Last May, The Lancet published the outcome of an unprecedented international consensus process: polycystic ovary syndrome (PCOS) will no longer be known by that name and will instead be renamed polyendocrine metabolic ovarian syndrome (PMOS). Led by Monash University and endorsed by the World Health Organization, this change is far more than a cosmetic adjustment in terminology; it is the result of fourteen years of scientific work.

Behind the new name lies an extensive process involving iterative global surveys, modified Delphi methods, and the participation of more than 14,000 individuals—both patients and healthcare professionals—from every region of the world. The goal was to identify a name that accurately reflects what is truly happening in the bodies of those living with this condition.

Dr. Carlos Martí – Neolife Medical Team

A new name to better reflect clinical reality

For decades, the term “polycystic” focused attention—and diagnosis—on a specific ultrasound finding: the presence of multiple follicles within the ovary. Yet these follicles are not pathological cysts, but rather immature structures that failed to complete their development, and many women with the condition do not even exhibit this ovarian morphology.

This discrepancy between the name and the clinical reality had important consequences: delayed diagnoses, fragmented care, and a stigma that remains associated with the word “polycystic.” The new name aims to put an end to this confusion and to acknowledge, from the terminology itself, that this is a multisystem disorder involving hormonal, metabolic, and reproductive dysfunction simultaneously.

The magnitude of the problem justifies the change. According to the WHO, PMOS affects one in eight women of reproductive age worldwide, and up to 70% of cases are estimated to remain undiagnosed. The transition to the new terminology will be implemented gradually over the next three years, with updates to clinical guidelines, diagnostic classifications, and educational materials for patients.

From PCOS to PMOS: the anatomy of a global consensus

The process, published on May 12, 2026, and led by Professor Helena Teede together with the Global Name Change Consortium, involved 56 academic, clinical, and patient organizations. The aim was not merely to select a new name based on the opinion of a few experts, but rather to build it upon scientific evidence and the real-world experiences of individuals living with the condition.

The new terminology was officially presented during the European Congress of Endocrinology in Prague and simultaneously published in The Lancet. According to the authors, the priority was to find a precise term, even if this meant leaving behind the familiar PCOS acronym that had defined the condition for decades.

The three pillars of the new name

The term polyendocrine metabolic ovarian syndrome encapsulates three key concepts.
“Polyendocrine” acknowledges that the disorder extends beyond the ovaries and involves multiple hormonal systems, including androgens, insulin, and, in some cases, thyroid function.
“Metabolic” places insulin resistance and cardiovascular risk at the center of the condition, rather than treating them as secondary complications.
“Ovarian” preserves the reproductive origin of the syndrome while removing the misleading reference to cysts.

This new terminology is not only more accurate; it also provides a better framework for treatment. A condition that simultaneously affects metabolism, multiple endocrine pathways, and the reproductive system cannot realistically be managed from a single specialty.

What is PMOS and how is it diagnosed?

Beyond the name change, PMOS continues to be diagnosed using the well-established Rotterdam criteria. At least two out of three conditions must be present:
Ovulatory dysfunction (irregular menstrual cycles or anovulation).
Excess androgen levels, either clinically (acne, hirsutism, hair loss) or demonstrated biochemically.
Characteristic ovarian morphology on ultrasound or elevated anti-Müllerian hormone levels.
In adolescents, diagnostic criteria are applied more cautiously, and only the first two criteria are considered.

These combinations give rise to different phenotypes; not all women with PMOS share the same profile. Some present with hyperandrogenism and irregular cycles together with polycystic ovarian morphology, whereas others exhibit the same hormonal abnormalities without the ultrasound findings. Still others maintain normal ovulation while showing androgen excess and multiple follicles. This variability is precisely what the new terminology aims to capture more effectively.

Although insulin resistance is extremely common in PMOS, it is not part of the formal diagnostic criteria. Nevertheless, it strongly influences prognosis and treatment, which explains why the metabolic component now occupies a central place in the disease’s name.

Why naming matters for health

Women with PMOS experience a wide range of manifestations: irregular cycles, difficulty conceiving, persistent acne, excessive hair growth, and hair loss, but also an increased risk of type 2 diabetes and cardiovascular disease. The previous terminology, focused mainly on the ovaries, tended to overlook these metabolic implications, which are often the most significant determinants of long-term health.

Accurately naming a disease is not merely symbolic. When terminology reflects the true complexity of a condition, it improves clinical recognition, accelerates diagnosis, and facilitates coordinated care among different specialties.

The cardiovascular component: why it is not a minor detail

Cardiovascular risk is not a secondary consequence of PMOS but one of the fundamental reasons behind the name change. Insulin resistance is present in approximately 85% of affected individuals and represents one of the central mechanisms driving the syndrome. Compensatory hyperinsulinemia stimulates ovarian and adrenal androgen production, reduces sex hormone-binding globulin (SHBG), and increases circulating free testosterone levels.

Ese mismo desequilibrio favorece la acumulación de grasa visceral y hepática, un estado proinflamatorio de bajo grado y disfunción del endotelio vascular, ingredientes que, sostenidos en el tiempo, derivan en hipertensión arterial, dislipemia y aterosclerosis prematura. El riesgo de diabetes tipo 2 y de diabetes gestacional también aumenta de forma proporcional al peso corporal.

For this reason, current guidelines recommend that all women newly diagnosed with PMOS undergo a metabolic evaluation including a lipid profile and an oral glucose tolerance test, regardless of age or body mass index. Early identification of these abnormalities allows intervention before overt cardiovascular disease develops, in line with the preventive approach that we apply at Neolife to cardiometabolic risk factors.

How PMOS is treated

Treatment of PMOS has never relied on a single solution, and this does not change with the new terminology. Management remains individualized and depends on the patient’s predominant symptoms, reproductive goals, and degree of metabolic impairment.

For most women, the first step consists of lifestyle interventions: adopting a diet that improves insulin sensitivity, engaging in regular physical activity, and achieving moderate weight loss when appropriate. These measures alone can improve menstrual regularity, reduce hyperandrogenism, and lower long-term cardiometabolic risk.

When metabolic dysfunction is significant, insulin-sensitizing agents such as metformin are often used. Combined hormonal contraceptives and antiandrogens are commonly prescribed to regulate menstrual cycles and manage acne or hirsutism, with spironolactone remaining one of the most widely used medications because of its effectiveness against excessive hair growth and acne. However, it should be avoided in women seeking pregnancy because of its teratogenic potential.
For women wishing to conceive, ovulation induction therapies such as letrozole or clomiphene citrate are available, and if necessary, assisted reproductive technologies such as in vitro fertilization may be considered.

Importantly, PMOS does not necessarily imply infertility. Many women with the condition achieve spontaneous or assisted pregnancies. The key lies in comprehensive follow-up involving gynecology, endocrinology, and nutrition, together with psychological support whenever necessary, given the emotional burden associated with living with a chronic condition.

What changes—and what does not—for patients

The symptoms do not change. A woman with PMOS experiences exactly the same manifestations previously associated with PCOS. What changes is the framework used to understand and integrate these manifestations into a single clinical picture, as well as the way healthcare professionals communicate and coordinate care.

