Medical Research Supporting Patient Experience
This page will list professional research, articles, opinions and links which support what we already know…or they are at least in the right direction. And you can use these to support your argument with your black-and-white physician that certain thyroid treatments do NOT work, and there IS a better way to do all this.
***FOUND MORE RESEARCH ARTICLES THAT WOULD HELP THIS PAGE?? Use the Contact below to send the link to the article or comment. Remember: I’m only seeking research that can be used to help doctors understand better thyroid treatment and that which is related, as well as which challenges their bad information.
THE FAILURE OF T4-ONLY
- This eye-opening 1995 study firmly reveals that T4-only treatment does not ensure that all tissues are free from hypothyroidism aka euthroidism, and is thus not a recommended treatment! http://www.ncbi.nlm.nih.gov/pmc/articles/PMC185993/ (And it is following up by showing that only having T3 in one’s treatment does the job: https://www.ncbi.nlm.nih.gov/pubmed/8641203)
- Conclusions from this study show that more than 20% of patients, despite normal TSH levels, do not maintain FT3 or FT4 values in the reference range, reflecting the inadequacy of peripheral deiodination to compensate for the absent T3 secretion. It concludes that a more physiological treatment than levothyroxine monotherapy may be required. Study is titled “Levothyroxine monotherapy cannot guarantee euthyroidism in all athyreotic patients”. http://www.ncbi.nlm.nih.gov/pubmed/21829633 (See #5 below which shows 70%) Comment from Janie: And from reported patient experience, even with what appear to be adequate levels of T3, patients on T4 state they do NOT get the good results they do on desiccated thyroid.
- Thyroxine was no more effective than a placebo in improving cognitive function and psychological well-being in patients with symptoms of hypothyroidism. Thyroxine did NOT improve cognitive function and well-being in healthy participants. http://www.bmj.com/cgi/content/full/323/7318/891
- Despite a two-fold increase in total serum T3, free T3 in the cerebrospinal fluid (CSF) remained unchanged when one is on T4-only, which agrees with previous results in rats showing that T3 is less exchangeable between serum and CSF. http://informahealthcare.com/doi/abs/10.3109/00365513.2010.541931
- At the 90th annual meeting of the Endocrine Society, June 2008, it was announced that T3 can be an effective substitute for T4. And…the target TSH was .5 – 1.5. http://www.endocrinetoday.com/view.aspx?rid=28931 Comment from Janie: Even though being on desiccated thyroid, with its T4, T3, T2, T1 and calcitonin, is even better according to the experience of many patients, this announcement is at least a good step in the right direction. Hopefully, they will take the final step!
- Swedish Doctor at Karolinska Hospital in Stockholm states: Levaxin is the medicine that is offered to patients with Hypothyroidism. Approximately seven out of ten patients are not symptom-free. Stefan Sjoberg, endocrinologist and associate professor at the Karolinska Institute has therefore, together with his research team, shows that patients blood tests may show normal levels of thyroid hormones with T4-only due to not enough conversion to T3. Research underway at Halmstad Hospital. http://www.sourze.se/Forskare_ser_omvandlingsproblem_med_Levaxin_10742982.asp
- This study with patients who have no thyroid due to removal after cancer revealed that T4-only didn’t cut it: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3148220/
- 2015 RESEARCH CATCHES UP WITH YEARS OF PATIENT EXPERIENCES AND WISDOM ABOUT T4-ONLY AND THE TSH LAB TEST….and you wonder how long it will take doctors to GET THIS. Namely, this research underscores that1) T4-only treatment leaves residual symptoms
2) the TSH doesn’t reflect whether all tissues are getting enough thyroid hormones, aka, it states “While the molecular basis for the residual hypothyroid symptoms is lacking, it is generally hypothesized that these patients suffer from tissue-specific states of hypothyroidism and that serum TSH might not adequately reflect thyroid status at the level of different tissues
3) A T4/T3 combination, and even better NDT, is the way to go. http://www.jci.org/articles/view/77588
