Archives For biology

math prodigy

According to overenthusiastic hacks at Wired, scientists have recently developed a way to scan your brain to predict just how intelligent someone is or how good you’ll be at certain tasks. This sounds like the beginning of a dystopian nightmare, rather than an actual field of research, that will end up with mandatory brain scans for everyone to “facilitate an appropriate job function” in some dark, gray lab in front of medical paper pushers, true. But it only sounds like this because the writer is more interested in page views than the actual study, which really has nothing to do with one’s intelligence but actually tested whether you could identify someone by scanning how this person’s brain is wired. Rather than trying to develop IQ tests in a box, the researchers put the theory that your brain wiring is so unique that getting a map of it could identify you every bit as well as a fingerprint, to the test. Not surprisingly, they found that a high quality fMRI scan of your brain at work performing some standard tests can definitely be used to identify you.

All right, that’s all fine and well, after all, the fMRI scan is basically giving you insight into unique personalities, and no two people’s brains will work the same way. But where exactly would this whole thing about measuring intelligence come into play? Well, the concept of fluid intelligence, mentioned only three times in the study, was brought up as an additional avenue of research in light of the findings and revolves around the idea that certain parts of the brain having a strong connection will make you notably better at making inferences to solve new problems. Unlike its counterpart, crystallized intelligence (called Gc in neuroscience), fluid intelligence (or Gf) is not what you know, but how well you see patterns and come up with ideas. Most IQ tests today are heavily focused on Gf because it’s seen as a better measure of intelligence and the elaboration on what exactly the fingerprinting study had to do with predicting Gf was an extended citation of a study from 2012 which found a link between the lateral prefrontal cortex’s wiring to the rest of the brain and performance standardized on tests designed to measure Gf in 94 people.

Here’s the catch though. Even though how well your lateral prefrontal cortex talks to the rest of your brain does account for some differences in intelligence, much like your brain size, it really only explains 5% of these differences. Current theory holds that because your prefrontal cortex functions as your command and control center, what Freud described as the ego, a strong link between it and several other important parts of the brain will keep you on task and allow you to problem-solve more efficiently. Like a general commanding his troops, it makes sure that every other relevant part of your mind is fully engaged with the mission. But even if that theory is right and your preforntal cortex is well wired in a larger than median brain, close to 90% of what you would score on an IQ test can come down to level of education and other factors that generally make household income and education a better predictor of IQ scores than biology. Although in many ways it’s not that accurate either because style of learning and culture also play a role. All we can conclude is that the interplay between Gf, Gc, and education is very complex.

We should also take note of one study of popular theories of biological contributors to Gf which spanned 44,600 people and found no evidence that a combination of fMRI maps has predictive power when it comes to IQ points. In other words, we have a lot of ideas that seem plausible as to the biological origins of intelligence, but because our brains are very plastic, we are not all on a level playing field when it comes to the amount and quality of education we receive, and even our longest-running efforts for accurate Gc assessments have shown that we’re really bad at it, studies that claim predictive powers when it comes to our IQs using brain scans of 100 college students or fewer are extremely likely overselling their results. Not only that, but even when the studies do actively oversell, they still claim to explain only a tiny fraction of the score differences because they recognize how small and homogeneous their data sets really are. Not only do we not have an fMRI based tests for intelligence, we’re not even sure it’s possible. But those facts bring in far, far fewer page views than invoking kafkaesque sci-fi lore in a pop sci post…


When we think of ancient biological killers, we typically think of a Black Plague or a smallpox, an often recurring disease that wipes out millions of people and has been recorded since humanity started recording things. The plague killed more than a third of all Europeans in outbreaks from the fall of Rome while smallpox killed well over a billion people over the last 10,000 years. What rarely gets brought up in this pantheon of ancient killers, however, is cancer. It’s been with us a very long time, found in Egyptian mummies over 4,000 years old and named by Greek doctors puzzled by patients who died of “crab-like growths” as they were described, from which we get the disease’s name. But cancer doesn’t just affect us. It kills all living things. Even dinosaurs got tumors because cancer isn’t one disease but abnormal cell growth that is often fatal. If you’re a complex multicellular organism, chances are that there’s a cancer you can develop in time.

