tag:tealady.blog.co.uk,2009-11-21:/This Blog gives my thoughts on causes / symptoms of some medical conditions, with references where available. I hope to promote discussion with a view to better understanding. It is not intended to be a beginner's guide to thyroid related health symptoms OR to provide individual medical advice. Just at present I'm only using this blog as a place to store a few of my jumbled thoughts together:) as well as save a few links I like to jog my memory. So if you happen to read some of ramblings and they don't quite make sense.. its OK, they don't to me either:, feel free to add your view!.. but I'm almost there.. .. .. :) MokoFeed2009-11-21T08:24:56+01:00tag:tealady.blog.co.uk,2008-05-04:/2008/05/04/t4-and-t3-at-night-and-during-day-4128136/tealady2008-05-04T05:36:44+02:002008-05-04T23:05:20+02:00 <p>Taking part of one's thryoid meds at night is something many have been doing. (with docs OK)<br> <br> As well many folks experiences of improved wellbeing, and for some, just plain convenience of not having to worry about what they eat in the morning or rushing to work etc., here's why from <a href="http://forums.about.com/n/pfx/forum.aspx?tsn=23&nav=messages&webtag=ab-thyroid&tid=71961">this post</a></p> <blockquote><p>There is a diurnal cycle of TSH secretion from the anterior pituitary. In humans, peak TSH concentration occurs in the night and the nadir in the late afternoon (Fisher, 1996). Diurnal cycles have been reported for thyroid hormone levels in rats Cokelaere et al., 1996 ), amphibians (Gancedo et al., 1997) ...</p></blockquote> <p><em><br> It is normal to have some thyroid hormone released at night, so taking some at night makes sense.</em>(apologies to comparing humans to rats and amphibians but common things do seem to occur amongst animals especially between rats and humans which are surprisingly fairly close mammals as far as the way our bodies work!)<br> <a href="http://www.ncbi.nlm.nih.gov/pubmed/8858374?ordinalpos=28&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum">Cokelaere-Influence of feeding pattern on thyroid hormones </a>in long-term food-restricted rats<br> <a href="http://www.thieme-connect.de/ejournals/abstract/hmr/doi/10.1055/s-2007-979802"><a href="http://www.thieme-connect.de/ejournals/abstract/hmr/doi/10.1055/s-2007-979802">http://www.thieme-connect.de/ejournals/abstract/hmr/doi/10.1055/s-2007-979802</a></a>  at Uni of Syd Medical library 574.192705 2<br> <br> Here's some of the old posts from 2003-2005 on taking at least part of thryoid meds at night, some took Armour (THYROID + T4+t3), some took just T4, some took a combo.<br> Shows that thyroid med consumers have found the benefit of at least some thyroid hormones at night time for a long time, presumably way before this:-) </p> <p><a href="http://forums.about.com/n/pfx/forum.aspx?tsn=1&nav=messages&webtag=ab-thyroid&tid=46477"><a href="http://forums.about.com/n/pfx/forum.aspx?tsn=1&nav=messages&webtag=ab-thyroid&tid=46477">http://forums.about.com/n/pfx/forum.aspx?tsn=1&nav=messages&webtag=ab-thyroid&tid=46477</a></a><br> I have found that taking Cytomel at night helped me get restful good sleep. My daughter takes Armour at night also and it helps her sleep better.<br> What is your story?!!! CoachLinda</p> <p><a href="http://forums.about.com/n/pfx/forum.aspx?tsn=2&nav=messages&webtag=ab-thyroid&tid=46477"><a href="http://forums.about.com/n/pfx/forum.aspx?tsn=2&nav=messages&webtag=ab-thyroid&tid=46477">http://forums.about.com/n/pfx/forum.aspx?tsn=2&nav=messages&webtag=ab-thyroid&tid=46477</a></a><br> Hi, Linda!<br> Taking my third dose of Armour in the evening between 7 and 10pm helps me sleep better because it appears to prevent the breathing problems that I had previously.<br> endophobia!</p> <p><a href="http://forums.about.com/n/pfx/forum.aspx?webtag=ab-thyroid&nav=messages&msg=46477.6"><a href="http://forums.about.com/n/pfx/forum.aspx?webtag=ab-thyroid&nav=messages&msg=46477.6">http://forums.about.com/n/pfx/forum.aspx?webtag=ab-thyroid&nav=messages&msg=46477.6</a></a><br> me too endo. I need 15mg Armour equivalent (1/4 g)at night...slow released. Definitely aids sleep, and keeps me a tad warmer during the night. Also I don't feel quite so dead in the morning, so it is easier to get up.<br> Jan<br> ------------ </p> <p><a href="http://forums.about.com/n/pfx/forum.aspx?tsn=36&nav=messages&webtag=ab-thyroid&tid=67042"><a href="http://forums.about.com/n/pfx/forum.aspx?tsn=36&nav=messages&webtag=ab-thyroid&tid=67042">http://forums.about.com/n/pfx/forum.aspx?tsn=36&nav=messages&webtag=ab-thyroid&tid=67042</a></a>  Choccy with thryoid meds at night for better absorption, or at least it sure sounds like a great excuse with some originality!</p> <p>Ok, I gotcha per <a href="http://forums.about.com/n/pfx/forum.aspx?tsn=39&nav=messages&webtag=ab-thyroid&tid=67042">taking T4 at nite with chocolate. (Dumb me for not figuring out what you were saying). For the 1st time in my life, I'm not constantly cold. Aren't cold legs, feet & hands the pits? Once my T3 got out of the gutter, warmth followed</a>. Now, I get hot & still am unable to sweat. Maybe adding tyrosine helped, since I began taking it about the same time that T3 inched up. Believe me, I'm not complaining about being warm. It's wonderful to not search out clothing with long sleeves. </p> <p> <small> <a href="http://tealady.blog.co.uk/2008/05/04/t4-and-t3-at-night-and-during-day-4128136/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2008-05-04:/2008/05/04/tsh-and-ft3-circadian-rhythm-4127930/tealady2008-05-04T01:08:46+02:002008-05-04T23:03:32+02:00 <p>Accepted on March 17, 2008 <a href="http://jcem.endojournals.org/cgi/rapidpdf/jc.2007-2674v1">FREE FULL PDF</a><br> <a href="http://jcem.endojournals.org/cgi/content/abstract/jc.2007-2674v1">Free triiodothyronine has a distinct circadian rhythm that is delayed but parallels thyrotropin levels</a><br> W. Russell, R. F. Harrison, N. Smith, K. Darzy, S. Shalet, A. P. Weetman, and R. J. Ross*<br> Academic Unit of Diabetes, Endocrinology & Metabolism, and Department of Automatic Control & Systems Engineering, The University of Sheffield, Sheffield S1 3JD, UK; Chemical Pathology, Royal Hallamshire Hospital, Sheffield S10 2JF, UK; Department of Endocrinology, Christie Hospital, Manchester M20 4BX, United Kingdom </p> <p>* To whom correspondence should be addressed. E-mail: <a href="mailto:r.j.ross@sheffield.ac.uk.">r.j.ross@sheffield.ac.uk.</a><br> ----------------------------------</p> <p>Context: TSH is known to have a circadian rhythm but the relationship between this and any rhythm in T4 and T3 has not been clearly demonstrated.</p> <p>Objective: With a view to optimising thyroid hormone replacement therapy we have used modern assays for FT4 and FT3 to investigate circadian rhythmicity.</p> <p>Setting: University Hospital.</p> <p>Design and subjects: Cross sectional study in 33 healthy individuals with 24 hour blood sampling (TSH in 33 and FT4 and FT3 in 29 individuals) and cosinor analysis.</p> <p>Results: 100% of individuals showed a sinusoidal signal in TSH, for FT4 76% and for FT3 86% (p<0.05). For FT4 and FT3 the amplitude was low. For TSH the acrophase occurred at a clock time of 0240 h and for FT3 approximately 90 minutes later at 0404h. The group cosinor model predicts that TSH hormone levels remain above the mesor between 2020 h and 0820 h and for FT3 from 2200 h to 1000 h. Cross correlation of FT3 with TSH showed that the peak correlation occurred with a delay of 0.5–2.5 hours. When time adjusted profiles of TSH and FT3 were compared there was a strong correlation between FT3 and TSH levels (=0.80, p<0.0001). In contrast, cross correlation revealed no temporal relationship between FT4 and TSH.</p> <p>Conclusion: FT3 shows a circadian rhythm with a periodicity that lags behind TSH suggesting the periodic rhythm of FT3 is due to the proportion of T3 derived from the thyroid. Optimising thyroid hormone replacement may need to take these rhythms into account.<br> ---------------------------------<br> <em><br> I have been taking a part of my thyroid meds at night since 2002, and try to include some T3 with the T4 taken at night(about a human ratio of T4:T3 but that is very approximate!)<br> A few of us on a thryoid forum started before 2003- <a href="http://tealady.blog.co.uk/2008/05/04/t4-and-t3-at-night-and-during-day-4128136">here's some of the old posts</a><em><br> My thoughts and practise are in this <a href="http://forums.about.com/n/pfx/forum.aspx?tsn=23&nav=messages&webtag=ab-thyroid&tid=71961">post from Apr 07 </a>& <a href="http://tealady.blog.co.uk/2008/01/12/my_post_on_ukthyroid_t3_timing_and_corti~3564235">this post below</a><br> AS I also take estradiol this post is on the benefits of at taking part of one's meds to approximate any natural circadian rhythm that occurs , with both thyroid meds and oestradiol :-)<br> In practise since 2002, I have always taken somewhere between 1/4 Grain THYROID(Armour equiv) and one half of my thyroid meds at night, but others have taken them all at night. I feel I need to spread mine to last better(some also before large meals for digestion and before a lot of exercise), but maybe one day I also will be able to take them all at night!</em></em> </p> <p> <small> <a href="http://tealady.blog.co.uk/2008/05/04/tsh-and-ft3-circadian-rhythm-4127930/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2008-05-03:/2008/05/03/metabolic-effects-of-thyroid-hormone-and-4125715/tealady2008-05-03T12:04:17+02:002008-05-03T12:06:21+02:00 <p><a href="http://www.ncbi.nlm.nih.gov/pubmed/18279024?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DiscoveryPanel.Pubmed_Discovery_RR&linkpos=1&log$=relatedreviews&dbfrom=pubmed">Metabolic effects of thyroid hormone derivatives</a>.Moreno M, de Lange P, Lombardi A, Silvestri E, Lanni A, Goglia F.<br> Dipartimento di Scienze Biologiche ed Ambientali, Università degli Studi del Sannio, Via Port'Arsa, Benevento, Italy.</p> <p>The processes and pathways mediating the intermediary metabolism of carbohydrates, lipids, and proteins are all affected by thyroid hormones (THs) in almost all tissues. Particular attention has been devoted by scientists to the effects of THs on lipid metabolism. Among others, effects related to cholesterol, lipid handling, and cardiac performance have been the subject of study. Many reports are present in the literature concerning the calorigenic effect of THs, with most of them aimed at identifying the molecular basis of this effect. However, at the moment the mechanism(s) underlying the metabolic effects of THs remain to be elucidated. THs exert most of their effects though TH receptors (TRs). However, some effects of THs cannot be explained by a nuclear-mediated pathway, and recently an increasing number of nonnuclear actions have been described, which can provide a regulatory system of which the effects differ from those mediated on the transcriptional level by TRs. Some of the TH derivatives (naturally occurring metabolites and analogs) possess biological activities. TH-related biological effects have been described for physiological products such as tetraiodothyroacetic acid (Tetrac) and triiodothyroacetic acid (Triac) (via oxidative deamination and decarboxylation of thyroxine [T4] and triiodothyronine [T3] alanine chain), 3,3',5'-triiodothyronine (rT3) (via T4 and T3 deiodination), 3,3'-diiodothyronine (3,3'-T2) and 3,5-diiodothyronine (T2) (via T4, T3, and rT3 deiodination), and 3-iodothyronamine (T1AM) and thyronamine (T0AM) (via T4 and T3 deiodination and amino acid decarboxylation), as well as for TH structural analogs, such as 3,5,3'-triiodothyropropionic acid (Triprop), 3,5-dibromo-3-pyridazinone-l-thyronine (L-940901), N-[3,5-dimethyl-4-(4'-hydroxy-3'-isopropylphenoxy)-phenyl]-oxamic acid (CGS 23425), 3,5-dimethyl-4[(4'-hydroxy-3'-isopropylbenzyl)-phenoxy] acetic acid (GC-1), 3,5-dichloro-4[(4-hydroxy-3-isopropylphenoxy)phenyl] acetic acid (KB-141), and 3,5-diiodothyropropionic acid (DITPA). Most of these compounds have interesting properties: counteracting lipid accumulation, reducing cholesterol level, and increasing lipid metabolism without cardiotoxic effects. Hopefully, further studies on basic mechanisms of such compounds will be harbingers of more knowledge on the metabolic effects of TH derivatives and on their possible clinical application.</p> <p>PMID: 18279024 [PubMed - indexed for MEDLINE]<br> -------------------<br> <em>my thoughts<br> It will be great if they CAN investigate some of the thryoid hormone metabolites as they would be way preferable to statins in reducing cholesterol, and, at least partly the lowering thryoid hormone levels (or less effective binding or a form of thryoid hormone resiatnce (similar to insulin resistance)) in some of the elderly is the cause of higher cholesterol levels. However unless they ALTER the metabolite I guess they wont be able to patent it?.. and any altered one will have consequences again like side effects and not working as expected..similar to all the other patented drugs!, and without patents and their associated money, where is the incentive to investigate thyroid hormones?</em> </p> <p> <small> <a href="http://tealady.blog.co.uk/2008/05/03/metabolic-effects-of-thyroid-hormone-and-4125715/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2008-01-26:/2008/01/26/addison_s_psychosis_hashimotos~3633775/tealady2008-01-26T04:45:42+01:002008-05-04T02:13:04+02:00 <p><a href="http://neuro.psychiatryonline.org/cgi/content/full/18/4/450">http://neuro.psychiatryonline.org/cgi/content/full/18/4/450</a> about a woman presenting with psychosis and addison. In the end of the article they wonder if she maybe had HE.</p> <p><em>Increasing thyroid meds may precipiate Addisons</em> </p> <p> <small> <a href="http://tealady.blog.co.uk/2008/01/26/addison_s_psychosis_hashimotos~3633775/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2008-01-12:/2008/01/12/my_post_on_ukthyroid_t3_timing_and_corti~3564235/tealady2008-01-12T03:23:34+01:002008-05-04T03:32:23+02:00 <p><a href="http://forums.about.com/n/pfx/forum.aspx?msg=4104.3&nav=messages&webtag=ab-thyroiduk#a3"><a href="http://forums.about.com/n/pfx/forum.aspx?msg=4104.3&nav=messages&webtag=ab-thyroiduk#a3">http://forums.about.com/n/pfx/forum.aspx?msg=4104.3&nav=messages&webtag=ab-thyroiduk#a3</a></a>  <br>my post on UKthyroid forum</p> <p>now that would get me off Armour fur sure! Apply T3 patch at times need additional FT3 :-) ..well I'd at least try it <img src="/img/smilies/icon_smile.gif" alt=":)" class="middle" border="0"></p> <p>I've tried time release capsules of T3.. but still not good enough as receptors don't need to be inundated ALL the time, and you still need it as required, even if T3 taken with T4 in my case. What I didn't try was taking parts of capsules at needed times, like with meals, before exercise ONLY :-).. times our bodies needs the higher FT3 ;-)</p> <p>For some reason T3 makes me ravenous(both time released or not time released) This reportedly seems to happen ina lot of people on commencement of T3 containing meds, but esp. straight T3, but the effect lessens to non-noticeable over time. With me appetite lessened slightly, it is still too strong to tolerate:-)., even taking with T4. <br>Armour also increases appetite similar to T3, but nowhere near the same extent:-) Most people don't notice it much. </p> <p>Some do though. I know someone on a forum who takes appetitive suppressants as well..but I'm not prepared to go that way!</p> <p>No exogenous thyroid hormones.. no noticeable appetite :-)</p> <p>Lately I've worked out with oestradiol patches to only apply at bedtime and remove in morning.. coping a LOT better now!, also apply a incy bit of oestrogel (estradiol)gel at lunchtime and dinner (if remembered)as that is a rise in estradiol as well. Oestradiol has a daily rhythm too.. and its probably best to very roughly emulate it.. <br><strong>wonder why noone has cottoned on to this?</strong> <strong>I can't find any research on any suggestions of it?</strong></p> <p>It seems to stop most of all the neg. side effects(and hopefully any increased risk of cancer etc with luck), while providing the benefits</p> <p>If I ever do get that T3 patch, I'd be applying any T3 patch at start of meal, until digested:-).. or when I want to do some strenuous exercise.,or go for a long walk for hrs in a blizzard, both equally as unlikely at present:-), or a liitle extra T3 at night with the rise in  Oestradiol and shortly after TSH rises(see below**)<br>Also see our trials of T4+T3 taken at bedtime back in 2002 in the thyroid forum</p> <p>yes, I realise this is too complicated for most.. but it depends on how bad you feel and difficult it is for you to cope otherwise I guess. If you feel great with once a day dosing of T4 then stick with it!</p> <p>I look on T3 taking as similar to insulin in diabetes type 1... only take if really needed and its worth the effort for me:-)</p> <p><em>For more info on oestradiol.. it rises at night..<strong> seems to be with the cortisol pattern and perhaps TSH spike pattern, perhaps in part  to aid in raising Total-thyroid hormone levels?!</strong></em><strong> <br></strong><em>Suggested Hypothesis..the rise in oestradiol probably binds thyroid hormones released by the spikes in TSH, thus preventing too high free levels in body when not needed , and binding free cortisol as well also peaking in early morning hours , sure to be many other reasons and other endocrine hormones which also rise during sleep...<br>Oestradiol peaks about 2am -6am ish in most (females,premeno I guess,  will need to check) then rises , again probably with the FT3 probably after lunch and dinner a little ... as far as I can make out. !! ..still looking out, brain permitting!</p> <p>Seems I was onto something here as <a href="http://tealady.blog.co.uk/2008/05/04/tsh-and-ft3-circadian-rhythm-4127930"><u>this study</u> </a>also shows <strong>fT3 rising after TSH at night</strong><br></em><em><br>----------------------</em> </p> <p><em>The point I'm trying to get across...<br>endocrine hormones, similar to insulin, for some of us anyway , maybe should be timed to optimise   <strong>TAKING IT when will be used(on demand) </strong><strong>by the body, or when the body would naturally be producing it(circadian rhythm) ..</strong>. not just taking once a day for convenience? (just like diabetes 1 give insulin injections before meals), but especially for T3, which would be a FT3 immediate rise, whether or not time released.. with time released the rise would just be more spread out!<br>Then we don't have a lot of free T3 floating about when it is NOT needed and causing receptors to have T3 bound when really they would do far better with a break as would occur naturally( reduces receptor<br>"resistance" and allows other molecules that may be needed to bind to also work more effectively), but still have it when needed..<br>This would happen if fT3 is released on demand by the thryoid gland or  converted on demand optimally in our bodies! (all enzymes functionally optimally which doesn't happen until hypothryoidism has been treated for a long time perhaps in those who have been hypothryoid for a long time?? OR if fT3 is released as close as possible to its natural release in a circadian rhythm (by thyroid gland or from conversion)).<br></em></p> <p><em>This is why I am against time released T3 over a longer time frame. A lot of people find oit beneficial over a short time frame but I have not heard of anyone who has felt well on time released T3 over years, where it is timed to be released over the entire 24 hr period.<br>It's also why I think in that Wilson's protocol they worked out it was beneficial to cycle on and off, and even then noone stays on the protocol over a long period of time.(years)... or shouldn't!</p> <p>I think I find it a LOT easier on myself timing my T3 intake to coincide with meals or periods of exercise and a little with my T4 at night(to approximate a "typical human ration".!.. not completely sure.. but reasonably sure..</em></p> <p><em>and this hadnt been suggested at all? I know it's difficult . but its done with insulin, so for those of us who need it, like insulin, its worth trying..especially if it really helps!</em></p> <p><em>can you find ANYWHERE that this has been suggested before <br>or better still tried before!</em></p> <br>-----------------------<br>For the past few months (since 2007 sometime) I have been <strong>applying an oestradiol only patch at night as late as possible(bedtime) and removing in morning when I wake up.  This is instead of oestrogel(estradiol gel, as this is absorbed more continually and I need to be be able to stop the release, as I can on removal of the patch)<br></strong>Sometime I fall asleep early and tend to wake about 3AM or 4AM , so I apply patch at 3AM or 4AM if I fall asleep and forget at bedtime!<br>The patch is easily placed back onto its plastic backings for use the next night. It resticks around 5 or 6 times, and you need a new patch anyway about 5 to 6 times of use! They are designed for 3.5days approx release continually, but they always seemed to run out after 3 days to me , and usually about 2.5days!<br>Some people may be able to get a max of a week out of one patch wearing only to bed at night, it depends on the relase rate into your skin, which would be indivual and depend on temperature etc.</p> <p>This routine of patches only while in bed at night really seems to be working for me!!</p> <p>I get all the benefits with none of the side effects of the constant estradiol binding to receptors I guess. I used to get "wierd" sensations, as I've seen others write about as well as some weight gain etc.. now I'm fine, I get the lift in mood, the lessening of fatigue, the increased vasopressin(ADH) so I don't have to run to the loo for urine all the time and can sleep thru the night with only one rise for a piddle :-), as well as the reduction in thirst..yes still thirsty but not so extreme!<br>I feel "better" overall, and I think it's more than just the reduction in broken sleep. <br>I think I've worked it out eventually!<br>(Of course, still having a uterus, I also use progesterone pessaries for around 14 days of each month in form of pessaries to release progesterone mostly near uterus where needed)<br> </p> <p> <small> <a href="http://tealady.blog.co.uk/2008/01/12/my_post_on_ukthyroid_t3_timing_and_corti~3564235/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2008-01-08:/2008/01/08/thyroid_hormone_primer~3544309/tealady2008-01-08T01:28:14+01:002008-01-08T01:28:14+01:00 <p><a href="http://209.85.165.104/search?q=cache:gdqTElTNgzIJ:www.endocrinology.med.ucla.edu/Thyroid.htm+%22UCLA%22+Endocrinology+sertraline+thyroid&hl=en&ct=clnk&cd=2&gl=us">http://209.85.165.104/search?q=cache:gdqTElTNgzIJ:www.endocrinology.med.ucla.edu/Thyroid.htm+%22UCLA%22+Endocrinology+sertraline+thyroid&hl=en&ct=clnk&cd=2&gl=us</a></p> <p>UCLA Endocrinology Thyroid Hormone summary </p> <p> <small> <a href="http://tealady.blog.co.uk/2008/01/08/thyroid_hormone_primer~3544309/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-09-05:/2007/09/05/microregulation_of_thyroid_hormone_secre~2929357/tealady2007-09-05T15:21:52+02:002007-09-05T15:21:52+02:00 <p>The Immune System as a Regulator of Thyroid Hormone Activity</p> <p>John R. Klein<br> Department of Diagnostic Sciences, Dental Branch, University of Texas Health Science Center,Houston, TX 77030</p> <blockquote><p>Although the mechanisms behind this are poorly understood, they appear to reflect a process of local intrathyroidal synthesis of TSH mediated by a population of bone marrow cells that traffic to the thyroid. </p> <p>This hitherto undescribed cell population has the potential to microregulate thyroid hormone secretion leading to critical alterations in metabolic activity independent of pituitary TSH output, and it has expansive implications for understanding mechanisms by which the immune system may act to modulate neuroendocrine function during times of host stress. In this article, the basic underpinnings of the hematopoietic-thyroid connection are described, and a model is presented in which the immune system participates in the regulation of thyroid hormone activity during acute infection.