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21 hours ago, Relentless1k said:On 19 January 2016 at 8:41 AM, trantran83333 said:"I just ordered parasite and anti fungal cleanse from Humaworm. I heard it's great from one of the threads I been following, It's herbal and also read that they can't become immune to herbal remedies "Cant actually post for some reason without using this quote mechanism so:
Again do you actually have stool testing done to prove you have said issues. And no herbals will not beat prescription ones. Antibiotics and such are natural even tho its pharma too, at least some of them. Herbs are great in general and as an add on. Also if you are looking for ways to deal with biofilms you prob can just buy enzymes for it cheaper than the cleanses.Its great that you try stuff but get diagnosed first with testing and then try out ways. Now you wont ever know if you had it in the first place and then you cant really know if you got rid of it either. Its like shooting in the dark and you dont know if there is a target or not.
- Relentless1k
Ok I will make an effort to go get my condition clinically tested by another doctor to be 100% sure. To be honest I was a little sceptical with kinesiology. I have never heard of it but apparently it is widely practiced in Australia with chiropractors as such.
I also read somewhere that you can also get colloidal silver IV's for chronic candida infections. Haven't looked into that much.
As for smoking, I started because of the depression. I hate it I want to quit, but easier said than done. Tried two times to go cold turkey, but one time with bad migraine that lasted all day, and second time I was just real tired all day. Might have to fork out another $200 for a hypnotherapy session. A work colleague of mine did it and succeeded. She was a heavy smoker for 40yrs and quit with no side effects nothing.
Would be nice if Roche would pay for all my expenses, yeah rite!
Which digestive enzymes were you talking about specifically? I do have a bottle of it here along with ox bile.
thanks relentless1k
41 minutes ago, Modeaa said:guitar man,-
http://lib.dr.iastate.edu/cgi/viewcontent.cgi?article=4063&context=etd
mentioned in this forum before. i think there is some mass of people who used it on this forum, strangely i haven't create a big buz.
does it just treat the symptoms or cure,,, not saying symptoms management is not importent for preventing more deterioration...
''Supplemental SAM partially prevents increased GNMT activity due to 13CRA treatment''
Very nice this is actually SAM-E they are talking about. this could be a big part of the equation that we are looking into right now. Thanks for the help. This is a very good research paper. says whole brain serotonin levels were decreased by 46% in rats receiving ATRA, an effect that was partially attenuated by oral SAM. 46 percent!!! thats nice to know
37 minutes ago, trantran83333 said:Ok I will make an effort to go get my condition clinically tested by another doctor to be 100% sure. To be honest I was a little sceptical with kinesiology. I have never heard of it but apparently it is widely practiced in Australia with chiropractors as such.
I also read somewhere that you can also get colloidal silver IV's for chronic candida infections. Haven't looked into that much.
As for smoking, I started because of the depression. I hate it I want to quit, but easier said than done. Tried two times to go cold turkey, but one time with bad migraine that lasted all day, and second time I was just real tired all day. Might have to fork out another $200 for a hypnotherapy session. A work colleague of mine did it and succeeded. She was a heavy smoker for 40yrs and quit with no side effects nothing.
Would be nice if Roche would pay for all my expenses, yeah rite!Which digestive enzymes were you talking about specifically? I do have a bottle of it here along with ox bile.
thanks relentless1k
here are some legit medical test. that could maybe diagnose bacterial overgrowth if you decide to get any of these done
http://www.mayoclinic.org/diseases-conditions/blind-loop-syndrome/basics/tests-diagnosis/con-20024503
Colloidal silver yea dont look into that. not safe. look up blue man. thats what it did to him.
18 hours ago, tryingtohelp2014 said:by adding lots of SAM-E. today i went to get a serum b-12/homocysteine/full cbc panel and a methylmalonic lab test done.
Could you go get a plasma methionine test done as well? Be aware, you have to water fast for at least 12 hours when checking amino acids so it's accurate. Keep us updated with results!
