Understanding Endometriosis: Looking Beyond the Symptoms

Looking Beyond the Symptoms

By Jonathan Jackson BSc (Hons) Chinese Medicine | Acupuncturist & Fertility Coach

Introduction

Endometriosis is one of the most widespread and misunderstood conditions affecting women and those assigned female at birth during their reproductive years. It is estimated to affect 1 in 10 people in this group globally — yet despite this prevalence, the average time from first symptoms to a confirmed diagnosis remains, in many countries, between seven and ten years. That diagnostic gap reflects how much we still have to learn about this condition, and how poorly it has historically been recognised and resourced.

At Jonathan Jackson Health, education sits at the heart of everything we do. Understanding the biology of endometriosis — what it is, how it develops, and how it interacts with broader aspects of health — is an essential foundation for anyone navigating this condition, whether they have received a diagnosis, are seeking one, or are supporting someone who has. Knowledge is never a replacement for medical care, but it is an indispensable companion to it.

This article provides a thorough, evidence-grounded overview of endometriosis: its symptoms, its biology, its relationship to fertility and quality of life, and the ways in which the body’s wider internal environment may be relevant. It also includes a clearly labelled personal hypothesis, Jonathan Jackson’s Theory, which explores a speculative but clinically interesting idea about cellular health and hormonal responsiveness. That section is explicitly presented as a conceptual framework for discussion, not as established science.

What Is Endometriosis?

Endometriosis is a chronic, inflammatory condition in which tissue resembling the endometrium — the lining of the uterus — develops outside the uterus itself. These deposits, known as lesions or implants, are most frequently found on the ovaries, fallopian tubes, the outer uterine wall, the bowel, the bladder, and the peritoneum (the lining of the pelvic cavity). In uncommon cases, endometriotic tissue has been identified at distant sites including the lungs and diaphragm.

Unlike the endometrial lining inside the uterus, which builds and sheds in response to the hormonal cycle, these external deposits have no route of exit. They respond to the same cyclical hormonal signals, becoming inflamed and breaking down each month, but the resulting blood and cellular debris cannot leave the body. Over time, this repeated inflammatory process often leads to the formation of scar tissue and adhesions. Where the ovaries are involved, blood-filled cysts known as endometriomas — or ‘chocolate cysts’ — may develop.

One of the most clinically confounding aspects of endometriosis is the poor correlation between the extent of disease and the severity of symptoms. Women with widespread lesions may experience manageable discomfort, while others with minimal visible endometriosis suffer severe, life-altering pain. This inconsistency is one of many reasons researchers continue to look beyond the lesions themselves when trying to understand this condition.

Recognising the Symptoms of Endometriosis

The symptoms of endometriosis vary widely between individuals and overlap significantly with other gynaecological and gastrointestinal conditions — a key contributor to the prolonged diagnostic journey many people face. Commonly reported symptoms include:

Dysmenorrhoea: severe menstrual pain that is typically disproportionate to standard period cramping and may be debilitating
Chronic pelvic pain: persistent lower abdominal or pelvic discomfort that occurs throughout the cycle, not only during menstruation
Dyspareunia: pain during or following sexual intercourse, particularly with deep penetration
Dyschezia and dysuria: painful bowel movements or urination, particularly pronounced around menstruation
Heavy or irregular menstrual bleeding, or spotting between periods
Abdominal bloating and gastrointestinal symptoms, commonly referred to as ‘endo belly’
Persistent fatigue, which may be severe and chronic
Difficulties with fertility or conception
Anxiety, depression, and mood disturbance — experienced both as direct features of the condition and as responses to living with chronic pain

It is worth emphasising that a proportion of women with endometriosis are entirely asymptomatic, discovering the condition incidentally during investigation for infertility or through unrelated surgery. Equally, the severity of symptoms is not a reliable indicator of disease extent — a reality that underlines the complexity of this condition.

What Does Current Science Tell Us About Endometriosis?

Despite sustained research effort over many decades, the precise origin of endometriosis has not been definitively established. The current scientific consensus is that endometriosis is a multifactorial condition — one shaped by genetic predisposition, immune system function, hormonal environment, and potentially wider systemic and environmental factors. Several theories have been proposed, each contributing something meaningful to an incomplete picture.

Retrograde Menstruation

The most longstanding and widely accepted theory — proposed by John Sampson in the 1920s — suggests that during menstruation, endometrial cells travel in reverse through the fallopian tubes into the pelvic cavity rather than exiting through the cervix. These misplaced cells then attach to pelvic structures and begin to proliferate.

Evidence suggests that retrograde menstruation occurs to some degree in the majority of women who menstruate. Yet most of those women do not develop endometriosis. This means that retrograde flow alone cannot explain the condition — something else determines whether displaced cells survive, implant, and grow. Current evidence points strongly to the immune system as a key determining factor.

