triglicéridos de cadena media (MCT)

Medium Chain Triglycerides (MCT): An Encyclopedic Reference

1. Identity: Chemical Names, Natural Sources, and Common Forms

1.1 Chemical Definition

The MCT molecule is composed of glycerol esterified with saturated linear-chain fatty acids containing 6 to 12 carbon atoms — specifically: caproic acid (C6:0), octanoic acid (C8:0), decanoic acid (C10:0), and dodecanoic acid (lauric acid, C12:0). More precisely, a medium-chain triglyceride (MCT) is a triglyceride in which all three fatty acid moieties are medium-chain fatty acid moieties — defined as fatty acids that have 6 to 12 carbon atoms.

The four constituent medium-chain fatty acids (MCFAs), and their formal chemical identities, are:

• Caproic acid (C6:0) — hexanoic acid; the shortest MCFA, present only in minor amounts in most commercial preparations.
• Octanoic acid (C8:0), also known as caprylic acid, is a saturated fatty acid of the formula CH₃(CH₂)₆COOH.
• Decanoic acid (C10:0), also known as capric acid, is a saturated fatty acid of the formula CH₃(CH₂)₈COOH.
• Lauric acid (C12:0) — dodecanoic acid; technically a borderline MCFA; it is the predominant fatty acid in coconut oil but is considered by some researchers to behave metabolically more like a long-chain fatty acid.

Commercial MCT preparations contain predominantly caprylic (C8) and capric (C10) fatty acids, with lesser amounts of caproic (C6) and lauric (C12) fatty acids.

1.2 Natural Sources

MCTs are lipids that are commonly present in nature, for instance in milk and in some vegetable oils. More specifically, natural sources of MCT include plant sources such as coconuts, coconut oil, palm kernels, and palm kernel oils, as well as animal sources such as milk. Decanoic acid and octanoic acid form about 5–8% and 4–10% of the fatty acid composition of coconut oil, respectively.

In adult life, the major food-derived sources of MCTs are palm kernel oil and coconut oil. Human breast milk is also a natural source of MCTs.

1.3 Production and Commercial Forms

Originally, MCTs were developed as by-products of coconut oil manufacturing to utilize low melting point fatty acids present in coconut oil. These fatty acids, obtained from the lower boiling or top fraction of hydrolyzed coconut oil, consisted predominantly of C8:0 and C10:0.

MCT oil is typically made through a process called fractionation, which separates the MCTs from their original source — often coconut or palm kernel oil — concentrating the MCT content. MCTs may also be synthesized by esterification of glycerol with one or more medium-chain fatty acids with a tail of 6 to 12 carbon atoms.

Common commercial forms and preparations include:

• Liquid MCT oil — the most widely sold dietary supplement form, typically containing a blend of C8:0 and C10:0.
• MCT powder — spray-dried oil combined with a carrier (e.g., acacia fiber, whey protein) for use in beverages; used in some clinical trials.
• Structured lipids — synthetic fats in which MCFAs and long-chain fatty acids (LCFAs) are esterified on the same glycerol backbone.
• Intravenous (IV) lipid emulsions — formulated as MCT/LCT emulsions (e.g., Lipofundin® MCT/LCT) for parenteral nutrition.
• Enteral nutrition formulas — incorporated into complete enteral feeds for patients with malabsorption.
• MCT-enriched ketogenic diet foods — medical foods (e.g., Ketonia, K.Vita) used in epilepsy management.

MCTs are widely used for parenteral nutrition in individuals requiring supplemental nutrition and are being more widely used in foods, drugs, and cosmetics.

2. Traditional and Historical Use

The specific fractionation and concentration of MCTs as a distinct supplement is a modern industrial development. Originally, MCTs were developed as by-products of coconut oil manufacturing to utilize low melting point fatty acids present in coconut oil — obtained from the top fraction of hydrolyzed coconut oil, consisting predominantly of C8:0 and C10:0.

