If a newborn baby is too large or a woman's pelvis too narrow, it can be dangerous or deadly.

In theory, these are the sorts of characteristics that evolutionary pressures might make less common over time.

And yet, as researchers point out in a study published December 5 in the journal Proceedings of the National Academy of Sciences, obstructed labor caused by these traits still occurs pretty frequently (3-6% of births worldwide, according to an analysis of World Health Organization data).

The researchers conclude that there are certain evolutionary factors working against each other to keep these rates high. But more controversially, they conclude that more Cesarean section (C-section) births could be changing the balance of these factors and increasing the rates of obstructed labor. Still, there's reason to be skeptical about how much we know here.

In the paper, the researchers explain that competing pressures may cause these high rates of obstructed labor in the first place. On the one hand, higher birth weights and brain sizes are advantageous to newborns, right up until they are too big to fit through the birth canal. At the same time, since the genes that affect the size of the human pelvis come from both men and women and the researchers think there may be advantages to not developing ever-wider hips, that space hasn't become constantly wider to support larger babies.

The modern change that they predict is that C-sections make it easier to pass on the genes that would account for a small birth canal, potentially increasing rates of these potentially dangerous births.

According to a model the researchers created, they predict that C-sections may have caused these cases of obstructed labor to become 10 to 20% more common since roughly the 1950s, going from affecting about 30 out of every 1,000 births to affecting 33-36 out of every 1,000 births. (They don't actually know whether these rates have gone up, but they expect that if their model is correct, they have.)

"Without modern medical intervention such problems often were lethal and this is, from an evolutionary perspective, selection," Philipp Mitteroecker, a theoretical biologist at the University of Vienna and lead author of the study, told the BBC.

But of course, showing evolutionary changes in a short time span — about 60 years — is very difficult. Most evolutionary change occurs on scales of thousands or even millions of years, though in small populations it can happen more quickly. In addition, it's hard to know if obstructed labor is in fact becoming more common at all, and if so, it's even harder to know if that is strictly the result of C-sections.

What the data shows

C-sections have been a part of the human birth process for thousands of years. Greek mythology, ancient Hindu and Egyptian texts, Chinese etchings, and Roman history includes references to these types of births. But the modern era of safe and common C-sections began much more recently, after the development of antibiotics and after births in hospitals became the norm.

But the majority of C-sections do not occur because of obstructed labor, meaning that a rise in the number of C-sections doesn't necessarily mean these rates have gone up.

If obstructed labor occurs in 3% of births (or, if rates have increased, 3.3-3.6%), that still only accounts for a very small percentage of all of the C-sections performed. In the US, close to a third of all births happen by C-section. (Researchers say that ideally, these rates should be closer to 19%.) Many C-sections are the result of medical necessity caused by factors like obesity and diabetes. Others have to do with obstetrics ward policies or — perhaps — financial incentive or fear of malpractice lawsuits. In other words, obstructed labor is not the main factor here.

So are C-sections changing evolution? Maybe.

The researchers here simply say that their model can explain why obstructed labor persists as part of the human condition and they say it predicts how C-sections could make this more common.

It's certainly possible, likely, that a change in the way large numbers of people give birth has some effect on humanity.

"It would never occur to me that cesarean sections would not have an effect," biological anthropologist Karen Rosenberg tells The Daily Beast. "The idea that human behavior affects our evolution is a central idea in understanding of evolution. All kinds of things — when we cook our food, when we share food, when we build shelters — everything we do as cultural animals has the potential to affect our biology."

But for now, we don't even know that obstructed labor is becoming more common. There's probably some effect or multiple effects that C-sections are having on humanity, but without more data, we can't specifically say what they are.

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Forensic science has become a mainstay of many a TV drama, and it’s just as important in real-life criminal trials. Drawing on biology, chemistry, genetics, medicine and psychology, forensic evidence helps answer questions in the legal system. Often, forensics provides the “smoking gun” that links a perpetrator to the crime and ultimately puts the bad guy in jail.

Shows like “CSI,” “Forensic Files” and “NCIS” cause viewers to be more accepting of forensic evidence. As it’s risen to ubiquitous celebrity status, forensic science has become shrouded in a cloak of infallibility and certainty in the public’s imagination. It seems to provide definitive answers. Forensics feels scientific and impartial as a courtroom weighs a defendant’s possible guilt – looking for proof beyond a reasonable doubt.

But the faith the public and the criminal justice system place in forensic science far outpaces the amount of trust it deserves.

For decades, there have been concerns about how the legal system uses forensic science. A groundbreaking 2009 report from the National Academy of Sciences finally drew the curtain back to reveal that the wizardry of forensics was more art than science. The report assessed forensic science’s methods and developed recommendations to increase validity and reliability among many of its disciplines.

These became the catalyst that finally forced the federal government to devote serious resources and dollars to an effort to more firmly ground forensic disciplines in science. After that, governmental agencies, forensic science committees and even the Department of Defense responded to the call. Research to this end now receives approximately US$13.4 million per year, but the money may not be enough to prevent bad science from finding its way into courtrooms.

This fall, the President’s Council of Advisors on Science and Technology (PCAST) released its own report on forensic science. It’s a more pronounced acknowledgment that the discipline has serious problems that require urgent attention. Some scientific and legal groups are outraged by or doubtful of its conclusions; others have praised them.

As someone who has taught forensic evidence for a decade and dedicated my legal career to working on cases involving forensic science (both good and bad), I read the report as a call to address foundational issues within forensic disciplines and add oversight to the way forensic science is ultimately employed by the end user: the criminal justice system.

Is any forensic science valid?

The President’s Council of Advisors on Science and Technology recognized ongoing efforts to improve forensic science in the wake of the 2009 NAS report. Those efforts focused on policy, best practices and research around forensic science, but, as with any huge undertaking, there were gaps. As PCAST noted, forensic science has a validity problem that is in desperate need of attention.

PCAST focused on what’s colloquially termed “pattern identification evidence” – it requires an examiner to visually compare a crime scene sample to a known sample. PCAST’s big question: Are DNA analysis, bite marks, latent fingerprints, firearms identification and footwear analysis supported by reproducible research, and thus, reliable evidence?

They were looking for two types of validity. According to PCAST, foundational validity means the forensic discipline is based on research and studies that are “repeatable, reproducible, and accurate,” and therefore reliable. The next step is applied validity, meaning the method is “reliably applied in practice.” In other words, for a forensic discipline to produce valid evidence for use in court, there must be (1) reproducible studies on its accuracy and (2) a method used by examiners that is reproducible and accurate.

Among the forensic science they assessed, PCAST found single-sourced DNA analysis to be the only discipline that was valid, both foundationally and as applied. They found DNA mixture evidence – when DNA from more than one person is in a sample, for instance from the victim and the perpetrator, multiple perpetrators or due to contamination – to be only foundationally valid. Same with fingerprint analysis.

Firearms identification had just the potential for foundational validity, but the research that could support it hasn’t been done yet. Footwear analysis lacked studies even showing potential for foundational validity. And bite mark analysis has a low chance of achieving any validity; the PCAST report advised “against devoting significant resources” to it.

All these types of evidence are widely used in thousands of trials each year. Many additional cases never even go to trial because this supposedly definitive evidence seems damning and compels defendants to plead guilty. But the lack of reliable science supporting these disciplines undermines the evidence which, in turn, undermines criminal convictions.

Risks of lacking validity

When forensic methods are not validated but nevertheless perceived as reliable, wrongful convictions happen.

For example, the field of forensic odontology presumes that everyone has a unique bite mark. But there’s no scientific basis for this assumption. A 2010 study of bite marks from known biters showed that skin deformations distort bite marks so severely that current methods of analysis could not accurately include or exclude a person based on the pattern left by their teeth.

In 1986, Bennie Starks was convicted of rape and other crimes after forensic odontology experts testified he was the source of a bite mark on the victim. In 2006, DNA test results showed Starks could not have been the perpetrator. Starks spent 20 years in prison for a crime he did not commit because of faulty evidence from an unreliable discipline. More recently, the Texas Forensic Science Commission recommended a flat-out ban on bite mark evidence.

Like in Starks’ case, questionable forensic evidence plays a significant role in at least half of overturned convictions, according to the Innocence Project. Once a verdict comes in, it becomes a Sisyphean task to undo it – even if newly discovered evidence undermines the original conviction. It’s next to impossible for people once convicted to get their cases reconsidered.

At the moment, only two states (Texas and California) permit a defendant to appeal a conviction if the scientific evidence or the expert who testified is later discredited. More laws like these are needed, but it’s politically a hard sell to grant more rights and avenues of appeal to convicts. So even if the science is undermined or completely discredited, a prisoner is often at the mercy of a court as it decides whether to grant or deny an appeal.

What should be admissible?

The PCAST report recommended judges consider both the foundational and applied validity of the forensic discipline that produced any evidence before admitting expert testimony. This includes ensuring experts testify to the limitations of the analysis and evidence. For example, the justice system traditionally considers fingerprint evidence as an “identification” – for instance, the thumbprint recovered from the crime scene was made by the defendant’s thumb. No one ever testifies that there are little scientific data establishing that fingerprints are unique to individuals. The same holds true for other types of pattern identification evidence such as firearms, toolmarks and tire treads.

