Category: Molecular Genetics


Since August 2015, a large number of babies in Northeast Brazil have been born with very small heads, a condition known as microcephaly, and with other serious malformations. 4,180 suspected cases have been reported.

Epidemiologists have found a convincing correlation between the incidence of the natal deformities and maternal infections with the Zika virus, first discovered in Uganda’s Zika Valley in 1947, which normally produces non-serious illness.

The correlation has been evidenced through the geographical distrubution of Zika infections and the wave of deformities. Zika virus has also been detected in the amniotic fluids and other tissues of the affected babies and their mothers.

This latter finding was recently reported by AS Oliveira Melo et al in ascientific paper published in the journal Ultrasound in Obstetrics & Gynecology, which noted evidence of intra-uterine infection. They also warn:

“As with other intrauterine infections, it is possible that the reported cases of microcephaly represent only the more severely affected children and that newborns with less severe disease, affecting not only the brain but also other organs, have not yet been diagnosed.”

The Brazilian Health Minister, Marcelo Castro, says he has “100% certainty” that there is a link between Zika and microcephaly. His view is supported by the medical community worldwide, including by the US Center for Disease Control.

Oliveira Melo et al draw attention to a mystery that lies at the heart of the affair:

“It is difficult to explain why there have been no fetal cases of Zika virus infection reported until now but this may be due to the underreporting of cases, possible early acquisition of immunity in endemic areas or due to the rarity of the disease until now.

“As genomic changes in the virus have been reported, the possibility of a new, more virulent, strain needs to be considered. Until more cases are diagnosed and histopathological proof is obtained, the possibility of other etiologies cannot be ruled out.”

And this is the key question: how – if indeed Zika really is the problem, as appears likely – did this relatively innocuous virus acquire the ability to produce these terrible malformations in unborn human babies?

Oxitec’s GM mosquitoes

An excellent article by Claire Bernish published last week onAntiMedia draws attention to an interesting aspect of the matter which has escaped mainstream media attention: the correlation between the incidence of Zika and the area of release of genetically modified Aedes aegypti mosquitos engineered for male insterility (see maps, above right).

The purpose of the release was to see if it controlled population of the mosquitos, which are the vector of Dengue fever, a potentially lethal disease. The same species also transmits the Zika virus.

The releases took in 2011 and 2012 in the Itaberaba suburb of the city of Juazeiro, Bahia, Northeast Brazil, about 500 km west of ther coastal city of Recife. The experiment was written up in July 2015 in the journal PLOS Neglected Tropical Diseases in a paper titled ‘Suppression of a Field Population of Aedes aegypti in Brazil by Sustained Release of Transgenic Male Mosquitoes’ by Danilo O. Carvalho et al.

An initial ‘rangefinder of 30,000 GM mosquitos per week took place between 19th May and 29th June 2011, followed by a much larger release of 540,000 per week in early 2012, ending on 11th February.

At the end of it the scientists claimed “effective control of a wild population of Ae. aegypti by sustained releases of OX513A male Ae. aegypti. We diminished Ae. aegypti population by 95% (95% CI: 92.2%-97.5%) based on adult trap data and 78% (95% CI: 70.5%-84.8%) based on ovitrap indices compared to the adjacent no-release control area.”

So what’s to worry about?

The idea of the Oxitec mosquitoes is simple enough: the males produce non-viable offspring which all die. So the GM mosqitoes are ‘self-extinguishing’ and the altered genes cannot survive in the wild population. All very clever, and nothing to worry about!

But in fact, it’s not so simple. In 2010 geneticist Ricarda Steinbrecherwrote to the biosafety regulator in Malaysia – also considering a release of the Oxitec mosquitoes – with a number of safety concerns, pointing out the 2007 finding by Phuc et al that 3-4% of the first generation mosquitos actually survive.

The genetic engineerig method employed by Oxitec allows the popular antibiotic tetracycline to be used to repress the lethality during breeding. But as a side-effect, the lethality is also reduced by the presence of tetracycline in the environment; and as Bernish points out, Brazil is among the world’s biggest users of anti-microbials including tetracycline in its commercial farming sector:

“As a study by the American Society of Agronomy, et. al.,explained, ‘It is estimated that approximately 75% of antibiotics are not absorbed by animals and are excreted in waste.’ One of the antibiotics (or antimicrobials) specifically named in that report for its environmental persistence is tetracycline.

In fact, as a confidential internal Oxitec document divulged in 2012, that survival rate could be as high as 15% – even with low levels of tetracycline present. ‘Even small amounts of tetracycline can repress’ the engineered lethality. Indeed, that 15% survival rate was described by Oxitec.”

