June 21, 2013

Aging, intelligence, cooperation, and ecology

The age-specific force of natural selection and biodemographic walls of death "Nonlinear interactions cause the collapse of Hamilton-style predictions in the most commonly studied case..."

GWAS of 126,559 Individuals Identifies Genetic Variants Associated with Educational Attainment "A linear polygenic score from all measured SNPs accounts for ≈2% of the variance in both educational attainment and cognitive function."

Fusing enacted and expected mimicry generates a winning strategy that promotes the evolution of cooperation "reducing conflict intensities among human populations necessitates (i) instigation of social initiatives that increase the perception of similarity among opponents"

Global human appropriation of net primary production doubled in the 20th century

Several scales of biodiversity affect ecosystem multifunctionality

May 3, 2013

Sampling Daphnia from a canoe, in the snow, May 3...

...for our research on the evolution of aging. Sandra Brovold is sampling, I'm trying to remember the J stroke, and Bob Sterner took the video.

April 17, 2013

High-school student undermines our "famine-food longevity" hypothesis, maybe

Back in 2009, I suggested that, to the extent that organic foods provide greater health benefits, this might be due to tradeoffs with reproduction. See my original post for a more-detailed explanation. Since then, I've seen at least one paper on a diet that increases both longevity and reproduction in some species, but there were no data on the timing of reproduction, which is key to our hypothesis.

This week, however, high school student Ria Chhabra and colleagues published a paper in PLoS One reporting both greater longevity and increased egg-laying at all ages, in fruit flies fed various organic foods. It's not inconceivable that some conventionally-grown produce could be so poor, nutritionally, that it would reduce both lifespan and reproduction. But their data seem inconsistent with our hypothesis that organic-vs-conventional differences were mainly differences in toxins (synthetic in conventional, natural in organic) and that natural toxins mainly acted as environmental cues, switching physiology towards longevity at the expense of reproduction.

I'd like to see this experiment repeated by a different lab, however, before drawing firm conclusions. There are a couple of strange things in their data. First, as noted in the paper, survival curves for Drosophila are usually sigmoidal, whereas theirs are more linear. Also, their peak egg-laying rate was reportedly at an age of 1 day. Other studies I've seen show essentially no egg-laying that early, with peaks at day 5 or so. See this paper or this open-access one.

April 5, 2013

Tradeoff-free longevity?

I have argued that understanding evolutionary tradeoffs is key to improving agriculture and increasing longevity.

For example, in 2009 I discussed a paper showing that food deprivation extends lifespan of C. elegans nematode worms by delaying their reproduction. I've seen other papers claiming to extend lifespan without reducing reproduction, but those papers have ignored possible effects on timing of reproduction. In a growing population, reproducing later reduces fitness, because your offspring are added to a larger gene pool. On the other hand, if the population is decreasing...

But a recent paper in PNAS reports that chemicals called ascorides (thought to be used as a crowding cue) increase the lifespan of C. elegans, without an apparent reproductive cost. Treated animals produced at least as many offspring as controls, at all ages. I don't understand this result. If there's no tradeoff, why haven't they evolved to turn on this response all the time, even without the crowding cue?

In humans, though, "Exceptional longevity is associated with decreased reproduction." That was the conclusion of a 2011 paper. They found that Ashkenazi Jewish centenarians (average age ~100 years) averaged 2.0 children, while a control group (parents of their children's spouses and friends, who died in their 70's) averaged 2.5 children. The centenarians also reproduced later in life (28-32 vs. 26-30). So, is it worth having 0.5 fewer children, to live 30 more years? Natural selection apparently doesn't think so.

September 14, 2012

This week: fossils, epidemics, cooperation, and aging

Arthropods in amber from the Triassic Period "arthropods some 100 Ma older than the earliest prior records in amber"

Unifying the spatial epidemiology and molecular evolution of emerging epidemics "spatial parameters of an emerging epidemic [can] be directly estimated from sampled pathogen genome sequences"

Evolution of cooperation and skew under imperfect information "full cooperation may not be achievable due to private information over individuals' outside options"

No third-party punishment in chimpanzees "Dominants retaliated when their own food was stolen, but they did not punish when the food of third-parties was stolen, even when the victim was related to them. "

Ageing: Mixed results for dieting monkeys
Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study "Our study suggests a separation between health effects, morbidity and mortality"

August 28, 2012

The importance of titles

Years ago, someone reinvented a method I'd published in a journal he regularly read (and published in), without citing my paper. I complained. He pointed out that the title of my article didn't hint at that aspect of the contents.

Since then, I've tried to get the main point of each paper into the title. For example:

When Stress Predicts a Shrinking Gene Pool, Trading Early Reproduction for Longevity Can Increase Fitness, Even with Lower Fecundity

But journal editors don't always cooperate. For example, we wanted to call our recent Perspective in Science (discussed here) "Are Antibiotics Weapons, Signals, Cues, or Manipulation?" The editor insisted on "Alternative Actions for Antibiotics."

We worried that people would glance at the title and think, "Oh, another one of those antibiotics-as-signals articles." A "signal" is information whose transmission benefits sender and receiver. A "cue" is information used in ways that don't necessarily benefit the source. For example, bacteria may respond to low doses of antibiotics by turning on protective mechanisms, by fleeing, or by hiding in a biofilm. I would only call antibiotic production a "signal" if scaring away competitors, rather than killing them, is the main way it increases the producer's fitness.

Just as we feared, a recent paper miscites our work:

"Antibiotics, especially at subinhibitory concentrations, can act as signal molecules aside from their antibacterial effect (Davies et al. 2006; Yim et al. 2007; Ratcliff and Denison 2011)."

Choose your title carefully.

August 9, 2012

Darwinian agriculture and Darwinian medicine: beyond resistance management

DarwinianMedicine.jpg Thumbnail image for BookCover.gif

Evolution happens. Careless use of antibiotics selects for antibiotic-resistant pathogens, careless use of insecticides (including crops that make their own insecticides) selects for pesticide-resistant insect pests, and careless use of herbicides selects for herbicide-resistant weeds.

Many people seem to assume that this well-known problem, evolution of resistance, is all there is to "Darwinian medicine" or "Darwinian agriculture." But check the tables of contents of the books above. You'll only find one chapter on the "arms race" between pathogens and their hosts and one chapter (titled "Stop Evolution Now!") that focuses on slowing the evolution of resistance to pesticides and other pest-control measures.

Both books (Nesse and Williams, 1994, Denison, 2012) and the earlier review articles on which they were based (Williams and Nesse, 1991, Denison, et al., 2003) devote much more space to the implications of past evolution.

"If evolution by natural selection can shape sophisticated mechanisms such as the eye, heart, and brain, why hasn't it shaped ways to prevent nearsightedness, heart attacks, and Alzheimer's disease?"

Similarly, biotechnology allows us to increase the expression of crop genes that enhance drought tolerance, but

"mutations that increase gene expression happen all the time, and natural selection maintains those that are beneficial to the plant. So why does corn normally have lower expression of this gene than was obtained by genetic engineering?"

