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what about and ige type blood test that would maybe show something related to allergy? someone else here said they tested high.
anyone have this test that came back negative or normal?
The Pfeiffer Treatment Center identifies two different supplement regimes depending on if you are an "over-methylator" or an "under- methylator." These are VERY rough estimations and nothing concrete...they may not be accurate either; further research is needed.
Q: How can you find out if you are over or under?
A: Histamine levels may be a good indicator of whether someone is an over or under-methylator.
Low histamine points to over-methylator: If your histamine level is low you are probably an over-methylator (according to Pfeiffer research). This means that many supplements would be detrimental to him (those containing methyl). These would include taurine, GABA [both precursors to methyl activity in the brain], folic acid, B12, B6, DMG, TMG (and SAMe) - to name a few.
Q: What test checks histamine levels?
A: There is a blood test to measure histamine. Your pediatrician can do it.
Have we looked at the other end of the spectrum?
Overmethylation (Histapenia): Too much methyl (a carbon group with three hydrogen atoms). It is very active in the brain, and too much leads to too much of a good thing. This causes an overproduction of serotonin, norepinephrine, and dopamine in the brain. In many cases,high serotonin levelscan cause psychological problems including reduced motivation, reduced libido,weight gain, and confusion.
This is what I was talking about earlier and maybe why it was the Folate that possibly gave me a limp di*k
yetanotheraccutanevictim said his depression disappears with nican/ nicanmade. True? This vitamin is said to cancel out methyl groups
22 minutes ago, guitarman01 said:what about and ige type blood test that would maybe show something related to allergy? someone else here said they tested high.
anyone have this test that came back negative or normal?The Pfeiffer Treatment Center identifies two different supplement regimes depending on if you are an "over-methylator" or an "under- methylator." These are VERY rough estimations and nothing concrete...they may not be accurate either; further research is needed.
Q: How can you find out if you are over or under?
A: Histamine levels may be a good indicator of whether someone is an over or under-methylator.Low histamine points to over-methylator: If your histamine level is low you are probably an over-methylator (according to Pfeiffer research). This means that many supplements would be detrimental to him (those containing methyl). These would include taurine, GABA [both precursors to methyl activity in the brain], folic acid, B12, B6, DMG, TMG (and SAMe) - to name a few.
Q: What test checks histamine levels?
A: There is a blood test to measure histamine. Your pediatrician can do it.Have we looked at the other end of the spectrum?
Overmethylation (Histapenia): Too much methyl (a carbon group with three hydrogen atoms). It is very active in the brain, and too much leads to too much of a good thing. This causes an overproduction of serotonin, norepinephrine, and dopamine in the brain. In many cases,high serotonin levelscan cause psychological problems including reduced motivation, reduced libido,weight gain, and confusion.
This is what I was talking about earlier and maybe why it was the Folate that possibly gave me a limp di*k
why would we have too many methyl groups after taking accutane? about 100 studies say accutane drains methyl groups??
idk man thats why your here to tell me this
BAM!
Therefore, if there is a mutation in the MTR or MTRR genes, they will potentially be unable to correctly synthesise methionine, which we need to utilise up the methyl-groups we create and supplement.
http://www.nature.com/ajg/journal/v103/n2/fig_tab/ajg20085077f1.htm l" height="287" src="http://www.mthfrsupport.com.au/wp-content/uploads/2014/09/MTr-MTRR-2.gif" style="margin:0px;padding:0px;border:none;font-size:16px;vertical-align:middle;height:auto" width="383">Source: http://www.nature.com/ajg/journal/v103/n2/fig_tab/ajg20085077f1.html
Therefore, supplementing with methylfolate without first supporting your patients MTR and MTRR genes could do more harm than good, as their body will be unable to create the methionine needed to use the methyl-portion of their supplemented methyl-folate.
