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New Research and Treatments for Parkinson’s Disease


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Find out what the latest research has shown in terms of the pathogenesis and etiology of Parkinson’s. What are some of the predisposing factors? What are some of the things to look out for that can be causative? And what kind of clues might those things give us in terms of treatment?

Revolution Health Radio podcast, Chris Kresser

Parkinson’s is obviously a neurological, neurodegenerative condition. If you’ve been following my work, listening to this show for any length of time, you’ll know that I spend a lot of time thinking and talking about the gut-brain axis. Whenever we talk about any kind of brain condition, we always have to look at the gut. And vice versa. If we’re talking about gut condition, we have to look at the health of the brain. That’s because the gut and the brain exists in this axis that’s interrelated and bidirectional. So the gut affects the brain and the brain affects the gut. This can give us, again, some clues in terms of what to look for whenever we’re dealing with a condition that manifests anywhere on this axis. It turns out there is actually a lot of research, most of it fairly recent, that makes a strong connection between gut dysfunction and Parkinson’s.

In this episode, we cover:

6:25  The latest Parkinson’s research and what to look for
13:34  Is Parkinson’s an autoimmune condition?
23:22  Parkinson’s treatment

Steve Wright: Good morning, good afternoon, and good evening. You are listening to the Revolution Health Radio show. I’m your host, Steve Wright, co-author at SCDlifestyle.com. This episode of RHR is brought to you by 14Four.me. Now if you haven’t heard of this 14-day healthy lifestyle reset program that Chris has put together, you’ll want to listen in for a little bit here. This program is really meant for somebody who’s still struggling with their digestion, maybe they’re struggling with acne, maybe a little weight gain, or any one of these nagging lifestyle symptoms. 14Four is the program for you. Basically, it’s 14 days with four different areas of focus. That includes diet, sleep, stress, and movement. If you listen to this show at all, you know that these are very important topics for your overall well-being, from recovering from weight gain to leading a healthy lifestyle. The problem typically is actually implementing them in your life and doing them all at the same time. So that’s what 14Four does. I urge you to go check it out at 14Four.me. With that said, with me is integrative medical practitioner, healthy skeptic, and New York Times bestselling author, Chris Kresser. Chris, how’s your day?

Chris Kresser: It’s great. It’s beautiful, cloudless sky here in California. It’s a little chilly, but a gorgeous day. How about you?

Steve Wright: My day is going great. It’s a ridiculous snowstorm out there, but I got my new tea kettle right here.

Chris Kresser: Oh, very nice. It’s very nice. I like it. I’m having some kukicha, or twig tea, at the moment.

Steve Wright: Oh my gosh. I was about to brag about my blend of turmeric and yerba mate, but you just stole the show, man.

Chris Kresser: No, no. Twig tea is green tea. Most green tea comes from the leaves of the plant, but this is from the stem or the twigs. It’s a lot lower in caffeine. It has kind of an earthier flavor. It’s one of my preferred afternoon beverages because it doesn’t jack me up like stronger caffeine would, but it gives me a nice little lift.

Steve Wright: I didn’t even know there was such a thing as twig tea. See? That’s why I love doing this show.

Chris Kresser: You learn something every day. And I’ve got my favorite new cup. Can you see it?

Steve Wright: Oh, I see it! Is that a Christmas gift?

Chris Kresser: I made it as Christmas gifts for other people, and I had to give myself one too. Other people in my family. So pictures of Sylvie all around the cup.

Steve Wright: Sylvie has officially made the show.

Chris Kresser: Yeah, she has. We have a good show planned today. It’s a question about Parkinson’s disease, which is a—there’s some really interesting new research coming out. It’s a tricky disorder to work with, no doubt. It sounds like Anthony’s doing a lot of the right things, which we’ll hear about in a second. But I’m going to give him and the rest of the listeners hopefully some new ideas for some things to focus on, and just kind of summarize some of what the latest research is telling us. Let’s hear from Anthony. We’ll go from there.

Anthony: Hi, Chris. This is Anthony DiClementi from Chicago. I’m a big fan of your show. Thank you for doing what you’re doing. Please keep it up. My question is this. It’s actually about my dad. My father has been experiencing some Parkinsonian symptoms now for the past few years. His mother is in the process of passing away after dealing with Parkinson’s herself. We have done a number of interventions that have helped, ranging from introducing the ubiquinol form of CoQ10 at 300 mg/day. We’ve also gotten him doing B12 shots, taking the bioactive form of folate and B6, along with some B12 lozenges and omega-3 supplements, and some other things that we found to be helpful. He’s also taking acetyl-L-carnitine, the Memory Pro product. Some of that has helped. It’s slowed the progression, but it hasn’t necessarily reversed things. He was always a really strong guy. The past five or ten years, he’s experienced a very steep physical and cognitive decline. My question is, what protocol do you use with your patients that are expressing Parkinsonian-like symptoms when haven’t yet been diagnosed with Parkinson’s? Because you want to try to intervene before it progresses to that point. Is there a way that you could recommend us finding a good physician to help with this in the Chicagoland area? Thank you so much for your time. I really appreciate this. We’ve really tried to do everything we can in our power from a dietary and supplemental perspective. We’ve decreased his protein intake significantly, trying to get him to eat more vegetables. Then we’ve got him on those supplements that I mentioned plus some more. But anything you can share would be very, very helpful, particularly in terms of the protocol that you use and finding a good physician for us to work with. Thank you so much, Chris. I really appreciate it.

