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Is it possible to increase lifespan through controlled evolution?

Is it possible to increase lifespan through controlled evolution?


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A few years back when I was reading The Selfish Gene by Richard Dawkins, there's this short passage where he theorizes about a way to achieve an increased lifespan through controlled evolution.

The theory goes like this: we don't tend to have medical problems until after 30 because we all tend to reproduce before that age. Thus, people who tended to die before 30 never passed on their dying-prone genes.

So, if you didn't let people reproduce before a age X (where X starts at 30) and then slowly move that age up, you could use evolution to increase lifespan.

The ethical issues notwithstanding, is there any reason why this wouldn't work? If it would work, how long do you think you would need to sit at each value of X? How far apart do you think each value could be? Finally, how many generations, using this technique, would it take before someone would live to be 1000 naturally?


I think this would probably work. The grandmother effect, which is one of the main theories for human longevity after fertility might indicate that human lifespan would increase if the children come later.

Just have to disclaim here: We will never do this. Many unthinkable consequences would result…

If you simply forbid anyone to have children before they are 40 or 45 (fertility doesn't drop until age 35 or so), forbid invitro fertilization and medical assistance to conception we would probably be looking at a prolonged lifespan. Infertility rates in women at age 40 are not clear, but one estimate is that 40% of women can have children at 40 years of age. If we want to seen an effect early, we would push the age up a year or two. Forbidding in vitro fertilization and other medical assistance to offspring we could look like a 80-90% cut of people - lots of people would never have children. This might make people unhappy an destabilize the social fabric.

Its not clear how long this would take. The generation time would go to 40 years from about 20 now - 40 to get to childbearing age, but results would take 80 years - when we find out how the children would fare. Given the C elegans longevity experiments and the fact that we are starting with 8 billion people, we probably would find some great late age breeders who may also live long. But for the longevity phenotype to set in it would take several generations as we are looking for an indirect effect: later breeding causing longevity. The Belyaev experiments which produced domesticated foxes by strong selective breeding took some 30ish generations to complete though they saw a significant effect in just 10. It could take a similar numbers of selection rounds in this cse. 4-500 years. Ethical issues aside, this is why most geneticists study flies.

There would also be a lot of other negative socioeconomic consequences to this thought experiment. One good thing is that the population of the earth would plummet - many people would be eliminated from the gene pool, though eldercare would be a major part of the world workforce. Lots of work, not clear who is going to pay for it, but low unemployment and low low wages may result.

So you see Mister President, this is quite a distinct possibility, though some sacrifices would have to be made.

The science of human eugenics is not scientifically wrong, but selective animal breeding and lab experiments don't usually evaluate or care about the consequences of large peturbations in the gene pool.

You would also have a lot more autism and Downs syndrome and other congenital defects which tend to show up in offspring of older parents. These issues might improve with application of biotechnology which screens weak sperm and eggs without ruining the effect you are looking for, maybe not.

Since we are selecting against fecundity, the human race could be dogged by fertility problems or chronic genetic diseases which the genetic contribution of some of the more robust people in the gene pool being removed and the tendency to such age-related birth defects might not go away given the drastic selection pressure we are putting on the gene pool.

Other consequences you might not expect; some physical traits associated with longevity and prolonged fertility would cause us to look more alike and not necessarily in a good way. Browse the internet; its probable that we would get shorter and possibly uglier?

There are many more direct ways to increase the human lifespan - better diet, exercise, the elimination of poverty, vaccinations, proper medical care, access to clean drinking water and a lower birth rate (fewer children not later) all are known to directly effect longevity, having more than doubled the human life expectancy in the past few hundred years.


This has been done in fruit flies. At least two labs have used selection to breed longer-lived flies.

Rose, M. Laboratory Evolution of Postponed Senescence in Drosophila melanogaster. Evolution (1984).

Luckinbill, L. et al. Selection for Delayed Senescence in Drosophila melanogaster. Evolution (1984).

We won't do this to humans, because eugenics is evil.

The "methuselah flies", as Rose calls them, live about twice as long. I don't know how long it would take to get them to live 10 times as long. In any breeding program you run up against the problem that eventually you'll run out of standing genetic variation to select from, and you have to wait for new mutations to appear.

But obviously selection can eventually lead to the evolution of much longer life. This has happened many times in evolutionary history, for example.


Is it possible to increase lifespan through controlled evolution? - Biology

Does evolution occur in rapid bursts or gradually? This question is difficult to answer because we can't replay the past with a stopwatch in hand. However, we can try to figure out what patterns we'd expect to observe in the fossil record if evolution did happen in bursts, or if evolution happened gradually. Then we can check these predictions against what we observe.

What should we observe in the fossil record if evolution is slow and steady?
If evolution is slow and steady, we'd expect to see the entire transition, from ancestor to descendant, displayed as transitional forms over a long period of time in the fossil record.

In fact, we see many examples of transitional forms in the fossil record. For example, to the right we show just a few steps in the evolution of whales from land-dwelling mammals, highlighting the transition of the walking forelimb to the flipper.

What would we observe in the fossil record if evolution happens in "quick" jumps (perhaps fewer than 100,000 years for significant change)?
If evolution happens in "quick" jumps, we'd expect to see big changes happen quickly in the fossil record, with little transition between ancestor and descendant.

In the above example, we see the descendant preserved in a layer directly after the ancestor, showing a big change in a short time, with no transitional forms.

When evolution is rapid, transitional forms may not be preserved, even if fossils are laid down at regular intervals. We see many examples of this "quick" jumps pattern in the fossil record.

Does a jump in the fossil record necessarily mean that evolution has happened in a "quick" jump?
We expect to see a jump in the fossil record if evolution has occurred as a "quick" jump, but a jump in the fossil record can also be explained by irregular fossil preservation.

Read more about competing hypotheses on the pace of evolution or delve into one of these ideas, punctuated equilibrium.

Learn more about transitional features in Understanding macroevolution through evograms, a module exploring five examples of major evolutionary transitions in the fossil record.


Is it possible to increase lifespan through controlled evolution? - Biology

The Stress-Vulnerability Model
of Co-occurring Disorders

  • What causes psychiatric disorders?
  • Why do some people develop a psychiatric disorder but others don't?
  • What affects the course of the disorder?

These are common questions raised by people with co-occurring disorders and their family members. The stress-vulnerability model provides answers to these questions. This model can help in understanding the causes of psychiatric disorders, how psychiatric disorders and addiction can influence each other, and how co-occurring disorders can be managed and treated together.

This information is also available as a PDF, which is included in the Hazelden Co-occurring Disorders Program.

If we are vulnerable to something, it means we're more likely to be affected by it. For example, some people might be biologically vulnerable to certain physical illnesses-such as heart disease or asthma. Maybe the disease runs in the family, or maybe something in our early life "set us up" for it.

Some people are biologically vulnerable to certain psychiatric disorders: bipolar disorder, major depression, schizophrenia, or anxiety disorders (panic, post-traumatic stress), for example. This vulnerability is determined early in life by a combination of factors, including genetics, prenatal nutrition and stress, birth complications, and early experiences in childhood (such as abuse or the loss of a parent). This is why some families are more likely to have members with a particular psychiatric disorder. Although vulnerability to psychiatric disorders is primarily biological in nature, people can take steps to reduce their vulnerability, including taking medication and not using alcohol or drugs. It's also worth noting that the greater a person's vulnerability to a particular disorder, the earlier it is likely to develop, and the more severe it may become.

Similarly, some people also have a biological vulnerability to developing an addiction: they are more likely to develop alcohol or drug abuse or dependence. This is why addiction, similar to psychiatric disorders, sometimes "runs in families."

What Are the Elements of the Stress-Vulnerability Model?

These two main areas -- biological vulnerability and stress -- are influenced by several other factors that people have some control over. These factors include

This means that by addressing these factors, people can reduce symptoms and relapses and improve the course of their co-occurring disorders.

Alcohol and Drug Use

Using alcohol or drugs can increase a person's pre-existing biological vulnerability to a psychiatric disorder. Thus, substance use can trigger a psychiatric disorder and lead to more severe symptoms and other impairments. Because most people with co-occurring mental and substance use disorders have a biological vulnerability to psychiatric disorders, they tend to be highly sensitive to even small amounts of alcohol and drugs.

