Taking part of one's thryoid meds at night is something many have been doing. (with docs OK)

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 this post

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) ...

It is normal to have some thyroid hormone released at night, so taking some at night makes sense.(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!)
Cokelaere-Influence of feeding pattern on thyroid hormones in long-term food-restricted rats
http://www.thieme-connect.de/ejournals/abstract/hmr/doi/10.1055/s-2007-979802  at Uni of Syd Medical library 574.192705 2

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.
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:-)

http://forums.about.com/n/pfx/forum.aspx?tsn=1&nav=messages&webtag=ab-thyroid&tid=46477
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.
What is your story?!!! CoachLinda

http://forums.about.com/n/pfx/forum.aspx?tsn=2&nav=messages&webtag=ab-thyroid&tid=46477
Hi, Linda!
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.
endophobia!

http://forums.about.com/n/pfx/forum.aspx?webtag=ab-thyroid&nav=messages&msg=46477.6
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.
Jan
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http://forums.about.com/n/pfx/forum.aspx?tsn=36&nav=messages&webtag=ab-thyroid&tid=67042  Choccy with thryoid meds at night for better absorption, or at least it sure sounds like a great excuse with some originality!

Ok, I gotcha per 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. 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.

Accepted on March 17, 2008 FREE FULL PDF
Free triiodothyronine has a distinct circadian rhythm that is delayed but parallels thyrotropin levels
W. Russell, R. F. Harrison, N. Smith, K. Darzy, S. Shalet, A. P. Weetman, and R. J. Ross*
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

* To whom correspondence should be addressed. E-mail: r.j.ross@sheffield.ac.uk.
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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.

Objective: With a view to optimising thyroid hormone replacement therapy we have used modern assays for FT4 and FT3 to investigate circadian rhythmicity.

Setting: University Hospital.

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.

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.

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.
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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!)
A few of us on a thryoid forum started before 2003- here's some of the old posts
My thoughts and practise are in this post from Apr 07 & this post below
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 :-)
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!

Metabolic effects of thyroid hormone derivatives.Moreno M, de Lange P, Lombardi A, Silvestri E, Lanni A, Goglia F.
Dipartimento di Scienze Biologiche ed Ambientali, Università degli Studi del Sannio, Via Port'Arsa, Benevento, Italy.

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.

PMID: 18279024 [PubMed - indexed for MEDLINE]
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my thoughts
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?

http://neuro.psychiatryonline.org/cgi/content/full/18/4/450 about a woman presenting with psychosis and addison. In the end of the article they wonder if she maybe had HE.

Increasing thyroid meds may precipiate Addisons

http://forums.about.com/n/pfx/forum.aspx?msg=4104.3&nav=messages&webtag=ab-thyroiduk#a3  
my post on UKthyroid forum

now that would get me off Armour fur sure! Apply T3 patch at times need additional FT3 :-) ..well I'd at least try it

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 ;-)

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.
Armour also increases appetite similar to T3, but nowhere near the same extent:-) Most people don't notice it much.

Some do though. I know someone on a forum who takes appetitive suppressants as well..but I'm not prepared to go that way!

No exogenous thyroid hormones.. no noticeable appetite :-)

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..
wonder why noone has cottoned on to this? I can't find any research on any suggestions of it?

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

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**)
Also see our trials of T4+T3 taken at bedtime back in 2002 in the thyroid forum

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!

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:-)

For more info on oestradiol.. it rises at night.. seems to be with the cortisol pattern and perhaps TSH spike pattern, perhaps in part  to aid in raising Total-thyroid hormone levels?!
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...
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!

Seems I was onto something here as this study also shows fT3 rising after TSH at night

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The point I'm trying to get across...
endocrine hormones, similar to insulin, for some of us anyway , maybe should be timed to optimise   TAKING IT when will be used(on demand) by the body, or when the body would naturally be producing it(circadian rhythm) ... 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!
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
"resistance" and allows other molecules that may be needed to bind to also work more effectively), but still have it when needed..
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)).

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.
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!

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..

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!

can you find ANYWHERE that this has been suggested before
or better still tried before!

This routine of patches only while in bed at night really seems to be working for me!!

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!
I feel "better" overall, and I think it's more than just the reduction in broken sleep. 
I think I've worked it out eventually!
(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)

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

UCLA Endocrinology Thyroid Hormone summary

The Immune System as a Regulator of Thyroid Hormone Activity

John R. Klein
Department of Diagnostic Sciences, Dental Branch, University of Texas Health Science Center,Houston, TX 77030

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.

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.

Exp Biol Med 231:229–236, 2006

http://www.ebmonline.org/cgi/reprint/231/3/229

Psychological Well-Being Correlates with Free Thyroxine But Not Free 3,5,3'-Triiodothyronine Levels in Patients on Thyroid Hormone Replacement

http://jcem.endojournals.org/cgi/content/abstract/91/9/3389

Ponnusamy Saravanan, Theo J. Visser and Colin M. Dayan

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

Yes, this agrees with what I have found in myself
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
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, ...
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)

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I've only glanced at the abstract of this one

Calcitonin deficiency in early stages of chronic autoimmune thyroiditis
Borges MF, Abelin NM, Menezes FO, Dahia PL, Toledo SP.
Department of Medicine, Federal School of Medicine of Triângulo Mineiro, Uberaba, Brazil.

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 (, 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.

PMID: 9797849 [PubMed - indexed for MEDLINE]

Sudden unexpected death associated with lymphocytic thyroiditisVestergaard V, Drostrup DH, Thomsen JL.
Institute of Forensic Medicine, University of Southern Denmark, Winsløwparken 17, DK-5000 Odense C. vibeke.vestergaard@ouh.regionsyddanmark.dk

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.

PMID: 17520957 [PubMed - indexed for MEDLINE]

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