Menopause is a universal phenomenon in humans alone, with occasional cases in domestic animals that seem to be “an artifact of civilization.”[1] Despite menopause being currently understood as a process separate from senescence due to its comparably more sudden onset, it is still difficult to separate menopausal changes from those of senescence. This means that identifying the biological start of menopause is equally, if not more, difficult, and the actual prompt for menopause is still debated. In spite of this, theories abound, and studies regarding the biological changes caused by and resulting in menopause are becoming more and more common. In order to better understand why menopause would evolve in human females versus the world’s mammals, it is crucial to understand how menstruation evolved in the first place and how outside factors might affect the evolution of menopause.
The two major theories regarding the evolution of menopause are Profet’s anti-pathogen hypothesis, and Strassman’s hypothesis that menstrual bleeding is a side-effect of endometrial regression. Marjorie Profet suggests that menstrual bleeding evolved as a means of cleaning the uterus and vagina of sperm-borne pathogens. She states that if this is the case, then uterine pathogens are more prevalent before menses than after, that menstruation tracks pathogen burden, and that the copiousness of menstruation increases with the promiscuity of the breeding system. In response to this hypothesis, Beverly Strassmann brings up several studies and experiments in which it was found that nutrient-rich blood only feeds bacteria, and brings up the cases of gonorrhea and Chlamydia, both of which are more prevalent after menstruation. She continues to say that menstruation does not track pathogen burden because women still have sex while pregnant, during post-partum amenorrhea, and in their postmenopausal years in both modern and preindustrial societies. Finally, Strassmann uses Profet’s own primate data to demonstrate a lack of correlation between promiscuity of the breeding system (different subspecies of macaques and baboons have different breeding systems and the same menstruation regardless).
Strassmann then proposes her own hypothesis that menstrual bleeding is a side effect of endometrial regression, which is more cost effective than maintaining the endometrium. She says that as women get closer to ovulation, the endometrium that lines the uterus is accompanied by the growth of an endometrial microvasculature that provides it with nourishment. When implantation does not occur, “then the endometrium actually erodes and its injured vasculature bleeds into the uterine cavity.”[2] Only 1/3 of the endometrium is shed – the rest, as in other primates – is reabsorbed. In healthy West European women, only 9% - 14% lose more than 80ml of blood, the threshold for iron deficiency in women, and the fecal protein loss over one cycle in women is higher than the menstrual protein loss over the same period, suggesting that it is not very costly to shed the endometrium.
Why would menopause be beneficial, given this information? Penn and Smith discuss the fitness costs of reproduction between the sexes, using “genealogical data from the Utah Population Database, for which survival information is complete for couples and their offspring.”[3] Using this data, they compared reproductive costs of men and women one year and five years after their last birth. They found that the survival rates of both parents decline with increasing parity during both intervals, and that increasing parity had a higher impact on the survival of the mothers than the fathers. This data suggested that “women had significantly higher risks of mortality than men at all levels of parity and worsened with increasing parity.”[4] The costs are persistent, and the more children that couples had, the higher the survival costs to both parents.
Penn and Smith made sure to control for socioeconomic status and other random effects, finding that the data was not confounded by outside variables. They also looked into survival of offspring based upon parental mortality, and found that the survival of the offspring was more dependent upon the survival of the mother than of the father. Their data also suggested that offspring reproductive success depends more upon the mother’s presence than the father’s, and is likely because mothers leave behind fewer surviving offspring (prudent mother hypothesis) as opposed to the enhancement of survival of grandchildren (grandmother hypothesis). This evidence provides an increasingly good evolutionary reason for menopause to exist in human females, but doesn’t explain the biological mechanism.
Wise et al. discuss two theories of causation of menopause: an unrenewable source of follicles in the ovaries, and the chemical interactions of the hypothalamus and ovaries. The first theory discusses how women are born with a certain number of follicles, and then explains that many will degenerate. In fact, there is a doubling of the “rate of loss of follicles in middle-aged women around the age of 35, when about 25,000 primordial follicles remain and, coincidentally, when perimenopausal symptoms begin to appear.”[5] This is a very common theory that is often discussed by the non-scientific community, but the second theory Wise et al. discuss also has substantial support. They mention that some investigators hold to the idea that the hypothalamus is what initiates the events leading to menopause, saying that changes that occur in the hypothalamus present themselves in women when they are between 35 and 40 years old, which is the same time that rates of follicular loss increase. The authors suggest that neither theory is mutually exclusive, and suggest that these processes may even occur independently of each other, while leading to the same end.
Leidy provides data that suggests that there is a genetic component to menopause in women who experience premature ovarian failure,[6] and that atresia (degeneration of the follicles) may be “an evolved mechanism that facilitates reproduction by means of relatively small numbers of offspring,”[7] – which would correlate to Wise et al.’s discussion of degeneration of follicles over time and correspond with Penn and Smith’s discussion of reproductive fitness costs on women with more offspring. I have also been able to relate Jared Diamond’s statement on offspring survival – “the birth of each child immediately jeopardizes the mother’s previous children due to increased risk of death in childbirth,”[8] – to Penn and Smith’s discussion of the same topic.