</p></blockquote> <p>Exp Biol Med 231:229–236, 2006 </p> <p><a href="http://www.ebmonline.org/cgi/reprint/231/3/229">http://www.ebmonline.org/cgi/reprint/231/3/229</a> </p> <p> <small> <a href="http://tealady.blog.co.uk/2007/09/05/microregulation_of_thyroid_hormone_secre~2929357/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-07-04:/2007/07/05/psychological_well_being_correlates_with~2575492/tealady2007-07-05T00:27:48+02:002008-01-12T11:47:03+01:00 <p>Psychological Well-Being Correlates with Free Thyroxine But Not Free 3,5,3'-Triiodothyronine Levels in Patients on Thyroid Hormone Replacement </p> <p><a href="http://jcem.endojournals.org/cgi/content/abstract/91/9/3389">http://jcem.endojournals.org/cgi/content/abstract/91/9/3389</a></p> <p>Ponnusamy Saravanan, Theo J. Visser and Colin M. Dayan </p> <p>Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology (P.S., C.M.D.), University of Bristol, Bristol BS1 3NY, United Kingdom; and Department of Internal Medicine (T.J.V.), Erasmus University Medical Centre, 3000 DR Rotterdam, The Netherlands </p> <p><em> Yes, this agrees with what I have found in myself</em><br> feel bad with a FT4 of 10,11, 12 .. much better when FT4 is 16. I agree too.. you wouldnt exctly call it depressed, at least not bad depression<br> I've noted that within the people I know who are "normal" (not on any thyroid hormone replacement and feel fine) that there TSH (edit T4? ~ Bob) is around the 18 or 19 level.. mum 19, daughetr 19, ...<br> range is 10-22, or 10-25, usually , but TSH is always identical no matter what the particular lab normal range is set at. (so are my TSH results)</p> <p>----------------<br> <em>I've only glanced at the abstract of this one</em></p> <p> <small> <a href="http://tealady.blog.co.uk/2007/07/05/psychological_well_being_correlates_with~2575492/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-07-04:/2007/07/04/calcitonin_deficiency_in_autoimmune_thyr~2572197/tealady2007-07-04T15:13:07+02:002007-07-04T15:13:07+02:00 <p><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=9797849&ordinalpos=13&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum">Calcitonin deficiency in early stages of chronic autoimmune thyroiditis</a><br> Borges MF, Abelin NM, Menezes FO, Dahia PL, Toledo SP.<br> Department of Medicine, Federal School of Medicine of Triângulo Mineiro, Uberaba, Brazil.</p> <p>OBJECTIVES: Although calcitonin (Ct) deficiency has been described in chronic autoimmune thyroiditis (CAT) it is unclear at what stage in the disease it develops. We have analysed the Ct secretory responses of patients in two different evolutionary stages of CAT, namely the goitrous and atrophic phases. DESIGN: We studied the Ct response to combined calcium (2 mg/kg) and pentagastrin (0.5 microgram/kg) intravenous infusion in 27 patients with CAT and 30 normal adult controls. The cases were divided into two groups. The first comprised eleven women with CAT and goitrous subclinical hypothyroidism (GH), aged 28.6 +/- 10.1 years--at diagnosis they had increased thyroid autoantibody titres and cytological features compatible with stages 1 and 2 of Hashimoto's thyroiditis. The second comprised 16 females with CAT and an atrophic thyroid confirmed by ultrasound scan, aged 38.0 +/- 9.2 years--these patients were severely hypothyroid at diagnosis and were termed AH (atrophic hypothyroidism). Both groups (GH and AH) received replacement doses of thyroxine sufficient to restore euthyroidism for at least six months before the stimulation tests. Control group (C) consisted of 20 healthy women (A), aged 30.0 +/- 9.6 years, and 10 healthy men (<img src="/img/smilies/icon_cool.gif" alt="B)" class="middle" border="0">, aged 34.7 +/- 8.0 years. Serum Ct was measured by IRMA. The Ct secretory response was related to thyroid size and cytological data, when available. RESULTS: Basal Ct concentrations in groups GH (0.08 ng/l, median) and AH (0.07 ng/l, median) were significantly lower than those of female controls (0.58 ng/l, median). Stimulated Ct peak values in groups GH (0.08 ng/l, median) and AH (0.19 ng/l, median) were significantly lower than those of female controls (13.61 ng/l, median). Also, both basal (2.72 ng/l, median) and stimulated Ct levels (35.73 ng/l, median) in male controls were significantly higher than in female controls given already. A positive correlation between the Ct secretory reserve and thyroid dimensions, evaluated by ultrasound scan, was found only in patients with thyroid atrophy (AH; rs = 0.61, P < 0.05). CONCLUSIONS: We have found low basal and stimulated calcitonin values in patients with chronic autoimmune thyroiditis and thyroid enlargement, which represents an early phase of chronic autoimmune thyroiditis. Our data have also confirmed previous findings of deficient calcitonin secretion in advanced stages of chronic autoimmune thyroiditis in which thyroid atrophy is usually found. These findings may be associated with C-cell destruction following progressive, nonspecific follicular cell damage caused by lymphocytic infiltration and fibrosis of the gland.</p> <p>PMID: 9797849 [PubMed - indexed for MEDLINE]</p> <p> <small> <a href="http://tealady.blog.co.uk/2007/07/04/calcitonin_deficiency_in_autoimmune_thyr~2572197/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-07-04:/2007/07/04/can_lymphocytic_thyroiditis_be_deadly~2572167/tealady2007-07-04T15:07:52+02:002007-07-04T15:07:52+02:00 <p><a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=17520957&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus">Sudden unexpected death associated with lymphocytic thyroiditis</a>Vestergaard V, Drostrup DH, Thomsen JL.<br> Institute of Forensic Medicine, University of Southern Denmark, Winsløwparken 17, DK-5000 Odense C. <a href="mailto:vibeke.vestergaard@ouh.regionsyddanmark.dk">vibeke.vestergaard@ouh.regionsyddanmark.dk</a></p> <p>A forensic autopsy study comprising 125 cases was carried out retrospectively in order to evaluate pathological changes in the thyroid gland in different groups of death. The five groups selected consecutively were: (i) opiate addicts who died from an overdose, (ii) alcoholics who died as a result of their alcohol abuse, (iii) cases of fatal poisoning other than opiate addicts, (iv) unknown cause of death and (v) controls without prior disease. Tissue samples from the thyroid gland were cut and stained with haematoxylin and eosin and van Gieson. Histology examinations were subsequently performed blind with semiquantitative assessment of the following six parameters: (a) height of the follicular epithelium, (b) the amount of lymphocytes, (c) the presence of plasma cells, (d) hyperplastic follicular changes, (e) oxyphilic changes, and (f) fibrosis. The most striking result was the finding of extensive lymphocytic infiltration of the thyroid parenchyma in five of the 124 cases, of which four belonged in the group of 'unknown cause of death'. This discovery leads to reflections regarding lymphocytic thyroiditis as a cause of death, either by itself or in combination with other disorders. Silent (painless) thyroiditis, especially, is easily overlooked at autopsy as there are no macroscopic changes and often no prior symptoms or history of thyroid disease pointing towards this condition. Analyses of thyroid hormones are unreliable in predicting endocrine status in life. Routine microscopy of the thyroid gland is therefore advocated in cases of sudden unexpected death in order to diagnose thyroid disease, in particular silent (painless) thyroiditis.</p> <p>PMID: 17520957 [PubMed - indexed for MEDLINE]</p> <p>also see <a href="http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&DbFrom=pubmed&Cmd=Link&LinkName=pubmed_pubmed&LinkReadableName=Related%20Articles&IdsFromResult=17520957&ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus">related</a> </p> <p> <small> <a href="http://tealady.blog.co.uk/2007/07/04/can_lymphocytic_thyroiditis_be_deadly~2572167/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-07-04:/2007/07/04/hashimotos_thyroiditis_can_cause_fever~2570924/tealady2007-07-04T11:35:04+02:002007-07-04T14:57:41+02:00 <p><a href="http://www.springerlink.com/content/d7734x86t871t110/">Sustained fever resolved promptly after total thyroidectomy due to huge Hashimoto’s fibrous thyroiditis</a><br> Journal Endocrine<br> Publisher Humana Press Inc.<br> ISSN 0969-711X (Print) 1559-0100 (Online)<br> Issue Volume 31, Number 1 / February, 2007 </p> <p>Abstract</p> <p>We encountered a 55-year-old female patient with Hashimoto’s thyroiditis who showed persistent fever, and could not find any source of fever other than the large nontender goiter. Her fever continued with positive CRP for 6 months. Although we did not assume that the inflammation was related to Hashimoto’s thyroiditis, total thyroidectomy was performed for cosmetic reasons; however, fever was resolved immediately after thyroidectomy.<br> Pathological diagnosis was Hashimoto’s chronic thyroiditis. Immunohistochemical staining showed that the follicular cells were positive for IL-1alpha, IL-1beta, and TNF-alpha. </p> <p>We believed that fever was induced by inflammatory cytokines produced in thyroid. The case indicated that Hashimoto’s thyroiditis with nontender goiter could cause idiopathic fever. </p> <p><em>I've also had thyroidits attacks lasting a while with fever.. I thought that was a part of thryoiditis, like it is with tonsillitis?, but not so severe in height of temp </em> They've become less frequent with time...(many years on and off)</p> <p> <small> <a href="http://tealady.blog.co.uk/2007/07/04/hashimotos_thyroiditis_can_cause_fever~2570924/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-07-04:/2007/07/04/estradiol_neuroprotective_effect_against~2570884/tealady2007-07-04T11:28:42+02:002007-07-04T11:28:42+02:00 <p>The <a href="http://www.springerlink.com/content/710t27888w44v0h5/">effects of glutamate can be attenuated by estradiol via estrogen receptor dependent pathway in rat adrenal pheochromocytoma cells </a><br> Abstract Estrogens have been suggested to exhibit neuroprotective activities against several insults including beta-amyloid and glutamate, one of the excitatory neurotransmitters in the central nervous system.<br> In the present study, we showed that exposure to <strong>glutamate not only inhibited the cell growth of exponentially growing rat pheochromocytoma PC12 cells in a time- and dose- dependent manner, but also influenced cell adherence capacity</strong>. <strong>Glutamate-induced growth inhibition was significantly attenuated by the co-administration of estradiol in PC12 cells. Pre-exposure of the PC12 cells to the estradiol was not required for protection against glutamate-induced growth inhibition</strong>. Administration of anti-estrogen ICI182,780 efficiently blocked the neuroprotective effects of estradiol. <strong>Glutamate-induced changes in cell adherence, on the other hand, were not significantly affected by estradiol</strong>.