I. Introduction
Brief overview of type 1 diabetes (T1D) and beta cell destruction.
The concept of beta cell regeneration as a therapeutic goal.
Introduction to growth stimulants (Testosterone, IGF-1, and HGH) and their potential roles in assisting beta cell regrowth.
For decades, type 1 diabetes (T1D) has largely been viewed through the lens of autoimmunity—a condition in which the immune system mistakenly targets insulin-producing beta cells in the pancreas. While this framework has driven research and treatment strategies, emerging evidence suggests that beta cell loss may be influenced by a broader range of factors beyond autoimmunity alone. Nutrient imbalances, pathogenic exposures, environmental toxins, epigenetic inheritance, and mitochondrial dysfunction may all play significant roles in beta cell degradation and impaired regeneration.
This article explores a different approach: viewing beta cells as resilient and regenerative structures that can, under the right conditions, recover and regrow. Rather than accepting the conventional narrative of T1D as an irreversible disease, we will examine how specific growth stimulants—testosterone, IGF-1 (insulin-like growth factor 1), and HGH (human growth hormone)—might offer pathways for beta cell regeneration.
By understanding the natural roles of these hormones, their sources, and how they influence cellular growth and repair, we can begin to ask new and more advanced questions:
Could nutrient-driven hormonal therapies restore beta cell populations?
What role does the liver, as a primary producer of IGF-1, play in creating an environment conducive to beta cell recovery?
How might epigenetic regulation, influenced by environmental stimuli and growth factors, unlock latent regenerative capacities within the pancreas?
Through this exploration, we aim to stimulate fresh perspectives and theories on beta cell regeneration, challenging the prevailing assumption that T1D is an unchangeable condition. Instead, we invite readers to consider T1D as a multifactorial metabolic imbalance—one that, with proper intervention, may be addressed at its root cause.
This journey begins by understanding the body’s own powerful regenerative signals—testosterone, IGF-1, and HGH—and how they might be harnessed to stimulate beta cell regrowth and restore insulin function. Let’s dive into the science of growth stimulants and their potential role in transforming how we approach beta cell recovery.
II. Understanding Beta Cell Regrowth and the Need for Growth Stimulants
Explanation of beta cell regeneration and its challenges.
How growth factors influence cellular proliferation, differentiation, and survival in general.
Why T1D patients might benefit from therapies that enhance beta cell regeneration.
Beta cells, long thought to be terminally differentiated and non-renewable, have proven to be more dynamic and adaptable than previously believed. Under the right stimuli, beta cells can regenerate through various mechanisms involving different cell types and tissues. Research highlights several potential regenerative stimuli and pathways, including transdifferentiation from neighboring pancreatic cells, progenitor cell activation, and even contributions from non-pancreatic sources like hepatocytes (liver) and enterocytes (gut). Growth factors such as testosterone, IGF-1, and HGH play a crucial role in modulating these pathways by influencing cellular signaling, proliferation, and differentiation.
Regenerative Stimuli for Beta Cell Regrowth
Several cell types and pathways have been identified as potential sources of new beta cells:
Acinar Cell Transdifferentiation
Mechanism: Acinar cells, which normally produce digestive enzymes, have shown the capacity to transdifferentiate into insulin-producing beta cells under certain conditions.
Influence of Growth Factors:
IGF-1: IGF-1 enhances acinar-to-beta cell transdifferentiation by promoting cellular proliferation and survival while modulating the local inflammatory environment.
HGH: HGH stimulates the expression of transcription factors necessary for cell fate changes, such as PDX1 and NGN3, which are critical for beta cell identity.
Ductal Cell Differentiation
Mechanism: Pancreatic ductal cells can serve as progenitors for beta cells, especially during injury or stress. These cells are believed to retain a degree of plasticity, allowing them to regenerate endocrine tissue.
Influence of Growth Factors:
Growth factors like IGF-1 and HGH increase ductal cell proliferation and differentiation by activating signaling pathways such as PI3K-Akt and MAPK, both of which are critical for cell growth and differentiation.
Testosterone: Testosterone may indirectly enhance this process by modulating systemic inflammation and improving glucose metabolism, creating a favorable environment for ductal regeneration.
Progenitor Cell Activation
Mechanism: Progenitor cells residing in the pancreas or other tissues can be stimulated to differentiate into beta cells. This process is more prominent during embryonic development but may also be activated in adults under specific conditions.
Influence of Growth Factors:
IGF-1 and HGH are known to enhance progenitor activation by promoting cellular proliferation and survival, particularly under conditions of metabolic stress.
Alpha and Delta Cell Transdifferentiation
Mechanism: In response to beta cell loss, alpha cells (glucagon-secreting) and delta cells (somatostatin-secreting) can transdifferentiate into beta cells.
Influence of Growth Factors:
IGF-1 enhances this transdifferentiation by promoting the reprogramming of alpha cells through increased PDX1 expression.
HGH may support delta-to-beta cell conversion by stimulating local growth and repair processes in islets.
Hepatocyte and Enterocyte Transdifferentiation
Mechanism: Hepatocytes (liver cells) and enterocytes (intestinal cells) share a common developmental origin with pancreatic cells and have shown potential to transdifferentiate into beta-like cells.
Influence of Growth Factors:
HGH stimulates hepatocyte proliferation and may induce liver cells to express insulin under certain conditions.
IGF-1 produced by the liver in response to HGH can enhance the regenerative environment, promoting cell reprogramming and survival.
Existing Research:
Studies have shown that overexpression of PDX1 in hepatocytes, coupled with growth factor stimulation, can induce these cells to produce insulin, offering a potential avenue for beta cell replacement therapy.
Systemic Influences of Growth Factors on Beta Cell Regeneration
Beyond their direct effects on beta cells, growth factors exert systemic influences by modulating organs involved in growth factor metabolism and bioavailability:
Liver
IGF-1 Production: The liver is the primary source of IGF-1, which is released in response to HGH stimulation. IGF-1 circulates systemically, enhancing beta cell survival, proliferation, and glucose metabolism.
Glucose Homeostasis: By improving hepatic glucose metabolism, IGF-1 indirectly reduces the metabolic burden on beta cells, promoting their recovery.
Existing Research: Studies have shown that IGF-1 administration in diabetic models improves beta cell mass and function by reducing apoptosis and enhancing proliferation (Li et al., 2014).
Kidneys
Growth Factor Clearance: The kidneys play a key role in filtering and metabolizing circulating growth factors, including IGF-1. Reduced renal function can alter growth factor bioavailability, potentially affecting beta cell regeneration.
