Category Archives: AEPS Blog

Evolutionary Psychiatry Group Started

It’s the Evolutionary Psychiatry Special Interest Group (EPSIG) at the Royal College of Psychiatrists in the UK.

They list their objectives:

  1. Raise awareness of the value of understanding the contribution of evolutionary theory to psychiatry.

  2. Encourage research into the evolutionary psychiatry.

  3. Provide a forum for psychiatrists and others to discuss evolutionary models, research ideas and data with fellow evolutionists.

  4. Facilitate networking with academic institutions and evolutionary scientists, biologists, psychotherapists, psychologists and other disciplines such as philosophy.

  5. Keep members and supporters of the SIG informed via a webpage and newsletter.

  6. Organise workshops, symposia and conferences on Evolutionary Psychiatry and related subjects.

  7. Organise sessions at the WPA and the RCPsych’s International Congress as well as with other college Faculties and Divisions.

Via psychiatrist and researcher @RandyNesse, whose own work applying evolutionary theory to psychiatry and medicine can be seen here.

The Evolution Of “Creepiness”

Evolutionary social psychologist Francis T. McAndrew has a new paper out in on “creepiness.” The abstract:

Surprisingly, until now there has never been an empirical study of “creepiness.” An international sample of 1341 individuals responded to an online survey. Males were perceived as being more likely to be creepy than females, and females were more likely to associate sexual threat with creepiness. Unusual nonverbal behavior and characteristics associated with unpredictability were also predictors of creepi- ness, as were some occupations and hobbies. The results are consistent with the hypothesis that being “creeped out” is an evolved adaptive emotional response to ambiguity about the presence of threat that enables us to maintain vigilance during times of uncertainty.

Smithsonian.com’s Linda Rodriguez McRobbie quotes McAndrew:

“[Creepy is] about the uncertainty of threat. You’re feeling uneasy because you think there might be something to worry about here, but the signals are not clear enough to warrant your doing some sort of desperate, life-saving kind of thing,” explains McAndrew.

 

Being creeped out is different from fear or revulsion, he says; in both of those emotional states, the person experiencing them usually feels no confusion about how to respond. But when you’re creeped out, your brain and your body are telling you that something is not quite right and you’d better pay attention because it might hurt you.

 

This is sometimes manifest in a physical sensation: In 2012, researchers from the University of Groningen in the Netherlands found that when subjects felt creeped out, they felt colder and believed that the temperature in the room had actually dropped. (Dickens might not have used the word in quite the way it soon came to mean, but he did get the chills part right.)

 

That physical response further heightens your senses, and, continues McAndrew: “You don’t know how to act but you’re really concerned about getting more information … It kind of takes your attention and focuses it like a laser on this particular stimulus, whatever it is.”

 

Whatever it is can be things, situations, places and, of course, people. Most creepy research has looked at what makes people seem creepy. For example, the 2012 study successfully creeped people out by exposing them to others who didn’t practice normal non-verbal behavior.

 

…Perhaps the biggest predictor of whether someone was considered creepy was unpredictability. “So much of [what is creepy] is about wanting to be able to predict what’s going to happen, and that’s why creepy people creep us out – because they’re unpredictable,” explains McAndrews, noting that the 2012 study also seemed to underscore that point. “We find it hard to know what they’re going to do next.”

 

Creepiness in people is also related to individuals breaking certain tacit social rules and conventions, even if sometimes that rule breaking is necessary. This becomes more evident when we look at the kinds of jobs a majority of respondents found creepy. However unfairly, taxidermists and funeral directors  were among the creepiest professions listed in McAndrew and Koehnke’s survey, likely because these people routinely interact with macabre things that most other people would avoid.

 

“If you’re dealing with somebody who’s really interested in dead things, that sets off alarm bells. Because if they’re different in that way, what other unpleasant ways they might be different?” says McAndrew.

Cooperate To Compete: The Evolution Of “Ultrasociety”

This overview of Peter Turchin’s new book, Ultrasociety: How 10,000 Years of War Made Humans the Greatest Cooperators on Earth, is followed by practical applications for your business. (There are also links below to books and articles referenced or mentioned within this post.) 

How did we evolve from small-scale societies of foragers and hunter-gathers into large-scale industrial societies in an evolutionary blip of 10,000 years?

In Ultrasociety, historian Peter Turchin advances a scientific approach to history to identify the causal mechanisms that enabled large-scale society–a strand of research Turchin calls Cliodynamics.

The standard explanation of how large-scale societies evolved from small-scale egalitarian tribes is the advent of agriculture- as proposed by Jared Diamond (1998) in Guns, Germs and Steel. The premise is that agriculture created high population densities as well as production surpluses that enabled hierarchy. “On this premise, agriculture got the ball rolling and the entire history of civilisation followed from that” (p. 20).

However, Turchin argues that this theory is incomplete. Although agriculture was a prerequisite for large-scale society, it is not a sufficient explanation. For example, why would agriculture necessarily lead to the rise of states and costly institutions being implemented, such as bureaucracy, the rule of law, and organized religion? Additionally, agriculture had a markedly negative impact on human health due to agricultural produce providing poorer nutritional value, resulting in smaller stature, more illness and the spread of pathogens through high density settlements.

How did agricultural societies succeed against small-scale hunter-gatherers despite these costs?

Turchin argues that, paradoxically, the main driver of large-scale society has been war. “It is competition and conflict between human groups that drove the transformation of small bands of hunter-gatherers into huge nation-states. Not to put too fine a point on it, it was war that first created despotic, archaic states and then destroyed them, replacing them with better, more equal societies… War is a force of destructive creation, a terrible means to a remarkable end” (p. 22).

