Can I please buy one of your kidneys?

Should we legalise the sale of human organs?

In the UK alone the average waiting time for a kidney transplant is 3 years, this costs the NHS around £24,000 per patient per year and in 2013 – 2014 1000 people died whilst on the transplant waiting list. Dialysis patients also often say they feel that they are just existing rather than living. But, if these patients could get a transplant from a living donor, their life expectancy would increase up to 23 years and their lives could really begin. With increasing cuts to the NHS budget is it possible that the cost-effectiveness of kidney transplant might persuade the government to legalise a market in human organs?  The implementation of a legal organ market would also increase the human organ supply and eliminate the consequences of the black market.

Due to a shortage in organs, the black market and transplant tourism is thriving. Annually, 15,000 – 20,000 illegal kidney transplants take place around the world, often in developing countries such as India and the Philippines. There are even slums in the Philippines dubbed “kidney-vile”, as the majority of the slum’s residents have been driven to sell a kidney. But the black market is built on systematic deception. Brokers coerce desperate workers to sell a kidney then give them much less money than they were promised. Nor do they care about the surgical quality and often leave donors with little or no aftercare. Consequently, donors often become ill and are unable to continue their usual hard labour, which perpetuates their poverty, rather than alleviating it. Recipients are also affected by black market fraud: often these kidneys are not screened properly and donors are coerced to cheat their medical records. As a result of these schemes and poor hygiene standards, recipients often contract diseases such as hepatitis B/C and HIV.

Group of men from Baseco “Kidney-ville” in Philippines, displaying their scars from selling a kidney.
Group of men from Baseco “Kidney-ville” in Philippines, displaying their scars from selling a kidney.

Iran is currently the only country with a compensated and regulated kidney donation program. In this system, there are no brokers and it is charity organizations that coordinates donors with recipients. The government pay a fixed price for organs and cover the costs of all necessary aftercare for donors. Due to this system, Iran is currently the only country with no kidney transplant waiting list. It has also successfully eliminated its black market, and has still maintained a respectable percentage of altruistic donations. Nevertheless there are flaws to the Iranian system as discussed here.

Erin & Harris proposed an ethical, highly regulated, system in which only individuals within a nation are eligible to sell or receive organs. The market would have one purchaser (e.g. the NHS in the UK) and organs would be allocated fairly, giving recipients an equal chance of receiving a transplant regardless of their economic background. This system would also remove the draw for brokers, and subsequently reduce the exploitation of vulnerable people. Medical screening would ensure only healthy individuals could sell an organ, which would to minimise risk (Gill & Sade, 2002). Such a system would also provide proper medical care for donors who would also benefit from a full psychological evaluation, to make sure they are aware of the consequences of their actions.

A study of 478 donors from the Iranian regulated system has shown their health did not deteriorate after the sale, and that 90% of them were content with selling their kidney. These results contrast markedly with the study of 305 Indian donors in an unregulated market. The health of 90% of these donors declined, people living below the poverty line rose up to 20% and 79% of donors would not recommend selling a kidney. This shows that within a regulated program, both vendors and patients are better cared for and are more satisfied with the transplant process.

The strongest argument against the sale of organ is the possible exploitation of the poor. Critics argue that legalisation could lead to a market that would exploit poorer people, as they might view organ sale as a last resort. But, is it exploitation if a person makes a reasoned decision to take an action they consider to be the best option to improve their life? One can’t assume that money would simply overrule a person’s judgment. A black market would also lead to greater exploitation than any legalised market ever would. Prohibiting an organ market is paradoxical, to restrict an individual’s autonomy and cause moral harms to liberty.

Another prominent argument against the sale of human organs is that it would lead to commodification of the human and therefore corrupt human dignity. Commodification is an unsuitable term to use for the sale of a kidney, since there are numerous other circumstances when paying money does not insinuate loss of dignity, such as surrogacy.The scarcity of organs and, death and exploitation of people will not be resolved through rhetoric of moral repugnancy and human dignity.

