Can Alzheimer's Be Cured?

An excellent article over at Scientific American. As I eventually hope to be involved with Alzheimer's in my career, I found it so good that I fancied reproducing it here on this blog.

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P. Murali Doraiswamy is the head of biological psychiatry at Duke University and is a Senior Fellow at Duke’s Center for the Study of Aging. He’s also the co-author of The Alzheimer’s Action Plan, a guide for patients and family members struggling with the disease. Mind Matters editor Jonah Lehrer chats with Doraiswamy about recent advances in Alzheimer’s research and what people can do to prevent memory loss.

What do you think are the biggest public misconceptions of Alzheimer's disease?

The two biggest misconceptions are “It’s just aging” and “It’s untreatable, so we should just leave the person alone.” Both of these misconceptions are remnants of an outdated view that hinders families from getting the best diagnosis and best care. They were also one of the main reasons I wanted to write this book.

Although old age is the single biggest risk for dementia, Alzheimer’s is not a normal part of aging. Just ask any family member who has cared for a loved one with Alzheimer’s and they will tell you how different the disease is from normal aging. Alzheimer’s can strike people as young as their forties; there are some half a million individuals in the United States with early-onset dementia. Recent research has pinpointed disruptions in specific memory networks in Alzheimer’s patients, such as those involving the posteromedial cortex and medial temporal lobe, that appear distinct from normal aging.

The larger point is that while Alzheimer’s is still incurable it’s not untreatable. There are four FDA-approved medications available for treating Alzheimer symptoms and many others in clinical trials. Strategies to enhance general brain and mental wellbeing can also help people with Alzheimer’s. That’s why early detection is so important.

Given the rapid aging of the American population - by 2050, the Alzheimer's Association estimates there will be a million new cases annually - what are the some preventative steps that people can take to prevent or delay the onset of the disease?

Unfortunately, there isn’t yet a magic bullet for prevention. You can pop the most expensive anti-aging pills, drink the best red wine, and play all the brain games that money can buy, and you still might get Alzheimer’s. While higher education is clearly protective, even Nobel Laureates have been diagnosed with the disease, although it’s likely their education helped them stave off the symptoms for a little bit.

My approach is more pragmatic - it’s about recognizing risks and designing your own brain health action plan. The core of our program is to teach people about the growing links between cardiovascular markers (blood pressure, blood sugar, body weight and BMI, blood cholesterol, C-reactive protein) and brain health. A population study from Finland has developed a fascinating scale that can predict 20-year risk for dementia – sort of a brain aging speedometer. Obesity, smoking, lack of physical activity, high blood pressure, and high cholesterol are some of the culprits this study identified. So keeping these under control is crucial.

Depression is another risk factor for memory loss, so managing stress and staying socially connected is also important. B vitamins may prevent dementia in those who are deficient and there are some simple blood tests that can detect this. For the vast majority of people, however, there are no prescription medications that have been proven to prevent dementia. This means that a brain-healthy lifestyle is really our best bet for delaying the onset of memory loss.

In the near future we will likely have prevention plans that are personalized based on genetic, metabolic and neurological information. In familial Alzheimer’s disease, pre-implantation genetic diagnosis has already been used to successfully deliver babies free of a deadly Alzheimer causing mutation—though only time will tell if deleting such dementia risk genes in humans has other consequences.

Your book talks about a new technique that allows doctors to image amyloid plaques in the brain. How will these change the diagnosis of the disease?