- Again, showing that T4-only (levothyroxine) and a so-called normal TSH, can result in continued problems. And since this came from an Endocrinology journal, I guess they would choke to dare mention that NDT would have been a great alternative: http://www.medscape.com/viewarticle/870924?src=wnl_mdplsnews_161028_mscpedit_wir&uac=92500HJ&impID=1224287&faf=1
- What’s interesting about this research is that pushing your T4-only too high (as a false way to treat continuing symptoms) can result in artery stiffness: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4275408/
MENTAL HEALTH RELATED
a) DEPRESSION and T4-ONLY
This article outright points out a study which shows that “…therapy with levothyroxine alone was not sufficient to induce a total remission of depressive symptoms in this population”. Plus…“In patients treated with T4, psychological symptoms may persist even when they achieve a euthyroid state.” Sadly, parts of the article are lacking…for example, it states “…the vast majority of patients with depression do not have biochemical evidence of thyroid dysfunction”. Clearly, they aren’t looking in the right places and probably going by the ridiculous TSH range, which can never show the lack of T3 in many tissues and organs including the brain!! http://www.hindawi.com/journals/jtr/2012/590648/
b) BIPOLAR CAN BE STRONGLY RELATED TO UNDIAGNOSED OR POOR THYROID TREATMENT:
Dr. Peter Whybrow, a world-renowned expert on bipolar disorder, published his findings in the journal Molecular Psychiatry about the connection between thyroid and bi-polar. But it’s hard to find on the net. Instead, here is one of several other articles which talks about this connection: http://www.psycheducation.org/thyroid/introduction.htm
c) HOW ANTI-DEPRESSANTS CAN NEGATIVELY AFFECT THE HPA AXIS (SKEWING YOUR SALIVA CORTISOL RESULTS)
This study, titled Antidepressant use and salivary cortisol in depressive and anxiety disorders reveals that antidepressants can drive cortisol too high or low.
HEART ISSUES FROM T4-ONLY TREATMENT:
The Journal of Clinical Endocrinology & Metabolism has reported that long-term levothyroxine replacement therapy in young adults is associated with cardiovascular abnormalities. http://jcem.endojournals.org/cgi/content/abstract/93/7/2486 2008 COMMENT: Of course, thyroid patients have known this a longggg time as they watched their cholesterol and Triglycerides rise while on a lousy T4-medication, and some end up with heart problems. But this finally gives some research on a FACT.
T4 COMBINED WITH T3 GIVES BETTER RESULTS:
- Here’s a study from 1996 which underscored that both T4 and T3 are needed to remove hypothyroidism: http://www.ncbi.nlm.nih.gov/pubmed/8641203 (And it followed research from the previous year showing that T4-only did NOT do the job–see http://www.ncbi.nlm.nih.gov/pmc/articles/PMC185993/)
- As far back as 1999, the New Journal of Medicine reported superior results of a synthetic T4 and T3 combination treatment, especially on the brain and other tissues. http://content.nejm.org/cgi/content/full/340/6/424
- And another one titled Thyroid Insuffiency: Is Thyroxine the Only Valuable Drug, http://www.encognitive.com/ Journal of Nutritional & Environmental Medicine (2001), 11, 159–166
- And here’s another one from 2009 sent by Paul: http://www.eje-online.org/cgi/content/abstract/EJE-09-0542v1 (has a fee) but here’s where you can at least see the abstract: http://www.ncbi.nlm.nih.gov/pubmed/19666698 They evaluated depression and anxiety rating scales as well as patients ownpreference.
- Also this one: http://www.endocrine-abstracts.org/ea/0013/ea0013P316.htm
- At first blush, this Amsterdam study appears to give the same propaganda of T4 only. But as you read on, it mentions this: Third, recent animal experiments indicate that only the combination of T4 and T3 replacement, and not T4 alone, ensures euthyroidism in all tissues of thyroidectomized rats. From 2001, Developmental Endocrinology to Clinical Research: http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowAbstract&ArtikelNr=48140&Ausgabe=227546&ProduktNr=224036
- John C. Lowe’s Four 2003 Studies of Thyroid Hormone Replacement Therapies: Logical Analysis and Ethical Implications Excellent article (16 pages) about the efficacy of using T4 and T3 in treatment, and not using the TSH, and so much more.