Stress in the environment can worsen biological vulnerability, worsen symptoms, and cause relapses. Stress is anything that challenges a person, requiring some kind of adaptation. Serious stressful events include losing a loved one, getting fired from a job, being a victim of crime, or having conflicts with close people.

Stress is often associated with negative events, but positive events and experiences may be stressful as well. For example, performing well in school, getting a new job, starting a new relationship, having a baby, or being a parent all involve some degree of stress.

It is also possible for stress to be caused by not having enough to do. When people with co-occurring disorders have nothing purposeful or interesting to do, they tend to have worse symptoms and are more prone to using substances. So a lack of meaningful involvement in life-in areas such as work or parenting, for example-can be another source of stress.

Coping Skills

Developing coping strategies can help with handling stress and reducing its negative effects on vulnerability. Examples of coping skills include

Stress is a normal part of life. Effective coping enables people to be engaged in interesting, rewarding activities that may involve stress, such as working or being a parent. Coping efforts can make it possible for someone with co-occurring disorders to live a normal life without suffering the negative effects of stress.

Involvement in Meaningful Activities

Having something meaningful to do with one's time gives one a sense of purpose, and reduces the stress of having nothing to do. Meaningful activities can include:

Social Support

Another way to reduce the negative effects of stress on vulnerability is through social support, which comes from having close and meaningful relationships with other people. Supportive people can help in a variety of ways, such as

People who have good social support are less vulnerable to the effects of stress on their psychiatric disorder. Therefore, having strong social support enables people with co-occurring disorders to handle stress more effectively, and live a normal life.

Treatment Implications of the Stress-Vulnerability Model

Based on an understanding of the stress-vulnerability model, there are many ways to help people manage their psychiatric illness and co-occurring substance use disorder. In the broadest terms, the severity and course of a co-occurring mental health disorder can be improved by reducing biological vulnerability and increasing resiliency against stress.

Reducing Biological Vulnerability

Biological vulnerability can be reduced in two primary ways: taking medication and avoiding alcohol or drug use. Medication can be a powerful way of reducing biological vulnerability by helping to correct the imbalances in neurotransmitters (chemicals in the brain responsible for feelings, thinking, and behavior) believed to cause psychiatric disorders. By taking medication, the symptoms of a psychiatric disorder can be lowered and the chances of having a relapse can also be reduced.

Avoiding alcohol and drug use can reduce biological vulnerability in two ways. First, because substances affect the brain, using alcohol or drugs can directly worsen those vulnerable parts of the brain associated with psychiatric disorders. Second, using substances can interfere with the corrective effects of medication on vulnerability. This means that somebody who is using alcohol or drugs will not get the full benefit of any prescribed medications for his or her disorder, leading to worse symptoms and a greater chance of relapses.

Increasing Resiliency against Stress

It is impossible for anyone to live a life that is free of stress. However, there are many ways people can learn how to deal with stress more effectively, and to protect themselves from the effects of stress on worsening symptoms and causing relapses, including

Webinar
Focus on Integrated Treatment:
This webinar provides an overview of FIT and explains its role in providing the tools and training needed to become certified to treat clients with co-occurring disorders.
Professional Development

Hazelden offers many courses to help you expand your knowledge about alcohol and drug addiction and mental health disorders, including:


How cancer was created by evolution

The latest figures show just how distant a prospect victory is right now. In the US, the lifetime risk of developing cancer is 42% in men and 38% in women, according to the American Cancer Society. The figures are even worse in the UK. According to Cancer Research UK, 54% of men and 48% of women will get cancer at some point in their lives.

And cases are on the rise. As of 2015 there are 2.5 million people in the UK living with the disease, according to Macmillan Cancer Support. This is an increase of 3% each year, or 400,000 extra cases in five years.

Cancer is not only extremely pervasive, but also becoming more and more common

Figures like this show that cancer is not only extremely pervasive, but also becoming more and more common. But why will so many people develop the disease at some point in their lives?

To get to the answer, we must understand that cancer is an unfortunate by-product of the way evolution works. Large and complicated animals like humans are vulnerable to cancer precisely because they are large and complicated.

But even though it is evolutionary processes that have made cancer such a problem, it is also evolutionary thinking that is now leading to pioneering treatments that could stack the odds against cancer and in favour of our health.

To understand how cancer exists at all, we need to go back to a fundamental process that occurs in our bodies: cell division.

A cancerous cell breaks all the rules of controlled division that our other cells follow

We each started out when an egg and sperm cell met and fused. Within a few days, that egg and sperm had turned into a ball containing a few hundred cells. By the time we reach adulthood about 18 years later, those cells have divided so many more times that scientists cannot agree, even to the nearest few trillion, exactly how many cells our bodies contain.

Cell division in our bodies is very heavily controlled. For instance, when you were first growing your hands, some cells went through "cell suicide" &ndash a process called apoptosis &ndash to carve out the spaces between your fingers.

Cancer is also all about cell division, but with one important difference. A cancerous cell breaks all the rules of controlled division that our other cells follow.

"It is like they are a different organism," says developmental biologist Timothy Weil of the University of Cambridge in the UK. "The better that cell gets at dividing faster than its neighbours and gaining nutrients, the more successful it will be as a cancer, and the more likely it will survive and grow."

Healthy cell division is marked by control and restraint, but cancerous cell division is wild, uncontrolled proliferation.

"Adult cells are constantly under strict control," Weil says. "Basically cancer is a loss of control of those cells."

Cancer can only grow in this uncontrolled fashion if some of the genes that usually stop any accidental cell growth &ndash such as the p53 gene &ndash get mutated in the cancer cells.

If just a few survive they have the potential to rapidly multiply again and regrow the tumour

However, our bodies are pretty good at spotting these mutations. There are biological systems within us that step in to destroy most mutated cells before they can cause us harm.

We have several "corrective" genes which send instructions to kill any corrupted cells. "There's millions of years of evolution that's gone into this," says Charles Swanton of the Francis Crick Institute in the UK. "It's pretty good but it's not quite perfect."

The threat comes from the tiny number of corrupt cells that do not get fixed. Over time, one of these cells can grow and divide into thousands, then tens of thousands of cancer cells. Eventually there may even be billions of cells in a tumour.

This leads to a truly challenging problem. Once that initial corrupt cell has divided and multiplied into a tumour, a person will have cancer until every single one of the cancer cells has been obliterated. If just a few survive, they can rapidly multiply and regrow the tumour.

Cancer cells are not all alike: far from it. Whenever a cancerous cell divides, it has the potential to pick up new mutations that affect its behaviour. In other words, they evolve.

No two cancer cells in a tumour are the same

As the cells inside a tumour mutate, they become ever more genetically diverse. Then evolution goes to work to find the most cancerous ones.

Genetic diversity is "the spice of life, it's the substrate upon which natural selection acts", says Swanton. By this he means evolution by natural selection, first proposed by Charles Darwin in 1859.

Just like individual species &ndash humans, lions, frogs, even bacteria &ndash gain genetic variation over time, so too do cancer cells. "Tumours don't evolve in a linear manner," says Swanton. "They evolve in a branched evolutionary manner, which means that no two cells in a tumour are the same."

In effect, the cells of a tumour are evolving to become more cancerous. "Essentially we are dealing with branches of evolution that create diversity and that create fitness, and allow cell populations to survive therapy and ultimately outwit the clinician," says Swanton.

The fact that tumours are constantly changing their genetic makeup is one of the reasons why cancers are so hard to "kill".

It is for this reason that Swanton, and others in the field, take an evolutionary approach to tackling cancer. Swanton, who specialises in lung cancer, is both a clinician and a research scientist. His work has revealed something that he hopes will help create effective, targeted treatment.

Think of the evolution that goes on inside a cancer tumour as like a tree with many branches

Think of the evolution that goes on inside a cancer tumour as like a tree with many branches. At the base of the tree are the original mutations that triggered the tumour in the first place: mutations that should be shared by all of the cancer cells in the tumour.

In theory, a therapy that targets one of those base mutations should destroy every cell in the tumour. This is an approach that some therapies already use. For instance a drug called EGFR therapy targets lung cancer, and a BRAF inhibitor protein attacks the faulty gene which can lead to melanoma.

The trouble is, these therapies do not work as well as we might hope. Even in these targeted therapies, resistance often appears over time.

"It occurs because there will be one or more cells in the tumour branches that has a resistance mutation that allows it to outwit the therapy," Swanton says.