Amyloid PET scans are in the late stages of validation testing to see if they can improve the accuracy of clinical diagnosis. The Alzheimer’s brain is defined by beta-amyloid plaques and tangles but, at present, these can only be definitively diagnosed with an autopsy. If an amyloid PET scan is “plaque negative” that will tell a doctor that Alzheimer’s is unlikely to be the diagnosis and help reassure the family. Early findings suggest that people who carry risk genes are more likely to have plaque positive scans even before they develop symptoms - suggesting that the scans could possibly be useful for predicting future risk. If true, this might eventually lead to a change in diagnostic terminology where “preclinical” Alzheimer’s is diagnosed purely based on biomarker and scan findings long before memory symptoms start. Therapies to treat Alzheimer’s by blocking amyloid plaques are already in trials but are currently given blindly to patients without knowing their brain plaque status—raising their risk for side effects and treatment failure. So this scan may also help drug development by helping select the most appropriate subjects for treatment and then monitoring treatment effects. Amyloid accumulation with aging is seen in many animal species and the scan offers us a tool to study what role plaque plays in normal brain aging. So this could do for the brain what colonoscopy did for the gut!

Will science ever find a cure for Alzheimer's?

It’s an incredibly tough puzzle to crack but the pace of research is so great that new drug targets are being reported daily. I think a form of cure is more likely to come from delaying the onset rather than by growing new brain cells to repair lost tissue. Realistically speaking there are several fundamental questions we don’t fully understand and have yet to answer: What causes the disease? Why do plaques and tangles form? Why are the memory centers the first to be destroyed? On the positive side, there are several dozen drugs in clinical trials.

What recent scientific advances in treating or understanding Alzheimer's are you most excited about?

I’m most excited about diagnostic advances. By using a combination of biomarkers, genetic tests and new brain scans, we are inching very close to predicting not only who will develop Alzheimer’s but the exact age when they may start developing symptoms. This offers huge opportunities for conducting prevention trials. Of course, it also brings a whole host of ethical challenges, since our diagnostic and predictive abilities are advancing far faster than our ability to prevent Alzheimer’s.

On the treatment side, there are several developments that I am excited about. The interactions between vascular disease and memory loss suggest that at least some aspects of Alzheimer’s may be modifiable through diet and exercise. Dimebon, a drug that improves mitochondrial function, has yielded promising results and is in final stages of testing. In addition, therapeutic strategies which target the brain’s own ability to repair itself – for example, by delivering nerve growth factor through viral vectors – are in clinical trials. Until we have a cure, however, it’s really important to focus on improving the quality of life of people with Alzheimer’s.

Gonna (Evolve To) Sing You My Love Song

Why do we like to sing soppy love songs to our loved one? What is it about them that evokes a mood of affinity and bonding? Why do tears spring to our eyes when we hear a lyric that reminds us of a friendship, relationship or other close bond?

The composition and interpretation of music through song, dance, and playing a musical instrument, are complex and high-level tasks of the creative brain. Indeed, the 'creative' aspects of personality are thought to constitute a particular division of intelligence in itself. Although it is possible to gain a certain level of proficiency in playing the works of Beethoven and Mozart through social and/or environmental factors (parental support, music school), the phenomenon of the child prodigy does in fact suggest an innate genetic basis for talent. Creativity itself is a complex process that draws largely from areas of the right hemisphere, not activating the frontal lobes or cortices very much. And since we are talking mainly of cognitive processes,we can expect hormones such as arginine vasopressin (AVP), which helps to control higher functions such as memory and learning, to take a lead role. Given that this hormone is mediated by the AVP receptor 1A (AVPR1A) gene, that affects many behavioural, social and emotional traits such as male aggression, pair bonding, altruism, parenting, sibling relationships, love etc., it stands to reason that this key gene is the one to watch.



A team of researchers at Helsinki University, headed by Liisa Ukkola, carried out a study purporting to investigate the neurobiological basis of music in human evolution by analysing the role of the AVPR1A gene and five others and their effects on general creativity and musical aptitude by testing 343 multigenerational participants from 19 Finnish families, professional and amateur musicians alike. Ages varied from 9 to 93 (mean age 43) and DNA was obtained by 298 (86.9%) of those over age 15. Three measures were administered: an extensive online questionnaire to assess creativity in those who composed, improvised or arranged music; Carl Seashore's pitch and time discrimination subtests (SP and ST respectively); and a Karma Music Test (KMT) designed by one of the research team. The results showed that high scores on the music tests associated well with high levels of creativity, and also higher in creative individuals than non-creative individuals. Genetic testing confirmed that creativity was a heritable trait.

Wait a minute - what does all this have to do with the brain?

This study showed how auditory structuring ability (gleaned from the KMT test) were associated with the AVPR1A gene, with the strongest effect found in the RS1+RS3 haplotype. The ST and SP tests also suggested this association, and this was further confirmed when the associations were replicated with combined music test score (COMB). The kicker is that the AVPR1A gene is instrumental in modulating social and cognitive behaviours, and music is certainly a medium that initiates, enhances and accelerates certain behaviours! We all know about the peculiar social customs of singing songs of romantic content in order to attract the opposite sex, music played to enhance group cohesion and initiate vigorous hip-spinning activity, and mothers singing soothing lullabies to their offspring in order to induce a state of quietness.

But aside from all of that, the genetic studies provided interesting tidbits of information relating to the homologies of the AVPR1A gene as various alleles were recognised to associate with either composing, arranging and performing music. Higher spatial scores were found among musicians than non-musicians, a possible explanation being that musicians tend to need to read and memorise notes and/or sheet music. Research into the recently discovered TPH2 gene may uncover the details behind the numerical sense necessary to perceive rhythm. The A1 allele associated with the dopamine receptor D2 (DRD2) gene is suggested to be linked to courtship.

The releases related to this story hyped up the evolutionary implications in a big way but I can find very little basis for that in this paper. As usual, evolutionary extrapolations are mainly speculative but interesting nevertheless. The text specifically mentions that evolutionary contributions are speculated on the basis of PET imaging that show partial overlapping between music and language-related areas of the brain. As improvising music usually consists of collaboration with other musicians or between a performer and their audience it makes sense that the role of these brain areas and the genes associated with musical talent be highlighted as it has. As the paper itself says:

"Creativity is a multifactorial genetic trait involving a complex network made up of a number of genes."

And it is because of that and the connections to social/cognitive areas of the brain that there is justification for the idea that music enables and enhances social communication in a way that increases attachments. This can explain why people automatically feel closer when they find they share the same types of music.

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Ukkola, L., Onkamo, P., Raijas, P., Karma, K., & Järvelä, I. (2009). Musical Aptitude Is Associated with AVPR1A-Haplotypes PLoS ONE, 4 (5) DOI: 10.1371/journal.pone.0005534

A Beautiful 'Brainbow'

(Inspired by Encephalon #64)

Neurons are clever little cells, the very material that processes what we think, see, hear, feel, understand, and so much more. Has anyone considered if they look as artistic as they are artful? In 2007 a team of Harvard neuroscientists found a way to activate multiple fluorescent proteins in neurons and which allows over 90 distinct colours to be 'tagged'. Similar to television, a palette of colours and hues can be generated from three primary colours such as red, green and blue. As one might expect, the activity generated by brain activity causes an explosion of colours, referred to as 'brainbows', and not only does this technique present an impressive light show but also allows researchers to gain an insight into the mechanics by which neurons receive and transmit information. Below are my favourite images:


Auditory portion of a mouse brainstem. A special gene (extracted from coral and jellyfish) was inserted into the mouse in order to map intricate connection. As the mouse thinks, fluorescent proteins spread out along neural pathways. Mammals in general have very thick axons in this region which enables sound to be processed very quickly.


A single neuron (red) in the brainstem. The helter-skelter of lines that criss-cross through the image are representative of signal traffic from other neurons. In this image, one brainstem neuron is surrounded by the remnants of signals from other neurons (mainly blue and yellow-coloured). When viewed with a special microscope, cyan, red and yellow lasers can cause each neuron to shine a specific colour, enabling researchers to track the activity of individual neurons.


This view of the hippocampus shows the smaller glial cells (small ovals) in the proximity of neurons (larger with more filaments). The hippocampus is an important brain structure that plays a major role in memory formation, and is also an essential component of the limbic system which is responsible for a variety of functions including emotion.

