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You’re a what?… I’m a medical writer (oh, and I’m in NZ)

Imagine the scenario… you’re at a party and you’re introduced to someone new. Exchanging pleasantries, you’re asked THE question you hate to answer. You start to twitch, stutter, and eventually you say, ‘I’m a medical writer…’. Before you’ve finished saying the words, you already know their reply; in fact, you can – if you’re on the ball – mime the response at the same time as they say it (but that would be rude…) ‘YOU’RE A WHAT?’

That’s right, I’m a medical writer! I write about medical things… there’s more to it than that, but that’s how my explanation often starts. However, if I’m a little more alert, it seems the best way of explaining what I do, is to explain where I came from…

…Always a geek and at the age of 11, I knew I wanted to  be a cancer researcher. Why? My Grandad died of it, from this personal experience, I could see cancer REALLY sucks – I wanted to bosh it on the head. Simple. A few years’ of education ensued (and a few more)… I did a degree in Biology, a PhD in cancer research, and postdoctoral research in leukaemia. I loved it, but at the time I was 26 and saw too many people 10 years older than me on 1-month rolling contracts. The instability was not for me so I got out as soon as I could and moved into medical communications.

Medical commucations, or medcomms, as those in the know call it, is a thriving industry full of spods such as myself who support doctors, nurses, patients, and pharmaceutical companies in all of their medical writing activities. From writing a scientific manuscript for a journal such as The New England Journal of Medicine, through to writing a patient counselling tool, or even helping doctors with scientific presentations at big international meetings – a medical writer does allsorts! I love what I do. Someone else does the research, and I help them write it up! I’m a professional medical writer (see this paper for a down and dirty explanation of professional medical writing). I’ll write more about this another time. But this is how I ended up in New Zealand. It turns out medical writers are lacking over here, and New Zealand Immigration recognised that and gave me a residency visa (a.k.a my golden ticket) that allowed myself, my lovely wife, and The Spaniel to move New Zealand.

To give you an idea of what I do, here is a lightly edited version of a post from a recent initiative by a cool guy called Peter Llewellyn in the UK, which plotted A Day in The Life of Medcomms as it happened throughout the world. Hopefully it will provide you with a taster of what I do.

“Imagine… it’s a dank, dark, day, its mid-January 2011, and you’ve worked over Christmas as part of the run up to American Society of Clinical Oncology (ASCO) submissions (or FI-ASCO as I endearingly call it) [for readers not familiar with it, this is the largesst cancer conference in the world]. Your client is on the West Coast of the US and you’re working until silly o’clock again for the nth time in a row to cover the US time zone.

Well, that’s how my journey to Auckland, New Zealand began. I will spare you the full details of my journey (for now…), but working long nights was getting pretty tedious, and the solution seemed simple – flip time zones! I could then start work earlier in the day and finish earlier! I guess that’s the magic of MedComms, with a laptop and a phone you can work almost anywhere with a few minor exceptions (Antarctica anyone?).

At 7:30 am this morning, I checked my emails from home. My clients are a US MedComms agency, and so given the overlap in time zones, there is a window of opportunity up to 11am New Zealand time to read and respond to any emails, or chat to the client if needed. And then it was off to the beach to walk the dog! Auckland has fantastic beaches, and even in the middle of winter it is pretty mild. This also gives me the opportunity to mull over my work for the day, and consider what my priorities should be.

At 8:30 am(ish), suitably refreshed after walking the dog and a short trip to the office, I got straight into my day of medical writing. I received a brief overnight to write an outline for a manuscript for a top-tier general medical journal. First, I listened to a recording of the kick-off call with the authors and client, and the rest of my day was then spent writing the outline. The great thing about working in New Zealand is that I can do the part of a medical writing job I REALLY enjoy… the writing! For the client, having a writer in New Zealand allows projects to be kept moving forward around the clock. They can effectively work all 24 hours in the day, and no-one drops through exhaustion.

As your working day begins, I’m now on the beach (see below). I’ve now handed the baton over, and it’s now up to you to keep that MedComms wheel spinning, until tomorrow that is…”


Possible Link Between Childbirth And Risk of Certain Types of Breast Cancer?

Giving birth may influence the risk of getting certain types of breast cancer according to recent research

When a breast cancer patient has their tumor biopsied or removed, a pathologist will take a sample of the removed cancer cells and will test them for receptors for estrogen, progesterone, or for HER2. The results of these tests will help determine the best treatment for the patient and the overall prognosis (or chance of recovery).