We don't have definite answers to these questions. Both books present hypotheses with various amounts of supporting data, but additional research is needed. With aging populations and rising food prices, maybe there will even be some money available to fund that research.

Should evolutionary biologists working on fundamental problems and/or wild species consider adding applied work to their research portfolios? If so, you or your students might get some useful ideas from Nesse and Williams or from my book, just published by Princeton University Press.

Literature Cited

Denison RF. 2012. Darwinian agriculture: How understanding evolution can improve agriculture. Princeton: Princeton University Press.

Denison RF, Kiers ET, West SA. 2003. Darwinian agriculture: when can humans find solutions beyond the reach of natural selection? Quarterly Review of Biology 78: 145-168.

Nesse RM, and Williams GW. 1994. Why we get sick: The new science of Darwinian medicine. New York: Vintage Books.

Williams GW, Nesse RM. 1991. The dawn of Darwinian medicine. Quarterly Review of Biology 66: 1-22.

July 7, 2012

Evolution of aging talks at Evolution 2012 in Ottawa

Hwei-yen Chen described her experiments to explain why aging (an increase with age in the chance of death per year) sometimes levels off at an "aging plateau." For example, humans are more likely to die in their 101st year than their 70th, but not more likely to die in their 101st than their 100th. Do we "get our second wind" and stop aging? Or is it just that older cohorts have already lost the frailer individuals (the heterogeneity hypothesis).

Chen exposed nematode populations to high vs. low death rates caused either by temperature stress (preferentially killing the weak) or random assassination. The aging plateau was only seen in the temperature-stress populations, consistent with effects from elimination of weaker individuals earlier in life.

I think I missed something, though. As I've described it, seems like this experiment could have been done with a single cohort of individuals, which would be increasingly enriched with stronger individuals as the weaker were killed off. But this was described as experimental evolution. If the evolution treatments preferentially killed weaker genotypes, wouldn't that eliminate the variation the heterogeneity hypothesis needs to work? Maybe someone else who saw this talk can clarify or maybe I can find her poster. Or maybe we'll have to wait for her paper.

Alan Cohen gave an interesting talk in the same session. He showed chance of death per year data as a function of age for a bunch of species. In humans and many other species, death rate increases with age. This has been explained by, for example, tradeoffs between longevity and early reproduction. But apparently many species don't have an increasing risk of death with age. So maybe such tradeoffs aren't universal?

In a theoretical talk, Olivier Cotto discussed the evolution of aging in metapopulations. Local extinction and recolonization processes were shown to favor evolution of different life-history strategies (reproductive effort as a function of age) for dispersing and nondispersing individuals.

Later, Will Ratcliff presented our latest data on the evolution of aging after experimental evolution of multicellularity, research led by Mike Travisano. Excellent experimental work by Jennifer Pentz has been key to our success. As discussed in our recent PNAS paper, we started with unicellular yeast and imposed selection for rapid settling in liquid media. Within about two weeks, most of our replicate populations evolved a "snowflake" phenotype: clusters of connected cells that settle much faster than their unicellular ancestor. Under continued settling selection, clusters competed with each other based on differences in growth, reproduction (via multicellular propagules), and survival (settling fast enough to make it into the 5% of the population that made it into the next generation).

The first snowflake clusters to evolve didn't age significantly faster than their unicellular ancestor. In other words, only a few of the cells within a cluster would die over the course of a few days, and the ability to compete with a reference genotype wasn't much less for older than younger clusters. But, under continued settling selection, faster aging evolved. Older clusters accumulated more dead cells and were less competitive than younger clusters.

Why did aging evolve? The dead cells form break-points that facilitate reproduction (release of multicellular offspring). And aging doesn't really set in until after 24 hours, when settling selection is imposed. Only 5% of cluster survive that selection, so there's only very weak selection against traits that only reduce fitness after 24 hours. Imagine if humans only lived 30 years. There wouldn't be much selection against genes that cause cancer in 80-year-olds.

March 7, 2012

Is diet soda bad for us? An evolutionary perspective.

A recent paper reports that "Diet Soft Drink Consumption is Associated with an Increased Risk of Vascular Events in the Northern Manhattan Study." The correlation persisted even after they corrected for "age, sex, race/ethnicity, education, smoking, physical activity, alcohol consumption, BMI, daily calories, consumption of protein, carbohydrates, total fat, saturated fat, and sodium... and this persisted after controlling further for the metabolic syndrome, peripheral vascular disease, diabetes, cardiac disease, hypertension, and hypercholesterolemia."

Previous studies have found correlations between diet soft drink consumption and other health problems. What's going on? A specific artificial sweetener could have some specific negative effect. But could the sweet taste itself cause health problems? An evolutionary perspective suggests that it could.

Continue reading "Is diet soda bad for us? An evolutionary perspective." »

January 20, 2012

Also this week...

Variation in cognitive functioning as a refined approach to comparing aging across countries "The degree to which demographic aging translates into societal challenges depends to a considerable extent on the age at which mental functioning becomes significantly impaired.... In several countries with older populations, we find better cognitive performance on the part of populations aged 50+ than in countries with chronologically younger populations."

Large-scale, spatially-explicit test of the refuge strategy for delaying [sprayed] insecticide resistance
"refuges delayed resistance and treated cotton fields accelerated resistance"

The evolutionary basis of human social learning "We tested nine hypotheses derived from theoretical models, running a series of experiments..."

Collaborative learning in networks "In contrast to prior work, however, we found that efficient networks outperformed inefficient [slower] networks, even in a problem space with qualitative properties thought to favor inefficient networks."

Historical contingency affects signaling strategies and competitive abilities in evolving populations of simulated robots "populations with the more complex [but less efficient] strategy outperformed the populations with the less complex strategy"

The spread of a transposon insertion in Rec8 is associated with obligate asexuality in Daphnia "this element may be in the process of spreading through the species"

December 24, 2011

BRCA linked to reproduction-versus-longevity tradeoff

This is amazing. BRCA mutations have been linked to increased risk of breast cancer and ovarian cancer. Yet these mutations are not that rare. Hasn't natural selection been doing its job? Or is there some benefit that balances the risk?

The authors of "Effects of BRCA1 and BRCA2 mutations on female fertility," recently published in Proceedings of the Royal Society, hypothesized that women with a BRCA mutation might have more children, even if they don't live as long, on average.

Today, enough couples use birth control that the number of children born depends on preferences for family size, not just innate fertility. So the authors compared women (with and without the mutation) born before 1930. They used the Utah Population Database, which has data on births, deaths, and family relations for large numbers of Utah residents. Most of those women are no longer alive, however, so how can we know whether they had the BRCA mutation or not?

The authors used a variation on ancestral state reconstruction. When two women had the same BRCA mutation -- apparently there are various versions -- the authors assumed that their most-recent common ancestor had that mutation also. They also identified a number of controls -- women who presumably did not have a BRCA mutation, because none of their descendants did -- from the same time period.

