During the European winter of 1944, Allied troops were pushing toward Germany. In Nazi-occupied Holland, Dutch drivers went on strike to further hinder the German war effort. In retaliation, the Germans began a blockade of the Western Netherlands which, together with a severe winter, resulted in a period of catastrophic deprivation and starvation. The population was reduced to a diet of about a third of their needed daily calorie intake, resulting in approximately 20,000 deaths between November 1944 and May 1945 when the blockade was lifted. People were forced to eat grass and tulip bulbs, and were burning furniture for heat in order to stay alive. This period is known as the Dutch Hunger Winter. The iconic actress Audrey Hepburn1 was a teenager in Holland at the time. The ill health she suffered throughout her life was likely a result of the deprivations of these few months.
One can easily imagine how a severe lack of nutrition could affect the health of the victims. But what about the lives of babies who were still in the womb during that terrible period, and even generations beyond them? Due to excellent registry and health records in the Netherlands, scientists have been able to use this episode as a ‘living laboratory’, following birth weights and health issues for decades after the end of World War II. This has yielded some startling results.
Babies who were in the first months of gestation during this period were found to have normal birth weights, while more likely to suffer from obesity in their later years. Those exposed to starvation in the last months of gestation were found to be under the average weight at birth, and for the rest of their lives. They were less likely than the general population to be obese.2 Even more startling, these same characteristics seemed to also have passed on to the following generation, the grandchildren of the women starved during those six awful months. This was so despite the fact that the diets of these women, and those of their descendants, returned to normal when the blockade ended.
These and other variations from average suggested that these changes were not just a result of a nutrition deficiency during the development of these children, but that the ‘environmental’ change represented by the starvation had led to something changing in the expression of their genetic information. In other words, external changes had led to long-term inherited effects.
It was not likely that an environmental change could alter the sequences in their DNA code, which were still going to be the result of the combination of codes from their mother and father. So it must have been the way in which genes were expressed which had been altered by the environment, i.e. while the DNA sequence remained the same, certain genes were switched on or off as a result of outside, environmental stimuli. Scientists have identified the insulin-like growth factor II (a protein coded for by the IGF2 gene) as playing an important role in this.3
A new discipline was born, the study of epigenetics (over, or above genetics). One of those doing research on this intriguing mechanism, Dr Bas Heijmans, says, “Epigenetics could be a mechanism which allows an individual to adapt rapidly to changed circumstances … It could be that the metabolism of children of the Hunger Winter has been set at a more economical level, driven by epigenetic changes.”4 Tel Aviv University neurobiologist Oded Rechavi stated that “the children of Dutch famine victims showed various effects of their heredity that appeared to be a kind of compensation for their parents’ starvation.”5
Research pointing to changes in the access to genetic information in the DNA (genotype) driven by outside or environmental stimuli, and resulting in a change in the organism (phenotype), is proliferating. Experiments have been done on worms: “Previously, nobody had yet shown that it’s enough to change the worms’ environmental conditions to cause heredity that isn’t dependent on DNA … Because restricting calorie intake apparently extends life, the great-grandchildren of our famished worms lived 1.5 times longer than ordinary worms—despite the fact that they ate no less than any other worm.”6
In another example, an RNA silencer, induced in worms as a response to an introduced virus, continued to express itself for more than 100 generations.7
Studies on bison bones found in permafrost in a Canadian gold mine indicated that epigenetic changes in the bison population enabled them to adapt rapidly to changes in climate. These are changes far too rapid for traditional Darwinian models of natural selection to explain. “The bones play a key role in a world-first study, led by University of Adelaide researchers, which analyses special genetic modifications that turn genes on and off, without altering the DNA sequence itself. These ‘epigenetic’ changes can occur rapidly between generations—without requiring the time for standard evolutionary processes.”8
Scientists conducting experiments on agouti mice found that by manipulating nutrition they could switch off a certain gene. When the gene is active (‘on’) the mice are normally obese and a yellowish colour; by switching the gene off the mice are of a normal, slim appearance, and brown. By feeding a combination of nutrients including vitamin B12 to the mother before mating, the gene was able to be turned off in the babies.9
Evolutionists holding to the paradigm of the Modern Synthesis (neo-Darwinism; that mutations and natural selection explain the diversity of life on earth) have tended to resist strongly the conclusions coming from epigenetic research. In their view, evolution is a slow process of random mutations in the genome, resulting sometimes in a tiny advantage in the phenotype. This is favoured by natural selection, and passed on by Mendelian inheritance to future generations. The gene is seen as the master that controls the outward expression in the cell and the larger organism, an idea made popular in Dawkins’ book, The Selfish Gene. The idea that the interaction of the outward form of an organism with the environment passes information back to the genome, or even just affects how the genome ‘acts’, is anathema to them.
Even worse for evolutionists, epigenetics suggests that latent genetic information of sorts is sitting in the DNA waiting for a particular environment in order to be switched on or off. It is like information in a book with certain pages stapled together, only to be opened and the information acted upon in certain environmental circumstances. If evolution occurs by natural selection, via the environment culling or conserving the effect of random mutations, how can there possibly be a ‘suite’ of genetic information just waiting there to be switched on by an environment to which the organism has yet to be exposed? It poses another ‘chicken or egg’ conundrum to the myriad that already challenge evolutionists.