Receptors are proteins that help cells communicate with the outside world. When a receptor binds a specific molecule, various processes within the cell are triggered. For example, when estrogen binds to estrogen receptors and progesterone binds to progesterone receptors normal cellular processes involved in cell growth and division are triggered. However, in breast cancer, one of both of of these receptors  are overproduced triggering breast cells to grow and divide rapidly, which eventually leads to the development of a tumor or cancerous growth.  Relatively recently it has been discovered that another receptor, HER2- which seemingly does not have any molecules which bind it naturally- is also overproduced in some breast cancers.  HER2 overproduction also tells breast cancer cells to grow and divide rapidly, also leading to tumor growth. 

Most breast cancers have one or more of these receptors; however one type, called triple negative breast cancer does not have any of them.

Tumors that that have estrogen receptors generally respond well to treatment with antiestrogens, which prevent estrogen binding the estrogen receptors and triggering growth of breast cancer cells. Likewise, tumors that have HER2 generally respond well to trastuzumab, more commonly known as Herceptin, which stops HER2 triggering growth of breast cancer cells. However, triple negative breast cancers seem to be more difficult to treat and has a higher chance of the cancer coming back (recurrence). In addition, a large proportion of these tumors contain the BRCA1 mutation; a genetic fault which generally signifies an increased risk of a women getting breast cancer in her lifetime.

Hormone levels change during pregnancy, with estrogen being produced by the placenta throughout a pregnancy until birth. Because triple negative breast cancers, don’t have any estrogen receptors and hormone levels change during pregnancy, it is thought that childbirth could influence the risk of getting this type of breast cancer.

To address this question, Phipps and colleagues at the Fred Hutchinson Cancer Center in New York used data from over 150,000 women enrolled in the Women’s Health Initiative, a large study of postmenopausal women from 40 centers across the United States. 155,723 women were monitored over 8 years. Of these women, breast cancer developed in 6,194 women and complete data on estrogen receptor, progesterone receptor, and HER2 status was available in 307 women who developed triple-negative breast cancer, 2,610 women with estrogen receptor positive breast cancer, and the remaining cancers were estrogen receptor negative/progesterone receptor positive or estrogen receptor negative/progesterone receptor negative/HER2 positive (n=154). 150,529 women were used as controls.

They found that women without children had an increased risk of estrogen receptor positive breast cancer, but decreased risk of triple-negative breast cancer compared to those who had given birth to children. Specifically, having not given birth to children was associated with a 39% lower risk of triple negative breast cancer, but a 35% higher risk of estrogen receptor positive breast cancer compared with women who had given birth to children. For the statistically minded, see full statistics below. However, of those women who had given birth, those with more children had a higher risk of triple-negative and lower risk of estrogen receptor positive breast cancer (see below).

The authors note that they only studied postmenopausal women, so the findings reported here may not apply to younger premenopausal women. The findings should also be approached with considerable caution, as the study used a relatively small number of women so results need to be confirmed with a larger proportion of women. In essence, this is an interesting hypothesis-generating study (a study which scientists will use to further evaluate the influence of having children on the risk of having certain types of breast cancer), if indeed having children does influence the risk.



For patient information: please see:


Twinkle, Twinkle, Little Star…

If you don’t know already, Tefalhead is a medical writer, tinkering away at his keyboard writing ‘stuff’ for other folks. Most of his writings are based on clinical trial data for whatever product he is working on, and for whomever chooses to use his writing talents; usually a pharmaceutical company. As a result, Tefalhead does not have much artistic license when it comes to inventive manuscript titles. But, Tefalhead has a burgeoning artistic side, which is often desperate to show itself (in a non Jekyll and Hyde kind of way, it’s ok folks…).