In other words, some of the branches of the cancer tree have evolved in a way that makes them less vulnerable to attack through the base mutation. They can dodge the therapy.

An average tumour might contain something like a thousand billion cancer cells. Some of those cells might well have evolved in a way that makes them immune to attack through a specific basal mutation.

Targeting three base mutations at the same time will "chop the trunk down" and destroy every single cell in the tumour

But what if a therapy targeted two of those basal mutations at the same time? Far fewer cells will have evolved in a way that makes them immune to both forms of attack.

Swanton and his colleagues crunched the numbers to see how many base mutations in the cancer "trunk" they would have to target simultaneously to ensure that they could successfully destroy every one of the cancer cells. Three was the magic number. Their calculations suggest that targeting three base mutations at the same time will "chop the trunk down" and destroy every single cell in the tumour.

However, this approach is not going to be cheap. To work, it requires the researchers to study a person's specific cancer to establish which base mutations their tumour has, so that the right cocktail of therapies can be applied.

"What we've come up with is an approach where we sequence tumours and produce the truncal antigens on a patient-by-patient basis," Swanton explains.

Colorectal cancer researcher Alberto Bardelli of the University of Turin in Italy, has also been using evolutionary theory as inspiration for a potential solution to overcoming drug resistance.

"I was very disappointed by the fact that all tumours became resistant," he says of his previous work. Now Bardelli has used the reality of drug resistance to develop a new anti-cancer therapy.

He begins by teasing out the resistant cancerous cells, which he calls "clones". Patients are given a particular drug therapy and then monitored to see when a particular cancerous "clone" rises to dominance in the tumour because it has developed drug resistance.

We use the tumour against itself&hellip it's a war of cancer clones

Then Bardelli stops treating the cancer with the drug. This removes the evolutionary pressure that allowed the clone to become so successful. Without that pressure, other types of cancer cell in the tumour also have a chance to flourish. They "fight back" against the dominant clone. In effect, the cancer effectively begins to war with itself.

When some of those other clones have gained ground, it is time to administer the drugs again, as these new clones should not yet have developed resistance. Bardelli calls it "the war of clones".

"We use clones against clones, we wait for the winners, then take out the pressure the drug. The winners at this point are unfit and start to disappear, and then others take over. So we use the tumour against itself.

"I want to use the portion of the cells that are not affected by the therapy to fight back the others."

For now we do not know if this tactic will work or not. His team is starting a clinical trial in the summer of 2016.

These evolutionary approaches may show great promise, but at the same time it is important to better understand the many triggers that can cause cancer in the first place.

In 2013 one of the biggest genetic studies took an important step forward in doing so. Researchers scoured cancer patients' genomes to look at "signatures" of the 30 most common cancer mutations.

It is important to better understand the many triggers that can cause cancer in the first place

These signatures represent small chemical changes to the DNA in cancers including lung, skin and ovarian cancer. Andrew Biankin, a surgeon at the University of Glasgow in the UK, was one of the researchers involved. He says it was possible to observe the "insult to the DNA" that left a tell-tale sign of the damage.

"In skin cancer like melanoma, we can see evidence of UV light exposure, in lung cancer can see a particular signature of smoking exposure," explains Biankin. "We can see evidence of there being an inherited inability to repair DNA."

As well as these known cancer signatures, the team could see unusual cancer-forming patterns where the cause was unclear. "There's [now] a lot of effort in trying to work out what these causes are," he says.

The core challenge for researchers like Biankin and Cancer Research UK, who funded the study, will be to understand exactly what leads to these types of genetic change.

While it is vital to understand the causes of cancer and to find new treatments, others stress that for now it is more important to focus on prevention. That is because there are known risk factors that contribute to cancer-causing mutations, such as smoking and sunburn.

Otis Brawley, chief medical officer at the American Cancer Society, says focusing on some of these risks could prevent many instances of cancer forming in the first place. He cites two startling statistics: in 1900 the age-adjusted death rate for cancer in the US was 65 per 100,000, but this had jumped to 210 deaths per 100,000 only 90 years later.

Tobacco is the single most preventable cause of death in the world

"If you have something that has increased that quickly over 90 years, there's something that causing it," says Brawley. "If you can remove the cause you can decrease the cancer."

In the US there has been a 25% decline in death rate in the last two decades. "More than half of that decline is driven by cancer prevention activities," says Brawley.

This points to the fact that some of the cancers that would previously have killed people had been prevented. Almost a third of death from cancer in the US has been attributed to cigarette smoking, for example. This makes tobacco "the single most preventable cause of death in the world", according to Cancer Research UK.

Although it is obviously good that death rates are falling, overall cancer diagnoses are on the rise.

There is a degree to which this is because certain cancers are now better diagnosed, and so cases are more likely to be identified and counted. This is true of prostate cancer, for instance.

But a more telling reason for the rise is that humans, on average, live a lot longer than they used to. "If you live long enough you will get cancer," says Biankin.

"If we decide that we all want to live to more than 70, then we have to accept that sooner or later we will get some sort of cancer," says Bardelli. It is inevitable because our cells have not evolved to maintain their DNA for as long as we now live, he says.

If we decide that we all want to live to more than 70 then we have to accept that sooner or later we will get some sort of cancer

Brawley goes even further, and says that everyone over 40 will get a mutation that can cause cancer at some point. That sounds alarming, but fortunately our natural defence mechanisms will usually stop the mutation in its tracks by destroying the mutant cell before it can grow into a full-blown tumour.

Even though the rise in cancer is an almost inevitable consequence of other improvements in our health, progress towards better treatments is continuing apace.

And peering back into how life works to "fight evolution with evolution" may well provide further breakthroughs. "Our host, our body has to make use of resources that have been growing for millions and millions of years," says Bardelli.

"There is hope. I have no doubt we will beat cancer, no doubt," he says. "Sometimes we fail because we don't identify the problem as it should be. It's nobody's fault, it's how science works."

Melissa Hogenboom is BBC Earth's feature writer. She is @melissasuzanneh on Twitter.


New Natural Selection: How Scientists Are Altering DNA to Genetically Engineer New Forms of Life

Before human beings wrote books or did math or composed music, we made leather. There is evidence hunter-gatherers were wearing clothes crafted from animal skins hundreds of thousands of years ago, while in 2010 archaeologists digging in Armenia found what they believed to be the world's oldest leather shoe, dating back to 3,500 B.C. (It was about a women's size 7.) For a species sadly bereft of protective fur, being able to turn the skin of cows or sheep or pigs into clothing with the help of curing and tanning would have been a lifesaving advance, just like other vital discoveries Homo sapiens made over the course of history: the development of grain crops like wheat, the domestication of food animals like chickens, even the all-important art of fermentation. In each case, human beings took something raw from the natural world&mdasha plant, an animal, a microbe&mdashand with the ingenuity that has enabled us to dominate this planet, turned it into a product.

The natural world has its limits, though. Tanned animal skin may make for stylish boots, motorcycle jackets and handbags&mdashsupporting an industry worth about $200 billion a year&mdashbut it's still animal skin. That would seem to be an insurmountable problem if you're one of the hundreds of millions of vegetarians around the world, or even just someone who worries about the environmental impact of raising tens of billions of animals for clothing and food. But it's not the animal skin that makes leather leather&mdashit's collagen, a tough, fibrous protein that is a major biological component of animal connective tissue, including skin. If there was a way to manufacture collagen alone, it might be possible to produce leather that even the most dedicated animal-rights activist could love.

And that's exactly what's happening on the eighth floor of the cavernous Brooklyn Army Terminal on New York's waterfront, where Modern Meadow has its labs and offices. There, the 60-person startup takes tiny microbes and edits their DNA&mdashthe genetic code that programs their behavior&mdashso they will yield collagen as a metabolic product, just as the yeast that brew beer create alcohol from grain sugar. The result is a microbiological factory, as the tweaked cells multiply in vats and the harvested collagen is processed. After a tanning procedure&mdashone more sustainable than that used in standard tanning, since there is no animal hair or fat to remove from the microbe-grown collagen&mdashwhat's left is a material that is biologically and chemically similar to conventional leather, save chiefly for the fact that no animals were harmed in its making. In fact, this biofabricated leather may be better than animal leather&mdashModern Meadow's microbes can produce collagen much faster than it would take to raise a cow or sheep from birth, and the company can work with brands to design entirely new materials from the cell level up. "It's biology meets engineering," says Andras Forgacs, the co-founder and CEO of Modern Meadow. "We diverge from what nature does, and we can design it and engineer it to be anything we want."

