I had several symptoms of Parkinson’s Disease as a teenager, but played Squash and later Racketball all my life and didn’t get the tremor until 2009. Took 2 years to get the dreaded diagnosis and then took increasing doses of Ropinirole and Sinemet as prescribed by the neurologist. Basically I ignored the PD and got on with my life until the vicious back pain induced by the muscle tension started to seriously interfere with my quality of life. It’s quite inconvenient being unable to walk until you’ve spent an hour or two on a heat pad at maximum power EVERY morning! Then I decided to try the Ketosis Diet recommended by Colin Potter. I’ve been eating no carbs and lots of fat for a fortnight and gradually reducing from 16mg of the dopamine agonist Ropinirole and 12 Sinemet down to ZERO meds for the last 3 days. I’m feeling a bit lethargic, but it is 30degC to be fair and I’m still able to play Racketball - with 2 rackets, hence my handle: 2bats. I’ve ordered some vitamin B5 as they say it helps with lethargy when changing from running on sugar/carbs to running on fat. Initially I felt very jittery and I find it takes 20 minutes to stop my left arm jerking when I start playing Racketball but the great news is that the vicious back pain is fading fast because the leg and back muscles are no longer tight as a drum. Another sufferer mentioned shoulder issues and I’ve had rotator cuff surgery on my right shoulder twice, lost the long biceps and the supraspinatus on the right arm and had to learn to play left-handed - and then lost the long biceps on the left arm so now I play with 2 rackets, which is curiously satisfying:). I spend the UK Winter in New Zealand and play Squash there but because of the volley serve I just use one racket with whichever arm can play forehand for the shot.
Having researched Ketogenesis my belief is that SUGAR is POISON and our modern diet is directly responsible for most illness. I’d be fascinated to hear whether others have succeeded in getting their lives back and I strongly recommend giving the KETO DIET a try for a month. You can buy 50 ketostix for a fiver - what have you got to lose?
Oh - it will also improve your waistline, I went from 72kg to 67kg in a fortnight, without losing any muscle...
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2bats
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2bats I love your outlook on life. I love your way of expressing yourself.
You’ve had quite a journey. I’d love to ‘do’ the diet. My hangup is Sugar.
It’s increased in the last 2 years only. Was pretty good until something was nagging me to buy Coke ...hated it all my life. I enjoyed it so much I think I’m addicted. I do pass it by from time to time now, trying to be strong.
I live in Queensland Sugar Cane Farms keep this town going. The crop is being cut as I write and so pretty with its Lilac flowers although if you suffer with Hay Fever best to stay indoors.
I was diagnosed 2005 but it was smooth sailing until about 2 years ago. I’m feeling like ‘I’m up the creek without a paddle’. It’s quite awful.
3 falls in 8 days. First black eye, bruising, cuts and a lump on my head. It happens so quickly. My Neurologist told me that that’s the way most PD recipients leave this paradise and now I know what she meant. I have no idea of what’s ahead and I don’t want to know.
I had a smile reading your post so post more for us all to pick up your vibes.
Very interesting, especially the bit about coming off the medication. We are told that we must never come off the medication. I have done so, but I only succeeded doing so after 8 years. I am on the HFLC (High Fat Low Carb) diet, not too strictly, but I did come off the Sinemet after 2 years of taking it every day.
We are all different, which can mean anything, but unfortunately some people use that as an excuse for not really trying to do something about their Pd. Taking pills is the easy way out, but it gets us NOWHERE!
Hi JohnPepper, Thank you so much for the response - I’m delighted to make contact as I’ve read a lot about you and admire your determination. Like me, you don’t take what the medical profession says at face value! Isn’t it extraordinary that we don’t see what should be blindingly obvious - what we eat has a huge impact on our health. When you look around at the general population you can see that even if they are not afflicted with Parkinson’s Disease or MS or ALS or any of the other TLA*’s they are almost all in terrible shape and they could be so much better. * Two/Three Letter Acronyms
I’m really annoyed that it took me so long to discover KETO and hope that I can repair the damage I’ve done with 7 years of prescription medication...
2bats, you’re right on! I am addicted to sugar, but thirty years ago, after a bout of cancer and my weight ballooning up 80 pounds over what is healthy, I got off sugar almost completely with the help of a group, lost the weight, then a few years ago decided that I deserved to taste ice cream again. Since then it’s been a struggle. I go a few weeks, then give in to some gooey dessert. I’ve been sugar free for two weeks and counting. I’m convinced that sugar and its effect, inflammation causes PD in some people. I’m not willing to give up grains and starchy vegetables but I eat mostly whole grains, small servings.
WE have been discouraged from eating FAT. Fat is the most satisfactory food to eat. It does not burn up immediately, leaving us craving more. Change your mindset!
