Endometriosis involves the growth of the uterine lining (endometrium) on pelvic structures outside of the uterus. With mild, early ( Stage 1) endometriosis these endometrial deposits  grow on  pelvic structures with little, if any, visible evidence of anatomical distortion that could compromise the release of an egg (ovulation) or its transportation from the ovary to the fallopian tube. With advanced endometriosis (Stage 2, 3 & 4), there are usually pelvic adhesions and ovarian endometriomas (see below), sufficient to distort normal pelvic anatomy and interfere with egg development/maturation as well as egg/embryo transportation.

Since early endometriosis is not associated with significant anatomical distortion and is infrequently associated with absent or dysfunctional ovulation, it would be reasonable to conclude that (in such cases) normally ovulating women should have no difficulty in conceiving and that in cases of moderately severe endometriosis associated with anatomical disease amenable to surgically correction, the infertility could be successfully reversed …nothing could be further from the truth.

Toxic pelvic environment: It is common place for women with early endometriosis to achieve a pregnancy and thereupon, battle to conceive again. This is why endometriosis is one of the commonest causes of secondary infertility. The main reason is that women with endometriosis all have “toxins” in their pelvic secretions. This renders the egg envelopment (zona pellucida) relatively impervious to sperm penetration. Thus as eggs, as they traverse this “toxic” environment e to reach the awaiting sperm in the Fallopian tube(s) are rendered much less fertilizable (by a factor of at least 3-4). Consider the fact that in the absence of endometriosis, young women with fertile male partners have about a 15% chance (per month) and 80%, per year  of propagating a baby while in the presence of (even mild) endometriosis the comparable chance would be chance of success would be < 5% per month and 40% within 3-4 years.

IVF, which involves extracting eggs prior to ovulation and their subsequent exposure to pelvic toxins, can bypass this effect. This is why a woman with endometriosis, who in spite of reduced odds of conceiving (naturally or following the use of fertility drugs-(with or without intrauterine insemination), frequently experiences secondary infertility later in her reproductive career. It also explains why with early endometriosis, ovulating women who have patent Fallopian tubes do not really benefit from intrauterine insemination, the use of fertility drugs, or from surgery.

Also, endometriotic deposits are often non-pigmented and are thus cannot be readily identified during surgery. It follows that when a normally ovulating woman with mild to moderate endometriosis conceives following , surgery or the use of fertility drugs (with or without IUI) , it is probably in spite of  (rather than due to)  such treatment.

Immunologic Implantation Failure: About 1/3 of women with endometriosis (regardless of its severity) have of increased uterine natural killer cell activity (Nka). Activated NK cells, produce an excess of TH-1 cytokines which can lead to an immunologic implantation dysfunction (IID) with rejection of embryo attachment prior to hCG being detected in the woman’s blood. Rather than this being “true infertility” such women are in fact experiencing a “mini miscarriages “so early on, that they do not even realize that they in fact conceived. Sometimes the pregnancy attaches temporarily and is then lost (a chemical pregnancy or early miscarriage). In such cases the initial TH-1 cytokine onslaught was not immediately lethal to the embryo’s root system (trophoblast).

Endometriomas: Here, “menstrual blood” produced by endometrial cells that line cyst-like cavities in the ovary(ies) undergo decomposition and come to look like molten chocolate. Hence the name “chocolate cysts’ (syn., endometriomas). These endometriomas activate the surrounding ovarian stroma (connective tissue) resulting in e male hormone (predominantly testosterone) production. If produced in excess, such local overproduction of ovarian testosterone, compromises egg development and maturation in the affected ovary. Accordingly, I hold that sizeable endometriomas (>1.5cm) should be eliminated prior to embarking on ovarian stimulation. A few years ago, I introduced “sclerotherapy”, an effective, safe and relatively inexpensive, outpatient alternative to surgical treatment of endometriomas. Sclerotherapy involves needle aspiration of the liquid content of the endometriotic cyst, followed by the injection of 4-5% tetracycline into the cavity. The lesions permanently disappear in >70% of cases, within 6-8 weeks. A follow-up aspiration of any recurring fluid accumulation almost always results in a permanent cure of persistent lesions. Sclerotherapy can be conducted under local anesthesia or under general anesthesia.

Adhesions and scar tissue: Endometriosis and/or its surgical treatment, can produce pelvic adhesions and/or scarring which are capable of compromising tubal function. Such scarring can also compromise ovarian blood flow, reduce ovarian reserve and hasten the onset of menopause.