So, was there any difference in fertility between women with versus without a BRCA mutation?

Continue reading "BRCA linked to reproduction-versus-longevity tradeoff" »

November 14, 2011

A cure for aging? Not yet.

"Clearance of p16Ink4a -positive senescent cells delays ageing-associated disorders" is an accurate statement of the results presented in a recent paper in Nature. I guess the title would have been too long if they'd added " mice genetically engineered to have short-life spans, but the treated mice didn't live longer."

The authors argue that "removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan." They hypothesize that senescent cells release chemicals that cause excessive aging of other cells nearby. So they genetically engineered mice, which were already genetically engineered to age faster than normal, so that their senescent cells could be killed by a drug. Giving the mice the drug eliminated senescing cells faster and had various health benefits, such as better performance on treadmills, relative to the same fast-aging mice not given the drug.

But our ancestors already evolved mechanisms, long ago, to eliminate cells that are no longer needed or are causing problems, like cancer. Are those evolved mechanisms too slow? If so, why? That is, why haven't mutants that clear these cells faster out-competed those that clear them slower? Speeding up an existing natural process is well within the capabilities of natural selection.

Sometimes, there can be trade-offs between longevity (or late-life vigor) and reproduction, especially early reproduction. In such cases, natural selection will often -- but not always -- favor early reproduction over longevity. Could keeping senescing cells around longer increase fertility, or something? If so, then a drug that would speed the elimination of senescing cells could still be useful. We just wouldn't take it until we were finished having children.

But speeding the clearance of senescent cells in older but not younger individuals doesn't seem too difficult for natural selection to have managed either, given millions of years to work on the problem. I'm assuming that older individuals have been contributing to the survival of their children and grandchildren for at least a few million years.

I'm betting that faster-than-natural clearance of senescent cells, which didn't extend actual life-span even in mice engineered to age faster than normal, won't do much for the health-span of normal mice.

August 12, 2011

This week's picks

Reciprocal Rewards Stabilize Cooperation in the Mycorrhizal Symbiosis Toby Kiers, who previously demonstrated host sanctions against cheating rhizobia, now shows that plants give less carbon to less-beneficial mycorrhizal fungi. I hope I can find time to discuss this paper in more detail soon.

Natural variation in Pristionchus pacificus dauer formation reveals cross-preference rather than self-preference of nematode dauer pheromones "strains may have evolved to induce dauer formation precociously in other strains in order to reduce the fitness of these strains"

Nest Inheritance Is the Missing Source of Direct Fitness in a Primitively Eusocial Insect

Polyandrous females benefit by producing sons that achieve high reproductive success in a competitive environment

Kin selection in den sharing develops under limited availability of tree hollows for a forest marsupial

Aging of the cerebral cortex differs between humans and chimpanzees "significant aging effects in humans were... individuals that were older than the maximum longevity of chimpanzees. Thus... brain structure shrinkage in human aging is evolutionarily novel and the result of an extended lifespan"

Bacterial persistence by RNA endonucleases

Host-parasite local adaptation after experimental coevolution of Caenorhabditis elegans and its microparasite Bacillus thuringiensis

Sperm chemotaxis, fluid shear, and the evolution of sexual reproduction

June 3, 2011

Darwinian agriculture: health benefits of organic vegetables

I'm making final revisions to my book, "Darwinian agriculture: where does nature's wisdom lie?" [they made me change the title, too] and my editor, at Princeton University Press, has asked me to cut two chapters. I agree that doing so will give the book a narrower focus, but I think some people might find them interesting. So here's the first of the missing chapters.

Beneficial toxins, evolutionary tradeoffs, and the health benefits of organic vegetables

"Early births are worth more than late in an increasing population, and vice versa in a decreasing one." -- Hamilton. 1966

What about food quality?

Early in 2011, a majority of the world's population could afford to buy enough food to meet their basic needs for protein and food energy, although this may not always be true in the future. But some diets are better than others. Vegetables appear to be particularly health-promoting.

Some of the income from my brother Tom's family's organic farm (near Corvallis, Oregon) comes from "community supported agriculture" subscriptions, where families pay an annual fee for a weekly food box from his farm. I once asked him whether people save money by buying these subscriptions.

"They save money on their medical bills," he explained. This is because one of his boxes contains more vegetables than most families would otherwise eat. Rather than waste vegetables they've already paid for, they eat them, presumably improving their health.

Why are vegetables so good for us? They provide fiber, vitamins, and antioxidants, all apparently beneficial, but can these explain all of their health benefits?

Continue reading "Darwinian agriculture: health benefits of organic vegetables" »

March 11, 2011

Aging primates, agricultural ants, efficent cooperation, etc.

Lots of interesting papers this week, but I only have time for some brief comments.

I can't believe Obama's response to the earthquake in Japan was to go ahead with a speech on gasoline prices. (BBC cut him off!) Higher prices for nonrenewable resources are an efficient way (relative to rationing, say, or complicated mandates) to encourage us to use them more slowly, so they'll last longer. And although adding more carbon dioxide to the atmosphere may increase photosynthetic efficiency and make our winters here in Minnesota a little less cold, I'm not willing to bet that those benefits will outweigh risks such as rising sea level from melting glaciers. If civilization must be at war with nature, I'm on the side of civilization, but let's not shoot ourselves in the foot. For example, we can stay warm inside insulated houses, while agricultural pests perish in the cold, reducing the need for pesticides later. Cold winters are good! Hmmm... maybe I should turn comments back on; but I'm still deleting all commercial links.

Aging in the Natural World: Comparative Data Reveal Similar Mortality Patterns Across Primates "in neither females nor males did we find evidence of a negative correlation between IMR [initiral mortality risk, at onset of adulthood] and RoA [rate of aging, increase in mortality with age],which would be indicative of a trade-off..."
[I wouldn't have expected a trade-off between those parameters, but what about a tradeoff with reproduction (mentioned only in the definition of adulthood)?]

How within-group behavioural variation and task efficiency enhance fitness in a social group "females of both phenotypes [aggressive versus docile] experience increased fitness when occupying colonies containing unlike individuals"

Experimental peripheral administration of oxytocin elevates a suite of cooperative behaviours in a wild social mammal

Co-Residence Patterns in Hunter-Gatherer Societies Show Unique Human Social Structure

The influence of maternal effects on indirect benefits associated with polyandry

Primate extinction risk and historical patterns of speciation and extinction in relation to body mass

Evolution of cold-tolerant fungal symbionts permits winter fungiculture by leafcutter ants at the northern frontier of a tropical ant-fungus symbiosis

Structural basis for nonribosomal peptide synthesis by an aminoacyl-tRNA synthetase paralog

Global CO2 rise leads to reduced maximum stomatal conductance in Florida vegetation

February 18, 2011

Free downloads of applied evolution papers...