One of the most common alt med tropes employed to convince you to buy some new snake oil preaches that frequent cancer diagnoses are a result of our world becoming too polluted and a toxic cocktail of Cthulhu-knows-what circulating through your tissues is to blame. In reality, the reason why so many people get cancers today is because humans are living longer than ever, and are armed with the technology and knowledge to catch more varieties of it earlier, allowing them to subdue it and extend their lifespans even further. In fact, someone I personally know is a survivor of three cancer diagnoses, each a different type, and each was cured with outpatient surgeries. Just a few decades ago, this person would’ve been diagnosed too late and die swiftly even after surgery and chemotherapy, and it’s very likely that with age, there will be yet another cancer diagnosis because cancer is degenerative. The longer you live and the more cells are in your body, the more chances there are for a tumor to spawn after a botched cell division.

But it seems that no one told that to our pachyderm friends, who, despite being large and with fairly long lifespans, have cancer mortality rates half to a fifth of ours. How? Is their blood full of chemo drugs? Not exactly. Their secret weapon against cancers is their genome. Instead of a single copy of the gene encoding the protein p53 like we do, they have 38 in 20 versions. Since this is a protein used to suppress tumor growth, it’s critically important for fighting cancer during its first and most vulnerable stage. More versions of it means better ability to recognize growths that could turn cancerous and a chance to destroy all affected cells earlier. Elephant cells prune such mutations so aggressively, it’s difficult for a new tumor to take hold and this results in their much lower susceptibility to the disease. Given that we’re currently experimenting with medical gene therapy, a hypothetical pop sci afficionado might wonder, could we engineer our very own versions of p53 encoding genes to create a similar resistance to cancers and deal our decisive blow to nature’s murderous defect that’s plagued us since the dawn of complex life?

Sadly, probably not. These p53 variants evolved in elephants against types of tumors that often affect them and which went through millions of years of trial and error in pachyderms, not in us, which means that whether our own gambit to follow this strategy would be successful is unclear at best. Instead, humans could more easily adopt the biochemical strategy employed by naked mole rats, which uses p53 alongside several other mechanisms, including a special sugar, that simply prevent cells from clumping together, breaking up cancerous tumors as a side-effect. It’s a more viable method of combating earliest stage cancers and wouldn’t require inserting some dozen new genes into our DNA, a cocktail of drugs could change how existing genes work. We should continue to study the elephants’ genome to see if we can actually figure out a way to be more proactive with our own evolution to help resist cancer, but for now, we need to take what certainly is a very neat little tidbit of information and keep in mind that anyone in the media who tells us that we could just edit our genes to be more like a pachyderm’s — which we all know will happen sooner rather than later nowadays — is using coming book science for attention…


Anti-vaccine activists would have us believe that autism is the result of some sort of undefined, or scary sounding toxicity and should be cured by a gluten-free diet and detoxification typically conducted by a profiteering quack. However, the real scientific evidence points to genetics and brain development, meaning that no one develops autism or turns autistic, but is born this way and will fall at some point along the spectrum when the condition can be diagnosed. Recently, another study provided additional evidence for this theory by comparing how modified skin cell cultures taken from those with autism, reverted into stem cells, and induced to grow into micro brains developed to skin cells from their non-autistic parents, subjected to the same treatment. Right away, the researchers noted an over-abundance of inhibitory neurons which created the roadblocks to forming necessary connections for sensory and social input processing.