The following passage explains the evolutionary logic (pp. 38-39, emphasis added):

“When people first started cultivating plants and settled in permanent villages, war between tribes became more intense. Defeat now could easily result in a loss of land for growing crops, which meant starvation… Because of the consequences of losing were so grave, societies came under great evolutionary pressure to get better at surviving at war. This meant inventing better weapons and armor, building up social cohesion, and adopting better battlefield tactic. But the best thing you could do was simply become a larger group, so that you could bring more battalions to the fight.

 

This inexorable evolutionary logic forced villages to combine into larger-scale societies. These combinations could take the form of loose alliances, more cohesive federations, or centralized, hierarchical chiefdoms… The same evolutionary logic induced chiefdoms to combine in yet larger-scale societies–complex “chiefdoms of chiefdoms.” Those, in turn, scaled up into early states and empires, and eventually into modern nation-states. At every step, greater size was an advantage in the military competition against other societies.”

One must appreciate that although wars between empires and nation states dwarf inter-tribal conflicts in scale, the proportion of people engaged and directly affected by warfare has declined remarkably. Turchin writes: “There is no contradiction between larger armies and larger butcher’s bills from warfare, on the one hand, and on the other, a greater part of the population enjoying peace.” (p. 41).

Cultural Multilevel Selection

The evolutionary theory advanced by Turchin to explain why we humans are the world’s champion cooperators is cultural multilevel selection

Multilevel selection (also known as group selection) is a theory in evolutionary biology proposing that natural selection acts at the level of the group, instead of at the more conventional level of the individual. There is some controversy about group selection. However, the ‘game-changer’ is applying multilevel selection to cultural evolutionas opposed to genetic evolution. As stated by Turchin; “[…][T]he most important point is that the evolution of cooperation is driven by competition between groups. These groups can be teams, coalitions, even aggregations without any clear boundaries, or whole societies. No matter what form groups take, it is competition on the collective scale that is necessary for cooperation to evolve. We cooperate to compete” (p. 93).

A troubling implication of cultural group selection is that in the absence of an external threat, the level of selection moves to within the group, causing cooperation to erode and inequality to rise. The spirit of ‘we are all in the same boat’ disappears and is replaced by a ‘winner takes all’ mentality, resulting in growing social dysfunction and in extreme cases, societal collapse. As stated by the historian Arnold Toynbee, “great civilisations are not murdered–they die by suicide” (quoted pp. 42-43).

A thought-provoking analysis of American politics is provided in Ultrasociety, arguing that rising income inequality and political polarisation since the 1970s indicates that the US has become a dysfunctional state (bear in mind Ulitrasociety was written before the rise of Donald Trump). Similarly, Turchin also links the rise of extreme individualism in the US and elsewhere to the increase in corporate scandals during the early 2000s, and to “the greatest case of corporate hubris and fraud–the Global Financial Crisis of 2007-08” (p. 51).

Let’s explore a case study from Ultrasociety–the Enron scandal.

The Enron Scandal

Jeff Skilling was widely regarded as a business genius. An executive at Enron who worked closely with Skilling called him “the smartest son of bitch I’ve ever met.” (Bryce, 2002, p. 47, cited p. 45). Skilling obtained an MBA from Harvard, graduating in the top five percent of his class. He went on to become a management consultant at McKinsey, becoming one of the youngest partners in the firm’s history. He joined Enron in 1990 and was promoted to president and Chief Financial Officer in 1997, becoming CEO in 2001.

Smart Skilling may be. However, Skilling held a warped view of evolutionary theory, which Turchin suggests sowed the seeds of disaster.

The story of the Enron scandal is well known. Enron went under in 2001, with its shareholders losing tens of billions of dollars and 20,000 employees not only losing their jobs but their entire life savings. Its top executives ended up in prison, where Skilling is still serving his sentence.

Although other Enron executives bear responsibility for Enron’s failure, Skilling was widely seen as the company’s visionary. Turchin argues that the managerial system Skilling created turned Enron into an “an epic of corporate greed, fraud, and corruption” (p. 46).

Jeff Skilling famously claimed that Richard Dawkins’ The Selfish Gene was his favourite book (see Conniff, 2006). Although Turchin argues that The Selfish Gene was flawed and caused significant harm, Dawkins’ classic work has arguably been widely misinterpreted (for example, selfish genes don’t necessarily make selfish people).

Skilling took his variant of Social Darwinism and applied it to increase competition within Enron, enacting systems such as the Performance Review Committee–colloquially known as ‘Rank-and-Yank’. Skilling recruited hundreds of newly minted MBAs from the leading business schools every year, and fired the bottom fifteen percent of performers whilst lavishly rewarding the top five percent of performers.

Skilling told reporters that the PRC was “the glue that holds the company together.” Turchin argues that Skilling couldn’t have been more wrong. “The PRC wasn’t glue. It was poison” (p. 46).

As one former employee said; “If I’m going to my boss’s office to talk about compensation, and if I step on some guy’s throat and that doubles it, then I’ll stamp on the guy’s throat” (Johnson, 2009, quoted p. 46).

Turchin summarizes the Enron scandal eloquently (p. 47):

“It is cooperation that underlies the ability of human groups and whole societies to achieve their shared goals. This is true for all kinds of groups, for economic organizations, firms and corporations, as well as for political organisations, such as states. But what Skilling did at Enron was to foster within-group competition, which bred mutual distrust and back-stabbing (if not throat-stomping). In other words, Skilling completely destroyed any willingness among his employees to cooperate–not with each other, not with their bosses, not with the company itself. And after that, collapse was inevitable.”

What is the relevance to your business?

With the benefit of hindsight, corporate scandals at notorious firms may seem obvious. However, the Enron scandal took the world by surprise. Fortune Magazine named Enron ‘America’s Most Innovative Company’ for six years in a row. Enron is not an isolated case. For example, Lehman Brothers was ranked #1 ‘Most Inspired Securities Firm’ in 2007–less than a year before its collapse. With the prevalence of corporate management systems encouraging intra-organizational competition, one must ask where the next corporate scandal will arise. As stated by Turchin; “It looks like Fortune doesn’t learn from its mistakes” (p. 51).