It's so true 2bats that we don't pay enough attention to our health - I've always loved reading about health things and knew a lot of what was good or bad for us but never put it entirely into practice. Now I'm so sorry I didn't but no use moaning, I haven't taken any medications as yet but I've only got an essential tremor in my jaw, though have noticed a few finger trembles in my hands of late. Want to get onto healthy diet, etc. as soon as possible. Suffering Socks
Hi Bridielena, It’s strange, but we are often addicted to things that are bad for us. Please use the mindset that SUGAR IS POISON. I also had a sweet tooth, but I just don’t miss it a bit now I’m off the lethal stuff. You can do it, Just clear the fridge and the cupboards of all the carbs and go keto. I know that this won’t play well in Queensland, but Big Sugar is right up there with Big Tobacco - they just don’t have any morals or ethics, either of them...
No thanks . Only a beer now and then. It does get very humid here which adds to PD stress. I had heard though, beer was ok for us and I silently said ‘thank goodness’.
In the UK there’s a non-alcoholic beer called Becks Blue - .05% alc and 8.5g of carbs per 275ml botttle. Tastes really good when ice cold and cheap too. I’ve never liked spirits, so the only items in the bar I can consume are the Becks and the peanuts!
Thanks. There is one here similar to that I think .. we can only buy alcohol at special outlets not in supermarkets but that is where I can get this ‘beer’ . Have tried it....it’s ok .....I’m in Queensland . Some of the other states have supermarket alcohol outlets.. Not important really but I did read where a beer is beneficial for PD. So many contradictions though.
I had constipation from childhood, lost my sense of smell in my twenties, would occasionally get shaky hands from my teens, sweated more than anyone I’ve ever seen when playing Squash and crucially never had a dropshot, which I regard as very significant as it indicated a lack of motor control as did my inability to ever write in a properly formed style. Plus alopaecia, Reynaud’s, shoulder damage and as a side note I used to eat an enormous amount and never put on weight. I know I’m missing some other things, but cannot remember them at the moment! I used to think the PD was caused by a serious motorbike accident when I was 17 - now I’m not so sure, though I’m sure it didn’t help
Thank you for replying so quickly! My husband is 78, officially diagnosed about three years ago. He is tremor dominant, and still doing well. But your post about having PD since you were a teen was interesting. He didn’t have anything definite but has always jumped or “jerked” an excessive amount when falling asleep, since we first married. He was 32. He also has never been able to put on weight and is very slender. He has always walked sort of leaning forward, and with shorter steps, and when the Dr was first examining him, she said his gate was pretty characteristic of PD, but I said no, he’s always walked that way! He was very, very focused at work, and never was a multi-tasker, but almost concentrated in a way that seemed a little more than normal. (He’s a retired veterinarian) When we were with other people, I’d have to sort of elbow him to keep him paying attention and interested in the conversation, as he often seemed to be looking out the window or “daydreaming” about something else. He has suffered for years with leg cramps, mostly at night. He’s had shoulder problems in his tremor dominant arm for years. Lots of things that make me wonder if there isn’t at least some “pre-conditions” or characteristics that point to Parkinson’s, when taken all together. He’s still an exceptionally intelligent and driven individual, and like you, I think his outlook on life is a great blessing for him (and me) in dealing with this little “beast” that has now has a name, in our lives! Sorry this is so long. But knowing these things may help someone in the future. I sure hope so!
I agree, I feel that it should be possible to look at a cluster of oddities and say - check for Parkinson’s Disease or whatever. I do recommend the Keto - have you tried it?
I’ve tried it a little, but didn’t do it very well. It’s just too drastic a change, I’m afraid. My husband has not. And he’s so thin that I’m afraid he’d lose too much more weight on that diet. We do try to eat well and are not into much junk food.
I too struggle to keep weight on but only in the past two years. I was diagnosed 18 months ago but had noticeable symptoms since 2014. Why does PD cause weight loss?
I was interested to read in your post that your husband suffered for years with leg cramps - I have also suffered with leg cramps for years, always wear warm socks to bed, do stretches and now take Magnesium tablets. Have heard that you should have a drink before retiring which should help so am doing that also with good results. I agree that there seems to be little symptoms which crop up before you're actually diagnosed with PD.
I started the Keto Diet and simultaneously started reducing the meds over 2 weeks. I’ve been off all meds since 4th July (5 days) and feeling pretty shaky, but my back doesn’t hurt nearly as much, my skin’s improving and overall it’s good. I’m waiting for some B5 Pentathenic Acid to be delivered as that is said to help with lethargy from the diet and I’ll also try B1 Thiamine as that is supposed to assist too. I’m only just in ketosis according to the ‘stix so I’m going to be even more careful about the carbs - and fast a bit as well.
