Monthly Archives: May 2013

Herceptin: the long and the short of it

If I, or anyone I loved, had breast cancer I’d want to make damned sure they got the best possible treatment. This is at the core of issues surrounding how the drug trastuzumab (trade name Herceptin) is to be used.  This morning Radio New Zealand reported that the Breast Cancer Aotearoa Coalition has made a submission to the Northern B Ethics Committee to stop New Zealand women entering a trial comparing short duration (9 week) and long duration (12 month) Herceptin treatments.

I understand that the submission is based on the results of another study, the PHARE trial.  I will shortly summarise this study.   I will also summarise the SOLD trial which the BCAC want stopped (in NZ).  Before I do so, a disclaimer.  I have no a priori position on whether a short or long duration treatment should be funded, I am not involved or have been involved in any Herceptin studies and I have no links whatsoever to the manufacturers of Herceptin (Roche pharmaceuticals).  I have spoken publically against the process that resulted in the funding of 12 months of treatment.  This was in 2008 when the National political party (not in government at the time) had as an election promise that they would fund 12 months of Herceptin rather than 9 weeks as Pharmac had proposed.  My argument then, as now, was that it was wrong for a political party to make such a call.  The independent entity, Pharmac, has been given the responsibility to make such calls and is required to base them on the best available evidence.  If the politicians believe that those calls are not being made correctly, then they need to improve the funding for Pharmac or its structure so that we can all be confident the best calls are made.  They should not try and override their calls for political gain, which is exactly what happened in 2008.

 What is Herceptin and who benefits?

  • Herceptin (transtuzumab) is a drug marketed by Roche for the treatment of HER-2 positive breast cancer.
  • HER-2 refers to Human Epidermal growth factor Receptor 2 which is a protein that promotes the growth of breast cancer cells.
  • HER-2 is present in only about 1 in 5 breast cancers.
  • Herceptin is, therefore, only an option for up to 1 in 5 people with breast cancer.
  • Herceptin improves survival.  From the Cochrane review* of the efficacy and safety of trastuzumab (I paraphrase): “If 1000 women were given standard therapy alone (with no trastuzumab) then about 900 would survive. If 1000 women were treated with standard chemotherapy and trastuzumab for one year, about 933 would survive (33 more women will have their lives prolonged), about 740 would be free of disease recurrence (95 more women will not experience the disease return).”
  • Herceptin increases heart toxicity: “If 1000 women were given standard therapy alone (with no trastuzumab) then five would have experienced heart toxicities. If 1000 women were treated with standard chemotherapy and trastuzumab for one year 26 would have serious heart toxicity (21 more than the chemotherapy alone group) due to the drug.”

 The SOLD (Synergism Or Long Duration) trial

In women diagnosed with early breast cancer with high risk of recurrence who are HER2-positive this compares a 9 week course of trastuzumab with a 51 week course.

The study began recruiting in 2008 and is expected to be completed by January 2015.

The primary outcome is a comparison of the Disease-Free-Survival (DFS) at the end of the study in the two groups. DFS for an individual is the length of time they survive without symptoms of cancer after the end of the treatment.  Secondary outcomes look at overall survival and measures of heart function and adverse events.

This is a world wide trial run by the Finnish Cancer Research Group and New Zealand patients may be eligible to enter.  I understand Pharmac is providing  $3.2M to support this trial**.

The Northern B Health and Disabilities Ethics Committee approved the ethics application for this study.  It consists of lay and professional members and judges if a study is meeting a number of specific criteria designed to ensure study participants rights and interests are safeguarded.

The PHARE (Protocol for Herceptin as Adjuvant therapy with Reduced Exposure) trial

This study aimed to compare two treatments: six months and 12 months of Herceptin.  The primary outcome was again Disease-Free-Survival.  The aim was to recruit 7000 people, only 3400 were recruited.

