Popular Misconceptions About Evolution

Ask the average lay person what they take the word evolution to mean, and few will reply “the change in the genetic frequency of a population over time”. This general lack of understanding is further evidenced by US figures showing that only 45% of people hold true the statement that “human beings, as we know them, developed from earlier species of animals”. More worrying was a study conducted by the Jewish Theological Seminary and HCD Research in Flemington, New Jersey where 34% of doctors reportedly believed that the Intelligent Design was a superior explanation. This is despite the growing realisation that nothing in medicine makes sense, except in the light of evolution.

The greatest barrier to the understanding of the theory usually tends to be in its conceptualisation. If we are the cumulation of billions of years of selective pressure from our original ancestors to our branch, then one could expect that we would be a complex aggregate of patchwork fixes meshed together to form an organism that may appear “irreducibly complex”.  Ironically, it is our evolution that has shaped our outlook. Many cite the body as a perfect machine unlike any we can construct. However, the question of what is perfection is one philosophers have been unable to answer since Plato, but in context a philosopher is not required to answer this. What we hold to be perfect — how we make sense of things — is shaped by our experiences and selection biases. We tend to remember the good and disregard the negatives. Selection biases of this nature were revealed in studies of people who perceived themselves to be lucky versus those who believed themselves to be unlucky. There was no statistical difference in positive versus negative events in the two groups, but what they recollected. It was also determined that once someone was conditioned to take on the “lucky” outlook, they didn’t revert to their previous pessimistic point of view. This recollection bias can reinforce the placebo effect, and explain why people find alternative therapies to work for them. Essentially we “data mine” our recollections for self affirmation. This may have had importance when it came to our ancestors’ forming of habits including food gathering, and experiments have found this mechanism at work in pigeons which could be trained to exhibit superstitious traits. Now days this vestige may be behind superstitions of our own, like alternative medicine.

Human evolution has been given a bad rap. Critics often cite eugenics as evolutions’ logical extreme when applied in human populations. Eugenics does not follow from evolution, but rather a poor understanding of it. Eugenics presupposes some form of goal in evolution, and that in some way there exists some perfected outcome to which all should conform. Evolution in no way predicts a perfectible phenotype, merely that gene frequency will change with time, it is purely a function of random genetic mutation and non-random reproduction, and nothing more. Any defects that manifest after reproduction are immune from negative selection pressures that shape the organism’s evolutionary future. Those that are deleterious to survival of the phenotype, making it not viable before it can reproduce, will fail to propagate. Evolution is merely a means, and not an ends as many believe. If it can reproduce, it will be sustained.

Lacking a goal, evolution thus becomes a function of genetic diversity. Diversity in any population is a metric of its resilience. The higher the diversity, the more pressures that the population, in theory, is able to overcome. Diversity, however, is not equally present in all genes. Genes that are required for critical steps in metabolism, or are in some other way “core”, are highly conserved (some with over 50% homology between humans and the humble E. coli). Furthermore, within genes certain domains will be more highly conserved than other regions. Regions of intense conservation serve functions like membrane spanning, signal transduction or other domains to which changes will disrupt function. Disruption to these genes would cause lethal phenotypes. Consequently, as an organism becomes more complex, tighter regulation is required to coordinate development and function. The organism becomes less able to develop new useful mutations as it risks rendering dysfunctional a gene that is essential to development, regulation or some other essential process (especially true in species with long generation times). This isn’t to say that new mutations are impossible, it just restricts where they can occur. Most of the useful mutations occur in pseudogenes and in terminal repeats, the average person has 150 mutations of their own to contribute to the gene pool.

New, useful genes do not necessarily come at the expense of existing ones. The immunoglobulin superfamily, hemoglobins, and homebox genes that regulate embryological development are just a few examples of gene duplication events. Successful pathways in evolution are highly conserved, but thanks to mobile genetic elements like long interspersed nucleic elements (LINES), gene duplications can occur. Without promoter sequences the duplicated gene stays repressed, and unable to access editing enzymes it takes on mutations at a more rapid rate. Occasionally these new duplicates come under the regulation of a new promoter. Depending on their evolutionary meanderings,  a new functional gene may be formed. Some apparently negative mutations are beneficial in a different context (e.g. sickle cell anaemia in the heterozygous state and malaria). Could it be possible that with gene duplication events, and enough time, a potentially deleterious protein may serve an as yet unforeseen but highly positive function in our evolutionary history? Again, this is an unknown, but the possibilities exist.

Bacterial and viral adhesion and pathogenicity are mediated by receptors. Essentially these receptors could be anything. Homogenising these receptors at a population level comes with dire consequences. Attempts at selecting fish and breeding them for resistance against vibriosis unwittingly created a population that, although resistant to the disease of interest, was woefully susceptible to other infections and was entirely overcome. This raises the spectre of designer babies. Could the human selection of favoured traits create a homogeneous internal host environment that encourages the evolution of pathogens to exploit these new common features?For example, recent studies suggest that there is a genetic marker that determines an individual’s susceptibilty to infection by Neisseria meningitidis — a single protein found in some hosts. If we unwittingly select for these markers, not only might we be more likely to suffer as a population from the disease as a result of vulnerability, but increased colonisation might open up new possibilities for transmissibility, compounding the potentially devastating effect.

Hopefully a well grounded understanding of evolution will allow us to realise there is no “perfect” human we should be aiming for, but rather a diverse population. Evolution isn’t an end, but a process. In the future a better understanding of the human genome combined with a means of measuring differential gene expression, and predicting cross over interactions, might allow us to understand each individual’s susceptibilities and optimal treatments. We’re slowly taking steps in this direction each and every day, in this era of the sub-$1000 genome. These evolutionary insights also reveal that with our 99.99% genetic similarity we are truly a human fraternity. The next chapter in our evolution, like all those that have come before, won’t be defined by competition but by mutual aid. The more we allow our fellow man to remain in the grip of disease, the greater opportunity we give disease to adapt to us. The evolution of our social groups allowed our survival through a conspiracy against nature, now as a species we must conspire against disease.

Molecular microbiologist, Post-Doc in infectious diseases research . Research focus on ESBL and carbapenemases. Current UWA Medical student | @CdrHBiscuitIII | LinkedIn |

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.