Steve Wright: Before Chris gets into this, if you want to be Anthony, if you would like advice like this from Chris on your situation or what you’re doing, make sure you go to ChrisKresser.com/podcastquestion. This radio show is brought to you by you and for you, so make sure you do that. All right, Chris. Take it away.

Chris Kresser: All right. As I mentioned, a lot of the things that Anthony and his family are doing are definitely good ideas and things that can be really helpful. I’m just going to mention a few other things. I’m going to talk a little bit more about what the latest research has shown in terms of the pathogenesis and etiology of Parkinson’s. In other words, what are some of the predisposing factors? What are some of the things to look out for that can be causative? And what kind of clues might those things give us in terms of treatment?

The Latest Parkinson’s Research and What to Look For

Parkinson’s is obviously a neurological, neurodegenerative condition. If you’ve been following my work, listening to this show for any length of time, you’ll know that I spend a lot of time thinking and talking about the gut-brain axis. Whenever we talk about any kind of brain condition, we always have to look at the gut. And vice versa. If we’re talking about gut condition, we have to look at the health of the brain. That’s because the gut and the brain exists in this axis that’s interrelated and bidirectional. So the gut affects the brain and the brain affects the gut. This can give us, again, some clues in terms of what to look for whenever we’re dealing with a condition that manifests anywhere on this axis. It turns out there is actually a lot of research, most of it fairly recent, that makes a strong connection between gut dysfunction and Parkinson’s. For example, constipation has been shown to precede the development of the somatic motor symptoms of Parkinson’s disease for several years. We have studies showing that the intestinal microbiome, the gut flora, is altered in Parkinson’s disease and is directly related to motor phenotype. So the specific kind of type of microbiome presentation relates to the different ways that Parkinson’s manifests. We know that the abundance of particular phyla of bacteria in the stool of Parkinson’s patients—we see an abundance of certain types of bacteria, rather, in the stool of Parkinson’s patients versus controls. There is even some experimental evidence in animals that altering the balance of these bacteria can have an effect in terms of treatment. We know that Parkinson’s patients have significantly greater intestinal permeability, i.e. their guts are more leaky than patients without Parkinson’s. We know that intestinal permeability in Parkinson’s patients is correlated with markers of oxidative stress and endotoxin exposure, like exposure to lipopolysaccharide.

Finally, there’s quite a lot of research correlating Parkinson’s with small intestinal bacterial overgrowth (SIBO). I’ve mentioned this before, but one study detected SIBO in 25% of Parkinson’s patients. Another study found even higher prevalence of SIBO in Parkinson’s disease versus controls. So 55% of the patients with Parkinson’s had SIBO versus 20% of controls, which is, by the way, a pretty high percentage for controls. Another study found an even bigger difference. It was 54% in Parkinson’s with SIBO versus just 8% of controls. And Parkinson’s patients with SIBO have much worse motor function than Parkinson’s patients without it. We know that eradication of SIBO in Parkinson’s patients results in an improvement in motor function. And for some reason, probably related to motility via the gut-brain axis and the vagus nerve, the relapse rate of small intestinal bacterial overgrowth in Parkinson’s patients is unfortunately very high. It’s 44% even at just six months after treatment. The relapse rate for SIBO in general is quite high, but it’s even higher for Parkinson’s patients. That probably is because of that bidirectional connection between the gut and the brain. In other words, SIBO is making Parkinson’s worse or contributing to Parkinson’s, but Parkinson’s is probably contributing to SIBO as well via perhaps a reduction in gut motility. So when you put all that together, it’s a pretty strong relationship between digestive and gut function and the risk of developing Parkinson’s disease, and also just exacerbating it if it’s already present.

Steve Wright: That’s just another reason why I want to keep pooping on a daily basis. I did not know that connection.

Chris Kresser: Yeah, one of many reasons. This show, we can almost sound like a broken record sometimes, because just about any condition that we talk about at this point has a strong correlation to gut health, you know, the gut microbiota, the intestinal barrier, and SIBO. And really, that’s good news. Because from a functional medicine perspective, we’re always—you know, a patient might walk through my door. Let’s say two different patients. They might have very different symptoms. But as a functional medicine practitioner, I know that I need to be really looking at the same basic systems for most patients. Like, I’m looking at the gut, I’m looking at the HPA axis, I’m looking at oxygen deliverability and blood sugar regulation, I’m looking at methylation. These are all the underlying mechanisms that tend to be at the root of most modern disease, regardless of whether we’re talking about diabetes, cardiovascular disease, autoimmunity or neurodegenerative conditions like Parkinson’s and Alzheimer’s. So it actually really simplifies things in a way, if you’re approaching things from a functional medicine perspective.

