The Mitochondrial Free Radical Theory of Aging - Supernova: Pliki

CHAPTER 7
The Status of Gerontological Theory
in 1995
The central motivation of this chapter is a fact that may surprise, if not appall, non-biologists:
that theoretical biology has a bad name. Theoretical gerontology, moreover, has a
particularly bad name: it is considered to be a magnet for sloppy thinkers with half-baked
ideas. As a theoretical gerontologist, I am therefore obliged to dissuade the reader from
prejudging what I have to say; this I hope to do in the following sections.
7.1. What Is a “Theory of Aging”?
In gerontology, as in any field of science, the development of a hypothesis involves a
perpetual oscillation between creative and analytical thinking. Advances of understanding
are rarely achieved by purely deductive analysis of existing data; instead, scientists formulate
tentative and incomplete generalisations of that data, which allow them to identify which
questions are useful to ask by further observation or experiment. (In this respect, gerontology
differs from most other scientific disciplines only in how little we have so far progressed
along the path to that understanding.) The further any such path is travelled, the more
complete and detailed are the hypotheses under active investigation.
The above is, in fact, so universally accepted as a cornerstone of the scientific method
that some may wonder why I have chosen to belabour it. I have three reasons.
The first is that there is a long-standing and widespread tendency, in the study of aging,
to over-sell a hypothesis. Many of the physiological or molecular changes that occur in our
bodies as we age can be proposed, with reasonable plausibility, to influence the rates of other
changes—and, in some cases, their own rate. But there is a huge difference between proposing
that a process influences the rate of aging and proposing that it is the dominant influence.
This difference has too often been glossed over: the process under consideration is presented
as being the dominant determinant of the rate of aging, when the supporting arguments
actually only suggest that it makes a non-zero contribution. This is all the more regrettable
because hypotheses which propose a non-zero contribution by a particular process are perfectly
legitimate stepping-stones to more ambitious hypotheses; the only requirement is to
keep the two types of hypothesis distinct. A recent review of the free radical theory 1 took care
to stress the distinction between the weak statement: “oxidants contribute significantly to the
process of degenerative senescence” and the strong statement: “oxidants determine maximum
lifespan potential”; the field will benefit greatly if this example is widely followed.
My second motivation is to dispel a view which has gained some popularity recently: 2,3
that aging is, broadly, already understood. The foundation of this view is that we have
discovered most, if not all, of the major mechanisms by which our macromolecular
organisation gradually breaks down, so that all that remains is to flesh out the finer details
The Mitochondrial Free Radical Theory of Aging, by Aubrey D.N.J. de Grey.
©1999 R.G. Landes Company.