The National District Attorneys Association (NDAA) was critical of the PCAST report. It countered that there actually is scientific data validating these forensic fields, but members of PCAST did not adequately consult subject-matter experts. The NDAA also worried that if courts required stronger scientific validity before allowing evidence into court, it would hamstring the entire investigative process.

The NDAA concluded that judges should continue to be the ones who decide what makes evidence reliable and thus admissible. It asserted that the stringent requirements to become expert witnesses, along with the ability to cross-examine them in court, are enough to guarantee reliable and admissible evidence.

But should the admissibility of scientific processes – which ought to be grounded in their proven ability to produce reliable evidence – be determined by people who lack scientific backgrounds? I would argue no.

Pattern identification evidence shouldn’t be excluded from cases wholesale, but forensic evidence needs to be placed into context. When the human eye is the primary instrument of analysis, the court, the attorneys and the jury should be fully aware that certainty is unattainable, human error is possible, and subjectivity is inherent.

Reliance upon the adversary system to prevent wrongful convictions and weed out junk science requires a leap of faith that ultimately undermines the integrity of the criminal justice system. Counting on cross-examination as an effective substitute for scientific rigor and research can’t be the answer (although it has been for more than a century).

The PCAST report is yet another wake-up call for the criminal justice system to correct the shortcomings of forensic science. We demand that guilt be proven beyond a reasonable doubt; we should also demand accurate and reliable forensics. Without improvement, we can’t trust forensic science to promote justice.

Jessica Gabel Cino, Associate Dean for Academic Affairs and Associate Professor of Law, Georgia State University

This article was originally published on The Conversation. Read the original article.

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When most people think about air pollution, they tend to imagine rapidly developing cities such as Delhi and Beijing.

But urban areas in the Western world are equally having to deal with increasing levels of smog. Paris is currently experiencing an “exceptionally serious” crisis, as a massive spike in pollution has become the most prolonged event for at least a decade.

In response, the city has announced that all public transport will be free for the second day running, while on Tuesday the Velib bike-share and Autolib electric cars were also free to use. In addition, the city has implemented a system in which only half of all cars are allowed to enter the city center.

On Tuesday, only cars with an even-numbered plate could drive in the capital region, while on Wednesday it will be the turn of all cars with an odd-numbered plate. Anyone flouting this rule is to be fined€35, with 1,700 fines handed out on the first day alone.

The temporary ban placed on half of all vehicles comes just days after the mayor of Paris pledged, along with three other major cities, to ban all diesel cars by 2025 in a long-term bid to cut the dangerously high levels of air pollution present in the capital. The plan is to instead promote alternative vehicles, while at the same time promote walking and cycling.

“Today, we also stand up to say we no longer tolerate air pollution and the health problems and deaths it causes – particularly for our most vulnerable citizens,” the mayor of Paris, Anne Hidalgo, announced when the pledge was made in Mexico City last week. “Big problems like air pollution require bold action, and we call on car and bus manufacturers to join us.”

The current situation has not been helped by the windless conditions across the city, meaning the smog blanketing the capital has not been dispersed as it usually would be. Air pollution is thought to kill at least 3 million people globally, with the majority of these being in cities. As the public health implications of pumping dangerous gasses and particles into the streets becomes more obvious, more urban centers are going to have to start taking action.

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Sex is everywhere.

Ads. Tinder. "Game of Thrones." Flowers in a garden.

But just because we see it everywhere doesn't mean that we can definitively explain why it's everywhere.

Sexual reproduction is a costly endeavor: You need two parents to reproduce, and the male half of a sexually reproducing species is fundamentally incapable of directly producing offspring.

Given the Darwinistic and cutthroat rules of natural selection and the high evolutionary cost of sexual reproduction, why sex continues to exist, and why so many different organisms reproduce that way, is a fascinating and difficult question.

Bio 101

Before we jump to the research, let's run through a refresher of the terminology.

Reproduction is the process by which organisms (parents) produce new organisms (offspring.)

There are two types of reproduction: asexual and sexual. With asexual, a given organism can reproduce by itself (without the assistance of another organism). Examples include budding— in which a new organism develops as a growth from the original organism — and cloning. The key thing about asexual reproduction is that the offspring is identical or extremely similar genetically to the parent.

Meanwhile, sexual reproduction requires two organisms, a male and a female. The male fertilizes a female of the same species to create offspring. The key thing here is that the offspring's genetic composition derives from both parents, meaning it is not identical to either parent. A simple example: A child could have the hair color of one parent but the eye color of the other.

So what's the big problem with sexual reproduction?

Natural selection is ruthless and efficient, but sexual reproduction is not the most efficient way of reproducing. After all, in asexual reproduction, all the organisms can reproduce, while in sexual reproduction, only half of the organisms can reproduce — the females.

In less abstract terms, two hydra can both reproduce asexually, which gives you two offspring. But a human female and a human male together only create one offspring (excluding the possibility of having twins, etc.) since the male cannot directly create offspring.

"This is a huge cost in evolutionary terms, so there must be something very valuable about [sexual reproduction]," Robert Axelrod, a political scientist at the University of Michigan and the mind behind a computer study of the iterated Prisoner's Dilemma, told the Evolution Institute a few years ago. "The fact that sex is so universal means that it must be something that large animals and plants have in common."

A look at the reproduction of yeast

So what gives?

As noted above, sexual reproduction leads to genetic variation in the offspring. And so it's possible that sex, although costly in terms of the rate of reproduction, could help the offspring organism adapt to an environment better than its parents. (Anyone who took biology in high school likely remembers the example of the peppered moth during the Industrial Revolution.) This makes intuitive sense, but the trick is actually getting empirical evidence.

Notably, there are a few organisms that reproduce both asexually and sexually, which makes them the prime candidates to test the benefits of sexual reproduction. One such organism is yeast.

Yeast reproduce asexually when there's an abundance of food. But if there's not enough food, then they reproduce sexually.

Back in 2005, a team of researchers led by Matthew Goddard, then a postdoc at Imperial College London, genetically engineered yeast so that it would continue to reproduce asexually in dire circumstances. This, then, allowed them to compare how yeast that can reproduce sexually fare in tough conditions compared to those that could only reproduce asexually.

And here's where it gets interesting: under normal conditions, both yeasts did equally well; but in the harsher conditions, the yeast that could sexually reproduce adapted more quickly and survived better.

"Our results indicate that sexual reproduction can provide a selective advantage during adaptation to new environments," the team wrote in Nature. "A challenge now is to understand the nature of the mutations that underlie adaptation and to extend these techniques to larger plants and animals."

Parasites?

Another stunning idea about sexual reproduction came from a paper produced by William Hamilton, Robert Axelrod, and Reiko Tanese back in 1990, which explored the idea of sexual reproduction as an adaptation helping organisms resist parasites.

"Darwinian theory has yet to explain adequately the fact of sex. If males provide little or no aid to offspring, a high (up to 2-fold) extra average fitness has to emerge as a property of a sexual parentage if sex is to be stable," the team wrote in the abstract.

"The advantage must presumably come from recombination but has been hard to identify. It may well lie in the necessity to recombine defenses to defeat numerous parasites."

As Axelrod explained at the Evolution Institute:

"Parasites evolved to mimic our cells so that our immune system wouldn’t attack them. As a result, they can evolve around thirty times faster than we can since their generation time is so short. If you were to reproduce asexually it would mean you’d have an offspring that was almost identical to you, so the parasites that are adapted to you would also be adapted to your offspring. However, by reproducing sexually our offspring are quite different from us. Therefore, the parasites have to start all over. [Hamilton's] idea was that sexual reproduction is an adaptation to resist parasites. It is just a brilliant idea."

Here, too, offspring appear better set up for survival because of sexual reproduction. However, what's notable in this theory is that offspring do not evolve just for an advantage to a changing environment — as with the yeast example — but rather just to survive as other rival organisms also change and therefore threaten the survival of the their species.

Why do males still exist?

One final interesting thing to think about is why men continue to exist if their primary contribution to reproduction is sperm. A possible explanation is sexual selection: Males competing for females, and females choosing among males.

In research published in Nature in 2015, a team from the University of East Anglia, led by professor Matthew Gage, evolved replicate populations of flour beetles over several years under controlled conditions. The only difference between populations was the intensity of sexual selection at each adult reproductive stage — which ranged from 90 males competing for 10 females to the "complete absence of sexual selection, with only single males and females in monogamous pairings, where females got no choice and males experienced no competition."

And after seven years they found that populations with stronger sexual selection were fitter and more likely to survive than those without:

"Lineages from populations that had previously experienced strong sexual selection were resilient to extinction and maintained fitness under inbreeding, with some families continuing to survive after 20 generations of sib × sib mating [Editor's note: sibling x sibling]. By contrast, lineages derived from populations that experienced weak or non-existent sexual selection showed rapid fitness declines under inbreeding, and all were extinct after generation 10."

"Multiple mutations across the genome with individually small effects can be difficult to clear, yet sum to a significant fitness load; our findings reveal that sexual selection reduces this load, improving population viability in the face of genetic stress," they added.

Ultimately, it's important to note that it would not be appropriate to oversimplify or extrapolate from any of these studies. And, moreover, none of this even begins to touch on how sexual reproduction came about. However, it is still fascinating to consider the evolutionary benefits from sexual reproduction.

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Eric Trump recently suggested that when his father, Donald Trump, bragged about grabbing women's genitals without consent, it was an example of "two alpha guys in a thing."

