The court has however upheld the ruling that synthetically created exons-only strands of nucleotides known as composite DNA (cDNA) are patentable. The ruling found that “A naturally occurring DNA segment is a product of nature and not patent eligible merely because it has been isolated, but cDNA is patent eligible because it is not naturally occurring”

The full ruling is available here.

Dr Luigi Palombi is a patent lawyer and author of ‘Gene Cartels: Biotech Patents in the Age of Free Trade’. He is also an academic at the Centre for the Governance of Knowledge and Development at The Australian National University. He comments:

“This decision is to be welcomed. It removes 30 years of uncertainty over the patenting of biological materials existing in nature and deals a blow to the semantics over the word ‘isolated’. According to the Court merely isolating genetic material from the human body does not render the genetic material patentable subject matter. The Court also make it clear that while cDNA is patentable subject matter, if the genetic sequence housed in the cDNA is “indistinguishable” from the information in the natural DNA, that cDNA is also not patentable subject matter. In other words, before genetic material is patentable the genetic sequence housed in that material must be distinguishable from what exists in nature.”

Professor Ian Olver is CEO of the Cancer Council, comments:

“This is a welcome decision that addresses the issue of commercial monopolies over genetic mutations that are vital to cancer prevention, diagnosis and treatment. If there had been greater clarity on the issue back in 2008, the Australian licensee for the BRCA1 and BRCA2 patents would not have been able to demand public laboratories cease conducting the tests. Eventually the patent enforcement claim was withdrawn, but there was, and still is, nothing in Australian law to prevent commercial interests trying to monopolise the use of genetic materials.

“The US Supreme Court’s ruling paves the way for Australia’s federal parliament to change the Patents Act and clarify that human genetic materials are not inventions and are not patentable. We welcome innovation in medical research, which should rewarded by a robust patents system. However, discovery and isolating genetic material is not innovation. The US Supreme Court’s decision is a landmark ruling that provides a clear precedent for Australia.”

The 168 pigs in the study were fed a diet of either GM or non-GM corn and soy over the course of their normal commercial lifespan (just over five months) at a pig farm in the United States. They were then autopsied by veterinarians after slaughter and tested for any significant differences across a wide range of measures.

The study found evidence that stomach inflammation classified as ‘severe’ was higher in pigs fed the GM diet. It also found that pigs in the GM feed group had, on average, a heavier uterus. There were no other significant differences between the disease status or weight of the organs of pigs in the two groups.

The results further showed no significant differences in blood biochemistry, weight, illness, veterinary interventions or mortality between the two groups.

The full study is available here.

A Before the Headlines analysis of the paper is available here.

The Science Media Centre approached experts for reaction to the study. We will update our website with further comments as they are received.

Assoc Prof Peter Dearden, Director, Genetics Otago, University of Otago, comments:

“This study investigates is GM feed has adverse affects on pigs, and shows that both the rates of severe stomach inflammation and uterine weight appear to differ between the GM and non-GM fed pigs.

“I have a few issues with the outcomes of this paper. The first is that the procedure has been to feed the pigs the differing diets (and it must be noted that the diets between the groups differed more than just due to the GM) and then measure a vast array of parameters and report only those that are significant. In this kind of statistical analysis it is important to note that tests can have a positive result by chance. thus the more tests you, the more times a difference will be seen just by chance. Statisticians have known this for a while and there are a range of ways to account for multiple testing; none of which have been applied here. This is a problem.

“Secondly, the author report that GM fed pigs have more severe inflammation of the stomach than non GM fed pigs. But non-GM fed pigs have more moderate inflammation than GM fed pigs, reversing this trend. I would expect that the more GM you gave the more inflammation you would get, if there was a direct affect of GM food. We would expect, I think, to see a relationship between dose and response. The data from the paper doesn’t show this, which is puzzling.

“In summary, there may be something in this paper, but it needs repeating, and a more robust study needs publishing in a high impact, international journal. That would encourage me to think that that the weak effects seen here are not just an artifact.”

Prof Thomas Lumley, Professor of Biostatistics, University of Auckland, comments:

“This study is much better designed and analysed than the controversial French GM/glyphosate study from last year. It has just two groups and a reasonable sample size in each group. There’s a good level of detail given about the study process, and the assessments were carried out in a way that would reduce bias, with approximately matched numbers of pigs from each diet at each occasion, and with measurements made by someone who didn’t know which diet each pig had received. I can’t comment on how appropriate these diets are either for pigs or as a guide to human effects, but enough detail is given for this assessment to be made by a knowledgeable person. The researchers do comment that the finely-ground feed used in the pig industry is known to lead to stomach inflammation. This inflammation would be common to the GM and non-GM diets, so it would not cause bias, but it may make the results less generalisable to other animals and to humans.

“The statistical analysis is reasonable, and follows standard practice. The results are consistent with a harmful effect of the GM corn or soy. The results provide only modest evidence of harm, even for pigs on a 100% GM diet, because many possible effects were tested, making it quite possible that some difference would turn up just by chance. The researchers give a plausible explanation for an effect on stomach inflammation, but would likely have been able to give equally plausible explanations for other findings. The study should not change policy on its own, but it is worth taking seriously for future research. If the same results were found in a replication they might signal a harmful effect of high doses of the specific insecticidal proteins in these GM feed varieties.”

Further comments gathered by the UK Science Media Centre

Prof Patrick Wolfe, Professor of Statistics at University College London, said:

“I am not an expert on animal health, husbandry, toxicology etc, and therefore I cannot comment on these aspects of the study. As a statistical methodologist I can however comment on the data analysis undertaken and presented in the article.

“The biggest issue is that the study was not conducted to test any specific hypothesis. This means that the same sample (in this case nearly 150 pigs) is, in effect, being continually tested over and over for different findings.

“The statistical tests employed assume that a single test is done to test a single, pre-stated hypothesis; otherwise the significance levels stemming from the tests are just plain wrong, and can be vastly over-interpreted.

“Thus there is a higher-than-reported likelihood that the results are due purely to chance. The number of pigs being in the low hundreds (instead of, say, the thousands, as is often the case in large medical studies) can make this effect even more prominent.

