Healthy Aging for All: How Fatty15 & C15:0 Support Healthy Aging At All Stages

When we hear “healthy aging”, we tend to think of our middle to older years. In reality, from the moment we are conceived, we are aging. 

During our youngest years, healthy aging means healthy growth and development. As young to middle-aged adults, our primary goal is to slow biological aging to protect our good health. And as older adults, we aim to reverse biological aging and restore our overall health and wellness. The result? Optimal health throughout our lives, for everyone in our life.

While the science explaining how we age (and therefore, how to slow and reverse aging) has been rapidly advancing, there is currently a disturbing dichotomy between 1) the emergence of healthspan-extending technologies, and 2) the rise in aging-related conditions among younger and younger people. In this day and age, we should be meaningfully advancing health, not seeing the slipping health of new generations.

Here at fatty15, we are on a mission to democratize healthy aging for all. To challenge previously accepted norms. To make discoveries that drive evidence-based nutrients to the forefront. To unabashedly support healthy growth and development for our youngest. To maintain good health for young to mid-age adults. And yes, to even reverse biological aging for older adults. 

In this article, we cover the why behind our current “Healthy Aging for All” campaign, including 1) the unexpected and groundbreaking discovery of C15:0 (pentadecanoic acid) as a healthy aging nutrient, 2) how C15:0 meets the evidence-based criteria of an essential nutrient that supports healthy aging at all ages, 3) the science behind optimizing C15:0 to tap into longevity-enhancing mechanisms, 4) evidence of nutritional C15:0 deficiencies that may be accelerating aging in as many as 1 in 3 people globally, and 5) the science behind the amounts of daily C15:0 needed to restore and optimize C15:0 levels to meaningfully enable healthy aging for all.

Let’s dive in.

An Unexpected Discovery

Our initial discovery of C15:0 (pentadecanoic acid) as a core healthy aging nutrient was made while our co-founder, Dr. Stephanie Venn-Watson, was caring for older Navy dolphins. She found that about 1 in 3 older dolphins developed a cluster of aging-associated changes related to metabolic, liver, red blood cell, cardiovascular, and immune health. 

Thanks to the Office of Naval Research funding, Dr. Steph’s team used metabolomics to study thousands of small molecules in the dolphins’ archived serum and all-fish diets to see which molecules predicted the healthiest aging dolphins. This is where they unexpectedly found that higher dietary and circulating levels of C15:0, an odd-chain saturated fatty acid, predicted the healthiest aging dolphins. Even better? When dolphins were provided a higher C15:0 diet, their red blood cell, metabolic and cardiovascular health improved. You can watch Dr. Steph’s TEDx talk about her initial discoveries while helping dolphins here. 

Fast forward 10 years and more than 100 peer-reviewed studies since that initial discovery, and C15:0 is emerging as the first essential fatty acid to be discovered in over 90 years, since omega-3.

C15:0 As An Emerging Essential Nutrient

C15:0 is not only an active and beneficial fatty acid, it is emerging as an essential nutrient. 

By definition, a nutrient is a substance that provides nourishment essential for growth and the maintenance of life. By helping to ensure that we 1) have healthy growth and development and 2) maintain long-term health, nutrients support healthy aging throughout our lives. To help standardize how nutrients are determined to be, well, nutrients, a consortium of nutrition experts developed a list of evidence-based criteria for nutrients. As you can see below, the evidence supporting C15:0 as a core nutrient has been rapidly growing over the past decade: 

Prospective cohort studies. Meta-analyses (studies of multiple prospective studies) tracking tens of thousands of people over many years repeatedly show that people with higher C15:0 are associated with better protected long-term cardiovascular and metabolic health.

Randomized clinical trials. Across six randomized and controlled clinical trials, higher C15:0 intake has been shown to increase C15:0 levels, and these higher C15:0 levels have been associated with protected red blood cell, liver, cholesterol, gut microbiome, and vascular health.

