Fundamentals
Have you ever noticed a subtle shift in your daily rhythm, a quiet change in your energy, or a gradual alteration in how your body responds? Perhaps the morning vitality feels a little less vibrant, or recovery from exertion takes longer than it once did.
These are not merely signs of passing years; they are often whispers from your internal messaging system, the endocrine network, signaling deeper biological adjustments. Your lived experience, the feelings of diminished vigor or a lingering sense of being “off,” holds profound biological meaning. These sensations are direct reflections of cellular conversations happening within you, conversations orchestrated by hormones.
Understanding your own biological systems is the first step toward reclaiming vitality and function without compromise. We often perceive aging as an inevitable, uniform decline, yet the science reveals a far more intricate process. Cellular aging, the very mechanism by which our cells lose their youthful capacity, is not a simple, linear progression.
Instead, it is a complex interplay of molecular pathways, significantly influenced by the delicate balance of your hormonal environment. When this balance falters, the cellular machinery that maintains health and resilience begins to falter too, accelerating what we perceive as age-related changes.
Consider the cell’s internal clock, ticking away, meticulously regulating its functions. This cellular rhythm directly influences how you feel each day. Hormones act as the master conductors of this cellular orchestra, sending signals that dictate everything from energy production to repair processes.
When hormonal levels become insufficient, these signals weaken, and the cellular orchestra can fall out of sync. This can manifest as the very symptoms you might be experiencing ∞ persistent fatigue, changes in body composition, altered mood, or a general sense of not being your best self.
Hormonal balance is a critical determinant of cellular health and resilience, directly influencing the pace of biological aging.
At the core of cellular health are several fundamental biological processes that govern how cells function and endure. These processes, often referred to as the hallmarks of aging, include the maintenance of chromosomal ends, the integrity of genetic material, the efficiency of cellular powerhouses, and the body’s ability to clear cellular debris.
Each of these cellular functions is profoundly influenced by the presence and activity of various hormones. A deficit in these chemical messengers can disrupt these vital processes, leading to a cascade of effects that contribute to accelerated cellular aging.
Cellular Foundations of Longevity
Our cells possess protective caps at the ends of their chromosomes, known as telomeres. These structures safeguard genetic information during cell division. With each division, telomeres naturally shorten. When they become critically short, cells can no longer divide and enter a state of irreversible growth arrest, known as cellular senescence.
This process is a natural part of the aging continuum. Hormones, particularly sex steroids, play a significant role in regulating the enzyme responsible for maintaining telomere length, called telomerase. For instance, estrogen has been shown to influence telomerase activity, potentially slowing the rate of telomere shortening in certain tissues. A decline in estrogen levels, as seen in menopause, can therefore contribute to accelerated telomere attrition and subsequent cellular aging.
Another fundamental aspect of cellular health involves the mitochondria, often described as the power plants of the cell. These organelles generate the energy currency of the cell, adenosine triphosphate (ATP), through a process called oxidative phosphorylation. Efficient mitochondrial function is paramount for all cellular activities.
As we age, mitochondrial function can decline, leading to reduced energy production and an increase in harmful byproducts known as reactive oxygen species (ROS). This imbalance between ROS production and the body’s antioxidant defenses results in oxidative stress. Hormones are deeply intertwined with mitochondrial health.
Steroid hormone biosynthesis itself occurs within mitochondria, and these organelles provide the energy for hormone production and secretion. Deficiencies in hormones can impair mitochondrial efficiency, creating a vicious cycle where reduced energy leads to more oxidative stress, further damaging cellular components and accelerating aging.
Hormonal Signals and Cellular Resilience
The endocrine system acts as a sophisticated communication network, with hormones serving as messengers that transmit instructions throughout the body. When these messages are clear and consistent, cells operate optimally. When hormonal signals become weak or distorted, cellular processes can become dysregulated. This dysregulation extends to the body’s inflammatory responses.
Chronic, low-grade inflammation, often termed “inflammaging,” is a hallmark of biological aging and a contributor to many age-related conditions. Hormones play a regulatory role in the immune system and inflammatory pathways. An imbalance in hormones can exacerbate this chronic inflammatory state, creating an environment that promotes cellular damage and accelerates the aging process.