“Bottom line: a better-designed study would have hypothesized a particular effect (such as changes in stomach size), and then applied a statistical test solely to check this hypothesis. Perhaps another independent team of researchers will go down this path. Until then, this study definitely does not show that GM-fed pigs are at any greater risks than non-GM fed pigs.”
Prof Tom Sanders, Head of the Nutritional Sciences Research Division at Kings College London, said:

“It does not look like a convincing adverse effect as it was a minor incidental finding. There were no differences in growth and mortality rates and pigs at sacrifice appeared in similar health. The dietary groups were also not identical as different supplements had been used. If you do not specify outcomes at least one in 20 will come up as being statistically significant by play of chance.

“The probabilities for the abnormal findings were low. Gastric inflammation is often due to infections and uterine weight can be influenced by factors such as rate of weight gain. The number of pigs with mild to severe inflammation did not different between groups with 69/73 showing inflammation in the control group and 64/79. The authors have unwisely highlighted differences in the number with severe inflammation. It seems unlikely that the effects observed were treatment-related.”

Prof David Spiegelhalter, Winton Professor of the Public Understanding of Risk at the University of Cambridge, said:

“The study’s conclusions don’t really stand up to statistical scrutiny. The authors focus on ‘severe’ stomach inflammation but all the other inflammation categories actually favour the GM-diet. So this selective focus is scientifically inappropriate.

“When analysed using appropriate methods, the stomach inflammation data does not show a statistical association with diet. There are also 19 other reported statistical tests, which means we would expect one significant association just by chance: and so the apparent difference in uterus weight is likely to be a false positive.”

Councillors voted this morning to stop adding fluoride to Hamilton’s drinking water, overturning the outcome of a 2006 referendum in support of continued fluoridation.

The decision will create the second-largest population in the country without access to fluoridated water (after Christchurch). Hamilton joins a growing number of smaller communities that have voted to reduce or eliminate fluoridation, including New Plymouth, Central Hawkes Bay, Dunedin and Tauranga.

You can read a round up of recent news coverage here.

Further links:

• A media release from the council regarding the decision.
• A council agenda document outlining the decision, including an analysis of submissions.
• National Fluoridation Information Service review of scientific papers.
• A map showing fluoridated water supplies in New Zealand.
• National Fluoridation Information Service report on community water fluoridation in New Zealand 2011-2012.
• Previous SMC expert commentary on fluoridation.
• Responses from the NZ College of Public Health Medicine and Waikato DHB.

The Science Media Centre approached experts for reaction to the announcement.

Dr Jonathan Broadbent, Senior Lecturer in Preventive and Restorative Dentistry, University of Otago and President, Otago Branch of NZ Dental Association, comments:

“This decision will undermine public health in New Zealand. We are going in the wrong direction. Right now our nearest neighbors, the Australian State of Victoria, are spending Au$3.6 million build more fluoridation plants across rural parts of their State.

“The World Health Organisation, the World Dental Federation, and the International Association for Dental Research have all stated that ‘universal access to fluoride for dental health is part of the basic human right to health’. In New Zealand, a central part of the universal right to fluoride is community water fluoridation. The New Zealand Ministry of Health Guidelines and Statements (2010) on fluoridation are clear: community water fluoridation is effective and safe, and community water supplies in New Zealand should be fluoridated at 0.7-1.0 parts per million (ppm) wherever feasible. The 7 Councillors who voted against this in Hamilton were either unaware of this, or disregarded it (as well as disregarding the opinion of their own citizens from a 2006 referendum).

“Those who are unwilling to drink fluoridated water should not be permitted to impose the risks, damage, and costs of failure to fluoridate on others. The ethics and science in support of fluoridation are clear, but antifluoridation arguments often present a highly misleading picture of water fluoridation.

“While the extent of tooth decay has reduced in recent decades, the disease remains more prevalent than other significant health conditions in New Zealand (such as asthma), particularly in unfluoridated areas and among disadvantaged New Zealanders. The recent New Zealand Oral Health Survey found much less tooth decay in fluoridated than non-fluoridated areas. There is generally 0.3 ppm background fluoride in New Zealand (although it varies), and adjusting that to Ministry of Health-recommended levels has a significant effect of reducing tooth decay among people of all ages.

“There is a very strong public health case for expanding the use of fluoridation. To a large extent, the improved oral health we now enjoy in New Zealand compared to the past is due to water fluoridation. We forget that very few New Zealanders are affected by water-borne diseases, thanks to water chlorination. If chlorination was not used, we would have more water-borne diseases. Fluoride does the same for tooth decay.

“While community water fluoridation is known to be effective and safe, Hamilton is the fourth town in the past 2 years to remove it. It is time for the Ministry of Health and central government politicians to properly support the policy of community water fluoridation and provide a cohesive public health policy for universal access to fluoride in our communities, and legislate to fluoridate. We have very little in the way of a ‘safety net’ for adults who cannot afford dental care. Now that water fluoridation in Hamilton is being removed, we can expect dental caries experience in that city will increase, and health inequalities will increase too. Following this decision, I hope that Hamilton can put a plan in place for the dental care of those that cannot afford it.”

Non-steroidal anti-inflammatory drugs (NASIDs) –  such as diclofenac and ibuprofen — have been the cornerstone in managing pain in people with inflammatory disorders like rheumatoid arthritis, and are some of the most commonly used drugs worldwide. However, NASID use has been linked to heart attacks and gastrointestinal bleeding.

Now a new study has drawn on data from hundreds of trials to clarify the association between NASID use and vascular complications identified in previous research.

The study, published this week in the Lancet, reviewed data from 639 previous randomised controlled trials of NASIDs covering over 353 000 patients. In addition to identifying specific risks for different NSAIDs and doses, the review found that overall NSAIDs approximately double the risk of heart failure and produce an increased risk of serious upper gastrointestinal complications such as bleeding ulcers. The study also identified the types of patients most at risk of adverse events, information which will help doctors prescribe the best NSAID regime for patients based on a risk profile.

