How do you define what is “Indian”?

In his wonderful new book, The Sceptical Patriot, Sidin Vadukut, a journalist with LiveMint, tries to assess the haughty claims Indians make. Was the zero really invented in India? What about plastic surgery? Did India never invade another nation? And was it the richest country in the world at some point?

As a trained scientist, I’ve learned to be sceptical about everything. So it is no wonder I enjoyed the book. But, for me, the best part of the book was the last few pages. In them, Vadukut tries to explain the value of knowing history. One of his epiphanies from the exercise of writing the book is that “there is no such thing, ethnically speaking, as an Indian.”

There is a genetic basis to this argument, because for thousands of years the native south Asian population has mixed with Mongols, Greeks, Persians, British, Mughals, French, Portuguese and Arabs, and those populations have previously mingled with others around the world. Indeed, centuries of casteism has left its mark on Indians today, but it would be near impossible to find a citizen today who is “purely Indian”.

But some people will easily dismiss this biological mixing, and point out to our distinct Indian cultural heritage. Surely that is different and unique from the rest of the world?

Columbus, Columbus

Well, not really. Vadukut argues that “an entire planet’s worth of history courses through our veins”, and there is no better way to look at that than to look at our everyday meals. Consider the ingredients of just two such quintessentially Indian dishes: rajma and aloo gobi.

Kidney beans, tomato, green chilli, potatoes and cauliflower are all foreign imports. Apart from gobi, which came from Turkey, all the ingredients were given to the world by the Spanish and the Portuguese, after Christopher Columbus’s famous 1492 voyage to the Americas (or as he assumed, then, to India). The contribution is known as the Columbian Exchange, and marks the time when a whole bunch of other foods started being used in cuisines around the world. These also include maize, cocoa, vanilla, oranges, bananas and pineapples.

Many of the spices that make up garam masala are not of Indian origin. But, without potatoes and tomatoes, we wouldn’t have delicacies such as pav bhajidum aloo or masala dosa. 

I pick out these two ingredients because their arrival in India is a lot more recent. According to British records, potatoes became a mainstay in Indian diets only in the 1700s. And, according to the great food historian KT Achaya, Indian cooking adopted tomatoes as late as the 1880s.

“In less than a century, an entire country, with about 18% of the world population and impossibly diverse culinary cultures and preferences, went from looking at the tomato with suspicion to consuming it with absolutely everything,” writes Vadukut. How, then, do you define what is “Indian”?

First published in Lokmat Times. Image from Wikipedia.

To become an elite sportsperson, you need to win the genetic lottery

A review of The Sports Gene by David Epstein

Winners, it is said, are not born but made. That, however, is not the whole truth, as David Epstein, an investigative reporter with Pro Publica, shows in his book The Sports Gene.

In recent decades, the role of genes in causing diseases has been elucidated time and again. So it should not be surprising that they must also play a role in creating gifted individuals. And, yet, the science to support the latter hypothesis is limited and more recent. The reason for this disparity is not because we don’t have the tools to find evidence for that hypothesis, but because the message it supports is not one that society is ready for.

Epstein make his case through many examples. These are not just of rare individuals with extraordinary achievements. He also looks at physiological characteristics of all players at the international level across various sports. Consider, for instance, the average male basketball player. Had he lived at the time, he would not have made a good candidate for Leonardo da Vinci’s Vitruvian Man. That is because a professional basketball player won’t fit in da Vinci’s circle—the length of the player’s outspread arms is greater than his height. Those two measures were considered to be equal in an “ideal human”. But Epstein’s calculations show that if you want to be an internationally successful basketball player, you need to be an exception—you need to be tall and have longer arms still.

This phenomenon is true of other sports. Be it sprinting, where those endowed with the ability to draw more oxygen from the air than the average are more likely to win. Or be it high jump, where rare jumpers with excessively long Achilles tendon end up succeeding. Or be it marathons, where most winners come from within a single tribe in western Kenya. The story is clear—to sculpt an elite athlete, the roll of nature’s dice must be played in their favour.

