Rapid Wound Healing Observed Following Oral LathMized NAD+ Supplementation: A Case Study

Summary:

Postoperative wound infections after common body contouring procedures are a key contributor to chronic open wounds, placing major burdens on patients and presenting serious challenges to plastic surgeons. Patients may experience consequent serial infections, prolonged treatment plans, readmissions, high medical costs, and decreased quality of life. An aging population and rising prevalence of obesity and metabolic syndrome contribute to growing risks of developing postoperative wound infections and chronic wounds. We present the case of a 59-year-old woman with hypertension, hyperlipidemia, and a distant history of a prolonged postoperative complications and hospitalization who underwent implant removal, bilateral mastopexies with capsulectomies, and concurrent bilateral brachioplasties with liposuction. Despite use of evidence-based perioperative and postoperative interventions, the patient presented with significant incisional dehiscence and fibrinous exudate at postoperative day (POD) 14. On POD 18, the patient, on her own initiative, began 1500 mg of modulated oral LathMized NAD+ (LNAD+) and continued dosage throughout the wound healing period. Healing progressed from full-thickness wound dehiscence before supplementation to granulation on days 2–5 of supplementation (POD 19–22) and complete closure without scar formation on day 22 (POD 40). No adverse reactions were reported. To our knowledge, this case represents the first reported use of oral LNAD+ that potentially supported reduced healing time of deep surgical wound dehiscence in a patient predisposed to delayed healing and scarring. Proposed mechanisms of action might involve suppression of inflammatory mediators known to impede wound healing and metabolic upregulation via an increase in SIRT1 levels and activity.

Postoperative wound complications have complex and multifactorial patient-dependent pathophysiology. Delayed healing, particularly in the inflammatory phase, prevents cellular proliferation and remodeling, increasing risk of adverse scarring.¹ Older adults and those with comorbidities are more susceptible to chronic nonhealing wounds, resulting in complications that increase infection risk and reduce quality of life, contributing to US healthcare costs exceeding $25 billion annually.²

Age-related NAD+ depletion drives cellular senescence, resulting in a proinflammatory microenvironment that impairs wound healing capacity.^3,4 In RENEWAL-NAD+, a recent double-blind placebo-controlled randomized controlled trial in healthy aging adults (NCT07336836),⁵ oral LNAD+ (500mg, four times a day) significantly increased intracellular NAD+ levels by 53% within 5 days compared to placebo, demonstrating enhanced bioavailability and cellular uptake.

In this report, we present a case wherein oral LNAD+ was taken in an attempt to support resolution of a brachioplasty wound complicated by dehiscence and infection.

CASE DETAILS

Retrospective review of the patient chart for this case study was approved by The Institute of Cellular and Regenerative Medicine institutional review board (IRCM-2025-450).

The patient is a 59-year-old woman with hypertension, hyperlipidemia, and a distant history of a prolonged postoperative complications and hospitalization resulting in Clostridioides difficile and resistant Enterobacter species surgical site infection. She presented a decade later with bilateral grade III capsular contracture and implant rupture and underwent implant removal, bilateral mastopexies with capsulectomies, and concurrent bilateral brachioplasties with liposuction. Despite tailored perioperative prophylactic antibiotics and the use of incisional negative pressure dressings she dehisced her brachioplasty incisions bilaterally. On postoperative day (POD) 8, the negative pressure incisional dressings were removed; minimal wound breakdown areas and edema were identified along both incisions, but were worse along the left incisions. The arms were dressed with silver-based dressings and ace wrap for edema control.

On POD 14, the patient presented with worsening left-upper arm erythema, with a significant incisional dehiscence and fibrinous exudate. The patient was started on Bactrim; a disposable negative pressure dressing was applied in the area of deepest dehiscence; and Aquacel was applied along the rest of the incision. At 48-hour wound check (now POD16), her erythema had improved, but the dehiscence was unchanged.

On POD 18, the patient, on her own initiative, began 1500 mg of modulated oral LNAD+ and continued the dosage throughout the wound healing period. Patient disclosure of LNAD+ initiation was documented in the electronic medical record. Within 24 hours of starting the LNAD+, a reduction in wound depth and early contraction of the wound was observed, resulting in removal of negative pressure dressing. Three days after initiating LNAD+ supplementation (POD 21), marked approximation of the wound edges and reduced erythema and edema became clinically relevant. Healing continued, with progressive re-epithelialization, scant exudate, and the presence of a linear wound margin observable by the fifth day of supplementation (POD 23). On the 22nd day postsupplementation (POD 40), the wound was completely closed, defined as 100% re-epithelialization of the wound surface with no discernible exudate, drainage, or dressing, drainage, and minimal residual erythema (Fig. 1). Complete closure was confirmed at a follow-up appointment no less than 14 days later (POD 54+). (See appendix, Supplemental Digital Content 1, which displays the full timeline of patient milestones and interventions, https://links.lww.com/PRSGO/F325.)

Fig. 1.

Wound healing progression following oral LNAD+ supplementation in postbrachioplasty dehiscence. A, Day 1 of LNAD+ supplementation (POD 18). B, Day 5 of LNAD+ supplementation (POD 22): continued epithelialization occurs as inflammation resolves and the healing surface smooths with minimal exudate. C, Day 22 of LNAD+ supplementation (POD 40): complete closure is observed with minimal scarring and no adverse events reported.