The transition will be gradual. Over the next three years, clinical guidelines, classification systems, medical records, and educational resources for both patients and professionals will be updated. The goal of the consensus initiative is not to transform clinical practice overnight, but rather to ensure an orderly evolution toward this new diagnostic framework.

The Neolife approach

At Neolife, we have long approached female hormonal disorders through a comprehensive perspective, integrating endocrinology, gynecology, and nutrition to understand what happens beyond the ovary itself. This change in terminology reinforces something that has always been part of our clinical practice: evaluating each patient’s hormonal, metabolic, and reproductive profile as a whole, rather than treating individual symptoms in isolation.

Because giving a disease the right name is often the first step toward treating it better.

BIBLIOGRAPHY

(1) Teede HJ, Bahri Khomami M, Morman R, et al; Global Name Change Consortium. Polyendocrine metabolic ovarian syndrome, the new name for polycystic ovary syndrome: a multistep global consensus process. Lancet. 2026 Jun 6;407(10545):2329-2339. doi: 10.1016/S0140-6736(26)00717-8. Epub 2026 May 12.

(2) Teede HJ, Moran LJ, Morman R, et al. Polycystic ovary syndrome perspectives from patients and health professionals on clinical features, current name, and renaming: a longitudinal international online survey. EClinicalMedicine. 2025;84:103287.

La entrada The polycystic ovary syndrome gets a new name: the polyendocrine metabolic ovarian syndrome (PMOS) is finally born se publicó primero en Neolife.

The menopausal transition promotes changes in body composition. We analyze the hormonal factors involved and the most effective nutritional strategies.

During menopause, many women experience weight gain, particularly in the abdominal area. Although this is often attributed exclusively to “hormones,” the phenomenon is more complex. The decline in estrogen levels, changes in muscle mass, and metabolic adaptations all play a significant role. We review what actually happens and how to intervene effectively.

Adriana Martín Peral – Neolife Nutrition Unit

Hormonal Changes in Menopause: What Really Happens?

Menopause is characterized by a progressive decline in estrogen levels, particularly estradiol. This hormonal shift impacts:

• Redistribution of body fat toward a more android (abdominal) pattern.
• Decreased basal energy expenditure.
• Increased insulin resistance.
• Higher cardiometabolic risk.

Estrogens play a protective role at the metabolic level. Their decline favors greater accumulation of visceral fat, which is metabolically active and associated with inflammation.

Is It Only a Hormonal Issue?

Not exclusively. In addition to hormonal changes, other factors are involved:

• Loss of Muscle Mass (Sarcopenia)

From the ages of 40–50 onward, there is a progressive decline in muscle mass if no strength stimulus is present. Since muscle is metabolically active tissue, its reduction decreases daily energy expenditure.

• Decreased Total Energy Expenditure

Lower levels of spontaneous physical activity, changes in sleep patterns, and increased stress contribute to a sustained positive energy balance.

• Changes in Appetite and Satiety

Some women report increased cravings for energy-dense foods, possibly related to hormonal fluctuations and sleep disturbances.

Evidence-Based Nutritional Strategies

• Prioritize Adequate Protein Intake: A sufficient protein intake (approximately 1.2–1.6 g/kg/day depending on individual profile) helps to:
  • Preserve muscle mass.
  • Improve satiety.
  • Support glycemic control.

Distributing protein evenly throughout the day optimizes muscle protein synthesis.

• Strength Training + Nutrition: Resistance training is key to counteracting age- and menopause-related muscle loss. When combined with adequate protein intake, it improves body composition beyond what is reflected on the scale.
• Control Energy Density: Reduce ultra-processed foods and prioritize:
  • Vegetables
  • Whole fruit
  • Legumes
  • Healthy fats (extra virgin olive oil, nuts)
  • Lean protein sources

This approach supports satiety while lowering overall caloric load.

• Fiber and Metabolic Health: A high fiber intake (25–35 g/day) improves:
  • Insulin sensitivity
  • Lipid profile
  • Gut health

The gut microbiota also appears to play a relevant role in weight regulation during this stage.

Sleep and Stress

Sleep deprivation is associated with greater insulin resistance and increased appetite. Therefore, intervention should be comprehensive and lifestyle-oriented.

What Does NOT Work

• Extremely restrictive diets maintained over time.
• Complete elimination of food groups without clinical indication.
• Focusing exclusively on weight without assessing body composition.

During menopause, the goal should be to improve body composition and metabolic health—not simply reduce body weight.

Conclusion

Weight gain during menopause is not inevitable, but it does require a different approach. The combination of appropriate nutrition, strength training, and a comprehensive lifestyle strategy can improve body composition and reduce cardiometabolic risk during this stage of life.

BIBLIOGRAPHY

(1) Lovejoy JC et al. Increased visceral fat and decreased energy expenditure during menopause.

(2) Lizcano F, Guzmán G. Estrogen deficiency and the origin of obesity during menopause.

(3) Stuenkel CA et al. Treatment of symptoms of menopause.

(4) Messier V et al. Menopause and sarcopenia: impact on metabolic health.

La entrada Menopause and Weight Gain: The Real Role of Hormones and How to Address It Through Nutrition se publicó primero en Neolife.

The Department of Health and Human Services (HHS) and the FDA have conducted an in-depth review of the scientific evidence and have decided to remove the former “black box” warnings that had accompanied many hormone treatments since 2002.

For more than 20 years, those black boxes warned of a possible increased risk of heart attack, stroke, thrombosis, breast cancer, and dementia in all women using estrogen, regardless of age, timing of treatment initiation, or the type of hormone used. These warnings were largely based on early results from the well-known Women’s Health Initiative (WHI) study, conducted in women over 60 years of age, many with pre-existing cardiovascular disease, and using hormone preparations that are now largely obsolete.

Dr. Sánchez – Neolife Medical Team

What exactly has the HHS/FDA decided?

After reviewing decades of clinical studies and meta-analyses, the HHS concluded that these generalized warnings did not reflect current scientific knowledge and may have discouraged many women from receiving a treatment beneficial to their health.

The key changes include the removal of “black box” warnings from multiple systemic estrogen and estrogen–progestogen preparations. Package inserts still include warnings, but no longer as a global, alarmist message for all women. It is also stated that in women under 60 years of age or within 10 years of menopause, the overall evidence from clinical trials indicates that hormone therapy reduces coronary heart disease events and overall mortality, markedly lowers the risk of osteoporotic fractures, and may reduce cognitive decline and Alzheimer’s disease when initiated close to menopause (the so-called “window of opportunity”), although debate remains in this area. In addition, the FDA has created a dedicated expert panel on menopause and Menopausal Hormone Therapy (MHT) to update information for patients and healthcare professionals and to continue reviewing the evidence on an ongoing basis.

In summary, the official message has shifted from “avoid it unless absolutely necessary and for the shortest possible time” to “for many younger postmenopausal women, the benefits may clearly outweigh the risks when therapy is properly indicated and supervised.”

What evidence supports this new perspective?

As mentioned, the data review includes meta-analyses of clinical trials showing that women who start Menopausal Hormone Therapy before age 60 or within 10 years after menopause experience a 30% reduction in coronary heart disease and a 30–40% reduction in all-cause mortality compared with placebo. Trials in women with recent menopause (such as the Danish DOPS study and others) were also included, showing fewer cardiovascular events and fewer fractures in women treated with estrogen compared with untreated women. In addition, observational and neuroimaging studies were considered, suggesting a lower amyloid/tau burden or reduced dementia risk when therapy is initiated close to menopause, although results are not uniform and research is ongoing.

