Endometriosis is a disease of profound biological and social complexity. Yet too often, its discussion is flattened by oversimplified headlines or speculative claims. A rising trend both in popular media and some corners of academic discourse suggests that trauma, emotional dysregulation, or mental illness may be the cause of endometriosis. While chronic illness and mental health do frequently intersect, it’s essential to approach this relationship with nuance and scientific precision.
Currently, there is no conclusive evidence that childhood trauma, PTSD, or emotional sensitivity cause endometriosis. Some studies have identified correlations between adverse experiences and worsened symptoms, likely mediated through stress-related inflammatory pathways. However, correlation does not equate to causation. These narratives, if misinterpreted or overextended, risk echoing a long history of stigmatizing beliefs—ones that have blamed individuals, especially women, for their own pain and medical conditions.
Understanding Inflammation and Neuroimmune Complexity
Modern science is finally beginning to explore the interplay between inflammation, cellular signaling, and genetic expression in endometriosis. For instance, inflammatory cytokines, molecules released by immune cells, can dramatically alter how cells behave. According to Grandi et al. (2023), these molecules can change gene expression and interfere with anti-inflammatory pathways, fueling persistent pain and chronic immune activation. These findings underscore that pain in endometriosis is not just physical, it is the result of a persistent, whole-body inflammatory response.
A recent interview from our The Invisible Voice columnist Madison Rodriguez with Clinical naturopath, nutritionist, neuroscientist, and founder of the Womens’ Integrative Health Clinic in Australia, Renee Grandi, stated it best: “This is why you have to be looking at endometriosis as a neuroimmune hormonal complex multifaceted condition that is extremely intertwined with the central nervous system.” We aren’t dealing with a condition that stems from trauma, we’re dealing with a systemic disorder that affects both physical and cognitive function.
Revisiting the Embryogenesis Theory
One increasingly compelling theory is that endometriosis may originate during embryogenesis, when early cell layers are forming the foundations of the body’s organs and systems. According to Dr. David Redwine, this developmental window, particularly the first eight weeks of fetal life, is critical.
During week 3, a process called gastrulation begins. This is when the embryo, initially a single layer of epithelial cells known as a blastula, reorganizes into a multilayered and multidimensional structure called the gastrula. From this point forward, three key layers form: the ectoderm, mesoderm, and endoderm.
Between weeks 3 and 8, a second major process called organogenesis occurs. This is when these three germ layers differentiate into specific organs and systems. The mesoderm, in particular, is the middle layer that gives rise to many structures—including skeletal muscle, smooth muscle, blood vessels, bones, joints, connective tissue, the uterus, fallopian tubes, kidneys, endocrine glands, and heart muscle, among others.
The Müllerian ducts, precursors to female reproductive organs, are also present in both sexes during this time. Around 8.5 weeks into development, these ducts regress in males as the body develops Wolffian ducts, which form male reproductive structures. But if embryonic Müllerian tissues, or other mesodermal cells, are misplaced during gastrulation or organogenesis, it could lead to a range of structural abnormalities. These anomalies have been observed in animals, human males and females of all ages, and even in fetuses — a fact that challenges traditional assumptions about who can develop endometriosis.
Critically, all reported sites of endometriosis are derived from mesodermal tissue. While the endometrium refers specifically to the inner lining of the uterus, the uterine mucosa, endometriosis occurs outside this lining, across a range of mesodermal development sites. This distinction is crucial: the disease was named over a century ago based on a now-disproven theory that presumed it arose from misplaced uterine lining cells due to retrograde menstruation. But growing evidence now supports the view that abnormal differentiation or migration of the mesoderm during fetal development could instead be the root cause. Explaining not only the range of disease locations, but also its presence in people without uteruses, including men and intersex individuals.
The latest June 2025 study in Human Reproduction supports this direction. Researchers identified cellular and molecular evidence that suggests endometrial-like cells outside the uterus may arise from misplaced embryonic tissue rather than retrograde menstruation…emotional trauma. These dormant cell clusters, when activated by immune or environmental signals, can become invasive and inflammatory.
To break this down simply: the disease could already be present before birth. What “activates” it later in life isn’t emotional stress alone either, but likely inflammatory signals in the body, ranging from immune challenges, infections, toxins, or metabolic changes. While stress can certainly amplify pain perception and immune responses, it does not create endometriosis.
Gut Health, Inflammation & the Hype of Causation
The gut microbiome has emerged as another area of interest but again, many headlines misrepresent findings as causation. It’s crucial to understand that gut dysbiosis (imbalanced microbiota) is an effect and amplifier of systemic inflammation, not a proven root cause. In fact, many with endometriosis do not show signs of gut microbiome imbalance, and treatments like broad-spectrum antibiotics can further harm beneficial bacteria and compromise immune balance.
If gut-targeted treatments were truly curative, we wouldn’t have close to one billion people worldwide still struggling. Repackaging microbiome studies as the “cause” of endometriosis does a disservice to both science and patients. This trend reflects a broader problem in endometriosis research: decades of recycling hypotheses and sensationalizing minor breakthroughs without delivering meaningful clinical change.