This will typically show as classic symptoms of over-methylating, as the methyl folate will be unable to be given to methionine by MTR and MTRR due to their underfunctioning.
http://www.mthfrsupport.com.au/mtr-mtrr/
http://www.ncbi.nlm.nih.gov/pubmed/12221207
Hepatic glycine N-methyltransferase is up-regulated by excess dietary methionine in rats.
ok so this. too much methionine is bad?
1 hour ago, thedayacneceased said:So basically, I shouldn't try Accutane even after the Acne.org regiment and home remedies have failed me because it'll likely ruin my life with side-effects.
uh C correcto. I wouldnt say my life is ruined, but I picture my other self who never took accutane and he's better then me.
Hey, i want to help with a testimonial of an very rare accutane side effect that i have in 2011.
and for the record i ended my second course in december 2015,
my first contact with accutane was in 2011 when my face exploded with severe cystic acne and nothing worked 1 month before the accutane i was taking tetracycline which only worsened my acne
after 2 weeks i god a persistent headache and my vision was blurry so i was diagnosed with pseudo tumor cerebri, i got a papiledema in my eyes and i was experiencing a high pressure of liquor in my head, i stopped accutane right after that.
the doctors said that couldve be a tumor in my brain so my family and me was desperated i do remember like it was yesterday i experiencing a nightmare
2011 was a hell to me, after being affected with acne i got this rare side effect of accutane so i passed all 2011 taking drugs to relieve the pressure in my head, i dod alot of x-rays, ressonances etc and nothing was found, and i take a drug called diamox for around 4 months
the side effects of diamox was terrible my head was pricking my arms and legs was pricking and i was very weak
in 2012 my head was doing okay and i went to a new dermatologist and she said that this head pressure side effect was due to the hypervitaminosis caused by accutane and te tetracycline that wasnt full out of my system and she said that she was able to manage to put me in accutane again in low doses(20mg day) and she guaranteed that this time i would not go pass to this again and i accepted, let me say something before you judge me
i was about to kill myself i wasnt eating, i wasnt doing anything, i was paralyzed by depression due to my state, i accepted because i was nihilist enough to just give up everything and end my life.
i take 20mg accutane from jan 2012 to 2013. I got no harsh side effects beside dry lips, hair and skin
in beggin of 2015 my face exploded again and my derm put me in accutane again but in 40mg this time, i ended the course december 2015
i got no internal side effects again except by a very itchy scalp and a mild hair loss with a baldspot that she diagnosed as alopecia areata but she said that it wasnt because accutane which i doubt because it started after 1 month on accutane.
my hair loss is stabilishing right now and for the moment i didnt experienced longterm side effects
this is a true and sincerely testimonial and i only recommend accutane if your acne isnt deable and very severe to the point of destroying your life
20 hours ago, thedayacneceased said:So basically, I shouldn't try Accutane even after the Acne.org regiment and home remedies have failed me because it'll likely ruin my life with side-effects.
Permanent debilitating side effects are rare, so I don't know how you can deduce that you will "likely" ruin your life with side effects...You are *unlikely to ruin your life, and the odds are in your favor as millions have taken this drug, but odds nonetheless. If you have severe acne, and are old enough to walk into a casino and gamble, then you are old enough to understand the potential risks of taking Accutane, and cleared for treatment under the supervision of a dermatologist in my opinion. However, be aware that nary a dermatologist, nor physician, understands this drug or its mechanisms of action intrinsically on a chemical level.
...
Just talking to some of these kids man...such a waste of time.
Really a shame how they can market and solicit this stuff to teenagers and young adults who have no capacity of situational awareness or how the world works around them. And the parents just go along with whatever, because well, they were raised in an era where preventative medicine (vaccines) in the 50's and 60's saved so many lives, so they just inherently trust whatever a doctor tells them or gives them. I hate how we are perceived as if we are against allopathic medicine as a whole, which is not the case...and its so disheartening that the common sense in people can't see that currently the whole industry is just so saturated and perverse imo.