Until now Tefalhead had gotten used to writing according to CONSORT guidelines, guidelines for transparent reporting of medical trials. But Tefalhead often muses on the lack of opportunity to write creative titles in his medical manuscripts. While thinking this, Tefalhead cast back his mind back to years gone by when he was a lonely, nerdy, little PhD Student, residing in Dallas, at the University of Texas Southwestern Medical Center. Here, the research was exciting, bold, inventive, creative even… and it is this creativeness that often ended up in manuscript titles, such as this….by Ron Estabrook and Bill Rainey:

Boy, these guys were good – gods in Tefalhead’s scientific world. In describing how one protein, called StAR controls how  hormones are produced in the cell, they don’t just stop with the imaginative title. Oh no, check out the last sentence…. “…and colleagues have demonstrated that StAR will continue to shine—but a twinkle remains in the eyes of those pursuing the detailed mechanism through which this long sought labile protein participates as an acute regulator of steroidogenesis.” So much better than the star trek sounding ‘New frontiers in…’ or the really uninviting ‘A perspective on…’, and leaves you with a pleasant picture of a twinkle in someone’s eye…. (mmm…)

Proof scientists are creative beings indeed… but that article is from 1996- eon’s ago in the scientific world! Have any other scientists demonstrated artistic flare in their manuscript titles? Well, it seems so… Tefalhead did a quick literature search and quickly found these little gems…

Through a glass darkly: advances in understanding breast cancer biology

Presumably in reference to the Bible passage from 1 Corinthians 13, in which seeing through a glass darkly refers to our understanding of God when we are alive, but the view will only be clear when we die. When reading this Tefalhead found his head slunking over his keyboard in a wave of despair… boy, this sounds depressing given we are talking about developments in breast cancer biology! Tefalhead reckons the authors presumably wanted to convey the fact that our vision of breast cancer at the moment is an imperfect or obscure vision of what is ‘reality’. Not so depressing I guess… hey, these guys are on another level! Here is another…

Transporters, Trojan horses and therapeutics: suitability of bile acid and peptide transporters for drug delivery

 Sounds like a bit of The Matrix mashed up with a bit of greek mythology doesn’t it?

We’ll ignore all reference to ‘Achilles Heel’… you guys are wasters, but Tefalhead reckons there are lots of opportunities for you scientists out there to be creative in writing your manuscript titles, and is a little jealous, after all it’s little restrictive when all you really have to play with is…

Phase 3 randomized controlled study of [insert drug] in patients with [insert disease]…  yada yada yada

But, hey, who said being a medical writer was all rock and roll! (But I like it…)

Chronic Fatigue Syndrome: Stop PACEing Around and Move On?

Tefalhead is not an angry man, in fact, Tefalhead is a mild-mannered medical writer who nonchantly keeps on plodding on in his own Tefalhead world; indifferent to most happenings in the world. But, that all changed last week when he saw headlines like the one below:

Tefalhead was not the only one to be stirred by the release of the PACE(Pacing, Activity, and Cognitive behavioural therapy, a randomised Evaluation) study of various treatments for myalgic encephalomyelitis (M.E)/chronic fatigue syndrome (CFS) in the Lancet this week. The Twittersphere, and the internet as a whole was full of chatter spinning off in every direction following on from the PACE study publication, with blog titles such as “Invest in ME: PACE trials are .Yup, that’s right claims that a study published in the prestigious journal The Lancet’ are BOGUS! Controversy surrounding the study was not confined to random bloggers, tweeters, or such like but the M.E. Association had this cracking press release:


 Yup, you read it correctly “Results are at serious variance to patient evidence…“. Let me get this right, one of the main M.E/CFS patient advocacy groups in the UK disagree with the results published in the Lancet, one of the “world’s best known, oldest, and most respected general medical journals“ according to Wikipedia!

 It’s now Sunday, and Tefalhead has recovered from the red mist that blinded his thoughts on Friday. Tefalhead is a scientist by training and although he desperately wanted to blog about this on Friday, he knew his scrawlings would lack objectivity. However, after two days of chillin’, his objectivity head is back on, but first, Tefalhead has one thing to disclose…nope, we’re not talking about receipt of consultancy fees from The Department of Health, or that Tefalhead is one of the co-authors’ of the study. No, this is much more personal. Tefalhead’s wife has M.E/CFS a condition that is misunderstood by all, massively impacts lives of those afflicted with this condition and has no known magic bullet in terms of a cure. In brief, this condition sucks BIG time- and to see the love of your life affected by it – well, there are no words for it. Needless to say, because of this fact, there will be inherent biases in what I repor. It’s inevitable folks- so treat what I say next, with CAUTION.

What did the study involve?

