Dirty laundry a powerful magnet for bedbugs

Bedbugs are small insects and suck human blood for their sustenance. They hide around beds in small cracks and crevices. Their existence can be identified by the presence of small bugs or tiny white eggs in the crevices and joints of furniture and mattresses. You might also locate mottled bedbug shells in these areas. A third sign of existence is the presence of tiny black spots on the mattress which are fecal matter, or red blood spots. And if you have itchy bites on your skin, then that is a clear sign. Unfortunately it is the fourth that provides people with the impetus to check their living areas for bugs, rather than the need to maintain hygiene by changing sheets.

The incidences of bedbugs have increased globally and one theory is that that visitors to countries where the hygiene levels are less stringent bring them back to their own country. The cost of cheap travel, both in terms of rail tickets and air flights, has enabled people to visit far-flung places. But one thing that has not been so apparent is how the bed bugs are carried back. It had been thought that bugs are more drawn to the presence of a human being – but surely they don’t piggyback on one across regions and continents?

The authors of a recent research into the matter have a new perspective of the matter. They believe that bugs are drawn to evidence of human presence, and not necessarily just to the presence of a human host. They believe that bed bugs, in places where hygiene is slightly lacking, collect in the dirty laundry of tourists and are then transported back to the tourists’ own location, from where they feed and multiply.

While this was an experimental study, the results are interesting because it had been previously thought that bed bugs prefer to be near sleeping people because they can sense blood.

The experiments leading to these results were conducted in two identical rooms.

Clothes which had been worn for three hours of daily human activity were taken from four volunteers. As a basis of comparison, clean clothes were also used. Both sets of clothes were placed into clean, cotton tote bags.

The rooms were identically set to 22 degrees Celsius, and the only difference was that one room had higher carbon dioxide levels than the other, to simulate the presence of a human being.

A sealed container with bed bugs in was placed in each room for 48 hours. After twenty four hours, when the carbon dioxide levels had settled, they were released.

In each room there were four clothing bags introduced – two containing soiled laundry and the other two containing clean laundry, presented in a way that mimicked the placement of clean and soiled clothes in a hotel room.

After a further 4 days, the number of bedbugs and their locations were recorded. The experiment was repeated six times and each experiment was preceded by a complete clean of the room with bleach.

The results between both rooms were similar, in that bed bugs gravitated towards the bags containing soiled clothes. The level of carbon dioxide was not a distinguishing factor in this instance, and the result suggested traces of human odour was enough to attract bed bugs. The physical presence of a human being was not necessary.

The carbon dioxide however did influence behaviour in that it encouraged more bed bugs to leave the container in the room with carbon dioxide.

In other words, the carbon dioxide levels in a room are enough to alert bed bugs to human presence, and traces of human odour in clothes are enough to attract them.

Why is this hypothesis useful to know? If you go to a place where the hygiene is suspect, then during the night when you are asleep, the bed bugs know you are present, and if they do not bite you, during the day they may come out and embed themselves in your dirty laundry. The researchers concluded that the management of holiday clothing could help you avoid bringing home bedbugs.

The simple way of protecting yourself against these pesky hitchhikers could just be to keep dirty laundry in sealable bags, such as those with a zip lock, so they cannot access it. Whether or not it means they will turn their attention to you during your holiday is a different matter, but at least it means you will avoid bringing the unwanted bugs back into your own home.

The study was carried out by researchers from the University of Sheffield and was funded by the Department of Animal & Plant Sciences within the same university.

More research of course is needed into the study. For example, if there were a pile of unwashed clothes while some was sleeping in the room, would the bugs gravitate towards the human or towards the clothes? It is more likely that they move for the human, but that kind of theory is difficult to test without willing volunteers!

Also, did the bugs in the room only head for the unwashed clothes because of the absence of a human, or did the proximity of the clothes to the container lull them into account the way they did? Also what is not accounted for are other factors by which bed bugs may be drawn to where they reside. Perhaps in the absence of a human being in the room, bed bugs would head for the next best alternative, which are clothes with trace human odours or skin cells, but perhaps with a human being in the room, bed bugs might rely on temperature differences to know where to zoom in on. In other words, instead of detecting human presence using carbon dioxide, they rely on the difference in temperature of the human body relative to its surroundings (the human body is at 36.9 degrees Celsius).

Carbon dioxide levels have been shown to influence mosquitoes and how they react but perhaps bed bugs rely on other cues.

