Posts Tagged ‘diabetes’
a post to send you to sleep, or not
Häggström, Mikael (2014). “Medical gallery of Mikael Häggström
Canto: Anything interesting you’ve learned lately?
Jacinta: Well, there’s so much, it’s hard to keep track of it all, before it slides down the slippery slope into a past of fragmented memories.
Canto: A pasta of memories? That’s food for thought. I know you’ve been reading up on sleep, among all your other heavy reading. Tell me.
Jacinta: Yes, I’ve been reading up on feminism and misogyny as you know, which is mostly depressing, but this sciencey but very accessible book, Why we sleep by Matthew Walker, is not so much depressing as worrisome, for those of us whose sleep patterns are all over the place, like mine. He’s a big-time sleep researcher, and what he says about sleep deprivation is all bad – even for a wee bit of it.
Canto: So, those dreams of doing away with sleep, of zapping your brain for a few seconds to provide the instant reinvigoration that sleep takes eight hours of wasteful oblivion to achieve, allowing us that much more time to ruin the biosphere and all, or just to read more books and shit, those dreams are just a waste of sleep?
Jacinta: No zapping will ever replace the complexity of sleep, with all its REMness and non-REMness, let Mr Walker assure you. Sleep is a restorative and builder, which has complexly evolved with the complex evolution of our brains and bodies. And by ‘our’ I don’t just mean humans, but every complex or not-so complex evolved organism. They all sleep.
Canto: Well, there are many questions here. You’ve mentioned REM sleep, which I think has something to do with dreaming – your eyes, presumably under their lids, are rapidly moving about. Why? It doesn’t sound healthy.
Jacinta: They’re responding to brain signals, and it’s perfectly normal. More specifically, they seem to be responding to the brain’s changing visual representations while dreaming. They used electrodes in the brain to discover this – which sounds Frankensteinish but in this case they were patients with epilepsy preparing to have very invasive treatment to stop their seizures. They looked at activity in the medial temporal lobe, a region deep in the brain which includes the hippocampus and amygdala, and is involved in encoding and consolidating memories, and found fairly clear-cut connections between that activity and patients’ eye movements.
Canto: But how could they ‘see’ the eye movements?
Jacinta: Oh god, I don’t know, for now I’m more interested in sleep deprivation, which raises concerns for everything from diabetes to Alzheimer’s. And, although I haven’t measured anything carefully, my guess is that I average 6 to 7 hours’ sleep a night, and I need to amp that up.
Canto: And you’ve recently been diagnosed as pre-diabetic, so do you think more sleep can help with that? It’s usually pretty strongly correlated with diet isn’t it?
Jacinta: Less time sleeping, more time for eating, Walker writes. I’m certainly trying to lose weight, but only by eating less. I think my diet’s not too bad, less wine though. And I suppose if I slept more, which is easier said than done, I wouldn’t eat so much. I’ve found in the past that just reducing the quantity of food I ingest, without changing its make-up – in other words, being more disciplined – can take the weight off quite quickly. The key is to make it life-long.
Canto: More fibre is good, I think. For the microbiome.
Jacinta: So type 2 diabetes is generally about blood sugar levels and their regulation, or lack thereof. In a healthy person, eating a meal adds glucose to the blood, which triggers the hormone insulin, produced in the pancreas, to somehow bring about cellular absorption of the glucose as an energy source. In the case of diabetes, there’s usually a break-down in the cellular response to the insulin signal, I think, and so you become hyperglycaemic – not that this has ever happened to me, so far.
Canto: So how does this relate to lack of sleep, apart from giving you more time to guzzle sugar?
Jacinta: Walker describes a series of studies, independent from each other, in different continents, which found high rates of type 2 diabetes in people who reported sleeping for less than six hours a night on a regular basis. They controlled for other factors such as obesity, alcohol use, smoking etcetera. But of course correlation isn’t causation so they investigated further. They conducted experiments with a bunch of healthy people – no blood glucose problems or signs of diabetes. Firstly, they mildly tortured them – they permitted them only four hours of sleep per night over six straight nights. Then they tested their ability to absorb glucose, and found a 40% reduction in that ability. This would immediately classify them as pre-diabetic, and these studies, I’m assured, have been replicated numerous times.
Canto: That sounds incredible. And these guinea pigs quickly recovered? Or are they now full-blown diabetics? Doesn’t sound like mild torture to me. And do they know why a week’s sleep deprivation had such a dramatic effect?
Jacinta: Ha, well, Walker doesn’t mention the afterlife of the experimental subjects, but I’m assuming normality came bounding back after they recovered their sleep. As to the mechanism of action, Walker describes two options – sleep loss may have blocked the release of insulin by the pancreas, providing no signal for cell absorption to take place, or it may have interfered with the released insulin’s message to the cells. And though it seems that sleep loss probably had an effect on both, it was clear from biopsies taken from subjects that it was the latter, the cells’ lack of response to insulin, their ‘refusal’ to take up the blood glucose, that was the principal problem.
