[GRG] NewAbs: Why Do Women Lose Fertility?

To Members and Friends of the Los Angeles Gerontology
Research Group:  Why do
women lose fertility? — Steve Coles

“Why Women Lose Fertility:

Mating Behavior Is an Unlikely
Driver of Women’s Reproductive Aging”by
Daniel Levitis and Alan Cohen
September 1, 2013; (The Scientist) — The late statistician George
E.P. Box, who famously wrote that “all models are wrong, but some are
useful,” also wrote that “science is a means whereby learning is
achieved, not by mere theoretical speculation on the one hand, nor by the
undirected accumulation of practical facts on the other, but rather by a
motivated iteration between theory and practice.”Richard
Morton, Jon Stone, and Rama Singh  at McMaster University in
Ontario, in their recent article in

PLOS Computational Biology (9:e1003092, 2013), present a
mathematical model exploring whether menopause could evolve as a result

male preferences for younger mates. Their model imagines that early
in human evolutionary history, women remained fertile well into their
70’s and even 80’s, but men had a strong fixed preference for mating with
younger women. The older women thus remained mateless, therefore gaining
little fitness by retaining fertility, and as a result, accumulated
mutations that reduced their ability to reproduce later in life. The
central assumptions of this model, unfortunately, appear to be
false. In
Box’s framework, Morton and his colleagues have excelled at theoretical
speculation, but seem to have skimped on the reference to practical
facts: Our female great-ape relatives experience loss of fertility
near the end of their lifespans, at just about the same chronological age
human women do, implying that it is highly unlikely that our female
ancestors reproduced at ages later than women do now. Sustained selection
for later reproduction, were it to occur, would have had to overcome
serious physiological and phylogenetic constraints. And far from being a
starting point for human evolution, the preference of men for younger
women is a peculiarly human trait, not something we got from our distant
ancestors. We know this because most primate males preferentially mate
with older, more experienced females. Given this, it seems evident that
male preference for younger mates evolved as a result of the long human
postfertile lifespan, and not the other way around. That is, if our
ancient foremothers lost fertility as they aged, as women do now, males
would be expected to evolve a preference for the younger mates who would
be more likely to produce viable offspring.Just as
the evolutionary assumptions of the model ignore what we know about
evolution, its social assumptions ignore what we can easily see in human
societies throughout history: older women still have lovers. Older women
may be underrepresented in advertising and discriminated against in the
workplace, but very few of them are unable to gain access to sperm, and
very many are in long-term sexual relationships with committed
partners.One cause
of confusion, we believe, is revealed by Morton and colleagues’ choice of
language. They don’t distinguish between reproductive senescence (the
decline in fertility with age), menopause (the physiological cessation of
cycling that occurs after fertility has already reached zero), and the
postfertile stage in women’s evolved life history. Each of these three
traits is “menopause” in their terminology, obscuring the fact that all
three are related but very different traits with different evolutionary
histories. The puzzle that Morton and colleagues attempt to address is
not menopause, but rather the postfertile lifespan -­ in other words, why
women’s reproductive senescence occurs so long before they die of old
age?This is
actually the right evolutionary question, as it is the aspect that is
unique to humans. In contrast to other primate species, and despite
popular belief to the contrary, women live well beyond their reproductive
years across environments and have done so even in the harshest of
conditions. The presence of age-related decline in fertility and
subsequent cessation of reproductive cycling, on the other hand, is not
unique and doesn’t require a human-specific explanation. Despite focusing
on the right question, however, Morton and colleagues offer a novel but
unlikely theory for the female human’s postfertile lifespan.Just as the evolutionary assumptions of the model ignore
what we know about evolution, its social assumptions ignore what we can
easily see in human societies throughout history: Older women still have