In addition to shedding some light on how Trump's son views his father and manhood, it's also interesting because "alpha males" aren't actually a thing.

As the writer Saladin Ahmed pointed out, the concept of "alpha male" wolves that assert dominance over their pack through aggression comes from a debunked model of lupine social groups.

David Mech introduced the idea of the alpha to describe behavior observed in captive animals. Alphas, he wrote in his 1970 book "The Wolf: Ecology and Behavior of an Endangered Species," win control of their packs in violent fights with other males.

But, as he outlined in a 1999 paper, he's since rejected that idea in light of research into the behavior of wolves in the wild.

In nature, Mech writes, wolves split off from their packs when they mature, and seek out opposite-sex companions with whom to form new packs. The male and female co-dominate the new pack for a much simpler, more peaceful reason: They're the parents of all the pups.

Mech writes on his website (with the lovely title Wolf News and Info) that his original book is "currently still in print, despite my numerous pleas to the publisher to stop publishing it."

Another Twitter user, Mike Westphal, pointed out another paper on the misuse of the phrase "alpha males" to describe breeding roosters.

In the 2003 book "Sexual Selections: What We Can and Can't Learn about Sex from Animals," the biologist Marlene Zuk points out that social groups of hens do have "pecking orders." That is, hierarchies among the females with dominance asserted through pecking.

But roosters are not part of those social groups, Zuk writes, and the idea that the top hen is somehow an "alpha male" bizarrely misgenders the dominant bird.

All of which is to say: Humans who enjoy the idea of "alpha males" might want to keep in mind that there isn't really any such thing. And to the extent the term has any meaning at all, it describes the behavior of captive, lonely creatures.

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Pimples can be unsightly and irritating, but Google search after Google search urges us to leave them alone. However, ingrown hairs can cause inflammation and bumps – and these kinds of blemishes require our attention, lest they grow painful and dangerous. 

Special thanks to Dr. Ricardo Mejia from Jupiter Dermatology and Hair Restoration for speaking with us about the different treatments for ingrown hair.

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When you look at that blob above, what do you see?

I don't see much of anything — just a bunch of reddish-brownish-greenish circles. (Ask me to tell you which ones are which and I'd have to think for a minute.) Other colorblind people, apparently, might spot the digits 21. Sighted people should see a 74.

Assuming you aren't colorblind as well, you can see what I can't because the cone cells in your eyes work better than mine. Cone cells detect color, while rod cells detect light and dark.

I've known I was color-blind since I was about three years old, on a walk to Bee Creek Park in College Station, Texas. My dad, holding my hand, pointed out trees with leaves turning red for the start of autumn. I had no blasted idea what he was talking about, and told him so. He wasn't too surprised. After all, there had been a 50% chance I'd turn out (as my school friends would later call it) color-stupid.

Colorblindness (or stupidity) is, in the great scheme of things, hardly a great problem in life. I'll never get to fly a commercial airliner or fighter plane. Some video games maps and heads-up-displays are confusing to me. Once or twice in my lifetime I've driven through a red light on an empty road at night. And pretty much every data visualization on the internet looks like a mess.

But the real frustrating part of colorblindness, for me at least, is how little most people seem to understand it. Here's a typical scene in the life of a colorblind person:

Dopey friend: Wait, you're colorblind?! You never told me!

Colorblind individual: It, uh, never came up.

DF: What color is this? Points to stapler

CI: That's a black stapler.

DF: Okay. What color is the sky?

CI: Blue.

DF: What color is grass?

CI: Green.

DF: What color is—

[THIRTY MINUTES ELAPSE]

DF: What color is this? Points to shirt.

CI: I don't know.

DF: Oh my god, you can't see my shirt! Do I look naked to you??

In the grand scheme of things, of course, this falls squarely into the not a big deal category of irritants. The oppression of colorblind people is decidedly not a thing. But still, lots of people don't understand what colorblindness is. And most colorblind people I've spoken with agree that over a lifetime that confusion gets pretty annoying. So I'm going to clear up a few things.

What even is colorblindness? How do you catch it?

The most commons forms of colorblindness are genetic conditions, passed along the x-chromosome. People with an x-chromosome and a y-chromosome only need their one x to be defective to catch it. People with two x-chromosomes need both to be defective.

Most women have two x-chromosomes, and most men have an x-chromosome and a y-chromosome. That's why colorblindness is much more common in men than in women.

My mother's father was colorblind. He had one defective x-chromosome, which he passed to my mother. But my mother has two x-chromosomes. Her other x, which she got from her mother, works fine. So she isn't colorblind. But she is a carrier.

That means that when she has a child, she has a 50% chance of passing that defective x-chromosome along.

My father passed me a y-chromosome. And my mother passed me her defective x, so I'm colorblind. If they had a child tomorrow with two x-chromosomes, that child would have a 50% chance of becoming a carrier like my mother. If my father were colorblind as well (he isn't), that two-x-chromosome child would have a 50% chance of being born colorblind. 

If they were both colorblind, all of their children would be colorblind.

Okay, okay. Enough genetics stuff. What is it like to be colorblind?

Okay. First things first. If it weren't for all of you color-sighted folks around telling me I'm colorblind, I'd never know it.

Like many colorblind people, I'm what's called "red-green colorblind" as a shorthand. True, black-and-white colorblindness where the world looks like an old-timey movie is actually pretty rare. And it's probably a lot easier for you to imagine.

My world looks pretty colorful. Red, green, yellow, orange, purple, blue, pink. Name any of those colors and I can form a clear picture of it in my head, think of a thing in the world that I've seen as that color. (Though green and orange look pretty similar in that sentence, and yellow is almost illegible.)

But there are a whole lot of reddish, greenish, brownish things in my world that other people seem to see as distinct shades. Nearly everything other people describe as purple I see as blue. Sometimes white things turn out to be pink in other people's eyes. 

The real mystery arises with all the in-between shades. Some of them I can spot well enough — royal blue, baby blue, and sky blue for example.

But there's a whole universe of hues that are mysterious to me. I can almost never recognize crimson, auburn, or salmon unless they're pointed out to me. The same holds for most purples. I'm told there are colors with names like indigo, teal, and yellow-green, but I'm not sure I believe it.

Can you show me what it's like to be colorblind?

Probably not. Some tools on the internet claim to convert images to show what they would look like to colorblind people. I can't step outside my own visual experience to evaluate them from a neutral perspective, but I'm doubtful.

Here's why.

Wavelengths of light, which our brains interpret as color, are objective features of the universe. And I can point toward certain wavelengths and say they're indistinguishable to me. But I can't describe for you or visually represent the reddish-greenish color my brain churns up when my cones send a signal saying "well, it's one of those."

Here's a photograph that has a lot of color in it:

What does it look like to you? What does colorfulness look like? What is it like to see in full color?

You can't explain that to me, not really. And I can't explain my muddier vision to you any better. I can turn down the saturation on reds, greens, and purples, like so:

But colorblindness is a confusion and conflation of colors, not just a desaturation. So neither of us can really know what each others' perspectives really look like.

Similarly, I have no idea what it's like to be blue-yellow colorblind (a rarer form). Confusing blue and yellow? Those people must be bonkers!

How can I be less annoying and more helpful to my colorblind comrades?

Ah! Finally, a simple question.

• Don't ask us to tell you what color our shirt is. We know what color our shirt is! It's [inaudible].
• Avoid color-coding things when possible. When color-coding is necessary, stick to bold, primary colors and try to spread them over as wide an area as possible. It's much harder for us to tellthese two colors apart, using only thin crowded text,  t h a n    t h e s e  t w o   c o l o r s, using nice spread-out color blocks.
• Remember, confusing colors is not the same thing as not seeing that color exists. If you put a colorful thing on a white background, we can probably tell it's there. (Probably.) We just may not know what it is.
• If we get a color wrong, just correct us! But, like, also keep in mind that this has happened about a million times in our lives and we may not find it as hilarious as you do.

That's all there is to it, really.

Wait, I think I might be colorblind!

Cool! Luckily, it's super easy to test for. This page (made by the same people who make those glasses) can tell you if you're colorblind, and what sort of colorblindness you have.

Actually, whether or not you're colorblind, you're super colorblind.

Even if all the cones in your eyes function perfectly, you can't see anything close to "all" of the colors. You see significantly more than I do, just like I see significantly more than a person with a more severe visual defect. But your eyes still round infinite wavelengths of light in the visual spectrum into just a few million colors.

Some people, known as tetrachromats, have extra cones in their eyes and see millions more colors within the same wavelengths that you see. Concetta Antico, a tetrachromat, described her vision to New York Magazine like this:

I see colors in other colors. For example, I’m looking at some light right now that’s peeking through the door in my house. Other people might just see white light, but I see orange and yellow and pink and green and some magenta and a little bit of blue. So white is not white; white is all varieties of white. You know when you look at a pantone and you see all the whites separated out? It’s like that for me, but they are more intense. I see all those whites in white but I resolve all these colors in the white, so it’s almost like a mosaic. They are all next to each other but connected. As I look at it, I can differentiate different colors. I could never say that’s just a white door, instead I see blue, white, yellow-blue, gray ...

... Let’s take mowed grass. Someone who doesn’t have this genetic variation might see bright green, maybe lights or darks in it. I see pinks, reds, oranges, gold in the blades and the tips, and gray-blues and violets and dark greens, browns and emeralds and viridians, limes and many more colors — hundreds of other colors in grass. It’s fascinating and mesmerizing.  