The business implications of all this should be clear: enact business policies that reduce inequality, foster an organizational culture that promotes cooperation, and suppress internal competition. As stated by Turchin (p. 93):

“As a corollary, while competition between teams create cooperation, competition among players within a team destroys it. In other words, to succeed, cooperative groups must suppress internal competition. Equality of group members is, therefore, a very important factor in promoting group cohesion and cooperation, which translates into the capacity of the group to win against other groups. This insight…should be intuitively obvious. Yet it is not. At least, it is not obvious to the majority of corporate managers, nor the owners of professional sports teams.”

I’ll wrap up this post with a few of my own suggestions–suggestions I hope you’ll find helpful for your business:

1. Reduce the discrepancy in employees’ basic pay, and increase compensation from bonuses linked to company (or team) performance.

 

2. During difficult times, it’s wise to appreciate the adverse impact mass redundancies have on group cohesion and consider alternative paths of action, such as organization-wide pay cuts. Employees may be prepared to accept change if the alternative is job losses.

 

3. Democratize team meetings so that all members are able to have their voices heard, and enable bottom-up communication processes that feed directly to senior leaders.

 

4. Also, make sure your leaders are visible and approachable. Make a priority what Nigel Nicholson calls ‘Managing By Wandering Around’ (see Nicholson, 2014). If you’re a leader, take the time to walk around and speak with employees in various contexts, and make them feel “we’re all in this together.” Don’t segregate yourself.

 

5. Similarly, make sure the amount of physical space allocated to senior management within the company is equitable and doesn’t trigger indignation (in other words, that your offices don’t resemble Enron’s headquarters).

This post was originally written by Max Beilby for Darwinian Business. To buy a copy of Ultrasociety, click here

References

Bryce, R. (2002) Pipe Dreams: Greed, Ego, and the Death of EnronPublic Affairs, New York

Conniff, R. (2006) “Animal Instincts”, The Guardian. Available here

Dawkins, R. (1976) The Selfish Gene. Oxford University Press

Diamond, J. M. (1998). Guns, Germs, and Steel: A short history of everybody for the last 13,000 years. Random House

Johnson, E.M. (2009) “Survival of the Kindest”, Seed Magazine. Available here 

Pinker, S. (2012) “The false allure of group selection”, Edge. Available here

Pinker, S. (2011) The Better Angels of Our Nature: A history of violence and humanity. Penguin

Nicholson, N. (2014) The ‘I’ of LeadershipJoey-Bass

 

The Evolution Of Shame: Why Shame Is Adaptive

In The Boston Globe, Megan Scudellari reports on recent research by UCSB evolutionary psychologist Daniel Sznycer and his colleagues on shame:

In a new study published in the Proceedings of the National Academy of Sciences, researchers argue that shame evolved as a defense to prevent individuals from damaging important social relationships.

 

“When people find out negative things about you — say, that you steal or are physically weak or sexually unfaithful — this causes them to be less helpful and more exploitative toward you,” says study author Daniel Sznycer, an evolutionary psychologist at the University of California Santa Barbara.

 

That could be a threat to one’s welfare and success in life — especially back in early human hunter-gatherer social groups. It is possible therefore that humans evolved shame as a way to defend themselves by avoiding or concealing things that would make others devalue them.

 

To test this “defense” hypothesis of shame, Sznycer and colleagues recruited over 900 adults across the US, India, and Israel to answer questions about two dozen fictional scenarios. Each scenario depicted traits expected to invoke shame, such as stinginess, infidelity, and physical weakness.

 

They asked one set of participants to report — on a scale of 1 to 7 — how much shame they would feel if they themselves were committing the act in the scenario, such as stealing money from another person. People in a second group were asked to be observers, and to rate how negatively they would view the offending person. How would they feel, for example, about a person they spotted stealing money?

 

In similar experiments, the team gauged individuals’ feelings of sadness and anxiety in response to each scenario.

 

If shame is, in fact, a defense against the judgment of others, the researchers expected the intensity of shame felt in the first group to match up with the intensity of negative perception, or “devaluation,” of the second group. Such a match would suggest shame evolved to deal with the threat of being devalued by one’s peers.

 

That is exactly what they found. “The shame scores in each of the three countries were very highly correlated with the magnitude of devaluation of those in the audience situation,” says Sznycer. Morever, feelings of anxiety and sadness did not match up, supporting the idea that shame evolved as a defense against being devalued.

 

The findings suggest that shame is an innate emotion that evolved across different cultures, and that it is an evolved, rational trait designed to protect the individual.

Supplemental information about the study is here.

More from Daniel Sznycer about his research and thinking on shame (from his UCSB page):

The psychology of shame.

Ancestrally, the degree to which other people valued one’s welfare would have affected one’s access to resources such as food, mates, and support in times of conflict. Becoming less socially valuable would have entailed fitness costs. This adaptive problem is expected to have shaped adaptations for decreasing the likelihood and the costs of being socially devalued. We proposed that one such adaptation is the emotion of shame. Using this basic functional framework, and in collaboration with John Tooby and Leda Cosmides, I developed a theory of shame—the information threat theory of shame (ITTS)—and tested predictions derived from it.

 

Failing to deploy countermeasures against devaluation when one is devalued is a costly mistake. Deploying shame measures when one is not devalued is another type of mistake. Thus, effective shame countermeasures require an understanding of what does and does not elicit devaluation. In fact, we found a strong match between the extent to which a particular situation elicits devaluation on one hand (audience’s perspective) and shame on the other (discredited individual’s perspective).

