an autodidact meets a dilettante…

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.