If homocysteine is low but methionine is also low, it indicates total sulfur depletion in the body. To cure this eat plenty of garlic, ginger, onions, brassica veggies, or eggs daily for over a month.
I hope you got the homocysteine drawn correctly. It's not accurate in most cases if they don't do it absolutely perfectly. Russell Jaffe has a great method where he uses an advanced cell preservative anti-coagulant that prevents leakage out of the RBCs into the plasma (which would falsely elevate the result).
Here he goes into more detail about methylhomocysteine (methionine) & homocysteine:
https://www.holisticprimarycare.net/topics/topics-o-z/prevention-practice-pearls/1587-homocysteine-rethinking-a-predictive-biomarker.html
"Homocysteine deserves to be a routine measurement in any primary care practice. Until now, however, it has been limited by an important pre-analytic variable: if proper cell preservatives are not used in the testing process, homocysteine may leak out of dead red cells into the plasma, giving a false increase in plasma levels that does not really reflect the patient's actual inflammation status.
Better labs require that specimens be processed within 30 minutes of drawing blood in order to return an accurate assessment of actual plasma levels. In practice, this has limited the utility of the test.
In the near future, look for emergence of high sensitivity homocysteine (hsHCY) tests that use better cell preservatives thus providing a more precise, accurate and predictive homocysteine measurement, with less variance at the important low end of the range"
--
EDIT: thought this was interesting:
"In many clinicians' minds, homocysteine is strongly linked with cardiovascular disease. Fewer are aware that this biomarker is predictive of many other things. It reflects the functional status of bone and retinal tissue, as well as the ears. It is also indicative of a host of autoimmune conditions"
Most people with chronic fatigue syndrome (PWCs), but not all, are found to have values of GSH that are below the reference range*. This means that they are suffering from glutathione depletion. As they undergo treatment to lift the partial methylation cycle block, this value usually rises into the normal range over a period of a few months. I believe that this is very important, because
glutathione normally participates in the intracellular metabolism of vitamin B12, and if it is low, a functional deficiency of vitamin B12 results, and insufficient methylcobalamin is produced to support methionine synthase in the methylation cycle. In my view, this is the mechanism that causes the onset of ME/CFS. This functional deficiency is not detected in a conventional serum B12 test, but will produce elevated methylmalonate in a urine organic acids test. In my opinion, many of the abnormalities and symptoms in ME/CFS can be traced directly to glutathione depletion.
SO GIVE TREATMENT A COUPLE MONTHS!!!
SAMe therapy resulted in a significant increase of hepatic glutathione levels both in patients with alcoholic and in those with non-alcoholic liver diseases as compared with placebo-treated patients. SAMe may therefore exert an important role in reversing hepatic glutathione depletion in patients with liver disease.
---retinoid-induced elevations in enzyme activity were reflected in the abundance of GNMT protein. To our knowledge, this is the first report of a nutritional compound that induces GNMT activity at the transcriptional and/or translational level.
Earlier work demonstrated that increased methionine catabolism by dietary CRA resulted in a significant increase in hepatic taurine concentrations that was achieved in part at the expense of reduced inorganic sulfate excretion and diminished hepatic glutathione levels (10,29). according to this Taurine equals bad, no good for us
was looking back at my folic acid test and my score was a bit above normal 22 ng/ml
ive seen reference ranges from 2-10,2-17, and 2-20.
not sure if this is significant at all, but according to Rich he says:
High values, especially in the presence of low values for THF, may be associated with inability to convert folic acid into reduced folate readily, such as because of a genetic polymorphism in the DHFR enzyme. They may also be due to high supplementation of folic acid.
