Why Asians are more prone to Type 2 diabetes than Westerners

Thirty-four year-old Alan Phua is what you might describe as a typical male Chinese man. He exercises for three to five times a week in a country that places a high emphasis on healthy lifestyles. He also carefully observes what he eats and is strict about his diet.

Alan lives in Singapore. In addition to military service for the duration of two and a half years when they turn eighteen, citizens have annual reservist training for two weeks until they turn forty. Failing to meet targets for physical exercises such as chin ups, standing broad jumps, sit ups, shuttle runs and a 1.5 mile run means remedial physical training every few months until these standards are meet. But not all is negative though. Meeting or exceeding these targets is rewarded by financial incentives. In other words, living in Singapore as a male means there is a strong push to keep fit and maintain it.

The reasons for this are very clear. Singapore is a small country surrounded by two large neighbours in Malaysia and Indonesia. Its population of five million citizens means that like Israel, it has to rely on a citizen reservist force should the threat of war ever loom. While most of the citizens there seem of the mindset that military war would never break out, as the country is so small that any military action would damage the infrastructure and paralyse it; furthermore, the military is only a deterrent force, the readiness to military action gives leverage in negotiations between nation. For example, if the countries disagree over the supply of water that Malaysia gives Singapore to refine, and the discussions escalate towards a military standoff, having a reservist army puts the country in a better negotiating position. But while many may claim that a war is hypothetical, there is a simpler reason for maintaining fitness. A fitter population means less stress on the healthcare system. Singapore is the sustainable healthcare system that many countries are seeking to adopt.

Like many others in Singapore, Alan’s body does not produce enough insulin. This, as a result, causes the accumulation of sugar in the bloodstream. The lack of insulin leads to other health issues, such as general fatigue, infections, or other effects such as the failure of wounds to heal. However, all is not lost. Eating properly and having a good level of exercise can prevent the blood glucose level from rising and developing into diabetes.

Local researchers from the country’s National University Hospital (NUH), working together with Janssen Pharmaceuticals, have discovered that the reason why Asians are moresusceptible than Westerners to developing Type 2 diabetes is the inability of their bodies to produce high enough levels of insulin.

Even though the finding was based only on a small sample size of 140 mostly Chinese participants, the data, if expanded and refined, will point the way and help patients with diabetes to manage it better; not just for local patients but also within the region. Doctors believe that better dietary advice and a better selection of drugs would help patients to treat diabetes. The preliminary findings are part of the country’s largest diabetes study launched last year. The five-year ongoing study has recruited around 1,300 participants, and aims to eventually nearly double that.

The researchers did however notice the ethnicity of the results was fairly restricted and more participants from a wider racial profile will be needed for the results to be applied to the general population.

Currently, the statistics show that one in three Singaporeans has a risk of developing diabetes. Currently, one out of every fourteen Singaporeans are diabetic. Type 2 diabetes comes about because insufficient insulin is produced by the pancreas, or because the body has insulin resistance.

A previous study that 8 per cent of Chinese people with a Body Mass Index (BMI) of 23 have diabetes. A BMI of 23 is within the normal weight range for Caucasians, and the rate of diabetes development within Chinese people is four times more than their European counterparts. The researchers claimed that it highlighted the importance of avoiding too much high-glucose food such as those rich in simple carbohydrates which include white rice and sugar.

The findings could also lay the foundation for efforts to test whether therapies that target insulin secretion and the ability to make more insulin could be more effective in the local population, and lead to customised diabetes treatment.

What bearing does this have on us, and what action can we take? A good start would be to avoid eating high glucose food such as rice too often and managing our diet. Also try adopting a more active lifestyle!

Women and favoured sleep positions

If you’ve ever woken up in the morning to stiffness in a particular side you would probably arrive at the conclusion that you had spent much of that night lying in that position. That discomfort may have arisen from the weight of your body pressed against that side for a prolonged period.

An incorrect – or to be more specific – uncomfortable sleeping position can raise your blood pressure through the night and consequently bring along some of the other risks associated with raised blood pressure if repeated for a prolonged period.

If the pressure of your own body pressed against your side in a night causes that level of discomfort in the morning, imagine what would happen if you were a pregnant woman bearing the weight of a baby?

We have already examined in the previous post how common themes around daily life such as diet, exercise, medicine and mental health are often researched and investigated and thoroughly mined for slants and angles as part of a media strategy of generating column inches from pre-existing information and common knowledge.

