The enzyme serrapeptase is used to relieve pain and inflammation; its effects on heart health are also being researched. Learn more here.

Dr. Sarah King, PT, DPT interviews Colin Potter about his experience being diagnosed with Parkinson's Disease and his hard-fought battle to dramatically improve his Parkinson's symptoms. Start building your own Parkinson's Plan of Attack with similar strategies to Colin's: http://www.InvigoratePT.com/start-here LEARN MORE ABOUT SARAH'S PARKINSON'S SPECIFIC EXERCISE PROGRAM: http://www.InvigoratePT.com/Booster FOR ADDITIONAL INTERVIEWS WITH COLIN: http://www.invigoratept.com/blog/colin-potter-fight-parkinsons-special-interview-2017

The main serrapeptase benefits is the anti-inflammatory property without the side effect. This supplement may prevent pain, similar to ibuprofen and aspirin; without thinning the blood. Additionally, it has been shown to help prevent plaque buildup in the heart arteries

Disease modification in Parkinson's disease (PD) is an unmet medical need. In the current study, we evaluated trehalose, a safe and well-tolerated disaccharide that has previously demonstrated efficacy in rodent models of neurodegenerative diseases, including PD. In a rat model of PD, based on deliv …

[Facebook LIVE Replay] Are you interested in combating PD symptoms without simply taking more medication? Dr. Sarah King, PT, DPT chats with Colin Potter, founder of Fight Parkinsons, about his holistic approach to PD. www.InvigoratePT.com Here's a breakdown of the conversation: 3:00 - Quick Disclaimer 7:30 - Colin’s Background - self-employed problem-solver 10:00 - Colin’s initial symptoms (3 years before official diagnosis) 12:55 - When Colin started taking medication 14:14 - The gift Colin received that changed everything 15:50 - The #1 thing Colin learned initially that launched his journey (hint: it’s at the heart of most chronic diseases) 19:04 - Peek into Colin’s diet 21:30 - How long it took for him to start seeing results (and his transition off medication) 24:00 - Colin’s advice on where to start with nutrition, exercise, supplementation, and toxin elimination upgrades 25:55 - How Colin developed an optimistic mindset and how he stays motivated to keep fighting 28:00 - What Colin’s able to do now physically that he couldn’t do 4 years ago 29:27 - The role of exercise in Colin’s recovery plan 31:49 - Colin’s #1 Reading recommendation 34:53 - Colin’s supplementation program - then and now 38: 55 - The physician who Colin sees primarily to help him guide his natural treatment program (and their plan of attack) 45:20 - A recent victory that Colin got wildly excited about! 47:30 - Steps that Colin recommends when just starting out on your journey 53:45 - The role of toxins in brain health and where they show up in our daily life 55:55 - Answer to the question "Do I have to go 100% for these efforts to be worth it?" 1:00:10 - Constipation, Urinary Frequency, and Colon Hydrotherapy… oh my! 1:04:00 - Colin’s take on dairy in his diet 1:09:50 - The role of medication in a thriving Parkinson's recovery program

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Could gluten's toxicity extend to the nervous system, producing symptoms identical to classical Parkinson's disease? A compelling case study adds to a growing body of research indicating that wheat's neurotoxicity is greatly underestimated.

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The Michael J. Fox Foundation is dedicated to finding a cure for Parkinson's disease through an aggressively funded research agenda and to ensuring the development of improved therapies for those living with Parkinson's today.

Researchers are just now starting to link inflammation in your gut with some of the most deadly and debilitating diseases we have.

Magnesium oil, cannabis and Iodine are natural medicinals that have been found to be a remarkable help in decreasing the pain and spasms and increasing functioning, language, and better attention in Parkinson's disease.