The precursor to modern MCT oil — whole coconut oil and palm kernel oil — has a considerably longer history of use across tropical cultures. Coconut oil has been used historically for cooking, skincare, and even traditional medicine. Coconut-producing cultures across South and Southeast Asia, the Pacific Islands, and parts of Africa have incorporated coconut oil as a dietary staple for centuries, valued both for its caloric density and its presumed medicinal properties.

From a clinical nutrition standpoint, purified MCT oil began to be developed and studied in the mid-20th century. The large interest in MCT in clinical nutrition is due to the unique physico-chemical, biochemical, and metabolic features which characterize MCT compared to conventional lipids (long-chain triglycerides, LCTs). Early medical applications focused on malabsorption syndromes, where the unique absorptive properties of MCTs made them therapeutically advantageous over LCTs for patients unable to properly absorb fat through the normal lymphatic route.

The ketogenic diet — in which MCT oil plays a major role — was first formally proposed by Wilder in 1921 for the treatment of epilepsy. The ketogenic diet was first proposed by Wilder in 1921 for the treatment of epilepsy and is currently recommended as a safe and effective dietary treatment for drug-resistant epilepsy.

3. Key Constituents and Mechanisms of Action

3.1 Distinctive Digestion and Absorption

The metabolism, digestion, and absorption of MCT is different from that of LCT. Human endogenous enzyme lipase brings about hydrolysis of MCT. After hydrolysis, the MCFA are released from the glycerol backbone and, because of their hydrophilic nature and shortened carbon chain, these MCFA are directly transported via the hepatic portal vein to the liver.

This distinguishes MCTs fundamentally from long-chain triglycerides. The hydrolysis of dietary triglycerides starts in the stomach by lingual lipase and continues in the duodenum with gastric and pancreatic lipases. These lipases show higher activity for short- and medium-chain fatty acids than for long-chain fatty acids, producing two free fatty acids and one 2-monoglyceride per triglyceride acted upon. Dietary MCT and LCT therefore have very different metabolic pathways in digestion and absorption.

Medium-chain fatty acids released from MCT in the gut are poor substrates for re-synthesis of triglycerides within enterocytes, and as a result they are absorbed into the portal vein as free acids and sent to the liver for disposal. Less than 1% of the ingested dose of MCT will reach peripheral circulation.

3.2 Hepatic Metabolism and Ketogenesis

These fatty acids undergo β-oxidation. This quick metabolism of MCFA results in the formation of ketone bodies, which act as an immediate energy source to the body.

MCTs are fatty acids with the unique property of bypassing the peripheral circulation and entering the liver through the portal vein, where they induce rapid ketone production. Dietary medium-chain triacylglycerols (MCTs; C8:0–C12:0) are absorbed and utilized differently compared with long-chain fats. They directly enter the portal vein as free medium-chain fatty acids, most of which are converted to ketone bodies in the liver, with a significant proportion entering the circulation.

3.3 Key Metabolic Properties Compared to LCTs

MCT differ from long-chain triglycerides as they are relatively soluble in water and, hence, rapidly hydrolyzed and absorbed. MCT are transported in the blood through the portal system; consequently, they bypass adipose tissue, making them less susceptible to hormone-sensitive lipase and deposition into adipose tissue stores.

Accumulating evidence links MCT intake to improved glucose homeostasis; increased energy expenditure and satiety with concomitant modest weight loss; and chain length-dependent modulation of circulating lipoprotein profiles and liver metabolism. Emerging data also suggest direct benefits for cardiac contractility, hinting at a broader cardiometabolic advantage.

3.4 Direct Neurological Mechanisms

The commonly accepted paradigm underlying MCT supplementation trials is that the benefits stem from ketogenesis and that MCT supplementation is safe. However, medium-chain fatty acids (MCFAs) may also exert effects in the brain directly. Research has revealed that not all effects of MCT supplementation can be linked to liver ketogenesis; chain length-specific effects (particularly of C8:0 and C10:0) on neuronal function and mitochondrial activity are an active area of investigation.

