Orphan Genes Part 2: Evolutionists’ Response

In Part 1 of this series we discussed how the relatively recent technological advances in DNA sequencing led to some very unexpected findings. In particular, the discovery of the prolific existence of “orphan genes.” Given the evolutionary assumption of shared genes among all living things with changes occurring incrementally over vast eras of time, these mystery genes are a direct contradiction to any scenario predicted by evolutionary theory on a foundational level. Therefore, such evidence requires a very serious response. As we’ll see, the explanations evolutionists offer have certainly been revelatory, but not from a scientific standpoint. What has been revealed is a highly unscientific, faith-based commitment to the theory of evolution.

Nelson Velasco Debate

In the 2014 design vs evolution debate between Paul Nelson (Discovery Institute) and Joel Velasco (Texas Tech), the subject of orphan genes arose. Velasco’s 5 points are perfectly representative of the initial evolutionist response. Cornelius Hunter, writing for Evolution News, recounts Velasco’s arguments:

  1. “… there isn’t much to be concerned with here because ‘Every other puzzle we’ve ever encountered in the last 150 years has made us even more certain of a fact that we already knew, that we’re all related.’”
  2. …the whole orphan problem is contrived, as it is nothing more than a semantic misunderstanding — a confusion of terms…”
  3. … many of the orphans are so categorized merely because the search for similar sequence is done only in ‘very distantly related’ species.”
  4. …orphans are really nothing more than a gap in our knowledge… the more we know about a species, the more the orphan problem goes away. And which species do we know the most about? Ourselves of course…: ‘…How many orphan genes are in humans?… Zero.’”
  5. …while new orphans are discovered with each new genome that is decoded, the trend is slowing and is suggestive that in the long run relatives for these orphans will be found..”

As you can see, Velasco doesn’t offer a scientific explanation for the existence of orphan genes. Initially, evolutionists were very reluctant to even concede that they legitimately existed in numbers large enough to warrant discussion. Instead, he frames his case around faith that an explanation which fits evolutionary theory will arise. His answer is a catch all attempt to cover all the bases. Hunter sums up the inadequacy of Velasco’s view:

So to summarize Velasco’s position, the orphan problem will be solved so don’t worry about it, but actually orphans are not a problem at all but rather a semantic misunderstanding, but on the other hand the orphan problem is a consequence of incomplete genomic data, but actually on the other hand the problem is a consequence of insufficient knowledge about the species, and in any case even though the number of known orphans keeps on rising, they will eventually go away because the orphans as a percentage of the overall genomic data (which has been exploding exponentially) are going down.”

Velasco’s 4th Point

The one point listed that most resembles an actual argument is Velasco’s 4th. Is it true that the human genome, the one we know most about, doesn’t have any orphan genes?

The short answer is no.

A 2007 study by the Lander group did indeed reject thousands of proposed orphan genes that had been identified within the human genome, but not all. Authors of the study noted that not all proposed orphans were able to be rejected. In fact, this 2015 study “identified 634 human-specific genes” that appear to have arisen de novo in the human genome. Most telling, however, is why the Lander study rejected the majority of the orphans:

If the orphans represent valid human protein-coding genes, we would have to conclude that the vast majority of the orphans were born after the divergence from chimpanzee. Such a model would require a prodigious rate of gene birth in mammalian lineages and a ferocious rate of gene death erasing the huge number of genes born before the divergence from chimpanzee. We reject such a model as wholly implausible. We thus conclude that the vast majority of orphans are simply randomly occurring ORFs that do not represent protein-coding genes…” (emphasis mine)

On what grounds would such a model be considered “wholly implausible”? Apparently, because their existence cannot be plausibly explained within the constraints of evolutionary theory. Hunter notes the following:

This is what philosophers refer to as theory-ladenness…There was no scientific evidence that those human sequences, identified as orphans, were ‘spurious.’ The methods used in the Lander study were full of evolutionary assumptions. The results entirely hinged on evolution. Although the paper did not explicitly state this, without the assumption of evolution no such conclusions could have been made. Although the paper authoritatively concluded that the vast majority of the orphans in the human genome were spurious, this was not an empirical observation or inference…”

On Second Thought…

Over time evolutionists have been forced to accept that orphan genes do in fact exist in numbers great enough to require a revamping of long held beliefs regarding the formation of genes. In other words, the evolutionists’ explanation of the origin of genes had to… evolve.

