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the myth of holistic medicine

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It does get my goat rather that so-called naturopaths, in spite of having varied and often contradictory therapies, love to call themselves practitioners of holistic medicine. It’s a feel-good term that, like spirituality, seems to make a virtue of its own vagueness. Of course, holistic medicine can be defined in a superficial sense – it’s treating the whole person, right? But how does that work in reality, and how do naturopaths manage it?

Well, the obvious answer is, they don’t. It’s nothing more than a propaganda term.

Clearly, holistic, whole-person treatment would be fabulous if it could be achieved, but it would entail not only knowing the whole anatomy and physiology of the client, but her psychology and her entire medical history from birth, and even before. Would there be any other way of treating ‘the whole person’?

Personalised medicine may in fact become the way of the future – I’ve heard as much – but that has nothing to do with naturopathy. That has to do with science – your personal microbiome, your heart rhythms, your cholesterol, your triglycerides, your lung function, your bowel movements, your bone density (not to mention your sequenced genome), taking more responsibility for those things as far as is possible and in co-operation with healthcare providers. Naturopathy is something else altogether – it’s about herbs instead of pills (unless they’re homeopathic), ‘age-old’ treatments such as reflexology and TCM rather than invasive tests and vaccinations, getting in tune with or detoxifying your body rather than taking impersonal prescriptions to your local impersonal pharmacist.

So the question is – how did taking an entirely chemical herbal treatment from a naturopath come to seem more holistic than taking a chemical such as theophylline prescribed by your specialist?

I don’t see how a naturopath would or could treat a client as a ‘whole person’ any more than a conventional GP could. Limited info, limited time, it’s the same whether your treatments are science-based or traditional. But I do know at least one happy client who swears by her naturopath, who really does treat the whole person, unlike the medical establishment, according to her. I haven’t pressed her to explain this, but I have my own nasty theory. The woman is clearly obese, and wouldn’t take kindly to being told so, and she’s found a practitioner whose greatest skill is to tell her everything but what she most needs to hear. At last, someone who really understands her, who really listens and accepts her own expertise about her own body. And it must be said that many doctors, full to the brim of years and years of training and practice, do sometimes treat their clients in an offhand or specimen-like way. The psychological effects of healthcare practice are surely underestimated. So many people, but especially the unhealthy, want to be seen as, or made, whole. ‘Holistic medicine’ therefore, makes for a very effective propaganda label.

Yet many treatments that eagerly make use of the holistic banner are about as far from being individualised as can be imagined.

Acupuncture supposedly manipulates your ‘chi’ or ‘qi’, a system of energy flow that, if it existed, could be individualised to the client. Some clients might have a different chi from others, just as we have different blood types, different hormonal levels, different cholesterol levels, different insulin levels, etc, all of which can be measured. But acupuncturists don’t measure our chi levels and give us a read-out. Why ever not? Surely that would be the holistic, personalised thing to do. The fact is, nobody, in the supposedly thousands of years of acupunctural history, has ever thought to isolate this energy force and describe its wave function or the molecules or particles associated with its action. Nobody has even shown the slightest curiosity about the physical properties of what is advertised as a fundamental energy source in humans and perhaps all other living things. That’s fucking amazing – the only amazing thing I can say about acupuncture. Yet, apparently, there are particular points in the body where chi is more abundant, and that’s where you should stick your needles, and at a certain depth, otherwise you won’t be in touch with the chi. So acupuncture depends entirely upon chi being a physical, measurable entity…

Say no more. Your chi can’t be personalised and made a part of your whole-person profile because it doesn’t exist.

Homeopathy also likes to travel under the holistic banner, and you’ll find it advertised in all those brochures featuring glowingly healthy individuals, often dressed in white, meditating or staring lovingly at the sky-spirits. The trouble is, homeopathic treatments are designed to treat the illness, not the individual. The bogus ‘law of similars’ involves swallowing pills which are supposed to contain material ‘like’ whatever it was that made you sick. If that doesn’t sound very scientific, don’t blame me. It’s obviously a problem if you don’t know what made you sick, but the solution is simple. Just pay attention to your symptoms – say itchy skin or funny-coloured urine – and take pills containing a substance that produces similar symptoms. But hang on, won’t that just make you more sick? No, not at all, because the offending substance will be diluted to infinitesimal proportions. Okay, but won’t that render it useless? Ah but you’re clearly unaware of the ‘law of infinitesimals’ which defines a substance as increasing in potency the more it’s diluted. Welcome to the world of homeopathy, where the more truth is watered down, the more obviously true it becomes.

But the point I wanted to make here, before becoming entranced by the homeopathic mindset, was a simple one. Far from treating clients as ‘whole people’, it is solely concerned with physical symptoms. A homeopathic treatment would work just as well on a horse or a hedgehog as on a human. The client’s humanity, let alone her particular history or psychological make-up, isn’t a factor. It’s as far removed from holistic medicine as you can get.

I could go on – reflexology, iridology, reiki, chiropractic – these are all bogus, and the fact that they all jump eagerly onto the holistic bandwagon is further evidence of their crappiness. Holistic medicine is an impossible ideal, though personalised medicine, where you take personal responsibility to educate yourself about and keep records of your own health and physical maintenance, in collaboration with health specialists, is a great way to go. And that involves a lot more than just holding hands in a smiley circle.

Written by stewart henderson

March 28, 2015 at 12:38 pm

on vaccines and type 1 diabetes, part 3 – causes

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As mentioned earlier, it’s not precisely known what causes diabetes type 1, more commonly known as childhood diabetes. There’s a genetic component, but it’s clearly environmental factors that are leading to the recent apparently rapid rise in this type.

I use the word ‘apparent’ because it’s actually hard to put figures on this rise, due to a paucity of historical records. This very thorough and informative article, already 12 years old, from the ADA (American Diabetes Association – an excellent website for everything to do with the evidence and the science on diabetes), tries to gather together the patchy worldwide data to cover the changing demography and the evolving disease process. At the beginning of the 2oth century childhood diabetes was rare but commonly fatal (before insulin), and even by mid-century no clear rise in childhood incidence had been recorded. To quote the article, ‘even by 1980 only a handful of studies were available, the “hot spots” in Finland and Sardinia were unrecognized, and no adequate estimates were available for 90% of the world’s population’. Blood glucose testing in the early 20th century was far from being as simple a matter as it is today, and the extent of undiagnosed cases is hard to determine.

There’s no doubt, however, that in those countries keeping reliable data, such as Norway and Denmark, a marked upturn in incidence occurred from the mid 20th century, followed by a levelling out from the 1980s. Studies from Sardinia and the Netherlands have found a similar pattern, but in Finland the increase from mid-century has been quite linear, with no levelling out. Data from other northern European countries and the USA, though less comprehensive, show a similar mid-century upturn. Canada now (or as of 12 years ago) has the third highest rate of childhood diabetes in the world. The trend seems to have been that many of the more developed countries first showed a sharp increase, followed by something of a slow-down, and then other countries, such as those of central and eastern Europe and the Middle East, ‘played catch-up’. Kuwait, for example, had reached seventh in the world at the time of the article, confounding many beliefs about the extent of the disease’s genetic component.

The article is admirably careful not to rush to conclusions about causes. It may be that a number of environmental factors have converged to bring about the rise in incidence. For example, it’s known that rapid growth in early childhood increases the risk, and children do in fact grow faster on average than they did a century ago. Obesity may also be a factor. Baffled researchers naturally look for something new that has entered the childhood environment, either in terms of nutrition (e.g. increased exposure to cow’s milk) or infection (enteroviruses). Neither of these possibilities fit the pattern of incidence in any obvious way, though there may be subtle changes in antigenicity or exposure at different stages of development, but there’s scant evidence of these.

Another line of inquiry is the possible loss of protective factors, as part of the somewhat vague but popular ‘hygiene hypothesis’, which argues that lack of early immune system stimulation creates greater susceptibility, particularly to allergies and asthma, but perhaps also to childhood diabetes and other conditions. The ADA article has this comment:

Epidemiological evidence for the hygiene hypothesis is inconsistent for childhood type 1 diabetes, but it is notorious that the NOD mouse is less likely to develop diabetes in the presence of pinworms and other infections. Pinworm infestation was common in the childhood populations of Europe and North America around the mid-century, and this potentially protective exposure has largely been lost since that time.

The NOD (non-obese diabetic) strain of mice was developed in Japan as an animal model for type 1 diabetes.