4. Scientific Evidence by Area of Use

4.1 Neurological and Cognitive Health (Alzheimer's Disease and Mild Cognitive Impairment)

The brain in Alzheimer's disease shows glucose hypometabolism but may utilize ketones for energy production. Ketone levels can potentially be boosted through oral intake of medium chain triglycerides (MCTs).

A 2020 systematic review and meta-analysis (PMC7050425) searched Medline, Scopus, and Web of Science for literature up to March 2019, examining the effects of MCTs on peripheral ketone levels and cognitive performance in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). This meta-analysis demonstrated that MCTs can induce mild ketosis and may improve cognition in patients with mild cognitive impairment and Alzheimer's disease. However, risk of bias of existing studies necessitates future trials.

A later and more comprehensive meta-analysis (2023, published in the Journal of Alzheimer's Disease) searched PubMed, Cochrane Library, EMBASE, Scopus, and Web of Science for studies published up to December 2022, and identified nine studies meeting inclusion criteria. Meta-analysis showed cognitive improvements in general (SMD = 0.64; 95% CI [0.05, 1.24]), but not in memory, language, and attention domains after oral MCT administration, compared to placebo. The effect of MCT was greater among APOE ε4 (−) subjects than APOE ε4 (+) subjects (SMD = 1.87; 95% CI [0.35, 3.40]). Better characterized clinical studies are warranted before making a definitive conclusion on the use of MCT for MCI and AD management.

A 2024 systematic review (PMC11074881) included 21 studies — eight uncontrolled trials and 13 RCTs — on the effects of MCT on AD and MCI. A substantial increase in plasma ketone levels and brain metabolic rates was observed. Cognitive assessments showed only occasional or domain-specific performance improvements. The effects on functional abilities or psychological outcomes were inadequately studied. The evidence was severely weakened by heterogeneous and poorly designed study protocols, bias, and conflicts of interest. In conclusion, the ketogenic properties of MCTs may have beneficial effects on brain metabolism in AD and MCI, but do not always result in measurable clinical improvement. Current evidence is insufficient to recommend MCT as a comparable symptomatic treatment option.

One notable individual RCT (Juby et al., 2022 — the longest duration MCT/AD study conducted at that time) used a 6-month randomized, double-blind, placebo-controlled, crossover design with a 6-month open-label extension in subjects with probable Alzheimer's disease on stable medications. MCT dose was 42 g/day, or maximum tolerated; cognition was assessed with the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA), and Cognigram®. Twenty subjects with average age 72.6 years and baseline MMSE of 22.6/30 were enrolled; average MCT oil consumption was 1.8 tablespoons/day (25.2 g, 234 kcal). Eighty percent remained stable or improved. The results raise the intriguing possibility of a prolonged neuroprotective effect, given that those on continuous 11-month MCT supplementation appeared to have a better cognitive outcome than those whose MCT intake was interrupted. The study's small sample size (n=20) and open-label extension design limit the strength of conclusions.

There is growing interest in the use of ketogenic supplements, including medium-chain triglycerides (MCT), to achieve intermittent ketosis without adhering to a strict ketogenic diet. MCT supplementation is an inexpensive and simple ketogenic intervention, proven to benefit both individuals with normal cognition and those suffering from mild cognitive impairment, Alzheimer's disease, and other cognitive disorders.

Evidence strength (Alzheimer's disease/MCI): Preliminary to moderate. Multiple systematic reviews and meta-analyses confirm that MCTs reliably raise plasma ketones and may improve general cognitive function, especially in APOE ε4 non-carriers. However, the overall evidence base is hampered by small sample sizes, short durations, heterogeneous protocols, and risk of bias. No definitive clinical recommendations have been established.

4.2 Epilepsy and the MCT Ketogenic Diet

MCTs have been incorporated into the MCT ketogenic diet (MCTKD) as a dietary therapy for drug-resistant epilepsy. The MCT ketogenic diet includes 70% fat, 15% protein, and 15% carbohydrate, with 30–60% of fat coming from MCT oil, enhancing ketone production with greater dietary flexibility than the classic ketogenic diet.

