Until three years ago I was one of the many scientists who took the gene-centric view of the universe for granted. I had spent the last 17 years producing hundreds of twin studies trying to convince a sceptical public and scientific world that virtually every trait and disease had a major genetic influence. My colleagues and I around the world were largely successful in this, and the prospect of finding the genes underlying most diseases looked increasingly certain. But I had a nagging doubt that we were missing something.
Scientific dogma has long stated that genes are fixed entities and cannot be changed. Once we have inherited them, they can’t be affected by our environment and remain with us until we die or pass them on – unchanged – to the next generation. While we can influence our lives by choosing our friends, spouses, lifestyles, or training our memory, our genes are always immutable. Genes are viewed as central to how the body and cells develop and work, our ‘blueprint’, ‘the code of life’ – or so it was thought.
By studying twins we found that for just about every disease we looked at, identical twins (who share the same genes) both developed the disease more often than non-identical (fraternal) twins (who share only half their genes). The degree of sharing is called a correlation, and by a bit of simple maths comparing these correlations we can produce a measure of the genetic fraction called heritability.
For example, if you were measuring the heritability of weight you might compare the weights of 50 identical twin pairs with 50 non-identical twin pairs by adding up the similarities in one group with the similarities in the other. If the average similarity in identical twins is 90 per cent and in non-identicals is 60 per cent, the heritability is found by doubling the difference between them, i.e. 30 × 2. So we would say that weight in this example is 60 per cent heritable. Calculating the heritability of diseases is slightly more complicated but the principle is the same. This is simply the proportion of differences between people explained by genes.
Diseases like rheumatoid arthritis have heritabilities of 60–70 per cent, so appear to be strongly genetic. Yet when we looked at identical women twins with the disease, 85 per cent of the women never developed their sister’s disease – even though they had the same genes and very similar lifestyles.1 I found this same pattern was true for most diseases studied: there was rarely more than a 50 per cent chance of both twins getting the same disease, and usually the figure was much lower. This was a worry: I realised that my traditional view of genetics and the dominant role of genes might have to change.
Just over ten years ago researchers found that the diets of pregnant mothers could alter the behaviour of genes in their children and that these changes could last a lifetime and then be passed on in turn to their children. The genes were literally being switched on or off by a new mechanism we call epigenetics – meaning in Greek ‘around the gene’. Contrary to traditional genetic dogma, these changes could be transferred to the next generation. In this case the mothers just happened to be rats, but recent similar findings in humans have created a revolution in our thinking.
Darwin’s theory of natural selection and evolution, published 150 years ago, was based on a number of simple but broad concepts that have since been frequently refined and sometimes misquoted.2 His theory was the result of a more general diffuse set of ideas than commonly appreciated, based on the laws of reproduction, inheritance, variability between individuals, and a struggle for survival. The slow process of natural selection will occur in a world in which organisms can reproduce themselves, and there are differences (variation) between individuals. When these individuals reproduce they pass on characteristics of the parents, and these inherited characteristics affect the offspring’s success in survival and reproduction. A key factor in the process of natural selection is that it is blind and driven by random variations. Darwin himself knew nothing of genes, Mendel’s laws of inheritance or DNA, all of which would only become attached to the theory of evolution in the next century.
The gene-centric view is in fact a relatively new phenomenon, firmed up by the coming together of a number of discoveries in the early twentieth century.3 These included finding that genes are segments of DNA that code for proteins, the chemicals that drive all the body’s reactions, made up of a number of amino acids put together in the cell. They also found that these genes come in pairs, each called alleles, which are lined up along 23 paired chromosomes (strands like pipe-cleaners) in each cell in the body. One pair of alleles is inherited from the father and one from the mother. These pairs conveniently split apart when sperm or egg cells are made, so that each contains only one half of the 46 chromosomes, and therefore when they fuse to make a fetus the number of chromosomes and genes stays the same. The splitting and fusing also involves randomly shuffling the (unchanged) parents’ genes, so that no two eggs or sperm contain the same combinations of genes.
James Watson and Francis Crick in 1953 worked out that DNA was a double helix made up of four interlocking chemical bases (abbreviated as T,A,G,C), which zips and unzips – a process that explains why the copies of DNA and genes are so reliable. It was found that these bases lined up opposite each other in a complementary way, which was always the same. This led to the discovery of a smaller molecule called RNA, which translates the DNA code to make the proteins (and so the enzymes) that drive the cell. It was also discovered that genes could, in rare cases, spontaneously ‘mutate’, causing diseases and traits like dwarfism, and this random event was believed to be one source of the natural variation that could be inherited.
