The BPC-157 Surgery Protocol

How I'm Stacking Peptides, Hormones & Timing To Rebuild Stronger

Surgery on your calendar. Depressed you’ll be out of the gym for months. Angry you must scale back intensity. Grudgingly accepting the “take it slow” advice that feels more like surrender than strategy.

My hernia surgery was just yesterday. I’ve spent a lot of time researching and planning my recovery protocol as to NOT follow that same script.

Most people accept the standard timeline. 6–8 weeks of minimal activity. Walks only. Gradual return to training. Fingers crossed the repair holds.

The medical advice is sound but passive - rest, don’t lift, let nature take its course.

But here’s what that advice misses: your body’s healing machinery can be optimized. Collagen synthesis, angiogenesis, inflammation control - these aren’t fixed. They respond to signals. You can stack those signals intelligently.

I’ve used targeted recovery protocols before:

• Peptides for chronic back pain

• Tissue-repair compounds for shoulder injuries

• Collagen-support stacks for ligament tears.

This time, I’m deploying everything I know about wound healing, mapped onto the specific phases of fascial repair.

This newsletter breaks down the full protocol: hormones, peptides, and supplements, with dosing, timing, and the mechanistic rationale behind each choice.

Fair warning - this gets technical. But if you want to understand how to accelerate recovery without compromising repair quality, keep reading.

How Wounds Actually Heal (And Where Standard Advice Falls Short)

Most people treat recovery as passive waiting. But healing happens in distinct biological phases (inflammation → proliferation → remodeling), each with different rate-limiting factors.

This protocol matches specific compounds to the phase where they have maximum impact, then tapers them as the next phase takes over. The idea is to time the right signals to the repair phase.

Before we get into the protocol, we must have a basic understanding of wound recovery mechanisms. Most tissue repair follows overlapping phases. This is a quick review of what happens in each phase, with definitions to bring you up to speed.

1. Inflammation occurs over hours to days. This is the cleanup and setup for recovery. Immune cells are recruited and travel to the injury site. Cytokines begin coordinating activity between immune cells. Dead cells and debris gets cleared.

2. Proliferation occurs over days to weeks. In short, this phase is focused o building new tissue. Fibroblasts begin synthesizing new collagen and extracellular matrix. Collagen is deposited to fill the wound gap. Skin cells proliferate and migrate from the wound edges across the wound surface, restoring the protective outer barrier. Angiogenesis (the formation of new blood vessels) peaks.

3. Remodeling occurs over weeks to months. This phase is where the newly formed tissue strengthens under load. Collagen matures and crosslink, reorganizing and aligning across stress lines. Tensile strength is tested and improved. The final scar architecture completes.

Standard advice treats all three phases the same: rest, eat protein, hope for the best. But each phase has different rate-limiting factors.

Early on, it’s angiogenesis and fibroblast recruitment.

Mid-phase, it’s collagen deposition and matrix organization.

Late phase, it’s mechanical loading and cross-linking.

If you can identify what limits each phase, you can target it with specific compounds, then taper them as the phases shift. That’s what this protocol does. I call it “Phase-matched signaling” - the right molecule, at the right dose, at the right time.

The Endocrine Foundation: Setting the Metabolic Stage for Repair

Hormones mainly act by shifting:

• Inflammatory tone - Too much results in delayed healing.

• Fibroblast/collagen behavior - Too little and the repair is weak. Too dysregulated results in fibrosis.

• Angiogenesis (for adequate blood flow)

• Muscle and bone support around the injury, which determines function and load tolerance.

Why I’m Keeping Testosterone at TRT (Not Higher)

Testosterone Cypionate
160 mg once weekly

I will be keeping my testosterone at my TRT dose (160 mg/week). This keeps my testosterone levels in the 900-1000 ng/dL range.

Higher testosterone doses are generally not recommended, as androgens can inhibit wound healing, increase inflammatory responses, and change collagen dynamics during wound repair.