The study was carried out by researchers from several UK institutions, and was funded by the UK medical research council, The Department of Health for England, the Scottish Chief Scientist Office, and The Department of Work and Pensions. The study was published in The Lancet online this week at . Whoa, right, let’s backtrack for one second…. “funded by… The Department of Work and Pensions’? For non-UK readers, the Department of Work and Pensions is an UK government department that manages welfare and pension policy in the UK, including provision of financial support for people claiming disability benefits. So what on earth are these guys doing funding a clinical study to assess the effectiveness and safety of treatments for patients with M.E/CFS.? Hmmm… Tefalhead, asked the very same question. After digging around a bit, he stumbled across this document from Malcolm Hooper, an Emeritus Professor Of Medicinal Chemistry…. This document seems to open up a whole lot of controversy surrounding the PACE study, including suggestions that the Department of Work and Pensions could use the data from the study to essentially remove many CFS patients from benefits system in the UK. That would save some money right? Not a bad thing in this era of austerity measures. Tefalhead does not want to distract from the main analyses reported in the Lancet study, but the fact that an external body that has inherent interests in the data reported actually funded the study… is a little bit fishy. However, it happens all the time with pharmaceutical companies for example, who are continually reporting the results from their clinical studies in manuscript articles. When reading such articles one needs to take into account the phenomenon of funding bias and acknowledge that the conclusions of a study could be biased towards the outcome the funding agency wants. To be clear, Tefalhead is not saying the funding bias has occurred in the PACE Lancet study, but we need to take this into account when considering the data.

So… where did this study come from?

Details of the Study Design are given in Box 1. In brief, 641 patients were given one of four treatments: specialist medical care (SMC)(provided by doctor with specialist expertise in CFS), SMC plus adapative pacing therapy (aims to assist CFS patients in optimally using their limited stores of energy); SMC plus cognitive behaviour theapy (CBT; believes that fear responses are linked to physiological response and make the fatigue worse and involves strategies such as establishing a healthy sleep patterm addressing fears, problem solves and working with a therapist to increase mental and physical activity), and SMC plus graded exercise therapy (GET; believes that fatigue can be reversed or reduced using gradual increases in activity and uses strategies to establish a baseline of acheivable exercise followed by negotiated incremental increases in the time spent being physically active).

Patients were given questionnaires to fill in to assess the effectiveness of treatment and were unmasked to treatment, ie it was obvious what treatment they were receiving. As a result, their own expectations of what treatment they were receiving, could have influenced the final results. To account for this, the investigators did assess patient  expectations before treatment started. The study clinicians also used questionnaires and scoring methods to assess the impact of treatment on the patients’ overall health, Any adverse events were also monitored forthroughout the study (any adverse change in health or side effect during treatment).

There were no biological measures assessed during the study, which would have been expected for a condition such as CFS where the biological basis of the condition is unknown. Tefalhead thinks this is a big shame given the large amount of patients involved in the study.

What did the researchers find?

After 1 year, the study found that fatigue was significantly lower for CBT and GET compared with SMC alone (See Box 2). However, there was no significant difference between APT and SMC. Physical functioning (the ability to perform a range of activities from self care to more vigorous acitivities) was significantly higher for CBT and GET versus SMC, but there was no significant difference between APT and SMC. Compared with APT, CBT and GET were associated with less fatigue and better physical functioning. The Oxford criteria for diagnosi of ME/CFS are broader than other criteria used, and as a result, may cover a broader range of conditions that may be unexplained and thus categorized as ME/CFS. When different diagnostic criteria for CFS were applied (the international CFS criteria and the London criteria for ME), two-thirds of patients met the international CFS criteria and about half met the M.E criteria, which requite the presence of post-exertional relapse and excludes patients with depressive of anxiety disorders. When these new criteria were applied, the authors found similar results with no significant differences in results results between the different criteria used.

Of note, after treatment 16% of patients in the APT group, 30% of patients in the CBT group, 28% of patients in the GET group, and 15% undergoing SMC were within ‘normal’ ranges for the fatigue and physical functioning outcomes measured. Let’s switch that around, 70% of patients in the CBT group and 72% of patients in the GET group had abnormal levels of fatigue and physical functioning. In addition, a clinically useful difference in results for the primary outcomes equated to 2 points on the Chalder fatigue questionnaire and 8 points for the short form 36 questionnaire, ie it just took a small change for the therapies to be clinically useful. Using these relatively loose criteria, only 42% of patients on APT, 59% of patients on CBT, 61% of patients on GET, and 45% of patients receiving standard medical care ‘improved’  at 52 weeks.


How were the results interpreted by the authors?