Read more about the study in a Lancet media release.

In commentary article for the journal, Marie Griffin from Vanderbilt University Medical Center in the USA says, “The meta-analysis offers considerable certainty about relative and absolute major vascular risks of high doses of the most commonly prescribed NSAIDs, but leaves large gaps about risks associated with lower NSAID doses, longer durations of use, and residual effects after stopping treatment.”

She adds, “Identification of safe and effective strategies for chronic pain is sorely needed. In the meantime, long-term use of high dose NSAIDs should be reserved for those who receive considerable symptomatic benefit from the treatment and understand the risks.”

Our colleagues at the UK SMC collected the following expert commentary. Feel free to use these quotes in your reporting. If you would like to contact a New Zealand expert, please contact the SMC (04 499 5476; smc@sciencemediacentre.co.nz).

Professor Simon Maxwell, member of the British Pharmacological Society and Professor of Student Learning/Clinical Pharmacology, University of Edinburgh, said:

“This study adds further information by confirming that commonly used standard NSAIDs such as diclofenac and ibuprofen appear to carry the same excess risk as the newer and more selective coxibs. The interesting finding is that a rather less commonly used NSAID, naproxen, appears to carry no excess risk of heart attack or stroke compared to placebo. This might lead to a review of prescribing advice by some NHS organisations who currently advocate the use of diclofenac and ibuprofen.”

Professor Donald Singer, member of the British Pharmacological Society and Professor of Clinical Pharmacology and Therapeutics at the University of Warwick, said:

“These findings confirm previous reports that newer painkillers – coxibs – are associated with a clinically important increase in risk of coronary disease. A major new finding is that among traditional non-steroidal anti-inflammatory painkiller drugs (tNSAIDs) – diclofenac, and possibly ibuprofen, but not naproxen – appear to be associated with a similar increase in fatal and non-fatal coronary heart events to the coxibs. However naproxen, like all coxibs and tNSAIDs studied, was associated with an increased risk of heart failure and gastro-intestinal complications such as bleeding. The authors themselves acknowledge they cannot be sure whether the reported risks would persist in patients on longer term treatment or on lower doses of these medicines. In addition, the extent of adjustments across treatment groups for different cardiovascular risk factors (e.g. smoking as a source of bias) is not revealed. Despite this, the findings underscore a key point for patients and prescribers: powerful drugs may have serious harmful effects. It is therefore important for prescribers to take into account these risks and ensure patients are fully-informed about the medicines they are taking.”

R&D expenditure grew at an average rate of 7.6 per cent per annum between 2007 and 2011, largely driven by the public sector, but growth slowed to 3.7 per cent in 2011 – 2012 as the economy started to recover. The equivalent of 4600 full-time R&D jobs were created during this period. However, when the economy started to recover during 2011-12, the growth in R&D expenditure slowed to an average of 3.7 per cent per annum.

An interactive graphic displays the data used in the Innovation Index breaking down innovation by sector and type of activity.

Some highlights from the second IBM Innovation Index (the first was undertaken in 2010):

- R&D created the equivalent of 4600 full-time jobs between 2007-10, when the equivalent of 12,600 full-time jobs were lost across the economy as a whole.

- By 2012, nearly 50,000 New Zealanders were employed to conduct R&D, 35,000 in research roles and the remainder in support roles.

- Applied R&D expenditure grew by 46% between 2008-12; much faster than either Experimental R&D (14% growth) or Basic R&D (3.4% growth).

- Intellectual Property (IP)- trademarks, patents, Plant Variety Rights and designs- registrations per business in each industry fell 5% between 2007 and 2011.

Professor Shaun Hendy, Victoria University innovation expert, in a commentary piece on the research said:

In a market economy, innovation policy should maximise economic rather than market value. While an improvement in on-farm productivity may generate a large market return, the economic value of such an improvement may not greatly exceed this. In contrast, the economic value of an innovation that leads to the establishment of a new technology company and seeds a new industry sector may substantially exceed its market value. The difficulty, of course, lies in the ability of policy to identify economic benefits in excess of market value.

Specialised economies are vulnerable to macroeconomic volatility, and those that specialise in agriculture are especially exposed to climate change and biosecurity threats. New Zealand’s long-term future will depend on its ability to exploit economic opportunities outside its traditional primary sector strengths. To create such opportunities and to maximise the economic value of its investments in innovation, New Zealand will need to diversify its research and development portfolio.

Chief Science Advisor to the Prime Minister, Professor Sir Peter Gluckman said:

Technology transfer from the public to private sector is often seen as the issue, but this may be an over-simplification. The issue appears to be more about the need to increase the flow of ideas and to have appropriate vehicles to take those ideas to commercial scale rapidly, rather than any cultural resistance to that transfer. Certainly, we need to improve the knowledge that both the academic community and the private sector have of each other. Developments such as Callaghan Innovation are part of a robust pathway to change that is reflected in the growing research intensity of our private sector.

However, there remain real limitations in our access to risk capital, to expertise in technological global marketing and in company expansion. Our private sector is dominated by small and medium sized organisations and, relative to other small countries, they are indeed vibrant and research-intensive. The problem is that our ecosystem lacks research-intensive global corporations, which in other countries, both large and small, not only are large research consumers and providers but also offer very important spill-over effects for the whole innovation ecosystem. The lack of such corporations within the New Zealand ecosystem is a major constraint.

IBM New Zealand’s chief technologist, Dougal Watt, said:

When IBM expanded its research activities after the Second World War, our focus was on fundamental scientific research, where effort was guided by interest in the problem and not by external considerations. This model worked well for many years but eventually proved inadequate, in part because research conducted

in isolation from the needs of clients could not, on its own, drive the sort of innovation that creates new markets and new opportunities. The other flaw in this model was that it did not clearly link our research efforts with IBM’s strategic business direction. We did not use our researchers’ knowledge of the future to help us make important decisions about how to evolve and adapt IBM’s business model to keep pace with changes in technology and business.

