“Is Fatty15 Legit” Series: How much science backs fatty15's benefit claims, using studies beyond what fatty15 scientists have published?

If you’re here, chances are that you recently heard about fatty15, a healthy aging supplement containing C15:0. And you may be wanting to know if this supplement is legit.

In this series, we help answer some of the most common questions about the science behind fatty15. We also address misconceptions and misinformation about fatty15 that are coming from folks who aren’t living and breathing C15:0 science 24/7. To help you dive even deeper, you can visit DiscoverC15.com/resources to read the cited peer-reviewed studies.

How much science backs fatty15's benefit claims, using studies beyond what fatty15 scientists have published?

The short answer: an abundance of science. More specifically, 100+ peer-reviewed studies have been published by independent scientists throughout the world on the benefits of C15:0, including the pure C15:0 ingredient in fatty15. While we literally wrote a fully referenced Simon & Schuster book summarizing these independent studies (The Longevity Nutrient), which can also be found at DiscoverC15.com/resources, a summary of the robust science to date behind C15:0 and fatty15 is provided below.

C15:0 is emerging as the first essential fatty acid to be discovered in over 90 years. 

Background: This discovery, while first made by fatty15’s co-founder, Dr. Stephanie Venn-Watson, has been revalidated by three independent teams from Canada, China, and France across four studies, including gold standard studies used to determine whether a fatty acid meets the criteria of essentiality [1,2,3,4,5]. You can read our deep dive on the research behind C15:0 as an essential fatty acid by clicking here.

What skeptics have said: In a video, a skeptic incorrectly stated that there was no evidence to support that C15:0 is an essential fatty acid, including gold standard studies in which nutritional deficiencies are induced and resolved.

Setting the record straight: These gold-standard studies have been published by independent teams, who have similarly concluded that C15:0 meets the criteria of being an essential fatty acid [3,4,5]. Note: There is no single body who determines that a fatty acid is essential. Instead, this process involves an initial discovery that is published in the peer-reviewed literature which is further proven or disproven by independent teams conducting and publishing their own research in the peer-reviewed literature.

C15:0 is a pleiotropic nutrient with multiple dose-dependent mechanisms of action.

Background: Using best-of-practice dose-dependent cell-based studies routinely used by pharmaceutical companies and conducted by third parties, multiple independent research teams have demonstrated that C15:0’s broad health benefits are thanks to its ability to:

• Strengthen cell membranes against lipid peroxidation, which slows age-related breakdown at the cellular level [1,6,7]

• Support healthy mitochondrial function, which supports cellular energy [1,2,8]

• Activate AMPK, AKT, and PPARɑ/δ, which supports healthy glucose metabolism [1,9,10]

• Inhibit mTOR, JAK-STAT, NF-kB, and HDAC6, which results in healthy immune response [6,11,12,13]

• Inhibit MAO-B and FAAH, which results in maintaining healthy dopamine and endocannabinoid levels and supports cognitive, sleep, mood, and joint health [14]

What skeptics have said: There are a couple of sources who have erroneously said that it is unknown how C15:0 works.

Setting the record straight: These gold-standard studies demonstrate not only how C15:0 works as a pleiotropic nutrient with well-established mechanisms of action to support long-term health, but they have also shown the concentrations needed to optimize specific mechanisms of action (e.g., > 5 µg/ml or > 20 µM).

C15:0 has dose-dependent efficacy across numerous human cell systems and in relevant animal models.

Background: Using best-of-practice and dose-dependent primary human cell-based systems routinely used by pharmaceutical companies to screen compounds for safety and efficacy, independent research teams have demonstrated that C15:0:

• Lowers 18+ proinflammatory cytokines in human cell systems representing cardiometabolic, gut, lung, liver and skin health. C15:0 also lowered proinflammatory cytokines in the blood, liver, and gut of animal models [15].