Cellular senescence, a state where cells stop dividing but remain metabolically active, is another critical aspect of aging. Senescent cells accumulate over time and secrete a cocktail of pro-inflammatory molecules, growth factors, and proteases, collectively known as the senescence-associated secretory phenotype (SASP).
This SASP can negatively influence neighboring healthy cells, contributing to tissue dysfunction and age-related diseases. Hormonal changes, such as those occurring with age, can influence the accumulation of senescent cells in various tissues. For example, the decline in estrogen and progesterone can increase markers of senescence in certain tissues, contributing to their degeneration.
Maintaining cellular cleanliness is also vital for longevity. A process called autophagy, meaning “self-eating,” is the cell’s internal recycling system. It removes damaged organelles, misfolded proteins, and other cellular debris, ensuring cellular efficiency and health. The activity of autophagy naturally declines with age, leading to an accumulation of cellular waste and a loss of homeostatic control.
Hormones exert control over autophagic processes. For instance, deficiencies in hormones have been linked to impaired autophagy in specific cell types, contributing to their dysfunction and accelerated aging. Restoring optimal hormonal signaling can support the body’s innate ability to perform this essential cellular housekeeping, thereby promoting cellular resilience and delaying the onset of age-related decline.
Intermediate
Having explored the foundational cellular mechanisms influenced by hormonal balance, we now turn to the practical applications of this understanding ∞ the clinical protocols designed to address hormonal deficits and support cellular vitality. These protocols represent a strategic approach to recalibrating the endocrine system, aiming to restore the clear communication signals that cells require for optimal function. The objective is to mitigate the molecular pathways that drive accelerated cellular aging, translating scientific insight into tangible improvements in well-being.
The concept of hormonal optimization protocols extends beyond simple replacement; it involves a precise, individualized strategy to support the body’s inherent capacity for self-regulation and repair. This requires a deep appreciation for the interconnectedness of the endocrine system, recognizing that a shift in one hormone can influence many others, impacting cellular processes across various tissues. Our focus here is on targeted interventions that work with your body’s biology, rather than against it, to promote sustained health.
Targeted Endocrine System Support
Hormonal support protocols are tailored to distinct patient groups, acknowledging the unique physiological requirements of men and women. The overarching aim remains consistent ∞ to address specific hormonal deficits that contribute to symptoms and accelerated cellular aging. This involves a careful assessment of individual hormonal profiles through comprehensive laboratory testing, followed by the judicious application of specific agents.
Testosterone Recalibration for Men
For men experiencing symptoms of diminished vitality, often associated with age-related testosterone decline, Testosterone Replacement Therapy (TRT) can be a transformative intervention. As men age, Leydig cells in the testes, responsible for testosterone production, can experience aging-related dysfunction, leading to reduced hormone synthesis. This decline is not merely about sexual function; it impacts metabolism, mood, bone density, and cardiovascular health, contributing to a broader acceleration of cellular aging.
A standard protocol often involves weekly intramuscular injections of Testosterone Cypionate (200mg/ml). This exogenous testosterone helps to replenish circulating levels, alleviating symptoms and supporting cellular functions that rely on adequate androgen signaling. However, a comprehensive approach recognizes the body’s intricate feedback loops.
To maintain natural testosterone production and preserve fertility, concurrent administration of Gonadorelin is often included. Gonadorelin, a gonadotropin-releasing hormone (GnRH) analog, stimulates the pituitary gland to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH), thereby encouraging the testes to continue their own hormone synthesis.
Another consideration in male hormonal optimization is the conversion of testosterone to estrogen, a process mediated by the enzyme aromatase. Elevated estrogen levels in men can lead to undesirable side effects. To mitigate this, an aromatase inhibitor such as Anastrozole (2x/week oral tablet) may be prescribed.
This helps to block estrogen conversion, maintaining a healthier androgen-to-estrogen ratio. In some cases, Enclomiphene may be added to further support LH and FSH levels, particularly when preserving endogenous production is a primary concern. This selective estrogen receptor modulator (SERM) acts at the pituitary to stimulate gonadotropin release.
Precision in male hormonal support balances exogenous testosterone with strategies to preserve endogenous production and manage estrogen levels.
Hormonal Balance for Women
Women navigating the transitions of pre-menopause, peri-menopause, and post-menopause often experience a wide array of symptoms stemming from fluctuating or declining estrogen and progesterone levels. These hormonal shifts can directly influence cellular aging pathways, affecting everything from bone density to cognitive function and skin integrity.
