Why I am experimenting with intermittent fasting to see if it helps Parkinson’s

no eatingWhy I am experimenting with intermittent fasting to see if it helps my Parkinson’s symptoms…

Let me state this categorically, I am not suggesting that anyone should begin fasting in an attempt to help with their Parkinson’s symptoms. Amongst other concerns, many people who are diagnosed with PD experience unexpected weight loss, and fasting does not seem safe in that scenario. There also may be concerns about fasting and some prescription medications. If you are considering this at all, please discuss with your doctor first.

That said, fasting, or more specifically intermittent fasting (IF) is something that I am experimenting with myself, and I am happy to share my experience and motivation with those who are considering it.

My motivation is two-fold.

On the one hand, fasting does promote autophagy. I say this with a caveat, because there are a plethora of health gurus and “YouTube celebrity doctors” that state this as a fact, then point to references that do not substantiate their claims.

Autophagy is the process through which the body recycles damaged cells, proteins, and toxins. There is a considerable amount of research that suggests the normal process of autophagy is disrupted in Parkinson’s Disease.

The Role of Autophagy in Parkinson’s Disease (2012):

Role of Autophagy in Parkinson’s Disease (2018):

Dysregulation of autophagy and mitochondrial function in Parkinson’s disease (2016):

These research papers can be a hard read. Charbel Moussa, Assistant Professor of Neurology, Georgetown University, does a great job of explaining the connection in his article “Nobel prize-winning autophagy research laid groundwork for potential Parkinson’s treatment”: http://theconversation.com/nobel-prize-winning-autophagy-research-laid-groundwork-for-potential-parkinsons-treatment-66474

In neurodegenerative diseases, toxic proteins accumulate within brain cells called neurons.

Neurons are irreplaceable. They must continue to recycle proteins and break them down into small amino acids to avoid a toxic buildup of abnormally large proteins. That is what autophagy lets them do.

The process works by sequestering unwanted proteins into pipelines called “autophagosomes.” Then they dump those proteins into a part of the cell called a “lysosome,” where they are recycled. When this process doesn’t work properly, harmful proteins can accumulate.

Defects in autophagy are a common factor in neurodegenerative diseases regardless of aging, gene mutations, environmental toxins, infections and abnormal proteins.

When my lab examined postmortem Alzheimer’s and Parkinson’s brains, we found that the molecular steps of autophagy are broken, leading to accumulation of the toxic proteins.

So if we can find a way to activate autophagy or repair the molecular cascade that kicks it off, cells could once again clear out harmful proteins. Work from my lab suggests that certain cancer drugs may actually do this.

Georgetown University has been running a clinical trial on nilotinib, a cancer drug, as a potential treatment. That’s great, I hope the study sees positive results. Just this week, a press release from Georgetown University suggests they are making progress: https://www.eurekalert.org/pub_releases/2019-03/gumc-rdh030819.php

But what about that “Nobel prize-winning autophagy research” referenced in the title of that article?

Dr. Yoshinori Ohsumi was awarded the 2016 Nobel Prize in Physiology or Medicine for his discoveries of mechanisms for autophagy. Nobel Prize press release:

There are plenty of health gurus who point to this Nobel Prize as if Dr. Ohsumi was a fasting researcher.

But, read the press release. The most recent of Dr. Ohsumi’s key research papers on autophagy was published in 2000. He was awarded the prize for “a series of brilliant experiments in the early 1990’s”, which have paved the way for further research.

Contrary to what all these so-called health gurus and “YouTube celebrity doctors” say, Dr. Ohsumi’s research is 20 years old, and he did not research human fasting. He researched the process of autophagy, and when he studied autophagy in yeast, he starved the yeast cells to induce autophagy. This starvation of yeast cells some does not directly apply to human fasting.

Starvation was long believed to be associated with increased autophagy, but there was an assumption that the brain was a protected organ that would be walled off from these effects.

In 2010, a team in California studied fasting, or more correctly, caloric restriction, in mice. They found that it did increase autophagy in the brain…of mice. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3106288/

I do think autophagy is very significant, and expect we will see great scientific progress in this area in coming years. I have doubts that my intermittent fasting will increase autophagy in my brain…maybe it will, but I’m not counting on it.

My decision to experiment with intermittent fasting is based more on the research of Mark Mattson, a professor of Neuroscience in the Johns Hopkins School of Medicine and chief of the Laboratory of Neurosciences at the National Institute on Aging. There’s a great overview of his research here: https://www.johnshopkinshealthreview.com/issues/spring-summer-2016/articles/are-there-any-proven-benefits-to-fasting

His TEDx Talk  from 2014 is legendary:

And his 2016 research paper helped convince me: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5411330/

There is a lot of good research details on intermittent fasting (IF) in that study, but the key take-away for me is this particular conclusion:

IF [intermittent fasting] can delay onset and slow the progression of neuronal dysfunction and degeneration in animal models of Alzheimer’s, Parkinson’s and Huntington’s diseases.