So IBM changed its innovation model to ensure our researchers were more closely connected with the needs of our clients and the marketplace, and to ensure that our researchers had direct input into decisions about IBM’s strategic direction

These changes have allowed us to more effectively commercialise our research efforts and open up new markets. They have also helped us forge deep, highly collaborative relationships with our clients – relationships that have delivered better research outcomes. The success of this model can be seen in IBM’s continued leadership in U.S. patents: 2012 marked the 20th consecutive year that IBM topped the annual list of U.S. patent recipients, with a record 6,478 patents granted, more than to any other research organisation.

The study claims that the mice were given a dose of BPA that is comparable to human exposure. BPA is found in many plastics including bottles and food cans, and it can get into food through these containers.

Our colleagues at the Canadian, Australian and UK SMCs collected the following expert commentary. Feel free to use these quotes in your reporting. If you would like to contact a New Zealand expert, please contact the SMC (04 499 5476; smc@sciencemediacentre.co.nz).

Warren Foster, Department of Obstetrics and Gynecology, McMaster University:

“The paper itself is very good with state of the art methods and published in PNAS, a highly respected journal. Moreover, BPA, as you know, is highly controversial and thus this article is likely to attract quite a bit of attention.

“There are a number of limitations with the paper, the first of which is with the use of the term “low-dose”. Many investigators use this term freely today without giving it much thought. In the present paper the authors use it because they’re looking at doses of 20 and 200 micrograms per kilogram per day, and the FDA’s safe limit is 50 micrograms/kg/day. In effect they’re saying its environmentally relevant because their doses bracket the FDA rfd.

“The concern is when we humans are exposed to anything in our diet, we’re exposed to it at small amounts over the course of the day. What they’ve done here is give the dose as a bolus, i,e. the entire dose at once. The dosing solution is simply flushed down the animal’s throat. It’s convenient for research but people are not exposed like that. You’re getting your whole safe level or more all at once. When a risk assessment is done, the FDA estimates exposure over the course of a person’s daytime exposure. Regardless, the method of dosing the animals is a limitation of the study and of the interpretations.

“Another comment I have is, in the statistical methods – it’s hard to tell but it doesn’t look they took litter effects into consideration. A dam is giving birth to 12 to 17 pups per litter. Classically, what you’re supposed to do is take one pup from each litter and compare results across pups from different litters. The reason to do this is that it’s possible you have a dam that’s unusually sensitive or resistant to the effects of your test chemical that could unjustly skew results and mislead investigators.

“Finally, the other thing I take some exception with is – coming back to the issue of dose and human exposure. In a previous report, Justin Teeguarden and others have carried out pharmacological studies in humans with large BPA diets – canned peas and corn and stuff, diets graded 95th percentile for exposure to BPA. Of all the exposure they looked into, it was very hard to measure free BPA in the serum at all. So when studies in mice make the comment that its relevant for humans – I have some problems with those studies, if others have been unable to quantify the free (bioactive) form of BPA in the serum. It’s a question of whether free BPA is even present in most people and able to bind to receptors in target tissues.

“One final thing; there’s a line in the paper where they talk about BPA being associated in human children with behaviour and aggression. It is important to recognize that the investigators of those studies also look at many chemicals at once beside BPA, such as phthalates. Results of these studies are published as separate papers each reporting association between the chemical of concern and behavioural abnormalities. So at this point it’s hard to know if the association between BPA and behavioural problems is anything more than a simple statistical association. Drawing causal inferences then is very difficult.”

From the AusSMC:

Dr Ian Musgrave, Senior Lecturer in the Faculty of Health Sciences at the University of Adelaide, comments:

“This is a well-designed study that uses concentrations of BPA that cover the upper levels of permitted exposure for BPA in humans, as well as very high doses. The doses are given in a way which mimics human exposure.

“The most interesting results are those relating to behaviour. While there is huge variation in the responses of the mice, this study re-enforces our understanding that low doses of BPA, which are still higher than humans would be expected to be exposed to, have no significant effect on behaviour. ”

From the UK SMC:

Prof Andrew Smith, MRC Toxicology Unit, University of Leicester, and Royal Society of Chemistry’s Toxicology Group, said:

“This publication is in line with other reports suggesting that in pregnant experimental animals bisphenol A may influence the methylation of genes so controlling their action and leading to subtle differences in physiology of offspring.  The work is well organised but its findings emphasize the need for more fundamental research in this area.  Although administered by the authors at relatively low doses possibly compatible with human experience, there are important issues of the degree of exposure to bisphenol A versus the direction of methylation and behavioural/brain changes. These must be confirmed, clarified and mechanisms resolved before any extrapolation can be made to the human context especially in relation to mental and cognitive disorders.  Indeed, it is unclear how understanding consequences of low bisphenol A exposure fit in the landscape of human exposure to other chemicals.”

Prof Richard Sharpe, Research Group Leader/Professor, MRC Centre for Reproductive Health, University of Edinburgh, said:

“This study shows that exposure of pregnant mice to bisphenol A can cause changes in gene expression/function in the brains of offspring after birth and also lead to changes in certain aspects of behaviour. In general the study is well conducted and uses a route of exposure that is human relevant (>95% of our bisphenol A exposure is via our diet), although the method of results analysis is not the most reliable.

“Whilst these findings raise the possibility that comparable effects of bisphenol A could occur in humans, several factors suggest this is unlikely. First, the lowest dose use is still 10-20 times higher than normal human bisphenol A exposure. Second, the endpoints measured showed huge between-animal variation and considering that there were low numbers per group for some endpoints, the likelihood of false positive results is high, and no information on reproducibility of the results is provided (i.e. if the experiment was repeated would the same changes be detected).  Third, if the effects described work through an oestrogen mechanism, they are unlikely to be human relevant because pregnancy levels of oestrogens in humans are far higher than in mice and would swamp any weak oestrogenic effects of bisphenol A.”