While this isn’t confirmation that this is in fact what causes autism, it’s a substantial step toward identifying the culprits. It also narrowed down the gene responsible and gave the researchers a good idea for how to control its expression. While some pop sci outlets trumpet this as work we can use to develop a cure for autism, I’m not so sure that it’s so simple. After all, autism isn’t a structural disorder in which an excess of inhibitory neurons blocks important functions and pills or even gene therapy would suddenly turn autistic individuals into neuro-typical ones. With their brains affected from birth, their lives have been built around their neurons compensating for all the neurotransmitter dead ends. It would take many years for their brains to re-wire themselves and fashion a new personality. And while those with severe autism would greatly benefit, would this be a desired, or even an ethical treatment for high functioning autistic people?

If autism shapes how you see the world and you have always had it, yes, it can make life really confusing and difficult. But when one learns to overcome, to recognize one’s problems and find coping mechanisms, the journey has made this person who he or she is today. It’s tempting, in the words of autism quacks to “fix” them, but considering how integral autism has been to how they became who they are, the “fix” in question would mean undoing a lifetime of learning, and in some way undoing what they are today for the ability to better process certain stimuli, social interactions, and better emotional coping skills. Again, for low functioning autistic people, there are arguments in favor of the benefits outweighing the risk, but for those who’ve learned to see this condition as a part of who they are and can easily function on their own, even benefiting a little from some of its positive side effects, being “cured” won’t always be the best choice…

woman on bench

Once in a while, the internet remembers random things, such as a woman who wanted to trim the male population by at least 90% and use the survivors as breeding stock to reduce gender inequality across the world. While MRAs believe that this is what all feminists secretly want and most people understand that this is little more than a joke that went too far and has absolutely zero chance of happening, ever, all of the online discussions on the subject have focused on a trip down the histrionics-laden minefield of gender politics instead of a relevant scientific issue that should be front and center. Sure, being one of the few males left on Earth and given a life filled with relative luxury and constant sex sounds like the plot of a particularly wishful porn film which I’m sure has been made a few hundred times by now. But would it actually work? What’s the consequence of eliminating up to 99% of men from the gene pool? Well, it could very likely doom our species in the long run, even with heavy reliance on artificial insemination and gene therapy. We thrive thanks to variety, and reducing our genetic diversity will only harm us.

Let’s say that 90% of men are somehow culled. With about 10 women for every remaining man we’d quickly end up with the same problem as Iceland worldwide. In just a few generations, the attractive stranger with whom you’re flirting is likely your half-sibling. Sure, you can curate who gets to reproduce and how, but the sheer lack of new male genes will quickly have you trying to fight math. Artificial insemination using same sex donors is possible and has been done, but it’s still a very touchy, expensive process that doesn’t always work. Women in poverty or in remote, undeveloped parts of the world are going to have extremely limited access to this resource and women in wealthy nations will be looking at high costs and failure rates. Nature got really, really good at this whole reproduction thing over 3.5 billion years and re-inventing the wheel is not an easy feat. Today, the best we can do with tried and true technology is successful about 15% of the time per implanted zygote on average. After just ten generations, there’s going to be a very serious threat of a genetic bottleneck which spells evolutionary doom for any organism.

An even more base, but still relevant question in the face of us no longer being able to just out-breed our way through genetic defects and weaknesses as we do today, is what about women who want monogamous, long-term heterosexual relationships? That’s close to 90% of those on the planet in this post-male apocalypse world. Instead of having a boyfriend or a husband they just plain want, they’re now on waiting lists among rationed men who also can’t have any sort of meaningful relationship. While more women than men admit to same-sex fantasies, and acting on them, you might end up with artificially high same-sex pairings among women simply out of emotional and physical necessity. It’s one thing if you’re homosexual and have your choice of a partner everywhere you look. But if you’re not, your choices are to get on a waiting list for some person to whose gender you have a strong innate attraction, pair up with a same sex partner to release some stress until you can’t do it anymore, or be lonely. Again, there are good reasons why nature prefers a 50/50 ratio between the sexes, one of which is more choices in mating.