One more aspect of gut health, but also just immune function that’s linked to Parkinson’s, is gluten intolerance. There’s a fair amount of literature suggesting that gluten intolerance, non-celiac gluten sensitivity, especially when it is connected, when transglutaminase 6 (tTG6) antibodies are present. Transglutaminase 6 is an enzyme that has a lot of activity in the brain. And in patients who are gluten intolerant who also produce antibodies to transglutaminase 6, when they eat gluten, their body essentially attacks this transglutaminase 6 enzyme in the brain and causes neurodegeneration. This is present in some patients with Parkinson’s. Gluten, therefore, can contribute to and exacerbate Parkinson’s if a person is gluten intolerant. Cyrex Array 3 is the best test available right now for testing reactions against the full wheat proteome, not just gluten, but other proteins in wheat. They also run antibodies to transglutaminase-2, -3, and -6. So this can be helpful. I don’t think I’ve had a Parkinson’s patient with tTG6 antibodies, but I’ve had certainly a lot of children on the autism spectrum and other people with neurodegenerative, neurological disorders test positive for antibodies to various epitopes of gliadin, agglutinin or wheat germ agglutinin (WGA) and also tTG6. There’s a very close correlation between that and their symptom presentation.

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Is Parkinson’s an Autoimmune Condition?

Steve Wright: Is this a good chance to ask a question? If gluten is causing potential reactions to the brain, is Parkinson’s, in your opinion, an autoimmune condition?

Chris Kresser: Well, it’s interesting that you ask that. I don’t know. It has some characteristics that could be—you know, autoimmunity may play a role. Actually, one of the things I was going to talk about next was low-dose naltrexone (LDN) as a potential therapy for Parkinson’s. I’ll just skip to that now. Because the fact that low-dose naltrexone seems to work in some cases may actually suggest that there is autoimmunity present or autoimmunity may play a role in Parkinson’s. We know that LDN halts progression in some cases of multiple sclerosis, and it’s been used more recently with other neurodegenerative conditions like Parkinson’s and amyotrophic lateral sclerosis (ALS), which is Lou Gehrig’s disease. These conditions are still not that well-understood in terms of their etiology, but there is some evidence that suggests an autoimmune mechanism, which could explain why low-dose naltrexone works.

For those who aren’t familiar with LDN and haven’t heard me talk about it in the past, there are a few mechanisms of action of LDN. One is that it promotes T regulatory cell function. The T regulatory cells are cells that help balance and regulate immune function. That’s why LDN tends to work so well in autoimmunity. But LDN also reduces central nervous system inflammation, and we know that Parkinson’s is characterized by both inflammation and oxidative damage in the central nervous system in the brain. So that’s another reason that LDN might work for Parkinson’s. LDN is also a prokinetic, which means that it increases intestinal motility. It’s being used by people who are on the front line of SIBO treatment, like Dr. Mark Pimentel at Cedars-Sinai, for patients who don’t respond to typical SIBO treatment because their motility is impaired. Or let’s say they do respond, like they get rid of SIBO, but it comes back. They relapse because their motility is slowed down, which means the cleansing peristaltic wave doesn’t happen, which means they’re much more likely to get bacterial overgrowth in the first place. LDN is being used as a prokinetic to promote better motility and reduce the chances of relapse for SIBO therapy. And because, as I mentioned, Parkinson’s is related to SIBO, and Parkinson’s patients have a high probability of relapsing for SIBO, then LDN could be effectively used as a prokinetic in Parkinson’s treatment.

There’s a researcher, Dr. Hong at the National Institutes of Health, who believes that Parkinson’s and MS are caused by overactivated microglial cells, which are the immune cells, killer cells in the brain, which in turn, causes chronic brain inflammation. And we have evidence that low-dose naltrexone (LDN) significantly inhibits brain inflammation, neuroinflammation. So I wouldn’t call Parkinson’s like a straight up autoimmune disease in the way that we understand other autoimmune diseases like MS and celiac, but I would say that there is enough evidence that it does have some characteristics of autoimmunity, and may respond therefore to some of the same kinds of dietary, supplement, and perhaps medication and lifestyle interventions that autoimmune disease responds to.

So there’s another whole piece here to look at in terms of etiology and treatment. It’s iron overload. I’ve spoken a lot about this in the past. In fact, I gave a talk on iron overload at the Ancestral Health Symposium. I think it was 2012 or 2013, I can’t recall. The talk is available online for free. I think if you search for “Chris Kresser iron overload”, you’ll find it. What I argued in that talk is that there’s a lot of evidence that high-normal and just slightly elevated iron levels, which are completely ignored in the conventional medical establishment, can actually be a pretty serious risk factor for a number of different diseases, including things like Parkinson’s disease. We know that iron is a catalyst of oxidative damage. It’s a free radical, so it causes oxidative stress and inflammation. You know, all of the tissues in the body are sensitive to that, but some of the tissues that are the most sensitive would include the liver, the heart, the pancreas, and, of course, the brain and the small organs in the brain. So iron has been strongly implicated in several neurodegenerative disorders, including Parkinson’s disease.