Prof Tamara Galloway, Professor of Ecotoxicology, University of Exeter, said:

“The doses of BPA in the study are in an appropriate concentration range, spanning the suggested recommended tolerable limit for BSA in humans of 50 micrograms/kg body weight/day. As the authors quite rightly point out, there are differences in metabolism of BPA between humans and rodents, and they have taken account of this as far as they can in their planning. The doses have been administered orally, which is in line with current thinking on appropriate route of exposure. Earlier experiments by other groups have been criticised for administering BPA intravenously, which would bypass normal routes of metabolism in the gut.

“The non-monotonic dose response curves that the authors have obtained for many of the measured endpoints have also been reported by many other researchers, including ourselves, in both in vivo human population studies and in vitro laboratory experiments. I agree with their conclusion that environmentally relevant doses of BPA may induce very different effects dependent on the level of exposure and support the view that appropriate risk assessment of BPA toxicity should consider multiple low dose exposures.”

Earlier this year, a scientific review raised concerns that double-stranded RNA molecules produced in new genetically modified crops could pose a risk to human health.

The paper’s authors, including Professor Jack Heinemann at University of Canterbury, called on regulators to require experimental evaluations – including bioinformatic sequencing, in vitro tests, animal feeding trials and potentially even clinical trials — before approving any genetically modified foods using the technology.

Further background and comments on the original paper are available here.

FSANZ has now released a report responding to the concerns raised, concluding:

• The weight of scientific evidence published to date does not support the view that small double-stranded RNAs (dsRNAs) in foods are likely to have adverse consequences for humans.
• There is no scientific basis for suggesting that small dsRNAs present in some GM foods have different properties or pose a greater risk than those already naturally abundant in conventional foods.
• The current case-by-case approach to GM food safety assessment is sufficiently broad and flexible to addresses the safety of GM foods developed using gene silencing techniques.

Full conclusions and a copy of the FSANZ report can be found here.

The SMC contacted scientists for further comment on FSANZ response to the criticisms in Heinemannet al‘s article. Feel free to use these quotes in your reporting. If you would like help reaching these or other experts, please contact the SMC (04 499 5476; smc@sciencemediacentre.co.nz).

The SMC contacted scientists for further comment on the FSANZ response to the criticisms in Heinemann et al’s article. 

Dr Tony Conner, Science Group Leader, Agresearch. Dr Conner’s research career has focused on the applications of plant biotechnology and genomics to crop improvement and the integration of these emerging technologies into plant breeding programmes. He comments:

“The FSANZ response to Heinemann et al 2013 is well considered and very thorough. It demonstrates that the risk claims in the article are an overreaction based on dubious scientific evidence about the biosafety risks in plants genetically modified with gene silencing approaches.

“The public can take comfort from two key aspects:

1. Double-stranded RNAs do not present a new issue for food safety. They are very common in a wide range of organisms, including many fresh foods that have a long history of safe use in our diet.

2. The current approaches used by regulatory bodies, including FSANZ, are sufficiently robust to address food safety of GM products with dsRNAs.”

Assoc Prof Peter Dearden, Director, Genetics Otago, University of Otago:

“Food Standards Australia and New Zealand (FSANZ) have responded, remarkably promptly, to Prof Jack Heinemann’s review published in ‘Environment International’. Their response is comprehensive, well researched, and dismisses Prof Heinemann’s points entirely.

“Prof Heinemann’s paper suggested that double stranded RNAs produced in GM crops to change the way genes are regulated might pose a human health risk through that RNA passing into human cells and changing the way our genes are regulated. FSANZ dismiss this possibility stating that such RNA molecules are ubiquitous in nature, including in the food we eat, suggesting such molecules do not pose a health risk.  They review the evidence that shows that the development of RNA therapies targeting viruses and other diseases, designed to manipulate genes in just the way suggested by Prof Heinemann, have been unsuccessful, because humans do not easily take up such RNAs. FSANZ then suggest that Prof Heinemann has underestimated the ability of GM food safety testing to detect off-target and unintended effects.

“FSANZ’s report provides a sensible and well-argued counterpoint to Prof Heinemann’s claims, and I find their report very convincing. The difference of views expressed by FSANZ and Prof Heinemann spring, I think, from one controversial paper (Zhang et al, 2012, Exogenous plant MIR168a specifically targets mammalian LDLRAP1: evidence of cross kingdom regulation by microRNA. Cell Research 22(107):126). This paper is central to Prof Heinemann’s claims, as it shows that an RNA molecule made by rice can be detected in human serum, and that that RNA can regulate one of our genes. This paper is disputed, as some authors have criticized the techniques used, and other experiments have failed to find evidence of plant RNAs in animals (Zhang et al, 2012, Analysis of plant derived RNAs in animal small RNA datasets, BMC Genomics, 13:381). More pertinently, the paper does not show that the rice RNA, when eaten, regulates a human gene, just that the RNA can be detected, and in cell culture experiments adding a synthetic version of the RNA will change the expression of a human gene. We have no evidence that ingested RNAs from food affect human genes.

“My opinion is that FSANZ have got it right. Their assessment is that the risk to human health of double stranded RNA constructs used in GM plants is negligible, and I agree. I do, however, think that one of Prof Heinemann’s suggestions, that bioinformatic examination of potential human targets of the RNAs made in GM plants should be carried out to ensure that such RNAs cannot affect human genes, is worth doing. In my experience it is possible to design numerous double-stranded RNA molecules to affect the expression of a gene. I would like to think that when designing such RNAs it would be common practice to avoid regions with strong similarity to human genes, just to remove any possibility of an effect on humans. While I firmly believe that the risks of such RNA constructs are negligible, performing this analysis is trivially easy, and thus worth doing.

“The safety of our food is a key issue. I am pleased to see our regulatory agencies responding to scientific criticism and new scientific knowledge. Such criticism and response is vital to ensure we have effective, evidence based, regulation of food safety issues.”

Prof Jack Heinemann, School of Biological Sciences, University of Canterbury (co-author of the original paper), comments:

“Our food safety watchdog, FSANZ, is relying on assumptions instead of seeking evidence when confronted by a newly identified risk in GM foods.

“When FSANZ says it is not “likely” that small dsRNAs in foods will harm humans, it effectively acknowledges this is still possible, and so a risk. Yet it proposes not even testing for that risk until the “weight of evidence” suggests it is doing harm. We say consumer protection should be forward looking – do the tests now: don’t wait for harm to be proven.

