Thyro-Gold or Nutri-Meds

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Thyro-Gold or Nutri-Meds

Unread postby JohnS » Thu May 09, 2013 9:25 am

Does anyone use these products? I'm interested in trying NDT but not sure how to go about it. I'm not getting much support from my doctor, all my Thyroid labs are normal, so I was thinking of trying something on my own.

My main symptoms are feeling sluggish especially when my hands and feet are freezing and lower than normal body temps.

Any help would be appreciated.
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Re: Thyro-Gold or Nutri-Meds

Unread postby MyUsernameHere » Thu May 09, 2013 11:03 am

Hello, I have used Thyrogold 150mg for the past month or so. I'm currently taking 2 caps and trying to work up to 3 but I'm having some problems.

The pills give me some issues like brain fog, difficulty thinking and concentrating. They also didn't do much to raise temps or pulse. When I try to take 3 caps a day, the brain fog simply gets even worse, but I think they helped a bit in reducing my heart palpitations.

I don't feel any rush or any effect of T3 when I take the pill, so I think there is too much T4 and too little T3.

They would probably work a lot better combined with cytomel. I haven't tried any other kind of thyroid yet so maybe it just doesn't work for me.
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Re: Thyro-Gold or Nutri-Meds

Unread postby FunkOdyssey » Thu May 09, 2013 12:39 pm

MyUsernameHere wrote:The pills give me some issues like brain fog, difficulty thinking and concentrating. They also didn't do much to raise temps or pulse. When I try to take 3 caps a day, the brain fog simply gets even worse, but I think they helped a bit in reducing my heart palpitations.


What's your diet like?
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Re: Thyro-Gold or Nutri-Meds

Unread postby key » Thu May 09, 2013 12:44 pm

nutri-meds seems to work for me
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Re: Thyro-Gold or Nutri-Meds

Unread postby MyUsernameHere » Thu May 09, 2013 2:55 pm

FunkOdyssey wrote:
MyUsernameHere wrote:The pills give me some issues like brain fog, difficulty thinking and concentrating. They also didn't do much to raise temps or pulse. When I try to take 3 caps a day, the brain fog simply gets even worse, but I think they helped a bit in reducing my heart palpitations.


What's your diet like?


I think it's pretty by the book, but I am experimenting a lot with eliminating/adding things as I'm still trying to figure out what is causing this pounding heart that I've had since November (pretty much since I started this diet), it's not on/off, I feel it every single moment of the day. Always worse after meals and hard exercise. There isn't anything I haven't tried and I'm starting to lose my mind over that.

But yeah, it seems dairy makes it worse so I try to avoid milk for now. I just have cheese for dinner. The rest of it is eggs, pork and chicken, some vegetables like tomatoes & bell peppers, a lot of fruit, the OJ, etc.
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Re: Thyro-Gold or Nutri-Meds

Unread postby Edward » Thu May 09, 2013 3:52 pm

Thyro-Gold contains forskolin, which is known to increase cAMP and CYP2C and interferes with other cytochrome p450 hepatic enzymes. Forskolin used to be a popular dietary supplement because of its ability in some experiments to reduce body fat, the downside? When you have a compound that increases cAMP which modulates adrenaline and modulates calcium channels and interferes with p450 you can run into problems. Because ultimately this can interfere with estrogen metabolism. The other thing with forskolin is that in some experiments it caused reduced body fat but increased fat deposition in the liver.
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Re: Thyro-Gold or Nutri-Meds

Unread postby MyUsernameHere » Thu May 09, 2013 4:06 pm

That's interesting. I never liked the fact that they put that in there. I will probably switch to Cynoplus after I finish the bottle.
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Re: Thyro-Gold or Nutri-Meds

Unread postby FunkOdyssey » Thu May 09, 2013 4:08 pm

+1 to Edward -- Forskolin can cause a huge array of side effects and throws a monkey wrench in a variety of systems. Definitely want to avoid.
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Re: Thyro-Gold or Nutri-Meds

Unread postby Edward » Thu May 09, 2013 4:13 pm

Forskolin and derivatives as tools for studying the role of cAMP
http://www.ingentaconnect.com/content/g ... 1/art00001

