Coconut oil has developed a reputation as a superfood in recent years, with health gurus praising its benefits for everything from weight loss to brain health. But what does the science actually say about how coconut oil affects our bodies?
New research sheds light on one potential health boon of coconut oil and other sources of MCTs (medium chain triglycerides) – the ability to reduce inflammation by changing the behavior of immune cells called macrophages.
Chronic inflammation is now believed to underlie many modern diseases. Finding dietary ways like coconut MCTs to modify inflammation could be a huge win for public health. Let’s take a deep dive on this exciting new science showing the potential for coconut oil to harness the power of macrophages and reduce inflammation.
The Role of Inflammation in Health and Disease
Inflammation is a normal bodily response designed to protect us from injury and infection. We need the acute inflammatory response to stimulate healing when we get a cut or to deploy immune cells to fight off a cold virus.
However, chronic low-grade inflammation that lingers in the body is now recognized as a root cause of many diseases. Diseases associated with inflammation include:
- Heart disease and stroke: Inflammation damages blood vessels and promotes atherosclerosis, clogged arteries leading to heart attacks and strokes.
- Diabetes: Inflamed fat tissue and metabolic disorders trigger insulin resistance and high blood sugar.
- Autoimmune diseases: Inflammation causes the immune system to overreact and attack the body’s own healthy cells, as in rheumatoid arthritis, lupus, and multiple sclerosis.
- Neurodegenerative diseases: Inflammation in the brain is linked to dementia, Alzheimer’s disease, and Parkinson’s disease.
- Depression and anxiety: Inflamed pathways in the brain can contribute to mental health disorders.
- Cancer: Inflammation promotes mutations, angiogenesis (growth of new blood vessels to feed tumors), and metastasis.
With inflammation at the root of so many diseases, reducing excessive inflammation is key for protecting health. That’s why this new research showing coconut oil can curb inflammation by changing immune cell behavior is so promising.
Macrophages: The Control Center for Inflammation
To understand how coconut oil MCTs impact inflammation, we first need to understand some basics about the immune cells called macrophages.
Macrophages are a type of white blood cell that act as “first responders” when infection or injury strikes. They have two main jobs:
- Phagocytosis – Macrophages literally gobble up and digest invading germs, foreign particles, dead tissue, and other cellular debris.
- Stimulating inflammation – Macrophages release signals and chemicals that trigger the inflammatory response. These include inflammatory cytokines like interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a).
Because of their central role in detecting threats, consuming pathogens, and sounding the alarm for inflammation to start, macrophages are critical controllers of immune activation and inflammation.
Research is revealing that macrophages don’t have just one activation state, but can morph and adapt to perform different functions depending on the signals they receive. Classically, macrophages were categorized into two major phenotypes:
- The M1 phenotype is inflammatory, releasing high levels of inflammatory cytokines and reactive oxygen species to destroy pathogens. The M2 phenotype is anti-inflammatory, suppressing excessive immune reactions and promoting tissue healing.
M1 and M2 macrophages have different metabolic profiles. M1 macrophages rely more on glycolysis, quickly converting glucose to lactate to provide energy. M2 macrophages utilize more oxidative metabolism and mitochondrial beta-oxidation of fats.
These two major macrophage phenotypes sit on a spectrum, with many possible activation states in between. The ability to shift macrophage activation from inflammatory to anti-inflammatory states is highly relevant for controlling chronic inflammation.
Study Design: How Researchers Tested Effects of MCTs on Macrophages
With this background on the central influence of macrophages on inflammation, let’s look at how the researchers designed the study to test whether coconut oil MCTs can affect macrophage activation and inflammation.
They conducted two sets of experiments:
- In vitro study: Isolated macrophage cells were treated with MCTs in the lab culture to directly test effects on the cells.
- In vivo mouse study: Mice were fed diets supplemented with MCT oil. Then macrophages were collected from the mice and tested.
This combined approach allowed them to look at direct effects of MCTs on macrophage cells themselves, as well as effects in the context of a whole living organism through diet.
For the in vitro study, the researchers used a mouse macrophage cell line called RAW 264.7. In the lab, they could directly expose these cells to MCTs and stimulating agents and measure outcomes like oxygen consumption and inflammatory signals.
For the animal study, they used mice genetically bred to have uniform immune systems, called C57BL/6 mice. One group of mice ate normal mouse chow, while others ate chow with 20% or 80% of the fat replaced by MCT oil from coconuts.
After 4 weeks eating these diets, the researchers harvested macrophages from the mice to test their behavior. This allowed them to see if dietary MCT oil ingested long-term could modify innate macrophage function.
Together, these in vitro and in vivo approaches provided a thorough and rigorous investigation of the effects of MCTs on macrophage inflammation from both direct-exposure and dietary perspectives.
Testing Macrophage Inflammatory Activation
To test the effects of MCTs on macrophage activation, the researchers looked at several key indicators of increased inflammation vs. suppressed inflammation:
- Oxygen consumption: Increased oxygen usage indicates enhanced mitochondrial metabolism linked to anti-inflammatory behavior.
- Surface proteins: Changes in levels of proteins on the macrophage cell surface reflect inflammatory or anti-inflammatory status.