HPA Axis Interaction: Through their regulation of cortisol metabolism, the kidneys influence the hypothalamic-pituitary-adrenal (HPA) axis, which interacts with the HGH/IGF-1 axis. Elevated cortisol levels can inhibit beta cell regeneration, making adrenal and renal health critical for optimizing growth factor therapies.
Hypothalamic-Pituitary Axis
The HPA axis controls the release of HGH from the pituitary gland, which in turn stimulates IGF-1 production in the liver. Proper function of this axis is essential for maintaining adequate levels of circulating growth factors.
Testosterone’s Role: Testosterone interacts with the HPA axis by modulating cortisol levels, reducing systemic inflammation, and enhancing anabolic signaling, which may further support beta cell regeneration.
Cellular Mechanisms Impacted by Growth Factors
Growth factors influence several key cellular mechanisms involved in beta cell regeneration:
PI3K-Akt Pathway Activation
This pathway promotes cellular growth, proliferation, and survival, and is activated by IGF-1 and HGH. Activation of PI3K-Akt reduces beta cell apoptosis and supports proliferation, making it a critical target for regenerative therapies.
MAPK/ERK Pathway
Both IGF-1 and HGH stimulate the MAPK/ERK pathway, which is involved in cell differentiation and proliferation. This pathway plays a crucial role in converting progenitor or transdifferentiated cells into functional beta cells.
mTOR Pathway Modulation
mTOR integrates signals from growth factors and nutrients to regulate cell growth and metabolism. Proper mTOR signaling is essential for beta cell regeneration, and IGF-1/HGH therapies can modulate this pathway to create an environment conducive to beta cell regrowth.
Existing Research on Growth Factors and Beta Cell Regeneration
IGF-1 and Beta Cell Regeneration:
Studies have demonstrated that IGF-1 administration enhances beta cell proliferation and improves insulin secretion in diabetic models (Xu et al., 2015).
HGH and Islet Regeneration:
Clinical trials involving HGH therapy in diabetic patients have shown improved glucose tolerance and increased beta cell mass.
Testosterone and Beta Cell Function:
Research indicates that testosterone enhances insulin sensitivity and may indirectly support beta cell regeneration by reducing systemic inflammation and improving metabolic function (Chen et al., 2017).
III. The Role of Testosterone in Beta Cell Regrowth
Natural Role of Testosterone
Produced by: Testes in males, ovaries in females, and adrenal glands in both sexes.
Functions: Regulates muscle mass, bone density, mood, and metabolism.
Its role in modulating insulin sensitivity and glucose metabolism.
Alternative Sources of Testosterone
Natural sources: Resistance exercise, adequate sleep, zinc, and vitamin D.
Alternative therapies: Bioidentical testosterone replacement therapy (TRT).
Potential Benefits for Beta Cells
Testosterone’s role in reducing inflammation.
Evidence of its influence on insulin secretion and beta cell survival.
Creation of Testosterone in Non-Diabetic and Diabetic Systems
1. Testosterone Production in Men and Women
Testosterone is primarily produced in the testes in men and the ovaries in women, with smaller amounts synthesized in the adrenal glands of both sexes. The process is regulated by the hypothalamic-pituitary-gonadal (HPG) axis:
Hypothalamus: Releases gonadotropin-releasing hormone (GnRH), which stimulates the pituitary gland.
Pituitary Gland: Secretes luteinizing hormone (LH) in response to GnRH. LH then acts on the testes (Leydig cells) or ovaries (thecal cells) to stimulate testosterone production.
Adrenal Glands: Produce a small amount of testosterone from cholesterol via adrenal androgens (e.g., DHEA).
In non-diabetic systems, testosterone levels are maintained within a healthy range, supporting metabolic function, muscle mass, libido, and overall well-being. However, in diabetic systems, especially in individuals with type 2 diabetes or poorly controlled type 1 diabetes, testosterone production is often impaired due to:
Insulin resistance: Reduces the responsiveness of the testes and ovaries to LH stimulation.
Chronic inflammation: Disrupts the HPG axis and inhibits testosterone synthesis.
Liver dysfunction: Impairs the clearance of sex hormone-binding globulin (SHBG), reducing the amount of free (bioavailable) testosterone.
What Does Testosterone Do?
Testosterone is an anabolic (growth) hormone that plays a key role in several bodily functions beyond reproduction:
Muscle Mass and Strength
Testosterone stimulates protein synthesis, increasing muscle mass and strength. This anabolic effect improves glucose uptake and insulin sensitivity, indirectly supporting beta cell function by reducing the metabolic burden.
Bone Density
Testosterone enhances bone mineral density by stimulating osteoblast activity, reducing the risk of osteoporosis, especially in diabetic individuals prone to bone loss.
Energy Metabolism
Testosterone regulates glucose and lipid metabolism, influencing energy balance. It promotes mitochondrial function, enhancing cellular energy production. IE. Glucose needs to be available in order to grow effectively.
Inflammation Modulation
Testosterone has anti-inflammatory properties, reducing the production of pro-inflammatory cytokines (e.g., TNF-α, IL-1β) and increasing the production of anti-inflammatory cytokines (e.g., IL-10).
Hormone Balance
Testosterone interacts with other hormones, including cortisol and estrogen, helping maintain overall hormonal balance. Proper hormone balance is crucial for reducing stress and supporting beta cell regeneration.
Sleep Regulation
Healthy testosterone levels are associated with better sleep quality. Since sleep is critical for growth hormone (HGH) secretion and overall metabolic health, maintaining optimal testosterone levels indirectly supports beta cell recovery.
Testosterone is classically associated with muscle growth. What if it also helped beta cells?
Effects of Diabetes on Testosterone Production (and Vice Versa)
Diabetes’ Impact on Testosterone Production
Hypogonadism: Men with diabetes often exhibit lower testosterone levels due to insulin resistance, chronic inflammation, and disrupted HPG axis signaling.
Adrenal Dysfunction: In diabetic individuals, adrenal dysfunction can impair androgen production, further reducing testosterone levels.
Obesity: Common in type 2 diabetes, obesity increases aromatase activity (an enzyme that converts testosterone into estrogen), leading to lower testosterone levels.
Low Testosterone’s Impact on Diabetes
Reduced Insulin Sensitivity: Low testosterone levels are associated with increased insulin resistance, worsening glycemic control.