She then quotes the leaked Oxitec paper:

“After a lot of testing and comparing experimental design, it was found that [researchers] had used a cat food to feed the [OX513A] larvae and this cat food contained chicken. It is known that tetracycline is routinely used to prevent infections in chickens, especially in the cheap, mass produced, chicken used for animal food. The chicken is heat-treated before being used, but this does not remove all the tetracycline. This meant that a small amount of tetracycline was being added from the food to the larvae and repressing the [designed] lethal system.”

So in other words, there is every possibility for Oxitec’s modified genes to persist in wild populations of Aedes aegypti mosquitos, especially in the environmental presence of tetracycline which is widely present in sewage, septic tanks, contaminated water sources and farm runoff.

‘Promiscuous’ jumping genes

On the face of it, there is no obvious way in which the spread of Oxitec’s GM mosquitos into the wild could have anything to do with Brazil’s wave of micrcophaly. Is there?

Actually, yes. The problem may arise from the use of the ‘transposon’ (‘jumping’ sequence of DNA used in the genetic engineering process to introduce the new genes into the target organism). There are several such DNA sequences in use, and one of the most popular is known as known as piggyBac.

As a 2001 review article by Dr Mae Wan Ho shows, piggyBac is notoriously active, inserting itself into genes way beyond its intended target:

“These ‘promiscuous’ transposons have found special favour with genetic engineers, whose goal is to create ‘universal’ systems for transferring genes into any and every species on earth. Almost none of the geneticists has considered the hazards involved …

“It would seem obvious that integrated transposon vectors may easily jump out again, to another site in the same genome, or to the genome of unrelated species. There are already signs of that in the transposon, piggyBac, used in the GM bollworms to be released by the USDA this summer.

The piggyBac transposon was discovered in cell cultures of the moth Trichopulsia, the cabbage looper, where it caused high rates of mutations in the baculovirus infecting the cells by jumping into its genes … This transposon was later found to be active in a wide range of species, including the fruitfly Drosophila, the mosquito transmitting yellow fever, Aedes aegypti, the medfly, Ceratitis capitata, and the original host, the cabbage looper.

“The piggyBac vector gave high frequencies of transpositions, 37 times higher than mariner and nearly four times higher than Hirmar.”

In a later 2014 report Dr Mae Wan Ho returned to the theme with additional detail and fresh scientific evidence (please refer to her original article for references):

“The piggyBac transposon was discovered in cell cultures of the moth Trichopulsia, the cabbage looper, where it caused high rates of mutations in the baculovirus infecting the cells by jumping into its genes …

“There is also evidence that the disabled piggyBac vector carrying the transgene, even when stripped down to the bare minimum of the border repeats, was nevertheless able to replicate and spread, because the transposase enzyme enabling the piggyBac inserts to move can be provided by transposons present in all genomes.

“The main reason initially for using transposons as vectors in insect control was precisely because they can spread the transgenes rapidly by ‘non-Mendelian’ means within a population, i.e., by replicating copies and jumping into genomes, thereby ‘driving’ the trait through the insect population. However, the scientists involved neglected the fact that the transposons could also jump into the genomes of the mammalian hosts including human beings …

“In spite of instability and resulting genotoxicity, the piggyBac transposon has been used extensively also in human gene therapy. Several human cell lines have been transformed, even primary human T cells using piggyBac. These findings leave us little doubt that the transposon-borne transgenes in the transgenic mosquito can transfer horizontally to human cells. The piggyBac transposon was found to induce genome wide insertion mutations disrupting many gene functions.”

Has the GM nightmare finally come true?

So down to the key question: was the Oxitec’s GM Aedes aegyptimale-sterile mosquito released in Juazeiro engineered with the piggyBac transposon? Yes, it was. And that creates a highly significant possibility: that Oxitec’s release of its GM mosquitos led directly to the development of Brazil’s microcephaly epidemic through the following mechanism:

1 Many of the millions of Oxitec GM mosquitos released in Juazeiro in 2011/2012 survive, assisted, but not dependent on, the presence of tetracycline in the environment.

2 These mosquitos interbreed with with the wild population and their novel genes become widespread.

3 The promiscuous piggyBac transposon now present in the local Aedes aegypti population takes the opportunity to jump into the Zika virus, probably on numerous occasions.

4 In the process certain mutated strains of Zika acquire a selective advantage, making them more virulent and giving them an enhanced ability to enter and disrupt human DNA.

5 One way in which this manifests is by disrupting a key stage in the development of human embryos in the womb, causing microcepahy and the other reported deformations. Note that as Melo Oliveira et al warn, there are almost certainly other manifestations that have not yet been detected.