Yes…it says animal model…we’re talking about a mouse study again, and we don’t know if it will apply to humans. But, it seems a lot more relevant to me personally as someone with PD, than the uncertainties of autophagy.

OK, so that was long-winded…

What exactly is intermittent fasting?

From the Johns Hopkins Review magazine link earlier:

Mattson recommends people try one of two strategies for incorporating calorie restriction.

The first is called the 5:2 diet, which has gained popularity in recent years, particularly in England after the BBC aired a 2012 documentary called Eat Fast and Live Longer in which Mattson was featured. That diet calls for limiting your caloric intake to 500 calories two nonconsecutive days per week while eating a healthy diet in the normal caloric range (2,000 for women; 2,500 for men) the rest of the week. Five hundred calories means maybe a fried egg for breakfast and a small serving of lean protein with vegetables for lunch or dinner.

Another strategy is a time-restricted diet in which you pack all your meals into one eight-hour period a day so your body has time to exhaust its supply of glycogen, start burning fat, and produce ketones. Mattson says animal studies have shown that the time-restricted diet has effects similar to those of intermittent fasting.

If you do decide to try fasting, don’t dive in too quickly, Mattson advises. “The analogy with exercise applies here as well. If you’ve been sedentary and then all of a sudden you try to run five miles, it’s not very pleasant and you’ll likely get discouraged. It’s the same thing as if you’ve been eating three meals a day plus snacks, and then you’re not eating anything at all for two days; you’re not going to like it.”

While I have long been convinced the 5:2 diet makes sense for weight loss, I think the time-restricted diet makes the most sense to me for this experiment.

Apart from special occasions, I plan to eat only during an 8 hour period between the hours of 11am and 7pm (most days I’ll aim for a smaller time window). So, we’re basically talking about skipping breakfast and avoiding late night snacks.

My primary concern with this was how it would affect my morning workouts without breakfast. Depending on the day, I burn 750-2000 calories in a morning workout. It’s only week 1, but so far so good. This morning, I did better maintaining high intensity (80%+) for a longer period of time than usual, and actually wasn’t hungry after a 1600 calorie workout.

Will it help my Parkinson’s symptoms…that remains to be seen…

Update: March 20, 2019

First an update…today is day 10 of my intermittent fasting (IF) experiment (see more detail in the post above this one). I am following a time restricted diet (TRD), where I eat only during an 8 hour period between the hours of 11am and 7pm. If I eat dinner late, my first meal the following day is later, always leaving a fasting window of at least 16 hours.

I had hesitated to start this diet, because I am committed to vigorous exercise to attempt to delay Parkinson’s progression. These exercise sessions are scheduled between 9am and 11am, putting them near the end of my fasting window.

To my surprise, I have not been hungry or weak during exercise. Last Friday (day 5), my personal trainer asked me what I was doing different this week, because I was crushing the balance exercises. His eyes rolled back in his head when I started talking about intermittent fasting, because he’s a firm believer in eating small meals every 3 hours to speed metabolism.

That same day, I set a personal best in vigorous exercise points with my heart rate fitness tracker. And on Sunday, I went for a 4 mile run for the first time in months. That was probably an over-exercise mistake, as I am now fighting off soreness.

All told, it may be a placebo response, but I seem to have more energy for exercise, which I was not expecting. I haven’t noticed anything else, but my trainer’s balance comments are interesting.

This morning, I saw that Psychology Today just published an intriguing article “Exercise and Fasting Linked to Brain Detox”: https://www.psychologytoday.com/ca/blog/advancing-psychiatry/201903/exercise-and-fasting-linked-brain-detox

This article provides a layman’s explanation of a recent Harvard research study “26S Proteasomes are rapidly activated by diverse hormones and physiological states that raise cAMP and cause Rpn6 phosphorylation“. With a title like that, you know it’s a real page turner. 🙂

According to the Psychology Today article:

The study examined the cellular effects of both fasting and vigorous exercise – both considered metabolic interventions — which were each independently shown to improve the internal cellular disposal of so-called waste proteins.

And why is this so exciting? Because we don’t have to wait for the development of a new drug! There are two things that we can all do right now, just using our body’s natural processes and without side effects. Neurodegenerative diseases such as Lou Gehrig’s Disease, Parkinson’s and Alzheimer’s disease are all linked to the excess accumulation of misfolded (mutant, toxic, or unnecessary) proteins which interfere with cellular functions. The Harvard study shows that vigorous exercise significantly increased the levels of cAMP, a chemical trigger that induces a cellular process resulting in the elimination of these excess or waste proteins. The team’s senior researcher, Albert L. Golberg, demonstrated through earlier research that cAMP-stimulating drugs could also precipitate the removal of these defective or toxic proteins, including those that can lead to neurodegenerative conditions. This new study shows that through either vigorous exercise or a 12-hour fast, the body can naturally induce the very same process without an introduction of any exogenous medicines or supplements.

Other related articles:


From my personal experience of exercising with a heart rate monitor, I question how many people with PD are actually achieving vigorous intensity levels.

But my experience with the time restricted diet form of intermittent fasting suggests this may more easily achieved.