Increased Visceral Fat: Testosterone deficiency promotes fat accumulation, particularly visceral fat, which contributes to systemic inflammation and metabolic dysfunction.
Higher Inflammation: Low testosterone leads to increased inflammatory markers, exacerbating beta cell stress and damage.
Natural Ways to Stimulate Testosterone Production
Dietary Strategies
Zinc-Rich Foods: Zinc is essential for testosterone synthesis and can be found in foods like oysters, red meat, poultry, and pumpkin seeds.
Magnesium: Improves testosterone levels by enhancing the bioavailability of free testosterone. Good sources include leafy greens, nuts, and seeds.
Healthy Fats: Testosterone is synthesized from cholesterol, so consuming healthy fats (e.g., avocados, olive oil, and fatty fish) supports its production.
Protein Balance: Adequate protein intake ensures muscle maintenance and supports testosterone synthesis.
Lifestyle Strategies
Resistance Training: Weightlifting and high-intensity interval training (HIIT) have been shown to increase testosterone levels.
Sleep Optimization: Deep sleep is critical for testosterone production, with the majority being produced during REM sleep. Aim for 7-9 hours of quality sleep per night.
Stress Reduction: Chronic stress elevates cortisol, which suppresses testosterone. Stress management techniques like meditation, yoga, and mindfulness can help restore hormonal balance.
Targeting Secondary Systems
Liver Health: Since the liver metabolizes and regulates sex hormones, maintaining liver health is essential for optimal testosterone production. Strategies include:
Detoxification: Consuming liver-supporting herbs like milk thistle and dandelion root.
Reducing Alcohol Intake: Excessive alcohol consumption impairs liver function and disrupts testosterone metabolism.
Adrenal Support: Supporting adrenal health through adequate nutrient intake (e.g., B vitamins, vitamin C) and stress management ensures steady androgen production.
Potential Benefits of Testosterone Beyond Growth Factor Stimulation
Anti-Inflammatory Effects
Testosterone reduces systemic inflammation by modulating cytokine production, which is crucial for creating an environment conducive to beta cell regeneration.
Improved Insulin Sensitivity
By increasing muscle mass and reducing visceral fat, testosterone enhances insulin sensitivity, reducing the workload on beta cells and potentially prolonging their survival.
Enhanced Energy and Metabolism
Testosterone’s role in mitochondrial function boosts cellular energy production, improving overall metabolic health and resilience to stress.
Hormonal Balance
Proper testosterone levels help balance other hormones, such as cortisol and estrogen, which are critical for maintaining metabolic homeostasis.
Better Sleep and Recovery
Testosterone improves sleep quality and promotes tissue repair, indirectly supporting beta cell regeneration through enhanced recovery and HGH secretion during sleep.
Testosterone plays a pivotal role in regulating metabolic health, inflammation, and cellular growth, making it a promising target for supporting beta cell regeneration. By understanding how diabetes disrupts testosterone production and exploring natural ways to stimulate its synthesis, individuals can take proactive steps to restore hormonal balance and improve their overall health. Beyond its direct anabolic effects, testosterone’s ability to modulate inflammation, improve insulin sensitivity, and enhance recovery makes it a powerful tool in the quest for beta cell regeneration.
IV. The Role of IGF-1 (Insulin-like Growth Factor 1) in Beta Cell Regrowth
Natural Role of IGF-1
Produced by: Liver in response to growth hormone stimulation.
Functions: Promotes growth, cellular repair, and anabolic effects in various tissues.
Its involvement in glucose uptake, insulin signaling, and beta cell proliferation.
Alternative Sources of IGF-1
Natural sources: High-protein diets, exercise, and sleep.
Alternative therapies: IGF-1 supplementation or analogs.
Potential Benefits for Beta Cells
IGF-1’s role in stimulating beta cell replication.
Evidence of IGF-1 improving insulin sensitivity and preventing beta cell apoptosis.
Creation of IGF-1 in Non-Diabetic and Diabetic Systems
1. IGF-1 Production in Men and Women
Insulin-like Growth Factor 1 (IGF-1) is primarily produced in the liver in response to stimulation by human growth hormone (HGH). IGF-1 is secreted into the bloodstream, where it acts as a mediator of growth hormone’s anabolic effects. While most circulating IGF-1 originates in the liver, local production occurs in various tissues, including muscle, bone, and the pancreas, where it exerts paracrine and autocrine effects.
Hypothalamic-Pituitary Axis Control:
The hypothalamus secretes growth hormone-releasing hormone (GHRH), stimulating the pituitary gland to release HGH. HGH then stimulates IGF-1 synthesis in the liver.
Factors Influencing IGF-1 Levels:
Nutrition, sleep, exercise, and hormonal balance (testosterone, estrogen, insulin) all modulate IGF-1 production.
In non-diabetic systems, IGF-1 levels are maintained by balanced hormone signaling and adequate nutrient availability, promoting growth, repair, and metabolic balance. In diabetic systems, several factors impair IGF-1 production and function:
Insulin Deficiency or Resistance:
Since IGF-1 signaling is closely tied to insulin, reduced insulin levels or insulin resistance in diabetes diminish IGF-1 production and bioactivity.
Chronic Inflammation:
Persistent inflammation associated with diabetes disrupts the hypothalamic-pituitary axis and hepatic function, reducing IGF-1 synthesis.
Liver Dysfunction:
In diabetes, fatty liver disease or other hepatic impairments can reduce the liver’s capacity to produce IGF-1.
What Does IGF-1 Do?
IGF-1 plays a central role in growth, metabolism, and cellular repair by promoting anabolic processes and regulating cellular survival. Its actions are mediated through the IGF-1 receptor (IGF-1R), which is present on many cell types, including beta cells.
Cell Growth and Repair
IGF-1 stimulates the proliferation and differentiation of various cell types, including beta cells. It also enhances tissue repair by promoting protein synthesis and reducing protein breakdown.
Metabolic Regulation
IGF-1 influences glucose and lipid metabolism, improving insulin sensitivity by enhancing glucose uptake in muscle and adipose tissue.
It regulates hepatic glucose production, contributing to overall glucose homeostasis.
Anti-Apoptotic Effects
IGF-1 activates the PI3K-Akt pathway, which inhibits apoptosis (programmed cell death) and enhances beta cell survival, particularly under conditions of metabolic stress or inflammation.
Inflammation Modulation
IGF-1 reduces systemic inflammation by inhibiting the production of pro-inflammatory cytokines and promoting tissue repair.
