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

tanedout

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Just got some bloods back which were done last week when I was feeling really shit and stopped TEI

- Liver enzymes - all in range
- Electrolytes - all ok - potassium on the low side as usual (4 [range 3.5-5.5])
- Ferritin - high - 499 (range 10-322)
- White blood cell count - low (not sure of the value)

These things seem to be in-line with previous tests I've had really. I'm assuming the high ferritin is due to inflammation, and I've read supplementing with MSM brings this down, so I may start on this and re-test. Also remember Helen talking about ferritin, so I'll search this board for more info too.
 

tanedout

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Bit of an update - still off the TEI sups. Focusing on gut and liver. Seem to have bad histamine issues causing my nose to run when eating, and this is probably resulting in leaky gut, which potentially is down to mast cell activation in the gut releasing a load of histamine. As a result, current stack;

- TUDCA - this definitely helps me a lot. Reduced pain/discomfort in the liver/GB area. Obviously helps with bile flow.
- MSM - to reduce inflammation, help with phase 2 liver detox. Some sulfur for toxins to bind to.
- Glutathione (sublingual) - I know it's poorly absorbed, but had it anyway. Will add NAC at some point as per suggestion from below article.
- Quercetin - just started, supposed to reduce histamine response, and help heal leaky gut as a result. Also increases glutathione levels.

Great, and very detailed article on leaky gut here from someone who seemingly understands the condition, and isn't just linking to supplements;

Digestive System: Leaky Gut Syndromes: Breaking the Vicious Cycle

(5) Glutathione (GSH) is an important component of the anti-oxidant defense against free radical-induced tissue damage. Dietary glutathione is not well absorbed, so that considerable quantities may be found throughout the gut lumen following supplementation[144]. Hepatic GSH is a key substrate for reducing toxic oxygen metabolites and oxidized xenobiotics in the liver. Depletion of hepatic glutathione is a common occurence in Leaky Gut Syndromes contributing to liver dysfunction and liver necrosis among alcoholics and immune impairment in patients with AIDS. The most effective way to raise hepatic glutathione is to administer its dietary precursors, cysteine or methionine. Anti-oxidant supplementation for Leaky Gut Syndromes should therefore include both GSH and N-acetyl cysteine. Because protozoa are more sensitive to oxidant stress than are humans and because most anti-parasitic drugs and herbs work by oxidative mechanisms, high dose anti-oxidant supplementation should be witheld during the treatment of protozoan infection, especially during treatment with Artemisia.

(6) Flavonoids are potent, phenolic anti-oxidants and enzyme inhibitors with varied effects depending on the tissues in which they act. Quercetin and related flavonoids inhibit the release of histamine and inflammatory mediators. Taken before eating, they may block allergic reactions which increase permeability. Catechins have been used in Europe to treat gastric ulcerations. The flavonoids in milk thistle (silymarin) and in dandelion root (taraxacum) protect the liver against reactive oxygen species[145].
 

tanedout

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Reading up on Carnitine (with it having been discussed a bit recently) and the following is fairly interesting (bearing in mind that study on how SAMe potentially mitigated the effects of isotretinoin - potential deficiency for people with accutane sides, PFS etc). It seems SAMe is a pre-cursor to Carnitine

Carnitine exists in the body in two forms, either L-carnitine or the acetylated form known as Acetyl-L-Carnitine (ALCAR).[7] The synthesis of these molecules can occur endogenously from the two dietary amino acids L-methionine and lysine, where a peptide-bound lysine is converted to e-N-trimethyllysinevia donation of S-adenosylmethionine

L-Carnitine: Scientific review on benefits weight loss/fat burning, side effects, and more

So maybe this is a factor in messed up fatty acid metabolism. Also worth noting is that in that '8 tips to cure accutane sides' video on youtube, the guy used MSM (a similar form of methionine much like SAMe) to cure his sides (along with choline and some other stuff).

From tomorrow I'm going to start on actyle l-carnitine and see how it goes. I'm taking it alongside sunflower lecithin (good source of choline, and supposed to help fatty liver)
 

Helen

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to make carnitine you need to methylate lysine )) I wrote all of this to ORION,

you need to recyle methionine with methione synthase, and b12 should recycled with methionine synthase reductase

and of course folate cycle needs to be working


Also you need to understand that minerals should be working for this. to fix the metabolism

since the minute you stop SAME or carnitine you go back
 

Helen

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Also you need to understand that carnitine creates free radicals, thus it is made with glutathione components.

thus it could be taken with ALA.


To make androgens work, body has to have lipid to make membranes.



if body does not have lipid metabolism, it has to use cortisol to break down protein, and use protein as source of energy,

and this uses up manganese zinc citruline arginine. and creates ammonia. causing symptoms


if you fix fat metabolism , cortisol will fall, and there will be lipid membranes,

and also body will be able to work on fats. and this will allow instead of breaking down the body with cortisol, BUILD the body with androgens.



this is the reason for not working androgens.


and the problem in fat metabolism could be in any part of either adrenaline pathway, ( methylation, copper, vitamin C, ) zinc iron, depending on the person

carnitine synthesis( methylation and all the systems above, which also needs zinc, methylation of lysine, iron, vitamin B6)) , or NAD and b2 synthesis which do the beta oxidation.( burn the fats)



with differnt people the problem lays in different things.
 
