how isotretinoin, the active ingredient is Roaccutane (Accutane), can suppress sebaceous glands and be used for severe acne treatment.[15]
 
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Helen

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Also we need to look into copper. High ferritin, I saw was lowered only by copper.

and actually methionine synthase could be a copper enzyme.

and serine is made from glycine, using tetrafolate.

so when methionine synthase works, this makes tetrafolate which then makes serine. and cysteine.

so you can say that copper makes cysteine.
 

tanedout

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Messages
538
Also we need to look into copper. High ferritin, I saw was lowered only by copper.

and actually methionine synthase could be a copper enzyme.

and serine is made from glycine, using tetrafolate.

so when methionine synthase works, this makes tetrafolate which then makes serine. and cysteine.

so you can say that copper makes cysteine.

I get better clarity from eating cashews. I assumed it was something to do with the fat content stimulating the bile, but that could be down to copper as I notice they are very high in copper?

Cashews

Looking at what foods contain serine, it doesn't look like I get any. I'm also taking granulated lecithin, but sunflower lecithin, not soy (soy contains serine, sunflower doesn't). Do you think it's worth adding some serine into the mix then?
 

Helen

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@Orion Serine plays an important role in the catalytic function of many enzymes. It has been shown to occur in the active sites of chymotrypsin, trypsin, and many other enzymes. The so-called nerve gases and many substances used in insecticides have been shown to act by combining with a residue of serine in the active site of acetylcholine esterase, inhibiting the enzyme completely.


Aluminum is the metal which binds serine. I think also,

this could cause high acetylcholine symptomsin some people like POIS
 

Helen

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Staff member
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5,415
1. Alpha-Lipoic Acid
This micro-nutrient available over-the-counter at drugstores may be a best
option for Alzheimer’s patients. A small study from Germany using 600
mg/day supplementation stabilized Alzheimer’s – i.e. halting disease
progression over an 11 month period. Eight of the nine participants had
equal or better Miracle-Mineral-Supplement E and ADAScog scores at the end of the trial. Scores of
the ninth participant fell below the curve only in the last month [1]. All
participants had been taking anti-cholinergic drugs for one to three years
and were suffering a continuous decline in mental performance as would be
expected. The alpha-lipoic acid (ALA) abruptly arrested this decline.
ALA is a capable metal chelator of transition metals, and removes brain iron
in older laboratory animals which would make it a potential candidate for
chelation of aluminum: i.e. iron chelators often also chelate aluminum.
ALA is a potent anti-oxidant. It has been used as the antidote of choice for
mushroom poisoning, used for radiation poisoning, and for heavy metal and
chemical poisoning – the later at dosages of 300 to 600 mg/day.
These dosages appear to be relatively safe, with the only observed adverse
effect in the mushroom poisoning cases being hypoglycemia in some
individuals. Whether lower dosages may be equally effective for Alzheimer’s
therapy is not known. Scientists at the Linus Pauling Institute at Oregon
State University are working on estimates of proper dosage for the normal
aging process. ALA is available over-the-counter in drugstores in 50 or 100
mg tablets.
In old laboratory animals, combination of ALA with the micronutrient
acetyl-L-carnitine produced even better results in retarding aging of the
brain. Acetyl-L-carnitine supplements in the 1.5 to 3.0 g/day range have
been used as mono-therapies for Alzheimer’s therapy, but with only a
modest effect in slowing Alzheimer’s progression. ALC is also available
over-the-counter.
2. Aluminum Chelation
A University of Toronto program removed one third of the aluminum from
the brains of Alzheimer’s patients over two years, and slowed disease
progression by 50 percent as measured by living skills, assessed by an
independent review of video records of the patients over a period of time.
The most rapidly declining patients were benefited the most, suggesting that
the metal is a promoter of the disease. Pneumonia rates were dramatically
reduced by the therapy [2].
The injectable drug desferrioxamine was used at 1/20
th
the normal dose to
prevent toxicity. There is a need to find a non-injected chelator with less
toxicity. Several alternatives exist:
• Orally taken deferiprone has been approved by the European
Commission for control of iron overload in thalassemia, and could be
used for aluminum. Feralex-G is another possibly superior oral
option, and has been used with vitamin C to increase brain aluminum
removal from the nuclear matrix of brain cells.
• A British expert is attempting to use silicic acid (soluble silicon) in
mineral water as a therapy. Common European mineral waters often
contain high levels of soluble silicon, which will remove aluminum
from the brain over time.
• If alpha-lipoic acid proves to be an aluminum chelator which seems
likely, it would be an ideal choice: i.e. orally taken, readily available
at the drugstore, and with low toxicity.
• Peptide YY, the appetite hormone, has been used to reduce obesity
which is also a risk factor for Alzheimer’s. PYY powerfully reduced
brain aluminum in laboratory rats over a very short period of time. A
nasally administered version is being developed by Merck and
Nastech for control of obesity, and might be ideal for Alzheimer’s
chelation therapy.
• Magnesium D-aspartate combined with sodium L-glutamate reduced
brain aluminum in laboratory rats. They are available at the
drugstore, but dosage has not been established. Magnesium is
severely depleted in Alzheimer’s patients.
• Curcumin (constituent of turmeric and yellow curry and available at
the supermarket as turmeric) is likely to chelate brain aluminum
since it is effective in reducing iron in the brain of animals and has
been shown to bond with aluminum. But human testing is needed. It
also reverses brain tangles in laboratory animals.
Lithium at normal dosage and combined with anti-oxidant vitamins, can
provide some control of brain damage produced by aluminum, but this has
only been demonstrated in laboratory animals. Other items listed below,
including zinc, melatonin, and Ginkgo biloba will also reduce brain injury
from aluminum.