</p> <p> These data indicate that the neuroprotective effects of estradiol against glutamate-induced insults in PC12 cells, at least in part, involve estrogen receptor-dependent pathways. </p> <p>Keywords Estrogen - Glutamate - Neuroprotection - PC12 cells </p> <p> <small> <a href="http://tealady.blog.co.uk/2007/07/04/estradiol_neuroprotective_effect_against~2570884/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-07-04:/2007/07/04/timing_of_taking_thyroid_meds_circadian_~2569561/tealady2007-07-04T06:49:36+02:002007-07-19T20:28:03+02:00 <p>This study found TSH lower when taking T4 at night instead of morning<br><a href="http://www.blackwell-synergy.com/action/showPdf?submitPDF=Full+Text+PDF+%28230+KB%29&doi=10.1111%2Fj.1365-2265.2006.02681.x"><a href="http://www.blackwell-synergy.com/action/showPdf?submitPDF=Full+Text+PDF+%28230+KB%29&doi=10.1111%2Fj.1365-2265.2006.02681.x">http://www.blackwell-synergy.com/action/showPdf?submitPDF=Full+Text+PDF+%28230+KB%29&doi=10.1111%2Fj.1365-2265.2006.02681.x</a></a> </p> <p>new TSH, T4, TT4, sulfation etc paper .. measures every hr for 24 hrs<br><a href="http://forums.about.com/n/pfx/forum.aspx?msg=61884.1&nav=messages&webtag=ab-thyroid#a1">Link</a></p> <p>About Three years ago Leslie (US Forum) did a switch from morning dose to evening dose of Thyroid meds.....along with other members of her family, for a number of sensible reasons.</p> <p>Now, a Dutch team:- Bolk, Visser et al, from Erasmus Medical Centre in Rotterdam have taken that a step further and carried out a preliminary <a href="http://dx.doi.org/10.1111/j.1365-2265.2006.02681.x">study</a> to show that a larger investigation would not lead to faulty assumptions on the methods adopted.</p> <p>Their preliminary findings are somewhat more astonishing than they thought they might have been (even from a small sample)</p> <p>On shifting the time at which the meds were taken, </p> <p>a) it was better absorbed, </p> <p>b) it didn't change the circadian pattern of overnight TSH production</p> <p>c) it greatly improved the resulting TSH (lower) from the same dose of meds </p> <p>d) it unexpectedly demonstrated that FT4 was elevated and has a circadian rhythm</p> <p>and work carried out by Visser with Saravanan and<a href="http://jcem.endojournals.org/cgi/rapidpdf/jc.2006-0414v1"> Dayan </a>from Bristol University also added to the data, as elevated FT4 showed improved psychological well-being.<br>Bob<br>-------------------</p> <p><em>I think the increase in is not just the absorption/digestion of T4 o'nite compared to in the day.. although that's way up there in the possibilities.. </p> <p>but I also think it has to do with a couple of undiscussed factors<br> </em>1. "When T4 is released from the thyroid, it is primarily in a<strong> bound form with thyroid binding globulin (TBG),</strong> with lesser amounts bound to thyroxine-binding prealbumin (TBPA). It is estimated that only<strong> 0.03-0.05 percent of T4 within the circulatory system is in a free or unbound form; this unbound T4 is called free-T4 (fT4).</strong> "</p> <p><em>so when we take t4 meds .. <strong>what are they bound to when absorbed</strong>??.. main question I'd like answered..and surely must be known?..????</p> <p>If all free,T4.. that would increase the FT4 in blood a lot more than endogenous?.. or is the amount of T4 taken usually only sufficient to raise FT4 to ''normal" levels and not allow for thryoid binding.. I , at least, can see why FT4 may have to be above "normal for endogenously produced FT4 levels".. if we don't get a raise in total T4 somehow as well...then again,maybe it binds readily as absorbed???</p> <p>If not the higher T4 would probably result in some quick "getting rid of this high FT4 "that can't be handled by the deioinases.. like via sulfation (see 2.)</em></p> <p>2. "<strong>Evidence also indicates the sulfation pathway for T4 increases substantially following exogenous T4 therapy in premenopausal women</strong>. Although only low T4S levels are detectable in serum both pre- and post-T4 treatment, <strong>urinary T4S values increase significantly.</strong>[49] However, unlike T4, significant increases in <strong>both serum and urine T3S levels are observed following T4 therapy.</strong>[50] "</p> <p><a href="http://www.encyclopedia.com/doc/1G1-65068470.html"><a href="http://www.encyclopedia.com/doc/1G1-65068470.html">http://www.encyclopedia.com/doc/1G1-65068470.html</a></a>  </p> <p><em>Perhaps as well as absorbing more, maybe during the night some of the T4 can bind better to become total T4 instead of being converted to T4S and T3S?</em></p> <p>If you look at this a little more closely.. look at the graph for TBG (which binds most of the T4 released from the thryoid gland if one is "normal")... note how there is more TBG available from mid afternoon with the night time dosing. <br>This could be because estradiol has a peak (according to Larrian, an  ) at noon.. and estradiol rising maybe would raise TBG.. I know estradiol rising can raise TBG levels in blood.. (from studies i think).. <strong><em>but why more when T4 was taken only at night??</p> <p></em></strong>The extra TBG  available  in the graphs, no matter how it WAS higher, could bind the T4 absorbed (with luck) and you'd have more TT4 (as observed).. now this increase in TT4 is probably more of big thing than the incr in FT4..as the amount of TT4 is way bigger (see in nmol not pmol for starters.. hundreds of times more in other words).. and this TT4 can keep the FT4 and FT3 higher thru the days following.. There is No great rush to lower it to a "normal ":amount of FT4 and possibly not as much T4S and T3S in urine?<br>Pity they didn't check that?.. will have to look at in more detail though to be sure</p> <p>rough ideas here.. not finished post</p> <p><em>Also I've found with iodine that it helps a lot with night sweats.. which are definitely estradiol related.. so maybe this TBG is to do with the iodine released from the T4 being available to help with estradiol metabolism at night somehow..I think its to do with conversion to estriol, unsure though (apparently the iodine from thryoid hormones may get reused by body either in formation of new thyoid hormones or as iodine in breasts etc)? .. all too confusing for me... But if more is converted to estriol in correct pathways with the extra iodine available.. then maybe somehow there's more TBG available to be used by the T4... really over my head though..and surely mroe complicated than my brain can get around at present..</em></p> <p>There are other known pathways besides sulfation.. like carboxylation,glucuronidation, ,even I think hydoxylation? (not sure there's a effect of alcohol too somewhere but I've forgotten) and other metabolites.<br>eg. thyroid hormones can undergo deamination and decarboxylase reactions in the liver resulting in the formation of so-called acetic acid analogues of thyroid hormones ..In human liver, both triac and tetraiodothyroacetic acid are conjugated by glucuronidated reactions about 1500 and 200 times faster than T3 and T4, respectively. This preference of conjugation reactions for the acetic acid analogues might partially explain their short half-life in the body.[56] </p> <p>Then there's bromide replacing iodide (if it does), <br>but sulfation, at least for starters, ought to have been looked at(I don't think much is known about the other paths ).. yes there re all minor pathways compared to the deiodinases</p> <p>thing is..<br>"It is estimated that more than 70 percent of T4 produced in the thyroid is eventually deiodinated in peripheral tissues, either at the outer phenolic ring to form T3 or at the inner tyrosyl ring to form rT3.[2] "</p> <p>so the other 30% is..??.. but will have to look at original studies to be sure of percentages.  the way this other 30% is converted in the body must have a significant impact on the free levels when you consider that it is  "estimated that only 0.03-0.05 percent of T4 within the circulatory system is in a free", (FT4) <br>All quotes from <br><a href="http://www.encyclopedia.com/doc/1G1-65068470.html"><a href="http://www.encyclopedia.com/doc/1G1-65068470.html">http://www.encyclopedia.com/doc/1G1-65068470.html</a></a>   (above)<br>-----<br>It is a good study, however instead of suggestion absorption is defferent during the night than in the day, perhaps they should have looked at the excretion in thryoid hormones (and metabolites?) in the faeces first?.. and it would have been great to have urine metabolites tested as well.(like the T4S, T3S etc and see if these were different in those taken at night and day..considering it was known that there is a difference in those taking exogenous thyroid meds and those who are "normal".. own thryoid producing endogenous thryoid hormones). Perhaps this should be looked at in any future studies .. cheeky grins. <br>yep, good study!<br>If the difference was being excreted in faeces, the yes, the absorption rate would be cause?.. if not.. then no?<br>-------- </p> <p> <small> <a href="http://tealady.blog.co.uk/2007/07/04/timing_of_taking_thyroid_meds_circadian_~2569561/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-05-09:/2007/05/10/membrane_fluidity_of_thyroid_gland_in_ra~2242493/tealady2007-05-10T00:32:39+02:002007-05-10T14:03:35+02:00 <p>study on <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=11372391">membrane fluidity of thyroid gland in rats with iodine deficiency </a>or iodine excess][Article in Chinese]<br><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=11372391">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=11372391</a><br>Yan Y, Fang H, Xiang J. <br>Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, China.</p> <p>OBJECTIVES: To explore the effect of iodine deficiency and excess on thyroid membrane fluidity and its pathogenesis. </p> <p>METHODS: Wistar rats were fed different levels of iodine in the diet (normal iodine as control, low iodine and excess iodine). <br>Serum T4 and T3 levels, thyroid superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities and malondialdehyde (MDA) content were determined, and two parameters of polarization (Pr) and micro-viscosity (eta) using DPH as a florescence probe were tested. </p> <p>RESULTS: Serum T4 and T3 levels in the low iodine (LI) group were markedly decreased, and the thyroid SOD and GPx activities and MDA content were significantly increased compared with the other two groups. <br>However no changes were found in the high iodine (HI) group. There were no differences in Pr and eta values among three groups at 12th week of experiment, but at 24th week, both Pr and eta values in LI group were increased significantly compared to the other two groups. But the effect of iodine excess as expected was not found in this study. </p> <p>CONCLUSIONS: <strong>Long-term iodine deficiency caused a marked increase of membrane micro-viscosity and decrease of membrane fluidity in rat thyroid gland</strong>. <strong>Oxidative damage of thyroid by free radicals and retardation of lipid metabolism are considered as two important pathogenesis factors</strong>.