High folic acid consumption leads to pseudo-MTHFR deficiency, altered lipid metabolism, and liver injury in mice.
http://www.ncbi.nlm.nih.gov/pubmed/25733650
CONCLUSIONS:
We suggest that high folic acid consumption reduces MTHFR protein and activity levels, creating a pseudo-MTHFR deficiency. This deficiency results in hepatocyte degeneration, suggesting a 2-hit mechanism whereby mutant hepatocytes cannot accommodate the lipid disturbances and altered membrane integrity arising from changes in phospholipid/lipid metabolism. These preliminary findings may have clinical implications for individuals consuming high-dose folic acid supplements, particularly those who are MTHFR deficient.
It's not folic acid though. It's methyl folate which is different I believe from that study. My skin is still dry as hell from it and reduced libido there has to be some connection maybe in the Methylation cycle. I know I read folates are slow to clear from the body. And reduced libido is not a side effect normally. I'm sure this shit will pass but just wondering if it meant anything besides lay off the folate
8 hours ago, Modeaa said:GNMT activates NPC2 needed for not getting a non aclchoholic fatty liver and fibrosis
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356423/'' Overexpression of GNMT doubled the half-lives of both NPC2 isoforms and reduced cholesterol accumulation in cells. ''
'' GNMT was downregulated in the liver tissues from patients suffering with NAFLD as well as from mice fed a high-fat diet, high-cholesterol diet or methionine/choline-deficient diet.
In conclusion, our study demonstrated that GNMT regulates the homeostasis of cholesterol metabolism, and hepatic cholesterol accumulation may result from downregulation of GNMT and instability of its interactive protein NPC2. ''
http://www.ncbi.nlm.nih.gov/pubmed/20578266?dopt=Abstract
Fatty liver and fibrosis in glycine N-methyltransferase knockout mice is prevented by nicotinamide.http://www.nature.com/labinvest/journal/v95/n2/index.html
TRAIL-producing NK cells contribute to liver injury and related fibrogenesis in the context of GNMT deficiency
BUT according to this NPC2 PROMOTES GALLSTONES-
http://www.ncbi.nlm.nih.gov/pubmed/26453970
Transgenic overexpression of Niemann-Pick C2 protein promotes cholesterol gallstone formation in mice.
. These results suggest that NPC2 promotes cholesterol gallstone formation by decreasing the cholesterol nucleation time, indicating a pro-nucleating function of NPC2 in bile.also this been posted on this forum before-
http://www.ncbi.nlm.nih.gov/pubmed/14978883
[Ultrastructural findings in the liver due to long-term retinol (isotretinoin) treatment. Significance of the perisinusoidal (Ito) cells].Electron microscopic examination revealed changes characteristic of vitamin A toxicity: hyperplasia of the perisinusoidal (Ito) cells with evidence of their activation and transformation, increased storage of lipids and vitamin A, perisinusoidal fibrosis, damage of the sinusoidal wall, partial necrosis in hepatocytes and an increased number of lysosomes, megalysosomes and smooth endoplasmic reticulum (SER), the signs of cholestasis as well as an increased number of Kupffer cells in the lobules etc. Histochemical examination showed a high content of vitamin A in the transitional (Ito) cells and in hepatocytes.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3054388/These results suggest hyperplasia and metaplasia are closely related to the gallstone formation. Hyperplasia is probably reactive to irritating effect of lithogenic bile or stone. Metaplasia and cholesterol gallstone may develop simultaneously, and act synergistically.
https://en.wikipedia.org/wiki/Cholestasis
Cholestasis is a condition where bile cannot flow from the liver to the duodenum. The two basic distinctions are an obstructive type of cholestasis where there is a mechanical blockage in the duct system that can occur from a gallstone or malignancy, and metabolic types of cholestasis which are disturbances in bile formation that can occur because of genetic defects or acquired as a side effect of many medications.