 

According to the ITTS, what counts as socially valuable differs from domain to domain. For example, in the domain of cooperation, a track record of reciprocating is viewed favorably. In the domain of mating, value is indexed by things such as cues of fertility and pathogen-resistance. Consistent with this, we obtained evidence that both the elicitors and the motivational responses of shame vary across domains.

 

The more a discrediting piece of information becomes widely known, the stronger the shame response is expected to be. Supporting this ITTS prediction, we discovered that the extent of publicity of a discrediting behavior modulates the intensity of shame—but not the intensity of guilt.

 

The ITTS was also instrumental in making functional sense of cultural differences in shame. The cost of being devalued by an existing relationship partner can be attenuated by forming alternative relationships. Therefore, cultures where opportunities to build new relationships are perceived as being scarce are expected to also display higher proneness to shame—and vice versa. In collaboration with Kosuke Takemura, Andy Delton, Kosuke Sato, Tess Robertson, Leda Cosmides, & John Tooby, we found evidence supporting this prediction among American, English, and Japanese subjects.

How Understanding Evolution Can Help Us Treat Cancer

Evolutionary scientists Athena Aktipis, Randolph Nesse, and their colleagues and grad students are doing fascinating and important research in evolutionary medicine, and — the topic of this post — they have been applying an evolutionary framework to cancer, in order to think about it and treat it more effectively.

Athena’s post-doctoral fellows, Amy Boddy and Helen Wasielewski, pulled together these exciting examples just below of the work they’re all doing in this area (and are surely researchers to keep an eye on for more exciting work to come).

 

How Understanding Evolution Can Help Us Treat Cancer 
This is a foundational paper in the field of cancer evolution and explains how cancer progression is an evolutionary process and how understanding this evolutionary process can change how we think about and treat cancer.

Aktipis, C.A., Nesse, R. (2013). Evolutionary foundations for cancer biology. Evolutionary Applications. 6(1) 144-159. DOI: 10.1111/eva.12034 Open access.

Abstract: New applications of evolutionary biology are transforming our understanding of cancer. The articles in this special issue provide many specific examples, such as microorganisms inducing cancers, the significance of within-tumor heterogeneity, and the possibility that lower dose chemotherapy may sometimes promote longer survival. Underlying these specific advances is a large-scale transformation, as cancer research incorporates evolutionary methods into its toolkit, and asks new evolutionary questions about why we are vulnerable to cancer. Evolution explains why cancer exists at all, how neoplasms grow, why cancer is remarkably rare, and why it occurs despite powerful cancer suppression mechanisms. Cancer exists because of somatic selection; mutations in somatic cells result in some dividing faster than others, in some cases generating neoplasms. Neoplasms grow, or do not, in complex cellular ecosystems. Cancer is relatively rare because of natural selection; our genomes were derived disproportionally from individuals with effective mechanisms for suppressing cancer. Cancer occurs nonetheless for the same six evolutionary reasons that explain why we remain vulnerable to other diseases. These four principles—cancers evolve by somatic selection, neoplasms grow in complex ecosystems, natural selection has shaped powerful cancer defenses, and the limitations of those defenses have evolutionary explanations—provide a foundation for understanding, preventing, and treating cancer.

 

Applying Life History Theory At The Cancer Cell Level
This paper applies evolutionary life history theory at the cancer cell level and describes the likely tradeoffs between cell proliferation and cell survival and how these tradeoffs may affect the tumor’s response to different treatment strategies.

Aktipis, C. A., Boddy, A., Brown, J., Gatenby, R, Maley C. C. (2013). Life history tradeoffs in cancer evolution. Nature Reviews Cancer, 13, 883-892. DOI: 10.1038/nrc3606

Abstract: Somatic evolution during cancer progression and therapy results in tumour cells that show a wide range of phenotypes, which include rapid proliferation and quiescence. Evolutionary life history theory may help us to understand the diversity of these phenotypes. Fast life history organisms reproduce rapidly, whereas those with slow life histories show less fecundity and invest more resources in survival. Life history theory also provides an evolutionary framework for phenotypic plasticity, which has potential implications for understanding ‘cancer stem cells’. Life history theory suggests that different therapy dosing schedules might select for fast or slow life history cell phenotypes, with important clinical consequences.

 

Treating Cancer Like an Infectious Disease
Chemotherapy resistance is a major problem in cancer biology, yet we have no strategies to target resistance. Similar to resistance to antibiotics in infectious diseases, this paper describes costs and benefits of controlling a tumor population instead of attempting to kill all the cancer cells.

Jansen, G., Gatenby, B., Aktipis, C.A. (2015). Control vs. eradication: Adopting strategies from infectious disease treatment to cancer. Proceedings of the National Academy of Sciences of the United States of America 112.4 937. DOI: 10.1073/pnas.1420297111

Abstract: Clinical treatment for metastatic cancer has traditionally entailed administering the highest possible dose in the shortest period, a strategy known as high-dose density therapy. The implicit goal is complete eradication. Unfortunately, a systemic cure for most metastatic cancers remains elusive, and the role of chemotherapy has been reduced to prolonging life and ameliorating symptoms.

 

Cancer is Common to Multicellular Life
This paper is a review of cancer in species across the tree of life. It shows cancer or cancer-like phenomena are found in almost all multicellular organisms.

Aktipis, C. A., Boddy, A., Jansen, G., Hochberg, M., Maley, C., Hibner, U., Wilkinson, G. (2015). Cancer across life: Cooperation and cheating in multicellularity. Philosophical Transactions of the Royal Society B. Published online June 8 DOI: 10.1098/rstb.2014.0219 Open access.

