Full-scale Disneyland (with canals!), and sustainability issues

We recently returned from a 2-week trip to Italy.  Two of our children and their spouses live in Europe.  One couple lives in a small town in northern Italy, the other in central Switzerland.  The latter drove down to Italy where we all enjoyed seeing each other, which is not easy given the distances.  But while this vacation/family gathering was very pleasant and, to us, important, it raises some less pleasant thoughts about sustainability in our time in history.

My concerns are personal, but in a sense also global, and to some extent they relate to societal inequity: not everybody can just drop a few thou and travel across the ocean for a couple of weeks' dinners with family.  But beyond unfairness, my concerns are about other issues.  This was a very energy-bad vacation, and we weren't alone!

We flew from the east coast to Venice, the most convenient airport for our purposes.  We flew on a large plane, maybe 2/3 full of passengers. As we all know, one of the worst ways to contribute to global warming is to fly. The aircraft was largely filled with people taking cruises in the Mediterranean.  The trip was about 3700 miles each way, not including the various train and car junkets we took during those two weeks.

And then there's Venice itself.  We stayed a couple of days there to recover from jet lag, and to see the sites.  We'd been there for a science meeting once before.  Bella Venezia!  Once home to a world-leading trade empire, and to many great cultural and architectural wonders and of course its romantic lacework of canals.  The glory days were then, but what is the city today?  Venice takes in something like 100,000 tourists a day, well more than the number of people who actually live there.  The piazzas, side streets, walkways, and bridges--and they are very scenic indeed--are often a shoulder-to-shoulder river of tourists.  They (and we) sightsee in museums, shop, eat, shop, stay in hotels, eat, and shop.  It is obvious that a huge amount of money pours into the city, every day, all year, and has been doing so for decades if not centuries.

Even forgetting their thought-provoking historical value and more trivial entertainment value, and just thinking of them as Disneyesque curiosities for selfie-ops, these museums, shops, and hotels are staffed by an army of people who earn their living from the tourist trade.  So while Venice is in a sense unique and beautiful, it is also in a perhaps deeper sense something of a fake, a touristic Potemkin village, a hyper, full-time, full-scale Disneyland entertainment park, there today mainly to pluck the pockets of the relatively idle affluent and wasteful denizens of our planet (I certainly include myself in that category!).

St Mark's Square, Venice; By Nino Barbieri - Own work

Venice is but one rather small city on the global tourist map.  If you think about the amount of fuel used to transport everyone to, from, and around Venice (and even take into account that the gondolas don't require fossil fuel!), and then multiply that by the hundreds of tourist sites around the world, you have to wonder what hope there is for containing global warming.  There is no sign of self-restraint of any kind here--even on departure to return home, the airport luxury shops do a booming business as tourists part with whatever dollars they've not yet spent.

But what can one seriously do?

It is easy to chastise people who take such totally needless trips, even if accompanied by a self-incorporating mea culpa.  After all, this really is a nearly total luxury.  For most of human history those relatives who moved or sailed far away never saw their family again and corresponded by mail (if at all, if there was such a thing as 'mail').  That was just how life was!  Our family get-togethers are a new, pure luxury.  In a seriously conservation-dedicated world, we could dispense at least with the purely sightseeing, self-indulging kinds of global vacationing.  That would seem like something trivial, a luxury that a resource-conscious world could easily forego.  But even if we all were so equitable, fair, future-aware, and so on, things aren't nearly so simple.

The world is crowded with people and much of it is industrialized, with the number of people who live on the land, as subsistence farmers, declining every year.  We have hugely diverse economies, in a sense creating occupations that earn money so we can swap that for food and so on.  Most of it isn't really necessary.  Among these non-food related activities is tourism, which is huge because so many people are now wealthy and idle enough to take global junkets.

In turn that means that much of the world depends on travel and sightseeing.  Countless peoples' livelihoods are involved.  This is in a sense quite antithetical to global sustainability.  If we seriously slowed down travel to save fossil fuels and reduce warming, then tourism, air travel, cruise ships, and the people involved in the manufacture and operation of planes, ships, trains and buses, their ports and terminals, would lose their jobs. The manufacturers of tourist-related goods, including Venetian carnival masks, post-cards, luxury shopping goods, hotel supplies, restaurant foods, chefs, waiters, menu printers, clerks, etc. would be hit.  Venice, already a shell of its former self, would cease to have a reason to exist.  Even those who deliver all these goods during the night, and those who remove the trash, invisible to the tourists sleeping quietly in their beds, would be affected.  Society would somehow have to do something about their employment needs.  

This means that the idea of just paring back on consumption really is a dream--or, as every even mild economic depression shows, a nightmare.  And just the one example of tourism, essentially a luxury trade, involves countless thousands of people.  Needless to say, all of this is grossly unfair to the huge majority of people living on or below the margins.  It shows the inadvertent implications, even the distanced cruelty, of those idealists who want quick changes in sustainability directions.

It is difficult to have a non-selfish moral position on these issues.  If we say "let's change things slowly so as not to be too disruptive to too many people", the normal human tendency is to think the problem isn't so real, and not even go along with 'slowly' with much dedication. That's why car companies begin making and hawking, and consumers purchasing, bigger cars and trucks the moment gas prices drop.  [I insert this post-posting editorial change because today's NY Times had a story about the return of gas-guzzlers, in the same spirit of what this post is about]

If we say 'we must rush' then too many will find rationales for not going along ('OK, it's a good idea, but I can't do it--I have to see my family overseas!').  So where is a feasible ground to be found, and to what extent should we personally expect to be affected by it?  What will we give up for the cause?  The question, for me, is not abstractly how much one must cut out of what one does, but how much I must cut!  That gets pretty close to home, so to speak.

I can't help but add a rather gratuitous, if snide, side comment. The problems are compounded in an ironic way.  We have agricultural sustainability issues, as everyone by now should know.  The 'developed' world suffers common diseases largely due to bad nutrition and that means to over-eating. So while much of the world barely scrapes by, many in the rich world waddle along largely over-weight (these are not the minority of people struggling with genetic or epigenetic problems that make weight control a real challenge).  The obesity epidemic is why we hear complaints about airplane seats being too small!  So I remark snarkily that, as a consequence, one reason air travel is so environmentally unfriendly is the countless tons of human bulk that are being transported daily across the oceans in tourist-filled aircraft.  One thing leads to another.

We just took what was clearly a very energy-bad trip, no matter how understandable our desire to be with family and our decision to go.  We could, of course, have talked with our family members via Skype--indeed, we already do that often.  I complain that leaders in sustainability and climate change, including the very organization that documents it for the UN, fly all over the world and meet in fancy hotels to discuss the problem and tell everyone what they (that is, they) must do to 'save the planet'. The leading spokespersons for sustainability and climate-change avoidance could set a very public example and work only via Skype! 

In the context of global conservation, sustainability, and climate issues, who should feel guilty about what?  If do as I say not as I do is not acceptable, then what justifies our personal exceptionalism? For me, the answers are far from clear.

Have gorillas really inbred themselves into the future?

By Anne Buchanan and Ken Weiss

NOTE:  This is a revision of our original post, because a mistake on our part was pointed out by a commenter, to whom we offer thanks.  Our main point hasn't changed....unless there are still misperceptions on our part.

BBC Earth headline: "Inbreeding Makes Mountain Gorillas Genetically Healthy." We are so tempted to add an exclamation point to that, but we won't.  Anyway, you know it's there, whether we add it or not. Everyone 'knows' that inbreeding is bad; what a juicy story!

And, to summarize, the story is this: Mountain gorillas are an endangered species, surviving now in just two small groups in central Africa, a total population of only about 800 individuals.  Their numbers had fallen to just under 300 in the 1980's, for multiple reasons including poaching and loss of habitat, but Diane Fossey made their conservation her life's work, and the population more than doubled since its lowest point.

                  Location of eastern and western gorillas; Xue et al., Science 2015

But, their small numbers led to extensive inbreeding, which is always worrisome to conservationists because it may reduce a population's ability to adapt to changing environments.  But, the BBC writes:

Now scientists have discovered inbreeding has actually benefitted mountain gorillas by removing many harmful genetic variations. They are also genetically adapted to living in small populations.

And,

Fewer harmful genetic mutations, which stop genes functioning and can cause serious health conditions, were found in the mountain gorilla population than in the western gorilla populations.

Ok, let's step over to the actual paper ("Mountain gorilla genomes reveal the impact of long-term population decline and inbreeding," Xue et al.), in Science last week, to get the story without the go-between.  So, the investigators sequenced the whole genomes of 13 eastern gorillas, including seven mountain gorillas and six eastern lowland gorillas.  They compared these sequences with published sequences of lowland gorillas further west, and found lower genetic diversity in both the mountain and lowland gorillas from the east, which they report as consistent with the smaller population sizes there.  Their analysis, they report, confirms that the eastern lowland and mountain gorillas are two genetically distinct populations.  Genome wide linkage disequilibrium was higher in the eastern gorillas than the western, evidence of different demographic histories of these populations, and suggesting a recent population bottleneck in the eastern gorillas.

