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As far as your guys side effects go...
Did you just wake up with them one morning or did they get progressively worse with time? Once again I just find this super interesting because for me everything started with minor fatigue/depersonalization that kicked in while I was a month into the pill and then things started to get gradually worse while other things got better. It's just so strange. And it makes me wonder because they say thyroid/hormone problems get gradually worse when not treated. Has anyone actually had hypothyroidism as a result of accutane ?
3 hours ago, cnb30 said:If the core problem of accutane is the retinoid issue, does that mean this is permaneant. Is there any hope that this can be undone, or does anybody know if undoing retinoid changes is possible, or being researched?
For sure we will never get any research going if no one reports their side effects.
1 hour ago, Colinboko said:As far as your guys side effects go...
Did you just wake up with them one morning or did they get progressively worse with time? Once again I just find this super interesting because for me everything started with minor fatigue/depersonalization that kicked in while I was a month into the pill and then things started to get gradually worse while other things got better. It's just so strange. And it makes me wonder because they say thyroid/hormone problems get gradually worse when not treated. Has anyone actually had hypothyroidism as a result of accutane ?
Mine was gradual and worsened over time, started to notice after completing accutane. Started with diffuse hair loss including eyebrows, body hair, then unusual facial flushing, headaches, problems concentrating, then years down the line, developed coating on my tongue, light sensitivity. Have had many, many blood test, not one has come back abnormal. In all my studying though, at least when it comes to nutrients, blood test might not show the whole picture when it comes to tissue levels like the brain, spinal fluid, muscles,skin. So you can have a deficiency on a cellular level while still showing in range or normal on a blood test. So you look at clinical symptoms. I've seen cases of confirmed b12 deficiency while still having normal blood test. This can be the case for numerous vitamins/minerals. Same with toxicity that could show "normal". Thats why ive started to look at what are normal levels in the general population. But to start questioning all the results that come back normal or in range, becomes a little maddening as well. As far as thyroid, havent seen it as a main issue. The thing is people want it to be this or want it to be that, so they can figure it out on simpler terms, have a sense of closure and move on with their lives. Just like im doing right now looking at b12. It becomes a obsession.
here is another interesting mutation I have. Very rare.
more info
| Bad | Repute |
| 2 | Magnitude |
| 4.5% | Frequency |
I also have this on top of the other mutation I posted for b12.
more info
| Bad | Repute |
| 2 | Magnitude |
| 18.6% | Frequency |
Sound familiar? I got some interesting zinc and copper numbers to post when I get a chance, after taking 100mg of zinc for a few weeks and then checking my copper levels. This is just a example if there was excess copper storage/abnormal transport going on what its capable of. Or possibly asign of liver disease in general.
Wilson disease: changes in methionine metabolism and inflammation affect global DNA methylation in early liver disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566330/
Hepatic methionine metabolism may play an essential role in regulating methylation status and liver injury in Wilson disease (WD) through the inhibition of S-adenosylhomocysteine hydrolase (SAHH) by copper (Cu) and the consequent accumulation of S-adenosylhomocysteine (SAH). We studied the transcript levels of selected genes related to liver injury, levels of SAHH, SAH, DNA methyltransferases genes (Dnmt1, Dnmt3a, Dnmt3b) and global DNA methylation in the tx-j mouse (tx-j), an animal model of WD. Findings were compared to those in control C3H mice, and in response to Cu chelation by penicillamine (PCA) and dietary supplementation of the methyl donor betaine to modulate inflammatory and methylation status. Transcript levels of selected genes related to endoplasmic reticulum stress, lipid synthesis, and fatty acid oxidation were down-regulated at baseline in tx-j mice, further down-regulated in response to PCA, and showed little to no response to betaine. HepaticSahhtranscript and protein levels were reduced in tx-j mice with consequent increase of SAH levels. Hepatic Cu accumulation was associated with inflammation, as indicated by histopathology and elevated serum ALT and liver tumor necrosis factor alpha (Tnf-) levels.Dnmt3bwas down-regulated in tx-j mice together with global DNA hypomethylation. PCA treatment of tx-j mice reducedTnf-and ALT levels, betaine treatment increased S-adenosylmethionine and up-regulatedDnmt3blevels, and both treatments restored global DNA methylation levels. Conclusion: reduced hepaticSahhexpression was associated with increased liver SAH levels in the tx-j model of WD, with consequent global DNA hypomethylation. Increased global DNA methylation was achieved by reducing inflammation by Cu chelation or by providing methyl groups. We propose that increased SAH levels and inflammation affect widespread epigenetic regulation of gene expression in WD.
