Purpose and Disclaimer

Purpose and Disclaimer for http://www.downsyndromesupport.net

The purpose of this group is to share experiences to help educate parents about thyroid and adrenal testing and treatment options in order to facilitate the strongest of communications with our physicians regarding testing and treatment.

Leslie’s Thyroid and Adrenal Support does not claim to diagnose, treat, or cure any kind of disease. The information provided is for learning and educational purposes only; hopefully, between you and your doctor together.  The information learned here should be used as a launching pad to a deeper learning.

© Leslie Boswell 2014

Thyroid Research Links

Mother, Child, Butterfly imageThyroid Research Links

Prevalence of Iron Deficiency in Down Syndrome


Newborn Screening Fails to Identify Hypothyroidism in Down Syndrome


T21 Causes Persistent Hypothyroidism



Fetal Brain Development as a Result of Thyroid

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1241181/ http://www.bio.umass.edu/biology/zoeller/pdf/JNeuroendo.pdf

Neonatal Thyroid Function



Down Syndrome and Thyroid



Feingold, ADHD and Thyroid



Stop the Thyroid Madness Medical Research



Cardiovascular and Thyroid



Down Syndrome and Thyroid



Perinatal Asphyxia and Thyroid



Thyroid Hormone Regulates the Expression of the Sonic Hedgehog Signaling Pathway



Thyroid Hormone Regulates Oxytocin Gene



Thyroid Hormones Serotonin



Thyroid Hormone necessary for response to SSRI



Regulation of Gene Expression by Thyroid



Thyroid Functions of Neonates in Down Syndrome



Dosing Thyroid Medication by TSH



Skeletal Development and Thyroid



Salivary Cortisol in Children


Recommended Thyroid and Adrenal Labs


Recommended Thyroid and Adrenal Labs

These are the routine labs that have been helpful for myself and my family for a decent outlook on thyroid function and adrenal glands.  There is a limited amount of blood we can get out of our children, and we don’t want more blood ordered than is available. 


TSH, Free T4, Free T3, Reverse T3.  It is good to also rule out antibodies with TgAb (Hashimoto’s), TPO (Hashimoto’s), and TSI (Graves.) The antibodies tests may be bumped to another set of labs if it is hard to get an order for this many labs.


TIBC, serum iron, ferritin, and % saturation.  Pernicious anemia: serum B-12, MMA, folate.

General: CBC, CMP

Adrenal function: 24-hour Saliva Cortisol (see below)

For adults, looking at sex hormones could be important too: Estrogen, Progesterone, and Testosterone.

I also like to refer to The Down Syndrome Treatment Center of Oregon’s list of labs.  I wouldn’t limit this list to Down syndrome.  I feel it is a great list for us all.



Stop the Thyroid Madness has an excellent list of recommended labs. 




If it is questionable whether your kiddo can spit into a tube, you can practice spitting to see if and how much saliva you can get.  You could also check with the lab and see if the sample drawn by a bulb syringe could be used.  Smelling a lemon can help produce saliva.  There are pediatric collections kits listed below as well as a good spit test.

NeuroScience Adrenal Tests (doctor must order these tests)

NeuroAdrenal Basic 9028 (Cortisol x4, DHEA, Epinephrine, Norepinephrine, Dopamine, Serotonin, Glycine, GABA, Glutamate, PEA, Histamine)

https://www.neurorelief.com/index.php?p=testDet&testID=31&TestPanelName=NeuroAdrenal Basic

NeuroAdrenal Essential 9094 (Epinephrine, Norepinephrine, Dopamine, Serotonin, GABA, Glutamate, PEA, Cortisol x4) https://www.neurorelief.com/index.php?p=testDet&testID=239&TestPanelName=NeuroAdrenal Essential

 Adrenal Rhythm 7000 ( Cortisol x4)

https://www.neurorelief.com/index.php?p=testDet&testID=73&TestPanelName=Adrenal Rhythm


Here are some avenues to get a saliva cortisol test without going through your doctor.

Cotton:  MyMedLab’s *Sabre* cortisol saliva kits come with the cotton swab ones, but it has to be the Sabre ones.

Cotton:  MyMedLab carries others as well. It’s a 6-sample test, which would mean waking your child up twice during the night.


