What Is Aging? Definitions and Concepts in Gerontology

Although everyone is familiar with aging, defining it is not so straightforward. In fact, aging can have a positive connotation as in "aging wine." In the context of senescence.info, and unless otherwise noted, the term "aging" refers to the biological process of growing older in a deleterious sense, what some authors call "senescence" (Williams, 1957; Comfort, 1964; Finch, 1990). (Personally, I actually prefer the term "senescence." If this were an academic book, I would use the term "senescence." Being a website with visitors from various backgrounds, I use the term "aging" because it is easier for the average reader to grasp and because "senescence" now frequently refers to cellular senescence.) Aging is one of the most complex biological process, whose definition is intrinsically related to its phenotype, as developed below.

Aging has been defined as the collection of changes that render human beings progressively more likely to die (Medawar, 1952). Clearly, one hallmark of aging in humans and many other species is an age-related increase in mortality rates (Fig. 1).

Mathematically, aging can be quantified using mortality curves such as those of Figure 1. There are several mathematical functions that can be used (Wilson, 1994; Strehler, 1999, pp. 103-124). The simplest, most widely used method is based on the Gompertz function (Finch, 1990, pp. 13-22; Strehler, 1999, pp. 111-113):

Being m(t) the mortality rate as a function of time or age (t), A is the extrapolated constant to birth or maturity, and G is the exponential (Gompertz) mortality rate coefficient. From Figure 1 it is possible then to estimate the Gompertz equation for a human population by a simple regression analysis after maturity: m(t) = 8.84e^0.0800t with r² = 0.997. From this equation we can derive the initial mortality rate (IMR), which is the mortality rate independent of aging, often calculated from the mortality rate prior to its exponential increase with age; in this case, IMR = 0.0002/year since that is the mortality rate at ages 10-20. Another important variable taken from the Gompertz equation is the mortality rate doubling time (MRDT) given by MRDT = 0.693/G (Finch, 1990, pp. 22-24). Hence, MRDT = 0.693/0.0800 = 8.66 years. In fact, human populations have a MRDT of about 8 years. This means that after our sexual peak, or roughly age 30, our chances of dying double about every 8 years.

Demographic measurements of aging, such as the MRDT, may then serve as estimates of the rate of aging. Changes in the MRDT are expected to reflect changes in the rate of aging, but the same is not true for the IMR (Finch, 1990; Finch and Pike, 1996; de Magalhaes et al., 2005a). For example, the life expectancy at birth increased considerably in the past 100 years: in the US, the life expectancy at birth jumped from 47.3 years in 1900 to 77.3 years in 2002 (National Center for Health Statistics, Data Warehouse on Trends in Health and Aging). Still, the rate of aging and the MRDT have remained unaltered for thousands of years (Finch, 1990; Hayflick, 1994). What happened was that the IMR, which is not affected by the aging rate, was lowered due to breakthroughs in different areas, such as in the war against infectious diseases, thus lowering mortality rates across the entire lifespan and increasing the life expectancy.

This is an important concept to correctly interpret experimental results in gerontology, as briefly mentioned before: changes in lifespan may not reflect changes in the rate of aging. To determine whether rate of aging was affected one tool researchers have at their disposal is then calculating the MRDT and IMR with changes in the MRDT being indicate of changes in the rate of aging (Pletcher et al., 2000; de Magalhaes et al., 2005a). For experiments in, for instance, animal models to be relevant to aging it is crucial to discriminate between interventions affecting the aging process and interventions affecting health, as proposed by many others (Hayflick, 2000; Pletcher et al., 2000). These measurements are useful for comparisons between species. They have also been employed to determine whether interventions in rodents modified or not the aging process (de Magalhaes et al., 2005a). Lastly, and being IMR independent of aging, the conditions by which aging is studied should be ideal environmental conditions in order to minimize the IMR and allow us to better focus our research on aging (Strehler, 1986).

As mentioned above, human mortality rates begin to climb exponentially after about age 30. One peculiar phenomenon, however, is that this rate of increase of mortality actually levels off after about age 65 (Vaupel et al., 1998), as has been reported other species too. This is probably due, however, to statistics rather than any unknown biological process (Partridge and Mangel, 1999; Rossolini and Piantanelli, 2001).

As is common knowledge, women have a higher life expectancy than men. Pre-menopausal hormonal protection appears to be the reason behind this difference. Women have lower IMR than men but the MRDT appears to be similar for both sexes or even slightly higher for men^*. This indicates that women do not age slower than men; they are just better protected against certain diseases until menopause; interesting is the fact that there is some anecdotal evidence that, after menopause, women may suffer more from aging than men. Eunuchs also appear to live slightly longer than men (Hamilton and Mestler, 1969); a reduction in IMR due to hormonal alterations appears to be at the origin of this phenomenon (Grossman, 1984).

The way that the increase in life expectancy was due to changes in the IMR independent of changes in aging rates is also the reason why the average lifespan of humans is reaching a plateau. The only way to considerably increase human longevity in the future is to affect the aging process itself (Olshansky et al., 1990).

Aging can also be defined as a progressive functional decline, or a gradual deterioration of physiological function with age, including a decrease in fecundity (Partridge and Mangel, 1999), or the intrinsic, inevitable, and irreversible age-related process of loss of viability and increase in vulnerability (Comfort, 1964). Clearly, human aging is associated with a wide range of physiological changes that not only make us more susceptible to death, as described above, but that limit our normal functions and render us more susceptible to a number of diseases. The purpose of senescence.info is not to describe all age-related changes and pathologies typical of old age, as there are excellent resources on the topic (Craik and Salthouse, 1992; Spence, 1995; DiGiovanna, 2000; Timiras, 2002; also see the A.D.A.M Medical Encyclopedia's MedlinePlus Medical Encyclopedia). Nonetheless, a brief look at the most important physiological changes that occur with age and the pathological consequences of these changes may be useful to understand aging.