I was not supplementing at the time and rarely eat cereal
3 hours ago, guitarman01 said:Earlier work demonstrated that increased methionine catabolism by dietary CRA resulted in a significant increase in hepatic taurine concentrations that was achieved in part at the expense of reduced inorganic sulfate excretion and diminished hepatic glutathione levels (10,29). according to this Taurine equals bad, no good for us
no thats not what it means... it means or liver was mobilizing and creating taurine at the expense of other sulfur metabolites i.e. GSH... to get rid of the accutane metabolites. GSH doesnt attach to retinoic acid for excretion. taurine does, forming retinol taurate ... thought to be the inactive form ready for excretion. The liver was putting it there for a reason. to get rid of the insult.
"There was a significant correlation between the level of urinary taurine and the level of serum AST for individual animals given a hepatotoxic dose of CCl4 (2 ml.kg-1). The data presented suggest that: i) taurine is produced by the liver in response to a toxic insult and subsequent leakage from damaged cells leads to increased levels in the urine; ii) the urinary taurine level may be a useful non-invasive marker of liver damage.
Taurine : A possible urinary marker of liver damage. A study of taurine excretion on carbon tetrachloride-treated rats. "
https://www.researchgate.net/publication/21469654_Taurine_A_possible_urinary_marker_of_liver_damage_A_study_of_taurine_excretion_on_carbon_tetrachloride-treated_rats [accessed Jan 24, 2016].
and
finally also mentions the 4-oxo metabolite being recycled over and over. also shows why zinc and iron play a role. Iron and b-12 connection?
SAM-E (methionine, for GSH repletion, donor for cysteine and taurine and for the GAG glucuronic acid)
Taurine
b6 for one methylation pathway
b12 for another methylation pathway
folic acid im not too sure about... i think we need to fix other things first to get the process going and not get "trapped"
TMG same thing... i personally think we need the glycine on one hand, and on another it could be stripping any excess methionine we put in, that we might be needing. but TMG also turns the homocysteine from the SAM-e back into methionine. its also used in the patent , and also helpful for liver function.
then you get into a whole bunch of fix one thing, another needs to be supported... i.e. if we are b12 deficient (only the methylmalonic and serum b12 test can confirm) if you start supplementing b12...you could really deplete potassium.
but first things first.... if more people can get tested for methionine, b-12 folate, homocysteine, methylmalonic acid, and share your results on here (please upload scans taking names off of course.) i think we can find out why some of us have these long term problems, and others dont.
small anecdote... for the last two days i would wake up and take a SAM-e 400mg on an empty stomach... about an hour later, i would have a monster zero energy drink (contains taurine b6 b12) with breakfast... then a few hours later, another 400mg SAM-e before lunch. and i would have ridiculous energy for the rest of the day. completed things i put off for months. ive had monster energy drinks before by themselves, and havent felt this. could be a combination effect?
this is what i worry about with taking that cyclo... releasing all of the stored stuff.... side effects sound familiar???? hey modeaa... theres your capillary leakage
http://www.medical-hypotheses.com/article/S0306-9877(13)00393-9/abstract
Dengue hemorrhagic fever (DHF) is the most significant mosquito-borne viral disease worldwide in terms of illness, mortality and economic cost, but the pathogenesis of DHF is not well understood and there is no specific treatment or vaccine. Based on evidence of liver involvement, it is proposed that dengue virus and retinoids interact to cause cholestatic liver damage, resulting in the spillage of stored retinoids into the circulation and in an endogenous form of hypervitaminosisis A manifested by the signs and symptoms of the disease, including: fever, severe joint and bone pain, capillary leakage, thrombocytopenia, headache, and gastrointestinal symptoms. While retinoids in low concentration are essential for numerous biological functions, they are prooxidant, cytotoxic, mutagenic and teratogenic in higher concentration, especially when unbound to protein, and an endogenous form of vitamin A intoxication is recognized in cholestasis. The model tentatively explains the observations that 1) repeat infections are more severe than initial dengue virus infections; 2) the incidence of denue has increased dramatically worldwide in recent decades; 3) DHF is less prevalent in people of African ancestry than those of other racial backgrounds; and 4) infants are protected from dengue. The retinoid toxicity hypothesis of DHF predicts the co-existence of low serum concentrations of retinol coupled with high concentrations of retinoic acid and an increased percentage of retinyl esters to total vitamin A. Subject to such tests, it may be possible to treat DHF effectively using drugs that target the metabolism and expression of retinoids.
