[gondal4]

gondal, did you read my post in which I said that fenugreek+tea or nutmeg help my joint pain? I suspect my joint pain is caused by inflammation from POIS. Although it could also be caused by anything that POIS does to inhibit tissue growth and repair.

nO fenugreek tea didnt had any effect on me.......And iam talking not about joint pain only but generraly i feel older and cannot or play sports.it is since beginning of POIS when iwas 18,now iam 25..

[Vincent M]

gondal, I feel increased endurance(less fatigue) during exercise or sports the day after I take niacin if I take it and have a flush before an "o". The flush is a slight redness of the skin with a hot, itchy feeling. Safest to start with 50mg nicotinic acid which is the form of niacin you would want. If 50mg doesn't cause a flush I would bump it up to 100mg, and so on. I need about 500mg because my bottle of niacin is old and I didn't seal it properly so it lost potency quickly.

[gondal4]

what i meant was i cannot run and feel older and i have symptoms too like wrinkles on hand and feet,eye sight weakness,memory,etc.....and these all symptoms started at the time when POIS started? so i was asking is there a connection? and im talking generally about running,playing sports not in the days after POIS because i cannot move after O.

[Vincent M]

Found this about hypermethioninemia:

"Treatment of CBS deficiency usually begins with a trial of oral vitamin B6 (pyridoxine) supplementation, with daily measurement of plasma amino acids. CBS requires pyridoxine as a coenzyme for enzymatic activity. Overall, about 25% of patients respond to large doses of pyridoxine, although the percentage may be lower for patients identified through newborn screening. This pyridoxine response usually coincides with the presence of some residual enzyme activity. Dietary restriction of Methionine in conjunction with Cystine supplementation reverses the biochemical abnormalities to some extent and appears to reduce the clinical symptoms. Special formulas are available commercially, but the diet is difficult to maintain long term. In an attempt to decrease Homocysteine levels, folic acid, and betaine can be supplemented to induce recycling of this amino acid to Methionine for alternate metabolism. Vitamin B12 (cobalamin) may also be helpful.
Because the diagnosis and therapy of Homocystinuria is complex, the pediatrician is advised to manage the patient in close collaboration with a consulting pediatric metabolic disease specialist. It is recommended that parents travel with a letter of treatment guidelines from the patient’s physician."
http://www.perkinelmergenetics.com/Hypermethioninemia.htm

I wonder if this is why B-complex improves my symptoms, but methionine seems to make me slightly worse.

[kurtosis]

Wow, romies, congratulations on finding something that works for you!  Must be a big relief.  I'm still searching for my own solution, because it turns out I don't respond to the same treatments you and kurtosis have had success with.  I think my issue is that I am over-methylated, and combined with COMT and MAO-A mutations I quickly experience negative effects from methionine and other methyl donors.  I suffer from psychosis unless I'm taking dopamine-blocking drugs, and I have terrible reactions to some meds that block the reuptake of dopamine or norepinephrine (Wellbutrin).

My Genetic Genie results:



I have 3 homozygous mutations on my AHCY gene.  From my understanding this would increase methylation.  What's confusing is I also have 3 homozygous mutations on my BHMT gene, which would reduce the conversion of homocystine to methionine, a decrease in methylation.  I'm pretty sure that's right, correct me if I'm wrong!  The CBS mutation should also decrease methylation, so I'm guessing that homocystine levels are not indicative of very much for me.  My last check was very normal.  Is the methylation problem (be it over or under) resulting in a normal homocystine level by having mutations that both increase and decrease methylation?

I'm curious if I would respond to treatment that people with hypermethionemia have.  http://wiki.medpedia.com/Hypermethioninemia

I don't know exactly what that treatment is though, I havn't found a good resource on that.

Besides the BH4/mast cell connection, I still have no idea how this would cause increased symptoms after orgasm!

The AHCY gene provides instructions for producing the enzyme S-adenosylhomocysteine hydrolase. This enzyme converts the AdoHcy into the compound homocysteine.

But methionine is methylated homocysteine. I'm not sure it's as simple as saying that ACHY mutations will automatically increase methylation. SAM-e is the main methyl donor, not methionine. If you're body can't produce SAM-e from methionine then it may build up methionine and you may start to smell funny but you also won't have enough SAM-e and will have a range of symptoms from that including difficulty thinking, healing etc.