Case-control studies. Similarly, numerous case-control studies with pre-clinical models repeatedly show that C15:0 supplementation supports cholesterol, immune, red blood cell, liver, glucose, and gut health better than non-C15:0 supplemented controls.

Biological plausibility. Further, we know that C15:0 directly activates AMPK, AKT and PPARs, which are mechanisms of action well established to protect cardiometabolic health. C15:0 also inhibits mTOR, JAK-STAT, HDAC-6, NF-kB, MAO-B and FAAH, which help to balance immune responses and support cognitive function.

Replication and multiplicity of studies. Across prospective cohort studies, cell-based studies, mechanistic studies, and RCTs, C15:0’s beneficial role as a nutrient has been successfully repeated using a multiplicity of studies from different research teams. 

Dose-response relationships. Mechanism of action studies, human cell system studies, prospective cohort studies, and RCTs have shown that the higher the C15:0 level, the greater the associated benefit (aka dose-response relationship).

Presence of low-intake groups. Thanks to global dietary recommendations to decrease our intake of whole dairy fat, there are large swaths of populations that have had low C15:0 intake since the late 1970s, resulting in lower population-wide C15:0 levels.

Correct temporal sequence. The benefits of prospective control studies are that they can show that people who start with higher C15:0 levels at Day 1 are more likely to have protected cardiometabolic health at Year 10. Controlled animal studies and RCTs also prove that providing C15:0 resulted in health benefits that weren’t seen in non-exposed controls.

Low between-subject variance. A large genetic study by Otto et al. showed that there are no detectable genetic drivers for C15:0 levels, meaning that C15:0 levels are likely ubiquitously raised among individuals. This ubiquitous benefit of C15:0 as an essential nutrient has been emerging across species too, including C. elegans,  rats,  piglets, dolphins, and humans.

Intake estimate validation. Numerous large scale studies support that we need 100 to 200 mg of C15:0 a day to maintain healthy C15:0 levels of > 0.2% (> 20 uM, > 5 ug/ml). Based on reports from the USDA and declining whole fat milk intake over the past 50 years, the average person in the U.S. today may be getting as little as 25 mg of C15:0 per day.

Evidence of supporting early stage growth & the presence of poor growth caused by nutrient deficiency. Both prospective cohort studies of mother-infant pairs and controlled studies with multiple hallmark deficiency animal models support that lower or no dietary C15:0 among infants results in poorer growth, and supporting normal C15:0 levels results in healthier body growth and better cognitive development. This is one of the rarest and toughest criteria for a candidate nutrient to meet.

Evidence of protecting long-term health & the presence of diseases in adults caused by nutrient deficiency. All the above supports how C15:0 protects long-term health. Additionally, the detailed pathophysiology of a C15:0 nutritional deficiency syndrome, called Cellular Fragility Syndrome, was published in 2024. This described syndrome  involves a new form of cell death called ferroptosis and may be impacting as many as 1 in 3 people globally. Importantly, the ability for C15:0 to reverse this syndrome was recently revalidated, in detail, by a second independent team.

While we typically think of randomized clinical trials as being the single gold-standard way to determine the efficacy of a molecule (aka, a pharmaceutical drug), meeting the evidence-based criteria of a nutrient that is essential to sustaining health is much harder than meeting the criteria of a drug that is targeted to treat a disease. For nutrients, it’s the totality of data that repeatedly point to the same story that counts.

Importantly, multiple independent teams have published peer-reviewed studies supporting C15:0 as an emerging essential fatty acid. A list of references is provided at the end of this article.