Teasing apart the role of genes on complex human traits is no simple task. But recent studies have identified a handful genes that can make or break an athlete. Take the EPOR gene, for instance. Those who have the gene, also tend to have exceptionally high haemoglobin levels in the blood. This improves the efficiency with which oxygen is consumed, creating some remarkable athletes if they choose that path. Or take the HCM1 gene. It causes one of the chambers of the heart to grow in size without any apparent symptoms. This puts an athlete with HCM1 at the risk of falling dead on a track without a warning. On average one such athlete dies every other week in the US.

In general, however, the interaction of genes that creates such remarkable athletes is too complex to breakdown. For instance, hundreds of genes are involved in determining someone’s height. So, even if genetic engineering is available today, a designer baby can’t be created to make an “ideal athlete”. But, to be sure, neither can the natural bounty of genes alone ensure great athletic feats. And, yet, there is no doubt that Epstein’s thorough analysis raises uncomfortable questions for the long-held view—recently made famous by Malcolm Gladwell’s 10,000 hours rule—that talent is nothing and practice is everything.

The nature vs nurture debate is not new, but genetics is providing the tools to take the debate forward. The evidence, as Epstein puts it, appears to be that the contribution of both is equally important.

Nurture alone is not going to turn a Pygmy into an NBA player, and that is not a fact that we must shy away from. If anything, genes could help people find which sports would be a good fit for them. Society must not fear these inherent differences. Rather, such inequalities make human life interesting and worth living.

Image credit: piers_nye, CC-BY-NC

Modern humans’ ancestors

All scientific evidence points to the fact that, if you go far enough back, all life on Earth is related through common ancestry. Turns out that applying the same sort of analysis shows that all humans alive today are descendants of one man and one woman who walked our planet thousands of years ago. For several decades, there has been debate about when these ancestors, popularly known as Y-chromosomal Adam and mitochondrial Eve, existed. Two studies published this week find that there is a good chance Adam and Eve may have existed about the same time, evolutionarily speaking.

Genetic Adam and Eve may have walked on Earth at the same time. The Conversation, 1 August 2013.

Image credit: FurLined

Resetting humanity’s clock

Some time in humanity’s past, a small group of Homo sapiens migrated out of Africa before spreading out to every possible corner of the Earth. All the women of that group carried DNA inherited from just one woman, commonly known as mitochondrial Eve, whose DNA was inherited by all humans alive today. But the exact timing of this migration is not clear, and it has sparked debate among geneticists. Now, new research published in Current Biology may help calm both sides.

Fossil DNA used to reset humanity’s clock,  Ars Technica, 28 March 2013.

Image credit: Dongyi Liu

Manipulation of biological clocks teaches an important lesson

Synechococcus Elongatus in Petri dish

Evolution is a powerful force that optimises organisms to fit in their environment. But, in our attempts to understand life, biologists often stumble upon natural phenomena that leave them puzzled. According to a new study, solving one such puzzle has helped scientists understand why nature prefers to do things differently than humans would predict.

Proteins, the gears of a cell’s machinery work, are made from combinations of the same 20 building blocks called amino acids. These amino acids get stitched together by enzymes based on instructions from the organism’s DNA. A combination of three letters of the DNA sequence, called codons, instruct enzymes to use one amino acid. But because there are four types of letters (A, T, G and C) in DNA, there are 64 (4^3) ways of making up the three-letter combination of a codon. Because of this an organism has some room for error, because it can now make the same amino acid from three different codons. Consider an organism, for instance, in which the combination CCA codes for the amino acid proline. The same organism will also make proline from three more combinations, namely CCG, CCU and CCC.

It turns out, though not surprisingly, that each organism has a preference for which codon to use for a particular amino acid. Thus if an organism’s DNA carries these preferred codons, then its enzymes can read the code faster and make the protein more quickly. As organisms evolve, biologists assumed, its DNA would be altered to choose preferred codons over others by natural selection.

But that is not what nature does. In reports just published in Nature, two groups of researchers, one led by Carl Johnson at Vanderbilt University and the other by Yi Liu at the University of Texas Southwestern Medical Centre, have found two organisms that do not choose their preferred codons for making specific proteins. If the researchers forced these organism, through genetic manipulation, to use the preferred codons, they found that the mutants did far worse than their wild-types.

Dr Liu chose to work on Neurospora crassa, a fungus. Dr Johnson’s subject was Synechococcus elongatus, a photosynthetic bacteria. In both these organisms, proteins that make up the biological clock were made from codons that the organism did not prefer. “We wondered why evolution hadn’t hit upon that choice,” says Dr Johnson.

