BREAKING SCIENCE NEWS: The First Nutritional Deficiency Syndrome Discovered in 75 Years

Healthy Aging

Nutritional C15:0 Deficiency Causes Cellular Fragility Syndrome

This week, we’re excited to share our latest big science drop. As published in the peer-reviewed scientific journal Metabolites, we report the first nutritional deficiency syndrome to be discovered in 75 years. Let’s dive in.

What makes a deficiency, well, a deficiency?

Certain vitamins and minerals are so important that if we don’t get enough in our diet, we can develop a definable disease. Think: Vitamin C deficiency and scurvy, or Vitamin D deficiency and rickets. In fact, a key proof point of any nutrient deemed as “essential” should have evidence of disease in the absence (or too-low levels) of that nutrient. In turn, that disease should be readily fixed when appropriate nutrient levels are restored. This is the hallmark of a nutritional deficiency.

This is where C15:0 comes in.

As published in Scientific Reports back in 2020, we demonstrated how C15:0 meets the criteria of an essential fatty acid, including the following:

• People with low C15:0 levels have a higher risk of poorer metabolic, heart, and liver health.
• C15:0 has beneficial dose-dependent activities (especially between 20 to 50 µM) and has been shown to support metabolic, heart, and liver health.
• Our bodies cannot make enough C15:0 on their own to support these healthy levels.
• Our dietary C15:0 intake dictates our circulating C15:0 levels.

As would be expected of C15:0’s essential role in maintaining our long-term health, the past 12 years of studies have culminated in our discovery of Cellular Fragility Syndrome, a C15:0 deficiency syndrome.

What is Cellular Fragility Syndrome?

During 2012, a team of researchers at Columbia University discovered a new type of cell death, called ferroptosis. Since then, over 10,000 papers have been published on ferroptosis. Here’s how ferroptosis kills our cells:

• We have fragile fatty acids in our cell membranes, which leads to lipid peroxidation.
• Unwanted iron in our cells combines with lipid peroxidation to generate massive amounts of reactive oxygen species (ROS).
• ROS takes out our mitochondria, resulting in cell death.

Yikes. Ferroptosis accelerates our aging and speeds up the onset and severity of metabolic, heart, and liver conditions. Despite all this science, how and why ferroptosis showed up had remained unknown. Until now, that is…

In our paper, we demonstrate how too-low C15:0 in our diets and cell membranes cause ferroptosis, including creating fragile cells, unwanted intracellular iron, advanced cellular aging and the resulting chronic conditions. This C15:0 deficiency cascade is called Cellular Fragility Syndrome, and it may be affecting as many as 1 in 3 of us.

How do I know if I have Cellular Fragility Syndrome?

While Cellular Fragility Syndrome can result in general fatigue and other ails often attributed to “getting older”, it is best detected using blood tests.

First and foremost, Cellular Deficiency Syndrome can be detected by measuring your C15:0 blood levels (preferably red blood cell membrane levels). As described in our Metabolites paper:

• Deficiency Zone: C15:0 ≤ 0.2% of total fatty acids.
• Healthy Zone: C15:0 > 0.2% to 0.4% of total fatty acids.
• Optimal Zone (possibly): C15:0 > 0.4% – 0.64% is defined as potentially optimal based on recent studies related to long-term heart health and longevity.

Just as importantly, however, is detection of clinically relevant blood changes expected with Cellular Fragility Syndrome, which may include any combination of the following:

• Fragile red blood cells: Higher red blood cell distribution width (RDW), declining hemoglobin, and/or regenerative anemia.
• Iron tissue overloading: Higher ferritin with or without elevated transferrin saturation.
• Impaired liver function: Higher ALT, AST, and GGT.
• Impaired metabolism: Higher glucose, cholesterol, and/or triglycerides.

It is important that you work with your physician to assess and interpret these indices.