Ferroptosis: A Form of Cell Death Related to Iron

If you’ve ended up here, you’re curious about ferroptosis, a newly discovered form of cellular death discovered in 2012 and is now garnering mainstream attention. You may have also found this article because you’re curious about managing iron deficiency or supporting your cells in the best way possible. 

We’re going to answer all of these questions so you’ll know what ferroptosis is, how it works, and how researchers are working to find ways to use it therapeutically. We’ll also talk about iron deficiency and whether or not taking an iron supplement could place you at a higher risk of developing ferroptosis. 

Lastly, we’ll cover what you can do to protect your cells, the foundations of every system and tissue in your body, with a cellular supportive supplement that has the power to integrate into your cells and revitalize them, allowing you to age more healthfully.

What Is Cellular Death?

No one really likes to talk about death, but if we really think about how it happens (when it happens in age-related illnesses), death starts in our cells. Cells die and regenerate, but not all cells are capable of regeneration. 

Cells that do end up dying do so by one of several cellular death pathways:

Apoptosis

Apoptosis is the timed, purposeful, planned, and regulated death of a cell. It is the way your body naturally disposes of cells that it no longer needs. This is a natural part of how our bodies clean house and is necessary to ensure new cells are made and old cells are removed from the body.

Necrosis

Another way cells can die is through necrosis. Necrosis occurs when cells are exposed to injuries, infections, illnesses, or a lack of blood flow. 

This type of cell death is unregulated, unexpected, and can negatively impact a person’s health, especially if the cells that die are ones that cannot regenerate, like heart cells. These cells can be replaced with other types of cells, but the original cells cannot be replaced.

Autophagy

Cellular autophagy isn’t actually cellular death but rather a recycling of cell parts that are still usable and the disposal of cells that are no longer usable. Cells are filled with organelles that sometimes lose their function. 

Within the cell, lysosomes ingest and break down these parts and release the usable parts back into the cell to be made into new parts. Unusable parts are sent outside the cell. 

Autophagy is a good, needed cellular process that happens less frequently with age. There are ways to trigger autophagy. Autophagy happens when the cell is under stress. 

Fasting, exercise, and diseases can trigger autophagy. Obviously, we want to encourage cellular autophagy in our own bodies through the use of exercise and fasting, along with other healthy methods. 

Is Cell Death the Same as Cellular Senescence?

Depending on how far down the cellular health and longevity rabbit hole you’ve gone, you may have bumped into cellular senescence. Cellular senescence occurs when a cell loses its function but does not die through any of the known cellular death pathways. 

Instead, these “zombie cells” stay in our bodies, creating an inflammatory response in our immune systems, which can lead to chronic inflammation. This type of cell state is continually associated with age-related illnesses like unregulated blood sugar, unhealthy cholesterol levels, high blood pressure, and decreased liver function. 

What Is Ferroptosis? 

Ferroptosis is a regulated form of cellular death caused by an accumulation of too many fragile fatty acids (ie. polyunsaturated fatty acids (PUFAs)) in the cell membrane and ultimately too much iron in the cell. Specifically, the process of ferroptosis occurs because iron metabolism and lipid peroxidation in the cell become unbalanced. 

Glutathione peroxidase 4 (GPX4) is an enzyme that helps eliminate lipid peroxides in the cell and supports cellular balance. When a cell undergoes ferroptosis, the GPX4 pathway is compromised, leading to an imbalance between pro-oxidants and antioxidants in the cells.

What Causes Ferroptosis?

Insufficient amounts of C15:0 can lead to cellular weakness and initiate a process known as ferroptosis. Ferroptosis conversely expedites aging and has effects on our metabolic, liver, and heart health. Ferroptosis has also been linked to numerous illnesses like tumors, Alzheimer’s Disease, liver dysfunction, and kidney disease. 

How Iron Deficiency Could Play a Role

If you’re anemic, your healthcare provider may suggest that you take an iron supplement to restore your circulating levels of iron. This is important, as iron is an essential mineral your body needs for growth, development, and the creation of red blood cells. 

However, if you take iron, it’s important you don’t take too much. Not only can too much iron be toxic to your body, but there’s a possibility it could lead to ferroptosis in your cells. This is rare but notable and is a solid reason to ensure you are getting regular blood draws to keep your iron levels within a healthy range. 

How Much Iron Do I Need?

The amount of iron you need depends on your age. Most adults need about 45 mg of iron per day. The only way to tell if you are getting enough iron is to have a blood draw. 

If your iron levels are good and you don’t have underlying medical conditions that could trigger ferroptosis, you probably don’t need to worry about it. However, considering the health of your cells is something worth your attention. 

Why Are Cells So Important?

Our cells make up every part of us. As such, when your cells are healthy, your body is healthy, and when they experience age-related or disease-related decline, you experience a bodily “system-wide” decline in your health. 

Protecting your cellular health is multifaceted. There are numerous ways to support your cellular health and increase your health span or your ability to live longer and still stay healthy. The usual suspects are important to your cellular health as well as your overall wellness: eat a balanced diet, get plenty of exercise, and manage your stress levels. 

However, researchers studying longevity in bottlenose dolphins (that’s right, our big-brained and long-lived mammalian friends) discovered a particular essential fatty acid that could hold the key to repairing our cells, reversing cellular aging, and increasing our ability to lead longer, healthier lives. 

What Is the Role of C15:0?

The molecule these researchers discovered was pentadecanoic acid, aka C15:0. C15:0 is the first essential fatty acid to have been discovered since omega-3 and omega-6 over 90 years ago. 

C15:0 is an odd-chain, saturated fatty acid that our bodies need to maintain baseline health but can’t make on their own. That means we have to get C15:0 from either supplements or food. 