One study finds that in castrated, therefore androgen-deficient, rats :

• Increased collagen accumulation in wounds

• Increased fibronectin levels

• Faster healing overall

This further supports that androgens may delay healing. Proteolytic enzyme activity is increased. Collagen breakdown occurs. Accumulation of structural proteins is reduced.

Where testosterone is most clearly beneficial is muscle mass and strength maintenance, which can indirectly improve recovery capacity (mobility, rehab tolerance, less loss). A recent review in surgical contexts notes that TRT can help preserve lean mass post-op.

Why Estradiol Makes or Breaks Your Repair

At my 160 mg per week testosterone dose, this should be sufficient to preserve muscle as much as possible, while keeping my estradiol at the top of the range without an aromatase inhibitor.

The exact optimal estradiol range for surgical collagen remodeling is unknown, but the research shows that estrogen is an important factor in the healing process.

During the initial inflammation phase of recovery, estradiol tends to reduce prolonged inflammation. Estradiol also supports skin cell migration, re-epithelialization, and can improve the quality and tempo of the proliferative phase.

Estradiol is a direct regulator of collagen production, collagen organization, and tissue hydration - all of which determine how strong and resilient the repaired tissue becomes.

Estradiol directly binds to estrogen receptors in fibroblasts, tendon cells, ligament cells, skin, and fascia.

Upon binding, here’s what happens:

Type I and type III collagen gene transcription upregulates. Tensile strength and the quality of early wound scaffolding improves. Collagen cross-linking quality is enhanced. Fiber alignment improves. Brittle and disorganized scar tissue is reduced.

The result: less brittle, better-organized tissue that’s less likely to tear under load.

There’s also evidence in animal models that estradiol can upregulate pro-angiogenic pathways, important for faster closure and better-quality repair.

Preserving the Signal: How HCG Maintains the Hormonal Environment

HCG
250 IU subcutaneously 3 times weekly

I’ll be continuing to use HCG (human chorionic gonadotropin) through this process.

HCG is typically used to preserve LH signaling while on TRT, keeping the testes active and preventing shutdown of intratesticular testosterone and estrogen production.

This matters because adequate estradiol is required for high-quality collagen synthesis, crosslinking, and fascia strength, as described above. TRT alone can flatten that signal.

HCG also maintains pregnenolone, DHEA, and downstream neurosteroids, improving sleep, stress resilience, and recovery quality during healing.

Though HCG doesn’t directly help post-op recovery, it supports an optimal physiologic hormonal environment without adding excessive estrogen or water retention.

The Anabolic Engine: Why GH Stays in My Protocol

Growth Hormone
4 IU subcutaneously daily at bedtime

I will continue my established GH protocol (4 IU daily) throughout the recovery period.

Growth hormone is one of the most well-studied anabolic hormones in surgical and wound-healing contexts, with direct effects on collagen synthesis, tissue repair, and metabolic support during catabolic stress.

GH exerts its healing effects through multiple mechanisms.

• It directly stimulates fibroblast proliferation and collagen synthesis in wound tissue.

• It upregulates insulin-like growth factor-1 (IGF-1), which acts locally in healing tissues to promote cell migration, angiogenesis, and matrix deposition.

• GH also improves nitrogen retention and protein synthesis systemically, helping preserve lean mass during the post-operative catabolic window when the body is breaking down muscle to fuel repair.

Clinical data support GH’s role in accelerating wound healing.

Studies in burn patients, surgical wounds, and chronic ulcers show that GH administration increases collagen deposition, reduces healing time, and improves tensile strength of repaired tissue.

In surgical populations, GH has been shown to reduce nitrogen loss, preserve lean body mass, and improve recovery markers compared to placebo.

The 4 IU dose sits in the therapeutic range used in wound-healing studies (typically 0.05–0.1 mg/kg/day, or roughly 3–7 IU for a 70 kg adult). Bedtime dosing aligns with physiologic GH secretion patterns and minimizes interference with normal physiologic pulsatile release.

