Pregnancy risk in Female MDs

Caesarean section: a high stress. Procedure for the surgeon.

Would delivering a baby by cesarean section stress you out?
Think about your surgeon.

I just saw a post from “Medscape”, entitled “Female doctors have higher infertility rates and higher pregnancy risk: what can be done?”

On further reading, it turned out to be Medscape’s report on a paper, published online ahead of print by the Ann. Surg., 2022 Oct 17.
It was entitled “High infertility rates and pregnancy complications in female physicians indicate a need for culture change“, by Krista Lai 1 Erin M Garvey 1 Cristine S Velazco 1 Manrit Gill 2 Erica M Weidler 1 Kathleen van Leeuwen 1 Eugene S Kim 3 Erika L Rangel 4 Gwen M Grimsby 5 PMID: 36250327. DOI: 10.1097/SLA.0000000000005724

In the interest of brevity, I have paraphrased the report:

Pregnancy risk in Female MDs

4,533 female physicians completed a survey and here are the results:
Generally, Female MDs were older than non-physicians at the time of 1st pregnancy, were more often infertile and had more miscarriages and more premature babies.

However surgeons were worse off than nonsurgical MDs, on all counts.
Surgeons were more often discouraged from starting a family during training, and therefore were older at the time of their first pregnancy.
They had higher pregnancy risk: more premature births, more fetal growth problems and fewer children, than nonsurgical physicians.

Interestingly, only 8% had been educated about the risks of delaying pregnancy and that 8% had fewer miscarriages and fewer problems with infertility.

An even more disturbing finding was that Medical trainees appear to have “almost as high a rate of pregnancy complications as surgeons”. This is interesting: one would expect a lower pregnancy risk, based on their age, but when considered as a function of stress, the effects of which have nothing to do with age, it is unremarkable
(see “NOTES”, below).


The statement that “Female MDs have higher infertility rates and riskier pregnancies” is not in the slightest remarkable: in fact, to one who is aware of the metabolic effects of stress, it is to be expected.
Nor is the statement, “Medical trainees have almost as high rate of pregnancy complications as surgeons who have already completed the training”, surprising.

There is a simple explanation for the increased pregnancy risk in female MDs, both trained surgeons and trainees, and there is an easily and safely applied solution.


The facts are as follows:
(1) The medical profession and particularly the surgical branch of the profession, is well known for high stress: stress and burnout can lead to such psychological strain that medical doctors’ suicide rate is is highest, among the professions.

(2) Female MD trainees, just beginning a course with a reputation for the steepest of learning curves, in competition with their male peers in a reputedly male-dominated, risk-prone profession, are by definition, stressed from the start.

(3) Stress increases cortisol production (“hypercortisolemia”).
Hypercortisolemia, even of low degree, “twists” our thyroid hormone metabolism: cortisol blocks Deiodinase 1 (D1) and activates Deiodinase 3 (D3) – click the link above,
to see the normal metabolism of thyroid hormone.

(4) The intracellular effects of this “twist” are preventing T4 processing to T3 and preferential processing of T4 to reverse T3, which can’t do T3’s work.

(5) Deiodinase 3 also converts preexisting T3 within the cells to T2 (a thyroid hormone molecule with only 2 iodine atoms attached to it), which is also inactive.

(6) The net result is virtual elimination of T3 within the cells, effectively intracellular hypothyroidism (IH)

(7) Since T3 is mainly produced in peripheral cells, serum Free T3 (FT3) is reduced to a minimum.

(8) Hypothyroidism, whether true (low T4 production) or intracellular (stress-related), can cause infertility and early abortion.

(9) Also, the fetus doesn’t begin to make thyroid hormone for itself until 12 – 14 weeks of gestation, which is a critical period inthe development of the brain.

(10) Fetuses which survive the first eight weeks of pregnancy in the presence of maternal T3 deficiency are subject to imperfect brain development between the 8th and 12th week of pregnancy and may be hampered by other growth problems later on.

(11) IH is purely stress-related and is not age-dependent: the mother’s age doesn’t matter. Therefore the pregnancy risk from IH is the same for trainees and surgeons.


(1) The immediate question therefore is, how can we diagnose whether female MD medical trainees and surgeons are developing intracellular hypothyroidism due to their high-stress profession?

(2)Are infertility, pregnancy loss, high risk pregnancy and premature birth in medical trainees and surgeons due to IH?

(3)According to reports on the Internet, offspring subjected to triiodothyronine deficiency throughout the first trimester of gestation are liable to ADD/HD, depression, autism, and schizophrenia. If this is correct, there should be an increased incidence of these conditions among the children of female doctors.
So, is there an increased incidence of these conditions in the children of medical professionals, trainees and surgeons in particular?
And if there is, would proactive therapy reduce that incidence?

(4) In addition to stress-related intracellular T3 suppression, other hormonal aberrations produce deleterious effects on various organs, depending on the individual person’s particular organ’s sensitivity to hormone deficiency.
This is particularly important in the case of DHEA and its prime product, testosterone. DHEA and testosterone deficiency can often be observed in teenagers and in adults younger than age 25, but regardless of their level before age 25, everyone starts losing 1% production, of both DHEA and testosterone, per year at age 26.
In view of this, what is female physicians’ DHEA level before conception?
And can we improve their situation by prescribing DHEA supplements?

(5) What Maternal symptoms does intracellular T3 suppression (IH) cause?


(1) – Diagnosing IH: The serum rT3 level, a sensitive “marker”, goes up when more rT3 is generated by D3 and the serum T3 goes down when less T3 is made in the cells.
So when someone has IH, the serum rT3 goes up and the serum T3 goes down.