Dr Liu and Dr Johnson then rearranged the relevant bits of DNA to create a mutant versions of the two species. Surprisingly, Dr Liu and Dr Johnson got opposing results.

In Neurospora the rearranged letters led to more rapid production of the clock-running proteins, but, instead of making the biological clock more robust, it fell apart. Dr Liu noticed that this was because the faster-produced protein had the correct sequence of amino acids but its folding was not proper.

Proteins, as series of amino acids put together, are long-chain molecules. This gives them the freedom to fold in a number of ways, much like long piece of string can be folded in many ways. These folding patterns are as important for the function of the proteins as is their amino acid sequence. What Dr Liu found was not unusual. If the protein is not given enough time to get its folding tight then it does not function properly, leading to a broken biological clock.

With Synechococcus the result was the opposite. At first Dr Johnson’s experiment seemed to have worked. The mutant bacteria was producing more of the clock-running proteins and its biological cycle had become more robust (sticking closer to 24 hours than its wild variety). But strangely at at temperature of around 20° C the population of the mutant was growing much more slowly than the wild-type. At this temperature the wild-type Synechococcus had a 30-hour biological clock, whereas the mutant was being forced to a 24-hour cycle which Dr Johnson thought would help a photosynthesising bacteria.

Synechococcus’s optimal temperature for growth is about 30° C, which is perhaps what it experiences in its freshwater environment in the summer months. At that temperature the photosynthetic bacteria’s genes are expressed well enough to make its biological clock run closer to the 24-hour cycle where it works for 12 hours when the sun shines and sleeps for 12 hours when there is no sun. But at a lower temperature, which is perhaps what it experiences in the winter months, the gene expression is hampered which results in a 30-hour cycle.

“This 30-hour cycle seemed like an evolutionary adaptation at lower temperature,” says Dr Johnson. Although the reasons are not clear for the adaptation, it may be because of the reduced number of hours of sunlight that are available in winter months. Thus the mutant population with an apparently better biological clock of 24 hours was not doing as well as the wild population with its 30-hour clock. “Better understanding of this bacteria’s cycle is critical to be able to improve its efficiency in biofuels production,” says Dr Johnson.

The bigger lesson, though, is that what humans assumed would be an optimal way of doing things, turns out to be not optimal in evolutionary terms. Codon usage, it seems, is a fundamental part of gene regulation. Both Neurospora and Synechococcus chose to not use the preferred codons because that helped them adapt to their surroundings better. Natural selection works by choosing to make an organism better able to pass on its genes. If it has to do that through an inefficient way of making proteins, then so be it.

UPDATE (18 Feb; 8.53 am): It was incorrectly implied that proline has three codons. In fact, proline has four codons.


  1. Liu et al., Non-optimal codon usage affects expression, structure and function of clock protein FRQ, Nature, 2013.
  2. Johnson et al., Non-optimal codon usage is a mechanismto achieve circadian clock conditionality, Nature, 2013.

There are benefits to having three parents. You get to decide whether they are enough

In October I wrote an article in The Economist on a new method for curing mitochondrial disease. The method involves replacing faulty DNA from a mother’s egg with that from a healthy donor. And, if the baby is born, in principle, it paves way for a child to have three genetic parents.

Despite the public “uggh” factor raised by the idea of a three-parent child raises, there are good reasons for having such offspring. The technique may help cure a set of rare but nasty, inheritable diseases caused by faulty DNA our cells, and after decades of work researchers have developed a way of replacing those faulty bits.

Currently the law in Britain prohibits this vital research needed to develop a cure, because the process involves tinkering with human DNA. While such tinkering raises a number of issues, in this case, it should not stop that research from going forward. As I argued in the editorial that accompanied the article:

Mitochondrial transplants involve no tinkering with the DNA itself. Though on a microscopic scale, the process is quite like a heart, liver or kidney transplant, with the caveat that the transplant will be passed on to the recipient’s children, if she is female. Any organ transplant introduces new genes into the body. Mitochondrial genes are ubiquitous, it is true, but this difference is one of degree, not kind.

Another reason not to worry is that the mitochondria carry only 37 genes, compared with about 20,000 in the cell nucleus, and these genes are exclusively concerned with energy metabolism. Pushy parents will not be picking mitochondrial donors on the basis of looks, personality or intelligence.