The gene was the key. All these insights and the molecular biology and discoveries that followed tended to focus on the pivotal role of the gene as being the primary driver, causing its effects via the proteins. No one asked whether the environment would be influencing genes or proteins, or whether proteins might influence genes in the opposite direction. The fact that Darwin included a role for acquired inheritance in his theory of evolution is often overlooked.
However, Darwin’s big idea was that the main force of evolution was by random selection of the fittest elements of each generation, working over millennia. This (so-called ‘survival of the fittest’) theory perfectly explains our genetic similarity to other species. Whereas all humans share all of their approximately 25,000 genes (the current estimated number is close to 23,000, but this number is constantly being readjusted) with each other, they do vary in which variants of each of the genes are shared, so that whereas siblings share the same basic genes, they will have on average only 50 per cent of the variable bits in common. In all first-degree relatives (siblings and parents) some gene variants will be shared identically, others not at all. Our closeness in evolutionary time to our shared ancestors is exactly mirrored by our similarities in DNA. So we humans share 99 per cent of the same DNA sequence as chimpanzees, from whom we split 6 million years ago, 90 per cent with mice (100 million years), and even 31 per cent with yeast (1.5 billion years). This close genetic relationship with chimpanzees is an uncomfortable fact that creationists have great trouble explaining away, other than by invoking God’s playful nature – an effort to confuse us.
In 2000 Bill Clinton and Tony Blair proudly unveiled to the world one of the great advances for mankind: the sequencing of the 3 billion base pairs that make up the DNA in every cell of a single human. Within all this DNA, the sequence of all the genes was suddenly laid bare. Now, we thought, we had the tools to unlock how humans and animals worked. At the time it was billed as ‘the opening of the book of life’. All sorts of scientific and medical breakthroughs were predicted to follow.
The twentieth century may have been the century of the gene, but genetics has made astonishing advances in the twenty-first century. While the sequencing of the 3 billion bases of genetic code of the first human cost over $2,000,000,000 dollars and involved thousands of scientists working for over ten years, it can now be done for $2,000 and falling – a million-fold discount in ten years. This revolutionary technology has had many other spinoffs.
Curious to discover what the new technology could tell me about my own genetic health risks and family roots, I wanted to learn at first hand what the Internet could offer without seeing a specialist. I had heard of a couple of companies promising personalised genomics tests – Decode, based in Iceland, and 23andMe, in the US. Being a sceptical type of person I applied to both companies independently so that I could compare them. After paying a few hundred dollars for an ancestry and health check I received in the post a tube to spit into for several minutes from one company, and from the other a wooden stick to rub on the inside of my cheek.4
The companies extracted my DNA from the cells of my saliva or cheek tissue and then measured nearly 1 million genetic markers (called SNPs and pronounced ‘snips’) on each sample. They would then match them up with reports from published studies (some of which I had co-authored) that link these markers with diseases, personal traits and your ancestral origins.
Two weeks later the results arrived back via the Internet. They came with plenty of dire warnings about the consequences of knowing the results. Could they change my life? I had heard of journalists trembling when they opened the results, fearing the worst. What about me? Would I be doomed to cancer or Alzheimer’s? After some mild apprehension, in the end it wasn’t so bad, and the results were generally well explained with lots of warnings.
Consulting the findings from 23andMe, I decided to look at my ancestry first. This showed that I was 30 per cent North European, 60 per cent South European and unexpectedly 10 per cent Asian. This was reassuring, as results were similar between the companies. I get a good suntan, but I still can’t explain where the recent Asian genes came from, although I knew it was from my mother’s side of the family, who is supposedly white Australian.
I then checked the disease results and was relieved to see that out of the 20 or so diseases listed, my risk for most of them was low. I did however have a worrying increased risk for diabetes, glaucoma (high pressure) of the eye and bladder cancer. My risk was supposedly low for obesity, Alzheimer’s, Parkinson’s or heart disease. This came as some relief, as my father had died young of heart disease. I next looked at the personal traits and found I had an increased likelihood of having curly hair, brown eyes and not being bald, all of which were – so far – true.