Immune Dysfunction

In a healthy physiological state, the immune system identifies and eliminates endometrial cells that enter the peritoneal cavity. In women with endometriosis, this clearance mechanism appears to be impaired. Research has consistently documented altered immune profiles in affected individuals, including elevated macrophage activation in peritoneal fluid, reduced natural killer (NK) cell activity, and dysregulated T-cell responses.

These immune changes may allow displaced cells to evade destruction, adhere to peritoneal surfaces, and establish functioning lesions. Whether immune dysfunction precedes endometriosis or arises as a consequence of it — or both, in a self-reinforcing cycle — remains an active area of investigation.

Inflammation

Chronic inflammation is a central feature of endometriosis. The peritoneal fluid of affected women typically contains elevated levels of pro-inflammatory cytokines, including interleukin-1 (IL-1), IL-6, IL-8, tumour necrosis factor-alpha (TNF-α), and prostaglandins. These mediators support the survival, growth, and vascularisation of endometriotic lesions.

Inflammation also amplifies and sustains pain. Sensitisation of nerve fibres within and around lesions contributes to the intense local pain characteristic of endometriosis, while central sensitisation — changes in how the nervous system processes pain signals — may explain the broader, more diffuse pain that many affected women experience. The inflammatory environment is further associated with oxidative stress, which can damage surrounding reproductive tissues and impair egg quality.

Hormonal Influences and the Role of Oestrogen in Endometriosis

Endometriosis is fundamentally an oestrogen-dependent condition. Oestrogen drives the growth and maintenance of endometriotic lesions, and the condition creates a local hormonal environment that amplifies oestrogen activity. Endometriotic tissue has been shown to overexpress aromatase — an enzyme that converts androgens into oestrogen locally within the lesion — while simultaneously showing reduced activity of the enzyme responsible for oestradiol inactivation.

This produces a cycle of local oestrogen excess that perpetuates lesion growth, even when systemic oestrogen levels are within normal range. Endometriotic tissue also commonly displays resistance to progesterone — the hormone that counterbalances oestrogen and plays an essential role in preparing the uterine lining for implantation. This progesterone resistance means that the hormone’s normal regulatory and protective functions are diminished, allowing oestrogen-driven proliferation to continue.

Progesterone resistance in endometriosis is an important and active research area. Current evidence suggests it arises from changes at the cellular level — including altered progesterone receptor expression and disrupted downstream signalling — rather than from reduced circulating progesterone. This distinction is significant, and it underpins the personal hypothesis I share later in this article.

Genetic Factors

There is a clearly established hereditary component to endometriosis. Women with a first-degree relative affected by the condition are estimated to be five to seven times more likely to develop it themselves, and twin studies show higher concordance in identical twins than in fraternal twins — supporting a genetic contribution.

Large-scale genome-wide association studies have identified multiple genetic regions linked to endometriosis risk, implicating pathways involved in hormone metabolism, immune regulation, tissue remodelling, and cell proliferation. However, no single causative gene has been identified, which is consistent with endometriosis being a polygenic condition shaped by the interaction of genetic predisposition and environmental context.

Other Proposed Mechanisms

Researchers continue to explore several additional theories, including:

Coelomic metaplasia: the possibility that certain peritoneal cells retain a latent capacity to transform into endometrial-like tissue in response to hormonal or environmental stimuli
Lymphatic and vascular dissemination: the spread of endometrial cells through lymph or blood vessels, which may account for rare distant endometriotic deposits
Stem cell theories: the hypothesis that endometrial stem cells from the bone marrow or uterine basal layer may contribute to lesion formation
Gut and reproductive microbiome dysbiosis: emerging research describes associations between microbiome imbalance and endometriosis, though causal relationships have yet to be established

The range and complexity of these theories reinforces a central point: endometriosis does not have a single cause. It arises from the convergence of multiple biological systems — genetic, immune, hormonal, and inflammatory — and is almost certainly shaped by the wider physiological environment in which those systems operate.

Endometriosis and Fertility

Endometriosis is among the leading causes of female-factor infertility, with estimates suggesting it affects 30–50% of women who experience difficulty conceiving. The pathways through which it impairs fertility are varied and often interrelated.

In advanced disease, the most direct mechanism is anatomical: extensive adhesions may distort pelvic architecture, occlude the fallopian tubes, or restrict ovarian mobility, physically obstructing fertilisation. Endometriomas reduce ovarian reserve and may compromise egg quality, in part through the oxidative damage caused by the iron-rich fluid they contain.

