The financial considerations of investing in medicine and medical research

BBC News reports that a drug that would reduce the risk of HIV infection would result in cost savings of over £1bn over 80 years. Pre-exposure prophylaxis, or Prep, would reduce infection and hence lower the treatment costs for patients in the long term.

The catch? There is one. It’s the long term.

The cost of the treatment and prevention is such that its provision for the first twenty years – bundling together the cost of medical research and production of medicine – would result in a financial loss, and parity would only be achieved after a period of about thirty to forty years; this period is hard to define because it is dependent on what the drug would cost in the future.

Prep combines two anti-HIV drugs, emtricitabine and tenofovir. The medical trials behind it have concluded it has an effective rate of over one in five when it comes to protecting men who have unprotected sex with men from HIV infection. The exact figure is close to 86%.

Prep can be used either on a daily basis, or on what has been termed a sexual event basis – using it for two days before, during and after periods of unprotected sex.

The research model analysed the potential impact of Prep and found that it could reduce infection rates by over a quarter. The cost of the treatment itself, comparative to the cost of treating infection, would result in a saving over one billion pounds over eight years.

However, it does raise a few ethical questions. If the National Health Service is aiming to be a sustainable one – and one of the aims of sustainability is to empower citizens to take responsibility for their own health –  shouldn’t it be considering less about how it will balance the books, but spend more on education for prevention in the first place? The cost of producing Prep on the NHS would be £19.6 billion over 80 years; while the estimated savings from treatment would be £20.6 billion over the same period. Educating people not to have unprotected sex with those at the risk of HIV arguably would result in a higher saving over a lower time period. Perhaps the NHS should consider ways of reducing cost more significantly, rather than latching on to a cheaper prevention drug immediately. If consumer behaviour is not going to change, symptoms are still going to surface, and the provision of Prep on the NHS may only encourage less self-regulation and awareness.

The role of pharmacy in healthcare

Pharmacists are experts on the actions and uses of drugs, including their chemistry, their formulation into medicines and the ways in which they are used to manage diseases. The principal aim of the pharmacist is to use this expertise to improve patient care. Pharmacists are in close contact with patients and so have an important role both in assisting patients to make the best use of their prescribed medicines and in advising patients on the appropriate self-management of self-limiting and minor conditions. Increasingly this latter aspect includes OTC prescribing of effective and potent treatments. Pharmacists are also in close working relationships with other members of the healthcare team –doctors, nurses, dentists and others –where they are able to give advice on a wide range of issues surrounding the use of medicines.

Pharmacists are employed in many different areas of practice. These include the traditional ones of hospital and community practice as well as more recently introduced advisory roles at health authority/ health board level and working directly with general practitioners as part of the core, practice-based primary healthcare team. Additionally, pharmacists are employed in the pharmaceutical industry and in academia.

Members of the general public are most likely to meet pharmacists in high street pharmacies or on a hospital ward. However, pharmacists also visit residential homes (see Ch. 49), make visits to patients’own homes and are now involved in running chronic disease clinics in primary and secondary care. In addition, pharmacists will also be contributing to the care of patients through their dealings with other members of the healthcare team in the hospital and community setting.

Historically, pharmacists and general practitioners have a common ancestry as apothecaries. Apothecaries both dispensed medicines prescribed by physicians and recommended medicines for those members of the public unable to afford physicians’fees. As the two professions of pharmacy and general practice emerged this remit split so that pharmacists became primarily responsible for the technical, dispensing aspects of this role. With the advent of the NHS in the UK in 1948, and the philosophy of free medical care at the point of delivery, the advisory function of the pharmacist further decreased. As a result, pharmacists spent more of their time in the dispensing of medicines –and derived an increased proportion of their income from it. At the same time, radical changes in the nature of dispensing itself, as described in the following paragraphs, occurred.