I read a paper not too long ago that went as far as saying that the underlying pathogenic event in oxidative stress in the brain is cellular iron mismanagement. I test everyone who comes into my practice for iron—you know, they get a full iron panel. We’re testing for iron deficiency and for iron overload. In my patient population at least, who is typically on a Paleo diet, eating red meat and a lot of other iron-rich foods, iron deficiency is actually fairly rare. Worldwide, iron deficiency is a huge problem. Two billion people around the world suffer from it. If you were to look at the general population in the US, you’d find that iron deficiency is a much bigger problem than iron overload, especially in women. But in my patient population, iron overload is actually fairly common.

So one of the things that you want to look for, especially if you’re a man, is iron overload. You would be looking at markers like serum iron, iron saturation, total iron-binding capacity (TIBC) and unsaturated iron-binding capacity (UIBC), and ferritin as a starting place. If those numbers are indicative of iron overload, then you’ll want to look into an iron reduction protocol, which could include things like blood donation. That’s phlebotomy. Removal of blood is the most effective way of reducing your iron levels. Reducing your consumption of the most iron-rich foods, which unfortunately are some of the healthiest foods to eat, like organ meats and shellfish. You want to avoid high doses of vitamin C and HCL because they both significantly increase iron absorption. Bad news here: alcohol also significantly increases iron absorption. So sitting down to a meal of liver and onions with a glass of wine and taking some HCL capsules and vitamin C beforehand would definitely not be a good idea if you have iron overload.

Steve Wright: What if you’re strapped to a table and you’re currently bloodletting? Is it okay then?

Chris Kresser: Right. Then you should make sure to cook that meal in a cast iron skillet that’s really old and visibly flaking off before you do that. Yeah. Definitely check out that presentation if you’re curious about this, because there’s a lot more detail in there about how to approach this. We don’t have time to go into it today, but that’s definitely something you want to consider. The reason I said it’s more of an issue in men is that—and postmenopausal women, I should say—premenopausal women, women who are still menstruating, lose a little bit of iron each month in the menses. They’re a lot less likely to develop iron overload in the first place. But men, obviously that’s not happening. We just accumulate iron as we go through our lifetime. In most cases, we have a very intelligent mechanism for storing the appropriate amount of iron. Let’s say I eat liver. The cells in the intestine and other signaling cells or signaling molecules will kind of check in with my body and see how much iron I have stored. If I’ve got enough iron, then I just won’t absorb any of the iron from the liver; I’ll just excrete it. But there are a lot of different genetic mutations that can interfere with that iron-sensing function, and some people just go on absorbing more iron even if they have enough stored. Those are the people who are likely to develop iron overload. So it is more common in men. But when women enter menopause and stop the monthly menstruation, the rate of iron overload starts to equalize with men and postmenopausal women.

Steve Wright: This is just a side tangent. If people still can’t figure out how to get their liver, like the people who don’t have iron overload, for those of you who still can’t figure out liver consumption, EPIC Bar—I don’t know if you saw this, Chris—just came out with a liver beef bar.

Chris Kresser: Awesome.

Steve Wright: As far as I can tell, after several taste testings with myself and other people, it tastes better than all the other EPIC bars they’ve made so far. So check that out.

Chris Kresser: Cool. No, I didn’t know that. That’s a good tangent. Anything that can help people eat liver is always a good tangent. Let’s see.

Parkinson’s Treatment

A couple more things I want to cover before we finish, in terms of potential things to try. Curcumin is a compound that’s found in turmeric in the diet. It protects against inflammation and oxidative damage. It crosses the blood-brain barrier and is neuroprotective in several different neurological disorders. It’s really quite remarkable in its effects on a lot of different brain disorders. However, most oral forms of curcumin are poorly absorbed. If you eat a lot of turmeric, it might taste good if you like turmeric or if you drink it in your tea like Steve’s doing. It’s definitely a great thing to do, but you’re not going to absorb huge amounts of bioavailable curcuminoids, which are the active compounds. There have been a number of forms that have been introduced in recent years that have much better absorption. Things like the BCM-95 form, Theracurmin, the Longvida form, and then most recently, liposomal forms of curcumin. I think liposomal delivery is probably the best for a lot of these nutrients that can be difficult to absorb. We’ve been using liposomal curcumin more in our practice recently. I’ve seen some pretty good results. I’ve taken it myself, along with other forms of curcumin. I think the liposomal form probably works best. That’s something to consider.

Steve Wright: Do you have a brand there?

