This opinion piece is in response to an interesting report on fetal neurocognitive development, reviewed by Lily Ramsey, LLM, which I received today, Mar 29 2023..
It is entitled “Maternal weight gain in pregnancy and fetal neurodevelopmental disorders”
The report, based on children born in Sweden
from January 2007, to December 2010,
was authored by Dr. Chinta Sidharthan,
Rates of maternal weight gain over the course of pregnancy and offspring risk of neurodevelopmental disorders. Image Credit: Hazal Ak / Shutterstock
Dr. Siddharthan, reporting on a Swedish study says (paraphrased): “Neurodevelopmental disorders (NDD) are prevalent. The main three, ASD, ADHD, and intellectual disability, often coincide. While mutations are associated, biological, environmental and
social factors also contribute.”
Dr. Siddharthan relates 2nd and 3rd trimester gestational weight gain (GWG) rates,
to fetal ADHD and ASD.
A slow GWG in the 2nd trimester increased the risk by 9%, while
a high GWG in the 3rd trimester raised the risk by 28%.
Her conclusion is that poor GWG in the 2nd trimester,
with excessive GWG in the 3rd, are contributing factors to NDD.
She does not mention the First trimester.
This article and its expressed opinion should be evaluated in the light of current knowledge: a few related articles are offered, for comparison, below.
(1) Subclinical Hypothyroidism in Pregnancy: A Systematic Review and Meta-Analysis,
by Spyridoula Maraka,1,,2 Naykky M. Singh Ospina,1,,2 Derek T. O’Keeffe,1 Ana E. Espinosa De Ycaza,1 Michael R. Gionfriddo,2,,3 Patricia J. Erwin,4 Charles C. Coddington, III,5 Marius N. Stan,1 M. Hassan Murad,2,,6 and Victor M. Montori1,,2, in “THYROID”. 2016 Apr 1; 26(4): 580–590, doi: 10.1089/thy.2015.0418, PMCID: PMC4827301,
A new nationally representative study published online in the Journal of Affective Disorders found that one in four adults, aged 20-39, with attention deficit hyperactivity disorder (ADHD) had generalized anxiety disorder (GAD).
This question is therefore important, worldwide.
(2) Subclinical Hypothyroidism in Pregnancy May Have Long-Term Effects on Metabolic Parameters, by Sun Y Lee, in J Clin Endocrinol Metab. 2020 Jul; 105(7): e2628–e2629, Published online 2020 Apr 14. doi: 10.1210/clinem/dgaa198, PMCID: PMC7216923, PMID: 32285101
Adequate thyroid hormone is essential for normal fetal Neurocognitive development.
Because the fetal thyroid gland does not mature until 18 to 20 weeks’ gestation, there is a significant fetal need for maternal thyroid hormone production in early pregnancy.
Overt maternal hypothyroidism in pregnancy is known to be associated with adverse outcomes, both in the pregnancy and in the baby’s development, such as miscarriage, prematurity, low birth weight and lower IQ.
(3) Influence of maternal TH during gestation, on fetal brain development.
This excellent paper is a seminal treatise on thyroid hormone function, which Everyone should read.
It was authored by Nora K. Moog,a Sonja Entringer,a,b,c Christine Heim,a,d Pathik D. Wadhwa,b,c,e Norbert Kathmann,f and Claudia Bussa,b,, In Neuroscience. 2017 Feb 7; 342: 68–100. Published online 2015 Oct 3. doi: 10.1016/j.neuroscience.2015.09.070, PMCID: PMC4819012, NIHMSID: NIHMS731226, PMID: 26434624
The importance of maternal thyroid function to the fetus, especially as related to iodine deficiency, was reported over a century ago (Curling, 1850, McCarrison, 1909).
Maternal thyroid dysfunction may impair the child’s cognitive and motor development.
It has long been known that thyroid hormones (TH) are obligatory to brain development and maturation. (Zoeller, 2003, de Escobar et al., 2008, McLeod and McIntyre, 2010).
The developing fetus needs maternal T3, since its thyroid can’t make thyroid hormone until mid-gestation.
Without T3, normal brain development is impossible.
Recent evidence shows that early in gestation, even mild maternal hypothyroidism may adversely affect fetal neurocognitive development, retarding brain growth and causing the “misconnected wiring” which leads to cognitive disorders.
It is therefore important to understand that stress, in the first trimester, may cause maternal hypothyroidism and affect the fetal brain.
However the effect of stress on the thyroid, as it affects the fetal brain, has not been addressed to date.
MY VIEW OF THE EFFECTS OF STRESS, IN THE FIRST TRIMESTER
The thyroid and adrenal glands communicate with the hypothalamus and the pituitary gland, and their hormones regulate and counter-regulate one another: a change in one parameter is reflected in variation of the others.
A stress-related increase in cortisol production, via its down-regulation of Deiodinase 1 and up-regulation of Deiodinase 3, causes Reduction of intracellular and serum T3 levels to a minimum.
Therefore maternal stress can reduce the mother’s serum T3 sufficiently to produce fetal hypothyroidism and prevent normal neurodevelopment.
However this interaction has been overlooked in the literature, due to mainstream medicine’s taboo on testing of T3, reverse T3 and the T3/reverseT3 ratio *.
* Clicking the link, “taboo on testing”, will take you to the Canadian Ministry of health’s “CHOOSING WISELY” campaign page: Thyroid hormones are mentioned in item #11 , under the headline “13 Tests and treatments to Question”.
The entire page is an interesting read, for anyone interested in preventive care: it outlines the Canadian Ministry of health’s “CHOOSING WISELY” campaign to reduce the cost of medical tests, including thyroid investigations (the direct attack on thyroid testing is clearly stated: to view it, click here).
WHAT ALL THIS MEANS, WITH REGARD TO THE ARTICLE IN QUESTION
(1) Reduced, or retarded fetal neurocognitive development, reflected by ASD, ADHD, intellectual disability and possibly schizophrenia and gender dysphoria, can be viewed
as due to maternal hypothyroidism, including stress-related “low T3 syndrome” (intracellular hypothyroidism), a diagnosis which is easily made by testing for T3, reverse T3 and the T3/rT3 ratio.
(2) GWG variations in the 2nd and 3rd trimesters may reflect maternal hypothyroidism. However it is difficult to correlate 2nd and 3rd trimester GWG with a fetal deficiency whose origin lies between the 8th and the 20th week of gestation.
The increased GWG probably results from the hypothyroidism and in any case, the damage to the fetus by “T3 starvation” has been done before the 3rd trimester begins.
(3) As previously suggested in my blog post, “Preventive Care, as it should be”, maternal thyroid function should be assessed prior to initiating pregnancy, or at Least coincident with the diagnosis of pregnancy.
The investigation should include not only TSH and thyroid antibodies, but FT3, FT4 and reverse T3. The serum T3 and the T3/rT3 ratio will provide an accurate assessment of the prospective mother’s ability to supply the developing baby with T3 in the first 20 weeks of pregnancy.
(4) If this is done, we just might eliminate fetal neurocognitive maldevelopment and relegate dyslexia, ADD, ADHD, ASD, schizophrenia and gender dysphoria, all of which have been shown to be related to maternal hypothyroidism, to the annals of the past.