NMN Keeps Diabetic Retinopathy Patients' Retinas from Thinning Further
As the leading cause of blindness among adults, diabetic retinopathy causes vision damage that is almost irreversible once it reaches the late stage. What truly raises doctors' alarm is that long before vascular issues arise, the retinal neural layers in diabetic patients are already "silently thinning".
This invisible thinning is the very first alarm bell of retinal neurodegeneration.
Is there a way to make the retina "thin down slower"?
A randomized, double-blind, placebo-controlled clinical study by a team at Osaka University Hospital provided a noteworthy answer: NMN may help protect this thinning retina.
PART 01
What the Study Says
In 2026, building on their previously published randomized controlled trial (main trial DOI: 10.1111/ggi.14513), the Osaka University Hospital team conducted an in-depth analysis on an ophthalmological sub-dataset, focusing precisely on the metric of "retinal thickness".It should be noted that this ophthalmological sub-analysis currently has a limited sample size (7 participants per group, totaling 14 eyes) and is an exploratory analysis. However, as a rare piece of human double-blind controlled evidence targeting "NMN and retinal thickness," its signal value cannot be overlooked. Study Subjects: Elderly male diabetic patients over 65 years old (with physical frailty)
Intervention: Oral administration of 250 mg NMN or placebo daily for 24 consecutive weeks
Detection Method: Optical Coherence Tomography (OCT) to accurately measure thickness changes across 9 subfields of the macular area
The results emerged right where they mattered most.
PART 02
Core Data: The Temporal Retina "Stabilized"
In the outer temporal subfield of the retinal macular region (the side closer to the temple), a clear contrast emerged between the two groups: retinal thickness changed by +1.14 μm (basically stable) in the NMN group, whereas it changed by −2.77 μm (continued thinning) in the placebo group. The difference between the two groups reached statistical significance ($p = 0.006$).
In plain terms, the retina in the placebo group was gradually thinning as expected, while the retina in the NMN group was basically stabilized without significant thinning. The net difference between the two groups' changes was about 3.9 μm—a signal worth noting in a delicate structure measured in micrometers like the retina.
Even after excluding patients with other concurrent ocular conditions, this trend remained valid ($p = 0.07$), with an identical direction.
Beyond data, safety is equally crucial. Over 24 weeks, the NMN group recorded zero ocular adverse events and zero systemic adverse events; visual acuity, intraocular pressure, and retinal morphology were all stable, with no dropouts due to the study intervention. For a nutritional intervention that may require long-term use, safety is the first threshold. This record of "zero adverse events" undoubtedly bolsters confidence for conducting larger-scale future studies.
PART 03
Why "Temporal" Specifically?
This is precisely the most intriguing part of the study.Numerous studies have confirmed that in diabetic patients, the temporal region is often where retinal thinning occurs earliest and most noticeably. This region acts like a "vulnerable link" in the retina, being exceptionally sensitive to ischemia, hyperglycemia, oxidative stress, and aging.
The decline in NAD⁺ (Coenzyme I) levels is one of the underlying drivers of retinal neuronal degeneration—when energy supply is insufficient and neurons cannot sustain themselves, the retina gradually thins.
As a direct precursor of NAD⁺, supplementing NMN is equivalent to refueling the retina's "energy factories" (mitochondria). That the most fragile area is protected first makes biological sense and represents the most interesting observation here.
PART 04
From "Preliminary Signal" to "Evidence Accumulation"
Of course, science demands rationality.As the research team candidly admitted: the sample size is small, only male participants were included, and it is an exploratory analysis. It is not yet possible to draw the conclusion that "NMN can reverse retinopathy," but it does offer a clear direction—NMN warrants larger-scale, longer-term studies to verify its role in delaying diabetes-related retinal thinning.
It is through such rigorous clinical trials that NMN is gradually propelled from a "laboratory molecule" to an "evidence-based nutrient".
Rigorous clinical research relies on traceable, high-quality raw material support. This is precisely the domain where BONTAC has been deeply involved for over a decade.
As a national-level Specialized, Refined, Differential, and Innovated "Little Giant" enterprise that pioneered the large-scale production of NMN, BONTAC leverages 25 NMN invention patents, self-developed full-enzyme processes, and Bonpure® purification technology to achieve a stable supply with purity ≥ 99.9%. Certified by international safety standards such as GRAS and FSSC22000, BONTAC provides high-quality raw material support for the global scientific research and health industries.
Eye protection begins with the "visible" retinal thickness. BONTAC makes every batch of NAD⁺ raw material evidence-backed.
References:
[1] Shiraki A, Hara C, Akasaka H, et al. Effect of Nicotinamide Mononucleotide on Retinal Thickness of Older Patients With Diabetes Mellitus: A Placebo-Controlled, Double-Blind Study. Geriatrics & Gerontology International. 2026; 26: e70516. doi:10.1111/ggi.70516.
[2] Akasaka H, Nakagami H, Sugimoto K, et al. Effects of nicotinamide mononucleotide on older patients with diabetes and impaired physical performance: A prospective, placebo-controlled, double-blind study. Geriatrics & Gerontology International. 2023; 23(1): 38-43. doi:10.1111/ggi.14513.