Forskolin (7ß-acetoxy-1 ,6ß,9 -trihydroxy-8,13-epoxy-labd-14-en-11-one) is the first main labdane diterpenoid isolated from the roots of the Indian Plectranthus barbatus ANDREWS and one of the most extensively studied constituents of this plant. The unique character of forskolin as a general direct, rapid and reversible activator of adenylyl cyclase not only underlies its wide range of pharmacological effects but also renders it as a valuable tool in the study of the role of cAMP. The purpose of this review is to provide data presenting the utility of forskolin - as a cAMP activator - for studying the function of cAMP from different biological viewpoints as follows: 1) Investigation on the role of cAMP in various cellular processes in different organs such as gastrointestinal tract, respiratory tract, reproductive organs, endocrine system, urinary system, olfactory system, nervous system, platelet aggregating system, skin, bones, eyes, and smooth muscles. 2) Studies on the role of cAMP activation and inhibition to understand the pathogenesis (e.g. thyroid autoimmune disorders, leukocyte signal transduction defect in depression, acute malaria infection, secretory dysfunction in inflammatory diseases) as well as its possibly beneficial role for curing diseases such as the regulation of coronary microvascular NO production after heart failure, the attenuation of the development or progression of fibrosis in the heart and lungs, the augmentation of myo-protective effects of ischemic preconditioning especially in the failing hearts after myocardial infarction, the stimulation of the regeneration of injured retinal ganglion cells, the curing of glaucoma and inflammatory diseases, the reducing of cyst formation early in the polycystic kidney disease, and the management of autoimmune disorders by enhancing Fas-mediated apoptosis. 3) Studies on the role of cAMP in the mechanism of actions of a number of drugs and substances such as the effect of the protoberberine alkaloid palmatine on the active ion transport across rat colonic epithelium, the inhibitory effect of retinoic acid on HIV-1-induced podocyte proliferation, the whitening activity of luteolin, the effect of cilostazol on nitric oxide production, an effect that is involved in capillary-like tube formation in human aortic endothelial cells, the apoptotic effect of bullatacin, the effects of paraoxon and chlorpyrifos oxon on nervous system. Moreover, cAMP was found to play a role in acute and chronic exposure to ethanol, in morphine dependence and withdrawal and in behavioral sensitization to cocaine as well as in the protection against cisplatin-induced oxidative injuries.

Increased stimulatory G protein in neoplastic human thyroid tissues
http://europepmc.org/abstract/MED/1660629

Prior studies in our laboratory have shown that thyroid neoplasms produce increased amounts of cyclic adenosine monophosphate (cAMP). Thyroid-stimulating hormone receptors act through the stimulatory G protein (Gs) to activate adenylate cyclase, the enzyme responsible for cAMP production. The purpose of this study is to measure the activity and amount of Gs in human normal and neoplastic thyroid tissue to see whether alterations in Gs are responsible for the increased cAMP production seen in thyroid neoplasms. Four tumors with a high TSH-stimulated cyclase activity of 497.6 +/- 71.9 pmol/mg/30 min versus 35.9 +/- 13.5 pmol/mg/30 min for normal tissue from the same patients were studied. In reconstitution studies measuring Gs activity, neoplastic thyroid tissue produced 637 +/- 106 pmol cAMP/mg S49/mg thyroid membrane min versus 363 +/- 133 pmol cAMP/mg 549/mg thyroid membrane/min produced by normal thyroid tissue. Qualitative assessments of the amount of Gs present with cholera toxin-mediated adenosine diphosphate ribosylation showed increased Gs in thyroid tumors. Western blotting with antibodies directed against Gs showed a 3.3 +/- 0.6-fold increase in the amount of Gs in these thyroid tumors. These experiments identify an increase in the amount of an otherwise normal Gs as the biochemical defect responsible for the increased cAMP production in this group of tumors.

Hepatic cytochrome P450 mediates interaction between warfarin and Coleus forskohlii extract in vivo and in vitro
http://www.ncbi.nlm.nih.gov/pubmed/23146043

OBJECTIVES: This study aimed to determine whether Coleus forskohlii extract (CFE) influences the anticoagulant action of warfarin in mice in vivo and its relationship with hepatic cytochrome P450 (CYP).

METHODS: Mice were fed various doses of CFE standardised with 10% forskolin in a normal diet for one week, or in protein diets containing 7% and 20% casein (low and normal) for four weeks. They were then administered with warfarin by gavage on the last two days of the treatment regimen, and blood coagulation parameters, as well as hepatic CYP, were analysed at 18 h after the last dose. Direct interaction between CFE and forskolin with CYP2C was evaluated in vitro.

