Darwinian Evolutionary Theory (Wikimedia Commons Photo)
You know Darwinism has problems, but how do you explain them to your friends and family? Well, look no further than a bicycle lock.
What’s the greatest discovery in the history of biology? If you said “seedless watermelons,” you’re close. Actually, it’s probably the discovery of DNA.
It’s hard to imagine in this age of genetic engineering, but scientists in Darwin’s time saw life as quite simple. Cells were thought to be blobs of primitive chemicals called “protoplasm.” But as technology advanced and scientists were able to peer inside the cell, they discovered something amazing: Every living thing actually contains intricate, microscopic machines, performing functions without which life would not be possible.
The real breakthrough, came in 1953 when Watson and Crick uncovered the structure and function of DNA—the molecule that programs and regulates cells. It revolutionized our understanding of life. And it stretched Darwin’s theory to the breaking point.
DNA is essentially a form of incredibly efficient digital code, uniquely suited for storing the blueprints of living things. And for something microscopic, it’s huge. The human genome contains over a gigabyte of data! Of course, like digital code on a hard drive, DNA can be corrupted. The most recent iteration of Darwin’s theory claims that these corruptions—called mutations—are the engines of evolution. But here’s the problem: We don’t have a single example of a mutation resulting in a net gain of information. Not one.
As intelligent design theorists have pointed out, unguided, natural processes always degrade information—they never increase it. If life at its most fundamental level is a digital code, then mutations are glitches that, if they accumulate, will eventually kill the organism.
Information is at the heart of life, and our uniform and repeated experience tells us that matter, by itself, never produces information. The only known source capable of producing information is a mind.
Okay, fine, you say, but how do I explain this over the dinner table? One great place to start is a new video from the Discovery Institute that condenses the main argument for intelligent design to a snappy 20 minutes. It’s called “The Information Enigma,” and features noted ID authors Dr. Stephen Meyer and Dr. Douglas Axe.
Here are the basics: Using an analogy from Dr. Meyers’ book, “Darwin’s Doubt,” the video compares DNA with a bicycle lock.
“The reason a bike lock works,” explains Meyer, “is that there are vastly more ways of arranging those numeric characters that will keep the lock closed than there are that will open the lock.”
Most bicycle locks have four dials with ten digits. So for a thief to steal the bike, he would have to guess correctly from among 10,000 possible combinations. No easy task.
But what about DNA? Well, in experiments Axe conducted at Cambridge, he found that for a DNA sequence generating a short protein just 150 amino acids in length, for every 1 workable arrangement of amino acids, there are 10 to the 77thpossible unworkable amino acid arrangements. Using the bicycle lock analogy, that’s a lock with 77 dials containing 10 digits.
Thus, as the film states, it is overwhelmingly unlikely that a random mutational search would produce even one new functional protein in the entire history of life on earth. In other words, random mutation is not driving the biological bicycle.
It’s a powerful argument, and one I’d love you to understand and use. Come to BreakPoint.org, click on this commentary, and I’ll link you to Discovery Institute’s excellent new video. Then share it with your friends, and start some intelligent conversations about intelligent design.
Eric Metaxas is the bestselling author of “Bonhoeffer: Pastor, Prophet, Martyr, Spy.” He is the radio host of “The Eric Metaxas Show” and the co-host of “BreakPoint.”
Editor's Note: This piece was originally published byBreakPoint.
Famed neurosurgeon and 2016 presidential contender Dr. Ben Carson faced-off against the women of “The View” on Tuesday after he decried abortion and said that “we’re killing babies all over the place.”
Dr. Ben Carson on “The View” (“The View”/YouTube)
“In my case, I spent my entire career trying to preserve life and give people quality of life,” he said, explaining his past operations on premature babies and babies still in the womb. “There is no way you’re going to convince me that they’re not important, that they’re just a mass of cells.”
Host Whoopi Goldberg countered by asking whether Carson has “met with the women who have to make these horrendous decisions,” and questioned whether the Republican candidate is empathetic — to which he said that he is.
Carson then explained his belief that the private sector must provide adequate daycare so that mothers who choose to have their babies can get GEDs and finish their education.
“You’re assuming that these are mothers who aren’t educated,” Goldberg countered, with the crowd gasping and moaning when Carson said that most of them fit that description.