Chris Kresser: The Seeking Health brand is pretty good for liposomal curcumin. Then Longvida, L-O-N-G-V-I-D-A. It’s not a brand. It’s a patented form or delivery system. A lot of different supplement brands use Longvida. You can just search for Longvida. They have their own website. Then on the Longvida site, it shows what different brands contain the Longvida form. That’s one way to do it too. The last thing is the ketogenic diet. You know, I recently wrote a whole series about carbs and the pros and cons of low-carb diets. In one of the posts, we talked about when very low-carb diets are appropriate and effective. One of those situations was, of course, neurodegenerative conditions, which we’ve talked about before. Ketone bodies that we produce, if you’re on a ketogenic diet, bypass defects in mitochondrial complex I activity. These defects in mitochondrial complex I have been implicated in Parkinson’s disease. So ketone bodies can bypass that and promote more normal cellular metabolism. There’s very little research in actual human beings on the effects of ketogenic diet on Parkinson’s. But there is a very small study, with only seven patients, that showed that 28 days of ketogenic diet improved Parkinson’s, as measured by a disease rating scale that’s often used to subjectively determine disease activity.

Then we have some animal and in vitro studies that have shown benefits with a ketogenic diet. But of course, we need more research ideally to really show that this is effective. However, it’s a safe thing to try I think if it’s done responsibly, especially compared to some other drugs. And if you put together an approach that includes testing for and then treating any gut issues, like SIBO or intestinal permeability or dysbiosis, if you test for gluten intolerance and remove gluten from the diet, if you test for iron overload and then get iron levels back to normal, if you consider perhaps low-dose naltrexone as a way of reducing CNS inflammation and promoting T regulatory cell function, if you use something like liposomal curcumin to reduce oxidative damage and neuroinflammation, and then you try a period of time on a ketogenic diet, I think that could be a pretty effective strategy altogether. All of it is relatively low risk in terms of side effects and potential complications, compared to some of the drug treatments that are available. I hope this was helpful, Anthony, and gives you some ideas to focus on. I hope for those others that are listening, who have a family member or a friend who’s affected by Parkinson’s, this gives you some things to think about.

Steve Wright: I think it’s an amazing approach you just laid out there, Chris. I hope this really helps Anthony. One question. I know we’re out of time here, but I feel like it’s worth asking for people out there. What about some S-acetyl glutathione or some intravenous glutathione in a case like this?

Chris Kresser: Great question. Maybe I misread the question. I thought he had mentioned glutathione, but it’s possible that he didn’t. Glutathione would definitely be helpful. Glutathione and curcumin together can be really effective, a kind of one-two punch in terms of addressing oxidative stress and inflammation. Glutathione, of course, is the master antioxidant in the cells. We know that glutathione is depleted in several different conditions, like autoimmune diseases. It’s also depleted by numerous aspects of the modern lifestyle, like not sleeping enough, stress, not exercising enough, and poor diet of course. That’s because a lot of the precursors of glutathione, we know, especially from the recent NHANES Nurses’ Health Study data that just came out, that almost half of the population is deficient in most of the antioxidant vitamins, like vitamin A, vitamin C, vitamin D, and vitamin E. When I test people for glutathione status, it’s extremely common to see markers for both a high need and demand for glutathione, and also inadequate intracellular levels of glutathione. So yeah, liposomal glutathione, again, is probably my favorite way of taking glutathione. But you can also use precursors like alpha-lipoic acid and N-acetylcysteine. Whey protein is a good precursor for glutathione, if you tolerate that. Fresh fruits and vegetables in the raw form are a good source of glutathione as well. Exercise upregulates glutathione production. Stress reduction is important for glutathione. Great question, Steve.

Steve Wright: Thanks. I can’t remember if Anthony mentioned it or not, but I felt like that was a good thing to add in there.

Chris Kresser: It’s important. You’re right.

Steve Wright: All right.

Chris Kresser: That’s it.

Steve Wright: Thanks, everybody, for listening to this show. Like I mentioned earlier, go to ChrisKresser.com/podcastquestion to get help for you or your loved ones on the show. In-between episodes, if you’re wondering—for instance, I didn’t know about this new Nurses’ Health Study that Chris just mentioned. It’s probably because I don’t check Facebook enough, and when I’m on Facebook, I don’t go to Facebook.com/ChrisKresserLAc enough to see what Chris is reading and the new studies that are coming out. If you’re on social media, whether you’re a Twitter or a Facebook person, make sure you check him out in either place. Twitter.com/ChrisKresser. Thanks, Chris.

Chris Kresser: Thanks, Steve. Thanks, everyone. See you next time.

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Chris Kresser in kitchen


Join the conversation

  1. Try vegan whole foods diet like Nutritionfacts.org or Dr. McDoogle or Chef AJ on You Tube. It has changed my life. No more migraines, no more sciatica pain. I feel great! Do the diet for at least 10 days to two weeks to experience the change in your health and life outlook. Chef AJ spoke about how her food choices changed I was not convinced but I get it after two week on the diet. I eat fruits, vegetables, whole grains (not so much, but they don’t bother me, beans, lentils, nuts, seeds (sesame especially). I had been eating lots of avocados (2 a day) but probably overdid it because I started to not feel so great so I’ve cut back to 1 every four days (This may be coincidental, of course). I guess it’s always best to rotate foods. I do try to eat a beet a day and raw greens like kale (about a pound a day).