KEY FINDINGS: CFE dose dependently increased hepatic total CYP content and S-warfarin 7-hydroxylase activity at a dietary level of ≥0.05%. Warfarin-induced anticoagulation was attenuated by CFE in parallel with CYP induction. The findings were similar in mice fed diets containing CFE and different ratios of protein. CFE directly inhibited CYP2C activity in mouse and human liver microsomes in vitro, whereas forskolin was only slightly inhibitory.

CONCLUSIONS: CFE attenuates the anticoagulant action of warfarin by inducing hepatic CYP2C; thus, caution is required with the combination of warfarin and dietary supplements containing CFE.

Dietary Coleus forskohlii extract generates dose-related hepatotoxicity in mice
http://www.ncbi.nlm.nih.gov/pubmed/22729658

Coleus forskohlii root extract (CFE) represented by its bioactive constituent 'forskolin' is popularly used as a natural weight-lowering product, but the association of its use with liver-related risks is very limited. In the present study, the effect of standardized CFE with 10% forskolin on liver function of mice was examined. Mice were given 0-5% CFE in an AIN93G-based diet for 3-5 weeks. Food intake, body weights, relative organ weights and liver marker enzymes [aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP)] combined with histophatological analysis were assessed. CFE (0-0.5%) only had minimal effects on food intake and body weight whereas a significant difference was observed in mice receiving the highest dose (5% CFE). The extract 0.05-5% dose-dependently decreased visceral fat weight by between 16% and 63%, and a dose-dependent several folds increase was observed in liver weights and plasma AST, ALT and ALP activities with quick onset apparent after only 1 week of 0.5% CFE intake. The hepatic effect persisted throughout the 3-weeks course but was restored towards normalization within 1 week after withdrawal of treatment. Liver histology of mice fed 0.5% CFE for 3 weeks showed hepatocyte hypertrophy and fat deposition. In contrast, none of the hepatic responses measured were altered when mice were given a diet containing pure forskolin alone at the dose corresponding to its content in 0.5% CFE. The present study clearly indicated that forskolin was not involved in the CFE-induced hepatotoxicity and was caused by other unidentified constituents in CFE which warrants further studies.

Forskolin potentiates G-CSF-induced proliferation of a murine myeloblastic leukemia cell line
http://www.ncbi.nlm.nih.gov/pubmed/7509014

The role of the cAMP/A-kinase signaling pathway in G-CSF dependent proliferation of murine myeloblastic NFS-60 cells was investigated. G-CSF treatment resulted in a rapid and transient elevation of cAMP content of NFS-60 cells. G-CSF treatment of NFS-60 cells also resulted in the activation of A-kinase parallel to the increase in cAMP concentration. A low concentration (0.2-10 nM) of forskolin augmented the G-CSF-dependent cell proliferation, although forskolin by itself had no effect on NFS-60 cell growth. Forskolin did not affect the IL-3-induced proliferation of this cell line. Addition of forskolin resulted in further increases in the cAMP level, activation of A-kinase in NFS-60 cells stimulated by G-CSF. Proliferation of NFS-60 cells by G-CSF, but not by IL-3, was blocked by the axial diastereoisomer of adenosine 3',5'-phosphorothioate (Rp-cAMPS), a competitive cAMP antagonist. KT-5720(8R*,9S*,11S*)-(-)-9-hydroxy-9-n-hexyloxy-8-methyl-2, 3, 9, 10-tetrahydro-8, 11-epoxy-1H, 8H, 11H-2,7b, 11a-triazadibenzo(a,g) cycloocta(c,d,e)trinden-1-one), an A-kinase inhibitor, inhibited the G-CSF-dependent proliferation. These findings suggest that activation of the cAMP/A-kinase signaling pathway may be involved in G-CSF-mediated cell proliferation of NFS-60 cells, whereas IL-3-dependent proliferation is not mediated in such a manner.
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Re: Thyro-Gold or Nutri-Meds

Unread postby MyUsernameHere » Thu May 09, 2013 4:23 pm

Do you think it is a bad idea to finish the current bottle then? I have about a month's worth of pills left.
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