</p> <p>PMID: 11372391 [PubMed - indexed for MEDLINE]<br>----------------------<br> <em>However these 2 studies did find problems with excess iodine compared o optimal(normal) amounts</em></p> <p>Effect of chronic mild and moderate iodine excess on thyroid anti-oxidative ability of iodine deficiency and non-iodine deficiency Wistar rats] <span class="pub">[Zhonghua Yi Xue Za Zhi. 2006]</span> <span class="pmid">PMID: 16796889</span> </p> <p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=14642172" class="pl">[Effects of supplementation of different kinds of iodine on the antioxidative ability of retina in iodine deficient rats]</a> <span class="pub">[Zhonghua Yan Ke Za Zhi. 2003</span> </p> <p> <small> <a href="http://tealady.blog.co.uk/2007/05/10/membrane_fluidity_of_thyroid_gland_in_ra~2242493/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2007-05-04:/2007/05/04/only_t4_and_t3_combined_treatment_result~2208178/tealady2007-05-04T10:44:24+02:002007-05-05T11:04:35+02:00 <p>Well I've heard this before from research scientists who have done tissue sampling when studying thyroid hormones, but now I've finally found a study<br><a href="http://endo.endojournals.org/cgi/reprint/137/6/2490.pdf"><a href="http://endo.endojournals.org/cgi/reprint/137/6/2490.pdf">http://endo.endojournals.org/cgi/reprint/137/6/2490.pdf</a></a></p> <p>Note_ p 2495 , or p 6 of 13 in pdf<br>"We have shown that using T4 or T3 alone" (<em> and yes it was time released! as they used continuous infusion via  pumps.. comment added for proponents of time release T3 ONLY </em>) <br>" it is not possible to met either one of the two possibilities simultaneously for plasma and tissues (1,5) despite the wide ranges of doses used in the studies..." <br>"<strong>when infusing T4 alone, supraphysiological T4 concentrations have to be reached in most tissues to normalise their T3 concentrations, and this occurs at different T4 concentrations for different tissues</strong>(1). </p> <p><strong>When using T3 alone, T4 concentrations in plasma and tissues are always very low, and supraphysiological T3 concentrations have to be reached in the circulation to normalise T3 levels in many tissues</strong>(5) "</p> <p><em>My personal feelings/symptoms/blood test results  and my observations from reading of many others experiences on a thyroid forum would fit in with the above. They including <br>blood test results and dosages on various thyroid hormones from T4 alone, to T3 alone (usually time released), and including many "combos"  and doses both using synthetic T4 and T3 and using a pig's thyroid based thyroid hormone replacement both alone or with added T4 /T3.<br></em></p> <p><em>NOTE: The ratios  in above study are correct for a rat NOT a human, but the general principle of euthyroidism (normality) in all tissues on a physiological ratio of T4 and T3 still holds for humans in my opinion... </p> <p>Unfortunately we'll have to stick with rats at present; as obtaining tissues from humans is rather difficult!(perhaps those who undergo stomach stapling or removal of various parts.  Even if patients did volunteer their tissues after removal by independant surgical procedures, it is almost impossible to form a study from the subjects/patients and test the effects of various thyroid hormones.  As well as the logisitic difficulties,and only being able to test removed tissues, which would usually be only one tissue type per patient!,  the patients would have to undergo surgical thyroid removal  weeks before their other surgery! followed by thyroid hormone replacemnent at varying levels set as determined by the study. Thyroid removal for the sake of a study is clearly not acceptable!!. )<br>Hence the rats( this comment for those who dismiss studies as irrelevant as they were on rats and not humans!)</em></p> <p><em><br>slightly off topic<br>I recall it mentioned at uni that liver is way higher in T4 than the thyroid gland.. like eat liver to get T4 if desperate?..and this backs it up?<br>I still remember this and plan to go for lamb's fry in the case of a shortage of thyroid hormones if desperate; perhaps I could freeze dry it? I still wonder if it would work?</em></p> <p>comments welcome </p> <p> <small> <a href="http://tealady.blog.co.uk/2007/05/04/only_t4_and_t3_combined_treatment_result~2208178/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-11-11:/2006/11/12/endocrine_abstracts~1320588/tealady2006-11-12T00:21:08+01:002006-11-12T00:25:41+01:00 <p><a href="http://www.endocrine-abstracts.org/ea/0008/default.htm">http://www.endocrine-abstracts.org/ea/0008/default.htm</a></p> <p> a bit overwhelming for me. but maybe someone else may find it useful <img src="/img/smilies/icon_smile.gif" alt=":)" class="middle" border="0"></p> <p>examples<br> <a href="http://www.endocrine-abstracts.org/ea/0008/ea0008p84.htm">http://www.endocrine-abstracts.org/ea/0008/ea0008p84.htm</a><br> (click on [P84])<br> shows study wheich verfies the validity of home cortsiol tests , including saliva..provided of course they are correctly collected and a highly sensitive cortisol assay i accurately done.</p> <p> <small> <a href="http://tealady.blog.co.uk/2006/11/12/endocrine_abstracts~1320588/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-11-11:/2006/11/12/phytoestrogens_inhibit_aromatase~1320583/tealady2006-11-12T00:19:37+01:002006-11-12T00:19:37+01:00 <p>PHYTOESTROGENS INHIBIT mRNA EXPRESSION AND ACTIVITY OF AROMATASE IN HUMAN GRANULOSA-LUTEAL (GL) CELLS</p> <p>S Rice & SA Whitehead </p> <p>Basic Medical Sciences, St George's Hospital Medical School, London SW17 0RE, UK.</p> <p>--------------------------------------------------------------------------------</p> <p>Phytoestrogens bind weakly to oestrogen receptors and can initiate oestrogen-dependent transcription. They are promoted as natural alternatives to HRT and yet epidemiological evidence suggests that they may protect against breast and prostate cancer. Studies in cell-free preparations have shown that phytoestrogens can inhibit the activity of aromatase and that the inhibition is, at least partly, competitive with androgen substrates. The question as to whether chronic exposure to phytoestrogens may alter the expression of aromatase and thereby modulate the conversion of androgens to oestrogens has not been addressed.</p> <p>We have investigated the effects of three isoflavones, genistein, diadzein and biochanin A, two flavones, quercetin and apigenin and the mycotoxin zearalenone on mRNA and protein expression of aromatase after exposure of human GL cells to these phytoestrogens for 48 h. Real time RT-PCR was used to quantitate aromatase mRNA levels and normalized against two house-keeping genes beta-actin and GAPDH. The cellular concentration of aromatase was quantified with Western blots that were sequentially exposed to antibodies against aromatase and beta-actin. For all experiments the conversion of testosterone to oestradiol over a 4h period, prior to using cells for mRNA or protein expression, was measured. Thus biological activity was assessed in the same cells as either mRNA/protein expression was measured.</p> <p>Our preliminary results show that relatively high concentrations of phytoestrogens (10 micromolar) inhibit the expression of aromatase and that this is reflected in a reduced ability of GL cells to convert testosterone to oestradiol. Lower doses of phytoestrogens were ineffective in this respect. This is the first study to identify inhibitory effects of phytoestrogens on the mRNA and protein expression of aromatase in primary cultures of human cells. This may be of significance in the epidemiological evidence that diets high in phytoestrogens may protect against breast cancer.</p> <p>----------------</p> <p><em>I wonder if this reduces overakl oestradiol in females?<br> I also wonder if aromatase inibition would led to more DHT being produced and hair loss?</em> </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/11/12/phytoestrogens_inhibit_aromatase~1320583/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-11-02:/2006/11/02/reversible_subclinical_hypothyroidism~1286794/tealady2006-11-02T03:42:44+01:002006-11-02T04:02:14+01:00 <p><a href="http://www.medscape.com/viewarticle/545972">Reversible Subclinical Hypothyroidism in the Presence of Adrenal Insufficiency </a><br> Three case studies offer insights into the complexities of thyroadrenal interactions.<br> <a href="http://www.medscape.com/viewpublication/1224_toc?vol=12&iss=5">Endocr Pract 12(5) 2006</a> </p> <p>"In patients with both hypothyroidism and adrenal insufficiency, adrenal crisis can be precipitated if thyroid hormone replacement is instituted before the initiation of corticosteroid therapy.[1]"</p> <p>"In this report, we describe 3 young patients in whom mild hypothyroidism was detected but who, in fact, had severe adrenal insufficiency. More interestingly, the thyroid state normalized solely by treatment of the adrenal insufficiency"</p> <p>" Clinical signs and symptoms of adrenal insufficiency could be subtle, and the discovery of TSH elevation might deflect the caregiver from attending to the true diagnosis. Hence, physicians should contemplate the hypothalamicpituitary-adrenal axis in patients with mild hypothyroidism or compensated hypothyroidism, regardless of evidence of autoimmunity. It could be inferred that physiologic levels of glucocorticoids and mineralocorticoids are essential "</p> <p>1. Schatz DA, Winter WE. Autoimmune polyglandular syndrome. II: Clinical syndrome and treatment. Endocrinol Metab Clin North Am. 2002;31:339-352. </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/11/02/reversible_subclinical_hypothyroidism~1286794/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-10-21:/2006/10/21/thyroid_nodules_removed_by_ultrasound~1244909/tealady2006-10-21T08:30:06+02:002006-10-21T11:39:47+02:00 <p><em>I have thyroid nodules(only grown since beginning thyroid hormone replacement, which actually resulted in lowered FT4 levels and difficulty tolerating a higher dose of thryoid hormones).<br> I intend to keep an eye on this, although I'd be wary of ultrasound being successfully confined to just the nodules, especially considering the location of the parathyroid and nodules . Of course people's nodules will be in differing places and some may be easily isolated so every case is, as usual, individual.</p> <p>Also thyroid nodules, if not he cancerous type, produce thyroid hormones.. and I suspect are often just the body's defence against being kept hypothyroid.. either by insufficient replacement meds for the free levels in one's "bold to be as high as the body demands, or just by the body tending to be hypothyroid and no meds given.<br> Many reasons for this but they include a lack of a balanced form of natural iodine in diet (as in kelp and seafood), and fluoride in water replacing iodine in cells in body . or even a form of thyroid hormone resistance requiring the body to up its thyroid hormone levels to get the require response at receptor level...and why this exists or insulin resistance may be also manyfold, complicated, intricate and mostly as yet unknown!</p> <p>Just my thoughts(accurate as far as my limited understanding goes..) on why I wouldn't be jumping into surgery or ultrasound unless nodules were causing specific problems .. like obstruction in throat, or hyperthyroid symptoms etc"<br> </em></p> <p>Edited to add: </p> <p>from a <a href="http://forums.about.com/n/pfx/forum.aspx?tsn=1&nav=messages&webtag=ab-thyroid2&tid=4580">post </a>by Elaine<br> "The size of nodules and also levels of thyroid hormone are reduced on a low iodine diet. This is usually the standard approach. Or if there are any signs of hypothryoidism thryoid replacement hormone is used since TSH is known to cause thyroid cell growth. </p> <p>Nodules become hyperthyroid as a natural mechanism that helps reduce their size since TSH falls in hyperthyroidism. Using thryoid replacement level has the same effect"</p> <p>So it looks like thryoid nodules may also develop from a higher iodine diet, a least in the US where the high iodine levels are usually formed from adding in overhigh levels KI or KIO3 to salt and processed foods containing this salt, and be helped by avoidance/reduction of iodized salt.