We must ask: why does the language around causation persist so aggressively in endometriosis discourse when no single cause has ever been proven?
Teens, ACEs, and the Trauma Conversation: Where It Belongs
Let us be clear: chronic pain can absolutely lead to mental health consequences. Anxiety, depression, PTSD, and emotional dysregulation are tragically common in the endometriosis community, not as origins, but as outcomes of years of misdiagnosis, medical gaslighting, physical pain, social isolation, and financial burden.
Numerous studies support this link, especially in adolescents. A 2023 study in the Journal of Pediatric & Adolescent Gynecology found that 33% of teens with surgically confirmed endometriosis reported depression, while 19% reported anxiety. These teens were also more likely to experience pain-related comorbidities and school disruption. Another review emphasized that teens with endo often endure social withdrawal, decreased academic performance, and stigma, contributing to a feedback loop of emotional strain and worsening physical symptoms.
Adding another layer to this conversation, a massive study published in Human Reproduction in June 2025 followed over 1.3 million women and looked at how early life stress, known as adverse childhood experiences (or ACEs), related to endometriosis later in life.
The findings showed that:
Women who experienced one ACE (such as a serious illness, abuse, or neglect) had a 20% higher chance of being diagnosed with endometriosis.
Those who experienced five or more ACEs had up to a 60% higher chance.
Women who faced violence in childhood were more than twice as likely to be diagnosed later.
These are significant numbers, but they do not mean trauma causes endometriosis. The researchers emphasized that correlation does not equal causation. While some studies explore whether trauma could influence immune regulation or pain processing, there is no conclusive evidence that these factors contribute to the development of endometriosis itself. Their role may be limited to symptom severity or timing of diagnosis, not disease origin.
This distinction is essential. Misusing these findings to push trauma-first narratives places undue responsibility on patients and echoes harmful, outdated medical bias.
Historical Legacy Still Echoes Today
As Dr. Camran Nezhat and colleagues have extensively documented, women with unexplained pelvic pain have long been dismissed as hysterical. Endometriosis was once viewed as a condition caused by “sexual excess,” emotional instability, spiritual disconnection or repressed desire. The result? Women institutionalized, denied pain relief, and forced into harmful treatments or silenced.
That legacy lives on when we imply, whether subtly or overtly, that the body is creating disease because the mind is ‘unwell.’ Even in 2025, this narrative still quietly influences funding decisions, research priorities, patient experiences, and shockingly even holistic medicine practices. While some integrative approaches can be helpful when grounded in science, too often holistic narratives reinforce the same message: that healing is about mindset, that illness reflects inner imbalance, or that treating the “energy body” will resolve a complex physical disease. This can create pressure on patients to blame themselves or pursue unproven treatments at the expense of evidence-based care. Individualized care and cautious approaches are important for everyone.
A Call for Precision, Accountability, and Progress
Science evolves when we let go of oversimplifications. Mental health is a critical companion to physical disease, but not a convenient scapegoat. Emotional resilience can help individuals navigate the challenges of chronic illness, but it neither causes nor cures endometriosis, nor does its absence explain disease onset.
As we move forward, let us demand language and research that honor complexity, not narratives that pathologize emotions or recycle harmful myths. The endometriosis community deserves truth, accountability, science, and empathy that leads to tangible care, not hype.
Selected References
Grandi, G. et al. (2023). Endometriosis and the Brain: Connecting the Dots Between Pelvic Pain, the Nervous System, and Cognition. The Invisible Voice.
Nezhat, C. et al. (2021). Endometriosis: Ancient disease, ancient treatments. JSLS.
Journal of Pediatric and Adolescent Gynecology (2023). Adolescent comorbidity rates in endometriosis.
Diagnostics (MDPI, 2023). Psychological symptoms and endometriosis.
Human Reproduction (2025). Misplaced embryonic tissue as potential source of endometriosis. https://academic.oup.com/humrep/advance-article/doi/10.1093/humrep/deaf101/8159596
American Journal of Psychiatry (2025). Chronic pain as a contributor to psychiatric comorbidity. https://psychiatryonline.org/doi/10.1176/appi.ajp.20250289
Sørensen, H. T. et al. (2025). Adverse childhood experiences and risk of endometriosis: a nationwide cohort study. Human Reproduction. https://doi.org/10.1093/humrep/deaf101
Signorile PG, Baldi F, Bussani R, et al. “Ectopic endometrium in human fetuses is a common event and sustains the theory of müllerianosis in the pathogenesis of endometriosis.” Journal of Experimental & Clinical Cancer Research. 2009;28:49.
This post was written by Chelsea Hardesty
Chelsea, the president of Getting the Better of Endometriosis is a researcher with a strong passion for endometriosis awareness — as well as support for those suffering from the illness. Driven by her own personal experiences, she strives to make a meaningful impact on society to support the chronically ill.
Thank you for this. I really appreciate that you presented trauma as something that can amplify symptoms, but does not create the disease. I think this specification is imperative in making sure women are not blamed for their pain, while validating how our life experiences could make the effects of the disease harder on our bodies.