Stearic Acid & Mitochondrial Health
The current movement against polyunsaturated fatty acids has gained recent traction. However, the benefits of saturated fats often go ignored in all the drama. This is the story of one saturated fat.
Recently, there has been tremendous discussion concerning the health consequences of consuming polyunsaturated fatty acids (PUFAs) - otherwise known as seed or vegetable oils. Many have been cutting PUFAs out of their diets in favor of more saturated fatty acids (SFAs) , as well as the more beneficial omega-3 PUFA.
Despite this, the focus of contemporary debate seems concentrated on the detriments of omega-6 PUFAs. While this is a worthwhile discussion, the benefits of SFAs also deserve attention.
The focus of this article is on stearic acid (a long-chain SFA) and its impact on mitochondria, which ultimately impacts energy metabolism and overall health.
The Meat of It
Mitochondria are ancestral prokaryotic organelles that are believed to have been independent organisms which were engulfed by eukaryotic (mammalian) cells billions of years ago.
If you have taken an introductory college course on biology, the mitochondrion has likely been presented as the powerhouse of the cell, but it deserves more description than that.
Mitochondria are vital to life - we need them to produce most of our energy. They play roles in programmed cell death, molecular synthesis, calcium regulation, neurotransmitter metabolism, and play an integral role in the reduction-oxidation system.
Two complementative mitochondrial processes - fusion and fission - are essential for maintaining their form and integrity. Fission is required for mitochondrial reproduction, while fusion allows for cooperation.
When two or more mitochondria fuse, they are able to work together and produce energy more efficiently. While fragmented mitochondria may not have any issues generating energy, two fused mitochondria can share each other’s resources (metabolites, enzymes, etc.) throughout their compartment.
Mitochondrial fusion can also correct dysfunctional genetic mutations through a process called trans-complementation, wherein one mitochondrion deficient in a functional gene can fuse with another mitochondrion which contains a healthy copy of the same gene. The defective copy of the mt-DNA can be either corrected or compensated for, and the resulting fused mitochondrion can have restored function.
Saturated Fatty Acids
SFAs are fatty acids which contain a glycerol backbone and only carbon-carbon single bonds, with the maximum number of hydrogen atoms.
Over the past century, SFAs have been widely demonized as a driver of cardiovascular and metabolic disease. However, recent research has absolved SFAs of their long-believed consequences.
Take a look at one of our prior articles discussing the stability of saturated fats and the role of PUFAs (polyunsaturated fatty acids) in chronic disease:
Stearic acid, or C18:0, is a saturated fatty acid (SFA) with an 18 carbon chain. Significant dietary sources of stearic acid include tallow, lard, butter, meat, poultry, fish, & dairy.
An Interesting Experiment
To study the effects of stearic acid, researchers have conducted a study where subjects (healthy and diabetic) were fed a low-fat vegan diet for two days to lower the stearic acid baseline, then given a drink high in stearic acid.
The 2-day low-fat vegan diet, very low in C18:0, was designed to make sure the subjects had little to no circulating C18:0. Afterwards, they were given a banana milkshake drink with 24 grams of stearic acid.
The subjects’ blood were tested for mitochondrial fragmentation and fusion before and after the milkshake drink. They chose to observe neutrophils (a type of white blood cell) for convenience.
After the 2-day low-fat diet, neutrophilic mitochondria were found to be quite fragmented. About 50% of the mitochondria were fragmented, and <10% were fused. This effect was consistent across all 21 subjects.
Drinking the stearic acid-rich concoction induced mitochondrial fusion after 3-6 hours. The fragmentation had dropped to 25% while fusion had increased up to 27%. Results were once again robust among the subjects.
Additionally, to ensure that only the C18:0 in the drink was responsible for the mitochondrial fusion, as opposed to other components, one subject was given a C18:0 emulsion in water. The mitochondria fused as expected.
These data strongly indicate that C18:0 quickly causes mitochondrial fusion in human neutrophils. It is assumed that other human cells may also undergo mitochondrial fusion through a similar process.