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Helen

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look at Carnitine - Wikipedia

Beta oxidation - Wikipedia

and adrenaline pathway, and methylation to make adrenaline so you can get to FATS so you break them down.



plus you have to restore what you have spent detoxing ammonia since cortisol was the only fuel source

biotin, arginine, citrulin, manganese zinc.


plus methylation.
 

Helen

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TEI gives a better program IMO


it will take at least 6 months, on any of your trials.
 

tanedout

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Thanks @Helen Decided I'm actually going to start on SAMe tomorrow instead of carnitine, and I'll report back if I notice anything after a couple of weeks.

Reading some more on SAM-e and a few more things that tie in here. Apparently SAM-e is converted into glutathione in the liver, and as you posted recently, PFS people who have had glutathione tested have very low levels. Mutliple studies referred to in the below article show supplementing with SAM-e increases glutathione significantly

16 patients with liver disease (both alcoholic and non-alcoholic) were given 1,200 mg of oral SAMe per day for six months. Liver biopsies showed a significant increase in glutathione,

The Liver Super-Nutrient | Life Extension

Even more of interest is that studies show SAM-e is very effective for treating cholestasis and bilery obstruction. Issues with bile flow, and intermittently blocked bile ducts is a major issue for me right now (why I had to stop TEI), so if this helps it'll be great, and hopefully I can get back onto TEI then!
 

Helen

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yes, but if you dont recycle homocysteine, what is SAME going to do, create more homocysteine and keep atherosclerosis going?

you need to cycle homocysteine further into methionine or into CBS pathway with magnesium b6 into cysteine

or SAME will be broken down by GNMT not to create more homocysteine

remember all those test that I posted. they have high homocysteine


the problem is either with methionine synthase or methionine synthase reductase. IMO OR with SERINE, b6 magnesium for CBS pathway, if you have low cysteine

and low cysteine will cause low androgen binding. cortisol binding. etc

this is why Orion was doing great on vitamin b2. since methionine synthase reductase which recycled vitamin b12 is FAD enzyme

and then recycled b12 turns methionine synthase and lowers homocysteine.

and SAME starts going up and not being broken down by GNMT
 
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Helen

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So as you see it has to be all supported together, that is why I posted methylation protocol to get rid of methylation block
 

Helen

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I would test your cysteine, and see if homocysteine is high since it does not go into cysteine.

or just test cysteine. take some and see if you feel androgens right away like within days,

then you know you wil have to work on magnesium b6 serine pathway.

if cysteine is not going to do anything for you

then it is the methionine synthase or methionine synthase reductase problems.( b2, iron )) NADPH
 

tanedout

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yes, but if you dont recycle homocysteine, what is SAME going to do, create more homocysteine and keep atherosclerosis going?

you need to cycle homocysteine further into methionine or into CBS pathway with magnesium b6 into cysteine

or SAME will be broken down by GNMT not to create more homocysteine

remember all those test that I posted. they have high homocysteine


the problem is either with methionine synthase or methionine synthase reductase. IMO OR with SERINE, b6 magnesium for CBS pathway, if you have low cysteine

and low cysteine will cause low androgen binding. cortisol binding. etc

this is why Orion was doing great on vitamin b2. since methionine synthase reductase which recycled vitamin b12 is FAD enzyme

and then recycled b12 turns methionine synthase and lowers homocysteine.

and SAME starts going up and not being broken down by GNMT

So making taking along with magnesium and b6? I'm a bit confused by the SAH-SAM cycle, this seems to suggest that enough SAMe would actually result in the homocysteine being converted (ie reduced) if there is enough SAMe?

Methyl deficiency causes a reduction in SAMe levels, and an elevation in S-adenosylmethionine homocysteine (SAH). SAH is what's left over after SAMe donates a methyl group for biochemical reactions. An enzyme, SAH hydrolase, turns SAH into homocysteine. Homocysteine can be toxic if it builds up within the body, but is converted into cysteine (and eventually glutathione) if enough SAMe is present.

If SAMe is super-deficient, nothing gets converted, and SAH and homocysteine back up like a clogged drain. This is when cancer gets its toehold. A low SAMe-to-SAH ratio is step-one in the development of liver cancer. Maintaining SAMe can reverse the early changes in the process.

The Liver Super-Nutrient | Life Extension
 

Helen

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I thought SaME converts methionine into homocysteine.

and then homocysteine is converted either to cystein with serine, magnesium b6

or back to methionine with methionine synthase with b12. which recycled by FAD enzyme methionine synthase reductase,

and then this makes tetrafolate from methylfolate .


and this converts histidine into glutamic acid and glutamate. and further to gaba


so lets say if you dont have b6, then converts from glutamate to gaba stops.

and homocysteine is high . as an example, and tetra folate stops not to create too much glutamate.


You see how it is all connected
 

Helen

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SaME iself is a cofactor to make adrenaline, from noradrenaline. dont forget.
 

Helen

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by the way methionine synthase also could be copper enzyme. but homocysteine conversion is activated by zinc.
 

tanedout

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Currently been taking SAMe (along with co-factors B6, B12 and methylfolate in the form of an active b-complex). I'm just building up the dosage, but even at small doses I've noticed I'm starting to sweat a bit again (usually takes TUDCA or UDCA to get me sweating again), and I've noticed improved sense of smell and vision.

Going to keep slowly increasing the dosage and stick with it for a while. Keep reading loads of interesting stuff about SAMe, and the fact that study showed taking it alongside isotretinion mitigated side effects makes me think it could be quite beneficial.

S -Adenosyl- l -methionine: its role in the treatment of liver disorders
 

Orion

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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).