The trial was reported as a non-inferiority trial.  That is it tested if the six months treatment was not worse than the 12 month treatment.  It did not show that six months was equivalent to 12 months. It also failed to show it was inferior.  The trial had enough participants that if the lower bound of the 95% confidence interval of the Hazard Ratio*** had been greater than 1.15 then they could have drawn a positive conclusion about the  difference in the two studies.  It was not, the 95C%CI was 1.09-1.66 (ie the lower bound, 1.06, was not greater than 1.15).  This did not stop Roche and others reporting that the trial showed women receiving six months had a 28% higher risk of dying or having cancer return than those at 12 months (ie 1.28 being halfway between 1.09 and 1.66).

The results have only been presented in abstract form at a conference.  They have not gone through the rigorous peer review process yet, as far as I can tell.  I have not seen any information on the cardiac toxicity outcomes.

Summary of the evidence

The Ethics committee must decide if the PHARE trial and any other relevant information is sufficient that it would be unethical for patients to continue to be offered the opportunity to participate in a 9 week v 1 year SOLD trial.  This is a fair question to ask.  The difficulty they face is that the PHARE trial was not a 9 week vs 1 year trial, the results were inconclusive, the results have not as far as I can tell undergone peer review, and the published results appear not to say anything about differences in the rates of adverse events, especially cardiac ones.


*Cochrane reviews are independent and adhere to strict quality control.  They are about as “good as it gets” for assessing treatments.

**Under the NZ Public Health and Disability Act s48(c) one of the functions of Pharmac is “to engage as it sees fit, but within its operational budget, in research to meet [its] objectives…”

*** The Hazard Ratio in this case is simply how many times more or less a patient on 6 months compared to 12 months treatment is likely to not survive or still have cancer at the end of the study period.

Cheesecake files: Injury, function, and death

When they say your tests are positive for a disease just what do they mean?  If it is a simple blood or urine test often they mean that the concentration measured is outside (above or below) some  reference range.  In my field of Kidney Attack (a.k.a. acute kidney injury: AKI) two tests of the same substance (plasma/serum creatinine) are needed a day or two apart . The difference in the concentrations is what is important.  If the creatinine concentration has increased by >0.3 mg/dl within 48 hours or by more than 50% within a week then the diagnosis of AKI is made.  What happens, though, when someone comes along with a new test?  How do we know it is any better (or worse) than the original test? In my view what is required is that both the old and the new tests should be compared to a third, clinically relevant, variable.  For example, a new prostate cancer test may be compared to the present (poor) PSA test  by referencing both to the more definitive biopsy results.

In AKI the reason the creatinine threshold of 0.3 mg/dl was included as diagnostic was because research(1) had shown this level of increase to be associated with a four fold increase in the likelihood of premature death. If you’ve seen any of my previous posts on my research you will know that I am interested in new biomarkers (plasma and urine proteins mainly) that could be used to diagnose AKI earlier than creatinine.  While creatinine is a marker of changes in kidney filtration function, most of these new biomarkers reflect structural injury itself.  An analogy is that movement of a finger hurt in a rugby tackle tells us if the finger is functioning, whereas an x-ray is needed to tell us if it is broken or not.

Sam Whitelock damaged his finger during a game.  It had enough function to let him continue to play.  X-rays later showed it was broken. Picture: TV3

Sam Whitelock damaged his finger during a game. It had enough function to let him continue to play. X-rays later showed it was broken.
Picture: TV3


My latest publication(2) describes a method to determine appropriate biomarker thresholds.  It is quite simple.  First, I determine the sensitivity of the creatinine threshold to predict a meaningful clinical outcome – the need for dialysis or death within 30 days. The sensitivity is simply the proportion of all those who end up having the outcome who had a measure above the threshold.  I then take that sensitivity and work out what the biomarker threshold needs to be in order to yield that same sensitivity.

An early sketch of mine as I worked out how to determine structural biomarker thresholds

An early sketch of mine as I worked out how to determine structural biomarker thresholds

(1) Chertow, G. M., Burdick, E., Honour, M., Bonventre, J. V., & Bates, D. (2005). Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. Journal of the American Society of Nephrology : JASN, 16, 3365–3370. doi:10.1681/ASN.2004090740

(2) Pickering, J. W., & Endre, Z. H. (2013). Linking Injury to Outcome in Acute Kidney Injury: A Matter of Sensitivity. PloS one, 8(4), e62691. doi:10.1371/journal.pone.0062691.t001

H7N9 kills and attacks kidneys

27% of patients with H7N9 Influenza A died.  This is the finding of a report just released  in the New England Journal of Medicine is a study of 111 of the 132 confirmed cases of H7N9 Influenza A*.