I find that people say I’m thin because they’re comparing me to a generally obese population. I did lose 5kg - going from 72kg to 67kg in a fortnight on the Keto Diet (height 180cm) - but basically I just lost the belly and the muscle stayed the same. So my weight is now stabilised at 67kg and not decreasing any more at all. Parkinson’s Disease weight loss is probably caused by the tension in the muscles just burning energy constantly, plus other factors like depression and lack of exercise. It’s a pity that tense muscles don’t lead to increased strength!
For all the folks that read this thread . . . the neurological benefits of a ketogenic diet have long been known, and there have been numerous posts on this forum from people who tried a ketogenic diet and felt there was a benefit. Here are just a few of hundreds of related studies and post:
The obvious question anyone trying something new to treat their illness should ask is why it may be effective, and until recently there was little research on this topic. A paper published in 2017 offers one possible answer:
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Ketone-Based Metabolic Therapy: Is Increased NAD+ a Primary Mechanism?
Here we outline the overall implications and evidence for a rapid
and region-specific change in NAD+/NADH as a direct result of
consuming a KD. We hypothesize this as a new and fundamental
addition to potential key mechanisms underlying beneficial
antiseizure, neuroprotective and disease-modifying effects of
KD. Because NAD+ can modulate ion channels, enhance
mitochondrial health, decrease oxidative stress, and impact gene
expression, an increase in NAD+ and/or NAD+/NADH ratio is a
mechanism that can account for several diverse (and seeminglyunrelated)
effects of ketogenic therapy. Furthermore, benefits
of increasing NAD+ such as life-span extension and enhancing
cellular health have long been documented (Lin et al., 2000),
and pharmaceutical companies are currently manufacturing and
selling supplements that contain NAD+ precursors such as
nicotinamide or nicotinamide riboside in an attempt to increase
endogenous NAD+ levels and enhance metabolic resilience—an
outcome that may also be achieved physiologically by ketogenic
strategies.
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What does all that mean? It means folks should read my other post on Niagen and consider trying the vitamin. Also contrary to common belief on this forum Niagen (nicotinamide riboside) it is not simply another B3 like niacin (niotinamide), and one does not have to take a B complex to see benefits.
Niagen is a simple over the counter vitamin that has scientific proof it MAY slow the progression of PD. Not sure why everyone doesn't take it simply as a precaution. It CAN NOT reverse symptoms or make you feel "better" other than thru a placebo effect.
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HOWEVER, science says boosting NAD+ MAY help your cells repair themselves and thereby slow your PD.
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How would you know? You can't. There's no way to feel a slowing of progression.
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Joe in NY
P.S. Calorie restriction has also been shown to have the same benefit as a ketogenic diet.
That is one of the primary issues why this is a "new" B3 and why Simon felt a need to write a second article on nicotinamide riboside specifically. In one of the links above there is a chemical diagram that shows where NR falls in the molecular process that creates NAD+ and NADH. NR is further along in the cycle, and the most recent research indicates this makes it a more efficient booster of NAD+ which is the ultimate desire Also NR is a Sirtuin activator and niacin is a Sirtuin inhibitor. Sirtuin activation is one cellular process that is best known for benefitting from resveratrol and other stilbenes that also appears to have neurological benefits. However, as you read in the line about brain cancer, there is always some confounding alternative research, and that is the case with Sirtuin activation. Personally I think the best we can say is Niagen MAY be helpful and the benefits seem to greatly outweigh any potential danger so until science proves otherwise I will continue to take 375 mg a day.
Thank you Sunvox. I know you're a bit of an advocate for NR. Can you, personally, feel a difference since you've been on it? Or do you just feel like you're not getting worse?
I originally joined this forum because I got banned from a forum in the US (Living with Ataxia) (I know . . . hard to believe right ) I got banned because I wrote a post claiming a "partial cure" for my illness. I then got banned here for a few days for making the same claim and ultimately I realized if I used the words "alternative therapy" and told people never to try something without first consulting a doctor then the mods would be happy.