A 2025 study published in Frontiers in Neurology examined decanoic acid (C10)-enriched ketogenic diet versus the classic ketogenic diet in pediatric patients with refractory epilepsy. The C10-enriched KD demonstrated comparable efficacy and tolerability to the classic KD, offering a promising option for patients with refractory epilepsy who do not respond adequately to the classic KD alone. This study, the first to directly compare a C10-enriched KD with a classic KD, highlights the potential synergistic effects of decanoic acid. A 12-week study of a decanoic acid-enriched medical food (K.Vita) reported that six of 16 children (38%) and eight of 16 adults (50%) achieved a ≥50% reduction in seizures or paroxysmal events.

A large prospective study in 123 patients aged 2.5 to 65 years using a modified MCTKD (MCTs providing 20–30% of energy) found that response rates at 1, 3, and 6 months were 49.6%, 43.1%, and 30.9%, respectively; seizure freedom rates at 1, 3, and 6 months were 12.2%, 10.6%, and 6.5%, respectively. Side effects occurred in 21.14% of patients, predominantly gastrointestinal symptoms such as abdominal pain, diarrhea, vomiting, and constipation, most of which resolved after dietary adjustments.

A case report in PMC (2014) described an adult patient with drug-resistant epilepsy who experienced a significant daily seizure reduction (96% compared to baseline) after introduction of MCT oil. This improvement occurred in parallel to MCT oil titration over a period of one month. The maximal MCT dose was limited by gastrointestinal adverse effects. The seizure rebound after brief MCT oil discontinuation favored a direct cause-and-effect relationship rather than a placebo effect.

Evidence strength (epilepsy): Moderate to strong for drug-resistant epilepsy in children; the MCT ketogenic diet is a recognized and guideline-endorsed dietary treatment for this indication. Evidence for adults is more limited. Gastrointestinal tolerability and compliance remain practical challenges.

4.3 Weight Management and Body Composition

A 2015 meta-analysis in the Journal of the Academy of Nutrition and Dietetics (Mumme & Stonehouse) conducted a systematic review of randomized controlled trials comparing MCTs (specifically C8:0 and C10:0) to LCTs for weight loss and body composition in adults. Thirteen trials (n=749) were identified. Replacement of LCTs with MCTs in the diet could potentially induce modest reductions in body weight and composition without adversely affecting lipid profiles. However, further research is required by independent research groups using large, well-designed studies to confirm the efficacy of MCT and to determine the dosage needed for the management of a healthy body weight and composition.

A 2024 meta-analysis published in Clinical Nutrition specifically focused on individuals with overweight or obesity, and performed random-effects meta-analysis distinguishing pure MCTs from medium-long-chain triglycerides (MLCTs). Results revealed that diets enriched with MCTs are more effective in achieving weight reduction (WMD: −1.53%; 95% CI: −2.44, −0.63; p < 0.01), particularly those containing pure MCTs (WMD: −1.62%; 95% CI: −2.78, −0.46; p < 0.01), compared to long-chain fatty acids.

One individual crossover RCT examined 19 healthy overweight men (mean BMI 27.8 kg/m²) given diets rich in either MCT or LCT (olive oil) for 4-week periods each. MCT consumption had been shown to increase energy expenditure (EE) and lead to greater losses of adipose tissue in animals and humans; the objective of this research was to examine the relationship between body composition and thermogenic responsiveness to MCT treatment, using a randomized, crossover, controlled feeding trial.

MCT supplementation as an oil has been associated with reduced triglycerides and short-term increases in fatty acid oxidation, thermogenesis, and energy expenditure in humans. In trials of hypocaloric diets that randomized subjects to MCT or LCT, MCT were associated with greater weight loss, fat loss, and improvement in insulin sensitivity.