All of this has strengthened the “timing” or window-of-opportunity hypothesis: the effects of hormones depend greatly on when they are started (age and years since the last menstrual period) and on the type of estrogen and progestogen used.

It is also important to note that modern menopausal hormone therapy is based on the use of bioidentical hormones, primarily progesterone and estradiol, which are not equivalent to the synthetic hormones commonly referred to as progestins and estrogens that were also included in many of these studies. This distinction is critical, as many historical risks associated with hormone therapy stem from the use of progestins (such as Provera) or conjugated estrogens (such as Premarin), which are very different from the biological profile of molecules that the human body naturally produces or recognizes, such as bioidentical hormones.

The superiority of bioidentical hormones lies in the fact that the body recognizes them as its own, allowing them to exert specific effects on human receptors without significant off-target activation of unwanted pathways. In contrast, progestins and commercially available “progestogens” may also bind to androgenic or mineralocorticoid receptors, generating side effects.

Do risks still exist?

Yes, depending on the type of hormone, the route of administration, and the individual woman’s characteristics. Some hormones may increase the risk of venous thrombosis and stroke, particularly in older women, smokers, those with obesity, or those with pre-existing risk factors, and especially with high-dose oral estrogens.

Certain regimens combining estrogen with specific synthetic progestogens may slightly increase the risk of breast cancer after several years of continuous use. This is why choosing estradiol and progesterone in a balanced way, along with appropriate monitoring, is essential. The decision to treat a particular woman must remain individualized, taking into account personal and family history.

In fact, several experts have warned that enthusiasm for potential cardiovascular and neurological benefits should not be interpreted as a “free pass” to prescribe hormones to any woman. Consulting a healthcare professional who is experienced and up to date in this field remains essential.

What does this mean for you as a patient?

At Neolife, transparency and scientific rigor are central to how we share information with our patients, and we believe this update opens the door to more honest and nuanced conversations. If you are in perimenopause or within the first 10 years after menopause and experience bothersome symptoms (hot flashes, insomnia, vaginal dryness, mood changes) or have risk factors for osteoporosis, we can evaluate Menopausal Hormone Therapy not only as a symptomatic treatment but also as part of a long-term prevention strategy. Even if many years have passed since menopause, or if you have a history of thrombosis or hormone-dependent cancer, we will likely prioritize other treatment options, as the type of therapy (oral, transdermal, vaginal), dosage, and whether or not to combine with progesterone must be decided on a case-by-case basis after careful assessment.

Our approach at Neolife integrates these new recommendations with a thorough evaluation of personal and family history, as well as complementary studies. We favor bioidentical estradiol and micronized progesterone, which are the most extensively studied molecules and generally have the best safety profile. We also maintain close follow-up with each patient, with regular reviews to assess efficacy, potential side effects, and changes in risk factors, alongside lifestyle guidance.

In conclusion, the decision by the HHS and the FDA to remove the former “black box” warnings finally acknowledges what we at Neolife have long understood through continuous scientific updating: that current evidence paints a very different picture from that of 2002, and that when properly indicated and initiated at the right time, hormone therapy is a powerful tool not only for symptom relief but also for protecting bone and cardiovascular health in many women—adding more life to years.

If you are at this stage of life and have questions, we encourage you to reach out to us. The most important thing is to discuss it with a professional trained in hormone therapy, who can explain options, benefits, and risks transparently, and help you decide together what is best for you.

BIBLIOGRAPHY

(1) S. Department of Health and Human Services. (2024). HHS advances women’s health: Removes misleading FDA warnings on hormone replacement therapy. FDA Press Announcements

(2) Food and Drug Administration. (2025). FDA expert panel on menopause and hormone replacement therapy for women, 07/17/2025. FDA Expert Panels.

(3) Danish Osteoporosis Prevention Study (DOPS)

La entrada Hormone Therapy in Menopause se publicó primero en Neolife.

Estrogens are crucial for skin health due to their ability to modulate collagen synthesis. They have been shown to increase the activity of fibroblasts—cells responsible for producing collagen and elastin in the dermis—which enhances skin elasticity and hydration.

Studies have shown that estrogen therapy can increase collagen production in postmenopausal skin by approximately 48% after six months of treatment.

Dr. Galán – Neolife Medical Team

During menopause, collagen levels drop significantly, affecting both skin elasticity and hair density and quality.

Menopause is a transitional period in a woman’s life characterized by a decline in the production of sex hormones such as estrogens, testosterone, and progesterone. These hormones play fundamental roles in the homeostasis of various tissues, including skin and hair, which undergo noticeable changes during this phase.

The skin, the largest organ in the human body, and hair follicles highly depend on proper hormonal balance, particularly in terms of collagen synthesis and preservation. Collagen is an essential structural protein that provides elasticity, firmness, and strength. Its loss can lead to noticeable aesthetic changes such as wrinkles, skin laxity, and hair thinning.

Collagen in Skin and Hair

Type I and Type III collagen are the two predominant forms found in the dermis and play a vital role in maintaining skin’s structural integrity. The collagen fiber network not only provides mechanical support but also facilitates cellular regeneration, particularly in hair follicles. During menopause, collagen levels drop significantly, impairing skin elasticity and hair quality. Dermal collagen loss with age contributes to reduced follicle viability and a shorter anagen (growth) phase of the hair cycle, resulting in thinner, more fragile hair.

Changes in Postmenopausal Collagen Levels

Numerous studies have shown that, within the first five years after menopause onset, women experience up to a 30% reduction in dermal collagen, especially in the face and neck area (Brincat et al., 2005). This phenomenon is more pronounced in sun-exposed skin due to the combination of hormonal decline and accumulated UV damage. Accelerated postmenopausal skin aging is associated with decreased collagen and elastin synthesis, leading to a greater susceptibility to wrinkle formation, increased skin fragility, and noticeable volume loss in the facial area.

Additionally, in the scalp, the decline in sex hormones and collagen loss contribute to hair follicle miniaturization, a pathological process that can result in excessive hair shedding and the development of diffuse or female-pattern baldness.

The Role of Estradiol in Skin and Hair Health

Estrogens are crucial for skin health due to their ability to modulate collagen synthesis. Studies have shown that estrogens increase fibroblast activity, the cells responsible for producing collagen and elastin in the dermis, which improves skin elasticity and hydration (Thornton, 2013). Estradiol (E2) enhances fibroblast activity by binding to its specific receptors, primarily ER-α and ER-β. These receptors activate intracellular signaling pathways such as PI3K/Akt and MAPK/ERK, promoting fibroblast proliferation and differentiation. Additionally, estradiol stimulates the production of growth factors like TGF-β (Transforming Growth Factor Beta), which in turn increases Type I and III collagen synthesis.

• Increased collagen production: Studies have demonstrated that estrogen therapy can increase collagen production in postmenopausal skin by approximately 48% after six months of treatment (Phillips et al., 2001).
• Impact on skin elasticity: Research has shown an increase in skin elasticity and thickness, along with a reduction in collagen fiber fragmentation, thereby improving skin firmness and resilience.

