Coconut Oil Increases Tomato Carotenoid Uptake as Compared to Safflower Oil in Mongolian Gerbils Fed Whole Tomato Powder
A new study1 reports beneficial effects in accumulating carotenoids from a “salad” of powdered tomatoes for Mongolian gerbils eating a diet of 10% whole tomato powder along with a 20% safflower oil diet or an 18% coconut oil plus a 2% safflower oil diet (the latter was added to prevent essential fatty acid deficiency). The authors report that Mongolian gerbils are a good rodent model for humans ingesting tomatoes as “the lipoprotein profiles of the gerbil are more similar to humans than most other rodents, making carotenoid metabolism findings more relevant than those results in other species.” In addition, gerbils are reported to accumulate tomato carotenoids in levels proportionate to humans.1 Coconut oil is a good source of medium chain triglyceride fats, while safflower oil is the most commonly used vegetable oil in commercial salad dressings. The purpose of the study was to determine how the coconut oil plus low-dose safflower oil compared to the high-safflower oil for the tissue uptake of carotenoids from the powdered tomatoes. The authors note that recent studies have suggested that the combination of carotenoids derived from whole tomato powder may be more effective in disease prevention than lycopene alone.1 Tomatoes are known to contain the carotenoids phytoene, phytfluene, alpha-carotene, Z-carotene, and beta-carotene, as well as lycopene and lutein.
The results showed that “the coconut oil feeding resulted in significantly increased tomato carotenoid bioaccumulation compared to safflower oil in all tissues measured except the spleen and skin. Increased tissue accumulation may have been a result of increased solubility of tomato carotenoids in the intestinal lumen, portal absorption of medium-chain fatty acids, a cholesterol-mediated change in the flux of carotenoids between the liver and peripheral tissues, facilitated carotenoid cellular uptake by specific fatty acids, or the combination of the four.”1
Also observed was that serum cholesterol in the coconut-oil fed animals was significantly higher than that of the safflower-fed animals. The safflower oil-fed gerbils, however, had significantly higher liver cholesterol than the coconut-oil fed animals. These findings are consistent with what is known of the fatty acid content of these oils. You can avoid the increase in serum or liver cholesterol levels by not adding vegetable oils at all to your salad or using a smaller quantity than fed to the gerbils, but then you might absorb smaller amounts of the carotenoids than the gerbils did in this study. We get around this by both using smaller amounts of oil and eating larger amounts of carotenoid containing veggies (as well as taking supplements that contain particular carotenoids of interest, such as lycopene, lutein, zeaxanthin, and astaxanthin). And, of course, we both take niacin.
Keeping Cholesterol Under Control with Niacin
Another solution to high cholesterol levels that doesn’t require you to meddle with your salad is niacin and, as we explain below, the mechanism(s) responsible for the remarkable effectiveness if niacin in lowering LDL and increasing HDL is, despite decades of research, still unknown.
Durk’s Familial Hypercholesterolemia Succumbs to Niacin
We both take niacin on a daily basis, but it has been even more important for Durk who, before finding out about niacin quite a few years ago, had always had a problem with hypercholesterolemia, which ran in his family.
But How Does Niacin Work?
The mystery of how niacin works is under intensive investigation (even by pharmaceutical companies, hoping to find out mechanisms that it can use to design patentable drugs for the treatment of hypercholesterolemia in the many patients who are not treated effectively by statin drugs). Yet, as the years go by, one mechanism after another that is thought to explain how niacin works ends up explaining something but not how niacin works. A paper published two months ago2 explains that the GPR109A receptor that is activated by niacin (the “niacin receptor”) and was thought to be the reason for niacin’s decrease in triglycerides and LDL cholesterol and the increase in HDL cholesterol was found to be responsible for niacin’s antilipolytic effect but not for it’s effects on triglycerides or LDL or HDL. Hence, as reported in a commentary on the new niacin GPR109A findings,3 “[b]ecause the increase in HDL-C is regarded as the most important beneficial effect of nicotinic acid [niacin], the finding that it does not involve GPR109A questions the rationale for the development of synthetic GRP109A agonists; accordingly, most drug companies have stopped their GPR109A agonist programs.” However, the commentary also explains that there is reason to believe that the “increases in HDL-C may not be responsible for the long-term effects of nicotinic acid on the development of cardiovascular diseases.”
As the commentary explains, nicotinic acid has anti-inflammatory effects which do not involve GPR109A and has been shown to release adiponectin, the antiinflammatory cytokine released by fat cells. Moreover, the paper2 that was the subject of the commentary found that most effects of niacin on plasma lipid levels are not mediated by the GPR109A receptor. New data, the commentary3 suggests, points to the possibility that GPR109A may be of use in the treatment of diseases involving inflammation and immunological processes.
The niacin mystery lingers, tantalizingly. The title of the commentary paper,3appropriately points out “It Ain’t Over ’Til the Fat Lady Sings.”
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