That is the promise of synthetic biology, a technology that is poised to change how we feed ourselves, clothe ourselves, fuel ourselves&mdashand possibly even change our very selves. While scientists have for decades been able to practice basic genetic engineering&mdashknocking out a gene or moving one between species&mdashand more recently have learned to rapidly read and sequence genes, now researchers can edit genomes and even write entirely original DNA. That gives scientists incredible control over the fundamental code that drives all life on Earth, from the most basic bacterium to, well, us. "Genetic engineering was like replacing a red light bulb with a green light bulb," says James Collins, a biological engineer at the Massachusetts Institute of Technology and one of synthetic biology's early pioneers. "Synthetic biology is introducing novel circuitry that can control how the bulbs turn off and on."

We can use that control to harness nature to our own ends and do so in a way that will help solve some of our most pressing sustainability challenges. Cells could be engineered to make meat in a lab, eliminating the need for environmentally intensive and often cruel factory farms. Bacteria could be manipulated to secrete oil, providing a truly renewable source of liquid fuel. Yeast could be designed to produce artemisinin, a vital antimalarial drug that in its natural form must be made from limited supplies of the sweet wormwood plant&mdashwhich, as it happens, is already being done. "What is at stake here is finding a way to make everything humans need without trashing our civilization," says Drew Endy, a synthetic biologist at Stanford University who helped launch the field. "We can transition from living on Earth to living with Earth."

Market-Driven Eugenics

The dawn of the Synthetic Age is not just the province of scientist-dreamers and Brooklyn startups. A 2016 Transparency Market Research report predicted that the synthetic biology market would grow from $1.8 billion in 2012 to $13.4 billion by 2019. Last year, synthetic biology companies took in $1 billion from investors&mdashincluding tech titans like Eric Schmidt, Peter Thiel and Marc Andreessen&mdashdouble the total from 2014. Even the giants of the fossil-fuel world have gotten in on the game&mdashExxon Mobil has a $600 million deal with Synthetic Genomics, a partnership that bore fruit in June when the company announced a major breakthrough in engineering strains of algae to produce oil for use in sustainable biofuels.

The true benefits&mdashand consequences&mdashof synthetic biology will come as scientists move from mimicking nature in the lab to redesigning it. Imagine plants that change color in the presence of explosives or microbes that can secrete the scent of a long-extinct flower. Picture a cell line that is immune to all bacteria and viruses, or even the 3 billion DNA base pairs of a human being's genome, fully synthesized in a lab. All of those projects are underway at various stages, and the last target&mdashwriting an entire human genome&mdashwould be an epochal achievement for science, potentially opening the door to re-engineering the human body itself, making us healthier, smarter, stronger. It's one of the goals of GP-write, an international project launched in 2016 by a group of synthetic biologists who want to stimulate the development over the next decade of technology that could synthesize the genomes of large organisms&mdashincluding humans. "Being able to write large genomes means moving from natural selection and artificial selection&mdashthink traditional plant and animal breeding&mdashto intentional design," says Andrew Hessel, distinguished research scientist at the design company Autodesk and one of the founders of GP-write.

If the idea of synthesizing an entire human genome alarms you, you're not alone&mdasheven some synthetic biologists, like Stanford's Endy, are wary of the notion. The researchers behind GP-write have made it clear that they have no intention of creating artificial people with their synthesized DNA rather, their work will be confined to synthesizing human cells, in an effort to better understand how the human genome works&mdashand, potentially, how to make it work better. But any attempt to engineer the genetic code of living beings raises ethical concerns&mdashfirst over safety, and even more so, over success. What happens if an engineered plant or animal escapes into the wild, where its impact on the environment would be hard to predict? Engineering human cells to eliminate deadly genetic disorders might seem straightforward, but where would we draw the line between treatment and enhancement? "We're developing powerful tools that are changing what it is to be human," says Jim Thomas, a researcher with the technology watchdog the ETC Group. "The worry is that you could have market-driven eugenics."

Of course, those ethical questions assume that synthetic biologists will be able to replicate a human genome&mdashand that's far from certain. Scientists have yet to fully synthesize the genomes of much simpler single-celled organisms like yeast, so it could take far longer than a decade to learn how to write the 20,000 or so genes in a human genome. And like all technologies moving from the lab to the real world, synthetic biology will need to compete with conventional products in the market and at scale. Over the past several decades, startups that employed the tools of synthetic biology to produce advanced biofuels burned through hundreds of millions of dollars in a mostly futile effort to beat cheap gasoline. But whether it happens in the near term or the long term, the science behind synthetic biology&mdashthe ability to read and write the code of life&mdashis already with us. And it's poised to re-engineer the world as we know it.

Synthetic Biology

Look out your window. Every bit of living matter you see&mdashthe tree bending toward the sun, the sparrow winging on the breeze, the person walking past&mdashoperates on the same genetic code, the nucleobases of DNA: cytosine (C), guanine (G), adenine (A), thymine (T). This is the programming language of life, and in its basics it hasn't changed much since it arose out of Earth's primordial ooze. Just as the English language can be used to write both "Baa, Baa Black Sheep" and Ulysses, so can DNA in all its combinations write the genome of a 2 mm long E. coli bacterium and a 30-meter-long blue whale . "The same DNA in humans is the same DNA in every organism on the planet," says Jason Kelly, the CEO of Ginkgo Bioworks, a synthetic biology startup based in Boston. "This is the fundamental insight of synthetic biology."

The language of DNA may have been written billions of years ago, but we learned to read it only in recent years. Sequencing DNA&mdashdetermining the precise order of the C, G, A and T&mdashwas first done only in the 1970s, and for years it was laborious and expensive. It took more than 10 years and about $2.7 billion for the scientists behind the Human Genome Project to complete their mission: the first full sequence draft of the genes that encode a human being. But thanks in part to technology advances driven by that public-private effort, the price of sequencing DNA has plummeted&mdashit now costs around $1,000 to sequence a person's full genome&mdasheven as the speed has multiplied, to little more than a day.

If that sounds familiar, it should&mdashthe same thing happened to the cost and speed of microchips over decades past, as Intel co-founder Gordon Moore predicted in the law that bears his name. And just as faster and cheaper microchips drove the computer revolution from the days of room-size mainframes through the dawn of the iPhone, so does cheap DNA reading&mdashand increasingly, writing&mdashmake possible the revolution of synthetic biology. "It wasn't merely that you could do it, but that the costs came down so much starting 15 to 20 years ago," says Rob Carlson, the managing director of Bioeconomy Capital. "The improvements were even faster than Moore's Law."

Carlson should know. The Carlson Curve, the biotech equivalent of Moore's Law, was named after him&mdashthough like many in the field, he doesn't care for the name. (Carlson preferred "intentional biology," but biologists demurred&mdashthey thought the term made it sound as if their work hadn't been intentional before.) Synthetic denotes fake and artificial, the imitation of natural&mdashthink synthetic fabrics like nylon and polyester&mdashbut that's not how most synthetic biologists view their craft. To Stanford's Endy, who helped launch the movement when he was at MIT more than a decade ago, synthetic biology is about understanding the messy process of life at the cellular level and above through the process of engineering it. "We don't know how to do it, so we try, and one learns by doing," says Endy.

There's a quote that synthetic biologists repeat like a mantra, from the great theoretical physicist Richard Feynman: "What I cannot create, I do not understand." Feynman didn't exactly say those words&mdashthe phrase was found on the physicist's blackboard at CalTech at the time of his death. But to synthetic biologists, it means that the process of editing and writing DNA&mdashengineering life&mdashis necessary for us to better understand how DNA works. To that end, scientists have worked to synthesize genomes&mdashmeaning writing and printing whole artificial genes, rather than copying existing DNA, as in cloning&mdashof organisms, starting with the simplest ones, in an effort to understand what the words in the genetic book of life really mean. An initial success came in 2010, when the geneticist Craig Venter&mdashwho helped lead the Human Genome Project&mdashand his colleagues created the first synthetic cell, writing the entire genome of a tiny bacterium called Mycoplasma mycoides and inserting it into the empty cell of another bacterium. (They nicknamed the cell Synthia.) That was a remarkable achievement in its own right, but in 2016 Venter and his team went one better, taking Synthia's genome and methodically breaking it down until they reached the minimum number of genes required to sustain life. By stripping life to its basics, researchers could discover what each gene actually did. "The aim is to make something simple, to remove complexity, so you can begin engineering," says Sophia Roosth, a historian of science at Harvard University and the author of the new book Synthetic: How Life Got Made.