Since a designed genome is not an option for evolutionists, an alternative explanation for the existence of these orphan genes had to be considered. In late 2014, Tautz D. published the following conclusion in his The discovery of de novo gene evolution:

Genes can evolve via duplication and divergence mechanisms, but also de novo out of non-coding intergenic sequences. This latter mechanism has only recently become fully appreciated, while the former mechanism was an almost exclusive dogma for quite some time. This essay explores the history of this development: why a view developed, with the alternative hardly being explored. Because of the prevailing view, an important aspect of the nature of genes and their evolutionary origin escaped our attention. Evidence is now rapidly accumulating that de novo evolution isa very active mechanism for generating novelty in the genome, and this will require anew look at how genes arise and become functional.” (emphasis mine)

With evolution assumed, Tautz concludes that new genes must be able to arise “from scratch” (“de novo”) from non coding sequences. He also makes three admissions: (1) they have only recently become forced to abandon (due to the discovery of the existence of these orphan genes) the exclusive evolutionary dogma that dominated genetic understanding; (2) this dogma caused a blindness with regard to their understanding of the nature and origin of genes; (3) they will have to figure out how these genes could exist.

As the 20th century evolutionist Theodosius Dobzhansky famously said, “Nothing in biology makes sense except in the light of evolution.” This is the bias mainstream science operates under. The theory of evolution is never questioned- it is an assumed foundational truth. Since orphan genes are now acknowledged to exist, evolutionists assume that there must be a naturalistic mechanism to explain new genes appearing from scratch in the genome.

What Next?

Evolutionists are left with the task of explaining a naturalistic mechanism by which these “de novo” genes come to exist. In Part 3, we’ll take a look at the plausibility of these proposed mechanisms.

Orphan Genes Part 1: Unexpected Results in DNA Sequencing

In his book, Why Evolution is True, biologist Jerry A. Coyne describes modern evolutionary theory with the following statement:

Life on earth evolved gradually beginning with one primitive species—perhaps a self-replicating molecule—that lived more than 3.5 billion years ago; it then branched out over time, throwing off many new and diverse species.”

Based on this foundational principle, various species are expected to share similar (or homologous) structures due to common ancestry. Berkeley’s Evolution 101 page notes, “Evolutionary theory predicts that related organisms will share similarities that are derived from common ancestors. Similar characteristics due to relatedness are known as homologies.”

Wikipedia’s homology entry lists the following example: “…the forelimbs of vertebrates, where the wings of bats, the arms of primates, the front flippers of whales and the forelegs of dogs and horses are all derived from the same ancestral tetrapod structure.”

Image via wikipedia: “The principle of homology: The biological relationships (shown by colours) of the bones in the forelimbs of vertebrates were used by Charles Darwin as an argument in favor of evolution.”

The Berkeley source provides the following example in the case of plants:

However, the relatively recent advent of DNA sequencing has produced some very unexpected results- surprisingly contrary to this evolutionary theory prediction.

DNA Sequencing- We’ve Come a Long Way Baby

DNA is the blueprint, or instruction manual, containing the instructions which make every species unique. DNA (pictured below) is defined as, “…a thread-like chain of nucleotides carrying the genetic instructions used in the growth, development, functioning and reproduction of all known living organisms and many viruses.”

In the 1960’s scientists developed the ability to “read” this DNA instruction manual in a process called DNA sequencing. This was a monumental scientific breakthrough. Britannica defines DNA sequencing and reveals its significance with the following entry:

…technique used to determine the nucleotide sequence of DNA… The nucleotide sequence is the most fundamental level of knowledge of a gene or genome. It is the blueprint that contains the instructions for building an organism, and no understanding of genetic function or evolution could be complete without obtaining this information.” (emphasis mine)

The last sentence is imperative. While Darwin and his predecessors could hypothesize that common ancestry is the most reasonable explanation for similarities shared among various species based on visual comparison, common ancestry cannot be proven and the very concept of evolution cannot be understood without the ability to “read” an organism’s instruction manual (DNA).

For several decades DNA sequencing was a very slow and expensive process. However, the Human Genome Project, initiated in 1990 and completed in 2003, had a revolutionary effect. The goal of this international project, to map the entire human genome, spurred tremendous technological advances in gene sequencing which has continued far beyond the project’s completion. James Heather concludes his History of Sequencing DNA by stating, “Over the years, innovations in sequencing protocols, molecular biology and automation increased the technological capabilities of sequencing while decreasing the cost, allowing the reading of DNA hundreds of basepairs in length, massively parallelized to produce gigabases of data in one run.”