@Orion
 

Orion

Well-Known Member
Messages
879
@Orion Serine plays an important role in the catalytic function of many enzymes. It has been shown to occur in the active sites of chymotrypsin, trypsin, and many other enzymes. The so-called nerve gases and many substances used in insecticides have been shown to act by combining with a residue of serine in the active site of acetylcholine esterase, inhibiting the enzyme completely.


Aluminum is the metal which binds serine. I think also,

this could cause high acetylcholine symptomsin some people like POIS

Would supp'd serine help remove stored aluminum? I have high aluminum hairtest, and not sure, since I don't consume Al
 

Ingeno

Well-Known Member
Messages
394
1. Alpha-Lipoic Acid
This micro-nutrient available over-the-counter at drugstores may be a best
option for Alzheimer’s patients. A small study from Germany using 600
mg/day supplementation stabilized Alzheimer’s – i.e. halting disease
progression over an 11 month period. Eight of the nine participants had
equal or better Miracle-Mineral-Supplement E and ADAScog scores at the end of the trial. Scores of
the ninth participant fell below the curve only in the last month [1]. All
participants had been taking anti-cholinergic drugs for one to three years
and were suffering a continuous decline in mental performance as would be
expected. The alpha-lipoic acid (ALA) abruptly arrested this decline.
ALA is a capable metal chelator of transition metals, and removes brain iron
in older laboratory animals which would make it a potential candidate for
chelation of aluminum: i.e. iron chelators often also chelate aluminum.
ALA is a potent anti-oxidant. It has been used as the antidote of choice for
mushroom poisoning, used for radiation poisoning, and for heavy metal and
chemical poisoning – the later at dosages of 300 to 600 mg/day.
These dosages appear to be relatively safe, with the only observed adverse
effect in the mushroom poisoning cases being hypoglycemia in some
individuals. Whether lower dosages may be equally effective for Alzheimer’s
therapy is not known. Scientists at the Linus Pauling Institute at Oregon
State University are working on estimates of proper dosage for the normal
aging process. ALA is available over-the-counter in drugstores in 50 or 100
mg tablets.
In old laboratory animals, combination of ALA with the micronutrient
acetyl-L-carnitine produced even better results in retarding aging of the
brain. Acetyl-L-carnitine supplements in the 1.5 to 3.0 g/day range have
been used as mono-therapies for Alzheimer’s therapy, but with only a
modest effect in slowing Alzheimer’s progression. ALC is also available
over-the-counter.
2. Aluminum Chelation
A University of Toronto program removed one third of the aluminum from
the brains of Alzheimer’s patients over two years, and slowed disease
progression by 50 percent as measured by living skills, assessed by an
independent review of video records of the patients over a period of time.
The most rapidly declining patients were benefited the most, suggesting that
the metal is a promoter of the disease. Pneumonia rates were dramatically
reduced by the therapy [2].
The injectable drug desferrioxamine was used at 1/20
th
the normal dose to
prevent toxicity. There is a need to find a non-injected chelator with less
toxicity. Several alternatives exist:
• Orally taken deferiprone has been approved by the European
Commission for control of iron overload in thalassemia, and could be
used for aluminum. Feralex-G is another possibly superior oral
option, and has been used with vitamin C to increase brain aluminum
removal from the nuclear matrix of brain cells.
• A British expert is attempting to use silicic acid (soluble silicon) in
mineral water as a therapy. Common European mineral waters often
contain high levels of soluble silicon, which will remove aluminum
from the brain over time.
• If alpha-lipoic acid proves to be an aluminum chelator which seems
likely, it would be an ideal choice: i.e. orally taken, readily available
at the drugstore, and with low toxicity.
• Peptide YY, the appetite hormone, has been used to reduce obesity
which is also a risk factor for Alzheimer’s. PYY powerfully reduced
brain aluminum in laboratory rats over a very short period of time. A
nasally administered version is being developed by Merck and
Nastech for control of obesity, and might be ideal for Alzheimer’s
chelation therapy.
• Magnesium D-aspartate combined with sodium L-glutamate reduced
brain aluminum in laboratory rats. They are available at the
drugstore, but dosage has not been established. Magnesium is
severely depleted in Alzheimer’s patients.
• Curcumin (constituent of turmeric and yellow curry and available at
the supermarket as turmeric) is likely to chelate brain aluminum
since it is effective in reducing iron in the brain of animals and has
been shown to bond with aluminum. But human testing is needed. It
also reverses brain tangles in laboratory animals.
Lithium at normal dosage and combined with anti-oxidant vitamins, can
provide some control of brain damage produced by aluminum, but this has
only been demonstrated in laboratory animals. Other items listed below,
including zinc, melatonin, and Ginkgo biloba will also reduce brain injury
from aluminum.