As it turned out, even the world's simplest bacterial genome was more complicated than scientists might have suspected. Of the 473 genes in Venter's pared-down, synthetic cell, the functions of 149 were completely unknown. That's almost a third, which underscores how far scientists have to go before they can truly claim to understand the genetic code that we can now sequence so easily&mdashlet alone effectively synthesize the genomes of much bigger and more complex organisms. It brings to mind another Feynman quote&mdash"the difference between knowing the name of something and knowing something."

Rewriting the Book of Life

To actually know, scientists will need to sequence, synthesize and program vast amounts of genetic data. You design an organism, build it&mdashthrough DNA synthesis or through gene-editing tools like CRISPR&mdashtest it out in the lab and, hopefully, learn from the experiment. Then you do it again, and again, in a cycle called design-build-learn-test. In the case of Venter's synthetic cell, for instance, scientists would add or subtract a gene at a time and then look to see what happened to their organism. If the synthetic bacterium died, that was a pretty good sign that the gene in question was important. "That to me is the heart of engineering biology," says Nancy Kelley, another of the founders of GP-write.

But you'll only be able to learn as fast as you can design and build and test. That's why Carlson's Curve is so important. Think computer programming, which advances on a similar cycle. When Tom Knight, one of Jason Kelly's co-founders at Ginkgo Bioworks, was helping to build what would become the internet at MIT in the 1960s, he was programming on refrigerator-sized computers that required users to manually enter deck after deck of punched cards. It was slow and laborious&mdashand that was about the speed of biological programming until fairly recently. "We would spend an entire afternoon doing by hand site-directed mutagenesis that would enable you to change a single A to a T in the genome of a bacteria," says Kelly. "That's like spending an afternoon changing a bit from a zero to a one on a computer."

Today, as Kelly notes, "a guy at Facebook can create a new product in a single afternoon," simply because computers have gotten so much faster. We may never be able to program biology as fast as we can a computer&mdashin part because biology is made up of matter, however tiny, whereas computer code is just code&mdashbut we will keep getting faster. "Back in 2002 and 2003, it used to cost me $4 to press the DNA synthesis button once for one letter," says Endy. Now, says Emily Leproust, the CEO of San Francisco&ndashbased DNA synthesis startup Twist Bioscience, her company can synthesize a base pair&mdashthe essential building blocks of the DNA helix&mdashfor just 9 cents.

In the design-build-test-learn cycle of synthetic biology, Twist supplies the building materials. Labs and companies send orders for specific genes to Twist, and the company does the work of synthesizing them, printing tiny molecules of DNA on silicon. The turnaround time is a matter of weeks, and as Twist and other DNA synthesis companies get better, that will be shortened. As the barriers of cost and time fall, what is liberated is the imagination of synthetic biologists, who are able to rapidly try out ideas. Just as the dawn of the internet led to an array of tech startups in the 1990s&mdashsome of which are now pillars of the global economy, like Amazon and Google&mdashso the commercialization of DNA-writing technology is giving birth to a fresh industry. Apple Founder and CEO Steve Jobs, shortly before his death from cancer, told his biographer that "I think the biggest innovations of the 21st century will be at the intersection of biology and technology. A new era is beginning."

Many companies and investors are convinced that synthetic biology could revolutionize some of the fundamental ways we live and do business. Technologists at companies including Microsoft believe that DNA could even overtake silicon in our hard drives as a storage medium. The genetic code, after all, is really just a means to preserve and transmit information&mdashthe information of how a living thing works. DNA is an incredibly dense medium&mdashresearchers this year developed a method theoretically capable of storing all of the data in the world on a single room's worth of DNA&mdashand unlike existing physical recording mediums, there's no danger of it being made obsolete. Biology, after all, has been writing DNA for billions of years.

Twist has begun working with Microsoft to perfect the process of DNA storage, and in April the software company purchased 10 million strands of DNA from Twist as part of that agreement. "As much as the last century was about plastics, this century will be about biology," says Leproust.

At Ginkgo Bioworks, the biggest consumer of synthetic DNA on the planet, they can smell the future coming. Founded in 2008 by Kelly and four of his colleagues from MIT's pioneering synthetic biology program, Ginkgo designs customized living organisms&mdashengineered baker's yeast&mdashthat can produce flavors and fragrances that are usually derived from plants. Ginkgo has partnered with French perfume company Robertet to create a rose fragrance by extracting the genes from real roses, injecting them into yeast and then engineering the microbe's biosynthetic pathways to produce the smell of a rose&mdashwhich apparently smells just as sweet when emitted from a yeast. That might come as a surprise to some consumers who don't know that the active ingredient in their perfume came from engineered microbes. But it's worth noting that the yeast itself isn't a part of the perfume, and the rose oil it produces has a claim to be far more natural than any chemical substitute. "We said, What if instead of going into a field of roses to get rose oil, you can run a brewery?" says Kelly. "And instead of brewing beer, you brew rose oil? We develop those designed yeast using our platform, and we license it out to our customers."

Synthetic biologists won't be satisfied with simply copying existing forms of life they want to engineer something new, and even bring long-dead organisms back to life. Ginkgo is working on extracting DNA molecules from plant specimens preserved in herbariums, to synthesize the fragrances of flowers that have gone extinct, like an olive bush from the South Atlantic island of St. Helena that disappeared from the wild in 1994. The Bay Area startup Bolt Threads has engineered yeast microbes that can secrete spider silk, a material that is stronger than steel and yet extremely lightweight. Bolt has already used the spider silk thread to make ties, but the superstrong material could have a future in pharmaceutical products and the military. (The company is also an excellent example of why the decrease in the cost of DNA synthesis is so important&mdashit has gone through some 4,000 formulations to properly engineer yeast capable of making spider silk.) In the lab, Colorado State University biologist June Medford is working with the Defense Department (and its $7.9 million grant) to engineer plants that would turn white in the presence of a bomb. Medford imagines that the engineered plants&mdashwhich are likely years away&mdashcould be used in airport security lines, perhaps in place of multimillion-dollar wave scanners. "Plants have developed over 4 billion years to sense and respond to their environment," she says. "We identify a synthetic biology component that enables that and plug it into the natural infrastructure."

Infrastructure is an apt term. Right now, ours is powered mostly through minerals and petrochemicals, but synthetic biology offers the possibility of an infrastructure with built-in sustainability. As a farmer's field reliably demonstrates every spring, biology is renewable in a way that coal or oil or iron simply isn't. Biology is also simply very, very good at what it does, which is sustainable growth. All the plants on Earth, Endy says, harness 90 terawatts of energy, which he notes is about four and a half times the energy currently used by humanity. A biological cell can carry out complex operations far beyond the scope of our smartest artificial intelligence. "Biology is better at making small precise things than Intel is, and it makes more big physical stuff than car companies&mdashall in a sustainable way," says Kelly. A pine tree, for example, is infinitely more complex and has a longer life than a Lexus.

Looking into the future, synthetic biologists think they may be able to program cells to grow into almost anything. "Imagine your iPhone being grown from an engineered design, with cases made from synthetic leather and a screen that produces its own light," says John Cumbers, the founder of SynBioBeta and co-author of the forthcoming book What's Your Bio Strategy?

It's going to be a long time before we're harvesting iPhones in the fields. As cheap and as fast as DNA synthesis has gotten, it needs to be much cheaper and much faster. It may cost less than a dime to synthesize a single DNA base pair now, but Kelly points out that if a tech company like Facebook had to spend even a penny every time it changed a single bit in a software program, there would be no money left for anything else. "We're still in the IBM era of this technology," he says. DNA synthesis companies are limited in the length of DNA strands they can produce at a time&mdashTwist's maximum, for instance, is about 3,200 base pairs long. To put that in perspective, the entire human genome is roughly 3 billion base pairs long. That means researchers need to take those strands and link them together&mdashnot impossible, but hardly seamless either. "There's a messiness to biology, and engineering it is hard," says MIT's Collins. "It's a lot harder than we thought it would be."