6 It may be that the piggyBac transposon has itself entered the DNA of babies exposed in utero to the modified Zika virus. Indeed, this may form part of the mechanism by which embryonic development is disrupted.

In the latter case, one implication is that the action of the gene could be blocked by giving pregnant women tetracycline in order to block its activity. The chances of success are probably low, but it has to be worth trying.

No further releases of GM insects!

While I am certainly not claiming that this is what actually took place, it is at least a credible hypothesis, and moreover a highly testable one. Nothing would be easier for genetic engineers than to test amniotic fluids, babies’ blood, wild Aedes mosquitos and the Zika virus itself for the presence of the piggyBac transposon, using well established and highly sensitive PCR (polymerase chain reaction) techniques.

If this proves to be the case, those urging caution on the release of GMOs generally, and transgenic insects bearing promiscuous transposons in particular, will have been proved right on all counts.

But most important, such experiments, and any deployment of similar GM insects, must be immediately halted until the possibilities outlined above can be safely ruled out. There are plans, for example, to release similarly modified Anopheles mosquitos as an anti-malarial measure.

There are also calls for even more of the Oxitec Aedes aegyptimosquitos to be released in order to halt the transmission of the Zika virus. If that were to take place, it could give rise to numerous new mutations of the virus with the potential to cause even more damage to the human genome, that we can, at this stage, only guess at.


Oliver Tickell edits The Ecologist, where this article originally appeared.

Gene Splicers, Mosquitoes and Wall Street


Sometimes I think humans are the stupidest species on the planet. We are the only species that, solely for the sake of profit, endeavor to develop technologies that not only are completely unnecessary for our survival but have a potential risk factor of bringing about our own destruction. This has been going on for much of the last century, and we have amply demonstrated over the same time we will believe any lie told to us provided it comes from a “credible” source.

And one of those “credible” sources is “science.”

I normally am not a science writer, but for the past few days stories about genetically modified mosquitoes have been buzzing around the Internet with regard to Zika, the latest virus that seems to be threatening certain populations in lesser developed areas of the world. Depending upon which source you believe, such mosquitoes are either, a) the solution to the Zika outbreak, or, b) the cause of it.

Let’s examine theory “a” first. The idea that GM mosquitoes (GMM) might rescue the people of Brazil and other countries seems to stem from  a January 19 press release put out by Oxitech, a British company that describes itself as “a pioneer in controlling insects that spread disease and damage crops.”

The gist of the press release is that the company will be opening a “mosquito production facility” in the city of Piracicaba, Brazil, the function of which will be to produce “self-limiting mosquitoes whose offspring do not survive.” The male mosquitoes have been genetically altered in such a way that they are incapable, theoretically at any rate, of producing viable offspring. Thus, the GMM’s will be released into the wild, where they will mate with female Aedes aegypti mosquitoes, the main vector of the Zika virus, and henceforth they will dramatically reduce the mosquito population.

That’s the theory, at any rate. Fox News, NPR, CBS, The Guardian, Time, CNN and others all went with the story, all plugging the use of GMM’s and suggesting it might be useful in the fight against the Zika virus.

“There is no biological mechanism by which the Oxitec bug’s modified pieces of DNA can transfer into human DNA, or into other mammals and insects,” Ford Vox asserts confidently in an opinion piece at CNN.

In other words, it’s not only safe, it has the potential to help rid the world of a terrible disease. Vox, by the way, according to CNN, is a doctor.

Now let’s examine theory “b.” On January 25, an article got posted at Reddit with a link to an earlier Oxitec press release, dating back to July 2015. That earlier press release announced the release of GMMs in Brazil, this in the effort to fight dengue fever. Specifically, the mosquito-release took place in Juazeiro, in northeast Brazil, in virtually the same area where babies are now being born with microcephaly.

Map showing location of Juazeiro, Brazil


Map showing areas of Brazil where Zika has been reported

On January 29, alternative media outlets began to publish the story, and on January 30, RT came out with a piece as well, under the headline, GMO mosquitoes could be cause of Zika outbreak, critics say. The rather interesting thing about the RT report is that it contains a link to an article published in The Guardian back in 2012. That article includes some rather astounding information, so let’s take a look at it.

Under the headline, Can GM Mosquitoes Rid the World of a Major Killer?, the story was published in the Guardian on July 14, 2012. The “major killer” referred to is dengue fever. Like the other stories I’ve linked to above, i.e. those published in the past week or so, the 2012 piece mentions the work by Oxitec, including its efforts in Brazil and other countries. But now here’s the real eye-popper. It seems Oxitec, already at that time in 2012, was releasing mosquitoes into the air, and not just in Brazil, either:

The mosquitoes developed and raised here at the laboratories of Oxitec, a British biotech company based near Didcot, have already infiltrated wild populations in Brazil, Malaysia and the Cayman Islands, and will soon be unleashed in Panama and India. The company hopes that it will reduce populations of disease-carrying mosquitoes by 80% but public opposition to anything “genetically modified” remains a significant obstacle to the possibility of saving thousands of lives.