PERTAINING TO DESICCATED THYROID
- DESICCATED THYROID IS A SAFE ALTERNATIVE Thanh D. Hoang, DO, staff endocrinologist of the Walter Reed National Military Medical Center in Bethesda, Md., told Endocrine Today at ENDO 2013.
- A HEALTHY THYROID PRODUCES A ROUGH EQUIVALENT TO 3-5 GRAINS OF DESICCATED THYROID A few years ago, we found detailed medical info that revealed this, explaining why so many of us ended up in that range (tho not all). This article states: Estimates of average normal secretion for euthyroid humans are 94-110 µg T4 and 10-22 µg T3 daily (300). If you need more, it can be due to exogenous desiccated thyroid (giving it to yourself) vs. the superior absorption of natural release of thyroid hormones. Scroll down to slightly more than half way: http://www.thyroidmanager.org/chapter/thyroid-hormone-synthesis-and-secretion/
- COMPARING LEVOTHYROXINE TO NATURAL DESICCATED THYROID aka DTE Though this study clearly had problems (probably not raising high enough and/or going by the TSH), it did find that nearly 49% preferred desiccated thyroid. We have no doubt that figure would have been higher if the study understood what informed patients do about the use of NDT. https://www.ncbi.nlm.nih.gov/pubmed/23539727
PERTAINING TO T3:
- LOW T3 CAN BE IMPLICATED IN DEATHS WHILE IN ICU In unselected ICU patients, FT3 was the most powerful and only independent predictor of ICU mortality among the complete indicators. Addition of FT3 to the APACHE- score could significantly improve the ability to predict ICU mortality. http://www.ncbi.nlm.nih.gov/pubmed/22257427
- T3 IS NOT ONLY ANTI-CANCER IN YOUR LIVER, BUT CAN HELP YOUR LIVER TO REGENERATE: From the American Association for Cancer Research, this research study shows that T3 can not only be anti-cancer, but actually help your liver to form new cells: http://cancerres.aacrjournals.org/cgi/content/abstract/60/3/603 COMMENT: This article shows that T3 REDUCES liver nodules, and you can wonder what T3 might do against cancer elsewhere in your body.
- T3 IS BETTER FOR CRITICALLY ILL PATIENTS THAN IS T4: And there have been plenty of patient reflections when sick and forced to be on T4 in the hospital which confirms this! http://www.ncbi.nlm.nih.gov/pubmed/6822088
- WHY YOU DON’T WANT TO SWALLOW IRON TABLETS WITH YOUR THYROID Though this research is with the lousy T4-only medication, besides only evaluating the TSH lab test when there are much better ones to look at, it still underscores that iron in your stomach at the same time as thyroid can make you go more hypothyroid. http://annals.org/article.aspx?articleid=706001&year=1992
FIBROMYALGIA and HYPOTHYROIDISM CONNECTION
Finally, from Med Hypotheses. 2003 Aug;61(2):182-9….a mention of the connection, though it’s referring to thyroid hormone resistance, and patients who’ve had Fibro and saw it go away didn’t all have resistance. But it’s a great start and only underscores the brilliance that Dr. John C. Lowe gave us about the connection between hypothyroidism and fibromyalgia. http://www.ncbi.nlm.nih.gov/pubmed/12888300
GENE VARIATION AFFECTS THE ABILITY TO CONVERT T4 to T3 IN SOME (i.e. justifying adding T3 to T4, or even better, using desiccated thyroid).
From the Journal of Clinical Endocrinology and Metabolism comes this article titled: “Common Variation in the DIO2 gene predicts baseline psychological well-being and response to combination thyroxine plus triiodothyronine therapy in hypothyroid patients” May 2009,94(5):1623-1629.
Research conclusion: “Commonly inherited variation in the deiodinase 2 gene (DIO2 ) is associated with impaired baseline psychological well-being on T4 and enhanced response to combination T4/T3 therapy but did not affect serum thyroid hormone levels. A large patient study found that 16% of the study population had a variant DIO2 gene which impairs the ability of T4 to be converted to T3. Thanks to Terry for sending this!