</p> <p>In Tasmania thyroid nodules grew in women around 50 yrs of age who had lived in a low iodine environment ..possibly a way of the body getting enough thryoid hormones<br> Thyrotoxicosis developed with the addition of iodine to the diet. </p> <p>so it looks like either too little or too much regarding iodine, but again the added iodine was the form of KI or KIO3, not the iodine found naturally in kelp or seafood.<br> ----------------</p> <p><strong>Ultrasound Successful in Thyroid Nodule Trial</strong><br> 10.12.06, 12:00 AM ET</p> <p>THURSDAY, Oct. 12 (HealthDay News) -- A new technology designed to remove growths from the thyroid gland with high-intensity focused ultrasound beams has passed its first test in humans, French researchers report.</p> <p>The hope is that the treatment will eliminate the need for surgery that often is performed to remove the growths, formally called nodules, said Dr. Oliver Esnault, an endocrine surgeon at Saint-Louis Hospital in Paris and a leader of the trial.</p> <p>But the technology is in its early stages, Esnault said. "We just treated 25 patients with this technology," he said. "It may take three or four years to be sure the technology is convenient to patients, and we are not certain yet that we will be able to use it routinely."</p> <p>Thyroid nodules are fairly common. Many go unnoticed, and only 5 percent are cancerous. But since the thyroid sits at the base of the neck, some nodules can grow large enough to interfere with breathing. And overproduction of thyroid hormones by some nodules can cause symptoms such as unexpected weight loss and abnormal heartbeats.</p> <p>The 25 people in the trial were designated for surgery to remove their enlarged thyroids, which had multiple nodules. Surgery was, in fact, performed two weeks after their nodules were exposed to the high-intensity focused ultrasound. The main object of the study was to determine how patients reacted to the treatment, Esnault said. A single nodule was targeted in each patient.</p> <p>Three patients were frightened enough that their treatment was stopped, he reported, but it was "well tolerated in all other patients." Skin blisters were seen in seven participants, which led to a slight redesign of the ultrasound equipment.</p> <p>When the highest level of focused ultrasound was used, 70 percent of the nodular tissue was destroyed, Esnault said. "This study confirmed the feasibility and safety of the high-intensity focused ultrasound procedure," he concluded.</p> <p>Esnault presented the findings Thursday at the American Thyroid Association annual meeting, in Phoenix.</p> <p>The research is being financed by INSERM, the French equivalent of the U.S. National Institutes of Health. INSERM designed the prototype equipment, and "we have an industrial partner involved in the project," Esnault said. "They are building a series of prototypes."</p> <p>Esnault and his colleagues have begun two new studies designed to determine which patients are the best candidates for the ultrasound treatment. One study, for example, includes people whose nodules produce excessive amounts of thyroid hormone.</p> <p>Dr. Gregory Brent is secretary of the American Thyroid Association. "The [study] results look good, but it is obviously a small study," he said. "But with this kind of result, it gives you confidence that you can try non-surgical treatments for thyroid nodules. This is certainly a very important study, showing that ultrasound can shrink nodules without damaging surrounding tissue."</p> <p>Ultrasound treatment probably will be usable for a subset of people with thyroid nodules, Brent said, and "right now it is hard for anyone to know how large that subset will be."</p> <p> <small> <a href="http://tealady.blog.co.uk/2006/10/21/thyroid_nodules_removed_by_ultrasound~1244909/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-10-12:/2006/10/12/tsh_stimulates_inositol_phosphate_genera~1211911/tealady2006-10-12T05:57:59+02:002006-10-12T05:57:59+02:00 <p><strong>TSH stimulates inositol phosphate generation ButThyroid stimulating antibodies did NOT</strong></p> <p>The Journal of Clinical Endocrinology & Metabolism Vol. 91, No. 3 1099-1107<br> Copyright © 2006 by The Endocrine Society<br> <strong><a href="http://jcem.endojournals.org/cgi/content/abstract/91/3/1099">Thyrotropin Stimulates the Generation of Inositol 1,4,5-Trisphosphate in Human Thyroid Cells </a></strong>Jacqueline Van Sande, Didier Dequanter, Philippe Lothaire, Claude Massart, Jacques E. Dumont and Christophe Erneux<br> Institute of Interdisciplinary Research (J.V.S., C.M., J.E.D., C.E.), University of Brussels, School of Medicine, 1070 Brussels, Belgium; and Institut Bordet (D.D., P.L.), University of Brussels, 1000 Brussels, Belgium </p> <p>Address all correspondence and requests for reprints to: Christophe Erneux, Institute of Interdisciplinary Research, Campus Erasme Building C, 808 Route de Lennik, 1070 Brussels, Belgium. E-mail: <a href="mailto:cerneux@ulb.ac.be.">cerneux@ulb.ac.be.</a></p> <p>Context: <strong>Dual activation by TSH of the phospholipase C and cAMP cascades has been reported in human thyroid cells</strong>. In contrast, Singh et al. reported convincing data in FRTL-5 thyrocytes arguing against such an effect in this model. Their data in FRTL-5 cells indicated no increase in inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] in response to TSH. Therefore, the authors questioned results previously obtained on human cells by cruder methodology. </p> <p>Objective: We investigated the formation of inositol phosphates by HPLC techniques in human thyroid slices to separate the inositol phosphate isomers. </p> <p>Results: Ins(1,4,5)P3, inositol 1,3,4-trisphosphate, and inositol 1,3,4,5-tetrakisphosphate were increased after TSH stimulation. The effect of TSH in human thyroid cells was reproduced by recombinant TSH and prevented by antibodies blocking the TSH receptor. Thyroid-stimulating antibodies at concentrations eliciting a cAMP response equivalent to TSH failed to stimulate inositol phosphate generation. </p> <p>Conclusions: TSH, but not thyroid-stimulating antibodies, activates both cAMP and the phospholipase C cascade in human thyroid as now demonstrated by an increase in Ins(1,4,5)P3 and its inositol phosphate metabolites. Therefore, this effect cannot be extrapolated to the FRTL-5 cell line. The apparent discrepancy may be due to a difference between species (human vs. rat) or to the loss of the fresh tissue properties in a cell line. The dual effect of TSH in human cells, through cAMP on secretion of thyroid hormones and through the diacylglycerol, Ins(1,4,5)P3 Ca2+ pathway on thyroid hormone synthesis, implies the possible separation of these effects in thyroid disease.<br> --------------------<br> <em>I've no idea what the implications of this is??</em> </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/10/12/tsh_stimulates_inositol_phosphate_genera~1211911/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-10-08:/2006/10/08/blocking_action_of_t4_on_t3_effect~1198718/tealady2006-10-08T05:23:05+02:002006-10-08T05:23:05+02:00 <p>Membrane cooperative enzymes. High molecular specificity for blocking action of thyroxine on triiodothyronine effect in rat erythrocyte and Escherichia coli systems.<br> J Biol Chem 1978 Sep 10;253(17):6255-9<br> de Mendoza D, Moreno H, Farias RN.</p> <p>The molecular specificity for the blocking action of thyroxine on the triiodothyronine effect in the cooperativity of membrane-bound rat erythrocyte acetylcholinesterase and Escherichia coli Ca2+-ATPase was analyzed. Changes in the values of n (Hill coefficient) were obtained at strict physiological levels of these hormones. The structural requirements of the thyroid hormones to modify the membrane-bound systems were studied using various analogues of these hormones. In the erythrocyte system, a very high molecular specificity for triiodothyronine and thyroxine actions was found. The L-alanine side is essential to carry out both the allosteric desensitization and the blocking effects. The blocking ability of thyroxine is characterized by the presence of iodine in the 5' position. The bacterial system presented only specificity for the triiodothyronine allosteric desensitization. A system of membrane-bound enzymes for the study of the actions of thyroid hormones, is presented here.</p> <p>PMID: 150417 [PubMed - indexed for MEDLINE] </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/10/08/blocking_action_of_t4_on_t3_effect~1198718/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-10-03:/2006/10/03/low_thyroxine_levels_in_b2_deficiency_fe~1183050/tealady2006-10-03T09:44:13+02:002006-10-03T09:44:13+02:00 <p>Acta Psychiatr Scand. 1992 May;85(5):360-3</p> <p>Low thyroxine levels in female psychiatric inpatients with riboflavin deficiency: implications for folate-dependent methylation<br> <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1605056&dopt=Abstract">http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1605056&dopt=Abstract</a></p> <p>Bell IR, Morrow FD, Read M, Berkes S, Perrone G<br> Department of Psychiatry, Harvard Medical School, McLean Hospital, Belmont.</p> <p>Intermediates in the folate-dependent methylation pathways may play a role in the etiology and treatment of such mental disorders as major depression. These pathways include a step dependent on a riboflavin (B2)-derived coenzyme, flavin adenine dinucleotide (FAD), which is reportedly sensitive to thyroid status and to phenothiazine and tricyclic drug exposure. In a sample of 52 male and female acute psychiatric inpatients, 17% (n = 9) showed B2 deficiency (i.e., insufficient FAD activity) on a functional red blood cell enzyme assay, but only one B2-deficient individual showed deficiency in another B-complex vitamin (folate). All patients with B2 deficiency were women, who were also significantly younger than the rest of the sample. The B2-deficient women had significantly lower thyroxine levels, even when controlling for sex and covarying for age. B2-deficient patients exhibited a nonsignificant trend toward more unipolar depression (44% vs 14%), but not toward bipolar or schizophrenic disorders. As in a previous study, drug exposure did not show a relationship to riboflavin deficiency in this sample. The findings suggest that B2 (FAD) activity may serve as a sensitive marker of thyroxine status in certain female psychiatric inpatients and that B2 deficiency may play an etiological role in defects of the methylation pathways in a subset of mentally ill individuals.</p> <p>PMID: 1605056 [PubMed - indexed for MEDLINE] </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/10/03/low_thyroxine_levels_in_b2_deficiency_fe~1183050/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-09-26:/2006/09/26/pcos_triglycerides~1161547/MKBob2006-09-26T11:04:28+02:002006-09-26T11:04:28+02:00 <p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=15670186">link</a></p> <p><strong>Tryptophan 64 --> arginine polymorphism of beta-3-adrenergic receptor in Chilean women with polycystic ovary syndrome.</strong></p> <p>Objective To establish the frequency of the Trp64Arg polymorphism of the β3 adrenergic receptor (ADRB3) in women with polycystic ovary syndrome (PCOS) from a Chilean population, focusing particularly on the interaction with body weight. In addition, we evaluated the relationship of the Trp64Arg variant with other metabolic components of this syndrome.</p> <p>Patients and Design In a case–control design study, a total of 106 women with clinical and hormonal evidence of PCOS and 82 healthy women (HW) were evaluated.</p> <p>Measurements An oral glucose tolerance test (OGTT) was performed and serum glucose and insulin were measured before the glucose load and 30, 60, 90 and 120 min after. Lipid profile was determined in the basal sample. Insulin resistance was assessed by the homeostatic model assessment (HOMAIR) and insulin sensitivity index (ISI) composite. A polymerase chain reaction restriction fragment length polymorphism (PCR-RFLP) analysis was performed to determine the Trp64Arg polymorphism of ADRB3.