The bottom line from all this is that more research and monitoring of the disease needs to be done. Type 1 diabetes is a complex challenge to our understanding of the human immune system, and of the infinitely varied feedback loops between genetics and environment, requiring perhaps a broader questioning and analysis than has been applied thus far. Again I’ll quote, finally, from the ADA article:

In conclusion, the quest to understand type 1 diabetes has largely been driven by the mechanistic approach, which has striven to characterize the disease in terms of defining molecular abnormalities. This goal has proved elusive. Given the complexity and diversity of biological systems, it seems increasingly likely that the mechanistic approach will need to be supplemented by a more ecological concept of balanced competition between complex biological processes, a dynamic interaction with more than one possible outcome. The traditional antithesis between genes and environment assumed that genes were hardwired into the phenotype, whereas growth and early adaptation to the environment are now viewed as an interactive process in which early experience of the outside world is fed back to determine lasting patterns of gene expression. The biological signature of each individual thus derives from a dynamic process of adaptation, a process with a history.

However, none of this appears to provide any backing for those who claim that a vaccine is responsible for the increased prevalence of the condition. So let’s wade into this specific claim.

It seems the principle claim of the anti-vaxxers is that vaccines suppress our natural immune system. This is the basic claim, for example, of Dr Josef Mercola, a prominent and heavily self-advertising anti-vaxxer whose various sites happen to come up first when you combine and google key terms such as ‘vaccination’ and ‘natural immunity’. Mercola’s railings against vaccination, microwaves, sunscreens and HIV (it’s harmless) have garnered him quite a following among the non compos mentis, but you should be chary of leaping in horror from his grasp into the waiting arms of the next site on the list, that of the Vaccination Awareness Network (VAN), another Yank site chock-full of of BS about the uselessness of and the harm caused by every vaccine ever developed, some of it impressively technical-sounding, but accompanied by ‘research links’ that either go nowhere or to tabloid news reports. Watch out too for the National Vaccination Information Centre (NVIC), another anti-vax front, full of heart-rending anecdotes which omit everything required to make an informed assessment. The best may seem to lack conviction, being skeptics and all, but it’s surely true that the worst are full of passionate intensity.

There is no evidence that the small volumes of targeted antigens introduced into our bodies by vaccines have any negative impact on our highly complex immune system. This would be well-nigh impossible to test for, and the best we might do is look for a correlation between vaccination and increased (or decreased) levels of disease incidence. No such correlation has been found between the MMR vaccine and diabetes, though this Italian paper did find a statistically significant association between the incidence of mumps and rubella viral infections and the onset of type 1 diabetes. Another paper from Finland found that the incidence of type 1 diabetes levelled out after the introduction of the MMR vaccine there, and that the presence of mumps antibodies was reduced in diabetic children after vaccination. This is a mixed result, but as yet there haven’t been any follow-up studies.

To conclude, there is just no substantive evidence of any kind to justify all the hyperventilating.

But to return to the conversation with colleagues that set off this bit of exploration, it concluded rather blandly with the claim that, ‘yes of course vaccinations have done more good than harm, but maybe the MMR vaccine isn’t so necessary’. One colleague took a ‘neutral’ stance. ‘I know kids that haven’t been vaccinated, and they’ve come to no harm, and I know kids that have, and they’ve come to no harm either. And measles and mumps, they’re everyday diseases, and relatively harmless, it’s probably not such a bad thing to contract them…’

But this is a false neutrality. Firstly, when large numbers of parents choose not to immunise their kids, it puts other kids at risk, as the graph at the top shows. And secondly, these are not harmless diseases. Take measles. While writing this, I had a memory of someone I worked with over twenty years ago. He had great thick lenses in his glasses. I wear glasses too, and we talked about our eye defects. ‘I had pretty well perfect vision as a kid,’ he told me, ‘and I always sat at the back of the class. Then I got measles and was off school for a fortnight. When I went back, sat at the back, couldn’t see a thing. Got my eyes tested and found out they were shot to buggery.’

Anecdotal evidence! Well, it’s well known that blindness and serious eye defects are a major complication of measles, which remains a killer disease in many of the poorest countries in the world. In fact, measles blindness is the single leading cause of blindness in those countries, with an estimated 15,000 to 60,000 cases a year. So pat yourself on the back for living in a rich country.

In 2013, some 145,700 people died from measles – mostly young children. In 1980, before vaccination was widely implemented, an estimated 2.6 million died annually from measles, according to the WHO.

Faced with such knowledge, claims to ‘neutrality’ are hardly forgivable.

Written by stewart henderson

January 30, 2015 at 6:02 pm

on vaccines and diabetes [type 1], part 2

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1.d                         42943_type1diabetes

Okay, before I look at the claimed dangers of vaccines in general, I’ll spend some time on diabetes, which, as mentioned, I know precious little about.

Diabetes mellitus, to use its full name, is a metabolic disease which causes blood sugar levels to be abnormally high. Some of the immediate symptoms of prolonged high blood sugar include frequent urination and feelings of hunger and thirst, but the disease can lead to many serious complications including kidney failure, heart disease and strokes. Diabetes is generally divided into type 1, in which the pancreas fails to produce enough insulin, and type 2, in which the body’s cells fail to process the insulin produced. Type 2, which accounts for some 90% of cases, can lead to type 1. There’s a third recognised type called gestational diabetes, a sudden-onset form occurring in pregnant women, which usually disappears after giving birth. As I’m not sure whether the claim about the MMR vaccine was related to type 1 or type 2, I’ll examine both.

type 1 diabetes and vaccination

A factsheet from Australia’s National Centre for Immunisation Research and Surveilance (NCIRS), a joint service of Westmead Hospital and Sydney University, and part of the World Health Organisation’s Vaccine Safety Net system of public information websites, summarises type 1 diabetes thus:

This is thought to be an autoimmune disease, where the immune system malfunctions to cause destruction of the insulin-producing cells in the pancreas. This is the usual type of diabetes in children, and requires treatment with insulin injections. Without insulin, people with Type 1 diabetes will die. Diabetes is thought to be due to an interaction between inherited and environmental factors, not all of which have been identified.

It goes on to describe an ‘unexplained’ increase in cases in Australia and many other (but not all) countries. There are regional variations in rates of increase, with higher rates in Northern European countries, lower in Asia and Africa, probably due to genetic factors. A number of  environmental factors that may also contribute to the incidence of the disease have been studied, including breast feeding, infections, immunisation, nitrates and vitamin D. Breast feeding slightly reduces the risk of contracting diabetes, and drinking cow’s milk may increase the risk. As to infections, few have been proven to cause diabetes – though one of them, interestingly, is mumps. Diabetes incidence is affected by seasonal variation, and it’s likely that seasonal viral infections may trigger the onset of diabetes in some people. It’s also possible that some strong medications may compromise the immune system and so cause or promote the onset of the disease. High levels of nitrates in drinking water have been shown to increase the incidence.

The factsheet is entitled ‘Diabetes and vaccines’, so it deals head-on with the vaccination issue, and its conclusion is uncompromising: ‘No, there is no evidence that vaccines cause diabetes’. It cites 15 separate studies in its reading list, three of which are authored or co-authored by a Dr John Classen. These three are the only studies to suggest a link. Here’s the NCIRS response:

There have been a number of studies which have searched for links between diabetes and immunisations. The only studies suggesting a possible increase in risk have come from Dr John B Classen. He found that if the first vaccination in children is performed after 2 months of age, there is an increased risk of diabetes. His laboratory study in animals also found that certain vaccines, if given at birth, actually decrease the risk of diabetes. This study was based on experiments using anthrax vaccine, which is very rarely used in children or adults. Dr Classen also compared diabetes rates with vaccination schedules in different countries, and interpreted his results as meaning that vaccination causes an increased risk of diabetes. This has been criticised because the comparison between countries included vaccines which are no longer used or used rarely, such as smallpox and the tuberculosis vaccine (BCG).

The study also failed to consider many reasons other than vaccination which could influence rates of diabetes in different countries. Later, in 2002, Dr Classen suggested that vaccination of Finnish children with Hib vaccine caused clusters of diabetes 3 years later, and that his experiments in mice confirmed this association.

Other researchers who have studied the issue have not verified Dr Classen’s findings. Two large population-based American studies failed to support an association between any of the childhood vaccines and an increased risk of diabetes in the 10 years after vaccination. The highly respected international Cochrane Collaboration reviewed all the available studies and did not find an increased risk of diabetes associated with vaccination.

Dr Classen, it turns out, is an established anti-vaxxer who has more recently tried to prove a link between vaccines and autism.