THAT’S NEAT! just test T3 and rT3: divide the T3 number by the rT3 number ** and you will get a number (the T3/rT3 ratio), which will be high when everything is okay and low when the person has intracellular hypothyroidism.
In fact, the T3/rT3 ratio provides a very accurate measure of the severity of IH:
Normal T3/rT3 = >20 and <20 indicates intracellular hypothyroidism.
We rate IH thus: 15–20 = “mild”, 10–15 = moderate, <10 = severe.
** T3 as reported in picomoles/L and rT3 is reported in Ng/DL , so you need to convert the T3 result into Ng/DL, to calculate the ratio.

So, let’s test female doctors for IH, with TSH, T4, T3 and reverse T3, at some point between when they start studying medicine and when they decide to get pregnant.
The first test should be about 6 weeks before a planned conception, or on diagnosis of pregnancy
From the results, we’ll calculate T3/rT3: then we’ll know who starts out with IH and who doesn’t.

(2-3) – When the T3/r3 ratio is “borderline”, we can’t tell which mother is going to lose her pregnancy, and which baby will fail to develop normally. In this situation it Is difficult to say whether or not treatment should be prescribed.

(4) – Treatment for IH: Treating pre-existing IH should be a prerequisite to pregnancy planning, so as to avoid the risk of losing a pregnancy or producing a handicapped baby because you didn’t treat the mother’s hypothyroidism.
Similarly, IH diagnosed after conception should be treated immediately.

The following protocol is suggested:
(A) Test everyone who is planning a pregnancy, 6 weeks before the expected date of conception. Test again on diagnosis of pregnancy and at 4, 6 and 8 weeks of gestation.
(B) Regardless of when a positive test is found, initiate treatment immediately, with oral Triiodothyronine (, beginning at 5 µg daily, testing weekly and increasing the dose by 5 µg/day, until serum T3 = >5 PMol/L, or T3/rT3 = >24.
(C) If no pregnancy ensues, continue triiodothyronine at the appropriate dosage.
(D) If all goes well, continue therapy until the 14th week of gestation, at which point the fetus will making its own T4 and T3, if the mother’s iodine and selenium levels are good.
(E) In the interest of the mother, it would be better to continue therapy with slow-release triiodothyronine throughout the pregnancy, balancing the prescription according to T3/rT3 test results: but I can’t advise on this, since I have no experience of doing it.

(5) – What about DHEA and testosterone? – DHEA is indispensable for almost all cells in our bodies and DHEA deficiency is responsible for a proportion of IH cases.
Prospective mothers who are younger than 25 years may or may not be DHEA deficient.
Everyone older than 26 years will be deficient in DHEA and testosterone, as compared with their status before the age of 25, because of the “natural”, yearly, 1% loss of DHEA production which begins at age 26.
DHEA deficiency significantly increases the pregnancy risk in Female MDs, as it does in the general population.
Supplemental DHEA has been found to reduce both conception failure and spontaneous abortion:
Infertility clinics in the USA routinely prescribe 75 mg of DHEA daily, until the beginning of the 2nd trimester.
At the least, prospective mothers should be tested for DHEA and supplemented, with a micronised product (50 mg daily is sufficient), if they are deficient per primam.
However, there is some question as to how long DHEA supplementation should continue during pregnancy, because DHEA production increases significantly during gestation.


(1) Intracellular hypothyroidism is purely stress-related, not age-dependent.
This explains the comparable pregnancy risk to both trainees and practising surgeons.

(2) The literature suggests that the normal range of reverse T3 is 8 – 25 ng/DL.
This range is incorrect: it should be 8–13 , or perhaps 7–13 ng/DL.
However, rT3 is nonfunctional and does not contribute to our metabolism.
The reverse T3 level is only useful as a marker for abnormal T4 processing.
Therefore it isn’t necessary to define its “normal range”: we only need to test it to see if T4 is being normally processed to T3, or whether unsuspected stress-related cortisone excess is “twisting” T4 into rT3.

(3) DHEA is utilized by all cells, to produce “micro-hormones” vital to their function.
In particular, DHEA is essential to the thyroid’s production of T4 and is a deterrent to intracellular hypothyroidism, because it reduces cortisol production. *
In any event, since DHEA levels fall progressively at a rate of 1% per annum beginning at age 26, and since it is sometimes deficient even before age 25 **, it would be wise (as suggested above) to check DHEA before every pregnancy and supplement it if necessary.

(4) The above explanation and information is provided in the interest of supplying our “lady doctors” with information which they may find useful and helpful.
This opinion piece should not be construed as constituting “advice” or “therapy” and the ideas herein should be discussed with a qualified “functional medicine” or “metabolic medicine” practitioner, whose advice should be considered carefully prior to instituting any of my suggestions.

(5) I am retired and no longer licensed: as such, I cannot (and have no wish to) act as medical advisor to anyone, our female surgeons included. however I would be happy to discuss pregnancy risk in female MDs via email, if anyone has questions:

*The prime symptoms of DHEA deficiency (hair loss, poor fingernails and dry skin) are in fact hypothyroid symptoms and they regress rapidly when DHEA is supplemented, without any change in T4 availability.

** Margarita (not her real name), an athletic, extremely healthy 25-year-old, had no trouble getting pregnant, but complained that she wasn’t interested in sex.
Tests showed that she had a low DHEA and zero testosterone.
Margarita responded well to a low dose of DHEA, with normalization of her serum testosterone and an improvement in her libido.

%d bloggers like this: