Wednesday, March 29, 2017

The (bad) luck of the draw; more evidence

A while back, Vogelstein and Tomasetti (V-T) published a paper in Science in which it was argued that most cancers cannot be attributed to known environmental factors, but instead were due simply to the errors in DNA replication that occur throughout life when cells divide.  See our earlier 2-part series on this.

Essentially the argument is that knowledge of the approximate number of at-risk cell divisions per unit of age could account for the age-related pattern of increase in cancers of different organs, if one ignored some obviously environmental causes like smoking.  Cigarette smoke is a mutagen and if cancer is a mutagenic disease, as it certainly largely is, then that will account for the dose-related pattern of lung and oral cancers.

This got enraged responses from environmental epidemiologists whose careers are vested in the idea that if people would avoid carcinogens they'd reduce their cancer risk.  Of course, this is partly just the environmental epidemiologists' natural reaction to their ox being gored--threats to their grant largesse and so on.  But it is also true that environmental factors of various kinds, in addition to smoking, have been associated with cancer; some dietary components, viruses, sunlight, even diagnostic x-rays if done early and often enough, and other factors.

Most associated risks from agents like these are small, compared to smoking, but not zero and an at least legitimate objection to V-T's paper might be that the suggestion that environmental pollution, dietary excess, and so on don't matter when it comes to cancer is wrong.  I think V-T are saying no such thing.  Clearly some environmental exposures are mutagens and it would be a really hard-core reactionary to deny that mutations are unrelated to cancer.  Other external or lifestyle agents are mitogens; they stimulate cell division, and it would be silly not to think they could have a role in cancer.  If and when they do, it is not by causing mutations per se.  Instead mitogenic exposures in themselves just stimulate cell division, which is dangerous if the cell is already transformed into a cancer cell.  But it is also a way to increase cancer by just what V-T stress: the natural occurrence of mutations when cells divide.

There are a few who argue that cancer is due to transposable elements moving around and/or inserting into the genome where they can cause cells to misbehave, or other perhaps unknown factors such as of tissue organization, which can lead cells to 'misbehave', rather than mutations.

These alternatives are, currently, a rather minor cause of cancer.  In response to their critics, V-T have just published a new multi-national analysis that they suggest supports their theory.  They attempted to correct for the number of at-risk cells and so on, and found a convincing pattern that supports the intrinsic-mutation viewpoint.  They did this to rebut their critics.

This is at least in part an unnecessary food-fight.  When cells divide, DNA replication errors occur.  This seems well-documented (indeed, Vogelstein did some work years ago that showed evidence for somatic mutation--that is, DNA changes that are not inherited--and genomes of cancer cells compared to normal cells of the same individual.  Indeed, for decades this has been known in various levels of detail.  Of course, showing that this is causal rather than coincidental is a separate problem, because the fact of mutations occurring during cell division doesn't necessarily mean that the mutations are causal. However, for several cancers the repeated involvement of specific genes, and the demonstration of mutations in the same gene or genes in many different individuals, or of the same effect in experimental mice and so on, is persuasive evidence that mutational change is important in cancer.

The specifics of that importance are in a sense somewhat separate from the assertion that environmental epidemiologists are complaining about.  Unfortunately, to a great extent this is a silly debate. In essence, besides professional pride and careerism, the debate should not be about whether mutations are involved in cancer causation but whether specific environmental sources of mutation are identifiable and individually strong enough, as x-rays and tobacco smoke are, to be identified and avoided.  Smoking targets particular cells in the oral cavity and lungs.  But exposures that are more generic, but individually rare or not associated with a specific item like smoking, and can't be avoided, might raise the rate of somatic mutation generally.  Just having a body temperature may be one such factor, for example.

I would say that we are inevitably exposed to chemicals and so on that will potentially damage cells, mutation being one such effect.  V-T are substantially correct, from what the data look like, in saying that (in our words) namable, specific, and avoidable environmental mutations are not the major systematic, organ-targeting cause of cancer.  Vague and/or generic exposure to mutagens will lead to mutations more or less randomly among our cells (maybe, depending on the agent, differently depending on how deep in our bodies the cells are relative to the outside world or other means of exposure).  The more at-risk cells, the longer they're at risk, and so on, the greater the chance that some cell will experience a transforming set of changes.

