If you have had a miscarriage, there is a very good chance you were told one of the following:
"It was just bad luck."
"It was a chromosomal abnormality nothing you could have done."
"It happens to one in four pregnancies. It is very common."
And while none of those statements is entirely wrong chromosomal abnormalities are the most common identified cause of early miscarriage, and it is indeed common they are profoundly incomplete.
Not always identifiable causes. Not always preventable causes. But causes nonetheless and in a significant proportion of cases, causes that are modifiable, treatable, and entirely missed by standard investigation.
This post is the foundation of everything I will cover in this series. It is the map the overview of why miscarriage happens, what drives it, and where the opportunities for investigation and intervention actually lie.
WHAT IS MISCARRIAGE?
Miscarriage is the loss of a pregnancy before 20, 24 or 28 weeks of gestation depending on which part of the World. The majority approximately 80% occur in the first trimester, before 12 weeks.
Miscarriage affects approximately 10-20% of known pregnancies. The true figure is higher, because many very early losses occur before a woman knows she is pregnant and are mistaken for a late or heavy period.
THE CAUSES; A COMPLETE PICTURE
The causes of miscarriage can be broadly grouped into six categories. Understanding these categories is what allows investigation to be targeted and meaningful.
1. CHROMOSOMAL AND GENETIC CAUSES
This is the most commonly cited cause and it is real.
Approximately 50-60% of first trimester miscarriages are associated with chromosomal abnormalities in the embryo, most commonly trisomies (an extra chromosome), monosomies (a missing chromosome), and polyploidy (an abnormal total number of chromosomes).
These abnormalities arise during the formation of the egg or sperm, or during the first cell divisions after fertilisation. They are not caused by anything the mother did or did not do. They are, in most cases, random errors in a biologically complex process.
However and this is critical the frequency of these chromosomal errors is not fixed. It is influenced by egg quality. And egg quality is profoundly modifiable.
The mitochondrial function of the egg, its energy production capacity is the primary determinant of whether chromosomal division occurs correctly. Mitochondrial function declines with age, but it is also influenced by oxidative stress, nutritional status, environmental toxin exposure, and metabolic health.
This means that even chromosomal miscarriage is not purely bad luck. The conditions that produce chromosomally normal eggs are, at least in part, within our influence.
2. HORMONAL CAUSES
Hormonal imbalances are a significantly under investigated cause of miscarriage, particularly in women whose losses are attributed to chromosomal abnormality without further investigation.
Progesterone deficiency. Progesterone is produced by the corpus luteum, the remnant of the follicle after ovulation and is essential for maintaining the uterine lining in the early weeks of pregnancy before the placenta takes over progesterone production at around 10-12 weeks. Insufficient progesterone in the luteal phase and early pregnancy is associated with early pregnancy loss.
A Day 21 progesterone below 30 nmol/L suggests suboptimal luteal function even if ovulation has occurred.
Thyroid dysfunction. Both overt and subclinical hypothyroidism are associated with increased miscarriage risk. Thyroid autoimmunity elevated TPO or thyroglobulin antibodies increases miscarriage risk independently of TSH levels. This is one of the most evidence-based and most commonly missed contributors to recurrent loss.
Elevated prolactin. Hyperprolactinaemia suppresses ovulation and impairs luteal phase function. It can cause recurrent early loss through inadequate progesterone support in early pregnancy.
Insulin resistance and elevated androgens. In women with PCOS and insulin resistance, the hormonal environment of early pregnancy is disrupted elevated LH, elevated androgens, and impaired endometrial receptivity all contribute to higher miscarriage rates.
3. IMMUNE CAUSES
The immune system's role in miscarriage is one of the most active and rapidly evolving areas of reproductive medicine.
Antiphospholipid syndrome (APS). APS is the most well-established immune cause of recurrent miscarriage. It is an autoimmune condition in which antibodies attack phospholipids components of cell membranes promoting a prothrombotic state that causes small clots in placental vessels, impairing placental development and blood flow to the embryo. APS is present in approximately 15-20% of women with recurrent miscarriage and is entirely treatable with low-dose aspirin and low molecular weight heparin.
Uterine natural killer cell abnormalities. The endometrium contains specialised immune cells uterine natural killer cells (uNK cells) that play a critical role in implantation and early placental development. Abnormalities in the number or activity of these cells are associated with recurrent implantation failure and recurrent miscarriage. Investigation and treatment options exist but are not universally offered.
Alloimmune factors. In some cases of recurrent miscarriage, the immune system mounts an inappropriate response against the embryo's paternal antigens treating it as foreign rather than tolerating it. This is an area of active research with emerging treatment options.
Systemic inflammation. Elevated inflammatory markers particularly hsCRP are associated with impaired implantation and increased miscarriage risk. Chronic inflammation from any source gut dysbiosis, autoimmunity, endometriosis, metabolic syndrome can contribute to a hostile environment for early pregnancy.