Try to picture that. Really imagine what it's like. See how impossible that is? That's what it's like when you describe your color vision to us.

And there are animals with even more cones that can see even more colors in our wavelengths, as well as many creatures that can see deep into the ultra-violet and infra-red ranges. Radiolab dedicated a beautiful segment to this phenomenon.

I hope this was helpful for some of you poor color-sighted folks out there. If not, oh well! At least you get to know what "chartreuse" looks like.

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Today most people do not get enough sleep. The Centers for Disease Control and Prevention (CDC) has called insufficient sleep an epidemic. While we are finally paying attention to the importance of sleep, the need for dark is still mostly ignored.

That’s right. Dark. Your body needs it too.

Being exposed to regular patterns of light and dark regulates our circadian rhythm. Disruption of this rhythm may increase the risk of developing some health conditions including obesity, diabetes and breast cancer.

Light regulates our sleep and wake patterns

The physiological processes that control the daily cycle of sleep and wake, hunger, activity levels, body temperature, melatonin level in the blood, and many other physiological traits are called the endogenous circadian rhythm.

On its own, the endogenous circadian rhythm is nearly, but not exactly, 24 hours. Our bodies rely on the Sun to reset this cycle and keep it at precisely 24 hours, the length of our days. The light – and the dark – are important signals for the cycle. This circadian rhythm has developed over three billion years as life evolved on Earth in the context of the Sun’s day/night cycle. It is built deeply into our genetic makeup.

During the night, in the dark, body temperature drops, metabolism slows, and the hormone melatonin rises dramatically. When the Sun comes up in the morning, melatonin has already started falling, and you wake up. This natural physiological transition into and out of night is of ancient origin, and melatonin is crucial for the process to proceed as it should.

If you were to put someone in a dark cave with no time cues at all, the cycle will last about 24 hours, but not exactly. Without time cues like those from the Sun, eventually that person would become out of sync with people outside. In fact many profoundly blind people, who cannot perceive light, must cope with this de-synchronization in their daily lives.

What does your body do in the dark?

Many things happen to our bodies during the dark. Levels of the hormone leptin, which helps control hunger, go up. High levels of leptin mean we do not feel hungry while low levels make us hungry.

Why does leptin go up in the dark? Since we evolved without artificial light at night, one theory holds that leptin goes up at night because it would be good to not be hungry during the night, rather than needing to forage in the dark and possibly get into trouble.

This fasting that should happen every night, and why we call the first meal in the morning “breakfast.” Experiments in human beings have shown that sleep disruption and turning on lights lowers leptin levels which makes people hungry in the middle of the night.

In the last decade or two it has become clear that the genes which control the endogenous circadian rhythm (the “clock genes”) also control a large part of our entire genome including genes for metabolism (how we process the food we eat), DNA damage response (how we are protected from toxic chemicals and radiation), and cell cycle regulation and hormone production (how our cells and tissues grow).

Light at night disrupts these processes. The changes that result from exposure to electric light at night have biological connections to disease and conditions that are common in the modern world today including obesity, diabetes, cancer and depression.

Blue light, red light, no light

Not all light is the same – some kinds of light make you more alert and more awake, and others have less of an effect.

Light from the Sun is strong in blue, short wavelength light, although it includes all other colors as well. That’s important in the morning when we need to be alert and awake. But when it comes in the evening or during the night, it fools the body into thinking it’s daytime. We now know that this bright blue light has the strongest effect on lowering melatonin during the night.

Your tablet, phone, computer or compact fluorescent lamp (CFL) all emit this kind of blue light. So using these devices in the evening can prevent that primordial physiological transition to night from occurring. This makes it harder to sleep and might also increase the longer term risk of ill-health.

Other kinds of light, like dimmer long wavelength yellow and red light, have very little effect on this transition. This is the kind of light from a campfire or a candle; even the old fashioned incandescent light bulb is dimmer and redder than the new CFL.

Only in the last 20 years have we acquired a basic biological understanding of how the eye’s retina tells the circadian system it is daytime. Now we know that blue, short wave-length light is captured by the newly discovered photopigment melanopsin in the retina, and that when blue light stops, we start our physiological transition to nighttime mode.

Electricity changed the way we sleep

Before electricity, people experienced bright, full-spectrum days of sunlight and dark nights. We slept in a different way than we do now. The dark lasted about twelve hours and during this time people slept for eight or nine hours in two separate bouts, and were awake, but in the dark, for another three or four hours.

Everything changed when electric lighting was invented in the latter part of the 19th century. Since then there has been an ever increasing assault on dark. Outdoor environments are relentlessly lit, and more and more people use computer tablets and smart phones at all hours, bathing their faces in bright blue light at times of day when they should be transitioning to nighttime physiology.

When people get away from the city and its artificial light to go camping, they often notice a marked improvement in their sleep. A recent study has verified this effect.

Today, most of us get too little light during the day and too much at night for our circadian rhythm to function at its best. It is the rare person who sleeps in a completely dark bedroom, and many people get very little sunlight because they work inside all day long.

What can you do for your circadian health? Get bright, blue light in the morning (preferably from the Sun), and use dim, longer wavelength light (more yellow and red like incandescent) in the evening. And sleep in the dark.

This will certainly improve sleep, and may reduce risk of later disease.

Richard G. "Bugs" Stevens, Professor, School of Medicine, University of Connecticut

This article was originally published on The Conversation. Read the original article.

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We like to say we know less about the ocean here on Earth than we do about the surface of Mars, because while we have a vague idea of its overall structure, we’ve only properly seen less than 0.05% of it.

Imagine we discover an alien planet that’s teeming with life, and we’ve only explored an area the size of Tasmania - that’s what we’re dealing with when it comes to the ocean. And now, thanks to this awesome deep-sea diver, we’re getting a glimpse at what’s really down there.

Roman Fedortsov is a deep-sea fisherman based in the port city of Murmansk in Russia, which looks out over the Barents Sea - a relatively shallow sea that opens into the Arctic Ocean.

Fishing throughout the coastal Arctic ocean region, all the way to the coast of Morocco, Fedortsov has been sharing images of the deep-sea creatures that wander into his nets.

And let’s just say, you might think you know what an anglerfish looks like, but it’s a whole other story to see one close-up, sitting in the palm of someone’s hand:

Imagine being hunted by this:

Or this:

If you're wondering why they're all black, aside from red, it's the best colour to be in the deep sea if you don't want to get spotted.

These creatures live in the 'twilight zone' of the ocean - otherwise known as the Mesopelagic - which extends from a depth of 200 to 1,000 metres (roughly 660 to 3,300 feet) below the surface.

Below the Mesopelagic is the bathyal zone, which spans from 1,000 to 4,000 metres deep (3,300 to 13,000 feet), at which point there is zero sunlight.

That means these guys are dealing with only the tiniest hints of light penetration, and because black absorbs every wavelength of light without reflecting any back, they're effectively invisible in their natural habitat.

This also applies to red-hued deep-sea creatures too, as the US National Ocean and Atmospheric Administraation (NOAA) explains:

"The black animals absorb all colours of light available, and the red animals appear black as well; there is no red light to reflect and their bodies absorb all other available wavelengths of light. Thus red and black animals predominate."

Case in point:

Before we have a look at some more of these incredible creatures, let's just put it out there that it sucks that these animals died because they were caught up in a fisherman's net, and the best place for them is obviously back safe in their habitat.

But these images give us the opportunity to appreciate and learn more about life on Earth, and the more excited we are about the breadth of life that's lurking in the depths of the ocean, the more likely researchers will be to get the funding they need to actually go down there and study them.

So here are some more of our favourite pics from Fedortsov, and you can see them all in his Twitter feed:

Aww.

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If you've never woken up unable to turn your head without pain, those of us with an intimate understanding of the term "crick in the neck" are extremely jealous.

But why does it happen? Why are there days we wake up unable to turn our heads to the left or right?

"It's an age-old question that has probably plagued mankind since its existence," says Dr. Charles Kim, a musculoskeletal expert and assistant professor in the departments of rehabilitative medicine and anesthesiology at NYU School of Medicine who specializes in integrative pain management, physiatry, sports medicine, and medical acupuncture.

So what is a crick in the neck in the first place?

Kim says it can be caused by a variety of things, but most involve a minor injury to the system of muscles, joints, ligaments, and tendons that hold your head on top of your body. A muscle or ligament strain is the usual culprit in younger people, while arthritis is more likely to be a factor for older patients.

The Causes

We put extra strain on the muscles and ligaments in our neck whenever we have our heads or necks twisted or bent out of a neutral, natural position.

Sadly, this mostly happens during the activities we spend most of our time engaged in: working and sleeping.

At work we frequently spend much of the day with our heads bent forward, looking down at a screen or a desk. This is the exact same effect that we've seen recently described as"text neck." Since our head weighs 10-12 pounds, the muscles in our neck have to work extra hard to hold it up whenever it isn't in a neutral position, as shown in the graphic below.

Kim explains that though it's frequently described as a new phenomenon, "text neck" is just another name for an overuse injury, where one part of our body is strained beyond its capacity. The muscles in our neck can be compared to a rope-and-pulley system, he says, and if we lean forward all day we may put too much strain on one part of that system.

Stress can also be a contributing factor, either at work or at home.