So in other words, if The Guardian article is correct, the release of genetically engineered mosquitoes in Brazil didn’t begin in 2015; it started at least as far back as 2012.

According to its website, Oxitec “was formed in 2002 as a spin out from the University of Oxford,” and hence the company’s name (in reality a shortened version of Oxford Insect Technologies). It’s aim is to pioneer “environmentally safe methods of insect control,” and to this end it has developed genetically modified versions not only of the Aedes aegyptimosquito, but also the Mediterranean fruit fly and the pink bollworm.

Last year, in August to be exact, Oxitec was purchased by Intrexon Corp. In an article published January 28, 2016, theMotley Fool financial site reported that shares of Intrexon had “surged as much as 24% during Thursday’s trading session as a direct result of the spreading Zika virus.” The article is headlined, “Intrexon Corporation Catches Zika Fever.”

The CEO of Intrexon is Randal J. Kirk, who describes himself as “a lifelong student of business,” while one of the company’s top-ranking executives is Sr. Vice President Nir Nimrodi, formerly employed by the biotech firm Life Technologies,  now a part of Thermo Fischer Scientific. Nimrodi, according to Reuters, previously served with the Israeli Ministry of Defense.

The 2012 article in the Guardian informs us also that the Oxitec mosquitoes–though deliberately engineered not to produce offspring–could in fact generate viable young if they somehow gained access to the antibiotic tetracycline. Or as the story puts it:

The altered males are fed tetracycline in the lab and then introduced into the wild where they mate with wild females. The offspring need tetracycline to develop but cannot find it and so die. Only males are introduced into the environment and in a few days both they and their offspring are dead.

But of course, ranchers and farmers have been feeding antibiotics to cattle for a good many years now, so what happens if, for instance, one of Oxitec’s mosquitoes should come into contact with domestic animals pumped full of tetracycline? The issue is in fact raised by a biotech industry critic quoted in the story:

Critics of Oxitec say that the company is rushing to commercialise its products to provide a return on investment, massaging research while leaving key questions unanswered. Dr Helen Wallace, the director of GeneWatch, says she has several problems with Oxitec’s findings from its trials. One major issue, she says, is the occurrence of the tetracycline – the antibiotic that the young mosquitoes need to survive – in livestock and meat. Theoretically, if a female mosquito, daughter to a modified one, bit meat or an animal that contained tetracycline, she could survive. Oxitec says that the chance of this happening is very slim and in its most recent trial in the Caymans, it did not find a single mosquito that had survived.

Wallace says: “It’s a very experimental approach which has not yet been successful and may cause more harm than good. They are pushing ahead to commercialise their approach so they can start paying back their investors.

“I would be happier if there were more experiments in controlled areas, caged areas and labs, before general release in the populated areas. For example, in an area where dengue fever is endemic there’s a possible danger to the public.”

Wallace believes that existing control methods could be just as effective as releasing genetically modified insects and points out there are other innovations on the horizon which could be even more successful.

Tetracycline, by the way, can also be produced by bacteria in soils, and thus can occur naturally in the environment.

Back in 2014, when Ebola was ravaging countries in West Africa, news surfaced on some alternative websites that the epidemic had been preceded by a period of time in which the US government and certain pharmaceutical corporations had conducted ebola tests on humans, presumably in the interest of developing a vaccine. This was the subject of an article at the time by Paul Craig Roberts, who discusses the findings of Francis Boyle, of the University of Illinois, and Dr. Cyril Broderick, of the University of Liberia.

“Reports narrate stories of the US Department of Defense (DoD) funding Ebola trials on humans, trials which started just weeks before the Ebola outbreak in Guinea and Sierra Leone,” said Broderick. “The reports continue and state that the DoD gave a contract worth $140 million dollars to Tekmira, a Canadian pharmaceutical company, to conduct Ebola research. This research work involved injecting and infusing healthy humans with the deadly Ebola virus.”

Why, we might wonder, don’t these corporations, if their work is so benign and altruistic, do their research in their own countries on their own populations? Why do they continuously seem to go to countries in Africa and Latin America?

Roberts’ article came out just a month after reports in the mainstream media regarding a group of health officials and journalists that came under attack in Guinea by local villagers who “feared that outsiders” had brought the disease into their community. Where on earth would they get such an idea?