    • Try the diet for a week or two and if you miss animal protein you can always add some in once a week if you don’t feel better. I think this diet works because it clears out the bowels and it is nutrient dense. My skin is looking better than ever and I have no bloating. My eyes are now deep green and my complexion is pink instead of sickly pale-yellow. Also, I try to do 10-16 minutes of high intensity interval kettlebell workout and 10-16 minutes of running every other day, along with pilates once a week.

  2. I see so much said about gluten intolerance tests not being conclusive. Is there really a reason to get the specific one(s) you recommend? Why waste money if you might get a false negative?

  3. I have Parkinson’s and have read about the particular interventions you mention by researching the internet. Hearing you discuss them gives me the added confidence to give them a try at last.
    Thank you

    • Hey Celia, I am sorry about your condition. Did you try for second opinion??? Actually my uncle’s daughter suffered a lot with Parkinson’s disease. It’s so horrible to handle the situation at that time. By god grace one of my friend gave suggestion ta take Medical second opinion. After took suggestions from top experts from Bestdoctor.com now her condition is better than before.

      Thanks Chris Kresser for sharing this informative stuff…

  4. I would like to take alpha lipoic acid as a glutathione precursor. However, I have reactive hypoglycemia (low blood sugar) and I found the ALA at the store today in the diabetes section. A short search online says it will lower blood sugar. So perhaps not a good fit for me after all? My question is, does anyone have experience with ALA affecting blood sugar? Chris, any thoughts?

    • ALA crashes my blood sugar (I am prone to hypoglycemia).
      I tried it with a moderate carb snack, not on empty stomach, and the result was low blood sugar an hour later. That same moderate carb snack on its own does not cause me problems.

  5. If you or your loved one has Parkinson’s Disease or parkinsonism, please search “amino acid therapy” developed by Dr. Marty Hinz. It has given my sister her life back! It does not come without expense and effort, but the changes have been nothing short of miraculous for her.

    • Hey Sue,

      How’s your sister doing since your post, I came across a co that test your Neurotransmitters with a urine test and sets up an amino acid therapy. I’ve had PD tremors since Sept 2013. Thanks for your response! Mark

      • Hello Mark,
        I’m sorry that I am just seeing this now. She continues to do great! She is still working on finding the perfect doses – but is functioning at ~95% at least 90% of the time. This is after progressing to the point of needing help with all of her activities of daily living – and being wheelchair-bound outside of the home. If you contact CHK Nutrition, they can put you in touch with a physician using this treatment. It is expensive – but, like I said in my post, it has given my sister her life back!

  6. My Father has Parkisons, dementia, and hydrocephalus. Do you think that the protocol mentioned here would help?

  7. Great podcast – I love this: “as a functional medicine practitioner, I know that I need to be really looking at the same basic systems for most patients”

    I was not aware of the constipation/SIBO connection but the whole gut-brain connection makes so much sense.

    I know you couldn’t address everything but because of my work with anxiety (and the fact that 45% of those with Parkinson’s have anxiety) I always consider low zinc and low vitamin B6:
    Zinc/copper imbalance http://www.ncbi.nlm.nih.gov/pubmed/24954589
    A case study on Parkinson’s and low vitamin C and zinc http://www.ncbi.nlm.nih.gov/pubmed/25070397
    Many studies on homocysteine and Parkinson’s – here is a recent one http://www.ncbi.nlm.nih.gov/pubmed/24992727

  8. Meg: Good points. As a PT, I have seen the results of exercise and Parkinsons. The Big and Loud program and the PRW4Life programs have compelling research. I would add to that cranial electrical stimulation as researched by the VA. Also very interesting.

  9. Curcumin bioavailability. Read somewhere that mixing black pepper w turmeric significantly improves the bioavailability of curcumin/tumeric. Something in black pepper that affects this.

    • I have heard that also. I make a paste of turmeric and black pepper to make golden milk everyday, at least once, if not twice!

  10. There’s a tendency to refer to PD as a homogenous disorder (I dislike “disease”) whereas it’s heterogenous.
    It is possible to have the tremor dominant variation and sprint. Even at an advanced age (80-ish) – a feat in itself!
    The typical Neurologist will tend to provide a range of prescriptions or refer for DBS. The prescriptions may persist even if there is no tangible response, and in spite of severe side effects.
    They are less likely to recommend nutritional therapies.
    Exercise does seem to be gaining ground but the problems surrounding PD also mitigate against compliance. There can be an aversion to groups; it can be difficult to reach centers, due to declining driving skills etc.
    It disappoints me that even celebrity foundations (MJFF et al.,) seem to work primarily with Big Pharma. Rather than pursuing non-chemical and non-invasive possibilities that require funding as there is less of a profit in the offing. Catch-22!

  11. clinical glutathione by terry naturally is a sublingual form of glutathione. i have been taking it for several months and found it to lower my inflamation.(i have me/cfs and hashi’s.

  12. I hadn’t read all the comments, but I do know that AFA, Aphanazomenon Flos Aqua, the Blue Green Algae professionals and others scorn and ignore, is one of the most effective foods that decrease Parkinson symptoms. It increases Adult Stem Cell Circulation, which seems to be very effective with Parkinson. Take in large doses and it takes 3-4 weeks before symptoms start to decrease.