It is this burgeoning wealth of genetics information that has revealed the “mystery” of orphan genes.

What are Orphan Genes and Why are They Problematic for Evolutionary Theory?

Cornelius Hunter, writing for Evolution News, provides the following definition, “The term orphan refers to a DNA open reading frame, or ORF, without any known similar sequence in other species or lineages. Hence ORFan, or ‘orphan.’” The author of this article in Uncommon Descent explains orphan genes this way, “Orphan genes are presumed protein coding genes that exist in only one species and have such non-similarity to anything in any other species they are called orphans…”

Why is this troubling? If the theory of evolution and (by default) common ancestry are true, a coding gene that is species specific, with no recognizable counterpart in other species should be an extreme rarity. Ann Gauger writes in Orphan Genes: A Guide for the Perplexed, “The working assumption had been that, given common descent and the fact that most housekeeping genes are shared among living things, and the assumption hitherto that evolution occurs by incremental small changes, orphan genes…should be rare if not non-existent.”

So, just how common are they? This 2009 study published in Trends in Genetics found, “Comparative genome analyses indicate that every taxonomic group so far studied contains 10-20% of genes that lack recognizable homologs in other species.” According to Richard Buggs (writing for Ecology and Nature), researchers originally believed that the mystery of these orphan genes would be resolved over time as more genomes were sequenced, finding precursors for the sequences that are now categorized as orphans. However, the opposite has proven true.

For example, Dr. Jeffrey Tompkins discusses ants, “When comparing the ant genes to other insects, researchers discovered 28,581 genes that were unique only to ants and not found in other insects. While the various ant species shared many groups of genes, only 64 genes were common to all seven ant species…The researchers concluded that on average, each ant species contained 1,715 unique genes—orphan genes.”

In Buggs’ 2017 ash tree genome paper published in Nature, he and his colleagues report that of the over 38,000 protein-coding genes found, “…one quarter (9,604) were unique to ash. On the basis of our research so far, I cannot suggest shared evolutionary ancestry for these genes with those in ten other plants we compared ash to: coffee, grape, loblolly pine, monkey flower, poplar, tomato, Amborella, Arabidopsis, barrel medic, and bladderwort. This is despite the fact that monkey flower and bladderwort are in the same taxonomic order (Lamiales) as ash.”

Not only are orphan genes common, they also appear to be functional. Dr.Tompkins writes, “These orphan genes are also being found to be particularly important for specific biological adaptations that correspond with ecological niches in relation to the creature’s interaction with its environment. The problem for the evolutionary model of animal origins is the fact that these DNA sequences appear suddenly and fully functional without any trace of evolutionary ancestry (DNA sequence precursors in other seemingly related organisms).”

Conclusion

Orphan genes are certainly a fly in the ointment for evolutionary theory, but no surprise to either creation science or intelligent design. As Gauger points out, “ Then there is the elephant in the room that evolutionary biologists don’t want to acknowledge. Perhaps we see so many species- and clade-specific orphan genes because they are uniquely designed for species- and clade-specific functions. Certainly, this runs contrary to the expectation of common descent.”

In Part 2 of this series, we’ll take a look at how evolutionary biology responds to orphan genes.

Ethical Guidelines for Clinical Trials Prevent Many Vaccines From Being Adequately Tested For Safety

The CDC (Centers for Disease Control), the WHO (World Health Organization), the National Institutes of Health (NIH), and the FDA (Food and Drug Administration) are considered by most Americans to be the most credible, trusted sources of “unbiased” information regarding disease, medical treatment, and the safety of pharmaceuticals. Your doctor and the entire medical community base their decisions about your care on recommendations from these organizations, which are theoretically based on the studies brilliant, highly-qualified scientists perform for these organizations. These organizations publicly publish this information so that anyone who wishes to educate themselves can do so.

That is precisely what millions of Americans, including myself, are now doing when it comes to the subject of vaccine safety. Unfortunately we are finding that these “trusted” recommendations are not adding up with the information provided by their own sources and many times are blatantly at odds with this publicly published information. I’m going to clearly demonstrate that to you today.

