That’s quite a stretch

A great post from Evolution (https://www.facebook.com/evolutionarybiology):

“Intelligent” design? Not really.

Let us follow the pathway of the recurrent (inferior) laryngeal nerve, an important nerve that is a branch of the Vagus nerve (tenth cranial nerve), to see how evolution works and its limitations, and also see how “intelligent design” doesn’t fit anywhere into our biological observations.

I’ll use the analogy of ‘Climbing Mount Improbable’ by Richard Dawkins- suppose Evolution is to be compared to a Mountain with different peaks, and the higher we go on the mountain the greater is the complexity. Suppose you’re already halfway up there, and suddenly realize while standing on the vantage point that there’s a a better route! But you can’t climb all the way down and start afresh, because that’s just not evolution, as it has no foresight, and you’ll have to make do with whatever you’ve got.

Similar is the case with the aforementioned recurrent (inferior) laryngeal nerve. This nerve connects the brain with the larynx (voice box). Damage to the recurrent laryngeal nerve means there’s damage to our voice/speech box. Hence, the obvious path for the nerve to travel is straight from the brain into the neck and into the larynx, right? If you were designing the animal from scratch and “intending” that mammals would arise someday, that makes all the sense in the world. In mammals, however, the nerve goes from the brain down past the heart and then to the larynx. This is because that’s the way it was in earlier fish-like ancestors, in whom making a trip around the heart was indeed the closest route from the brain to the larynx. But as the neck evolved and lengthened in a mammalian-like morphology, the current structure could not be made to start from scratch and the nerve developed its current highly unnecessary circuitous route. And nowhere is it more prominent than in Giraffes, where the nerve had to travel just 2 inches but instead makes a long tour all the way down the neck, and back up.
https://i0.wp.com/4.bp.blogspot.com/_QrCOp9vQWTc/TLC8niUj5TI/AAAAAAAAApw/YpwT8H8Uwhk/s400/450px-GiraffaRecurrEn_svg.png
It’s shown here in this video explained by Dawkins himself, do watch it:
https://www.youtube.com/watch?v=cO1a1Ek-HD0

As Dawkins would say, evolution didn’t start out millions and millions of years ago with the plan that mammals would someday rock the world. No. Fish got the basic, simple design and the rest of us millions of years later have to suck it up and deal with it. (Source 3)

Sources:
(suggested by one of our fans- Brian Wilson)
1) http://scienceblogs.com/grrlscientist/2010/06/22/the-laryngeal-nerve-of-the-gir/
2) http://qilong.wordpress.com/2012/06/05/the-stupid-unintelligent-recurrent-laryngeal-nerve-evolution-working-as-not-intended/
3) (Image source too) http://www.laughinginpurgatory.com/2010/10/what-is-example-of-natural-selection.html

Human Statue

Imagine your muscles, ligaments and tendons slowly turning to bone, and you can do nothing as you become a living statue. This sounds like magic, but once again the truth is stranger than fiction. The skeleton you see belonged to a man named Harry Eastlack (1933-1973) who suffered from a condition called fibrodysplasia ossificans progressiva (FOP). The extra bone on his skeleton used to be tissue, but because of a rare genetic mutation it ossified over the course of his life until he could only move his lips.

The first sign of FOP is a malformed big toe in newborns. Later, extra bone tends to appear in the neck, spine and shoulders. This bone production will then continue all over the body throughout the sufferer’s life. Secondary issues can arise such as difficulties breathing or malnutrition due to problems eating or difficulty. Any injury causes the body to “heal” the area with more bone – the reason extra bone cannot be removed surgically. At the moment there is no definitive treatment, and any reports of successful drug treatments are anecdotal.

The cause of FOP appears to be a mutation in the ACVR1 gene, which controls production of a member of the bone morphogenetic protein (BMP) Type 1 receptors family. Under certain conditions, this mutated gene may change the shape of the receptor – preventing inhibitor proteins binding and leaving the receptor constantly activated. This prolonged activation causes an overgrowth of bone and the fusion of joints. But it’s important to note we now know the cause – there is hope that in the future we will have a way to block the overactive receptor.

https://sphotos-b.xx.fbcdn.net/hphotos-snc6/185154_531226923558954_1474114524_n.jpg

Photo credit: A.B. Shafritz et al., New Eng. J. Med. 1996, Massachusetts Medical Society (taken from HowStuffWorks’ article on FOP). http://ghr.nlm.nih.gov/condition/fibrodysplasia-ossificans-progressiva http://www.ucsfbenioffchildrens.org/conditions/fibrodysplasia_ossificans_progressiva/ http://science.howstuffworks.com/environmental/life/human-biology/fop.htm