    • Janice
      Thank you for your comment about AFA, blue/green algae, but what is not clear is it based on your personal experience or the manufacturers claims? Also, do you have to take them long term?

  13. I appreciate Meg’s comments concerning toxins and PD. This is from a post that has been forever in draft mode for my site: 11 ubiquitous pesticides increase PD risk at low concentrations’, and the levels are way below what is needed for the pesticides to do their job.  The pesticides are:  All metal-coordinating dithiocarbamates tested (e.g., fungicide maneb, pesticide ziram), 2 imidazoles (fungicide benomyl, triflumizole), 2 dicarboxymides (captan, folpet), and 1 organochlorine (dieldrin.)  “These pesticides are pretty ubiquitous, and can be found on our food supply and are used in parks and golf courses and in pest control inside buildings and homes. So this significantly broadens the number of people at risk.

    PD Researchers study agricultural chemicals and well-water contamination, see the population-based, case-control study called the Parkinson’s Environment & Genes Study which focuses on 3 rural California counties (Fresno, Tulare, Kern) as most R&D has looked at urban.

    From Well-Water Consumption and Parkinson’s Disease in Rural California: private well water resulted in approximately 70–90% increases in relative risk of PD. Many private wells are dug or driven at shallow depths (i.e., < 15–20 yards), which place them at risk of being contaminated by land activities such as pesticide applications in the vicinity of a well (U.S. Environmental Protection Agency 2002.) Measurable concentrations of pesticides have been detected in air, water, plants, and animals up to several hundred meters from the application sites (Chester and Ward 1984; Currier et al. 1982; MacCollom et al. 1986), emphasizing the need for methods to assess environmental exposures due to drift and contamination of soil, air, and water in agricultural communities.

    From High risk of Parkinson's disease for people exposed to pesticides near workplace, "This stuff drifts… it's borne by the wind and can wind up on plants and animals, float into open doorways or kitchen windows — up to several hundred meters from the fields… combined exposure to pesticide ziram, fungicide maneb and herbidice paraquat near any workplace increased the risk of PD threefold, while combined exposure to ziram and paraquat alone was associated with an 80 percent increase in risk. This is the first study that provides strong evidence in humans that the combination of the three chemicals confers a greater risk of Parkinson's than exposure to the individual chemicals alone.

    Interesting United States PD incidence maps can be found at: Geographic and Ethnic Variation in Parkinson Disease: A Population-Based Study of US Medicare Beneficiaries, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2865395/

  14. About five years ago I developed Parkinson symptoms (I did not have a clinical diagnosis, so I assume that I can claim that I had Parkinsonism). Two neurologist told me that it was too early to give a PD diagnosis, even though I had many of the early symptoms on the right-side which included: muscle-loss, stiffness in all the joints and my jaw. I also developed a tremor in my index finger about one year into the symptoms. MRIs were clear. I also had diverticulosis, IBS, gas, heartburn since my early 40’s.

    Up to this point in time (age 49) I ate a “normal” standard american diet (SAD) my entire life. I even started treating my gut symptoms with a low-fat / high-fiber (sugary) diet. This is when the PD symptoms really accelerated!

    I took health into my own hands; declared to the gods that it is possible to heal and took the kingdom by storm and decided that I WILL GET BETTER and then humbled myself to just learn. What I discovered is essentially everything Chris has described. I healed my gut and my Parkinsonism symptoms are now 99% reversed. The ketogenic diet with coconut oil and a ton of vegetables and targeted supplements was the pathway back to health.

    It took nearly three years to reverse all the symptoms, It was a long journey, but this 53-year old man feels like he is 20 again!

    It now think that my Parkinsonism may have been triggered by taking two rounds of Cipro to treat diverticulitis in my mid 40’s. I will never know, but will always be suspicious of the fluoroquinolone antibiotics.

    • So glad to hear you took your health back! Yes, I have had problems with Cipro in the past also and do not doubt for a minute it was the root cause.

    • Thank you for your comments on Cipro. Recent use for a tropical dysentry proved very detrimental . MY whole system was acutely and chronically ? affected. I would appreciate any information you might have on a functional coarser of action to regain my life ”Randy Brooks

  15. Interesting topic and I greatly appreciate having the transcript. I’m not much for listening to podcasts and when the subject is technical, I definitely prefer seeing it in writing so I can read and absorb at my pace.

    • Agreed! I can also read faster than they speak so that makes it easier to get through the information in one brainwave and not lose focus 🙂

  16. Anthony – to find a good movement disorder specialist, specifically one that specializes in PD – reach out to your regional APDA center (under “Local Resources”. They’re amazing people who will not only connect you with a referral to a PD Specialist – but also support groups and PD exercise classes.

    Chris – I’m honestly really disappointed in this episode. I’ve been waiting for some time for PD to be covered more by the paleo community – but this was a let down. I’m upset – as a member of the PD *and* paleo communities.

