Scientific Mechanism of Action of MCT C8 (Caprylic Acid)
Medium-chain triglycerides (MCTs) exhibit distinct metabolic characteristics compared with long-chain triglycerides. Caprylic acid (C8) is particularly notable for its rapid gastrointestinal digestion, efficient portal transport, and preferential hepatic mitochondrial oxidation. These properties collectively contribute to accelerated ketone body production and rapid systemic energy availability.
Biochemical & Physiological Basis
Step 1) In the gut: it is digested fast
After you swallow MCT Oil C8, pancreatic enzymes “lipases” hydrolyze it and release free caprylic acid (C8) and smaller fat pieces. Because C8 is shorter than normal dietary fats, caprylic acid demonstrates higher solubility (Digested and handled faster).
(Faster Digestion= Faster Energy + Faster Ketone Rise)
Step 2) Absorption: MCTs don’t need the full fat process
Most long-chain fats (like olive oil) usually need either strong bile micelles or chylomicron-mediated lymphatic transport. But MCT C8 oil are much easier:
- They are absorbed more directly from the intestine.
- They reach the liver faster (mainly through the portal circulation).
This “easy absorption” is exactly why MCTs have a role in some fat-malabsorption people (e.g. Celiac disease, Crohn’s disease, or short bowel syndrome, often the result of surgical removal of a portion of the small intestine, can leave too little intestinal surface area to absorb fats effectively).
Step 3) In the liver: C8 enters mitochondria fast → beta-oxidation
Within hepatocytes, the fatty acid readily enters mitochondria more easily than long-chain fatty acids. Once inside, C8 undergoes β-oxidation.
(β-oxidation = “fat cutting” into energy units)
What does this mean?
Normally, your liver makes energy this way:
Fat/Glucose → acetyl-CoA → TCA cycle (Krebs cycle) → ATP (energy)
*TCA= “Energy Engine”
What happens after MCT C8?
The liver breaks it down quickly (β-oxidation), which produces a lot of acetyl-CoA at an accelerated rate. Therefore, the liver has more acetyl-CoA than usual.
Why can’t the liver just burn ALL that acetyl-CoA in the TCA cycle?
Because the TCA cycle has a “gatekeeper” ingredient called oxaloacetate which is needed to combine with acetyl-CoA to start the cycle. If oxaloacetate is low, acetyl-CoA can’t enter the cycle fast enough. Thia low oxaloacetate commonly happens when carbs are lower than usual OR the body is using oxaloacetate for gluconeogenesis (making glucose).
In simple words, acetyl-CoA starts to “pile up”.
The liver solution: make ketones
The liver converts excess acetyl-CoA into ketone bodies, This process is called ketogenesis.
Step 5) Ketones as fuel: brain + muscle can use them
Ketones move in the blood and enter tissues through monocarboxylate transporters. In the brain and muscle, ketones are converted back to acetyl-CoA → enter the TCA cycle → make ATP. This is part of the “brain energy support” idea in aging/cognition papers.
Clinical Metabolic Implications
The unique metabolic handling of caprylic acid (C8) explains several clinically relevant characteristics observed with MCT supplementation. Rapid hepatic oxidation and ketone generation contribute to faster perceived energy availability compared with long-chain dietary fats.
From a practical perspective, ketone bodies serve as an efficient alternative energy substrate, particularly for tissues with high metabolic demand such as skeletal muscle and the central nervous system. This mechanism underlies the frequent use of MCT C8 in ketogenic dietary strategies, cognitive-energy support contexts, and low-carbohydrate nutritional models.
Additionally, the portal transport pathway of C8 partially bypasses traditional lipid transport constraints, which may explain improved tolerability in selected fat-malabsorption scenarios. However, dose-dependent gastrointestinal effects remain an important consideration in patient counseling.