Foraging gorilla, Congo; Wikipedia, Pierre Fidenci

In eastern gorillas, chromosomes were found to be homozygous across 34 to 38% of their length, while in western lowland gorillas, they were 13% homozygous, indicating that the eastern gorillas have a recent history of several generations of close inbreeding.  Xue et al. also report that the eastern and western populations diverged perhaps 150,000 years ago, with no mating history in the last 20,000 years or so.  And, overall, it seems that gorilla population sizes have been small for thousands of years, and thus probably have been inbreeding for all of that time.

Again comparing mountain with lowland gorillas, Xue et al found no evidence for natural selection or adaptation favoring functional genes in either group.

Such adaptation might be expected from the fact that mountain gorillas range over high altitudes (1500 to 4000 m), with consequences for diet, morphology, and physiology. However, we found no significant enrichment in any functional category of genes, although there are interesting examples related to nervous system morphology, immunoglobulin quantity, and red blood cell morphology. Mountain gorillas carry a significant excess of variants in genes associated with blood coagulation in humans (fig. S21), perhaps linked to high-altitude living. We also identified variants associated with cardiomyopathy, including in one deceased individual (Kaboko) in whom post mortem analysis revealed evidence of muscular hypertrophy. Cardiovascular disease has been identified as a notable cause of death in captive western lowland gorillas.

With respect to unfavorable effects of inbreeding, the authors report the opposite, saying that inbreeding seems to have purged deleterious mutations from the genome.  They suggest that gorillas have found workarounds for inbreeding effects, as well, such as by "natal dispersal and gene flow between isolated populations."

Xue told the BBC that gorillas have been coping with small populations for thousands of years, and,

"While comparable levels of inbreeding contributed to the extinction of our relatives, the Neanderthals, mountain gorillas may be more resilient. There is no reason why they should not flourish for thousands of years to come."

No reason? 
But, we can think of a number of reasons.  The Ebola virus has been devastating to chimps and gorillas, wiping out 95% of some groups of gorillas in which it has spread.  And, there's always the possibility that other infectious diseases may emerge, or reach these animals, and be equally, or even more devastating.

And, poaching continues to be a problem, and hunting for bushmeat.  Loss of habitat continues to be a problem.  Climate change will surely have consequences for these animals.  As with any other animal, including humans, environmental change and its consequences are unpredictable.  Whether or not any species has the genetic wherewithal to adapt to that change is unpredictable; it's impossible to know what any single gene will do in every possible environment, never mind what every gene, and every genetic interaction will do.  This is, of course, true with respect to predicting our own futures from our genomes as well. 

What is 'inbreeding' and what does it mean?
There are several things about this paper aside from the apparent obliviousness of the research report to the real threat to gorilla 'fitness', namely that they're widely projected to become extinct because of human incursion and predation, in addition to disease. We might also ask, if the western gorillas have so little relative homozygosity, why they aren't plagued with the sorts of defects that the easterners have already purged, and on the verge of collapse -- or long gone?  

The answer is that both populations (not just the eastern) did well enough to be here today.  Both low and high homozygosity are obviously good enough, because neither wiped out either population structure in their past.  So why tell the story as if one way's better? It seems to be the tired old evolutionary trope that we cannot seem to escape: To be different from is to be better than, to evolve away from is because it's a better way.  But, mutation is always happening, genetic drift is always happening, and if a variant works, it works. It isn't necessarily selected because it's better, or more adaptive, than anything that came before. 

This paper is in a sense an exaggeration of, and in a way confusion about inbreeding and its effects.  There are several meanings of 'inbreeding' that are relevant here** . The classical meaning refers to mating with close relatives relative to random-mating. The issue there is the classical one of increased incidence of recessive disorders with inbreeding.  In that context, the probability of an allele being homozygous more than just by chance: if the latter is p^2 when there is random mating, the former is p^2 + Fp(1-p), where p is the frequency of the variant in question, and F is the excess probability of being homozygous due to non-random mating. That may be because of socially constructed preferential kin-mating or just a deviation from random mating. In many, if not historically most, human populations, mating was prescribed as to be between cousins of various types. If variants are harmful but recessive so that their harm is only seen in homozygotes (both copies in a person being defective), then mating between close relatives can increase the frequency of such events, and the loss of the harmful variant from the population, but of course only at the expense of the carriers of those harmful genotypes. One can argue that if something like close-relative mating were so dangerous it would never have evolved to be, in a sense, the ancestral human way as it has.  Or, one can note that the reason for local group endogamy or exogamy (how mates are chosen in any population, human or otherwise) has to do with social structure, resource distribution, and control of internecine and intergroup strife--not because of disease genes.