In the early years, many prescriptions were for extemporaneously prepared medicines, either following standard ‘recipes’from formularies such as the British Pharmacopoeia (BP) or British Pharmaceutical Codex (BPC), or following individual recipes written by the prescriber (see Ch. 30). The situation was similar in hospital pharmacy, where most prescriptions were prepared on an individual basis. There was some small-scale manufacture of a range of commonly used items. In both situations, pharmacists required manipulative and time-consuming skills to produce the medicines. Thus a wide range of preparations was made, including liquids for internal and external use, ointments, creams, poultices, plasters, eye drops and ointments, injections and solid dosage forms such as pills, capsules and moulded tablets (see Chs 32–39). Scientific advances have greatly increased the effectiveness of drugs but have also rendered them more complex, potentially more toxic and requiring more sophisticated use than their predecessors. The pharmaceutical industry developed in tandem with these drug developments, contributing to further scientific advances and producing manufactured medical products. This had a number of advantages. For one thing, there was an increased reliability in the product, which could be subjected to suitable quality assessment and assurance. This led to improved formulations, modifications to drug availability and increased use of tablets which have a greater convenience for the patient. Some doctors did not agree with the loss of flexibility in prescribing which resulted from having to use predetermined doses and combinations of materials. From the pharmacist’s point of view there was a reduction in the time spent in the routine extemporaneous production of medicines, which many saw as an advantage. Others saw it as a reduction in the mystique associated with the professional role of the pharmacist. There was also an erosion of the technical skill base of the pharmacist. A look through copies of the BPC in the 1950s, 1960s and 1970s will show the reduction in the number and diversity of formulations included in the Formulary section. That section has been omitted from the most recent editions. However, some extemporaneous dispensing is still required and pharmacists remain the only professionals trained in these skills.

The changing patterns of work of the pharmacist, in community pharmacy in particular, led to an uncertainty about the future role of the pharmacist and a general consensus that pharmacists were no longer being utilized to their full potential. If the pharmacist was not required to compound medicines or to give general advice on diseases, what was the pharmacist to do?

The need to review the future for pharmacy was first formally recognized in 1979 in a report on the NHS which had the remit to consider the best use and management of its financial and manpower resources. This was followed by a succession of key reports and papers, which repeatedly identified the need to exploit the pharmacist’s expertise and knowledge to better effect. Key among these reports was the Nuffield Report of 1986. This report, which included nearly 100 recommendations, led the way to many new initiatives, both by the profession and by the government, and laid the foundation for the recent developments in the practice of pharmacy, which are reflected in this book.

Radical change, as recommended in the Nuffield Report, does not necessarily happen quickly, particularly when regulations and statute are involved. In the 28 years since Nuffield was published, there have been several different agendas which have come together and between them facilitated the paradigm shift for pharmacy envisaged in the Nuffield Report. These agendas will be briefly described below. They have finally resulted in extensive professional change, articulated in the definitive statements about the role of pharmacy in the NHS plans for pharmacy in England (2000), Scotland (2001) and Wales (2002) and the subsequent new contractual frameworks for community pharmacy. In addition, other regulatory changes have occurred as part of government policy to increase convenient public access to a wider range of medicines on the NHS (see Ch. 4). These changes reflect general societal trends to deregulate the professions while having in place a framework to ensure safe practice and a recognition that the public are increasingly well informed through widespread access to the internet. For pharmacy, therefore, two routes for the supply of prescription only medicines (POM) have opened up. Until recently, POM medicines were only available on the prescription of a doctor or dentist, but as a result of the Crown Review in 1999, two significant changes emerged.

First, patient group directions (PGDs) were introduced in 2000. A PGD is a written direction for the supply, or supply and administration, of a POM to persons generally by named groups of professionals. So, for example, under a PGD, community pharmacists could supply a specific POM antibiotic to people with a confirmed diagnostic infection, e.g. azithromycin for Chlamydia.

Second, prescribing rights for pharmacists, alongside nurses and some other healthcare professionals, have been introduced, initially as supplementary prescribers and more recently, as independent prescribers.