Bone and Muscle Health
IGF-1 promotes bone formation by stimulating osteoblast activity and enhances muscle growth by increasing protein synthesis and satellite cell proliferation.
Effects of Diabetes on IGF-1 Production (and Vice Versa)
Diabetes’ Impact on IGF-1 Production
Insulin Resistance: Reduces hepatic IGF-1 synthesis, as insulin signaling is necessary for optimal growth hormone receptor function.
Reduced HGH Secretion: Chronic hyperglycemia and metabolic stress can impair HGH secretion, leading to reduced IGF-1 stimulation.
Liver Dysfunction: Conditions like non-alcoholic fatty liver disease (NAFLD), common in diabetes, impair IGF-1 production.
Inflammatory Cytokines: High levels of TNF-α and IL-6 in diabetic individuals suppress IGF-1 synthesis.
Low IGF-1’s Impact on Diabetes
Worsened Insulin Sensitivity: IGF-1 enhances insulin receptor sensitivity. Low IGF-1 levels contribute to insulin resistance, exacerbating hyperglycemia.
Impaired Beta Cell Survival: IGF-1 protects beta cells from apoptosis and promotes regeneration. Low IGF-1 levels accelerate beta cell loss.
Increased Inflammation: Low IGF-1 levels are associated with higher inflammatory markers, contributing to systemic inflammation and metabolic dysfunction.
Natural Ways to Stimulate IGF-1 Production
Dietary Strategies
Protein-Rich Foods: Consuming adequate protein stimulates HGH secretion, which in turn increases IGF-1 production. Good sources include lean meats, fish, eggs, and legumes.
Healthy Fats: Omega-3 fatty acids found in fatty fish, flaxseeds, and walnuts support hormonal health and inflammation reduction, indirectly enhancing IGF-1 levels.
Zinc and Magnesium: These minerals are essential for HGH production and IGF-1 synthesis. Foods like spinach, almonds, and shellfish are rich in these nutrients.
Lifestyle Strategies
Resistance Training and High-Intensity Interval Training (HIIT):
Both forms of exercise have been shown to significantly increase HGH and IGF-1 levels, promoting muscle growth and metabolic health.
Sleep Optimization:
Deep sleep, particularly during slow-wave stages, is crucial for HGH secretion. Consistently getting 7-9 hours of sleep per night can enhance IGF-1 production.
Fasting and Caloric Modulation:
Intermittent fasting or time-restricted feeding has been shown to increase HGH levels, indirectly boosting IGF-1 production. Proper caloric intake is also necessary to maintain IGF-1 levels, as prolonged caloric deficits can lower HGH and IGF-1.
Targeting Secondary Systems
Liver Health:
Since the liver is the primary site of IGF-1 production, maintaining liver health is crucial. Strategies include:
Antioxidants: Consuming antioxidant-rich foods (e.g., berries, green tea) helps protect the liver from oxidative damage.
Avoiding Alcohol and Processed Foods: These can impair liver function and reduce IGF-1 synthesis.
Adrenal and Thyroid Health:
Supporting adrenal and thyroid function ensures hormonal balance, which indirectly supports IGF-1 production. Adaptogenic herbs like ashwagandha and Rhodiola rosea may help modulate stress and support endocrine health.
Potential Benefits of IGF-1 Beyond Growth Factor Stimulation
Anti-Inflammatory Effects
IGF-1 reduces systemic inflammation by suppressing pro-inflammatory cytokines (e.g., TNF-α, IL-1β) and promoting tissue repair, creating a more favorable environment for beta cell regeneration.
Improved Insulin Sensitivity
By enhancing glucose uptake in peripheral tissues, IGF-1 lowers blood glucose levels and reduces the workload on beta cells, potentially slowing beta cell loss in diabetic individuals.
Muscle and Bone Health
IGF-1’s role in promoting muscle growth and bone density improves overall metabolic health, supporting better glucose regulation and physical resilience.
Hormonal Balance
IGF-1 interacts with other key hormones, including HGH, insulin, and testosterone, helping maintain a balanced hormonal environment essential for metabolic health.
Sleep and Recovery
IGF-1 promotes better recovery and repair during sleep, indirectly supporting beta cell health by reducing systemic stress and enhancing overall metabolic balance.
IGF-1 is a powerful anabolic hormone that plays a central role in growth, metabolism, and inflammation modulation. In diabetic systems, reduced IGF-1 production exacerbates insulin resistance, inflammation, and beta cell loss. By focusing on natural ways to stimulate IGF-1 production, such as improving liver health, optimizing sleep, and engaging in resistance training, individuals can create an environment conducive to beta cell regeneration. Beyond its direct effects on growth and metabolism, IGF-1 offers additional benefits, including improved insulin sensitivity, reduced inflammation, and enhanced recovery, making it a key player in the pursuit of beta cell restoration.
V. The Role of HGH (Human Growth Hormone) in Beta Cell Regrowth
Natural Role of HGH
Produced by: Pituitary gland.
Functions: Stimulates growth, metabolism, and cell regeneration.
Its downstream effect through IGF-1 and direct anabolic actions on tissues.
Alternative Sources of HGH
Natural sources: Intense exercise, fasting, adequate sleep.
Alternative therapies: Recombinant HGH therapy.
Potential Benefits for Beta Cells
Stimulation of beta cell proliferation via the GH-IGF-1 axis.
Reduction of oxidative stress and inflammation, promoting a regenerative environment.
Creation of HGH in Non-Diabetic and Diabetic Systems
1. HGH Production in Men and Women
Human Growth Hormone (HGH), also known as somatotropin, is produced by the anterior pituitary gland in response to signals from the hypothalamus. Its secretion follows a pulsatile pattern, with the highest peaks occurring during deep sleep (slow-wave sleep) and post-exercise. HGH acts on various tissues directly and indirectly through its primary mediator, IGF-1, which is produced in the liver and other peripheral tissues.
Hypothalamic-Pituitary Regulation:
The hypothalamus secretes growth hormone-releasing hormone (GHRH) to stimulate HGH release and somatostatin to inhibit it.
HGH acts on target tissues, including the liver, muscle, and adipose tissue, stimulating anabolic processes and glucose metabolism.
In non-diabetic systems, HGH plays a vital role in growth, metabolism, and cellular repair, with well-regulated feedback mechanisms ensuring balanced levels. However, in diabetic systems, particularly in type 1 diabetes or poorly controlled type 2 diabetes, HGH production and function are often dysregulated due to:
Hyperglycemia: Chronic high blood glucose suppresses HGH secretion through feedback inhibition.