Estrogens also play an important role in regulating matrix metalloproteinases (MMPs), enzymes that degrade collagen fibers. MMPs, particularly MMP-1 (collagenase), MMP-3, and MMP-9, break down collagen in the extracellular matrix. During menopause, the decline in estrogen levels increases the activity of these enzymes, accelerating collagen degradation. Estradiol modulates MMP expression through estrogen receptor (ER) pathways, inhibiting MMP gene transcription and promoting the activity of tissue inhibitors of metalloproteinases (TIMPs), which helps preserve collagen integrity and delay wrinkle formation.

Additionally, estrogens prolong the anagen phase of the hair cycle—the active growth phase—contributing to denser and more voluminous hair.

The Role of Testosterone in Skin and Hair Health

• Sebaceous Secretion

Testosterone stimulates the sebaceous glands, increasing sebum production. In postmenopausal women receiving testosterone therapy, an increase in sebaceous gland activity has been observed. This effect is due to the conversion of testosterone into dihydrotestosterone (DHT) by the enzyme 5-alpha reductase in the skin, which enhances sebaceous activity.

• Skin Thickness, Collagen, and Elastin

The decline in estrogen levels during menopause leads to a reduction in collagen and elastin synthesis, essential proteins for skin firmness and elasticity. Although testosterone is not the primary hormone regulating these proteins, some studies suggest that testosterone therapy may partially counteract collagen loss and improve skin thickness. The proposed mechanism involves the conversion of testosterone into estrogens via the aromatase enzyme in skin tissues, which may stimulate collagen and elastin production.

• Wrinkle Depth

The reduction in collagen and elastin during menopause contributes to wrinkle formation and deepening. By potentially increasing the synthesis of these proteins, testosterone therapy may reduce wrinkle depth and improve overall skin appearance.

Comparing the Effects of Estradiol and Testosterone on Collagen Synthesis

Estradiol’s effect on collagen production is significantly stronger than that of testosterone. While estradiol directly activates the expression of collagen-related genes, testosterone has a less pronounced effect and largely depends on its conversion to estradiol via the aromatase enzyme in the skin. Comparative studies have shown that estradiol increases collagen production in postmenopausal skin by 48%, while testosterone has a modest effect, increasing synthesis by only 10-15% when administered in physiological doses (Shen et al., 2014).

The Role of Progesterone in Skin and Hair Health

Progesterone has a complementary role in hormonal balance and, as mentioned in previous discussions, is a vital hormone in the context of hormone replacement therapy (HRT). In this context, it plays an additional role in modulating the androgenic effects of testosterone by acting as an inhibitor of 5-alpha reductase, reducing the conversion of testosterone into DHT. This helps mitigate potential adverse effects on the scalp in predisposed women. Additionally, progesterone promotes skin hydration and may improve overall hair quality by preventing hair loss and maintaining proper hormonal balance.

Overall Impact of Hormone Replacement Therapy (HRT) on Skin and Hair

Clinical studies have evaluated the impact of HRT on the skin and have shown that estrogen treatment reduces wrinkle depth by 30% to 40% after one year of therapy (Sumino et al., 2004). This is associated with an increase in dermal collagen content and improved skin hydration.

Histological studies in postmenopausal women receiving HRT have shown a significant increase in Type III collagen, particularly in the first year of treatment, suggesting an improvement in skin elasticity and firmness (Sumino et al., 2004). Additionally, HRT has also been shown to reduce hair loss and improve hair thickness in women suffering from postmenopausal androgenetic alopecia.

BIBLIOGRAPHY

(1) Brincat, M., Baron, Y. M., & Galea, R. (2005). Estrogens and the skin. Climacteric, 8(2), 110-123. https://doi.org/10.1080/13697130500118195

(2) Thornton, M. J. (2013). Estrogens and aging skin. Dermato-endocrinology, 5(2), 264-270. https://doi.org/10.4161/derm.22805

(3) Sumino, H., Ichikawa, S., Abe, M., Endo, Y., Kumakura, H., Takayama, Y., … & Kurabayashi, M. (2004). Effects of hormone replacement therapy on skin composition and aging in postmenopausal women. Journal of Dermatological Science, 35(3), 191-198. https://doi.org/10.1016/j.jdermsci.2004.06.004

(4) Zouboulis, C. C. (2009). Androgens and the sebaceous gland. Dermatologic Therapy, 22(5), 288-294. https://doi.org/10.1111/j.1529-8019.2009.01245.x

(5) Bolke, L., Schlippe, G., Gerß, J., Voss, W. (2019). A collagen supplement improves hair growth and thickness in women suffering from temporary hair thinning. Journal of Cosmetic Dermatology, 18(6), 1501-1508. https://doi.org/10.1111/jocd.12930

(6) Shen, W., Wong, T., Cheng, S. (2014). Effects of estrogen and testosterone on collagen metabolism in dermal fibroblasts. Journal of Investigative Dermatology, 134(2), 403-410. https://doi.org/10.1038/jid.2013.345

La entrada Research has demonstrated that estrogen therapy can increase collagen production in postmenopausal skin by approximately 48% after six months of treatment. se publicó primero en Neolife.

A 2020 study involving more than 800 men followed since 2004 revealed that testosterone therapy not only does not increase the risk of prostate cancer but that the detected cases are less aggressive and have a better prognosis.

The fear of prostate cancer should not automatically be a reason to deny testosterone replacement therapy in hypogonadal men, as long as proper monitoring protocols are followed and any underlying prostate disease is first ruled out.

Dr. Sánchez – Neolife Medical Team

What does the new study say?

A long-term follow-up of men with testosterone levels consistent with hypogonadism (testosterone of 350 ng/dL or 3.5 ng/mL) shows that testosterone therapy does not increase the incidence of prostate cancer — a risk historically attributed to this treatment — and, when it does occur, the tumors tend to be less aggressive than in men not receiving testosterone therapy.

What was studied and what were the findings?

A total of 428 men received testosterone therapy (T group) and 395 did not (control group, CTRL). The results are clear: only 2.8% of men treated with testosterone developed prostate cancer, compared with 11.1% in the untreated group.

Even more, in the testosterone-treated group, prostate cancer appeared only within the first 18 months of treatment, and most tumors were low grade (less aggressive). In contrast, in the untreated group, tumors tended to be more invasive and aggressive (higher Gleason scores).

Importantly, in the testosterone-treated group, no recurrences or prostate cancer–related deaths occurred, unlike the control group, where recurrences and 12 deaths were recorded during follow-up. Notably, almost all men treated with testosterone were able to resume therapy after surgery.

Conclusion: What are the implications?

Estos datos respaldan la seguridad de la terapia con testosterona en varones adecuadamente seleccionados que durante más de 30 años se ha ido demostrando (p.ej. el estudio TRAVERSE, ya comentado anteriormente en la newsletter de Julio 2024 ‘‘Cómo la TRHB puede reducir la mortalidad y el riesgo de padecer cáncer’’, disipando uno de los grandes temores en la práctica médica y abriendo la puerta a mejorar la calidad de vida de muchos hombres con seguridad y controles periódicos.