One trial found that MCT increased resting energy expenditure over 4 hours compared with long-chain TAG (LCT) (124.8 kJ, 95% CI 13.5, 236.0; P = 0.031). Consumption of MCT over approximately one month increased energy expenditure and fat oxidation in women and men, and consumption of 18–24 g MCT oil over 16 weeks enhanced weight loss in overweight adults.

Evidence strength (weight management): Modest but consistent. Multiple RCTs and two meta-analyses support modest reductions in body weight and fat when MCT replaces LCT in the diet, primarily through thermogenesis and fat oxidation. Effect sizes are small and heavily depend on whether MCTs replace, rather than add to, total caloric intake. Long-term data and dose-response relationships require further study.

4.4 Athletic Performance and Exercise

MCT have been proposed as a means to maximizing an athlete's ability to maintain their glycogen stores so they can be more competitive. However, the evidence for exercise performance enhancement is largely negative.

A systematic review published in PMC (PMC9579472) searched PubMed, Embase, CINAHL, and the Cochrane Library for MCT oil supplementation in healthy populations. Most studies reported that MCT oil did not improve exercise performance and had no effect on respiratory exchange ratio, glucose concentration, fat/carbohydrate oxidation, and lactate concentration. Although ketones were increased when supplementing with MCTs, most studies demonstrated that the body could not utilize the MCT oil-induced ketones as its primary energy source during an acute bout of endurance exercise.

One small study of recreational athletes (n not specified in available data) tested the effect of 2 weeks of consuming 6 g MCT daily. The exercise time to exhaustion at a workload corresponding to 80% peak VO₂ was significantly longer in the MCT trial (10.2 ± 7.6 min) than in the LCT trial (5.8 min). However, this is a single, small study and is not representative of the broader literature.

Evidence strength (athletic performance): Weak to negligible. The majority of systematic review evidence indicates MCT supplementation does not reliably improve endurance performance or substrate utilization during exercise. Individual studies report conflicting results.

4.5 Malabsorption Syndromes and Clinical Nutrition

Due to their ability to be absorbed rapidly by the body, medium-chain triglycerides have found use in the treatment of a variety of malabsorption ailments. MCT supplementation with a low-fat diet has been described as the cornerstone of treatment for Waldmann disease.

A retrospective review of clinical data on MCT administered for 2 weeks as nutritional therapy to hospitalized patients included 46 patients from a cohort of 1,152 admitted for nutritional therapy. Of those 46 patients, 21 had gastrointestinal dysfunction (improved in 15 patients), 15 had lymphatic abnormalities (improved in seven patients), five had dyslipidemia (improved in three patients), four had exocrine pancreatic insufficiency (improved in two patients), and one had epileptic seizures (no improvement). It was stated that administration of MCTs may be useful in the management of gastrointestinal malabsorption, pancreatic exocrine insufficiency, and dyslipidemia.

Intravenous MCT preparations, either as physical mixtures or structured lipids, have been used clinically in patients with immunosuppression, critical illness, liver and pulmonary disease, and in premature infants. Medium-chain triglycerides, long advocated as a superior substrate for parenteral use, possess many unique physiochemical and metabolic properties that make them theoretically advantageous over their LCT counterparts. Despite great promise, the clinical data comparing the efficacy of MCT-based lipid emulsions to their LCT counterparts has been equivocal, in part due to the limited nature of published clinical trials.

Evidence strength (malabsorption/clinical nutrition): Moderate, with long-standing clinical use supporting MCT as an established nutritional tool for specific malabsorption conditions. Intravenous MCT/LCT lipid emulsions are in routine clinical use in Europe and elsewhere for parenteral nutrition.

4.6 Satiety and Appetite Regulation

Medium-chain triglycerides may result in negative energy balance and weight loss through increased energy expenditure and lipid oxidation. Research into satiety effects has yielded mixed findings.

In a previous study, MCT oil consumption resulted in lower food intake than consumption of a fat rich in long-chain triglycerides in overweight men; similarly, another showed that MCT oil supplementation decreased food intake in 12 healthy adult males.