Most of us probably inherit mutations in some of these genes from conception, and have to await other events to occur (whether these are mutational or of another nature as mentioned above).  The age patterns of cancers seem very convincingly to show that.  The real key factor here is the degree to which specific, identifiable, avoidable mutational agents can be identified.  It seems silly or, perhaps as likely, mere professional jealousy, to resist that idea.

These statements apply even if cancers are not all, or not entirely, due to mutational effects.  And, remember, not all of the mutations required to transform a cell need be of somatic origin.  Since cancer is mostly, and obviously, a multi-factor disease genetically (not a single mutation as a rule), we should not have our hackles raised if we find what seems obvious, that mutations are part of cell division, part of life.

There are curious things about cancer, such as our large body size but delayed onset ages relative to the occurrence of cancer in smaller, and younger animals like mice.  And different animals of different lifespans and body sizes, even different rodents, have different lifetime cancer risks (some may be the result of details of their inbreeding history or of inbreeding itself).  Mouse cancer rates increase with age and hence the number of at-risk cell divisions, but the overall risk at very young ages despite many fewer cell divisions (yet similar genome sizes) shows that even the spontaneous mutation idea of V-T has problems.  After all, elephants are huge and live very long lives; why don't they get cancer much earlier?

Overall, if if correct, V-T's view should not give too much comfort to our 'Precision' genomic medicine sloganeers, another aspect of budget protection, because the bad luck mutations are generally somatic, not germline, and hence not susceptible to Big Data epidemiology, genetic or otherwise, that depends on germ-line variation as the predictor.

Related to this are the numerous reports of changes in life expectancy among various segments of society and how they are changing based on behaviors, most recently, for example, the opiod epidemic among whites in depressed areas of the US.  Such environmental changes are not predictable specifically, not even in principle, and can't be built into genome-based Big Data, or the budget-promoting promises coming out of NIH about such 'precision'.  Even estimated lifetime cancer risks associated with mutations in clear-cut risk-affecting genes like BRCA1 mutations and breast cancer, vary greatly from population to population and study to study.  The V-T debate, and their obviously valid point, regardless of the details, is only part of the lifetime cancer risk story.

ADDENDUM
Just after posting this, I learned of a new story on this 'controversy' in The Atlantic.  It is really a silly debate, as noted in my original version.  It tacitly makes many different assumptions about whether this or that tinkering with our lifestyles will add to or reduce the risk of cancer and hence support the anti-V-T lobby.  If we're going to get into the nitty-gritty and typically very minor details about, for example, whether the statistical colon-cancer-protective effect of aspirin shows that V-T were wrong, then this really does smell of academic territory defense.

Why do I say that?  Because if we go down that road, we'll have to say that statins are cancer-causing, and so is exercise, and kidney transplants and who knows what else.  They cause cancer by allowing people to live longer, and accumulate more mutational damage to their cells.  And the supposedly serious opioid epidemic among Trump supporters actually is protective, because those people are dying earlier and not getting cancer!

The main point is that mutations are clearly involved in carcinogenesis, cell division life-history is clearly involved in carcinogenesis, environmental mutagens are clearly involved in carcinogenesis, and inherited mutations are clearly contributory to the additional effects of life-history events.  The silly extremism to which the objectors to V-T would take us would be to say that, obviously, if we avoided any interaction whatsoever with our environment, we'd never get cancer.  Of course, we'd all be so demented and immobilized with diverse organ-system failures that we wouldn't realize our good fortune in not getting cancer.

The story and much of the discussion on all sides is also rather naive even about the nature of cancer (and how many or of which mutations etc it takes to get cancer); but that's for another post sometime.

Friday, March 24, 2017

Paid To Prey (PTP) journals

In the bad old days if you as a scientist had something worth saying, a journal would (after vetting through a mainly fair confidential review system) publish it.  If you had good things to say, whether or not you had grants, your ideas were heard, and you could make a career on the basis of the depth of your thought, your careful results, and so on.

If you needed funds to do your research, such as to travel or run a laboratory, well, you needed a grant to do your work.  This was the system we all knew.  You had to have funding, but you couldn't just pay your way through to publishing.  Also, if you were junior, start-up funds were typically made available if you needed them, to give you a leg up and a chance to get your career going.

Publishing has always had costs, of course, but the journals survived by library and personal subscriptions, often based on professional society memberships, where the fees were modest, especially for the most junior members.