Potential concerns include fluid retention, joint stiffness, and transient insulin resistance - all manageable at this dose but worth monitoring. I’ve acclimated to this dose over months of administration, so these side effects are not a concern.

GH’s pro-anabolic effects are synergistic with adequate protein intake and the collagen and vitamin C supplementation outlined below, creating a complete environment for tissue repair: hormonal signal (GH, IGF-1), enzymatic cofactors (vitamin C), and substrate availability (collagen peptides, dietary protein).

Unlike supraphysiologic androgens, which can impair certain aspects of wound healing, GH consistently demonstrates pro-healing effects across tissue types.

The decision to continue rather than initiate GH reflects an already-established protocol. Starting GH solely for surgery would require more careful risk-benefit analysis with timing and dose considerations, but maintaining a stable dose avoids the metabolic disruption of withdrawal during a high-demand recovery phase.

Now that we have the baseline hormonal stack out of the way, let’s review the OTC supplements critical for optimal repair. These are basic building blocks. Repair cannot happen without them.

The Raw Materials: Collagen, Vitamin C, and the Building Blocks You Can’t Skip

Collagen peptides and vitamin C will be initiated 14 days pre-op and used through full recovery. The pairing addresses the fundamental bottleneck of surgical recovery.

These are synergistic.

Collagen is the primary structural protein of fascia. Vitamin C is depleted by surgery.

Without adequate vitamin C, collagen peptides cannot be properly hydroxylated, resulting in instability and a lack of tensile strength (scurvy pathophysiology).

Without adequate glycine and proline substrate (from collagen peptides), vitamin C has insufficient precursor to process.

Collagen Peptides - Giving Your Fibroblasts Something to Work With

Collagen Peptides
20 g 1-3 times daily

Studies show that 10 g daily of bioactive collagen hydrolysate (rich in prolyl‑hydroxyproline) significantly improved Pressure Ulcer Scale for Healing (PUSH) scores and reduced wound area versus placebo by week 16, with divergence apparent by week 8.

Pharmacokinetic work confirms that oral collagen hydrolysate elevates bioactive dipeptides (Gly‑Pro‑Hyp, Pro‑Hyp) in the bloodstream and skin within hours, providing direct building blocks and substrate for collagen synthesis. Specifically, the Pro-Hyp dipeptide acts as a growth‑initiating factor specific to wound‑healing fibroblasts, stimulating proliferation and matrix production.

Vitamin C - The Cofactor That Prevents “Scurvy-Like” Healing

Vitamin C Ester
2000 mg daily

Vitamin C dosing is derived from the only randomized controlled trial specifically examining collagen synthesis in inguinal hernia repair patients. It showed that 1,250 mg vitamin C daily started 14 days pre‑surgery and continued 14 days post‑surgery, significantly increased serum procollagen propeptide concentrations versus control.

Vitamin C is a required cofactor for procollagen hydroxylation in fascial tissue. Not only is it a cofactor, plasma vitamin C is shown to fall precipitously after surgery. It’s been found that ingesting at least 500 mg/day is required to normalize levels post‑operatively, and that Vitamin C-deficient states produce scurvy‑like impaired healing with poor scar formation.

As the inflammatory phase ends and proliferative phase begins and progresses through week 4, collagen type III deposition accelerates. The initial oxidative burst resolves. Dosage is kept high to support newly synthesized procollagen.

As the remodeling phase begins around week 5, we transition to load-driven remodeling. This requires maintaining substrate availability while allowing mechanical forces to dictate fiber alignment. Vitamin C remains necessary for cross-linking. Collagen peptides remain necessary for substrate.

Though the dosages described above are higher than the dosages used in studies, I see no problem with being above the dosage ranges based on mechanistic reasoning and safety data.