Here is a questionable gene mutationright here indicating that I might have a problem with copper
23andme does not include all these genes, it would be nice to be able to look at them all. You can be heterozygous for Wilsons disease, which means you can have a issue with copper, it just doesn't manifest into full blown wilson's disease that needs treatment. But this coupled with Accutane?
| Other | ClinVar Significance |
| 50.4% | Frequency |
| 0.4803 | GMAF |
| 2 | References |
| ATP7B | Gene |
| 13 | Chromosome |
| 51949672 | Position |
| 0 | Max Magnitude |
| 20161218 | Rs time |
| minus | Stabilized |
| minus | Orientation |
Association of K832R and R952K SNPs of Wilson's disease gene with Alzheimer's disease.
Abstract
Copper homeostasis appears abnormal in Alzheimer's disease (AD) patients. The aim of this study was to assess whether loci of susceptibility for AD lie in the Wilson's disease (WD) ATP7B gene. We studied single nucleotide polymorphisms (SNPs) K832R (c.2495 A>G, rs1061472) and R952K (c. 2855 G>A, rs732774) of the WD gene in 251 AD patients and 201 healthy controls. We also evaluated their relation with apolipoprotein E (ApoE) 4 allele frequency. R allele in K832R [adjusted Odds Ratio (OR) = 1.71 (1.12-2.60); p = 0.012] and the K allele in R952K [adjusted OR = 1.82 (1.19-2.80); p = 0.006] ATP7B SNPs were associated with an increased risk of developing AD, as well as the haplotype R832/K952, containing the 2 risk alleles (X2 = 4.85; p = 0.028). Conversely, the K832/R952 haplotype appeared to confer protection against the disease (X2 = 7.21; p = 0.007). No difference in the frequency of the ATP7B alleles between carriers and non-carriers of the ApoE 4 variant was revealed. The linkage disequilibrium (LD) analysis revealed an association between K832R and R952K substitutions in both AD patients (D' = 0.79) and controls (D' = 0.81). A high LD between K832R and R952K was also confirmed in all HapMap populations. Our investigation demonstrated the presence of loci of susceptibility for AD in the WD ATP7B gene, supporting a role of copper dysfunction in contributing or accelerating neurodegenerative processes leading to AD.
22 hours ago, guitarman01 said:Sound familiar? I got some interesting zinc and copper numbers to post when I get a chance, after taking 100mg of zinc for a few weeks and then checking my copper levels. This is just a example if there was excess copper storage/abnormal transport going on what its capable of. Or possibly asign of liver disease in general.
Wilson disease: changes in methionine metabolism and inflammation affect global DNA methylation in early liver disease
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3566330/
Hepatic methionine metabolism may play an essential role in regulating methylation status and liver injury in Wilson disease (WD) through the inhibition of S-adenosylhomocysteine hydrolase (SAHH) by copper (Cu) and the consequent accumulation of S-adenosylhomocysteine (SAH). We studied the transcript levels of selected genes related to liver injury, levels of SAHH, SAH, DNA methyltransferases genes (Dnmt1, Dnmt3a, Dnmt3b) and global DNA methylation in the tx-j mouse (tx-j), an animal model of WD. Findings were compared to those in control C3H mice, and in response to Cu chelation by penicillamine (PCA) and dietary supplementation of the methyl donor betaine to modulate inflammatory and methylation status. Transcript levels of selected genes related to endoplasmic reticulum stress, lipid synthesis, and fatty acid oxidation were down-regulated at baseline in tx-j mice, further down-regulated in response to PCA, and showed little to no response to betaine. HepaticSahhtranscript and protein levels were reduced in tx-j mice with consequent increase of SAH levels. Hepatic Cu accumulation was associated with inflammation, as indicated by histopathology and elevated serum ALT and liver tumor necrosis factor alpha (Tnf-) levels.Dnmt3bwas down-regulated in tx-j mice together with global DNA hypomethylation. PCA treatment of tx-j mice reducedTnf-and ALT levels, betaine treatment increased S-adenosylmethionine and up-regulatedDnmt3blevels, and both treatments restored global DNA methylation levels. Conclusion: reduced hepaticSahhexpression was associated with increased liver SAH levels in the tx-j model of WD, with consequent global DNA hypomethylation. Increased global DNA methylation was achieved by reducing inflammation by Cu chelation or by providing methyl groups. We propose that increased SAH levels and inflammation affect widespread epigenetic regulation of gene expression in WD.