The January 19 press release from Oxitec quotes company CEO Hadyn Parry as well as Piracicaba Mayor Gabriel Ferrato, both of whom express delight at the partnership formed between the biotech firm and the Brazilian city. “The city of Piracicaba has always sought innovative solutions to serious problems,” Ferrato proclaims.

You have to wonder about the sales pitches thrown at local officials like Ferrato. “Trust us, we’re smart Western scientists,” or some variation thereof perhaps.

So if the mosquitoes that caused, or at least possibly caused, the Zika outbreak were genetically engineered, what about the virus itself? Was it also genetically engineered? Hard to say. According to Wikipedia, the Zika virus was first isolated in 1952, but Wikipedia is so full of spin on a such a variety of issues, particularly political ones, that it’s difficult to take anything the “encyclopedia” presents with much more than a grain of salt. What’s clear is that the biotech industry falls into the same category as the nuclear industry: though it might yield some positive benefits, it also has the potential to do humanity completely in. And at the same time it doesn’t seem to be nearly as tightly regulated as the nuclear industry. Apparently any greed-driven fool can set up a lab and start splicing genes without having to go through much in the way of regulatory oversight.

Recently Stephen Hawking, one of the somewhat more intelligent members of the stupidest species on earth, cautioned that humanity is heading toward a disaster of its own making, and he warned ominously of three dangers in particular that pose a dire challenge to life on the planet. The first two items of concern were pretty much what you would expect: nuclear war and climate change.

It was the third item, however, that possibly raised a good many eyebrows, or at least it raised mine, for the third item on the list–which Hawking ominously warned imperils humanity’s future–was…genetically engineered viruses. Quite fascinating, really, that the mainstream media, which in large part have never even acknowledged the existence of such viruses, would report Hawking’s words, but in fact they did.

“We are not going to stop making progress, or reverse it,” Hawking told listeners that night, “so we have to recognize the dangers and control them.”

It’s a warning the stupid human species would do well to keep in mind–but I’m reasonably sure we won’t.

Richard Edmondson is the author of The Memoirs of Saint John: When the Sandstone Crumbles, a novel about an archaeological expedition to Syria, set amidst the current conflict in the country

Political Paralysis and the Genetics Agenda

Variations in individual “educational attainment” (essentially, whether students complete high school or college) cannot be attributed to inherited genetic differences. That is the finding of a new study reported in Science magazine (Rietveld et al. 2013). According to this research, fully 98% of all variation in educational attainment is accounted for by factors other than a person’s simple genetic makeup.

This implies that most of student success is a consequence of potentially alterable social or environmental factors. This is an important and perhaps surprising observation, of high interest to parents, teachers, and policymakers alike; but it did not make the headlines.

The likely reason is that the authors of the study failed to mention the 98% figure in the title, or in the summary. Nor was it mentioned in the accompanying press release.

Instead, their discussion and interest focused almost entirely on a different aspect of their findings: that three gene variants each contribute just 0.02% (one part in 5,000) to variation in educational attainment. Thus the final sentence of the summary concluded not with a plea to find effective ways to help all young people to reach their full potential but instead proposed that these three gene variants “provide promising candidate SNPs (DNA markers) for follow-up work”.

This is as spectacular a misdescription of a scientific finding as is to be found anywhere in the scientific literature. But the question is why? Why did the more than two hundred authors decide to highlight the unimpressive 0.02% and bury the 98%? The easy answer is that the authors are geneticists and that geneticists will not have distinguished careers if variation in genes is irrelevant to health and human achievement. The full answer, however, is considerably more interesting, and much more significant, than simple conflicts of interest.

The broader explanation, which needs to account, for example, for the fact that Science magazine would publish such a discrepant conclusion, is that the science of human biology is in the grip of hidden political forces. These forces are powerful enough to enable (this and other) comprehensively misrepresented genetic studies to evade the corrective potential of the scientific peer review process, and be published in the foremost journals of science.

How money and politics can dictate the conclusions of a scientific study

The easiest starting point to explain this miscarriage of science is to begin with funding. The Rietveld research, we know for a fact, was part of a genetic epidemiology project called the Social Science Genetic Association Consortium (SSGAC). The consortium obtains its money almost entirely from the National Institutes of Health (NIH) and the National Science Foundation, i.e. the US government.

The self-described funding premise of SSGAC is that: “for most outcomes in life, over half the resemblance of two biological siblings reared in the same family stems from their genetic similarity” (Benjamin et al. 2012).

In other words, SSGAC believed even before Rietveld was published that inherited genetic predispositions make the dominant contribution to ones’ lifetime achievements, in education and apparently “most” spheres of human behavior. Consequently, the aim of all its projects is to physically locate these specific genetic factors on human DNA.