• Improves glucose metabolism in muscle cells. C15:0 benefits included improved glucose uptake and improved insulin sensitivity [9]. C15:0 also supported healthy glucose levels in an animal model [1].

• Improves mitochondrial function and lowers oxidative stress in cell systems with impaired mitochondria and increased reactive oxygen species (ROS) [1]. C15:0 also lowered oxidative stress and lipid peroxidation in multiple animal models [6,7].

• Lowers proliferation of rogue fibroblasts in human cell systems representing lung, liver and skin health [1]. C15:0 also supported healthy tissue function in the liver of animal models [1,6].

What skeptics have said: In a video, a skeptic incorrectly states that C15:0 studies are limited to “sprinkling C15:0 on cells in a petri dish.”

Setting the record straight: Published C15:0 cell-based and in vivo efficacy studies used gold-standard assays and protocols that were conducted by independent third parties and accepted by the pharmaceutical industry to assess the safety and efficacy of active compounds. These studies, many of which were not from fatty15 scientists and doctors, consistently demonstrate C15:0 health benefits that are expected given C15:0’s established mechanisms of action.

There are an increasing number of human clinical trials supporting the health benefits of C15:0 that directly align with its established mechanisms of action and demonstrated efficacy.

Background: Today, there are seven published studies across six controlled clinical trials evaluating the effects of increased C15:0 intake, including the pure C15:0 ingredient in fatty15. While C15:0 clinical trials are described in depth in another article in this series (click here to view), here is a brief overview of what these clinical trials have shown or are supporting:

• C15:0 supplementation increases circulating C15:0 levels. Robust clinical trials to determine the bioavailability and pharmacokinetics of the pure, free fatty acid C15:0 ingredient in fatty15 have been published. These studies included healthy women, men, and children and consistently showed that the pure, free fatty C15:0 nutrient is, on average, 100% bioavailable [16,17]. This is how we know that for every 100 mg of C15:0 ingested, circulating levels increase, on average, by 1 µg/ml (or 10 µM).

• C15:0 is safe. All clinical trials have shown that C15:0 is safe [16,17,18,19,20,21,22].

• Evidence that C15:0 improves liver and red blood cell function. In a randomized, placebo-controlled clinical trial, when daily supplementation with fatty15 raised C15:0 concentrations to > 5 ug/ml, liver and red blood cell function improved. Specifically, this group had lowered ALT and AST, as well as increased hemoglobin within 12 weeks [18].

• Evidence that C15:0 lowers LDL cholesterol and supports a healthy gut microbiome. This clinical trial showed that, above and beyond caloric restriction and the Mediterranean diet, C15:0 lowered LDL cholesterol and increased the abundance of Bifidobacterium adolescents, a healthy gut microbe [19].

• Early support that C15:0 may help improve mood. In a post-hoc analysis of the clinical trial above, study participants who were supplemented with C15:0 had the most significant improvement in mood [20].

• Evidence that raised C15:0 levels support healthy vascular function. A controlled, cross-over clinical trial showed that Increased C15:0 dietary intake and subsequent increases in C15:0 levels independently predicted lowered arterial stiffness within 12 weeks [21].

• Evidence that C15-rich oral supplementation supports skin health. A randomized, placebo-controlled clinical trial showed that daily use of a C15-rich supplement resulted in improved collagen, elasticity, and water content of skin within 12 weeks [22].

What skeptics have said: A few sources have incorrectly stated that there are either no clinical trials or only two clinical trials with C15:0. Some also erroneously reported that these clinical trials showed no benefits, despite pointing to abstracts on the screen in which the authors conclude that C15:0 benefits were observed.

Setting the record straight: A growing number of clinical trials demonstrate that C15:0 supplementation, when taken routinely, raises C15:0 levels and is safe. Further, these clinical trials are providing evidence that C15:0 can support liver, red blood cell, cholesterol, gut, and skin health, and possibly mood health [16,17,18,19,20,21,22]. These outcomes are consistent with C15:0’s established dose-dependent mechanisms of action, cell-based and in vivo efficacies and robust epidemiological studies described throughout this article.