In the rest of this newsletter for paid subscribers, I’ll be diving into the 3 peptides, their mechanisms, dosing protocols, timing, and rationale for optimal healing.

Targeted Signaling: The Phase-Specific Peptide Protocol

With the hormonal and substrate foundation set - testosterone for muscle preservation, estrogen for collagen quality, HCG to keep the system balanced, GH to drive anabolic signaling, and OTC supplements to provide the building blocks - we’ve created the metabolic environment for repair.

Now we add the targeted signals.

BPC-157 | Weeks 1–2: Jump-Starting Angiogenesis (The “Now” Signal)

BPC-157
Week 1 - 1000 mcg twice daily
Week 2 - 1000 mcg twice daily
Week 3 - 500 mcg twice daily
Week 4 - 500 mcg twice daily
Week 5 - 250 mcg twice daily
Week 6 - 250 mcg twice daily

Dosing here is a combination of personal and client experience with BPC-157, and also extrapolated from animal tendon and GI models, then mapped onto human wound‑healing phases, as no human trials presently validate this exact regimen.

The acute inflammation phase begins within minutes to hours. Animal studies consistently start BPC-157 within 10-30 minutes of injury and show robust healing, with no evidence that early administration interferes with hemostasis (the stopping of bleeding).

As the proliferative phase begins on day 3, angiogenesis, fibroblast proliferation and migration, granulation tissue, collagen III deposition, and ECM formation are at maximum. This high dosing continues through day 14. This timing is supported by animal studies - which show results in increased load-to-tendon failure and higher functionality.

By day 14, we are in the late proliferative phase and begin transitioning into early remodeling. During this period, collagen deposition continues aggressively. Angiogenesis continues, but normalizes. Fibers start aligning. Mechanical loading begins to matter more.

BPC-157 is reduced but kept at moderately high to support angiogenesis, fibroblast survival, and ECM remodeling. This reduction in dose is still at the top range of current recommended dosages. The rationale is to maintain strong chemical assistance through the bulk of collagen deposition and early alignment.

By weeks 5-6, we are established in the remodeling and maturation phase. Dose is reduced again. Angiogenesis is normalized. Collagen cross-linking and stiffness development under load become priority. This reduced dose will provide cytoprotective and inflammatory support without overwhelming the load signal.

The decision to decrease the dose is made from a phase‑aware translation of the animal data and general wound‑healing physiology, not a regimen that has been prospectively tested in humans.

It reflects how human wounds actually heal: angiogenesis and fibroblast activity dominate early, while later phases are about collagen alignment and stiffness under load.

Because BPC‑157 is strongly pro‑angiogenic and long‑term human data are limited, we front‑load its use during the most biology‑sensitive window, then shift to the lowest doses likely to maintain benefit as the fascia matures.

TB-500 | Weeks 2–6: Maintaining Pliability While Tissue Organizes

TB-500
Week 1 - None
Week 2 - 500 mcg twice daily
Week 3 - 500 mcg twice daily
Week 4 - 500 mcg twice daily
Week 5 - 250 mcg twice daily
Week 6 - 250 mcg twice daily

Dosing here is a combination of personal and client experience with TB-500 and extrapolated data from animal models of dermal wound healing, tendon repair, and cardiac regeneration, then mapped onto human wound‑healing phases, as no human trials presently validate this exact regimen.

Note: Scientific studies on TB-500 are scarce. Most studies focus on thymosin beta-4, the “parent” peptide of TB-500. So I’ll be using studies on thymosin beta-4 in my rationale.

TB‑500 is introduced in Week 2 rather than immediately post‑surgery. This delayed start is intentional: BPC‑157 handles the initial angiogenic and fibroblast recruitment surge during days 0–14, while TB‑500 (thymosin beta‑4) is reserved for when tissue pliability, cell motility, and actin cytoskeleton remodeling become the dominant biological needs.