The authors appear not to have done this kind of calculation, however, and samples would have been too small for it to make sense.  Instead, they looked along the genome to see what fraction was homozygous (that is, variant sites along the region in the sequenced animals).  This reflects a different use of the term 'inbreeding', and we think what this paper is referring to, is the rise in homozygosity due to genetic drift in small populations.   In a small population, rarer alleles (genetic variants) are lost more rapidly from the population, mainly just by chance. Homozygosity at a given site is an inevitable reflector of population size, and in a small population the region of a chromosome that is homozygous (not varying) would be larger than in a large outbred population. That is not an automatic indicator of a history of loss of harmful mutations, recessive or otherwise. In any population harmful variants have a shorter staying time than helpful ones, but their duration depends on many different factors that can't be inferred from the stretches of homozygosity alone.

Do western lowland gorillas, with their lack of a history of 'inbreeding' as presented by this story, show some detectable load of sub-par individuals? If so, that would be relevant news. In fact, both groups have coefficients higher than human cousins relative to each other, as a commentary on this paper notes. But so what?  In fact, and perhaps to the contrary, being too inbred in the small-population sense could, as far as just-so stories go, mean there would not be enough variation in the population to respond to environmental challenges.

What the study does no doubt actually show is that the two gorilla populations have had different demographic histories. That is ecologically interesting and perhaps useful for understanding wildlife conservation issues.  But in itself it says basically nothing about purging harmful variation except that it would be somewhat faster, on average, in one group than the other -- but only slightly so, because if that were not the case the burden of loss could have threatened the very survival of the group in the past so that it never made it to the present, which obviously isn't the case.  'Inbreeding' in headlines may have a juicy sound and catch the lascivious eye, and that's why the news media go for it so readily.

It should also be noted that extensive, detailed, biomedically documented studies in human isolate populations have found each to have particular instances of elevated recessive diseases or other traits due to inbreeding effects, but the overall burden of genetic disease has not been particularly increased, if at all.

***The often and perhaps still confusing issue of inbreeding have been clarified long ago, e.g., by Albert Jacquard in 1975, in J. Theoretical Biology, "Inbreeding: one word, several meanings", by various wrtiting of Warren Ewens back in the 70s, or see Templeton and Read, Conservation Genetics, 1994; they are discussed in any good population genetics text.

Ptolemaic genetics: epicycles of lobbying

That was then...

Ibn al-Shatir's model for the
appearances of Mercury,
showing the multiplication of
epicycles in a Ptolemaic
enterprise. 14th century CE
(Wikimedia Commons).

Way back then, in the dark ol' days of science, the Roman astronomer Claudius Ptolemy (90-168AD) tried to explain the position of the planets in terms of divinely perfect circles of orbit around God's home (the Earth).  The idea that we were at the center of perfect celestial spheres was a standard 'scientific' explanation of the cosmos and our place in it.

But the cantankerous planets refused to play by the rules, and their paths deviated from perfect circles.  Indeed, occasionally the seemed to move backward through the skies!  Still, perfect circular orbits around Earth simply had to be true based on the fundamental belief system of the time, so astronomers invented numerous little deviations, called epicycles, to make the (we now know) elliptical orbital pegs fit the round holes of theory.

And then along came Nicolaus Copernicus (1473-1543 AD).  And the cosmos was turned inside out: the earth was not the center of things after all!

Thomas Kuhn famously described in The Structure of Scientific Revolutions how the best and the brightest scientists struggle valiantly to fit pegs into holes they don't really fit, until some bright person ccomes along and shows the benighted herd a better way to account for the same things.  Copernicus, Galileo, Newton, Einstein, and others were the knights in shining armor who inaugurated some of the most noteworthy of these occasional 'scientific revolutions.'  Darwin's evolutionary ideas are also a classic example.

The same kind of struggle is just what is happening now in genetics and evolutionary biology--indeed in many other fields in which statistical evidence runs headlong into causal complexity.  Whether, when, or what knightly change will occur is anyone's guess.