However, endometriosis affects fertility even in the absence of significant structural changes. The inflamed peritoneal environment is hostile to both eggs and sperm. Elevated reactive oxygen species impair egg development and may damage sperm DNA. Altered tubal function may disrupt the transport of gametes and embryos. The immune-inflammatory milieu of the uterus can reduce endometrial receptivity, making successful implantation less likely even when fertilisation has occurred.

Progesterone resistance adds a further layer of complexity. An effective luteal phase requires adequate progesterone signalling to transform and sustain the endometrial lining in preparation for implantation. Where progesterone responsiveness is impaired at the cellular level, physiologically normal hormone levels may nonetheless fail to exert their full biological effect.

It is important to note that endometriosis does not make conception impossible for the majority of affected women. Many conceive naturally or with targeted support. The impact on fertility varies considerably depending on disease severity and location, the degree of ovarian involvement, age, and the wider health context of both partners.

Quality of Life and the Broader Impact of Endometriosis

The consequences of endometriosis reach well beyond its physical manifestations. Living with chronic pain, unpredictable fatigue, and the burden of a poorly understood condition takes a significant psychological and social toll. Research consistently demonstrates that women with endometriosis experience substantially higher rates of anxiety, depression, and impaired quality of life compared with the general population.

The path to diagnosis is frequently a source of additional harm in itself. Years of pain dismissed as normal menstruation, inconclusive investigations, and the experience of not being believed are widely reported within endometriosis communities. The cumulative effect of this medical invalidation is real, and it matters.

Endometriosis touches every dimension of a person’s life: relationships, sexual intimacy, career, social engagement, and sense of self. Painful intercourse can place significant strain on partnerships. Unpredictable symptom flares lead to missed work and lost opportunities. Fertility challenges bring grief, uncertainty, and relational pressure that many couples are ill-equipped to navigate alone.

Any meaningful approach to endometriosis must hold the full person in view — not only the pelvic lesions, but the life being lived around them.

The Body’s Internal Environment

While endometriosis has identifiable biological drivers, it does not exist in isolation from the rest of the body. A growing body of clinical and research interest is focused on how the wider physiological environment — shaped by nutrition, metabolic health, stress physiology, sleep quality, and systemic inflammation — may influence the development, progression, and lived experience of endometriosis.

Nutrition and Metabolic Health

Several nutritional patterns have been studied in the context of endometriosis risk and symptom burden. Diets characterised by high intakes of trans fats and omega-6 fatty acids have been associated with elevated risk in some cohort studies, while higher omega-3 intake — with its well-established anti-inflammatory properties — has been associated with reduced risk. Antioxidant-rich dietary patterns may help to offset the oxidative stress that is a consistent feature of the endometriotic environment.

Blood sugar regulation and insulin sensitivity are also clinically relevant. Insulin resistance promotes systemic inflammation and may unfavourably influence oestrogen metabolism — both of which have direct implications for endometriosis. Supporting liver function, which governs oestrogen clearance, and gut microbiome health, which influences the reabsorption of oestrogen metabolites via the oestrobolome, are additional considerations within a nutritional framework.

Stress and the HPA Axis

Sustained psychological stress activates the hypothalamic-pituitary-adrenal (HPA) axis and disrupts normal cortisol rhythmicity. The downstream consequences include altered immune regulation, increased inflammatory tone, and shifts in reproductive hormone balance. Emerging evidence suggests that HPA axis dysregulation may interact meaningfully with the immune and hormonal features of endometriosis.

Stress is not a cause of endometriosis. However, it may shape the physiological environment in which the condition operates — potentially amplifying inflammatory activity, altering immune surveillance, and intensifying pain through central sensitisation pathways. Stress reduction is therefore a relevant consideration within a comprehensive endometriosis management strategy.

Sleep

Sleep is a period of critical cellular repair, immune recalibration, and hormonal restoration. Melatonin — produced primarily during sleep — has demonstrated direct anti-endometriotic activity in laboratory studies, inhibiting cell proliferation, reducing oxidative stress, and modulating immune behaviour. Chronic sleep disruption, by contrast, promotes pro-inflammatory states and limits the body’s capacity for repair and regulation.

Systemic Inflammation

Although endometriosis generates its own localised inflammatory environment, it also exists within the context of the body’s broader systemic inflammatory status. Women with endometriosis frequently show evidence of wider inflammatory dysregulation. Lifestyle factors that sustain systemic inflammation — poor dietary quality, physical inactivity, chronic stress, and environmental toxin exposure — may create conditions in which endometriosis is more likely to establish, persist, and produce symptoms.

Reducing systemic inflammatory burden through evidence-informed lifestyle choices will not resolve endometriosis. But it may represent a meaningful and modifiable contribution to a comprehensive management approach, sitting alongside appropriate medical and surgical care.