Thymosin beta‑4 regulates cell shape, migration, and matrix organization - processes that become critical as freshly deposited collagen undergoes alignment.

TB‑500 accelerates wound healing and reduces inflammation through multiple mechanisms:

• Upregulates actin to help cell migration to injury sites

• Promotes matrix metalloproteinase expression during repair

• Enhances endothelial cell migration and adhesion for angiogenesis

In dermal wound models, thymosin beta‑4 is upregulated four‑ to six‑fold after initial vessel formation and remains active throughout the remodeling phase.

Unlike BPC‑157’s early‑phase dominance, TB‑500’s effects on tissue pliability and mechanical adaptation are most valuable when the repair site is vascularized and ready to respond to stress.

As the proliferative phase continues through weeks 2–4, the priority shifts from simply generating new tissue to organizing that tissue for function. Collagen deposition continues. Fibers begin aligning along stress lines. Cell migration and actin cytoskeleton remodeling occur. Fibroblasts reposition. The matrix begins to reorganize under early mechanical cues.

TB‑500 during this window supports these processes - enhancing cell motility, maintaining tissue pliability, and preparing the fascia to handle progressive loading without premature stiffening or aberrant scarring.

By weeks 5–6, again we are entering established remodeling and maturation. Collagen cross‑linking and stiffness development under load become the priority.

As with BPC-157, the TB-500 dose is reduced.

I believe this taper is critical: if TB‑500 remains at full strength, the tissue may retain excessive plasticity and cellular motility, delaying the transition from chemical regulation to mechanical regulation.

By stepping down the dose, we allow mechanical loading to become the primary driver of collagen alignment and cross‑linking. The tissue is forced to self‑organize under stress, developing true mechanical resilience rather than remaining in a chemically maintained, pliable state.

GHK-Cu | Day 3 Onward: The Matrix Modulator

GHK-Cu
2 mg daily starting day 3 post-op

GHK-Cu is a copper peptide that shows evidence of increased wound healing in rats within a 21-28 day period. It has anti-inflammatory effects, helps with collagen III synthesis, stimulates fibroblast activation and angiogenesis. Many of these effects overlap with BPC-157.

For these reasons, I’ll be starting GHK-Cu on day 3, as the transition from the inflammatory phase to the proliferative phase begins. Anti-inflammatory and pro-collagen effects become maximally useful during this transition.

GHK-Cu will be continued through weeks 2-8 for continued support throughout the proliferative and remodeling phase.

Studies on rats used 50 mcg/kg topical dosing. For me, a ~70 kg male, this would come to approximately 3.5 mg daily.

I’ll be using 2 mg subcutaneous injections to remain conservative and account for the difference between administration routes.

The Complete Playbook: Dosing, Timing, and Delivery Methods

There you have it. My full surgery recovery stack. Here it is in one spot:

Testosterone

160 mg intramuscularly 1 time week weekly

HCG

250 iu subcutaneously 3 times weekly

Growth Hormone

4 IU subcutaneously daily at bedtime

Collagen Peptides

20 g by mouth 1-3 times daily

Vitamin C

2000 mg by mouth daily

BPC-157 starting immediately post-op

Week 1 - 1000 mcg subcutaneously twice daily
Week 2 - 1000 mcg subcutaneously twice daily
Week 3 - 500 mcg subcutaneously twice daily
Week 4 - 500 mcg subcutaneously twice daily
Week 5 - 250 mcg subcutaneously twice daily
Week 6 - 250 mcg subcutaneously twice daily

TB-500 - Starting Week 2

Week 2 - 500 mcg subcutaneously twice daily
Week 3 - 500 mcg subcutaneously twice daily
Week 4 - 500 mcg subcutaneously twice daily
Week 5 - 250 mcg subcutaneously twice daily
Week 6 - 250 mcg subcutaneously twice daily

GHK-Cu

2 mg subcutaneously daily starting day 3 post-op
Continued through recovery

Why Not Just Let It Heal Naturally?