“In responding to our peer-reviewed research, FSANZ does not deny that it uses assumptions, rather than scientific testing, to address the risks we identified.

“FSANZ is silent on what specific tests and techniques it uses to guard against unintended effects from the new dsRNA molecules that it is approving as safe for use in GM food crops. What we do know is that it does not require animal feeding studies of any kind. In the approvals that we reviewed, it had never even required tests for detecting dsRNA in the blood of animals, much less required tests that would reliably detect unintended harmful effects from dsRNA. FSANZ does not monitor for effects on people after approval or specify any particular monitoring be done by the developing companies. FSANZ needs to do more than just say its processes work; it needs to be forthcoming on what evidence it relies on to show that all these new dsRNA molecules are no threat to humans.

“To come to its position, FSANZ takes our statements out of context, deflects the issues, and makes misleading assertions.

“The “weight of evidence” it rests its opinion upon is either not appropriate for the testing of new dsRNAs in food, or invokes an absence of evidence when no evidence was ever sought. FSANZ should require this testing as it has the power to in its legislation, it has the option to under international food safety guidelines, and it has a responsibility to the people of Australia and New Zealand to do this.

“Contrary to what FSANZ asserts, there is scientific basis for suggesting that small dsRNAs present in some GM foods may pose a greater risk than those already naturally abundant in conventional foods. Some of these molecules are proven as pesticides. They can have potent effects on animals and should be tested before use on humans.

“RNA molecules are in the food we eat, but to extrapolate from the safe use of food with naturally occurring forms to those that are engineered and unique to new kinds of food is wrong. Proteins of all kinds are also in the food we eat but new proteins are evaluated for the potential to be toxic or allergenic in food. These dsRNA molecules can participate in fundamental biological reactions in human cells and so must be tested to be determined safe.

“Let’s use scientific evidence to see if the new dsRNAs in approved and future foods are safe. Science and public health will then be the winner, whatever the outcome.”

John Reeve, Principal Advisor (toxicology) Ministry of Primary industries, comments:

“The method of assessment of GE Foods conducted by Food Standards Australia and New Zealand (FSANZ) on behalf of Australia and New Zealand is exactly the same as internationally established as appropriate and used by all the major regulatory authorities in the world. The need for data has been carefully considered to ensure that any genetic modification getting into the human food chain does not pose any unacceptable risk.  The risk assessors involved in the FSANZ process are highly competent and very experienced both domestically and internationally.

“I note the suggestion that clinical testing be conducted on each new food, but this would seem to be quite impractical.  This sort of testing is not required for any current dietary risk assessments systems.  Any risk assessments carried out on foods are always based on the data available at the time, and are never set in stone.

“Thus, at any time, new information on a substance or food will always be considered carefully, and if necessary a risk assessment will be appropriately updated.  Revision of risk assessments is occurring around the world and within the WHO expert committees on a regular basis and the acceptability of foods are constantly being updated. This would apply in the case of any genetically modified food that has an approval.”

Updated: A Huge tornado has devastated the US state of Oklahoma killing at least 24 people and injuring many more.

Earlier reports indicated more than 90 fatalities, however this number was revised downward.

Our colleagues at the UK SMC collected the following expert commentary. Feel free to use these quotes in your reporting. If you would like to contact a New Zealand expert, please contact the SMC (04 499 5476; smc@sciencemediacentre.co.nz).

Professor David Schultz, Professor of Synoptic Meteorology, University of Manchester, said:

“Tornadoes are unfortunately to be expected in this area of the US at this time of year.  Compared to the 1999 Oklahoma tornado, which was of similar magnitude, yesterday’s tornado sadly led to a greater number of deaths.  This is partly because of the time of day it occurred – at around 3pm, parents were out and about picking up children from school and some children were still in class.  Because people were less likely to be near a television or listening to a radio, they might not have heard warnings and therefore unfortunately might not have been able to take precautions.  In 1999 the tornado hit at around 7pm, when most people were sitting down to dinner or watching the evening news, which would have been reporting live on the track of the tornado.  Sheltering within their homes with their families would have been easier.  Clearly, the time of day that the tornado hits can affect people’s ability to be prepared.

“In the US, the National Weather Service issues outlooks days in advance of anticipated severe weather.  The outlooks highlight regions of the country that face the risk of tornadoes, large hail, strong winds, and lightning.  With possible tornadoes three to six hours away, watches are issued that highlight portions of a state or two.  Tornado warnings are issued when the threat of tornadoes is imminent.  Warnings often appear tens of minutes before the tornadoes hit.  In the case of large and violent tornadoes, such warnings can be quite accurate.  Weaker tornadoes sometimes may happen without warning.  Research within the National Severe Storms Laboratory and the Storm Prediction Center aims to improve the tornado warning process, giving more lead time to the public.”

Dr John Marsham, School of Earth and Environment, University of Leeds, said:

“We do not yet know the full details of this particular event and it is impossible to attribute any one event to climate change. Tornadoes are too small to be explicitly represented in climate models. However, research shows that in much of the USA climate change is likely to lead to increase in the frequency of severe storms, and tornadoes form as a result of severe storms. Climate change therefore may well increase tornadoes, but the effects are expected to be regionally varying and much remains uncertain.”

Dr Andrew Russell, Lecturer in Climate Change, Brunel University, said:

“It is unclear whether tornadoes will become more likely as our climate changes because computer climate models don’t have the power (i.e. high enough resolution) to represent tornadoes. So you can’t just go through climate model data and count the tornadoes that it thinks will occur. It is possible, though, to look at the changes in the larger scale conditions that usually result in tornadoes, but this also gives us a unclear picture: whilst the increased warmth and moisture predicted by climate models will mean more energy would be available to developing tornadoes, the climate projections also shown a decrease in the occurrence of the wind patterns that are needed to form tornadoes. Nonetheless, there is some good evidence showing that reducing greenhouse gas emissions now will reduce the risk of more severe storms and tornadoes in the future.”

