Antibiotic Resistance Evidence of “Devolution”

Updated near the bottom.

The issue involved in the above video is not evolution, but in fact, DEVOLUTION. In other words, “no newly evolved complex information has been demonstrated,” EVOLUTION NEWS AND VIEWS continues with a quote and then some commentarry [I am working on getting the graphic mentioned]:

A key aspect of bacterial survival is the ability to evolve while migrating across spatially varying environmental challenges. Laboratory experiments, however, often study evolution in well-mixed systems. Here, we introduce an experimental device, the microbial evolution and growth arena (MEGA)-plate, in which bacteria spread and evolved on a large antibiotic landscape (120 × 60 centimeters) that allowed visual observation of mutation and selection in a migrating bacterial front. While resistance increased consistently, multiple coexisting lineages diversified both phenotypically and genotypically. Analyzing mutants at and behind the propagating front, we found that evolution is not always led by the most resistant mutants; highly resistant mutants may be trapped behind more sensitive lineages. The MEGA-plate provides a versatile platform for studying microbial adaption and directly visualizing evolutionary dynamics.

The key to understanding the paper is its Figure 3C. There it shows the genes that have undergone more than one mutation across tested bacteria. They break the mutations down into silent changes, changes of amino acids (point mutations), and insertion-deletion or nonsense mutations, which almost certainly are loss of function (LOF). Over half of genes contain such LOF mutations, along with some point mutations, which likely also degrade or destroy function. In other words, devolution….

In another post over at EVOLUTION NEWS AND VIEWS, it is mentioned that “Evolutionists often speak in generalities about beneficial mutations. They may be rare, we are assured, but they happen.” But is this the case? Continuing we read:

…when they do [happen], “natural selection is daily and hourly scrutinising, throughout the world, every variation, even the slightest; rejecting that which is bad, preserving and adding up all that is good; silently and insensibly working, whenever and wherever opportunity offers, at the improvement of each organic being in relation to its organic and inorganic conditions of life” (Darwin, Origin of Species). All right, we have some data to look at. We can put a number to the frequency of beneficial mutations in a large sample. The number is zero.

Genome sequencing technology has progressed very rapidly in only the last few years. NATURE just published results of the Exome Aggregation Consortium (ExAC), the largest survey of human genes to date. (An “exome” is the portion of the genome that codes for proteins.) The exomes from 60,706 individuals from a variety of ethnic groups have been collected and analyzed. If we multiply 60,000 people by the 20,000 genes in the human genome (the lowest estimate), we get a minimum of 1.2 billion genes that have been examined by ExAC for variants. That sounds like a pretty good sample size for scrutinizing some of those beneficial variations that Darwin said his law of natural selection could add up and preserve.

Large-scale reference data sets of human genetic variation are critical for the medical and functional interpretation of DNAsequence changes. Here we describe the aggregation and analysis of high-quality exome (protein-coding region) DNA sequence data for 60,706 individuals of diverse ancestries generated as part of the Exome Aggregation Consortium (ExAC). This catalogue of human genetic diversity contains an average of one variant every eight bases of the exome, and provides direct evidence for the presence of widespread mutational recurrence. We have used this catalogue to calculate objective metrics of pathogenicity for sequence variants, and to identify genes subject to strong selection against various classes of mutation; identifying 3,230 genes with near-complete depletion of predicted protein-truncating variants, with 72% of these genes having no currently established human disease phenotype. Finally, we demonstrate that these data can be used for the efficient filtering of candidate disease-causing variants, and for the discovery of human ‘knockout’ variants in protein-coding genes. [Emphasis added.]

Out of this high ratio of variants (one in eight bases shows variation, they said), there should be some proportion, even if small, that improves fitness. But we search the paper in vain for any mention of beneficial mutations. There’s plenty of talk about disease. The authors only mention “neutral” variants twice. But there are no mentions of beneficial mutations. You can’t find one instance of any of these words: benefit, beneficial, fitness, advantage (in terms of mutation),improvement, innovation, invention, or positive selection.

They mention all kinds of harmful effects from most variants: missense and nonsense variants, frameshift mutations, proteins that get truncated on translation, and a multitude of insertions and deletions. Quite a few are known to cause diseases. There are probably many more mutations that never survive to birth. As for natural selection, the authors do speak of “negative selection” and “purifying selection” weeding out the harmful mutations, but nowhere do they mention anything worthwhile that positive selection appears to be preserving…

Yep. I note this “devolution” in a conversation with a biology graduate student in regards to evidences for the GENERAL THEORY OF EVOLUTION (GTE).