If you look at the heartfixer website then your genetics would indicate the following:

VDR (+/+) and COMT (+/-)

COMT (+/-) and VDR (+/+) behaves like COMT (-/-)

Therefore

Lowest dopamine levels
Poor tolerance to toxins and microbes
Needs and tolerates dopamine precursors and methyl donors
Lowest susceptibility to mood swings

MAO A you know about.

Monoamine Oxidase A breaks down serotonin, a neurotransmitter that is generated from the dietary amino acid tryptophan, in a BH4 requiring reaction.  Many anti-depressant drugs, including the SSRIs (Serotonin Selective Reuptake Inhibitors) work by blocking the breakdown of serotonin.  Defects in serotonin metabolism have been associated with mood and neurological disorders.  How best to address the MAO A R297R abnormality is not clear to me.  As serotonin metabolism is adversely affected, individuals with the R297R defect should avoid large doses of high tryptophan foods (see appendix).  High doses of St. John’s Wort, often taken to address depression, could lead to mood swings as serotonin levels fluctuate.

BHMT

Phosphatidylcholine, or as a less expensive alternative, Phosphatidylserine 100 mg daily, to stimulate the BHMT reaction

Betaine or TMG is also possible in those without COMT (+/+)

On to AHCY

S-Adenosyl Methionine (SAMe), the key methyl donor generated from methionine, is metabolized in to S-Adenosyl Methionine, and then on to homocysteine by AHCY.  Individuals (+) for both AHCY and CBS often have low baseline urine sulfate levels, which then rise and fall  in response to treatment.  Early on the levels rise, as the “bottle neck” abnormal AHCY enzyme has been “limiting the supply” of homocysteine.

There are reports on phoenixrising.me of people with COMT (-/-) and AHCY taking SAMe with some success. The CBS mutation tends to shove the outputs towards ammonia which requires BH4 to clear. You've already sent me some material on this. There's synthetic BH4, supplements which may increase the creation of BH4 and NADH which may increase BH2-BH4 recycling.

MTRR and MTHFR A1298c indicate a need for methyl-b12

MTRR generates the methyl-B12 needed by MTR and many other methyl-B12 requiring enzymes.  Blood B-12 levels may be normal, but if MTRR is (+/+) or (+/-), methyl-B12 formation will be compromised, homocysteine levels will be elevated, methylation in general will be compromised, and your physiology will be compromised.   

[kurtosis]

Found this about hypermethioninemia:

"Treatment of CBS deficiency usually begins with a trial of oral vitamin B6 (pyridoxine) supplementation, with daily measurement of plasma amino acids. CBS requires pyridoxine as a coenzyme for enzymatic activity. Overall, about 25% of patients respond to large doses of pyridoxine, although the percentage may be lower for patients identified through newborn screening. This pyridoxine response usually coincides with the presence of some residual enzyme activity. Dietary restriction of Methionine in conjunction with Cystine supplementation reverses the biochemical abnormalities to some extent and appears to reduce the clinical symptoms. Special formulas are available commercially, but the diet is difficult to maintain long term. In an attempt to decrease Homocysteine levels, folic acid, and betaine can be supplemented to induce recycling of this amino acid to Methionine for alternate metabolism. Vitamin B12 (cobalamin) may also be helpful.
Because the diagnosis and therapy of Homocystinuria is complex, the pediatrician is advised to manage the patient in close collaboration with a consulting pediatric metabolic disease specialist. It is recommended that parents travel with a letter of treatment guidelines from the patient’s physician."
http://www.perkinelmergenetics.com/Hypermethioninemia.htm

I wonder if this is why B-complex improves my symptoms, but methionine seems to make me slightly worse.

I improve with methylfolate and methyl-b12. I get worse with over 25mg of pyroxidine / day. I don't like folic or even folinic acid. NADH makes me feel good and I think this is because it increases BH4. I feel much happier when I get only the methylfolate form of folate in my multi-vitamin and methyl b12 every day. I've learned these from trial and error. A week or so at a time and plotting general happiness and cognitive performance results.

I also take molybdenum and manganese in my multivitamin as I have all the signs of the SUOX mutation. Just the smell of red wine or perfume make me feel nauseous. 

[Nightingale]

Thanks for your analysis, kurtosis.  I with I had known about the heartfixer website sooner, it's really where I should have started when I began my path to understanding all this.

"Understanding how to incorporate the science of Methyl Cycle Genomics in to your treatment program, and how best to monitor your individual response, will be a challenge to both of us.  If we accept this challenge, and spend time, energy, and resources in dealing with your Methyl Cycle Abnormalities, then you can take strides forward in improving your health."