I compared the results with those from the other company, Decode, which used very similar genetic methods but a different prediction algorithm. About half of the tests didn’t agree well on my risk. For the diseases, they only agreed on an increased risk for adult-onset diabetes, which my grandmother had suffered from. For the personal non-disease traits, according to the Decode results I was 85 per cent likely to have blue eyes. This was a shock, as mine are very dark brown and I’m dark-skinned – so this was one of the few predictions I could show were wrong.
With my scepticism heightened, I looked more carefully at the diabetes results that showed me to be at high risk. In fact, my lifetime risk only increased from an average 15 per cent to 19 per cent – so this extra 4 per cent was unlikely to be life-changing. But the sheer range of other results produced from this single DNA test is impressive. I was found to be at twofold risk of overreacting to blood-thinning drugs like warfarin, but not to a range of other common drugs. This might be useful if I were one day to need this drug, say after getting a blood clot in my leg or lung after sitting for too long on a plane. The results also reassured me that while I was, like most Europeans, able to digest milk and not intolerant to the protein lactose, I had a greater than average chance of being a heroin addict. More worrying than my potential drug habit was me being diagnosed as a carrier of a rare disease I’d never heard of: Canavan’s disease, which could affect my children.
As part of the screening test, the 23andMe company included 20 so-called ‘monogenic’ diseases caused by a mutation in a single gene. There are several thousand of these so-called Mendelian diseases, named after the monk Gregor Mendel, including diseases like sickle-cell or cystic fibrosis. Although most are incredibly rare, they often lead to serious mental, visual, lung or nerve problems and early death. These illnesses make up only 2 per cent of all genetic diseases and are very predictable, which is why they have been portrayed as poster boys for the way all the other 98 per cent of genes and diseases behave. Often a tiny change (mutation) in one single chemical base of a gene or pair of genes could lead to a faulty protein being produced, resulting in the disease.
So I found out I was the proud carrier of this rare and lethal genetic brain syndrome called Canavan’s disease, caused by producing an abnormal chemical, aspartate, in the brain. As a carrier I have the mutation only on one of the two copies (alleles) of my genome – the other normal gene means that the enzyme is still being produced normally. It could however be lethal for my children if my wife also was a carrier and had the same mutation on one copy of her genes. Fortunately, although carriers are fairly common (1 in 40) in East European Jews (my father was Jewish, so probably to blame as the likely carrier), the chances of both partners having it are slim (1 in 40 × 1 in 40 = 1 in 1,600), and very much less if one partner is not Jewish. Thousands of other rare genetic diseases act in this way, which is called recessive inheritance.
This real story of personal genetics highlights the successes and limitations of the modern revolution in genetics and personalised medicine. The fact that, only ten years after the first mapping of DNA, any member of the public can now easily access one million genetic tests for a few hundred dollars is pretty incredible. New advances continue at a dizzying pace. Companies like 23andMe are now offering direct to the public for less than $1,500 even more detailed tests using sequencing technology, which can pick up millions of very rare gene variants by only looking at the 1 per cent of your total DNA (your genome) that contains genes. These regions are called your exomes.
Extraordinarily, most doctors and health professionals (unlike the general public, or at least many cab-drivers that I meet) are unaware of these rapid advances and the availability of genetic data. In regular seminars I give to junior doctors, only one in twenty knows how many genes there are in the body – most overestimate by a factor of at least 1,000 and assume there are millions rather than thousands. It just shows how easy it is for the overworked medical professional to be left behind by scientific progress. This gene technology has practical implications and has been great for screening for rare diseases, targeting expensive cancer drugs to most receptive patients and predicting the exact safe dosage of blood-thinning drugs like warfarin.5 But it also has much to tell us about evolution and where we come from.
