Science Tribune - Article - March 1998
The evolution and ecology of the menopause
Andrew J. Petto
National Center for Science Education, PO Box 8880, Madison WI 53708-8880
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Outreach Specialist, Wisconsin Teacher Enhancement in Biology, Department of Genetics, U Wisconsin, 445 Henry Mall, Madison WI 53706-1574
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Why menopause ?
One of the enduring questions in understanding the evolution of the human life span has been explaining the mechanisms that are responsible for the biological changes that we experience late in life. How is it possible, we ask, for a characteristic that appears late in life to be affected by natural selection and other processes that contribute to evolution when we know that evolution requires that traits under selection produce differences in survival and reproduction? One such set of biological changes receiving a great deal of renewed attention lately is the menopause.
We humans seem to be the only species in which the female reproductive system goes into decline while the rest of the body remains healthy and vigorous. It is estimated that a 75-year-old human female still retains at least 90% of her basal metabolic rate, 85% of nervous system function, 70% of her cardiovascular function and muscle coordination, and 50% of pulmonary function compared to her physiological state in her 20s (see (1) for details). Yet at this point in her life, a woman's reproductive system has been inactive for at least 2 decades. What could account for the early cessation of such a fundamental biological function in the absence of any serious malfunction in most of the other systems of the body?
Biology of reproduction
The menopause has received considerable attention in the past decade from researchers in a variety of fields of study. Although there is some disagreement among researchers over what causes the menopause, there is broad agreement on the nature of the physiological changes. Since female reproductive function depends on the interactions among the hypothalamus, anterior pituitary gland, ovaries, and uterus, research teams have explored each of these links. Because uterine function mainly affects fertility after conception, most research focuses on the hypothalamus-pituitary-ovarian links.
In normal reproductive function, the hypothalamus monitors the levels of hormones in circulation and integrates signals from the rest of the body. In response to input from the sensory neurons of the nervous system, changes in brain chemistry as a result of the emotional state, and circulating levels of hormones, the hypothalamus acts to control the secretions of the pituitary gland. The hypothalamus sends Gonadotropin-Releasing Hormone (GnRH) to the anterior pituitary gland which causes the release of specific hormones that stimulate the maturation and release of eggs and the production of sex hormones in the ovary. The anterior pituitary also releases prolactin which influences the sensitivity of the ovaries to these hormones by its effects on the number of molecules available in the ovaries that can respond to the other hormones.
In humans, as in other mammals, peak fecundity occurs in early adulthood, around the mid-20s. Fecundity then declines more or less gradually for the next 25 years. One consequence of this phenomenon is that women who have delayed reproduction into their middle or late 30s (or older) uniformly report difficulties in becoming pregnant despite "normal" levels of circulating hormone, adequate endocrine function, and lack of any cell, tissue, or organ abnormalities or dysfunctions.
After age 40, O'Rourke and colleagues (2) report that the daily levels of female hormones are significantly lower, but that the peak levels - the maximum level associated with ovulation - remain similar compared to those in younger women. Furthermore, they report that the peak levels of hormones designed to support implantation of the fertilized egg and to sustain a pregnancy may actually be higher in these older women.
Others have focused on the dual role of the follicles, as the source of primordial egg cells and as the structures that produce the hormones necessary to trigger ovulation. Studies by Gosden & Faddy (3) and Judd & Fournet (4) have explored the effects of the reduction of available follicles or the decline in follicular function as a cause for the reproductive changes associated with the menopause.
Female reproductive ecology
In most mammal species, females reproduce regularly until they die. In our work at the New England Regional Primate Research Center of Harvard Medical School, we found that regular reproduction continues in macaque monkeys well into the mid-teens. Between ages 15 and 20 years, most of the females will begin to succumb to old age, and very few will survive into their 20s. Although reproductive output does decline somewhat in these older females, it is only in monkeys over 19 years old that reproductive function is seriously disturbed.
One important difference, of course, is that the other primates have much shorter generation times. By the time a macaque female is 4-5 years old, she is a mother. She is a grandmother by age 9, and a great-grandmother by 14. By the time that she begins a serious decline in reproductive function, her daughters will be grandmothers. On average, only 42% of the total life span of a macaque female will have been spent when she becomes the grandmother of a granddaughter who is likely to survive to reproductive age. This is true of most of the other Old World monkeys, but the African apes use up over 2/3 of their life spans before reaching this milestone. Humans have "reset the clock" to the 42% typical of macaques by living so far beyond the end of reproduction but, unlike macaques, they have also given up the ability to reproduce much beyond this milestone (see (5) for details).
Menopause and the human life span
Pavelka & Fedigan (6) have taken an evolutionary perspective on the question. Menopause itself appears to be universal in human females in all populations studied, even though the majority of human females throughout the history of our species (and even alive today throughout the world) seem not to survive long enough for this characteristic to be expressed fully. Life expectancy at birth for a baby girl born in North America is now close to 80 years, but this "average" life span is not attained, even in industrialized countries today, by as many as half of those female children. If the menopause is not expressed in most females (because, even today, most don't survive long enough for reproductive function to cease), how did it become such a fundamental and universal constituent of the reproductive span of human females?