That's pretty much where I'm at.  There is a lot to learn, and I need to understand why I'm taking a particular supplement because 1) I have health care providers whose trust I need and 2) I don't want to know I unwittingly made things worse for myself.

My head is fogged and my motivation is low.  But I will be chipping away at this stupid methylation cycle until I get it...

[romies]

I believe the improvement we're noticing from NADH is increased energy and increased glutathione production. I also worry about fluctuating homocysteine levels that may contribute to the dull headache that some of us get. Just some thoughts. I realise that none of this is conclusive.

I know NADH can be used to recycle bh4 and reduce ammonia levels. Another possibility is synthetic BH4. I think there's a product called Kuvan but I have not tried it. It's prescription only so, as usual, discuss it with your doctor.

We both have CBS mutations.
However, I think that some of our illness (and this may not apply to other POIS sufferers, just those that have A1298c and/or MTHFR C677T mutations) may be caused by low levels of glutathione.
My skin and stomach problems improve very quickly when I add supplementary glutathione. I just don't think I'm making enough of this normally and need a helping hand.

good points about CBS mutations. and I remember your earlier Histamine analysis, which is brilliant.

I used to need to take daily omeprazole to deal with night-time heart burn, and daily Cetirizine for stuffy nose during sleep. I was dependent on both for ~8 years (unable to quit, because of severe symptoms ensued). Clearly having too much histamine in my system.

After starting on Methyl-guard, in a few days, I don't need either omeprazole or Cetirizine. I am taking loratadine for my allergy now. Previously loratadine was way too weak to alleviate my nasal blockage at night.

One question here: CBS mutation will up-regulate homocysteine metabolism and generate too much glutathione, according to Amy Yasko?

[romies]

Wow, romies, congratulations on finding something that works for you!  Must be a big relief.  I'm still searching for my own solution, because it turns out I don't respond to the same treatments you and kurtosis have had success with.  I think my issue is that I am over-methylated, and combined with COMT and MAO-A mutations I quickly experience negative effects from methionine and other methyl donors.  I suffer from psychosis unless I'm taking dopamine-blocking drugs, and I have terrible reactions to some meds that block the reuptake of dopamine or norepinephrine (Wellbutrin).

My Genetic Genie results:



I have 3 homozygous mutations on my AHCY gene.  From my understanding this would increase methylation.  What's confusing is I also have 3 homozygous mutations on my BHMT gene, which would reduce the conversion of homocystine to methionine, a decrease in methylation.  I'm pretty sure that's right, correct me if I'm wrong!  The CBS mutation should also decrease methylation, so I'm guessing that homocystine levels are not indicative of very much for me.  My last check was very normal.  Is the methylation problem (be it over or under) resulting in a normal homocystine level by having mutations that both increase and decrease methylation?

I'm curious if I would respond to treatment that people with hypermethionemia have.  http://wiki.medpedia.com/Hypermethioninemia [nofollow]

I don't know exactly what that treatment is though, I havn't found a good resource on that.

Besides the BH4/mast cell connection, I still have no idea how this would cause increased symptoms after orgasm!

Nightingale,

I am not completely out of the woods yet.. The recipe is quite complex, so if I forget one or two ingredient, I sometimes still get some POIS symptoms, but for 12-18 hrs only, as opposed to 4-5 days before.

Your COMT, VDR and MAO A profile is almost completely opposite from mine. so I guess your are more of the over-methylation type. Maybe taking Niacin before and after an O will help to mop up extra methyl and lessen the crash?

I do think there are several sub-types of POIS. maybe there is a over-methylation type, where too much dopamine was generated. Dopamine response curve is U-shaped. too much DA does degrade cognitive and may also causes dopamine receptor to down-regulate, and causes a hang-over for 4-5 days after..

[kurtosis]

I have the C699T up-regulation. I read Yasko's "Genetic Bypass" book and while I'm not 100% convinced that anybody knows
1) the exact interaction between all these genes
2) that other genes are not involved that may complicate these interactions further.
I think that the methylation pathyway diagrams make a lot of sense and seem somewhat, if not entirely, complete.
Here's her quote on C699T from (page 48)

"Increased CBS enzyme activity would act to convert homocysteine more efficiently to cysteine, thereby lowering homocysteine levels. Ultimately individuals with the CBS C699T upregulation of the CBS enzyme can generate more sulfur breakdown products with potential sulfur toxicity issues, enhanced ammonia production, and a lack of glutathione."