For women, a personalized approach to hormonal support may involve Testosterone Cypionate, typically administered at low doses (10 ∞ 20 units or 0.1 ∞ 0.2ml) weekly via subcutaneous injection. While often associated with male health, testosterone plays a vital role in female well-being, influencing libido, mood, energy, and body composition. Its careful application can significantly improve quality of life and support cellular resilience.
Progesterone is another critical component, prescribed based on the woman’s menopausal status. Progesterone influences cellular processes, including its role in regulating cellular senescence and supporting endometrial health. For some women, long-acting pellet therapy, which delivers a steady release of testosterone, may be considered. When appropriate, Anastrozole may also be used in women to manage estrogen levels, particularly in the context of testosterone administration or specific clinical presentations.
Post-Therapy and Fertility Support
For men who have discontinued TRT or are actively trying to conceive, a specific protocol is employed to stimulate natural hormone production and support fertility. This protocol typically includes Gonadorelin to stimulate the hypothalamic-pituitary-gonadal (HPG) axis, encouraging the testes to resume their function.
Additionally, selective estrogen receptor modulators (SERMs) such as Tamoxifen and Clomid are often used. These agents block estrogen’s negative feedback on the pituitary, leading to increased LH and FSH secretion, which in turn stimulates testicular testosterone production and spermatogenesis. Anastrozole may be optionally included to manage estrogen conversion during this phase.
Growth Hormone Peptide Therapy
Beyond traditional hormone replacement, targeted peptide therapies offer a sophisticated means of influencing cellular aging pathways. These small chains of amino acids act as signaling molecules, guiding specific biological processes that often decline with age. For active adults and athletes seeking anti-aging benefits, muscle gain, fat loss, and improved sleep, Growth Hormone Peptide Therapy presents a compelling option.
Key peptides in this category work by stimulating the body’s natural production of growth hormone (GH), rather than directly administering GH. This approach aims to restore more youthful GH pulsatility, which naturally diminishes with age, a phenomenon sometimes called “somatopause.”
- Sermorelin ∞ This peptide is a growth hormone-releasing hormone (GHRH) analog. It stimulates the pituitary gland to release GH in a pulsatile, physiological manner, supporting muscle mass, fat metabolism, and recovery.
- Ipamorelin / CJC-1295 ∞ Often used in combination, Ipamorelin is a GH secretagogue that selectively stimulates GH release without significantly impacting other hormones like cortisol. CJC-1295 is a GHRH analog that provides a sustained release of GH. Together, they promote muscle growth, fat reduction, and improved sleep quality.
- Tesamorelin ∞ This GHRH analog is particularly noted for its effects on reducing visceral adipose tissue, a type of fat associated with metabolic dysfunction and accelerated aging.
- Hexarelin ∞ A potent GH secretagogue, Hexarelin also has direct effects on cardiac tissue, potentially offering cardioprotective benefits.
- MK-677 (Ibutamoren) ∞ While not a peptide, MK-677 is a non-peptide GH secretagogue that orally stimulates GH release, increasing both GH and IGF-1 levels. It supports muscle mass, bone density, and sleep architecture.
These peptides influence cellular mechanisms such as protein synthesis, cellular repair, and mitochondrial function, all of which are critical for combating age-related decline. They represent a targeted approach to optimizing the body’s regenerative capacities.
Other Targeted Peptides
The therapeutic landscape of peptides extends to other specific applications, addressing particular aspects of health and cellular function.
- PT-141 (Bremelanotide) ∞ This peptide acts on melanocortin receptors in the brain to influence sexual arousal and function. It offers a unique mechanism for addressing sexual health concerns in both men and women, working centrally rather than directly on the vascular system.
- Pentadeca Arginate (PDA) ∞ PDA is recognized for its role in tissue repair, healing processes, and modulating inflammation. It supports the body’s ability to recover from injury and manage inflammatory responses at a cellular level, contributing to overall tissue integrity and resilience against age-related damage.
These clinical protocols, from hormonal recalibration to targeted peptide therapies, represent a sophisticated understanding of how to support the body’s intrinsic capacity for health. By addressing hormonal deficits and optimizing cellular signaling, we aim to slow the progression of age-related changes and restore a sense of vitality that reflects a healthier biological age.