Ok, so what do people who have Wilson's disease take??
Regardless of what condition you have after Accutane you're either going to have to take a drug/supplement combined with possibly eliminating things to get out of this mess - what would that be in relation to Wilson's disease?
Also due to the ever increasing confusion of which path to follow, do people with Wilson's disease have thyroid issues, do they have testosterone issues and B12 issues and all these other conditions that we discuss on this forum??
Just trying to connect the dots and eliminate more confusion....
51 minutes ago, TrueJustice said:Ok, so what do people who have Wilson's disease take??
Regardless of what condition you have after Accutane you're either going to have to take a drug/supplement combined with possibly eliminating things to get out of this mess - what would that be in relation to Wilson's disease?Also due to the ever increasing confusion of which path to follow, do people with Wilson's disease have thyroid issues, do they have testosterone issues and B12 issues and all these other conditions that we discuss on this forum??
Just trying to connect the dots and eliminate more confusion....
im going to be looking into this further through various doctors and testing before commenting too much. I glanced at a study not too long ago that isotretinoin might be capable of enhancing some of these mutations people have or increasing the chance of negative effects from normally dormant mutations. Basically if you got this,this and this going on and then you take accutane,(gene mutations, problems processing copper,predisposed liver or mental conditions) it might lead to the "perfect storm" in a sense and the way your body functions is changed, like in the hypomethylation studies that have been posted as a example. DNA healing and repair changes. These changes I image could be wide ranging and have numerous systemic effects on the body. Probably as time goes on as well, which is really what concerns me the most.
I honestly dont have any concrete answers at the moment. If I could snap my fingers and take any and every blood test I wanted to take, I think I would find something. But some of these are very expensive and I need to find the right doctor or doctors that are willing to play detective for me and have the knowledge, understanding, compassion and time to help me explore and get some of these tests so I can get them covered by insurance. I have a MRA test pending and regardless of what the results show, Ive already contacted and started the process of setting up a appointment at the mayo clinic, that has one of the top neurologist departments in the world. They turn down alot of people though so we will see. If not I have a couple university options not far from me as well to finally try to fully investigate things.
4 hours ago, Colinboko said:Why am I experiencing such terriblevoice loss/hoarseness..? I'm a singer (like professionally) so this definitely won't fly...
Mumbling and stuttering are common side effects for sure.
Please report your side effects by reporting o adverse side effects in your country plus directly to the Review committee in Europe.
I have posted all the emails.
Many thanks
On 4/19/2017 at 0:16 PM, hatetane said:On 4/10/2017 at 2:06 AM, hatetane said:Time to be proactive!!
There is going to be a review of accutane in JUNE this year.
I want each and everyone of you from Europe to write the best email you can.
Send it to the representatives of your country and to as many independents as possible.
For those of you outside of the UK please send to all independents and to as many others as you can especially
to the MHRA in the UK.
This as a minimum, everyone send to as many representatives as you can. Once you have composed an email it is simply a matter of re-sending.
You must include your name ( data protection will protect you) age, dosage, duration and how long post A.
A complete and thorough list of all your side effects.
You must tell your story about how and when your sides evolved.
Write about your full experience but I especially ask that you concentrate on sexual dysfunction (brain - penis disconnect) and any sides that are not listed on the PIL.
For anyone who has or still is - talk about depression and try and describe it. I believe that many doctors think you are all depressed because of your acne and you really have to convey how this unique depression gets hold of you and how long it lasts.
For those of you who feel they have had there personalties change and or depersonalisation please describe it.
Most importantly talk about any suicidal ideation or attempts.
Please mention how accutane has effected and or interrupted your study/work.
Mention how you feel about accutane and any regrets you might have about taking it.
Write about any recovery and the time this has taken.
Add a brief detail about the response of you doctors and finish of with:
1 I have reported my sides to .......
2 I have never reported my side effects.This is your opportunity to protest and have your voice heard. It will probably take you an hour which is less time than it would take to visit you GP.