We have already reported that glucosamine (GlcN) distinctly abrogates the pigmentation of human epidermal equivalents stimulated by stem cell factor + endothelin-1 (SE). In this study, we characterized the molecular mechanism involved in the anti-melanogenic effects of GlcN using normal human melanocytes (NHMs) in culture. The SE-stimulated gene (12 h) and protein (24 h) expression levels of melanocyte-specific proteins (at the indicated times post-stimulation) were significantly abrogated by pretreatment with GlcN for 72 h. Western blotting analysis of the phosphorylation of intracellular signaling molecules in the MAPK pathway revealed that despite the significantly decreased level of total CREB protein at all times post-stimulation, the SE-stimulated phosphorylation of ERK, CREB and MITF is not attenuated at 15 min post-stimulation in GlcN-treated NHMs. However, the SE-stimulated protein expression level of total MITF at 2 and 6 h post-stimulation was significantly abrogated by 72 h pretreatment with GlcN. Consistently, pretreatment with GlcN for 72 h abrogated the stimulated gene and protein expression levels of MITF at 1 h and 2 h post-stimulation, respectively. Analysis of gene and protein expression levels also demonstrated that pretreatment with GlcN for 72 h significantly reduced the protein levels of CREB and MITF without affecting their gene expression levels prior to the SE stimulation. Silencing with a CREB siRNA distinctly abrogated the SE-stimulated expression of MITF (at 2 h post-stimulation) and melanocyte-specific proteins (at 24 h post-stimulation). Similarly, transfection of MITF siRNA markedly abrogated the SE-stimulated expression of MITF protein and melanocyte-specific proteins at 2 and 24 h post-stimulation, respectively. Finally, the decreased levels of CREB and MITF proteins induced by 72 h pretreatment with GlcN were abrogated by the co-addition of the proteosomal degradation inhibitor MG132. These findings suggest that the anti-melanogenic effect elicited by GlcN is mediated via the decreased expression of MITF which results from the attenuated transcriptional activity of CREB due to proteolytic degradation.

Parkinson's disease (PD) is a progressive movement disorder resulting primarily from loss of nigrostriatal dopaminergic neurons. PD is characterized by the accumulation of protein aggregates, and evidence suggests that aberrant protein deposition in dopaminergic neurons could be related to the dysre …

Medical Medium Blog: read True Cause of Parkinson's now at www.medicalmedium.com

We now can convincingly demonstrate that a ketogenic diet is helpful in Parkinson’s, and we now have a better understanding of the underlying mechanisms.

Parkinson's disease (PD) is the second most common neurodegenerative disorder of aging. The pathological hallmark of PD is neuronal inclusions termed Lewy bodies whose main component is alpha-synuclein protein. The finding of these Lewy bodies in the intestinal enteric nerves led to the hypothesis that the intestine might be an early site of PD disease in response to an environmental toxin or pathogen. One potential mechanism for environmental toxin(s) and proinflammatory luminal products to gain access to mucosal neuronal tissue and promote oxidative stress is compromised intestinal barrier integrity. However, the role of intestinal permeability in PD has never been tested. We hypothesized that PD subjects might exhibit increased intestinal permeability to proinflammatory bacterial products in the intestine. To test our hypothesis we evaluated intestinal permeability in subjects newly diagnosed with PD and compared their values to healthy subjects. In addition, we obtained intestinal biopsies from both groups and used immunohistochemistry to assess bacterial translocation, nitrotyrosine (oxidative stress), and alpha-synuclein. We also evaluated serum markers of endotoxin exposure including LPS binding protein (LBP). Our data show that our PD subjects exhibit significantly greater intestinal permeability (gut leakiness) than controls. In addition, this intestinal hyperpermeability significantly correlated with increased intestinal mucosa staining for E. coli bacteria, nitrotyrosine, and alpha-synuclein as well as serum LBP levels in PD subjects. These data represent not only the first demonstration of abnormal intestinal permeability in PD subjects but also the first correlation of increased intestinal permeability in PD with intestinal alpha–synuclein (the hallmark of PD), as well as staining for gram negative bacteria and tissue oxidative stress. Our study may thus shed new light on PD pathogenesis as well as provide a new method for earlier diagnosis of PD and suggests potential therapeutic targets in PD subjects. Trial Registration Clinicaltrials.gov NCT01155492