Academic
The intricate relationship between hormonal deficits and accelerated cellular aging extends into the deepest molecular pathways, where the very machinery of life begins to falter. This section delves into the precise biochemical and cellular mechanisms by which a decline in endocrine signaling contributes to the hallmarks of aging, providing a granular understanding of this complex interplay. Our exploration centers on how hormonal insufficiency disrupts cellular homeostasis, leading to systemic decline.
Cellular aging is not a singular event but a constellation of interconnected processes. When hormonal communication weakens, these processes become dysregulated, creating a cellular environment conducive to decline. We will examine the specific molecular cascades involved, drawing connections between endocrine signals and the integrity of cellular components.
Telomere Dynamics and Endocrine Influence
The integrity of our genome is safeguarded by telomeres, repetitive DNA sequences at the ends of chromosomes that protect against degradation and fusion. Each cell division typically results in telomere shortening, a process that eventually triggers cellular senescence or apoptosis when telomeres reach a critical length.
The enzyme telomerase, a reverse transcriptase, counteracts this shortening by adding new telomeric repeats. While telomerase activity is high in germline and stem cells, it is generally low or absent in most somatic cells, contributing to their finite replicative lifespan.
Hormones exert a direct regulatory influence on telomerase activity and telomere length. Estrogen, for instance, has been shown to activate telomerase through transcriptional regulation of the hTERT gene, which encodes the catalytic subunit of telomerase. This occurs via estrogen response elements within the hTERT promoter.
Consequently, estrogen deficiency, a hallmark of menopause, can lead to accelerated telomere shortening in hormone-sensitive tissues. This molecular mechanism provides a direct link between declining estrogen levels and the progression of cellular aging, affecting tissue function and regenerative capacity. The maintenance of telomere length by sex hormones is a significant area of research, with implications for understanding sex-specific differences in longevity.
Mitochondrial Bioenergetics and Hormonal Crosstalk
Mitochondria are central to cellular metabolism, generating the vast majority of cellular ATP through oxidative phosphorylation. They are also a primary source of reactive oxygen species (ROS), byproducts of metabolic activity. Under normal conditions, antioxidant defense systems neutralize these ROS. However, with age, mitochondrial function declines, leading to increased ROS production and impaired antioxidant capacity, resulting in oxidative stress. This oxidative stress damages cellular macromolecules, including DNA, proteins, and lipids, contributing significantly to the aging phenotype.
The endocrine system and mitochondrial health are inextricably linked. Steroid hormone biosynthesis, including that of testosterone and estrogens, occurs within mitochondria, requiring efficient mitochondrial function for adequate hormone production. A decline in mitochondrial integrity, often observed with aging, can therefore directly impair hormone synthesis. Conversely, hormonal deficits can compromise mitochondrial bioenergetics.
For example, estrogen plays a role in maintaining mitochondrial membrane fatty acid composition, making them less susceptible to peroxidation and improving respiration and ATP production rates. Testosterone also influences mitochondrial function in various tissues, and its decline can contribute to mitochondrial dysfunction in Leydig cells, leading to further reductions in testosterone synthesis. This creates a feedback loop where hormonal decline exacerbates mitochondrial dysfunction, and impaired mitochondria further compromise hormonal balance, accelerating cellular aging.
Mitochondrial health and hormonal signaling are interdependent, forming a critical axis in the regulation of cellular aging.
Inflammaging and Hormonal Dysregulation
Inflammaging, a state of chronic, low-grade systemic inflammation, is a consistent feature of biological aging and a major driver of age-related diseases. This persistent inflammatory milieu is characterized by elevated levels of pro-inflammatory cytokines, chemokines, and other mediators. Hormones are key regulators of immune responses and inflammatory pathways. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, often seen with chronic stress and aging, leads to altered cortisol levels, which can exacerbate systemic inflammation.
Sex hormones, such as testosterone and estrogen, possess immunomodulatory and anti-inflammatory properties. A decline in these hormones can therefore contribute to an increase in pro-inflammatory cytokines and a reduced capacity to resolve inflammation.
This sustained inflammatory state contributes to cellular damage, impairs tissue repair, and promotes the accumulation of senescent cells, which themselves secrete pro-inflammatory factors, creating a self-perpetuating cycle of inflammation and cellular decline. The interplay between hormonal deficits and inflammaging represents a significant molecular pathway through which the endocrine system influences the pace of cellular aging.
