Archive for the ‘Evolution’ Category
Interesting. In my meme-oriented view, the internet would be an emergent phenomenon of memes, drawing in more and speeding up their evolution. And, of course, the most successful of those memes would (by definition) capture the attention of the greatest number of people. That’s quite a fertile environment for meme evolution—and of course it’s attractive by (more or less) necessity/definition: the most successful memes are the most attractive, so the Internet, which allows more or less free evolution, would quickly (in human terms) evolve to a high level of addictiveness.
Or maybe not. But it’s clear that the entire Internet is a creation built of memes. That’s what the whole thing is—nothing but memes (in the Richard Dawkins sense). And it’s clear that the Internet (i.e., the memes that comprise it) is evolving rapidly—just look at the Internet’s underlying technology as one group of its memes and see the rapid advance there—and that’s mainly, I would think, because the environment is uncontrolled. That is, it’s not a medium where the big content makers totally predominate: we are all on-line, and networks have developed that quickly draw the attention of the Internet denizens to things of greater interest (thus the origins of its addictive nature). Those networks are all the various link-exchange sites of whatever level—even news stories now include many hyperlinks. So this network of connections surfaces things more quickly, thus allowing more rapid memetic evolution.
It all sort of hangs together, doesn’t it? What we’re seeing and a part of (and a part of us if I’m right that one’s identity is constructed from memes) is a meme Cambrian Explosion.
Very interesting, given my low-carb way of eating. John Upton writes in the Pacific Standard:
In a Western world of plentiful crop cultivation, packeted convenience, and overconsumption, carbohydrates can be a curse. The sugar in today’s doses is often toxic, and plentiful servings of carb-rich wheat, rice, and corn can conspire with it to fuel plagues of obesity and diabetes.
But in worlds inhabited by our distant ancestors, before agriculture and production lines and Cap’n Crunch, carbs delivered charitable bursts of energy that weren’t so easy to find. It’s not difficult to imagine how evolution ensured that mammals came to perceive sugar as delicious. But now science is unlocking secrets about this hardwired allure of carbs that goes beyond their obviously alluring flavor.
Our mouths possess a subtle sense—one that’s unlike taste or smell. It’s linked to signaling pathways that recognize the presence of sugars, even sans flavor, and trigger a cerebral response. The response doesn’t just reward our carb consumption with gratifying deliciousness and dopamine. It green-lights the burning of additional energy and improves our physical performance.
Research published four years ago, for example, showed that even rodents with no sense of sweetness showed a glutton-like preference for sugary foods over similarly-caloric proteins. The brains of these taste-stunted rats still released dopamine when sugar was consumed, just as a normal rat’s brain would after chowing down on a cupcake. A body of research dating back to 2008 has shown that merely gargling carbohydrate solution during exercise can boost performance.
To test whether this mysterious carb-detecting sense activated parts of the brain that are independent of those that detect sweetness, New Zealand researchers put healthy volunteers into MRIs. The volunteers were instructed to pinch a device with a particular force whenever a cross was lit up in front of their eyes. During some of the tests, the volunteers swished solutions containing maltodextrin, a relatively flavorless type of sugar, in their mouths. In others, a flavor-matching but sugar-free placebo was used. . .
Continue reading. Perhaps Taubes was wrong about the insulin, but he seems to have been right to be suspicious of carbs.
Fascinating answer at the top.
Fascinating article, and it’s worth noting that global warming will bring more tropical diseases to the US, particularly in the Southeast, where climate is (so far) humid. Indeed, mosquitoes carrying dengue fever are already here, I believe. And Ed Yong explains well how difficult it is to stop malaria:
The meandering Moei river marks the natural boundary between Thailand and Myanmar. Its muddy waters are at their fullest, but François Nosten still crosses them in just a minute, aboard a narrow, wooden boat. In the dry season, he could wade across. As he steps onto the western riverbank, in Myanmar, he passes no checkpoint and presents no passport.
The air is cool. After months of rain, the surrounding jungle pops with vivid lime and emerald hues. Nosten climbs a set of wooden slats that wind away from the bank, up a muddy slope. His pace, as ever, seems relaxed and out of kilter with his almost permanently grave expression and urgent purpose. Nosten, a rangy Frenchman with tousled brown hair and glasses, is one of the world’s leading experts on malaria. He is here to avert a looming disaster. At the top of the slope, he reaches a small village of simple wooden buildings with tin and thatch roofs. This is Hka Naw Tah, home to around 400 people and a testing ground for Nosten’s bold plan to completely stamp out malaria from this critical corner of the world.
Malaria is the work of the single-celled Plasmodium parasites, and Plasmodium falciparum chief among them. They spread between people through the bites of mosquitoes, invading first the liver, then the red blood cells. The first symptoms are generic and flu-like: fever, headache, sweats and chills, vomiting. At that point, the immune system usually curtails the infection. But if the parasites spread to the kidneys, lungs, and brain, things go downhill quickly. Organs start failing. Infected red blood cells clog the brain’s blood vessels, depriving it of oxygen and leading to seizures, unconsciousness, and death.