See all of the images at Wired.

Why Are Some People Black?

As a follow-up of sorts to the last post on evolution, an excellent article by Steve Jones from the same book discusses the reasons for why evolution results in different skin complexions. It was written around 1996 or so.

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Everyone knows - do they not? - that many people have black skin. What is more, black people are concentrated in certain places - most notably, in Africa - and, until the upheavals of the past few centuries, they were rare in Europe, Asia, and the Americas. Why should this be so? It seems a simple question. Surely, it we cannot give a simple answer, there is something wrong with our understanding of ourselves. In fact, there is no straightforward explanation of this striking fact about humankind. Its absence says a lot about the strengths and weaknesses of the theory of evolution and of what science can and cannot say about the past. Any anatomy book gives one explanation of why people look different. Doctors love pompous words, particularly if they refer to other doctors who lived long ago. Black people have black skin, their textbooks say, because they have a distinctive Malphigian layer. This is a section of the skin named after the seventeenth-century Italian anatomist Malphigii. It contains lots of cells called melanocytes. Within them is a dark pigment called melanin. The more there is, the blacker the skin. Malphigii found that African skin had more melanin than did that of Europeans. The question was, it seemed, solved.

This is an example of what I sometimes think of as 'the Piccadilly explanation.' One of the main roads in London is called Piccadilly - an oddly un-English word. I have an amusing book that explains how London's streets got their names. What it says about Piccadilly sums up the weakness of explanations that depend, like the anatomists', only on describing a problem in more detail. The street is named, it says, after the tailors who once lived there and made high collars called piccadills. Well, fair enough; but surely that leaves the interesting question unanswered. Why call a collar a piccadill in the first place? It is not an obvious word for an everyday piece of clothing. My book is, alas, silent.

Malphigii's explanation may be good enough for doctors, but will not satisfy any thinking person. It answers the question how but not the more interesting question why there is more melanin in African skin.

Because the parents, grandparents, and - presumably - distant ancestors of black people are black, and those of white people are white, the solution must lie in the past. And that is a difficulty for the scientific method. It is impossible to check directly just what was going on when the first blacks appeared on earth. Instead, we must rely on indirect evidence. There is one theory that is, if nothing else, simple and consistent. It has been arrived at again and again. It depends solely on belief; and if there is belief, the question of proof does not arise. Because of this, the theory lies outside science.

It is that each group was separately created by divine action. The Judeo-Christian version has it that Adam and Eve were created in the Garden of Eden. Later, there was a gigantic flood; only one couple, the Noahs, survived. They had children: Ham, Shem, and Japheth. Each gave rise to a distinct branch of the human race, Shem to the Semites, for example. The children of Ham had dark skins. From them sprang the peoples of Africa. That, to many people, is enough to answer the question posed in this essay.

The Noah story is just a bald statement about history. Some creation myths are closer to science. They try to explain why people look different. One African version is that God formed men from clay, breathing life into his creation after it had been baked. Only the Africans were fully cooked - they were black. Europeans were not quite finished and were an unsatisfactory muddy pink. The trouble with such ideas is that they cannot be disproved. I get lots of letters from people who believe passionately that life, in all its diversity, appeared on earth just a few thousand years ago as a direct result of God's intervention. There is no testimony that can persuade the otherwise. Prove that there were dinosaurs millions of years before humans, and they come up with rock 'footprints' showing, they say, that men and dinosaurs lived together as friends. So convinced are they of the truth that they insist that their views appear in school textbooks.

If all evidence, whatever it is, can only be interpreted as supporting one theory, then there is no point in arguing. In fact, if belief in the theory is strong enough, there is no point in looking for evidence in the first place. Certainty is what blocked science for centuries. Scientists are, if nothing else, uncertain. Their ideas must constantly be tested against new knowledge. If they fail the test, they are rejected.

No biologist now believes that humans were created through some miraculous act. All are convinced that they evolved from earlier forms of life. Although the proof of the fact of evolution is overwhelming, there is plenty of room for controversy about how it happened. Nowhere is this clearer than in the debate about skin colour.

