Showing posts with label gene. Show all posts
Showing posts with label gene. Show all posts
Thursday 18 January 2024
Wednesday 7 June 2023
Thursday 4 June 2020
Genetics is not why more BAME people die of coronavirus: structural racism is
Yes, more people of black, Latin and south Asian origin are dying, but there is no genetic ‘susceptibility’ behind it writes Winston Morgan in The Guardian
Indeed, race is a social construct with no scientific basis. However, there are clear links between people’s racial groups, their socioeconomic status, what happens to them once they are infected, and the outcome of their infection. And focusing on the idea of a genetic link merely serves to distract from this.
You only have to look at how the statistics are gathered to understand how these issues are confused. Data from the UK’s Office for National Statistics that has been used to highlight the disparate death rates separates Indians from Pakistanis and Bangladeshis, and yet groups together all Africans (including black Caribbeans). This makes no sense in terms of race, ethnicity or genetics.
The data shows that those males categorised as black are more than 4.6 times more likely to die than their white counterparts from the virus. They are followed by Pakistanis/Bangladeshis (just over four times more likely to die), and then Chinese and Indians (just over 2.5 times).
Most genome-wide association studies group all south Asians. Yet, at least in the UK, Covid-19 can apparently separate Indians and Pakistanis, suggesting genetics have little to do with it. The categories used to collect government data for the pandemic are far more suited to social outcomes such as employment or education.
This problem arises even with a recent analysis that purportedly shows people from ethnic minorities are no more likely to die, once you take into account the effects of other illnesses and deprivation. The main analysis only compares whites to everybody else, masking the data for specific groups, while the headline of the newspaper article about the study refers only to black people.
Meanwhile, in the US the groups most disproportionately affected are African Americans and Hispanics/Latinos. All these groups come from very different population groups. We’ve also seen high death rates in Brazil, China and Italy, all of which have very different populations using the classical definition of race.
The idea that Covid-19 discriminates along traditional racial lines is created by these statistics and fails to adequately portray what’s really going on. These kinds of assumptions ignore the fact that there is as much genetic variation within racialised groups as there is between the whole human population.
There are some medical conditions with a higher prevalence in some racialised groups, such as sickle cell anaemia, and differences in how some groups respond to certain drugs. But these are traits linked to single genes and all transcend the traditional definitions of race. Such “monogenic” traits affect a very small subset of many populations, such as some southern Europeans and south Asians who also have a predisposition to sickle cell anaemia.
Death from Covid-19 is also linked to pre-existing conditions that appear in higher levels in black and south Asian groups, such as diabetes. The argument that this may provide a genetic underpinning is only partly supported by the limited evidence that links genetics to diabetes.
However, the ONS figures confirm that genes predisposing people to diabetes cannot be the same as those that predispose to Covid-19. Otherwise, Indians would be affected as much as Pakistanis and Bangladeshis, who belong to the same genome-wide association group.
Any genetic differences that may predispose you to diabetes are heavily influenced by environmental factors. There isn’t a “diabetes gene” linking the varying groups that are affected by Covid-19. But the prevalence of these so-called “lifestyle” diseases in racialised groups is strongly linked to social factors.
Another target that has come in for speculation is vitamin D deficiency. People with darker skin who do not get enough exposure to direct sunlight may produce less vitamin D, which is essential for many bodily functions, including the immune system. In terms of a link to susceptibility to Covid-19, this has not been proven. But very little work on this has been done and the pandemic should prompt more research on the medical consequences of vitamin D deficiency generally.
Other evidence suggests higher death rates from Covid-19 including among racialised groups might be linked to higher levels of a cell surface receptor molecule known as ACE2. But this can result from taking drugs for diabetes and hypertension, which takes us back to the point about the social causes of such diseases.
In the absence of any genetic link between racial groups and susceptibility to the virus, we are left with the reality, which seems more difficult to accept: that these groups are suffering more from how our societies are organised. There is no clear evidence that higher levels of conditions such as type-2 diabetes, cardiovascular disease and weakened immune systems in disadvantaged communities are because of inherent genetic predispositions.
But there is evidence they are the result of structural racism. All these underlying problems can be directly connected to the food and exercise you have access to, the level of education, employment, housing, healthcare, economic and political power within these communities.
The evidence suggests that this coronavirus does not discriminate, but highlights existing discriminations. The continued prevalence of ideas about race today – despite the lack of any scientific basis – shows how these ideas can mutate to provide justification for the power structures that have ordered our society since the 18th century.
A TfL worker sprays antiviral solution inside a tube train. Photograph: Kirsty O’Connor/PA
From the start of the coronavirus pandemic, there has been an attempt to use science to explain the disproportionate impact of Covid-19 on different groups through the prism of race. Data from the UK and the US suggests that people categorised as black, Hispanic (Latino) and south Asian are more likely to die from the disease.
The way this issue is often discussed, but also the response of some scientists, would suggest that there might be some biological reason for the higher death rates based on genetic differences between these groups and their white counterparts. But the reality is there is no evidence that the genes used to divide people into races are linked to how our immune system responds to viral infections.
There are certain genetic mutations that can be found among specific ethnic groups that can play a role in the body’s immune response. But because of the loose definition of race (primarily based on genes for skin colour) and recent population movements, these should be seen as unreliable indicators when it comes to susceptibility to viral infections.
From the start of the coronavirus pandemic, there has been an attempt to use science to explain the disproportionate impact of Covid-19 on different groups through the prism of race. Data from the UK and the US suggests that people categorised as black, Hispanic (Latino) and south Asian are more likely to die from the disease.
The way this issue is often discussed, but also the response of some scientists, would suggest that there might be some biological reason for the higher death rates based on genetic differences between these groups and their white counterparts. But the reality is there is no evidence that the genes used to divide people into races are linked to how our immune system responds to viral infections.
There are certain genetic mutations that can be found among specific ethnic groups that can play a role in the body’s immune response. But because of the loose definition of race (primarily based on genes for skin colour) and recent population movements, these should be seen as unreliable indicators when it comes to susceptibility to viral infections.
Indeed, race is a social construct with no scientific basis. However, there are clear links between people’s racial groups, their socioeconomic status, what happens to them once they are infected, and the outcome of their infection. And focusing on the idea of a genetic link merely serves to distract from this.
You only have to look at how the statistics are gathered to understand how these issues are confused. Data from the UK’s Office for National Statistics that has been used to highlight the disparate death rates separates Indians from Pakistanis and Bangladeshis, and yet groups together all Africans (including black Caribbeans). This makes no sense in terms of race, ethnicity or genetics.
The data shows that those males categorised as black are more than 4.6 times more likely to die than their white counterparts from the virus. They are followed by Pakistanis/Bangladeshis (just over four times more likely to die), and then Chinese and Indians (just over 2.5 times).
Most genome-wide association studies group all south Asians. Yet, at least in the UK, Covid-19 can apparently separate Indians and Pakistanis, suggesting genetics have little to do with it. The categories used to collect government data for the pandemic are far more suited to social outcomes such as employment or education.
This problem arises even with a recent analysis that purportedly shows people from ethnic minorities are no more likely to die, once you take into account the effects of other illnesses and deprivation. The main analysis only compares whites to everybody else, masking the data for specific groups, while the headline of the newspaper article about the study refers only to black people.
Meanwhile, in the US the groups most disproportionately affected are African Americans and Hispanics/Latinos. All these groups come from very different population groups. We’ve also seen high death rates in Brazil, China and Italy, all of which have very different populations using the classical definition of race.
The idea that Covid-19 discriminates along traditional racial lines is created by these statistics and fails to adequately portray what’s really going on. These kinds of assumptions ignore the fact that there is as much genetic variation within racialised groups as there is between the whole human population.
There are some medical conditions with a higher prevalence in some racialised groups, such as sickle cell anaemia, and differences in how some groups respond to certain drugs. But these are traits linked to single genes and all transcend the traditional definitions of race. Such “monogenic” traits affect a very small subset of many populations, such as some southern Europeans and south Asians who also have a predisposition to sickle cell anaemia.