C15:0 As A Geroprotector To Slow and Reverse Biological Aging

Mounting studies support that C15:0 is meeting the criteria of a geroprotector, which is considered the holy grail of healthy aging. Geroprotectors are molecules that slow biological aging (or aging rates) to stem the onset of aging-related breakdown that leads to our demise. By doing so, geroprotectors help us stay healthier, longer. Here’s how C15:0 is meeting the criteria of geroprotectors:

• Targets core mechanisms that enable longevity. C15:0 activates AMPK and inhibits mTOR, which are two core mechanisms within the Human Longevity Regulating Pathway.
• Protects against and reverse key hallmarks of aging. There are a dozen hallmarks of aging, which explain how we age at the cellular level. To date, C15:0 has been shown to reverse numerous hallmarks of aging by repairing mitochondrial function, balancing immune responses, and improving cellular signaling.
• Improves clinically relevant indices within months. Both preclinical studies in animal models and randomized controlled clinical trials support that raised C15:0 can improve red blood cell, liver, cholesterol, gut microbiome, and vascular health.
• Has evidence of slowing biological aging rates. A population study using both AgeAccelPheno and AgeAccelGrim has shown that people with higher amounts of C15 in their complex lipids have a younger biological age than their chronological age. This may be due to C15:0’s demonstrated ability in preclinical models to lower red blood cell distribution width (RDW), a key biomarker of aging rate.
• Tangibly protects long-term health. As shared above, C15:0’s role as a nutrient is to promote and support our long-term health, especially our long-term cardiovascular and metabolic health.
• Safe to use over long periods of time. As a nutrient that every infant gets at birth, C15:0 has been extensively tested for safety and has Generally Recognized as Safe (GRAS) status.

Additionally (and perhaps most importantly) C15:0 is a sturdy fatty acid that plays a core role in stabilizing cell membranes against age-driving lipid peroxidation. This cell-strengthening role is aligned with Hulbert’s Cell Membrane Pacemaker Theory of Aging, where he showed that the more sturdy the fatty acids in cell membranes the longer a mammalian species’ lifespan. By strengthening cell membranes, C15:0 leverages a core evolutionary tool for longevity.

All of the above can help explain why people who live in Sardinia’s High Longevity Zone and have C15:0 levels 2 to 3 times higher than the average person, have better protected cardiovascular health and live longer.

All this is to say that C15:0 is not only emerging as an essential nutrient to support healthy aging at all stages, but as a geroprotector that can help slow and reverse aging at the cellular level.

Evidence of How Nutritional C15:0 Deficiency Accelerates Aging

One of the key criteria of an essential nutrient is the presence of a syndrome in the fact of a nutritional deficiency. Like vitamin D deficiency and rickets, or vitamin C deficiency and scurvy. We shared above that both prospective cohort studies of mother-infant pairs and controlled studies with multiple hallmark deficiency animal models support that lower or no dietary C15:0 among infants results in poorer growth (aka a deficiency syndrome).

Further, the detailed pathophysiology of a newly recognized nutritional C15:0 deficiency syndrome, called Cellular Fragility Syndrome, has been described. This syndrome was first discovered in Navy dolphins who were inadvertently receiving a low C15:0 diet.  Here are the key points related to Cellular Fragility Syndrome:

• Low C15:0 levels in red blood cell membranes results in fragile cells, detectable with increasing RDW and decreasing hemoglobin.
• These fragile red blood cells are engulfed by Kupffer cells in the liver, resulting in iron overload and a newly recognized form of cell death called ferroptosis.
• Ferroptosis is caused by fragile fatty acids in cell membranes and unwanted intracellular iron, resulting in lipid peroxidation, massive reactive oxygen species production, mitochondrial death, and death of the cell.
• In turn, ferroptosis can accelerate aging and compromise long-term liver, metabolic, heart and cognitive health.
• Multiple models from independent teams have shown that restoring healthy C15:0 levels via supplementation reverses Cellular Fragility Syndrome, including ferroptosis, liver iron overload, and lipid peroxidation.

Thus, there is building evidence that nutritional C15:0 deficiencies may result in a distinct and detailed syndrome, including ferroptosis, which is becoming increasingly prevalent in human populations and can accelerate aging. Importantly, studies support that this syndrome is reversible by restoring healthy C15:0 levels to stabilize cell membranes.

Achieving Healthy & Optimal C15:0 Levels

Fatty15 is an award-winning and patented C15:0 supplement backed by a once-in-a-century discovery and developed over 10 years with Office of Naval Research funding to meaningfully support healthy and optimal C15:0 levels, resulting in healthy aging for all.