.Causes
https://www.ncbi.nlm.nih.gov/pubmed/19944093 Hypervitaminosis A inducing intra-hepatic cholestasis--a rare case report.https://en.wikipedia.org/wiki/ Perisinusoidal_space
The Space of Disse also contains Ito cells, also called hepatic stellate cells, which store fat or fat soluble vitamins (like vitamin A). A variety of insults that cause inflammation can result in Ito cells transforming to myofibroblasts, resulting in collagen production, fibrosis, and cirrhosis.EDIT:
http://www.journaltocs.ac.uk/index.php?action=browse&subAction=subjects&publisherID=155&journalID=7774&pageb=2&userQueryID=&sort=&local_page=1&sorType=&sorCol =
Methionine and S-adenosylmethionine levels are critical regulators of PP2A
activity modulating lipophagy during steatosis...normalization of methionine and SAMe levels in Gnmt-KO mice using a methionine deficient diet normalized the methylation capacity, PP2A methylation, autophagy, and ameliorated liver steatosis. Conclusions These data suggest that elevated levels of methionine and SAMe can inhibit autophagic catabolism of lipids contributing to liver steatosis.
GNMT GETTING RIDD OF METHIONINE- TRYING TO PREVENT FATTY LIVER? (ON THE WAY IT CREATES GALLSTONES?)
https://en.wikipedia.org/wiki/Protein_phosphatase_2
is a ubiquitous and conserved serine/threonine phosphatase with broad substrate specificity and diverse cellular functions. Among the targets of PP2A are proteins of oncogenic signaling cascades, such as Raf, MEK, and AKT.
we are NOT GNMT -/- knockout mice. we are at the absolute other end of the spectrum due to accutane. we are +++++/+++++GNMT knockout mice. you need to understand this when reading anything negative about methionine or SAM-E
http://onlinelibrary.wiley.com/doi/10.1002/hep.510290111/pdf
http://link.springer.com/chapter/10.1007%2F978-0-387-75681-3_30
A deficiency of methionine leads to reduced levels of SAM and an increased risk of depression. In an animal study conducted at McGill University, researchers Simon N. Young and Marjan Shalchi supplemented half of a group of laboratory rats with methionine and the other half with synthesized SAM, a relatively expensive and unstable supplement. In findings published in the January 2005 issue of the "Journal of Psychiatry & Neuroscience," Young and Shalchi reported that the methionine supplement raised SAM levels in various parts of the central nervous system at lower doses than were attained with the SAM supplement.
Although glycine is non-essential, your liver cant make an unlimited amount, and the typical diet usually comes up short 8-10 grams of glycine per day. Meanwhile, glycine has critical functions in the body only recently discovered. Most relevant to human diet and health is the fact that glycine is the most important endogenous regulator of inflammation. In fact, Im convinced that glycine deficiency lies at the core of most conditions that make people sick and die these days, from diabetes and arthritis to heart disease and cancer. Thats because theyre all traceable to chronic excess inflammation. If you are glycine-deficient, it will show up as chronic inflammation sooner or later, one way or another.
So thats why I have been quick to say that most people eat too much methionine, and really should avoid supplements such as SAMe, TMG, etc, which boost methylating power. But in one of the comments after one of my posts on this site a few months ago, the suggestion that some people are under-methylators prompted me to have another look at what is going on. After all, it is well known that mutations of the gene for the enzyme MTHFRwhich is critical for the regeneration of methionine from homocysteineare quite common in all human populations (between 10 and 20%). People with defective forms of MTHFR do not regenerate methionine efficiently. Consequently, during periods of fasting (or even shorter periods of say, 4-6 hours between meals), they may actually be somewhat methionine-deficient, precisely because excess methionine is so efficiently removed after absorbing a meals worth of high protein.
Therefore, such people may endure chronic health problems by being both glycine AND methionine-deficient!
on a side note.... To lighten things up a bit.