It turns out that testosterone not only appears to be safe, but may also be protective against the feared prostate cancer, as it is associated with less severe tumors when proper patient selection and follow-up are ensured.

Los estudios más recientes aportan tranquilidad: no existe una relación entre los niveles endógenos de Recent studies bring further reassurance: there is no link between endogenous testosterone levels and the development of prostate cancer. Moreover, exogenous testosterone therapy has not been shown to increase PSA levels or the risk of developing this type of cancer. In fact, contrary to what was once believed, high-grade prostate cancer has been associated with low testosterone levels in the blood (1).

To date, clinical studies have also confirmed that testosterone does not increase the risk of heart attack, and there is no evidence linking its use to a higher risk of prostate cancer—concerns that previously made physicians hesitant to prescribe this therapy. These findings align with the American Urological Association (AUA) recommendations, which since 2018 have stated that men undergoing testosterone therapy do not have a higher risk of developing prostate cancer—something these studies now strongly support.

The fear of prostate cancer should not automatically be a reason to deny testosterone replacement therapy in hypogonadal men, as long as proper monitoring protocols are followed and any hidden prostate disease is ruled out beforehand.

At Neolife, we consider it essential to inform patients that current evidence does not show an increased risk of prostate cancer associated with testosterone therapy in these contexts. We emphasize the importance of proper urological monitoring and individualized patient assessment in every case.

BIBLIOGRAPHY

(1) Raynaud, J.-P. (2009). Testosterone deficiency syndrome: Treatment and cancer risk. The Journal of Steroid Biochemistry and Molecular Biology , 114(1–2), 96–105.

(2) S. Haider, A. Haider, X. Xu, 376 Prostate Cancer (PCa) Incidence and Severity in 823 Hypogonadal Men With and Without Testosterone Therapy (TTh) in a Controlled, Observational Registry Implying 7,116 Patient-years, The Journal of Sexual Medicine, Volume 17, Issue Supplement_1, January 2020, Page S105, https://doi.org/10.1016/j.jsxm.2019.11.221

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Melatonin has evolved from being considered merely the “sleep hormone” to a systemic modulator with significant effects on cardiovascular, metabolic, immune, and cognitive health. Recently, some controversy arose following the publication of preliminary observational data suggesting a possible association between long-term melatonin use and an increased risk of heart failure.

However, a critical review and detailed analysis of the information published by the American Heart Association (AHA) indicate that these types of studies do not establish a causal relationship and have important limitations. This is because they rely on large population databases and lack control over key factors such as dosage, duration of use, comorbidities, and participants’ sleep quality. These limitations reduce the clinical relevance of the findings, which should be interpreted as hypothesis-generating rather than definitive conclusions. For this reason, at Neolife we aim to share, with scientific rigor, the beneficial properties of melatonin beyond its role in regulating the circadian rhythm.

Dr. Sánchez – Neolife Medical Team

Beyond Sleep: A Key Molecule in Global Homeostasis

To date, no randomized clinical trials have confirmed any direct adverse effect of melatonin on the cardiovascular system. On the contrary, improving sleep quality—one of its main functions—helps reduce the risk of hypertension, diabetes, inflammation, and cardiovascular mortality.

What we do know about melatonin is that it shortens sleep latency and improves overall sleep quality, particularly in cases of sleep-onset insomnia. Moreover, it has a clear antioxidant effect and acts as an immune regulator with potential neuroprotective properties. And, importantly, it has a superior safety profile compared to benzodiazepines—melatonin does not cause dependence or cognitive impairment.

In recent years, melatonin has been found to play a fundamental role in maintaining the balance of the gut microbiome, opening up new therapeutic perspectives. It is now known that the gut contains concentrations of melatonin up to 400 times higher than those found in the brain. Melatonin is not only produced in the pineal gland but also in the gastrointestinal tract, where it acts locally on enteric receptors to modulate motility, immunity, and intestinal permeability.
This production occurs through intestinal bacteria, which can influence the conversion of tryptophan into serotonin—and subsequently into melatonin—directly affecting both its systemic production and function. This explains why patients with dysbiosis (an imbalance in the gut flora) often experience sleep disturbances, circadian rhythm alterations, and mood disorders.
Melatonin promotes the growth and maintenance of beneficial bacteria such as Lactobacillus and Bifidobacterium, while reducing pro-inflammatory species (LPS-producing bacteria), thus promoting a state of eubiosis (microbial balance). This activity helps reduce intestinal inflammation, improve mucosal integrity, and enhance immune response.

Melatonin is the only hormone with antioxidant properties, and its interaction with the microbiota reduces oxidative stress and inflammatory markers (TNF-alpha, IL-6), improving insulin sensitivity, lipid metabolism, and neuroendocrine regulation through the gut–brain axis.

Multiple studies suggest potential benefits of melatonin as an adjunct treatment in irritable bowel syndrome, stress- or antibiotic-induced dysbiosis, metabolic diseases (such as insulin resistance and obesity), and neurodegenerative disorders including Parkinson’s and Alzheimer’s.

Paradoxically, the same mechanisms that some observational studies have linked to cardiovascular harm are, in fact, those that protect the endothelium and reduce systemic inflammation, as supported by physiological evidence. Through its antioxidant action and its influence on the gut microbiome, melatonin reduces lipid peroxidation, enhances mitochondrial function (ATP production, i.e., energy), promotes a healthier lipid profile, regulates blood pressure and heart rate variability, and modulates the autonomic balance between the sympathetic and parasympathetic systems (vagal tone).

The bidirectional interaction between melatonin and the microbiome is emerging as an essential mechanism in the regulation of multiple physiological functions. Modulating this axis represents a promising therapeutic pathway in inflammatory, metabolic, and neurological disorders.

In this context, melatonin transcends its traditional role as a sleep regulator—it acts as a global modulator of the circadian–immune–microbial axis, with far-reaching effects on cardiovascular, metabolic, and neuroendocrine health.

Taken together, melatonin’s overall impact on the body is protective and homeostatic, especially when dosing and treatment are personalized by healthcare professionals.
At Neolife, the regulation of the circadian rhythm and quality sleep are considered fundamental pillars of treatment, with proven benefits for our patients’ well-being. We know that melatonin supplementation can help restore gut ecosystem balance (eubiosis) and serve as an adjunct therapy in conditions such as irritable bowel syndrome, stress-induced dysbiosis, and certain metabolic or neurodegenerative diseases.

The current clinical challenge lies in personalizing its use, adapting it to each individual’s age, chronotype, gut microbiome status, comorbidities, and clinical goals. While we await further research, current evidence supports a rational, safe, and medically supervised use of melatonin within a comprehensive, integrative approach to overall health and healthy longevity.

BIBLIOGRAPHY

(1) Iesanu, M. I., Zahiu, C. D. M., Dogaru, I.-A., Chitimus, D. M., Pircalabioru, G. G., Voiculescu, S. E., Isac, S., Galos, F., Pavel, B., O’Mahony, S. M., & Zagrean, A.-M. (2022). Melatonin–Microbiome Two-Sided Interaction in Dysbiosis-Associated Conditions. Antioxidants, 11(11), 2244. https://doi.org/10.3390/antiox11112244

(2) American Heart Association. Long-term use of melatonin supplements to support sleep may have negative health effects. News release, 3 Nov 2025.