We have a fight-or-flight response to stress that causes muscles to tense and posture to stiffen, but while that response would have been helpful when escaping a lion on the savanna, it now sabotages us.

Since we can't always "escape" the thing that causes this stress response — a job, for example — the constant tension can lead to our musculoskeletal system being strained beyond its capacity.

Even when we sleep, we aren't home free. We tend to move around during much of the night, rolling from one side to another and onto our backs or stomachs. While doing so, it's easy to tilt the head too far forwards, backwards, or to the side, which means that some other body part has to compensate for that unnatural position.

How To Treat It

It's not all bad news. Even though a neck crick is pretty awful when it first shows up, it usually subsides within a few days.

In the meantime, Kim recommends light stretches to ease pain. He says you should generally be able to loosen some of the tension that way. Gently massaging that sore part of your neck in a hot shower can help, especially if the injury caused some inflammation. A short course of acetaminophen or ibuprofen should reduce your discomfort in that case, too.

Bad inflammation can make the pain easily last a week.

You should see a doctor if the pain lasts longer than a couple weeks, or if it's accompanied by numbness, tingling, or arms falling asleep — that's potentially a sign of a pinched nerve, an injury that can cause especially sharp and lasting pain. In those extreme cases, a doctor will sometimes prescribe muscle relaxants.

How To Avoid It In The Future

If this happens more than occasionally, it may be a sign that you need to make some changes.

To start, set up a workstation that allows you to keep your spine in a neutral position. Have your computer monitor at eye level.

"Your workspace should fit you like a shoe," Kim says.

Focusing on posture is important, too. A standing desk can help, but even better is a workstation that allows you to alternate between sitting and standing.

In bed, changing pillows can help. If you use too many pillows, your head will bend one way, while one very soft pillow might not provide enough support.

A specifically designed ergonomic pillow is probably not necessary, according to Kim. It may help, but that improved situation could probably have been achieved with another pillow change too, and one that wasn't quite as expensive.

Finally, exercise is key. While athletes generally strain their muscles more than the rest of us, they're usually well conditioned enough that their muscles are less likely to suffer these office-derived overuse injuries. Spend some time strengthening your back, neck, and core, and your body will thank you.

Unfortunately, the problem may simply be a common consequence of the modern lifestyle.

"We're not designed as humans to be sitting in front of a computer all day, we need to be active," says Kim. "You may think that inactivity doesn't cause pain, but it causes a lot of pain."

This post originally appeared in December of 2014.

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Scientists have figured out the specific gene mutation responsible for red hair — and why it's more common in beards than on heads.

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Approximately 66 million years ago, a massive asteroid or comet smashed into the Earth near what we now think of as the Yucatan peninsula of Mexico. On the other side of the world, in India, at a place called the Deccan Traps, a period of intense volcanic eruption began — one that would last tens of thousands of years.

These catastrophic and powerful events are often considered the primary causes of the mass extinction event at the end of the Cretaceous period that wiped out most of the dinosaurs along with 75% of life on the globe.

But brand-new research reveals another factor that may have played a role in ending the era of the most massive creatures to ever walk the surface of the planet. It seems dinosaur eggs took a particularly long time to hatch. That means that when they had to compete for sparse resources in a post-extinction event world with the more efficient amphibians, reptiles, birds, and mammals that made it through that era into the next one, dinosaurs may have lost out.

Compared to reptiles, birds lay few eggs, and they are particularly large. This could hamper their competitiveness, since it exposes them to destructive risks. But bird eggs hatch about twice as fast as reptiles (their behavior keeps eggs warm and stable), which researchers think helps enough survive to hatch. Dinosaurs still exist in the form of birds — avian dinosaurs — and so researchers thought that the eggs of the non-avian varieties would still hatch at about the same fast rate as bird eggs do. After all, from what we can tell, non-avian dinosaur and bird eggs have similar structures and birds are the only remaining dinosaurs for us to base these hypotheses on.

But the new study, published January 2 in the journal Proceedings of the National Academy of Sciences, reports that dinosaur eggs took far longer to hatch. For one species studied, researchers estimate that a comparable bird egg would take between 40 and 82 days to hatch. The dinosaur egg, it seems, would have incubated between 83 and 171 days before it was ready, more like a reptile.

And that changes a lot of what we know about dinosaurs.

It's all about the teeth

The amount of time it takes for young to be born has a significant impact on how a species lives. It can define mating season, migratory behavior, and other characteristics.

Dinosaurs had large eggs and, in general, adults expended more energy than comparably sized reptiles or amphibians, putting a limit on their competitiveness.

By studying the growth of embryonic teeth in other species, researchers have been able to determine how long it took for the infants of those species to develop. So the team behind this study, consisting of researchers from Florida State, the University of Calgary, and the American Museum of Natural History, decided to try to calculate embryonic tooth growth in two dinosaur species, Hypacrosaurus stebingeri (a sort of "duck-billed" dinosaur) and Protoceratops andrewsi (a less-famous relative of the Triceratops).

The researchers saw that a certain measure that can be used to calculate embryonic tooth development in both human and crocodilian species exists in dinosaur species as well. So they evaluated fossil teeth from the above species.

Their calculations showed that the Protoceratops egg would have taken more than twice as long to incubate as a comparable bird egg, and would have been just a bit quicker to develop than a similar reptile. The Hypacrosaurus egg would have incubated even longer, needing more time than a similar reptile.

As the study authors write, this means that many hypotheses of dinosaur behavior may need to be re-evaluated. It was thought that perhaps these species made long migrations back and forth from the Arctic between seasons, but long egg incubation periods may have made this impossible. And while these new findings are just based on evaluations of fossils from two species of dinosaur, the authors say they think these long incubation periods would most likely be found in all toothed dinosaurs — though further research could always change that conclusion.

The other big effect this may have had is on the extinction of these creatures. We already believe dinosaurs expended more energy and needed more resources than reptiles or amphibians. They took a long time to mature, unlike many mammals and birds. When the resources of the world were devastated by a changed climate after the asteroid struck and during the period of volcanic activity, it became hard for any large species to survive. Slow hatching rates would have been just another blow to the non-avian dinosaurs. And that may help further explain why none made it through that time.

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Two researchers — Dr. Calvin Coffey and Dr. Peter O'Leary — are forever changing the way we understand an important tissue in the human body called the mesentery. In a recent study, Coffey and O'Leary suggest that the mesentery deserves to be recognized as an new human organ. There are 78 organs in the human body, and the mesentery would make 79. Here's why the mesentery is so important. 

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One of the first things you learn about evolution in school is that the human body has a number of 'vestigial' parts— appendix, wisdom teeth, tailbone — that gradually fell out of use as we adapted to more advanced lifestyles than our primitive ancestors.

But while our wisdom teeth are definitely causing us more pain than good right now, the human appendix could be more than just a ticking time bomb sitting in your abdomen. A new study says it could actually serve an important biological function — and one that humans aren’t ready to give up.

Researchers from Midwestern University traced the appearance, disappearance, and reemergence of the appendix in several mammal lineages over the past 11 million years, to figure out how many times it was cut and bought back due to evolutionary pressures.

They found that the organ has evolved at least 29 times— possibly as many as 41 times — throughout mammalian evolution, and has only been lost a maximum of 12 times.

"This statistically strong evidence that the appearance of the appendix is significantly more probable than its loss suggests a selective value for this structure,"the team reports.

"Thus, we can confidently reject the hypothesis that the appendix is a vestigial structure with little adaptive value or function among mammals."

If the appendix has been making multiple comebacks in humans and other mammals across millions of years, what exactly is it good for?

Conventional wisdom states that the human appendix is the shrunken remnant of an organ that once played an important role in a remote ancestor of humans millions of years ago.

The reason it still exists — and occasionally has to be removed due to potentially fatal inflammation and rupturing — is that it’s too 'evolutionarily expensive' to get rid of altogether. There's little evolutionary pressure to lose such a significant part of the body.

In other words, the amount of effort it would take for the human species to gradually lose the appendix though thousands of years of evolution is just not worth it, because in the majority of people, it just sits there not hurting anyone.

But what if it's doing more than just sitting there?

A haven for 'good' bacteria?

For years now, researchers have been searching for a possible function of the human appendix, and the leading hypothesis is that it’s a haven for 'good' intestinal bacteria that help us keep certain infections at bay.

One of the best pieces of evidence we’ve had for this suggestion is a 2012 study, which found that individuals without an appendix were four times more likely to have a recurrence of Clostridium difficile colitis— a bacterial infection that causes diarrhoea, fever, nausea, and abdominal pain.

As Scientific American explains, recurrence in individuals with their appendix intact occurred in 11 percent of cases reported at the Winthrop-University Hospital in New York, while recurrence in individuals without their appendix occurred in 48 percent of cases.

Now the Midwestern University team has taken a different approach to arrive at the same conclusion.

First they gathered data on the presence or absence of the appendix and other gastrointestinal and environmental traits across 533 mammal species over the past 11,244 million years.

Onto each genetic tree for these various lineages, they traced how the appendix evolved through years of evolution, and found that once the organ appeared, it was almost never lost.

"[T]he appendix has evolved independently in several mammal lineages, over 30 separate times, and almost never disappears from a lineage once it has appeared,"the team explains in a press statement.

"This suggests that the appendix likely serves an adaptive purpose."