We now know exactly when we split from other primates (6 million years ago) and from Neanderthals (half a million years) and that we are much more similar genetically to our Neanderthal cousins than we care to admit – as we can often observe on any Friday night in big cities. We know that South American Indians migrated from Asia across Siberia 5–15 thousand years ago and that Europeans branched off from Asian Indians, who were one of the first modern human groups to leave Africa. So this more precise knowledge of our DNA has altered our understanding of human history.6
What about helping us understand diseases? Just in the last few years there have been over a thousand genes discovered that have a role in over 100 common diseases. The early discoveries showed large effects (explaining over 25 per cent of the possible genetic influence) of certain unexpected genes for a few diseases like macular degeneration – the commonest cause of blindness7 – or for that important public health and personal distress problem – male pattern baldness, which my team helped discover.8 Having a high risk of both of these ‘diseases’ can now be predicted with reasonable accuracy from DNA testing. There have been many scientific breakthroughs in just a few years.9
However, despite the extensive list of successes, a few signs were emerging that the paradigm was wrong. Most of the gene discoveries for common diseases turned out to be interesting in terms of biology, but the more we discovered the less useful each new gene became in accounting for the disease, since each gene is of tiny individual effect. For example, the 30 or so genes discovered for obesity, even when combined, account for only 2 per cent of the disease.10
This was frustrating to all of us working in the field, as it meant that each common disease was controlled not by one gene but by hundreds or even thousands of genes. This would require teams from many countries to combine forces and perform studies of tens, and sometimes hundreds of thousands, of subjects in order to find these tiny effects. Another consequence was that for common diseases (unlike rare monogenic diseases) these gene tests were pretty useless for prediction, as I found out from my Internet results.
Another widely held belief that bit the dust was that only the part of DNA containing the genes was important. The remaining 98 per cent of our DNA was thought to be worthless, containing remnants of old unused genes and boring repeat areas. Yet these non-gene regions are also faithfully copied and inherited, so presumably they once had some use in evolutionary history. The fact that genes and their regions are not all-powerful was highlighted when the estimate for the number of genes we are supposed to possess dropped fourfold from 100,000 to less than 25,000 – pretty much the same number as a worm. For the scientists who believed that genes represented the Book of Life it seemed unlikely that worms and humans were reading the same best-sellers. Even the least sophisticated human we can think of is clearly more complex than a worm.
So our complexity and our many differences cannot now be attributed solely to our genes. The big genetic difference between us and worms is that although we have very similar numbers of genes and gene regions, we have masses of what was until recently and quite mistakenly described as ‘junk DNA’ – what we now call non-coding (or intronic regions), as opposed to the exonic regions mentioned earlier.
The traditional paradigm of one gene equals one protein and so one disease has also been exposed as actually a rare phenomenon. The same gene can produce hundreds of different proteins via rearrangements (called splicing) due to this ‘junk’ and to other chemical signals in the cell. So the same gene can produce very different proteins in different environments and therefore different diseases.
Another gene mystery was how, if every cell in our body was derived from replication of the same fertilised egg and had the same identical DNA, did the original cells manage to differentiate into 200 different cell types as diverse as skin, liver cells and brain cells, each with a completely different function? Until now scientists have ignored this awkward problem, as they did not have the tools to investigate it. Recent discoveries are changing this. The secret could lie in the junk or non-coding DNA carried along in the genes, but this appears to be identical (just like the gene regions) in all DNA throughout every cell in the body. So something else must be going on that makes cells different – something that can’t be driven by the genes themselves. This ability to signal genes to perform different functions and make different tissues has to be coming from the cell itself.
More and more, as we acquire the molecular tools to look more closely, we see greater levels of complexity. Eye colour was until recently thought to be genetically simple, a reliable guide to whether your dad was the milkman; it was believed to be controlled by only three genes. As part of an international research project, my team has shown that it is influenced by at least 20 and possibly hundreds of genes.11 I have also met a few rare identical twin pairs with different coloured eyes to each other – a phenomenon that was said to be impossible.
While the hundreds of recent gene discoveries have given us great insights into new disease mechanisms and possible drug targets, the common genes found to date usually account only for less than 5 per cent of the genetic influence. Exactly where the missing 95 per cent comes from is a mystery that is perplexing the field. Most scientists agree that we simply aren’t yet smart enough to realise what we don’t know.
Meanwhile newspapers and the media continue to happily pump out more and more stories proclaiming ‘The gene for fat / depression / strokes / homosexuality / anorexia found’, assuming a determinism that makes most of us feel instinctively uncomfortable when we think about it. Throughout this book, I will refer to some of these simplistic deterministic ideas and slogans to challenge these outdated newspaper headlines and introduce some more modern concepts.
Generally resistant to the genetics revolution have been another group of scientists: the epidemiologists, those who study the environmental causes of disease, as opposed to genetic epidemiologists like me, who study its genetic causes. Until the last ten years they were the most powerful research group studying disease causes, and attracted most of the funds and glory. The different views of the two groups on the relative importance of genes versus environment accentuated the ‘Nature versus Nurture’ debate.