Cellular Senescence and the SASP
Cellular senescence is a state of irreversible cell cycle arrest, where cells remain metabolically active but lose their proliferative capacity. Senescent cells accumulate in tissues with age and in response to various stressors, including DNA damage, oxidative stress, and telomere shortening.
A defining characteristic of senescent cells is the senescence-associated secretory phenotype (SASP), a complex secretome comprising pro-inflammatory cytokines (e.g. IL-6, IL-1β), chemokines, growth factors, and proteases. The SASP contributes to tissue dysfunction, chronic inflammation, and the spread of senescence to neighboring cells.
Hormonal deficits directly influence the induction and accumulation of senescent cells. For example, the loss of 17β-estradiol and progesterone during menopause has been shown to increase senescence markers in cartilage, contributing to its degeneration. In the male reproductive system, Leydig cell aging, characterized by increased senescence, is a primary mechanism for age-related testosterone decline.
This senescence is mediated, in part, by pathways such as p38 MAPK, which promotes Leydig cell aging and impaired testosterone synthesis. The accumulation of senescent cells in endocrine tissues can further impair hormone production and responsiveness, creating a detrimental feedback loop that accelerates systemic aging.
Autophagy and Proteostasis in Hormonal Context
Autophagy, a fundamental catabolic process, is essential for maintaining cellular homeostasis by degrading and recycling damaged organelles and misfolded proteins. This cellular “self-eating” mechanism is critical for cellular quality control and adaptation to stress. A decline in autophagic activity is a hallmark of aging, leading to the accumulation of cellular debris and impaired cellular function.
Hormones play a significant role in regulating autophagic pathways. For instance, glucagon, a hormone involved in glucose metabolism, is known to activate autophagy. In steroid-secreting cells, such as Leydig cells in the testes, autophagy, particularly mitophagy (the selective degradation of damaged mitochondria), is crucial for maintaining cellular health and steroidogenesis.
Age-related reductions in autophagy, specifically mitophagy, lead to an accumulation of dysfunctional mitochondria and increased ROS in Leydig cells, directly contributing to reduced testosterone production and conditions like late-onset hypogonadism. Similarly, endometrial cells dynamically modulate autophagy in response to cyclic changes in estrogen and progesterone concentrations, highlighting the hormonal control over this vital cellular process. Supporting optimal hormonal balance can therefore help maintain robust autophagic activity, promoting cellular cleanliness and resilience against age-related decline.
| Hormonal Deficit | Affected Molecular Pathway | Cellular Impact |
|---|---|---|
| Testosterone Decline | Leydig cell senescence, p38 MAPK activation, oxidative stress, impaired mitochondrial function | Reduced steroidogenesis, increased cellular damage, systemic metabolic dysfunction, muscle loss |
| Estrogen Deficiency | Reduced telomerase activity, increased telomere shortening, mitochondrial dysfunction, increased oxidative stress, enhanced cellular senescence | Accelerated cellular aging, bone density loss, impaired cognitive function, tissue degeneration |
| Progesterone Decline | Increased senescence markers, extracellular matrix disassembly, altered autophagy regulation | Cartilage degeneration, impaired endometrial function, potential for increased cellular dysfunction |
| Growth Hormone/IGF-1 Decline | Reduced protein synthesis, impaired cellular repair, mitochondrial dysfunction, altered metabolic signaling | Decreased muscle mass, increased fat accumulation, reduced energy, slower recovery, systemic aging |
The interconnectedness of these molecular pathways underscores the systemic impact of hormonal deficits. A decline in one hormone does not simply affect a single organ; it initiates a cascade of molecular events that collectively accelerate cellular aging across multiple tissues and systems. Understanding these deep biological connections allows for a more precise and effective approach to personalized wellness protocols, aiming to restore the cellular harmony that underpins vitality and longevity.
References
- Liu, B. et al. “Estrogen decreases cell senescence in endothelial progenitor cells.” Aging Cell, vol. 15, no. 4, 2016, pp. 701-710.
- Midzak, A. S. et al. “Leydig cell aging and the mechanisms of reduced testosterone synthesis.” Journal of Andrology, vol. 30, no. 2, 2009, pp. 129-139.