“A lot of those young girls who are having babies out of wedlock — when they have that first baby, they stop their education and that child is four times as likely to grow up in poverty,” Carson said. “We, as a society, have an obligation to do what’s necessary to stop that cycle.”
That’s when Joy Behar stepped in to defend Planned Parenthood against recent Republican attacks.
“So, how important is birth control then to the Republican Party?” she said. “They should be out there applauding Planned Parenthood for supplying birth control, mammograms and everything else.”
It should be noted, as TheBlaze previously reported, that Planned Parenthood president Cecile Richards confirmed during a congressional hearing last week that none of her organization’s 650 to 700 clinics across America has a mammogram machine.
In a mouse model of frontotemporal dementia, giving salsalatereversed memory loss and protected the hippocampus, a part of the brain essential for memory formation. The drug appears to work by reducing toxic buildup of tau, a protein also implicated in Alzheimer's.
Most Alzheimer's research has focused on tau's more famous cousin,beta amyloid, long the prime suspect in Alzheimer's. Both are abnormal forms of normal proteins. When altered, they become toxic and damage neurons, leading to their death. Several drugs targeting beta amyloid have reached the clinic, but none to date have been proven effective.
Salsalate is now being tested in several clinical trials, including one for another tau-related neurological disease, progressive supranuclear palsy, or PSP.
Meanwhile, no drugs targeting tau are available for Alzheimer's, say researchers led by scientists from the Gladstone Institutes at UC San Francisco.
The study was published Monday in Nature Medicine. It is available online at j.mp/alzsalsalate.
Salsalate inhibits a process called acetylation, which makes tau more toxic, the study found.
"One of the main enzymes that acetylates tau is p300, which can be inhibited by salicylate or SSA, an ancient drug commonly used as anNSAID," the study stated.
"Pharmacokinetically, SSA is quickly metabolized into its active component, salicylate. Unlike salicylate, aspirin (acetylsalicylate) leads to higher levels of ac-tau in cultured neurons. SSA and aspirin have been widely used to treat rheumatoid arthritis and related illnesses in the past decades, and work presumably via inhibition of cyclo-oxygenase (COX). Interestingly, patients taking NSAIDs, including salicylate and derivatives, have a reduced risk of AD."
Trials with more specific inhibitors of COX didn't find a protective effect against Alzheimer's, the study noted. That could be explained if the protective effect is actually due to inhibiting p300.
"Targeting tau acetylation could be a new therapeutic strategy against human tauopathies, like Alzheimer's disease and FTD," said Dr. Eric Verdin, a co-senior author, in a press release. "Given that salsalate is a prescription drug with a long-history of a reasonable safety profile, we believe it can have immediate clinical implications."
"Interesting but very preliminary," Aisen said by email. "In my view, the likelihood that salsalate will prove to be an effective therapy for AD or other tauopathies is small. It is misleading to say that this work has 'immediate clinical implications.' ”
Aisen is a proponent of the theory that beta amyloid is the main driver of Alzheimer's. He is leading a study funded by Eli Lilly & Co. that uses an experimental Lilly drug to reduce amyloid accumulation in people with signs of amyloid buildup, but who have no Alzheimer's symptoms.
Like Aisen, Dave Schubert, a Salk Institute scientist researching Alzheimer's drugs, said the study's conclusions went beyond the evidence given.
"My impression is that it is an interesting study, but likely with overstated conclusions with regard to therapy and even mechanism," Schubert said by email.
"The claim in the press release 'We identified for the first time a pharmacological approach that reverses all aspects of tau toxicity,' can not be true because in the mouse model and humans nerve cells die, and unless salsalate induces the production of new nerve cells to replace the old ones, there is now way to 'reverse' the pathology."
Schubert said the study didn't show that the acetylated tau hypothesized to harm neurons is concentrated in human neurons or synapses. Moreover, there are safety concerns about using salsalate against Alzheimer's.
"While salsalate has been used for years as an anti-inflammatory, it is quite toxic at high doses over extended periods of time as would be required for a chronic disease like AD," he wrote. "Also, as the authors point out, there are a lot of other potential targets for salsalate that could account for the animal data.
"As with all drug candidates, the only way to find out if they have any therapeutic value it to get them into people with the disease in a clinical trial."
The salsalate study was funded by the Tau Consortium and the National Institutes of Health.