When Nosten first arrived in Southeast Asia almost 30 years ago, malaria was the biggest killer in the region. Artemisinin changed everything. Spectacularly fast and effective, the drug arrived on the scene in 1994, when options for treating malaria were running out. Since then, “cases have just gone down, down, down,” says Nosten. “I’ve never seen so few in the rainy season—a few hundred this year compared to tens of thousands before.”
But he has no time for celebration. Artemisinin used to clear P. falciparum in a day; now, it can take several. The parasite has started to become resistant. The wonder drug is failing. It is the latest reprise of a decades-long theme: We attack malaria with a new drug, it mounts an evolutionary riposte.
Back in his office, Nosten pulls up a map showing the current whereabouts of the resistant parasites. Three colored bands highlight the borders between Cambodia and Vietnam, Cambodia and Thailand, and Thailand and Myanmar (Burma). Borders. Bold lines on maps, but invisible in reality. A river that can be crossed in a rickety boat is no barrier to a parasite that rides in the salivary glands of mosquitoes or the red blood cells of humans.
History tells us what happens next. Over the last century, almost every frontline antimalarial drug—chloroquine, sulfadoxine, pyrimethamine—has become obsolete because of defiant parasites that emerged from western Cambodia. From this cradle of resistance, the parasites gradually spread west to Africa, causing the deaths of millions. Malaria already kills around 660,000 people every year, and most of them are African kids. If artemisinin resistance reached that continent, it would be catastrophic, especially since there are no good replacement drugs on the immediate horizon.
Nosten thinks that without radical measures, resistance will spread to India and Bangladesh. Once that happens, it will be too late. Those countries are too big, too populous, too uneven in their health services to even dream about containing the resistant parasites. Once there, they will inevitably spread further. He thinks it will happen in three years, maybe four. “Look at the speed of change on this border. It’s exponential. It’s not going to take 10 or 15 years to reach Bangladesh. It’ll take just a few. We have to do something before it’s too late.”
Hundreds of scientists are developing innovative new ways of dealing with malaria, from potential vaccines to new drugs, genetically modified mosquitoes to lethal fungi. As Nosten sees it, none of these will be ready in time. The only way of stopping artemisinin resistance, he says, is to completely remove malaria from its cradle of resistance. “If you want to eliminate artemisinin resistance, you have to eliminate malaria,” says Nosten. Not control it, not contain it. Eliminate it.
That makes the Moei river more than a border between nations. It’s Stalingrad. It’s Thermopylae. It’s the last chance for halting the creeping obsolescence of our best remaining drug. What happens here will decide the fate of millions.
THE WORLD TRIED TO eliminate malaria 60 years ago. . .
I wonder how those who deny evolution explain the development of resistance to pesticides and antibiotics. From an evolutionary point of view, it’s simple: organisms that are vulnerable die without reproducing, but in a population there’s enough genetic diversity to (almost always) result in some who are less affected. These go on to reproduce, with offspring also less affected. Any that are totally unaffected leave a lot of similar progeny, so soon we say “the mosquitoes have become resistant to DDT.” And evolutionarily, it’s easy to understand. But how do non-evolutionists explain it? and the genetic changes in the immune population?
Things always seem to be more complex than expected as one delves more deeply into them. Take genes, for example: Michael White writes in Pacific Standard:
Today, DNA is central to modern biology, but scarcely a century ago biologists were debating whether or not genes actually existed. In his 1909 textbook on heredity, Danish botanist Wilhelm Johannsen coined the term gene to refer to that hereditary “something” that influences the traits of an organism, but without making a commitment to any hypothesis about what that “something” was. Just over a decade later, a prominent biologist could still note that some people viewed genes as “a convenient fiction or algebraic symbolism.”
As the century progressed, biologists came to see genes as real physical objects. They discovered that genes have a definite size, that they are linearly arrayed on chromosomes, that individual genes are responsible for specific chemical events in the cell, and that they are made of DNA and written in the language of the Genetic Code. By the time the Human Genome Project was initiated in 1988, researchers knew that a gene was a segment of DNA with a clear beginning and end and that it acted by directing the production of a particular enzyme or other molecule that did a specific job in the cell. As real things, genes are countable, and in 1999 biologists estimated that humans had “80,000 or so” of them.
Yet, when the dust from the Human Genome Project cleared, we didn’t have nearly so many genes as we thought. By the latest count, we have 20,805 conventional genes that encode enzymes and other proteins. Our inflated gene count, though, wasn’t the only casualty of the Human Genome Project. The very idea of a gene as a well-defined segment of DNA with a clear functional role has also taken a hit, and as a result, our understanding of our relationship with our genes is changing.
One major challenge to the concept of a gene is the growing evidence that many genes are shapeshifters. Instead of a well-defined segment of DNA that encodes a single protein with a clear function, we should view a gene as “a polyfunctional entity that assumes different forms under different cellular states,” according to University of Washington biologist John Stamatoyannopoulos. While researchers have long known that genes are made up of discrete subunits called “exons,” they hadn’t realized until recently the degree to which exons are assembled—like Legos—into sometimes thousands of different combinations. With new technologies, biologists are cataloging these various combinations, but in most cases they don’t know whether those combinations all serve the same function, different functions, or no function at all.
Our concept of a gene is also challenged by the fact that . . .