So it is no surprise, hence, to see yet another article in the media dispensing advice on sleep.

The Mail Online advises women not to sleep on your back in the last trimester as it could cause stillbirth. Backed of course, by experts.

Remember the line of thinking mentioned in the previous post?

A shark is a fish. A whale is a fish. With time, sharks can become whales, according to experts.

This is how the media works.

The Mail Online seems to have done exactly that. Perhaps sensationalising the headline first, then teasing the reader along the way by purporting to reveal the organisation and result of a blitz of information at the end. Except that after reading the article, you’ve probably thought it flowed well, but didn’t really reveal any insight.

The study – who financed it? – examined the sleep positions of twenty-nine women in their final trimester and the effects these had on their baby’s behaviour.

The overall result was that all babies were born healthy. On that basis there was no significant impact on sleeping positions on baby development. Remember the attention grabbing headline? It seemingly amounted to nothing in the end.

The tenuous link used in the research was that when women slept on their right side, babies were slightly more likely to be active and awake, and if mothers slept on their backs, babies were more likely to be quietly asleep.

The research was carried out by researchers in New Zealand and involved placing ECG monitors on mothers in the third trimester.

Despite the non-entity of significant results, sleeping on your back for a pregnant mother may compress major blood vessels and this may change the baby’s heart rate.

But don’t role out the possibility that in years to come, the media may use this piece of research to bulk up an article fronted by the headline “Sleeping on your back gives you calmer babies”, using the tenuous link that the blood flow and pressure of stressed, tense pregnant women to the baby was reduced when they slept on their backs.

There are 7 billion in this planet and using a study sample size of twenty nine women is also ridiculously small. If 1 of those women had experienced complications then the headline might have been “3% of all foetuses at risk”!

Just sleep in a comfortable position. And get lots of sleep. And go see your GP for advice instead of seeking health advice from a newspaper.

You know how media spin works.

What your breakfast reveals about media companies

Wordsmiths would tell you that the origins of the word “breakfast” lie in the words “break” and “fast”. Then again, you wouldn’t actually need an expert to tell you the combined word comes from its intention – to end the fasting period. What fast? Presumably in Roman days the fast represented the period from after sunset to sunrise, where people had to endure going without food in the cold of night, at a time when the thinking was “Eat as much as you can during the day, while you can”. The line of thinking about what to eat for breakfast certainly does vary from place to place. Some believe that after a period of doing without food – okay, so a few hours every evening now after a “Just Eat” gorge of Indian takeaway washed down with bottles of Kingfisher can hardly be called a fast anymore –  the body has to stock up on its resources. Enter the full English breakfast; sausages, bacon, eggs, tomatoes, beans (mustn’t forget your greens), black pudding – everything you wanted to eat during the day, presented to you literally on a plate, in case you miss the opportunity to eat later on. In contrast, there are others of the thinking that after an overnight period of doing without, the body cannot be forced into what is a gorge. Just as someone who is parched and dehydrated has to resist the natural urge to guzzle down water when presented with it, breakfast, some think, is only a primer for a heavy lunch. Hence the idea of a light continental croissant, a little way of appeasing the hungry body but regulating the intake of food so the body is not lulled into a yo-yo pattern of starvation and gorging that is more typical of eating disorders.

Makes sense? Both points of view actually do, despite the conflicts about whether or not to eat heavy first thing in the morning. But to further complicate the issue, a third group believes that since your body, when at rest, will require resources to draw on when you are asleep, then it makes perfect sense to load up with a heavy meal as the last meal of the day. Start light, finish heavy. Viewed in the context, it makes sense too.

If there is any one consistent factor about diet, it is probably that the debate, ideas and media reports will continue into the future, and ideas will come and go and come back again. The fad for various diets has sold books and filled magazine columns and given the media lots to write about, which is great for the industry because media is not a sector that relies on bringing to you information that is necessarily correct, it is a sector that relies on attracting readership and human traffic in order to build up a reader base which it leverages to companies to sell advertising. Advertising is what drives media, not the exposition or exploration of facts. Hence media companies will present information that they feel is of interest and will hook in readers. It doesn’t necessarily have to be substantiated, as long as there is a fellow source to mention, as if the validation of facts had been corroborated by them.

