Health concerns are an important issue with high-fat diets and diets high in MCTGs. Considering that it has been claimed that MCFAs do not increase plasma cholesterol, Tholstrup et al. compared the effects of a diet rich in either MCFAs or oleic acid on fasting blood lipids, lipoproteins, glucose, insulin, and lipid transfer protein activities in healthy men. The trial employed a double-blind, randomized, crossover design, with 17 healthy young men. The treatments consisted of replacing part of their usual dietary fat intake with 70 g of MCTGs (66% 8:0 and 34% 10:0) or high-oleic acid sunflower oil (89.4%18:1). Intervention periods lasted for 21 days. After completing one of the diets, there was a 2-week washout period. Blood was obtained before and after the intervention periods. Compared with the intake of high-oleic sunflower oil, MCTG intake resulted in 11% higher plasma TC (p = 0.0005), 12% higher LDL-C (p = 0.0001), 32% higher very low density lipoprotein cholesterol (VLDL-C) (p = 0.080), a 12% higher ratio of LDL-C to HDL-C (p = 0.002), 22% higher plasma total TG (p = 0.0361), and higher plasma glucose (p = 0.033). Plasma HDL-C, insulin concentrations, and activities of cholesterol ester transfer protein and phospholipids transfer protein did not differ significantly between the diets. The authors concluded that compared with the high-fat oleic acid diet, the MCTG diet unfavorably affected lipid profiles in healthy young men by increasing plasma LDL-C and TG.87
The changes in FA composition of TGs when fed MCTGs are another concern, as mentioned previously. It has been hypothesized that excess dietary MCTGs cause an increase in hepatic synthesis of MCFAs through de novo synthesis or chain elongation and desaturation. The elongation process is costly energy-wise and may account for the increase in energy expenditure when MCTGs were overfed. The authors cited another study that is consistent with this finding88 in which case an increase in postprandial thermogenesis was theorized to be due to hepatic de novo lipogenesis.80 Since the writing of this article, additional work supports this theory.89
Nine middle-aged men with mild hypercholesterolemia were studied to determine the effects of a natural food diet supplemented with MCTGs, palm oil, or high-oleic acid sunflower oil on blood lipids. TC and LDL-C concentrations obtained on the MCTG diet and the palm oil diet were not significantly different, but they were significantly higher than those produced by a high-oleic acid (sunflower oil) diet. The MCTG diet resulted in nonsignificant increases in TG concentrations when compared to the palm oil or high-oleic acid diet. No differences were found in the HDL-C concentrations. The authors concluded that, on the basis of percent of energy in the diet, the study suggested MCTGs are cholesterol-raising FAs that can raise TC and LDL-C similar to palm oil and also have the tendency to raise TGs.90
Naohisa et al. completed a study to investigate the effects of dietary MCTGs on serum lipid levels, liver function, and hepatic fat accumulations in healthy men. Eleven men consumed diets between 2200 and 2600 kcal daily. The diets consisted of 70 to 80 g of fat and included either 40 g of MCTGs or 40 g of LCTGs as blended vegetable oil. The FA content of the oil was predominately unsaturated. The diet was administered for 4 weeks. No significant differences were found between the diets for serum TC, VLDL-C, LDL-C, HDL-C, or TGs. No other blood, urine, or liver tests indicated a problem from the ingestion of 40 g of MCTGs for 4 weeks.91 Note that the subjects were not athletes.
A single-blind, randomized, crossover study to test the effects of a single dose feeding was completed whereby 20 healthy men were fed a single dose of 71 g of either MCT oil or canola oil. Blood was drawn at baseline before the participants ingested the oils. The dose of 71 g of oil was chosen because it was equivalent to a large order of French fries or a salad with oil-based dressing and a cookie. Blood was drawn at 1, 2, 3, 4, and 5 h postingestion and analyzed for TGs. Two weeks later, the project was repeated with the oils consumed being reversed, that is, those who received the canola received the MCT oil and vice versa. The canola oil caused a 47% increase in TGs above baseline (p < 0.001) and the MCT oil caused a 15% decrease in TGs below the baseline. Remember that these results are based on lipid profiles just hours after ingestion of the test oils, and the authors point out that the effect of long-term usage of MCT oil on TGs is yet to be established.92 This finding is in disagreement with the work of Hill et al.80 and Swift et al.93 It should also be remembered that with a trial such as this, where the amount of oil used was equivalent to the oil in a large order of French fries or a salad with an oil-based dressing and a cookie, the French fries, the salad, or the cookie were not consumed. Had they been consumed, there could possibly have been a difference in the postprandial TG levels. Thus, it would not be correct to assume that eating a large order of French fries would produce exactly the same results as reported here, and it was not the authors' intention to imply such. The subjects in this trial also were not athletes.
A study was conducted to observe the effects of MCTGs and corn oil on plasma lipids in patients with primary hypertriglyceridemia. Ten subjects ate a low-fat diet for 2 weeks followed by different proportions of corn oil and MCTGs for 12 weeks. Fasting plasma TC, TGs, and HDL-C concentrations were measured at the end of each period. Compared with corn oil, MCTGs were associated with an increased mean for fasting TC concentration (p < 0.05) and non-HDL cholesterol concentrations were also higher with MCTGs than with corn oil (p < 0.005). It was concluded that MCTGs can raise TC concentrations in primary hypertriglyceridemic subjects.94 Again, since these subjects were not athletes, these results should not be assumed necessarily to be true for athletes, but this should be thoroughly investigated with athletes before recommendations for increasing fat or MCTGs in the diet are made.