There could be other factors that cannot or were not be be recreated in the same controlled environment of the experiment.

Ever wonder what it was like in the past centuries? Did people have to deal with bed bugs if they lived in the times of the Baroque ?

Nobody knows but one thing is for sure. Getting rid of bed bugs is a bothersome business but if you can prevent them getting in your home in the first place, all the better!

Revising Traditional Antibiotic Advice

What do you do when you have a cold and feel under the weather? Perhaps you decide to tough it out, and head to work as usual. You grin and bear it, because as far as you are concerned, it’s just a common cold and you can’t do anything about it.

But suppose you don’t get any better after a week, when you expected that the cold would have already run its course. You decide to stay at home to rest, and after a further two days when no improvement is seen, you go to visit the doctor.

The doctor’s advice? A course of antibiotics. Two tablets three times a day after meals, and by the way, keep finishing the course even when you feel better.

This is the advice that has been dispensed through decades to patients. Finish the whole prescription of antibiotics. And as patients, we put our trust in doctors so whatever they said went. Who were we to argue with seven years of medical training?

But what would you say if this medical advice turned out to be incorrect? I know what I’d think – firstly the sceptic in me would say medical advice is fickle and flows with what is fashionable at the time. At times, medicine seems also subservient to politics and economy. Remember the case with red wine? When the economy was flagging, a glass of red wine was said to be good for you. Yet when the NHS was under strain this so-called health benefit was reversed.

In this day and age it is also fashionable for everyone to carve a niche for themselves, and for many the way to do so is to turn traditional advice upside down on its head and revise or reformat existing information. And so, with these in mind, it is unsurprising that we learn of yet another study that claims the rule that patients must finish antibiotics course is wrong.

The new slant on the old problem is that patients should stop taking the prescribed medication when they feel better rather than as what doctors previously used to recommend.

The new panel of experts suggest that  the long embedded rule is incorrect, because continually taking medication after we have felt better only lowers the body’s resistance in the long run. They argue that if the body already feels better, giving it medication it does not need has counter-productive effects.

This differs with the advice that doctors have traditionally recommended, which is based on the idea that bacteria remains in our bodies even though we feel better and these bacteria may develop adaptation to antibiotics if they are not fully killed off. In other words, if you have not fully killed off the bacteria, it develops tolerance and immunity to the drug which partially fended it off, and ultimately the antibiotics’ effectiveness is negated.

Imagine two medieval armies: Trojans and Greeks. One day the Trojans manage to get inside the Greek city walls and wreak havoc (according to the Greeks anyway) with their torches, spears and swords. But the Greeks have a special weapon, say for arguments’ sake, an M16 with a laser sight. If the Greeks completely defeat the Trojans, the effectiveness of their weapon is guaranteed against successive waves of Trojan attacks. But if the Greek army stops to celebrate the moment the city battle swings in their favour, retreating Trojans may bring back information about the weapon, and how it works, and plan successive attacks that limit the effectiveness of the weapon or destroy it completely.

Martin Llewelyn, professor in infectious diseases at Brighton and Sussex medical school have called for a re-examination of the traditional advice. In an analysis in the British Medical Journal, they say “the idea that stopping antibiotic treatment early encourages antibiotic resistance is not supported by evidence, while taking antibiotics for longer than necessary increases the risk of resistance”.

In other words, stop taking the medicine the moment you feel better.
In the past, the theory supporting the completion of a course of antibiotics has been that too short a course would allow the bacteria causing  disease to mutate and become resistant to the drug.

For certain diseases, bacteria can clearly become resistant if the drugs are not taken for long enough to completely eradicate them. One such example of this is tuberculosis.

But a large majority of the bacteria that cause illnesses are found in the environment around us and have no impact until the bacteria gets into the bloodstream or the gut. The case putting forward a cessation in medication once the patient’s health improves is that the longer the bacterial exposure to antibiotics within the body, the higher the chance of developed resistance.

The hypothesis put forth by Professor Llewelyn has not been without its backers.

Peter Openshaw, president of the British Society for Immunology, said he had always considered the notion  that stopping antibiotic treatment early would make organisms more drug-resistant rather “illogical”.

He supported the idea of a more sparing use of antibiotics because the evidence of a link between long-term complete use and benefit was tenuous.