I want you all to post on here when you have done it so as to encourage others to participate.
This is not a lot to ask, no excuses are acceptable .
We are trying to get better 'Patient Information' for anyone being giving accutane in the future - if you feel stronger than this then say so.Please, Please participate.
http://www.ema.europa.eu/ema/index.jsp?curl=pages/contacts/PRAC/people_listing_000112.jsp#MNMSPlease copy and paste on any other forums you use and let us know that you have done this.
Many many thanks.
Who is participating - PM me please
ANYONE REPORTED YET - IF NOT WHY NOT?
IF YOU WANT RESEARCH CARRIED OUT YOU NEED TO PARTICIPATE!
THIS IS OUR CHANCE TO BE HEARD.
4 hours ago, Colinboko said:Why am I experiencing such terriblevoice loss/hoarseness..? I'm a singer (like professionally) so this definitely won't fly...
This could be acid reflux, muscle weakness or some kind of chronic inflammation maybe similar to a allergy, similar maybe to a mast cell activation disorder. Ive had it too. actually got diagnosed with eosinophilic esophagitis, this is a type of allergic reaction to something. been diagnosed twice now with eosinophils in my esophagus, which they are not suppose to be there.
7 minutes ago, hatetane said:Mumbling and stuttering are common side effects for sure.Please report your side effects by reporting o adverse side effects in your country plus directly to the Review committee in Europe.
I have posted all the emails.
Many thanks
4 hours ago, Colinboko said:Why am I experiencing such terriblevoice loss/hoarseness..? I'm a singer (like professionally) so this definitely won't fly...
Mumbling and stuttering are common side effects for sure.
Please report your side effects by reporting o adverse side effects in your country plus directly to the Review committee in Europe.
I have posted all the emails.
Many thanks
6 minutes ago, guitarman01 said:4 hours ago, Colinboko said:Why am I experiencing such terriblevoice loss/hoarseness..? I'm a singer (like professionally) so this definitely won't fly...
This could be acid reflux, muscle weakness or some kind of chronic inflammation maybe similar to a allergy, similar maybe to a mast cell activation disorder. Ive had it too. actually got diagnosed with eosinophilic esophagitis, this is a type of allergic reaction to something.
MANY PFS GUYS REPORT THIS SYMPTOM
1 hour ago, hatetane said:Mumbling and stuttering are common side effects for sure.Please report your side effects by reporting o adverse side effects in your country plus directly to the Review committee in Europe.
I have posted all the emails.
Many thanks
I think reporting is important, in Australia I've insisted my doc reports my side effects - especially as my record for discussing issues goes all the way back to 2001, I'll be following this up shortly when I go back to discuss recent blood tests.
I have to ask though, at what point do you think the authorities will say " oh my god can you believe all these people experiencing side effects, we had no idea - lets get a group of scientists on to it immediately, these people need our help" As if they're not aware of the dangers of this drug - it's known already. Unfortunately the argument will always be, most people who go on Accutane won't experience too many ongoing side effects and if I'm being completely honest about this, statistically they are probably right, that doesn't help us though does it.
Given this drug has been on the market for something like 35 years and given the side effects known are put on packaging etc or documented, this could only of come about due to people reporting negative side effects over many years correct? and yet did that stop the drug from being sold - NO it hasn't.
Suicide, bowel cancer, kids crashing planes into buildings, congressman's children dying all due to Accutane and yet it's still available??I don't see how the dozen or so regulars on this forum can change all this by reporting?
All the frustration of trying to tell doctors/specialists by mentioning Roaccutane is a waste of time really, I've learnt that you're better off just trying to focus on what you can change. Debating issues and side effects and coming back to Accutane each time just creates more mental anguish - even with those smart, sympathetic doctors who I respect, the best response I've had is "I'm really sorry you have to deal with this".......
6 hours ago, TrueJustice said:I think reporting is important, in Australia I've insisted my doc reports my side effects - especially as my record for discussing issues goes all the way back to 2001, I'll be following this up shortly when I go back to discuss recent blood tests.I have to ask though, at what point do you think the authorities will say " oh my god can you believe all these people experiencing side effects, we had no idea - lets get a group of scientists on to it immediately, these people need our help" As if they're not aware of the dangers of this drug - it's known already. Unfortunately the argument will always be, most people who go on Accutane won't experience too many ongoing side effects and if I'm being completely honest about this, statistically they are probably right, that doesn't help us though does it.