So it seems its highly likely that isotretinoin has resulted in signifiant elevation in GNMT activity for us which leads to a loss of methyl groups vital for many SAM-dependent transmethylation reactions (messing up SAMe : SAH ratios), and likely resulting in our side effects. The following study concluding;
- Both CRA [i.e. Accutane] and ATRA significantly elevated the activity of GNMT 74 and 124%, respectively, compared with controls.
http://jn.nutrition.org/content/132/3/365.full
So then you would assume looking for ways to reverse this would be, in simple terms, to reduce/decrease GNMT activity, to move things back in the right direction. The following study is aimed at studying the effects of reduced GNMT activity, but in it there are some interesting pieces of information in the study, namely;
- GNMT was downregulated in the liver tissues from patients suffering with NAFLD [Non-alcoholic Fatty Liver Disease]as well as from mice fed a high-fat diet, high-cholesterol diet or methionine/choline-deficient diet.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356423/
So that would seem to suggest we potentially want to avoid methane and choline, and eat a high fat high/cholesterol diet to reduce GNMT activity from its currently elovated state?!
Also in another study (this is on diabetic rats, so I dont how relevant this is) has some interesting points about GNMT activity;
- folate deficiency resulted in the greatest elevation in GNMT activity. The elevation is likely due to a lack of folate which would otherwise impose postranslational inhibition of GNMT
The study also advises that folate binds to GNMT, so excess GNMT may result in too little folate as a result as its all binding to the GNMT enzyme and hence unavailable for other things? The study suggests that in their tests supplemental folate did not reduce GNMT, but they suggest that higher amounts might do.
[Edited link out]
So again that last study was on diabetic rates, but in conclusion maybe a high fat, high cholesterol diet with supplemental [active] folate (in a fairly high dosage) and avoiding methionine and choline might result in some benefits?!..
8 minutes ago, Accutainted4ever said:tryingtohelp2014, is there any particular reason why you havenot replied to the PM I sent you a few weeks backasking the simple question whether or notyou think we should be supplementing vitamin K2?
i dont know. i think vitamin D and K2 could be dangerous without fixing the underlying problem! we know for a fact accutane causes excess calcium in serum. this causes the bone spurs etc. if you add vitamin D or k2... you could exacerbate the problem by causing more calcium to be deposited.
again... anything that doesnt have anything to do with excretion of retinoic acid or its metabolites....probably wont do anything for us. at best will mask symptoms, at worst, fuck your liver up really bad. there was a lady named patti lodes who took vitamin D i think, and she got really messed up.
if we could just start with a clean slate, everything else would fix itself in short order.
3 minutes ago, tryingtohelp2014 said:i dont know. i think vitamin D and K2 could be dangerous without fixing the underlying problem! we know for a fact accutane causes excess calcium in serum. this causes the bone spurs etc. if you add vitamin D or k2... you could exacerbate the problem by causing more calcium to be deposited.
Ok thanks good point, but do you think this would apply to someone who has been off Accutane for as long as 20 years? Would someone who has been off Accutanefor this long also have high serum calcium?
Should foods high in retinol, such as liver also be avoided by people who have been off Accutane for many years?