And this is now
Everyone remembers the hoopla the sequencing of the human genome was met with when it was announced (or rather, each time it was announced) -- we were promised that we would by now not only know why people were sick, but we'd be able to predict what we'd get sick with in future.  It was promised that this would be a silver-bullet reality by the early 21st century by no other than Francis Collins.  Others were promising lifespans in the centuries: all of us would be Methuselahs!

So, all those illnesses would now be treatable or preventable in the first place. How?  Well, the genome would allow us to identify druggable pathways, and common diseases must be due to common genetic variants (an idea that came to be known as common disease common variant, or CDCV), and if we could just identify them, we'd be in business.  After all, didn't Darwin show us that everything about everything alive was due to genetic causation and natural selection?  If that's the case, we should be able to find it, and our wizardry at engineering would take the ball and run with it.  Big Pharma jumped on the 'druggable' genome bandwagon and people running big sequencing labs jumped on the CDCV idea, and genomewide association studies (GWAS) were born.  And then the 1000 Genomes project, and all the -omics projects....  Big is better, of course!  Not that these efforts weren't questioned at the time, based on what everyone should have known about evolution and population genetics, but the powers-that-be plowed ahead anyway.

Well, we're no longer in a minority of naysayers.  It's widely recognized that GWAS haven't been very successful, relative to the loud promises being trumpeted only a few years ago.  And even the successes they have had -- and numerous genes associated with traits have been identified, it must be said -- typically explain only a small amount of the variation in disease, or any trait, in fact.  So now researchers are working on automating the prediction of disease from gene variants based on protein structure and other DNA-based clues.  But the assumption--the belief system, really--is still that the answer is in the DNA, and disease prediction is still going to be possible.

A piece in Feb 9 Nature describes a number of state-of-the-art approaches to predicting the effects of DNA variants, in part based on what amino acid changes do to proteins.  The idea now is that diseases are going to be found to be due to rare variants, and the challenge is to figure out what these variants do.  In part, evolution will help us to do this.

"Sequencing data from an increasing number of species and larger human populations are revealing which variants can be tolerated by evolution and exist in healthy individuals."

But, are we trying to explain a current disease, or predict the diseases someone will eventually get? These are different endeavors, though it may often be inconvenient to acknowledge that.  Rare pediatric diseases that are due to single genetic mutations, or genetic diseases that cluster in families (and, again, usually with young onset age and rare) are easier to parse than the complex chronic diseases that most of us will eventually get.  But, based on the comparison of the genomes that have already been sequenced, we now know that we all seem to differ from each other at something like 3 million bases.  That is, we all have a genome that has never existed before and never will again. Assigning function to all that variation is from daunting to impossible -- not least because a lot of it might not even have a function.  And the idea that we'll eventually be able to make predictions from those variants is based on questionable assumptions.

It's true in one sense that every disease we get is genetic -- everything that happens in our body is affected by genes -- but in another sense, much of what happens is a response to the environment, and so is environmentally determined--that is, is not due to genetic variation in susceptibility.  Predicting a disease from genes when it's due to combined action of genes and environment, therefore, is a very challenging problem.

Here is just one example of why: Native Americans throughout the Americas are about 65 years into a widespread epidemic of obesity, type 2 diabetes and gallbladder disease, diseases that were quite rare in these people before World War II.  There are a number of reasons to suspect that their high prevalence is due to a fairly simple genetic susceptibility.  But, if gene variants (still not identified) are responsible, they have been at high frequency in the descendants of those who crossed the Bering Straits from Siberia for at least 10,000 years -- which means that variants that are now detrimental were "tolerated by evolution and exist[ed] in healthy individuals" for a very long time.

If geneticists had wanted to predict 70 years ago what diseases Native Americans were susceptible to, these variants would have been completely overlooked, because they weren't yet causing disease.  And indeed these 'risk' genes, whatever they be, were benign -- until the environment changed.  We're all walking around with variants that would kill us in some environment or other, and since we can't predict the environments we'll be living in even 20 years from now, never mind 50 or 100, the idea that we'll be able to predict which of our variants will be detrimental when we're old is just wrong. In fact, we're each walking around with substantial numbers of mutant or even 'dead' genes, with apparently no ill effect at all -- but who knows what the effect might be in a different environment.

But, ok, some of us do have single gene variants that make us sick now.  Many of these have been identified, most readily when a family of affected individuals is examined (though the benefit of knowing the gene is rarely of use therapeutically), but many more remain to be.  The current idea is that this can be done by looking for mutations in chromosome regions that are conserved among species, and figuring out which of these change amino acids (and thus the protein coded for by the gene).  The idea is that unvarying regions are unvarying because natural selection has tested the variants that arose and found them wanting, thus eliminating them from the population.  They must, therefore, be functionally important!