Non-biological objections are sometimes raised as well. Some worry, for instance, that a person with three genetic parents might suffer an identity crisis. But that seems less likely than in the case of people conceived by in vitro fertilisation using sperm donated by strangers who have contributed half of their offspring’s genes, not a paltry three dozen. And for that reason mitochondrial donors are even less likely than sperm donors to want to be involved with bringing up children in whom they have but a fractional genetic interest.

The Human Fertilisation and Embryology Authority (HFEA) ends its consultation on mitochondrial replacement therapy today. Please take a few minutes to fill up the survey.

Your decision in the consultation is not to decide whether or not to allow this therapy to be used in public today, but to decide whether or not to allow the research to test for the therapy’s safety and efficacy.

The genetics of politics

Slowly, and in some quarters grudgingly, the influence of genes in shaping political outlook and behaviour is being recognised

In 1882 W.S. Gilbert wrote, to a tune by Sir Arthur Sullivan, a ditty that went “I often think it’s comical how Nature always does contrive/that every boy and every gal that’s born into the world alive/is either a little Liberal or else a little Conservative.”

In the 19th century, that view, though humorously intended, would not have been out of place among respectable thinkers. The detail of a man’s opinion might be changed by circumstances. But the idea that much of his character was ingrained at birth held no terrors. It is not, however, a view that cut much ice in 20th-century social-scientific thinking, particularly after the second world war. Those who allowed that it might have some value were generally shouted down and sometimes abused, along with all others vehemently suspected of the heresy of believing that genetic differences between individuals could have a role in shaping their behavioural differences.

Such thinking, a product compounded of Marxism (if character really is ingrained at birth, then man might not be perfectible) and a principled rejection of the eugenics that had led, via America’s sterilisation programmes for the “feeble minded”, to the Nazi extermination camps, made life hard for those who wished to ask whether genes really do affect behaviour. Now, however, the pendulum is swinging back. In the matter of both political outlook and political participation it is coming to be seen that genes matter quite a lot. They are not the be-all and end-all. But, as a review of the field published in September inTrends in Genetics, by Peter Hatemi of Pennsylvania State University and Rose McDermott of Brown University, shows, they affect a person’s views of the world almost as much as his circumstances do, and far more than many social scientists have been willing, until recently, to admit.

Family values

The evidence for this claim comes from two types of source, one relatively old and one spanking new. The old is studies of twins, comparing identical and non-identical pairs. The new is a direct examination of people’s DNA, searching for genes whose variation correlates with observable behavioural differences.

Twins studies, which seek to control for the effects of upbringing by comparing identical twins (who share all their DNA) with fraternal ones (who share, on average, half), have been going on since the 1950s. In that time, quite a number, in many countries, have looked in part at political questions. Dr Hatemi and Dr McDermott pored over 89 peer-reviewed papers on the effects of genes and environment (both family upbringing and wider circumstances) on political matters. These included twins’ political knowledge, their attitudes to racial, sexual and religious questions, their views on defence and foreign policy, and their identification with particular political parties.

On all counts, identical twins were found to be more alike than fraternal twins. That knowledge, refracted through the prism of statistical theory, allows calculations of the proportionate influences of genes, family environment and general environment on particular traits to be made (see chart). Some show strong genetic influence. Some show little. Intriguingly, political knowledge and party identification are at opposite ends of the spectrum. As the chart shows knowledge (or rather, presumably, an innate predisposition to acquire such knowledge) is highly genetically determined. Identification with a particular political party, by contrast, is largely a question of family upbringing—much more so than are opinions about the sorts of policy that it might be thought would determine voting patterns.

But even family ties weaken when people leave home—and they do so in a way that helps disentangle genetic influence. Dr Hatemi showed this in 2009 when, along with a group of colleagues, he looked at twins aged between 11 and 75. His results demonstrated that until their late teens both kinds of twins had equally similar political views. Soon after they flew the nest, though, as might be expected, their views began to diverge. And, just as would be expected if genes have political influence, the views of fraternal twins diverged more than did those of identical ones. Between the ages of 18 and 20 identical and fraternal twins both shared nearly 70% of their political ideology. Between the ages of 21 and 25, that had shrunk to 60% for identical twins and 40% for fraternal twins. Clearly, then, genes matter.