Under prohibition, patients are suffering and dying whilst waiting for a transplant. Both vendors and recipients are exploited by the black market, and the human rights of poor people are violated. These problems will continue to exist as long as there is a dearth of organs. So, should a market in human organs from living persons be legalised? Or is it merely a naive and impractical idea, only appropriate for a dystopian future. Either way, the possibility of legalising a regulated and ethical market should be explored.

Post by: Alyssa Vongapai


Erin, C. A., & Harris, J. (2003). An ethical market in human organs. Journal of Medical Ethics , 29 (3), 137–138.

Ghods, A. J. (2009). Ethical issues and living unrelated donor kidney transplantation. Iranian Journal of Kidney Diseases , 3 (4), 183–191.

Goyal, M. (2002). Economic and Health Consequences of Selling a Kidney in India. Journal of the American Medical Association , 288 (13), 1589.

Higgins, R., West, N., Fletcher, S., Stein, A., Lam, F., & Kashi, H. (2003). Kidney transplantation in patients travelling from the UK to India or Pakistan. Nephrology Dialysis Transplantation , 18 (4), 851–852.

Hippen, B. E. (2005). In defense of a regulated market in kidneys from living vendors. The Journal of Medicine and Philosophy , 30 (6), 593–626.

Kidney Org. (2010). Transplantation Cost Effectiveness. [Online] Available from: [Accessed on 5 Aug 2016]

MacKellar, C. (2014). Human Organ Markets and Inherent Human Dignity. The New Bioethics: A Multidisciplinary Journal of Biotechnology and the Body , 20 (1), 53–71.

Moazam, F. (2009). Conversations with Kidney Vendors in Pakistan. Hastings Center Report, (June), 29–44.

New Internationalist. (2014). Human traffic: exposing the brutal organ trade. [Online] Available
from: [Accessed on 5 Aug 2016]

Organ Donation. (2015). Transplant save lives. [Online] Available from:
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Pat Roque. (1999). Group of men from Baseco “Kidney-ville” in Philippines, displaying their scars from selling a kidney [Photograph]. At: [Accessed on 5 Aug 2016]

The Wall Street Journal. (2015). Cash for kidneys: The case for a Market for organs. [Online] Available from:
[Accessed on 5 Aug 2016]

World Socialist Web Site. (2015). Dramatic increase in worldwide illegal organ trade. [Online]
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Insight from behind the lab bench: Could a period pain treatment be re-purposed to treat Alzheimer’s disease?

Today we are lucky enough to have the opportunity to publish a post written by Mike Daniels – one of the researchers behind the recent discovery that a drug used for the treatment of period pain may have a role to play in the treatment of Alzheimer’s disease. We hope you enjoy the opportunity to slip behind the lab bench and see what happens behind the scenes of a big scientific discovery.

My name is Mike Daniels, I am a PhD student working at the University of Manchester. We’ve just published a paper in the journal Nature Communications on how currently available drugs may be used to treat Alzheimer’s disease. The Brain Bank North West got in touch with us and gave us a fantastic opportunity to add our voice to the current media storm surrounding this research. I hope I can give you a detailed look at the ins and outs of this important research and offer some insight into the workings of a big research project.

Screen Shot 2016-08-19 at 20.48.07Our lab group are particularly interested in AD, not just because it affects over 26 million people worldwide without any truly effective treatment but also because our speciality is immunology and research suggests that an overactive immune system may play an important role in AD. One particular part of that immune system recently implicated in AD is something called an inflammasome. The inflammasome is a large bundle of proteins which forms a kind of machine within cells whose job it is to produce proinflammatory cytokines. These cytokines go on to promote inflammation in the brain which can worsen AD.

What’s particularly exciting for us is that this inflammasome appears to be largely redundant in everyday immune functions like fighting bacteria or viruses. This means we should be able to inhibit it in patients without rendering them susceptible to infection.