Abstract: Multicellularity is characterized by cooperation among cells for the development, maintenance and reproduction of the multicellular organism. Cancer can be viewed as cheating within this cooperative multicellular system. Complex multicellularity, and the cooperation underlying it, has evolved independently multiple times. We review the existing literature on cancer and cancer-like phenomena across life, not only focusing on complex multicellularity but also reviewing cancer-like phenomena across the tree of life more broadly. We find that cancer is characterized by a breakdown of the central features of cooperation that characterize multicellularity, including cheating in proliferation inhibition, cell death, division of labour, resource allocation and extracellular environment maintenance (which we term the five foundations of multicellularity). Cheating on division of labour, exhibited by a lack of differentiation and disorganized cell masses, has been observed in all forms of multicellularity. This suggests that deregulation of differentiation is a fundamental and universal aspect of carcinogenesis that may be underappreciated in cancer biology. Understanding cancer as a breakdown of multicellular cooperation provides novel insights into cancer hallmarks and suggests a set of assays and biomarkers that can be applied across species and characterize the fundamental requirements for generating a cancer.

 

Reproducing versus Maintaining the Body is Important to Cancer Risk
All species vary in the investment of cancer defense mechanisms. Why certain species are more susceptible to cancer, while others are cancer resistant is an open question. This paper explore whether reproductive tradeoffs cancer influence an organism’s risk for getting cancer.

Boddy, A., Kokko, H., Breden, F., Wilkinson, G. Aktipis, C. A., (2015). Cancer susceptibility and reproductive tradeoffs: A model of the evolution of cancer defenses. Philosophical Transactions of the Royal Society B. Published online June 8 Open access. DOI: 10.1098/rstb.2014.0220

Abstract: The factors influencing cancer susceptibility and why it varies across species are major open questions in the field of cancer biology. One underexplored source of variation in cancer susceptibility may arise from trade-offs between reproductive competitiveness (e.g. sexually selected traits, earlier reproduction and higher fertility) and cancer defence. We build a model that contrasts the probabilistic onset of cancer with other, extrinsic causes of mortality and use it to predict that intense reproductive competition will lower cancer defences and increase cancer incidence. We explore the trade-off between cancer defences and intraspecific competition across different extrinsic mortality conditions and different levels of trade-off intensity, and find the largest effect of competition on cancer in species where low extrinsic mortality combines with strong trade-offs. In such species, selection to delay cancer and selection to outcompete conspecifics are both strong, and the latter conflicts with the former. We discuss evidence for the assumed trade-off between reproductive competitiveness and cancer susceptibility. Sexually selected traits such as ornaments or large body size require high levels of cell proliferation and appear to be associated with greater cancer susceptibility. Similar associations exist for female traits such as continuous egg-laying in domestic hens and earlier reproductive maturity. Trade-offs between reproduction and cancer defences may be instantiated by a variety of mechanisms, including higher levels of growth factors and hormones, less efficient cell-cycle control and less DNA repair, or simply a larger number of cell divisions (relevant when reproductive success requires large body size or rapid reproductive cycles). These mechanisms can affect intra- and interspecific variation in cancer susceptibility arising from rapid cell proliferation during reproductive maturation, intrasexual competition and reproduction.

 

Cancer as an Evolutionary Process
Cancer is an evolutionary process, yet this concept is overlooked in cancer research.

Aktipis, C. A., Kwan, V.S.Y., Johnson, K. A., Neuberg, S.L., Maley, C.C. (2011) Overlooking evolution: A systematic analysis of cancer relapse and therapeutic resistance research. PLoS ONE 6(11): e26100. doi:10.1371/journal.pone.0026100 Open access.

Abstract: Cancer therapy selects for cancer cells resistant to treatment, a process that is fundamentally evolutionary. To what extent, however, is the evolutionary perspective employed in research on therapeutic resistance and relapse? We analyzed 6,228 papers on therapeutic resistance and/or relapse in cancers and found that the use of evolution terms in abstracts has remained at about 1% since the 1980s. However, detailed coding of 22 recent papers revealed a higher proportion of papers using evolutionary methods or evolutionary theory, although this number is still less than 10%. Despite the fact that relapse and therapeutic resistance is essentially an evolutionary process, it appears that this framework has not permeated research. This represents an unrealized opportunity for advances in research on therapeutic resistance.

 

How Do Elephants Avoid Cancer?
Larger, long-lived species have more cells and more time to accumulate mutations. This should make them more cancer prone than small, short lived species. However, larger, long-lived species typically get much less cancer than expected (known as Peto’s Paradox). This paper explore the elephant genome and finds that elephants have an extra 19 copies of P53, an important tumor suppressor gene.

Abegglen, Lisa M., et al. Potential mechanisms for cancer resistance in elephants and comparative cellular response to DNA damage in humans. JAMA 314.17 (2015): 1850-1860. DOI: 10.1001/jama.2015.13134

Abstract: Importance Evolutionary medicine may provide insights into human physiology and pathophysiology, including tumor biology.

Objective: To identify mechanisms for cancer resistance in elephants and compare cellular response to DNA damage among elephants, healthy human controls, and cancer-prone patients with Li-Fraumeni syndrome (LFS).

Design, Setting, and Participants: A comprehensive survey of necropsy data was performed across 36 mammalian species to validate cancer resistance in large and long-lived organisms, including elephants (n = 644). The African and Asian elephant genomes were analyzed for potential mechanisms of cancer resistance. Peripheral blood lymphocytes from elephants, healthy human controls, and patients with LFS were tested in vitro in the laboratory for DNA damage response. The study included African and Asian elephants (n = 8), patients with LFS (n = 10), and age-matched human controls (n = 11). Human samples were collected at the University of Utah between June 2014 and July 2015.

Exposures: Ionizing radiation and doxorubicin.

Main Outcomes and Measures: Cancer mortality across species was calculated and compared by body size and life span. The elephant genome was investigated for alterations in cancer-related genes. DNA repair and apoptosis were compared in elephant vs human peripheral blood lymphocytes.

