Veteran Member
  • Content count

  • Joined

  • Last visited

Community Reputation

140 Excellent


About guitarman01

Veteran Member


Silver Poster
Posted at least 500 different posts
20 posts
100 posts
500 posts
2000 posts
No reviews awards
Review at least 1 product
1 product
5 products
10 products
25 products

Recent Profile Visitors

2,288 profile views
  1. 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;spage=587;epage=588;aulast=Uyar 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 Genç2, Ayse Gökduman4 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 Fevzipaşa Bulvarı Basmane, Izmir Turkey Source of Support: None, Conflict of Interest: None Check 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 “p” 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.
  2. 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. 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. 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.)
  3. 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. 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?
  4. Vitamin B12 and 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. Table 2: Vitamin B12's Purported Mechanisms of Action
  5. 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.
  6. 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.
  7. Here is a questionable gene mutation right 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? rs732774(A;G) more info 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 Topics Pharma DMET ClinVar Other Wilson disease not specifie Association of K832R and R952K SNPs of Wilson's disease gene with Alzheimer's disease. Bucossi S1, Polimanti R, Mariani S, Ventriglia M, Bonvicini C, Migliore S, Manfellotto D, Salustri C, Vernieri F, Rossini PM, Squitti R. Author information 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) ε4 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 ε4 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.
  8. 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 a sign of liver disease in general. Wilson disease: changes in methionine metabolism and inflammation affect global DNA methylation in early liver disease 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. Hepatic Sahh transcript 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-α) levels. Dnmt3b was down-regulated in tx-j mice together with global DNA hypomethylation. PCA treatment of tx-j mice reduced Tnf-α and ALT levels, betaine treatment increased S-adenosylmethionine and up-regulated Dnmt3b levels, and both treatments restored global DNA methylation levels. Conclusion: reduced hepatic Sahh expression 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.
  9. here is another interesting mutation I have. Very rare. Reduced conversion of beta-carotene to retinol Reduced BCMO1 activity results in 32% lower ability to convert Beta-carotene to retinyl esters and higher serum beta-carotene levels. See also rs12934922. rs12934922 (R267S) and rs7501331 (A379V) double mutant have a reduced catalytic activity of beta-carotene by 57%. Female volunteers carrying the T variant of rs7501331 (379V) had a 32% lower ability to convert Beta-carotene, and those carrying at least one T in both SNPs show a 69% lower ability to convert Beta-carotene into retinyl esters. rs7501331: the frequency of the wild-type C allele and variant T allele was 76 and 24%, respectively; 56% of the population was CC wild-type genotype, and 39% was heterozygote CT with the TT variant present in 5% of the population. rs12934922: the frequency of the wild-type A allele and variant T allele was 58 and 42%, respectively; 38% of the population was AA wild-type genotype, 40% was heterozygote AT, and 22% was TT homozygote more info Bad Repute 2 Magnitude 4.5% Frequency I also have this on top of the other mutation I posted for b12. rs602662(G;G) Lower vitamin B12 levels We found that the SNP '''rs602662''' was significantly associated with the levels of vitamin B(12) (p value<0.0001). We also found that individuals adhering to a vegetarian diet with GG (homozygous major genotype) have significantly '''lower''' levels of vitamin B(12) in these individuals. [PharmGKB:Non-Curated GWAS results: Genome-wide Association Study of Vitamin B6, Vitamin B12, Folate, and Homocysteine Blood Concentrations. (Initial Sample Size: 2,934 individuals; Replication Sample Size: 686 individuals); (Region: 19q13.33; Reported Gene(s): FUT2; Risk Allele: rs602662-A); (p-value= 3E-20).This variant is associated with Folate pathway vitamins.] [OMIM:VITAMIN B12 PLASMA LEVEL QUANTITATIVE TRAIT LOCUS 1; B12QTL1] [GWAS:Folate pathway vitamins] more info Bad Repute 2 Magnitude 18.6% Frequency