Next, the researchers considered various ecological factors — the species' social behaviours, diet, habitat, and local climate — to figure out what that "adaptive purpose" could be.

They found that species that had retained or regained an appendix had higher average concentrations of lymphoid (immune) tissue in the cecum— a small pouch connected to the junction of the small and large intestines.

This suggests that the appendix could play an important role in a species' immune system, particularly as lymphatic tissue is known to stimulate the growth of certain types of beneficial gut bacteria.

"While these links between the appendix and cecal factors have been suggested before, this is the first time they have been statistically validated,"the team concludes in their paper.

"The association between appendix presence and lymphoid tissue provides support for the immune hypothesis of appendix evolution."

The study is far from conclusive, but offers a different perspective on the hypothesis that humans have been keeping the appendix around for its immune support this whole time.

The challenge now is to prove it, which is easier said than done, seeing as most people who have had their appendix removed don't suffer from any adverse long-term effects.

But it could be that when people get their appendix removed, immune cell-producing tissues in the cecum and elsewhere in the body step up to compensate for the loss.

One thing's for sure in all of this — while we're probably not going to regain our tails, it's too soon to write off the appendix just yet.

The research has been published in Comptes Rendus Palevol.

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The dietary supplements had ominous names, like Black Widow and Yellow Scorpion. They contained an illegal and potentially dangerous molecule, similar in structure to amphetamines.

But when a Harvard researcher dared to point that out, in a scientific, peer-reviewed study and in media interviews, the supplement maker sued him for libel and slander.

STAT has conducted the first detailed look at the legal showdown that followed by interviewing key players and reviewing hundreds of pages of trial transcripts and other court documents. The jury trial had momentous implications for the future of research into the safety of weight-loss and muscle-building pills; for the freedom of academics to speak out about matters of public health; and for our ability to learn what's in the supplements on our kitchen counters.

In case things weren't interesting enough, swirling in the backdrop was a bizarre backstory involving a slew of sensational allegations against the wealthy founder of the supplement company — who dreamed up the business while in prison on a charge stemming from selling ecstasy.

The Harvard researcher, Dr. Pieter Cohen, won the defamation trial in federal court in Massachusetts in November.

But the man who sued him, Jared Wheat, the owner and CEO of Hi-Tech Pharmaceuticals, doesn't see the jury verdict as a loss: He's openly hopeful that the long and costly legal battle will scare away other academics from investigating the supplement industry.

If that doesn't work, he's counting on President-elect Donald Trump to follow through on vows to to "open up" the nation's libel laws to make it easier for parties who feel they have been defamed to win lawsuits. Trump has discussed this goal in the context of his grievances against the news media. But it could also have ramifications for published research.

Asked whether Trump should make easing libel laws a priority, Wheat told STAT: "Absolutely."

Meanwhile, the six adulterated supplement brands from Hi-Tech are still on the market, despite alarms raised not just by Cohen, but by the Food and Drug Administration. The FDA has ordered Hi-Tech to recall several such products. Wheat has refused, though he said the company has voluntarily made minor tweaks to the formulas for some of them to satisfy distributors.

The entire episode opens a window into the Wild West world of supplements. Unlike drug companies, supplement manufacturers don't have to show that their formulations are safe or effective before putting a product on the market. They don't have to run clinical trials. They don't have to consult federal regulators.

With little oversight, they can jump right into a highly lucrative industry: Wheat, a convicted felon, said his company brings in more than $100 million a year in annual revenue. His company's social media pages are lined with images of bodybuilders with veins bursting out of their biceps.

And Wheat has no regrets about spending what he estimated as between $300,000 and $400,000 in corporate funds to go after an academic who challenged the safety of his products in a meticulously documented study.

"I spent a lot of money, but hopefully it will deter others from going out there and making baseless allegations," Wheat said in a phone interview from his company's headquarters in Georgia. His advice to other academics: "Think twice and do better research, knowing you can get sued if you do this."

A hidden danger in weight-loss pills

Pieter Cohen was browsing an email newsletter when he learned he was being sued for $200 million.

Sitting at his computer that day in the spring of 2015, he stumbled upon a report of the lawsuit in a supplement industry trade publication. He wasn't even sure at first if it was real.

It was. Hi-Tech was suing him and his three coauthors in federal court in Georgia over the study they had published a few weeks earlier in the scientific journal Drug Testing and Analysis.

Cohen had launched that study with the goal of prodding the FDA to enforce the law by cracking down on supplements illegally containing a compound known as BMPEA. Chemically similar to amphetamines, BMPEA has never been demonstrated to be safe or effective in humans.

And there are plenty of reasons to suspect it can be dangerous. It's been shown to send blood pressure and heart rate soaring in dogs and cats. It's been linked to a stroke in a Swedish woman. Such evidence prompted Canadian health officials to call it a "serious health risk."

Supplement makers often claim that BMPEA is a natural botanical product that comes from a Southwestern shrub called Acacia rigidula. In fact, it has never been shown scientifically to come from that shrub, or from any other natural source. And the shrub itself is illegal to include in supplements because no manufacturer has gone through the necessary steps to prove that it's safe for humans to ingest.

There are a number of theoretical reasons that companies might want BMPEA in their products. It's possible that it might have weight-loss effects similar to those of amphetamines, which decrease appetite and increase metabolism. It may also aid in athletic performance. In other words: BMPEA might be more potent than natural botanical ingredients.

In 2014, FDA scientists had reported detecting BMPEA in a handful of supplement products labeled as containing Acacia rigidula — but they couldn't find any evidence of BMPEA in the actual shrub. That research made a minor splash, but the FDA team hadn't named names.

Cohen — who's known as perhaps the most dogged detective scrutinizing supplements — wanted to see if he could replicate some of those findings and publicize the specific brands containing BMPEA.

So his team chemically analyzed 21 popular supplements, made by a handful of manufacturers and labeled as containing Acacia rigidula. Eleven of them turned out to contain BMPEA — including six of the 10 Hi-Tech products in the study. (All six were marketed for weight loss.)

Hi-Tech's "Fastin-XR" pills, for example, contained 82 milligrams of BMPEA in the maximum daily dose recommended on the label. The maximum recommended dosage of "Yellow Scorpion" pills contained 69 milligrams, and "Black Widow," 56 milligrams. Because BMPEA has not been studied in humans, it's hard to compare the strength of these pills to, say, ADHD medication, but it was clear this was more than a trace.

Such pieces of evidence "strongly suggest" that BMPEA is synthetically produced and used to spike the products, Cohen's paper concluded.

The study immediately made waves: Cohen went on "Good Morning America" and was quoted in an article that appeared on the front page of some editions of the New York Times. Two senators issued a stern statement urging the FDA to keep such products off the shelves.

And within two weeks, the FDA issued warning letters to Hi-Tech and four other companies, ordering them to recall products containing BMPEA.

Cohen's study listed products and their manufacturers in the table of results. That's the only place in the paper where Hi-Tech is named. Cohen did not mention Hi-Tech by name in any of his media interviews.

Still, all the attention was giving Hi-Tech's customers cold feet. Distributors and retailers, including Rite Aid, sent back Hi-Tech products. A few other supplement companies that paid Hi-Tech to manufacture their products took their business elsewhere. So Wheat sued. He would later blame Cohen for costing Hi-Tech an immediate $14 million in lost business.

News about the suit spread quickly in the dietary supplement industry. Wheat said he got "hundreds" of supportive calls and emails from people "hoping that we were able to silence this guy."

A watchdog becomes a target

The guy the supplement industry wants to silence speaks thoughtfully, punctuating his points with emphatic hand gestures. Cohen is friendly and informal, at one point rolling up his pant leg to show a large skin graft on his left calf, a battle scar from a fall during a hiking expedition with his wife and their three school-aged children.

"He's the kind of person you want as your doctor," said Dr. Joshua Sharfstein, a former principal deputy FDA commissioner and now a professor of public health at Johns Hopkins. "He's not a clock-puncher by any stretch of the imagination."

Cohen, 46, is an assistant professor at Harvard Medical School and an internist at Cambridge Health Alliance, a network of hospitals and clinics just north of Boston. He first got interested in studying supplements after seeing Brazilian immigrant patients with alarming symptoms, such as palpitations, panic attacks, and even kidney failure. It turned out they had been taking a Brazilian weight-loss supplement spiked with amphetamines, antidepressants, and benzodiazepines.

With hardly any research funding, Cohen has turned out study after high-impact study identifying hidden synthetic stimulants in popular weight-loss products. And he's repeatedly called for tighter regulation. He's become the most widely recognized critic of the supplement industry, in part because he's very media-savvy, boosting the reach of his studies by pitching them to journalists. (He also pitched STAT on writing about this lawsuit.)

Cohen's well regarded, even among some people who disagree with him. Steve Mister, president of the Council for Responsible Nutrition, a trade group for dietary supplement makers, praised him for performing an "important watchdog function" and added that he does "some very good research"— even though Mister generally doesn't think it should translate to policy changes. (Hi-Tech has never been a member of the trade group.)

Cohen had dealt with supplement companies unhappy with his research before, but it had never gone anywhere. And Hi-Tech's suit seemed destined for the same fate last spring when a judge in Georgia dismissed it because Cohen didn't do any of his work there.

But then Hi-Tech refiled in Massachusetts, with a few small changes. Cohen's coauthors were no longer named as defendants. The demand for precisely $200 million in damages was dropped, too.