Nor do they merely affect a person’s opinions. They also affect his level of political engagement. This was shown in a study published in 2008 by James Fowler of the University of California, San Diego. Dr Fowler and his team analysed the voter-registration records of identical and fraternal twins from Los Angeles, and also from a more nationally representative database. They found that identical twins are 53% more likely either both to register or both not to register than are fraternal twins.

Political signals

Twins studies like these unequivocally demonstrate the heritability of politically related behaviour. What they do not do, though, is explain the underlying biology. That is an area which is only now starting to be explored.

In 2010 a study published by Dr Fowler and his colleagues implicated a gene known asDRD4 in the development of political affiliation. DRD4 encodes a receptor molecule for a neurotransmitter called dopamine. (Neurotransmitters are chemicals that carry signals from one nerve cell to another.) Those with a variant of DRD4 called 7R, and also a large network of friends acquired during their adolescence, tended to be (in the American sense of the word) liberals—ie, left wing.

One interesting point about this observation is that it requires both a genetic input (the 7R variant) and an environmental one (the network of friends) to take effect. DRD4-7R has previously been associated with novelty-seeking behaviour. The authors of the paper speculate that the interaction of that tendency with possible exposure to lots of different ideas held by lots of different people might push an individual in a leftwardly direction.

Following up on Dr Fowler’s work, research published earlier this year by a team led by Dr Hatemi found a further 11 genes, different varieties of which might be responsible for inclining people towards liberalism or conservatism in the way that Gilbert described. These included genes involved in the regulation of three neurotransmitters—dopamine, glutamate and serotonin—and also G-protein-coupled receptors, which react to a wide variety of stimulants. Most astonishingly, the researchers found that olfactory receptors are also implicated, giving a whole, new twist to the idea that someone’s political platform “smells” wrong.

The word “inclining” is important. No one is suggesting that there are particular genes, or versions of genes “for” liberalism or conservatism. But inclinations there do seem to be. Moreover, direct studies of genes also support what the twins studies suggest about political engagement, independent of opinion. In particular, work by Dr Fowler implicates another dopamine receptor, DRD2, and also 5HTT, which regulates serotonin levels, in influencing voter turnout. People with versions of these genes that increase the effect of the neurotransmitter are more likely to vote than those with low-activity versions.

The will and the way

The third part of the question, though, is how this all links up with the fundamental driver of biology, evolution. The suggestion of Dr Hatemi and Dr McDermott is that political action is the collective expression of some pretty primal biological motives: those of survival and procreation. Deciding whether or not to be part of a particular group, whom else to admit to your group, how to keep or share resources, and how much sexual freedom to afford oneself, one’s neighbours and one’s children are all, and always have been, lively matters of political debate. But they are also all matters that have an impact on the crucial Darwinian business of getting genes into the next generation.

Dr Hatemi and Dr McDermott are not suggesting genetic factors directly create ideologies that relate to these matters. They are suggesting, though, that genes assist in deciding which opinions an individual will find it most attractive to cleave to.

Unlike the social determinists of old, however, who frequently refused to concede even the possibility of genetic influence on behaviour, the new generation of genetic political scientists are perfectly happy to acknowledge nurture along with nature. Dr Hatemi’s own work, for instance, has shown that external shocks, such as unemployment and divorce, effectively abolish the genetic influences he has detected on many ideological questions as other responses, more appropriate to survival in the changed circumstances, kick in. These responses too, of course, are probably under evolutionary—and hence genetic—control. But they are different from the ones being looked for at present.

That sort of granularity, and the need to accept partial rather than universal explanations for biological phenomena, led the two researchers to one other thought. This is that part of the problem social science has had in the past in accepting biological explanations is that its practitioners do not understand the nature of the claims being made. There are, to repeat, no genes for socialism or conservatism, or for prejudice or tolerance, any more than there are genes for Christianity or Islam. But a person’s genes can sometimes propel him more easily in one direction than another. His free will is, if you like, a little freer to turn right than left, or vice versa. Gilbert was therefore not quite right. But he was not exactly wrong, either.

First published in The EconomistAlso available in audio here.

This story was mentioned on the cover page of the print issue and featured on the front page of

Image credit: The Economist