Canto: Just looking at the Sleep Foundation website, and they seem to get things the other way round, that diabetics are suffering from sleep loss. I must say, that, off the top of my head, I’d find being pre-diabetic easier to manage than my sleep behaviour. I mean, I can imagine changing my diet and exercise habits easily enough, but my sleep habits not so much. How do you turn off your brain?
Jacinta: Well, Mr Walker has some suggestions on that, which we’ll explore next time. And by the way, there seems to be tons of videos and websites providing knowledge and advice on the issue, which always makes me feel superfluous to requirements as a human being…
Canto: Well, try not to lose sleep over it.
References
Why we sleep, by Matthew Walker, 2017
https://www.sciencealert.com/scientists-have-worked-out-why-your-eyes-move-when-you-re-dreaming
https://en.wikipedia.org/wiki/Sleep_deprivation
https://www.sleepfoundation.org/physical-health/lack-of-sleep-and-diabetes
covid-19: vitamin D, fructose and oxidative stress
So looking at the Medcram coronavirus update 82, approaching mid-June, we find that many of the monitoring websites give the impression that case rates are falling in the USA and elsewhere….
The update also looks at diabetes as a risk factor for covid-19. It discusses data from China linking mortality to blood sugar levels. Glycated haemoglobin (HbA1c) was brought up in a previous post, though there are different ways of measuring it – I’ll keep to the percentages. The normal HbA1c should be below 6%, though presumably not too far below, as can happen for diabetics that over-medicate. Your HbA1c measure tells you what your blood sugar level has been over the last two-month period, approximately. So, to quote from the study:
the researchers found an increased mortality risk associated with any form of previously undiagnosed elevated blood glucose at the time of admission among 453 patients hospitalised with laboratory-confirmed SARS-CoV2 infection
One would imagine that, with the oxidative stress that SARS-CoV2 brings on, diabetics or pre-diabetics not on medication might be more at risk than those on regular medication with a consequently relatively low HbA1c. This is the kind of association found here.
The update goes on to discuss an article on race and covid-19 mortality in England, which has a supposedly open-access National Health Service (NHS), which in fact has been subject to savage cuts from successive conservative governments. The article concludes, unsurprisingly, that BAME (i.e Black, Asian and Minority Ethnic) persons are ‘at increased risk of death from covid-19 even after adjusting for geographic region’. Suggestions for reducing these apparent inequities include ensuring adequate income protection, reducing occupational risks, reducing barriers in accessing healthcare and providing culturally and linguistically appropriate services. Of course, these problems exist within all countries with substantial immigrant populations, many of whom are more exposed to the virus than others.
Vitamin D is next revisited, with an article entitled ‘Vitamin D deficiency in Europe: pandemic?’, which was actually published back in 2016. Now I note from some of the comments on this update that there’s a lot of hype and apparent misinformation on vitamin D out there, so I want to dwell on this, for my own education.
The article refers to a Vitamin D Standardisation Program (VDSP) which has developed protocols to look at serum vitamin D data from differently-aged European populations, ‘to better quantify the prevalence of vitamin D deficiency in Europe’. So they applied these protocols to 14 different population studies, looking at serum 25-hydroxyvitamin D [25(OH)D]. Vitamin D has five different types, but the pertinent one for human health is D3, aka cholecalciferol, which is made by the skin when exposed to sunlight, and is also found in foods and supplements. D3 is hydroxylated by the liver at the ’25 position’, according to Seheult. Presumably this is a position on the D3 molecule where a hydroxyl group is added. 25(OH)D refers to the molecule after this hydroxylation, but before it becomes activated by further hydroxylation at position 1 by the kidney. So they looked at this molecule in a number of studies using ‘certified liquid chromatography – tandem mass spectrometry on biobanked sera’. Combined with other standardised serum data, data was collected from almost 56,000 patients, and the findings were that 13% of them, regardless of category, had serum levels seriously below normal, especially during the winter months. 40% were below the generally accepted norm. The problem was considerably exacerbated in dark-skinned ethnic sub-groups.
Back to 2020, and an article looking at the role of vitamin D in the prevention of covid-19 infection and mortality. It noted that ‘Vitamin D levels are severely low in the aging population especially in Spain, Italy and Switzerland’, so this is obviously a covid-19 co-morbidity factor. The article goes on to describe the mechanism of vitamin D’s action in the body, the details of which I’ll pass over, but it does involve ACE-2 and angiotensin 1,7, and also many other factors including macrophage development. With all this they raise the question of widespread vitamin D supplementation, which is apparently a hot topic beyond strictly scientific media, as mega-doses of vitamin D are being argued for on certain social media platforms, and even in the comments to this update. There are messy arguments going around about safe upper limits. Dr Seheult simply reports the article’s concern about ‘popular information channels’ spruiking the use of vitamin D3 above the generally accepted safe upper limit of 4000 international units per day. There is of course a battle here, not only in relation to vitamin D3, between those who demand proper trialling and vetting of medications and supplements and those looking for quick fixes. In any case, modest, regular dosing of the vitamin seems to be most effective.