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The combination of bioidentical estradiol and micronized progesterone has shown, according to scientific literature, no association with thrombotic events or an increased risk of breast cancer.

The warnings about hormone replacement therapy (HRT) date back to 2002, when the Women’s Health Initiative (WHI) study linked the combined therapy CEE + MPA (Conjugated Equine Estrogens + Medroxyprogesterone Acetate) to an increased risk of breast cancer and cardiovascular events.

Dr. Alfonso Galán – Neolife Medical Team

Women suffering from debilitating symptoms were kept away from an effective treatment due to unfounded fears, losing quality of life as well as bone and vascular protection.

In July 2025, the U.S. Food and Drug Administration (FDA) convened a panel of experts to reevaluate the evidence surrounding Hormone Replacement Therapy (HRT) in menopausal women. This marks a turning point in the institutional narrative that, for decades, has been dominated by fear, black box warnings, and a distorted perception of risk.

At Neolife, we welcome this step as an act of scientific and medical justice — but also as a reminder of the great harm that misinformation about HRT has caused. In this article, we analyze in depth the panel’s conclusions, the key studies discussed, and, above all, the fact that the formulations we use at Neolife (bioidentical estradiol and micronized progesterone) have shown no increase in cardiovascular or cancer risk.

What Was Said at the FDA Panel?

1. Removal of the most severe warnings (black box warnings) for certain forms of HRT.
2. Recognition of previously minimized benefits: cardiovascular protection, improved bone health, reduction of hot flashes, and enhanced mood—especially in women under 60 or within the first 10 years after menopause.
3. Lack of differentiation between formulations: one major criticism was the failure to distinguish between treatments using conjugated equine estrogens (CEE) and medroxyprogesterone (MPA), versus bioidentical options.

The Legacy of the WHI and Its Consequences

The warnings about HRT trace back to 2002, when the Women’s Health Initiative linked CEE + MPA to an increased risk of breast cancer and cardiovascular events. However, in the years since, it has become clear that:

• The observed risk does not apply to all formulations or all women.
• The late age of treatment initiation (average age in WHI: 63 years) distorted the outcomes.
• The study did not use bioidentical estrogens or micronized progesterone.

As a result, millions of women gave up a beneficial therapy based on fears that we now consider unfounded for many patients.

Current Evidence: What Does Science Say About Bioidentical HRT?

Studies such as E3N (France) have demonstrated that oral bioidentical estradiol combined with micronized progesterone does not increase breast cancer risk (RR: 0.9).

A meta-analysis (Scarabin, 2018) confirms that the safest combination is transdermal estradiol plus micronized progesterone, with no significant increase in thromboembolic risk.

Differences between formulations

The Neolife Approach: Evidence, Personalization, and Safety

At Neolife, we use HRT in a personalized and evidence-based manner, with:

• Bioidentical estradiol
• Micronized progesterone
• Regular clinical and laboratory monitoring

This combination has consistently shown no association with thrombotic events or increased breast cancer risk in the short- to medium-term scientific literature.

What Happens Next?

If the FDA is now willing to reconsider its most severe warnings based on current evidence, the next logical step would be to retract and acknowledge the harm caused over the past two decades.
Women with debilitating symptoms were denied an effective treatment due to misplaced fears, losing not only quality of life but also bone and vascular protection.

Medicine must have the courage to correct its course. Today, we know that well-prescribed, bioidentical, and personalized HRT is a powerful, effective, and safe tool for many women.

Conclusion

The FDA panel marks a shift in direction, but there is still a long road ahead — many physicians and patients remain to be educated. At Neolife, we have long applied an evidence-based approach, free from dogma and with safety as our top priority. It is time to rewrite the narrative of HRT — with science, prudence, and respect for women’s health.

BIBLIOGRAPHY

(1) Scarabin, P. Y. (2018). Progestogens and venous thromboembolism in menopausal women: an updated oral versus transdermal estrogen meta-analysis. Climacteric, 21(4), 341–345.

(2) Fournier, A. et al. (2008). Use of different postmenopausal hormone therapies and risk of histology- and hormone receptor-defined invasive breast cancer. Journal of Clinical Oncology, 26(8), 1260–1268.
(E3N cohort, Francia)

(3) Manson, J. E. et al. (2013). Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women’s Health Initiative randomized trials. JAMA, 310(13), 1353–1368.

(4) The NAMS 2022 Hormone Therapy Position Statement Advisory Panel. (2022). The 2022 Hormone Therapy Position Statement of The North American Menopause Society. Menopause, 29(7), 767–794.

(5) FDA Expert Panel on Menopause and Hormone Replacement Therapy (2025). U.S. Food & Drug Administration Public Meeting Archive: July 17, 2025.

La entrada The FDA Reconsiders Its Warnings on Hormone Therapy in Menopause: The Beginning of a New Era for Women’s Health? se publicó primero en Neolife.

The impact of testosterone on mood and mental health is also significant.

Men with low testosterone levels often experience symptoms such as fatigue, irritability, difficulty concentrating, and depression. Low testosterone is also a significant risk factor for cardiovascular diseases, including atherosclerosis.

Dr. Alfonso Galán – Neolife Medical Team

Testosterone levels typically peak between the ages of 20 and 30. From around age 30–35, levels begin to decline gradually at an approximate rate of 1% per year. This gradual decline, known as late-onset hypogonadism or “andropause,” can be accelerated by various factors.

Testosterone (T) is an essential hormone in the male body, playing a fundamental role not only in the development of secondary sexual characteristics but also in a wide range of functions affecting physical and mental health.

Although often associated with youth and vitality—and trivialized as a hormone that only enhances sexual performance or helps build muscle—maintaining healthy levels of free testosterone in older men can have deep and lasting benefits for overall health and quality of life. In the following lines, we’ll explain how testosterone influences areas such as cardiovascular health, mood, body composition, and more, as well as the factors that contribute to its age-related decline.

The Decline of Testosterone With Age

Testosterone levels typically reach their peak between the ages of 20 and 30. After 30–35, levels begin to gradually decrease at a rate of about 1% per year. This slow decline, referred to as late-onset hypogonadism or “andropause,” can be accelerated by factors such as chronic stress, obesity, physical inactivity, excessive alcohol intake, poor diet, and chronic diseases like type 2 diabetes.

Testosterone circulates in the blood in three main forms: bound to proteins such as sex hormone-binding globulin (SHBG), loosely bound to albumin—the most abundant protein in the body—and free. It is this free testosterone that is biologically active and available to the body’s tissues, and it is the primary metric we focus on in lab testing to assess the real status of our male patients. With age, not only do total testosterone levels decrease, but SHBG levels also increase, further reducing the free fraction, while the weaker bond with albumin only partially compensates for the loss of bioavailable testosterone.