▼ It has been proven that resistance to many modern antibiotics was present decades before their [the antibiotics] discovery. In 1845, sailors on an ill-fated Arctic expedition were buried in the permafrost and remained deeply frozen until their bodies were exhumed in 1986. Preservation was so complete that six strains of nineteenth-century bacteria found dormant in the contents of the sailors’ intestines were able to be revived! When tested, these bacteria were found to possess resistance to several modern-day antibiotics, including penicillin. Such traits were obviously present prior to penicillin’s discovery, and thus could not be an evolutionary development. (Medical Tribune, December 29, 1988, p. 1, 23.)

In 1998, the National Academy of Sciences published and distributed a book to public schools and other institutions entitled Teaching About Evolution and the Nature of Science. Jonathan Sarfati, Ph.D., F.M., wrote a book, Refuting Evolution, which is a topic by topic rebuttal to this Academy of Sciences publication. Under the evidence for evolution in the evolutionist text is the following quote:

▼ Similar episodes of rapid evolution are occurring in many different organisms. Rats have developed resistance to the poison warfain. Many hundreds of insect species and other agricultural pests have evolved resistance to the pesticides used to combat them – even to chemical defenses genetically engineered into plants.

(Sarfati’s reply – any words in the [boxes] are mine):

▼ However, what has this to do with the evolution of new kinds with new genetic information? Precisely nothing. What has happened in many cases is that some bacteria already had the genes for resistance to the antibiotics. In fact, some bacteria obtained by thawing sources which had been frozen before man developed antibiotics have shown to be antibiotic-resistant [6 different antibiotics in fact, penicillin in modern doses – which is way beyond the strength of natural penicillin found in nature]. When antibiotics are applied to a population of bacteria, those lacking resistance are killed, and any genetic information they carry is eliminated. The survivors carry less information [or specificity], but they are all resistant. The same principle applies to rats and insects “evolving” resistance to pesticides. Again, the resistance was already there, and creatures without resistance are eliminated.

[Much like if we killed all dogs (including Canis Domesticus and Canis Lupus) except for Chihuahuas, we would permanently lose the information of the parent population. You could then breed Chihuahuas for a millennium and not get an Irish Wolfhound]

▼ …In other cases, antibiotic resistance is the result of a mutation, but in all known cases, this mutation has destroyed information. It may seem surprising that destruction of information can sometimes help. But one example is resistance to the antibiotic penicillin. Bacteria normally produce an enzyme, penicillinase, which destroys penicillin. The amount of penicillinase is controlled by a gene. There is normally enough produced to handle any penicillin encountered in the wild, but the bacterium is overwhelmed by the amount given to patients. A mutation disabling this controlling gene results in much more penicillinase being produced.

[Thus, the bacteria found frozen in 1845 already had the mutation to overcome modern medical doses of penicillin. So the mutation wasn’t the result of the penicillin in modern doses, thus seemingly becoming resistant… it already had the resistant mutation – informational or specificity losing – in the population. In other words, no new information was added to the parent population!]

(See more in this entire chapter discussing the issue: “VARIATION AND NATURAL SELECTION VERSUS EVOLUTION“)

Updated info with a h-t to ‎TOMI AALTO’S site‎ and it comes by way of PHYS.ORG:

Excerpt: “Pioneering work being carried out in a cave in New Mexico by researchers at McMaster University and The University of Akron, Ohio, is changing the understanding of how antibiotic resistance may have emerged and how doctors can combat it in the future.

In research published in Nature Communications today, the scientists examined one bacterium found 1,000 feet underground (called Paenibacillus) that demonstrated resistance to most antibiotics used today, including so-called ‘drugs of last resort’ such as daptomycin. These microorganisms have been isolated from the outside world for more than four million years within the cave.

The results show the bacterium is resistant to 18 different antibiotics and uses identical methods of defense as similar species found in soils.

Among the different ways that the bacteria could be resistant to antibiotics, the scientists identified five novel pathways that were of potential clinical concern. Finding these new pathways is particularly valuable, as it gives researchers time to develop new drugs to combat this type of resistance, potentially decades before it will become a problem for doctors and their patients.

“The diversity of antibiotic resistance and it’s its prevalence in microbes across the globe should be humbling to everyone who uses these lifesaving drugs,” said Gerry Wright, an author of the paper and scientific director of McMaster’s Michael G. DeGroote Institute for Infectious Disease Research.

“It reflects the fact that we must understand that antibiotic use and resistance go hand in hand.”

My [Tomi’s] comment: How could anyone talk about bacterium evolution after this finding? We can’t observe evolution, we can only observe reaction and adaptation. We can also see strong evolutionary stasis here. Bacteria have not experienced changes in assumed millions of years. They have not evolved the ability to rapidly adapt to modern medicines. Instead, they already have all necessary genomic information and capabilities for ecological adaptation. These features are built in by Intelligent source and the Creator. The evolutionary theory is a dangerous heresy.

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