Results: Across mammals, cancer mortality did not increase with body size and/or maximum life span (eg, for rock hyrax, 1% [95% CI, 0%-5%]; African wild dog, 8% [95% CI, 0%-16%]; lion, 2% [95% CI, 0%-7%]). Despite their large body size and long life span, elephants remain cancer resistant, with an estimated cancer mortality of 4.81% (95% CI, 3.14%-6.49%), compared with humans, who have 11% to 25% cancer mortality. While humans have 1 copy (2 alleles) of TP53, African elephants have at least 20 copies (40 alleles), including 19 retrogenes (38 alleles) with evidence of transcriptional activity measured by reverse transcription polymerase chain reaction. In response to DNA damage, elephant lymphocytes underwent p53-mediated apoptosis at higher rates than human lymphocytes proportional to TP53 status (ionizing radiation exposure: patients with LFS, 2.71% [95% CI, 1.93%-3.48%] vs human controls, 7.17% [95% CI, 5.91%-8.44%] vs elephants, 14.64% [95% CI, 10.91%-18.37%]; P < .001; doxorubicin exposure: human controls, 8.10% [95% CI, 6.55%-9.66%] vs elephants, 24.77% [95% CI, 23.0%-26.53%]; P < .001).

Conclusions and Relevance: Compared with other mammalian species, elephants appeared to have a lower-than-expected rate of cancer, potentially related to multiple copies of TP53. Compared with human cells, elephant cells demonstrated increased apoptotic response following DNA damage. These findings, if replicated, could represent an evolutionary-based approach for understanding mechanisms related to cancer suppression.

 

Making Cancer Go Extinct
One goal of cancer therapies is to drive tumors to extinction. What can we learn from species extinction in the paleontological record that can help us improve cancer therapy and prognosis?

Walther, V., Hiley, C.T., Shibata, D., Swanton, C., Turner, P.E., and Maley C.C.: Can oncology recapitulate paleontology? Lessons from species extinctions. Nature Reviews Clinical Oncology, Published online: 17 February 2015 | doi:10.1038/nrclinonc.2015.12

Abstract: Although we can treat cancers with cytotoxic chemotherapies, target them with molecules that inhibit oncogenic drivers, and induce substantial cell death with radiation, local and metastatic tumours recur, resulting in extensive morbidity and mortality. Indeed, driving a tumour to extinction is difficult. Geographically dispersed species of organisms are perhaps equally resistant to extinction, but >99.9% of species that have ever existed on this planet have become extinct. By contrast, we are nowhere near that level of success in cancer therapy. The phenomena are broadly analogous—in both cases, a genetically diverse population mutates and evolves through natural selection. The goal of cancer therapy is to cause cancer cell population extinction, or at least to limit any further increase in population size, to prevent the tumour burden from overwhelming the patient. However, despite available treatments, complete responses are rare, and partial responses are limited in duration. Many patients eventually relapse with tumours that evolve from cells that survive therapy. Similarly, species are remarkably resilient to environmental change. Paleontology can show us the conditions that lead to extinction and the characteristics of species that make them resistant to extinction. These lessons could be translated to improve cancer therapy and prognosis.

 

The Use of Common Pain Medications Could Slow Cancer Growth
This paper explores the potential for slowing down the evolution of cancer cells through the use of NSAIDS.

Kostadinov, R.L., Kuhner, M.K., Li, X., Sanchez, C.A., Galipeau, P.C., Paulson, T.G., Sather, C.L., Srivastava, A., Odze, R.D., Blount, P.L., Vaughan, T.L., Reid, B.J., Maley, C.C.: NSAIDs modulate clonal evolution in Barrett’s esophagus. PLOS Genetics, 9:e1003553, 2013. DOI: 10.1371/journal.pgen.1003553 Open access

Abstract: Cancer is considered an outcome of decades-long clonal evolution fueled by acquisition of somatic genomic abnormalities (SGAs). Non-steroidal anti-inflammatory drugs (NSAIDs) have been shown to reduce cancer risk, including risk of progression from Barrett’s esophagus (BE) to esophageal adenocarcinoma (EA). However, the cancer chemopreventive mechanisms of NSAIDs are not fully understood. We hypothesized that NSAIDs modulate clonal evolution by reducing SGA acquisition rate. We evaluated thirteen individuals with BE. Eleven had not used NSAIDs for 6.2±3.5 (mean±standard deviation) years and then began using NSAIDs for 5.6±2.7 years, whereas two had used NSAIDs for 3.3±1.4 years and then discontinued use for 7.9±0.7 years. 161 BE biopsies, collected at 5–8 time points over 6.4–19 years, were analyzed using 1Million-SNP arrays to detect SGAs. Even in the earliest biopsies there were many SGAs (284±246 in 10/13 and 1442±560 in 3/13 individuals) and in most individuals the number of SGAs changed little over time, with both increases and decreases in SGAs detected. The estimated SGA rate was 7.8 per genome per year (95% support interval [SI], 7.1–8.6) off-NSAIDs and 0.6 (95% SI 0.3–1.5) on-NSAIDs. Twelve individuals did not progress to EA. In ten we detected 279±86 SGAs affecting 53±30 Mb of the genome per biopsy per time point and in two we detected 1,463±375 SGAs affecting 180±100 Mb. In one individual who progressed to EA we detected a clone having 2,291±78 SGAs affecting 588±18 Mb of the genome at three time points in the last three of 11.4 years of follow-up. NSAIDs were associated with reduced rate of acquisition of SGAs in eleven of thirteen individuals. Barrett’s cells maintained relative equilibrium level of SGAs over time with occasional punctuations by expansion of clones having massive amount of SGAs.