- Li, Y. et al. “Involvement of p38 MAPK in Leydig cell aging and age-related decline in testosterone.” Aging Cell, vol. 20, no. 1, 2021, e13278.
- Varughese, R. and Rahman, S. “Endocrine Dysfunction in Primary Mitochondrial Diseases.” Endocrine Reviews, 2025, bnaf002.
- Pickart, L. and Margolina, A. “GHK-Cu and skin aging.” Biofactors, vol. 44, no. 6, 2018, pp. 548-557.
- Yang, J. et al. “Epithalon activates telomerase and extends lifespan in mice.” Biogerontology, vol. 4, no. 6, 2003, pp. 345-352.
- Korkushko, O. V. et al. “Peptide bioregulators and aging.” Journal of Gerontology and Geriatrics, vol. 59, no. 2, 2011, pp. 123-130.
- Jeong, J. H. et al. “Peptide therapy for anti-aging ∞ How it works and what to expect.” Journal of Clinical & Aesthetic Dermatology, vol. 12, no. 7, 2019, pp. 28-35.
- Teichman, S. L. et al. “Pharmacokinetics and pharmacodynamics of CJC-1295, a long-acting growth hormone-releasing factor analog.” Journal of Clinical Endocrinology & Metabolism, vol. 91, no. 3, 2006, pp. 799-805.
- Dominari, A. et al. “Hormonal regulation of telomerase activity and hTERT expression in steroid-regulated tissues and cancer.” International Journal of Molecular Sciences, vol. 21, no. 16, 2020, 5779.
- Hayflick, L. and Moorhead, P. S. “The serial cultivation of human diploid cell strains.” Experimental Cell Research, vol. 25, no. 3, 1961, pp. 585-621.
- Baker, D. J. et al. “Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.” Nature, vol. 479, no. 7372, 2011, pp. 232-236.
- Hoenicke, L. and Zender, L. “Senescence-associated secretory phenotype (SASP) in cancer and aging.” Aging, vol. 4, no. 10, 2012, pp. 709-713.
- Farr, J. N. et al. “Estrogen slows deficits associated with aging and cell senescence in bone.” Journal of Bone and Mineral Research, vol. 34, no. 10, 2019, pp. 1850-1861.
- Song, Y. et al. “Menopause-induced 17β-estradiol and progesterone loss increases senescence markers, matrix disassembly and degeneration in mouse cartilage.” Nature Aging, vol. 5, no. 1, 2025, pp. 65-86.
Reflection
As we conclude this exploration into the molecular pathways linking hormonal deficits to accelerated cellular aging, consider the profound implications for your own health journey. The scientific insights shared here are not merely academic; they are a lens through which to view your personal experience, validating the subtle shifts you may have felt and providing a framework for understanding their biological origins. This knowledge is a powerful tool, transforming vague concerns into actionable insights.
The journey toward reclaiming vitality is deeply personal. It begins with an honest assessment of your current state, guided by comprehensive testing that reveals the unique symphony of your internal systems. Armed with this understanding, you can then consider personalized strategies to recalibrate your endocrine environment, supporting your cells in their fundamental work of maintaining health and resilience.
This is not about chasing an elusive ideal; it is about restoring your body’s innate intelligence, allowing it to function at its full potential.
Your body possesses an incredible capacity for adaptation and repair. When provided with the right signals and support, it can often recalibrate and regain a more youthful function. This understanding moves us beyond a reactive approach to health, inviting a proactive stance where you become an informed participant in your own well-being. The path to sustained vitality is a collaborative one, where scientific authority meets empathetic guidance, leading you toward a future of enhanced health and uncompromised function.
Glossary
cellular aging
molecular pathways
cellular health
accelerated cellular aging
cellular senescence
telomere shortening
telomere attrition
mitochondrial function
oxidative stress
hormone production
endocrine system
inflammaging
senescence-associated secretory phenotype
senescent cells
estrogen and progesterone
age-related decline
hormonal deficits
hormonal balance
testosterone production
bone density
testosterone cypionate
gonadorelin
estrogen levels
anastrozole
growth hormone peptide therapy
growth hormone
sermorelin
ipamorelin
cjc-1295
pt-141
pentadeca arginate
mitochondrial dysfunction
leydig cells
leydig cell aging