He dismissed claims that not finishing a course of antibiotics would lead to bacteria gaining antibiotic resistance but thought the reverse would be more true. “Far from being irresponsible, shortening the duration of a course of antibiotics might make antibiotic resistance less likely.”

A great British authority, Prof Harold Lambert had made the suggestion as far back as in 1999 in a Lancet article entitled “Don’t keep taking the tablets”. Even though the idea had been broached then, it had not been taken seriously and with hindsight it is surprising that nearly two decades later the medical world has not investigated the alternatives fully and that the optimum duration of antibiotics courses or doses in many conditions remains an investigated fast.

Jodi Lindsay, a professor of microbial pathogenesis at St George’s, University of London, stated that the new research by Professor Llewellyn was good in principle, and that the previous advice to complete a course of antibiotics may have been based on a fear of under-treatment. But nevertheless she cautioned against an over-reaction towards the results of the findings. “The evidence for shorter courses of antibiotics being equal to longer courses, in terms of cure or outcome, is generally good, although more studies would help and there are a few exceptions when longer courses are better – for example, TB.”

To complicate matters, the ideal length of a course of antibiotics varies in individuals depending on what antibiotics they have taken in the past. Hospitalised patients can be tested to find out when the drugs can be stopped. Outside of a hospital setting, this testing is not feasible.

The World Health Organisation advice is still based on the pre-existing guidelines and has not changed.

The Royal College of GPs, however, expressed caution over the findings. “Recommended courses of antibiotics are not random,” said its chair, Prof Helen Stokes-Lampard. She further elaborated that antibiotic treatment courses were already being customised according to individual conditions and if patients took it upon themselves to adjust the prescribed periods, stopping when they felt better, it would be dangerous because a slight turn in outlook did not necessarily demonstrate the complete eradication of the disease. Professor Stokes-Lampard also stressed that it was important for patients to have clear guidelines to adhere to and any adjustment using feel as an indicator might be confusing.

The National Institute for Health and Care Excellence is currently developing guidance for managing common infections, which will look at all available evidence on appropriate prescribing of antibiotics.

The cynics among us might ask, has such a review on current guidelines been made with the objective to cut the cost of medical care? It is well known the health budget is ever dwindling, and one cannot help but feel that the review on existing guidelines of antibiotics has been made with an objective to save on the cost of medicine rather than put patient health first.

The health service is currently riding the trend of developing sustainability in infrastructure and treatment, and this revision of traditional guidelines may seem to be a reframing of the evidence to suit a pre-determined outlook.

Let us return to the example of Greeks and Trojans. If the battle is raging within the Greek city walls and the tide turns against the Trojans, should the Greeks fire their ammunition at the retreating Trojans until they all fall to the ground? Ammunition in the form of gunpowder and metal casings cost money and if the ammunition could be used sparingly, then there is more money to funnel towards other  daily activities like farming and livestock. The question we are being asked to address is the equivalent of this hypothetical situation: Should the Greeks keep firing their weapons, until all the Trojans fall before they manage to retreat and leave the Greek city walls, or should the Greeks try to save the cost of a few rounds of ammunition if they are certain the Trojans are so heavily wounded they would never survive the escape and make it to their own city walls to compromise the information they know about the secret weapon?

You may decide, as I did, that the cost of a few extra rounds of ammunition outweighs all the mental confusion of wondering “what if …?” for the next few months. “What if I didn’t take the medication long enough? What if the bacteria has mutated?”

You can see why it is easier that when it comes to health, be cautious, don’t customise. Don’t experiment on the one life you’ve got!

New breakthrough in heart attack treatment

Are we edging closer towards lowering the risk of recurring heart attacks? Scientists definitely think so. In what has been described as the biggest advance since the discovery of statins, a study has shown that anti-inflammatory injections could lower the incidence of recurring heart attacks in heart attack survivors. Furthermore, these injections have been suggested to also slow the progression of cancer.

It has been discovered that heart attack survivors who were administered injections of a targeted anti-inflammatory drug called canakinumab had a lower risk of such attacks in the future. With this particular drug as well, the incidence of cancer deaths were also reduced to less that fifty percent.

Canakinumab is not normally prescribed for this purpose; its function normally lies in the use for rare inflammatory condition. Instead, the current drugs for the prevention of heart attacks are statins. The main method in which statins prevent heart attacks from recurring is by lowering cholesterol levels. Despite this, statin users who regularly take the drug have a one in four chance of suffering another heart attack within half a decade. While the cause for this is unknown, and research has been done on heart attacks and statins, the current line of thinking is that inflammation within the heart’s arteries are the cause of this recurrence.