The council of the Royal Pharmaceutical Society of Great Britain (RPSGB) decided that it was necessary to allow all members to contribute to a radical appraisal of the profession, what it should be doing and how to achieve it. The ‘Pharmacy in a New Age’consultation was launched in October 1995, with an invitation to all members to contribute their views to the council. These were combined into a subsequent document produced by the council in September 1996 called Pharmacy in a New Age: The New Horizon. This indicated that there was overwhelming agreement from pharmacists that the profession could not stand still.

The main output of this professional review was a commitment to take forward a more proactive, patient-centred clinical role for pharmacy using pharmacists’ skills and knowledge to best effect.

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.

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.

Wort on earth: St John’s wort and its use as an anti-depressant

St John’s wort, also known as Hypericum perforatum, has for years been used as a treatment for nerves. Its use dates back to over hundreds of years. In medieval times, its reputation as a remedy for wounds, as well as sores, burns, bruises and nerve pains, gave it its popularity. Evil spirits were also thought to be repelled by it, and the insane would often drink an infusion of St John’s wort in an attempt to ward off madness. In modern times, St John’s wort has been used to manage seasonal affective disorder (SAD), improve sleep quality and improve mood.

St John’s wort is a tall wild plant and the flowers are yellow. It is often found growing wild in many parts of the world including Europe, Asia and the US, and is named after St John the Baptist as the traditional collection day was on St John’s Day, June 24th.

It is sometimes used by people with mild to moderate depression as an alternative to anti-depressants. It is in this group that scientists believe the best effects of St John’s wort are best demonstrated. We have seen in earlier posts that less severe depression, where sufferers are not in immediate danger, may not require anti-depressants or other medication and if they are not necessary, it is best not to use them as they can lead to addiction or have other side effects.

St John’s wort has been one of the most well-researched herbal medications. While the results of its use are not necessarily consistent, studies have demonstrated that if it is taken in the right form and with the correct dosage, it can have effective results on sufferers with mild to moderate depression. Scientists believe that it works in a similar way to SSRI drugs. SSRI (“selective serotonin re-uptake inhibitor”) drugs lift the levels of certain brain chemicals, such as serotonin, dopamine and noradrenalin, and in doing so make the user feel more positive. Drugs such as Prozac have the same effect. For mild to moderate depression sufferers this sort of herbal treatment is usually enough.

While St John’s wort is available as a traditional medicine, it is classed under “herbal” alternatives which are not necessarily regulated by law. This means that different variants are available, all with different consistencies. If you are considering this as a non-medical alternative, and are slightly puzzled by the variants on offer, it is best to start off with one that has been certified as a Traditional Herbal Remedy, or THR. The symbol for this is a leaf in a black square on the label, and is a useful starting point in guaranteeing the safety and purity of the product.
Effective products will contain a concentration of the active ingredient, hypericin, of about 0.3%. And a good guideline is a product that has a dose of around 300 – 900 mg of hypericin. Start with the median dosage of around 600mg and then adjust it according to how you feel.

It must be emphasised that the usage of St John’s wort has to be considered with the same caution of any prescription SSRI anti-depressants that it is meant to substitute. This means you should use it carefully, and not think that just because it is a natural herbal remedy, taking it – either within the guidelines or above the recommended threshold – will not do you any harm. The use of St John’s wort can cause interference with other drugs and lead to complications. St John’s wort may interfere with statins, blood thinners and also things like oral contraceptives like the pill. Possible side effects could also include nausea, skin allergies and hypersensitivity to sunlight. St John’s wort should also not be taken with drugs prescribed for depression, as that would result in an overdose of hypericin. If you are considering using it as a herbal substitute to reduce mild or moderate depression, it would be a good idea to check with your GP, or consult any other medical practictioner so you have some idea of the associated risks.

St John’s wort, in Germany, is classed as a prescription drug but outside of Germany, it can be readily bought at pharmacists without the need for a prescription. Is it more advantageous to the average person that it is classed as a herbal remedy?