  10. 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.
  11. 520. Range 180 up to 1100 pg/ml Is that too low for a 20 year old. I guess it would be better to be nearer the top of the range. One Japanese study states the normal limits as 500–1,300 pg/mL.[42] I would like to look at a lot more serum results in the normal population at different ages and male/female compared to post accutane users. I would like to know how this blood level would and should normally respond to oral supplements.
  12. I would say this is could be insignificant unless a couple other people had this same mutation. Then it could be very significant. What was your b12 level btw? Did you ever have this tested?
  13. You guys got this gene mutation? I do. affects b12 transport and serum levels frequency is only 4.4 percent of being a carrier rs526934(G;G) Genome-wide significant predictors of metabolites in the one-carbon metabolism pathway. G allele associated with lower serum Vitamin B12. 'The TCN1 rs526934 G variant may reduce transport of cobalamin, resulting in lower plasma vitamin B12 levels.' [PharmGKB:Non-Curated GWAS results: Genome-wide Association Study of Vitamin B6, Vitamin B12, Folate, and Homocysteine Blood Concentrations. (Initial Sample Size: 2,934 individuals; Replication Sample Size: 686 individuals); (Region: 11q12.1; Reported Gene(s): TCN1; Risk Allele: rs526934-A); (p-value= 0.000002).This variant is associated with Folate pathway vitamins.] [GWAS:Folate pathway vitamins] more info 4.4% Frequency
  14. epigenetic modification may regulate the expression of GNMT Nutritional and hormonal modulation of glycine N-methyltransferase: implications for aberrant methyl group metabolism Bunch of information on Retinoids effects on here.
  15. anyone even hitting over 600 pg/ml of vitamin b12 in their blood tests? My highest is maybe around 550 pq/ml, my lowest was in the 400s I just posted that study how accutane reduces b12 levels. maybe my normal pre-accutane used to be alot higher then 550. alot of these people are hitting in the 1000s for b12 serum levels.
  16. Not really sick in the traditional sense no. But people have had ongoing issues with sinuses, ear fullness, breathing,headaches, so its hard to tell what qualifies as sick anymore. Not sure if this correlates with testosterone, i've hit fairly T high numbers in the past, not supplementing anything.
  17. who is that? Im starting to notice alot of different supplements having similar effects. From b12, to vitamin D, zinc and numerous others. there is not one supplement I still take to this day since day 1 many years ago since looking into supplements, and I think that says alot. I believe there is some type of chronic inflammation going on in and around the stomach, that depending on what you take might just worsen this. One thought is for some reason there is increased acid production being generated by alot of different supplements that might already be chronically increased due to accutane. This could trigger a immune type response that could effect the whole body in various ways. Still looking into this.
  18. On a different note. If you want to find out if accutane is still floating around in your blood, you find a university that can replicate this study. Determination of 13-cis-retinoic acid and its major metabolite, 4-oxo-13-cis-retinoic acid, in human blood by reversed-phase high-performance liquid chromatography. Vane FM, Stoltenborg JK, Buggé CJ. Abstract A high-performance liquid chromatography (HPLC) method for the quantitation of 13-cis-retinoic acid (13-cis-RA) and its major metabolite, 4-oxo-13-cis-RA, in human blood has been developed. The method includes extraction of 1 ml of blood with diethyl ether at pH 6 and the analysis of the extract by reversed-phase HPLC with solvent programming and detection at 365 nm. The quantitation ranges for 13-cis-RA and 4-oxo-13-cis-RA are 10--2000 and 50--2000 ng/ml of blood, respectively. The method also provides estimates of the concentrations of all-trans-RA and 4-oxo-all-trans-RA. The mean intra- and inter-assay variabilities for all four compounds were 6% or less. The method separates 13-cis-RA and 4-oxo-13-cis-RA from 9-cis-RA, all-trans-RA, 4-oxo-all-trans-RA, and some other possible metabolites, such as hydroxy and epoxy retinoic acids. The method has been successfully applied to the analyses of over 1200 blood samples from four 13-cis-RA clinical studies.