Our following guidance related to 1) defining low, healthy, and optimal C15:0 levels and 2) daily fatty15 dosing, are based on 100+ peer-reviewed studies with C15:0. 

C15:0 level guidelines:

• Low C15:0 levels: < 0.2% total fatty acids, < 20 µM, or < 5 µg/ml
• Normal (healthy) C15:0 levels: 0.2%-0.4% total fatty acids, 20-40 µM, or 5-10 µg/ml
• Optimal C15:0 levels: 0.4%-0.6% total fatty acids, 40-60 µM, or 10-15 µg/ml

Recommended fatty15 dosing: 100-200 mg C15:0 per day for the average person to achieve and maintain healthy to optimal C15:0 levels.

Summary

In summary, C15:0 is emerging as an essential healthy aging nutrient that supports growth and development during our earliest years and our long-term health throughout our lives. It does so by tapping into core longevity-enhancing mechanisms to help slow and reverse biological aging at the cellular level. 

Nutritional C15:0 deficiencies, caused by population-wide decreased dietary intake of C15:0 from whole dairy fat, may be a key driver of ferroptosis, a newly discovered form of cell death that can accelerate aging. This may also explain why younger people are aging faster.

Fatty15 was developed with funding from the Office of Naval Research to provide a pure, bioavailable and science-backed C15:0 healthy aging ingredient to help restore and optimize our long-term health and wellness. We're here to empower healthy aging for all.

Read the Science

Links to full articles are available at DiscoverC15.com/resources

Selected Venn-Watson et. al studies

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

Venn-Watson et al. PLOS One 15:e0230769 (2020).

Venn-Watson et al. Sci Rep 10:8161 (2020).

Venn-Watson & Jensen Int J Mol Sci 26:3746 (2025).

 Venn-Watson et al. Metabolites 14, 355 (2024).

C15:0 Mechanisms of Action & Efficacy

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

Bishop et al. Nutrients 15, 2052 (2023).

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

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

Li et al. Bioorg Med Chem Letters 72:128881 (2022).

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

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

Wu et al. Nat Comm 15:9291 (2024).

Wei et al. Nature Microbiol 8, 1534–1548 (2023)

Singh et al. Nutrients 16, no. 17 (2024): 3031.

Prospective Cohort Meta-Analyses

Chen et al. Critical Rev Food Sci Nutr 61, 2705–2718 (2021).

Huang et al. Nutrients 11:998 (2019).

Imamura et al. PLOS Med 15, e1002670 (2018).

Li et al. Front Nutr 9, 963471 (2022).

Trieu et al. PLoS Med 18:e1003763 (2021).

C15:0 Clinical Trials

Arghavani et al. Nutr Metab, Cardiovasc Dis In Press (2025).

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

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

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

Mitri et al. Nutrients 13, 1145 (2021).

Robinson et al. Journal of Clinical Nutrition 154, 2763-2771 (2024).

Salamanca-Sanabria et al. Front Nutr 12 (2025).

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

C15:0 As An Emerging Essential Fatty Acid & Nutritional C15:0 Deficiency

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

Ciesielski et al. J Nutr Biochem 137:109814 (2025)

Ciesielski et al. Biochimie 227:123-129 (2024)

Dornan et al. J Am Chem Soc 98:813-824 (2021)

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

George et al. Nutrients 13:4183 (2021).

Ruan, M. et al. PLOS Biol 22:e3002841 (2024)

Yuan et al. Eur J Clin Nutrition 79:320-328 (2025).

C15:0 Reverses Multiple Hallmarks of Aging

Venn-Watson et al. Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? 

Duan et al. Odd-chain fatty acid-enriched fats improve growth and intestinal morphology and function in milk replacer-fed piglets.

Venn-Watson et al. Pentadecanoic Acid (C15:0), an Essential Fatty Acid, Shares Clinically Relevant Cell-Based Activities with Leading Longevity-Enhancing Compounds.