Soldiers Who Don't Need to Eat

On May 10, 2016, nearly 150 synthetic biology experts met behind closed doors at Harvard Medical School to discuss launching what could be one of the most ambitious and consequential missions in the history of human science. The project's initial name, HGP-write, declared the scope of that ambition: to successfully synthesize an entire human genome before the next 10 years were up. HGP-write came under initial criticism for that first closed summit&mdashthough the organizers claimed the secrecy was because an as yet unpublished paper was being discussed at the meeting&mdashand the H was later dropped to take some of the emphasis off the human genome specifically and put more on the notion of simply accelerating the pace of DNA writing, just as the Human Genome Project massively accelerated DNA sequencing. But there's no doubt that many of the organizers hope that a mission to write human genes will be as galvanizing as reading them was. "We're humans, and we see through the lens of humanity," says Autodesk's Hessel. "This is the next grand challenge for synthetic biology."

GP-write hopes to raise $100 million for the project, though at its most recent meeting, in New York in May&mdashwhich was open to the public&mdashnot much actual funding had yet materialized. One exception was Columbia University's Harris Wang and New York University's Jef Boeke, who received a $500,000 grant from the Defense Department to study how human cells could be engineered to become self-sufficient nutrient factories. Early in their evolution, animal cells lost the ability to manufacture certain vitamins and essential amino acids, which we now need to get through our diet. But plant, fungi and bacteria cells are still capable of producing those nutrients through photosynthesis, and through borrowing those gene pathways, it might be possible to engineer human cells that could do the same. That would have an immediate benefit in reducing the cost of developing human cell lines used in laboratory studies, as scientists might not have to feed self-sufficient cells with serum. But it doesn't take a conspiracy theorist&mdashor a science fiction writer&mdashto picture how the Pentagon might put to use soldiers who don't need to eat. For his part, Wang imagines the possibility of phototrophic cells helping human beings survive the rigors of long-term space travel&mdashthough he wants to make it clear that he is not trying to engineer the perfect astronaut. "We could make quantum leaps in terms of the type of things that evolution would take a long time to develop, or might never do," says Wang.

The sensitivity around GP-write is a reminder that as synthetic biology moves from bacteria into the realm of the human, the accompanying ethical concerns will only grow. If we can synthesize a human genome, how long will it be before we're able to engineer ourselves&mdashor our offspring? A group of Chinese researchers shocked the science world in 2015 when they became the first to use the synthetic biology tool CRISPR to edit the genomes of human embryos, but just this year a major federal panel ruled that similar studies could be ethically allowable "for compelling reasons." But what would those reasons be? While few people might be against using the techniques of synthetic biology to eliminate genetic disorders or reduce disease, where do we draw the line between medicine and enhancement? The possibility that the rich could have first access to technology to "perfect" themselves and their children risks making political and economic inequality a concrete biological fact. Beyond what we might do to ourselves, how will the world change if many of the products that we now gather from the wild, or grow on farms, are instead engineered in biological factories? "The best time to have these conversations about a new technology is right before it becomes plausible," says Hank Greely, a bioethicist at Stanford. "Now is the time to talk about it."

And so we will, as the products of synthetic biology steadily migrate from the laboratory into the world around us. If the skepticism surrounding genetically modified foods is any lesson, that migration won't happen without a fight. According to a 2015 Pew Research Center poll, only 37 percent of the general public believes GM foods are safe to eat, compared with 88 percent of scientists. But while the burden of proof will be on the proponents of synthetic biology, it's worth keeping in mind that while the solutions are debatable, the existential environmental challenges our planet faces&mdasharound food, fuel and the climate&mdashare not. Right now, some 40 percent of the world's land is taken up for food production, which leaves less and less space for any other species&mdashand despite that, one in nine people still lacks enough to eat. Yet somehow we'll need to feed an additional 2 billion people by midcentury. The world may need to reach zero total carbon emissions as early as 2050 to escape dangerous climate change&mdashyet we've barely begun to stop the increase in global emissions, let alone ratchet them back, and 1.2 billion people still lack any access to electricity, renewable or not. The status quo will not get us to where we need to be.

Harvard's George Church is one of the giants of synthetic biology and a force behind the GP-write group. He's also the kind of bold scientist who makes bioethicists and environmentalists worry, by planning to resurrect the extinct wooly mammoth through gene editing and openly musing on the possibility of genetically enhancing human beings by making them invulnerable to disease. When Stephen Colbert had Church on The Colbert Report in 2012, the TV host asked the scientist: "How do you think your work will eventually destroy all mankind?" He was joking&mdashmostly.

Whether the kind of radical biological changes that scientists like Church envision should happen&mdashor ever will happen&mdashhe's right to note that the dangers go more than one way. "I am a critic of the uncritical precautionary principle," he says. "There are risks of doing nothing or going slowly." A radical age may demand radical solutions.


Darwin's theory of gradual evolution not supported by geological history, scientist concludes

Charles Darwin's theory of gradual evolution is not supported by geological history, New York University Geologist Michael Rampino concludes in an essay in the journal Historical Biology. In fact, Rampino notes that a more accurate theory of gradual evolution, positing that long periods of evolutionary stability are disrupted by catastrophic mass extinctions of life, was put forth by Scottish horticulturalist Patrick Matthew prior to Darwin's published work on the topic.

"Matthew discovered and clearly stated the idea of natural selection, applied it to the origin of species, and placed it in the context of a geologic record marked by catastrophic mass extinctions followed by relatively rapid adaptations," says Rampino, whose research on catastrophic events includes studies on volcano eruptions and asteroid impacts. "In light of the recent acceptance of the importance of catastrophic mass extinctions in the history of life, it may be time to reconsider the evolutionary views of Patrick Matthew as much more in line with present ideas regarding biological evolution than the Darwin view."

Matthew (1790-1874), Rampino notes, published a statement of the law of natural selection in a little-read Appendix to his 1831 book Naval Timber and Arboriculture. Even though both Darwin and his colleague Alfred Russel Wallace acknowledged that Matthew was the first to put forth the theory of natural selection, historians have attributed the unveiling of the theory to Darwin and Wallace. Darwin's notebooks show that he arrived at the idea in 1838, and he composed an essay on natural selection as early as 1842—years after Matthew's work appeared. Darwin and Wallace's theory was formally presented in 1858 at a science society meeting in London. Darwin's Origin of Species appeared a year later.

In the Appendix of Naval Timber and Arboriculture, Matthew described the theory of natural selection in a way that Darwin later echoed: "There is a natural law universal in nature, tending to render every reproductive being the best possibly suited to its condition…As the field of existence is limited and pre-occupied, it is only the hardier, more robust, better suited to circumstance individuals, who are able to struggle forward to maturity…"

However, in explaining the forces that influenced this process, Matthew saw catastrophic events as a prime factor, maintaining that mass extinctions were crucial to the process of evolution: ". all living things must have reduced existence so much, that an unoccupied field would be formed for new diverging ramifications of life. these remnants, in the course of time moulding and accommodating . to the change in circumstances."

When Darwin published his Origin of Species nearly three decades later, he explicitly rejected the role of catastrophic change in natural selection: "The old notion of all the inhabitants of the Earth having been swept away by catastrophes at successive periods is very generally given up," he wrote. Instead, Darwin outlined a theory of evolution based on the ongoing struggle for survival among individuals within populations of existing species. This process of natural selection, he argued, should lead to gradual changes in the characteristics of surviving organisms.

However, as Rampino notes, geological history is now commonly understood to be marked by long periods of stability punctuated by major ecological changes that occur both episodically and rapidly, casting doubt on Darwin's theory that "most evolutionary change was accomplished very gradually by competition between organisms and by becoming better adapted to a relatively stable environment."

"Matthew's contribution was largely ignored at the time, and, with few exceptions, generally merits only a footnote in modern discussions of the discovery of natural selection," Rampino concludes. "Others have said that Matthew's thesis was published in too obscure a place to be noticed by the scientific community, or that the idea was so far ahead of its time that it could not be connected to generally accepted knowledge. As a result, his discovery was consigned to the dustbin of premature and unappreciated scientific ideas."