Now what we have is a large pay-to-play (PTP) industry.  Pay-to-play journals are almost synonymous with corruption.  The mass of nearly-criminal ones prey on the career fears of desperate students, post-docs, and faculty (especially junior faculty, perhaps).  Even the honest PTP journals, of which there are many, essentially prey on investigators, and taxpayers, but the horde of dishonorable ones are no better than highwaymen, robbing the most vulnerable.  A story in the NY Times exposes some of the schemes and scams of the dishonorable PTPers.  But it doesn't go nearly far enough.

How cruel is this rat race?  Where does the PTP money come from?
We have every moral as well as fiscal right to ask where the PTP subscriptions are coming from.  Are low-paid, struggling post-docs, students, junior or even more senior faculty members using their own personal funds to keep in the publication score-counting game?  How much taxpayer money goes, even via legitimate grants, to these open-source publishers rather than to the research costs for which these grants were intended.  In the past, you might have had to pay for color figures, or for reprints, and these costs did come generally from grant funds, but they were not very expensive.  And of course grants often pay for faculty salaries (a major corruption of the system that nobody seems able to fix and on which too many depend to criticize).

The idea of open-source journals sounded good, and not like a private-profiteering scam.  But too many have turned out to be the latter, chickens laying golden eggs even for the better journals, when there is profit to be made. The original, or at least more publicly proclaimed open-source idea was that even if you couldn't afford a subscription or didn't have access to a university library--especially, for example, if you were in a country with a paucity of science resources--you would have access to the world's top science anyway.  But even if the best of the open-source organizations are non-profit, non-predatory PTP operations, and how would we know?, we are clearly preying on the fears of those desperate for careers in heavily oversubscribed, heavily Malthusian overpopulated science industries.

There is no secret about that, but too many depend on the growth model for there to be an easy fix, except the painful one of budget cuts.  The system is overloaded and overworked and that suggests that even if everyone were doing his/her best, sloppy or even corrupt work would make it through the minimal PTP quality control sieve.  And that makes it easy to see why many may be paying with personal funds or submitting sloppy (or worse) work--and too much of it, too fast.

There isn't any obvious solution in an overheated hyper-competitive system.  We do have the web, however, and one might suggest shutting down the PTP industry, or at least somehow closing its predatory members, and using the web to publicize new findings.  Perhaps some of the open review sources, like ArXiv, can deal with some of the peer reviewing issues to maintain a quality standard.

Of course, Deans and Chairs would have to actually do the work of evaluating the quality of their faculty members' works (beyond 'impact factors', grant totals, paper counts, and so on) to reward quality of thought rather than any quantity-based measures.  That would require the administrators to actually think, know their fields, and take the time to do their jobs.  Perhaps that's too much to ask of a system now sometimes proudly proclaiming it's on the 'business model'.

But what we're seeing is what we deserve because we've let it happen.

Thursday, March 16, 2017

Higher resolution discrimination: The GOP wants to allow employers to require genetic testing

This morning, Ed Yong published an article that takes on issues that we at the The Mermaid's Tale care very deeply about.
Link to article
The consequences for important medical research are not going to be pretty.

And I can't help but be angry about this for threatening to take away the fun of genetics too. If we can't have some control over our genetic testing, we can't do it for fun, for education, for finding out more about ourselves, for the awe of it, for innerspace exploration in the technology age. They're taking that away from us by eroding GINA.

I have lots of other thoughts... like about how this fits in so nicely with (not all of) the right's racist/eugenics inclinations.

And juxtapose this view from the political right where there is full-on acceptance of actually-more-than-genetics-can-even-deliver against their anti-science politics and policy...

It's like science is totally fine for Republicans as long as Mother Nature is a dictator.

If it's more complicated than that, then deny it, defund it, bulldoze it. The reality is, genetics is largely probabilistic; it is not a dictatorship. It's just so hard to convince people that it isn't. The ideological drive to justify behavioral differences and socioeconomic inequality with Nature above all is just too strong. If it's Nature, then we don't have to do the hard work of addressing the problems because Nature is Nature is Nature. This is really old thinking that really new knowledge (both through lots of science and lots of lived experience and lots of humanities and lots of art) has overturned but has not managed to catch on all that well. Along with new knowledge we get increasing understanding of genetics so these ancient beliefs can just be spouted by politicians using new-fangled science jargon.