Cotton: DirectLabs has a 4-sample one from MetaMatrix which is the cotton one, too. https://www.directlabs.com/TestDetail.aspx?testid=308&locale=en-US

Spit:  MyMedLab spit, four times a day.  https://sttm.mymedlab.com/sttm-profiles/sttm-24-hour-cortisol-dhea

© Leslie Boswell 2014 



Vitamin D, Gene Regulation, and Thyroid

Vitamin D, Gene Regulation, and the Thyroid

 There is much ado about vitamin D these days and the fallout physically from being vitamin D deficient.  Vitamin D deficiencies are high among the special needs kids’ population, as well as the hypothyroid population.

I am very thrilled to read the Vitamin D Council’s blog regarding a new study that finds that vitamin D helps regulate three genes involved in autism.  These genes, as you will read in the blog, relate to regulation of the serotonin synthesis.   This discovery is considered to be “groundbreaking.”  I am deeply saddened that the equation that the thyroid hormone also plays into causing vitamin D deficiency, as well as these other “mysteries,” such as low oxytocin levels in children with autism, has been ignored.  I have included various studies to show these physiological functions relating back to the thyroid hormone of these “groundbreaking” “mysteries.”

Here are a few excerpts from their blog.

“The authors also solved some of the mysteries surrounding autism. One mystery is why autistic individuals have low levels of serotonin in their brain but elevated serotonin levels in their peripheral blood. The authors discovered that there are two genes involved in turning tryptophan into serotonin, a central gene and a peripheral gene.

Vitamin D up-regulates the central serotonin gene and down-regulates the peripheral serotonin gene. That may explain why autistic kids have elevated blood serotonin but decreased brain serotonin when their vitamin D levels are low. To date, many studies of vitamin D levels in autism show autistic kids are vitamin D deficient.”

“Drs Patrick and Ames may have solved another mystery of autism: why autistic children have low levels of oxytocin. Oxytocin is a hormone that does a lot of things, such as promote socialization. The authors explain that oxytocin is also directly controlled by vitamin D. If children are deficient in vitamin D, they will also have low levels of oxytocin.”

You can read entirety of the New Study Finds Vitamin D Regulates Three Genes Involved in Autism, Vitamin D Council’s blog, yourself here.


 Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism.

Patrick RP1, Ames BN.

Author information

1Nutrition and Metabolism Center, Children’s Hospital Oakland Research Institute, Oakland, California, USA.


“Serotonin and vitamin D have been proposed to play a role in autism; however, no causal mechanism has been established. Here, we present evidence that vitamin D hormone (calcitriol) activates the transcription of the serotonin-synthesizing gene tryptophan hydroxylase 2 (TPH2) in the brain at a vitamin D response element (VDRE) and represses the transcription of TPH1 in tissues outside the blood-brain barrier at a distinct VDRE. The proposed mechanism explains 4 major characteristics associated with autism: the low concentrations of serotonin in the brain and its elevated concentrations in tissues outside the blood-brain barrier; the low concentrations of the vitamin D hormone precursor 25-hydroxyvitamin D [25(OH)D3]; the high male prevalence of autism; and the presence of maternal antibodies against fetal brain tissue. Two peptide hormones, oxytocin and vasopressin, are also associated with autism and genes encoding the oxytocin-neurophysin I preproprotein, the oxytocin receptor, and the arginine vasopressin receptor contain VDREs for activation. Supplementation with vitamin D and tryptophan is a practical and affordable solution to help prevent autism and possibly ameliorate some symptoms of the disorder.-Patrick, R. P., Ames, B. N. Vitamin D hormone regulates serotonin synthesis. Part 1: relevance for autism.”


Thyroid Hormone Regulates the Oxytocin Gene.


Adan RA, et al. Show all

Adan RA, Cox JJ, van Kats JP, Burbach JP.


J Biol Chem. 1992 Feb 25;267(6):3771-7.