Death from Covid-19 is also linked to pre-existing conditions that appear in higher levels in black and south Asian groups, such as diabetes. The argument that this may provide a genetic underpinning is only partly supported by the limited evidence that links genetics to diabetes.
However, the ONS figures confirm that genes predisposing people to diabetes cannot be the same as those that predispose to Covid-19. Otherwise, Indians would be affected as much as Pakistanis and Bangladeshis, who belong to the same genome-wide association group.
Any genetic differences that may predispose you to diabetes are heavily influenced by environmental factors. There isn’t a “diabetes gene” linking the varying groups that are affected by Covid-19. But the prevalence of these so-called “lifestyle” diseases in racialised groups is strongly linked to social factors.
Another target that has come in for speculation is vitamin D deficiency. People with darker skin who do not get enough exposure to direct sunlight may produce less vitamin D, which is essential for many bodily functions, including the immune system. In terms of a link to susceptibility to Covid-19, this has not been proven. But very little work on this has been done and the pandemic should prompt more research on the medical consequences of vitamin D deficiency generally.
Other evidence suggests higher death rates from Covid-19 including among racialised groups might be linked to higher levels of a cell surface receptor molecule known as ACE2. But this can result from taking drugs for diabetes and hypertension, which takes us back to the point about the social causes of such diseases.
In the absence of any genetic link between racial groups and susceptibility to the virus, we are left with the reality, which seems more difficult to accept: that these groups are suffering more from how our societies are organised. There is no clear evidence that higher levels of conditions such as type-2 diabetes, cardiovascular disease and weakened immune systems in disadvantaged communities are because of inherent genetic predispositions.
But there is evidence they are the result of structural racism. All these underlying problems can be directly connected to the food and exercise you have access to, the level of education, employment, housing, healthcare, economic and political power within these communities.
The evidence suggests that this coronavirus does not discriminate, but highlights existing discriminations. The continued prevalence of ideas about race today – despite the lack of any scientific basis – shows how these ideas can mutate to provide justification for the power structures that have ordered our society since the 18th century.
Sunday 18 February 2018
Ramanujan and Salam — what inspired them?
Pervez Hoodbhoy in The Dawn
SRINIVISAN Ramanujan (1887-1920) and Muhammad Abdus Salam (1926-1996), two intellectual giants of the 20th century, were born in the same corner of the world. Of humble origin and educated in local schools, they nevertheless rose to dizzying heights in the arcane world of theoretical science. Few others on the subcontinent enjoy their iconic status.
What I shall address below is that both attributed their works to some divine agency. Some of their devotees see this in validating their own respective belief system. With the rise of Hindutva in India, and the violent persecution of Ahmadis in Pakistan, these claims assume considerable importance. Hence a careful, impartial examination is called for.
No mathematician has a story more romantic than Ramanujan’s. Many books, plays, and movies — such as The Man Who Knew Infinity (2015) — dwell upon this enigmatic figure. Drawing upon deep intuition, Ramanujan created new concepts in the theory of numbers, elliptic functions and infinite series. Even full-blown mathematicians take years to grasp his complex ideas.
Exceptional genes plus fortunate circumstances is why some become maths-science superstars.
Born in Madras to a low-level clerk, this young Brahmin boy was steeped in tradition, sang religious songs, attended temple pujas, and was a strict vegetarian. But by age 12, he was inventing sophisticated theorems and unwittingly duplicating some results of European mathematicians of the previous century. He flunked college twice for lack of interest in anything but mathematics — in which he excelled. His awestruck teachers could not decide whether he was a genius or fraud.
At 16, encouraged by one of his teachers, Ramanujan sent off a letter to the renowned pure mathematician G.W. Hardy at Cambridge University. It was accompanied by theorems densely packed into nine pages. Hardy was stunned and arranged for him to travel to England. Ramanujan duly obtained permission from the family goddess Namagiri, consulting appropriate astrological data before his voyage overseas.
At age 32, Ramanujan was dead. He had returned to Madras exhausted, half-famished and fed up with English winters. But even on his deathbed, his pen scrawled out profound results. A century later these still intrigue the brainiest of mathematicians and string theorists. He attributed his exceptional qualities to the psychic visitations of Namagiri who would whisper equations to him. Sometimes, he said, “she wrote on my tongue”. He told colleagues, “An equation for me has no meaning unless it represents a thought of God.”