Guitarman Actually playing guitar. Check it out im actually kind of proud of it. one of my favorite songs. Its Beachy
Nice tunes guitarman. I like what you bring to the thread. And for a bit more levity, how about this? 112 wpm. Not bad for a tane brain, eh?
On 1/28/2016 at 5:20 PM, Modeaa said:i'm aware to the fact that we might have an upregulated GNMT and not downregulated GNMT, AND I WAS AWARE THAT THE STUDY(s) WAS ABOUT GNMT -/-KNOCOUT or deficient mice . THE POINT was to show what GNMT activity might be used for by the body, and according to the information it seems like it is needed for the prevention of fatty liver, because methinionine and samE can contribute to fatty liver creation, so GNMT is getting ridd of them.
that's what i understood from the text, could be wrong affcourse, or that GNMT activiry post accutane might have other reasons.http://www.sciencedirect.com/science/article/pii/S0168827815006224
'' Gnmt deficiency in mice (Gnmt-KO) results in abnormally elevated serum levels of methionine and its metabolite S-adenosylmethionine (SAMe), and this leads to rapid liver steatosis development. Autophagy plays a critical role in lipid catabolism (lipophagy), and defects in autophagy have been related to liver steatosis development. Since methionine and its metabolite SAMe are well known inactivators of autophagy, we aimed to examine whether high levels of both metabolites could block autophagy-mediated lipid catabolism.''
'' We detected a significant increase in serum methionine levels in steatotic patients. We observed that autophagy and lipophagy were impaired in hepatocytes cultured with high methionine and SAMe, and that Gnmt-KO livers were characterized by an impairment in autophagy functionality, likely caused by defects at the lysosomal level. Elevated levels of methionine and SAMe activated PP2A by methylation, while blocking PP2A activity restored autophagy flux in Gnmt-KO hepatocytes, and in hepatocytes treated with SAMe and methionine. Finally, normalization of methionine and SAMe levels in Gnmt-KO mice using a methionine deficient diet normalized the methylation capacity, PP2A methylation, autophagy, and ameliorated liver steatosis.
Conclusions
These data suggest that elevated levels of methionine and SAMe can inhibit autophagic catabolism of lipids contributing to liver steatosis. ''if this GNMT Is active in us because of this- this is a state where the body constatly fighting for prventing a liver dammage? and it decrease lipogenesis also?
we might see a perfect liver tests results post accutane due to our body fighting so well? but this fight compramise other things cause it decrease samE, the smaE Is needed on one hand but on the other the liver is in a state where it can be hurt by SAM-E?GNMT can be activated by foxo due to necrosis (of liver cells?)
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3219165/
isotretinoin-induced upregulation of nuclear FoxOs would just impair lipogenesis and reduce the lipophilic follicular milieu for P. acnes overgrowth and P. acnes-mediated proinflammatory TLR2/PI3K/Akt/NFºB signal transduction.
I know.
This was one of my earlier theories.... that the liver shuts down bile synthesis to stop our bodies from absorbing Vitamin A... it senses we are already toxic.
...but after reading about SAM-E and methionine... they are totally needed by the liver to prevent a fatty buildup.... not the other way around. you see the studies of what our body does even after the first few doses of accutane...it produces massive amounts of taurine in the liver. look on any avitaminosis A page, and look at what they say to take.....
- Phosphatidylcholine, in the form of PPC, or DLPC.
- Taurine
https://en.wikipedia.org/wiki/Hypervitaminosis_A
methionine is needed for both of these.
i found something else interesting....
http://www.google.com/patents/EP2598115A1?cl=en
[Edited image out]
Speaking of that. What was one of the first side effects you noticed after accutane. Long time ago I know. But was it facial flushing? I think mine was. Clues... My hair didn't fall out till after this I believe. My eyes didn't become sensitive till much later. I didn't even have to wear sunglasses for a long time
GNMT. This enzyme participates inglycine, serine and threonine metabolism.