And this time, Cohen's Harvard lawyers couldn't get the suit dismissed. Last summer, a federal judge ruled that the company had a 7th Amendment right to a jury trial.

Academics around the country have come under similar threats, said Hank Greely, a law professor who heads the Center for Law and the Biosciences at Stanford University.

"Some threats come through litigation, some of them come through legislative requests or demands, and we don't really have any good ways of dealing with them," Greely said. "There are lots of ways that scientists are getting harassed."

And faculty members can't always count on their university to provide legal assistance; it depends on a number of factors, including the kind of research they're doing, according to Robert O'Neil, former general counsel for the American Association of University Professors.

Cohen was lucky to have Harvard in his corner. Still, the several months leading up to the trial were grueling for him. He had to put aside all his research projects. He was deposed for an intense six and a half hours. And he worried about the financial hit he could take, should the jury decide against him. It took months for Harvard's insurer to commit to covering a jury award for Hi-Tech, and even then it would only cover up to $5 million. The trial started out with Hi-Tech demanding more, though by the end, the company's demands were whittled to below $5 million.

Worst of all, Cohen was required to turn over hundreds of pages of his notes, peer-review feedback, and his written correspondences with the journal, coauthors, and journalists.

"That's when I really just had a new sense of what we were talking about here," Cohen said.

An antagonist with a checkered past

The seven-day trial, which started last October, wasn't about whether Hi-Tech's supplements actually contained BMPEA.

Hi-Tech admitted they did in the initial lawsuit — in fact, a few of the products in question actually listed it on their labels — but claimed, without evidence, that it had naturally extracted the substance from Acacia rigidula.

Instead, the case hinged on what Cohen had said about BMPEA: Had it really never been tested for safety or efficacy in humans? Was it really potentially dangerous? Was it really synthetic, not derived from Acadia rigidula?

These are not controversial questions in the scientific community. (The answers are yes, yes, and yes.) But they are scientifically complex questions, and it was far from certain how the jury would assess the evidence.

Hi-Tech's lawyers and witnesses claimed, without evidence, that BMPEA had been evaluated in proprietary studies that have never been published. They also tried to persuade the jury that the compound had been tested by pointing to studies of molecules that are chemically similar to, but ultimately distinct from, BMPEA.

By contrast, Cohen's lawyer, Brian Sullivan, focused on the high stakes for public health. In his opening statement, Sullivan urged the jury to consider the evidence "in the context of Dr. Cohen's ability and his right to speak the truth to powerful interests and the interests of his patients and people in general … [who are] putting things in their bodies without knowing really what's in there."

The trial and its preparations also aired unsavory details about Hi-Tech's checkered past.

First convicted for selling ecstasy while still a teenager, Wheat went on to violate the terms of his release and spent several years in prison, where he conceived of Hi-Tech.

The business was rolling by 1998, but Wheat didn't stay out of trouble for long. In 2003, the FDA forced his company to destroy supplements spiked with an unapproved erectile dysfunction drug. In 2006, the agency seized $3 million worth of his company's products containing ephedra, a banned and potentially dangerous stimulant.

Later that year, Wheat and several Hi-Tech associates were arrested for running an illegal online pharmacy based out of Belize. Federal prosecutors later alleged that Wheat had been involved in discussions about killing an FDA agent and blackmailing a federal prosecutor.

Wheat denied knowledge of these alleged and unrealized schemes, and the government didn't pursue them. He pleaded guilty to the illegal pharmacy charge and was sentenced to four years in prison. (He did another two-month stint behind bars in 2014 for not complying with a court order to recall Hi-Tech products.)

Asked about the conviction, Wheat said, "it would take hours to explain, and I just don't have time to deal with it, and nobody ever tells the accurate side of the story." He also told this reporter to "go write your slander piece all you care to — that's what all y'all do."

In his opening statement, Sullivan framed Hi-Tech's clashes with the law as important context for the jury to consider.

Hi-Tech's lawyer, by contrast, made a point in his closing statement to note that the company had "rebuilt [its] reputation" after "coming back from those setbacks."

The trial was tough on Cohen. At one point, he had to rush to the emergency room when the lymphatic system in his leg got infected, stemming from the hiking injury. And he knew that his own research career — and the whole field of independent research into the safety of supplements — hung in the balance. After all, if Hi-Tech could successfully sue over research it didn't like, what would stop other companies from trying the same?

In his closing statement to the jury, Sullivan turned to a quote often (perhaps erroneously) attributed to Winston Churchill. "'You have enemies? Good. That means you stood up for something in your life.' Dr. Cohen has enemies because he stood up sometimes in his life," he declared.

Two and a half hours after they left to deliberate, the jurors returned a verdict in Cohen's favor.

Cohen was still too wound up to feel anything. It wasn't until a few days later, when it dawned on him that the trial was really, finally, over, that he felt relief.

Then he got back to work.

More research is on the way

Wheat explains away his loss in part by pointing to the makeup of the Massachusetts jury pool: They probably had a hometown bias for a local university professor — not to mention the fact that "they're liberal people up there," Wheat said. He insists he would have won had the trial been in Georgia, where the company is based.

Meanwhile, consumers are still buying the supplements in question. Wheat claimed his company altered several of them by slightly tweaking the chemical structure of BMPEA to satisfy distributors who refused to carry the products otherwise. He likened it to making green tea decaffeinated.

He insists those changes didn't come in response to the FDA's April 2015 warning to recall several products containing BMPEA. FDA spokesperson Lyndsay Meyer said the agency is "continuing to work with each of the companies [warned about BMPEA] to ensure that their products comply with federal law."

But Wheat characterized those letters as toothless — an attitude that exposes the FDA's limited ability to police potentially unsafe supplements.

After Wheat lost the suit against Cohen, he said, "a few dozen" people in the industry called to say they hoped it had at least "deterred" Cohen from actively publicizing his critical research.

They might be unwise to count on it.

Cohen submitted a new study for publication just days after he won his trial, and has three new projects in motion in the new year. He believes it will be more important than ever under the new Trump administration to hold the FDA responsible for enforcing the law.

"My experience," Cohen said, "has really reinforced to me why it is so important to not only continue the research we're doing but to be very aggressive about speaking out about it."

He said he hopes his experience will spur discussion about legal protections for academic researchers. "How many people can continue in the field if this is what it takes," he said. "If one paper leads to this?"

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Many mammals — like humans — can easily survive on a broad diet, getting nutrition from whatever plants or animals happen to be available and seem most delicious at the time.

But some other creatures survive on much more specialized diets. Of those, few are as particular as the three species of vampire bats that have evolved to subsist entirely on blood.

Two of those three species have been known to jump from one source of blood to another, but the third, the hairy-legged vampire bat or Diphylla ecaudata, has always been considered a bird-specialist.

Until now.

A new study published in December in the journal Acta Chiropterologica and first reported in New Scientist finds that the bats have started to feed on human blood, something scientists didn't even think was possible.

As people have started to move into the Caatinga dry forests of northeastern Brazil, they've been cutting down trees and hunting the tinamou and guan birds these bats would normally drain for a meal.

So a group of researchers from the Universidade Federal de Pernambuco in Recife, Brazil, decided to test the bats' feces to see what they'd been eating as their normal meal sources disappeared, thinking they may have decided to turn to the animals that humans bring with them.

The authors of the study write that they wanted to know "[h]ow the species would behave in a situation of scarcity of wild birds and increase in the availability of domestic animals."

DNA analysis showed they'd been consuming chicken blood — not a big surprise. But it also showed that the bats had been preying on humans.

"We were quite surprised," Enrico Bernard, who led the study, told Sandrine Ceurstemont of New Scientist. "This species isn't adapted to feed on the blood of mammals."

Ceurstemont writes that the bats "are adapted to process fat, the main component of bird blood, as opposed to the thicker, high-protein blood of mammals."

As a dietary change, this isn't just creepy. Bats have a remarkable capacity to carry viruses that can be deadly to humans. In northeast Brazil, similar cases have led to rabies outbreaks in the past. In 2005, deforestation and human movement led another sort of vampire bat (pictured above) to bite more than 1,000 people, infecting a number with rabies and causing at least 23 deaths.

The hairy-legged vampire bat has been known to carry the deadly hantavirus, according to New Scientist.

Sleep tight.

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Why do you glance off to the side when you speak? It's like you're trying to pull a word out of some blank space in the distance.

Breaking eye contact mid-sentence is a strange habit, but almost everyone seems to do it every once in a while.

And a pair of researchers at Kyoto University in Japan offer an intriguing answer as to why in a new study, which will be published in the journal Cognition.

They suggest that maintaining eye contact requires a level of mental effort and uses up your brain's resources.

So sometimes, when you speak, the tasks of coming up with the next word and maintaining eye contact become too much for your brain to handle. Then — snap — your attention shifts to the middle distance, and all the extra oomph in your head goes toward picking your next word.

Here's how the researchers came to their conclusions.

We know from a previous study that different word-associations are more or less hard to come up with. And there's different reasons you might take time to come up with a word.

Some word association tasks are hard because there are too many options. That means the mechanism in your mind for picking a word has to run longer, but it doesn't tax your conscious thought.

For example: Try to come up with a verb for the word scissors.

Now come up with a verb for the word ball.

Typically people think of a word faster for scissors, because there's only really one good option: cut.