This was how Ramanujan saw it. But how does one explain that Euler, Bernoulli, Gauss, Cantor, Hilbert and Gödel were non-Brahmin mathematicians who stood still taller? The edifice of modern mathematics owes largely to them, not to Ramanujan. Some were ardent Christians, others agnostic or atheistic. Nobody knows how to explain their feats.
Curiously, Abdus Salam, then a 19-year-old student at Government College Lahore, wrote his very first paper proposing a simpler solution to an intriguing mathematical problem posed about 20 years earlier by Ramanujan. He ended his paper by triumphantly declaring: “His [Ramanujan’s] solution is much more laborious”.
This was Salam’s debut into the world of high mathematics. Born into a conservative religious environment in Jhang — then a village-town — this child prodigy rapidly outpaced his teachers. Fortunately they bore him no grudge and helped him move on to Lahore. The next stop was Cambridge, where he excelled. By the early 1960s, he was one of the world’s top particle physicists, ultimately winning 20 international prizes and honours including the Nobel Prize in 1979.
In his later years, Salam gave numerous public lectures and interviews, recorded on camera and in print, locating his source of inspiration in his religious belief. In particular he said the concept of unity of God powered his quest for the unification of nature’s fundamental forces as well as his search for ever fewer numbers of elementary particles.
For me, to engage on a sensitive matter with one so senior and superior was not easy. But sometime in 1986 I picked up the courage to ask Salam the obvious question: both he, who thought himself a believer, and Steven Weinberg, an avowed atheist, had worked independently on unifying two of nature’s four fundamental forces and yet had arrived at precisely the same conclusions. How?
Salam gave his answer in the preface he wrote for my book on Islam and science (1990), where he stated: “I can confirm that he [Hoodbhoy] is right…”, and then went on to explicitly clarify that any bias towards the unification paradigm in his thinking was only unconsciously motivated by his religious background.
There is not the slightest doubt that Salam used exactly the same tools as Weinberg did — principally quantum mechanics and relativity theory — and did physics exactly as other physicists do (but better than most). His political and religious views were irrelevant to his work. Let’s note that although they are giants of physics, Salam and Weinberg stood on the shoulders of still greater giants — Einstein, Pauli, Dirac, Wheeler, and Feynman — whose personal philosophies of life vastly differed from each other.
Salam sourced his inspiration to his religious beliefs, while Ramanujan claimed direct transmission from his gods. These claims cannot ever be proved or disproved. It is also irrelevant here that Salam thought of himself as a Muslim whereas, by Pakistani law, he is not.
How can prodigious talent blossom in the absence of rigorous scientific training? Two factors explain Ramanujan’s and Salam’s successes. First, nature sometimes gifts an individual with exceptional innate mathematical ability. This is associated with brain circuits in the parietal lobe and acquired through genetic transmission. Second, by good fortune, Ramanujan and Salam managed to escape into a scholarly environment — Cambridge University — where their genius could flower. Had either stayed back home he would be unheard of today.
It is usual to take pride in the geniuses belonging to one’s own tribe. The ancient civilisations of China, India, Greece, Arabia, and modern European civilisation all claim superiority over others because of the creations of their most brilliant minds. But in fact an individual’s exceptional genes and fortunate circumstances — not some supreme transcendence — are the real reasons. While sources of inspiration do differ, empirically and logically deduced results don’t. Science and its heroes belong to all humankind, not to any one tribe.
SRINIVISAN Ramanujan (1887-1920) and Muhammad Abdus Salam (1926-1996), two intellectual giants of the 20th century, were born in the same corner of the world. Of humble origin and educated in local schools, they nevertheless rose to dizzying heights in the arcane world of theoretical science. Few others on the subcontinent enjoy their iconic status.
What I shall address below is that both attributed their works to some divine agency. Some of their devotees see this in validating their own respective belief system. With the rise of Hindutva in India, and the violent persecution of Ahmadis in Pakistan, these claims assume considerable importance. Hence a careful, impartial examination is called for.