Acute Kidney Injury or “Kidney Attack” was amongst the most common complications.

Of the 111 patients we evaluated, 85 (76.6%) were admitted to an intensive care unit (ICU); of these patients, 54 were directly admitted to the ICU, and 31 were admitted during hospitalization. Moderate-to-severe ARDS [Acute Respiratory Disease Syndrome] was the most common complication (in 79 patients), followed by shock (in 29 patients), acute kidney injury (in 18 patients), and rhabdomyolysis (in 11 patients).

In an analysis in the Appendix to the paper a comparison was made between the 30 patients who had died and 49 who had recovered (others were still in hospital).  100% of those who died had had ARDS compared with 40% of those who recovered.  One third of those who died had Acute Kidney Injury compared with 4% of those who recovered.  From a statistical perspective these numbers illustrate a real difference with a low probability (~ 1-2 out of 1000) of observing such a difference by chance.**

Note, all patients had been in close contact withe live chickens or pigeons within 2 weeks of hospitalisaton.

NEJM 23 May 2013

NEJM 23 May 2013

* Clinical Findings in 111 Cases of Influenza A (H7N9) Virus Infection

Hai-Nv Gao, M.D., Hong-Zhou Lu, M.D., Ph.D., Bin Cao, M.D., Bin Du, M.D., Hong Shang, M.D., Jian-He Gan, M.D., Shui-Hua Lu, M.D., Yi-Da Yang, M.D., Qiang Fang, M.D., Yin-Zhong Shen, M.D., Xiu-Ming Xi, M.D., Qin Gu, M.D., Xian-Mei Zhou, M.D., Hong-Ping Qu, M.D., Zheng Yan, M.D., Fang-Ming Li, M.D., Wei Zhao, M.D., Zhan-Cheng Gao, M.D., Guang-Fa Wang, M.D., Ling-Xiang Ruan, M.D., Wei-Hong Wang, M.D., Jun Ye, M.D., Hui-Fang Cao, M.D., Xing-Wang Li, M.D., Wen-Hong Zhang, M.D., Xu-Chen Fang, M.D., Jian He, M.D., Wei-Feng Liang, M.D., Juan Xie, M.D., Mei Zeng, M.D., Xian-Zheng Wu, M.D., Jun Li, M.D., Qi Xia, M.D., Zhao-Chen Jin, M.D., Qi Chen, M.D., Chao Tang, M.D., Zhi-Yong Zhang, M.D., Bao-Min Hou, M.D., Zhi-Xian Feng, M.D., Ji-Fang Sheng, M.D., Nan-Shan Zhong, M.D., and Lan-Juan Li, M.D.New England Journal of Medicine Online May 22, 2013 DOI: 10.1056/NEJMoa1305584

** something called a multivariate analysis was attempted which trys to take into account correlations between diseases to see which diseases are the major factors.  However, with “only” 30 deaths such an analysis is very limited and I do not think of value in this situation.

New way to spread the word

Changes to Flipboard mean it’s now a great tool for science outreach, or indeed any outreach.

If you don’t know what Flipboard is, then checkout or better yet, download the app.  It combines the beauty of a magazine with the usefulness of a reading list.  I use it on an iPad, there’s also an Android version.  Flipboard began life with in-house  magazines – Time, National Geographic, Popular Science, Cult of Mac etc etc etc.  Now, you can create your own magazines and share them if you wish (or keep them to yourself as a great way of maintaining a round-tuit reading list).  I’ve created two magazines called “Kidney Punch” and “Poland” both of which can be found using the search feature within Flipboard (the magnifying glass). There are a number of subscribers to them.  With two “clicks” I can flip any article I want from other Flipboard magazines, from my Twitter feed (beautifully presented in Flipboard as a magazine),  other social media feeds, or using their bookmarklet from any website (including your own blog of course). If you are going to be public, then keeping the articles flowing is important if you want readers to return.