This is really hard to write about today as all the stories about the proposed (and highly probable) budget cuts to science and the arts are blasting through my newsfeeds. It's overwhelming me today. I'm feeling hopeless and angry on behalf of science, art, knowledge, medicine, humanity, humans, children, teenagers, grown-ups, geezers. It's too much today.

But, back to Ed's article, I do need to put this here because it mentions that I have taught with 23andMe and longtime readers of the MT might know about that:

I don't teach with 23andMe anymore. I was doing it for as long as my university would pay for the kits. It was totally voluntary and students had to read Misha Angrist's book and endure long discussions and pass a quiz before deciding whether to go through with the testing. It was so powerful for teaching evolution, genetics, anthropology, etc... and we critiqued the hell out of it. My university said I needed to pay for the kits through course fees from now on. Before any of these threats to GINA, I decided not to do that and to stop using 23andMe. Now, even if my university reconsidered and funded the kits, I still wouldn't take it up again as a teaching tool.

Tuesday, February 28, 2017

Replacing the Affordable Care Act -- what's so complicated?

Nobody knew health care could be so complicated? Er, except everybody but Mr Trump.  And yes, it's a huge behemoth of a system, but the devil is in the detail.  It's when you throw in all the special interests, political considerations, back-scratching, etc. that it quickly gets complicated.  But before all that happens, there are only three basic choices when it comes to providing medical insurance, and they are easy to grasp.  Choosing among them, though, has become much more of a political choice than an unloaded purely economic one.

Here's what we had before the Affordable Care Act (ACA): private insurance, either from one's employer or purchased individually.  For this to work, of course, just as any other business, insurance companies must make a profit, and that's harder when customers get sick; purchasers actually using their insurance isn't good for the bottom line.  That's why there's so much talk about people with "pre-existing conditions".  These are people who insurers know will cost them money and that's why people with "pre-existing conditions" were essentially uninsurable before the ACA, except as members of large employee pools comprised primarily of healthy people who had to buy in as a condition of their employment.  And that's why insurance companies used to charge women, older people, smokers, and so on more; they were more likely to cost money.  And that's why insurance companies also had policies such as lifetime caps on benefits.  To stay in business, insurers have to make a profit.  It's their reason for being.  This system can work well for healthy people and insurance companies.

The second option is something like the ACA, where everyone, pre-existing condition or not, can buy insurance -- an appropriate thing to point out on Rare Disease Day 2017.  As with auto  insurance, the only way this is financially viable is if everyone is required to buy in; just as good drivers subsidize unsafe drivers, healthy people subsidize people more likely to use healthy insurance.  Thus, the hated "mandate", the requirement that everyone buy in or be penalized on their taxes.  Many detractors of the ACA believe the mandate can simply be eliminated, that a replacement for the ACA can cover as many people, as cheaply, without one.  But, that's impossible. This is the same kind of privitized system that has worked without major snags for many years in Switzerland, for example. There, insurance is compulsory, and insurance companies must offer a basic plan which they aren't allowed to profit from although people can purchase bells and whistles, which is how the insurers make a profit.

The third option is the public option, often these days described as Medicare for all.  Government-supplied health insurance, paid for by tax dollars.  It's cheaper than the first two options in large part because it's non-profit, and the infrastructure required by private insurers to validate or deny claims doesn't exist.  National health has worked well in many rich countries for decades, keeping costs down and providing access to medical care to all.

And that's it.  There's no other "terrific" "cheaper" alternative anyone has thought of that can replace the ACA. The only options are a system that's totally private; something like the ACA with its mandate; and national health.  Unfortunately, this wasn't very well explained when President Obama was working on the Affordable Care Act, and it's not being explained now.  The Republicans in control of Congress aren't going to give us national health; and while it seems that many of them would be happy going back to what we used to have before the ACA, opinion polls are showing that people are less and less happy with that option.  Will Trumpcare be Obamacare renamed, then?  We'll have to wait and see.  

In any case, whatever system we adopt, we've still got problems.  Although the rising cost of medical care in the United States has slowed some with the ACA, at almost 18% of GDP health care spending here is the most expensive in the world, far exceeding that of any other high-income country, most of which have national health care (e.g., source).  In part it's because of the high cost of medical care, the higher use of expensive technology (e.g., MRI's, mammograms and C sections) and the exorbitant cost of pharmaceuticals.  And this is even with limitations imposed by insurance companies to control costs.  In addition, the cost of individual premiums has soared for people who aren't eligible for government subsidies to help cover the cost of insurance, in part, because fewer healthy people have purchased insurance than companies anticipated.  And deductibles and co-pays have risen sharply.  Insurance companies still have to turn a profit to stay in the health insurance marketplace.