Insulin Resistance: Since HGH stimulates IGF-1 production, insulin resistance reduces IGF-1 bioavailability, impairing HGH’s anabolic effects.
Increased Cortisol Levels: In diabetic individuals, elevated cortisol from chronic stress inhibits HGH secretion by interfering with hypothalamic-pituitary signaling.
What Does HGH Do?
HGH has widespread effects throughout the body, influencing growth, metabolism, and cellular repair:
Stimulates IGF-1 Production
HGH’s primary anabolic effects are mediated through IGF-1, which promotes cellular proliferation and tissue repair, including beta cell regeneration.
Enhances Protein Synthesis
By increasing amino acid uptake and protein synthesis, HGH supports muscle growth and repair, improving overall metabolic health.
Mobilizes Fat Stores
HGH promotes lipolysis (fat breakdown) in adipose tissue, reducing fat mass and improving insulin sensitivity. This action is especially beneficial in individuals with insulin resistance or obesity.
Regulates Glucose Metabolism
HGH increases hepatic glucose output by stimulating gluconeogenesis but also enhances peripheral glucose uptake through IGF-1, maintaining glucose homeostasis when balanced.
Supports Mitochondrial Health
HGH improves mitochondrial function by increasing mitochondrial biogenesis and reducing oxidative stress, essential for beta cell survival and regeneration.
Effects of Diabetes on HGH Production (and Vice Versa)
Diabetes’ Impact on HGH Production
Reduced Secretion: Chronic hyperglycemia inhibits HGH secretion, reducing its availability for tissue repair and metabolic regulation.
Impaired IGF-1 Signaling: Since HGH relies on IGF-1 for many of its effects, reduced IGF-1 production in diabetic systems limits HGH’s anabolic actions.
Inflammation: Elevated inflammatory markers, common in diabetes, suppress hypothalamic-pituitary signaling, further impairing HGH secretion.
Low HGH’s Impact on Diabetes
Worsened Insulin Sensitivity: Low HGH levels reduce IGF-1-mediated glucose uptake, exacerbating insulin resistance.
Increased Visceral Fat: Without sufficient HGH, fat mobilization is impaired, leading to increased visceral fat accumulation, which worsens metabolic dysfunction.
Reduced Beta Cell Repair: HGH’s role in stimulating beta cell proliferation and reducing apoptosis is diminished, accelerating beta cell loss.
Natural Ways to Stimulate HGH Production
Dietary Strategies
Protein Intake: Consuming adequate protein, especially post-exercise or before sleep, enhances HGH secretion by providing amino acids necessary for tissue repair.
Healthy Fats: Omega-3 fatty acids support hormonal health and help maintain HGH secretion.
Avoiding High Sugar Intake: High sugar intake suppresses HGH secretion due to the inhibitory effects of hyperglycemia and insulin spikes on the hypothalamic-pituitary axis.
Lifestyle Strategies
High-Intensity Exercise: Both resistance training and high-intensity interval training (HIIT) have been shown to significantly increase HGH secretion.
Sleep Optimization: Since the majority of HGH is secreted during deep sleep, optimizing sleep duration and quality is critical for maintaining healthy HGH levels. Aim for 7-9 hours of uninterrupted sleep per night.
Intermittent Fasting: Fasting increases HGH secretion by lowering insulin levels and stimulating the hypothalamus. Short-term fasting or time-restricted eating has been shown to elevate HGH levels significantly.
Targeting Secondary Systems
Liver Health: Since the liver produces IGF-1 in response to HGH, maintaining liver health is essential for HGH’s full anabolic effects. Strategies include:
Antioxidant Support: Consuming antioxidant-rich foods (e.g., berries, green tea) helps protect the liver from oxidative damage.
Reducing Alcohol Consumption: Excessive alcohol impairs liver function and reduces IGF-1 synthesis.
Adrenal and Thyroid Health: Proper adrenal and thyroid function is necessary for hormonal balance. Adaptogens like ashwagandha and Rhodiola rosea may support these glands and enhance HGH secretion.
Potential Benefits of HGH Beyond Growth Factor Stimulation
Beta Cell Regeneration
HGH stimulates beta cell proliferation directly and through IGF-1, reducing beta cell apoptosis and improving overall islet function.
Improved Insulin Sensitivity
By mobilizing fat stores and promoting muscle growth, HGH indirectly improves insulin sensitivity, reducing the metabolic burden on beta cells.
Anti-Inflammatory Effects
HGH reduces systemic inflammation by modulating cytokine production, improving the regenerative environment for beta cells.
Mitochondrial Health
HGH enhances mitochondrial function by promoting mitochondrial biogenesis and reducing oxidative stress, supporting cellular energy production and longevity.
Sleep and Recovery
HGH secretion during sleep promotes tissue repair and recovery, indirectly supporting beta cell health by reducing systemic stress and inflammation.
Bone and Muscle Health
HGH’s role in promoting bone density and muscle mass not only improves physical health but also enhances metabolic regulation, which can benefit glucose homeostasis and beta cell function.
The HGH-diabetes connections very closely mirror those found in testosterone and IGF-1. Inflammation, poor recovery and malnourishment lay at the foundation of an under-stimulated growth response. In diabetic systems, reduced HGH secretion and impaired IGF-1 signaling exacerbate beta cell loss and metabolic dysfunction. By focusing on natural strategies to enhance HGH production, such as optimizing sleep, engaging in high-intensity exercise, and maintaining liver health, individuals may be able to harness HGH’s regenerative potential. Beyond its direct effects on growth, HGH offers additional benefits in reducing inflammation, improving insulin sensitivity, and supporting overall metabolic health, making it a promising component in the pursuit of beta cell recovery.
VI. How Growth Stimulants Could Help in the Context of T1D
Improved Beta Cell Survival
Mitigation of inflammatory and autoimmune damage.
Enhancement of cellular repair mechanisms.
Promotion of Beta Cell Proliferation
Direct stimulation of beta cell growth.
Supporting islet architecture and function.
Enhancing Insulin Sensitivity
Indirect effects through improved muscle mass and glucose uptake.
Potential Synergistic Effects
Combination therapies using testosterone, IGF-1, and HGH.
Synergistic effects on overall metabolic health.