On 1/25/2016 at 3:44 AM, tanedout said:So it seems its highly likely that isotretinoin has resulted in signifiant elevation in GNMT activity for us which leads to a loss of methyl groups vital for many SAM-dependent transmethylation reactions (messing up SAMe : SAH ratios), and likely resulting in our side effects. The following study concluding;
- Both CRA [i.e. Accutane] and ATRA significantly elevated the activity of GNMT 74 and 124%, respectively, compared with controls.
http://jn.nutrition.org/content/132/3/365.full
So then you would assume looking for ways to reverse this would be, in simple terms, to reduce/decrease GNMT activity, to move things back in the right direction. The following study is aimed at studying the effects of reduced GNMT activity, but in it there are some interesting pieces of information in the study, namely;
- GNMT was downregulated in the liver tissues from patients suffering with NAFLD [Non-alcoholic Fatty Liver Disease]as well as from mice fed a high-fat diet, high-cholesterol diet or methionine/choline-deficient diet.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356423/
So that would seem to suggest we potentially want to avoid methane and choline, and eat a high fat high/cholesterol diet to reduce GNMT activity from its currently elovated state?!
Also in another study (this is on diabetic rats, so I dont how relevant this is) has some interesting points about GNMT activity;
- folate deficiency resulted in the greatest elevation in GNMT activity. The elevation is likely due to a lack of folate which would otherwise impose postranslational inhibition of GNMT
The study also advises that folate binds to GNMT, so excess GNMT may result in too little folate as a result as its all binding to the GNMT enzyme and hence unavailable for other things? The study suggests that in their tests supplemental folate did not reduce GNMT, but they suggest that higher amounts might do.
[Edited link out]
So again that last study was on diabetic rates, but in conclusion maybe a high fat, high cholesterol diet with supplemental [active] folate (in a fairly high dosage) and avoiding methionine and choline might result in some benefits?!..
i know what youre saying... GNMT is there for a reason in your body... and that reason is to get rid of excess methionine... to keep a homeostasis of sorts. In a normal person... when you dont eat methionine, of course you wouldnt need the GNMT to be elevated! but thats not our problem! theres a HUGE difference.
we took something that caused the GNMT to be upregulated, and stay upregulated, regardless of methionine levels! DEPLETING METHIONINE! (but now , we might be a level below even this... adequate methionine, but cant convert it due to liver dysfunction) avoiding methionine wont make us better, it would make us waste away. it wont shut off GNMT by itself as long as theres something inside of us causing it to be screwed up. it would produce all of our side effects.
if taking deplin was the answer, this would be extremely easy to fix no problem. its not.
1. deplin/folate would not bind or excrete whats causing the elevated GNMT in the first place
2. folate/deplin wouldnt correct the deficiency of the sulfur metabolites caused by accutane. i.e. folate cannot form cysteine
3. elevated GNMT in and of itself doesnt account for our problems. it causes our symptoms indirectly. its the deficiencies that cause our symptoms directly!
even rich himself said (hes dead now by the way) for some reason it didnt work... he suggested a polymorphism.
18 minutes ago, Accutainted4ever said:Ok thanks good point, but do you think this would apply to someone who has been off Accutane for as long as 20 years? Would someone who has been off Accutanefor this long also have high serum calcium?
Should foods high in retinol, such as liver also be avoided by people who have been off Accutane for many years?
We need to find a study where GNMT stays elevated post TANE. I know Rich commented on this and said it was elevated in one case even years post Accutane. But I would like to see an actual study. I think we have a few good leads here anyways to follow up on. One thing at a time. Ive taken high dose vitamin D 25kiu for a bit i believe? didnt mess me up but dont believe it was help treating the cause.
If we really have a methylation problem we should be looking at that and that alone atm. Not to throw in too many varibles.
6 minutes ago, tryingtohelp2014 said:even rich himself said (hes dead now by the way) for some reason it didnt work... he suggested a polymorphism.
he went on to say though he thought a higher dose might work he just didnt know how high
I would think taking a dose comparable to deplin could be a backup plan or something to at least try down the road if other things ie( high dose sam-e) fail to work. especially if noone has even come close to trying this.
Or we get some of those blood test he recommended and put this theory to bed.
but it would be cheaper this to try high dose folate/plan b
17 minutes ago, Accutainted4ever said:Ok thanks good point, but do you think this would apply to someone who has been off Accutane for as long as 20 years? Would someone who has been off Accutanefor this long also have high serum calcium?