I should point out also that the above factsheet, which is a few years old, doesn’t include a more recent study, on a very large scale, which showed a significant decrease in the incidence of type 1 diabetes with various vaccinations, including MMR.

Classen, though, wasn’t looking at the MMR vaccine, his claims were about the Hib vaccine, which prevents invasive disease caused by the Haemophilus influenzae type b bacterium. It also significantly reduces the incidence of early childhood meningitis. The NCIRS factsheet doesn’t even mention MMR, stating that the vaccines being debated are Hib, BCG (for tuberculosis) and hepatitis B.

The Philadelphia Children’s Hospital’s Vaccine Education Centre (whose director, Dr Paul Offit, is one of the world’s leading immunologists and experts on vaccines), cites a long list of studies – have a look yourself – which together find no evidence of a causal connection between diabetes (mostly type 1) and various vaccines. I’ve yet to find any published studies, even poorly conducted ones, that claim a specific negative connection between the MMR vaccine and diabetes. If anybody out there can point me to such a study, I’d be grateful.

So, while I wait for someone to get back to me on this (ho, ho), I’ll explore what immunologists and epidemiologists are saying about the rise of type 1 diabetes in recent decades in my next piece.

Written by stewart henderson

January 23, 2015 at 5:11 pm

on vaccines and diabetes, part 1

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A picture lies better than 1000 words

A picture lies better than 1000 words

The other day, when I grumbled about anti-vaccination views during after-work drinks, a colleague said she was ‘semi-anti-vaccination’, specifically in relation to the connection between the MMR (measles, mumps and rubella) vaccine and diabetes. When I expressed skepticism, she challenged me on my knowledge of the science, which admittedly isn’t great – and I made matters look pretty bad for myself by egregiously claiming that children couldn’t be vaccinated before two years of age, instead of two months, a mistake I wouldn’t have made if I’d had kids of my own to vaccinate (or not), like most of my workmates.

When I inquired about this mysterious connection, I was curtly informed that it was nothing vague, but crystal clear causation. The link so often made between diabetes and increased sugar in our diets was bogus, I was told, because the timing didn’t make sense. Presumably the timing of the rise in diabetes did match the introduction of the vaccine, though such a correlation, if it exists, is far from proving causation. Proof would require that some component of the MMR vaccine was having a direct effect on our immune system in such a way as to increase susceptibility to the disease. If this were true, it would be absolutely sensational news, demanding domination of newspaper headlines worldwide. Extraordinary claims, as they say, require extraordinary evidence

Now, I must say that my sceptical antennae were immediately raised when I heard this claim, because I hadn’t heard it before, and as a regular reader of science magazines and relatively up-to-date popular science books, and a regular listener to science and scepticism podcasts, I’m reasonably sure I’m more scientifically literate than the average layperson. I’m aware, of course, of the vociferous anti-vaccination crowd and their claims of a causal connection between vaccines and autism, asthma and just about everything else that currently ails us. And I’m familiar too with the medical and immunisation experts, such as Doctors Paul Offit, Steve Novella and David Gorski, who are fighting the good fight against the tide of misinformation with evidence-based science. However, I’m perfectly willing to admit to a possible blind spot re diabetes, as it hasn’t personally affected me or anyone close to me.

I must say, though, that my ‘sceptical training’ enabled me to turn up this article from the Scientific American website within 5 seconds of looking (the first 4 seconds were spent avoiding the many innocuous-sounding websites that I knew to be fronts for anti-vaccination propaganda). The article reports on a review, conducted by the US institute of medicine, of over 1,000 published research studies on the adverse effects of eight vaccine types (including MMR). These vaccine types constitute the majority of vaccines against which claims have been made to the USA’s National Vaccine Injury Compensation Program (VICP). The report concludes that ‘vaccines are largely safe, and do not cause autism or diabetes’. Specifically on the MMR vaccine, the report had this to say:

The committee found that evidence “favors rejection” of discredited reports that have linked the MMR vaccine to autism and, along with the DTaP vaccine, to type 1 diabetes.

The DTaP vaccine covers three deadly bacterial diseases – diphtheria, tetanus and pertussis, or whooping cough.

End of story? Well, there’s always the possibility of a medical conspiracy, or of sloppy and complacent scientific analysis – doubtless influenced by Big Pharma. Needless to say, I’m very doubtful about this.

The final chapter of Dr Ben Goldacre’s landmark book Bad Science is entitled ‘The media’s MMR hoax’. It deals essentially with the claimed link between the vaccine and autism, but it has much of value to say about health scares in general and the role of the media in promoting them, either deliberately or inadvertently. For example, the MMR-autism connection scare was almost entirely confined to Britain at first, though it has since spread to the USA and Australia. It is almost unheard of in non-English-speaking countries, in spite of their using the exact same vaccine. Conversely, in France in the 1990s, the hepatitis B vaccine was being linked by some members of the public, supported by some in the media, to a rise in multiple sclerosis. No such link was being made outside of France, though the vaccine was the same everywhere. And there are many other examples to show that these scares are more culturally than scientifically based.

The anti-vaccination movement has a long and, it must be said, inglorious history, with the same sorts of arguments, and the same sorts of results, occurring from the beginning. Goldacre cites this interesting Scientific American article from 1888:

The success of the anti-vaccinationists has been aptly shown by the results in Zurich, Switzerland, where for a number of years, until 1883, a compulsory vaccination law obtained, and smallpox was wholly prevented– not a single case occurred in 1882. This result was seized upon the following year by the antivaccinationists and used against the necessity for any such law, and it seems they had sufficient influence to cause its repeal. The death returns for that year (1883) showed that for every 1,000 deaths two were caused by smallpox; In 1884 there were three; in 1885, 17, and in the first quarter of 1886, 85.

But, hey, measles is hardly smallpox, is it? It’s harmless. Is it worth disrupting our ‘natural immune system’ with vaccines just to protect ourselves against a few character-building ailments? Isn’t our over-reliance on vaccines potentially catastrophic for our bodies?

Well, I’ll delve more into such claims, and into diabetes more specifically, in my next piece.

Written by stewart henderson

January 23, 2015 at 3:27 pm

bronchiectasis updated

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Spiriva3   160px-Capsule_of_tiotropium_bromide_(with_puncture_holes_from_inhaler_device)      220px-%22Spiriva_HandiHaler%22-brand_dry_powder_inhaler_(open)

A lot has happened regarding my bronchiectasis recently, so I need to write about it here to learn more about the medication I’m on and what it might be doing to me.

I posted on this a couple of weeks ago, and that was an update on my first important post on the subject. But last time I wrote about an ‘acute exacerbation’, as the literature has it, of my condition, and what I believed was its cause. As it turned out, I was completely wrong. My doctor thought it might be viral, while I was privately convinced it wasn’t. I was given a doctor’s certificate and told to take a couple of days off, because I could benefit from the rest and because I might be infectious. I reluctantly did so, but was back at work the next day when I noticed a missed private call on my phone. It took me another day to respond, and it turned out to be my doctor telling me that my sputum tested positively for two viruses, influenza A and a human rhinovirus. Oh dear. I had to take more time off work, and my doctor told me not to worry about the antibiotics (it was a small course and I’d finished them anyway) and gave me a puffer with 60 doses of Alvesco®, which is ciclesonide, a synthetic corticosteroid which ‘prevents the release of substances in the body that cause inflammation’, according to this website. This was on top of the ingestible steroids, the subject of my previous post, though I didn’t go into detail about those pills, which I’ll rectify shortly. He also gave me a nasal spray for my rhinovirus, and arranged for me to have a consultation with a professor of Chesty Things at the RAH Chest Clinic.

So I’d like to look more carefully now at the medication I’ve been prescribed, apart from the antibiotics.

Firstly, Panafcortelone®, 30 white tablets each containing 25mg of prednisolone, an anti-inflammatory steroid much like ciclesonide. The worry about steroids is that they can interact with other medications to our detriment. They can also weaken our immune systems under some circumstances. I must say, though, that I’ve never yet had an adverse reaction to any medication I’ve taken. There’s quite a list of ailments that can be adversely affected by steroid use, no matter whether it’s prednisolone, ciclesonide or any other steroid, it seems. However, they shouldn’t be confused with anabolic steroids, notoriously misused by athletes.

Secondly, the nasal spray, Avamys®. Its active ingredient is Fluticasone furoate, yet another corticosteroid. According to the accompanying leaflet:

Avamys is used to treat symptoms of allergic rhinitis including stuffy, runny or itchy nose, sneezing, and watery, itchy or red eyes. The effects are usually felt within the first day, although some people will not feel the effects until several days after first taking it.