Source
And, all this spending hasn't made us healthier than people in countries that spend even considerably less.


Source

So,  even if Trumpcare is as terrific and as cheap as we've been promised, it's hard to see how it will cut the high cost of medical care, and make us a healthier nation.  That is complicated, especially when private profit, rather than public health, is its fundamental basis.

Friday, February 24, 2017

Reproductive Health Funding and Why it Matters

Conflict and war can have an enormous impact on demography and population health. When active fighting breaks out in an area it can lead to large and chaotic population movements - if you’ve been paying attention to the news about conflict in the Middle East you’ve most likely seen images of huge populations fleeing countries like Syria and Iraq and the resulting influx of millions of refugees arriving in places such as Europe.

The chaotic settings in which these populations find shelter are often rife with sanitation, hygiene and other problems. Difficult, strategic decisions must be made on behalf of humanitarian agencies regarding how best to allocate limited funding to properly address the needs of these populations. Unfortunately reproductive health isn’t normally a high priority – although it really should be. One of the best ways to improve the health of a population is to address morbidity and mortality in very early childhood. Everyone in a population goes through the childbirth bottleneck. Everyone has a biological mother. Targeting these age and sex groups can have far-reaching impacts.

An IDP (internally displaced person) camp along the Thailand-Myanmar border. Photo by Suphak Nosten


Most of my work focuses on health issues along the Myanmar-Thailand border and while there has been a decrease in fighting recently, in the very near past there was active civil war and sporadic flows of refugees seeking safety in the mountains on the Thai side of the border. By the early 1980s there were many small refugee and internally displaced person camps scattered along the border. In the mid-1990s (between 1994 and 1998) most of these smaller camps were consolidated into one of 9 currently existing camps. Today, Maela refugee camp, roughly 60 kilometers north of Mae Sot, Thailand, is the largest of these camps with a current population of roughly 37,000. It has been in existence now for over 30 years.

One thing that is easy to miss in an age of constant news bombardment is that these populations, these refugee camps, don’t just disappear with the news cycle. Sometimes refugee camps last for a very long time. Today there are second-generation refugees who were born, and continue to live, in Maela camp.

Shoklo Malaria Research Unit, a field station of the Mahidol-Oxford Tropical Medicine Research Unit, operated the only antenatal clinic in Maela camp until this past December (2016). Recently we analyzed records and data from our experiences in providing contraceptives to refugee women in this long, drawn-out refugee setting. Given the current dire refugee situation of the world, we thought our experiences might have relevance not only for the current refugee situation but also for the future, given that many people will likely be living in large refugee settings for the foreseeable future.

The first thing that became obvious from our analysis is that obtaining a good understanding of basic demographics can be rather difficult.  Information really is a first casualty of war – gaining a handle on data about the population can be difficult even decades later. Furthermore, population counts can have political implications, or conversely, population estimates are sometimes the result of political sentiments.  For Maela camp there are two main sources of population counts – one comes from the humanitarian agency that provides food (the Thai-Burma Border Consortium (TBBC)) and the other is from the United Nations High Commissioner for Refugees (UNHCR) that provides humanitarian and social services. Until very recently UNHCR counts have systematically been much smaller than TBBC counts.

Population estimates have varied widely by the reporting source. We estimated the reproductive age female population for Maela camp by year using data from both TBBC (black) and UNHCR (blue) population estimates.  A loess curve (solid line) is fit to the data points and 95% confidence intervals for the curve are shown in dark gray.


Our data also show that, when provided in a socio-cultural appropriate manner, men and women in refugee settings willingly uptake contraceptives. The population we work with can properly be considered a high fertility (or natural fertility) population meaning that, with some exception, families are large and people are happy with that. But even in a high fertility population contraceptives have important health implications.  Men and women should be able to regulate their family size and spacing if they choose. Unintended pregnancies can result in incredible burdens, especially in already difficult settings, with health consequences for children, families, and entire communities leading to intergenerational transfers of poverty and nutritional deficits [1,2]. Households with few working-age adults and many dependents tend to be households with economic and nutritional deficiencies.