OK so we have a plan – inhibit the inflammasome complex in the hope of improving outcomes for people living with AD. But how do we do this? We could design new drugs (something our lab is involved in right now) but the process of getting a new drug from bench to clinic can take around 20 years and cost around 1.6 billion dollars. Another quicker, cheaper option is to do something called ‘repurposing’, this basically means taking a drug already approved and on the market and using it to treat a different disease. With this in mind our lab head Dr. David Brough decided to test a number of drugs from a large class called non-steroidal anti-inflammatory drugs (NSAIDs) to see if they could inhibit the inflammasome and thus potentially be used in AD. So, this was the project I was tasked with in my first week of PhD life nearly two years ago.

We began by testing a number of these NSAIDs on immune cells cultured in a petri dish. This gave us the important opportunity to screen a large number of drugs without unnecessary use of animals. When we ran these screens we had a bit of a surprise. The more famous NSAIDs such as ibuprofen (Nurofen) had no effect. However, one drug, mefenamic acid, was able to inhibit the inflammasome and prevent release of inflammatory cytokines in the cells. Mefenamic acid is only available by prescription and is prescribed largely to treat period pain.

So, how does mefenamic acid inhibit the inflammasome?

Research suggests that ion channels on the cell surface play an important role in inflammasome activation and that mefenamic acid may inhibit some types of ion channels. To better understand this we formed a collaboration with a London-based research group led by Dr. Claudia Eder – an expert in electrophysiology (researching ion channels). It was with the help of Dr. Eder’s lab that we identified the target of the drugs as a chloride channel called the volume-regulated anion channel (VRAC).

Screen Shot 2016-08-19 at 20.56.56Now we had the drug and the mechanism but we still don’t know whether this drug would be effective in treating AD. This is where we needed to look at the drugs action in a living system. The first model system we chose was a rat model of amyloid-beta induced memory deficits. Build-up of amyloid-beta is a thought to be a major factor in memory impairment and AD. Indeed, if injected into the brain of rats, amyloid-beta causes permanent memory deficits. As part of a collaboration with Dr. Mike Harte’s lab here at Manchester, we injected a group of rats with either mefenamic acid or a placebo and found that those which received the drug were completely protected from amyloid induced memory deficits.

We then moved to look at the effect of the drug in a genetic mouse model of AD. These mice had been altered to express some of the same genes found in humans with the genetic form of AD and, like human sufferers, these mice develop memory deficits with advancing age. When treated with mefenamic acid at the age of onset, these mice did not develop memory deficits, unlike animals treated with a placebo. We also found that the brains of placebo mice displayed signs of intense inflammation while those of drug treated mice remained completely normal.

So to conclude, AD is a terrible and currently incurable disease which we believe to be partially caused by an overactive immune system – specifically over-activity of a protein complex called an inflammasome. We found that the commercially available drug mefenamic acid was able to inhibit the inflammasome and reduce memory loss in both mouse and rat models of Alzheimer’s-like memory deficits.

But what’s the next step? We are hoping to begin to move mefenamic acid into clinical trials to see if it could really work in humans. Luckily, because the drug is already known and approved we can skip the safety testing stage of the clinical trial process. Unfortunately however, clinical trials remain extremely expensive and, as mefenamic is off patent and can no longer be sold for profit, gaining funding through pharmaceutical companies is nigh-on impossible. This means we are relying on grants from fantastic charities such as Alzheimer’s Society and Alzheimer’s Research UK in order to move this study forward.

A lot of work is needed and it will still be a while before we have results in people currently living with AD, but this remains an exciting step and we can only hope that it will go some way to treating this horrible disease.

Guest post by: Mike Daniels

Screen Shot 2016-08-19 at 20.25.13Mike is currently studying for a PhD in neuroinflammation at the the University of Manchester, UK. His work is based mainly on the role of a huge protein complex called the inflammasome in diseases such as Alzheimer’s, stroke and haemorrhagic fever. When he’s not in the lab he’s usually found up a mountain or out in the countryside somewhere and is always on the lookout for any new science outreach ideas!