The researchers conclude that CBT and GET can be safely added to SMC to moderately improve outcomes for ME/CFS, and that APT is not an effective treatment. They also state that findings were similar for patients meeting the different diagnostic criteria for ME/CFS , and for those with depression. Importantly, they note that there were no important differences in safety outcomes between treatment groups

Author conclusions aside, how relevant are these results?

 This study had many strengths including: (1) a low dropout rate in the study, which is impressive given that patients could drop out part way if they felt they no longer wanted to continue treatment; (2) there were high rates of patient satisfaction; (3) well defined treatment protocols were used to name but a few. However, there are several limitations of this study to consider:

  • Patients who were unable to attend hospital were excluded, so the results from this study cannot really be applied to ME/CFS patients who are bed bound (there are quite a few out there)
  • Standard medical care is not the same as the usual medical care given by a family doctor or GP
  • Children who are also afflicted by ME/CFS were not included in the study
  • Conventional criteria were used to define clinically useful differences between treatments
  • Masking of patients or clinicians to the treatment given was not possible given the types of treatment given and research assessors were not masked, which may have led to reporting bias

One major objection to the study seems to be that the criteria used to select ME/CFS patients does not accurately reflect the ME patient (again see the response from Malcolm Hooper here). However, the authors do apply the results to alternative criteria for diagnosing CFS. Although this is no substitute for using the other ME/CFS criteria for inclusion into the study.

Perspective from Action for ME

Action for  ME, a UK-based patient advocacy group have serious concerns about the PACE study, stating “The largest ever clinical trial into the effects of CBT, GET and adaptive pacing therapy (APT) has produced results that are clearly at serious variance from those reported by the largest ever survey of patient opinion on these forms of treatment.

We find the trial results extremely worrying because pacing, in the form that the MEA recommends, may as a result no longer be offered as a treatment option in NHS clinics. And at the same time, NICE may well strengthen its inflexible and unhelpful recommendations regarding CBT and GET.

We also fear that the way in which the results are already being reported in media headlines – eg Got ME? Just get out and exercise, say scientists – will lead some doctors to advise inappropriate exercise regimes that will cause a serious relapse.

This is not a good day for people with ME/CFS.

They have a complex multisystem illness that requires a range of treatment options based on their individual symptoms as well as the stage and severity of their illness”

So, there you go, Action for ME have a lot of serious concerns not only about the design of the study, but also the implications for ME/CFS patients throughout the UK. 

Stop PACEing Around and Move On

The results from this study highlight the plight of patients with ME/CFS, and should fuel further research into the basic biology of what causes ME/CFS, together with clinical studies to determine what treatments really are effective for these patients. The lack of any harms with any of these treatments, should allay patient fears, that some of the treatments can do them harm. However, any confusion in findings can only be bolstered by rigorously designed clinical studies.

Tefalhead just hopes that something can be done to help his wife regain some type of  ‘normality’ in her life, and is reminded that it isn’t just numbers reported in this study, but results from patients whose lives are hugely affected.

There is a great deal of disunity amongst ME/CFS patients, clinicians and patient groups, and it seems that the main people losing out here are the ME/CFS patients themselves. Tefalhead is at a loss as what to suggest in terms of a way forward… thoughts anyone? However, a line clearly needs to be drawn under the furore of the PACE study, and a fresh start made [Tefalhead suggests a group hug, but that may not be everybody’s idea of a good time].

Tefalhead has one last little grumble…headlines such as ‘Got ME? Just get out and exercise”. Are not only irresponsible but downright dangerous. Tefalhead spoke to a leading expert in the ME/CFS field at the weekend, who reiterated that any exercise therapy must be done under medical supervision. Scientific journalists- careful reporting PLEASE. If your headlines are taken literally by vulnerable patients, serious harm could be done.

Note from TefalHead: Your comments on this topic are appreciated, BUT please remember Tefalhead is as concerned with this issue as you are, and he is just trying to put the topic out there for debate. In other words… be nice, thanks. Oh, and Tefalhead has purposefully steered well clear from the XRMV issue, mainly to report the results of the PACE study and not distract from that.  Tefalhead will review the XRMV story at some point in the future








Human Enzyme Made in Plants May Protect Against Nerve Agents

On Monday March 20, 1995, 5 members of the Japanese cult, Aum Shinrikyo walked onto their appointed trains with deadly parcels of the nerve agent Sarin wrapped in plastic bags and newspapers. At prearranged stations, the sarin packets were dropped and stabbed with umbrella tips to release deadly sarin vapours. Twelve people were killed, and nearly 5,000 were hospitalized.