Modern evolutionary biology began with the nineteenth-century English biologist Charles Darwin. He formed his ideas after studying geology. In his day, many people assumed that grand features such as mountain ranges or deep valleys could arise only through sudden catastrophes such as earthquakes or volcanic eruptions, which were unlikely to be seen by scientists as they were so rare. Darwin realised that, given enough time, even a small stream can, by gradually wearing away the rocks, carve a deep canyon. The present, he said, is the key to the past. By looking at what is going on in a landscape today. It is possible to infer the events of millions of years ago. In the same way, the study of living creatures can show what happened in evolution.

In The Origin of Species, published in 1859, Darwin suggested a mechanism whereby new forms of life could evolve. Descent with modification, as he called it, is a simple piece of machinery, with two main parts. One produces inherited diversity. This process is now known as mutation. In each generation, there is a small but noticeable chance of a mistake in copying genes as sperm or eggs are made. Sometimes we can see the results of mutations in skin colour; one person in several thousand is an albino, lacking all skin pigment. Albinos are found all over the world, including Africa. They descend from sperm or eggs that have suffered damage in the pigment genes. The second piece of the machine is a filter. It separates mutations which are good at coping with what the environment throws at them from those which are not. Most mutations - albinism, for example - are harmful. The people who carry mutant genes are less likely to survive and to have children than do those who do not. Such mutations quickly disappear. Sometimes, though, one turns up which is better at handling life's hardships than what went before. Perhaps the environment is changing, or perhaps the altered gene does its job better. Those who inherit it are more likely to survive; they have more children, and the gene becomes more common. By this simple mechanism, the population has evolved through natural selection. Evolution, thought Darwin, was a series of successful mistakes.

If Darwin's machine worked for long enough, then new forms of life - new species - would appear. Given enough time, all life's diversity could emerge from simple ancestors. There was no need to conjure up ancient and unique events (such as a single incident of creation) which could neither be studied nor duplicated. Instead, the living world was itself evidence for the workings of evolution. What does Darwin's machine tell us about skin colour? As so often in biology, what we have is a series of intriguing clues, rather than a complete explanation.

There are several kinds of evidence about how things evolve. The best is from fossils; the preserved remnants of ancient times. These contain within themselves a statement of their age. The chemical composition of bones (or of the rocks into which they are transformed) shifts with time. The molecules decay at a known rate, and certain radioactive substances change from one form into another. This gives a clue as to when the original owner of the bones died. It may be possible to trace the history of a family of extinct creatures in the changes that occur as new fossils succeed old.

The human fossil record is not good - much worse, for example, than that of horses. In spite of some enormous gaps, enough survives to make it clear that creatures looking not too different from ourselves first appeared around a hundred and fifty thousand years ago. Long before that, there were apelike animals which looked noticeably human but would not be accepted as belonging to our own species if they were alive today. No one has traced an uninterrupted connection between these extinct animals and ourselves. Nevertheless, the evidence for ancient creatures that changed into modern humans is overwhelming. As there are no fossilised human skins, fossils say nothing directly about skin colour. They do show that the first modern humans appeared in Africa. Modern Africans are black. Perhaps, then, black skin evolved before white. Those parts of the world in which people have light skins - northern Europe, for example - were not populated until about a hundred thousand years ago, so that white skin evolved quite quickly. Darwin suggested another way of inferring what happened in the past: to compare creatures living today. If two species share a similar anatomy, they probably split from a common ancestor more recently than did another which has a different body plan. Sometimes it is possible to guess at the structure of an extinct creature by looking at its living descendants. This approach can be used not just for bones but for molecules such as DNA. Many biologists believe that DNA evolves at a regular rate; that in each generation, a small but predictable proportion of its subunits changes from one form into another. If this is true (and often it is), then counting the changes between two species reveals how closely they are related. What is more, if they share an ancestor that has been dated using fossils, it allows DNA to be used as a 'molecular clock,' timing the speed of evolution. The rate at which the clock ticks can then be used to work out when other species split by comparing their DNA, even if no fossils are available.