It seems like I am taking a lot of drugs, peptides, and vitamins to heal properly.

You might be thinking, “Why don’t you just let the body heal naturally?”

Fair question. I get it - Humans have done just fine for thousands of years healing from wounds with just rest, adequate nutrition, and smart progressive loading.

I could do that, but I won’t.

Natural healing is slow healing. Fibroblasts don’t know you have a life to get back to. They’ll deposit collagen at their own pace, organize it however mechanical cues happen to guide them, and you’ll get whatever scar quality randomness delivers.

Or you can bias the process. Give your fibroblasts more substrate (collagen peptides). Ensure the enzymes have their cofactors (vitamin C). Front-load angiogenic signals when blood flow is the bottleneck (BPC-157). Support matrix remodeling when organization dominates (TB-500, GHK-Cu).

If I wanted to live completely naturally, I would leave the hernia and all other ailments alone and let nature take its course. We have tools to optimize the healing process. I will leverage what’s available.

Others may say I should wait 2 weeks before peptide initiation to allow the natural healing processes to occur. There are some anecdotal reports of keloid development attributed to early peptide initiation, but no published case series or controlled data support this.

For the BPC-157 studies, the peptide was given as soon as 10 minutes post-injury. To me, this is a critical early window where I want signaling to be maximized. In these studies, BPC-157 showed improved scar quality, not worse.

TB-500 and GHK-Cu are started later, with consideration of the healing phases we talked about.

My Recovery Starts Now (Your Move)

Outside of the above protocol, I’ll be eating at a slight surplus with high protein, moderate to high carbohydrates, and low to moderate fat. I want to maintain overall anabolic signaling through the repair process. Low insulin and low repair substrate would be counterproductive.

Now for you...

If you’re reading this pre-surgery: Start collagen peptides and vitamin C today. Even two weeks of loading makes a measurable difference in tissue stores. Everything else can wait until post-op.

If you’re reading this post-surgery: Don’t panic if you missed the pre-op window. Start the OTC stack immediately, add peptides within 72 hours if you’re comfortable, and focus on the phases ahead.

Now let me ask you:

• Have you used peptides for surgery?

• If so, what was your experience like?

• What changes would you make to the above protocol?

I’m looking forward to getting back in the gym in a few months, stronger than ever. Now for some rest and recovery. Day 2 begins.

Until next time,

-Marlon

References:

Hormones

1. Gilliver et al. (2003). Androgen receptor–mediated inhibition of cutaneous wound healing. Journal of Clinical Investigation.

2. Gilliver et al. (2006). Androgens modulate the inflammatory response during acute wound healing. Journal of Cell Science.

3. Gilliver et al. (2007). Androgens influence expression of matrix proteins and proteolytic factors during cutaneous wound healing. Laboratory Investigation.

4. Westermann et al. (2024). The Relationship Between Exogenous Testosterone Use and Risk for Primary Anterior Cruciate Ligament Rupture. Orthopaedic Journal of Sports Medicine.

5. Wilkinson et al. (2014). Estrogen effects on wound healing. Periodontology 2000.

6. Wilkinson et al. (2020). Advantages in Wound Healing Process in Female Mice. International Journal of Molecular Sciences.

Growth Hormone

1. Gilpin DA et al. (1994). Recombinant human growth hormone accelerates wound healing in children with large cutaneous burns. Annals of Surgery.

2. Demling RH et al. (1990). Effects of Recombinant Human Growth Hormone on Donor-site Healing in Severely Burned Children. Annals of Surgery.

3. Barrow RE et al. (2009). Randomized Controlled Trial to Determine the Efficacy of Long-Term Growth Hormone Treatment in Severely Burned Children. Annals of Surgery.

4. Cochrane Database Systematic Review. (2010). Human growth hormone for treating burns and skin graft donor sites. Cochrane Library.