Note, you may read the in-house mags by downloading the app.  To make your own and read other mags you must create and account and then restart Fliboard – it’s all free.

The front page of Kidney Punch magazine on Flipboard

The front page of Kidney Punch magazine on Flipboard

A page inside Kidney Punch .

A page inside Kidney Punch .

@kiwiskiNZ twitter feed inside Flipboard.  By clicking on the + symbol I can flip anything I want to Kidney Punch or any other of my magazines

@kiwiskiNZ twitter feed inside Flipboard. By clicking on the + symbol I can flip anything I want to Kidney Punch or any other of my magazines

The physics of maiming a child

Dear driver,

When you backed out of a driveway and did not even see how I swerved around behind your car to avoid T-boning you, how dare you have the temerity to tell me you were careful!  I was 7 feet tall, dressed in bright yellow and traveling at no more than 10 km/h.  Perhaps a simple lesson in physics will help you and your fellow “driveway backers” to realise how dangerous you are and to adopt safer driving practices.

In the diagram you can see a car backing out of a driveway.  Typically when you are at the edge of your property and have a fence (see photo below) blocking your view of the footpath you are able to see about 1.7 metres along the footpath.  Let us imagine that there is a child on a trike riding at 5 km/h just out of your line of sight.  How long  does it take them to travel that 1.67 metres?  The physics is quite easy.

Car backing out of a driveway.  Illustration of how little of the footpath can be observed.

Car backing out of a driveway. Illustration of how little of the footpath can be observed.

Velocity = distance/time, therefore time = distance/Velocity.

5 km/h is 5000 metres in 60 x 60 seconds, ie about 1.4 m/s.  Putting this in the formula above means that it takes about 1.2 seconds for the child to travel that 1.67 metres.

Now consider this. According to design guidelines for safe bicycle use 2.5 seconds must be allowed for someone to observe the danger, react, apply brakes and stop.  In other words, if you covered the distance from your driveway to the middle of the footpath, about 1 metre, in under 1.2 seconds you will almost certainly hit the child.  That is a speed of just 3 km/h!!!!!

Now consider who else is on the footpath, all legally:

  • Pedestrians 5 km/h
  • Joggers 5- 15 km/h
  • Kids on skateboards or scooters 10 km/h
  • Child on bicycle with small wheels, 10 km/h
  • Mobility scooter, 5-10 km/h
  • Me on my Trikke, 10 km/h
  • Postie on a bike 5-10 km/h.

For those going 10 km/h your speed needs to be just over 1.5 km/h to hit someone!

So, before you do some damage here is what you can do:

  • Never back out of a driveway unless you really really must.  If you think you must because of the design of your driveway, change the design!
  • Cut back those hedges, remove some of that fence so that you can see further.
  • Always always always stop at the end of your driveway (BEFORE THE FOOTPATH) and toot a horn.  Then proceed very very slowly.

By the way, you are legally obliged to give way:

 Land Transport (Road User) Rule 2004

4.4 Giving way when entering or exiting driveway

A driver entering or exiting a driveway must give way to a road user on a footpath, cycle path, or shared path (as described by clause 11.1A(1)).

Thank you for considering the physics of maiming a child, may you never find your self in such a terrible situation.


Dr John Pickering

A typical driveway with almost non-existant visibility

A typical driveway with almost non-existent visibility

Why you should care about Oregon

I love the way this med student writes. This is a fascinating account of an “accidental” randomised controlled trial of government spending on health (Medicaid in the US).

Two new Health Research Council grants worth crowing about

This week’s announcement by the HRC of Feasibility Study and Emerging Researcher grants have many great projects.  Two in particular are worth crowing about (because they have some relationship to kidneys and they involve two excellent people).  I have put summaries in their own words below, but first my comments.