“Endocrine factors involved in the transcriptional regulation of the oxytocin (OT) gene were investigated in heterologous expression systems. Plasmids having a 5′-flanking region of the rat OT gene (-363/+16) or the human OT gene (-382/+41) cloned in front of the firefly luciferase gene were co-transfected with an expression vector for the rat thyroid hormone receptor alpha in P19 embryonal carcinoma (EC) cells. Thyroid hormone (T3) stimulated the activity of the rat and human OT promoters about 10-fold. In MCF-7 breast tumor cells transfected with the human OT promoter-luciferase fusion gene, T3 stimulation through endogenous thyroid hormone receptors was about 5-fold. Co-transfection experiments in P19EC cells using 5′ deletion mutants of the rat OT gene showed that thyroid hormone responsiveness was located in two regions, one located between nucleotides -195 and -172, the other between nucleotides -172 and -148. Each region accounted for about 3-fold T3 stimulation. Gel retardation analysis using extracts from HeLa cells over-producing the c-erbA/TR alpha protein showed specific binding to the -172/-148 element, while no binding occurred on the -195/-172 element. The -172/-148 element which contains the imperfect estrogen response element, GGTGACCTTGACC, has inverted as well as direct repeats of the TGACC motif. Mutagenesis of TGACC motifs separately reduced thyroid hormone responsiveness by about 50%. However, simultaneous mutation of two TGACC motifs abolished the responsiveness to T3 completely. There was no cooperativity between the activated thyroid hormone and estrogen receptors in transfected MCF-7 cells nor in thyroid hormone receptor and estrogen receptor co-transfected P19EC cells. Negative interactions between these two receptors were observed and gel retardation assays showed interaction between the two receptors proteins. It was shown in an in vivo experiment that treatment of rats with thyroid hormone increased hypothalamic OT mRNA levels, the pituitary OT content, as well as OT levels in blood. The results reveal thyroid hormone as a physiological regulator of OT gene expression, which stimulates OT promoter activity directly through interaction with a thyroid hormone-response element in the OT gene.”


1371278 [PubMed – indexed for MEDLINE]

Free full text: HighWire


Vitamin D and Autoimmune Thyroid Diseases.


Kivity S, et al. Show all

Kivity S, Agmon-Levin N, Zisappl M, Shapira Y, Nagy EV, Dankó K, Szekanecz Z, Langevitz P, Shoenfeld Y.


Cell Mol Immunol. 2011 May;8(3):243-7. doi: 10.1038/cmi.2010.73. Epub 2011 Jan 31.




“The role of vitamin D as an immune modulator has been emphasized in recent years, and low levels of the hormone were observed in several autoimmune diseases including multiple sclerosis and systemic lupus erythematosus. Vitamin D mediates its effect though binding to vitamin D receptor (VDR), and activation of VDR-responsive genes. While VDR gene polymorphism was found to associate with autoimmune thyroid diseases (AITDs), few studies examined levels of vitamin D in these patients and those that did yielded conflicting results. We therefore undertook to evaluate the levels of vitamin D in patients with AITDs compared to patients with non-AITDs and healthy controls. Serum vitamin D (25-OH) levels were measured in 50 patients with AITDs, 42 patients with non-AITDs and 98 healthy subjects, utilizing the LIAISON chemiluminescence immunoassay (DiaSorin, Saluggia, Italy). Vitamin D deficiency was designated at levels lower than 10 ng/ml. Antithyroid antibodies, thyroid functions and demographic parameters were evaluated in all patients. The prevalence of vitamin D deficiency was significantly higher in patients with AITDs compared with healthy individuals (72% versus 30.6%; P<0.001), as well as in patients with Hashimoto’s thyroiditis compared to patients with non-AITDs (79% versus 52%; P<0.05). Vitamin D deficiency also correlated to the presence of antithyroid antibodies (P=0.01) and abnormal thyroid function tests (P=0.059). Significantly low levels of vitamin D were documented in patients with AITDs that were related to the presence of anti thyroid antibodies and abnormal thyroid function tests, suggesting the involvement of vitamin D in the pathogenesis of AITDs and the advisability of supplementation.


21278761 [PubMed – indexed for MEDLINE]

Full text: Nature Publishing Group


Thyroid hormones, serotonin and mood: of synergy and significance in the adult brain.


Bauer M, et al. Show all

Bauer M, Heinz A, Whybrow PC.


Mol Psychiatry. 2002;7(2):140-56.