But if you have a ball you can kick it, throw it, catch it, or play with it.

And then there are the word associations that don't overwhelm you with choice anxiety, but have weak enough connections that you have to consciously think about them to pick a verb.

So if you're given the word car, it's not too hard to get to drive, so you probably don't have to think about it. But if the word is leaf, you might have to mull it over a bit before getting to fall.

For the eye contact study, the researchers had 26 participants play the word association game while making eye contact with a computer-generated face.

They found that eye contact did make it harder to think of words, so the participants would take longer to think of them. But the effect was only significant when trying to make weak connections, like that between leaf and fall ;— the sort that require conscious thought to come up with.

That means eye contact doesn't directly interfere with the mental task of picking words. But it takes some cognitive effort to maintain. So when you're speaking and you come to a word you have to actively think to come up with, the two tasks come into conflict.

And then, perhaps, you might glance away.

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Many people take it as a given that after a certain point in our lives, we lose strength.

Sure, if you never ran until your 40th birthday and then trained for a marathon over the next few years, you might be more fit at 45 than you were at 25. But if you're functioning at more or less peak fitness at 50, there's no way you'll be stronger or faster at 60, right? And that seems like it should be even more true as you get older — as we age, we lose both muscle and aerobic capacity, right?

In general, that's true. But it doesn't have to be, as now 105-year-old French cyclist Robert Marchand shows.

Marchand's case, documented in a report recently published in the Journal of Applied Physiology, shows that even at far advanced ages it's possible to get in better shape.

At age 101, Marchand created the world record for the furthest distance cycled by a centenarian in one hour, covering an impressive 24.25 kilometers (14 miles). There hadn't been a centenarian record before, according to The Guardian, but the 100+ category was created so the impressive athlete could show his ability. You'd think that might be enough. But as the case study reports, two years later at age 103, Marchand broke his own record, going a full 26.92 kilometers (16 miles) in the same time.

By doing that he showed that with training, you can do more than just stave off age-related decline — it's possible to actually improve, even after 100 years of life.

And that's pretty inspiring.

As the researchers write in what has to be one of my favorite lines I've ever read in an academic study, that's a big deal for anyone wondering whether things have to go downhill as they age.

"[B]eyond the establishment of new performance records at an extremely old age, the possibility for improving their performance and maximal oxygen uptake (VO2max) during this last period of life is a way for 'adding life to the life' rather than searching to 'kill the death.'"

Older and faster

Marchand was not a lifelong cyclist. From age 15 to age 25, he was into it, but one of his coaches told him he should give it up, saying he wasn't good enough. For decades, life working as a gardener and wine dealer kept him off the bike. It wasn't until he was in his late 60s that he began to pick the sport back up.

He was good and accomplished impressive feats — good enough that, years later, researchers wanted him to be part of a study that he volunteered for that would show how much of an impact training could have on a centenarian. He was in good health at the time, with no heart, respiratory, or circulatory issues, and not on any medication.

Before his first centenarian record, he went through a series of tests. They happened at least two hours after a meal on a day he'd been asked to avoid caffeine. At the time, he was able to crank out 90 W of power at his peak and hit an impressive VO2max — a measure of how much oxygen his muscles could use — of 31 milliliters of oxygen per kilogram of body mass per minute (mL/(kg·min)).

Shortly thereafter, he set that first record. The "hour" performance test in cycling is generally considered one of the best ways to measure athletic performance, since it follows specific rules and demonstrates something very clear.

After that first performance, Marchand embarked on a training program. For the next two years, he covered 5,000 kilometers per year, spending 80% of his time at a light pace and 20% going hard.

He stepped back up for a new series of tests at the end of the training. His weight, lean body mass, and heart rate were unchanged, but he was stronger. His VO2max had improved by 13%, to 35mL/(kg·min) and peak power went up 39%, to 125 W. And when he set out for another 60 minute race, he set a new record.

"This study shows for the first time that, at a very old age, VO2max and performance could still be increased with training," the authors of the case study write.

So if you've been feeling like you're over the hill, take heart.

And Marchand hasn't stopped since then. Earlier this month, the 105-year-old created a new record for a new 105+ age category, going 22.547 km in 60 minutes (he says he could have been faster if he hadn't missed the 10 minute warning; his physiologist says he would have been faster if he hadn't given up meat a month ago).

Upon finishing, the AP reports that he said "I'm now waiting for a rival."

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The phrase "First, do no harm"doesn't actually appear in the text of the Hippocratic Oath, yet it's frequently considered a fundamental principle of medicine.

At the same time, we believe firmly in the principle of informed consent, the idea that people should know the risks of a drug or medical procedure.

But sometimes, trying to follow one of these principles violates the other.

Specifically, if you tell people that they are likely to experience a number of side effects, those people are significantly more likely to experience those side effects, according to Ted Kaptchuk, a professor of medicine at Harvard Medical School and the director of the Program in Placebo Studies at Beth Israel Deaconess Medical Center.

"Almost anything can be a side effect," says Kaptchuk. And whatever side effects you tell a person are associated with a drug — dizziness, depression, dry mouth, drowsiness, insomnia, gastrointestinal trouble, foggy mind — "that's what people get," he says.

This effect is called a "nocebo" effect, a negative placebo. Instead of getting healthier because people expect to get healthier, they get sicker because they expect to get sicker.

And contrary to what some people may think about placebo or nocebo effects, these effects are very much "real" things that have an impact on people's health, affect their lives, and can be costly.

"Nocebo effects are very, very important," says Kaptchuk.

How belief can harm

"Information can be self-fulfilling," writes Rebecca Wells, along with Kaptchuk, in a paper titled "To tell the truth, the whole truth, may do patients harm: The problem of the nocebo effect for informed consent," published in The American Journal of Bioethics.

As that paper explains, there's some pretty clear research demonstrating ways that telling people about an effect could create it.

In one study involving aspirin the paper describes, some of the 555 patients involved were told they might experience gastrointestinal trouble as a result of the medication. That group was six times more likely to withdraw from the study because of gastrointestinal trouble.

In another study of 96 people testing beta-blockers, 3.1% of people who didn't know what drug they were taking experienced erectile disfunction. From the group that was told the name of the drug, 15.6% had similar troubles. The third group of patients in that study was told that erectile disfunction was a side effect of the drug they were on —from that group, a whopping 31.2% reported having those troubles. Without knowing the risk, a small number of people experienced that side effect. But with knowledge, people were ten times as likely to have a problem.

The mind is a powerful thing that can affect the body.

People told that something is going to hurt experience much more pain than people told they'll feel a cooling sensation or that they will be too numb to feel pain. If someone asks, "will it hurt," and the answer is (convincingly) "no," then the answer is no. But if they believe the answer to be "yes," they'll feel pain. As the paper explains, studies of the brain show that people experiencing this nocebo effect show brain activity indicating pain and show decreased dopamine and natural opioid activity — their brain physically is making them feel that hurt.

"There is no absolute 'truth' about a medication's side effect profile independent of what the physician says or does not say," the authors write.

So what should people be told?

Just because there's no "absolute" truth about side effects doesn't mean that all side effects are changed by the nocebo effect.

"It's only things the brain can modulate," says Kaptchuk. "The brain can make you feel more pain or less pain, more depressed or less, more or less nausea." Some drugs have side effects that exist independent of neuromodulation — potential liver damage from acetaminophen or increased ulcer risk from ibuprofen. Those things aren't changed by placebos or nocebos, meaning that people should always be told about those risks.

It's what to tell patients about those other slightly more vague side effects — which some people will experience anyway, though not nearly as many if they aren't aware of it — that is more complicated.

In the paper, Wells and Kaptchuk argue that one potential solution is "contextualized informed consent." Tell people about definitive side effects, but depending on their individual risks (some people are probably more susceptible to nocebos and placebos than others), they may not need all the details. In some cases, a doctor might tell a patient to call if they experience anything unexpected, though even this is likely to increase the chance of unwanted side effects.

Still, it's complicated. Ethically, doctors don't want to be accused of withholding information from patients — something that might open them up to costly malpractice lawsuits. And yet at the same time, they don't want to make people sicker, even if that's something that Kaptchuk says is unfortunately a side effect of the way that medicine works.

"A placebo [or nocebo] is about predicting the future at some level," he says.

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LONDON — Despite being able to appreciate art, fake cry and understand basic physics, it takes infants years to see clearly.

Mr Romesh Angunawela — a consultant eye surgeon at Moorfields Eye Hospital in London — has worked with eye clinic Clinic Compare to develop a GIF that shows how babies learn to see the world around them every month for their first year on earth.

It shows that children cannot really focus on their parents' faces, even close up, until they're around three months old. Even then, a child's vision doesn't fully mature until they're almost two.

Angunawela told Business Insider that, from the moment a child opens their eyes for the first time, the visual cortex of the brain begins to learn to process the flood of visual information it encounters.

"At birth, a baby sees things more clearly at eight-10cm, but their range of vision extends as they grow."

The visualisation shows how babies eyes tend to be less co-ordinated at first, as their brains get used to processing new information.

But after three months, a child can start to focus and recognise parents' faces. "This may coincide with their first smile, as facial muscle coordination also develops apace," said Angunawela.

Vision continues to develop steadily and by two years old, a child's sight is nearly fully developed. "This coincides with increased interest and exploration of the world around them."

Watch the GIF below to see how a newborn starts to focus on the new world around them.

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