Thursday, May 28, 2009

Type 1 Diabetes on the Rise

28/05/2009 5:39PM

Type 1 childhood diabetes is increasing. Type 2 actually has a closer genetic connection than type 1, at least that is what one doctor told me. There was an interesting Italian study sometime ago which found that in obese individuals the risk of type 2 was 49 times higher for those in the highest 10% (I think) then the lowest group for organic pollutant measurements in their body tissues. Another study found increased complications in diabetes individuals if they lived close to a dump.

Type 1 diabetes is perceived as a Th 1 inflammatory mediated autoimmune disease, the beta cells appear particularly sensitive to oxidative attack. However the cytokine profile goes across the board. The Th 1-Th 2 stuff is useful but not the real thing. There might be an epigenetic process going on here because I recall one study which indicated that if the grandmothers had gone through a severe famine this increased the risk of diabetes but only in the grandchildren line(so far measured). I can think of two possible causes, there must be more. The point is this: Across wide populations, if we increase the potential risk factors through environmental changes, we can then create epidemics. It's a neat trick and we're pulling it off.

Strange stuff but just today I read this:

The water flea, daphnea will develop large defensive spines when predators are around. If they then reproduce, their off spring develop these spines even when not exposed to predators.

New Scientist May, 2008l p 31

There is a way to understand this but you have to give up the one gene - one protein idea. It's wrong so you may as well.

Now, speaking of persistent organic pollutants, has anyone bought any bottled water lately?



TedHutchinson said...

Vitamin D and Diabetes-Can We Prevent it? this 45 minute video explains how Diabetes can be prevented by increasing the amount of vitamin D mothers and babies have.
Human breast milk flows replete with D3 above 55ng~137.5nmol/l most EU mothers only reach around 75nmol/l at the end of summer.
When Finnish babies were given 2000iu/daily/D3 in the first year of life that grew up with 80% less type one Diabetes 30yrs later.

John said...

Interesting. Thanks. The Multiple Sclerosis Vitamin D link is strong. If I correctly recall, a study last year indicated that vitamin D levels during adolescence is particularly important. There are also faint statistical linkages for vitamin D levels during pregnancy and schizophrenia. Another linkage for Parkinson's, which I can't make sense of it except by reference to a paper released by Greg Willis; abstract below. It is a fascinating hypothesis and great read. Schizophrenia is not typically perceived as an "auto-immune disease" but "auto-immune like" activity is implicated; at least in a subset of patients.

Recent epidemiological studies indicate widespread deficencies in vitamin D. Puzzling because one study done in South East Qld, until recently a very sunny place, found up to 20% were vitamin D deficient. The RDA for vitamin D is a joke, way too low, so it could be considerably worse.

This is a third and very important cause. Thanks Ted.


John said...

Rev Neurosci. 2008;19(4-5):245-316.Links
Parkinson's disease as a neuroendocrine disorder of circadian function: dopamine-melatonin imbalance and the visual system in the genesis and progression of the degenerative process.
Willis GL.

The Bronowski Institute of Behavioural Neuroscience, Neurosciences Section, Coliban Medical Centre, Kyneton, Victoria, Australia.

For more than 50 years, Parkinson's disease (PD) has been conceptualized as a product of nigro-striatal dopamine (NSD) system degeneration. In spite of a growing body of evidence depicting the mammalian brain as an interrelated complexity of circuitous systems, dopamine (DA) deficiency of the NSD is still regarded as the main problem, with DA replacement being the purpose of therapeutic intervention. For at least 191 years circadian involvement in various aspects of PD, including depression and insomnia, has been recognized as an integral part of the symptom matrix of PD and yet attempts to elucidate the involvement of this system is uncharted territory. The present review attempts a major reorganization of mammalian brain into a coordinated complex involving the NSD and the retinal hypothalamic tract (RHT) as the primary systems involved in the retino-diencephalic/mesencephalic-pineal (RDMP) axis. Secondary systems including the lateral hypothalamus (LH), the area postraema (AP) and the subthalamic nucleus (STN) also form an integral part of this system as they have been shown to be either intimately related to the primary systems of the RDMP axis or have been shown to be significantly involved in the expression and treatment of PD. A large volume of evidence suggests that the RDMP axis is activated during the course of PD and during therapeutic intervention. Four types of neurotoxicity associated with melatonin are identified and the susceptibility of various parts of the RDMP axis to undergo neuropathological change, the tendency for melatonin to induce PD-like behavioural toxicity, and the relationship of this to PD symptomotology are described. This includes adverse effects of melatonin on motor function, hypotension, the adjuvant use of benzodiazepines, depression, insomnia, body weight regulation and various biochemical effects of melatonin administration: all problems currently facing the proposal to introduce melatonin as an adjuvant. It is suggested further that traditional DA replacement may well work by exerting its effect upon the circadian system, rather than simply replacing deficient DA. Activation of the circadian function by antagonizing melatonin with bright light not only has therapeutic value in treating the primary symptoms of PD but it shares a common mechanism with L-dopa in reducing the occurrence of seborrheic dermatitis. Concepts at the centre of understanding pineal function in PD, including pineal calcification, melatonin deficiency, symptomatic versus protective features of melatonin and antioxidative effects, are explained in a counterintuitive context. Intriguing propositions including the role of the retina in the aetiology of PD and that the nigra functions as a retina in this disorder are presented with the intention to provide a new understanding of the underlying compromised function in PD and to provide new treatment strategies. For the first time, abundant evidence is presented describing PD as an endocrine disorder of melatonin hyperplasia. The role of circadian interventive therapies and internal desynchrony in the aetiology and progression of PD provides a new direction for understanding the underlying physiology of a disease which is currently in a state of impasse and provides new hope for those who suffer from its debilitating effects.

PMID: 19145986 [PubMed - indexed for MEDLINE