It also adds another nail in the coffin of the so-called ‘junk DNA’ idea. As only a very small percentage of DNA codes directly for protein, evolutionists had been quick to promote the notion of junk DNA. They claimed that most DNA is ‘vestigial’; left over from eons of random trial and error mutations. In fact, neo-Darwinist evolution demands this because the vast majority of mutations are thought to confer no selection advantage or disadvantage and so would just ‘sit there’ in the DNA.
A corollary of this belief is ‘pseudogenes’; DNA sequences that look like genes but do not appear to code for protein, like normal genes; i.e. they are believed to be non-functional, having mutated from once-functional genes. This idea based on ignorance is used by scientists such as Francis Collins to argue that modern humans are related to certain apes which share the same ‘pseudogenes’. If these are indeed genes that have degenerated by random copying errors, this would seem to have some merit. Common functional genes could indicate common design but organisms sharing the same genes that are a result of random errors would point by the laws of probability to them being related, much as common mistakes on exam papers would indicate a cribbing relationship between those sharing the mistakes. However, many different functions for ‘pseudogenes’ are being discovered, including roles in epigenetic modification of gene expression.10 These discoveries are relentlessly helping destroy one of the major claimed ‘proofs’ of the common descent of apes and men.
Denis Noble, a British biologist who held the Chair of Cardiovascular Physiology at the University of Oxford from 1984 to 2004, wrote a paper on the implications of epigenetics for neo-Darwinism. Though an evolutionist, he says, “It was clearly premature to label this DNA as ‘junk’”.11 He is recommending a complete re-think of the neo-Darwinian mechanisms of evolution—random mutations and natural selection. Unsurprisingly he is coming under attack for daring to challenge the status quo.
Another reason many neo-Darwinian evolutionists have been so opposed to epigenetics (though the undeniable evidence is forcing at least a grudging acceptance) is that it seems to be a resurrection of the idea of ‘inheritance of acquired characteristics’. This was the view of the French naturalist Jean-Baptiste Lamarck. He believed that characteristics acquired by an organism during its lifetime (for example an animal ‘acquiring’ a longer neck by having to stretch for high leaves on trees) could be passed on to its descendants. For Lamarck this was an evolutionary mechanism. Darwin himself seemed sympathetic to the idea and alluded to it a number of times in his Origin of Species. But due to the implied movement toward a goal that Lamarck called Le pouvoir de la vie (the power of life), with possible metaphysical implications, the notion was rejected by neo-Darwinists.
Noble argues that epigenetics seems to vindicate aspects of Lamarckian ideas. He quotes John Maynard Smith, himself an influential neo-Darwinian, as having said in 1998 that Lamarckism ”is not so obviously false as is sometimes made out”.12 Noble continues to use the term ‘inheritance of acquired characteristics’. This seems to completely miss the point! Epigenetic research indicates that these new characteristics are not acquired, but merely ‘turned on’; all the information for the new characteristic shown in an organism was already there in the DNA, and activated by environmental stimuli. Someone turning on a vehicle air conditioner in response to high temperatures would not claim at that moment that the car had ‘acquired’ an air conditioner. The vehicle was manufactured with one; the activation of the air conditioner was in response to environmental conditions, and improved the ‘survival’ conditions in the vehicle. ‘Inheritance of switched-on characteristics’ would seem to be a better label for epigenetics.
Professor Alan Cooper of the University of Adelaide’s Australian Centre for Ancient DNA (ACAD) says: "The climate record shows that very rapid change has been a persistent feature of the recent past, and organisms would need to adapt to these changes in their environment equally quickly. Standard mutation and selection processes are likely to be too slow in many of these situations.”13 And so the study of epigenetics promises to potentially answer many questions for scientists working on models of biblical creation. Could it be one of the mechanisms that our omniscient and omnipotent God used to prepare the various kinds He created to adapt rapidly to different environments after the Fall (and subsequently the Flood)? Children born soon after the Dutch Hunger Winter, and their children after them, with their smaller physiques, would have been more likely to survive an extended famine. In the same manner, epigenetic processes in many organisms, with feedback from the environment regulating the switching on and off of certain genes, could have been one of God’s mechanisms enabling creatures to respond rapidly to environmental change. This contrasts with the mere ‘chance’ expression of various possible combinations within the God-given mechanism of Mendelian genetics, ‘selected’ by a survival of the fittest process (and the survivors then passing those characteristics on to their offspring).
Could skin, feather and fur colours have been more the result of epigenetic pre-programming activating after the Flood in animals and after Babel in humans, with those ‘switched-on’ genes then passed on to further generations by conventional genetics (transgenerational epigenetics)? Could apparently significant differences in different species, otherwise very similar to each other, have been the result of epigenetic switching within the same kind, but in different environments? For example, the thick fur and sebaceous (oil) glands in the woolly mammoths would have enabled them to survive very cold climates. Modern elephants lack these characteristics and yet in so many other ways are extremely similar to them.
The physiology associated with carnivory—tooth design, shortened gut and so on—could it also potentially be explained by epigenetics? Perhaps these characteristics were switched on simultaneously in many members of a population in response to environmental change at the Fall.14
Epigenetic research is gathering momentum, revealing another layer of breath-taking design. The ‘junk DNA’ and ‘pseudogene’ paradigm is fast crumbling along with neo-Darwinism itself. One senses that scientists are just beginning to scratch the surface of the “fearfully and wonderfully made”15 phenomenon that is life.