 

Cancer Evolves, Yet Treatment Often Doesn’t
Another foundational paper that describes the Darwinian nature of cancer and discussing the reason for this therapeutic failure. Greaves, M. & Maley, C.C.: Clonal evolution in cancer. Nature. 481:306-313, 2012. PMCID: PMC3367003. DOI: 10.1038/nature10762 Open access

Abstract: Cancers evolve by a reiterative process of clonal expansion, genetic diversification and clonal selection within the adaptive landscapes of tissue ecosystems. The dynamics are complex, with highly variable patterns of genetic diversity and resulting clonal architecture. Therapeutic intervention may destroy cancer clones and erode their habitats, but it can also inadvertently provide a potent selective pressure for the expansion of resistant variants. The inherently Darwinian character of cancer is the primary reason for this therapeutic failure, but it may also hold the key to more effective control.

 

Human Microbiome Papers

Microbes are Tiny Yet Powerful: Can They Change Human Behavior?
Explores novel possibilities for microbial manipulation of host behavior in humans.

Alcock, J., Maley, C.C., Aktipis, C.A. (2014). Is eating behavior manipulated by the gastrointestinal microbiota? Evolutionary pressures and potential mechanisms. BioEssays 36(10). DOI:10.1002/bies.201400071 Open access

Abstract: Microbes in the gastrointestinal tract are under selective pressure to manipulate host eating behavior to increase their fitness, sometimes at the expense of host fitness. Microbes may do this through two potential strategies: (i) generating cravings for foods that they specialize on or foods that suppress their competitors, or (ii) inducing dysphoria until we eat foods that enhance their fitness. We review several potential mechanisms for microbial control over eating behavior including microbial influence on reward and satiety pathways, production of toxins that alter mood, changes to receptors including taste receptors, and hijacking of the vagus nerve, the neural axis between the gut and the brain. We also review the evidence for alternative explanations for cravings and unhealthy eating behavior. Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating.

 

What We Eat Affects Whether Our Body’s Microbes Help or Harm Us
Considers diet as a fundamental source of cooperation or conflict between the gut microbiome and its human host, with important implications for health and disease.

Alcock, J., Wasielewski, H., Aktipis, C.A. (accepted pending revision). Conflict and cooperation between host and gut microbiota: Implications for nutrition and human health. Annals of the New York Academy of Sciences.

No link yet available. Not yet published.

 

For More in Evolutionary Medicine: Tweets and other references to the Evolutionary Medicine Symposium at the AAAS, The American Association for the Advancement of Science conference, February, 2016.

Follow: @RandyNesse, @AthenaAktipis@amy_boddy— and check out their papers posted on their sites linked at the top of this post.

Gossip Is An Evolved Social Skill, Not A Character Flaw

Evolutionary psychologist Frank T. McAndrew explains at The Conversation:

Let’s face it: gossips get a bad rap.

 

Smugly looking down from a moral high ground – and secure in the knowledge that we don’t share their character flaw – we often dismiss those who are obsessed with the doings of others as shallow.

 

Indeed, in its rawest form, gossip is a strategy used by individuals to further their own reputations and interests at the expense of others. Studies that I have conducted confirm that gossip can be used in cruel ways for selfish purposes.

 

…When disparaging gossip, we overlook the fact that it’s an essential part of what makes the social world tick; the nasty side of gossip overshadows the more benign ways in which it functions.

 

In fact, gossip can actually be thought of not as a character flaw, but as a highly evolved social skill. Those who can’t do it well often have difficulty maintaining relationships, and can find themselves on the outside looking in.

We are, in fact, “hardwired to gossip,” McAndrew continues:

Like it or not, we are the descendants of busybodies. Evolutionary psychologists believe that our preoccupation with the lives of others is a byproduct of a prehistoric brain.

 

According to scientists, because our prehistoric ancestors lived in relatively small groups, they knew one another intimately. In order to ward off enemies and survive in their harsh natural environment, our ancestors needed to cooperate with in-group members. But they also recognized that these same in-group members were their main competitors for mates and limited resources.

 

Living under such conditions, our ancestors faced a number of adaptive social problems: who’s reliable and trustworthy? Who’s a cheater? Who would make the best mate? How can friendships, alliances and family obligations be balanced?

 

In this sort of environment, an intense interest in the private dealings of other people would have certainly been handy – and strongly favored by natural selection. People who were the best at harnessing their social intelligence to interpret, predict – and influence – the behavior of others became more successful than those who were not.

 

The genes of those individuals were passed along from one generation to the next.

Yes, so the fact that you exist today, suggests that you had ancestors mumbling on to each other about the Kardashians of their day.

More on what fuels our thirst for gossip about celebrities at the link.

The Evolutionary Ecology Of Cancer

Theoretical evolutionary biologist Athena Aktipis, a co-founder of the Center for Evolution and Cancer at UCSF, talks to David Sloan Wilson about how cancer is evolution that’s taking place inside an organism, but a perversely adaptive form of it, since it ends in the death of both the organism and the cancer.

Aktipis explains the selection pressures on cancer cells:

Let’s say that a tumor has evolved and grown so much that the interior is totally absent of nutrients, like you see in some cities, where the slums are totally absent of resources and filled with garbage. There is intense selection for cells to survive better in those conditions, which we call hypoxic conditions. These cells become pre-adapted to live in regions that are far away from blood vessels, so when you give chemotherapy, they are able to hide out, a phenomenon called “refugia” in cancer treatment. There are some really important aspects of the environment, ecology, and diversity of ecological niches that get created in the course of cancer progression and changed during treatment that haven’t been fully considered from an evolutionary perspective. There’s a lot of opportunities.