For better or worse, the survival of humanity depends on having plenty of men available, and a significant amount of genetic diversity. Look at every successful species in history. They thrived in enormous numbers because they reproduced efficiently and had many mates available on a moment’s notice. Small, inbred populations nearly always die out because they lack the genetic diversity and numbers to absorb a change in diet, or the environment, or new diseases to come out on the other end as strong as ever. Humans survived a supervolcanic eruption which left an uncomfortably small population that might have dropped to as few as 10,000 individuals, awful plagues, and an ice age. Had we become too dependent on over-structured breeding systems, or had our species grown far too sex-lopsided, we would’ve went extinct. So an idea involving a reduction of up to 99% of one sex shouldn’t just be met with political and social objections, but it should be first dismissed from the most important point of all: that of evolutionary biology.

alien bacteria

We’re using far too many antibiotics. That has been the cry from the FDA and the WHO for the last several years as more and more antibiotic-resistant strains have been found after they had colonized or killed patients. Of course these bacteria aren’t completely immune to our arsenals of drugs, they’re just harder to kill with certain antibiotics or require different ones, but a rather small, yet unsettling number, have required doctors to use every last antibacterial weapon they had available to even make a dent in their populations. There’s not much we can do because in effect, we’re fighting evolution. The more antibiotics we throw at the bacteria, the more chances we give for resistant strains to survive and thrive. Doctors are starting to prescribe less and the pressure on farmers to stop prophylactic use of antibiotics is mounting, but we’re still overdoing it and the problem is growing and in need of some very creative new solutions.

Enter a genetic engineering technique known as CRISPR-Cas9 which replaces DNA sequences that short snippets of RNA are encoded to identity with ones provided by scientists. It’s not new by any means, but this is the first time it has been used in an evolutionary experiment intended to stem the rise of antibiotic resistance. Israeli researchers essentially gave bacterial colony an immunity to a virus, but at the cost of deleting genes which gave it antibacterial resistance. The bacteria happily propagated the immunity as they grew while maintaining the new weaknesses to antibiotics which were only marginally effective on them before. There’s a real advantage for the bacteria to propagate this new mutation because the virus to which it was now immune was lethal, acting as the greater selective pressure, and the susceptibility to antibiotics just wasn’t an important factor, so the bacteria acted like it got a fair deal.

Even better, edits were made by a specially engineered virus, meaning you can, in theory, just infect bacteria-prone surfaces with it and demolish their antibiotic resistance, right? Well, yes, it would be possible. However, the researchers worry that new antibiotic resistant mutations can still evolve and that there’s no way to prevent the bacteria’s genetic drifts from accepting genes for viral immunity while holding on to its existing antibacterial mechanisms. But this technique is still useful for reducing the number of resistant bacteria or targeting strains with very well known resistance mechanisms to allow doctors to use existing antibiotics. Ultimately, what will help the most would be more research into new antibiotics, curtailing their use in doctors’ offices for any viral infection regardless of the patients’ complaints, and eliminating preventative use of animal antibiotics on farms. Still, research like this can still help us identify new resistant strains and give us a fighting chance to slow them down while we find new ways to fight them.

See: Yosef, I., et. al. (2015). Temperate and lytic bacteriophages programmed to sensitize and kill antibiotic-resistant bacteria PNAS DOI: 10.1073/pnas.1500107112

lab mouse

While studying what effect cell division has on cancer risk, a team of scientists decided to make mice that that produced excess levels of a protein called BubR1 and got results that seem way too promising at first blush. Not only were the engineered mice a third less likely to develop lung and skin cancers after exposure to potent carcinogens than control animals, but they had twice the endurance, lived 15% longer, and were less than half as likely to develop a fatal cancer. So what’s the catch? Well, there is none. It’s as if an over-expression of BubR1 is a magical elixir of good health and longevity. This doesn’t mean that this protein couldn’t become our most potent weapon against cancer with enough study or that it must have some sort of side-effect, which is entirely possible since too little BubR1 in humans is associated with premature aging and some forms of cancer, but this is a signal to proceed with optimistic caution.