A study examining the effect of MCT on energy intake and gastric emptying found that gastric emptying was delayed by MCT in both resting and exercise trials, which may contribute to satiety effects. However, the same study found no significant overall effect on energy intake or subjective appetite ratings.

Evidence strength (satiety): Weak to modest. Some studies show reduced food intake with MCT versus LCT consumption; however, overall the evidence is mixed, and studies in uncontrolled feeding contexts do not consistently replicate findings from controlled trials.

4.7 Glycemic Control and Insulin Sensitivity

Epidemiologic studies have shown that dietary consumption of short-chain fatty acids and MCFA was associated with a reduced risk of type 2 diabetes. However, MCT compose only a minor fraction of the dietary intake of most people. In the Malmö Diet and Cancer Cohort, dietary consumption of short-chain fatty acids and MCFA with 4–12 carbons (predominantly from dairy) was associated with reduced risk of developing type 2 diabetes.

A feasibility study (PMC6927614) explored MCT supplementation and insulin sensitivity. Accumulating evidence links MCT intake to improved glucose homeostasis. In trials of hypocaloric diets randomizing subjects to MCT or LCT, MCT were associated with greater improvement in insulin sensitivity, though the specific mechanisms remain under investigation.

Evidence strength (glycemic control): Preliminary. Small RCTs and epidemiological data suggest a potential benefit, but large-scale, well-controlled human trials specifically targeting glucose homeostasis are lacking.

5. Body Systems and Health Areas of Association

• Central Nervous System: Alzheimer's disease, mild cognitive impairment, epilepsy (drug-resistant), emerging research in Parkinson's disease and healthy aging cognition.
• Metabolic/Endocrine System: Energy expenditure, thermogenesis, body weight regulation, insulin sensitivity, glucose homeostasis, lipid metabolism.
• Gastrointestinal System: Malabsorption syndromes (e.g., short bowel syndrome, Waldmann disease, lymphangiectasia, pancreatic insufficiency), gastric emptying modulation.
• Hepatic System: MCTs are primarily metabolized in the liver; hepatic ketogenesis; used in parenteral nutrition formulations where liver disease is a concern; IV MCT/LCT emulsions are used in intestinal failure-associated liver disease management.
• Cardiovascular System: Emerging data on cardiac contractility; effects on circulating lipid profiles require careful attention, as discussed in the safety section.
• Musculoskeletal/Athletic Performance: Studied as an ergogenic aid; evidence for benefit is currently weak.

6. Dosage Forms and Dosages Reported in Studies

Dosages across clinical studies vary considerably based on indication and population. The following are drawn directly from peer-reviewed sources:

• In the Juby et al. (2022) Alzheimer's disease RCT, the MCT dose was 42 g/day, or maximum tolerated. Average MCT oil consumption achieved was 1.8 tablespoons/day (25.2 g, 234 kcal).
• In a randomized controlled trial on nutritional ketosis induction, participants received either an MCT supplement containing 65% caprylic acid (C8:0) and 35% capric acid (C10:0), 30 ml three times per day (90 ml/day), for 20 days.
• One study reported that 100% of participants experienced gastric distress (cramping and diarrhea) with dosages of 50 and 60 g MCT, with only small GI effects noted at 30 g.
• The MCT ketogenic diet for epilepsy typically includes 30–60% of fat from MCT oil, within a diet providing 70% fat, 15% protein, and 15% carbohydrate.
• The modified MCT ketogenic diet in a 123-patient clinical study contained fat that provided 50–70% of total energy, with MCTs providing 20–30% of fat and LCTs providing 30–40%.
• In Alzheimer's disease studies, doses have been reported as a percentage of daily energy intake of 10–40%.
• A study in recreational athletes used food containing a small amount — 6 g — of MCT per day over two weeks.
• 6 g/day of MCTs over a period of 2–6 weeks was reported as necessary to increase acyl ghrelin in patients with anorexia nervosa.
• Preliminary dose-determination studies suggest that 6 g oil per day is well-tolerated in frail elderly people.
• Consumption of 18–24 g MCT oil over 16 weeks was studied for weight loss in overweight adults.
• Thirty grams of MCTs appears to be the safe maximal dosage to minimize adverse reactions during or after exercise.

