Journal

Understanding menopause at the level of the cell to live it better

Menopause remains one of the most poorly understood biological transitions in the female body. It is still widely associated with negative representations: loss of energy, inevitable weight gain, mood disturbances, accelerated ageing, and even cognitive decline. These narratives, often simplistic and reductive, are rooted in a fragmented view of female physiology. They perpetuate enduring misconceptions that obscure contemporary scientific understanding and distance women from a clear, rational and reassuring comprehension of what is truly taking place within their bodies at this stage of life.

This anxiety-laden framing leads to a double dead end. On the one hand, there is an often excessive and standardised medicalisation, largely focused on hormone levels, with insufficient consideration of the broader biological context. On the other, there is a tendency to normalise symptoms, dismissed as “inevitable”, “age-related” or simply something women must endure. In both cases, individual experience is insufficiently heard, and the deeper biological mechanisms — energetic, inflammatory and metabolic — remain largely unexplored.

Yet menopause is neither a disease nor a failure of the female body. It is a physiological, universal hormonal transition, fully embedded in the continuum of life. Its impact does not depend solely on the decline in oestrogen levels, but primarily on the cell’s capacity to adapt. What matters, therefore, is not the cessation of menstrual cycles itself, but the biological terrain at the moment this transition occurs: mitochondrial function, the degree of chronic low-grade inflammation, metabolic balance, gut integrity, detoxification efficiency and micronutrient availability.

Adopting a cellular perspective on menopause fundamentally changes the way we understand it. By addressing the underlying biological mechanisms — mitochondrial energy, low-grade inflammation, the microbiome and micronutrition — it becomes possible to dismantle prevailing misconceptions and to transform this phase into a genuine lever for prevention, physiological stability and female longevity. This is precisely the approach proposed by Cellular Nutrition®.

I. Menopause and misconceptions: why the dominant narrative is misleading

For a long time, menopause was portrayed as a sudden hormonal collapse leading inevitably to a global deterioration in health. This linear, downward and overly simplistic framework has shaped a collective imagination in which declining oestrogen levels are equated with unavoidable decline, loss of vitality and progressive impairment of physical and cognitive functions.

Such a reductive view has led either to uniform medicalisation — often focused almost exclusively on hormone levels — or to the minimisation of symptoms, regarded as a natural consequence of ageing or simply of being a woman. In both scenarios, many women are left without support that is truly adapted to their individual physiology or their unique biological history.

Biological reality, however, tells a very different story. Two women of the same age, at the same hormonal stage, may experience menopause in radically different ways. Some go through this transition with few clinical manifestations, while others develop profound and persistent fatigue, chronic sleep disturbances, progressive abdominal weight gain or marked emotional instability.

This variability is neither random nor psychological. It is explained by one fundamental factor: the state of the cell before menopause. Long-standing chronic stress, years of low-grade inflammation, gut microbiota imbalance, functional liver overload, impaired insulin sensitivity or micronutrient deficiencies all create a fragile biological terrain long before the hormonal transition begins. Menopause then acts as a biological revealer rather than an isolated cause.

Misconceptions arise precisely when hormonal change is confused with cellular dysfunction.

To go further — biological variability and menopausal symptoms

Avis, N.E. et al. (2015). Duration of menopausal vasomotor symptoms over the menopause transition. JAMA Internal Medicine, 175(4), 531–539. https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2108915

Thurston, R.C. & Joffe, H. (2011). Vasomotor symptoms and menopause. Obstetrics & Gynecology Clinics, 38(3), 489–501. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3185243/

II. What really happens during menopause: a cellular perspective

Oestrogens play a central role in female physiology far beyond reproduction alone. They are involved in the regulation of energy metabolism, bone protection, skin quality, brain function, cardiovascular health and immune regulation. Their action is diffuse, cross-functional and deeply integrated into the body’s major regulatory systems.

At the cellular level, oestrogens support mitochondrial function, promote ATP production, enhance glucose and fatty-acid utilisation, and limit oxidative stress. They also regulate the expression of numerous genes involved in cellular repair, neuronal survival and metabolic stress responses.

As oestrogen levels decline, cells must adapt to a new hormonal environment. When mitochondria are efficient and antioxidant systems are robust, this adaptation occurs gradually and relatively quietly. When cells are already compromised, however, hormonal decline becomes an additional stressor: available energy decreases, inflammation rises, and repair and intercellular communication mechanisms are impaired.

This is when persistent fatigue, sleep disturbances, mood fluctuations, anxiety, abdominal weight gain, joint pain or accelerated skin ageing may emerge. These manifestations are not an inevitable consequence of ageing; they reflect a pre-existing cellular imbalance that the hormonal transition merely makes more visible and symptomatic.