Should foods high in retinol, such as liver also be avoided by people who have been off Accutane for many years?
ive been off of it 20 years as well.
are your joints getting worse? is the tightness of the ligaments or tendons getting better? if anything is getting worse... i would avoid anything that could add to the problem. i just dont see a benefit of eating liver.
its funny they dont even know why accutane upregulates GNMT.
remember our body has GNMT enzymes in places other than the liver (the pancreas) that dont get upregulated during or post accutane treatment. only the liver one does. this would make sense...as everything is takingplace in the liver.
I just had a revelation.....
isnt this a simple theory------> we take accutane------> our body mobilizes methionine to produce taurine, to the liver to get rid of the insult -------> our body senses the elevated methionine levels in the liver, not knowing why -------> thus upregulating GNMT in the liver to get rid of the excessive methionine-------> causing our bodies to get rid of the very co-factor needed to excreteaccutane from the liver! ----> causing a vicious loop
if this theory is right..... only taking massive amounts of methionine (SAM-E) and or taurine, to overwhelm our bodies own defensive elevated GNMT , to get at the stored metabolites in the liver and conjugate them out.
makes sense.
On 1/25/2016 at 4:05 AM, tryingtohelp2014 said:we took something that caused the GNMT to be upregulated, and stay upregulated, regardless of methionine levels! DEPLETING METHIONINE! (but now , we might be a level below even this... adequate methionine, but cant convert it due to liver dysfunction) avoiding methionine wont make us better, it would make us waste away. it wont shut off GNMT by itself as long as theres something inside of us causing it to be screwed up. it would produce all of our side effects.
if taking deplin was the answer, this would be extremely easy to fix no problem. its not.
1. deplin/folate would not bind or excrete whats causing the elevated GNMT in the first place
2. folate/deplin wouldnt correct the deficiency of the sulfur metabolites caused by accutane. i.e. folate cannot form cysteine
3. elevated GNMT in and of itself doesnt account for our problems. it causes our symptoms indirectly. its the deficiencies that cause our symptoms directly!even rich himself said (hes dead now by the way) for some reason it didnt work... he suggested a polymorphism.
Yeah I'm probably looking at this in a much more simplistic view to yourself, but the way I see it is that GNMT activity has been up regulated by accutane (as the studies would seem to show), and despite this no longer being in the system (I know there is some debate on this, but in my opinion we are looking at dealing with persistent effects of it, not problems due to a continued presence - I for example only took a very small amount, but still got sides - it's like a switch has been flicked 'on' and it's staying on), so by reducing GNMT activity we might at least have a shot pushing things back in the right direction, then maybe things might stabilise even when we ween off the support.
5-methyltetrahydrofolate [active folate] looks to be quite safe even in high doses. I've been taking 400mcg daily for some time, however some people are getting results from 50mg (12 times the dose I'm taking) for depression according to this information (just googled this quickly, link below) so I'm well below amounts that may potentially yield a benefit.
[Edited link out]
Anyone tried a fairly high dose of methylfolate for a time out of interest, and how much?
On 1/25/2016 at 4:56 AM, tanedout said:Yeah I'm probably looking at this in a much more simplistic view to yourself, but the way I see it is that GNMT activity has been up regulated by accutane (as the studies would seem to show), and despite this no longer being in the system (I know there is some debate on this, but in my opinion we are looking at dealing with persistent effects of it, not problems due to a continued presence - I for example only took a very small amount, but still got sides - it's like a switch has been flicked 'on' and it's staying on), so by reducing GNMT activity we might at least have a shot pushing things back in the right direction, then maybe things might stabilise even when we ween off the support.
5-methyltetrahydrofolate [active folate] looks to be quite safe even in high doses. I've been taking 400mcg daily for some time, however some people are getting results from 50mg (12 times the dose I'm taking) for depression according to this information (just googled this quickly, link below) so I'm well below amounts that may potentially yield a benefit.