A particular cancer therapy can make sense — that is, until it’s viewed from an evolutionary perspective. Aktipis gives the example of the medical bias toward going with the most aggressive treatment possible:

For a long time it was almost a moral imperative to use the highest dose and most aggressive treatment possible, but now that’s being reexamined and many top cancer treatment hospitals in the country and the world are backing off from that. Not all of them are backing off because of an explicitly evolutionary framework, but some of the work that has been done over the last decade has helped to show why an overly aggressive approach can be problematic. As for drug-resistant infectious agents and resistance to pesticides in agriculture, high doses in cancer treatment imposes the highest selective-pressure on a population of cancer cells. If you have a small population that’s not very diverse, then using a high dose can make sense. But if you have a large and diverse population of cancer cells then the higher the dose, then the greater the selection pressure for resistant cells. That’s one of the really important insights that comes from taking an evolutionary approach to treatment. We shouldn’t just think about killing cells; we should be more strategic about what we want to select for and against.

Dr. Aktipis is also the author of the forthcoming book from Princeton University Press, “Evolution in the flesh: Cancer and the transformation of life.”

Genuine Disorders or Environmental Discrepancies? Review of an Evolutionary Psychology Explanation of Female Sexual ‘Dysfunction’

Like many other nonhuman primates, men and women engage in sexual intercourse for a myriad of reasons: to satisfy their own sexual desires, to satisfy the desires of their partners, to gain access to resources, and every once in a while, to procreate. A woman’s ability pass her genes on to healthy offspring contributes to her genetic fitness, and this ability is closely tied to the timing and frequency of sexual intercourse. From an evolutionary perspective, there should then be selection pressure for alleles that are associated with high sexual arousal and desire in women.

Epidemiological data, however, indicate that is not the case—recent estimates have suggested that up to 50% of women experience sexual dysfunction, characterized by dampened sexual arousal or desire, or inability to reliably experience orgasm during intercourse. But if natural selection favors alleles related to high sexual desire and arousal (and subsequently, the creation of offspring), why does the prevalence of sexual dysfunction in women remain so high?

A recent article in Adaptive Human Behavior and Physiology by anthropologist Menelaos Apostolou suggests that these clinical concepts we’ve labeled as ‘dysfunctions’ did not represent genuine dysfunctions in the pre-industrial environments where the majority of human evolution has taken place. In such pre-industrial environments, women’s sexuality was strictly regulated by parental and societal forces. Women were required by their parents to refrain from intercourse outside of the context of marriage, and were often married off to partners chosen by the parents. Once in that marriage, it was not illegal for husbands to force intercourse upon their wives. In this sort of environment, what we today would consider ‘sexual dysfunctions’ were not dysfunctions at all, as they did not contribute to a woman’s reproductive fitness—having high sexual arousal or desire would not significantly modulate a woman’s frequency and timing of sexual activity. In fact, low sexual desire and arousal may have even been a good thing, as such women would not be motivated to seek intercourse before marriage or with partners other than one’s husband.

Fast forward to the post-industrial society we live in currently, and the regulation of women’s sexuality in many parts of the world has changed considerably. Rather than being potentially maladaptive as they were during much of human evolution, high sexual desire and arousal are traits that now actually increase a woman’s reproductive fitness. In a society where women freely choose their mates and regulate their own sexual behavior, those with greater arousal and desire may engage in intercourse more often, and thus be more likely to pass on their genes.

This concept, of traits being disadvantageous currently when they were advantageous in ancestral societies, is called ancestral neutrality. The argument that Apostolou makes is that we have not lived in post-industrial societies with unregulated female sexuality long enough for evolution to catch up and ‘weed out’ alleles for low sexual desire and arousal, which explains the high prevalence of sexual ‘dysfunctions’ reported. However, depending on the extent to which low sexual arousal and desire decrease a woman’s reproductive fitness in this post-industrial context, it is likely that the alleles for these traits will become increasingly rare over time.

Apostolou’s paper highlights the important point that our conceptualizations of ideas such as health and illness are strongly time and culture-dependent. Low sexual arousal and desire have transformed from being advantageous traits in pre-industrial societies to being natural variants in female sexuality in the late 20th century, to then being dysfunctions warranting DSM-V categorizations and development of drugs to ‘cure’ them. (Sidenote: women’s sexual function has not been the only arena in which societal views modulate what we view as normal or abnormal. Rather than being labeled as having a mental illness, individuals with what the DSM-V would categorize as schizophrenia in ancestral societies were often regarded as shamans with significant spiritual and healing powers.) It will be interesting to keep tracking how societies define health and illness as they relate to female sexuality as our conceptualizations of sexuality continually develop.

Upcoming Evolutionary Psychology Conferences

HBES, June 29th to July 3rd, 2016, Vancouver, Canada: The 28th annual HBES conference will be held June 29th to July 3rd, 2016 at the Westin Bayshore in Vancouver, Canada. (HBES is the biggie of ev psych conferences, with the most international attendees.)

NEEPS, June 2-5, 2016, in Halifax, Nova Scotia (Canada): The NorthEastern Evolutionary Psychology Society will hold its 10th annual conference, beginning 6/2/16, in Halifax, Nova Scotia. (Our AEPS meetings and sessions will also be held there.)

SEEPS, Feb 12, 2006, Tuscaloosa, Alabama: The SouthEastern Evolutionary Perspectives Society (SEEPS) will hold its inaugural meeting February 12th, 2016 (Darwin Day) through the 14th at the Alabama Museum of Natural History in Tuscaloosa, AL. (SEEPS is the newest ev psych organization.)

ISHE, August 1-5, 2016, University of Stirling, Scotland: The 23rd Biennial Congress on Human Ethology will be held at the University of Stirling, in Scotland, from the 1st – 5th of August 2016. What is ethology? More from ISHE’s website.

SPSP (with Evolutionary pre-conference, Jan 28), Jan 28-30, San Diego, California: The annual Society for Personality and Social Psychology conference will be held in will be held in San Diego, Jan 28-30, 2016.

EHBEA, April 5-8, 2016, at the London School of Hygiene and Tropical Medicine: The annual European Human Behavior and Evolution Association’s annual conference will take place in London, April 5-8, 2016.