We also note that funding has a huge impact on the uptake of contraceptives and even the type of contraceptives that are chosen. Yes, men and women in the camp chose to readily use contraceptives, but the availability of contraceptives and the type of contraceptives available were directly influenced by funding. In this setting and in others, most of that funding could best be described as “rescue funding”, with reproductive health services normally operating on small and dwindling budgets but occasionally being “rescued” by a new source of funding. Given the importance of reproductive health (including the availability of contraceptives) and the dependence of reproductive health services on funding, funding agencies should carefully consider what they fund and should give careful consideration to funding cuts.


It is hard to draw direct, causal relationships between something like reproductive health funding and reductions in morbidity and mortality because there are complex relationships between health care delivery and health outcomes. However, we do know that during the time that SMRU operated the antenatal clinic in Maela camp both maternal and neonatal mortality decreased drastically. From 1986 to 1990 there were about 499 maternal deaths for every 100,000 births while in 2006 – 2010 there were 79 per 100,000 births [3].  In 1996 there were approximately 43.5 deaths for every 1,000 neonates and by 2011 there were 6 per 1,000 [4,5].

When funding was available, refugees in Maela camp willingly chose to use contraceptives leading to safer, better-planned pregnancies, which leads to health improvements of mother and child. A focus on reproductive health in conflict and refugee settings is extremely important and can have a drastic impact on population health. When people are given the opportunity to be more in charge of important parts of their lives, they are more likely to break out of difficult poverty cycles, and subsequently go on to live healthier lives. We believe this is a good thing.

photo by Suphak Nosten


1. Wagmiller Jr RL, Adelman RM. Childhood and intergenerational poverty: The long-term consequences of growing up poor [Internet]. Columbia University Academic Commons. 2009. Available: http://hdl.handle.net/10022/AC:P:8870

2. Corak M. Do poor children become poor adults? Lessons from a cross country comparison of generational income mobility [Internet]. IZA Discussion Paper. 2006. Available: http://ftp.iza.org/dp1993.pdf

3. McGready R, Boel M, Rijken MJ, Ashley E a., Cho T, Moo O, et al. Effect of early detection and treatment on malaria related maternal mortality on the north-western border of Thailand 1986-2010. PLoS One. 2012;7. doi:10.1371/journal.pone.0040244

4. Luxemburger C, McGready R, Kham A, Morison L, Cho T, Chongsuphajaisiddhi T, et al. Effects of malaria during pregnancy on infant mortality in an area of low malaria transmission. Am J Epidemiol. 2001;154: 459–465. 

5. Turner C, Carrara V, Aye Mya Thein N, Chit Mo Mo Win N, Turner P, Bancone G, et al. Neonatal Intensive Care in a Karen Refugee Camp: A 4 Year Descriptive Study. PLoS One. 2013;8: 1–9. doi:10.1371/journal.pone.0072721


Friday, February 3, 2017

Save the Planet? Nonsense! But still.....

One hears a lot of Doomsday pleas that we should cut back on our consumption of carbon fuels, eat less meat, fish less, and so on--or else!  Or else what?  Or else, as it's often expressed, we'll destroy the planet!  Scientists speaking to each other about agricultural sustainability or climate change use less excessively inflammatory rhetoric, though even they can engage in catastrophism when the public media cameras are on.  Concern for the future is understandable, but exaggeration is not sensible if you stop to think about it. Crying "Wolf!" can backfire, because the Earth is not in imminent danger!




Human activity, even if we let our population rise to 10 or more billion and burn every single last chunk of coal and drop of oil, will not destroy the Earth.  No amount of energy conservation and sustainability will save the Earth from destruction, because it's not headed that way anyhow, and people haven't the power to destroy it (though, would we be able to come close with a nuclear WWIII?).

Indeed, it's possible that imminent catastrophe rhetoric reinforces the reactionary view that this is scientific nonsense and we should just close climate-change government-sponsored web sites and de-fund environmental science.

Part of the problem is that this is like the frog in a boiling kettle: the water gets hot so gradually that the frog doesn't notice it until it's too late.  We humans are not very good at long-term thinking or planning, perhaps because longterm thinking wasn't possible or useful as we evolved, when each day's food, safety and mates were what was at stake.  When change is slow, as global warming is, people often feel less inclined to self-denial today in exchange for a viable tomorrow.