I took this medication regularly as prescribed for 5 or 6 days, then dropped off, as I obviously felt a lot better. It contains 30 sprays, and I wasn’t told to keep taking it to the end, as far as I can recall. The leaflet says that ‘once symptoms are controlled you may be able to decrease your dose to one spray in each nostril per day [down from 2]’. However it says elsewhere: ‘Do not stop using Amavys or change the dose without first checking with your doctor’. So I’ll try to keep taking it, though I don’t feel that I need it. My symptoms have always been mild compared to the description above.

Thirdly, the first medication prescribed by the Professor. Spiriva® is the brand name for capsules containing 18 micrograms of tiotropium (equivalent to 22.5 micrograms of tiotropium bromide, monohydrate), which are punctured and inhaled rather than orally ingested. It’s an anticholinergic bronchodilator used generally to manage COPD (chronic obstructive pulmonary disease), but not for acute exacerbations. Here’s what Wikipedia has to say on anticholinergics:

An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system. Anticholinergics inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary movement of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, etc. Anticholinergics are divided into three categories in accordance with their specific targets in the central and/or peripheral nervous system: antimuscarinic agents, ganglionic blockers, and neuromuscular blockers.

Tiotropium is described as a muscarinic receptor antagonist (MRA), which means that it blocks the muscarinic acetylcholine receptor, found in the cell membranes of some neurons and other cells. Muscarinic receptors are divided into types, and the one I’m concerned with is the M3 receptor, which plays a role in bronchoconstriction.

Finally, the second medication prescribed by the professor is Nuelin™, aka theophylline (200mg in a sustained release form), which causes the muscle lining of the airways to relax, according to the leaflet. It is used to treat asthma and other conditions where breathing is difficult. According to the netdoctor site,

Theophylline is a type of medicine called a xanthine bronchodilator. It is used to open the airways.
Theophylline causes the muscles surrounding the airways to relax by a mechanism that is not fully understood. This allows the airways in the lungs to open.
In conditions where the airways tighten, such as asthma or chronic obstructive pulmonary disease (COPD, eg emphysema and chronic bronchitis), it is difficult for air to get in and out of the lungs. By opening the airways, theophylline makes it easier to breathe.

So all these medications are to help me breathe easier, but of course I’m hoping to be cured, and the professor, a lively and interesting gentleman, informed me that my lung function test, like the previous one earlier this year, came up very positively. That’s to say, my lung functionality is above average even for a normal person, so I’m really not having any difficulty breathing at all, I think… In fact, the professor mentioned a lung capacity of 106%, which doesn’t make much sense to me, and I forgot to ask for clarification (I’ve never given a student more than 100% for any test I’ve given them).

In any case I’m to go back to him around April for another consultation, by which time all these medicaments will be consumed. I think the hope is that some of the blocked areas as revealed on my CT scan will be a little less blocked. So maybe there’ll be another CT scan in the pipeline. The professor took me on a tour of my lungs via the previous scan, pointing out that because the whole of the right lung is affected by little blockages all through it, no operation would be possible, as might be the case if it was one localised very badly blocked region. presumably he was talking about an operation to remove a section of the lung. The left lung is not affected at all, which is apparently quite unusual.

Anyway, I’m always the optimist, and I’m hoping that maybe I can yet be cleared of all this gunk, and so cured.

Written by stewart henderson

December 24, 2014 at 7:38 am

Posted in health, medicine

Tagged with , ,

a plague of mysteries

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Well, maybe not quite

Well, maybe not quite

I’m writing this because of some remarks made in the workplace which – well, let’s just say they set my sceptical antennae working overtime. They were claims made about the bubonic plague, of all things.

Bubonic plague, dubbed the Black Death throughout European history, is a zoonotic disease, which means it spreads from species to species – in this case from rodents to humans via fleas. Actually there are three types of ‘black death’ plagues, all caused by the enterobacterium Yersinia pestis, the others being the septicemic plague and the pneumonic plague. Other zoonotic diseases include ebola and influenza. Flea-borne infections generally attack the lymphatic system, as does bubonic plague. The term ‘bubonic’ comes from Greek, meaning groin, and the most well-known symptom of the disease were ‘buboes’, grotesque swellings of the glands in the groin and armpit.

It wasn’t called the Black Death for nothing (the blackness was necrotising flesh). It’s estimated that half the European population was wiped out by it in the 14th century. If untreated, up to two-thirds of those infected will be dead within four days. With modern antibiotic treatments, the mortality rate is of course greatly reduced. The broad-based antibiotic, streptomycin has proved very effective. Of course treatment should be immediate if possible, and prophylactic antibiotics should be given to anyone in contact with the infected.

The plague is first known to have stuck Europe in the sixth century, at the time of Justinian. The Emperor actually caught the disease but recovered after treatment. It’s believed that the death toll was very high, but little detail has been recorded. The fourteenth century outbreak appears to have originated in Mongolia, from where it spread through Mongol incursions into the Crimea. An estimated 25 million died in this outbreak from 1347 to 1352.  More limited outbreaks occurred in later centuries, and the last serious occurrences in Europe were in Marseille in 1720, Messina (Sicily) in 1743, and Moscow in 1770. However it emerged again in Asia in the nineteenth century. Limited for some time to south-west China, it slowly spread from Hong-Kong to India, where it killed millions of people in the early twentieth century. Infected rats were inadvertently transported to other countries by trading vessels, resulting in outbreaks in Hawaii and Australia. By 1959, when worldwide casualties dropped to under 200 annually, the World Health Organisation was able to declare the disease under control, but there was another outbreak in India in 1994, causing widespread panic and over 50 deaths.

So that’s a v brief history of the rise and fall of bubonic plague, but I’m interested in looking at early treatments and the discovery of its cause. For the fact is that, even in 1900, when the plague first came to Australia, there was no clear consensus among the experts as to its means of transmission, with many believing that it was as a result of contact with the infected. However, a growing body of evidence was showing a connection with epizootic infection in rats, and as it happened, work done by Australian bacteriologists Frank Tidswell, William Armstrong and Robert Dick, working for a new public health department in Sydney under Chief Medical Officer John Ashburton Thompson, established as a direct result of the plague outbreaks in Sydney from 1900 to 1925, contributed substantially to the modern understanding of Yersinia pestis and its spread from rats to humans. This Australian work was another step forward in the germ theory of disease, first suggested by the French physician Nicolas Andry in 1700, and built upon by many experimental and speculative savants over the next 150 years. The great practical success of John Snow’s work on cholera, followed by the researches of Louis Pasteur and Robert Koch, established the theory as mainstream science, but zoonotic infections, especially indirect ones where the infection passes from one species to another by means of a vector, have always been tricky to work out.

In fact it was in Hong Kong that the Yersinia pestis bacterium was identified as the culprit. A breakout of plague occurred there in the 1890s, and Alexandre Yersin, a bacteriologist who had worked under both Pasteur and Bloch, was invited to research the disease. He identified the bacterium in June 1894, at about the same time as a Japanese researcher, Kitasato Shibasaburo. The cognoscenti recognise that both men should share the honour of discovery. 

What is fascinating, though, is that the spread of plague from Asia in the 1890s to various ports of the world in the earlier 20th century was very different from the spread of earlier pandemics. Did this have anything to do with science or human practices? Well, what follows is drawn from by far the most comprehensive analysis of the disease I’ve found online, Samuel Cohn’s ‘Epidemiology of the Black Death and successive waves of plague’, in the Cambridge Journal of Medical History.