The research team followed over 10,000 patients and were led from Brigham and Women’s hospital in Boston. One of the hypotheses tested was whether targeting the inflammation with a potent anti-inflammatory agent would provide an extra benefit over statin treatment. In other words, the trial aimed to see if statins combined with canakinumab would be better than just statins alone. The 10,000 patients who had had a heart attack and had all received a positive blood test for inflammation into the trial. In addition to the doses of statins, patients also received either canakinumab or a placebo, both administered by injection every three months. The trial, also known as the Cantos study, lasted for four years.

For the first group – patients who had received the canakinumab injections – the results demonstrated that there had been a 15% reduction in the risk of a cardiovascular event; this means that the risks of heart attacks, either fatal or non-fatal, and strokes had been reduced. But the benefits of canakinumab did not merely end there. The need for expensive interventional procedures, such as surgery such as bypass surgery, or the insertion of stents, was reduced by over three-tenths. The drug did not, however, change cholesterol levels, meaning that it must still be used alongside statins, and the use of statins as cholesterol limiters will still continue to remain so. There was also no significant statistical difference in the number of death rates between patients who had received canakinumab and those who had been given placebo injections.

Dr Paul Ridker, who led the research team, said the study did “usher in a new era of therapeutics”.
This study is the first incidence where scientists have been able to show conclusively that the risk of cardiovascular risk is reduced when inflammation independent of cholesterol is lowered. Why the results have been considered ground-breaking is due to the insight that they have provided; there could be an entirely new way to treat patients and significantly improve health outcomes through the targeting of inflammation, jointly with the lowering of cholesterol. The statistical benefits for patients who took canakinumab were described as being “above and beyond” those seen in patients who only took statins.

Dr Ridker also mentioned that the study showed that the use of anti-inflammatories was the next big breakthrough following the linkage of lifestyle issues and then statins.

“In my lifetime, I’ve gotten to see three broad eras of preventative cardiology,” he said. “In the first, we recognised the importance of diet, exercise and smoking cessation. In the second, we saw the tremendous value of lipid-lowering drugs such as statins. Now, we’re cracking the door open on the third era. This is very exciting.”

But despite the promising results of the treatment, it was not without its negatives. The researchers reported that there was a rise in the potential chance of dying from a severe infection for about a tenth of a percentage point, although this increase was counterbalanced by decrease by over 50% of cancer deaths across all cancer types. The most promising cancer reduction rates were seen in the case of lung cancer. The odds of dying from lung cancer, with the use of canakinumab, were reduced by over three quarters. There was no scope within this study to investigate that further, although subsequent trials to investigate canakinumab’s effect against cancer are being considered.

Prof Martin Bennett, a cardiologist from Cambridge, had no involvement in the study, and while he said the trial results were a promising insight in understanding the occurrence of heart attacks, he expressed concerns both about the side effects, whether the high cost of the drug would pass the Quality Adjusted Life Years (QALY) test that the NHS administers to determining cost effectiveness of drugs, and also the fact that there were no significantly lesser incidences of deaths between those prescribed canakinumab and those who had received the placebo.

“Treatment of UK patients is unlikely to change very much as a result of this trial, but the results do support investigation of other drugs that inhibit inflammation for cardiovascular disease, and the use of this drug in cancer,” he said. In other words, despite the results of the study and what we can glean from them, he believes statins will still remain the mainstay of recurrent heart attack prevention.

Prof Jeremy Pearson, who is the associate medical director at the British Heart Foundation, showed more positive belief about the trial and the possibilities of it opening the doors to new types of treatment for heart attacks.

He mentioned that heart attacks account for a high number of hospitalisations every year. The figure is thought to be close to two hundred thousand people each year in the United Kingdom. He further explained that the use of cholesterol-lowering drugs like statins, when prescribed to these people to reduce their risk of another heart attack, does save lives, but the reduction of high cholesterol rates as a mere medical focus alone is not always a measure that effectively deals with the whole of the problem.

He added that one could be forgiven in feeling a flutter of excitement when it came to these trial results, which have been eagerly awaited by the medical community. The confirmation of previous medical hunches that the continual inflammation is a significant contributor to the risk of heart disease, and that the intent to reduce it could help save lives, is a significant way forward towards the treatment of heart attack patients.