DISCUSSION

Postoperative wound complications pose a significant burden on patients, surgeons, and the healthcare system. The overall complication rate of brachioplasty is approximately 33%.⁶ Most are minor (eg, aberrant scarring, 9.9%), but moderate (eg, infection, 3.64%) and severe (eg, nerve injury 2.5%) complications are observed, and operative reintervention is required in 7.5% of patients.⁶

In this case, the complete closure of a deep incisional wound—complicated by dehiscence secondary to surgical site infection—was achieved within 3 weeks of initiating the LNAD+ supplementation without secondary surgical intervention or adverse effects, and with minimal scarring.

The temporal correlation between oral LNAD+ initiation and visible evidence of the initiation of wound contraction within 24 hours, combined with the rapid resolution during follow-up (40 d versus an expected 6–12 wk for secondary intention healing) and the absence of significant scarring, aligns with NAD+-mediated metabolic enhancement. (See figure, Supplemental Digital Content 2, which displays the wound 24–48 hours post-LNAD, https://links.lww.com/PRSGO/F326.)

This prompted further investigation into the potential contribution of LNAD+ to this patient’s outcome. The bioanalytical observations from RENEWAL-NAD+ RCT (NCT07336836), summarized in Table 1, provide potential biological mechanisms for the rapid wound healing observed in this report. Critically, RENEWAL-NAD+ identified a 32% increase of plasma SIRT1 protein alongside coordinated suppression of inflammatory mediators known to impede wound healing.⁵ SIRT1, an NAD+-dependent deacetylase, orchestrates tissue repair through multiple pathways, including fibroblast migration, collagen deposition, and inflammatory resolution. In animal models, SIRT1 suppresses p66Shc activity, reducing mitochondrial reactive oxygen species (ROS) generation⁷; p66Shc knockout mice also show accelerated wound closure with reduced inflammatory infiltration.⁸ In line with this, therapeutic administration of the NAD+ precursor nicotinamide mononucleotide mitigated inflammatory damage to endothelial cells and enhanced bactericidal activity of phagocytes, leading to improved survival in a rodent sepsis model.⁹ Collectively, this suggests that LNAD+ may be addressing multiple critical pathways in wound repair.

Table 1.

LNAD+ Mechanisms to Support Wound Healing (from RENEWAL-NAD+ RCT⁷)

Pathway	RCT Finding	Wound Healing Relevance
NAD+ uptake	53% increase (P < 0.001)	Substrate for SIRT1 and PARP
SIRT1 upregulation	32% increase (P < 0.05)	p66Shc suppression, inflammation control
Anti-inflammatory	CXCL10/12, MMP9 suppression	Reduced proteolysis, optimized ECM deposition
Metabolic reprogramming	FABP1 ↑59%, enhanced β-oxidation	Energy supply for proliferating cells
Angiogenic signaling	VEGF pathway activation	Neovascularization support
DNA repair	Base excision/homology-directed DNA repair↑	Genomic stability in dividing cells
Cellular defense	Phase I/II detoxification enzymes ↑	ROS management, oxidative stress control

LIMITATIONS

Study limitations include the single-case design with correlative evidence, absence of wound healing biomarkers, and lack of standardized wound measurements or control comparison. Although the temporal relationship is suggestive of a role for LNAD+ in this patient’s wound healing, we acknowledge that supplementation timing may have coincided with secondary-site infection resolution from antibiotic therapy and the transition from a persistent, proinflammatory state associated with chronic wounds to the proliferative and early contractile phases. The use of other evidence-based interventions, including negative pressure wound therapy and advanced dressings, patient’s controlled comorbidities, and relatively preserved vascular function could have also contributed to robust healing.

CONCLUSIONS

This case outlines a potential role of oral LNAD+ supplementation in surgical wound healing. Although this single case does not establish causality, preliminary data obtained in the RENEWAL-NAD+ RCT showing that LNAD+ significantly elevates intracellular NAD+ and SIRT1 abundance provides a biologically plausible mechanism for wound healing support.⁵ Further disentangling the pattern of molecular biomarker changes in healthy adults and their potential relationship with the clinical healing response reported here will be the focus of future targeted prospective studies into use of LNAD+ for adjunctive postoperative risk reduction.

DISCLOSURES

The views expressed in this retrospective institutional review board–approved case study are those of the authors and do not necessarily reflect the official policy or position of the Department of the Navy, Department of Defense, or the US Government. No ghostwriters were used to write this article. Komac is the founder and CEO of BioNADRx d.b.a. Bryleos. Hastings and Kornilov are paid consultants of Bryleos who received consultancy fees during the preparation of the manuscript. Komac holds stock, and Hastings, Kornilov, and Fahey McGrath hold stock options in Bryleos. The patient in this study took LathMized NAD+ of their own volition without consulting their licensed physician (Ortiz-Pomales), and Bryleos had no role in the course of patient treatment.

ACKNOWLEDGMENTS

The authors would like to express their deepest gratitude to the late Dr. Lynne Fahey McGrath. Although she did not live to see this work in print, her tireless contribution to advancing BioNADRx, compassion for her colleagues, and love of science remain at the heart of everything we do.