The traditional epidemiologists had also made bold claims, such as that 80 per cent of common disease and 30 per cent of cancer in a population is preventable by changing diet, exercise, and controlling smoking and alcohol consumption.12 In fact, apart from successfully reducing cigarette smoking, which accounts for 30 per cent of cancer deaths, most public health preventions for common diseases have failed. Despite this failure and the costs to society,13 there has been a scarcity of new insights and ideas in the last 30 years. In particular, little thought has been devoted to explaining exactly how different environments exert their effect and how they can interact with genes.
As a junior doctor in the East End of London in the 1980s I was struck by the number of wheelchair-bound patients I saw suffering from the crippling and deforming joint disease rheumatoid arthritis. They had usually developed this in middle age in the 1950s and 1960s. Nowadays the rate of new cases of the disease has halved and cases are much milder, and in my clinics nowadays I virtually never see anyone in a wheelchair. Doctors like me often take the credit and claim that greater skill, insight, earlier diagnosis, scans and better treatments are the reasons for the change.
Ironically, the reality is that the changes had already started before the new technologies and all the new powerful drugs came into use. Yet the reasons for this change remain unknown. Recent changes in asthma, allergies, short-sightedness, heart disease, diabetes, schizophrenia, autism and many cancers also remain largely unexplained by known environmental factors. All the usual suspects – alcohol, coffee, tea, sunshine, exercise, diet – get huge media coverage, but usually have tiny individual effects on any disease. In fact, if you put all of the known measurable environmental risk factors together (apart from smoking or age), they can predict or explain less than a twentieth of most diseases. The rest remain a complete mystery.
I have always been interested in solving puzzles: at 14 my career guidance test told me I should be a detective or a psychiatrist (I ruled out being a priest, which sounded less glamorous). The first research paper I published while a medical student showed that consumption of coffee or soya was linked to cancer of the pancreas. I now realise this was almost certainly wrong, and not a cause of the cancer, but the paper did get me hooked on research. Since then epidemiologists have slowly run out of new factors to study, and to further complicate matters it turns out that many of their prime suspects were actually heavily influenced by genes, so not ‘purely’ environmental at all. We now know that whether you eat garlic or take regular exercise, drink milk or smoke cigarettes is influenced by your genes regardless of your environment. There are few if any examples of environmental factors without a genetic component, and conversely genes don’t work alone and are usually dependent on the cells they live in and their environments. So in a world where hundreds of genes are working together to influence a trait or disease, the old distinction between nature and nurture is simply no longer relevant.
To understand which traits are predominantly genetic and which acquired, scientists have, since the 1920s, turned to the simple model of twins. This is a unique ‘natural’ experiment: the key is to compare the similarities or differences between the pairs. There are two main types of twin: monozygotic (MZ), meaning one-egg, or identical, who share 100 per cent of their genes; and dizygotic (DZ), two-egg, non-identical or fraternal twins, who share on average 50 per cent of their genes and are the same as all ordinary siblings in that respect. In contrast, both sets of twins share very similar environments, so if the factors you are testing (such as height) are similar in both types of twin, a trait can’t be very genetic. But if identical twins are more similar than fraternal twins – and given that the other, non-genetic, factors are equally similar – then a trait must be partly genetically controlled. The standard twin study assumes that the family environment is the same for both twins and that the general environment they are exposed to is very similar – which it usually is.
But just how important is the environment, and how do you test it independently? An ideal but cruel experiment would be to obtain two identical clones born at the same time, separate them at birth and give them different environments, and then see what happens. While we are still some way from deliberately creating human clones (and aren’t yet allowed to), nature has created its very own unique experiment for us to observe. There are now globally around 11 million natural identical-twins experiments to choose from. From these, a few rare sets have been studied in great detail. They are especially unique as they were separated soon after birth to single mothers by overzealous adoption agencies, particularly in the US and Sweden in the 1940s and 50s, and raised in different families for ‘their benefit’. The largest collection of these reared-apart twins features in the Minnesota Twin Study.
The tale of the Jim twins is one of the iconic stories that changed perceptions of the Nature versus Nurture debate in the 1980s and helped launch the Minnesota Twin Study.14 In Southern Ohio in 1979 a 39-year-old called Jim Lewis tracked down his long-lost identical twin brother, who was living locally. They had been separated after their unmarried mother gave them up for adoption as month-old infants in 1940.