 

This research into canakinumab is one of many that have been conducted into heart attack prevention. We should be cautious about its possible side effects; aspirin, for example, has been shown to cause bleeding when prescribed to heart attack patients. It has also been suggested that  beta blockers for heart attack patients, on the other hand, do not have the ascribed health benefit. Furthermore, if the drug does end up prescribed to heart attack sufferers, what are the side effects when taken for the long term?

Could we possibly see canakinumab being prescribed as a matter of course for heart attack patients to prevent a recurrent? The answer perhaps lies not with whether or not the drug has benefit – it has already proven this in some areas – but whether the side effects can be mitigated. More importantly, the issue of cost will probably determine its future. If the cost of canakinumab could be lowered, so that its prescription to the over two hundred thousand heart attack sufferers per year would not be a significant burden on the financial limitations on the health service, then we could see it being prescribed as a matter of course. If not, then we may have to wait for a less expensive substitute to hit the market. And while it is somewhat disheartening that medical intervention in recent times is more geared not towards finding medicine that works, but medicine that is cost effective, the promise of canakinumab nevertheless is a positive health step.

Are we nearing a medical cure for Parkinson’s disease?

Are we edging towards a cure for Parkinson’s disease? A study in the medical journal Lancet suggests that while we may still be a bit away from a total cure from the disease, there is enough evidence to suggest that it may soon be possible to halt its progression, which is the next step towards managing or eliminating a disease that causes damage to the brain, tremors, difficulty with movements and eventually memory problems.

Parkinson’s disease is caused by the loss of cells which produce the chemical dopamine. The decline to the brain is slow but eventually the accumulated damage causes mental and physical problems. There is no cure for it but current therapies can help to contain the damage and manage the symptoms. They work by boosting dopamine levels, but only manage the symptoms without addressing the damage to the brain.

The Lancet reports that there is evidence now to suggest the progression of Parkinson’s can be delayed. The damage to the brain can be restricted so that no further damage is done. This means that Parkinson’s sufferers retain their mental capacities at the point of diagnosis. This is promising news and the answer lies with a drug normally used in type 2 diabetes.

The trial in the research published in the Lancet was only conducted on 62 patients, so while the evidence is promising and optimistic, further evaluation and studies need to be carried out in order to confirm the findings and the news should be received cautiously. The long-term benefits or side effects are also not completely certain yet. The drug will need more testing; it is easy to be carried away with initial findings but all medication has side effects, either on mental states or physical well-being that we should be mindful of.

The study was conducted by a team from University College London (UCL) team. “There’s absolutely no doubt the most important unmet need in Parkinson’s is a drug to slow down disease progression, it’s unarguable,” Prof Tom Foltynie, one of the researchers, told the BBC.

Currently, there is no drug which achieves that effect. The drugs that are currently prescribed only manage the symptoms, but do not address damage to the brain.

The study divided the 62 patients into two groups. One group received the drug exenatide, which is normally used in the treatment of type 2 diabetes. Another group was given a placebo. Patients were unaware of which treatment they were receiving. For precautionary reasons, all patients also continued to remain on their usual medication.

The 31 patients who received only their usual medication showed symptoms of decline usually associated with Parkinson’s disease. This decline manifested itself both in mental states such as forgetfulness and memory loss, or through the loss of locomotor movement. The results were apparent over a period of 48 weeks.

Patients for whom exenatide was prescribed displayed stability in their results. In other words, their decline due to Parkinson’s was halted. Not only was the further damage to the brain restricted, the loss of physical movement was contained. This suggested that exenatide could have some role in the damage limitation of Parkinson’s disease.

The initial study took place over a year and after that those on exenatide came off the treatment. Yet the benefits of taking the drug continued for up to three months.

 

Prof Foltynie said, “It gives us confidence exenatide is not just masking symptoms, it’s doing something to the underlying disease.”

Nevertheless, he urged, while we have reason to be encouraged by these positive findings, they still need to be replicated on a larger scale, and the drug also needs to be trialled for a much longer period before any suitable effect and link can be stated.

Another reason to be cautious is that the drug exenatide only made a difference over a maximum trial period of sixty weeks. But in real life Parkinson’s disease afflicts individuals over a prolonged period. The introduction of any new drug into the human body usually causes a noticeable effect at the onset anyway, as the body is flooded by chemicals, but the effect needs to be maintained for prolonged periods without losing consistency. In this particular, case, for a drug to be effective against Parkinson’s disease, it will need to hold back the damage to the brain for years in order that patients who are prescribed the drug would experience a significant improvement on the quality of life.