...from the Applied Evolution Summit (Heron Island, 2010) are available, temporarily, from Evolutionary Applications.

I've already discussed part of my paper, "Past evolutionary tradeoffs represent opportunities for crop genetic improvement and increased human lifespan".

I also made minor contributions to two overview papers:
Evolutionary principles and their practical application
and Evolution in agriculture: the application of evolutionary approaches to the management of biotic interactions in agro-ecosystems.

Check out these and other exciting papers and download the ones you want, before they go behind a pay-wall. Some of these would be great for participatory seminars.

February 10, 2011

Evolution of cooperation, disease, relatives, birds...

Some recent papers that look interesting:

The evolution of host protection by vertically transmitted parasites

Cooperation among non-relatives evolves by state-dependent generalized reciprocity

Before senescence: the evolutionary demography of ontogenesis

Costs of memory: lessons from 'mini' brains

Land inheritance establishes sibling competition for marriage and reproduction in rural Ethiopia

Major global radiation of corvoid birds originated in the proto-Papuan archipelago

Within and transgenerational immune priming in an insect to a DNA virus

Multiple strategies in structured populations

Long-term isolation of a highly mobile seabird on the Galapagos

January 21, 2011

Modeling reproduction/longevity tradeoffs and phenotypic plasticity in fluctuating environments

A year ago, I was passing through beautiful Brisbane (in the news recently because of disastrous flooding) on my way back from the Applied Evolution Summit on Heron Island. This week, I'll discuss one figure from a paper I wrote for that meeting. An online-early version of "Past evolutionary tradeoffs represent opportunities for crop genetic improvement and increased human lifespan" is up at Evolutionary Applications, which will publish a special issue of papers from the meeting.

Continue reading "Modeling reproduction/longevity tradeoffs and phenotypic plasticity in fluctuating environments" »

August 19, 2010

"Bigger splash in the gene pool" made a splash on the web

Our paper showing that delaying reproduction can increase fitness (when environmental cues predict population decline) was apparently the most-viewed story on the University of Minnesota website.

June 4, 2010

Cancer's deep evolutionary roots

This week's paper, "Phylostratigraphic tracking of cancer genes suggests a link to the emergence of multicellularity in metazoa" was published in BMC Biology by Tomislav Domazet-Lošo and Diethard Tautz. Each of our cells is descended from an unbroken lineage going back to the first living cell. Most cells in an adult, however, are at the end of the line and will have no descendants. Exceptions include sex cells, stem cells, and cancer cells.

We consider cancer an aberration, but think back to the first multicellular life, which may have resembled Trichoplax. A Trichoplax has an upper and a lower layer of cells, and not much in between. They can reproduce by dividing in half, producing two offspring with hundreds of cells each (video). Or they can bud off propagules containing a small number of cells. They also seem to be able to reproduce sexually, from a fertilized single-cell egg, although complete development from an egg hasn't been documented. A Trichoplax can reform from separated cells, sometimes combining cells from two individuals. In such a chimeric organism, cells with different genotypes could compete for resources and reproductive opportunities, undermining collective success. Similar problems can occur when social amoebae get together to form a stalk for their spores. Even in a genetically uniform organism, a mutant cell could start reproducing (perhaps generating many propagules) at the expense of the whole. Today, we call cells that reproduce at the expense of the whole cancers, but something similar would presumably have been a problem for the earliest multicellular organisms.

Presumably? The authors of this week's paper used "phylostratigraphic tracking" to see when the ancestors of our cancer-suppressing genes evolved. Sure enough, there was an evolutionary burst of such genes right around the time when multicellular animals first evolved.

March 10, 2010

Why hasn't natural selection eliminated Alzheimer's?


The Alzheimer's Disease-Associated Amyloid beta-Protein Is an Antimicrobial Peptide
[See comment below for an earlier paper making this suggestion.]

Life-long protection against brain infections, in exchange for increased risk of dementia at an age few of our ancestors reached? Sounds like a reasonable tradeoff to me. Except that now we may have better options:

"it raises the possibility of preventing amyloidosis from initiating by pre-emptive targeting of pathogens/insults that stimulate the brain's innate immune system."

All we need is a good noninvasive way to detect brain infections early, so we can treat them with nonAlzheimer's-inducing antibiotics before amyloid beta-protein gets into the act.

December 18, 2009

Tradeoff-free longevity?

I'm working on my talk for the Applied Evolution Summit, so don't have time to write a detailed post, but here are some papers that looked interesting, with brief comments on some of them:

Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila
(published in Nature by Richard Grandison, Matthew Piper & Linda Partridge)
Dietary restriction reduces reproduction and increases longevity in many species. This study, using fruit-flies, showed that adding the amino acid, methionine, to a restricted diet restored total lifetime reproduction to that of fully-fed flies, but with the greater longevity of restricted-diet flies. Extrapolating to humans, the paper suggests that

the benefits of dietary restriction for health and lifespan may be obtained without impaired fecundity

But, if there would be no reproductive cost to doing so, why haven't flies evolved the ability to discard the "extra" food they get when fully-fed -- except for the methionine -- and live longer? I suspect that the restricted-plus-methionine diet affects the timing of reproduction, but data on timing weren't reported. (Instead, they give an "index of lifetime fecundity.") If overall population size is increasing (as fully-fed flies might expect), individuals that reproduce earlier make a disproportionate contribution to the gene pool. So the evolutionary trade-off may be between longevity and earliness of reproduction, not total reproduction. If population is decreasing, however, individuals who delay reproduction make a larger contribution to the gene pool, as laid out in our "shrinking pool" hypothesis. My guess is that flies respond to the restricted-plus-methionine diet as a cue predicting population decline and reproduce later, thereby gaining the observed increase in longevity. Extrapolating to humans again, we might be able to develop diets or other treatments that increase life-span and health, but which cost us teenage pregnancy. Hmmm... might be worth it.

Click "aging" at right for other posts relevant to this topic.

Regulating Alternative Lifestyles in Entomopathogenic Bacteria

Mozambican Grass Seed Consumption During the Middle Stone Age
If our ancestors were eating grass seeds 100,000 years ago, as this paper seems to show, what kind of selection, inadvertent or perhaps deliberate, were they imposing on those grasses?

Phylogeographic reconstruction of a bacterial species with high levels of lateral gene transfer

On the Origin of Species by Natural and Sexual Selection

Coots use hatch order to learn to recognize and reject conspecific brood parasitic chicks
"When experimentally provided with the wrong reference chicks, coots can be induced to discriminate against their own offspring"

Increasing phylogenetic resolution at low taxonomic levels using massively parallel sequencing of chloroplast genomes

Have giant lobelias evolved several times independently? Life form shifts and historical biogeography of the cosmopolitan and highly diverse subfamily Lobelioideae (Campanulaceae)
DNA analysis suggests that giant Lobelias evolved once and then spread, even to remote places like Hawaii, rather than evolving separately in different locations.