Cohn’s research and analysis casts credible doubt on the whole plague story, specifically the assumption that we’re dealing with one disease, from the sixth century through to modern outbreaks. He recounts the standard story of three separate pandemics, in the sixth century with a number of recurrences, ditto in the fourteenth century, and in the nineteenth. However, the epidemiology of the most recent pandemic, definitely attributed to Y Pestis and its carrier the Oriental rat flea, Xenopsylla cheopis, is substantially different from that of pandemics one and two, a fact which, according to Cohn, has been obscured by inaccurate analysis of the records. Cohn’s own analysis, it must be said, is fulsome, with 30 pages of references in a 68-page online essay. He doesn’t have a solution as to what caused the earlier pandemics, but he asks some cogent questions. For my own understanding’s sake, I’ll try to summarise the issues in sections.

speed of transmission

 Pandemic 3, if we can call it that, was a much slower mover than the previous two. It seems to have sprung up in China’s Yunnan province from where it reached Hong Kong in 1894. It was noted in the early 20th century that Y pestis was travelling overland at a speed of only 12 to 15 kilometres a year. This can be explained by the fact that Y pestis is a disease mainly of rats, though other rodents can also be infected, and rats don’t move far from their home territories. At this rate pandemic 3, even in a world of railways, cars, and dense human populations, would have taken some 25 years to cover the distance that pandemic 1 covered in 3 months. Pandemic 1 made its first appearance in an Egyptian port in 541 and quickly spread around the Mediterranean from Iberia to Anatolia. Within two years of first occurrence it had reached to the wastelands of Ireland and eastern Persia. Pandemic 2, believed to have originated in India, China or the Russian steppes, made its first European appearance in Messina, Sicily in 1347. Within three years it had impacted most of continental Europe, and had even reached Greenland. The fastest overland travel recorded for plague occurred in 664 (pandemic 1), when it took only ninety-one days to travel 385 kilometres from Dover to Lastingham (4.23 km a day)— far faster than anything seen from Y pestis since its discovery in 1894. Pandemic 2’s speed was similar, as Cohn details it:

like the early medieval plague, the “second pandemic” was a fast mover, travelling in places almost as quickly per diem as modern plague spreads per annum. George Christakos and his co-researchers have recently employed sophisticated stochastic and mapping tools to calculate the varying speeds of dissemination and areas afflicted by the Black Death, 1347–51, through different parts of Europe at different seasons. They have compared these results to the overland transmission speeds of the twentieth-century bubonic plague and have found that the Black Death travelled at 1.5 to 6 kilometres per day—much faster than any spread of Yersinia pestis in the twentieth century. The area of Europe covered over time by the Black Death in the five years 1347 to 1351 was even more impressive. Christakos and his colleagues maintain that no human epidemic has ever shown such a propensity to cover space so swiftly (even including the 1918 influenza epidemic). By contrast to the spread of plague in the late nineteenth and twentieth centuries the difference is colossal: while the area of Europe covered by the Black Death was to the 4th power of time between 1347 and 1351, that of the bubonic plague in India between 1897 and 1907 was to the 2nd power of time, a difference of two orders of magnitude.

All of which raises the question – why was pandemic 3 so much slower than the others? Could it be that Y pestis wasn’t the cause of the earlier pandemics?

mode of transmission

We know that Y pestis is a disease of rats,  and we know that the Black Death was all about rats, so that’s an obvious connection, no? Well, according to Cohn, what we think we know is just wrong. ‘… no scholar has found any evidence, archaeological or narrative, of a mass death of rodents that preceded or accompanied any wave of plague from the first or second pandemic.’ I must say I found this incredible when I first read it, yet Cohn seems to have investigated the sources thoroughly.

Cohn notes that:

while plague doctors of “the third pandemic” discovered to their surprise that the bubonic plague of the late nineteenth and twentieth centuries was rarely contagious, contemporaries of the first suggest a highly contagious person-to-person disease. Procopius, Evagrius, John of Ephesus, and Gregory of Tours characterized the disease as contagious and, in keeping with this trait, described it as clustering tightly within households and families; the evidence from burial sites supports their claims.

Pandemic 2 made the word contagium popular among the general public, and the incredible speed of transmission became one of the principle signs of the Black Death, differentiating it, for example, from smallpox, which had some similar physical characteristics. This contagion suggests person to person contact, more typical of pneumonic plague, which is highly infectious and can be transmitted through coughing and sneezing. A later chronicler of pandemic 2, Richard Mead, writing in the 1700s, advised against crowding plague sufferers in hospitals, as it ‘will promote and spread the Contagion’. However, those treating pandemic 3 noted, to their surprise, that plague wards were the safest places to be, and that this particular plague rarely took on the pneumonic form.

Cohn notes that the earlier pandemics were often associated with famine. For example in Alexandria and Constantinople in 618 and 619 famine preceded the plague and appeared to spark it into life. However, pandemic 3, definitely caused by Y Pestis, tended not to thrive in situations of dearth and was instead fed by increased yields. Such yields lead to higher rat populations, and higher rates of possibly infected rat fleas and so higher rates of transmission to humans.

death rates

According to contemporary accounts the first pandemic wiped out entire regions, decimating the inhabitants of cities and the countryside through which it so swiftly passed.  These accounts are backed up by archaeological and other evidence. It’s pretty clear that millions died in the second pandemic too. Compare this to the third pandemic, which spread so slowly and was limited to coastal areas and even just shipping docks. Restricted to temperate zones, this last pandemic resulted in deaths in the hundreds, with never more than 3% of an affected population dying.


Although few quantitative records describe the signs or symptoms of plague for pandemic one, those that do (and Cohn cites 6 different ancient authors) are in general agreement in their descriptions of ‘swellings in the groin, armpits, or on the neck just below the ear’, the classic symptoms of bubonic plague. Procopius of Caesaria also observed that victims’ bodies were covered in black pustules or lenticulae. Pandemic 2, which begins with the Black Death of 1347-52, is marked, on the other hand, by extensive records, both professional and popular – writings about it were amongst the first forms of popular literature.

range and seasonality

Another problem for the view that this has all been the doing of Y pestis, is that pandemics 1 and 2 could strike all year round, but generally settled into a pattern of prevailing in summer in the southern Mediterranean and the Near East, which is not the best season for the flea vector X cheopis. The seasonal cycle of modern plague is quite different, and the range is much more limited.

So all this opens up a mystery. Scientists are agreed that we don’t have a clear-cut story of Y pestis causing horrific disease through rats and fleas over millennia (archaeological and other evidence suggests that rats were scarce in 14th century Europe) , but they’re much in disagreement about what the real story might be. If not Y pestis, then maybe a hemorrhagic virus (one of which causes ebola). Such viruses are notorious for their rapid transmission, their resurgences and their high mortality rates. Pneumonic plague,  the more infectious, lung-infecting form of plague may also be implicated, but this doesn’t appear to agree with most of the described symptoms of pandemics 1 and 2. Other types of fleas, not associated with rats, as well as lice, are also being considered as possible vectors. Some geneticists believe that a variant of pestis may have been responsible. It looks as if genetic analysis is the most likely pathway to finding a solution.

This article got started, as I wrote at the beginning, because someone keen on naturopathy said something about bubonic plague in our staff room. Some plant she brought in, which had great anti-oxidant properties (she clearly hasn’t kept up with the latest findings on anti-oxidants) was also a cure for bubonic plague, or maybe it was a variant of the plant, and the person who discovered the secret of its healing properties died suddenly (presumably not from plague) and the secret was lost to us for centuries…

Written by stewart henderson

December 11, 2014 at 8:50 am

bronchiectasis and steroids

with 3 comments


My bronchiectasis has just ‘acutely exacerbated’.

Today I’m off work because I’ve got another infection, the first since I finished the course of broad-spectrum antibiotics back in May. The symptoms are an increase in phlegm, a slightly sore throat, a nasty cough and a scratchy voice, not good for teaching. And generally I feel rundown and a little depressed. This morning I visited the doctor for the first time since February. It was a new doctor, as my usual doctor apparently doesn’t work in the mornings. I didn’t want to take any time off work as I’m saving my pennies for an overseas trip, so I was planning to go to work straight afterwards because I didn’t start teaching until 1 o’clock. However the doc put the kibosh on that by giving me a sick certificate for Thursday and Friday, telling me I needed the rest and that I might be infectious. He also prescribed steroids along with the usual antibiotics, in this case Augmentin forte – though I bought the cheapie alternative called Curam Duo Forte – tablets containing a mix of amoxycillin (875mgs) and clavulanic acid (125mgs).

I’m often overly passive and docile with doctors, as with everyone else, and I often don’t clarify my thoughts until after the consultation. So in my usual docile fashion I rang in sick for work straight afterwards, even though this would mean I would lose hundreds of dollars in pay when I could ill-afford it. It’s true that my voice can barely stand the strain at the moment but I enjoy the energy my work gives me. More importantly, I don’t think I’m infectious.

While I recognise of course that our brains often play tricks on us, or more accurately that our brains and our memories aren’t always reliable, that doesn’t always mean that the doctor knows better than we do.

During the consultation the doctor asked me what I thought had caused this latest infection. I said I thought it might be something I ate. He didn’t seem too impressed with that and thought it might be something I picked up from my students, something viral. Hence the idea that I might spread the infection. Here’s the rub though – I actually felt quite certain that it was something I ate, and I know what it was and when it was. And this is not the first time I’ve felt such certainty about one of my many infections. Once it was a glass of wine which gave me a furry tongue, followed by the usual full-blown symptoms, and on other occasions it was food that I’d left a day or so too long in the fridge. These were clearly bacterial not viral infections. On this occasion it was an odd concoction of tabouleh salad, tuna, beans and roast potato that I’d constructed and taken to work for lunch, but had forgotten to eat. I found it later in my bag and scoffed it, half-knowing that I was making a mistake. The first symptoms soon followed.