The focus of this article is the following claim publicly stated by the CDC:

“Before vaccines are approved by the Food and Drug Administration (FDA), they are tested extensively by scientists to ensure they are effective and safe.”

How do scientists test vaccine safety?

There are 3 phases in prelicensure vaccine safety testing as described by the FDA. According to the FDA, “Clinical trials are conducted according to plans that FDA reviews to ensure the highest scientific and ethical standards. The results of the clinical trials are a part of FDA’s evaluation to assess the safety and effectiveness of each vaccine.” Herein lies the rub.

What are the highest scientific standards when it comes to determining safety?

According to the NIH, randomized double blind placebo control studies are the “gold standard.” The NIH goes on to state that, “RDBPC studies remain the most convincing research design in which randomly assigning the intervention can eliminate the influence of unknown or immeasurable confounding variables that may otherwise lead to biased and incorrect estimate of treatment effect.”

The problem is, most vaccine studies are not RDBPC due to the ethical standards that must be maintained.

The fact is most vaccine safety clinical trials do not and cannot use a placebo in the truest sense of the word. According to the CDC’s own glossary of terms, a placebo is, “a substance or treatment that has no effect on human beings.” In the case of vaccine testing, a true placebo would have to be an injectable substance that is completely inert, such as saline solution for example. However, that is NOT what is predominantly used in vaccine trials.

If they aren’t using true placebos, what are they using?

According to the 2013 WHO Expert Consultation on the Use of Placebos in Vaccine Trials, the following replacements are used in lieu of a true placebo:

    • “In place of a placebo, a vaccine against a disease that is not the focus of the trial is given to participants who do not receive the trial vaccine.”

Or, an “add-on” vaccine can be used:

    • “In this design, the trial vaccine or placebo product is mixed with an existing vaccine not studied in the trial, and the subjects are given either (a) the trial vaccine mixed with the existing unrelated vaccine or (b) the combination of a placebo and the existing unrelated vaccine.”

Yes, you read those correctly! These vaccines are not being tested for safety against substances that are known to be safe. They are tested against other vaccines which contain the same or similar toxic ingredients common to all vaccines. Some trials are performed using “add-on” vaccines as a placebo. In these cases, potentially everyone in the trial is injected with the actual vaccine being tested! It doesn’t take a rocket scientist to deduce that these methods are unacceptable when the goal is to ascertain safety.

The WHO freely admits this:

“A methodological disadvantage, however, is that trials using these types of placebos provide a less perfect control. It may be difficult or impossible to assess fully the safety and reactogenicity of the trial vaccine, although its efficacy can usually be assessed satisfactorily.” (emphasis mine)

(Reactogenicity is the ability of the vaccine to cause adverse reactions.)

“Methodological disadvantage!?” That’s the understatement of the century!

Let’s look at some very disturbing clinical trial data for a few of the vaccines the CDC recommends. Each vaccine is linked to its package insert so that you can read this information for yourselves:

Engerix B Hepatitis B vaccine (Recombinant) GlaxoSmithKline

“Ten double-blind studies involving 2,252 subjects showed no significant difference in the frequency or severity of adverse experiences between ENGERIX-B and plasma-derived vaccines…All subjects were monitored for 4 days post-administration.”

This study doesn’t prove that this vaccine is safe. Plasma derived vaccines were used in the control group instead of a placebo. It demonstrates that this vaccine doesn’t cause any more or any worse adverse effects than other vaccines cause- at least within the 4 day time frame the subjects were monitored.

This vaccine is given to babies on their very first day of life whether they are at risk for Hep B or not. Only babies born to Hep B positive mothers are at risk for Hep B. For millions of babies this vaccine is a completely unnecessary risk that provides them with absolutely zero benefit.

Infanrix (DTaP) GlaxoSmithKline

Table 4, on page 18 shows that Infanrix was not compared to a placebo, it was compared to the whole cell DTP vaccine.

According to WHO, acellular vaccines (like Infanrix) were introduced “to address the adverse reactions observed with whole cell vaccines…” This WHO report also notes that acellular vaccines have replaced whole cell vaccines in industrialized countries. However, due to the increased cost of acellular vaccines, the whole cell is still used in many developing countries. This vaccine is being tested against a control vaccine that we already know to be more dangerous than the type of vaccine being studied!