December 11, 2009

Delaying reproduction: the "disposable germline" hypothesis

This week's paper sheds new light on trade-offs between longevity and reproduction in Caenorhabditis elegans. This nematode worm is popular with medical researchers because it has a simple nervous system, insulin-like hormones, etc., yet it can be grown in Petri dishes, where it can mature and start reproducing two days after hatching from a tiny egg.

At various stages during this maturation process, C. elegans can essentially put life on hold. Environmental cues, particularly food shortage, switch them off their normal developmental pathway onto a side-track, where they can survive for months without food, but without maturing. Once food returns, they resume development.

This week's paper reports a new kind of developmental delay in individuals on the verge of reproductive maturity. "Starvation Protects Germline Stem Cells and Extends Reproductive Longevity in C. elegans" was published in Science, by Giana Angelo and Marc R. van Glist, working at the Fred Hutchison Cancer Resarch Center, in Seattle.

When worms with developing eggs are starved just before reproducing, some of them "die in childbirth", as the eggs hatch inside their bodies and emerge. Others, however, delay reproduction. Most of the developing germ cells apparently end up getting digested "for fuel", rather than becoming eggs. The adults can then survive for a month or more. Once fed, they resume reproduction, although they then lay fewer eggs than if they hadn't been starved. So an individual who would have started to lay eggs on day 2 can start on day 30 instead, a 15-fold delay in reproductive maturity.

Why do they do this? The authors have identified some genes that help control this process. But evolutionary biologists ask a different kind of "why" question: why have genes for delaying reproduction under starvation displaced genes for reproducing at the usual age?

A common answer is that they are waiting for "better conditions." But better how? Maybe they can produce more eggs if they wait until there's more food. But the relative success of different genes depends on the timing of reproduction, not just the number of offspring. An individual that produces a few eggs early might have lots of great-grandchildren by the time an individual who delayed reproduction started to lay eggs. A key point is that evolutionary changes in the genetic composition of populations depend on the relative performance of individuals with different genes. Maybe there will be more food later, but there will be more food later for everyone: for individuals who delayed reproduction and for the descendants of those who didn't.

It turns out that the one "better condition" that really makes it worthwhile to delay reproduction is a decrease in overall population size. -- not the increased resources per individual that you might get with lower population, but lower population itself. This is because each offspring added to a smaller gene pool will have a disproportionately large effect on the composition of future generations. As we put it in a recent paper, "When Stress Predicts a Shrinking Gene Pool, Trading Early Reproduction for Longevity Can Increase Fitness, Even with Lower Fecundity."

Under our "smaller pond" hypothesis, starvation provides worms with information, specifically, information predicting a decreasing population. That makes delaying reproduction a promising strategy. Even if the worm ends up laying fewer eggs (which isn't necessarily the case, depending on the direct effects of food supply on egg production), they will join a smaller gene pool. Individuals delaying reproduction will therefore be over-represented in future generations.

Food supply isn't the only factor predicting whether population will increase or decrease. If it's crowded, even a large food supply may not last long. Nematodes have previously been shown to detect the degree of crowding, essentially by smelling each other. Crowding can contribute to delays in maturation earlier in life. This week's paper shows that this is also true for adults that delay reproduction. If starved individuals are removed from the crowd, they resume reproduction, even without food. If there are few other worms around -- they probably can't tell the difference between "few" and "none" -- this is their big chance to found a dynasty.

The authors propose a "disposable germline" hypothesis. This is an allusion to Kirkwood's discredited "disposable soma" hypothesis, which attempted to explain trade-offs between reproduction and longevity as the result of limited resources: not enough calories to reproduce and also maintain healthy bodies. Although the "disposable soma" hypothesis has been cited hundreds of times, it hasn't been quite the same since people discovered that starvation increases longevity. To explain this result under the "disposable soma" hypothesis, you would have to assume that starving individuals save so many calories by not reproducing that they actually have more calories available for maintenance than if they had all the food they could eat.

August 21, 2009

Are these the same evolutionary biologists who advised Hitler?

Actually, Hitler drew on preDarwinian sources like Martin Luther as well as on people who may have been influenced by people who were influenced by a German mistranslation of the Origin of Species. But I want to discuss a less-serious case of falsely attributing incorrect ideas to evolutionary biologists.

"Evolutionary biologists, the experts on the theory of aging, have strong reasons to suppose that human life span cannot be altered in any quick and easy way. But they have been confounded by experiments with small laboratory animals, like roundworms, fruit flies and mice. In all these species, the change of single genes has brought noticeable increases in life span."
This confounded quotation is from Nicholas Wade's recent New York Times article. Actually, "the change of single genes" isn't so "quick and easy" in humans yet. Even so, I don't know who these unnamed evolutionary biologists are who claim human lifespan can't be altered easily. Swimming with crocodiles usually works.

But perhaps Wade meant "increased" rather than "altered." Increasing lifespan doesn't seem to be that hard either. Exercise and protection from infectious disease (vaccines, clean water supplies, antibiotics) both seem to help. Where are the evolutionary biologists who supposedly deny this? What evolutionary biologists have said is that there are trade-offs between potential longevity and potential reproduction, most recently confirmed for macaques.(1) George Williams' classic paper on these tradeoffs(2) is discussed here by John Dennehy.

The relative importance (i.e., fitness benefit) of current reproduction vs. longevity allowing later reproduction depend on whether population size is increasing or decreasing.(3) If population is increasing, offspring produced later contribute genes to a larger gene pool, where they will have proportionally less effect. Conversely, if population is likely to decrease, forgoing current reproduction may increase fitness, if it significantly increases the chances of reproducing later. This is because each offspring produced later will be added to a smaller gene pool, thereby having a greater evolutionary effect. We recently suggested that many species have therefore evolved the unconscious ability to predict population declines and delay reproduction, thereby increasing longevity.(4) Our hypothesis explains some otherwise-puzzling results:

1) soft drinks with artificial sweeteners are just as likely to cause metabolic syndrome as those with sugar(5,6) - "food is plentiful, so population will increase, so I should reproduce now, so adjust insulin levels etc. accordingly, whatever the long-term consequences"
2) food odors reverse the longevity increase otherwise seen with food deprivation(7) - "even though I'm not eating, someone nearby is, so population isn't likely to decrease after all; cancel plans to sacrifice current reproduction to increase longevity"
3) many plant toxins improve health in low doses, a phenomenon known as "hormesis"(8) - "if I'm eating these bitter leaves, there must be a famine in progress; this will lead to population decrease, so I should switch the reproduction/longevity switch to the longevity position; I'll wait until after the famine, when the gene pool is smaller, to reproduce"

A key point is that delaying reproduction can increase fitness even without increasing the number of offspring produced. This is because fitness is a relative measure, with increasing per-offspring impact in smaller populations.

If our hypothesis is correct, what are the practical implications for increasing human longevity?