The effect of Parkinson’s disease is slo. Sufferers experience damage to the brain and slow decline on mind and body over years, sometimes extending up to a decade. The team from University College London said that their research in this 60-week trial produced statistical improvements in quality of life scores, but they will need to extend the benefit over a longer period.

Exenatide’s traditional role as part of a diabetes treatment is in controlling the blood sugar levels in the body. It does this through the action on a hormone sensor known as GLP-1. It is believed that Exenatide makes the hormone sensors work more efficiently or perhaps it improves their ability to survive.

But the GLP-1 sensors are not just found in the body. They are also in existence in brain cells. Those sensors are also present in brain cells too. The current thinking behind using Exenatide in some form as a Parkinson’s disease treatment is that if it can make hormone sensors in the body more efficient, so that they manage blood sugar levels better, then they may have a significant role if used to improve the sensors in brain cells.

It is specifically for this reason that the research of the drug is also being widened beyond its effect on Parkinson’s disease, but also in other neurodegenerative diseases such as Alzheimer’s disease.

David Dexter, the deputy director of research at Parkinson’s UK indicated that there was hope offered through the finding that drugs like exenatide, or perhaps similar ones, could slow the course of Parkinson’s that we currently take for granted. They offer some posibilities that other drugs do not.

“Because Parkinson’s can progress quite gradually, this study was probably too small and short to tell us whether exenatide can halt the progression of the condition, but it’s certainly encouraging and warrants further investigation.”

But amidst all the optimism generated by the possible positive effects on exenatide, Dr Brian Fiske, from the The Michael J Fox Foundation for Parkinson’s Research, cautioned that “the exenatide studies justify continued testing” but that clinicians and patients should not rush to “add exenatide to their regimens” until the impact and safety of exenatide had been proven.

How does Parkinson’s disease gradually lead to the decline of physical movements and memory loss? The disease affects the brain by a slow process of decline and brings on debilitating loss of movement. It has since been discovered that the damage to the brain is also synonymous with accumulation of high levels of the protein alpha-synuclein in the brain.

Scientists at Columbia University Medical Center and the La Jolla Institute for Allergy and Immunology found that T-cells, a part of your immune system, tries to destroy the alpha-synuclein in Parkinson’s disease sufferers, but it is through the killing of alpha-synuclein as an auto-immunity measure that the T-cells inadvertently kills brain cells where the alpha-synuclein accumulates. In other words, a malfunctioning immune system is destroying brain cells, which then have a knock-on impact on the brain’s health and physical functions.

In recent years scientists have made significant progress in their understanding of Parkinson’s disease. One emerging possibility that is gradually gaining ground in that Parkinson’s may have its origins in the gut.

“We imagine that T-cells may first identify alpha-synuclein out in periphery, particularly in the nervous system of gut which is not a problem until the T-cells enter the brain.”

Dr Alessandro Sette, from La Jolla, said: “Our findings raise the possibility that an immunotherapy approach could be used to increase the immune system’s tolerance for alpha-synuclein, which could help to ameliorate or prevent worsening symptoms in Parkinson’s disease patients.”

David Dexter also said that the research lent weight to the idea that “the condition may involve the immune system becoming confused and damaging our own cells.

He stressed however that more needed to be done in order for us to have some understanding about how, in the complicated chain of events that lead or contribute to Parkinson’s, the immune system – or a faulty immune one – played its part in the overall grand scheme of things.

Nevertheless, he added that the new research presented new avenues and opened up new insights into current Parkinson’s treatments. He was optimistic, perhaps cautiously so, that “this presents an exciting new avenue to explore to help develop new treatments that may be able to slow or stop the condition in its tracks.”

Is a medical cure for Parkinson’s disease on the horizon then? Perhaps in fifteen or twenty years’ time, we will look back upon these discoveries – that exenatide halts the decline of the brain by improving the proficiency of GLP-1 hormone sensors in the brain; that Parkinson’s disease originates in the gut; that managing the tolerance for alpha-synuclein by T-cells in the brain prevents them from destroying brain cells which lead to impaired mental and physical function – perhaps in the future we will look upon them as defining moments in the cure of Parkinson’s disease.