@Orion
I've been using ALA and Acetyl-l-carnitine when rolling with mdma/amphetamines in the past to counter the oxidative stress induced by those drugs and causes the hangover to be more managable. Problem with regular ALA is the half-life, only 30 minutes or something. There are other versions of ALA with longer half-life and might be even better.
 

tanedout

Well-Known Member
Messages
538
Bit an update, I’ve been taking TUDCA which always helps when I get liver/bile issues really bad, and these things have got a lot worse over the last couple of years. I’m pretty sure these drugs (tane, fin etc) cause ‘drug induced cholestasis’

Drug-Induced Cholestatic Liver Disease - Madame Curie Bioscience Database - NCBI Bookshelf

Of note though, usually TUDCA or UDCA makes my hair go really dry brittle and comes out when drying or styling it (& that tends to make me stop taking it). If I take SAMe alongside however then it stops this, and my hair is actually very soft and healthy looking, so I’m guessing TUDCA does something which depletes SAMe?

Going to slowly increase the doses and see how it goes. Sweating again which always happens on Tudca
 

Helen

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Staff member
Messages
5,415
Bit an update, I’ve been taking TUDCA which always helps when I get liver/bile issues really bad, and these things have got a lot worse over the last couple of years. I’m pretty sure these drugs (tane, fin etc) cause ‘drug induced cholestasis’

Drug-Induced Cholestatic Liver Disease - Madame Curie Bioscience Database - NCBI Bookshelf

Of note though, usually TUDCA or UDCA makes my hair go really dry brittle and comes out when drying or styling it (& that tends to make me stop taking it). If I take SAMe alongside however then it stops this, and my hair is actually very soft and healthy looking, so I’m guessing TUDCA does something which depletes SAMe?

Going to slowly increase the doses and see how it goes. Sweating again which always happens on Tudca


yes, of course it does. This is what electrolytes protocol was all about. FIN impairs bile
 

Helen

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Staff member
Messages
5,415
Tudca is acidic. SamE increases adrenaline and decreases acidity you breathe faster, since SamE increases adrenaline. and fat metabolism

More adrenaline , less cortisol needed, better for the hair , no need to break down hair for protein.
 

Admiral

Well-Known Member
Messages
955
Bit an update, I’ve been taking TUDCA which always helps when I get liver/bile issues really bad, and these things have got a lot worse over the last couple of years. I’m pretty sure these drugs (tane, fin etc) cause ‘drug induced cholestasis’

Drug-Induced Cholestatic Liver Disease - Madame Curie Bioscience Database - NCBI Bookshelf

Of note though, usually TUDCA or UDCA makes my hair go really dry brittle and comes out when drying or styling it (& that tends to make me stop taking it). If I take SAMe alongside however then it stops this, and my hair is actually very soft and healthy looking, so I’m guessing TUDCA does something which depletes SAMe?

Going to slowly increase the doses and see how it goes. Sweating again which always happens on Tudca

I'm focussing more on the liver now and bought me some TUDCA. What's the reason you take SAMe along with it other than hair benefits?
 

tanedout

Well-Known Member
Messages
538
I'm focussing more on the liver now and bought me some TUDCA. What's the reason you take SAMe along with it other than hair benefits?

Couple of reasons., firstly there is that accurate study that showed that taking SAMe alongside isotretinoin seemed to mitigate the side effects, and may help with the side effects once you've got them. Also Helen found a number of PFS bloods that showed people who had SAM levels tested were all very low.