"My rule of thumb is to ignore the evolutionary biologists -- they're constantly telling you what you can't think," Gary Ruvkun of the Massachusetts General Hospital remarked.
He can think whatever he wants, but the FDA should check antiaging drugs for their effects on fertility. As predicted by our hypothesis, resveratrol, a naturally occurring chemical that extends lifespan in some species, has already been shown to decrease early fecundity.(9) This wouldn't necessarily be a bad thing in humans, however.


1. Blomquist, G. E. Trade-off between age of first reproduction and survival in a female primate. Biology Letters 5, 339-342 (2009).
2. Williams, G. C. Pleiotropy, natural selection, and the evolution of senescence. Evolution 11, 398-411 (1957).
3. Hamilton, W. D. The moulding of senescence by natural selection. Journal of Theoretical Biology 12, 12-45 (1966).
4. Ratcliff, W. C., Hawthorne, P., Travisano, M. & Denison, R. F. When stress predicts a shrinking gene pool, trading early reproduction for longevity can increase fitness, even with lower fecundity. PLoS One 4, e6055 (2009).
5. Dhingra, R. et al. Soft drink consumption and risk of developing cardiometabolic risk factors and the metabolic syndrome in middle-aged adults in the community. Circulation 116, 480-488 (2007).
6. Lutsey, P. L., Steffen, L. M. & Stevens, J. Dietary Intake and the Development of the Metabolic Syndrome: The Atherosclerosis Risk in Communities Study. Circulation 117, 754-761 (2008).
7. Libert, S. et al. Regulation of Drosophila life span by olfaction and food-derived odors. Science 315, 1133-1137 (2007).
8. Mattson, M. P. & Cheng, A. Neurohormetic phytochemicals: low-dose toxins that induce adaptive neuronal stress responses. Trends in Neurosciences 29, 632-639 (2006).
9. Gruber, J., Tang, S.Y., & Halliwell, B. Evidence for a trade-off between survival and fitness caused by resveratrol treatment of Caenorhabditis elegans. Annals NY Acad Sci 1100:530-542 (2007)

July 20, 2009

Join my lab?

I hope to welcome one or possibly two new graduate students in autumn 2010.

As I noted on the Ecology, Evolution and Behavior web page, much of my research can be seen as following up on ideas first discussed by W.D. Hamilton. This includes our work on the evolution of cooperation (Nature 425:78-81) and on longevity-versus-reproduction tradeoffs as a possible explanation for the health benefits of eating low doses of plant toxins (PLoS One 4:e6055). Often, my grad students use crop plants and/or noncharismatic microfauna (bacteria, yeast, etc.), so if aesthetics is more important to you than science, choose a different major professor. I am also interested in agricultural implications of past and ongoing natural selection (Q. Rev. Biol. 2003 and forthcoming book), although I don't currently have any grant funding for this work.

I also accept students in the Plant Biology grad program, which has been unusually generous in financial support for grad students, providing first-year and summer stipends, paying for meeting travel, etc. (Budget cuts could change this.) Also, unlike most Plant Biology programs, their vision extends beyond molecular biology of Arabidopsis, with significant strength in evolution and in legume (especially Medicago) symbiosis. So students interested in plants should consider both programs.

July 10, 2009

What really causes tradeoffs between longevity and reproduction?

Now the New York Times is reporting on the two aging studies I mentioned yesterday. It's a good article, except for this part:

Dietary restriction seems to set off an ancient strategy written into all animal genomes, that when food is scarce resources [calories?] should be switched to tissue maintenance from breeding.
This is the "disposable soma" hypothesis of Kirkwood, and I don't think it applies to the monkey experiment. The monkeys in the study aren't reproducing anyway, so those on a low calorie diet should have fewer resources available for maintenance, yet they have lower rates of death from aging-related causes.

More generally, if the only way reproduction shortened lifespan were by consuming resources, then eating more (enough to outweigh the metabolic cost of reproduction) should increase longevity. It doesn't.

There is plenty of evidence for a tradeoff between reproduction and longevity, but I don't think it's mainly due to competition between reproduction and maintenance for calories. It's more likely that blood pressure or levels of insulin and testosterone have different optima for reproduction and longevity. Even in males for whom reproduction has negligible energy costs -- I know this is not true of males of all species -- testosterone levels that maximize reproduction have a long-term cost, reducing lifespan.

I suspect that many aging researchers would agree that there's more to the reproduction-vs.-longevity tradeoff than calories, so this isn't the really novel part of the hypothesis we published last week.

What's new in our paper is the reason that delaying reproduction increases fitness. The key point is that Darwinian fitness is the relative contribution to the next generation, not the absolute number of offspring produced. So, if population is decreasing, delaying reproduction can increase fitness, simply because each offspring makes a bigger splash in the smaller gene pool.

I think we're the first to link the fitness benefits of delaying reproduction in a declining population to environmental cues that predict such decreases: calorie restriction, crowding, or consumption of "famine foods" with toxins like resveratrol, asprin, glucosinolates, or alcohol.

July 9, 2009

Has natural selection been asleep at the switch?

"This new forage has great insect resistance", effused a former colleague, "we just need to eliminate the toxins that keep sheep from eating it."

Genetically engineered drought-tolerant crops are introduced with great fanfare, only to disappear when they turn out to have low yield under nondrought conditions.

When natural selection falls short of perfection, it may be because "you can't get there (some desirable adaptation) from here (current genotypes)" without passing through a series of intermediate generations that would have lower fitness. Natural selection favors genotypes best-adapted to current conditions, which are not necessarily steps towards any long-term improvement.

But natural selection often seems to miss even "simple" improvements, that might be achieved by changing as little as one DNA base. Such small changes are often enough to increase or decrease expression of key genes, for example. This sort of evolutionary progress may be blocked by tradeoffs, e.g., between seed production under different conditions (e.g., wet vs. dry), or between the competitiveness of individual plants and their collective seed production.

So what are we to make of two recent papers (in Science and Nature, respectively, discussed in Science News) on extending lifespan, one using calorie restriction and the other using the antibiotic, rapamycin?

Calorie restriction has been shown to increase longevity in model species like nematode worms and mice, but this latest study shows clear benefits in monkeys. The obvious question -- at least, it was obvious to me -- is why has past natural selection given monkeys (and fruitflies, and nematodes, and mice...) appetites that make them eat more than is good for them?

At least, that seemed to be the question, until it was shown that food odors can reverse the beneficial effects of calorie restriction, at least in fruitflies and nematodes. In humans, soft drinks with artificial sweeteners turn out to be just as likely to cause "metabolic syndrome" (related to diabetes) as those with sugar. So apparently our lives can be shortened by a perception of abundance, not just by actually eating too much. What is going on here?

In this case, the evolutionary tradeoff seems to be between current and future reproduction. As discussed in last week's post, delaying reproduction usually decreases fitness (representation in the next generation, relative to others) when population is increasing, but delaying reproduction can increase fitness when population is decreasing. Calorie restriction predicts population decline, triggering physiological responses that delay reproduction and thereby increase longevity. So do bitter-tasting foods, traditionally eaten only during famines. Food odors or sweet tastes have the opposite effect, because they predict population increase.