Other factors heavily influence when menopause occurs, as well. The median age of menopause in industrialized societies is roughly 47 – 51, where women are relatively well-nourished and have more of a choice in their pregnancies. In non-industrialized societies, this age is even younger.[9] Why? Penn and Smith suggest that fertility declines “are most closely linked to the improvements in women’s education and reproductive autonomy, suggesting that when given the opportunity, women prefer smaller families perhaps to reduce their costs (or perceived costs) of reproduction.”[10] The New England Research Institute, Leidy says, performed a study regarding women and smoking, and found that women who smoked not only have an earlier menopause, but also an earlier perimenopause.[11] Gillespie et al. found that women who are widowed early on have a higher chance of earlier menopause as well.[12] Lennon’s study (1982) discusses the psychological aspects of menopause and how it affects women, saying that when menopause is early or late, it causes psychological distress, but when it is on time (the years discussed above), “it is expected and appropriate.”[13] The influence of outside factors, then, can lead to psychological distress in women who are less healthy.
Menopause, then, is a necessary factor. While it does not cost as much to shed the endometrium as it would to maintain it, the process of childbirth can be very stressful on the human body, and as parity increases, so too does the risk of survival for both the mother and her offspring. Smith writes that without menopause, women would “be forced to divide declining faculties between the care of extant offspring and increasingly hazardous production of new ones.”[14] Therefore, menopause is significant in the scope of human evolution in that it allows women to stop reproducing when it would risk their fitness and the survival of their offspring.
References:
Agee, Eve. "Menopause and the Transmission of Women's Knowledge: African American and White
Women's Perspectives." Medical Anthropology Quarterly, New Series 14, no. 1 (2000): 73-95.
Davis, Dona L.. "Blood and Nerves Revisited: Menopause and the Privatization of the Body in a
Newfoundland Postindustrial Fishery." Medical Anthropology Quarterly, New Series 11, no. 1
(1997): 3-20.
Diamond, Jared. Why is Sex Fun? The Evolution of Human Sexuality. 1st ed. New York: Basic Books,
1997. Print.
Dillaway, Heather E.. "Menopause is the "Good Old": Women's Thoughts About Reproductive Aging."
Gender & Society 19, no. 3 (2005): 398-417.
Franceschi, Silvia, Demenico Schinella, Ettore Bidoli, Luigino Dal Maso, Carlo La Vecchia, Fabio
Parazzini, and Romano Zecchin. "The Influence of Body Size, Smoking, and Diet on Bone Density in Pre- and Postmenopausal Women." Epidemiology 7, no. 4 (1996): 411-414.
Gillespie, Duncan O.S., Mirkka Lahdenperä, Andrew F. Russell, and Virpi Lummaa. "Pair-Bonding
Modifies the Age-Specific Intensities of Natural Selection on Human Female Fecundity." The American Naturalist 176, no. 2 (2010): 159-169.
Leidy, L. E.. "Biological Aspects of Menopause: Across the Lifespan." Annual Review of Anthropology
23, no. (1994): 231-253.
Lennon, Mary C.. "The Psychological Causes of Menopauce: The Importance of Timing of a Life Stage
Event." Journal of Health and Social Behavior 23, no. 4 (1982): 353-366.
Nesse, Randolh M. and George C. Williams. Why We Get Sick, The New Science of Darwinian
Medicine. 1st ed. New York: Vintage Books, 1994. Print.
Penn, Dustin J. and Ken R. Smith. "Differential Fitness Costs of Reproduction between the Sexes."
Proceedings of the National Academy of Sciences of the United States of America 104, no. 2 (2007): 553-558.
Strassmann, Beverly I.. "The Evolution of Endometrial Cycles and Mentruation." The Quarterly Review
of Biology 71, no. 2 (1996): 181-220.
Williams, George C.. "Pleiotropy, Natural Selection, and the Evolution of Senescence." Evolution 11, no.
4 (1957): 398-411.
Winterich, Julie A.. "Sex, Menopause, and Culture: Sexual Orientation and the Meaning of Menopause
for Women's Sex Lives." Gender & Society 17, no. 4 (2003): 627-642.
Wise, Phyllis M., Kristine M. Krajnik and Michael L. Kashon. "Menopause: The Aging of Multiple
Pacemakers." Science, New Series 273, no. 5271 (1996): 67-70.
Zeserson, Jan M.. "How Japanese Women Talk about Hot Flushes: Implications for Menopause
Research." Medical Anthropology Quarterly, New Series 15, no. 2 (2001): 189-205.
[1] Williams, George C., “Pleiotropy, Natural Selection, and the Evolution of Senescence,” p. 407.
[2] Strassmann, Beverly, “The Evolution of Endometrial Cycles and Menstruation,” p. 192.
[3] Penn, Dustin J. and Ken R. Smith, "Differential Fitness Costs of Reproduction between the Sexes,” p. 553.
[4] Ibid, p. 554.
[5] Wise, Phyllis et al, “Menopause: The Aging of Multiple Pacemakers,” p. 68.
[6] Leidy, L.E., “Biological Aspects of Menopause: Across the Lifespan,” p. 235.
[7] Ibid.
[8] Diamond, Jared, “Making More by Making Less: the Evolution of Female Menopause,” Why is Sex Fun?, p. 117.
[9] Leidy, L.E., “Biological Aspects of Menopause,” p. 240.
[10] Penn, Dustin J. and Ken R. Smith, "Differential Fitness Costs of Reproduction between the Sexes,” p. 553.
[11] Leidy, L.E., “Biological Aspects of Menopause,” p. 246.
[12] Gillespie, Duncan O.S. et al., “Pair-Bonding Modifies Age-Specific Intensities of Natural Selection on Human Female Fecundity,” p. 159.
[13] Lennon, Mary Clare, “The Psychological Consequences of Menopause,” p. 353.
[14] Smith, George C., “Pleiotropy, Natural Selection, and the Evolution of Senescence,” p. 408.