</p> <p>Results The frequency of the heterozygous condition was similar between PCOS and HW (39%vs. 35%). Only two subjects were homozygous for arginine, both belonging to the PCOS group and having a body mass index (BMI) > 30 kg/m2. In the crude analysis, hypothesis tests and odds ratios show that there is no evidence of association between the ADRB3 Trp64Arg variant and PCOS (P = 0·47). Moreover, when data were stratified by BMI categories, the statistical test for interaction between Trp64 carrier status and obesity was not significant (P = 0·29). This variant was present in 52% of the obese PCOS patients and 40% of the obese HW. In normal weight and obese PCOS carriers, the presence of the Trp64Arg variant was associated with high triglyceride (TG) levels. A major effect of the Trp64Arg variant on insulin resistance parameters could not be demonstrated.</p> <p>Conclusions The frequency of the Trp64Arg polymorphism was similar in healthy women and PCOS women, and a possible interaction between the effect of this variant and obesity in PCOS could not be demonstrated. However, our results showed an association between triglyceride levels and the presence of this genetic variant in PCOS women.</p> <p>Francisco Pérez-Bravo*†, Bárbara Echiburú†, Manuel Maliqueo*, José Luis Santos† and Teresa Sir-Petermann</p> <p>Clinical Endocrinology<br> Volume 62 Page 126 - February 2005</p> <p><a href="http://dx.doi.org/10.1111/j.1365-2265.2004.02183.x">http://dx.doi.org/10.1111/j.1365-2265.2004.02183.x</a></p> <p>Volume 62 Issue 2 </p> <p>Bob </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/09/26/pcos_triglycerides~1161547/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-08-16:/2006/08/16/iron_cellular_iron_metabolism_mitochondr~1042918/tealady2006-08-16T01:32:08+02:002006-08-16T01:32:08+02:00 <p><a href="http://www.bloodjournal.org/cgi/content/full/105/5/1844">http://www.bloodjournal.org/cgi/content/full/105/5/1844</a> </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/08/16/iron_cellular_iron_metabolism_mitochondr~1042918/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-08-08:/2006/08/08/iodine_deficiency_and_hyperthyroidism~1022248/tealady2006-08-08T09:53:00+02:002006-12-02T04:10:54+01:00 <p><br>1: Thyroid. 2000 Nov;10(11):951-63. <br><strong><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?itool=abstractplus&db=pubmed&cmd=Retrieve&dopt=abstractplus&list_uids=11128722">Thyroid disorders in mild iodine deficiency</a></strong>.<br>Laurberg P, Nohr SB, Pedersen KM, Hreidarsson AB, Andersen S, Bulow Pedersen I, Knudsen N, Perrild H, Jorgensen T, Ovesen L. <br>Department of Endocrinology and Medicine, Aalborg Hospital, Denmark. <a href="mailto:Laurberg@aas.mja.dk">Laurberg@aas.mja.dk</a><br><br>Comparative epidemiologic studies in areas with low and high iodine intake and controlled studies of iodine supplementation have demonstrated that the major consequence of mild-to-moderate iodine deficiency for the health of the population is an <strong>extraordinarily high occurrence of hyperthyroidism in elderly subjects, especially women, with risk of cardiac arrhythmias, osteoporosis, and muscle wasting.<br></strong><br> The <strong>hyperthyroidism is caused by autonomous nodular growth</strong> and function of the thyroid gland and it is accompanied by a high frequency of goiter. </p> <p>Pregnant women and small children are not immediately endangered but the consequences of severe iodine deficiency for brain development are grave and a considerable safety margin is advisable.<br> <br>Moreover, a shift toward less malignant types of thyroid cancer and a lower radiation dose to the thyroid in case of nuclear fallout support that mild-to-moderate iodine deficiency should be corrected. </p> <p>However, there is evidence that a high iodine intake may be associated with more autoimmune hypothyroidism, and that Graves' disease may manifest at a younger age and be more difficult to treat.<br> <br>Hence, the iodine intake should be brought to a level at which iodine deficiency disorders are avoided but not higher. Iodine supplementation programs should aim at relatively uniform iodine intake, avoiding deficient or excessive iodine intake in subpopulations. To adopt such a strategy, surveillance programs are needed.</p> <p>PMID: 11128722 [PubMed - indexed for MEDLINE] </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/08/08/iodine_deficiency_and_hyperthyroidism~1022248/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-08-08:/2006/08/08/iodine_deficiency_was_associated_with_a_~1022256/tealady2006-08-08T09:35:59+02:002006-08-08T09:35:59+02:00 <p>CLINICAL STUDY </p> <p><strong>The Danish investigation on iodine intake and thyroid disease</strong>, <br>DanThyr: status and perspectives <br>Peter Laurberg, Torben Jørgensen2, Hans Perrild3, Lars Ovesen1,4, Nils Knudsen2,3, Inge Bülow Pedersen, Lone B Rasmussen1, Allan Carlé and Pernille Vejbjerg2,3 <br><em>Department of Endocrinology and Medicine, Aalborg Hospital, DK-9000 Aalborg, Denmark, 1 Danish Institute for Food and Veterinary Research, Copenhagen, Denmark, 2 Research Centre for Disease Prevention and Health, Glostrup Hospital, Copenhagen, Denmark, 3 Medical Clinic I, Bispebjerg Hospital, Copenhagen, Denmark and 4 The National Heart Foundation, Copenhagen, Denmark</em> <br><em>(Correspondence should be addressed to P Laurberg; Email: <a href="mailto:laurberg@aas.nja.dk">laurberg@aas.nja.dk</a> )</em><br><br><em>Objective</em>: Denmark was an area of iodine deficiency, and mandatory iodine fortification of table salt and salt in bread (13 p.p.m. iodine) was initiated in 2000/2001. The Danish investigation on iodine intake and thyroid disease (DanThyr) is the monitoring of the iodine fortification program. <br><em>Design and methods</em>: DanThyr consists of three main parts: a study of population cohorts initialized before (n = 4649) and after (n = 3570) iodization of salt, a prospective identification of incident cases of overt hyper- and hypothyroidism in a population of around 550 000 people since 1997, and compilation of data from the national registers on the use of thyroid medication, thyroid surgery, and radioiodine therapy. <br>Studies were carried-out in parallel in subcohorts living in areas with differences in iodine content of ground water. <br><em>Results</em>: <strong>The study showed profound effects of even small differences in iodine intake level on the prevalence of goiter, nodules, and thyroid dysfunction</strong>.<br><strong>Mild and moderate iodine deficiency was associated with a decrease in serum TSH with age</strong>.<br>Other environmental factors were also important for goiter development (increase in risk, smoking and pregnancy; decrease in risk, oral contraception and alcohol consumption), and the individual risk depended on the genetic background. <br>Environmental factors had only a minor influence on the prevalence of thyroid autoantibodies in the population. <br>There were more cases of overt hypothyroidism in mild than in moderate iodine deficiency caused by a 53% higher incidence of spontaneous (presumably autoimmune) hypothyroidism.<br>On the other hand, there were 49% more cases of overt hyperthyroidism in the area with moderate iodine deficiency. <br>The cautious iodine fortification program, aiming at an average increase in iodine intake of 50 µg/day has been associated with a 50% increase in incidence of hyperthyroidism in the area with the most severe iodine deficiency. <br>The incidence is expected to decrease in the future, but there may be more cases of Graves&rsquo; hyperthyroidism in young people. </p> <p><em>Conclusion</em>: A number of environmental factors influence the epidemiology of thyroid disorders, and even relatively small abnormalities and differences in the level of iodine intake of a population have profound effects on the occurrence of thyroid abnormalities. Monitoring and adjustment of iodine intake in the population is an important part of preventive medicine. </p> <p>Ref: <a href="http://eje-online.org/cgi/content/full/155/2/219"><a href="http://eje-online.org/cgi/content/full/155/2/219">http://eje-online.org/cgi/content/full/155/2/219</a></a><br>      <a href="http://eje-online.org/cgi/content/abstract/155/2/219"><a href="http://eje-online.org/cgi/content/abstract/155/2/219">http://eje-online.org/cgi/content/abstract/155/2/219</a></a><br>     <a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=retrieve&db=pubmed&list_uids=16868134&dopt=Abstract">[pubmed]</a> </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/08/08/iodine_deficiency_was_associated_with_a_~1022256/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-08-03:/2006/08/03/lowered_stomach_gatric_acid_in_thyroid_d~1012012/tealady2006-08-03T23:30:30+02:002008-05-04T02:11:10+02:00 <p><a href="http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16694026">http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=16694026</a></p> <p>THE GASTRIC SECRETION IN EXOPHTHALMIC GOITRE AND MYXOEDEMA</p> <p>By J. LERMAN AND J. H. MEANS</p> <p>(From the Thyroid Clinic and Metabolism Laboratory of the Massachusetts General Hospital, Boston)</p> <p>(Received for publication August 13, 1931)<br> <br> Our knowledge of the gastric secretion in endocrine disturbances is limited, and this applies to exophthalmic goitre and myxoedema as well as to other endocrine conditions. In both the old and recent literature one finds conflicting statements regarding the gastric contents in thyroid disease&hellip;&hellip;..</p> <p><em>CONCLUSIONS</em><br> 1. In patients with exophthalmic goitre and myxoedema, there is a definite lowering of the gastric acidity to about half its normal value.<br> 2. The incidence of <a href="http://en.wikipedia.org/wiki/Hypochlorhydria">achlorhydria</a> in exophthalmic goitre is 38 per cent and in myxoedema is 53 per cent. Corrected for the age distribution of a normal group, the incidence is 46 per cent and 75 per cent respectively.<br> 3. The frequency of achlorhydria is out of proportion to the depression in the average acidities and suggests that other factors are also important in its causation. There is perhaps a threshold of gastric secretion, and if the secretion is depressed beyond it, anacidity results.<br> 4. In exophthalmic goitre, there is no definite correlation between gastric acidity and such factors as age, red blood cell count, hemoglobin and level of basal metabolism. On the other hand, there is a high degree of correlation between the incidence of achlorhydria and age and basal metabolic rate and a probable inverse correlation between the incidence of achlorhydria and red blood cell count and hemoglobin. There is also a higher incidence of achlorhydria and hyperchlorhydria among males than among females.<br> 5. In myxoedema, there is an unusual tendency to anemia among patients with achlorhydria.<br> 6. There is indirect evidence that achlorhydria may persist in some cases at least after the primary condition has been cured.<br> 7. The knowledge of the gastric secretion in an individual case maybe of practical importance in prevention of the development of anemia</p> <p>Bob </p> <p><em>I think this may be related to lowered vitB1 (thiamin) use in hypothryoid.. hence lowered gastric acid production.