Low levels of C15:0 can lead to cellular fragility. This explains why many people with declining levels of C15:0 often have poorer heart, liver, and metabolic health. These weakened cells are prone to lipid peroxidation (and the release of ROS that also occurs in ferroptosis) and early breakdown.

How C15:0 Works

C15:0 works by integrating into our cells to restore and revitalize them. In studies, C15:0 has been shown to:

• Strengthen cells by 80%. Cellular membranes become flimsy over time, causing cells to lose their shape. When cells lose their shape, they also lose their function. C15:0 is a sturdy fatty acid that is solid at room temperature. It integrates into cell membranes to fortify them. 

• Improve mitochondrial function. The mitochondria in our cells become sluggish as we get older. They produce less cellular energy, known as ATP, and produce more ROS (the bad, cell-killing molecules). C15:0 has been shown to reduce ROS output by 45% and increase ATP within cells by 350% in studies. 

• Improve liver enzymes and lower “bad” LDL cholesterol

• Improve the gut microbiome.

• Target six out of the 12 hallmarks of aging (better than rapamycin)

C15:0 also binds to special receptors called PPARs that regulate mood, sleep, glucose uptake, and appetite. By binding to these receptors, C15:0 helps restore total body homeostasis.

Are You Deficient in C15:0?

C15:0 is found primarily in small amounts in whole-fat dairy products like butter and whole milk. As such, you may not be getting much C15:0 through your diet. 

Who drinks whole milk anymore? Additionally, the move toward more plant-based products has caused 40% of American households to switch to plant-based milks, which are completely void of C15:0.

A significant research article was recently released regarding a newly discovered nutritional deficiency syndrome known as Cellular Fragility Syndrome, connected with C15:0 deficiency. It's a substantial development because nutritional insufficiency syndromes — such as those related to vitamin C resulting in scurvy or vitamin D leading to rickets — are seldom uncovered.

Insufficient amounts of this essential fatty acid can lead to cellular weakness and initiate ferroptosis. However, a recent study published in the scientific journal Metabolites, shows that treating C15:0 deficiencies reinforces your cells, counteracts ferroptosis, decelerates cellular aging, and safeguards our enduring metabolic, liver, and heart health. 

Even more encouraging? There are measures to support optimal C15:0 proportions that can promote an even healthier and prolonged life. 

C15:0 levels should be above 0.2% of your total fatty acids to prevent nutritional deficiencies and Cellular Fragility Syndrome. It’s worth noting that in blue zones (where people consistently live to be 100), C15:0 levels usually measure between 0.4% and 0.6% of total fatty acids. 

The only way to know for certain if you are deficient is by ordering the fatty15 C15:0 at-home test or having your doctor perform a blood test. Additionally, you can determine the result of increasing your C15:0 levels by monitoring your complete blood count, fasting lipid panel, and liver enzymes.

How Do I Get C15:0?

Not getting enough C15:0 through our diets means that we may need C15:0 supplementation. The first and only supplement to contain the pure, vegan-friendly version of C15:0 is fatty15. Additionally, there are a few reasons why taking fatty15 is actually a better way to get C15:0:

• It’s readily absorbable. In milk (and other foods), C15:0 is attached to branches of lipids called triacylglycerides, aka triglycerides. That means our gut has to use digestive enzymes to break down these triacylglycerides to release C15:0 as a free fatty acid. Once C15:0 is released, it is ready to be absorbed. These multiple steps can make our absorption of C15:0 from foods less efficient. In fatty15, the pure FA15™ (vegan version of C15:0) is made ready to absorb. 

• It's not mixed with bad saturated fats. While the good C15:0 fatty acid is present in whole-fat dairy products in trace levels, there are much higher levels of “bad” even-chain saturated fatty acids that continue to be associated with poorer health. That is probably why studies evaluating the effects of milk on our health are mixed (some say dairy fat is bad for us, while others say it is good for us). Fatty15 provides just the good fat without the bad fats.
  
  
• It skips the cows and calories. Whole fat dairy products provide a wallop of calories, including sugars (aka lactose), that also require cows. Further, the movement to more plant-based milk and meat replacements is driven by a desire for more animal-free products, as well as a desire to veer from cows and cattle because of concerns around methane production. Interestingly, plant-based milk replacements lack C15:0 altogether. Fatty15 offers a vegan-friendly C15:0, with only one calorie per dose.

• It’s proven to prevent and treat Cellular Fragility Syndrome. In a randomized, double-blind, and placebo-controlled study, fatty15 was proven to safely increase C15:0 levels, restore liver function, and improve red blood cell health.

Protect Your Cells

Your cells are important, and even though some cellular death is natural, ferroptosis is not. You can strengthen your cells and prevent C15:0 deficiency and ferroptosis by taking fatty15, the once-a-day ferroptosis-fighting supplement.

Sources:

Ferroptosis in cancer therapy: a novel approach to reversing drug resistance | Biomedcentral.com

Ferroptosis: past, present and future | Cell Death & Disease

Necrosis: What Is Necrosis? Types & Causes | Cleveland Clinic

Definition of apoptosis | NCI Dictionary of Cancer Terms

Iron - Consumer | ODS.NIH.gov

Double-edge sword roles of iron in driving energy production versus instigating ferroptosis | Cell Death & Disease

Efficacy of dietary odd-chain saturated fatty acid pentadecanoic acid parallels broad associated health benefits in humans: could it be essential? | Scientific Reports

The Cellular Stability Hypothesis: Evidence of Ferroptosis and Accelerated Aging-Associated Diseases as Newly Identified Nutritional Pentadecanoic Acid (C15:0) Deficiency Syndrome | Metabolites

Pentadecanoic Acid Supplementation in Young Adults with Overweight and Obesity: A Randomized Controlled Trial | The Journal of Nutrition