Yasko believes that ammonia and taurine are elevated in CBS up-regulations and that glutathione is decreased.
Ammonia buildup is bad and the best way to clear it is with BH4, which can be recycled using NADH. NADH has also been shown to increase glutathione in one study I read.
See

Freedenfeld s. [et al.], Biochemical effects of Ribose and nADH Therapy in children with Autism, 2011

I don't think there are enough studies to decide it's conclusive  but it's worth thinking about.

[romies]

I have the C699T up-regulation. I read Yasko's "Genetic Bypass" book and while I'm not 100% convinced that anybody knows
1) the exact interaction between all these genes
2) that other genes are not involved that may complicate these interactions further.
I think that the methylation pathyway diagrams make a lot of sense and seem somewhat, if not entirely, complete.
Here's her quote on C699T from (page 48)

"Increased CBS enzyme activity would act to convert homocysteine more efficiently to cysteine, thereby lowering homocysteine levels. Ultimately individuals with the CBS C699T upregulation of the CBS enzyme can generate more sulfur breakdown products with potential sulfur toxicity issues, enhanced ammonia production, and a lack of glutathione."

Yasko believes that ammonia and taurine are elevated in CBS up-regulations and that glutathione is decreased.
Ammonia buildup is bad and the best way to clear it is with BH4, which can be recycled using NADH. NADH has also been shown to increase glutathione in one study I read.
See

Freedenfeld s. [et al.], Biochemical effects of Ribose and nADH Therapy in children with Autism, 2011

I don't think there are enough studies to decide it's conclusive  but it's worth thinking about.

Very interesting. I hope the biomedical people can be more quantitative about the details of these pathways. I am an electrical engineer, and I see all these processes basically as systems of rate equations, which probably can be simplified into constant-coefficient ordinary differential equations (not even PDE). And our genetic profile ( and the regulation of our gene expression) determines these coefficients. Supplements are forcing functions. If these coefficients are known, one can solve for an optimal supplement regiment in MATLAB in second.

And blood testing may help in determine some of the constants in the equations...

I admit my thinking is probably too mechanistic for biologic systems....

[kurtosis]

Well, octave was developed so chemical engineering students would have a free version of MATLAB to solve exactly these kinds of equations. However,there are feedback loops as CBS takes from homocysteine which reduces the amount for remethylation to methionine which further slows the methylation cycle. That's why understanding the methylation cycle perfectly can help give an optimal supplementation path.
Ideally, that's what nutrigenomics should do. A combination of functional testing and genetic testing should lead to an optimisation problem such that over time the supplementation produces metabolic equilibrium with normal (or indeed optimum) levels of certain enzymes and their co-factors in serum and tissue.

CBS up-regulation may produce downstream byproducts of CBS at 10 times the rate so that's a lot more ammonia being built up. 10 times more? That's not clear as there are other mutations and a split between sulfur byproducts such as ammonia and taurine . To clear ammonia requires more BH4 to recycle BH2. But supplements don't appear to be absorbed uniformly and it seems that it's a bit early to say we can fix these problems in a MATLAB simulation in a flash. In theory, yes but in practice medical researchers are in the early stage of understanding the efficiency implications of any genetic mutation, never mind combinations.

So there's a lot of intelligence and research which would go into writing the ODE's you speak of and
1) they may be a best guess approximation for what's actually happening.
2) because of reasons including (1) they'd still require functional testing to determine they were working. It'll still be iterative ...

[romies]

Yes, Octave is pretty good as a MATLAB replacement.

In your current routine, the blueberry extract is a replacement for Ginkgo Biloba extract, right?

What's your daily dosage? any special dose before/after an O?

Thanks!

[kurtosis]

Yes, Octave is pretty good as a MATLAB replacement.

In your current routine, the blueberry extract is a replacement for Ginkgo Biloba extract, right?

What's your daily dosage? any special dose before/after an O?

Thanks!

Yes, that's a good point. I believe that both blueberries and ginkgo can reduce inflammation. I like ginkgo but it sometimes makes me itchy whereas blueberries or pterostilbene (there's a patented extract in some supplements) seem to reduce POIS and I haven't noticed any side effects.

[Nightingale]

Nightingale,

I am not completely out of the woods yet.. The recipe is quite complex, so if I forget one or two ingredient, I sometimes still get some POIS symptoms, but for 12-18 hrs only, as opposed to 4-5 days before.

Your COMT, VDR and MAO A profile is almost completely opposite from mine. so I guess your are more of the over-methylation type. Maybe taking Niacin before and after an O will help to mop up extra methyl and lessen the crash?