Chimpanzees and gorillas seem, from their body plan, to be our relatives. Their genes suggest the same thing. In fact, each shares 98 percent of its DNA with ourselves, showing just how recently we separated. The clock suggests that the split was about six million years ago. Both chimp and gorilla have black skins. This, too, suggests that the first humans were black and that white skin evolved later. However, it does not explain why white skin evolved. The only hint from fossils and chimps is that the change took place when humans moved away from the tropics. We are, without doubt, basically tropical animals. It is much harder for men and women to deal with cold than with heat. Perhaps climate has something to do with skin colour. To check this idea, we must, like Darwin, look at living creatures. Why should black skin be favoured in hot and sunny places and white where it is cool and cloudy? It is easy to come up with theories, some of which sound pretty convincing. However, it is much harder to test them.

The most obvious idea is wrong. It is that black skin protects against heat. Anyone who sits on a black iron bench on a hot sunny day soon discovers that black objects heat up more than white ones do when exposed to the sun. This is because they absorb more solar energy. The sun rules the lives of many creatures. Lizards shuttle back and forth between sun and shade. In the California desert, if they stray more than six feet from shelter on a hot day, they die of heat stroke before they can get back. African savannahs are dead places at noon, when most animals are hiding in the shade because they cannot cope with the sun. In many creatures, populations from hot places are lighter - not darker - in colour to reduce the absorption of solar energy. People, too, find it hard to tolerate full sunshine - blacks more so than whites. Black skin does not protect those who bear it from the sun's heat. Instead, it makes the problem worse. However, with a bit of ingenuity, it is possible to bend the theory slightly to make it fit. Perhaps it pays to have black skin in the chill of the African dawn, when people begin to warm up after a night's sleep. In the blaze of noon, one can always find shelter under a tree.

The sun's rays are powerful things. They damage the skin. Melanin helps to combat this. One of the first signs of injury is an unhealthy tan. The skin is laying down an emergency layer of melanin pigment. Those with fair skin are at much greater risk from skin cancer than are those with dark. The disease reaches its peak in Queensland, in Australia, where fair-skinned people expose themselves to a powerful sun by lying on the beach. Surely, this is why black skin is common in sunny places - but, once again, a little thought shows that it probably is not. Malignant melanoma, the most dangerous skin cancer, may be a vicious disease, but it is an affliction of middle age. It kills its victims after they have passed on their skin-colour genes to their children. Natural selection is much more effective if it kills early in life. If children fail the survival test, then their genes perish with their carriers. The death of an old person is irrelevant, as their genes (for skin colour or anything else) have already been handed on to the next generation.

The skin is an organ in its own right, doing many surprising things. One is to synthesise vitamin D. Without this, children suffer from rickets: soft, flexible bones. We get most vitamins (essential chemicals needed in minute amounts) from food. Vitamin D is unusual. It can be made in the skin by the action of sunlight on a natural body chemical. To do this, the sun must get into the body. Black people in sunshine hence make much less vitamin D than do those with fair skins. Vitamin D is particularly important for children, which is why babies (African or European) are lighter in colour than are adults. Presumably, then, genes for relatively light skin were favoured during the spread from Africa into the cloud and rain of the north. That might explain why Europeans are white - but does it reveal why Africans are black? Too much vitamin D is dangerous (as some people who take vitamin pills discover to their cost). However, even the fairest skin cannot make enough to cause harm. The role of black skin is not to protect against excess vitamin D.

It may, though, be important in preserving other vitamins. The blood travels around the body every few minutes. On the way, it passes near the surface of the skin through fine blood vessels. There, it is exposed to the damaging effects of the sun. The rays destroy vitamins - so much so, that a keen blond sunbather is in danger of vitamin deficiency. Even worse, the penetrating sunlight damages antibodies, the defensive proteins made by the immune system. In Africa, where infections are common and, sometimes, food is short, vitamin balance and the immune system are already under strain. The burden imposed by penetrating sunlight may be enough to tip the balance between health and disease. Dark skin pigmentation may be essential for survival. No one has yet shown directly whether this is true.