Mice may have a lot of similarities to humans from a genetic standpoint, but they are a different species so what works well in mice may not always work as well in humans. Likewise, if we really wanted to be sure of the results, we’d have to test them on thousands of humans over decades, which is a massive undertaking in logistics alone. And since testing the protein modifications in humans would be such a major effort, the researchers need to know exactly how BubR1 does all the wonderful things it does, breaking down its role by chemical reaction and testing each factor on its own. The work may take decades to complete but if it’s correct, we may have found a way to extend and improve our lives in a humble protein. Combined with other ongoing work, there’s some very real science behind extending human lifespans and modifying our genomes for the better. I just hope we don’t get a little too carried away and treat editorials treating BubR1, gene therapy on a massive scale, and cell reprogramming technology as just around the corner with the necessary healthy skepticism, since the research is by no means complete…

See: Baker, D., et. al. (2012). Increased expression of BubR1 protects against aneuploidy and cancer and extends healthy lifespan Nature Cell Biology DOI: 10.1038/ncb2643

trilobite fossil

A while ago, creationists in South Korea persuaded textbook publishers to start removing entire chapters discussing proof for evolution in a move I likened to an overzealous and very dishonest prosecutor in court demanding that the judge refuse to admit evidence exonerating defendants simply because he would lose his case if such evidence were introduced. After a campaign by scientists with the relevant credentials, the South Korean Ministry of Education and Technology decided to formally review the creationists’ complaints and told them that science classes won’t be factually neutered at their request. Dismissing their arguments about dinosaurs being the starting lineage for birds as vague and invalid, the ministry did agree that a chapter about the evolution of horses was lacking in proper scientific rigor. But whereas the creationists tried to excise the chapter completely, the ministry said that the chapter should be rewritten with a more current picture of how horses evolved. In other words, their solution to creationist’s complaints of poor evidence is to have textbook publishers update the books with better science.

Of course no science will ever be good enough for creationists when it comes to biology, but it’s the right approach. If the proof presented in the textbooks isn’t compelling enough, we should be presenting better and more accurate evidence rather than bow to the Nirvana fallacy espoused by so many creationists. If we don’t know how every molecule in living things interacts with every other molecule, something we can never know for certain unless we were to manifest Laplace’s Demon and ask it some questions, it doesn’t mean that the other 95% of the theory isn’t a solid body of facts and has to be discarded. After all, you don’t rewrite an entire term paper if you find out you misspelled a word, or quoted something incorrectly. You fix the mistake and continue, revising along the way until you get a more accurate body of work. But to the fundamentalist mindset, that’s cheating. They’re used to a text they believe hasn’t changed for thousands and thousands of years — don’t tell them that it was rewritten numerous times and was edited by a self-appointed group that rejected more than a hundred parts and pieces of its first drafts — and when we correct our theories with better facts, they think we’re changing our story.

And yes, we are to an extent but our goal isn’t consistency, it’s accuracy, whereas to a religious adherent, perceived consistency means that the text must be accurate in a twist on the ad hoc, ergo prompter hoc line of reasoning. No one changed the holy book, therefore it must be true in the first place and when science revises its ideas, it must mean that the ideas were flawed from the start, otherwise they wouldn’t need correcting. And again, there’s a point there because few big ideas have been only expanded; many have been outright rewritten. Newton’s work was not replaced by general relativity, as popularly claimed. Without Newton, there would be no general or special relativity in the first place, and without Darwin’s natural selection and Mendel’s punnet squares, genetics wouldn’t have the kind of context that lets us decipher genomes to the extent we can today. We can also cite atomic theory and electromagnetism as examples of science that was updated rather than rewritten. But these are the exceptions. The aether gave way to mostly empty space, plate tectonics turned geology on its head, miasmas and the four humors fell to germ theory, ancient astrology lost the metaphysics and became astronomy, etc.