5. Demling RH. (2000). Growth hormone, burns and tissue healing. Journal of Burn Care & Research.

6. Kjaer M et al. (2009). From mechanical loading to collagen synthesis, structural changes and function in human tendon. Scandinavian Journal of Medicine & Science in Sports.

7. Svensson M et al. (2016). Effect of growth hormone on aging connective tissue in muscle and tendon: gene expression, morphology, and function following immobilization and rehabilitation. Journal of Applied Physiology.

8. Velloso CP. (2008). Regulation of muscle mass by growth hormone and IGF-I. British Journal of Pharmacology.

9. Owens DJ et al. (2016). In Vitro and In Vivo Effects of IGF-1 Delivery Strategies on Tendon Healing: A Review. International Journal of Molecular Sciences.

10. Rauch DA et al. (2010). Biologics in Achilles tendon healing and repair: a review. Foot & Ankle International.

11. Sato K et al. (2020). Tendon, Ligament, and Muscle Injury, Osteotendinous, Myotendinous, and Muscle-to-Bone Junction Therapy Perspectives with Growth Factors and Stable Gastric Pentadecapeptide BPC 157. Pharmaceuticals.

12. Sato K et al. (2023). Effect of systemic administration of recombinant growth hormone on rotator cuff repair: a rat model study. IP Journal of Surgery and Allied Sciences.

13. Efron DT et al. (2000). Wounds in infection and sepsis - role of growth factors and mediators. Surgical Clinics of North America.

14. Radzikowska-Büchner E et al. (2023). Overview of Recent Developments in the Management of Burn Injuries. International Journal of Molecular Sciences.

Peptides

1. Starešinic et al. (2003). Gastric pentadecapeptide BPC 157 accelerates healing of transected rat Achilles tendon and in vitro stimulates tendocytes growth. Journal of Orthopaedic Research.

2. Gwyer et al. (2019). Gastric pentadecapeptide BPC 157 and its role in accelerating musculoskeletal soft tissue healing. Cell and Tissue Research.

3. Cerovecki et al. (2010). Achilles Detachment in Rat and Stable Gastric Pentadecapeptide BPC 157: Promoted Tendon-to-Bone Healing and Opposed Corticosteroid Aggravation. Journal of Orthopaedic Research.

4. Sikiric et al. (2019). Stable gastric pentadecapeptide BPC 157 can improve the healing course of spinal cord injury and lead to functional recovery in rats. Journal of Orthopaedic Surgery and Research.

5. Philp et al. (2004). Thymosin beta4 promotes angiogenesis, wound healing, and hair follicle development. Mechanisms of Ageing and Development.

6. Malinda et al. (1999). Thymosin beta4 accelerates wound healing. Journal of Investigative Dermatology.

7. Smart et al. (2007). Thymosin beta4 induces adult cardiomyocyte proliferation and heart regeneration. Nature.

8. Goldstein et al. (2012). Thymosin β4: A multi-functional regenerative peptide. Basic properties and clinical applications. Expert Opinion on Biological Therapy.

9. Philp et al. (2003). Thymosin beta4: structure, function, and biological properties supporting current and future clinical applications. Academia.edu.

10. Biotech Peptides. (2022). TB-500 Research in Regards to Wound Healing. Biotech Peptides Monograph.

11. Pickart & Margolina. (2018). Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data. International Journal of Molecular Sciences.

Nutrition

1. Kjaer et al. (2020). Multinutrient Supplementation Increases Collagen Synthesis during Early Wound Repair in a Randomized Controlled Trial in Patients with Inguinal Hernia. The Journal of Nutrition.

2. Fukushima & Yamazaki. (2010). Vitamin C requirement in surgical patients. Current Opinion in Clinical Nutrition & Metabolic Care.

3. Bechara et al. (2022). A Systematic Review on the Role of Vitamin C in Tissue Healing. Antioxidants.