Part of the Parkinson’s Disease research that I mentioned a couple of weeks ago is a survey of all the food a participant has eaten in the past 24 hours. I received my login information and went to the site to log what I have been eating for the past 24 hours. To my amazement, there were almost no options to record food you had made yourself. My morning mug muffin is made from coconut and almond flours, pastured eggs, coconut and perilla oil, flax seeds, aluminum-free baking powder, and some sweetener. Every choice on the survey for muffins had a “brand” attached. There were hundreds of them. I think I am experiencing food industry overload.
I found this book on the goop page on Instagram (I know, I know). I’m not sure what grabbed my attention, but I read it and the science seemed sound. We have been following the diet for just over 3 weeks now. We have both lost weight, and are feeling good about what we feel going on in our gut. I am hopeful that eliminating lectins from my diet will boost my immune system, breed healthier mitochondria in the future, and stop causing stress on my vagus nerve. It is thought that if Parkinson’s Disease begins in the gut, it is this vagus nerve that allows it to travel to the brain. Obviously I need to learn more about this mechanism, but I like what I am eating and I like how I feel.
“If you are experiencing memory loss, Parkinson’s, or neuropathy, exciting research suggests that the exhausted Mighty Mice (mitochondria) in your nerve cells can come back to life if they are fed ketones instead of sugar.” Gundry, Steven R., M.D.
It is easy to look up research, references, and resources in this book, using the footnotes. In this case, here is what researchers Maalouf, Rho, and Mattson conclude from their study “The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies.”
“Calorie restriction and the ketogenic diet share two characteristics: reduced carbohydrate intake and a compensatory rise in ketone bodies. The neuroprotective effects of reduced carbohydrate per se are being investigated by several research groups (Mattson et al. 2003; Ingram et al. 2006). We have evaluated the possibility that ketone bodies might mediate the neuroprotective effects of calorie restriction and of the ketogenic diet. An expanding body of evidence indicates that ketone bodies are indeed neuroprotective and that the underlying mechanisms are similar to those associated with calorie restriction – specifically at the mitochondrial level.
However, several important questions remain unanswered. The effects of ketone bodies on gene expression have not been investigated, although inhibition of glycolysis with 2-deoxyglucose (which blocks phosphofructose isomerase) has been reported to inhibit BDNF expression and kindling progression in rats (Garriga-Canut et al, 2006). Moreover, the neuroprotective of ketone bodies in vivo have not been thoroughly examined. For instance, it is imperative to demonstrate that the neuroprotective effects of ketone bodies are associated with a preservation of clinically relevant functions such as cognition. Finally, it is crucial to determine if the anti-apoptotic properties of ketone bodies might potentially increase the risk of carcinogenesis. Intriguingly, both the calorie restriction and the ketogenic diet have been associated with anti-neoplastic properties and similarly, preliminary data suggest that the ketone bodies β-hydroxybutyrate and acetoacetate have anti-neoplastic effects on human glioblastoma cell lines (Patel et al. 2004; Jolly 2006 Zhou et al. 2007). Further research will hopefully further clarify the mechanisms underlying the neuroprotective properties of calorie restriction and ketone bodies and explain the counter-intuitive effects on carcinogenesis.”
I’m really excited to learn about this new research project from Dr Terry Wahls. Basically this team will survey all participants every six months for five years, and try to identify what impact alternative treatments might be having on the course of their Parkinson’s Disease. I am working on both my mitochondrial health through diet and lifestyle, and my brain’s neuroplasticity through learning and movement. It is my hope that I can model how to slow or halt this disease. I’d urge anyone with a Parkinson’s diagnosis to participate; it took me about 30 minutes to answer the first survey.