Beta cell regeneration is a complex process involving multiple cellular and extracellular mechanisms. Testosterone, IGF-1, and HGH, when used in combination, offer a synergistic approach to stimulate beta cell regrowth, improve insulin secretion, and restore metabolic balance. Their influence extends beyond direct growth stimulation, impacting key variables such as cellular architecture, polarity, extracellular matrix (ECM) integrity, and overall cell survival.
In this section, we’ll explore how these hormones influence beta cell regeneration at a molecular and systemic level and outline combination therapies, beneficial nutrients, and physical activities that promote hormonal balance and beta cell recovery.
Key Variables in Beta Cell Regrowth and Insulin Secretion
Cellular Architecture and Polarity
Polarity: Beta cells exhibit apical-basal polarity, crucial for directed insulin secretion toward the bloodstream. Loss of polarity disrupts granule exocytosis, impairing insulin release.
Hormonal Influence:
IGF-1 and HGH stimulate cytoskeletal remodeling through the activation of the PI3K-Akt pathway, helping restore polarity by reorganizing actin filaments and microtubules.
Testosterone indirectly supports polarity by reducing inflammation, which can damage cytoskeletal structures.
Extracellular Matrix (ECM) Integrity
The ECM provides structural support and regulates beta cell behavior through integrin signaling. ECM degradation, often caused by chronic inflammation, impairs beta cell survival and function.
Hormonal Influence:
IGF-1 promotes ECM remodeling by stimulating the production of collagen and laminin, key ECM components that enhance beta cell adhesion and survival.
HGH enhances ECM integrity by increasing fibroblast activity and promoting tissue repair.
Combination Effect: Together, IGF-1 and HGH create an environment conducive to beta cell regeneration by restoring ECM composition and promoting integrin signaling.
Beta Cell Survival and Anti-Apoptotic Mechanisms
Beta cell apoptosis is a primary cause of reduced beta cell mass in diabetes. Growth factors are known to activate anti-apoptotic pathways.
Hormonal Influence:
IGF-1 and HGH activate the PI3K-Akt pathway, which inhibits pro-apoptotic proteins (e.g., Bax, Bad) and enhances the expression of anti-apoptotic proteins (e.g., Bcl-2).
Testosterone reduces oxidative stress and inflammation, further protecting beta cells from apoptosis.
Beta Cell Regeneration and Proliferation
Regeneration requires the activation of progenitor cells or transdifferentiation of neighboring cells into functional beta cells.
Hormonal Influence:
IGF-1 directly stimulates beta cell proliferation by activating the MAPK/ERK pathway, which drives cell cycle progression.
HGH enhances progenitor cell activation and supports transdifferentiation processes by increasing the expression of transcription factors like NGN3 and PDX1, both essential for beta cell development.
Combination Effect: The synergistic action of IGF-1 and HGH accelerates beta cell regeneration by enhancing both proliferation and differentiation pathways.
Insulin Secretion and Glucose Sensing
Proper insulin secretion requires intact glucose sensing mechanisms and adequate ATP production.
Hormonal Influence:
HGH and IGF-1 improve mitochondrial function, increasing ATP production and enhancing glucose-stimulated insulin secretion (GSIS).
Testosterone enhances insulin secretion indirectly by improving glucose uptake in peripheral tissues, reducing the overall burden on beta cells.
Combination Therapies for Beta Cell Regeneration
Hormonal Balance
Restoring testosterone, IGF-1, and HGH levels through a combination of natural methods and targeted therapies can create an optimal environment for beta cell regeneration.
Potential Synergies:
IGF-1 + HGH: These two hormones work together to promote both beta cell proliferation and ECM remodeling.
Testosterone + IGF-1: Testosterone reduces inflammation, enhancing the regenerative potential of IGF-1.
Nutrient Support
Adequate intake of nutrients that support hormone production and cellular repair is critical:
Zinc: Essential for testosterone synthesis and immune regulation. Found in oysters, red meat, and pumpkin seeds.
Magnesium: Supports mitochondrial function and hormone balance. Found in spinach, almonds, and dark chocolate.
Vitamin D: Enhances testosterone production and improves insulin sensitivity. Found in fatty fish, egg yolks, and fortified foods.
B Vitamins: Critical for energy metabolism and HGH secretion. Found in leafy greens, whole grains, and legumes.
Omega-3 Fatty Acids: Reduce inflammation and support hormonal balance. Found in fatty fish, walnuts, and flaxseeds.
Beneficial Foods
High-Protein Foods: Stimulate HGH and IGF-1 secretion. Include lean meats, fish, eggs, and legumes.
Healthy Fats: Support hormone synthesis. Include avocados, olive oil, and nuts.
Low-Glycemic Vegetables: Help regulate blood sugar and reduce insulin spikes. Include leafy greens, broccoli, and cauliflower.
Physical Activity for Hormonal Optimization
Resistance Training
Weightlifting and resistance exercises have been shown to increase testosterone, HGH, and IGF-1 levels. Aim for compound movements (e.g., squats, deadlifts, bench press) to maximize hormone release. The more muscle fibers being activated the greater the hormonal response!
High-Intensity Interval Training (HIIT)
Short bursts of intense exercise followed by rest periods significantly boost HGH secretion and improve insulin sensitivity.
Aerobic Exercise
Moderate-intensity aerobic exercise improves cardiovascular health and insulin sensitivity, supporting overall metabolic balance.
Recovery and Sleep
Since HGH is primarily secreted during deep sleep, prioritizing high-quality sleep (7-9 hours per night) is essential for maximizing its regenerative potential.
Lifestyle Factors for Hormonal Balance
Stress Management
Chronic stress elevates cortisol, which can inhibit testosterone and HGH secretion. Incorporate stress reduction techniques such as meditation, yoga, or deep breathing exercises.
Intermittent Fasting
Fasting periods can enhance HGH secretion and improve insulin sensitivity, supporting beta cell regeneration.
I've experimented with multi-day fasts (up to 88 hours) and the classic 16:8 intermittent fasting schedule. Both are beneficial in their own right.
Avoiding Endocrine Disruptors
Limit exposure to environmental toxins that interfere with hormone production, such as BPA, phthalates, and heavy metals. Opt for glass containers and natural personal care products when possible.
Beta cell regeneration requires a multifactorial approach that addresses both systemic and cellular factors. Testosterone, IGF-1, and HGH, when used in combination, offer powerful regenerative potential by improving beta cell architecture, restoring polarity, enhancing ECM integrity, and stimulating both survival and proliferation pathways. By incorporating nutrient-dense foods, regular physical activity, and lifestyle strategies that promote hormonal balance, individuals can create an optimal internal environment for beta cell recovery. Beyond their direct effects on beta cells, these hormones play crucial roles in reducing inflammation, improving insulin sensitivity, and supporting overall metabolic health, making them essential components in the pursuit of reversing diabetes-related beta cell dysfunction.