2. Modes of Evolution

It is essential to understand that biologists recognize many ways that evolution can occur, evolution by natural selection being just one of them, although it is often held to be the most prevalent one. Evolution can also occur through genetic drift, mutation, or migration. It can also occur through sexual selection, which some consider to be a form of natural selection and others consider to be distinct from natural selection (the latter having been Darwin&rsquos 1859, 1874 view). Evolutionary theory, then, can be taken to be the study (including, but not limited to, mathematical models) of these and other modes of evolution.

To see why it makes sense to think of multiple modes of evolution, consider again one of the definitions of evolution presented above, where evolution is understood as &ldquoany change in the frequency of alleles within a population from one generation to the next&rdquo. With natural selection, the frequency of alleles that confer greater fitness would tend to increase over those which confer lesser fitness. Sexual selection would be the same, but with fitness understood strictly in terms of mating ability. With genetic drift, a form of evolution that involves chance (see the entry on genetic drift for explanation), there could be an increase in the frequency of alleles that confer greater fitness, an increase in the frequency of alleles that confer lesser fitness, or an increase in the frequency of alleles whose manifestation (if any) was neutral. If organisms migrate from one population to another, it is likely that there will be a change in the frequency of alleles in both populations. And if there is a mutation from one allele to another, then the frequency of alleles in the population will likewise change, albeit by a small amount. Distinguishing these different modes of evolution allows biologists to track the various factors that are relevant to evolutionary changes in a population.

The careful reader may have noted that the previous paragraph invoked probabilistic language: what tends to happen, what could happen, what is likely to happen. Indeed, mathematical evolutionary models today (see the entry on population genetics) are typically statistical models. This fact about evolutionary models has given rise to a debate in the philosophy of evolution over whether natural selection and genetic drift should be be understood as causes of evolution, as most biologists conceive them, or as mere statistical summaries of lower-level causes: births, deaths, etc. (The natural selection and genetic drift entries give more information about this debate). It is for this reason that this entry uses the more neutral phrase &ldquomodes of evolution&rdquo so as not to beg any questions under dispute between the causalist and the statisticalist.

Although there is widespread agreement that there are multiple modes of evolution, much contemporary work in biology and philosophy of biology has been focused on natural selection. Whether this focus is a good thing or not is in part what the debate over adaptationism is about. That is, do we have reason to think that natural selection is the most prevalent or most important mode of evolution? Should scientific methodologies be geared toward testing natural selection hypotheses or toward a variety of possible evolutionary modes? The focus on natural selection has also led to a large literature on the concept of fitness, given that population genetics&rsquo definitions and other definitions of natural selection typically invoke fitness a natural selection explanation of why X was more successful than Y might invoke X&rsquos higher fitness. What fitness means, what entities it applies to (genes, organisms, groups, individuals, types), what sort of probabilities it invokes, if any, and how it should be calculated, are all under philosophical dispute. There is also a large literature on conceptually and empirically distinguishing natural selection from genetic drift. Migration, mutation (as a mode of evolution), and sexual selection have received less attention from philosophers of biology.


Evolution of Language Takes Unexpected Turn

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It's widely thought that human language evolved in universally similar ways, following trajectories common across place and culture, and possibly reflecting common linguistic structures in our brains. But a massive, millennium-spanning analysis of humanity's major language families suggests otherwise.

Instead, language seems to have evolved along varied, complicated paths, guided less by neurological settings than cultural circumstance. If our minds do shape the evolution of language, it's likely at levels deeper and more nuanced than many researchers anticipated.

"It's terribly important to understand human cognition, and how the human mind is put together," said Michael Dunn, an evolutionary linguist at Germany's Max Planck Institute and co-author of the new study, published April 14 in Nature. The findings "do not support simple ideas of the mind as a computer, with a language processor plugged in. They support much-more complex ideas of how language arises."

How languages have emerged and changed through human history is a subject of ongoing fascination. Language is, after all, the greatest of all social tools: It's what lets people share and cooperate, divide labor, make plans, preserve knowledge, tell stories. In short, it lets humans be sophisticated social creatures.

One school of thought, pioneered by linguist Noam Chomsky, holds that language is a product of dedicated mechanisms in the human brain. These can be imagined as a series of switches, each corresponding to particular forms of grammar and syntax and structure.

The findings ɽo not support simple ideas of the mind as a computer, with a language processor plugged in.'Such a system would account for why, of the nearly infinite number of languages that are possible -- imagine, for instance, a language in which verb conjugation changes randomly it is possible -- relatively few actually exist. Our brains have adapted to contain a limited, universal set of switches.

A limited set of linguistic universals is exactly what was described by the late, great comparative linguist Joseph Greenberg, who empirically tabulated features common to language. He made no claims as to neurological origin, but the essential claim overlapped with Chomsky's: Language has universals.

If you speak a subject-verb-object language, one in which "I kick the ball," then you likely use prepositions -- "over the fence." If you speak a subject-object-verb language, one in which "I the ball kicked," then you almost certainly use postpositions -- "the fence over." And so on.

"What both these views predict is that languages should evolve according to the same set of rules," said Dunn. "No matter what the language, no matter what the family, if there are two features of language that are somehow linked together structurally, they should be linked together the same way in all languages."

That's what Dunn, along with University of Auckland (New Zealand) computational linguist Russell Gray, set out to test.

Unlike earlier linguists, however, Dunn and Gray had access to powerful computational tools that, when set to work on sets of data, calculate the most likely relationships between the data. Such tools are well known in evolutionary biology, where they're used to create trees of descent from genetic readings, but they can be applied to most anything that changes over time, including language.

In the new study, Dunn and Gray's team created evolutionary trees for eight word-order features in humanity's best-described language groups -- Austronesian, Indo-European, Bantu and Uto-Aztecan. Together they contain more than one-third of humanity's 7,000 languages, and span thousands of years. If there are universal trends, say Dunn and Gray, they should be visible, with each language family evolving along similar lines.

That's not what they found.

"Each language family is evolving according to its own set of rules. Some were similar, but none were the same," said Dunn. "There is much more diversity, in terms of evolutionary processes, than anybody ever expected."

In one representative example of divergence (diagram above), both Austronesian and Indo-European languages that linked prepositions and object-verb structures ("over the fence, ball kicked) tended to evolve preposition and verb-object structures ("over the fence, kicked ball.") That's exactly what universalism would predict.

But when Austronesian and Indo-European languages both started from postposition, verb-object arrangements ("the fence over, kicked ball"), they ended up in different places. Austronesian tended towards preposition, verb-object ("over the fence, kicked ball") but Indo-European tended towards postposition, object-verb ("the fence over, ball kicked.")

Such differences might be eye-glazing to people unaccustomed to diagramming sentences, but the upshot is that the two language families took opposite trajectories. Many other comparisons followed suit. "The things specific to language families trumped any kind of universals we could look for," said Dunn.

"We see that there isn't any sort of rigid" progression of changes, said University of Reading (England) evolutionary linguist Mark Pagel, who wasn't involved in the study. "There seems to be quite a lot of fluidity. That leads me to believe this isn't something where you're throwing a lot of parameter switches."

'What languages have in common is to be found at a much deeper level. They must emerge from more-general cognitive capacities.'Instead of a simple set of brain switches steering language evolution, cultural circumstance played a role. Changes were the product of chance, or perhaps fulfilled as-yet-unknown needs. For whatever reason, "the fence over, ball kicked" might have been especially useful to Indo-European speakers, but not Austronesians.

There is, however, still room for universals, said Pagel. After all, even if culture and circumstance shapes language evolution, it's still working with a limited set of possibilities. Of the six possible combinations of subject, verb and object, for example, just two -- "I kicked the ball" and "I the ball kicked" -- are found in more than 90 percent of all languages, with Yoda-style "Kicked I the ball" exceedingly rare. People do seem to prefer some structures.

"What languages have in common is to be found at a much deeper level. They must emerge from more-general cognitive capacities," said Dunn.

What those capacities may be is a new frontier for investigation. As for Dunn, his team next plans to conduct similar analyses on other features of language, searching for further evolutionary differences or those deeper levels of universality.

"This can be applied to every level of language structure," he said.

Images: 1) Mikul/Flickr. 2) Map of the geographic origin of languages analyzed in the study (Russell Gray). 3) Comparison of trends in Austronesian and Indo-European languages (Nature).

Citation: "Evolved structure of language shows lineage-specific trends in word-order universals." By Michael Dunn, Simon J. Greenhill, Stephen C. Levinson & Russell D. Gray. Nature, published online, April 14, 2011.


How old are the major human pathogens?