HOW HYPOTHYROIDISM AFFECTS THE BRAIN:
From 1980 and the J. Clin. Invest. (The American Society for Clinical Investigation, Inc.), this article explains how the brain is affected by thyroid hormones, whether from excess or a deficiency, and talks about the deiodinase enzymes converting T4 to T3. http://www.jci.org/articles/view/109887/files/pdf
a) SUPPRESSIVE TSH RESEARCH:
- This PubMed article from 2005 is about research which shows that even suppressive doses of T4 does not negatively affect bone mineral density. http://www.ncbi.nlm.nih.gov/pubmed/16269872 And this one from 1993: http://www.ncbi.nlm.nih.gov/pubmed/8252740
- The Society for Endocrinology in the UK in 2010 did research which revealed that having lower TSH levels while taking Thyroxine replacement is not detrimental to health, and that low level was .004 to .4 !! I also did a blog post about this here. http://www.sciencedaily.com/releases/2010/03/100315230910.htm
b) EARLY COMMENTS ABOUT PROBLEMS WITH THE TSH:
This was a short forum with comments by David Derry, Raymond Peat, and individuals: NOTE: the following link now fails to show the comments, but I’m leaving it to show it did used to exist. Hopefully we find the comments again. (http://www.bmj.com/cgi/eletters/314/7088/1175#26029) COMMENT: you can see the blossoming of doubt about the TSH in these posts from 1999 to 2002.
c. TSH RANGE NEEDS TO BE NARROWER
Written in 2005 in the The Journal of Clinical Endocrinology & Metabolism, this article says the evidence is compelling that the TSH range should be far more narrow, and it agrees with what Janie has said all along: that “reference populations previously considered normal were contaminated with individuals with various degree of thyroid dysfunction that served to increase mean TSH levels for the group”. http://jcem.endojournals.org/cgi/content/abstract/90/9/5483
d. A NORMAL TSH MEANS NOTHING
From Oct. 2016, this is underscoring how a so-called “normal” TSH doesn’t always equal the removal of hypothyroidism (and includes the problem of Levothyroxine). http://www.medscape.com/viewarticle/870924?src=wnl_mdplsnews_161028_mscpedit_wir&uac=92500HJ&impID=1224287&faf=1
From 1983, this medical article underscores that saliva testing is far superior to blood testing when it comes to cortisol levels. http://www.ncbi.nlm.nih.gov/pubmed/6316831
b) HYPOTHYROIDISM RAISES CORTISOL
Though this article is maddening the way it implies that the TSH lab is an ideal way to diagnose hypothyroidism (Hogwash!! Patients have had hypo with a TSH below 2!!), besides the way they say that you only have “subclinical hypo” if your TSH is up to 10 (give me a break!), it does come to a conclusion that patients already know: hypothyroidism raises cortisol! http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520819/ (which eventually turns into low cortisol–see the last chapter in the STTM II book!). And of course, they don’t realize that this is what happens to so many on the inadequate T4-only!!