No mathematician has a story more romantic than Ramanujan’s. Many books, plays, and movies — such as The Man Who Knew Infinity (2015) — dwell upon this enigmatic figure. Drawing upon deep intuition, Ramanujan created new concepts in the theory of numbers, elliptic functions and infinite series. Even full-blown mathematicians take years to grasp his complex ideas.
Exceptional genes plus fortunate circumstances is why some become maths-science superstars.
Born in Madras to a low-level clerk, this young Brahmin boy was steeped in tradition, sang religious songs, attended temple pujas, and was a strict vegetarian. But by age 12, he was inventing sophisticated theorems and unwittingly duplicating some results of European mathematicians of the previous century. He flunked college twice for lack of interest in anything but mathematics — in which he excelled. His awestruck teachers could not decide whether he was a genius or fraud.
At 16, encouraged by one of his teachers, Ramanujan sent off a letter to the renowned pure mathematician G.W. Hardy at Cambridge University. It was accompanied by theorems densely packed into nine pages. Hardy was stunned and arranged for him to travel to England. Ramanujan duly obtained permission from the family goddess Namagiri, consulting appropriate astrological data before his voyage overseas.
At age 32, Ramanujan was dead. He had returned to Madras exhausted, half-famished and fed up with English winters. But even on his deathbed, his pen scrawled out profound results. A century later these still intrigue the brainiest of mathematicians and string theorists. He attributed his exceptional qualities to the psychic visitations of Namagiri who would whisper equations to him. Sometimes, he said, “she wrote on my tongue”. He told colleagues, “An equation for me has no meaning unless it represents a thought of God.”
This was how Ramanujan saw it. But how does one explain that Euler, Bernoulli, Gauss, Cantor, Hilbert and Gödel were non-Brahmin mathematicians who stood still taller? The edifice of modern mathematics owes largely to them, not to Ramanujan. Some were ardent Christians, others agnostic or atheistic. Nobody knows how to explain their feats.
Curiously, Abdus Salam, then a 19-year-old student at Government College Lahore, wrote his very first paper proposing a simpler solution to an intriguing mathematical problem posed about 20 years earlier by Ramanujan. He ended his paper by triumphantly declaring: “His [Ramanujan’s] solution is much more laborious”.
This was Salam’s debut into the world of high mathematics. Born into a conservative religious environment in Jhang — then a village-town — this child prodigy rapidly outpaced his teachers. Fortunately they bore him no grudge and helped him move on to Lahore. The next stop was Cambridge, where he excelled. By the early 1960s, he was one of the world’s top particle physicists, ultimately winning 20 international prizes and honours including the Nobel Prize in 1979.
In his later years, Salam gave numerous public lectures and interviews, recorded on camera and in print, locating his source of inspiration in his religious belief. In particular he said the concept of unity of God powered his quest for the unification of nature’s fundamental forces as well as his search for ever fewer numbers of elementary particles.
For me, to engage on a sensitive matter with one so senior and superior was not easy. But sometime in 1986 I picked up the courage to ask Salam the obvious question: both he, who thought himself a believer, and Steven Weinberg, an avowed atheist, had worked independently on unifying two of nature’s four fundamental forces and yet had arrived at precisely the same conclusions. How?
Salam gave his answer in the preface he wrote for my book on Islam and science (1990), where he stated: “I can confirm that he [Hoodbhoy] is right…”, and then went on to explicitly clarify that any bias towards the unification paradigm in his thinking was only unconsciously motivated by his religious background.
There is not the slightest doubt that Salam used exactly the same tools as Weinberg did — principally quantum mechanics and relativity theory — and did physics exactly as other physicists do (but better than most). His political and religious views were irrelevant to his work. Let’s note that although they are giants of physics, Salam and Weinberg stood on the shoulders of still greater giants — Einstein, Pauli, Dirac, Wheeler, and Feynman — whose personal philosophies of life vastly differed from each other.
Salam sourced his inspiration to his religious beliefs, while Ramanujan claimed direct transmission from his gods. These claims cannot ever be proved or disproved. It is also irrelevant here that Salam thought of himself as a Muslim whereas, by Pakistani law, he is not.