“The use of thyroid hormones as an effective adjunct treatment for affective disorders has been studied over the past three decades and has been confirmed repeatedly. Interaction of the thyroid and monoamine neurotransmitter systems has been suggested as a potential underlying mechanism of action. While catecholamine and thyroid interrelationships have been reviewed in detail, the serotonin system has been relatively neglected. Thus, the goal of this article is to review the literature on the relationships between thyroid hormones and the brain serotonin (5-HT) system, limited to studies in adult humans and adult animals. In humans, neuroendocrine challenge studies in hypothyroid patients have shown a reduced 5-HT responsiveness that is reversible with thyroid replacement therapy. In adult animals with experimentally-induced hypothyroid states, increased 5-HT turnover in the brainstem is consistently reported while decreased cortical 5-HT concentrations and 5-HT2A receptor density are less frequently observed. In the majority of studies, the effects of thyroid hormone administration in animals with experimentally-induced hypothyroid states include an increase in cortical 5-HT concentrations and a desensitization of autoinhibitory 5-HT1A receptors in the raphe area, resulting in disinhibition of cortical and hippocampal 5-HT release. Furthermore, there is some indication that thyroid hormones may increase cortical 5-HT2 receptor sensitivity. In conclusion, there is robust evidence, particularly from animal studies, that the thyroid economy has a modulating impact on the brain serotonin system. Thus it is postulated that one mechanism, among others, through which exogenous thyroid hormones may exert their modulatory effects in affective illness is via an increase in serotonergic neurotransmission, specifically by reducing the sensitivity of 5-HT1A autoreceptors in the raphe area, and by increasing 5-HT2 receptor sensitivity.”


11840307 [PubMed – indexed for MEDLINE]

Free full text: Nature Publishing Group


Understanding TSH, T4, and T3

Understanding TSH, T4, and T3

It can be difficult to wrap your head around how the different hormones TSH, T4, and T3 function.  The TSH (thyroid stimulating hormone) is a pituitary hormone.  This stands for thyroid stimulating hormone.  It is a signal that comes from the pituitary gland to tell the thyroid that there is not enough active thyroid hormone in the cells and that it needs to kick some more thyroid hormone out.  The T4 (thyroxin) is the thyroid storage hormone.  The body in a perfect state of health has to convert the T4 hormone into the active thyroid hormone T3 (triiodothyronine).  The cells of the body receive this active T3 hormone through receptors.

One way I like to look at it is to correlate it to a light switch, a light fixture, and actual lighting that you have in front of your face to see an object.  The light switch is the TSH.  The light fixture is the T4.  The light in front of you is the T3.  When looking at thyroid function by means of a TSH test, you are merely looking at the light switch to see if it is turned in the on position.  When you measure the storage thyroid hormone T4 (Free T4 test), you are looking at the light fixture to make sure there is a light bulb in there.  When you measure the active thyroid hormone (Free T3 test), you are assessing whether or not you have light to see by.  If you don’t have enough light to see by, that would be referred to as having hypothyroid symptoms.

There are numerous reasons why the TSH is iffy in testing thyroid function.  In this post, I will only address a correlation as to determining dosage of thyroid treatment in regards to the “light source.”  Say that you determine that you have faulty lighting and you just don’t have enough light to see by, and so you provide an external source of lighting such as a skylight or other window.  This would be like taking thyroid hormone replacement.  If you have enough light to see by, you are not prompted to go flip the switch to turn the light bulb on.  The same kind of goes with thyroid replacement.  When the cells of the body are receiving the active thyroid hormone, the feedback loop has no need to tell the pituitary gland to tell the thyroid to produce more hormones.  Therefore, we see a drop in the TSH level.  Doctors are trained to perceive this is being hyperthyroid and are prompted to reduce the dosage, then throwing the body back into hypothyroidism.  When only TSH and Free T4 levels are tested, the main function of the thyroid is left out, the T3 levels.  This is the same as looking at a light switch or a light fixture to tell you whether you have enough light to see by.  Proper testing for a complete picture of thyroid function should contain the lab tests TSH, Free T4, Free T3, and a Reverse T3.  The ratio between Free T3 and Reverse T3 will help you to know how much active thyroid hormone T3 is getting received by the cells in your body.

Understanding TSH, T4, and T3        © Leslie Boswell 2014