In humans, our body's functional decline tends to begin after the sexual peak, roughly at age 19 and perhaps some functions decline even sooner. Contrary to demographic measurements of aging, that show mortality rates increasing exponentially, the human functional decline is linear (Strehler, 1999). Succinctly, aging is characterized by changes in appearance, such as a gradual reduction in height and weight loss due to loss of muscle and bone mass, a lower metabolic rate, lower reaction times, declines in certain memory functions, declines in sexual activity and, in women, menopause, a functional decline in audition, olfaction, and vision, declines in kidney, pulmonary, and immune functions, declines in exercise performance, and multiple endocrine changes (Craik and Salthouse, 1992; Hayflick, 1994, pp. 137-186; Spence, 1995). However, apart from presbyopia, or farsightedness, which is caused by the continuous growth of the eyes' lenses and appears to be universal of human aging (Finch, 1990, pp. 158-159; Hayflick, 1994, p. 179), and menopause, no single age-related change is inevitable.

The phenotype of human aging is one in which practically any system, tissue or organ can fail (Austad, 1997a; Strehler, 1999). This indicates an intrinsic phenomenon affecting the whole organism and leading to the "weakest link" failing, resulting in death. Interestingly, studies in supercentenarians--i.e., people over 110 years of age--suggest that these individuals age uniformly. In other words, what makes supercentenarians unique is the fact they do not have one debilitating organ or system that results in death; they do not have a "weakest link." Supercentenarians are nonetheless extremely frail and debilitated, showing multiple pathologies (Coles, 2004). Likewise, one "autopsy study" in centenarians revealed that all, even those described as healthy before death, had an acute organic failure causing death. These results also suggest that the idea that people can die of "old age" is incorrect (Berzlanovich et al., 2005).

Clearly, the incidence of a number of pathologies increases with age (Fig. 2). These include diabetes, heart disease, cancer, arthritis, and kidney disease. Also note how the incidence of some pathologies, like sinusitis, remains relatively constant with age, while that of others, like asthma, even decline. Therefore, it is important to stress that aging is not merely a collection of diseases. With age we become more susceptible to certain diseases, but, as described above, we also become more likely to die, frailer, and endure a number of physiological changes, not all of which lead to pathology.

	45-54 years		Over 85 years
Cause of death	Incidence	% of deaths	Incidence	% of deaths
Diseases of the heart	92.8	21.66%	5607.5	37.48%
Malignant neoplasm	126.3	29.48%	1747	11.68%
Cerebrovascular diseases	15.1	3.52%	1485.2	9.93%
Parkinson's disease	0.1	0.02%	1312.8	8.77%
Alzheimer's disease	0.2	0.05%	703.2	4.70%
Pneumonia	4.6	1.07%	676.5	4.52%
Chronic lower respiratory diseases	8.5	1.98%	638.2	4.27%
Diabetes melittus	13.6	3.17%	318.6	2.13%
Certain infectious and parasitic diseases	22.9	5.35%	243.8	1.63%
Atherosclerosis	0.5	0.12%	177.3	1.19%
Others	143.8	33.57%	2050.9	13.71%

Figure 3 shows the most important causes of death in the elderly. Not surprisingly, heart diseases are the number one cause of death in people aged 85 and older, followed by cancer, cerebrovascular diseases, Parkinson's and Alzheimer's diseases, pneumonia, and chronic lower respiratory diseases. While diseases like cancer and heart diseases are major causes of death at all ages, other diseases, like Parkinson's and Alzheimer's, only become significant at old age (Table 1). Lastly, it is important to note that an understanding of the physiology and pathology of aging is important to assess the relevance of model organisms for the study of human aging, as mentioned elsewhere.

Despite all the physiological and pathological changes, there is still no accurate way to quantify how aged someone is. Despite decades of research, and even though it seems likely that different people age at different paces, the most accurate method to determine how aged someone is is still chronological age. This is a major problem for studying aging and there are ongoing efforts to determine a better way to quantify aging (reviewed in Balin, 1994).

Now that we have a clearer idea regarding the aging phenotype, we can define the basic terms that will be used in senescence.info. To sum it up, aging is a complex process composed of several features: 1) an exponential increase in mortality with age; 2) physiological changes that typically lead to a functional decline with age; 3) increased susceptibility to certain disease with age. So, I define aging as a progressive deterioration of physiological function, an intrinsic age-related process of loss of viability and increase in vulnerability.

Gerontology, of course, is the branch of biomedical sciences that studies aging. In senescence.info, "gerontology" normally refers to the study of the biological process of aging, not its medical consequences. Generally, I use the term "geriatrics" to refer specifically to the medical study of diseases and problems of the elderly. Technically, "gerontology" includes both the biological and the medical branches of the study of aging, but since senescence.info is written in the context of the biology of aging, "gerontology" usually refers to the study of the biological aspects of aging.

Life expectancy is how long, on average, an animal can be expected to live. Longevity is the period of time an organism is expected to live under ideal circumstances. Lifespan is defined as the period of time in which the life events of a species typically occur. Lifespan and longevity can sometimes be used interchangeably. For humans, lifespan and longevity are about the same in industrious nations, but when studying species in the wild, one can expect that lifespan will be inferior than longevity since feral conditions are certainly not ideal for assessing longevity. For most purposes, life expectancy, average longevity, and average lifespan have the same meaning. Maximum longevity and maximum lifespan are the maximum amount of time animals of a given species can live--typically, the record longevity for that species.

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What Is Aging?

Demographic Measurements of Aging

Pathologic and Physiological Age-Related Changes

Basic Definitions in Gerontology