Meta-analyses of prospective cohort studies repeatedly link higher C15:0 to better long-term metabolic, liver and heart health.

Background: There are numerous epidemiological studies, including meta-analyses prospectively tracking tens of thousands of people over a decade or more, which repeatedly show that people who have higher C15:0 levels have better long-term metabolic and heart health [23,24,25]. Additional epidemiological studies link higher C15:0 to liver, cognitive, and red blood cell health [26,27,28].

What skeptics have said: A couple of skeptics appropriately pointed out that epidemiological studies only confirm association, not causation, of higher C15:0 with health benefits. They did not, however, share the abundant studies showing that C15:0 is a proven active and beneficial fatty acid with efficacies that support C15:0 can actively contribute to long-term health.

Setting the record straight: The combination of published dose-dependent C15:0 mechanisms of action, cell-based and in vivo efficacy studies and clinical trials all show that C15:0 is an active and beneficial fatty acid that can reasonably contribute to long-term benefits.

In summary

Fatty15 is backed by 100+ robust studies demonstrating C15:0 dose-dependent mechanisms of action, oral bioavailability, cell-based and in vivo efficacy, clinical trials efficacy, and protective effects via meta-analyses of prospective cohort studies demonstrate that fatty15 is backed by credible scientific evidence. The vast majority of these studies were conducted and published by independent research teams not affiliated with fatty15.

Cited peer-reviewed studies

[1] Venn-Watson et al. (2020) Sci Rep 10, 8161

[2] Dornan et al. (2021) J Am Oil Chem Soc 98, 813-824

[3] Ciesielski et al. (2024) Biochimie 227,123-129

[4] Ciesielski et al. (2025) J Nutritional Biochemistry 137:109814 (2025)

[5] Ruan et al. (2024) PLOS Biol 22:e3002841

[6] Aabis et al. (2025) Nauyn Schmied Arch Pharmacol doi: 10.1007/s00210-025-04143-6

[7] Wei et al. (2023) Nature Microbiology 8, 1534–1548

[8] Duan et al. (2025) J Nutr 155: 1298-1310

[9] Fu et al. (2021) Food Nutr Res 65:10.29219/fnr.v65.4527 

[10] Bishop et al. (2023) Nutrients 15, 2052

[11] To et al. (2022) Int J Mol Sci 23, 11340

[12] To et al. (2020) Nutrients 12, 1663

[13] Ediriweera et al. (2021) Biochimie 186, 147-156

[14] Venn-Watson et al. (2025). Int J Mol Sci 26:3746.

[15] Venn-Watson & Schork (2023) Nutrients 15, 4607.

[16] Stallings et al. (2013) Int J Clin Pharmacol Ther 51, 263-273.

[17] Mascarenhas et al. (2015) J Clin Pharmacol 55, 854-865.

[18] Robinson et al.(2024) J Nutr 154, 2763-2771.

[19] Chooi et al. (2024) Am J Clin Nutr 119, 788-799.

[20] Salamanca-Sanabria et al. (2025) Front Nutr 12, In Press.

[21] Arghavani et al. (2025) Nutr Metab, Cardiovasc Dis 35,104112.

[22] Kaneko et al. (2023) Med Cons New-Remed 60, 459-470.

[23] Li et al. (2022) Frontiers Nutr 9, 963471.

[24] Trieu et al. (2021) PLoS Med 18, e1003763.

[25] Huang et al. (2019) Nutrients 2019, 11, 998.

[26] Sawh et al. (2021) J Pediatr Gastroenterol Nutr 72, e90-e96.

[27] Zheng et al. (2017) BMC Med 15, 203.

[28] Shen et al.(2022) Diabetes Met Synd Obesity 15, 1423-1436.

[29] Soboleva (1994) Bull Exp Biol Med 117, 600-602.