The effects of MCT oil, myristic acid (14:0), and oleic acid (18:1) on serum lipoproteins were studied. The test fats were incorporated into solid foods. All subjects, 37 women and 23 men, were fed an initial diet high in oleic acid for 3 weeks. At the end of the initial diet, the subjects were divided into three groups. One group received a diet high in MCT oil, the second a diet high in myristic acid, and the third group continued on the oleic diet. The results indicated that the subjects on the diet high in myristic acid had LDL-C levels that were 0.37 mmol/l higher than those of the oleic acid diet (p = 0.0064). Those on the MCT oil diet had increased LDL-C levels, but not significantly higher than the oleic acid diet. HDL-C concentrations increased with the myristic acid diet by 0.10 mmol/l (p = 0.02), but there was no difference with the MCT oil diet. The MCT oil diet slightly elevated TG concentrations, but there was no significant difference between the diets. There was a significant decrease in the apoA-I-to-apoB ratio in the MCT oil diet compared to both of the other diets (p < 0.02). The authors concluded that MCT oil raises LDL-C concentrations slightly and affects the apoA-I-to-apoB ratio unfavorably compared with oleic acid. Myristic acid is hypercholesterolemic and raised both LDL-C and HDL-C concentrations compared with oleic acid.95
Thomas et al. conducted a study to evaluate the effect of MCTGs with and without exercise on postprandial lipemia (PPL). Twenty-five young men and women were chosen. Each subject had to perform three trials: (1) a control group ate a meal with only 1.5 g of fat/kg of body weight; (2) MCT oil was substituted for 30% of the fat calories; and (3) MCT oil was consumed as in trial 2, but 12 h of exercise was completed before the meal. ANOVA indicated that the substitution of MCT oil to the control meal did not affect the PPL. However, the PPL was significantly lower after the MCT oil + exercise vs. the other trials. The results suggest that MCT oil does not affect the TG response to a fat meal.96
On a different note, considering atherosclerosis as a result of the aging process and not due to the lipid theory, Kaunitz reviewed the research completed prior to 1986 and concluded that MCTGs could possibly prevent or slow down atherosclerosis.57
In summary, it can be noted that most of the research concerning health effects of acute and chronic ingestion of MCTGs has been completed with nonathletes and has involved nonpractical diets that have not been tested over the long term. Until long-term health effects of chronic practical ingestion of MCTGs can be adequately reported, athletes should exercise caution when using MCTGs as an ergogenic aid.
In the past decade, chemically defined structured lipids have become popular research items. These lipids were originally produced by mixing pure MCTGs and LCTGs and allowing hydrolysis to produce FFAs. This was followed by random transesterification of the FAs into mixed triglyceride molecules. This results in a TG containing combinations of short-, medium-, and long-chain fatty acids on a single glycerol backbone. The resulting TGs have unique chemical, physical, and physiological properties. Today the use of 1,3-specific or 2-specific lipases can be used to synthesize 1,3-specific or 2-specific triglycerides containing MC and LCTG on the same glycerol.97
A study was conducted to test performance after consumption of specific structured TGs consisting of a mixture of MCFAs and LCFAs (MLM), in an attempt to prevent the adverse effects observed by feeding larger doses of MCTGs (i.e., gastrointestinal distress and elevated plasma lipids). Seven well-trained cyclists worked 3 h at 55% of maximum O2 uptake. During this time, they ingested CHO or CHO plus the MLM. Immediately after the constant-load cycling, the subjects performed a time trial of ~50 min duration. Treatments did not significantly affect performance. Plasma FA concentrations were significantly higher after 3 h of cycling compared to the resting stage, but no differences in the sum total between groups was noted. No gastrointestinal disturbances were noted. The MLM consisted of M = 8:0 (caprylic) and L = 18:2 (linoleic). Breath and blood samples revealed no plasma 8:0 FAs, but the amount of phospholipid FAs was significantly higher after CHO + MLM than with CHO intake. The fact that 8:0 did not appear in the plasma when large doses were consumed may indicate the MLM treatment was not glycogen sparing. Possible explanations by the authors for a lack of 8:0 in the plasma include possible elongation of the 8:0 FAs to 14:0 FAs and longer, or possibly the 8:0 FAs were metabolized so fast they were not detected. In any case, the treatments did not improve performance.98 Kasai et al. found structured lipids to cause a reduction in body fat and to lower TC.99 Mu and Hoy reported that structured TGs are absorbed by the same mechanism as conventional LCTGs.100
Carvajal et al. found a difference in the fecal excretion of FAs in rats when they were fed diets containing different types of structured TGs.101 The future of structured lipids' use in diets remains to be seen, but most of the current research results are positive.
While weight reduction is usually not a goal for athletes, exercise, along with dieting, is a necessary component of any weight loss regimen. Researchers concerned with obesity have noted that MCTGs seem to promote an increase in energy expenditure, and thus a chronic intake of MCTGs may be a possible means of weight loss. Developments in this area could be of interest to athletes. For example, St.-Onge and Jones reported on a review of the literature concerning MCTGs and weight reduction. In their summary they state that diets with elevated levels of MCTGs cause an increase in energy expenditure, a depression of food intake, and a lower body mass. While these results should be of some interest to athletes, the authors point out that most of the research completed with MCTGs and weight reduction were done over short testing periods. The longest test period reported was 14 days. Clinical trials of longer duration need to be conducted before specific recommendations can be made.102 Others have shown that MCTGs in a diet help reduce body weight when compared to LCTGs103 and increase thermogenesis in humans104 105 and rats.106 This is also true for structured TGs.99 The future of MCTGs and structured lipids in weight reduction diets is also yet to be decided.
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