Given this drug has been on the market for something like 35 years and given the side effects known are put on packaging etc or documented, this could only of come about due to people reporting negative side effects over many years correct? and yet did that stop the drug from being sold - NO it hasn't.
Suicide, bowel cancer, kids crashing planes into buildings, congressman's children dying all due to Accutane and yet it's still available??I don't see how the dozen or so regulars on this forum can change all this by reporting?All the frustration of trying to tell doctors/specialists by mentioning Roaccutane is a waste of time really, I've learnt that you're better off just trying to focus on what you can change. Debating issues and side effects and coming back to Accutane each time just creates more mental anguish - even with those smart, sympathetic doctors who I respect, the best response I've had is "I'm really sorry you have to deal with this".......
How long you been debating side effects? Good luck with that!!
Get of your backside and try to get patients informed about the dangers of accutane.
That is what I am trying to do.
Every patient has the right to know ALL the possible side effects of all prescribed medications.
You can try and make changes like many greats have done before or you can except things as they are.
Accutane may have ruined your life but kids are still taking this drug everyday - think of them!!!
Guitarman - I have no time for any drugs/medications but have you you researched
http://www.webmd.com/drugs/2/drug-7560/penicillamine-oral/details
and
https://en.wikipedia.org/wiki/Vasopressin
I haven't had a proper look at these yet but though you might want to look them up.
Hyaluronidase.
Remember I have not researched any of this yet!
DRUGS FOR THE RELIEF OF SOFT-TISSUE INFLAMMATION 10.3.1 Enzymes Hyaluronidase
Vitamin B12and folic acid, with their interrelated metabolism, are important for the maintenance of various metabolic pathways in the body. In cases of deficiency, adverse effects on cardiovascular, neurological, psychological, hematological, gastrointestinal, locomotor (musculoskeletal) and immunological systems may occur.[8]
We all know these levels are coming back in range. I wonder if this needs to be further investigated though.
I've also had my homocysteine levels checked multiple times it hovers around 10, range is 0-15.
http://www.townsendletter.com/FebMarch2011/b12psych0211.html
Table 2: Vitamin B12's Purported Mechanisms of Action
1. Increases S-adenosylmethionine, which participates in the formation of phospholipids that comprise neuronal myelin sheaths and cell receptors, and the formation of monoamine neurotransmitters
2. Lowers plasma and brain levels of homocysteine, which might mitigate, reverse, and potentially normalize damaged brain neurons
3. Corrects inborn errors of metabolism
4. Corrects deficient methylation processes
5. Corrects altered gene expression
6. Resolves long-latency vitamin B12 debt (?)
7. Has anti-inflammatory propertiesReport #2: Sixty-One Patients: Serum vs. Brain Status of Vitamin B12
This study sought to determine to what extent vitamin B12 in the serum is a real reflection of vitamin B12 status of brain tissue.5It comprised 3 groups of patients and 1 control group. Group 1 involved 23 patients aged 60 to 85 with dementia, group 2 involved 16 patients aged 30 to 60 with organic affective syndrome, group 3 involved 10 female patients aged 25 to 40 with postnatal depression (and complaints of neurasthenia), and the control group was 12 patients aged 25 to 50. All patients were normal hematologically, had normal liver function and kidney function tests, but did have evidence of "soft" neurologic symptoms (i.e., some combination of encephalopathy and/or polyneuropathy or neuropathy).When the serum levels of vitamin B12 were tested, normal values (200800 pg/ml; 148590 pmol/L) were found in 45 of the 49 patients from groups 1 through 3. All 12 patients in the control group had serum B12 levels in the normal range. Deficient cerebrospinal fluid levels (CSF) of vitamin B12 (<5 pg/ml; <3.7 pmol/L) were found in 30 of the total 49 patients (or in 26 of the 45 patients with normal serum levels). All 12 patients in the control group had CSF levels in the normal range (>10 pg/ml; >7.4 pmol/L). Because there was a marked difference between both compartments when measured, these results indicate that a potentially treatable vitamin B12 deficiency will be overlooked in a significant portion of patients if CSF B12 levels are not included in the assessment.