    The biggest reason being exercise and movement were not mentioned at all as a treatment option for Parkinson’s. There are more studies supporting the benefits of exercise over ANY other treatments these days – especially with the tolerance people develop to pharmaceutical and supplemental PD treatments. Ignoring exercise and telling people to just focus on supplements and gut health is a huge blunder – usually a blunder coming from apathetic general neurologists when Sinemet doesn’t work and the patient doesn’t want DBS. Speak to any true movement disorders specialist, and the first thing they’ll recommend is daily exercise or increased movement. Am I saying exercise alone? Not at all – but part of a complete plan.

    Getting older PD patients to exercise when they’ve been voluntarily immobile most of their lives is a huge hurdle for those of us who work with them and their families. It doesn’t help us or them when “experts” ignore it completely. Believe me, it’s easier to get them to move than it is to get them to go keto or even gluten free. I’ve tried. For years.

    Sure a PD patient can’t sprint… but does that mean they shouldn’t consider exercise as a treatment because they can’t “move like a caveman”?? I can’t believe you would overlook something so important – especially something that’s a part of the 14Four.me foundations and your own teachings. I would expect that from the neurologists who believe the one-size-fits-all treatment of Sinemet… not from Chris Kresser. If you’re going to give advice on how to treat something, don’t get tunnel vision and focus on just the gut-brain connection – which I totally believe in, don’t get me wrong – there’s more to a person’s body than that. Especially with movement disorders.

    And on a smaller note, we can’t get enough volunteers for PD studies – you would have even stronger evidence for this podcast if we did. There have been MANY studies funded for the link between gut health and PD that weren’t completed because of lack of participants. The studies mentioned in this podcast were small and few – with many missed study opportunities in their wakes. The other problem is, most PD patients are diagnosed 7-8 years AFTER the dopamine depletion begins – hence why there’s only studies concluding that leaky gut exists at diagnosis, but nothing about how it could potentially be contributing to the beginning or progression of the disease – even though you claim there’s a “strong connection”. A few small studies does not make a “strong connection”.

    The only TRUE strong connection able to be drawn at this point in PD research is the connection between agricultural chemicals and PD. Take a look at the studies coming out of UCLA, and branch out from there. TONS of evidence about toxins and PD… I’d love to see a study into how intestinal permeability and these toxins might be connected, with and without the ALDH2 genetic mutation.

    Chris, if you ever want to observe the PD Community – you don’t have to go far from home. You’re not far from “Parkinson’s Alley” and many many support groups. We’ll all welcome you with open arms, especially if it means better awareness of the disease and putting an end to speculation.

    • It’s a damned shame Chris didnt take seriously your comment. It deserved a long reply. Good points you have here, Meg

      Very disappointed that he doesn’t address the few comments. He’s not taking it seriously.

      • Chris produced a great episode on Parkinsons based on his research. It’s helped me and I expect it will help others. Can’t expect him to nail every aspect of it in one hour.

        Curcumin + Keto + SIBO were new to me, and this advice could change peoples lives.

        Whats up with you guys being “very disappointed” he missed exercise. Contribute to the discussion like adults if he’s missed something.

  17. Interesting RHR – lots of food for thought. I have 2 unrelated questions-
    1- When you test iron status, if the ferritin is in high normal range (say 150-180) but other iron tests that you mention ( serum iron, iron saturation, TIBC and UIBC) are all well within normal, do you still consider that iron overload?
    2- you said ” Ketone bodies that we produce, if you’re on a ketogenic diet, bypass defects in mitochondrial complex I activity. These defects in mitochondrial complex I have been implicated in Parkinson’s disease. So ketone bodies can bypass that and promote more normal cellular metabolism”. Ketone bodies (in the form of b-OH-B) enter the cell (they do their thing with succinyl CoA), are ultimately converted to acetyl CoA and enter Krebs, thereby producing NADH, which feeds into the ETC on the inner mitochondrial membrane (the place of the mitochondrial complex 1) to create ATP. As far as I know, ketones don’t directly get involved with that complex, they enter the TCA cycle just as glucose and FAs would – at the acetyl Co A location. My question – in what direct way are ketones bypassing or in any way involved with mitochondrial complex 1 other than being shuttled into Krebs and generating NADH? Is there another pathway?

    • Hi Chris –
      I know you’re busy, but this issue does deserve an answer.
      You’ve recommended a challenging diet to address a serious disease, and you’ve presented a mechanism of action for that diet. Given these facts, the question is not out of line – please do explain how ketones directly interact with the mitochondrial electron transport complex – and please do provide one scientific paper that we can read in more detail. There are many of us who follow you, who have the scientific background to understand the nuances of cellular biochemistry, and respect your analyses, who are curious as to your statement.

      • This is the very reason I stopped reading his articles. Its like, ya know, is he making this sh*t up? I’ll go back to that now.

      • Honestly, a short search in pubmed can lead you to pretty much all the articles related to the question he is talking about. If you check ketogenic diet or ketones + neurodegenerative diseases or parkinsons you can find free articles and even systematic reviews on the topic, where the answer to your question is explained in detail. I can’t provide links now but I did the research some time ago and came accross quite a lot of information (free)