4. ANATOMICAL CAUSES
Physical abnormalities of the uterus account for approximately 10-15% of recurrent miscarriage cases.
Uterine septum. A septum, a band of tissue dividing the uterine cavity is the most common uterine abnormality associated with recurrent miscarriage. It is also the most treatable, as it can be surgically removed in a straightforward hysteroscopic procedure.
Uterine fibroids. Fibroids benign muscle tumours of the uterine wall can impair implantation and blood supply to the developing pregnancy depending on their size and location. Submucosal fibroids (those protruding into the uterine cavity) have the most significant impact on miscarriage risk.
Uterine polyps. Endometrial polyps can interfere with implantation and are associated with both infertility and early pregnancy loss. They are identified on ultrasound or hysteroscopy and can be easily removed.
Asherman's syndrome. Intrauterine adhesions often resulting from previous uterine surgery, infection, or a prior miscarriage can impair implantation and pregnancy maintenance. This is an underdiagnosed condition that warrants investigation in women with recurrent loss and a relevant history.
Cervical incompetence. In later first trimester and second trimester losses, cervical incompetence the inability of the cervix to remain closed under the weight of a growing pregnancy is an important anatomical cause that requires specific investigation and management.
5. THROMBOPHILIC CAUSES
Thrombophilias are conditions that increase the tendency of blood to clot and small clots in the developing placental vasculature are a recognised mechanism of early pregnancy loss.
Inherited thrombophilias including Factor V Leiden mutation, prothrombin gene mutation, and protein S and C deficiencies are associated with recurrent miscarriage, particularly second trimester loss and placental abruption.
Acquired thrombophilias most importantly antiphospholipid syndrome, covered above are more strongly associated with recurrent early loss.
Elevated homocysteine, as discussed in detail in the previous post in this series, promotes a prothrombotic state through its toxic effects on endothelial cells and is independently associated with recurrent pregnancy loss.
Thrombophilia screening is not universally offered after miscarriage but is warranted in women with recurrent loss, particularly those with second trimester losses or a personal or family history of clotting disorders.
6. NUTRITIONAL AND METABOLIC CAUSES
This is the category most commonly overlooked in conventional miscarriage investigation and the one with the greatest number of modifiable factors.
Folate and methylation. Impaired folate metabolism through dietary deficiency, MTHFR gene variants, or B12 deficiency leads to elevated homocysteine and impaired DNA methylation in the developing embryo. Both mechanisms are associated with early pregnancy loss.
Vitamin D deficiency. As covered in this series, vitamin D regulates endometrial immune tolerance and placental development. Deficiency is associated with both implantation failure and early miscarriage.
Iron deficiency. Severe iron deficiency impairs the oxygen-carrying capacity and mitochondrial function needed to sustain early pregnancy.
Oxidative stress. An imbalance between free radical production and antioxidant defence driven by poor diet, environmental toxin exposure, metabolic dysfunction, and chronic inflammation impairs egg quality, sperm quality, and early embryo development.
Thyroid nutrients. Selenium, zinc, and iodine are all essential for thyroid hormone production and conversion. Deficiency in any of these impairs thyroid function which, as covered in this series, is a significant contributor to miscarriage risk.
THE INVESTIGATION GAP
Here is the uncomfortable truth.
Standard miscarriage investigation even after three losses covers only a fraction of the known causes of recurrent pregnancy loss.
A typical recurrent miscarriage panel might include antiphospholipid antibodies, karyotyping, and a pelvic ultrasound. That is it.
Thyroid antibodies are frequently not tested. Homocysteine is almost never tested. Vitamin D is rarely checked. Fasting insulin is not included. Nutritional status is not assessed. Uterine NK cells are not investigated outside specialist centres.
The result is that a significant proportion of women with recurrent miscarriage are told no cause has been found when in fact the investigation has simply not been comprehensive enough to find it.
This series exists to close that gap. To give you the knowledge to ask for a more complete investigation. To help you understand what your results mean. And to identify every modifiable factor that might be contributing to your losses.
Because you deserve more than bad luck as an explanation.
WHAT COMES NEXT IN THIS SERIES
Over the coming posts I will cover each category of miscarriage cause in depth:
●The blood tests you should have after miscarriage
● Antiphospholipid syndrome, the clotting disorder behind recurrent loss
● Thyroid autoimmunity and miscarriage
● Natural killer cells and miscarriage
● Progesterone and the luteal phase
● How to prepare your body after miscarriage
● Questions to ask your doctor
Each post will give you the clinical knowledge to advocate for yourself so that if you face another appointment, another panel of results, another round of being told there is nothing to find, you will know exactly what to ask for next.
→ Get the Lab Interpretation Guide here $47
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A FINAL WORD
Miscarriage is not just bad luck.
It is a biological event with causes many of them identifiable, many of them modifiable, and many of them entirely missed by standard investigation.
You deserve a complete picture.
This series is where we begin building it.
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