But the actual Rietveld result implies that such genetic predispositions are pretty much irrelevant, at least as far as educational attainment is concerned. Moreover, SSGAC had previously searched for gene variants associated with “general intelligence”, and “economic and political preferences” (such as risk-aversion and trust). For all these traits the search was again unsuccessful; in only one instance did project members find a genetic variant that reached the threshold of statistical significance (which is itself far below what might be considered important as a predisposing factor) (Benjamin et al. 2012; Chabris et al. 2012). Thus we can say that SSGACs’ founding premise is not in alignment with the data.

But that just brings the question back one stage further: why is the US government funding excessively genetic determinist projects such as this in the first place?

The probable answer is that the US education system has many problems, which are exemplified by its low rankings on international scales. There is a danger that blame for these problems might be laid at the door of the secretary for education, the administration, or the President. This possibility could be neatly sidestepped, however, if educational attainment was genetically fated.

Essentially the same political logic applies to any human disease or disorder, or even any social complaint. If the disorder, for example autism, can be shown (or even just suggested) to have a partial genetic origin then a barn door is opened for any accused vaccine maker, or polluter, or policymaker, to evade the blame–both legally and in the perception of the public.

This opportunity within biology to make inequality (not just of wealth) look ‘natural’ has been recognized for a long time. Harvard Geneticist Richard Lewontin summed it up his 1992 book ‘The Doctrine of DNA: Biology as Ideology’: “The notion that the lower classes are biologically inferior to the upper classes…… meant to legitimate the structures of inequality in our society by putting a biological gloss on them”

Extreme genetics

Recognition that this reasoning aligns the interests of both corporations and governments has coincided with the extraordinary funding opportunities for scientists willing to apply DNA analysis and genomic approaches to vast areas of mental and physical health. Precise figures are not available, but over the last fifteen years close to half the budget of the NIH has gone to genetic analysis of human populations. That is likely in excess of $100 billion dollars in the US alone.

The financial outlay is ongoing: the same SSGAC consortium is also researching the possibility of genetic factors in “subjective well-being” (happiness) and “fertility”. Furthermore, the scope of the search for genetic predispositions is widening. In 2004 science writer John Horgan noted that (unsuccessful) searches have been made for “genes for” ”attention-deficit disorder, obsessive-compulsive disorder, manic depression, schizophrenia, autism, dyslexia, alcoholism, heroin addiction, high IQ, male homosexuality, sadness, extroversion, introversion, novelty seeking, impulsivity, violent aggression, anxiety, anorexia, seasonal affective disorder, and pathological gambling.”

Since he compiled that list the field of “behavioral economics” has been added to the list of genetic searches considered worthy of public support. For example, a 2013 publication in the journal PLOS one (with 68 authors) goes by the title “The Molecular Genetic Architecture of Self-Employment” (van der Loos et al. 2013). Meanwhile, the US National Human Genome Research Institute last year put out a call for evidence asking geneticists to support a search for predispositions to “behavioral adherence” to expert advice (i.e. compliance).

Thus there is operating within the disciplines of medicine, public health, social science, and now economics, a research framework that, if successful, would locate the causes of negative human outcomes internally. At fault will be genes and not circumstances. It is an officially sanctioned and scientific version of “blame the victim”.

Three major strands of evidence support this thesis.

Big tobacco and the origins of human genetics

Most directly of all, there is clear evidence that the search for genetic predispositions is the centerpiece of a longterm corporate agenda whose purpose is to sway public opinion. It began in the 1960s with the tobacco industry at a time when smoking was first implicated in lung cancer. The strategic purpose was to deflect the public fear of smoking, minimize the likely policy responses, and eliminate potential legal expenses, by funding, encouraging, and then exploiting, human genetic research. This could be done, so the industry thought, by building from scratch a science of genetic risk factors.

This agenda operated until the late 1980s when the tobacco industry became politically too controversial for medical organizations to maintain formal relations. According to research by Helen Wallace of the UK non-profit GeneWatch, the tobacco industry by 1994 had awarded around 1,000 researchers £225 million ($370 million) to nurture research in human genetics (Wallace 2009). This tobacco research money was directed in particular to searches for genetic associations with lung cancer.

As early as 1965, this strategy was sowing uncertainty about the causes of lung cancer. As Dr. George L. Saiger, a consultant paid over $50,000 by the tobacco industry, testified before the US Senate Commerce committee: “There is strong reason to believe that the constitutional hypothesis fits the evidence appearing in the Report of the Surgeon General’s Committee at least as well as the cigarette hypothesis…”

Proof that this statement was part of a conscious program to build the credibility of a “constitutional hypothesis” (i.e. the existence of genetic predispositions to lung cancer) was subsequently confirmed by searches of the Legacy Tobacco Documents (Gundle et al. 2010). These are internal documents of the tobacco industry, now kept by the University of California, San Francisco, that the industry was compelled to release in a lawsuit settlement.

