Diabetes linked with
increased Parkinson’s risk
Evidence is mounting for a link between diabetes and Parkinson’s disease, although the jury is still out on whether the association is causal.
Patients with a diagnosis of diabetes were at 36% increased risk of Parkinson’s disease compared with those without diabetes, according to a case-control study involving almost 2000 Danish patients with Parkinson’s disease.
The effect was found to be stronger in women, and with respect to early-onset Parkinson’s disease.
Writing in Diabetes Care, the authors said evidence was “accruing” for an association between diabetes and Parkinson’s disease.
They said their results were “strikingly similar” to another large trial using data from the Physician’s Health Study, which found a 34% increased risk of Parkinson’s disease associated with diabetes.
However whereas that study reported that most excess diabetes risk occurred around the time of Parkinson’s disease diagnosis (suggesting possible surveillance bias),the present study excluded first diabetes diagnoses and drug use up to five years prior to the index date.
Other prospective trials had also shown a link between diabetes and Parkinson’s, the authors noted, including one study of 51,000 Finnish adults, which linked diabetes diagnosis with an 85% increased risk of Parkinson’s disease.
However some case-control studies had found no link between the two diseases, and one actually found an inverse association, the authors noted.
Commenting on their own findings they said it was still unclear whether the association was causal. “A common biologic pathway appears to be the most plausible explanation at this point,” they said.
One pathway might be related to vitamin D levels, they said, noting these had been implicated in both diseases.
Alternatively, the effect could relate to insulin resistance, which had previously been implicated in Alzheimer’s disease risk, they said.
Diabetes Care 2011;
Nervous Tissue Support
Did you know...?
Phosphatidylserine (PS) is one of the key building blocks of cellular membranes, particularly in the nervous system, and occurs naturally in the brain, where it demonstrates an amazingly broad spectrum of beneficial functions. PS has a powerful effect in the improvement of memory, mood, attention span, and even reflexes. It is a safe, effective treatment for a wide variety of neurotransmitter imbalances and should be considered whenever a neurological condition is suspected.
PS is a phosphoglyceride phospholipid derived (for supplementation purposes) from non-genetically modified soy lecithin.
Any condition requiring neurological support
FUNCTIONS THAT MAY BE FACILITATED:
facilitates the production and release of acetylcholine within the cerebral cortex
stimulates the release of dopamine reduces the excessive release of adrenocorticotropic hormone and cortisol stimulates the production of protein-kinase-C enhances the function of nerve growth factor normalises the daily secretion of thyrotrophin enhances the efficiency of glucose metabolism within the brain increases the number of receptor sites for neurotransmitters within the brain can activate cells of the immune system.
PHOSPHATIDYLSERINE : NUTRITION FOR THE NERVOUS SYSTEM
Phosphatidylserine concentrates in all cell membranes, especially in the myelin sheaths of neurons.
Throughout the body generally, it is involved in the repair, strength, permeability, elasticity and maintenance of structural integrity of all cell membranes.
In neurons, it is the dominant phospholipid in the myelin sheaths, and appears to be important for anchoring proteins of both structural and functional importance.
Phosphatidylserine has been found effective in treating the symptoms associated with early Alzheimer’s disease and dementia.
For example, 300 mg per day for 8 weeks normalised the EEG patterns of Alzheimer’s Disease patients, whilst 400 mg of PS per day improved brain glucose metabolism, normalised EEG patterns and improved cognition1.
Another study showed that in aged patients with memory loss given 300 mg daily for 12 weeks, the best results (a 15% increase in memory) were observed in those with the worst impairment - and the improvement in memory lasted for up to 1 month after cessation of treatment.
Patients with early stages of dementia can also benefit from PS supplementation. Patients aged 55-80 years with mild cognitive impairment took 300 mg per day for 12 weeks. Benefits noted were: improved ability to learn and recall names of familiar persons; recall the location of misplaced objects; recall details from the prior week; recall telephone numbers; paragraph recall; ability to concentrate while reading; and in conversing and performing tasks.
Age-related decline in dendrites.
PS prevents the age-associated decline in the number of dendrites within the brain. Rats supplemented with PS from the age of 3 to 27 months exhibited no reduction in their number of dendrites for a further 24 months.
PS has been found very effective in the treatment of depression, especially in the elderly.
PS helps to prevent atherosclerosis by mediating the phagocytotic removal of dead cells in vascular smooth muscle.
People with hypertension exhibit lowered PS levels, and supplementation has proved helpful.
Stress and exercise
PS counteracts the exaggerated release of adrenocorticotropic hormone and cortisol that occurs as a result of the excessive stress, or from strenuous exercise.
Also, all cells of our body may benefit from less toxicity in our body, particularly nervous system cells are very sensitive to toxins.