Diabetes has always been considered hereditary. But some new detective work suggests that drugs, particularly antibiotics, could be behind the surge in cases among children.
With virtually no solid scientific evidence, diabetes has always been considered hereditary. While researching her doctorate in chemistry, Lisa Landymore-Lim decided to study groups of diabetic patients. Her surprising findings showing a possible link between early onset diabetes and high exposure to prescription drugs in utero and early childhood provide early evidence that diabetes could be caused by prescription drugs.
The results of epidemiological studies show tremendous variation in the incidence of diabetes in children internationally. In Hokkaido, Japan, about two of every 100,000 children have diabetes, compared with approximately 30/100,000 in Finland. In the US and Western Europe, the current incidence rate for diabetes is second only to asthma among severe chronic diseases of childhood, with considerable geographical variation. In terms of total numbers, in the UK some 1600 children under the age of 15 years were diagnosed during 1988, whilst it is estimated that in the US, some 22,000 children under the age of 15 years developed diabetes during the three years 1978-1980.
Another factor which points towards environmental agents as the cause is that Japanese children in the US have four times the risk of becoming diabetic as do children in Japan. Jewish and French children in Canada are two to three times more likely to suffer from diabetes than children of the same origin living in their native country.
When I began studying diabetic children attending children’s hospitals in the south of England and in Kent, I was surprised to discover that many children had been diagnosed as diabetic before the age of 10.
This led me to amalgamate all data obtained for diabetics diagnosed before 23 years of age, and to compare the age at which they were diagnosed with the year of onset. What I discovered was a decline in the average age at onset with each successive decade. In the Sixties, the average age of the onset of diabetes was up to 12; in the Eighties, this had dropped to up to the age of four.
This decline in incidence up to the age of four years suggests that there may have been an agent responsible for causing diabetes, to which children were subjected either in utero or around the time of birth.
In my interviews with some 170 mothers of diabetic children during the pilot study I observed
Many children had suffered from recurring tonsillitis, asthma, prolonged eczema or recurrent
Some mothers had taken certain drugs to prevent miscarriage or morning sickness, or had taken
antibiotics to treat infections during pregnancy.
Some children had always been sickly when compared to other children in the same family, and others had apparently been perfectly healthy before they were diagnosed.
Several mothers felt that their child had shown signs of sub clinical diabetes for two to four years before diagnosis, as they had been very thirsty children, tired easily, experienced “funny” spells, showed a disinclination to eat, or failed to gain weight.
When asked about significant events during labour, a small number of mothers reported having been induced or administered epidurals. It was observed that in general, children whose mothers had taken drugs during pregnancy or labour (other than the painkiller pethidine) generally became diabetic at a lower average age, and that the greater the degree of chemical exposure during pregnancy, labour or soon after birth either directly or via breast milk, the lower the age at onset. When mothers of the 20 children who had been diagnosed as diabetic before three years were then specifically asked whether they had been administered drugs during labour, half had been induced, been given epidurals or both.
I had not previously considered that drugs in use today may cause diabetes. I discovered that children who had suffered from tonsillitis or ear problems were very likely to have been exposed to antibiotics, and that eczema and exfoliative dermatitis are side effects of exposure to antibiotics. Asthmatics and sickly children were also probably more likely to visit the doctor, and be prescribed drugs. It was at this stage that I began to consider the possibility that drug exposure may be the common factor.
I then undertook further studies to look at the drug exposure of the diabetic child in utero, during birth and from birth to diagnosis of the disease.
Of 35 diabetic children attending a hospital in Kent, whose parents agreed to participate in the study which involved the examination of their child’s medical records, I discovered that if the child had been exposed to drugs in utero or during birth, he was more likely to have earlier onset of diabetes. Of the 65 per cent of children exposed to drugs (excluding pethidine) the average age of onset was 4.9 years, compared with an average age of onset of 6.5 years among those without drug exposure. Furthermore, the percentage of children in the study who were induced was 32 per cent, compared with a rate of 18 per cent for the S.E. Thames region in 1989.
If anything, my results represent considerable underreporting of drug exposure since in many cases mothers were being interviewed years after pregnancy or labour.
I went on to study diabetic children diagnosed before three years and attending a hospital in the Wessex region, and before four years and attending a hospital in the Cambridgeshire Area Health Authority.
Within these two groups of patients, some 58 per cent had a history of in utero or drug exposure (excluding pethidine) during labour. In one case, a six year old had been given amoxycillin five times before his first birthday, twice during his twos, and three more times during his third and fourth year. Besides nine other courses of antibiotics, he received a cephalosporin, antihistamines, a powerful anti vomiting drug and one for gastrointestinal spasms, and Bactrim, a very potent antibiotic (see Q&A, p 10).
I got hold of another study group from local diabetic groups and The Daily Telegraph newspaper readers in the UK. Both groups had a high proportion (60 per cent) of children who had experienced drug exposure either in utero or during labour.