A host of increasingly sophisticated algorithms predict whether a mutation is likely to change the function of a protein, or alter its expression. Sequencing data from an increasing number of species and larger human populations are revealing which variants can be tolerated by evolution and exist in healthy individuals. Huge research projects are assigning putative functions to sequences throughout the genome and allowing researchers to improve their hypotheses about variants. And for regions with known function, new techniques can use yeast and bacteria to assess the effects of hundreds of potential mammalian variants in a single experiment.

This is potentially useful, because for those with single gene mutations that cause disease -- 1 variant among 3 million other ways in which each person differs from everyone else -- homing in on the causative mutation is, again, difficult to impossible if you don't have a large family with similarly affected individuals in which to confirm the association of mutation and disease.

Well, if we can do with or without a protein (or other functional DNA element), depending on the variation we have across the genome, then even when the element is important its variation in a given individual may not be causal: there are many examples where that is clearly true.  Further, the same kind of evolutionary reasoning would say that centrally important -- and hence highly conserved -- parts of the genome probably cannot vary much without being lethal, largely to the embryo.  So, from that equally sound Darwinian reasoning, we would expect that disease-associated variation will be in the minor genes with only little effect!  So the 'evolutionary conservation' argument cuts both ways, and it's not at all clear which way its cut is sharpest.  It's a great idea, but in some ways the hope that searching for conservation will bail us out, is just more wishful thinking to save business as usual.

Methuselah (Della Francesca ca. 1550) 

To complicate things even more, not all amino acid changes cause disease, or even do much of anything.  And again, sometimes they will only be harmful in a given environment.  And, of course, not all diseases are caused by protein changing mutations -- sometimes they are caused by disturbances to gene regulation.

In fairness, the multitude of researchers trying to make sense of the limitless genetic variation that is pouring out of DNA sequencers recognize that it's complicated.  But then, why are they still saying things like this, as quoted in the Nature piece: “The marriage of human genetics and functional genomics can deliver what the original plan of the human genome promised to medicine.”

What's to the rescue?  Do we need another 'scientific revolution'?
We have no idea when or if our current model of living Nature will be shown to be naive, or whether our understanding is OK but we haven't cottoned on to a seriously better way to think about the problems, or indeed whether the hubris of computer and molecular scientists' love of technology will, in fact, be victorious.  If it comes, it could be.  But we are certainly in the midst of a struggle to fit the square truths about genetics and evolution into the round holes of Mendelian and Darwinian orthodoxy.

Perhaps the problem to be solved is how to back away from enumerative, probabilistic, reductionistic treatment of complex, multiple causation, and to make inferences in other ways.  We need to understand causation by numerous, small or even ephemeral statistical effects, without our current enumerative statistical methods of inference. In terms of the philosophy of science, doing that would require some replacement of the 400 year-old foundations of modern science, based on reductionistic, inductive methods that enabled science to get to the point today where we realize that we need something different.

The situation here is complicated relative to scientific revolutions in Copernicus', Newton's, Darwin's or even Einstein's time by the large, institutionalized, bureaucratized, fiscal juggernaut that science has become. This makes the rivalries for truth, for explanations that this time will finally, really, truly solve the complexity problem even more frenzied, hubristic, grasping, and lobbying than before.  That adds to the normal amount of ego all of us in science have, the desire to be right, to have insight, and so on.  Whether it will hasten the inspiration for a transforming better idea, or will just force momentum along incremental paths and make real insight even harder to come by, is a matter of opinion.

Sadly, the science funding system, including the role of lobbying via the media, is so entrenched in our careers, that dishonesty about what is claimed to the media or even said in grants is widespread and quietly acknowledged even by the most prominent people in the field: "It's what you have to say to get funded!", they say.  But where does dissembling end and dishonesty begin when it comes time to the design and reporting of studies (and, here, we're not referring to fraud, but to misleading results and over promising the importance of the work)?  The commitment to the ideology and the promises restrains freedom of thought, and certainly dampens innovative science.  But it's a trap for those who have to have grants and credit to make their living in research institutions and the science media.

Zip-line over rainforest canopy,
Costa Rica (Wikimedia)

But right now, scientists are like tropical trees, struggling mightily to be the one that reaches the sunlight, putting the others in their shade. What we need is a conceptual zip-line over the canopy.