“Is Fatty15 Legit” Series: Are there clinical trials supporting C15:0 & fatty15 benefits?

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.

Are there clinical trials supporting C15:0 & fatty15 benefits?

Yes, there are a growing number of clinical trials supporting C15:0 and fatty15’s health benefits.

To cut to the chase, controlled clinical trials have shown that increasing intake of C15:0 increases C15:0 levels, and by doing so, these studies also provide early support that higher C15:0 can promote healthy liver and red blood cell function, lower LDL cholesterol, support a healthy gut microbiome, promote vascular health, and possibly improve mood. 

Here’s a breakdown of the six clinical trials and seven studies to date:

Clinical Trial 1: Stallings et al. led a clinical trial with healthy humans to determine the oral bioavailability and pharmacokinetics of pure C15:0, the same ingredient provided in fatty15 [1]. Participants were provided a single oral dose of C15:0 and showed that circulating C15:0 levels reliably increased. For every 100 mg of ingested pure free fatty acid C15:0, C15:0 circulating levels increased on average by 1 ug/ml.

Clinical Trial 2: Mascarenhas et al. then led a clinical trial with an increased number of healthy humans, including adults and children, to extensively model the oral bioavailability and pharmacokinetics of pure C15:0, the same ingredient provided in fatty15 [2]. Participants were provided a single oral dose of C15:0 and repeated findings from the Stallings et al. study. Namely, that for every 100 mg of ingested pure free fatty acid C15:0, circulating C15:0 levels increased on average by 1 ug/ml. The authors concluded that pure free fatty acid C15:0 is, on average, 100% bioavailable.

Clinical Trial 3: Robinson et al. led a randomized, double-blinded and placebo-controlled clinical trial with young adults (ages 18 to 24 years old) at risk of metabolic syndrome and who were purposely avoiding whole fat dairy products [3]. The purpose of this clinical trial was to evaluate the ability for daily C15:0 (fatty15) supplementation to be safe, raise C15:0 levels, and change physiological markers. Participants were asked to take 200 mg of C15:0 per day for 12 weeks. At the beginning of this study, this population also had elevated liver enzymes, indicative of suboptimal liver function.

This study showed the following: 

• C15:0 supplementation was safe and raised C15:0 levels. 

• C15:0 levels increased among participants who strictly adhered to the protocol.

• Among participants who adhered to the protocol, their C15:0 levels increased at the same amounts demonstrated by Mascarenhas et al. and Stallings et al. Namely, 200 mg of C15:0 resulted in raised circulating C15:0 levels of 2.3 ug/ml. 

• This group with raised C15:0 levels also had significantly improved liver function (lower ALT and AST), as well as raised hemoglobin, demonstrating improved red blood cell function.

The authors conclude that C15:0 supplementation was safe, raised C15:0 levels, and had early evidence of providing clinically relevant benefits related to improved liver health and red blood cell function.

Clinical Trial 4: Chooi et al. led a randomized, controlled clinical trial that included women with suboptimal liver function to evaluate the ability for C15:0 supplementation to be safe, raise C15:0 levels, and change physiological markers above and beyond the benefits of concurrent caloric restriction and the Mediterranean diet. Participants took 300 mg of C15:0 per day for 12 weeks [4].

This study showed the following: 

• C15:0 supplementation was safe and raised C15:0 levels. 

• While all three groups had lowered liver fat and body weight loss, the C15:0 supplemented group trended to having the greatest loss of liver fat and body fat. It is important to note, however, that these shared improvements among all three groups were not statistically significantly between the groups.

• Compared to the other groups, the C15:0 supplemented group had lower LDL cholesterol and improved abundance of a healthy gut microbe called Bifidobacterium adolescentis.

The authors conclude that C15:0 supplementation was safe, raised C15:0 levels, and had early evidence of providing clinically relevant benefits related to lower LDL cholesterol and an improved gut microbiome.

Clinical Trial 5: Salamanca-Sanabria et al. did a post-hoc analysis of the Chooi et al. randomized and controlled clinical trial above to evaluate the ability for C15:0 supplementation to improve mood among women [5].

This post-hoc analysis showed that, while all three groups had lower body weight and improved mood, the C15:0 supplemented group had the most significant improvement in mood.

The authors conclude that C15:0 supplementation may have a positive effect on improving mood.

Clinical Trial 6: Arghavani et al. led a cross-over clinical trial that included healthy adults to evaluate the potential effects of dairy fat diets, as well as individual fatty acid components within dairy fat, on blood pressure and vascular stiffness [6]. In this trial, participants followed 1) a moderate dairy fat diet (< 4 servings of dairy products per day) and 2) a high dairy fat diet (≥ 4 servings of dairy products a day) for 12 weeks each, with a washout period between the two diets. This clinical trial showed the following:

• C15:0 intake from the diet directly correlated with circulating C15:0 concentrations.