In another case, a child diagnosed as diabetic at 11 years had very little history of drug exposure after birth. However, the child’s drug exposure from conception reveals a pattern similar to that of some other diabetic children in the study: his mother took antibiotics while she was pregnant, and was given oxytocin (to induce labour) and/or ergometrine (to control postpartum bleeding) during and after labour. If antibiotics are implicated in the onset of diabetes, the records I examined suggest that it may take many years after exposure before clinical diabetes becomes apparent (see box p 3).
This long latency period between exposure and disease is likely to occur if drugs were administered to the child at a very young age, causing the destruction of only a proportion of the insulin producing cells of the pancreas. The disease would only manifest itself only when the demand for insulin increased, possibly due to increasing consumption with age. And of course the younger the age at which drug exposure takes place, the earlier and greater the potential damage, since organs are small and immature and may therefore take longer to remove toxic chemicals from the body. The sheer profusion of drugs to which these children had been exposed prompted me to compare the chemical structures of drugs known or thought to be diabetogenic (capable of causing
diabetes) with those reported in the studies (see box above).
It has been suggested that some drugs have an affinity for zinc, so that when they enter the bloodstream and pass through the pancreas, a rich source of zinc, the foreign chemical binds to the zinc in the islet cells of the pancreas, displacing some or all the six insulin molecules temporarily bound to it.
This would result in irreversible damage to the cells and in turn may result in the activation of the body’s immune system as it detects a “deformed”cell which it regards as “foreign”. It would also cause the formation of antibodies proteins directed to “foreign” agents within the body, which may explain why many newly diagnosed diabetics have islet cell antibodies in their blood. If this was the case, these islet cell antibodies would be formed as a result of pre existing damage to the pancreas and would not be the agent responsible for destroying the insulin producing function of the pancreas, as is currently thought.
If these chemicals are indeed capable of destroying the ability of beta cells of the pancreas to secrete insulin, as have been known to occur in persons who have taken rat poison Vacor (see box, page 2), then it is feasible that the destruction may be gradual, with a portion of the pancreas being destroyed with each chemical attack.
Although information about the binding of drugs to zinc is limited, penicillin has been reported to bind zinc and copper. The drug pencillamine, which is also one of the breakdown products of penicillin, is an effective chelator of metal ions including zinc and is used in medicine in chelation therapy for the reduction of toxic levels of zinc salts.
Some of the drugs that diabetic children were exposed to during fetal development share structural similarities. For example, one child was exposed to the colitis drug mesalazine, and another to paracetamol. Mesalazine has structural similarity to para aminophenol, a highly toxic chemical, which is formed in the body in very small quantities following the breakdown of paracetamol (acetaminophen). Also, mesalazine is structurally similar to penicillamine.
Ephedrine, which is possibly capable of causing diabetes, is less commonly used today than some 50 years ago, when doctors prescribed it to treat asthma; in the US babies were given it in nasal drops. Under the right conditions, ephedrine can break down to methylamine and benzoic acid, both of which will complex to zinc under the right conditions.
One patient that I studied had become diabetic at the age of seven in 1944. This was a time when diabetes in children was rare and fewer children in the UK were probably administered drugs on a regular basis. The patient had a history of asthmatic attacks which sometimes required hospitalization, and recalled being administered ephedrine tablets on several occasions.
The use of steroids such as prednisolone have also been associated with the onset of diabetes. Interestingly, conditions in which excessive levels of the body’s glucocorticoids (the same chemicals which go into these steroids) are produced also can bring on diabetes. Since prednisolone and beclomethasone dipropionate (Becotide), the asthma steroid drug, are so structurally similar, one wonders whether appropriate clinical trials have been done to exclude the possibility that beclomethasone is also diabetogenic.
Oxytocin, which like insulin is composed of many small chemical groups called amino acids, is in my opinion quite likely to be able to bind zinc as insulin does. In fact, many amino acids which are present in oxytocin have been shown to bind to zinc. In addition, naturally occurring growth hormone, which like oxytocin derives from the pituitary gland, has been shown to be diabetogenic in animals. Indeed, some 20 per cent of patients who suffer from acromegaly or gigantism (disorders in which the body produces excessive levels of growth hormone), have been reported to be diabetic.
A scientific report published in 1936 revealed that when the front portion of rat pituitaries was homogenized and the extract injected into other rats, they became diabetic. Oxytocin derives from the pituitary gland, and although present in the rear of the pituitary, which was not selected for use in the experiments, the two halves of a pituitary are poorly defined and therefore difficult to separate. This could have resulted in contamination of the test material with oxytocin, or alternatively, may mean that one or several of the hormones present in the anterior portion of the pituitary may be diabetogenic.
Oxytocin has probably not been sufficiently studied to detect any possible long term adverse effects in children who were exposed at birth. Sandoz Pharmaceuticals, which markets oxytocin in the UK, admitted that “after an extensive literature search” they were unable to find any papers on long term follow up of offspring.
The full studies on which this article is based appear in Poisonous Prescriptions (PODD, PO. Box 1237, Subiaco, Western Australia 6008. £9.95 or $15.45 US).