Welcome to my blog!

I'm an acupuncturist, teacher, fertility specialist, patient centered advocate, mom, activist and more! This blog is a place for me to write down the things on my mind, the things I discuss over and over, and the things I find helpful, interesting, and inspiring all in the hope that someone else out there, maybe YOU, will find some of these things to be helpful, interesting and inspiring too. I love learning, I love sharing, and I am passionate about helping others lead more balanced, fertile, and healthy lives - while trying to do the same myself. So here goes... The Blogging Life...


Type 3 Diabetes - Alzheimers

One aspect of this "new" (to me!) approach to diet that is really powerfully resinating with folks I'm talking with is the idea of Alzheimer's disease being linked to insulin issues. If that aspect of this discussion is of interest to you here are a couple links you may like:

Here is a nice piece from the New York Times blog by foodie Mark Bittman about it (he has some further links in his piece too).

and, if you are interested in the more technical aspects...

Here is a link to the National Center for Biotechnology Information's review of the data on the hypothesis that insulin plays a role in Alzheimer's which concludes:


Altogether, the results from these studies provide strong evidence in support of the hypothesis that AD  [AD=Alzheimer's Disease] represents a form of diabetes mellitus that selectively afflicts the brain. Positive data stemmed from (1) direct analysis of postmortem human brains with documented AD; (2) an experimental animal model in which brain diabetes with cognitive impairment and molecular and pathological features that mimic AD was produced by intracerebral administration of a drug that is commonly used to produce T1DM or T2DM; and (3) a study showing that PPAR agonists, which are used to treat T2DM, prevent many of the AD-associated neurodegenerative effects of ic-STZ. The data are supported by abundant in vitroexperiments that demonstrated essentially the same or similar effects of STZ or oxidative stress treatments of neuronal cells. The human and experimental animal model studies also showed that CNS impairments in insulin/IGF signaling mechanisms can occur in the absence of T1DM or T2DM. Finally, we demonstrated that although obesity with T2DM causes brain insulin resistance with some features of AD-type neurodegeneration, the effects are relatively modest, not associated with significant histopathological lesions, and lack most of the critical abnormalities that typify AD. Therefore, T2DM was deemed not sufficient to cause AD, although it could possibly serve as a cofactor in its pathogenesis or progression. Altogether, the data provide strong evidence that AD is intrinsically a neuroendocrine disease caused by selective impairments in insulin and IGF signaling mechanisms, including deficiencies in local insulin and IGF production. 

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