Factors Affecting Testosterone Production With Age

In addition to natural aging, several factors can contribute to reduced testosterone production:

1. Chronic stress: Persistent stress raises cortisol levels, a hormone that inhibits testosterone production in the testes.
2. Obesity: Body fat, especially abdominal fat, converts testosterone into estrogen via the enzyme aromatase, lowering the availability of free testosterone.
3. Physical inactivity: Lack of exercise reduces stimulation for testosterone synthesis. Physical activity—especially strength training—is a powerful promoter of testosterone production.
4. Nutrient deficiencies: Minerals like zinc and magnesium, as well as vitamin D, are essential for testosterone synthesis. Deficiencies in these nutrients can limit hormone production.
5. Poor sleep quality: Testosterone is primarily produced during deep sleep. Inadequate rest can significantly reduce its levels.
6. Alcohol and tobacco consumption: Both negatively affect testicular function and testosterone production.

Here are some key strategies to optimize testosterone production: manage stress, engage in strength training, eat a nutritious diet, get adequate sleep, avoid smoking, and limit alcohol. It’s no coincidence that the absence of these good habits is linked to worse aging outcomes—testosterone is one of the mechanisms through which lifestyle profoundly impacts health.

Cardiovascular Benefits of Maintaining Optimal Testosterone Levels

The relationship between testosterone and cardiovascular health has been extensively researched. For many years, it was mistakenly believed that high testosterone levels increased cardiovascular risk. However, more recent studies have shown that low testosterone levels are, in fact, a significant risk factor for cardiovascular diseases, including atherosclerosis. Among these studies:

1. A meta-analysis published in The Journal of Clinical Endocrinology & Metabolism (2011) linked low testosterone levels to a higher risk of cardiovascular mortality.
2. A longitudinal study by Vikan et al. (2009) demonstrated an inverse relationship between free testosterone and the development of subclinical atherosclerosis.
3. Research by Shores et al. (2006), published in Archives of Internal Medicine, showed that testosterone replacement therapy (TRT) may reduce mortality in men with testosterone deficiency.
4. The “Testosterone Trials,” published in The New England Journal of Medicine (2016), involving over 700 older men with low testosterone, demonstrated significant improvements in bone density, anemia, and sexual function, without an increase in cardiovascular events.
5. A 2023 study in The Journal of the American College of Cardiology involving a large cohort showed that testosterone replacement therapy in men with hypogonadism was associated with a significant reduction in major cardiovascular events, such as heart attacks and strokes, reinforcing the safety and cardiovascular benefits of this intervention in selected populations.

Testosterone supports cardiovascular health by promoting vasodilation, improving blood flow, and reducing inflammation. It also helps regulate cholesterol levels by lowering LDL (“bad” cholesterol) and increasing HDL (“good” cholesterol). When testosterone levels are low, plaque buildup in arteries (atherosclerosis) increases, which can lead to heart attacks and strokes.

Moreover, TRT in testosterone-deficient men has been shown to significantly improve endothelial function, reduce arterial stiffness, and enhance overall cardiovascular health markers. This suggests that maintaining optimal testosterone levels is not only beneficial but crucial in preventing cardiovascular diseases in older men.

Testosterone and Emotional and Sexual Well-Being

Testosterone has a major impact on mood and mental health. Men with low levels often report fatigue, irritability, trouble concentrating, and depression. This is partly because testosterone affects the production of key neurotransmitters like serotonin and dopamine, which regulate mood and feelings of well-being.

Several studies have shown that testosterone replacement therapy can significantly improve depressive symptoms in men with hypogonadism.

For example, a study published in The Aging Male (2020) assessed 200 men treated with TRT and found significant improvements in depression, anxiety, and overall quality of life. Similarly, a randomized controlled trial published in The Journal of Clinical Psychiatry (2019) found that men with hypogonadism treated with TRT showed greater improvements in mood and general well-being compared to the placebo group. Adequate testosterone levels are also associated with increased confidence, motivation, and stress resilience. This positive effect on mood not only improves quality of life but also directly influences productivity, relationships, and—as we see in clinical practice daily—our patients’ ability to make lifestyle changes as they feel more driven and determined.

Testosterone also plays a critical role in sexual function, desire, and erection. This is far from frivolous, as a satisfying sex life adds years to our life and life to our years. Testosterone enhances libido by stimulating brain areas related to arousal, supports tissue elasticity—which improves both sexual performance and the appearance of the genitals—and increases blood flow to the genitals, enhancing erection quality. It also promotes erectile tissue health, improving responsiveness to stimulation. Adequate testosterone levels can even enhance the flaccid appearance of the penis by promoting better vascularization, making it appear fuller and better shaped.

Testosterone, Muscle, and Fat

Testosterone is essential for maintaining muscle mass and regulating body fat. It stimulates protein synthesis in muscles, promoting growth and recovery. At the same time, it helps mobilize fat stores by increasing insulin sensitivity and improving lipid metabolism.

As testosterone levels decline, men tend to lose muscle and gain fat, particularly around the abdomen. These changes in body composition not only affect appearance but also increase the risk of metabolic diseases such as type 2 diabetes. Studies have shown that TRT can reverse these effects, supporting fat loss and muscle gain—even in older men.

Conclusion

Maintaining healthy free testosterone levels in older men is neither a frivolity nor a luxury—it is a necessity for ensuring a long, healthy, and fulfilling life.

From preventing cardiovascular disease to enhancing mood, body composition, and overall quality of life, testosterone plays an integral role in male well-being.

With a combination of healthy lifestyle choices, regular exercise, a balanced diet, and—when necessary—medical interventions like TRT, it is possible to maintain optimal hormone levels well into old age. Prioritizing hormonal health not only helps prevent many aging-related conditions but also enables a more active and satisfying life.

BIBLIOGRAPHY

(1) Ohlsson, C., et al. (2011). Low testosterone levels are associated with increased mortality in men: a meta-analysis. The Journal of Clinical Endocrinology & Metabolism, 96(10), 3007-3019.

(2) Vikan, T., et al. (2009). Serum levels of testosterone and carotid atherosclerosis progression in men with and without cardiovascular disease. The 5th Tromsø Study, European Journal of Preventive Cardiology.

(3) Shores, M. M., et al. (2006). Testosterone treatment and mortality in men with low testosterone levels. Archives of Internal Medicine, 166(15), 1660-1665.

(4) Snyder, P. J., et al. (2016). Effects of Testosterone Treatment in Older Men. New England Journal of Medicine, 374(7), 611-624.

(5) Alexander, G. C., et al. (2023). Association Between Testosterone Replacement Therapy and Major Adverse Cardiovascular Events: A Large Cohort Study. The Journal of the American College of Cardiology, 81(1), 1-15.

(6) Zitzmann, M., et al. (2020). Effects of testosterone therapy on symptoms of depression in hypogonadal men: A longitudinal study. The Aging Male, 23(1), 1-7.

(7) McIntyre, R. S., et al. (2019). Testosterone augmentation in major depressive disorder: A randomized, double-blind, placebo-controlled trial. The Journal of Clinical Psychiatry, 80(5), e1-e8.

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From the age of 40, the symptoms of aging become more noticeable, often appearing earlier and negatively affecting many aspects of our lives. This is largely due to a decline in hormone levels.

Neolife offers optimal management of this hormonal imbalance, ensuring long-term effectiveness and safety. For over 10 years, we’ve been providing our patients in Madrid and Marbella with the best available options, which have consistently delivered successful results.