Fat vs fat in the fight against obesity and diabetes

Using fat to treat obesity and obesity-related conditions, such as type II diabetes, may sound like a strange idea. Nevertheless, this is exactly what scientists are working to achieve. So the question is, why?

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There are in fact two types of fat in the body. The more familiar of the two – white adipose tissue (WAT) – is the tissue we refer to colloquially as “fat” and associate with gaining weight. The second, and lesser known variety of fat, is brown adipose tissue (BAT). This unique tissue is densely innervated by the body’s sympathetic nervous system (SNS – initiator of the “fight or flight” response) and is well supplied by blood vessels. Originally believed only to exist in small mammals and human infants. BAT is used to produce heat without the need for shivering. This is particularly important for these organisms as a way of maintaining their core temperature in mild cold conditions.

The key to BAT’s ability to produce heat is a special protein called uncoupling protein 1 (UCP1), which is housed within the large number of mitochondria found in this tissue. In general, mitochondria act as the “powerhouses” of all cells, producing energy in the form of ATP which allows the cell to perform all its required functions.

However, in cold conditions, sensors on the skin send a signal to the part of the brain responsible for regulating body temperature. The brain, in turn, sends a message to BAT via the SNS, releasing noradrenaline and stimulating UCP1. Upon activation, UCP1 is able to “override” the usual ATP-synthesising function of BAT mitochondria, instead releasing energy as heat.

Importantly, this process of heat production requires a significant amount of energy to achieve. As the main fuel used by BAT are fat molecules, such as lipids and fatty acids, the idea that BAT could potentially be used to help reduce body weight in obesity is not as ludicrous as it may first appear. This is supported by the finding that both UCP1- and BAT-deficient mice models display increased weight gain.

Screen Shot 2016-08-14 at 20.48.58Despite evidence of the role BAT plays in controlling body weight in experimental rodent models, BAT was originally believed to be absent in adult humans. More recently, however, the use of radioactive tracer PET and CT scans have demonstrated the presence of functional BAT in adults in mild cold conditions using large cohorts of patients. Further analysis of PET and CT data has also uncovered an inverse association between BAT activity and BMI, with lower levels of activity in patients with severe obesity. Though the average human adult is estimated to possess just 50–80g of BAT, this mass is believed to use up to 20% of our daily energy intake, making BAT a desirable candidate to aid weight loss in obesity.

BAT has also been shown to express high levels of the glucose-transporter protein and displays comparable glucose uptake to muscle in response to insulin. Given that a key risk factor for type II diabetes is being overweight, and that this disorder is characterised by high blood glucose and insulin resistance, targeting BAT as a method of treatment is also under investigation. Notably, insulin-activated glucose uptake into BAT is significantly lower in those with obesity compared to subjects of a normal weight.

Given the mechanism of BAT activation discussed above, as well as the observation during PET and CT scans that BAT activity is inhibited when human subjects are warmed, the simplest way to stimulate this tissue for therapeutic reasons may be with the use of cold temperatures. In support of this theory, a small study involving healthy Japanese volunteers, who were repeatedly exposure to mild cold stimuli over 6 weeks, reported increased BAT and resulted in a loss of body fat in subjects. In another study, exposing healthy volunteers with active BAT to short-term mild cold led to increased insulin sensitivity.

Screen Shot 2016-08-14 at 20.49.22A second potential method of stimulating BAT with the aim to treat obesity or type II diabetes is via the SNS, specifically through beta-adrenergic receptors (βARs). It should be noted that anti-obesity medications which target these receptors have been tested in the past. However, these attempts failed due to unspecific activation of βARs throughout the body – particularly the heart – resulting in serious side effects, including increased blood pressure and heart rate. Nevertheless, the use of more specific βAR agonists have been used successfully to increase BAT activity and lessen obesity and insulin resistance in rodent models, without such side effects.