Dr Andrew Barrett, Department of Meteorology, University of Reading (commenting on the frequency and strength of tornadoes), said:

“Tornadoes are quite common in the Great Plains in May, averaging about 3-4 per day (often in clusters) – but not usually as strong as this one, and not usually in urban areas. Only 2% of tornadoes in the USA reach EF4 status (scale EF0 to EF5), with winds over 165mph.

“Tornados can occur in many places across the globe, but tornado alley of the Central Plains of the US is most famous. Central Plains in US is ‘Tornado Alley’ because it sees frequent collisions of warm, moist air from the south and cold air from further north and has no major east-west mountain range to block air flow between these two air masses.

“Moore, Oklahoma has been hit by significant tornadoes four times in the last 15 years (1999, 2003, 2010 and yesterday) including most intense storm ever with winds of 317 mph. The size of the tornado was not unprecedented, but at larger end of scales (widths vary from: 100m – 3 km).”

Dr Suzanne Gray, Senior Lecturer in Weather Systems, Department of Meteorology, University of Reading (commenting on climate change and tornadoes), said:

“Tornados are too small scale for current climate models to simulate, so it is not possible to say very much about how strength and occurrence might alter under climate change. But climate change means warmer temperatures and more moisture and that is providing more energy for the types of storms that produce tornadoes in a warmer climate.”

Dr Pete Inness, Lecturer and Senior Research Fellow, Department of Meteorology, University of Reading (commenting on tornadoes in the UK), said:

“The geography of the US High Plains is unique in creating the perfect environment for tornado formation. In the UK we simply don’t have the right set of circumstances to generate the intense storms in which big tornadoes form.

“According to the UK Tornado and Storm Research Organisation (TORRO) the UK experiences 30-40 tornadoes per year, although these are all far weaker and shorter lived than their US equivalents and most cause little or no damage to property. Recent occurrences include a small tornado in Oxfordshire in May 2012 which was tracked using Doppler radar by researchers at the University of Reading.

“In July 2005 a tornado hit Birmingham where damage to trees, houses and cars was widespread across an area to the south-east of the city centre. This was one of the few UK tornadoes to cause significant damage (estimated at 40 million pounds) and 19 people were injured.”

Dr Matt Watson, Lecturer in Natural Hazards, University of Bristol, said:

“Springtime in Oklahoma is pretty much prime time and place for tornadoes, therefore sadly this is not particularly unusual.  It is virtually impossible to attribute single events like this to climate change.”

Professor Bill McGuire, Professor of Geophysical & Climate Hazards, UCL, said:

“While there is no discernible upward trend in the number or strength of tornadoes in the US, I would not be surprised to see more in the way of the most powerful tornadoes as the world continues to warm. As climate change tightens its grip, extreme weather of all types is likely to be the order of the day.”

From the AusSMC:

Professor Dale Dominey-Howes, Natural Hazards and disaster management expert at the University of New South Wales, comments:

“Today’s tornado in Oklahoma is at the upper end of the magnitude scale of tornados. Given its size and the wide area of impact, searching for and rescuing survivors will stretch emergency services. Further, treating the injured and reuniting families will be extremely challenging. The response and recovery effort will require both State and US Federal resources and important questions must be asked about the effectiveness of early warnings and the building standards of property that are constructed in places where tornados like this occur.”

Dr Todd Lane, ARC Future Fellow, School of Earth Sciences, The University of Melbourne, comments:

“Tornadoes form below a class of severe thunderstorms known as supercells. Supercells feature intense upward moving columns of air that rotate, as the wind near the surface is drawn into those columns it begins to rotate and forms the tornado vortex. The damage attributed to tornadoes is caused by the strong winds in the vortex and flying debris.

“Oklahoma sits within an area of the United States commonly referred to as ‘tornado alley’ – this area is amongst the most frequent locations of tornado occurrence in the world. At this time of year, the warm and moist air from the Gulf of Mexico and cool and dry air from above the Rocky Mountains come together to make tornado alley the perfect environment to spawn supercells and tornadoes.

“Preliminary reports of damage from the Oklahoma tornado suggest it was of EF-4 intensity, which is the second highest intensity rating. EF-4 tornadoes have wind gusts between about 265 and 320 kilometres per hour.”

The study is the the largest of it kind and includes data from almost 1,500 SIDS cases across Europe, the UK, Australia and New Zealand.

In the article, published in BMJ Open, authors conclude: “88% of the deaths that occurred while bed sharing would probably not have occurred had the baby been placed on its back in a cot by the parents’ bed.”

The researchers do note that there is no risk from having an infant in bed for feeding or comfort provided the infant is returned to his or her own cot for sleep.

“SIDS remains a major cause of death among babies under one year of age in New Zealand and other high income countries,” said author Professor Ed Mitchell, from the University of Auckland in a media release.

“Parents need to know the risks from bed sharing, especially for babies under three months.

“Health professionals have a duty to inform them. Innovative strategies such as the wahakura and pepi-pod provide alternatives to bed sharing, and are attracting interest overseas.”

Our colleagues at the AusSMC collected the following expert commentary. Feel free to use these quotes in your reporting. If you would like to contact a New Zealand expert, please contact the SMC (04 499 5476; smc@sciencemediacentre.co.nz).

Professor Paul Goldwater, Senior Consultant, Microbiology & Infectious Diseases at SA Pathology (North Adelaide) and University of Adelaide School of Paediatrics and Reproductive Health

“The paper’s authors are well known to me (two are co-investigators with me on an international SIDS study) and have experience with large studies on the epidemiology of SIDS.

“Their findings are not surprising and confirm that co-sleeping is particularly dangerous for babies under three months of age. The main message is that co-sleeping (with or without other risk factors such as alcohol, other drugs or smoking) should never occur, but it is OK to breast feed in the parental bed and then to put the baby to sleep “face up” in its own cot (with clean linen) in the same room as the parent(s).