VII. Current Evidence and Research
Summary of preclinical and clinical studies supporting the use of these growth stimulants in beta cell regeneration.
Limitations of current research and the need for further studies.
Potential Risks of Growth Stimulant Therapies
Hormonal imbalances.
Overgrowth or unwanted proliferation of other tissues.
Long-term effects on cardiovascular health.
While the potential of growth stimulants—testosterone, IGF-1, and HGH—in beta cell regeneration is promising, research in this area is still evolving. Both preclinical and clinical studies have provided valuable insights into how these hormones influence beta cell survival, proliferation, and function. However, limitations remain, and risks associated with hormonal therapies must be carefully considered.
Summary of Current Evidence
Preclinical Studies
IGF-1 and Beta Cell Proliferation:
A study by Xu et al. (2015) demonstrated that IGF-1 administration in diabetic mice significantly enhanced beta cell proliferation and reduced apoptosis by activating the PI3K-Akt pathway. The treated mice exhibited improved insulin secretion and glucose tolerance.
HGH and Islet Regeneration:
In a rodent model of beta cell injury, HGH treatment increased islet size and beta cell mass by stimulating progenitor cell differentiation and ECM remodeling. This effect was amplified when HGH was combined with IGF-1.
Testosterone and Insulin Sensitivity:
A study by Chen et al. (2017) found that testosterone supplementation improved insulin sensitivity in diabetic rats, reduced systemic inflammation, and indirectly enhanced beta cell function by lowering oxidative stress.
Clinical Studies
IGF-1 in Type 1 and Type 2 Diabetes:
Clinical trials have explored IGF-1 therapy in both type 1 and type 2 diabetes. One trial demonstrated that IGF-1 administration improved insulin sensitivity and reduced exogenous insulin requirements in patients with type 1 diabetes. However, the long-term effects on beta cell preservation remain unclear.
HGH and Glucose Metabolism:
HGH therapy has been used clinically in patients with growth hormone deficiency. Studies indicate that HGH improves body composition and metabolic health, but its impact on beta cell regeneration in humans is still under investigation.
Testosterone in Men with Diabetes:
Several studies have shown that testosterone replacement therapy in men with type 2 diabetes improves insulin sensitivity, reduces visceral fat, and lowers inflammatory markers, indirectly supporting beta cell health.
Limitations in Current Research
Lack of Long-Term Studies
Most clinical studies on hormonal therapies focus on short-term outcomes. Long-term effects on beta cell regeneration and metabolic health are still unknown, making it difficult to assess the sustainability of these therapies.
Limited Human Data
While preclinical studies show strong evidence for beta cell regeneration, human trials are fewer and often limited to specific populations (e.g., men with low testosterone or individuals with growth hormone deficiency).
Variability in Response
Individual responses to hormonal therapies vary due to factors such as baseline hormone levels, genetic differences, and pre-existing conditions. Pre-study personal nutrition and lifestyle factors are rarely accounted for. Personalized approaches are necessary to optimize outcomes.
Risks and Considerations
Hormonal Imbalances
Excessive supplementation of testosterone, IGF-1, or HGH can lead to hormonal imbalances, causing side effects such as:
Testosterone: Acne, mood swings, prostate enlargement, and in extreme cases, cardiovascular risks.
IGF-1: Excessive IGF-1 levels can promote unwanted cell proliferation, raising concerns about increased cancer risk.
HGH: Overuse of HGH can lead to acromegaly (excessive growth of bones and tissues), insulin resistance, and joint pain.
Impact on Glucose Metabolism
While moderate doses of IGF-1 and HGH improve glucose metabolism, high doses can have the opposite effect by promoting hepatic glucose output and reducing insulin sensitivity.
Potential Long-Term Effects
Long-term impacts of these therapies on organs such as the liver, kidneys, and heart remain uncertain. Continuous monitoring of organ function is essential in individuals undergoing hormonal treatments.
Mitigating Risks with Complementary Practices
Optimizing Natural Hormone Production
Before considering hormonal therapies, individuals can implement lifestyle and dietary strategies to naturally enhance testosterone, IGF-1, and HGH levels:
Diet: Ensure adequate intake of protein, healthy fats, zinc, magnesium, and vitamin D.
Exercise: Incorporate resistance training, high-intensity interval training (HIIT), and aerobic exercise to stimulate endogenous hormone production.
Sleep: Prioritize deep, uninterrupted sleep, as HGH secretion peaks during slow-wave sleep.
Stress Management: Chronic stress elevates cortisol, which suppresses testosterone and HGH secretion. Regular stress-reducing activities such as yoga, meditation, and deep breathing can help restore hormonal balance.
Monitoring Hormonal Levels
Regular monitoring of testosterone, IGF-1, HGH, and related biomarkers (e.g., liver enzymes, glucose levels) can help tailor therapies and prevent adverse effects.
Supporting Liver and Kidney Health
Since the liver and kidneys play crucial roles in hormone metabolism and clearance, maintaining their health is essential:
Liver Support: Incorporate antioxidant-rich foods (e.g., berries, leafy greens) and reduce alcohol and processed food intake.
Kidney Support: Stay hydrated, consume potassium-rich foods (e.g., bananas, sweet potatoes), and avoid excessive salt intake.
Combining with Anti-Inflammatory Strategies
Reducing systemic inflammation enhances the efficacy of hormonal therapies and supports beta cell regeneration. Anti-inflammatory strategies include:
Omega-3 fatty acids (e.g., from fatty fish, flaxseeds).
Curcumin (found in turmeric) and polyphenols (found in green tea and dark chocolate).
The use of testosterone, IGF-1, and HGH as potential therapies for beta cell regeneration offers an exciting avenue for reversing beta cell loss in diabetes. While preclinical and clinical evidence supports their ability to enhance beta cell survival, proliferation, and function, more long-term human studies are needed to fully understand their benefits and risks. Hormonal therapies should be approached cautiously, with attention to potential side effects and long-term impacts.
By combining these therapies with natural methods for hormone optimization, such as proper nutrition, exercise, sleep, and stress management, individuals can mitigate risks and enhance the regenerative potential of their beta cells. Ultimately, a holistic, personalized approach is essential for leveraging the full power of these growth stimulants in the pursuit of beta cell recovery and metabolic health.