C15:0 Has Evidence of Slowing Aging Rates

Venn-Watson et al. Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? 

Aabis et al. Pentadecanoic acid supports liver and red blood cell health by modulating oxidative stress, immunity, and ferroptosis pathways in rat. 

Liu et al. The Lipidomic Correlates of Epigenetic Aging Across the Adult Lifespan: A Population-Based Study. 

C15:0 Directly Supports Biomarkers of Healthy Aging Within Months

Aabis et al. Pentadecanoic acid supports liver health by modulating oxidative stress, immunity, and ferroptosis pathways in rat. 

Duan et al. Odd-chain fatty acid-enriched fats improve growth and intestinal morphology and function in milk replacer-fed piglets.

Singh et al. Anti-Inflammatory Effect of Dietary Pentadecanoic Acid Supplementation on Gut Health in SAMP1/YitFc Mice.

Wei et al. Parabacteroides distasonis Uses Dietary Inulin to Support Liver Health via Its Metabolite Pentadecanoic Acid. 

Wu et al. Galactooligosaccharides and Limosilactobacillus reuteri synergistically support gut health and alleviate barrier dysfunction by enriching Bacteroides acidifaciens for pentadecanoic acid biosynthesis. 

Venn-Watson et al. Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? 

Arghavani et al. Impact of dairy intake on circulating fatty acids and associations with blood pressure: A randomized crossover trial. 

Chooi et al. Effect of An Asian-Adapted Mediterranean Diet and Pentadecanoic Acid on Health: The TANGO Randomized Controlled Trial. 

Kaneko et al. Effect of continuous ingestion of pentadecyl-containing aurantiiochytrium oil on skin health: A randomized, double blind, placebo-controlled study. 

Robinson et al. C15:0 Supplementation in Young Adults at Risk for Metabolic Syndrome: A Randomized Controlled Trial. Journal of Clinical Nutrition 154, 2763-2771 (2024).

C15:0 Has Evidence of Supporting Long-Term Health in Large Prospective Cohort Studies

Li et al. Saturated fatty acid biomarkers and cardiometabolic health: A Meta-Analysis of Prospective Studies. 

Zheng, J.S. et al. Association between plasma phospholipid saturated fatty acids and metabolic markers of lipid, hepatic, inflammation and glycaemic pathways in eight European countries: a cross-sectional analysis in the EPIC-Interact study. 

Chen et al. Associations between serum pentadecanoic acid (C15:0) and heptadecanoic acid (C17:0) levels and blood pressure: a cross-sectional analysis of NHANES data.)

Huang et al. Associations of erythrocyte membrane fatty acids with blood pressure in children. 

Kratz et al. Dairy fat intake is associated with glucose tolerance, hepatic and systemic insulin sensitivity, and liver fat but not β-cell function in humans. 

Sawh et al. Dairy fat intake, plasma pentadecanoic acid, and plasma iso-heptadecanoic acid are inversely associated with liver fat in children.

Soboleva et al. Fatty acids of the lipid fraction of erythrocyte membranes and intensity of lipid peroxidation in iron deficiency. 

Brydges, C.R. et al. Metabolomic signatures associated with mental health . 

Shen et al. The Associations Between Plasma Fatty Acid and Cognitive Function. 

C15:0 Taps Into the Cell Membrane Pacemaker Theory of Aging

Hulbert, A.J. On the importance of fatty acid composition of membranes for aging.

Venn-Watson et al. The Cellular Stability Hypothesis: Evidence of Ferroptosis and Accelerated Aging-Associated Diseases as Newly Identified Nutritional Pentadecanoic Acid (C15:0) Deficiency Syndrome. 

Venn-Watson et al. Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? 

Duan et al. Odd-chain fatty acid-enriched fats improve growth and intestinal morphology and function in milk replacer-fed piglets.

Venn-Watson et al. Pentadecanoic Acid (C15:0), an Essential Fatty Acid, Shares Clinically Relevant Cell-Based Activities with Leading Longevity-Enhancing Compounds.