7. Safety Considerations and Interactions

7.1 General Safety

MCFA have a shorter chain length and are quickly metabolized in the body, serving as an immediate energy source. They are known to have good physiological as well as functional characteristics.

The toxicological profile of MCTs has been formally reviewed. There was no evidence that intravenous or dietary administration of MCTs adversely affected the reproductive performance of rats or resulted in maternal toxicity, fetal toxicity, or teratogenic effects at doses up to 4.28 g/kg body weight/day (IV) or 12,500 mg/kg body weight/day (dietary). A 2-year study in rats conducted with tricaprylin (a triglyceride with C8 fatty acids) provided no evidence of a carcinogenic effect when administered by oral gavage at levels up to 10 ml/kg (9.54 g/kg) per day.

7.2 Gastrointestinal Adverse Effects

The most consistently reported adverse effects of MCT supplementation are gastrointestinal. Across MCT studies in dementia, besides gastrointestinal side effects, no harmful effects were observed. In a larger study of 86 AD participants receiving a proprietary MCT powder, GI events were reported in 49% of the MCT group vs. 27% of the placebo group; diarrhea occurred in 24% of the MCT group vs. 14% of the placebo group. However, GI side effects in the MCT group were reduced substantially after changing the base of dosing from water, milk, or juice to a meal replacement drink.

Adverse effects observed with MCT-enriched ketogenic diets have included transient hypoglycemia, metabolic acidosis, hypercalciuria, and gastrointestinal symptoms, all of which were manageable.

7.3 Lipid Profile Effects

Reported lipid profile effects with MCT consumption are variable, ranging from no effect to increases in lipoprotein levels. The variation may be due to either the population studied or dose. No statistically significant effect was found at a dose of 1.5–3 tablespoons per day in a cohort of 15 participants with AD at 3 months, whereas in a study of 18 healthy volunteers, an 11% increase in total cholesterol and 12% increase in LDL cholesterol was found at a dose of 70 g (65 ml) at 21 days.

Replacement of LCTs with MCTs in the diet could potentially induce modest reductions in body weight and composition without adversely affecting lipid profiles — but this conclusion applies specifically to C8:0 and C10:0 MCTs and dose-specific conditions.

7.4 Ketosis and Metabolic Acidosis

MCTs have a reported tendency to induce ketogenesis and metabolic acidosis, which may be contraindicated in some situations. However, there is other evidence demonstrating no risk of ketoacidosis or ketonemia with MCTs at levels associated with normal consumption, and that moderately elevated blood ketones can be an effective treatment for epilepsy.

7.5 Drug Interactions

Documented or clinically plausible interactions deserve attention in specific patient populations:

• Antiepileptic drugs: MCT-enriched ketogenic diets are therapeutic tools for some people with refractory epilepsy. In specialized clinics, most patients take antiepileptic drugs with no problem while using MCTs. Still, metabolic shifts can alter drug distribution or clearance in a minority of people.
• Fat-absorption-altering drugs: Gastrointestinal adverse effects become more likely when other interventions also alter fat handling, such as orlistat, bile acid sequestrants, or prior gastric surgery.
• Insulin and hypoglycemic agents: The ketogenic and glucose-lowering metabolic effects of MCTs may alter insulin requirements in patients on insulin or insulin secretagogues.

7.6 Special Populations

MCT supplementation is used in neonatal and pediatric parenteral nutrition. Intravenous MCT preparations have been used clinically in patients with immunosuppression, critical illness, liver and pulmonary disease, and in premature infants. Specific cautions exist for patients with severe liver disease, given that MCTs are primarily metabolized hepatically; however, the IV MCT/LCT emulsions are also studied precisely in populations with liver complications from parenteral nutrition.

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