Table 1: Changes in Serum and CSF Vitamin B12 Concentrations following Treatment
Group Pretreatment
serum B12 (pg/ml)Pretreatment
CSF B12 (pg/ml)Posttreatment
serum B12 (pg/ml)Posttreatment
CSF B12 (pg/ml)IM injection (n = 10) 310 (229 pmol/L) (average) <5 (<3.7 pmol/L) (average) >2400 (>1771 pmol/L) (average) 70 (52 pmol/L) (average) Oral
(Patient #1)430 (317 pmol/L) 14 (10 pmol/L) 2400 (1771 pmol/L) 21 (15.5 pmol/L) Oral
(Patient #2)450 (332 pmol/L) <5 (<3.7 pmol/L) >2400 (>1771 pmol/L) 9.6 (7.1 pmol/L) Ten patients were given 6 weeks of twice weekly IM treatment of hydroxocobalamin (1000 mcg) plus daily treatment with an oral supplement containing 50 mg zinc-DL-aspartate and 250 mg of taurine. Two patients were given 6 weeks of a daily supplement containing cyanocobalamin (0.1 mg) plus 50 mg zinc-DL-aspartate and 250 mg of taurine.Table 1highlights the changes in both serum and CSF that resulted from vitamin B12 treatment. Treatment with IM hydroxocobalamin produced more significant increases than oral cyanocobalamin in the patients' CSF levels of vitamin B12.
In group 1 (patients with dementia), the authors speculate that zinc deficiency and its corresponding high levels of copper block the transport of B12 in the choroid plexus (and therefore, the CSF), similar to the effects of free radical chain reaction inducers like mercury, cadmium, and other neurotoxins. Group 2 (patients with organic affective syndrome), all had exposures to toxic chemicals (i.e., alcohol, industrial solvents, or halogenated hydrocarbons), which were considered causative in their neurasthenic-depressive clinical presentation. The authors speculate that these neurotoxins may block the entry of vitamin B12 into the brain, leading to CSF deficiency of the vitamin. In group 3 (patients with postnatal depression), the authors suggest that estrogens or estrogen-receptor binding chemicals (e.g., halogenated hydrocarbons) have an effect on B12 transport through the bloodbrain barrier and choroid plexus, thus causing deficiency of the vitamin with the CSF.WE really need to see how serum b12 levels should normally respond to oral supplements. After having a chance of looking at multiple studies(which I havent yet) and if oral supplements are able to push b12 levels into the 1000 or 2000 pq/ml range, and if we are not capable of hitting these blood levels, that could be a big clue.
cyanocobalamin (0.1 mg) This is a solution consisting of 5000mcg of b12 btw. This is just a small sample, but in this study 5000mcg of oral b12 for 6 weeks pushed both of these patients b12 blood levels into the 2000s.
Excellent post guitarman on B12.
Very interesting how it has a relationship with CSF. Can I ask though what the tell tale signs of low CSF are?? Or is it too much CSF?
This must play a role in light sensitivity and pressure in head correct that some of us have??
Also, given that many of us have tried supplementing either Multi B Vitamins or taking diff B Vit on their own perhaps we need to look at B12 injections - up the anti and go for broke to really boost levels!!
In the meantime I'm going to hit TMG along with a B Multi. The other day I started upping the dose of TMG and not long after I started sneezing and releasing mucous which in turn released some head pressure and light sensitivity, this was a positive result for me.
2 hours ago, TrueJustice said:Also, given that many of us have tried supplementing either Multi B Vitamins or taking diff B Vit on their own perhaps we need to look at B12 injections - up the anti and go for broke to really boost levels!!
If something abnormal was going on here with b12 absorption or transfer. Id actually want to trial what should be a appropriate oral dose for a extended amount of time,( say a month) to substantially raise b12 serum levels and then get blood tested. To possibly "catch " something wrong that could be going on if blood levels arent significantly raised. getting a b12 injection first would mess up the blood test result. But yea b12 injections are definitely worth looking into.
and people would want to know what their b12 levels are before any injections or supplements if possible.
2 hours ago, TrueJustice said:Can I ask though what the tell tale signs of low CSF are??
possible premature loss of brain volume or cerebral atrophy. Many various neurologic symptoms.