I wonder how the doctor would have reacted if I’d insisted that it was food and not people that had infected me. It’s not a major issue, but now I also wonder if he’d have given me steroids for a purely bacterial infection. Strangely I didn’t wonder about the steroids until I got home. My neighbour was suspicious of this, saying that steroids were pretty strong stuff. I’ve certainly never had them prescribed for me before and now I wonder why.

According to medicine-net:

Steroids are used to treat a variety of conditions in which the body’s defense system malfunctions and causes tissue damage. Steroids are used as the main treatment for certain inflammatory conditions, such as systemic vasculitis (inflammation of blood vessels) and myositis (inflammation of muscle). They may also be used selectively to treat inflammatory conditions such as rheumatoid arthritis, lupus, Sjögren’s syndrome, or gout.

Bronchiectasis would be classified as an inflammatory condition I suppose, but pertaining to the upper airways, and nothing is mentioned specifically about this. Bronchiectasis is, however, a relatively rare condition (though possibly under-diagnosed). I’ve found a really good, thorough account of the treatment and management of bronchiectasis on medscape, but it says nothing about using steroids. So now I’m just a bit concerned, though I’m sure I’ve been prescribed a low dosage.

Actually on closer inspection I have found a section on medscape, dealing with anti-inflammatory therapy for bronchiectasis, where corticosteroids and other anti-inflammatory drugs crop up. I note that I’ve been given prednisolone tablets by the pharmacist (unfortunately I didn’t check the doctor’s prescription before handing it in, and I wasn’t given it back, so I can’t be sure if this was what the doctor prescribed). Prednisolone, according to Wikipedia, is a corticosteroid commonly prescribed for liver failure, but also used for treating auto-immune conditions such as asthma – so now we’re in the ballpark, so to speak. There are known side-effects for up to 5% of users, but i’ve never suffered any side-effects from any drugs I’ve been prescribed, not that I’ve been prescribed many. And side-effects are more often associated with long-term usage – aren’t they?

Medscape reports the literature on inhaled and oral corticosteroids for use with the many varieties of bronchiectasis and finds it promising but not entirely conclusive. I noted this line in conclusion:

A practical approach is to use tapering oral corticosteroids and antibiotics for acute exacerbations..

It almost seems as if my doctor has memorised this line. I’m feeling a bit more reassured now, but I have no idea what ‘tapering’ oral corticosteroids are. Well, I suppose it’s pretty obvious that it means gradual reduction..

Anyway, here’s hoping for a speedy recovery, and I’ve really got to take more care over food.

A few last words – the doc sent me to Healthscope next door to give a sputum sample, which, astonishingly, is the first time i’ve been asked to give one. The trouble is, if the medication works, I might not revisit the doctor for months, and will never find out the results of the tests on my sputum, just as i haven’t received the result of the blood tests I requested at my last consultation. I wanted to know if my mild anaemia had righted itself, as well as all the other health indicators – HDL and LDL cholesterol, triglycerides, etc. But they never provide you with the results if you don’t persistently ask for them. This is something I might explore further in another post.

Written by stewart henderson

November 28, 2014 at 12:02 am

want to live to 100?

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… It may destroy diseases of the imagination, owing to too deep a sensibility, and it may attach the affections to objects, permanent, important, and intimately related to the interests of the human species.

Humphry Davy,  on the value of science, in ‘Discourse introductory to a  course of lectures on chemistry’, 1802


A great many of us would like to live a long and healthy life, with a greater emphasis on health than length. But both please, if possible, thanks.

I’ve been reading the issues of New Scientist: the collection as they come out. The first issue dealt with the Big Questions, namely Reality, Existence, God, Consciousness, Life, Time, Self, Sleep and Death. Bit of a roller coaster ride, leaving me dizzy, confused, but often enlightened, and sometimes even exhilarated. So, better than a roller coaster. The second issue, entitled The Unknown Universe, took me far out beyond multiverses, quantum loops, energetic dark matter and the eventful horizons of black holes, and essentially taught me that modern cosmology is a mess of competing theories, often competing, it seemed, to be the most egregious ideas that are compatible with mathematical possibility. However, it may be that the studious avoidance of scary maths in these essays/summaries may have made them seem more loopy (or strangulatingly stringy) than they are.

The third issue was more down to earth, and not only earth but me, and you, dear reader. It’s entitled The scientific guide to a better you, and it’s all about longevity, health and success.

So what’s the secret, at least for the first two? Basically, eat healthily, with not too much meat, make sure you have good genes, don’t be too much of a loner (too late for me, I’ve been a loner for 40 years, and that’s unlikely to change, but I’l try, as I always say), be intelligent, active and exploratory. That’s the message of the first half of this issue anyway.

What interested me, though, was the detail. Measurements. Blood sugar, cholesterol, heart rate and many other factors and parameters, most of which I didn’t know I had to be concerned about. The various essays are peppered with these measures of health or lack thereof, but how does your average Jo like me get a measure of these things without pestering doctors on a weekly basis about wellness instead of sickness?

So, for fun, I thought I’d look into these ways of measuring ourselves and see if we can manage them from home. A sort of practical guide to centenarianism and beyond.

1. Body mass index (BMI)

Your BMI is a very rough-and-ready guide to whether or not you’re a healthy weight for your height. Various websites can calculate this for you instantly if you know your height and weight. My current BMI is 26, according to the Heart Foundation, which it regards as ‘overweight’, though very close to the borderline between ‘overweight’ and ‘healthy’. About three years ago my BMI was 29, well into the overweight category, in fact getting close to obese. I decided to eat less, without fasting or ‘going on a diet’, and to try to up my exercise, and over a 2-year period I brought my BMI down from 29 to 23, well into the healthy range. Since then it has crept back up to 26, and I’m struggling to get it back down again. I just need to lose a couple of kilos, and keep them off. The myriad other ways of measuring your health these days might make the old BMI seem outmoded – it doesn’t measure your fat to muscle ratio, for example, or the amount of fat around your heart and other organs – but I find it a useful guide for me, and the cheapest available.

2. Heart rate/blood pressure

Measured in beats per minute, your heart rate naturally varies with exertion, and also with anxiety, stress, illness, drug use and so on. The normal resting heart rate for an adult human ranges from 60 to 100 bpm. You can measure your own heart rate (your pulse) at any time by finding an artery close to the surface. The radial artery on the wrist, the one you see heading in the direction of the thumb, is commonly used due to ease of location, but don’t try it with your thumb which has its own strong pulse. I’ve just located my own wrist pulse and measured it as 62bpm. That’s the first time I’ve ever done it. However, I imagine it would be harder to measure after a bout of HIIT (high intensity interval training), which I sometimes indulge in, or after a moderately strenuous bike-ride. It would be even harder while you’re in the middle of exercise, so that’s where heart rate monitors, including those that can be worn on the wrist, come in handy. A quick google-glance tells me that such wrist devices are selling at $100 to $150. However, caveat emptor, as doubt is being cast on their accuracy. Electrocardiographs (ECGs, or EKGs), which measure the electrical activity of your heart, provide a much more accurate record than heart rate monitors, which are apparently only really effective when you’re at rest. One of the problems is that these optical monitors use light to track your blood, and to get an ‘accurate’ reading, you need to be very still, which sort of defeats the purpose. Reporter Sharon Profis, with the help of cardiologist Jon Saroff of Kaiser Permanente medical center in San Francisco compared various wrist monitor brands with the gold standard EKG measurements, and found them well off-beam especially at over 100 bpm. However, the Garmin Vivofit chest strap monitor, which measures electrical activity, was very accurate. This device can be bought for around $150 in Australia.

3. Cholesterol

Cholesterol’s an essential organic molecule, a sterol, a structural component of our cell membranes. It’s biosynthesised, mainly by our liver cell, often as a precursor to such vital entities as steroid hormones and vitamin D, and researchers have tracked the 37-step process of its synthesis. Cholesterol is transported through the blood within lipoproteins, and that’s where you get HDL (high-density lipoprotein) and LDL (low-density lipoprotein) cholesterol, of which the former is the one that causes problems. Some 32% of Australian adults have high blood cholesterol, the primary cause of atherosclerosis, leading to clogging of major blood vessels. Ways of lowering your LDL levels include not smoking, avoiding transfats, regular moderate exercise, and healthy eating including fruit, veg, grains and pulses and sterol-enriched foods. But of course you know all that. The big question is, can you measure your cholesterol from home? The current answer appears to be no, according to the Harvard Medical School (though I note that their article is 11 years old). The problem is that home testing kits can’t separate the ‘good’ HDL cholesterol from the ‘bad” (LDL). Measuring your overall cholesterol levels might be useful, but the real issue is the proportion that is LDL, not to mention that cholesterol can also be carried by other molecules such as triglycerides.