Where do research scientists fit in this grand scheme of things? There are various kinds of research scientists, ones that truly explore the world in order to further it, and others who conduct investigation in order that it may be latched on to by the media in reports. Ultimately it comes down to who is funding the work. Funded by a company such as Cancer Research? The investigative research conducted by such research scientists is likely to be subject to stringer validation. Funded by a pharmaceutical company? The data obtained by such research needs to be handled carefully in order that the outcomes are not flawed or biased towards any products the company is producing.

In other words, if a pharmaceutical company is working on producing a medical product that is, for example, has seaweed as an active ingredient, then the research must not be conducted in a way that only shows the positive benefits of seaweed; research that only gives supposed scientific validation to a pre-determined result.

Bias is all too easy to spot when the links are direct, when a pharmaceutical company employs scientists. But what happens when the grand paymaster is the media company?

Hang on, I hear you say. Why would a media company, perhaps a newspaper, employ a group of scientists? And how could they get away with it?

The end product for a pharmaceutical company is a medical one. The end product for a newspaper is news, and the research scientists are there to provide it.

The group of scientists don’t necessarily need to be under permanent employ, just occasional contract work when there are lull periods in the news. And the work that they do is not necessarily related to what is in the article that is published anyway. Tenuous links are exploited to maximise the draw of a headline.

This is how it works:

A shark is a fish. A whale is a fish. Your newspaper reports that there is the possibility that sharks could become whales.

And that’s it.

A media company – newspaper, magazine, channel, web agency – can hire research scientists to lend credibility to semi-extravagant claims.

As long as there is another attributable source, or somewhere to dismiss the evidence – easily done by mentioning “It is generally accepted that …” or “Common convention holds that …” before launching into the juicy bit – the bit that spins things out, through a long process by which the receiver, either reader or viewer, has hopefully forgotten what the gist of the argument was in the first place – everything can passed off. In fact, it is a psychological trick – the receiver keeps following in the hope of being able mentally ordering the great influx of information.

Ever watched a BBC drama series? After six episodes, numerous disjointed flashbacks, the final  episode always seems a bit of a letdown because you realise everything was obvious and the in-betweens were just filler bits to spin things out.

I digress. But returning to the point, media companies can hire research scientists on an occasional basis. Some may even do so, and have a scientist for full time hire as a generator of scientific news.

A direct link between a media agency and a research scientist may sound implausible. But think of the UK’s Channel 4 programme, Embarrassing Bodies, where a team of four doctors go around examining people, dispensing advice, running health experiments in a format of an hour-long slot punctuated by two minutes of advertisements for every thirteen minutes of the programme.

If the media company does not want its links to be so obvious, it can dilute them progressively through the form of intermediary companies.

For example, ABC newspaper hires DEF company to manage its search engine optimisation campaign. DEF hires GHI creative media, who hire  JKL, a freelance journalist who knows Dr MNO, who conducts research for hire. Eventually MNO’s “research” ends up in the ABC newspaper. If it proves to be highly controversial or toxic to some extent, ABC’s links to MNO are very, very easy to disavow.

So when the media recently reported that scientists say skipping the morning meal could be linked to poorer cardiovascular health, should we pay any heed to it?

The research findings revealed that, compared with those who had an energy-dense breakfast, those who missed the meal had a greater extent of the early stages of atherosclerosis – a buildup of fatty material inside the arteries.

But the link been skipping breakfast and cardiovascular health is tenuous at best, as the articles themselves admit.

“People who skip breakfast, not only do they eat late and in an odd fashion, but [they also] have a poor lifestyle,” said Valentin Fuster, co-author of the research and director of Mount Sinai Heart in New York and the Madrid-based cardiovascular research institute, the CNIC.

So a poorer lifestyle gives negative impact to your health. A poorer lifestyle causes you to miss breakfast. Sharks do become whales.

This supposed link between skipping breakfast and cardiovascular health was published in the Journal of the American College of Cardiology, and the research had partly been funded by the Spanish bank Santander. The health and diets of 4,052 middle-aged bank workers, both men and women, with no previous history of cardiovascular disease were compared.

You can bet that on another day where news is slow, someone will roll out an “Eating breakfast on the move harms your health” headline. Nothing to do with the way you move and eat, it is simply because you have a stressful lifestyle that impacts on your health which forces you to eat on the go. But it was a link and headline, a “sell” or bait that drew you in to either purchase a newspaper or magazine, watch a programme, or spend some dwell time on a site.

And that’s how media works.

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.