The authors further tested to check for mitochondrial fusion in response to another saturated fat - palmitic acid (C16:0). After consuming a drink with the same amount of C16:0, subjects did not exhibit mitochondrial fusion in their cells. Other studies have noted a similar effect for fats such as C18:1 (oleic acid) and C20:0 (arachidic acid).
Side-note on Acylcarnitines
Carnitines are a type of molecule involved in energy metabolism, which help transport long-chain fatty acids into the mitochondria for oxidation, and ultimately, energy production. Acylcarnitines are a complex of acetyl-CoA and carnitine that import fatty acids into the mitochondria.
The type of oxidation taking place in the mitochondrion is beta-oxidation. This process breaks down fatty acids into molecules involved in the electron transport chain, which is the primary mechanism by which we produce energy (ATP) aerobically.
Researchers measured acylcarnitine levels in the blood of subjects before and after ingestion of the stearic acid milkshake. Serum levels of acylcarnitine were higher after the 2-day low-fat diet, but they dropped significantly after the drink.
Presence of acylcarnitines in the blood after the low-fat diet is likely associated with impairment of beta-oxidation due to mitochondrial dysfunction. Alternatively, being on a low-fat diet may implicate carbohydrates as the main source of energy in these individuals, meaning carnitines would accumulate and remain unused.
While the acylcarnitine levels dropped after the drink, the C18:0 triacylglycerides in circulation spiked. This relationship suggests that the drop in acylcarnitine levels was in response to demand from mitochondrial beta-oxidation.
Once again, this was tested for other fatty acids such as C16:0 (palmitate). Serum acylcarnitine levels were not affected, however, which suggests that stearic acid has a specific effect.
Why Mitochondrial Dysfunction Matters
When mitochondria are excessively fragmented - meaning there is a deficit in fusion - it is likely that fusion-regulating proteins are disabled. Processes that disturb mitochondrial fusion can induce oxidative stress, metabolic issues, and overall mitochondrial dysfunction.
Mitochondrial dysfunction can either be inherited or induced through lifestyle. This has clinical relevance, as insulin-resistance-derived chronic illnesses have a deficit of mitochondrial fusion implicated in their pathophysiology. Notable examples include:
Type 2 Diabetes Mellitus (T2DM)
Neurodegenerative disorders (Alzheimer’s, Parkinson’s)
T2DM involves mitochondrial dysfunction, production of oxidative agents, and impaired ATP production. A study conducted on mice has shown that a deficit in the fusion proteins - excessive fragmentation - impairs glucose homeostasis, leading to insulin resistance and obesity.
Additionally, fusion/fission regulation is constantly impaired in pancreatic beta cells of diabetics. Hyperglycemia, for example, inhibits fusion and blocks mitochondrial O2 consumption.
A reduced expression of the mitofusin 2 protein has been associated with T2DM. In white blood cells of T2DM patients, higher mitochondrial fission and reduced fusion has been observed.
Exercise has been demonstrated to improve insulin sensitivity by increasing fusion proteins and decreasing fission proteins.
I think you get the point:
Many studies demonstrate the mitochondrial tendency to fission with T2DM.
Based on the above, I don’t expect you to buy the argument that mitochondrial fission is responsible for metabolic disease.
What I do expect you to understand is that…whether the chicken or egg came first…it doesn’t really matter. What matters is understanding what is causing the mitochondria to be under enhanced stress…and low support.
The physiology is such that, whatever is causing diabetes or the consequences of chronic metabolic disease…it is also associated with a phenotype that is weakening mitochondrial function.
Thus, it would behoove the reader to take part in activities that strengthen mitochondrial function.
Nutrients that optimize mitochondrial function are important to include in our diet to maintain our energy balance. Stearic acid is one of these nutrients, and you can source it from meat, fish, poultry, & butter. Its potential benefits on fatty acid oxidation and mitochondrial fusion should not be overlooked.
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