<br> Supplementing with vitB1 increased by gastric acid production.. too much at present from the rumblings down there, so I'll need to cut back on the B1. It could just be the form of thiamin I usually take though .. thaimin <u>HCL</u> both tablets and injections.. althought the sublinguals are thiamin cocarboxylase<br> (more on <a href="http://tealady-health.blog.co.uk/?tag=b1 headings">b1 headings </a>post)</em> </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/08/03/lowered_stomach_gatric_acid_in_thyroid_d~1012012/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-07-27:/2006/07/27/heart_changes_with_thyroid~994382/tealady2006-07-27T23:50:34+02:002006-07-27T23:50:34+02:00 <p>The assessment of cardiovascular risk factors in thyroid disease</p> <p><a href="http://www.endocrine-abstracts.org/ea/0011/ea0011s12.htm">http://www.endocrine-abstracts.org/ea/0011/ea0011s12.htm</a></p> <p>B Biondi, </p> <p>Department of Clinical and Molecular Endocrinology and Oncology, Naples, Italy.</p> <p>The cardiovascular system is one of the major targets of thyroid hormone action, sensitive enough to detect the effects of thyroid hormone excess or deficiency at tissue level. Triiodothyronine (T3) acts on the heart and vascular system by classic genomic as well as non-genomic mechanisms and influences heart rate, systolic and diastolic function and systemic vascular resistance thereby affecting cardiac performance. In human short-term overt hyperthyroidism, the increase in left ventricular performance is predominantly sustained by the increased preload with enhanced left ventricular diastolic function. The combination of reduced systemic vascular resistance, coupled with the increased venous return and preload, increases cardiac output. The cardiovascular risk of subclinical and overt long-term hyperthyroidism is related to short-term effects due to the electrophysiological effects of thyroid hormones, and to the long-term effects resulting from increased left ventricular mass and increased cardiac workload. The frequency of atrial fibrillation is increased to a similar degree in patients with overt and subclinical hyperthyroidism.The significant increase in left ventricular mass represents the most consistent cardiac abnormality reported in patients with long-standing overt and subclinical hyperthyroidism and is responsible for diastolic dysfunction and systolic dysfunction during effort. Long-standing hyperthyroidism exerts many relevant effects on the cardiovascular system and it may induce abnormalities that may lead to more severe cardiovascular disease, thus potentially contributing to the increased risk of cardiovascular morbidity and mortality observed in these patients. The cardiovascular risk in patients with overt and subclinical hypothyroidism results from the changes in cardiovascular function and from accelerated atherosclerosis The decreased cardiac output in hypothyroid patients at rest depends largely on changes in diastolic relaxation and hemodynamic loading conditions.The reduced cardiac preload, in combination with bradycardia and slightly depressed myocardial contractility, accounts for a subnormal cardiac output in overt hypothyroidism, whereas peripheral vascular resistance are remarkably increased. The most consistent cardiac abnormality recognized in patients with subclinical hypothyroidism is the impairment of left ventricular diastolic function with an impaired left ventricular systolic function on effort. The negative effect induced by subclinical hypothyroidism on the cardiovascular system is reverted, restoring euthyroidism with L-T4 therapy. Several epidemiological studies examined the linkage between SH and atherosclerosis showing conflicting results. Diastolic hypertension, dyslipidemia, endothelial dysfunction, elevated C reactive protein levels and coagulation abnormalities represent the atherosclerotic risk factors associated with subclinical hypothyroidism and may be reversible with euthyroidism after L-T4 therapy.</p> <p>Endocrine Abstracts (2006) 11 S12</p> <p> <small> <a href="http://tealady.blog.co.uk/2006/07/27/heart_changes_with_thyroid~994382/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-05-25:/2006/05/25/vita_low_iodine_suboptimal_thyroid_fatig~827366/tealady2006-05-25T04:07:51+02:002006-05-25T04:23:17+02:00 <p> .. don't suppliment with <a href="http://jcem.endojournals.org/cgi/content/full/89/11/5441?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=ferritin++thyroid+resistance&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT">VitA WITHOUT sufficient iodine </a>?</p> <blockquote><p>A question raised by these findings is the safety of VA repletion without concurrent iodine repletion in children with coexisting VAD and severe IDD. Our data suggest that moderate VAD in severely iodine-deficient children may reduce the risk for hypothyroidism. The data are consistent with the possibility that VAD may decrease activation of the pituitary retinoid receptor, thereby increasing transcription of the TSHß gene and increasing TSH secretion (19, 20, 21). Increased TSH stimulation of the thyroid increases thyroid size, but maintains circulating thyroid hormone, protecting against hypothyroidism. Additional studies are clearly needed to resolve this question. Until then, a prudent course would be to provide oral iodized oil along with VA supplements to children in areas of severe endemic goiter that do not yet have IS</p></blockquote> <p>(note <a href="http://tealady.blog.co.uk/2006/04/13/sunscreens_may_contribute_to_hypothryoid~723887">sunscreen</a> can also be a problem)</p> <p>other links on iodine<br> <a href="http://tealady-health.blog.co.uk/?tag=iodine">http://tealady-health.blog.co.uk/?tag=iodine</a> </p> <p> <small> <a href="http://tealady.blog.co.uk/2006/05/25/vita_low_iodine_suboptimal_thyroid_fatig~827366/#comments">Comments</a> </small> </p>tag:tealady.blog.co.uk,2006-05-03:/2006/05/03/gastric_acid_is_required_for_proper_abso~774270/tealady2006-05-03T23:25:34+02:002006-05-04T08:34:35+02:00 <p> So if you have impaired absorbrion, you may need to increase your dose of T4 by approx. 25%, especially if your body is reacted by growing nodules on your thyroid...trying to increase your own body's thyroid output maybe? Just another reason you may require a higher dose... umm shouldn't this be obvious??<br> I'd expect measuring the free's would pick it up? Still for some reason it helps doctors justify the increase in dose if they have a reason?<br> Also why its not wise to take calcium carbonate(or probably Magnesium carbonate pr any ant-acids) within at least couple of hours("advice is usually" 4 hrs for calcium supps) of your T4 thyroid meds:-)It's not only the calcium regarding calcium carbonate, but the carbonate also plays maybe a bigger part than the calcium as the carbonate may "reduce" stomach acids.</p> <p> Gastric acid is required for proper absorption of oral thyroxine, according to the results of a study reported in the April 27 issue of The New England Journal of Medicine.<br> N Engl J Med. 2006;354:1787-1795</p> <p>"Malabsorption of thyroxine has been described in patients treated with drugs that modify an acidic environment," write Marco Centanni, MD, from University La Sapienza in Latina, Italy, and colleagues. "Both H. [Helicobacter] pylori infection and treatment with proton-pump inhibitors are frequent in Western countries, and the association of thyroid diseases with atrophic gastritis has been reemphasized. The concomitant presence of such gastric disorders with thyroid diseases may lead to uncertainty about the daily dose of thyroxine and, thus, to a continuous need for care and monitoring."</p> <p>The investigators determined the dose of thyroxine required to obtain a low level of thyrotropin (0.05 - 0.20 mU/L) in 248 patients with multinodular goiter. Of the 248 patients, 53 also had H. pylori–related gastritis, and 60 had atrophic gastritis of the body of the stomach, including 31 with and 29 without evidence of H. pylori infection. The comparison group consisted of 135 patients with multinodular goiter and no gastric disorders.</p> <p>The investigators also prospectively studied variation in the level of serum thyrotropin in 11 patients treated with thyroxine before and after H. pylori infection, and both before and during treatment with omeprazole in 10 patients treated with thyroxine who had gastroesophageal reflux.</p> <p>Compared with the reference group, patients with H. pylori–related gastritis, atrophic gastritis, or both conditions had a higher daily requirement of thyroxine by 22% to 34%. Prospective studies revealed that H. pylori infection in the 11 patients treated with thyroxine was associated with an increase in the level of serum thyrotropin (P = .002), an effect that was nearly reversed when H. pylori infection was eradicated. Similarly, in all 10 patients treated with thyroxine, omeprazole treatment was associated with an increase in the level of serum thyrotropin. This effect was reversed by a 37% increase in the thyroxine dose.</p> <p>"Patients with impaired acid secretion require an increased dose of thyroxine, suggesting that normal gastric acid secretion is necessary for effective absorption of oral thyroxine," the authors write. "Although the clinical importance of these findings is fairly clear, the mechanism by which intestinal absorption of thyroxine is impaired in patients with hypochlorhydria is unknown.... Our findings indicate that patients with multinodular goiter require an increase in the dose of thyroxine if they have concomitant atrophic gastritis, chronic H. pylori infection, or both.</p> <p>La Sapienza University in Rome supported this study. The authors have disclosed no relevant financial relationships.</p> <p>-------------------</p> <p><em>the old calcium carbonate research</em><br> Thyroid. 2001 Oct;11(10):967-71. </p> <p>The acute effect of calcium carbonate on the intestinal absorption of levothyroxine.</p> <p>Singh N, Weisler SL, Hershman JM.</p> <p>Department of Endocrinology and Metabolism, Veterans Affairs Greater Los Angeles Healthcare System, California 90073, USA. <a href="mailto:Nalini.Singh@med.va.gov">Nalini.Singh@med.va.gov</a></p> <p>To determine the acute effect of calcium, we measured levothyroxine absorption after ingestion of thyroxine (T4) with and without simultaneous ingestion of calcium (as calcium carbonate) in seven volunteers without thyroid disease. Serum total T4, total triiodothyronine (T3), free T4, and thyrotropin (TSH) levels were measured after ingestion of 1,000 microg of levothyroxine on two separate visits at 4-week intervals: (1) levothyroxine alone and (2) levothyroxine together with 2.0 g of calcium as calcium carbonate. The amount of absorbed levothyroxine was calculated as the incremental rise in serum T4 level during the first 6 hours multiplied by the volume of distribution for the hormone. When 1,000 microg of levothyroxine alone was given to subjects, the maximum average total T4 absorption was 837 microg (83.7% of the dose ingested) at 120 minutes. When levothyroxine was coadministered with 2.0 g of calcium (as calcium carbonate), the maximum average T4 absorption decreased to 579 microg (57.9% of the dose ingested) at 240 minutes. The total levothyroxine absorption over 6 hours was significantly greater with thyroxine than that with thyroxine and calcium (p = 0.02). The administration of calcium and levothyroxine in these subjects was associated with a significant reduction in the peak increment in serum total T4 (p = 0.02) and free T4 levels (p = 0.03), as well as a significant reduction in the overall increment in serum total T4 (p = 0.003), free T4 (p = 0.002), and total T3 levels (p = 0.01) over four time points (120 minutes, 240 minutes, 360 minutes, 1,440 minutes). In summary, this pharmacokinetic study in seven volunteers indicates that calcium carbonate acutely reduces T4 absorption.<br> -------------------</p> <p> <small> <a href="http://tealady.blog.co.uk/2006/05/03/gastric_acid_is_required_for_proper_abso~774270/#comments">Comments</a> </small> </p>