c) WHAT HAPPENS TO CORTISOL WHEN PREGNANT
Great study which reveals that “salivary cortisol profiles exhibited a clear circadian rhythm during pregnancy with an increase in mean salivary cortisol from the 25th to 28th week onwards reaching concentrations in late pregnancy more than twice as high as in non-pregnant controls, rapidly returning to normal concentrations after delivery”….and “the elevated salivary cortisol levels in pregnancy may be explained by glucocorticoid resistance owing to the antiglucocorticoid action of high progesterone concentrations. http://www.ncbi.nlm.nih.gov/m/pubmed/2225483/
d) CIRCADIAN CORTISOL RHYTHM
This study explains the circadian rhythm of cortisol and is why we dose ACE or HC (if saliva proves we need either) similarly i.e. most in the morning and less each time: “cortisol levels reach lowest levels at around midnight, levels start to rise at around 02:00 to 03:00 and reach a peak at around 08:30. Cortisol levels then slowly decrease back to the nadir to complete the cycle over 24 h.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475279/
e) PHOSPHATIDYLSERINE AND THE TREATMENT OF HIGH CORTISOL
This study explains the effects of phosphatidylserine on endocrine response to moderate intensity exercise. i.e. it can also help us lower high cortisol, even from having had poor thyroid treatment, or the stress after thyroid removal, etc. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2503954/
CELIAC DISEASE IS A STRONG PREDICTOR OF HAVING HYPOTHYROIDISM:
From the Oct. 2008 issue of the Journal of Clinical Endocrinology and Metabolism come this article which states people with celiac disease had a greater than fourfold increased risk of being diagnosed with hypothyroidism, a threefold increased risk of suffering hyperthyroidism, and a 3.6-fold increased risk of developing thyroiditis. http://jcem.endojournals.org/content/93/10/3915
MISCELLANEOUS RESEARCH TO SUPPORT BETTER TREATMENT:
From Hot Thyroidology and the Journal owned by the European Thyroid Association, this is a 247 pages of research on topics such as Thyroid Cancer, Thyroid Metabolism, Iodine, Autoimmunity, and much much more. http://www.hotthyroidology.com/downloads/eta_abstractbook_2007.pdf COMMENT: I confess that I haven’t made my way through all of it, but if you do it, you may find some real gems in this!
RESEARCH VALIDATING THE IMPORTANCE OF T2, aka 3, 5-diiodothyronine (which you get in desiccated thyroid!)
The accumulated evidence permits the conclusion that the actions of T2 do not simply mimic those of T3 but instead are specific actions exerted through mechanisms that are independent of those actuated by T3 and do not involve thyroid hormone receptors. In addition, very recent evidence leads us to suggest that T2 may be a potentially useful agent for the treatment of diet-dependent overweight (and the consequent hypertriglyceridemia and high cholesterol level) without inducing thyrotoxicosis. http://www.ingentaconnect.com/content/ben/iemamc/2006/00000006/00000003/art00004
MISCARRIAGES CAN BE RELATED TO HYPOTHYROID or POOR THYROID TREATMENT:
The following link takes you to a website with a study of pregnant women with “normal” TSH, but who are positive for antibodies, who have fewer miscarriages following thyroid treatment. Medscape requires a log-in, but it’s free, and it sends regular e-mails on the latest research according to your preferred topics. www.medscape.com/ COMMENT: Once again, this article proves that a so-called normal TSH means squat, and miscarriages can have a strong connection to your undiagnosed or undertreated hypo state.
BREAST CANCER AND THYROID PROBLEMS CAN BE RELATED:
Many studies have been coming out about the connection, and especially as related to your iodine levels. Here is one titled from 2003 “The thyroid, iodine and breast cancer” from Breast Cancer Res and PubMed. http://www.ncbi.nlm.nih.gov/pubmed/12927031 plus “Breast Cancer in Association with Thyroid Disorders” http://www.ncbi.nlm.nih.gov/pubmed/12927040 From 2009: http://www.ncbi.nlm.nih.gov/pubmed/19810133
HAIR and THYROID HORMONES
This research explains how insufficient T4 and T3 can affect hair follicles. http://www.ncbi.nlm.nih.gov/pubmed/18728176
DO WE NEED MORE TRIALS ON T4 and T3 COMBINATION THERAPY IN HYPOTHYROIDISM?
Yup, this is a real live article title from the European Journal of Endocrinology, Oct. 6, 2009. And patients on desiccated thyroid can shout a resounding YES, YES, YES! We know the truth. When are you? Comically, the beginning of this article states that “10% of hypothyroid patients are dissatisfied with the outcome of levothyroxine replacement. It is unlikely that slight over- or under-treatment with T4 explains remaining complaints.” NOT. The rest is good. http://www.ncbi.nlm.nih.gov/pubmed/19808902?ordinalpos=9&itool=Email.EmailReport.Pubmed_ReportSelector.Pubmed_RVDocSum
See this Big Daddy of references from Thierry Hertoghe, MD of Belgium.