There are plenty of other theories as to why some people are black. For an African escaping from the sun under a tree, black skin is a perfect camouflage. Sexual preference might even have something to do with the evolution of skin colour. If, for one reasons or another, people choose their partners on the basis of colour, then the most attractive genes will be passed on more effectively. A slight (and perhaps quite accidental) preference for dark skin in Africa and light in Europe would be enough to do the job, This kind of thing certainly goes on with peacocks - in which females prefer males with brightly patterned tails - but there is no evidence that it happens in humans. Accident might be important in another way, too. Probably only a few people escaped from Africa a hundred thousand years and more ago. If, by chance, some of them carried genes for relatively light skins, then part of the difference in appearance between Africans and their northern descendants results from a simple fluke. There is a village of North American Indians today where albinos are common. By chance, one of the small number of people who founded the community long ago carried the albino mutation and it is still abundant there.

All this apparent confusion shows how difficult it is for science to reconstruct history. Science is supposed to be about testing, and perhaps disproving, hypotheses. As we have seen, there is no shortage of ideas about why people differ in skin colour. Perhaps none of the theories is correct, or perhaps one, two, or all of them are. Because whatever gave rise to the differences in skin colour in different parts of the world happened long ago, no one can check directly. But science does not always need direct experimental tests. A series of indirect clues may be almost as good. The hints that humans evolved from simpler predecessors and are related to other creatures alive today are so persuasive that it is impossible to ignore them. So far, we have too few facts and too many opinions to be certain of all the details of our own evolutionary past. However, the history of the study of evolution makes me confident that, some day, the series of hints outlined in this essay will suddenly turn into a convincing proof of just why some people are black and some white.

Quotes of Whoa #5: Evolution of Mind

"[I]f history and science have taught us anything, it is that passion and desire are not the same as truth. The human mind evolved to believe in the gods. It did not evolve to believe in biology. Acceptance of the supernatural conveyed a great advantage throughout prehistory, when the brain was evolving. Thus it is in sharp contrast to biology, which was developed as a product of the modern age and is not underwritten by genetic algorithms. The uncomfortable truth is that the two beliefs are not factually compatible. As a result those who hunger for both intellectual and religious truth will never acquire both in full measure."

-- Edward O. Wilson, 'Consilience: The Unity of Knowledge' (1998), p. 262.

Quotes of Whoa #4: Genetic Destiny?

"Once we realise that the basic wiring plan of the brain is under genetic influence, it's easy to see how not only animals but also people can have very similar brains and yet be so different, right from the start of their lives. Genetic forces, operating on the synaptic arrangement of the brain, constrain, at least to some extent, the way we act, think, and feel ... Still, it's important to recognise that genes only shape the broad outline of mental and behavioural functions, accounting for at most 50 percent of a given trait, and in many instances for far less. Inheritance may bias us in certain directions, but many other factors dictate how one's genes are expressed.

"For example, if a woman consumes excessive alcohol during pregnancy, or a child has a diet deficient in certain nutrients, a brain genetically destined for brilliance can instead turn out to be cognitively impaired. Likewise, a family history of extraversion can be squelched in an orphanage run with an iron fist, just as a natural tendency to be shy and withdrawn can be compensated for to some degree by the supportive encouragement of parents. Even if it becomes possible to clone a child who has died at a tender age, it's probable that the look-alike, having his own set of experiences, is going to act, think, and feel differently ... Genes are important, but not all-important."

-- Joseph LeDoux, 'Synaptic Self' (2002), p. 4-5.

Quotes of Whoa #2

"Just how do genes affect individual behaviour? In the simplest terms, they do so by making proteins that shape the way neurons get wired together."

-- Joseph LeDoux, 'Synaptic Self' (2002), p. 4.