Alternatively, it may be possible to target the thermoreceptors on the skin responsible for sensing cold, known as TRPs. As cold exposure cannot be controlled easily, activating these receptors artificially may provide a more efficient way of using BAT to treat obesity or type II diabetes. Interestingly, there are already a number of foods which activate TRPs, including menthol in mint and capsaicin in chili peppers. Animal and human studies of capsinoids – non-pungent analogues of capsaicin – have demonstrated that these compounds increase active BAT and reduce body fat.

Despite sounding rather contradictory, adipose tissue may prove useful in the treatment of obesity and the obesity-related disorder, type II diabetes. Unlike its white counterpart, BAT actually uses up lipids and glucose from the body as fuel in order to produce heat. However, in doing so, evidence suggests this can also result in weight loss, reduced insulin resistance and lowered blood glucose, making it a potential treatment for obesity and type II diabetes. Possible methods of activating BAT for this purpose may include cold stimuli or agonists which target βAR or TRP receptors. It is still early days for this treatment possibility but the idea certainly isn’t as strange as it may first appear.

Post by: Megan Barrett



Rheumatoid arthritis and Alzheimer’s disease, what’s the connection?

It has recently been reported that a drug currently used to treat rheumatoid arthritis (RA) may also pack a punch in the fight against Alzheimer’s disease (AD). This discovery may be hailed by the media as a big step forward for AD research but what does it really mean?

To pick apart this discovery, we first need to delve into some background on Alzheimer’s itself:

Screen Shot 2016-08-08 at 20.47.27Much of what we know about Alzheimer’s disease in the human brain comes from postmortem studies. This means that most of our knowledge is skewed towards late stages of the disease. We know that, in these late stages, patient’s brains are severely shrunken and littered with clusters of abnormal proteins known as amyloid plaques and tau tangles. Many academics acknowledge that if we want to successfully treat AD it’s important that we understand what causes these proteins to misbehave in the first place. This is where scientists picked up on an important link between RA and AD.

Rheumatoid arthritis is an autoimmune disease which causes inflammation, pain and swelling in joints. Interestingly, alongside chronic inflammation, many RA sufferers also experience what is known as secondary amyloidosis resulting from deposition of amyloid protein fibrils. This form of amyloid starts life in the liver before being cut into smaller pieces and then deposited in other tissues – importantly this process appears to parallel the deposition of amyloid in the AD brain. Another important parallel between the two diseases is the presence of tumor necrosis factor (TNF) – a pro-inflammatory cytokine. Researchers believe that RA may be driven by TNF and it is also known that AD patients show elevated levels of TNF in their cerebrospinal fluid.

So, is it possible that TNF could play a causative role in both RA and AD and, if so, can modulation of TNF be used as a treatment for both diseases?

In a recent study Richard C.Chou from Dartmouth-Hitchcock Medical Centre collected medical records from over 8,000,000 US patients and his team began crunching numbers in the hope of answering these questions. They found that patients suffering from RA (over 40,000 patients) had a significantly increased risk of also developing AD. In fact, RA patients over the age of 65 were more than twice as likely to suffer from AD than non-sufferers (2.95% of RA patients also suffered from AD in comparison to 1.37% of non-RA patients). What was even more interesting was that patients treated with the RA drug etanercept (an anti-TNF agent) were significantly less likely to suffer from AD than other RA patients.

These results suggest that both RA and AD may share a common mechanism, perhaps linked by the actions of TNF? It also raises the possibility that anti-TNF therapies could have a future in the treatment of AD.

Although this work is just one more piece in the Alzheimer’s puzzle, the implications seem to suggest a role for inflammation and perhaps TNF in disease progression – something which has also been highlighted in previous studies. So, although (as is often the case) more research is needed, it does seem like we are making some significant headway in understudying and hopefully treating Alzheimer’s.

Post by: Sarah Fox