As a result of the rise in global terrorism such chilling attacks remain a distinct possibility. However, the means to fully treat patients remains elusive as current anti-nerve agent treatments can only help symptoms but do not prevent long term nerve damage.

The human nervous system is constantly chattering away with the firing of impulses along lines of interconnected nerve cells. Signals are sent from the brain to various parts of the body through firing of impulses from one nerve cell to the next, and also from nerve to muscle cells which then results in a muscle contraction, for example contraction of muscles associated with breathing. Transmission of impulses from nerve to muscle cells requires the release of a substance called acetycholine at the end of the nerve cell which is immediately broken down by acetycholinesterase (AChE) into inactive components. The immediate breakdown of AChE is essential for coordinated movement of muscles. If this does not occur, acetycholine floods the nervous system resulting in paralysis and disorganized muscle contractions eventually leading to death when muscles required for breathing and heart muscles are affected. This occurs with nerve agents which prevent the breakdown of AChE.

Butyrylcholinesterase (BChE) occurs in blood, scavenging and binding to toxic nerve agents, such as sarin gas to prevent them from doing their dirty work of stopping the breakdown of AChE. However, there is not enough of BChE within the blood for it to be mass produced for stockpiling for the next bioterrorism attack, and of course there is the risk of transmitting blood disease- think back to the haemophilia scare of the 1980s when contamined blood products resulted in patients being needlessly infected with HIV.

However, recent research by Brian Geyer and colleagues in the November issue of The Proceedings of the National Academy of Sciences suggests an alternative for mass production of BChE to treat nerve agent attacks. They used tobacco plants which were genetically modified, also known as transgenic plants, to over produce BChE in their leaves. In their experiments Geyer et al. showed that this plant-derived BChE protected lab animals exposed to nerve agents and alleviated symptoms of poisoning such as difficulties in breathing and convulsions, and also prevented death. They also found that they could make the enzyme persist in the blood of the lab animals for longer by binding it to the chemical polyethylene glycol (PEG) to allow for further protection.

Much work remains before plant-derived BChE can be used to protect humans against nerve agents, but the fact that it can be produced in plants and demonstrates promising signs of benefit in lab animals is tantalizing.

As transgenic plants could be an abundant and relatively inexpensive source of BChE, they could be used for large-scale production and stockpiling of this treatment for the likely event of another terrorism attack.


Decaying Cellular Waste Disposal Pumps Linked to Cellular Aging

The maternal instincts of yeast cells to protect their offspring from the damaging effects of cellular toxic waste appears to promote their own demise, but this altruistic act also provides new insights in cellular aging and importantly age-related diseases such as cancer.

Most cells appear to have a finite ability to replicate, after which they enter a stage of cell aging, also known as cellular senescence during which toxic agents build up within cells.  Research reported by Li et al. this week in Nature Cell Biology provides further ideas on how and why this occurs.

Li et al., used bakers’ yeast, Saccharomyces cerevisiae, as a model to for studying aging, in which cells divide asymmetrically producing a ‘mother’ and ‘daughter’ cell which are not identical. Previous studies have shown that during yeast cell division, the mother keeps the damaged proteins which are toxic and could be harmful to the daughter cell. Dr Li and her team discovered that the mother yeast cell keeps an old set of  a specific type of protein called a Multi Drug Resistant (MDR) protein, but gives the daughter cells a completely new set. MDR proteins are well known already, as they have been implicated in resistance to some cancer drugs, by expelling the drug from the cell. However, they also transport compounds in and out of normal cells.

Li et al., found that these MDR proteins decayed and lost their function right at the end of the cells’ life, suggesting that they are limiting the lifespan of cells effectively resulting in the loss of a cell’s fitness. As a result, Li et al., hypothesized that if the loss of MDR proteins contributes to aging, then cells lacking MDR proteins should have a reduced lifespan (measured by the replicative ability of the mother cell), and that is exactly what happened- losing one MDR gene and the resultant lack of a particular MDR protein reduced the replicative ability of the mother cell by up to 66%. Conversely, when extra copies of MDR genes were inserted in the mother yeast cell, which led to over expression of MDR genes, the investigators saw an increase in replicative ability.

How this translates into humans, is not yet clear but the MDR proteins are conserved across organisms suggesting that they may have an important role in aging. This process mayalso explain why cancer cells which contain high levels of MDRs are immortal.