On reuniting, the twins discovered that they shared the same first name and an astonishing list of other similarities. They had such a close physical resemblance they both described it as ‘like looking into a mirror’. They were, 38 years after they last met, exactly the same height and weight. They had both married and divorced a Linda, and then married a Betty, and had a childhood dog called Toy. They called their first sons James Alan Lewis and James Allen Springer. They both drank Miller Lite, liked beach holidays in Bas-Grille Florida, smoked Salem cigarettes, suffered from migraines and were chronic nail biters. They also wrapped rubber bands around their wrists, hung keys from their belts and used the same rare Swedish toothpaste called Vademecum. At school they had both liked maths and hated spelling. They had carpentry as a hobby, had been part-time sheriffs and drove the same model and colour Chevy.
Sounds spooky? It certainly gives the impression of inevitable determinism, in which environment and upbringing didn’t count. Just think of the complex but identical genetic mechanisms that occurred to make them buy the same toothpaste. Going by this example, it doesn’t seem to matter what kind of parents you had, and whether you were raised in a hovel or the Hyatt: your genes remain totally dominant. The press loved this story and the two Jims became overnight celebrities and even appeared in Time magazine. They were physically so strikingly similar and had so many amazing quirks in common that one of the researchers was quoted as saying: ‘this would swing the pendulum even further away from radical environmentalism.’ But could this example possibly have been a combination of coincidence and hype?
They did have some small differences which we now know were downplayed at the time. One had married a third time – the knowledge of which was probably a worry for the other twin’s wife. They had different hairstyles – one Jim had a Beatles haircut while the other had long sideburns and a Robert De Niro look. One preferred written communication and the other preferred talking. Other differences would have emerged in the 15,000 questions they answered.
There are a number of reasons their similarities could have been exaggerated. The first is that the environment and peer groups they shared are likely to have been very similar: suburban Ohio is not San Francisco or London in terms of a varied social and cultural mix. Most guys there at some time drank Miller Lite and smoked Salems, did carpentry and had bought a Chevrolet.
The second factor is selective reporting. We all have thousands of personality traits and likes and dislikes that characterise us as individuals. On average we are likely to share many with unrelated strangers from the same country – say our favourite music, food, blend of coffee, newspapers, football teams or TV shows. Some strangers will by chance share more of these. So by picking the most striking pair, and focusing on the similarities while ignoring the traits that they don’t share, the similarities are easily exaggerated.
Producers of daytime TV shows are often desperate for twins who say they have psychic powers, and I receive regular requests for help. When we did an actual survey, 66 per cent of our identical twins said they had no psychic powers whatsoever. These ‘media boring’ twins unsurprisingly never get onto TV, to scupper the idea that most twins are telepathic. Psychologists and advertisers observe that people make subconscious choices. For example, they tend to select mates with similar names to themselves, to name their children and dogs in non-random ways, or to pick products that in some way remind them of themselves.15
A final factor in distorting the characteristics of the identical Jims is that once a twin pair has been told they are interesting or similar, they tend to subconsciously exaggerate their similarities and downplay their differences. Although the scientific papers that reported the findings did also mention subtle differences between them, the public and popular impression absorbed via the media was of an uncanny, nearly supernatural resemblance due to the power of genes, leaving little if any room for any other factors.
This book will show why the similarities between the two Jims are the exception and not the rule. To do so we have to look at genes in an entirely new way, and challenge some of the long-held traditional assumptions about our relationship with our genes.
Assumption One is that our genes single-handedly define the essence of human beings: that they are our ‘human blueprint’ or ‘book of life’ and are the only mechanism of inheritance. In order to fully understand this point we need to reconsider our entire gene-centric view of life. Assumption Two, following on from the central role of the gene, is that genes and heritable genetic destiny cannot be changed or modified. And therefore Assumption Three is that an environmental event can’t produce a long-lasting influence on your genes throughout the cells of your body. Assumption Four is that you cannot inherit the effects of your ancestor’s environments – in other words that you cannot inherit acquired characteristics. So the traditional view has always been that, to give one example, the smoking habits of your biological father, if you were adopted, and never met him, could not possibly influence your own health. The new science tells us something very different.
In short, we need to look again at our entire conception of genetic inheritance and question each assumption that has been handed down to us. To do so we will first hark back to a time before Darwin, to consider some alternatives to Darwinism.