The tobacco industry also pioneered ‘behavioral genetics’. The idea that even addiction to cigarettes was a genetic phenomenon (and not a characteristic of cigarettes or tobacco) originated with the tobacco industry. The consistent aim behind promoting genetics, according to a memo written by Fred R. Panzer, Vice President of Public Relations for the Tobacco Institute, was to change the focus of attention “from one product to a type of person”.

The tobacco industry was still actively pursuing the same public relations (PR) strategy when, for example, senior tobacco executives met with geneticist and Nobel Laureate Sydney Brenner in 1988, just a month before he set up the Human Genome Organization (HUGO) (Wallace 2009). HUGO was the organization formed to oversee the Human Genome Sequencing Project.

Human genetics is not public health

The second important point of evidence is that the public interest justification for identifying gene variants is hard to discern. For example, even if predispositions for educational attainment were to be found, it is not clear how public welfare would benefit. For example, it wouldn’t affect at all the need for high quality education, either for individuals found wanting, or for those of average or higher ability. This crucial point is glossed over by proponents of genetic explanations who, according to Chaufan and Joseph (2013), merely assume that genetic knowledge “will necessarily improve the prediction, diagnosis, prevention, or treatment of common disorders.”

As these weaknesses have become clearer, it has become more common for public health professionals to question the utility of these studies and argue that, at a minimum: “advocates of genomic medicine should be much more modest” about the likely impacts on public health (Hall, Mathews, and Morley 2010).

The genetic evidence deficit

The third reason to suspect that a political and not a scientific agenda underlies the continued push for genetic research is that the money has continued to flow even in the face of a tsunami of evidence against its major predictions. As Hall and colleagues also wrote, geneticists: “have not identified major susceptibility alleles (gene variants) for most common diseases.” (Hall, Mathews, and Morley 2010).

Even the findings that have been claimed (which are modest) have consistently not stood up to retrospective replication (Ioannidis and Panagiotou 2011). The absence of evidence is now so clear that even leaders in the field of human genetics sometimes find an acknowledgement is necessary (though only in the context of a request for more funding) (Manolio et al. 2009).

As the evidence for genetic causations has continuously and stubbornly refused to appear, critics have grown bolder. Chaufan and Joseph in 2013 felt confident enough to write: “these variants have not been found because they do not exist” (Chaufan and Joseph 2013).

It is important, nevertheless, to acknowledge that there are exceptions. The breast cancer mutations of the BRCA1 gene are one class of exception. But even BRCA1 is an exception that proves the rule. BRCA1 is well known precisely because it remains an almost unique example of a prominent genetic predisposition to a common disease. Yet even BRCA1 is oversold. More than 90% of all breast cancer cases are unrelated to it (Gage et al. 2012).

The other class of exceptions are those relatively rare disorders for which there is clear evidence of a simple genetic cause. Cystic fibrosis is an example of such a disease; Huntington’s disease is another.

However, to return to the main point, for common physical and mental health conditions, such as heart disease, cancer, autism and schizophrenia, the situation has proven very different. The epidemiological and genetic evidence suggests that genetic risk is at most a minor contributing component. For behavioral and economic traits the lack of positive genetic data is even more apparent.

Consequently, an extra-scientific explanation is required to explain why very large sums of taxpayer money have funded human genetic research in the face of such negative results.

Human genetics: a PR success built on a scientific failure

In purely research terms, the search for human genetic predispositions has foundered. Yet this failure has done curiously little to prevent medical and behavioral genetics from being an overwhelming PR success. Thanks to the tobacco industry (joined later by the chemical industry, the food industry, the pharmaceutical industry, all the way to the gambling industry), “genes for” any disease, or talent, or human oddity, is nowadays a standard topic of adult conversation.

This was not always the case. When the geneticist Mary-Claire King (co-discoverer of the BRCA1 gene) was interviewed recently in New Scientist, she was at pains to remind the interviewer that in the 1980s convincing funders to explore an inherited genetic basis for cancer was exceedingly difficult.

“The main experience of the period was that people completely ignored me” (Powerful genes New Scientist 22 June 2013).

It is hard to be certain but it is likely that this sea change in public opinion did indeed protect the tobacco industry, which continues to thrive. It also, we have previously argued, played a key role in protecting polluters and politicians of all kinds from facing regulations and responsibility. Much of the explanation for our societies’ generic failure to address social and environmental problems can probably be attributed to the simple overreliance on genetic determinist explanations.