Where we see progress, however, the fundamentalists see heathens who either lack the proper spiritual guidance to see the truth, the way, and the light, or nefarious heretics who only want the righteous to falter in their beliefs and abandon their faith, constantly changing their story when caught on a mistake or missing something important from their theories. This is why they seldom even bother to understand what the theories they so fiercely reject actually say, going so far as to constantly use an argument that actually provides evidence for evolution as a criticism of it if not just blithely dismissing it as fairy tales for adults as compared to the eternal truth of a talking snake and a naked woman dooming humanity to mortality and disease. Why bother learning the science if it’s just going to change? Seeing the massive flaws in this kind of reasoning, those in charge of education and scientific advancement in South Korea defaulted to the science, prone to change as it may be, but ground in proof, evidence, and able to revise itself as new facts come to light rather than the kind of intellectual cowardice that believe it’s just fine and dandy to censor the evidence it doesn’t like, and then prey on the subsequent factual vacuum.

Every time an experiment manipulating evolution hits the news, there’s always an eager throng of people who insist that the very fact that the biologists intervened and steered the forces of selection or mutations to doing the experiment means that we now have proof of a designed involved in evolution. Just take yesterday’s study on the possible emergence of multicellularity. According to the creationist crowd, if the biologists didn’t trigger the selective influences on the yeast, it would’ve remained the same and their meddling is therefore proof that without an external force, multicellularity wouldn’t have happened. Remember the study cited by Lehrer in his indictment of scientists’ seemingly slow progress? That’s exactly where it applies. Just because a biologist shook a beaker or changed a few genes to see what will happen according to the rules of evolution today isn’t proof that someone else also shook the beaker or changed a few genes billions of years ago, but it’s a rather neat and tidy story that’s easy to digest and hence it gets cited by those who are looking to justify a belief. It’s a backward and very self-centered approach, one that essentially promotes a two-tiered fallacy as a fact.

An applicable old cliché would be the one often used by creationists regarding a paining and a painter. If they see a painting, someone must have painted it since paintings don’t paint themselves. Therefore, since we’re not seeing stones turn into bacterial film out of the blue, someone must have created life. Airtight logic, right? Well, no, not at all. We know that paintings have a painter because we’ve seen painters make paintings. If we doubt a painting’s origins, we could always perform a chemical analysis on them and see that yes, it’s canvas with paint on it and we know that there’s a group of painters out there who do similar work. We can even track down the original painter of a more recent work and ask her to replicate her efforts. With life, matters are much less cut and dry because we’ve never seen a designer or an architect of living things. How do we confirm that living things are made rather than self-organizing? Where do we find the designer? No, in our hearts and in a spiritual universe all around us are not valid answers because they don’t pinpoint a culprit we could ask about the creation of life. And just because scientists did something interesting in the lab doesn’t mean that the very same experiment also happened in nature, much less that a hyper-intelligent being was behind it.

Having dealt with the non-sequitur we can now move on to the argument by assertion on which this entire line of thinking is based. Just like all intelligent design talking points, which are now living well past their sell by date and never actually worked, this one relies on asserting that there must be an entity capable of creating living things and that this entity is singular. This proposition alone requires a few hundred lines of evidence to establish in any way, shape or form, and merely asserting that there’s a singular designer is not proof. If your goal is to work backwards from the standpoint that some unnamed designer (or you could just say save both the time and the trouble and say God since this "designer" facade isn’t fooling anyone), created all life and we have to work backwards form this premise, the assertion that manipulating evolution for experiments is proof of your deity makes sense. But that’s not a valid point with which to start. We have to work from what we know onwards, otherwise we’re just deluding ourselves by inventing ways to wedge evidence into a predetermined conclusion. Under this pretense, a scientist tweaking evolution the lab has to be proof that a deity had to have done something similar in the past because if he didn’t, then the chain of events don’t match what we want to believe happened. That’s not a reasonable or logical argument. It’s just wishful thinking.