You ever get tested for b12 serum levels? Do you have access to the results?
3 hours ago, TrueJustice said:In the meantime I'm going to hit TMG along with a B Multi. The other day I started upping the dose of TMG and not long after I started sneezing and releasing mucous which in turn released some head pressure and light sensitivity, this was a positive result for me.
There is one scenario where TMG could raise methionine levels in the brain if for what ever reason we already had elevated methionine levels in the blood. So I would just be aware of this. The chance is probably slim though. This is due to a CBS deficiency which is very rare but alot of us do have mutations at this gene, and also if there was a induced GNMT deficiency, also very rare. Thats why id also like to get a amino acid blood test to rule this out completely, just in case. Im taking TMG myself at the moment 3grams twice a day.
3 hours ago, TrueJustice said:Also, given that many of us have tried supplementing either Multi B Vitamins or taking diff B Vit on their own perhaps we need to look at B12 injections - up the anti and go for broke to really boost levels!!
If something abnormal was going on here with b12 absorption or transfer. Id actually want to trial what should be a appropriate oral dose for a extended amount of time,( say a month) to substantially raise b12 serum levels and then get blood tested. To possibly "catch " something wrong that could be going on if blood levels arent significantly raised. getting a b12 injection first would mess up the blood test result. But yea b12 injections are definitely worth looking into.
and people would want to know what their b12 levels are before any injections or supplements if possible.
3 hours ago, TrueJustice said:Can I ask though what the tell tale signs of low CSF are??
possible premature loss of brain volume or cerebral atrophy. Many various neurologic symptoms.
You ever get tested for b12 serum levels? Do you have access to the results?
(Sorry for the double post, felt this might be important enough I wanted to get it on the next page.)
On 4/23/2017 at 8:16 PM, Chris16 said:Obviously this is just one persons opinion but could this be why some people experience positive changes when taking iodine?
[removed]
Everything on this thread is just "one person's opinion" because they want their problem to be in the spotlight. Thanks for sharing! Very interesting.
This is what you show your doctor if you want to fully investigate this. Including possible ultrasound. The one difference I see on here is looking at thyroid antibodies. This is not included in standard thyroid test.
| Year : 2016 | Volume : 82 | Issue : 5 | Page : 587-588 |
Effects of isotretinoin on the thyroid gland and thyroid function tests in acne patients: A preliminary study
Belkiz Uyar1, Aynur Solak2, Ali Saklamaz3, Muhittin Akyildiz4, Berhan Gen§2, Ayse G¶kduman4
1 Department of Dermatology, Faculty of Medicine, Sifa University, Izmir, Turkey
2 Department of Radiology, Faculty of Medicine, Sifa University, Izmir, Turkey
3 Department of Endocrinology, Faculty of Medicine, Sifa University, Izmir, Turkey
4 Department of Biochemistry, Faculty of Medicine, Sifa University, Izmir, Turkey
| Date of Web Publication | 4-Aug-2016 |
Correspondence Address:
Belkiz Uyar
35240, 172/2 FevzipaÅŸa Bulvar± Basmane, Izmir
Turkey
Source of Support: None, Conflict of Interest: None
DOI: 10.4103/0378-6323.182794
| Abstract |
Background: Isotretinoin is widely used in the treatment of acne. Aims: We investigated the effects of isotretinoin on thyroid function tests and thyroid volume in acne patients. Methods: In this prospective study, a total of 104 acne patients were included. Sixty-six patients were treated with isotretinoin for at least 4 months. Thirty eight patients were included in the control group. The levels of thyroid stimulating hormone, free triiodothyronine, free thyroxine, antithyroglobulin and antithyroid peroxidase antibodies were measured and a thyroid ultrasound was performed in all the subjects before treatment and 4 months after treatment. A œp value of < 0.05 was considered significant. Results: In the isotretinoin-treated group, thyroid stimulating hormone levels increased significantly during isotretinoin treatment (P = 0.018). Free triiodothyronine, free thyroxine, anti-thyroid peroxidase levels and thyroid volume decreased significantly during treatment (P = 0.016, P= 0.012, P= 0.006, P = 0.020 respectively). Limitations: The major limitation of this study is the lack of follow-up data after the cessation of isotretinoin therapy in acne patients. Conclusion: Patients treated with isotretinoin should be monitored with thyroid function tests.