To go further — oestrogens and mitochondria

Ventura-Clapier, R. et al. (2017). Estrogens, estrogen receptors and mitochondria. Biochimica et Biophysica Acta, 1863(7), 1567–1579. https://www.sciencedirect.com/science/article/pii/S0005273617300700

Brinton, R.D. (2008). Estrogen regulation of glucose metabolism and mitochondrial function. Trends in Endocrinology & Metabolism, 19(3), 99–106. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2605538/

III. Menopause, low-grade inflammation and accelerated ageing

Menopause is frequently associated with an increase in low-grade inflammation, also referred to as inflammaging. This chronic, diffuse and silent inflammatory state disrupts cellular communication, impairs mitochondrial function and accelerates senescence mechanisms, often without producing immediately identifiable acute symptoms.

When inflammation becomes chronic, its impact is systemic: weakened bone health and increased risk of osteopenia, dysregulation of glucose and lipid metabolism, elevated cardiovascular risk, cognitive impairment and progressive degradation of connective tissue quality.

It is essential to understand that menopause does not accelerate ageing per se. Rather, it represents a pivotal moment during which pre-existing inflammation becomes more apparent and more symptomatic, revealing imbalances that were previously partially compensated by the hormonal environment.

To go further — inflammaging and menopause

Furman, D. et al. (2019). Chronic inflammation in the etiology of disease across the life span. Nature Medicine, 25, 1822–1832. https://www.nature.com/articles/s41591-019-0675-0

Mauvais-Jarvis, F. et al. (2017). Sex and gender: modifiers of health, disease, and medicine. The Lancet, 390(10105), 565–582. https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)31446-8/fulltext

IV. The gut microbiome and oestrogen metabolism

The gut microbiome plays a decisive role during menopause. Through the oestrobolome, it actively participates in oestrogen metabolism, influences systemic inflammation, and modulates immune responses as well as neuro-emotional balance.

A diverse and functional microbiome supports more efficient oestrogen recirculation, finer inflammatory regulation and robust gut–brain axis function. Conversely, chronic gut dysbiosis can exacerbate menopausal symptoms: persistent fatigue, digestive disturbances, emotional fluctuations, sleep disorders and increased vulnerability to stress.

Addressing the microbiome is therefore a central and structuring lever in a cellular approach to menopause.

To go further — microbiome and oestrobolome

Baker, J.M. et al. (2017). The gut microbiome: role in estrogen metabolism. Maturitas, 103, 45–54. https://www.sciencedirect.com/science/article/pii/S0378512217301783

Chen, K.L. & Madak-Erdogan, Z. (2016). Estrogen and microbiota crosstalk. Trends in Endocrinology & Metabolism, 27(11), 743–753. https://pubmed.ncbi.nlm.nih.gov/27554320/

V. Fatigue, weight gain and sleep disturbances: a shared cellular origin

Chronic fatigue, abdominal weight gain and sleep disturbances during menopause share a common cellular origin. They reflect dysregulated energy production, persistent low-grade inflammation and disruption of neuro-hormonal axes involving cortisol, insulin and neurotransmitters.

In this context, further dietary restriction or the multiplication of isolated strategies often worsens metabolic stress and amplifies existing imbalances. By contrast, a global Cellular Nutrition® approach helps restore metabolic flexibility, support cellular recovery, improve sleep quality and stabilise key neuro-endocrine functions.

To go further — metabolism and menopause

Lovejoy, J.C. et al. (2008). Increased visceral fat and decreased energy expenditure during menopause. International Journal of Obesity, 32, 949–958. https://www.nature.com/articles/ijo200886

Carr, M.C. (2003). The emergence of the metabolic syndrome with menopause. Journal of Clinical Endocrinology & Metabolism, 88(6), 2404–2411. https://academic.oup.com/jcem/article/88/6/2404/2845084

VI. Cellular Nutrition®: supporting menopause differently

Cellular Nutrition®, developed by Dr. Espinasse, offers a global, personalised and scientifically grounded approach. Its aim is to support mitochondrial energy, reduce low-grade inflammation, restore microbiome balance and accompany neuro-hormonal axes without overriding physiology.

When integrated into this individualised strategy, dietary supplements are not used to “compensate” for isolated deficiencies. Instead, they support the body’s biological adaptive capacity. Used with precision, they become genuine tools of cellular modulation — without overstimulation or artificial manipulation of physiological processes.

To go further — integrative approaches

de Villiers, T.J. et al. (2016). Global consensus statement on menopausal hormone therapy. Climacteric, 19(2), 109–150. https://www.tandfonline.com/doi/full/10.3109/13697137.2015.1129166

Shifren, J.L. & Gass, M.L.S. (2014). The North American Menopause Society recommendations. Menopause, 21(10), 1038–1062. https://journals.lww.com/menopausejournal/fulltext/2014/10000/the_north_american_menopause_society.1.aspx

Key takeaways

Menopause is neither an inevitable decline nor a predetermined fate. It is a modifiable biological transition, whose impact depends largely on the cellular terrain. By adopting a rigorous, scientific and cellular perspective, this phase of life can be transformed into a period of active prevention, physiological stability and female longevity.