So could we expect medical prescriptions for Parkinson’s disease soon? At the earliest, a medical prescription for Parkinson’s will take at least ten to fifteen years to be made available. Pharmaceutical companies are normally granted a patent of twenty years to be the sole distributor of a medical product, in order to reward the impetus and the research undertaken into the product. At least half the amount of time is spent on research and further clinical trials. Most pharmaceutical companies apply for their patent from the time detailed research begins, so that the event that having done a significant part of their research, another company is awarded the patent, is avoided. So the moment a patent is awarded, in this case, for exenatide or a derivative product to tackle Parkinson’s disease – that is a sign we could expect a cure in about ten to fifteen years.

Is it possible too that there might be a non-medical cure for the disease? The BBC reported that more and more elderly people are taking up piano lessons to combat the onset of Parkinsons (http://www.bbc.co.uk/programmes/p04p50gg). Bearing that most cases of Parkinson’s are not hereditary, and that developing the skill of piano playing is not hereditary either, and depends on the effort of the individual himself, is it possible to build up a non-medical prevention for Parkinson’s? Only time will tell.

The problem with industry-funded drug trials

How much can we trust the results of clinical trials, especially ones that have been funded by companies with vested interests? This is the question we should continually ask ourselves, after the debacle of Seroxat.

The active ingredient of Seroxat is paroxetine. Medicines are known by two names, one of the active ingredient, the one that gives it the scientific name, and the other, the brand name. For example, the ingredient paracetamol is marketed under Neurofen, among other names. Companies that manufacture their own brand of medicine may decide to market it little more than their company name before the active ingredient, for example, Tesco paracetamol or Boots Ibuprofen, in order to distinguish it from other rival brands and aligning it with an already recognised scientific name, but without the associated costs of having to launch a new product brand.

Paroxetine is an anti-depressant and made its name as one of the few anti-depressants to be prescribed to children. However it was withdrawn from use after re-examination of the original scientific evidence found that the results published in the original research were misleading and had been misconstrued.

The prescription of medications to children is done under caution and monitoring, as there are various risks involved. Firstly, there is the danger that their bodies adapt to the medication and become resistant, thereby necessitating either higher doses in adult life, or a move on to stronger medication. In this instance there is the possibility that rather than addressing the problem, the medication only becomes a source of life-long addiction to medication. The second risk is that all medicines have side effects and can cause irreparable damage to the body in other regions. For example, the use of aspirin in the elderly was found to damage the lining of the stomach.

Equally worrying is the effect of these drugs on the health of the mind. Some drugs, particular those for mental health, are taken for their calming effect on the mind. The two main types of mental health drugs can be said to be anti-depressants and mood stabilisers, and while the aim of these drugs is to limit the brain’s overactivity, some have been found to trigger suicidal thoughts in users instead, ironically performing the function they were meant to discourage.

Children are often currently either prescribed adult medication in smaller doses of half strength instead, but the difficulty in assessing the dosage is that it does not lend itself to being analysed on a straight line graph. Should children under a certain age, say twelve for example, be prescribed as doseage based on age? Or if the most important factor in frequency is the body’s ability for absorption, should we prescribe based on other factors such as body mass index?

So when Seroxat came on to the market marketed as an anti-depressant for children you could almost feel the relief of the parents of the young sufferers. A medical product, backed by science and research, suitable for children, approved by the health authorities. Finally a medical product young sufferers could take without too much worry, and one – having been tested with young children – that parents could be led to surmise would be effective in managing their children’s mental health.

Except that Paroxetine, marketed as Seroxat, was not what it claimed to be. It has been withdrawn from use after scientists found, upon re-analysing the original data, that the harmful effects, particularly on young people were under-reported. Furthermore, researchers claim important details that could have affected the approval of its license were not made public, because it might have meant years of research might have gone down the drain.

When a medical product is launched, it is covered under a twenty-year no-compete patent, which means that it has a monopoly on that medicine for that period. While one might question why that is so, it is to protect the time spent by the pharmaceutical companies in investing in research and marketing the product, and give it a time period to establish a sizeable market share as a reward for developing the medication.