Dr Palmer (Department of Medicine, University of Otago Christchurch), who has appeared on this blog site before, conducts what in the trade are called “meta-analyses” and “systematic reviews.”  Simply put, these are methods to extract the best possible evidence from all the studies that have been done for the effectiveness of a treatment.  Just as one person may toss a coin 4 times in a row and get 4 heads, so too can any one trial give a mistaken impression that a treatment is efficacious (or not) when it really isn’t (or is).  By pooling together many treatments Suetonia provides the very best quality evidence available.  Given that Chronic Kidney Disease affects a large and growing proportion of us, knowing which treatments have the best outcomes is of national significance, not merely to our health but also to the national budget.  A particular problem is that after a trial it can be many many years until meaningful health outcomes are know (e.g. if the treatment delays dialysis need or reduces mortality).  Suetonia’s study will assess the effectiveness of surrogate endpoints for clinical trials.  Surrogate endpoints, such as plasma creatinine which I’ve discussed many time in this blog, are physiologically related to the functioning of an organ or to a disease state as well as statistically associated with future hard outcomes.  However, their use in trials is limited by how well they are associated and how they are used.  I look forward to finding out what Suetonia discovers.

Mrs Rachael Parke (Auckland DHB) is an experienced nurse undertaking a PhD. Ensuring patients have adequate fluids on board is particularly crucial to the kidneys and other organs. Obviously with surgery any blood loss needs to be compensated for. However, there are also physiological changes in where fluid is distributed throughout the body.  Cardiopulmonary bypass, used in cardiac surgery, is a particular risk factor for Acute Kidney Injury. In the past the practice has been to give large amounts of fluid in order to ensure adequate fluid is given.  However, recent research has shown that too much fluid can have a negative impact (increased mortality).  A more restrictive fluid regime may have very meaningful outcomes.  Rachael is investigating, in a randomised controlled trial, if restricting fluid improves outcomes.  The outcome she is most interested in is how long patients stay in the hospital.  This is a very practical outcome for both patient and budget.  I am particularly pleased that this study is nurse-led.  Nurses play an incredibly important role in research as well as patient management.

In their own words:

Dr Suetonia Palmer: Making better clinical decisions to prevent kidney disease

More than ten percent of adults will develop chronic kidney disease. The effectiveness of many treatments used to improve outcomes in kidney disease is tested against surrogate (indirect) markers of health (e.g., cholesterol levels or blood pressure).

Unexpectedly, subsequent systematic analysis has identified little evidence to show that treatment strategies based on these surrogate markers translate to improved health for patients. Serum creatinine and proteinuria levels are commonly-used markers of kidney function to guide treatment.

The research involves using systematic review methods to summarise the quality of evidence for using proteinuria and serum creatinine as markers of treatment effectiveness in clinical trials. It will be determined whether using these markers to guide clinical care improves patient health or, conversely, leads to treatment-related harm or excessive use of ineffective medication.

These summaries will help clinicians and patients make better shared decisions about which therapeutic strategies actually improve clinical outcomes in kidney disease.

Mrs Rachel Parke: Fluid therapy after cardiac surgery – A feasibility study

Following cardiac surgery, patients receive large amounts of fluid in the intensive care unit. This may cause problems with wound healing and delay hospital discharge. A planned randomised controlled trial of a restrictive fluid regime as compared to a more liberal approach utilising advance hemodynamic monitoring, aims to reduce the amount of fluid patients receive and reduce hospital length of stay. This feasibility study aims to determine whether this nurse-led protocol is practicable and feasible and will help answer the research question. This study is simple and inexpensive and if it demonstrates a decreased length of hospital stay then this will represent a significant benefit for both individual patients and the health system.