Sometimes I can only sympathize with the kind of frustrating setbacks experienced by biologists. Whereas an entire area of STEM disciplines can rely on formulas and basic theory to get them at least close to where they need to be, biology seems to change its mind on a dime, and what seem like very straightforward and simple ideas can end up grinding to a screeching halt when scaled up beyond a few cells. From promising research into greatly increasing lifespan to countless potential cancer therapies, some of the failed efforts by biologists make me wonder if working in the discipline ever feels like battling Murphy’s Law. The reason I say this has to do with a just published study citing a failure to implant reprogrammed stem cells from an organism’s own body, thereby protecting them from becoming a target for the subject’s immune system as they try to repair the targeted tissues and organs. It turns out that activating the signals that encourage stem cells to develop new structures sets off the immune response and the seemingly friendly cells are now seen as pathogenic.

Whoops. The problem, it seems, lies with two genes, Zg16 and Hormad1. During a period in which a fetus is developing the distinction between its own tissues and that of foreign entities, these genes may be turned off while in the reprogrammed stem cells they’re active. As the stem cells try to grow into new shapes, the body’s defenses see these cells as intruders because they’re trying to differentiate and form structures when internal chemistry has turned off this kind of radical development. Forget about being able to internally grow new arms and legs; the cell cultures trying to diversify into them will be annihilated by your immune system. While there’s data to suggest that your stem cells could conceivably be used to grow a new, mature heart or a lung or a liver and implanted back in with minimal fears of a rejection, using your own body’s processes to help out wouldn’t work and the technology needed to make it would have to be that much more complex than it is now. Now, it’s not that this finding completely eliminates the foundation for the key ideas behind regenerative medicine. This setback just tells scientists that there’s much more we need to know to make the process work and warns of the potential for more complications and problems down the road. Biology is just finicky like that.

This is partially why my last take on life extension and radical medicine focused on machinery rather than a biological answer. Every individual is somewhat unique and after billions of years of evolution, we have living things so bizarrely and intricately messy that changing something within them is fiendishly complex. Machine parts are mass produced and can be customized to work around and with biological limitations. We can use them to help build new organs and provide scaffolding and structure for developing stem cells, and one day, maybe even build new organs from bio-compatible materials that won’t be actively attacked by T cells, or with several mutations down the line develop tumors. So when something breaks and wears down, we can throw in new organs and joints to whatever extent biology will let us. But our cells are certainly not just plug-and-play as some popular science journals and overly eager scientists hoped, and we need to make sure that we are as thorough as possible with new clinical ideas and don’t take our conclusions as automatically correct, even if they simply build on the fundamentals of existing theories. And this experiment is just a reminder that we do not know nearly as much as we sometimes tend to think and have a very long time before we can really wield our knowledge of biology’s building blocks to do truly amazing things with our bodies from the bottom up.

Zhao, T., et al. (2011). Immunogenicity of induced pluripotent stem cells Nature DOI: 10.1038/nature10135

Oh concern trolls, those wonderful commenters who try their hardest to put up disclaimer after disclaimer that they’re not at all disagreeing with you but they just have some questions which oddly enough happen to sound an awful lot like the kind of talking points mounted to attack a solid scientific idea, where would science blogs today be without them? They provide not only material for blog posts but a showcase of why it’s still necessary to keep explaining the basics in post after post and how no matter how many times you explain something, a contingent of passionate zealots will always be there to J.A.Q. around before they lose their threads halfway to show their original intent, or just plain state it at their conclusion. Here’s a great example of pseudo-profound questions in a comment to an old post of mine in which I show why evolution is a repeatable science. Note all the pleas that you’re not reading the questions of a creationist at the beginning, followed by… questions I’d expect to find at one of Bill Dembski’s pontifications, questions such as…

Even if there are random repeatable mutations, which I don’t deny; how many of them are usable and beneficial to the organism? If species have been evolving over the past 100 million years, shouldn’t there be overwhelming samples of transitional fossils, instead of a random breaking edge one here and there? We should be finding these things all over, in every continent, even in our own back yards.