“The study pre-supposes that accidental smothering is the reason for these deaths while providing no autopsy evidence to that effect. The paper does not discuss the role of bacterial infection and only briefly alludes to it peripherally in terms of thermal stress (overheating) and the release of lethal toxins. In my view, it is likely that the theory of respiratory compromise due to smothering accounts for only a very small minority of cases.

“Many people will ask why the parental bed or sofa represents a dangerous sleeping surface; both of these are heavily contaminated with bacteria such as E. coli and Staphylococcus aureus, which are equipped with a variety of lethal toxins. A baby sleeping in such a contaminated environment could inhale or ingest shed skin cells covered in these bacteria. A genetically susceptible baby is at risk in the co-sleeping situation. This risk is further increased with every additional risk factor.”

Dr Mark Kohler, Lecturer at the Centre for Sleep Research, University of South Australia, comments:

“The opinion as to why bed sharing is a risk factor for SIDS is largely based on the likelihood of smothering the infant in some way and increased exposure to toxins. This thinking is highlighted by UK and Australian recommendations that types of parents place infants at greater risk than others – for example, those who smoke, are intoxicated, or take drugs/medication that alter awareness, cognitive ability and/or consciousness.

“The finding by Professor Carpenter and colleagues, which are hard to deny given this is the largest study of its kind, that bed sharing with any parent increases the risk of SIDS fivefold shows us that there are still important factors in our understanding of SIDS that have been missed. These may include overheating, exposure to pathogens in the bedclothes, changes in the child’s arousal response, amongst others.

“Similarly, the fact is that when adults are asleep their awareness and state of consciousness is altered, irrespective of whether drugs or alcohol have been taken. One important consideration of the study methods is that it does not answer the question as to why parents were bed sharing with their infant to begin with. Someone might say “always trust a mother’s intuition”, and while that someone is usually the mother, it begs the question as to why there was a felt need to bed share initially. Perhaps there was something about the infant the parent was sensing that if explored can help explain the true “type” of parent (and infant) at greatest risk.

“Combined, current bed sharing practises, particularly in western culture, still appear to place children at risk of SIDS and research should continue to provide greater understanding of why in order to avoid the devastating consequences.”

The findings, resulting from a broad international collaboration of scientists, have just been published in Nature Geoscience. Researchers used the most up-to-date information on temperatures, energy flows and energy accumulation in the climate system, to re-assess climate models.

Our colleagues at the UK SMC collected the following expert commentary. Feel free to use these quotes in your reporting. If you would like to contact a New Zealand expert, please contact the SMC (04 499 5476; smc@sciencemediacentre.co.nz).

Dr Richard Allan, Reader in Climate Science at the University of Reading, said:

“This work has used observations to estimate Earth’s current heating rate and demonstrate that simulations of climate change far in the future seem to be pretty accurate. However, the research also indicates that a minority of simulations may be responding more rapidly towards this overall warming than the observations indicate.”

“Sunlight reflected back to space by aerosol pollutant particles, which offsets some of the heating from greenhouse gases, is difficult to measure, as is the heating rate of the deep ocean. Both make it difficult to estimate the most realistic rate of future global warming, but they don’t change the overall picture and certainly don’t give us cause for complacency.”

“It is important to understand how much the planet will warm up in response to radiative forcing from rising greenhouse gas concentrations. This is often quantified as the total warming experienced in response to a doubling of the carbon dioxide concentration: how sensitive climate is to this heating effect (climate sensitivity).

“However, since the total response of the climate system can take hundreds of years to reach its final resting place (or equilibrium), more useful for making policy decisions involving adaptation strategies is the journey to this final resting place, or how quickly the climate responds (transient climate response).

“Are climate simulations, used to project future changes in climate, realistic in both of these respects?  To answer this question, Otto et al combine knowledge of the extra energy entering the climate system due to rising greenhouse gas concentrations and other factors (radiative forcing) with observations of surface temperature and of how heat is building up (primarily within the oceans).

“Despite the slow rate of surface warming in the recent decade, energy has continued to build up within the oceans and the authors find that the inferred sensitivity of climate to a doubling of carbon dioxide concentrations based on these observations (1.2-3.9 C total warming) is more or less consistent with the range from climate simulations (2.2-4.7 C).  However, the observations suggest that the rate of warming up to the point of doubled carbon dioxide concentrations over the coming decades may be slightly lower than predicted by a few of the climate models used to make future projections.

“The authors caution that uncertainties in the observations and the cooling effects of aerosol pollutant particles mean that it is difficult to precisely anticipate the most realistic rate of climate response over the coming decades, but with work like this our predictions become ever better.”

 From the AusSMC:

Professor Steven Sherwood, co-Director of the Climate Change Research Centre at the University of New South Wales, comments:

“These authors have looked at recent warming and ocean heat content data, and found that the oceans are sequestering heat more rapidly than expected over the last decade. By assuming that this behaviour will continue, they calculate that the climate will warm about 20% more slowly than previously expected, although over the long term it may be just as bad, since eventually the ocean will stop taking up heat. However, there is other research pointing out that this recent storage may be part of a natural cycle that will eventually reverse, either due to El-Nino or the so-called Atlantic Multidecadal Oscillation, and therefore may not imply what the authors are suggesting. So while their conclusions are interesting, they need to be taken with a large grain of salt until we see what happens to the oceans over the coming years.”

Dr Steven Phipps is a Research Fellow in the ARC Centre of Excellence for Climate System Science at the University of New South Wales, comments:

“This new study refines our estimates of the Earth’s sensitivity to increasing concentrations of atmospheric carbon dioxide. Using the latest observations of temperature and heat uptake, the authors calculate the short-term and long-term warming that follows a doubling of the CO₂ concentration. Their “best estimate” of the short-term warming is slightly lower than previous results. The most likely short-term response to a doubling of CO₂ is a global warming of 1.3ºC, while the most likely long-term response is a warming of 2.0ºC. Once uncertainty is taken into account, these new estimates are consistent with previous work.

“However, by including observations from the past decade, this study provides the most accurate estimates yet of the climate sensitivity. The extra precision confirms what we have long known: that our planet faces a very uncomfortable future if our emissions of greenhouse gases continue unabated.”