Imagine a group of drugs that could increase the energy available to your muscles, help you to lose weight, and let you live longer and more healthily. Sounds like the sort of futuristic promises we have been given for years. But such possibilities are becoming more likely, thanks to developments in a one-time research backwater that is becoming very much mainstream.
The drugs would target tiny units, known as mitochondria, that exist in virtually every cell in your body. Once, they were believed to be the vital but rather dull power-plants that provided the energy we need to move, think, digest, keep the heart beating, and so on. But recently, mitochondria have emerged as major-league players in most of the degenerative diseases that plague Western societies, such as heart disease and cancer, as well as Alzheimer's and Parkinson's. A whole new discipline is emerging known as "mitochondrial medicine", which will use specially targeted super- antioxidants that should have dramatic effects on ageing and weight loss.
Mitochondria are the size and shape of long, thread-like bacteria, and they are found in every cell that has a nucleus. Some only have a few, while others in energy-hungry organs such as the heart, have several thousand. Their astounding trick is to take the oxygen we breathe and use it to transform carbohydrates and fats into energy, which is stored in a chemical known as ATP. The other special feature of mitochondria is that each has its own DNA, known as mDNA, consisting of just a few genes.
Mitochondria are linked with obesity because ATP can either be stored as fat or released in the form of heat. The attraction, not to say profits, of developing a drug that could shift your muscle mitochondria in the direction of less storage and more heat production is obvious. Something like that seems to be going on naturally anyway.
Recently, a geneticist, Douglas Wallace, of the University of California, published a study showing that where your distant ancestors lived may affect your metabolism today. Analysing variations in mDNA in Asia and Africa, he found considerable variation in how efficiently individual's mitochondria produce heat or store fat. "People indigenous to tropical zones had gene variations that allowed their cells to use energy efficiently," he reported. "Individuals native to arctic zones, in contrast, had cells programmed to generate more heat."
The reason mitochondria have their own DNA can be traced back to their bizarre origin 2,500 million years ago. Then, they were free- living bacteria swimming in ancient seas. Somehow, one of them became incorporated into the body of another single-celled organism to form a totally new life form - the common ancestor of all multicellular creatures.
But this archaic symbiotic union was a Faustian pact that gave our distant ancestors energy, but in return created sex and death. Power plants are invariably polluting, and the free radicals (FRs) that are the damaging by-products from the manufacture of ATP are what link mitochondria to ageing. They damage tissue in much the same way that the oxygen in the atmosphere rusts iron. Defence against FRs is provided by antioxidants, supplied both by the diet - vitamins such as C and E - and by the body's own brands, such as SOD (superoxide dismutase) and glutathione. They mop up the free radicals, preventing further harm. However, as we age, we produce less, so damage accumulates in our vital organs, as well as in our DNA - especially mDNA.
Human mitochondria are quite leaky, giving off more FRs than those of birds, for instance. Mitochondrial DNA is particularly vulnerable to this type of damage, not just because it is next door to the major source of FRs, but also because its repair mechanisms are less efficient than regular DNA. If you boost the production of SOD in fruit flies or worms, or add extra antioxidants to their diet, their lifespan goes up by 40 per cent. …