  19. if nobody has gotten this sort of test in the past, this would be a good test to take when it comes to process of elimination. Amino Acids, Quantitative, Plasma Overview Specimen Clinical and Interpretive Performance Fees and Coding LIS Resources Setup Information: Excel | PDF Sample Report Abnormal Report Setup Reference Guide Useful For Evaluating patients with possible inborn errors of metabolism May aid in evaluation of endocrine disorders, liver diseases, muscle diseases, neoplastic diseases, neurological disorders, nutritional disturbances, renal failure, and burns Testing Algorithm Includes quantitation of the following amino acids: taurine, threonine, serine, asparagine, glutamic acid, glutamine, proline, alanine, citrulline, alpha-amino-n-butyric acid, valine, cystine, methionine, isoleucine, leucine, tyrosine, phenylalanine, beta-alanine, ornithine, lysine, histidine, argininosuccinic acid, allo-isoleucine, arginine, phosphoserine, phosphoethanolamine, hydroxyproline, glycine, aspartic acid, ethanolamine, sarcosine, 1-methylhistidine, 3-methylhistidine, carnosine, anserine, homocitruline, alpha-aminoadipic acid, gamma-amino-n-butyric acid, beta-aminoisobutyric acid, hydroxylysine, cystathionine, and tryptophan. Clinical Information Amino acids are the basic structural units that comprise proteins and are found throughout the body. Many inborn errors of amino acid metabolism, including phenylketonuria and tyrosinemia, have been identified. Amino acid disorders can manifest at any age, but most become evident in infancy or early childhood. These disorders result in the accumulation or the deficiency of 1 or more amino acids in biological fluids, which leads to the clinical signs and symptoms of the particular amino acid disorder. The clinical presentation is dependent upon the specific amino acid disorder. In general, affected patients may experience failure to thrive, neurologic symptoms, digestive problems, dermatologic findings, and physical and cognitive delays. If not diagnosed and treated promptly, amino acid disorders can result in mental retardation and death. Treatment for amino acid disorders includes very specific dietary modifications. Nonessential amino acids are synthesized by the body, while essential amino acids are not and must be obtained through an individual's diet. Therapeutic diets are coordinated and closely monitored by a dietician and/or physician. They are structured to provide the necessary balance of amino acids with particular attention to essential amino acids and those that accumulate in a particular disorder. Patients must pay close attention to the protein content in their diet and generally need to supplement with medical formulas and foods. Dietary compliance is monitored by periodic analysis of plasma amino acids.
  20. I wonder if a full amino acid profile would reveal anything? In the case of a GNMT deficiency there could be elevated methionine. This could indicate a ongoing problem with proteins and sulfur. I know this is GNMT induction. But could this lead to depletion?
  21. Been posted before. But it would be nice to test this once and for all. If not on a DNA level, I know there was some expensive and elaborate blood tests that Rich talked about. Vitamin A and its derivatives induce hepatic glycine N-methyltransferase and hypomethylation of DNA in rats. Rowling MJ1, McMullen MH, Schalinske KL. Author information Abstract Regulation of S-adenosylmethionine (SAM) and the SAM/S-adenosylhomocysteine (SAH) ratio by the key cytosolic enzyme glycine N-methyltransferase (GNMT) is essential in optimizing methyl group supply and subsequent functioning of methyltransferase enzymes. Therefore, inappropriate activation of GNMT may lead to the loss of