Jonathan Jackson’s Theory: A Cellular Perspective

Important: What follows is Jonathan Jackson’s personal hypothesis, not an established scientific fact. It is shared as a conceptual framework for discussion and future exploration only, and should not be read as a proven explanation for progesterone resistance or endometriosis.

The established science around progesterone resistance in endometriosis points to a disruption not of progesterone levels as such, but of how cells receive and respond to progesterone’s molecular signals. This distinction raises an interesting conceptual question: if the problem lies partly in the sensitivity and function of the cells themselves, what determines a cell’s capacity to receive and act upon a hormonal message?

My hypothesis begins with a foundational principle of cellular biology: cells require adequate raw materials to function well. Every cellular process — including the synthesis of receptor proteins, the transduction of hormonal signals, gene expression, and structural repair — depends upon the availability of appropriate nutrients. Healthy fats contribute to membrane integrity and the fluidity on which receptor function depends. Amino acids provide the structural building blocks from which receptor proteins are made. Vitamins and minerals serve as cofactors for the enzymatic processes that regulate signalling and gene expression. Sufficient energy is required for the cellular work of hormonal communication.

My proposal is this: where the body is chronically undernourished, exposed to poor dietary quality, burdened by persistent inflammation, or operating under conditions of metabolic dysfunction or high physiological stress, the quality of cellular function across many tissues may be compromised. Cells in such an environment may be less able to build and maintain adequate receptor infrastructure, receive hormonal signals clearly, or translate those signals into effective biological responses.

In the context of endometriosis specifically, I raise the possibility that impaired cellular health — arising from the quality of the body’s internal physiological environment rather than from endometriosis-specific mutations alone — could potentially contribute to the reduced progesterone responsiveness observed in the condition. If cells are not receiving the nutritional and metabolic support they require for optimal function, progesterone resistance may in some cases be, at least in part, a downstream expression of that broader cellular insufficiency.

This is not a claim that nutrition causes or cures endometriosis, nor that it is the primary driver of progesterone resistance. The genetic, epigenetic, and molecular changes documented in the research literature are real, well-evidenced, and significant. The suggestion here is more modest: that the cellular environment may be a modifiable factor that influences how those mechanisms are expressed and experienced.

From this perspective, supporting the body’s internal environment — through nutrient-dense, anti-inflammatory food, restorative sleep, effective stress management, and the reduction of factors that compromise cellular function — may be more than supportive care in a general sense. It may represent a meaningful attempt to optimise the conditions under which cells operate, with potential relevance to how well hormonal signals are received and acted upon.

I want to be clear: this is a conceptual hypothesis formed through clinical observation and engagement with the scientific literature, not a claim that has been subjected to controlled research. It is offered in a spirit of intellectual curiosity and honest clinical thinking, as a possible lens through which to consider the relationship between cellular health and hormonal responsiveness in endometriosis. It is not a treatment recommendation, a substitute for medical management, or a promise that lifestyle change will resolve this condition.

This is Jonathan Jackson’s personal theory and has not been scientifically proven. It is intended as a conceptual framework for discussion and future exploration, not as an established explanation for progesterone resistance or endometriosis.

Conclusion: Endometriosis Requires a Wider Lens

Endometriosis is a condition of genuine complexity. The science tells us it is shaped by genetic inheritance, immune dysregulation, oestrogen biology, chronic inflammation, and cellular signalling disruptions — none of which operates in isolation. What is increasingly clear is that the body’s internal environment — shaped by the quality of nutrition, sleep, stress management, and everyday health practices — is not a background detail. It is the ecosystem in which this biology unfolds.

This does not mean that endometriosis is a lifestyle disease, nor that it can be resolved through diet and wellness practices alone. It means that the body is an integrated system, and complex systemic conditions are influenced, at least in part, by the systemic environment. Supporting that environment thoughtfully, alongside evidence-based medical care, is not an alternative to conventional treatment — it is part of what it means to care for health comprehensively.

At Jonathan Jackson Health, our approach to fertility and hormonal wellbeing is built on this understanding: that genuine health education, personalised nutritional guidance, and support for the body’s internal environment can meaningfully complement the medical management of conditions like endometriosis. We are not here to replace your doctor. We are here to help you understand your body more deeply, and to support you in building the foundations that health depends upon.

For anyone living with endometriosis: you are not simply your symptoms. Your biology is not wholly fixed or beyond influence. And there are always meaningful questions worth asking about the environment your body is living in.

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Jonathan Jackson BSc (Hons) Chinese Medicine

Fertility Coach, Health Educator & Author of Drop in the Ocean

Jonathan Jackson Health