How can prodigious talent blossom in the absence of rigorous scientific training? Two factors explain Ramanujan’s and Salam’s successes. First, nature sometimes gifts an individual with exceptional innate mathematical ability. This is associated with brain circuits in the parietal lobe and acquired through genetic transmission. Second, by good fortune, Ramanujan and Salam managed to escape into a scholarly environment — Cambridge University — where their genius could flower. Had either stayed back home he would be unheard of today.
It is usual to take pride in the geniuses belonging to one’s own tribe. The ancient civilisations of China, India, Greece, Arabia, and modern European civilisation all claim superiority over others because of the creations of their most brilliant minds. But in fact an individual’s exceptional genes and fortunate circumstances — not some supreme transcendence — are the real reasons. While sources of inspiration do differ, empirically and logically deduced results don’t. Science and its heroes belong to all humankind, not to any one tribe.
Thursday 5 March 2015
Why you're almost certainly more like your father than your mother
The Independent
Genes from your father are more dominant than those inherited from your mother, new research has shown.
The findings could give scientists more insight into how diseases and conditions are caused by the expression of thousands of genes, of which several hundred imprinted genes – rather than out of the 95 initially thought – could be in favour of the father.
Genes from your father are more dominant than those inherited from your mother, new research has shown.
All mammals are likely to use the
majority of genetic material passed down from males, even if offspring look and
act more like the mother, according to the study on lab mice by University of North Carolina ’s
School of Medicine
This means that even though we inherit an equal amount of DNA
from each parent, the paternal line is mostly found to govern how a person
develops into an adult – especially in regards to their health.
The findings could give scientists more insight into how diseases and conditions are caused by the expression of thousands of genes, of which several hundred imprinted genes – rather than out of the 95 initially thought – could be in favour of the father.
Professor and
author of the study paper Fernando Pardo-Manuel de Villena said: “This is an
exceptional new research finding that opens the door to an entirely new area of
exploration in human genetics.”
The study on
the offspring of three genetically-diverse strains of “Collaborative Cross”
mice is hoped to shed light on how mutations show up in complex diseases such
as diabetes, heart disease, schizophrenia and obesity, according to
Science Daily.
James Crowley, assistant professor of genetics, selected strains
of mice that descended from a subspecies that evolved on different continents
and each type was used as both father and mother.
When the nine
baby mice reached adulthood, the researchers measured gene expression in four
different kinds of tissue, including RNA sequencing in the brain.
“This
expression level is dependent on the mother or the father,” Pardo-Manuel de
Villena said.
“We now know
that mammals express more genetic variance from the father. So imagine that a
certain kind of mutation is bad. If inherited from the mother, the gene
wouldn't be expressed as much as it would be if it were inherited from the
father.
“So, the same
bad mutation would have different consequences in disease if it were inherited
from the mother or from the father.”
The study is
published in the journal Nature Genetics.
Friday 2 August 2013
Selfish traits not favoured by evolution, study shows
Evolution does not favour selfish people, according to new research.
This challenges a previous theory which suggested it was preferable to put yourself first.
Instead, it pays to be co-operative, shown in a model of "the prisoner's dilemma", a scenario of game theory - the study of strategic decision-making.
Published in Nature Communications, the team says their work shows that exhibiting only selfish traits would have made us go extinct.
Game theory involves devising "games" to simulate situations of conflict or co-operation. It allows researchers to unravel complex decision-making strategies and to establish why certain types of behaviour among individuals emerge.
Freedom or prison
A team from Michigan State University used a model of the prisoner's dilemma game, where two suspects who are interrogated in separate prison cells must decide whether or not to inform on each other.
In the model, each person is offered a deal for freedom if they inform on the other, putting their opponent in jail for six months. However, this scenario will only be played out if the opponent chooses not to inform.
If both "prisoners" choose to inform (defection) they will both get three months in prison, but if they both stay silent (co-operation) they will both only get a jail term of one month.
The eminent mathematician John Nash showed that the optimum strategy was not to co-operate in the prisoner's dilemma game.