believe that neither menopause nor postfertile lifespan originated as a
result of mating preferences, especially given other convincing
explanations. The Grandmother Hypothesis and several variants suggest
that because human children need extended care, reproductive efforts of
older women are more profitably directed toward caring for existing young
than producing new babies. However, mammalian reproductive biology also
clearly plays a role. Almost all female mammals, if provided a safe
environment, show earlier aging of the reproductive system than of the
rest of the body. Humans didn’t need to evolve menopause or a postfertile
lifespan from scratch, they just needed to delay nonreproductive aging a
bit. Together, the numerous evolutionary forces and biological mechanisms
already identified by biologists and anthropologists elegantly explain
why all mammals undergo reproductive senescence and a menopause-like
cessation of cycling, but only humans and a couple of whale species
have postfertile lifespans of any ecological importance.  Many of
the false assumptions underlying the Morton team’s model are iterations
of long-standing misconceptions. Evolutionary theory often ignores some
very real biological constraints, assuming that age-specific fertility
and mortality schedules can freely evolve; in reality, they are governed
largely by trajectories, with what happens at one age affecting other
ages. Similarly, treating menopause and a postfertile life stage as the
same thing is common in the popular and scientific literature, and the
unfortunate myth that older women don’t have sexual partners is also not
new.To be
clear, we don’t suspect Morton and colleagues of being anti–older women
or ignorant of biology; instead, we believe they have fallen for the
great allure and inherent danger of Computational
Computational Biology allows us to think in ways that would have been
impractical not so many years ago. In tandem with molecular biology, it
is transforming the way biology is done and the role of biologists in the
modern world. While experimentalists must deal with the logistics and
expense involved in gathering data, computational biologists can do their
work with nothing but fast processors, big displays, elegant models, and
beautiful figures. But the ability to bypass the cumbersome steps
involved in going out to measure things cuts out some of the reality
checks that come from contact with the organisms being
described.So the
model presented by Morton, et al. is wrong, as Box posited all models
are, but is it nonetheless useful? Perhaps. Their false assumptions do
not mean that mate preference has had zero effect on the length of human
postfertile lifespan, and indeed, nothing prevents all these theories
from operating in concert. A reworked model with more realistic
assumptions could quickly show whether the idea is tenable. That
possibility of going back and doing it again is another beauty of
computational biology.


About Johnny Adams

My full-time commitment is to slow and ultimately reverse age related functional decline to increase healthy years of life. I’ve been active in this area since the 1970s, steadily building skills and accomplishments. I have a good basic understanding of the science of aging, and have many skills that complement those of scientists so they can focus on science to advance our shared mission. Broad experience Top skills: administration, management, information technology (data and programming), communications, writing, marketing, market research and analysis, public speaking, forging ethical win-win outcomes among stakeholders (i.e. high level "selling"). Knowledge in grant writing, fundraising, finance. Like most skilled professionals, I’m best described as a guy who defines an end point, then figures out how to get there. I enjoy the conception, design, execution and successful completion of a grand plan. Executive Director Gerontology Research Group (GRG). Manages Email discussion forum, web site, meetings and oversees supercentenarian (oldest humans, 110+ years) research. CEO / Executive Director Carl I. Bourhenne Medical Research Foundation (Aging Intervention Foundation), an IRS approved 501(c)(3) nonprofit. http://www.AgingIntervention.org Early contributor to Supercentenarian Research Foundation. Co-Founder Geroscience Healthspan Forum. Active contributor to numerous initiatives to increase healthy years of life. Co-authored book on conventional, practical methods available today to slow the processes of aging – nutrition, exercise, behavior modification and motivation, stress reduction, proper supplementation, damage caused by improper programs, risk reduction and others. Fundamental understanding of, and experience in the genomics of longevity (internship analyzing and curating longevity gene papers). Biological and technical includes information technology, software development and computer programming, bioinformatics and protein informatics, online education, training programs, regulatory, clinical trials software, medical devices (CAT scanners and related), hospital electrical equipment testing program. Interpersonal skills – good communication, honest, well liked, works well in teams or alone. Real world experience collaborating in interdisciplinary teams in fast paced organizations. Uses technology to advance our shared mission. Education: MBA 1985 University of Southern California -- Deans List, Albert Quon Community Service Award (for volunteering with the American Longevity Association and helping an elderly lady every other week), George S. May Scholarship, CA State Fellowship. BA psychology, psychobiology emphasis 1983 California State University Fullerton Physiological courses as well as core courses (developmental, abnormal etc). UCLA Psychobiology 1978, one brief but fast moving and fulfilling quarter. Main interest was the electrochemical basis of consciousness. Also seminars at the NeuroPsychiatric Institute. Other: Ongoing conferences, meetings and continuing education. Aging, computer software and information technology. Some molecular biology, biotech, bio and protein informatics, computer aided drug design, clinical medical devices, electronics, HIPAA, fundraising through the Assoc. of Fundraising Professionals. Previous careers include: Marketing Increasing skill set and successes in virtually all phases, with valuable experience in locating people and companies with the greatest need and interest in a product or service, and sitting across the table with decision makers and working out agreements favorable to all. Information Technology: Management, data analysis and programming in commercial and clinical trials systems, and bioinformatics and protein informatics. As IT Director at Newport Beach, CA based technology organization Success Family of Continuing Education Companies, provided online software solutions for insurance and financial professionals in small to Fortune 500 size companies. We were successful with lean team organization (the slower moving competition was unable to create similar software systems). Medical devices: At Omnimedical in Paramount CA developed and managed quality assurance dept. and training depts. for engineers, physicians and technicians. Designed hospital equipment testing program for hospital services division. In my early 20’s I was a musician, and studied psychology and music. Interned with the intention of becoming a music therapist. These experiences helped develop valuable skills used today to advance our shared mission of creating aging solutions.
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