Diabetes – A man made disease
Introduction
Symptomatic diabetes has been recognised for millennia, but the documented increase in incidence of both Type 1 and Type 2 diabetes is a very recent phenomenon. Where reliable records are available, it appears that Type 1 diabetes incidence has doubled over the last two to three decades which is similar to Type 2 incidence [1], [2]. This is far too rapid to be caused by genetic changes, so environmental causes need to be examined. In the context of islet beta cell damage, such environmental causes are likely to be of microbiological or ingested agent nature.
The major environmental candidates suggested summarised in Table 1, are made more likely if they have become more prevalent over the last few decades. This candidacy is also enhanced if the agent is diabetogenic in either normal animals or diabetes prone strains, and a plausible mechanism for this diabetogenicity exists.
It is not the purpose of this communication to review the evidence for a microbiological cause of the recent epidemic of diabetes. The excessive hygiene hypothesis meets all three criteria of secular trend congruity, animal model, and plausible diabetogenic mechanism, whilst the others listed in Table 1 lack one or more of these criteria, or have been disproved in other ways.
Among the ingested agents, too much food, associated with obesity provides an attractive hypothesis for both Type 1 and Type 2 diabetes – the accelerator hypothesis [7], whereas the other specific agents listed do not fit with secular trend – i.e. consumption of the agent has not increased 2–3-fold in the last three decades. Some do not fit with ecological considerations, e.g. arsenic, to provide a holistic aetiology.
Evidence that changes in modern food processing and storage techniques can provide potential diabetogens’ will be presented. This coupled with the ‘accelerator’ hypothesis provides a likely explanation for the recent epidemic of diabetes.
Section snippets
Glycation, Amadori rearrangement, and advanced glycation end products
Heating in air of many foods in the presence of sugars (e.g. glucose, fructose, lactose, etc.), lipids or protein will produce a range of glycated products. Ascorbic acid behaves as a sugar in this context.
An exemplar from the literature is shown in Table 2. The more extensive the heating, the longer the time, and the greater the concentration of reactants, the more formed and the more advanced these non-enzymatic products, e.g. UHT milk contains a thousand-fold higher amount of a glycation
Vitamin C
From the above it can be seen that ascorbic acid additions to food as an antioxidant have become increasingly widespread. (Table 3) Vitamin C is oxidised itself by food processing, and oxidation products of ascorbate are diabetogenic [23]. It is not clear that it is dehydro ascorbic acid itself or further degradation products that is responsible for this β-cell toxicity [24].
Lipoic acid
This acid is widespread in foods and is a potent lipid antioxidant. As with vitamin C the oxidised form of lipoic acid
Discussion
Although many environmental agents have been implicated in the rising incidence of diabetes, only a handful of these satisfy the three criteria of increase in the environment of the past three decades, causing diabetes in animal models, and having a plausible mechanism of action. Modern food processing and storage through glycation and oxidation may confer adverse effects on some food components, and lead to the speculation that diabetes is a man made disease. The accelerating effect of
Acknowledgements
Leo Hepner for providing vitamin C production data. Prof. Henryk Kostyra for provision of an English translation of the paper on glycated morphiceptin.
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Type 1 diabetes, the A1 milk hypothesis and vitamin D deficiency
2009, Diabetes Research and Clinical PracticeCitation Excerpt :Nevertheless it is not possible to discount the possibility of a change in the composition of milk (perhaps due to modern processing) that may lead to the increased presence of a diabetogenic factor in cow's milk. For example, Elliott hypothesises that a casomorphin released from the A1 genetic variant of β-casein, but not the A2 variant, can become glycated and have adverse immune effects [21]. Bovine β-casein exhibits allelic variation, with the A1 and A2 variants being particularly common.
A1 beta-casein milk protein and other environmental pre-disposing factors for type 1 diabetes
2017, Nutrition and DiabetesA European evidence-based guideline for the prevention of type 2 diabetes
2010, Hormone and Metabolic Research