Update 83 goes intensively into a very important and interesting health topic, which has been quite controversial and also revelatory of late; the role of fructose in our diet, and how it works in our bodies. So to refresh – which is always good for me, at least – about the issue of oxidative stress and how it is exacerbated by SARS-CoV2. So we have oxidative stress in the form of an excess of superoxide and reactive oxygen species (ROS). The SARS-CoV2 virus enters the cell via the ACE2 receptor, blocking angiotensin-converting enzyme 2 (ACE2) from converting angiotensin-2 (AT-2) to angiotensin 1,7 (AT-1,7). AT-2 promotes superoxide production, while AT-1,7 inhibits it. This problem is in addition to the effect of SARS-CoV2 itself in bringing about an increase in polymorphonuclear leukocytes (PMNs), which are white blood cells such as neutrophils, basophils and eosinophils. These also lead to increased superoxide production, and more oxidative stress. An essential feature of oxidative stress is that it can result in endothelial cell dysfunction. These cells line the vascular system that feeds the body’s major organs. This dysfunction brings about an increase in von Willibrand factor which leads to clotting and thrombosis. Recent analysis of autopsies found that covid-19 patients had nine times more lung clotting than control groups including influenza patients.
So the point of all this is that not having oxidative stress in the first place will be an important prophylactic against the virus. As Dr Seheult relates from the coalface, it’s those with a high BMI, with kidney and cardiovascular issues, and with diabetes, that seem to be at most risk of succumbing to the virus. Also, those with apparently normal HbA1c but with increased glucose were about 10 times more likely to have serious complications associated with the virus. This raises the question of diet, specifically bad diet.
We then go back to 2017 and an article, or compendium of articles, published in Nutrients. Its title is ‘fructose consumption in the development of obesity and the effects of different protocols of physical exercise on the hepatic metabolism’. So fructose is a simple sugar or monosaccharide which combines with glucose to form the disaccharide sucrose. There are two forms of fructose (and of glucose), which are enantiomers, which is to say they have opposite chirality, which gives them different reactive properties. They’e called D-fructose and L-fructose. They’re six-carbon sugars, and D-fructose is the prominent form in the body. Sucrose links together a molecule of glucose with one of fructose, so that sucrose (table sugar) is essentially 50% fructose. Fructose is added to many foods as a sweetener, particularly in the form of high fructose corn syrup (HFCS) and this has become controversial, in case you didn’t know. It’s not such as issue in Australia, where we mostly use cane sugar as a sweetener, but it features in imported processed foods, and in many sweetened drinks. So how does fructose impact on obesity and oxidative stress? To quote from the abstract of the above-named article, ‘studies indicate that fructose may be a carbohydrate with greater obesogenic potential than other sugars’. The article provides a compendium of such studies and how fructose affects glucose metabolism in the liver, adversely affects hepatocyte function and engenders inflammatory responses. It also advocates physical exercise for reduction of symptoms and as harm-minimisation practice. An experiment on rodents in which half were fed on fructose, the other half on sucrose (50% fructose, 50% glucose), the fructose-fed rodents gained more weight, and over time that extra weight involved an increase in abdominal adipose tissue and increased serum triglyceride levels:
Moreover, several studies corroborated the evidence that high fructose consumption might lead to accumulation of adipose tissue, systematic inflammation, obesity, oxidative stress and consequently insulin resistance in different tissues.
And there’s much more on the same lines, with relevant references. Dr Seheult describes other articles and studies over the last ten years identifying fructose and HFCS and their relationship to type 2 diabetes prevalence. One interesting article, which looked at HFCS alone, and surveyed diabetes on a global level, found that ‘diabetes prevalence was 20% higher in countries with higher availability of HFCS compared to countries with low availability’ and these results were adjusted for BMI, population, GDP and other factors. Greatest use of HFCS was in the USA, which of course has the highest rate of diabetes, and is leading the world in covid-19 cases.
References
Coronavirus Pandemic Update 82: Racial Disparities with COVID-19 & Vitamin D
Coronavirus Pandemic Update 83: High Fructose, Vitamin D, & Oxidative Stress in COVID-19
https://www.sciencedirect.com/science/article/pii/S0899900714001920
on vaccines and type 1 diabetes, part 3 – causes
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.
on vaccines and diabetes [type 1], part 2
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.