User:Glynwiki

Glynwiki's real name is Glyn Wainwright [1]

Cholesterol Depletion and leakage of the Na+ Transmembrane Potential

Reduction in eukaryotic membrane cholesterol causes Na+ to leak dramatically through the membrane. The explanation and mechanism and the mechanism has been written up by Dr Thomas HainesHaines, T. H. (2001). ""Do sterols reduce proton and sodium leaks through lipid bilayers?"". Prog. Lipid Res. 40: 299–324. {{cite journal}}: Cite has empty unknown parameter: |1= (help). Haines has shown that this causes a loss of the Membrane potential. Haines notes that the attempt to replenish Na+ can become runaway reaction which is ultimately lethal to the cell.
Link to Dr T H Haines Papers on Sterols and Membranes

Cholesterol Depletion and Dementias

Dr Henry Lorin's ^[1] interest in the relationship between cholesterol depletion and dementia began nearly ten years ago with his observation of the very low incidence of Alzheimer's disease in patients with type-2 diabetes. He noted that as a general rule this form of diabetes is associated with obesity and high blood cholesterol levels. He found that Cree Indians with their genetically predisposed diabetes of this type and high cholesterols have very low likelihood of Alzheimer's disease. He wondered could a high blood level of cholesterol offer some protective effect against the development of Alzheimer's disease? His enquiries discovered research publications describing the failure of myelination because of low LDL Cholesterol ( Apolipoprotein E)in blood plasma. The oligodendrocytes are unable to maintain and repair the myelin sheathing of the neurons. Neuron myelin sheathing loses cholesterol as a result of oxidative stress creating water soluble hydroxy-cholesterol which is eventually removed to the liver via HDL. Oligodendrocytes require huge amounts of myelin to maintain the situation. Dementia patients who tend to be losing weight and have lower cholesterol levels cannot maintain the protective myelin sheathing.

Our paper (currently in peer review) argues that the pathology develops initially due to damage caused by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer’s disease, and may also be due in large part to this same underlying cause. In this model the beta-amyloid production is a positive response to plasma membrane damage and ion leakages caused by cholesterol depletion.

Lipid Rafts hypothesis and cholesterol

As a result of reading biochemistry and recent Lipid_hypothesis research I have become interested in the paradigm shift that the lipid raft hypothesis has created in the world of biosciences. I am simultaneously concerned about the implications of this for those receiving long-term statin in chronic conditions or Preventative treatments which use statins in healthy people. Whilst acknowledging the success of statins in mainstream cardiology, there are concerns about extension of criteria and over-use of statins beyond any justification related to clinical trials of these drugs. There is a perception that these drugs are safe beyond the conditions examined in clinical trials and the non-cardiological implications are huge. The reporting and tracking of adverse events undertates the situation. In research for a BBC Radio 4 programme "The Investigation" in April 2008, the NNT in prevention showed a very poor outcome when set against the conservative estimates of adverse events caused by the side-effects of statins. See contributions at:-
User:Glynwiki/Mevalonate Inhibition
User:Glynwiki/Hypocholesterolemia
User:Glynwiki/Cholesterol Depletion


Wainwright G., Mascitelli L.,MD, Goldstein M. R.,MD, (2009). ""Cholesterol-Lowering Therapies and Cell Membranes" 
". Arch Med Sci. 5 (3). {{cite journal}}: Cite has empty unknown parameter: |1= (help); Unknown parameter |month= ignored (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)

Seneff S,. Wainwright G., and Mascitelli L. (2011). ""Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?"
". Arch Med Sci. 7 (in press). {{cite journal}}: Cite has empty unknown parameter: |1= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
Seneff S,. Wainwright G., and Mascitelli L. (2011). ""Nutrition and Alzheimer's disease: the detrimental role of a high carbohydrate diet"
". EJIM. {{cite journal}}: Cite has empty unknown parameter: |1= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)

Neutral Point of View

No doubt the WP:SYN and NPOV policies will ultimately prevail and commercial interests will be identified. I have no personal interest to declare beyond wanting to understand my personal experience of simvastatin in a preventative context. I hope I'm big enough to see both sides of the medical argument and appreciate the help of those who give me objective guidance whilst having a difference in perspective and experience.

Other Wikipedia Interests

Leeds Symphony Orchestra
Sunspots and Jupiter - The Planetary Tides of the Photosphere
http://www.newscientist.com/article/mg18124394.100-jupiters-influence.html

Can I suggest also the first book of a new "Lynda Collins Trilogy - The Girl who wasn't Good Enough" by Liz Wainwright, an established playwright as her first novel.Glynwiki (talk) 15:51, 14 February 2012 (UTC) at the moment

References

^ Lorin, Henry. Alzheimer's Solved. BookSurge Publishing, 2006 ISBN 1-4196-1684-6

External links

http://uk.youtube.com/profile_videos?user=glynwainwright Glyn publishes Science and Music Videos