To Your Health

A. Worldwide about 150,000 people have a genetic condition known as keratoconus, in which the cornea of the eye becomes progressively thinner and weaker and changes from a "dome" shape to a "cone" shape. The cornea can thin down to as little as half the normal thickness, and in addition develop scars that cloud vision even more. To make things even worse, many people with KC become sensitive to bright light, a sensitivity that is usually made worse by the hard contact lenses that are the standard remedy for KC.

The cornea is made entirely of collagen, a protein found abundantly in our bodies. There are at least 12 types of collagen, and the collagen in the cornea is unique because in the cornea the collagen must be transparent. The problem with KC almost certainly has to do with a defect in this collagen, but researchers have been unable to find a difference in the composition of collagen taken from a normal cornea and a cornea with KC.

New research has indicated that instead of the collagen being different there is just less collagen in a KC cornea than in a normal cornea, probably due to accelerated destruction of collagen by the enzymes that are used to continually "remodel" the cornea. Most of our structural body parts such as bone and skin are always in the process of being renewed by demolishing the old structure and then making it anew. Apparently the "destruction" phase in KC outpaces the "manufacturing" phase, so there is a need to either tone down the activity of the destructive enzymes or produce stronger collagen.

From the time of their discovery, bioflavonoids and vitamin C have been closely associated with strengthening collagen. Even those animals that make their own vitamin C, which is almost every species except us primates, produce stronger collagen with bioflavonoid supplements. Changing the activity of the enzymes that digest collagen may be more difficult, but a component of soy, genistein, has been proposed as an inhibitor of these enzymes, though as yet there is no proof that it is effective.

Magnesium deficiency has also been associated with corneal thinning. The role of magnesium deficiency in KC remains obscure, but some scientists think it may alter the structure of the collagen. An article in the Jan. 25, 2005 issue of Ophthalmic and Physiological Optics (pp. 7-12), suggests the ways in which magnesium deficiency could be involved in KC and points out that the cellular changes observed in KC are similar to the known physiological effects of magnesium deficiency.

Another significant observation made recently is that proinflammatory substances such as prostaglandin PGE2 are increased in the tears of people with KC. This indicates that our whole arsenal of anti-inflammatory substances, beginning the omega-3 fatty acids, could be used to slow the progression of KC. All things considered, there is hope that several of these treatments used together would help KC.