A week ago I posted my thoughts on the JAMA article about the potential of antioxidant supplements to decrease longevity. As a part of my commentary I pointed out that my study of the scientific literature (along with a dose of common sense) led me to believe that decreasing the amount of vulnerable polyunsaturated fatty acids in cellular and mitochondrial membranes would make them less prone to oxidation. If membranes are less prone to oxidation, they function better and last longer. If our membranes function better, so do we; and if our membranes last longer, so do we.
I just read a great paper in the Articles in Press section of one of my favorite journals, Experimental Gerontology, that adds confirming data to the greater-membrane-saturation-leads-to-longer-life hypothesis. Unfortunately, the abstracts are not available for the articles in press, so I’ll copy it below. Unlike a lot of abstracts, this one pretty much sums up the entire article. The paper discusses peroxidation, which is the technical term for oxidation of a fatty acid.
Extended longevity of queen honey bees compared to workers is associated with peroxidation-resistant membranes.
In the honey bee (Apis mellifera), depending on what they are fed, female eggs become either workers or queens. Although queens and workers share a common genome, the maximum lifespan of queens is an order-of-magnitude longer than workers. The mechanistic basis of this longevity difference is unknown. In order to test if differences in membrane composition could be involved we have compared the fatty acid composition of phospholipids [the fatty acid structure of cellular membranes] of queen and worker honey bees. The cell membranes of both young and old honey bee queens are highly monounsaturated with very low content of polyunsaturates. Newly emerged workers have a similar membrane fatty acid composition to queens but within the first week of hive life, they increase the polyunsaturate content and decrease the monounsaturate content of their membranes, probably as a result of pollen consumption. This means their membranes likely become more susceptible to lipid peroxidation in this first week of hive life. The results support the suggestion that membrane composition might be an important factor in the determination of maximum life span. Assuming the same slope of the relationship between membrane peroxidation index and maximum life span as previously observed for mammal and bird species, we propose that the 3-fold difference in peroxidation index of phospholipids of queens and workers is large enough to account for the order-of-magnitude difference in their longevity.
A couple of important findings in this paper are a) increasing consumption of pollen leads to a decreased saturation of cellular membranes, and b) decrease saturation (i.e. more polyunsaturated) in cellular membranes leads to a shorter life.
Honey bees destined to become workers eat mainly pollen, which is about 10 percent fat, mostly polyunsaturated. Queens-to-be are fed royal jelly, which contains about the same proportion of fat as pollen, but a more saturated fat. About half the fat in royal jelly is a naturally occurring trans fat that is monounsaturated; the rest of the fats are medium chain fatty acids that are either saturated or monounsaturated. So what we have are bees with the exact same genetics that have different degrees of saturation of their membranes depending upon their diet.
If you want to be a queen (if you’re a bee, at any rate), you’ve got to eat less polyunsaturated fat and more of the good stuff. For my money, the same holds if you’re a human. Perhaps that’s why despite my advanced age I look so much better than, say, Dean Ornish. It’s all that saturated fat I eat daily. I eat the human equivalent of royal jelly–he eats pollen. And consequently, like the queen bee’s, my membranes are more saturated.