Apart from a few putative ancestral pathogens, including Helicobacter pylori [15], that might have co-speciated with their human host, the infectious diseases afflicting us were acquired through host jumps from other wild or domesticated animal hosts or sometimes from the wider environment. The timing of these events and the original source remains unclear in many cases.

The traditional view has been that many human pathogens emerged during the Neolithic revolution. The main arguments for an origin of human pathogens linked to agriculture are based on the proximity between traditional farmers with their livestock and the emergence of higher human population densities in stable settlements enabled by agricultural subsistence. High population density is indeed required by some epidemic diseases which could not have maintained themselves on scattered groups of hunter-gatherers [12]. This argument, however, neglects the fact that pathogens can evolve fast. Also, while the proximity of humans and livestock is conducive to host jumps, humans transmitted more diseases to domestic animals than they acquired, with tuberculosis in particular having probably jumped from humans to cattle rather than the other way around [16]. Finally, this argument also neglects the high burden of pathogens in wild populations, including in the great apes.

Ancient direct evidence is scant for pathogens, and historical records rarely allow unambiguous attribution of described symptoms to a disease. That being said, recent progress in sequencing technology and in particular the ability to generate sequences, if not complete genomes, from ancient samples has greatly improved our understanding of the age of the major human pathogens, often leading to unexpected results. Figure 1 summarises the current knowledge on the age of the seven current ‘major killers’, as well as plague, which was included due to its major impact in the past. While some of these estimates may need to be updated in the future after the emergence of new evidence, it is unlikely the general pattern will change much. Some human diseases are old (for example Plasmodium falciparum malaria) and others recent, such as HIV or, more surprisingly, measles. There is also no obvious pattern pointing to the Neolithic revolution as a strong driver for the emergence of human pathogens.

Age of emergence of significant infectious diseases impacting on human populations. The time of emergence for the various major diseases is based on a synthesis of published research. When known with some confidence, point estimates are provided for each disease together with error bars depicting uncertainty in the inferred estimates. Orange error bars depict higher uncertainty compared to red. The black trend line plots an increase in human population size through time (x axis) in the order of billions of people (y axis). Key events in human history are highlighted and annotated at the top. Main references used were: smallpox [27] influenza [28] HIV [29] tuberculosis [30,31,32,33] P. falciparum malaria [34, 35] hepatitis B [36] measles [37] plague [38, 39]


As Technology Gets Better, Will Society Get Worse?

Imagine that two people are carving a six-foot slab of wood at the same time. One is using a hand-chisel, the other, a chainsaw. If you are interested in the future of that slab, whom would you watch?

This chainsaw/chisel logic has led some to suggest that technological evolution is more important to humanity’s near future than biological evolution nowadays, it is not the biological chisel but the technological chainsaw that is most quickly redefining what it means to be human. The devices we use change the way we live much faster than any contest among genes. We’re the block of wood, even if, as I wrote in January, sometimes we don’t even fully notice that we’re changing.

Assuming that we really are evolving as we wear or inhabit more technological prosthetics—like ever-smarter phones, helpful glasses, and brainy cars—here’s the big question: Will that type of evolution take us in desirable directions, as we usually assume biological evolution does?

Some, like the Wired founder Kevin Kelly, believe that the answer is a resounding “yes.” In his book “What Technology Wants,” Kelly writes: “Technology wants what life wants: Increasing efficiency Increasing opportunity Increasing emergence Increasing complexity Increasing diversity Increasing specialization Increasing ubiquity Increasing freedom Increasing mutualism Increasing beauty Increasing sentience Increasing structure Increasing evolvability.”

We can test the “Increasing” theory by taking a quick trip up north, to an isolated area south of the Hudson Bay. Here live the Oji-Cree, a people, numbering about thirty thousand, who inhabit a cold and desolate land roughly the size of Germany. For much of the twentieth century, the Oji-Cree lived at a technological level that can be described as relatively simple. As nomads, they lived in tents during the summer, and in cabins during the winter. Snowshoes, dog sleds, and canoes were the main modes of transportation, used to track and kill fish, rabbits, and moose for food. A doctor who worked with the Oji-Cree in the nineteen-forties has noted the absence of mental breakdowns or substance abuse within the population, observing that “the people lived a rugged, rigorous life with plenty of exercise.” The Oji-Cree invariably impressed foreigners with their vigor and strength. Another visitor, in the nineteen-fifties, wrote of their “ingenuity, courage, and self-sacrifice,” noting that, in the North, “only those prepared to face hardship and make sacrifices could survive.”

The Oji-Cree have been in contact with European settlers for centuries, but it was only in the nineteen-sixties, when trucks began making the trip north, that newer technologies like the internal combustion engine and electricity really began to reach the area. The Oji-Cree eagerly embraced these new tools. In our lingo, we might say that they went through a rapid evolution, advancing through hundreds of years of technology in just a few decades.

The good news is that, nowadays, the Oji-Cree no longer face the threat of winter starvation, which regularly killed people in earlier times. They can more easily import and store the food they need, and they enjoy pleasures like sweets and alcohol. Life has become more comfortable. The constant labor of canoeing or snowshoeing has been eliminated by outboard engines and snowmobiles. Television made it north in the nineteen-eighties, and it has proved enormously popular.

But, in the main, the Oji-Cree story is not a happy one. Since the arrival of new technologies, the population has suffered a massive increase in morbid obesity, heart disease, and Type 2 diabetes. Social problems are rampant: idleness, alcoholism, drug addiction, and suicide have reached some of the highest levels on earth. Diabetes, in particular, has become so common (affecting forty per cent of the population) that researchers think that many children, after exposure in the womb, are born with an increased predisposition to the disease. Childhood obesity is widespread, and ten-year-olds sometimes appear middle-aged. Recently, the Chief of a small Oji-Cree community estimated that half of his adult population was addicted to OxyContin or other painkillers.

Technology is not the only cause of these changes, but scientists have made clear that it is a driving factor. In previous times, the Oji-Cree lifestyle required daily workouts that rivalled those of a professional athlete. “In the early 20th century,” writes one researcher, “walking up to 100 km/day was not uncommon.” But those days are over, replaced by modern comforts. Despite the introduction of modern medicine, the health outcomes of the Oji-Cree have declined in ways that will not be easy to reverse. The Oji-Cree are literally being killed by technological advances.

The Oji-Cree are an unusual case. It can take a society time to adjust to new technologies, and the group has also suffered other traumas, like colonization and the destruction of cultural continuity. Nonetheless, the story offers an important warning for the human race. The problem with technological evolution is that it is under our control and, unfortunately, we don’t always make the best decisions.

This is also the principal difference between technological and biological evolution. Biological evolution is driven by survival of the fittest, as adaptive traits are those that make the survival and reproduction of a population more likely. It isn’t perfect, but at least, in a rough way, it favors organisms who are adapted to their environments.

Technological evolution has a different motive force. It is self-evolution, and it is therefore driven by what we want as opposed to what is adaptive. In a market economy, it is even more complex: for most of us, our technological identities are determined by what companies decide to sell based on what they believe we, as consumers, will pay for. As a species, we often aren’t much different from the Oji-Cree. Comfort-seeking missiles, we spend the most to minimize pain and maximize pleasure. When it comes to technologies, we mainly want to make things easy. Not to be bored. Oh, and maybe to look a bit younger.

Our will-to-comfort, combined with our technological powers, creates a stark possibility. If we’re not careful, our technological evolution will take us toward not a singularity but a sofalarity. That’s a future defined not by an evolution toward superintelligence but by the absence of discomforts.

The sofalarity (pictured memorably in the film “Wall-E”) is not inevitable either. But the prospect of it makes clear that, as a species, we need mechanisms to keep humanity on track. The technology industry, which does so much to define us, has a duty to cater to our more complete selves rather than just our narrow interests. It has both the opportunity and the means to reach for something higher. And, as consumers, we should remember that our collective demands drive our destiny as a species, and define the posthuman condition.

Tim Wu is a professor at Columbia Law School and the author of “The Master Switch.” This is Part II in a series on technological evolution. Part I was “If A Time Traveller Saw A Smartphone.”__



Comments:

  1. Zolokora

    Competent :) message, it's entertaining ...

  2. Hlithtun

    Bravo, great thought

  3. Ellis

    What a graceful thought

  4. Mekledoodum

    Yes it is fantastic



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