 4. Blood sugar/glucose

Glucose is a vital source of energy for the body’s cells, and its levels are associated with the hormone insulin, produced by the pancreas. Blood glucose levels naturally vary throughout the day, and having a level regularly above normal is termed hyperglycemia. Hypoglycemia is the term for low levels. Diabetes (technically Diabetes mellitus) is the disease most commonly associated with high blood sugar. General symptoms are frequent urination, hunger pangs and increased thirst.  The mean normal blood sugar level is around 5.5 mM (millimolars). That’s the international standard measure – the Americans measure it differently, which causes the usual confusion. Not surprisingly, considering the global rise in diabetes, blood glucose meters for use at home are readily available, but they’re mostly specially devised for use by diabetics, supervised by healthcare professionals. You can of course buy one and DIY but you must learn to be inured to pricks, and unless you’re at risk, which I’m not, as I don’t have much of a sweet tooth, don’t have particularly high cholesterol, and have never evinced any diabetic symptoms, it’s probably not worth the investment. The essential test associated with ‘pre-diabetes’ or hypoglycaemia is a glucose-tolerance test (GTT).

5. Sequence your genome

According to the Australian government’s National Health and Medical Research Council (NHMRC):

Rapid advances in DNA sequencing technologies now allow an individual’s whole genome to be sequenced. Although this is still relatively expensive, it is likely that in the near future it will become affordable and readily available.

Ah, that other country, the near future. But it is a fact that the price is coming down, from $10 million in 2005 to a mere $1 million in 2007 when James Watson’s genome was sequenced. The going rate in 2012 was under $10,000, and this year (2014) the Garvan Institute of Medical Research in Sydney became one of only three institutes in the world to deliver whole sequenced genomes at under $1000. However, there’s a problem. Your genome will mean nothing to you without expert analysis and interpretation, at a hefty price tag. So what would be the purpose, from a health perspective, of ‘doing your genome’? If you’re already quite healthy, do you want to spend up to $1000 only to find out that you carry a gene which may pre-dispose you to a disease that’s currently non-preventable? Our genome is very complex, so much so that current thinking on the subject, and especially on the introns, the sections that don’t code for proteins, has become more cloudy than ever. We know, or think we know, that the number of introns an organism has is positively correlated with that organism’s complexity, but that’s about all we know for sure, and  considering the enormous complexity of the interaction between genetics and environment, together with our lack of knowledge of the role of so much of our genome (over 98% of which is non-coding DNA), the question of whether it’s worth sequencing at this time is a live one. Of course if the price comes down to $100, or the price of a latte (which will soon be up around that figure) then it’d be well worth it; you would have it there awaiting scientific breakthroughs on all that non-coding stuff.

6. microbiome

If you’ve been paying attention to the world of human health, you’ll know that the microbiome is all the rage at the moment. the term was coined by Joshua Lederburg, who defined it thus, according to Wikipedia:

A microbiome is “the ecological community of commensal, symbiotic, and pathogenic microorganisms that literally share our body space.”

You may well have heard the impressive statistic that you have ten times more bacterial cells (and, most interestingly, archaean cells) growing on or in you than bodily (eukaryotic) cells, though this might become less impressive when you learn that the combined weight of those cells amounts to only a few hundred grams. Still, recent research on the microbiota has turned up some interesting results, especially for health. One finding, which may make it difficult to assess your own microbiome, is that different sets of microbes appear to perform the same function for different people. So you won’t just need to know the genetic content of your microbiome, but its function. Still, we can learn a lot already from our microbiome, according to Catalyst, the ABC science program. For example, we inherit a lot of bacteria from our mothers, via her breast milk, not only directly but because the sugars in breast milk encourage the growth of particular types of bacteria. Most of this gut bacteria does its work in the large intestine or bowel region. They’re anaerobic beasties, so they die when exposed to air. However, recent technological developments (and how often can that story be told) have allowed us to learn far more about them, by sequencing their genes inside the gut. From this we’ve learned that our gut bacteria are vital components of our immune system. And since these bacteria rely on our own diets for their nourishment, the kind of microbiome we have is profoundly related to what we eat. A diverse microbiome results, apparently, from eating a high-fibre diet, and low-fibre processed food, and the ingesting of antibiotics, is reducing that diversity, and contributing to multiple health problems. It appears that a less diverse microbiome finds itself under stress, leading to inflammation, an immune response that can damage our own tissue. As a sufferer from bronchiectasis, a chronic (and incurable) inflammation of the airways due probably to early childhood damage, I’m particularly concerned to limit the extent of inflammation through diet and exercise, so this is probably the aspect of my health I’m most concerned to monitor. And there’s also the relationship between gut bacteria and obesity. Some 62% of Australians are overweight or obese, and I’m one of that majority, and trying not to be.

It has been shown clearly, in mice at least, that a high-fibre diet reduces bronco-constriction, improving resistance to asthma and other airways conditions such as COPD. This is mainly due to the production of short-chain fatty acids by particular bacteria. The short-chain fatty acids are produced though the digestion of dietary fibre. Interestingly, acetate, found in vinegar, is a short-chain fatty acid, and a natural anti-inflammatory, so that’s something I should include regularly in my diet.

Finding out what your particular microbiome is, and how it might align with your health, is a simple if rather unpalatable and ‘intimate’ process. You can apply for a kit from the American Gut Project, an organisation dedicated to researching microbiota. The kit is for obtaining a sample of your ‘biomass’ as they call it, which you then send back to the AGP for analysis. All of this was spelt out in the above-linked Catalyst program, but since that program was aired two months ago, the AGP has been inundated with more biomass than it can deal with, so there’s been a backlog of logs, as it were. I plan to send for a kit anyway. The AGP sends back the results, apparently, with hopefully an analysis of the microbiome easy enough for a layperson to understand.


So there’s six areas to look at, either independently or with the help of your GP or other professionals, in terms of measuring how you’re going in terms of overall health, and there are many more aspects of your bodily chemistry and physiology to check up on – hormones, neurotransmitters, bone density, sight, hearing, lung capacity and so forth. Or you can follow the standard advice on diet and exercise, try to avoid stress and hope for the best. And above all don’t stop laughing and dancing, otherwise life would hardly be worth living.

Written by stewart henderson

November 1, 2014 at 6:36 pm


with one comment

it's all about Boyle's Law, apparently (P1V1 = P2V2)

it’s all about Boyle’s Law, apparently (P1V1 = P2V2)

Aerosinusitis, also called barosinusitis, sinus squeeze or sinus barotrauma is a painful inflammation and sometimes bleeding of the membrane of the paranasal sinus cavities, normally the frontal sinus. It is caused by a difference in air pressures inside and outside the cavities.

The above quote is from Wikipedia, and it describes something I experienced on two flights recently (see previous post), though I experienced it, or felt I experienced it, in the ears (I’ve learned not to trust my own perceptions). On the first flight, I experienced a build-up of pressure until a sudden change as of a bubble bursting in some inner cavity, and then everything was fine. I’ve had similar, but less intense, experiences in a car when driving up into the hills near my home. In fact, they’ve been so mild that I’ve often looked forward to them as a physical sensation, and I know it’s common because people would ask around – have your ears popped yet? On my second flight, the pressure built up again on the descent, and I fully expected the bubble to burst as it always did. But the pain just increased, to an excruciating level, so that my face was all scrunched up and I was gasping, squealing and whimpering like a pup. By the time we landed, though, the worst of the pain was gone, and it gradually got better over the next hour or so, and although I could still ‘feel’ it 24 hours later, it was more a memory of a feeling than the thing itself. I don’t know whether my pain was severe or relatively mild as I’ve never felt other people’s pain. This was one of the first things I had ‘deep’ thoughts about as a child. When I was nine or ten years old I fell, while running, and bashed my shin against the edge of our front porch, and I still think that was the most extreme pain I’ve ever felt in my life. I screamed and screamed, and amongst the comforting remarks came the inevitable ‘come on now, stop squealing, it’s not that bad’. Of course this made me angry and resentful but it also raised the questions, ‘am I over-reacting? Would others react like this in the same circumstances? Would they feel the same pain? How could we ever know?’ And along with those questions was one that always ate at me, and probably still does – can I control my pain, can I obliterate it with the power of my mind? I’d sell my soul, FWIW, for total control. But that’s a rather too large side-issue for this post. The Wikipedia article, though, does classify aerosinusitis in terms of pain, along with other more measurable symptoms:

Grade I includes cases with mild transient sinus discomfort without changes visible on X-ray. Grade II is characterized by severe pain for up to 24 h, with some mucosal thickening on X-ray. Patients with grade III have severe pain lasting for more than 24 h and X-ray shows severe mucosal thickening or opacification of the affected sinus; epistaxis or subsequent sinusitis may be observed.