University of Otago Papanui turns 800

Day one was ground breaking – 23 Feb 2011, the day after the big Christchurch earthquake.  Today is day 800 of what I lovingly refer to as the Papanui campus of University of Otago Christchurch.  For my children it’s just the office out the front of the house where their father works.  For me, it used to be my workshop & study.  Once upon a time it was computer and telephone free!  That all changed at midday on 22 February 2011 when I and my colleagues were unceremoniously thrown out of the University of Otago Christchurch building (you know the big building at the front of Christchurch hospital with the glass facade with the words “Research Saves Lives” written across it).  My ICU, ED and other medico colleagues went to work immediately, while the rest of us watched the first of the injured arrive at the hospital on the back of utes and sitting in the boots of cars. I hung around until I was sure my students and staff could all get home.  After an hour or so I walked home – first across Hagley park with hundreds of others exiting the city.  I chatted with a woman who got out of Ballantynes and another who escaped the carnage in Cashel Street.  A house not far from my own had partially collapsed – I went on to the property and called out to see if anyone was there.  I got hold of a neighbour who told me that the people who live there both work somewhere in town.  I prayed that they would be OK as they were in for a shock when they returned home.  Eventually I get home.  My family, including the dog, were not there – they had gone looking for me.  All the while the ground kept shaking.  My family returned and we rejoiced in each other’s presence.

My OfficeThe next day I opened my office thinking I may have to work at home for a few days.  My PhD student Dr Maryam Nejat was in touch.  She got home OK, but she was at a loss what to do about her thesis.  It was on her computer at work.  She’d been due to submit it within a month.  Fortunately, I had a laptop at home with a reasonably recent draft.  Maryam came around and we got to work, the first meeting at the Papanui campus.

The Papanui Campus

The Papanui Campus

When the quake hit I’d been in the middle of submitting an article to a journal for consideration for publication.  This too had to be retrieved and resubmitted somehow.  My colleagues involved in lab research suddenly had their facilities unavailable.  They were very concerned about the welfare of the animals.  My somewhat minimal role as group manager took on a new dimension.  Fortunately, those I work with were so very competent.  We discovered the animals had taken great priority and people were in the building feeding and caring for them all the while nobody else went inside.

As we watched the news, prayed for rescues, and held our breath every time the earth moved my thoughts turned to what else I could do.  I was fortunate to live in an area relatively unharmed, apart from the one house I mentioned.  The little liquefaction in the road around the corner had quickly been moved off the footpaths into the gutters and I’d hopped on the roof the neighbour’s house to remove chimney bricks threatening to fall on those below.  No medical skills, no search and rescue skills, no great shakes with a shovel (besides, my family didn’t want me out of sight for a while), I did what I could and went into work, 5 metres from the front door.  After all, Acute Kidney Injury is a great risk in crush victims and while I couldn’t help the people in the Christchurch quake, maybe I’ll do something for other quake victims in the future.

Messages started to come through from the Dean. The building had been yellow stickered for “remedial work”, but it looked like we would only be out of the building for about 4-8 weeks.  In the meantime, we were allowed to enter the building to retrieve essential items (computer!).

After 7 weeks (mid April) we were told occupancy of our offices and labs may not be till July. So I beefed up my broadband allowance.  Then we were told September (2011 remember!).  After that predictions no longer came.  The first staff went back into the building in November 2012, 21 months after the quake.  Nearly all academics (I may be the last left working elsewhere?) are back in the building now, the labs are open, the students are at lectures, the library is moving back in next week, and the Dean’s office should be back in about a month.

So, day 800 and lots to celebrate at the Papanui Campus:  Two PhD theses, 15 journal articles submitted and accepted, 1 book chapter, an ED & ICU study completed, another ICU study data collected, a lab study managed to completion in temporary location, new collaborations with colleagues in Germany, USA, Canada and Auckland, and a couple of online conferences.  An additional bonus has been the joy of working from home and seeing my family throughout the day (my children are Home educated).  Not so thrilling is the dog coming and nudging me when he wants some attention. Scariest moment was the large “after shock” in June 2011 where I held on to the monitor, ducked my head under the desk, and my group director on Skype from Sydney watched my printer fly off a filing cabinet behind me.  Perhaps the most difficult thing for a scientist working alone is the sense of isolation.  Email and Skype only partially ameliorate that.  I also make regular trips into town to visit colleagues and drink coffee.  Of the writing of blogs there is no end, but I have found participating in a couple of online blogging communities has kept me from having too narrow a focus.  How many more days there are for the Papanui Campus I do not know.  Little did I know when I built this Versatile sleepout 12 years ago that it would become a small outpost of Otago University. I don’t expect it will make the official history of the university, but it is now indelibly part of my personal history and I am very grateful that I have been able to work here.

