Endometriosis is commonly described as endometrial-like tissue growing outside the uterus. During this Mito-Hackers webinar, Dr. Ram Shankar Upadhyaya explained that this description tells us where the disease appears, but it does not fully explain why the tissue survives, why inflammation persists, or why symptoms can become so disruptive.
His presentation examined an emerging question in endometriosis research: Could mitochondrial dysfunction and altered cellular energy help explain parts of the disease that cannot be understood through hormones alone?
Endometriosis Is More Than a Hormonal Condition
Endometriosis has traditionally been viewed primarily as a hormone-related disease. Dr. Upadhyaya did not argue that hormones are unimportant. Instead, he described endometriosis as a multifactorial condition involving several interacting biological processes, including:
Hormonal signaling
Genetics
Immune dysfunction
Inflammation
Oxidative stress
Mitochondrial dysfunction
His central point was that mitochondria do not replace hormones in the endometriosis story. They may help explain how cells respond to hormonal and inflammatory signals.
Looking at both systems together may offer a more complete way to think about why endometriosis develops, persists, and affects women differently.
Why Mitochondria Matter
Mitochondria are usually introduced as the structures that produce cellular energy in the form of ATP. Dr. Ram described their role more broadly, discussing their involvement in:
Cellular energy production
Cell survival and repair
Oxidative stress
Inflammatory signaling
Immune function
Hormonal responses
He also discussed the balance between mitochondrial biogenesis, the production of new mitochondria, and mitophagy, the removal of damaged mitochondria.
When damaged mitochondria accumulate or cellular energy production falls, cells may have greater difficulty maintaining normal repair, communication, and immune regulation.
From Oxidative Stress to Inflammation and Pain
During the presentation, Dr. Ram outlined a possible cycle connecting oxidative stress, mitochondrial damage, inflammation, and pain.
In this model, oxidative stress can damage mitochondrial structures and interfere with energy production. Reduced cellular energy may then impair repair processes, while continued immune activation changes the environment around the affected tissue.
As inflammation persists, tissue damage, new blood-vessel formation, scar tissue, and nerve sensitization may contribute to continuing or worsening pain.
Dr. Ram stressed that pain should not be treated as an isolated symptom:
“Pain is not simply a symptom. Pain is a whole biology.”
This may help explain why the pain associated with endometriosis can be persistent and why reducing pain alone does not necessarily address all the biological processes involved.
Endometriosis, Cellular Energy, and Fertility
Dr. Ram also used reproductive biology to illustrate why cellular energy matters to women’s health.
He discussed the high energy demands associated with egg development, fertilization, pregnancy, and placental function. He described hormones and mitochondria as interconnected systems: hormones influence mitochondrial activity, while mitochondria provide the energy cells need to respond to hormonal signals.
This relationship may be especially relevant when considering endometriosis, infertility, reproductive aging, and the physical and emotional burden experienced by women seeking fertility treatment.
Common Myths About Endometriosis
Near the end of the presentation, Dr. Ram addressed several common misconceptions.
Myth 1: Endometriosis is just painful periods
He described it as a chronic inflammatory condition that may also be associated with infertility, fatigue, pelvic pain, pain during intercourse, and symptoms extending beyond menstruation.
Myth 2: Endometriosis is exclusively hormonal
Hormones are involved, but Dr. Ram also discussed the possible contributions of genetics, immune dysfunction, inflammation, oxidative stress, and mitochondrial dysfunction.
Myth 3: Surgery cures endometriosis
Surgery may remove lesions and relieve symptoms, but Dr. Ram noted that lesions and symptoms can recur after surgery.
Myth 4: More pain always means more extensive disease
The severity of pain does not necessarily correspond to the visible number or extent of endometriotic lesions.
Myth 5: Nothing new is happening in endometriosis research
Dr. Ram pointed to emerging work involving mitochondrial biology, immunology, immunotherapy, multiomics, and precision medicine.
Looking Toward a Broader Understanding
The presentation did not suggest that mitochondrial dysfunction is the sole cause of endometriosis. Instead, Dr. Ram presented it as one possible contributor within a much broader biological system.
Understanding how cellular energy interacts with hormones, inflammation, oxidative stress, immune function, and pain may help researchers ask new questions about the disease.
Dr. Ram described hormones and mitochondria as a kind of “twin engine,” with each system supporting the other. Hormones help regulate and protect mitochondrial function, while mitochondria provide cellular energy and support the production of steroid hormones. The first step in steroid hormone synthesis begins inside the mitochondria, making their relationship reciprocal rather than one-directional.
Hormones tell cells what to do, but mitochondria give those cells the energy to do it.
This energy relationship is only part of the connection. Mitochondria also support steroid hormone production, while hormones help regulate mitochondrial health and activity.
Considering both systems together may help provide a fuller understanding of endometriosis and the health challenges women experience.
Watch the Webinar
Mito-Hackers members can watch the complete webinar in two parts:
Part 1: Main Presentation
Endometriosis: An Energy Crisis Inside Women’s Cells
Part 2: Questions and Answers
Visit the Webinars & Events space to watch the recordings.
Continue the Conversation
Which part of this emerging model deserves the most attention: mitochondrial function, oxidative stress, immune signaling, pain biology, or the interaction between hormones and cellular energy?
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This briefing is intended for educational and scientific discussion only. It should not be interpreted as medical advice, diagnosis, or treatment guidance.