In addition, sociologically speaking, climate change messages can be seen as a scientific or 'left-wing' elite telling everyone else that they have to scale-down, while at least some have noticed the fact that the same elite fly all over the world to have meetings, promote their books, and deliver their message (and flying is among the worst CO2 polluters).

In fact, most of what is being said by science, even taking scientists' vanities, frailties, and grant-hungers into account, is basically right.  The climate clearly is changing, the seas rising, agricultural patterns changing, many species endangered.  Of course, there have always been changes in patterns of rainfall, temperature, and vegetation, though the time scale generally has been glacially slow, so to speak, with the possible occasional exception of major meteorite strikes or huge volcanic eruptions etc.  The current speed is one reason human activity seems surely to be at least partially responsible.
Another important point isn't that climate is changing, but that the pace we're seeing today may not be reversible even if our behavior is contributing, because our ability to change the course of geoclimate might be limited.

But that doesn't mean that the science-deniers and their ilk hiding their head in the sand are right. They're as self-willed ignorant as scientists say they are.  They are pretending that the science is wrong, when the real truth is that they don't like the answers the science is giving us.

The real risk
If climate is always changing, and Save the Earth is a misleading slogan, the problem is that even if the Earth is not in danger, we are!  And that is the very, very personal and selfishly short-sighted reason that we should slow down global warming if we can, increase use of renewable energies, keep funding climate sciences, and so on.  Let's take a look at the wolf that really is at our door, and making enough evidentiary noise that we can't miss it.  What is at stake is not the Earth, but the kind of constancy we, like any species, rightfully feel comfortable with.

In fact, climate change does pose very serious, very real, and potentially dire risks. There are at least a few likely, foreseeable consequences of climate change:
1. Threatened lifestyles.  On the more mundane side, having to change where and how we live, what we eat, how we interact with each other, and so on, are major dislocations of lifestyle.  Being animals, we like our 'territory' to be familiar and feel safe.  The levels of ill-will and unhappiness that would ensue major cultural upsets due to climate change and its consequences, would be upsetting to a great many people. There may indeed be changed patterns of wealth, lifestyle, disease in us and/or our animal and plant food sources.  We may exhaust some minerals vital to our technological support systems. Even peacefully, gradually adapting to a lower-consuming lifestyle could avoid this, but would be disruptive; even if we lived very well in lower-consuming times in the past, social and psychological factors will be strained if our life-ways are changed too much or too fast. 
2.  Mass dislocation.  Most cities and urban concentrations are near natural waterways.  That's because they were founded over many centuries when water-borne trade and transport of goods etc., the stuff that makes concentrated populations possible, was the only real means of large-scale transportation.  So, if water levels rise along coasts and major lakes or rivers, or if waterways dry up, there will be dislocations that make todays middle east refugees look like tiddly-winks by comparison.  If tens of millions of Londoners and New Yorkers (not to mention residents of China or India) need to relocate, they'll have to go where there already are people.  This mass internal migration will be seen by the 'recipients' as 'Yugely' more of a threat than refugees today pose. 
3.  Exacerbated inequality and suffering.  Other large-scale dislocations of many sorts will mean economic deprivation for some who were well off, and new privilege for others.  Climate change alters agricultural areas, drying some up and making others flourish. Food being one thing people really do fight over, one can anticipate major economic dislocation and very large-scale competition for the new food producing areas, by those whose breadbaskets dried up.  This means war and potentially on a massive scale.  With 10 billion people, and industrial-scale weaponry (including nukes), the suffering will potentially be massively unprecedented.
In the overall scheme of things, a few island populations imminently needing relocation is an enormous event for the islanders but not a terribly large event globally.  But when cities become inundated, and food hard to come by, when refugees number in the many millions, and they're armed, well, that may be a definition of Arm-aggedon (forgive the pun).

We should be talking turkey to the public. Even if climate change is human-accelerated, it is not the first time there has been major climate change.  The Earth, and even the human species, will survive it.  Scientists should not be pressed by the intentionally uneducated into over-stating the case.  The planet is not in danger.  But in a sense there really is a wolf knocking at the door, and it is worth saving the planet as we know it.

What is in danger is our way of life.  And that's something humans kill for.

Friday, January 27, 2017

Evolution as a pachinko history: what is 'random'?

We discussed a Japanese pachinko machine in an earlier post, a pinball machine, as an example of the difference between randomness and determinism, in an evolutionary context.   Here we want to use pachinko machine imagery in a different way.