[Edited link out]
Anyone tried a fairly high dose of methylfolate for a time out of interest, and how much?
you would be the ideal candidate for this then. i would still get a b12 test/ and methylmalonic test. if youre deficient in b12... all of the folate in the world will get "trapped"
why did u only take a small amount?
On 1/25/2016 at 5:01 AM, tryingtohelp2014 said:you would be the ideal candidate for this then. i would still get a b12 test/ and methylmalonic test. if youre deficient in b12... all of the folate in the world will get "trapped"
why did u only take a small amount?
I'm just taking a 'neurovit' supplement, which includes active B6, B12, folate and it just happens it's only 400mcg methylfolate. It seems it's possible to buy capsules with a high content, these at 10mg for example so I think I'll look into it further and potentially give this a go; [Edited link out]
Just out of interest, anyone who has had a 23andme test done, did you have the 'MTHFR gene mutation'? The MTHFR gene produces the enzyme that converts folate to methylfolate, andis also important for converting homocysteine into methionine (hence reduces it). Apparently people who have this mutation should actually avoid folate (as this can't easily be converted and binds to receptors) and take active, methylfolate http://wellnessmama.com/27148/mthfr-mutation/#comments
25 minutes ago, tanedout said:I'm just taking a 'neurovit' supplement, which includes active B6, B12, folate and it just happens it's only 400mcg methylfolate. It seems it's possible to buy capsules with a high content, these at 10mg for example so I think I'll look into it further and potentially give this a go; http://www.metabolicmaintenance.com/product/5-MTHF_10mg/cognitive_supportJust out of interest, anyone who has had a 23andme test done, did you have the 'MTHFR gene mutation'? The MTHFR gene produces the enzyme that converts folate to methylfolate, andis also important for converting homocysteine into methionine (hence reduces it). Apparently people who have this mutation should actually avoid folate (as this can't easily be converted and binds to receptors) and take active, methylfolate http://wellnessmama.com/27148/mthfr-mutation/#comments
right if homocysteine levels are in check meaning normal then they say it isnt a big deal to have the mthfr gene mutation. but in our case maybe it is. as is in effecting our methylation process componded by taking accutane. maybe all of us on this forum have the mutation but not bad enough to elevate homocysteine but enough to effect our different response to accutane. IDK it just comes down to, its just another supplement to try.
my b12 blood level is normal btw.
but if you go this route, per Rich dont just down 7.5 to 15mg at once.go slow and see how you respond to higher and higher doses.
im thinking of doing the same myself atm. before i go drop some cash on sam-e .cause its like the one supplement i dont have atm lol
folate also increases nitric oxide btw
there is a different test to test the actual folate in our blood the usable kind used by all cells
5-CH3-THF: This is a measure of the concentration of 5L-methyl
tetrahydrofolate in the blood plasma. The reference range is 8.4 to 72.6 nanomoles per liter.
This form of folate is present in natural foods, and is normally the most abundant form of folate in the blood plasma. It is the form that serves as a reactant for the enzyme methionine synthase, and is thus the important form for the methylation cycle. It is also the only form of folate that normally can enter the brain. Its only known reactions are the methionine synthase reaction and reaction with the oxidant peroxynitrite.
When there is a partial block in methionine synthase, 5L-CH3-THF drains from the cells into the blood plasma by the so-called methyl trap mechanism. As other forms of folate are converted to 5L-CH3-THF, this mechanism depletes the cells of folates in general.
Many PWCs have a low value of 5L-CH3-THF, consistent with a partial block in the methylation cycle. Most methylation treatment protocols include supplementation with 5L-CH3-THF, which is sold over-the-counter as Metafolin, FolaPro, or MethylMate B (trademarks), and in the prescription medical foods supplied by PamLab, including Deplin, CerefolinNAC and Metanx. There are some others on the market that include both racemic forms (5L and 5R) of this folate.