Twenty years for a patent might seem like a long term, but as companies apply for it while the product is in the early stages of development, in order that its research is not hijacked by a competing pharmaceutical company, they are often left with a period of ten years or less by the time the medical product has some semblance of its final form. The patent company has that amount of time to apply for a license and to market and sell the medication. After the original twenty years has elapsed, other companies can enter the fray and develop their own brands of the medicine. They, of course, would not need to spend the money on research as much of the research will have already been done, published, and accessible – enough to be reverse-engineered in a shorter space of time. Pharmaceutical companies are hence always engaged in a race against time, and if a product hits a snag in trials, mass production is put on hold – and if the company is left with anything less than five years to market its product, it is usually not long enough a period to recoup research costs. And if it is less with anything less than three years, it might as well have done the research for the companies that follow, because it will not recover the costs of research and marketing. While not proven, it is believed that pharmaceutical companies hence rush out products which have not been sufficiently tested, by emphasising the positive trial results, and wait for corrective feedback from the market before re-issuing a second version. It is not unlike computer applications nowadays which launch in a beta form, relying on user feedback for improvement, before relaunching in an upgraded form. The difference is software has no immediate implications on human health. Medication does.

Researchers who re-examined data from the medical trial of the antidepressant paroxetine, found reports of suicide attempts that had not been included in the original research paper. And because the makers of paroxetine, GlaxoSmithKline (GSK), had marketed paroxetine as a safe and also effective antidepressant for children, even though evidence was to the contrary, GSK had to pay damages for a record $3 billion for making false claims.

In the original research trials, GSK claimed that paroxetine was an effective medication for treating adolescents with depression and it was generally well-tolerated by the body with no side effects. Subsequent analysis found little advantage from paroxetine and an increase in harm in its use, compared to placebo.

The whole issues highlights the difficulty in trusting medical trials whose data is not independently accessed and reviewed.

The current stance on data is that pharmaceutical companies can select that clinical data they choose to release. Why is this so? We have already covered the reason for this. They have committed funds to research and are hence protective (and have right to be) protective of the raw data generated, particularly when competitors are waiting in the fold to launch products using the same data.

If you were a recording artist, and hired a recording studio for two weeks, musicians to play for you and sound engineers to record your work, at the end of the two weeks, you might have come up with a vast amount of recordings which will undergo editing, and from which your album will be created, then whatever has been recorded in the studio is yours, and you have the right to be protective about it in order that someone else might not release music using your ideas or similar to yours.

The problem is that when the pharmaceutical company initiating and funding the research is the one that will eventually market it first, and the clock is ticking against it, then it has a vested interest in the success of the product and is inherently biased to find positive outcomes that are advantageous to the product it creates.

Who would commit twenty years of time, research, marketing and finance to see a product fail?

The pharmaceutical company is also pressured to find these outcomes quickly and hence even the scientific tests may be already geared to ones that lead to pre-determined conclusions rather than ones that open it up to further analysis and cross-examination, and take up precious time or cause delay.

This creates a situation where only favourable data has been sought in the trials and only such data is made publicly available, leading to quick acceptance of the drug, a quick acquisition of a license and subsequently less delay heading into the marketing process.

The alternative is for independent review of the raw data, but this causes additional stresses on the time factor, and the security of the raw data cannot be guaranteed.

Despite the limitations of the current system, there are attempts to reform the system. The AllTrials campaign is a pressure group seeking independent scrutiny of medical data and has backing by medical organisations. The AllTrials group argue that all clinical trial data should be made available for the purpose of independent scrutiny in order to avoid similar issues to the misprescribing of paroxetine from repeated occurrence in the future.

The original study by GSK reported that in clinical trials 275 young people aged 12 to 18 with major depression were randomly allocated to either paroxetine, an older antidepressant drug called imipramine, or a placebo for eight weeks.

The researchers who reviewed the previous original study in 2001 found that it seriously under-reported cases of suicidal or self-harming behaviour, and that several hundreds of pages of data were missing without clear reason. It is likely these did not look upon paroxetine favourably.

Data was also misconstrued. For example, the 2001 paper reported 265 adverse events for people taking paroxetine, while the clinical study report showed 338.

The data involved examining 77,000 pages of data made available by GSK, which in hindsight, might have been 77,000 pages of unreliable data.

This study stands as a warning about how supposedly neutral scientific research papers may mislead readers by misrepresentation. The 2001 papers by GSK appear to have picked outcome measures to suit their results.

It subsequently come to light that the first draft paper was not actually written by the 22 academics named on the paper, but by a ghostwriter paid by GSK.

That fine for GSK might be seen as small in light of this. Certainly the reliability of industry-funded clinical trials, and how the process can be overhauled, is one we need to be considering for the future.