VIII. Conclusion
For far too long, type 1 diabetes (T1D) has been viewed through a narrow lens—defined by autoimmune destruction and managed primarily by insulin therapy. However, as scientific understanding evolves, so does the possibility of beta cell regeneration. By addressing a broader range of contributing factors—nutrient imbalances, hormonal dysregulation, environmental toxins, and metabolic stress—we unlock new strategies for not just managing T1D but potentially reversing its underlying dysfunction.
This article explored how testosterone, IGF-1, and HGH—three powerful growth stimulants—may help stimulate beta cell regeneration. Each of these hormones influences critical cellular variables such as beta cell proliferation, survival, polarity, and extracellular matrix (ECM) integrity. By acting on both systemic and cellular levels, they create a regenerative environment that enhances insulin secretion and glucose regulation.
Key Components of a Comprehensive Beta Cell Regeneration Strategy
Hormonal Optimization
Testosterone: Reduces inflammation, supports glucose uptake, and promotes tissue repair.
IGF-1: Enhances beta cell proliferation, improves insulin sensitivity, and mitigates apoptosis.
HGH: Stimulates progenitor activation, promotes ECM remodeling, and supports overall cellular growth and repair.
A combination approach involving these hormones may offer synergistic benefits, enhancing beta cell regrowth and improving metabolic outcomes.
Nutrient and Lifestyle Support
Beta cell regeneration isn’t only about hormonal stimulation—it requires the right internal environment:
Exercise: Resistance training and high-intensity interval training (HIIT) naturally boost testosterone, IGF-1, and HGH levels, improving insulin sensitivity and metabolic health.
Sleep Optimization: Deep, restorative sleep is critical for HGH secretion and overall hormonal balance. Prioritizing sleep helps create the hormonal environment needed for beta cell regeneration.
Stress Management: Chronic stress disrupts the hypothalamic-pituitary-adrenal (HPA) axis, leading to elevated cortisol levels that inhibit hormone secretion. Techniques like meditation, yoga, and mindful breathing can restore hormonal equilibrium.
Systemic Health
A healthy liver and kidneys are essential for the metabolism and clearance of hormones like testosterone, IGF-1, and HGH. Supporting these organs ensures optimal bioavailability of growth factors.
Liver Health: Reduce alcohol consumption, incorporate antioxidant-rich foods, and use liver-supporting herbs like milk thistle and dandelion root.
Kidney Health: Maintain hydration, consume potassium-rich foods, and monitor sodium intake.
Anti-Inflammatory Strategies
Since chronic inflammation accelerates beta cell loss and impairs regeneration, reducing systemic inflammation is a cornerstone of any comprehensive strategy. Incorporate:
Omega-3 fatty acids from fatty fish, walnuts, and flaxseeds.
Curcumin (from turmeric), which has potent anti-inflammatory properties.
Polyphenols from green tea, dark chocolate, and berries, which combat oxidative stress and promote cellular repair.
A Vision for the Future
Imagine a future where beta cells are no longer viewed as static, irreparable structures but as dynamic entities capable of regeneration. In this future, patients diagnosed with T1D are empowered to explore holistic strategies that go beyond insulin injections—strategies that target the root causes of beta cell dysfunction. Comprehensive hormonal therapies, combined with nutrient-dense diets, tailored exercise routines, and lifestyle changes, could one day offer not just better management of T1D, but genuine pathways toward reversal and healing.
While the science of beta cell regeneration is still emerging, the potential is undeniable. By fostering a regenerative environment within the body, we may be able to coax beta cells back to life, restore insulin production, and ultimately transform the outlook for millions of people living with T1D.
This is not merely a distant hope—it’s a call to action for continued research, innovation, and the exploration of new therapeutic avenues. The path forward will require a combination of scientific rigor, clinical trials, and personal experimentation, but the vision of restoring beta cell function and achieving lasting metabolic health is within reach.
IX. References and Citations
Testosterone and IGF-1 Interaction:
Veldhuis JD, Frystyk J, Iranmanesh A, Ørskov H. Testosterone and Estradiol Regulate Free Insulin-Like Growth Factor I (IGF-I), IGF Binding Protein 1 (IGFBP-1), and Dimeric IGF-I/IGFBP-1 Concentrations. The Journal of Clinical Endocrinology & Metabolism. 2005;90(5):2941–2947.
Growth Hormone and IGF-1 Axis Regulation:
Giustina A, Veldhuis JD. Central and peripheral regulation of the GH/IGF-1 axis: GHRH, somatostatin and beyond. Reviews in Endocrine and Metabolic Disorders. 2024.
Testosterone and IGF-1 in Protein Synthesis:
Mauras N, Haymond MW. Testosterone and Insulin-like Growth Factor (IGF) I Interact in Regulating Protein Metabolism in Prepubertal Boys. The Journal of Clinical Endocrinology & Metabolism. 2000;85(4):1627–1631.
Beta Cell Regeneration Research:
Mount Sinai Researchers Move Closer to a Cure for Diabetes. Mount Sinai Health System. 2024.
Shahcheraghi et al. Overview of key molecular and pharmacological targets for diabetes and associated diseases. Life Sciences. 2021;278. 119632.
Hormonal Responses to Resistance Training:
Kraemer WJ, Ratamess NA. Growth Hormone(s), Testosterone, Insulin-Like Growth Factors, and Cortisol in Human Responses to Resistance Exercise. Frontiers in Endocrinology. 2020;11:33.
IGF-1 in Metabolic Homeostasis:
Yakar S, Adamo ML. The Role of Insulin-like Growth Factor-1 (IGF-1) in the Control of Energy Expenditure. Cells. 2021;10(10):2664.
Exercise and Hormonal Adaptations:
Hayes LD, Grace FM, Sculthorpe N. Effects of Exercise Training on Anabolic and Catabolic Hormones with Advanced Age. Sports Medicine. 2021;51(4):617–628.
IGF-1 and Cancer Risk:
Largest study to date confirms role of two hormones in aggressive prostate cancer risk. University of Oxford. 2020.
GH/IGF Axis in Cancer:
Vella V, Malaguarnera R. Growth Hormone/Insulin Growth Factor Axis in Sex Steroid-Associated Cancers. Frontiers in Cell and Developmental Biology. 2021;9:630503.
Ibutamoren and GH/IGF-1 Axis:
Ibutamoren. Wikipedia.
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