So he won’t deny that repeatable mutations do exist but yet must preface the question with a conditional? That seems a little odd. Why would you place a conditional statement on something you don’t deny? Anyway, we’re well aware that beneficial mutations happen rarely, representing maybe a few percent of all mutations at best while the vast majority are negligible or benign, and another small percentage are actively harmful. But since over millions of years they happen trillions of times, they’re going to occur and be selected towards on a pretty regular basis. Evolution is all about numbers. It needs just that half a percent success rate to keep going and the overwhelming amount of genetic dead ends is the cost of evolving. As for the transitional fossils, we really do find them all over the place, and we can even predict where they’ll be found based on what we discover about the overall evolutionary timeline of our planet. Though in the purest sense, since organisms change on a constant basis, every fossil is a transition to something else or a dead end so this question is irrelevant and moot. Of course our commenter with questions about evolution doesn’t seem to understand speciation, which would explain the now ancient canard about transitional fossils.

Genetic drift and the inability to mate, doesn’t necessarily change a species into a new species, because there are physical restrains involved like size and appeal. Polar and Grizzly [bears] aren’t different species but two vastly different breeds within the same species.

Um, no. They’re related species, having branched off from the same ancestor, but until very recently, they lived in different environments and did not interact with each other. They still don’t by in large, and declaring them to be the same species seems a lot like creationists insisting that simply because two species look alike, they must be one and the same. Now, granted, the process of defining species is not perfect, but that’s because a perfect and clean separation between two species only exists on paper. Nature is much messier than that so we have to go by basic guidelines, like whether the populations mate with each other on a regular basis. And since we’re on the subject of speciation, what pray tell are breeds? They’re even more arbitrary, based on very cursory examinations of an animal’s morphology. Plus, here’s a funny thing. Since we’ve been separating our closest animal companions, dogs, into many separate and wildly different breeds, are they now a different or distinct species from wolves? By creationist logic, we’d have to say that dogs are actually just wolves, but yet, their populations are separate and some breeds of dogs could never mate with others because of the major differences in sizes and new pressures in sexual selection. Again, nature is rather messy.

Science cannot “prove” the past, because time is a specific, relative variable. The past can only be believed, not proven. If a person won’t believe solid evidence like yesterday’s newspaper[s], then that’s up to them.

I’m not going to sugarcoat it. That’s just an inane statement. If scientists can show that a particular creature in a fossil existed a certain amount of time ago with carbon or radiometric dating, they proved something about a world that existed in the past. End of story. If by a forensic examination I can trace the timeline of an event that happened a hundred years ago, I would’ve proven a number of facts. Even more plainly, if I go to a junkyard of the far future and dig up an old Zune player to show befuddled youths of the mid 21st century that yes, a rather long time ago there was an attempt to make an MP3 player which was not an iPod, I would’ve proven a factual statement about the past. Not believing solid evidence on a personal whim doesn’t seem like some scientific deficiency to me, more of a personality trait. And this statement seems like a post-modernist epistemological quip in which “everything’s like, only your opinion man.” Of course it’s a setup for the appeal you were probably expecting since the very beginning of this thinly disguised treatise…

I wonder how us, humans here on our little planet, in our little solar system, in our little galaxy can conclude from our tiny perspective that we know how the universe was formed, that a higher being, God doesn’t exist and couldn’t have been involved in creating this universe.

Define what you mean by God, identify the signs of involvement and how we know they’re real signs of his and only his involvement in the creation of the universe, explain how the universe was created, present your proof for it in terms of tangible data, and when you actually have a question that can be discussed with real science and real evidence rather than appeals to ignorance, we can discuss this. Until then, this is little more than yet another, perhaps quadrillionth, edition of the “I don’t know, ergo God” argument.