Yet beyond the example of BRCA1, few scientists or lay people could name a specific discovery to back up their genetic suppositions. This discrepancy, between the failure of the science program itself and its success as a PR project is truly a sobering testament to the power of modern public relations. It is also an indictment of science journalism and the inadequacy of the science media as a whole.

Free enquiry vs directed science

The above analysis proposes that it is a mistake to ascribe responsibility for their conclusions solely to authors of papers such as Rietveld et al. Equally culpable is the operating system within which these researchers find themselves. Science magazine and its editors and reviewers, for example, are clearly complicit in publishing misleading conclusions. Funding agencies are complicit in awarding public funds to speculative gene hunting projects at the expense of pressing public health questions. The evidence thus points to a broad system-wide failure.

Not sufficiently understood by outsiders is the fact that most of science is essentially now a top-down project. There persists a romantic notion (retained by many scientists) that science is a process of free enquiry. In this view, the endless grant applications and the requests for applications are merely quality control measures, or irritants imposed by bureaucrats.

But free enquiry in science is all but extinct. In reality, only a tiny proportion of research in biology gets done outside of straightjackets imposed by funding agencies. Researchers design their projects around funding programs; universities organize their hiring around them, and every experiment is carefully designed to bolster the next grant application.

The consequences of this dynamic are that individual scientists have negligible power within the system; but more importantly it opens a route by which powerful political or commercial forces can surreptitiously set the science agenda from above.

In the case of medical genetics that power has been used to deform our understanding of human nature itself. Thus public money has bought not scientific ‘progress’ but the domination of intellectual enquiry by an entirely malevolent project, conceived fully outside of science. This project was intended only to ensure political paralysis and the consolidation of economic power and whatever agenda scientists thought they were following was entirely incidental. What we observe is in fact a full-blown enlightenment malfunction.

Nevertheless, despite the almost daily PR barrage of genetic determinist headlines, our fate is not written in our DNA and the state of public understanding can in principle be reversed. The hopeful truth is that there are compelling reasons to remove subsidies for junk food, pesticides from the food and water, toxins from the workplace, and social and economic injustices from society, and that when we do, things will improve.

Jonathan R Latham, PhD Co-founder and Executive Director of the Bioscience Resource Project; Editor of the Independent Science News website, where this essay originally appeared. Dr. Latham holds a Masters degree in Crop Genetics and a PhD in Virology. He was subsequently a postdoctoral research associate in the Department of Genetics, University of Wisconsin, Madison.


Benjamin et al. (2012) The Promises and Pitfalls of Genoeconomics Annual Review of Economics 4: 627-662.
Benjamin D et al. (2012) The genetic architecture of economic and political preferences. Proc. Nat. Acad. Sci. 109: 8026–8031.
Chabris CF, et al. (2012) Most reported genetic associations with general intelligence are probably false positives. Psychol Sci. 23: 1314-23.
Gage M, Wattendorf D, Henry LR. (2012) Translational advances regarding hereditary breast cancer syndromes. J Surg Oncol. 105: 444-51. doi: 10.1002/jso.21856.
Gundle KR. Dingel, M and Barbara A. Koenig (2010) “To Prove This is the Industry’s Best Hope”: Big Tobacco’s Support of Research on the Genetics of Nicotine. Addiction. 105: 974–983. doi: 10.1111/j.1360-0443.2010.02940.x
Hall WD, Mathews R, Morley KI (2010) Being More Realistic about the Public Health Impact of Genomic Medicine. PLoS Med 7(10): e1000347. doi:10.1371/journal.pmed.1000347
Ioannidis JP and Panagiotou O (2011) Comparison of Effect Sizes Associated With Biomarkers Reported in Highly Cited Individual Articles and in Subsequent Meta-analyses. J. Am. Med. Assoc. 305: 2200-2210.
Chaufan C and Joseph J (2013) The ‘Missing Heritability’ of Common Disorders: Should Health Researchers Care? International Journal of Health Services 43: 281–303
Manolio T. et al. (2009) Finding the missing heritability of complex diseases. Nature 461: 747-753.
Rietveld et al. (2013) GWAS of 126,559 individuals identifies genetic variants associated with educational attainment. Science, 340, 1467-1471, . doi:10.1126/science.1235488
van der Loos MJHM, Rietveld CA, Eklund N, Koellinger PD, Rivadeneira F, et al. (2013) The Molecular Genetic Architecture of Self-Employment. PLoS ONE 8(4): e60542. doi:10.1371/journal.pone.0060542
Wallace H (2009) Big tobacco and the human genome: Driving the scientific bandwagon? Genomics, Society and Policy 5: 1-54.