"For many years, people have asked that if he [Nash] is right, then why do we see co-operation in the animal kingdom, in the microbial world and in humans," said lead author Christoph Adami of Michigan State University.
Mean extinction
The answer, he explained, was that communication was not previously taken into account.
"The two prisoners that are interrogated are not allowed to talk to each other. If they did they would make a pact and be free within a month. But if they were not talking to each other, the temptation would be to rat the other out.
"Being mean can give you an advantage on a short timescale but certainly not in the long run - you would go extinct."
These latest findings contradict a 2012 study where it was found that selfish people could get ahead of more co-operative partners, which would create a world full of selfish beings.
This was dubbed a "mean and selfish" strategy and depended on a participant knowing their opponent's previous decision and adapting their strategy accordingly.
Crucially, in an evolutionary environment, knowing your opponent's decision would not be advantageous for long because your opponent would evolve the same recognition mechanism to also know you, Dr Adami explained.
This is exactly what his team found, that any advantage from defecting was short-lived. They used a powerful computer model to run hundreds of thousands of games, simulating a simple exchange of actions that took previous communication into account.
"What we modelled in the computer were very general things, namely decisions between two different behaviours. We call them co-operation and defection. But in the animal world there are all kinds of behaviours that are binary, for example to flee or to fight," Dr Adami told BBC News.
"It's almost like what we had in the cold war, an arms race - but these arms races occur all the time in evolutionary biology."
Social insects
Prof Andrew Coleman of Leicester University, UK, said this new work "put a break on over-zealous interpretations" of the previous strategy, which proposed that manipulative, selfish strategies would evolve.
"Darwin himself was puzzled about the co-operation you observe in nature. He was particularly struck by social insects," he explained.
"You might think that natural selection should favour individuals that are exploitative and selfish, but in fact we now know after decades of research that this is an oversimplified view of things, particularly if you take into account the selfish gene feature of evolution.
"It's not individuals that have to survive, its genes, and genes just use individual organisms - animals or humans - as vehicles to propagate themselves."
"Selfish genes" therefore benefit from having co-operative organisms.
Wednesday 3 October 2012
The sequencing and analysis of the first Malayali personal genome
The new Malayali world of DNA
A Kochi-based laboratory has completed the full sequencing and analysis of the first Malayali personal genome, revealing the genetic diversity of the linguistic group and signalling a revolution in disease diagnosis and treatment.
The study by SciGenom Laboratories established that the Malayali is genetically similar to the Caucasians more than any other race on earth.
A detailed report on the analysis has been published after peer review by BMC Genomics, an international medical journal that identifies and pools research contributions in genomics. Investigators at SciGenom Labs had joined hands with Stephan C. Suschter's laboratory at Pennstate, USA, and others to analyse the genome sequencing data.
The report carries elaborate comparison of Malayali genome against other published genomes from other parts of the world. The study revealed that the gene sequence of the Malayali varies from Chinese and African genomes but stands closer to the Caucasian, a term denoting the white race.
Genetic diversity
According to the report, the availability of this genome and the variants identified is a first step in understanding the genetic diversity in the Indian subcontinent, a crucial factor in identifying clinically relevant changes. These changes, along with further studies on additional genomes from this region, should provide a comprehensive assessment of the disease burden in the Indian population, it concluded.
Dr. George Thomas, Director, SciGenom Labs, said this was the first complete sequencing of a South Asian Indian female (SAIF) genome. “The real challenge with regard to the data obtained from genome sequencing is its analysis for arriving at sound conclusions. The analysis enables listing out those genetic deformities and hidden diseases in an individual which would come out in future,” he said.
“So diseases such as cancer, diabetes, liver diseases, and Alzheimer’s would become predictable and there could be preventive treatment and personalised drugs. This is the field occupied by bioinformatics and India needs to develop a good number of experts in this field,” he said.
The sequencing and genotype data has been deposited at the European Genome-Phenome Archive, hosted by the European Bioinformatics Institute (EBI). The SAIF variant information could be viewed at http://gbrowse.scigenom.com. and the full report published by BMC Genomics was available at http://www.biomedcentral.com/1471-2164/13/440, a press note issued by SciGenom Laboratories said.
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