The prevailing, often unstated but just-under-the-surface assumption is that every trait in life is here because of natural selection.  Of course, for a trait to be here at all, bearers of its ancestral states up to the present (or, at least, the recent past) were successful enough to have reproduced.  It would not be here if it were otherwise, unless, for example, it's itself harmful, or without function but connected to a much better, related trait since genes are usually used in many different bodily contexts and may be associated with both beneficial and harmful traits.  Most sensible evolutionary geneticists know that many or even most sites in genomes tolerate variation that has either no effect or effects so small that in realistic population sizes they change in frequency essentially by chance.





However, the widespread default assumption that there must be an adaptive explanation for every trait usually also tacitly assumes that probabilism doesn't make much difference.  Some alert evolutionary biologists will acknowledge that one version among contemporary but equivalent versions of a trait can evolve by chance relative to other versions.  But the insistence, tacit or expressed, is that natural selection, treated essentially as a force, is responsible.  The very typical view is that the trait arose because of selection 'for' it, and that's why it's here.  And speaking of 'here', here's where a pachinko analogy may be informative.

If a bevy of metal balls tumbles through the machine, each bouncing off the many pins, they will end up scattered across the bottom ledge of the machine (the gambling idea is to have them end up in a particular place, but that's not our point here).  So let's take a given ball and ask 'Why did it end up where it did?"





The obvious and clearly true answer is 'Gravity is responsible'.  That is the analogue of 'selection is responsible'.   But it is rather an empty answer.  One can always say that what's here must be here because it was favored (that is, not excluded) by fitness considerations: its ancestral bearers obviously reproduced!  We can define that as 'adaptation' and indeed in a sense that is what is done every day, almost thoughtlessly.

Gravity is, like the typical if tacit assumption about natural selection, a deterministic force for all practical purposes here.  But why did this ball end up in this particular place?  One obvious answer is that each starts out in a slightly different place at the top, and no two balls are absolutely identical. However, each ball makes a different path from the top to the bottom of the obstacle course it faces. Yes, it is gravity that determines that they go down (adapt), but not how they go down.

In fact, each ball takes a different path, zigging and zagging at each point based on what happens, essentially by chance, at that point.   This one might think of as local ecosystems on the evolutionary path of any organism, that are beyond its control.  So, in the end, even if the entire journey is deterministic, in the sense that every collision is, the result is not one that can, in practice, be understood except by following the path of each ball (each trait, in the biological analogy).  And this means that the trajectory cannot be predicted ahead of time. And in turn, this means that our interpretation of what a trait we see today was selected 'for' is often if not usually either basically just a guess or, more often, equates what the trait does today to what it was selected to be, expressed as if it were an express train from then to now.

And this doesn't consider another aspect of the chaotic and chance-affected nature of evolutionary adaptation: the interaction with the other balls bouncing around at the same time in such an obstacle course.  Collisions are in every meaningful sense in the game of life, if not pachinko, chance events that affect selective ones, even were we to assume that selection is simple, straightforward, and deterministic.

The famous argument by Gould and Lewontin that things useful for one purpose, such as 'spandrels' in cathedral roofs, are incidental traits that provide the options for future adaptations--life exploits today with what yesterday produced for whatever reason even if just by chance.  The analogy or metaphor has been questioned, but that is not important here.  What is important is that contingencies of this nature are chance events, relative to what builds on them.  Selectionism as a riposte to creationism is fine but hyper-selectionism becomes just another often thought-free dogma.  Darwin gave us inspiration and insight, but we should think for ourselves, not in 19th century terms.

A far humbler, and far less 'Darwinian' (but not anti-Darwinian!), explanation of life is called for if we really want to understand evolution as a subtle often noisy process, rather than as a faith.  Instead, even serious biologists freely invent--and that's an apt word for it--selective accounts, as if true explanations, for almost any trait one might mention. It's invented because some reason is imagined without any direct evidence other than present-day function, but then treated as if directly observed, which is rarely possible. Here is an interview that I just came across that in a different way makes some of the same points we are trying to make here.

Everything here today is 'adaptive' in the sense that it has worked up to now.  Everything here today is also a 4 billion year successful lineage, that all made its way through the pachinko pins.  But these are almost vacuous tautologies.  Understanding life requires understanding one's biases in trying to force simple solutions on complicated reality.