Dr. César Montiel – Medical Team Neolife

Hormonal deficiency

Adult male androgen deficiency is caused by low testosterone levels, which are associated with a series of symptoms: irritability, sadness, loss of muscle mass, decreased sexual desire, worsening of erection quality, fatigue, and lack of vitality. These hormone-related issues don’t stop there—they are clearly linked to certain health conditions such as cardiovascular disease, fall risk, osteoporosis, depression, aggressive prostate cancer, metabolic disorders (type 2 diabetes, obesity, dyslipidemia), and neurodegenerative diseases.

On the other hand, the symptoms caused by a lack of female hormones such as estradiolthe progesteron and the testosteronewhich we address in our treatments menopauseare numerous and varied: hot flashes, mood swings, depression, anxiety, irritability, weight gain (fat), muscle loss, vaginal dryness, pain during intercourse, loss of libido, urinary incontinence, memory issues, difficulty concentrating, insomnia… in addition to less noticeable effects such as increased cholesterol levels, insulin resistance, higher cardiovascular risk, loss of bone mass, and cognitive decline associated with Alzheimer’s disease, among others.

What are the steps to begin a Bioidentical Hormone Replacement Therapy (BHRT) program at Neolife?

1. Completion of a preliminary questionnaire, after which our medical team will assess whether you are a suitable candidate and determine which biomarkers need to be tested.
2. Initial consultation, where a personalized prescription for Bioidentical Hormone Replacement Therapy will be made.
3. Start of the hormone treatment prescribed by our medical team.
4. Ongoing monitoring and treatment maintenance. After the initial 4–5 weeks, a blood test will be requested to assess the early results. From there, blood tests will be scheduled every 3–5 months, with intervals adjusted to each individual’s needs. These results will be used to personalize the next phase of treatment.

If you’re interested, contact us!

• Madrid Clinic: 917 32 59 50
• Marbella Clinic: 951 30 44 88

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Women with high progesterone levels during the luteal phase have up to a 30% lower risk of developing breast cancer compared to those with low levels.

Additionally,progesterone has calming and anxiolytic effects, mediated by its ability to modulate GABA receptors in the brain, which explains its role in improving sleep quality and reducing stress. It is also linked to more intense and satisfying orgasms.

Dr. Alfonso Galán – Neolife Medical Team

Women with balanced progesterone levels report greater relaxation and a better quality of life.

Progesterone is a vital steroid hormone that plays a crucial role in female physiology, particularly in the menstrual cycle, pregnancy, and reproductive health. However, its function is not limited to these aspects, as it also acts as a protective hormone in various organs and systems, contributing to disease prevention and overall well-being. Despite its importance in women, progesterone is not commonly used in men due to its effects on sexual function and male hormonal balance. Let’s delve deeper into all of this.

Physiological Functions of Progesterone in Women

Progesterone is mainly produced by the corpus luteum in the ovaries after ovulation and, in smaller amounts, by the adrenal glands and, during pregnancy, by the placenta. Its blood concentration varies throughout the menstrual cycle, peaking during the luteal phase. The luteal phase is the second half of the menstrual cycle, beginning after ovulation and ending with the onset of menstruation. During this phase, the ovarian follicle transforms into the corpus luteum, which produces progesterone. This hormone is essential for thickening and maintaining the endometrium (the innermost layer of the uterus), preparing it for the potential implantation of a fertilized egg. If pregnancy does not occur, the corpus luteum degenerates, causing progesterone levels to drop and leading to menstruation.

Below is a graph illustrating progesterone, estrogen, and other hormone levels throughout the menstrual cycle, along with changes in the endometrium and corpus luteum:

Among its physiological functions, the following stand out:

1. Regulation of the menstrual cycle: Progesterone prepares the endometrium for the implantation of a fertilized egg. If implantation does not occur, its levels drop, triggering menstruation.
2. Support of pregnancy: During gestation, progesterone maintains the endometrium and prevents premature uterine contractions.
3. Mammary gland development: Progesterone contributes to the development of mammary ducts and preparation for lactation.
4. Metabolic effects: Progesterone regulates glucose levels and plays a role in thermogenesis.

Progesterone and Endometrial and Breast Protection

One of the most relevant aspects of progesterone is its protective role in the endometrium and breasts. Adequate progesterone levels have been shown to reduce the risk of endometrial hyperplasia and endometrial cancer by counteracting the proliferative effect of estrogen.

In breast tissue, progesterone regulates cell proliferation, preventing excessive growth that could predispose individuals to breast cancer. Observational and clinical studies have shown that women with healthy progesterone levels have a lower incidence of breast cancer and reduced all-cause mortality.

A meta-analysis published in the Journal of Clinical Endocrinology & Metabolism indicated that women with high progesterone levels during the luteal phase have up to a 30% lower risk of developing breast cancer compared to those with low levels. Additionally, hormone therapies combined with natural progesterone have not shown the adverse event incidence observed in therapies using synthetic progestins.

Hormone Replacement Therapy and Progesterone

Hormone Replacement Therapy (HRT) is commonly used in postmenopausal women to relieve symptoms such as hot flashes, insomnia, and vaginal dryness. However, its effects go far beyond symptom relief. HRT has significant protective effects on bones, arteries, the heart, and the brain, reducing the risk of osteoporosis, cardiovascular diseases, and cognitive decline. The addition of progesterone to estrogen therapy is crucial for preventing endometrial hyperplasia. These protective effects make HRT an integral tool for well-being and disease prevention in postmenopausal women.

Numerous clinical studies have demonstrated that bioidentical progesterone—which is identical to the progesterone naturally produced by a woman’s body—is better tolerated and has a superior safety profile compared to synthetic progestins. Additionally, progesterone in HRT improves sleep quality, reduces anxiety, and contributes to an overall greater sense of well-being.

Calming Effects and Improved Sexual Health

Progesterone has calming and anxiolytic effects, mediated by its ability to modulate GABA receptors in the brain, explaining its role in improving sleep quality and reducing stress. Women with balanced progesterone levels report greater relaxation and a better quality of life.

In the sexual realm, progesterone plays an important role. It has been observed to contribute to better vaginal lubrication and increased sensitivity, which can enhance pleasure during sexual intercourse. Additionally, progesterone is linked to more intense and satisfying orgasms, thereby improving overall sexual health.

Progesterone in Men: Why Is It Not Used?

Despite its benefits in women, progesterone is not commonly used in men. This is because high progesterone levels can antagonize testosterone action, reducing libido and affecting erectile function.

There is some evidence that progesterone in men may have certain benefits in small amounts, such as reducing inflammation and supporting prostate health. However, excessive progesterone can lead to feminization symptoms, decreased sexual desire, and erectile dysfunction. Other studies have shown that progesterone administration in men can interfere with sperm production and reduce sexual responsiveness. This delicate balance is why progesterone is generally not used in men.

Conclusion

Progesterone is an essential hormone for women’s health, with functions that extend beyond reproduction. Its protective role in the endometrium and breast tissue makes it a key tool in cancer prevention and overall disease prevention. Additionally, its use in Hormone Replacement Therapy has been shown to improve quality of life, sexual health, and emotional well-being.

In men, however, its use is very limited and exceptional due to its adverse effects on sexual and hormonal function. Continued research in this field may provide new insights into the benefits and applications of progesterone in both sexes, but for now, its primary role remains in female health.

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