I do think there are several sub-types of POIS. maybe there is a over-methylation type, where too much dopamine was generated. Dopamine response curve is U-shaped. too much DA does degrade cognitive and may also causes dopamine receptor to down-regulate, and causes a hang-over for 4-5 days after..

Dopamine is an especially interesting part of this for me.  I have yet to find someone else to responds this way when they have 2 O's in a close timespan, especialy under 2 hours: The second O is harder to achieve, but it's intensity is FAR greater, both in POIS symptoms AND in pleasure.  I'm sure you know dopamine surges for an O.  It's like taking a illicit drug that leaves me senseless.  I often will lie there in what feels like a semi-coma.  It can be hard to move my self, as it's like I'm half-paralyzed.  It seems similar to what sufferers of cataplexy (sleep paralysis) experience, but I'm able to move with sustained effort.  Some mornings after when I was depressed and O'd more then once a day, it would take me 15 minutes longer to get out of bed because of the paralysis state.  I wonder how much histamine was surging through my system at those times...

I'm having Phe, ammonia, Heavy metals, and maybe sulfur levels tested this weekend.  I'm especially curious about ammonia, since after eating meat lately I'm getting this wave of brainfog and loss of concentration.

I have such days of low-functioning, I can't even learn how to make the next choice in my treatment.  I would love to complete my IT degree and finish my bachelors some day soon!

EDIT: I wonder, too, if my having to take 1.5g of niacin to achieve a flush now has something to do with an excess of methyl?  My first times trying niacin didn't require nearly as much, but early on I noticed I needed about 200mg to get a real flush were most were needing 100-150mg.  It quickly climbed to where I had to buy 500mg niacin tablets.  Actually, my flush isn't very strong anymore and I'm getting less reduction in symptoms, I might bump it up to 2g soon.

[romies]

I'm having Phe, ammonia, Heavy metals, and maybe sulfur levels tested this weekend.  I'm especially curious about ammonia, since after eating meat lately I'm getting this wave of brainfog and loss of concentration.

EDIT: I wonder, too, if my having to take 1.5g of niacin to achieve a flush now has something to do with an excess of methyl?  My first times trying niacin didn't require nearly as much, but early on I noticed I needed about 200mg to get a real flush were most were needing 100-150mg.  It quickly climbed to where I had to buy 500mg niacin tablets.  Actually, my flush isn't very strong anymore and I'm getting less reduction in symptoms, I might bump it up to 2g soon.

I need to take back what I said on Niacin for the following reasons:
1.Assuming you are over-methylated, your histamine will be easily disposed (metabolized) any time. Since you do not  suffer from high histamine, the causes of your POIS is likely to be different from Kurtosis and me.
2.Most people who are over-methylators suffer from insomina, anxiety. Niacin helps on those problems. But you don't have insomnia/anxiety symptoms, so I suppose Niacin will not help.
3.too much Niacin (1.5g is on the very high end) adds a lot of burden on your liver.

Your dopamine response is interesting. Do you experience high frustration and aggression,  or just low-tempo brain fog?

more test results, I think, are always better. What medicine/supplement are you taking daily?

[romies]

Yes, that's a good point. I believe that both blueberries and ginkgo can reduce inflammation. I like ginkgo but it sometimes makes me itchy whereas blueberries or pterostilbene (there's a patented extract in some supplements) seem to reduce POIS and I haven't noticed any side effects.

Yeah. ginkgo has so many different chemicals in it. variation from brand to brand can be huge. There is one brand causing diarrhea on me every single time. I will give blueberries and pterostilbene a try.

[Vincent M]

Nightingale, I wonder if your niacin might have lost some of its potency. I let mine sit in the closed bottle for a few months and needed 500mg or 600mg to get a flush instead of my usual 200mg even though I've only taken niacin maybe 7 or 8 times total.

I've wrapped the bottle in plastic now, but I haven't tried any yet to see if it lost more potency.

[kurtosis]

Niacin may increase prostaglandin release which may reduce inflammation (depends which prostaglandin is released). PGE1 and Histamine levels appear correlated. PGD2 may block histamine. I read a few papers about this in the past.  We had a long discussion about this over on poiscenter. I'm not sure it's as simple as under methylation or over methylation as there are interacting genetics here.

When I saw MTHFR a1298c on my own test I thought "I need more mb12" and deciding to increase that has been a good idea so far but it's not like I carefully measured what I was taking.

