This article will be shorter than it should be. I am not a medical doctor nor am I a neurobiologist. I am a daughter (and, to give myself a little credibility for literature review, a PhD Microbiologist currently practicing structural biology) who loves her dad. I want to make sure information that is generally ignored in medical practice is at least being discussed here. I have only added single references for some of my statements and, as a scientist, recognize that this would not cut it in peer review. However, if you like to read peer-reviewed literature, then you are welcome to use these articles as a jumping off point (or email me for more literature as I have quite a collection at this point.) I want to focus on, what I think, was the major contributor to Dad’s PD, whether genetically predisposed or not−extended proton pump inhibitor use. I will also mention a potential biological reason for Dad’s susceptibility to PD−increased MAO activity. And, finally, a good indicator of future neurological disease that Dad experienced, but society, in general, passes over because it is so common−sleep disturbance.
Proton Pump Inhibitors (PPIs)
Why reinvent the wheel when Chris Kesser has already written an informative series on the ineffective, harmful, and, unfortunately, overused PPI? You can begin reading about acid reflux and PPI use as written by Chris here. In summation, your stomach needs to be acidic and when it is not as acidic as it should be, due to PPI use, then you end up with dysbiosis (microbial imbalance, especially heightened risk of H. pylori infection) and malabsorption of nutrients. While I do not wholly agree with the low-carbohydrate approach to solving the reflux issue, I do agree that our stomach needs to be acidic and we should be addressing the issues using an individualized nutrition approach rather than prohibiting our bodies from doing what they should be doing with a drug.
Dad used PPIs for about 8 years, under the guidance of a doctor. Rather than addressing Dad’s weight (undue pressure placed on his stomach/esophageal sphincter), diet (especially consumption of dairy, wheat, and red meat), or alcohol consumption (which can cause esophageal inflammation and dysbiosis), Dad was prescribed multiple PPIs. The use of PPIs for this long, along with a diet that also promotes dysbiosis and inflammation can directly result in vitamin deficiencies (2) and indirectly result in neurological damage (e.g. PD), especially when considering infection with H. pylori (3).
Aside: I look forward to the scientific establishment of the relationship between PPI use and neurological disturbances (4). I look forward to it like I look forward to a stomach virus, but I look forward to it being an accepted concept none-the-less.
Alcohol and Monoamine Oxidases (MAOs)
Alcohol consumption, more specifically alcohol-dependence, has been genetically linked to increased MAO-B activity and this neurobiological basis for alcohol dependence primarily includes dopamine receptor dysfunction (5). Advanced PD drugs are aimed at decreasing MAO activity (specifically MAO-B) (6). MAOs degrade amines, but what is important for this discussion is that they can oxidize the most important neurotransmitter for PD sufferers, dopamine (7). The likelihood of someone who has consumed alcohol for a long period of time having increased MAO-B activity is good and this increased MAO-B activity can lead to the degradation of dopamine; hence, it is likely that Dad has lower concentrations of the neurotransmitter, dopamine, due to increased MAO-B activity. This may be a stretch and is still a bit muddled in my brain. I do, however, think there is a link and I hope by mentioning it here that someone with a deeper understanding of this area of science may offer some insight.
Sleep is more of an indicator of future PD and some other neurodegenerative diseases rather than a cause, per se (8). An abbreviated list:
- REM sleep behavior disorder (acting out dreams during sleep)
- Leg movement in sleep
- Nocturia (frequent nighttime urination)
It is good to be aware of these potential indicators of neurological disease, which can lead a person toward a more preventative lifestyle. In the case of PD, some measures can potentially be taken to stave off disease, or at least decrease severity and improve longevity (as I will discuss in Dad has Parkinson’s Part III: So, what do you do?).
- Matsuzaki et al (2015) PLoS ONE 10:e0133865
- Lam et al (2013) JAMA 10:2435
- Hashim et al (2014) PloS ONE 9:e112330
- Gomm et al (2016) JAMA Neurol 73:410
- Erjavec et al (2014) Progress in Neuro-Psychopharmocology and Biological Psychiatry 54:321
- Peripheral and Central Nervous System Drugs Advisory Committee Meeting: Background Package (2011) Azilect (rasagiline mesylate)
- Shih et al (1999) Polish J Pharmocol 51:25
- Postuma et al (2006) Neurology 66:845