• Increased circulating C15:0 levels from the high dairy fat diet independently predicted lowered arterial stiffness (measured as cfPWV).

The authors show that increased intake of dietary C15:0 raised C15:0 levels, and these raised C15:0 levels were associated with improved vascular function. They also concluded that different fatty acids in dairy fat had different effects (e.g. raised C16:0 from the high dairy fat diet independently predicted raised blood pressure), and that while some individual fatty acids within the whole dairy fat matrix can be beneficial (like, C15:0), others can be detrimental (like, C16:0).

Clinical Trial 7: Kaneko et al. led a randomized, placebo-controlled clinical trial that included older women to evaluate the potential effects of an oral high-C15 algal oil on skin elasticity, collagen density, and skin moisture [7]. This clinical trial showed that daily oral intake of high-C15 algal oil for 12 weeks improved skin elasticity, collagen density, and skin moisture.

The authors conclude that oral intake of high C15-containing supplements provides skin health benefits.

What the skeptics say

In videos, skeptics go over two clinical trials (Robinson et al. and Chooi et al.) and incorrectly conclude that these trials were not in relevant populations and did not demonstrate efficacy. Strangely, the skeptics made these statements while showing the papers’ abstracts, where the authors themselves concluded that C15:0 demonstrated promising results. The skeptics do not mention any of the other five studies and four clinical trials provided above, in part because two are recent publications.

Setting the record straight 

In the Robinson et al. clinical trial:

• This study was in young adults who were 18 to 24 years old and at risk of the same metabolic perturbations now affecting 1 in 3 people globally.

• Participants at the beginning of the study had elevated ALT and AST, showing that they started the study with suboptimal liver function.

• Participants who strictly adhered to the protocol of 200 mg of C15:0 per day had the same increase in C15:0 concentrations expected from in the Mascarhenas et al. and Stallings et al. clinical trials above (aka, an increase of 2.3 µg/ml). Those who didn’t adhere strictly to the study protocol did not have these increases.

• The authors conclude that C15:0 supplementation showed early support of clinically relevant effects, including lowered liver enzymes and raised hemoglobin.

• In support of C15:0 nutritional deficiencies, 2 out of 3 of the study participants had low C15:0 levels (< 5 µg/ml) at baseline. Those that achieved C15:0 levels > 5 µg/ml with supplementation had improved liver and red blood cell function.

• The study population had normal baseline levels of other indices, including glucose and cholesterol. As such, it was not expected that C15:0 supplementation would change these biomarkers, which were already normal.

In the Chooi et al. clinical trial:

The authors conclude in the abstract and discussion that C15:0 supplementation showed early evidence of clinically relevant effects, including lowering LDL cholesterol and improving gut microbiome health above and beyond caloric restriction and the Mediterranean diet. This clinical trial was published in The American Journal of Clinical Nutrition, the world’s most prestigious peer-reviewed nutrition research journal.

Beyond these two clinical trials, there are four additional C15:0 clinical trials described above.

Summary

In summary, there are seven peer-reviewed publications covering six clinical trials evaluating the safety and efficacy of increased C15:0 intake on various outcomes. These clinical trials, none of which were led or published by the fatty15 team, demonstrate that increased C15:0 intake increases C15:0 concentrations safely, and that these increases in C15:0 concentrations have supportive evidence of promoting liver, red blood cell, cholesterol, gut microbiome, vascular, and skin health, as well as possibly mood health.

Importantly, these clinical trial results align with C15:0's: 

• Dose-dependent mechanisms of action. C15:0 is an AMPK, AKT, and PPAR agonist and mTOR, NF-kB, JAK-STAT, HDAC6, FAAH, and MAO-B inhibitor [8,9,10,11,12,13,14]. By targeting these well-established receptors, C15:0 is expected to support liver, cholesterol, gut, vascular, skin and mood health. 

• Cell-based efficacy studies showing dose-dependent effects on improving mitochondrial function, lowering 18+ proinflammatory cytokines, and improving glucose uptake and insulin sensitivity [9,15]. 

• In vivo efficacy studies demonstrating C15:0 efficacy, including supporting healthy immune responses, glucose levels, and liver function, lowering oxidative stress, supporting healthy iron metabolism, improving mitochondrial health, and improving gut function [8,16,17,18,19,20]

• Prospective cohort and other epidemiological studies, including robust meta-analyses following tens of thousands of people over 6 to 14 years, showing that people with higher C15:0 levels have better long-term metabolic, cardiovascular, liver, and red blood cell health [21,22,23,24,25,26,27]

You can read more details about these studies by clicking here

Cited peer-reviewed studies

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

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

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

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

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

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

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

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

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

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

[18] Duan et al. (2025) J Nutr 155, 1298-1310

[19] Singh et al. (2024) Nutrients 16, 3031.

[20] Wu et al. (2024) Nature Communications 15, 929

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

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

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

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

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

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

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