Generally speaking, Serine plays an important role in various biosynthetic pathways. In addition, it is theprecursor to a number of amino acids like Glycine and Cysteine. Besides, it also helps an enzyme catalyze its reaction - the hydrolysis of peptide bonds in polypeptides and proteins, which is basically a major function in the digestive process.
Serine is recognized as a non-essential amino acid obtained from another amino acid called Glycine and is believed to be important to overall good health, both physical and mental. This amino acid is particularly essential for proper functioning of your brain and of your central nervous system.
One of the Serine's functions is to help form the phospholipids which are necessary for creating every cell in the human body. In addition, this amino acid is involved in the functioning of RNA and DNA, in the muscle formation as well as in the maintenance of a proper immune system. Tryptophan, an essential amino acid used to make serotonin (a mood-determining brain chemical), also cannot be produced without Serine. Meanwhile, both serotonin and Tryptophan shortages are believed to cause depression, insomnia, and anxiety. Numerous researches suggest that low levels of this amino acid are responsible for the chronic fatigue syndrome and fibromyalgia.
Serine is also known for assisting in production of immunoglobulins and antibodies for a healthy immune system, as well as for helping in the absorption of creatine that helps build and maintain the muscles.
Since Threonine is found largely in the central nervous system, it can be really helpful in treating different types of depression. This amino acid makes up elastin, collagen, and enamel protein, and even promotes the proper fat metabolism in the liver. Finally, Threonine is known for aiding the digestive and intestinal tracts to function more smoothly, as well as for helping in metabolism and assimilation.
Threonine is an essential amino acid, i.e., it is vital for your health, but it canott be synthesized by your body and therefore has to be obtained from a diet. This amino acid supports central nervous, cardiovascular, liver, and immune system functioning - just to name a few. Moreover, it helps in the synthesis of glycine and serine which, in their turn, assist in the production of collagen, elastin, and muscle tissue. In addition, Threonine aids building strong bones and tooth enamel and speeds up a wound healing process after trauma or surgery by boosting up the immune system.
Threonine works the following way: it combines with aspartic acid and Methionine to jointly help liver digest fats and fatty acids. This process helps reduce the accumulation of fat in the liver, which would otherwise affect the liver function. This amino acid is also useful in treating Lou Gehrig's disease, aka Amyotrophic Lateral Sclerosis. Scientific researches show that Threonine treatment also helps alleviate symptoms of Multiple Sclerosis - another disease affecting nerves and muscles. Besides, Threonine is recognized as an immunostimulant promoting the growth of thymus gland.
AND YOU KNOW ABOUT GLYCINE,
Have you guys looked at these other amino acids?
the activation and induction of GNMT by CRA and ATRA (11) may serve as the mechanistic basis for the increased methionine/SAM catabolism associated with retinoid treatment
So if this is the case still do you supplement with methionine or SAM?
Deficiency of methionine produces hepatic steatosis similar to that seen with ethanol
LOOK AT THIS SHIT!!!!
http://www.cell.com/cell-metabolism/abstract/S1550-4131(14)00122-3
Could this have to do with retinoid birth defects????
Methionine Metabolism Regulates Maintenance and Differentiation of Human Pluripotent Stem Cells
But wait, If that was the case then GNMT would go back to normal after treatment and debunk the whole theory
i.e babies are fine if conceived post accutane
On 1/29/2016 at 10:52 AM, guitarman01 said:LOOK AT THIS SHIT!!!!
http://www.cell.com/cell-metabolism/abstract/S1550-4131(14)00122-3Could this have to do with retinoid birth defects????
Methionine Metabolism Regulates Maintenance and Differentiation of Human Pluripotent Stem Cells
But wait, If that was the case then GNMT would go back to normal after treatment and debunk the whole theory
i.e babies are fine if conceived post accutane
[Edited link out]
read for what this Chinese guy says stops birth defects from retinoic acid