**Note figure 8.1 on page 18: “Pregnancy Category C Animal reproduction studies have not been conducted with INFANRIX. It is not known whether INFANRIX can cause fetal harm when administered to pregnant women or can affect reproduction capacity.

Despite this information listed in the product packaging, the CDC routinely recommends the DTaP vaccine to pregnant women. You can read about that on the CDC’s website in their article, Pregnant? Get Tdap in your 3rd trimester.

The CDC recommends either the BOOSTRIX vaccine or the Adacel vaccine (both DTaP) to pregnant women. While BOOSTRIX is rated one category safer than Adacel (Category B),the packaging still notes, “A developmental toxicity study has been performed in female rats at a dose approximately 40 times the human dose (on a mL/kg basis) and revealed no evidence of harm to the fetus due to BOOSTRIX. Animal fertility studies have not been conducted with BOOSTRIX. There are no adequate and well controlled studies in pregnant women. Because animal production studies are not always predictive of human response, BOOSTRIX should be given to a pregnant woman only if clearly needed.”

Still feeling safe? Still feeling like the CDC has your back?

GARDASIL- Merck

In 7 clinical trials (5 Amorphous Aluminum Hydroxyphosphate Sulfate [AAHS]- controlled, and 1 uncontrolled), 18,083 individuals were administered GARDASIL or AAHS control or saline placebo on the day of enrollment, and approximately 2 and 6 months thereafter, and safety was evaluated using vaccine report cards (VRC)- aided surveillance for 14 days after each injection of GARDASIL or AAHS control or saline placebo in these individuals.”

In these Gardasil trials, there actually WAS a control group which was given a true saline placebo. However there was another (much larger) control group given AAHS, which is the adjuvant in the Gardasil vaccine (the toxic portion that triggers immune response.) According to the insert, 15,706 subjects received Gardasil, 13,023 received AAHS and 594 received the placebo. However, they did not compare the three groups separately; they combined the AAHS and placebo group together and compared them to the Gardasil group. This means that the whole Gardasil vaccine was tested primarily against an injection containing its own toxic ingredients and determined to be “safe.”

Furthermore, 40 deaths occurred in the entire study which were broken down by cause. When you subtract the number of deaths that were due to car wrecks, overdoses/suicides and gunshot wounds, and compare the number of subjects who died: 18 subjects who were given either Gardasil or AAHS died and only 1 who had been given the placebo died.  Think about that! Subjects who received Gardasil or AAHS instead of placebo, died at a rate of 18 to 1!

Why Don’t Scientists Use Appropriate Placebos in Trials?

The “gold standard” in clinical trials cannot be implemented because the use of a placebo in many cases is unethical. The purpose of the 2013 WHO Expert Consultation on the Use of Placebos in Vaccine Trials was to detail the guidelines placed on the ethical use of placebos in vaccine trials. If using a traditional, inert placebo in the control group doesn’t “add any risk of serious or irreversible harm,” then clearly there is nothing unethical about using it. But what about when it does?

For example, according to WHO reports, in 2008 rotavirus was responsible for about 5% of all child deaths globally, with 90% of these deaths occurring in Africa and Asia. In a 2011-12 clinical trial in India for a new rotavirus vaccine, 2/3 of the infants received the test vaccine while 1/3 got a saline placebo injection. At the time, two approved oral rotavirus vaccines were already available. Not giving 1/3 of the Indian children in the trial a vaccine already known to be effective against rotavirus, constituted a human research violation that would not have been allowed in the US. Allowing preventable harm to occur in the name of research is unethical.

This means, for very legitimate ethical reasons, using true placebos according to the “gold standard” of clinical testing is not feasible. However, this in no way negates the fact that due to ethical constraints, it is impossible to accurately assess vaccine safety in many cases. It is also unethical to fail to provide this information to parents when discussing vaccine safety.

It crosses the line of unethical and meanders into the territory of illegal, when this information is intentionally censored from vaccine education sheets given to parents in the pediatrician’s office (as well as from conversations with your pediatrician) assuring that vaccines are “extensively tested for safety” knowing full well that safety and reactogenicity are “difficult or impossible to assess” by their own publicly published standards.

The next time someone tells you that vaccines have been proven safe in numerous extensive studies you can tell them that information is blatantly false, and the CDC, WHO, NIH, and FDA know it. Vaccines cannot be both adequately and ethically tested for safety.