Also it stops the TUDCA causing dry and brittle hair. Only issue is you're supposed to take it with co-factors B6, B12 and methylfolate, however I do really badly on methylfolate so currently I'm actually taking just TUDCA and Tribulus. I think for the liver tribulus is amazing - it's extremely bitter if you get good stuff (always open the capsule and taste, so brands I've had are a waste of time).

I'm also taking mastic gum and that seems to be helping with stomach issues - I've possibly got/had h.pylori, and mastic gum is supposed to be effective at killing it.

Overall doing much better than I have been for months. TBH I think the tribulus is a big factor. Bile flow has clearly been seriously impaired, and that's allowed bad bacteria to take hold in the gut and things go from bad to worse then. So focusing on getting the liver/bile going, and also tackling the bad gut bacteria. Food intolerances are much improved already

Edit: SAMe in itself has loads of benefits for the liver, so it's not hard to imagine why having low SAM is going to mean impaired liver function;

The evidence is definitely in. SAMe (S-adenosylmethionine) is serious medicine against liver disease. Almost a thousand published studies document the ability of this bioactive form of methionine to prevent and treat liver disorders, including cancer.

SAMe.gif

SAMe, the amazing "super-nutrient," can single-handedly normalize liver function. How? SAMe is the central player in liver biochemistry. It does two crucial things: It methylates, and it transforms itself into the liver's most vital substance, glutathione.

The liver contains the third highest amount of SAMe in the body, after the adrenal and pineal glands. SAMe is so important for liver function that it can be considered an essential nutrient for that organ. In addition to its many other functions, SAMe plays a leading role in liver regeneration. The liver has special SAMe enzymes just for regenerating tissue.

Loads of good info here

The Liver Super-Nutrient | Life Extension
 
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Goose12

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Messages
648
Couple of reasons., firstly there is that accurate study that showed that taking SAMe alongside isotretinoin seemed to mitigate the side effects, and may help with the side effects once you've got them. Also Helen found a number of PFS bloods that showed people who had SAM levels tested were all very low.

Also it stops the TUDCA causing dry and brittle hair. Only issue is you're supposed to take it with co-factors B6, B12 and methylfolate, however I do really badly on methylfolate so currently I'm actually taking just TUDCA and Tribulus. I think for the liver tribulus is amazing - it's extremely bitter if you get good stuff (always open the capsule and taste, so brands I've had are a waste of time).

I'm also taking mastic gum and that seems to be helping with stomach issues - I've possibly got/had h.pylori, and mastic gum is supposed to be effective at killing it.

Overall doing much better than I have been for months. TBH I think the tribulus is a big factor. Bile flow has clearly been seriously impaired, and that's allowed bad bacteria to take hold in the gut and things go from bad to worse then. So focusing on getting the liver/bile going, and also tackling the bad gut bacteria. Food intolerances are much improved already

Edit: SAMe in itself has loads of benefits for the liver, so it's not hard to imagine why having low SAM is going to mean impaired liver function;



Loads of good info here

The Liver Super-Nutrient | Life Extension
Nice info. The liver plays a huge role in this. At least in my situation.
 

tanedout

Well-Known Member
Messages
538
Couple of recent observations;

Tried a week of eating tofu, soya milk etc. Didn't notice anything at all from it. I know some people say they immediately get a benefit, but I got nothing. Maybe didn't eat enough.

Also stopped taking daily tribulus 2 days ago, and getting bad anxiety, but slight increase in libido. Previously in the past I did get a good rebound from trib, so interested to see if this increases. Get the feeling potassium was lowered too, but took some potassium chloride earlier, and feel better for it (lowered anxiety)

Not sure what this suggests really, but I wonder if I should cycle trib. Seem to always get noticeable benefits from it. The other thing that always helps with libido is grape seed extract. Always get a noticeable gain from that
 

Helen

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5,415
@tanedout we know that retinoic acid acts on RXR and RAR. receptors


usually retinoic acid is what increases ceruloplasmin .


So it goes like this, potassium and thyroid. ask for cortisol, this increases ACTH. so make cortisol more sensitive and take pressure off it it, body rises zinc.


as zinc rises this increases retinol binding protein and retinol comes out of the liver, then it gets transformed by adh aldh into retinoic acid, which increases ceruloplasmin and copper come out of the liver together with iron. ceruloplasmin helps to transport iron out of the liver.



So now if you feed retinoic acid. which is the end of this scenario, you might downregulate the receptor. PXR and RAR

and then you quit. and you have no retinoic acid action, and basically no ceruloplasmin action and no iron oxidation, and iron toxicity.
 

Helen

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Also of course the second variant is retinoic acid toxicity , if it really can be stored.
 

tanedout

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Messages
538
I’m going to push my doc to get iron tested. I’ve asked before and got declined, but i’ll keep trying!