As for histamine levels, well I don't know if the orthomolecular psychiatrists' description of "histadelia" isn't too simplistic but I remember Nightingale saying the descriptions he read online seemed very similar to what he was experiencing. Of course their description of high and low histamine levels are confusing as there are similarities between the 2 and without an assay of tissue histamine levels it would seem nigh on impossible for someone to figure out which category you fell into. And it's a rough theory, with several flaws. I don't think it's fair to write it off completely however as genetic testing may show increasing relevance of methylation mutations to mast cell stability. i.e. the BH4 connection.

[B_Daniel]

Wanted to give everyone an update on my current status.  So this update will be in 2 parts. 
Part 1:
First off, i sent Herman the blood tests he asked for.  He pointed out that my RT3 was high and my RT3 ratio low.  He also said my potassium was low, TSH high, and adrenals were low.  I was skeptical because I fell within the range on all these items.  But I spent time researching  what he said and he was right.  My RT3 ratio of 10 indicated that I'm hypothyroid.  My low cortisol indicate that I have an adrenal problem.  My TSH of 2.5 is on the high end of what some doctors believe the range should be.  So maybe I have an adrenal and thyroid problem??  I reached out to the woman, Valerie, who runs adrenalsweb.org and sent her my labs.  She agreed that I have low adrenals and am hypothyroid and that this could completely explain my fatigue, anxiety and brainfog.  I then figured that I COULD order hydrocortisone for my adrenals and T3 for my thyroid over online sites, and self medicate myself.  But, if I truly have a thyroid and adrenal problem that shows up in my blood tests, why don't I go to an endocrinologist and be treated the right way.  For one, hydrocortisone and T3 are hormones, and once you go on them you may always need them.  So nothing I wanted to mess around with.  I knew it'd be difficult to find a good Endo, but I wanted to try.  I had my dad send my blood work to one doctor he knew, who told me i was completely fine.  My GF, a medical resident at a top school, emailed the chief endo who is world reknown.  She sent him my cortisol and my labs and this note:

------------------------
Dear Dr. XXXX, (took out the name)
Have an interesting question for you about rT3 ratios (of which I'm unfamiliar with).  In general, is there any data to support the use of the T3/rT3 ratio in diagnosing hypo/hyperthyroidism?  I've done a brief lit search and haven't found much about it.

The reason I ask is that I've come across a case of a young adult man who reports low energy, constant fatigue, and most notably the inability to think clearly that he describes as "brain fog" impairing his ability to function normally.  These symptoms occur nearly daily.  He's been to several physicians who have done an extensive evaluation that has returned, unsurprisingly, normal (I've attached his thyroid studies, etc.).  However, he has done his own online research and has asked me to investigate whether or not there is any truth to the rT3 ratio.

 He also had his cortisol measures done using a home test kit with a 9AM cortisol of 4.6 (I've attached his graph compared to their controls).

Any thoughts?  Thanks for your time. 
------------------------------------------------

He e-mailed back a very thoughtful response....
-----------------

I am not aware of any scientific data indicating that the T3/rT3 is useful clinically. rT3 increases when the deiodinases that convert T4 to T3 are decreased by starvation and illness. One can then see an increase in rT3 and a decrease in T3 during illness. As you know TSH levels are the most accurate method for determining thyroid function as long as there is not pituitary/hypothalamic abnormalities. There is information on the WEB pushing the concept that rT3 inhibits the action of T3 by binding to the thyroid hormone receptor. If you want to read some fiction you can go to the following site

http://thyroid-rt3.com/canyou.htm

There are also WEB sites devoted to "adrenal fatigue". Again there is no scientific evidence for this syndrome. If you want to read even more fiction you can go to the following WEB site

http://www.adrenalfatigue.org/

 
I try to encourage my patients to to only use well recognized sites when they are reading about diseases on the WEB. There is an enormous amount of junk out there. One of the endocrine fellows a few years ago gave a talk on the endocrine myths on the WEB.

I hope this addresses your questions. If you need more information or have additional questions let me know.
---------------------------------

While it's convenient for me to say, he doesn't know what he's talking about but Valerie the webmaster at adrenalsweb.org does -that's tough for me to buy in to.  I'm beginning to side somewhat towards these doctors in that... I bet a lot of people with similar lab readings to me are perfectly perfectly fine.  However, given my symptoms, maybe the slight abnormalities in my readings should be given more scrutiny than you would give someone who feels fine.  Based on this, is it worth the risk of trying these hormones without medical supervision?  One of my doctors may even help me try it.  But do I want to go down that path yet?  I've decided I still have other ideas to test before I do anything extreme like that.  The next idea I'm going to include in the next post...