Austad (1) points out that there are several benefits for females ceasing reproduction while they are still otherwise healthy. For example, if a child takes a decade or more to be able to care for itself, then a mother that stops reproducing while still in good health can live long enough for her last child to reach this important milestone. It is also possible that an older woman in good health may devote time and effort to nurturing her grandchildren and improving their survival (7). Or, it is possible that the menopause is an unintended outcome of some other biological shift.
Menopause and evolution
There are only a few models in evolutionary biology that can explain selection for traits that have delayed expression or seem to be expressed only rarely. If we apply those explanatory models to the menopause, the first model would lead us to expect that menopause is an unintended outcome (or side effect) of selection for some other characteristic. In this view, the menopause may be caused by linked or pleiotropic genes (those that have effects on more than one characteristic or system). The menopause may represent a trade-off between reproduction later in life, when fertility is naturally lower and birth defects are higher, in favor of some other characteristic that enhances survival and reproduction at an earlier age. This trade-off works because the net gain in reproduction and fertility earlier more than offsets the potential loss from ending reproduction prematurely.
The second model derives from sociobiology and behavioral ecology. In this view, the reproductive success of a female is measured not only by the number of her children that survive, but the number of copies of her genes that survive into future generations in the form of her grandchildren and other relatives. Since her children will share, on average, one-half of her genes and each grandchild about one-quarter, a woman who successfully nurtures 2 grandchildren will have preserved as many of her genes in future generations as she would by having one more child. Women who devote their time to helping raise grandchildren, instead of having more children of their own, may therefore improve their representation in successive generations more than those who try to reproduce healthy children when they are over 40.
Maternal health and infant survival
In addition to the decline in fecundity through the reproductive span, we also observe an age-related increase in birth defects and other problems. In addition, the high energetic costs to mothers of caring for several children over a long period of time further decreases the potential for future reproduction. At some point, a simple cost-to-benefit analysis indicates whether it is better for a mother to invest her energy in having one more child or in assuring the survival of existing children. Theoretical concerns would predict that the switch to investing more in existing children would come when the total number of all one mother's children that survive would not be increased by bearing another child; or even the point at which that total would actually be decreased by her bearing another child.
Maternal investment across generations
How much difference can a grandmother make in the survival of her grandchildren ? Hawkes and colleagues (8) recently published results of their studies with Hadza grandmothers in Africa. These studies demonstrate that children whose grandmothers are able to participate in their care will be healthier, grow faster, and gain more weight than other children who are raised by mothers only. They argue that the "extended provisioning" of human children co-evolved with the postmenopausal life span. The successful survival of grandchildren who have the benefit of their grandmothers' care can assure the persistence of this biological characteristic into future generations by living to pass on these genes to their own children and grandchildren.
It is clear from the current research into the evolutionary ecology that the way that the menopause fits into the way that we humans live on earth is complex and multilayered (9). The universality of this physiological change among humans, back as far as reliable medical records can be found, indicates that it is a fundamental characteristic of our species, and its nearly complete absence from all but our closest African ape relatives further indicates that this is an evolutionarily recent phenomenon. As much as our long period of infant growth and development and continuous reproductive cycling, the menopause is an essential part of the reproductive strategy that defines our species.
It also appears to be an essential part of a very successful reproductive strategy, since our species has grown rapidly and spread throughout the planet at the same time that greater and greater proportions of our females are actually surviving past this reproductive milestone. So, by giving up the ability to reproduce past the fifth decade of life, our females have not given up any significant contribution to future generations, to population growth in general, or to the survival of their unique physiological attributes in their descendants.
Questions still abound, of course. The why of the menopause we may never know; the how we are beginning to understand; the variation in the when of this human universal remains as a fascinating issue for further exploration.
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2. O'Rourke MT, Lipson SF, Ellison PT. Ovarian function in the latter half of the reproductive lifespan. American Journal of Human Biology 8, 751-9, 1996.
3. Gosden RG, Faddy MJ. Ovarian aging, follicular depletion, and steroidogensis. Experimental Gerontology 29(3/4), 265-74, 1994.
4. Judd HL, Fournet N. Changes of ovarian hormonal function with aging. Experimental Gerontology 29(3/4), 285-98, 1994.
5. Petto AJ. Demographic consequences of life history variation in nonhuman primates [PhD Dissertation]. Amherst MA (USA): University of Massachusetts; 1986. 350 p, Available from University Microfilms, Ann Arbor, MI.
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7. Peccei JS. A hypothesis for the origin and evolution of menopause. Maturitas 21, 83-9, 1995.
8. Hawkes K, O'Connell JF, Jones NGB. Hadza women's time allocation, offspring provisioning, and the evolution of long postmenopausal life spans. Current Anthropology 38(4), 551-77, 1997.
9. Sherman S (ed). Proceedings of a conference on Menopause : Current knowledge and recommendations for research. Experimental Gerontology 29 (3/4) (special issue) 1994.