On the face of it, yes – being classed as a herbal remedy means that depression sufferers may try it first before going to their GP. If the remedy works for them, this means that they are more likely to avoid addiction to anti-depressants, and the side effects of the latter. They are also more likely to avoid requiring long-term medication due to the build-up of anti-depressant resistance. Furthermore, users of St John’s wort need not visit their GP to obtain a prescription, so there is a time saving for the GPs and more appointments can be made available.

However, one may argue that its listing as an alternative health herbal remedy only complicates matters. St John’s wort is found in the form of tablets, teas and tincture. Herbal remedies, like vitamins, cannot make the claim that they can cure a certain illness, but manufacturers can claim they are good for certain purposes. Therefore, St John’s wort can be said to “be good for mild depression”, but not cure it. But this is not the only disclaimer found in the text in St John’s wort products. In trying to absolve itself of litigious claims, it is not uncommon to see on the labelling that St John’s wort should not be taken if:

  • you are under 18 years of age
  • you are pregnant or breastfeeding
  • you are allergic to any of the ingredients
  • you are lactose intolerant
  • your skin is exceptionally sensitive to sunlight (photosensitive)
  • you are having light treatment (phototherapy) for any condition
  • you are suffering from depression

The printed label may also advise you that it may also interfere with medicines such as:

  • fentanyl, propofol, sevoflurane, and midazolam (anaesthetics/pre-operative medicines)
  • tramadol (an analgesic)
  • erythromycin, clarithromycin and telithromycin (antibiotics)
  • itraconazole and voriconazole (antifungals)
  • artemether and lumefantrine (antimalarials)
  • rasagiline (an anti-Parkinson’s medicine)
  • aripiprazole (an antipsychotic medicine)
  • buspirone (an anxiolytic)
  • aprepitant (used to treat post-operative vomiting)
  • butobarbital and phenobarbital (barbiturates)
  • methyl phenidate (a central nervous system or CNS stimulant)
  • exemestane (a hormone antagonist)
  • eplerenone (a diuretic)
  • lansoprazole and omeprazole (proton pump inhibitors)
  • theophylline (a bronchodilator)
  • gliclazide (an antidiabetic medicine)

A longer, more detailed list may advise that St John’s wort should not be used for:

  • All medicines for depression/anxiety – Amitriptyline, clomipramine, moclobemide, citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, duloxetine, venlafaxine
  • All hormonal replacement therapy treatments – HRT tablets, patches and gels
  • All medicines for thinning the blood (anticoagulants) – Warfarin, acenocoumarol
  • All medicines for epilepsy – Carbamazepine, phenobarbitone, phenytoin, primidone, sodium valproate
  • All immunosuppressant medicines – Ciclosporin, tacrolimus
  • All medicines for HIV infections – Amprenavir, atazanavir, darunavir, fosamprenavir, indinavir, lopinavir, nelfinavir, ritonavir, saquinavir, tipranavir, efavirenz, nevirapine, delavirdine
  • Cholesterol medicines such as Simvastatin, atorvastatin
  • Cancer medicines such as Irinotecan, dasatinib, erlotinib, imatinib, sorafenib, sunitinib, etoposide, mitotane
  • Heart disease medicines- Digoxin, ivabradine, amiodarone
  • Migraine treatments – Almotriptan, eletriptan, frovatriptan, naratriptan, rizatriptan, sumatriptan, zolmitriptan
  • High blood pressure treatments – Amlodipine, nifedipine, felodipine, verapamil
  • A medicine for regulating mood – Lithium
  • A thyroid hormone – Thyroxine

The list of precautions and possible medication conflict is so long, that one may find sufferers who are actually already on medication may decide against switching or downgrading to St John’s wort.

The dosing and safety of St John’s Wort has – in addition – not been studied in children/ adolescents below 18 years and hence the safety of use is not established.