From Wastelands to Worship

It had been one of those days. Uncertainty had emerged from its cocoon as full grown doubt, and doubt had spared no time bringing fear to a raging boil in this ol’ heart of mine. There are all sorts of reasons to be afraid. Tomorrow is an abyss we’re all teetering on the edge of. I questioned the future. I second guessed every decision I had ever made. Doubt’s chains of fear seemed too strong and too securely fitted for me to ever be able to break free. The looming threat of the unknown we call tomorrow felt too black and too ominous for me to ever expect a brighter day come morning.

So, sitting on my bed, Kindle in hand, I did the only thing I felt capable of doing. I forced my eyes over word after word in the book I was reading about a biochemist’s take on Darwinian evolution. It was then my eyes fell across the following passage, five paragraphs that describe in detail the process by which human beings are capable of seeing:

“When light first strikes the retina a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. (A picosecond is about the time it takes light to travel the breadth of a single human hair.) The change in the shape of the retinal molecule forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound. The protein’s metamorphosis alters its behavior. Now called metarhodopsin II, the protein sticks to another protein, called transducin. Before bumping into metarhodopsin II, transducin had tightly bound a small molecule called GDP. But when transducin interacts with metarhodopsin II, the GDP falls off, and a molecule called GTP binds to transducin. (GTP is closely related to, but critically different from, GDP.)

“GTP-transducin-metarhodopsin II now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to metarhodopsin II and its entourage, the phosphodiesterase acquires the chemical ability to “cut” a molecule called cGMP (a chemical relative of both GDP and GTP). Initially there are a lot of cGMP molecules in the cell, but the phosphodiesterase lowers its concentration, just as a pulled plug lowers the water level in a bathtub.

“Another membrane protein that binds cGMP is called an ion channel. It acts as a gateway that regulates the number of sodium ions in the cell. Normally the ion channel allows sodium ions to flow into the cell, while a separate protein actively pumps them out again. The dual action of the ion channel and pump keeps the level of sodium ions in the cell within a narrow range. When the amount of cGMP is reduced because of cleavage by the phosphodiesterase, the ion channel closes, causing the cellular concentration of positively charged sodium ions to be reduced. This causes an imbalance of charge across the cell membrane that, finally causes a current to be transmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision.

“If the reactions mentioned above were the only ones that operated in the cell, the supply of 11-cis-retinal, cGMP, and sodium ions would quickly be depleted. Something has to turn off the proteins that were turned on and restore the cell to its original state. Several mechanism do this. First, in the dark the ion channel (in addition to sodium ions) also lets calcium ions back into the cell. The calcium is pumped back out by a different protein so that a constant calcium concentration is maintained. When cGMP levels fall, shutting down the ion channel, calcium ion concentration decreases, too. The phosphodiesterase enzyme, which destroys cGMP, slows down at lower calcium concentration. Second, a protein called guantylate cyclase begins to resynthesize cGMP when calcium levels start to fall. Third, while all of this is going on, metarhodopsin II is chemically modified by an enzyme called rhodopsin kinase. The modified rhodopsin then binds to a protein known as arrestin, which prevents the rhodopsin from activating more transducin. So the cell contains mechanisms to limit the amplified signal started by a single photon. Trans-retinal eventually falls off of rhodopsin and must be reconverted to 11-cis-retinal and again bound by rhodopsin to get back to the starting point for another visual cycle. To accomplish this, trans-retinal is first chemically modified by an enzyme to trans-retinol–a form containing two more hydrogen atoms. A second enzyme then converts the molecule to 11-cis-retinol. Finally, a third enzyme removes the previously added hydrogen atoms to form 11-cis-retinal, [and] a cycle is completed” (1).

No, I didn’t actually comprehend the processes the author explained there. I didn’t have to. The fact alone that it takes four full paragraphs, at least eight different kinds of proteins, two different kinds of ions, four different types of enzymes (if I even counted correctly)—all of which have names whose pronunciation I can only guess—all interacting throughout a complex chain reaction of steps begun when a single photon hits the human retina and interacts within picoseconds with a molecule I’d never heard of before is enough for me. I had gotten the message loud and clear. I am the product of an unfathomably skilled craftsman.

I reached the end of the chapter, and only after reading a few paragraphs of the next chapter, I finally forced myself to put down my Kindle and call it night. As I lay in bed, a thought struck me. As if it wasn’t enough that the God of the universe had designed and then fashioned the human eye, the thought fell over me like showers from a looming raincloud that that very God was looking down on me in that very moment as his beloved son. I could call the designer and builder of human sight Father.

There, lying in the stillness of a darkened room, in a sleeping house in a row of other sleeping houses, I felt as if something dreadful and wonderful and holy had descended over me. Doubt lost its grip on its chains of fear. And they didn’t merely loosen—those chains. They snapped and fell off completely. And to think the truth I so needed to hear was tucked away in a book about biochemistry. Just like God intended, God had spoken through his creation, and his words were unmistakable: “I am here.” But that wasn’t all God was saying to me in that moment, for because I had read the words of a much older book, I also knew that the God who exists is also for me.

I cannot help but love the one true Creator God—the one who thought up the idea of sight and designed every last one of its mechanisms and who also holds every last one of my tomorrows in his sovereign hand. I love him for his mind-numbingly awesome, creative power, and I think I love him even more that he would stoop so low to hold someone like me in the stillness of a dark night and loosen the chains of doubt that were threatening to strangle him.

And to think he is not far from any one of us.

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(1) Behe, Michael. “The Vision of Biochemistry.” Darwin’s Black Box. Kindle ed., locations 325-358, Simon and Schuster.