- Cytokine release: Higher levels of inflammatory signals like IL-6 and TNF-a indicate increased inflammation. More anti-inflammatory signals like IL-10 suggest suppressed inflammation.
- Metabolic genes: Expression of genes related to inflammatory pathways reveals effects on macrophage function at the genetic level.
Using these metrics, the researchers could comprehensively analyze how MCTs affect inflammation based on macrophage energy use, cell signaling, immune messengers released, and gene activity.
Let’s walk through what they found…
Key Finding #1: MCTs Increase Oxygen Consumption and Mitochondrial Metabolism
The researchers used a tool called a Seahorse XF Analyzer to measure oxygen consumption in real-time in live macrophage cells. This oxygen consumption rate gives insight into how active the mitochondria are – running hotter indicates enhanced mitochondrial metabolism.
They found that macrophages treated with MCTs showed significantly increased oxygen consumption compared to untreated cells:
- Increased basal oxygen consumption indicates higher resting mitochondrial activity
- Heightened maximal respiration reveals energy production is revved up to a higher ceiling
- Increased ATP-linked respiration shows more oxygen is devoted to ATP synthesis for energy
This ramping up of oxidative mitochondrial metabolism is characteristic of anti-inflammatory macrophage phenotypes. The researchers observed this shift both in macrophage cells directly exposed to MCTs, and macrophages collected from mice that had consumed an MCT-rich diet.
This is a significant finding because it demonstrates that MCTs “reprogram” macrophage metabolism in favor of anti-inflammatory pathways.
Key Finding #2: MCTs Reduce Levels of Inflammatory Surface Markers
Macrophages display different proteins on their outer surface depending on whether they are in inflammatory or anti-inflammatory mode. One such protein marker for inflammation is CD86.
The researchers found that treating macrophage cells with MCTs significantly lowered levels of CD86. This suppression was even more pronounced when the macrophages were also exposed to a compound called LPS that intentionally stimulates inflammation.
Similar effects were seen in mice fed MCT oil, with lowered levels of the inflammatory marker CD11c. This shows that dietary MCTs can reduce inflammatory activation markers even in a living organism.
Key Finding #3: MCTs Lower Production of Inflammatory Cytokines
A major way macrophages promote inflammation is by pumping out cytokines, small protein molecules that act as immune signaling agents. Two examples are interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a).
The study found that macrophages treated with MCTs showed significantly lower release of IL-6 and TNF-a compared to untreated cells. Again, MCTs displayed an anti-inflammatory effect even in the presence of LPS designed to stimulate inflammatory cytokine secretion.
Key Finding #4: MCTs Increase Anti-Inflammatory Cytokines
While MCTs lowered pro-inflammatory cytokines like IL-6, they increased levels of the anti-inflammatory cytokine IL-10.
IL-10 works to deactivate inflammatory responses. Remarkably, macrophages exposed to MCTs increased IL-10 levels not only at baseline, but also when intentionally stimulated with an inflammatory trigger.
This suggests MCTs induce an anti-inflammatory state, preventing excessive reactions even when the macrophages encounter inflammatory stimuli.
Key Finding #5: MCTs May Uniquely Modify Cell Membranes
What mechanisms explain how MCTs induce anti-inflammatory metabolic and functional changes in macrophages? The exact molecular pathways still need further research.
But the scientists suggest possibilities like the rapid absorption of MCTs for increased mitochondrial metabolism, as well as effects on macrophage cell membranes themselves.
Unlike longer chain fats, MCTs are shorter and more rapidly transported into cells. Some research indicates the unique structure of MCTs may alter lipid rafts in cell membranes, disrupting inflammatory signaling.
More studies are needed to uncover the biological pathways, but the evidence clearly demonstrates MCTs potently reprogram macrophages away from inflammation.
Translating Science to the Dinner Table: Should You Use MCT Oil?
This scientific research provides compelling evidence that MCTs found in coconut oil can counter inflammation by shifting immune cells to a healthier status. What are the implications for the average person who simply wants to know how what they eat affects their health? Here are some key takeaways:
- Inflammation underlies chronic disease. With modern diseases like obesity, diabetes, heart disease and Alzheimer’s tied to unchecked inflammation, curbing inflammation is vital for protecting long-term health.
- MCTs may help reduce chronic inflammation. The study suggests dietary MCTs could be a tool for reducing the creeping inflammation that leads to disease by altering macrophage behavior.
- MCTs seem to make immune cells more resilient. Even when confronted with inflammatory stimuli, MCT-treated macrophages responded in a balanced, anti-inflammatory manner. This metabolic flexibility could support a more even-keeled immune system.
- Coconut oil has high levels of MCTs. While you can purchase concentrated MCT oil as a supplement, coconut oil provides a whole food source of inflammation-modulating MCTs.
- Effects depend on dosage. More research is needed to clarify optimal dosing for the greatest anti-inflammatory impact. Moderate intake provides benefit with minimal risk.
- MCTs are generally recognized as safe. Unless you have a specific condition like liver disease, there seem to be few health risks to reasonably increasing coconut oil and MCT intake. But don’t overdo it since fats are high in calories.
The fascinating new field of immunometabolism is revealing how nutrition can support health by optimizing immune function. This rigorous study expands the evidence that coconut oil’s MCTs hold promise as a dietary intervention to temper inflammation by working through macrophages.