When methylation treatment is used, the level of 5-CH3-THF rises in nearly every PWC. If the concentration of 5-CH3-THF is within the reference range, but either SAM or the ratio of SAM to SAH is below the reference values, it suggests that there is a partial methylation cycle block and that it is caused by inavailability of sufficient bioactive B12, rather than inavailability of sufficient folate. A urine organic acids panel will show elevated methylmalonate if there is a functional deficiency of B12. I have seen this combination frequently, and I think it demonstrates that the functional deficiency of B12 is the immediate root cause of most cases of partial methylation cycle block. Usually glutathione is low in these cases, which is consistent with such a functional deficiency. As the activity of the methylation cycle becomes more normal, the demand for 5-CH3-THF will likely increase, so including it in the treatment protocol, even if not initially low, will likely be beneficial.
This is interesting, apparently if you have the MTHFR gene defect you are more susceptible to candida! What trantran believes she may have..
http://mthfr.net/methylation-inhibited-by-candidas-toxin/2012/09/08/
Just ordered a23andme kit so I'll get the test donebefore jumping to too many conclusions, but it would be interesting if we did all have the MTHFR gene mutation. To be honest I'll likely try a high dose of methylfolate even if I don't have the mutated gene, but I'm interested to know.
I am homozygous for the MTHFR C677T enzyme SNP.
***If anyone gets a 23andme test done (I HIGHLY recommend it), be sure to get the full variant report done by visiting mthfrsupport.com/sterlings-app
It's the best genome analyzer available and it's constantly improving. It's WAY better than any other thing: NutraHacker, LiveWello, GEDmatch, Genetic Genie, Athletigen, Promethease, etc.. I've purchased them all and I can confirm this.
Also, I'm going to be talking to an expert on genetic SNPs soon (within the next week) and would like people here to PM me with any questions you'd like me to ask the doc. He's connected to many intelligent people as well.
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EDIT:
Here are some studies I gathered up on accutane causing hypercalcemia (and kidney damage).
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By the way, some here may want to check their parathyroid hormones (if you have muscle pain). Could be elevated which would elevate your serum calcium. Note: I had mine checked. Mine are normal.
Does anyone know the difference between Gamma LinolenicAcid ( Evening Primrose Oil ) and
Alpha Lipoic Acid??
The GLA that I've been taking on and off had no effect but I'm thinking of getting some ALA - has anyone had any success with this supplement?
Just like "folate" -GLA is often targeted/marketed for women but more evidence is suggesting that men should take these supplements too.
If anyone has an opinion please share!!
glycine N-methyltransferase starts a reaction that converts the compounds glycine and S-adenosylmethionin.
its right there, your not only losing sam your losing glycine.
so are we looking at this wrong? do we need glycine in a high dose? seen people take up to 20grams per day for fatty liver or fibrosis. TMG vs Glycine?
how high of dosage have you done per day on tmg or plain glycine?
its not taurine its glycine?
I got bad reflux issues due to digestion problems and alot of worse shit going on thats why ive been back on here. that being said I could tell pretty quick what works if it stops the reflux.
Glycine When TMG gives up all its methyl groups, glycine is left. This is the smallest of the amino acids and is very important for the formation of collagen, among other functions. Collagen is the most abundant protein in the human body and is necessary for connective tissue, such as tendons, ligaments, cartilage, arteries, veins and other similar structures.
Trimethylglycine aka Betaine Sets the Anabolic Stage for Increased Muscle Growth: Higher IGF-1 & Lower Cortisol -
http://suppversity.blogspot.com/2012/09/trimethylglycine-aka-betaine-sets.html
- stable growth hormone levels (vs. -17% in the placebo group)
- an 18% increase in IGF-1 (vs. a -10% decrease in the placebo group), and
- a -5% reduction in cortisol (vs. a 6%
now image if were already deficient in this to begin with post accutane because of hyper gnmt
maybe we are using up all our GLYCINE