But what about life extension by rapamycin? One known tradeoff is suppression of the immune system, so we might get longer lives only in a hypothetical germ-free environment. But could the protein target of rapamycin (TOR) also be important to reproduction? Is this yet another example of a longevity-vs.-reproduction tradeoff?

July 6, 2009

Throwing the longevity switch

If you could choose a longer, healthier life, but only by having fewer kids, would you? What if you could eventually have the same number of kids, but only by having sex more often, and with no possibility of becoming a parent as a teen-ager?

Is this really possible? Based on the paper we published last week, we are pretty sure it is, although we don't yet know how much of an increase in lifespan is achievable, nor how much it will "cost" in reduced fertility.

A key assumption is that there are tradeoffs between longevity and reproduction, especially early reproduction. There is plenty of evidence for this antagonistic pleiotropy hypothesis: some gene variants that increase longevity nonetheless stay rare, because individuals with those variants have fewer kids. There are many possible reasons for this tradeoff. Calories used for reproduction aren't available for maintaining our bodies. Blood pressure and insulin levels optimal for reproduction are unlikely to be exactly optimal for longevity. Other risks associated with reproduction include sexually transmitted diseases and direct risks of childbirth. When there is a conflict between reproduction and longevity, natural selection will often favor reproduction.

There are, however, two ways we may be able to choose differently, increasing longevity at the expense of (potential, but maybe not actual) reproduction. First, once germ-line gene therapy is perfected and available (initially, perhaps, only in one or two "outlaw states"), maybe we could reverse some of the effects of past natural selection. We might be able to produce genetically engineered kids who would reach puberty later and with low enough intrinsic fertility that occasional unprotected sex would rarely lead to pregnancy, but who would still be healthy at age 100.

Second, what about people already born? Is there some biological "switch" we can throw, that tilts the longevity-vs.-reproduction tradeoff more towards longevity? Or has past natural selection welded the switch in the "reproduce now" position?

We think the switch is free to move, depending on environmental cues that affected our ancestors' survival and reproduction. Our paper shows that the switch position that maximizes Darwinian fitness depends on whether the overall population is increasing or decreasing. If population is decreasing, then individuals that live longer and reproduce later can contribute a larger fraction to their species' (shrunken) gene pool than those that reproduce earlier, on average, even if a few of them die before they get a chance to reproduce, and even if their lifetime reproduction is less than they might have achieved earlier.

Therefore, even though gene variants that always sacrifice early reproduction to increase longevity may not have persisted in the gene pool, variants that delay reproduction (thereby increasing longevity) only when populations were decreasing are likely to be with us, in each of our DNA molecules, today.

If this is true, all we need to do to increase our longevity is to give our bodies (false) cues that, over our evolutionary history, usually predicted population declines. To the extent that population declines were caused by food shortage, eating less may work, as it does in most species tested. Eating "famine foods" (leaves rather than meat, maybe) may also trigger physiological responses that reduce fertility but extend lifespan. On the other hand, if population declines were usually caused by cold winters, is there some reasonably comfortable way to trigger similar responses?

Delaying reproduction can only increase fitness if it increases the chances of surviving the famine or cold winter and reproducing later. So stresses that often predicted the death of the stressed individual (those associated with violent conflict, perhaps) won't necessarily delay reproduction or increase longevity. But there are lots of examples of mild stress increasing longevity. These stresses presumably trigger health-and-longevity-promoting mechanisms, but we may be the first to explain why such beneficial mechanisms aren't turned on all the time: they tend to reduce fertility.

Now, here's a question for you: would increasing human longevity be a good thing? I've seen this issue discussed in various places, but rather superficially. Assume that this option was made available to everyone, given that the cost could be quite low: inexpensive drugs or lifestyle changes that might even save money. Death rates would go down, in the short run, but so would birth rates, especially in countries where birth control is now rare. Death from old age is a fairly small component of overall population trends in these countries (relative to birth rate and infant mortality), so their rate of population increase might actually slow. But, if people expected to live longer, would they have more children (despite lower intrinsic fertility) or fewer, and at what age? Assuming some increase in population, we might need to grow more food -- a significant challenge -- but how would the overall impact of two healthy 90-year-olds who are still working (perhaps as doctors or nurses) and driving compare to that of one 90-year old who doesn't drive but needs expensive medical care? If professors keep working into their 90's, will that slow the spread of good new ideas, or only of stupid ideas that younger faculty may not know were debunked long ago? Would a longer-lived population produce too many bloggers?

June 25, 2009

The bitter fountain of youth

"When stress predicts a shrinking gene pool, trading early reproduction for longevity can increase fitness, even with lower fecundity." That's the title of a paper that Will Ratcliff, Mike Travisano, Peter Hawthorne and I just published in PloS-One. This was a spin-off from Ratcliff's work on the timing of reproduction in bacteria, but our main conclusions should apply broadly to plants and animals, with important implications for human health. Our entire paper is available on-line, but here is some additional background and explanation.

Earlier, I blogged about our research at UC Davis showing that tomatoes grown using organic methods have higher concentrations of a specific chemical (Mitchell, et al. 2007). Plants make this chemical to defend themselves against insects, which may be why there was more of it in tomatoes not protected by artificial pesticides. Surprisingly, this chemical actually seems to benefit human health. At the time, I thought this might just be coincidence, and wrote that "some of the natural insecticides plants make... are likely to be harmful to humans, rather than beneficial."

Now, I'm not so sure. It turns out that many toxins, including natural insecticides, can have health benefits in low doses, a phenomenon known as hormesis (Mattson & Cheng. 2006). Other forms of mild stress, such as dietary restriction (calorie restriction, intermittent fasting) or high temperature, have also been shown to increase longevity.

How can stress be beneficial? Some stresses trigger various protection mechanisms, such as antioxidants or heat-shock proteins, which may increase lifespan, even relative to individuals not exposed to stress. But why aren't these protective mechanisms turned on all the time, rather than only under stress? Don't individuals with longer lifespans leave more descendants than those with shorter lifespans? Not necessarily.

What if some mechanisms that increase lifespan also delay sexual maturity or decrease the rate of reproduction? For example, what if the blood pressure that maximizes lifespan is lower than that which maximizes reproduction? Then a gene for lower blood pressure would not necessarily increase in frequency over generations. A trade-off between early reproduction and longevity (and later reproduction) was central to the "antagonistic pleiotropy" hypothesis of Williams (1957). Our paper builds on this widely accepted hypothesis.

Given trade-offs between early and late reproduction, when will natural selection favor genes that potentially increase longevity but delay reproduction? Sometimes, resources not used for reproduction can be invested in growth, increasing reproduction in future years. Also, more experienced individuals may care for their offspring better. But what if delaying reproduction doesn't increase either the number of offspring or their survival?