Annoyingly, my own intense but transitory experience doesn’t fit into any of those grades. I also find that this extremely technical article makes no mention at all of ear pain. Much of the focus is on the frontal sinuses, situated behind the brows and connected to the nose or nasal meatus, which naturally makes me uncertain about where my pain was located. Interestingly, the frontal sinuses still haven’t come into existence at birth, and aren’t fully developed until adolescence, and some 5% of people don’t even have them, which just complicates matters for me. As is mentioned above, the frontal sinuses are part of a whole labyrinth of hollows, bones, cartilaginous membranes and passageways known as the paranasal cavities. I’m hoping that the inner ear, or more accurately the middle ear cavity – technically called the tympanic cavity, is also part of that.

Though ‘ear-popping’ seems to be commonplace, aerosinusitis usually occurs in people who have head colds, or as the article puts it, it’s ‘typically preceded by an upper respiratory tract infection or allergy’. Of course, with my bronchiectasis, I’m effectively in a more or less permanent state of infection, so this may be a problem for me every time I fly.

So, what remedy? Well, the problem for me seems to be with the tympanic cavity or eustachian tube on one side. When I was eight, I perforated my ear drum and had to have an operation. I was told afterwards that I should never hold my nose tight while blowing it, as people do (making that horrible honking nose), as this might damage my eardrum. I remember being fascinated by this connection between the nose and the ears, and of course I’ve always followed the doctor’s advice. I didn’t want to blow my brains out of my ears.

Wikipedia suggests using decongestants or painkillers for mild forms of barotrauma, as does this useful site, which deals more with popping ears. First and foremost, though, it suggests gargling with warm salt water, which was my mother’s advice for many medical problems (she was a nurse).

I’m resisting any description of what I went through as ‘mild’.

Working the eustachian tube or tympanic cavity seems to be a good idea, for example by regular swallowing, chewing gum, sucking sweets, yawning, etc.

Sudafed is highly recommended. I’ll bear that in mind next time.

Written by stewart henderson

May 12, 2014 at 11:50 pm

acupuncture promotion in australia

with 2 comments

I tried to find a picture of the chi energy system online, but guess what, nothing to be found. Here's a chi-reflexology map instead - from the Australian College of Chi-Reflexology, no less!

I tried to find a picture of the chi energy system online, but guess what, nothing to be found. Here’s a chi-reflexology map instead – from the Australian College of Chi-Reflexology, no less!

On the ever-reliable US-based NeuroLogica blog, Steven Novella reports on an interesting case of acupuncture promotion here in Oz, via Rachel Dunlop. As Novella reports, acupuncture has been studied many times before, and Cosmos, our premier science mag, did a story on the procedure a while back, reporting no evidence of any benefits except in the notoriously vague areas of back pain and headaches.

Not surprisingly, lower back pain was one of the conditions that supposedly benefited from acupuncture, according to media hype about the latest study. The trouble is, this study was being reported on before being published and peer reviewed, which, to put it mildly, is highly irregular and raises obvious questions. The Sydney Morning Herald is the offending news outlet, and Dr Michael Ben-Meir the over-enthusiastic researcher. As the article points out, Ben-Meir is already a ‘convert’ to acupuncture, having used it for some time in acute cases at two Melbourne hospitals. That’s fine, if a bit unorthodox, but it doesn’t accord with other findings, and there are therefore bound to be questions about methodology.

One of the obvious difficulties is that acupuncture can hardly be applied to patients without them knowing it. It’s a much more hands-on and ‘invasive’ experience than swallowing a tablet, and this will undoubtedly have a psychological effect. It seems to me, just off the top of my head, that acupuncture, with its associated rituals, its aura of antiquity and its oriental cultural cachet, would carry greater weight as a placebo than, say, a homeopathic pill. But in fact I don’t have to speculate here, as there is much clinical evidence that injections have a greater placebo effect than pills, and big pills have a greater placebo effect than small ones. So it doesn’t greatly surprise me that people will report a lessening, and even a dramatic lessening, of acute pain, after an acupuncture treatment, however illegitimate. I presume there are illegitimate treatments, because the ‘key meridional points’ where the needles are applied are precisely know by legitimate acupuncturists, and they apply their treatments with rigorous accuracy.

Well, actually there’s a big question as to whether or not there are any legitimate acupuncturists, because acupuncture is based on an energy system known as ‘chi’, which supposedly has meridional points at which needles can be inserted quite deeply into the skin, but there’s no evidence whatever that such an energy system exists, let alone about how such a system might function – for example, its mode of energy transmission (whatever ‘energy’ might mean in this case). Considering that we know a great deal about the autoimmune system and the central and peripheral nervous systems, it seems astonishing that this other bodily system has gone undetected by scientists for so long, and especially in recent times, with our ultra-sophisticated monitoring devices. When you look up ‘chi, sometimes spelt ‘qi’ or with other variants, you’ll find nothing more specific than ‘energy’, ‘life force’ or something similar – nothing corpuscular or in any sense measurable by modern medicine. Even so, researchers into acupuncture have come up with an attempt to measure its efficacy by comparing it to ‘sham acupuncture’ in clinical trials. Sham acupuncture uses the ‘wrong’ meridians and the ‘wrong’ depths to which the needle goes.

But herein lies an obvious problem. Sham acupuncturists insert needles only millimetres deep, while real acupuncturists put their needles between one and three or four centimetres deep: ‘Depth of insertion will depend on nature of the condition being treated, the patients’ size, age, and constitution, and upon the acupuncturists’ style or school’, according to an acupuncture site I visited at random. These are rather wide parameters, but the point that interests me is this. If you don’t put your needle in deep enough, you won’t make contact with the chi that needs to be stimulated or other wise modified to heal the patient. So goes the rationale, surely. It’s like, if you don’t put the needle for a standard vaccination in the right place, you’ll miss the vein. But veins are clearly real. If you go dissecting, you’ll find veins and arteries and nerves and muscle and fat and so on. But you won’t find chi. Yet, apparently it does have real existence. It’s between one and four centimetres down, according to real acupuncturists, depending on the above-mentioned variables (and no doubt many others).

So we can’t actually see it, or find it on dissection, but it’s locatable in space, vaguely. Or is it that chi is everywhere in the body but the right kind of chi, the bit that’s causing the pain and needs to be treated with needles at certain precise meridional points, is at a certain distance from the surface of the skin?

It all begins to sound a bit like theology, doesn’t it?

Here’s the ‘take-home’ for me. If you read about treatments that ‘work’ but you get virtually nothing about the mechanism of action, as is the case, for example, with homeopathy and acupuncture, be very skeptical. In the end I’m not impressed with clinical trials that show a ‘real effect’, even a startling one, because I know about regression to the mean, and I particularly know about the placebo effect. I want ‘proof of concept’. In this case proof of the concept of chi and of meridians. I’ve heard homeopaths defend their pills on TV recently by claiming that, ‘whatever the mechanism, clinical trials consistently prove that this treatment works’, and I can’t be bothered chasing up those clinical trials  and testing their legitimacy, I go straight to the concepts and processes behind the treatment – the law of similars, the law of infinitesimals, and don’t forget succussion. These concepts are so intrinsically absurd that we needn’t bother looking at the clinical data. If there are positive results, they haven’t been produced by homeopathy. The fact that homeopaths themselves are largely uninterested in the mechanisms is a dead giveaway. You’d think that the law of infinitesimals and the law of similars would surely have myriad applications far beyond their current ones. They would revolutionise science and technology, if only they were real (and they’d also render obsolete much that we currently know).

The same goes for acupuncture, and chi. If this bodily system were real, and chi could be captured in a test tube, and its constituents examined and isolated under a microscope, how revolutionary that would be. How transformative. Chi pills, chi soap, chi breakfast cereal…

Ah but I’m thinking like one of those limited westerners, so modern, so smug, so lacking in the insight of the ancients…