methyl groups vital for many SAM-dependent transmethylation reactions. Previously, we demonstrated that the retinoid derivatives 13-cis- (CRA) and all-trans-retinoic acid (ATRA) mediated both the activity of GNMT and its abundance. The present study was conducted to determine whether vitamin A had a similar ability to up-regulate GNMT and to assess the biological importance of GNMT modulation by examining both the transmethylation and transsulfuration pathways after retinoid treatment. Rats were fed a control (10% casein + 0.3% L-methionine) diet and orally given retinyl palmitate (RP), CRA, ATRA or vehicle daily for 10 d. RP, CRA and ATRA elevated hepatic GNMT activity 32, 74 and 124%, respectively, compared with the control group. Moreover, the retinoid-mediated changes in GNMT activity were reflected in GNMT abundance (38, 89 and 107% increases for RP-, CRA-, and ATRA-treated rats, respectively). In addition, hepatic DNA, a substrate for SAM-dependent transmethylation, was hypomethylated (approximately 100%) after ATRA treatment compared with the control group. In contrast, the transsulfuration product glutathione was unaffected by retinoid treatment. These results provide evidence of the following: 1) vitamin A, like its retinoic acid derivatives, can induce enzymatically active GNMT; and 2) inappropriate induction of GNMT can lead to a biologically important loss of methyl groups and the subsequent impairment of essential transmethylation processes.
  22. I am realizing a picture here that could point to cardiovascular issues, starting with the blood vessels.(im thinking restricted blood flow,narrowing of arteries, connective tissue) Remember this? Accutane, Methylation Block and Glycine N-Methyltransferase I want to be able to look at each and every snp having to due with the GNMT gene to see if their are any mutations. Same with a few other genes. lets say accutane was capable of mutating the GNMT gene in certain susceptible individuals. Couple this with already inherited mutations at the CBS,MTHFR this could be bad and this could theoretically double your risk for the health related issues these gene mutations are capable of causing. oh and I was just reading my bottle of TMG: Betaine anhydrous, or TMG is known to facilitate methylation processes. Methylation is a normal biological process that is critical for DNA repair, liver detoxification mechanisms, lipid metabolism, and the production of SAM-E TMG (Trimethylglycine) has been shown to be a safe and effective methyl donor for the facilitation of methylation processes. I want to preface this is just another thought, but worth following up on if possible.
  23. Is there more complete DNA testing available to the consumer other then 23andme? what about ancestry or family tree? I ask because im trying to look up snps based on the GNMT gene and it looks like 23andme might be missing some data? I check snpedia and it mentions a certain SNP is on Ancestry v2? here is a example. I want to look into this but is 23andme just missing this information/didnt test this SNP? anyone can feel free to answer. rs121907888 Orientation plus Stabilized plus Geno Mag Summary (T;T) 0 common in clinvar Make rs121907888(C;C) Make rs121907888(C;T) Reference GRCh38 38.1/141 Chromosome 6 Position 42960916 Gene GNMT is a snp is mentioned by dbSNP rs121907888 ClinGen rs121907888 ebi rs121907888 HLI rs121907888 Exac rs121907888 Varsome rs121907888 Map rs121907888 PheGenI rs121907888 hapmap rs121907888 1000 genomes rs121907888 hgdp rs121907888 ensembl rs121907888 gopubmed rs121907888 geneview rs121907888 scholar rs121907888 google rs121907888 pharmgkb rs121907888 gwascentral rs121907888 openSNP rs121907888 23andMe rs121907888 23andMe all rs121907888 SNP Nexus SNPshot rs121907888 SNPdbe rs121907888 MSV3d rs121907888 GWAS Ctlg rs121907888 Max Magnitude 0 OMIM 606628 Desc Variant 0001 Related also ClinVar Risk rs121907888(C;C) Alt rs121907888(C;C) Reference Rs121907888(T;T) Significance Pathogenic Disease Glycine N-methyltransferase deficiency Variation info Gene CNPY3-GNMT GNMT CLNDBN Glycine N-methyltransferase deficiency Reversed 0 HGVS NC_000006.11:g.42928654T>C CLNSRC OMIM Allelic Variant UniProtKB (protein) CLNACC RCV000004386.3,
  24. Do you recall anyone getting b12 shots that's posted on this thread?