We showed that delaying reproduction can still increase Darwinian fitness, that is, proportional representation in the gene pool, provided that overall population size is decreasing. Hamilton (1966) pointed out that an offspring added to a smaller population represents a larger fraction of the total gene pool. Therefore, if total population is increasing, offspring produced earlier have a larger effect on fitness. But if population size is decreasing, then offspring produced later have a larger effect on fitness. This means that delaying reproduction can sometimes increase fitness, even if delay does not increase the number of offspring.

Most populations will alternate between increasing and decreasing in numbers. If the population is stable or increasing, delaying reproduction can only decrease fitness. This is especially true if there is a high risk of death from causes unrelated to reproduction. But if the size of the gene pool is likely to decrease, delaying reproduction can increase fitness. This is especially true if risks directly or indirectly associated with reproduction are large relative to other risks.

Our mathematical models show that the best strategy is to delay reproduction only when an individual's chance of surviving to reproduce later is high, and only when an individual has reliable information predicting a decrease in overall population size. This is where stress comes in.

Past population declines were often caused by shortages of food, which can affect both the amount and types of food eaten. For example, natural insecticides in plants often have an unpleasant taste. Over most of our evolutionary history, therefore, these plants may have been eaten only when preferred foods, like meat or fruit, were not available. Consumption of these "famine foods" would therefore have been a reasonably good predictor of population decline, so they may trigger physiological changes (lower testosterone, etc.) that increase longevity while tending to delay reproduction.

A remarkable result, seen in both nematode worms and fruit flies, is that food odors can reverse the beneficial effects of dietary restriction on longevity (Libert, et al. 2007). If an individual smells food, others may be eating that food, so population size may be increasing. In that case, delaying reproduction would be a losing strategy, even if reproducing now increases the chance of an early death.

What about humans? Our models assumed that individuals reproduce only once, then die, like salmon or soybeans. However, we expect that some of our results will apply to species, like humans, with more complex life histories. One result for humans that is consistent with our hypothesis is that artificially sweetened soft drinks are just as likely to cause metabolic syndrome (related to diabetes) as sugared soft drinks are (Lutsey, et al. 2008). Like food odors, sweet foods may have been correlated, over much of our evolutionary history, with abundance, and therefore with impending increases in population size. If we want to live longer, maybe we should instead eat foods whose chemical composition or flavor remind our bodies of past famines. The health benefits we get from eating vegetables like kale may be due, in part, to the chemicals that give them their slightly bitter taste.

High levels of toxins, including natural ones, are still presumably harmful. But low doses of plant toxins, perhaps especially those found in traditional famine foods, may often improve health. This assumes that our hypothesis is correct, so you might want to wait for the results of experiments we are planning before making major changes in your diet.

We are also assuming that most people would consider some decrease in potential reproduction to be acceptable. For the many humans that already choose to limit their own reproduction, this need not result in any decrease in actual family size. For example, if people don't expect to marry until after college, the risks of early fertility may outweigh the benefits, even apart from health effects of hormone levels etc. in the teenage years on health later in life. Delaying puberty might, however, result in larger adults, with possible negative implications for automobile fuel economy and other resource issues.

Another popular hypothesis has been that individuals benefit from delaying reproduction in a bad year and waiting until conditions are better. This may increase the number of offspring produced, but we show that it does not increase proportional representation if the entire population also reproduces more in the good year.

"How is putting our entire kingdom to sleep for 100 years better for my family than losing one daughter, however much we love her?" asked the queen. "In 100 years, our other children would have had countless grandchildren. Meanwhile, those in neighboring kingdoms will multiply. By the time the impenetrable thorn forest you put around our kingdom dies and we awake, our enemies will vastly outnumber us."

"Not necessarily", replied the fairy scientist, "My computer models predict 100 years of wars, famines, and plagues. It's true that your population won't grow, but those of your enemies will shrink. This would have been a winning strategy, even if there were another way to save your daughter's life."

Ratcliff, Travisano, Hawthorne, and Denison. Can you spot the model?


Hamilton WD. 1966. The moulding of senescence by natural selection. Journal of Theoretical Biology. 12 : 12-45

Libert S, Zwiener J, Chu X, VanVoorhies W, Roman G, Pletcher SD. 2007. Regulation of Drosophila life span by olfaction and food-derived odors. Science. 315 : 1133-7

Lutsey PL, Steffen LM, Stevens J. 2008. Dietary intake and the development of the metabolic syndrome: The atherosclerosis risk in communities study. Circulation. 117 : 754-61

Mattson MP, Cheng A. 2006. Neurohormetic phytochemicals: Low-dose toxins that induce adaptive neuronal stress responses. Trends in Neurosciences. 29 : 632-9

Mitchell AE, Hong YJ, Koh E, Barrett DM, Bryant DC, et al. 2007. Ten-year comparison of the influence of organic and conventional crop management practices on the content of flavonoids in tomatoes. Journal of Agricultural and Food Chemistry. 55 : 6154-9

Williams GC. 1957. Pleiotropy, natural selection, and the evolution of senescence. Evolution. 11 : 398-411

April 8, 2009


Which animals kill the most humans? Lions and tigers and bears? Oh no, malaria-transmitting mosquitoes! The risks of using insecticides to kill mosquitoes may be outweighed by the benefits, but those benefits only last until mosquito populations evolve resistance. Careful use (insecticide-treated bed-nets, for example, rather than spraying wetlands) can slow the evolution of resistance, but we haven't yet achieved a goal I recently saw on a bumper sticker, namely, to "Stop Evolution Now!"

Can we do better? A paper published today suggests a new approach. "How to make evolution-proof insecticides for malaria control" was written by Andrew Read and colleagues. It's in the open-access journal, PLoS Biology, so you can read the whole article for details, but here's my summary:

Continue reading "Evolution-Proof?" »

February 12, 2009

Happy 200th birthday, Charles Darwin!

Imagine a world in which senescence is eliminated, so that death rates do not increase with age but remain throughout life at the level for eighteen-year-olds, that is, about one per thousand per year. Some people would still die at all ages, but half the population would live to age 693, and more than 13 percent would live to age 2000!" -- Nesse and Williams (1994) Why we get sick: the new science of Darwinian medicine
Although Darwin's ideas are increasingly influential (at least among scientists), Darwin himself is dead. In a world without senescence, he might still be alive. In The dawn of Darwinian medicine. Q. Rev. Biol. 66, 1-22 (1991), Williams and Nesse offered the standard evolutionary explanation for aging:
Because the force of natural selection is stronger at earlier ages to which larger numbers survive, a gene that causes substantial morbidity and mortality during the tail end of the expected life span in the wild may nonetheless be favored if it has even minor earlier benefits.
The most important of these "earlier benefits" appears to be more reproduction earlier in life. One of my students came up with some interesting ideas about the implications of this tradeoff between reproduction and longevity, which I will discuss here once our paper is published.