Papanui campus in action. Left to right: Myself, Dr Azrina Md Ralib, Prof Zoltan Endre

Papanui campus in action. Left to right: Myself, Dr Azrina Md Ralib, Prof Zoltan Endre

NZ Scientists already well engaged in the National Science Challenges

Sorry to post twice in a day, but this is worth a look.  In the April Cabinet paper (here as a pdf) is an interesting graph which shows that 72.5% of current Vote Science and Innovation contestable and CRI core funding already goes to the newly announced National Science Challenges.  By my calcs the additional funding will push this to 78% assuming no increase in the “Research outside the Challenges” slice of the pie.  Have the challenges, therefore, merely reflected what is going on already in the science community?  One of the unanswered questions is “Which challenges will get the most funding from the new money?”  The graph shows the status quo.

The tao of science missed by National Science Challenges

The challenges are out. The committee has spoken. And now the critics respond.  Word on science street and in the media goes a bit like this:

Brilliant $73M more for science in New Zealand.  Well done Steven Joyce and the National Party.

Lacking in lustre.  These challenges are all a bit predictable. [eg Prof Hendy here]

Damn.  My research does not fit any of the challenges. [eg Dr Wiles here]

I sympathise with each of these opinions.  The National party has set a goal of 0.8 percent of GDP for science.  This is to be applauded. They have chosen a path of narrowing the scope of science to ensure it meets their own ideology of “government’s job is to grow the economy”.  This is reflected in the challenges and the language around them.  For example the challenge “High value nutrition: research to develop high value foods with health benefits” in the Peak Report document states:

There is enormous capacity to leverage both our primary industry and medical research to discover, validate and develop nutritional products with proven health benefits of significant market potential.

Some scientists seem to think that economic goals some how “devalue” science.  I am rather more pragmatic in suggesting that an economic return is an inevitable result of doing science.  The difficulty, though, is that any attempt to pick winners – and that is what the National Science Challenges does, fails to recognise that science at its best is not shackled but free to explore and expand.  Science by its very nature is at a frontier and a journey into lands unknown.  A pathway cannot be chosen for it and any attempt to do so will as often as not go straight past the pot of gold.

The National Science Challenges have been chosen by committee – there are “winners” and “losers” and the result is necessarily bland.  This is inevitable when science is done by committee.  Great science comes from great scientists who are driven to great discoveries.  It is driven by leadership, and leadership never comes from a committee.  On Morning Report this morning the interviewer and Prof Hendy both mentioned the US Space Program as an example of a truly exciting and great science challenge.  That challenge came from a great leader, President Kennedy, and while driven politically, the political goal was the same as the science vision.  Sadly, once the political goal had been reached the politicians turned elsewhere and the science community was left holding on to a few rocks and a vision shattered.

From my perspective what is needed for science in this country even more than challenges is vision and visionaries.  We need to fund scientists first and projects second.  Sadly, we have that priority completely around the wrong way.  Dr Wiles who ironically was one of the faces of science on the television campaign encouraging public submissions on the challenges is disappointed that her area of research, infectious diseases, is not acknowledged in a challenge.  I am disappointed that enthusiastic talented scientists like Dr Wiles are not directly receiving 3, 5, 10 year’s of salary and research cost support from this new money to pursue their vision. It’s not so much the topic of research as the researcher that counts.  I have a challenge for the New Zealand government.  And that is for their science policy to be evidence based (see Grant Jacobs’ blog post).  Part of that puzzle is whether it is best to fund researchers or to fund projects. This is why I say the Challenges have missed the tao of science – they are not in harmony with the way science is really done.  Let us run a trial.  Randomly select ten scientists and fund their salaries and $100K a year and let them pursue whatever they want.  Compare this to the results of randomly selected National Science Challenge funded projects with the same number of scientists involved.  The title of the trial could be “Is picking winners better than letting winners pick?