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Anyways, back then I had already gotten rid of 90% of my symptoms and I was only taking 2 supplements: trehalose and niagen. Originally I started with just trehalose and noticed a change in balance within a month, but not until I added niagen did I find that I could exercise and recover strength afterwards. In addition, my father and my aunt who had been in a wheel chair were both able to return to taking a few steps without the aid of a wheel chair. My disease is genetic and my father and my aunt both have SCA1 like me. SCA1 is caused by a bad protein in the brain and now scientists are beginning to believe that the one common cause in all Parkinson's is a bad protein in the brain, not the clumps they find, but the "mis-folding" of the protein BEFORE it clumps. (That theory is critical as to why I believe my therapy is relevant to PD.) In any case, my father remained stable with no progression for over a year until we put him in a nursing home where they refused to give him trehalose and niagen without a doctor's note. Tragically my father also suffers from alzheimer's and there is evidence that trehalose and niagen were probably neuroprotective for that illness as well. This past month which is 5 months after my father stopped taking trehalose and niagen he no longer recognizes me. On the other hand, my aunt remains stable at home almost 18 months after starting trehalose and niagen. She is taking nothing else but does do physical therapy twice a week. She is 76 and I am not aware of any clinical case of a person with SCA1 at her age not progressing rapidly worse to 100% reliance on a wheelchair and continually increased slurring of speech. (She is taking 3 to 4 Tbs of trehalose and 1000 mg of niagen - I do not recommend that much trehalose because it has been shown to cause weight gain, but at 76 my aunt feels it's worth it.)
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After my initial success with just trehalose and niagen, I increased my research and learned about the theory of attacking neurological diseases from as many angles as possible and that is why I added diet and exercise changes plus thiamine, magnesium, Tuarine, EGCG, and pterostilbene to my "therapy" in the belief that each plays a different but important role in overall cellular health.
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Bottom line: Yes, I saw enormous improvement from just taking trehalose and niagen, and I shared that information with folks around the world and I have found about half or more of the people that have tried just those 2 supplements reported improvement. Those folks included people with ataxia, Parkinson's, and Huntington's. Sadly, that and a $5 bill will get you a cup of coffee at Starbucks and not much else. Until some generous foundation offers serious money to study "supplements", we, the patients, have to rely on what little science exists and the reports we share.
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Joe
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P.S. Trehalose is essentially identical to mannitol in how it acts in the brain and obviously mannitol is getting a lot of attention in the world of Parkinson's. I consider trehalose and mannitol to be essentially identical in terms of potential benefit and think it's just a matter of which your body tolerates better as to whether you take one or the other. Mannitol might be slightly preferable since it has fewer calories although both are low calories sugar substitutes.
Hi Joe, I am buying some trehalose. I did try Mannitol it seems like I didn't do a thing for me . I was reading that your balance improved and I am hoping for my balance to improve with trehalose so I'm going to try some. I was going to buy some niagen and then I started reading some of the feedback on Amazon. Some people mentioned high blood pressure from taking niagen, and as you remember thiamine HCL give me very high blood pressure. So now I have no idea what to do if I should get a bottle of it or if I should not. What do you think? Mary
Hi Mary, There is no scientific evidence showing Niagen raises blood pressure in the least and there have now been hundreds of people run through clinical trials. In fact there is evidence that both Niagen and trehalose act to lower BP and improve vascular health. You even linked to one of the research reports:
With any supplement there is a strong propensity towards a placebo effect initially whether good or bad. I am not a doctor so talk to your doctor and have him/her monitor you over time, but my recommendation for all PwP is to try Niagen at the recommended dosage and a Tbs a day of trehalose or mannitol for a year and THEN make a judgement. Trying something for a month or two is truly meaningless. As I have said over and over, if these kinds of supplements actually work, they most likely will just slow progression meaning the average person will not FEEL any different, but after a year or two MAYBE they will notice they haven't gotten much worse. That would be the hope.
I agree with you entirely that sugar is poison, I'm having a difficult time cutting it out but am doing it gradually, it's in so many processed foods which I'm cutting out also. Want to try the Ketogenic diet pretty soon. Suffering Socks
I've been on keto diet for nearly 5 months having cut sugar out of my diet 12 months before. In all I've lost about 50lbs and seen my blood pressure drop significantly. First two weeks of keto diet were tough but then noticed muscles begin to relax (legs, arms, shoulder, neck, back) so persevered. Suffered from palpitations and anxiety for a few weeks but this was resolved by dropping amount of Sinimet and taking a small amount of Diazepam (boosts GABA which needs to balance Dopamine). Am now on about 1/3rd of Sinimet I had been prescribed and not sure if it is having any real benefit. Keto diet requires some dietary adjustments but is not that difficult.
PD researchers are trialling drugs (like Exenatide) which are used to treat T2 diabetes so it seems to make sense to go with diets that restrict carbs. My wife was diagnosed with T2 about 10 years ago and started the keto diet with me - she is now classed as "pre-diabetic".
2bats, thank you for sharing. I would be interested to know more about your journey to becoming free of the Anti-Parkinson medication. May I ask if you have a facebook page or twitter account where it may be possible to follow your progress?
Hi Paul, I do have facebook for family and friends but I don’t put anything health related on there - just here! I’m now 6 days off the Ropinirole and the Sinemet and while I feel pretty good still, I’m clearly out of their influence now as my right arm tremor is really noticeable. On the plus side, my back is so much less painful, the mild exzema continues to improve and my muscles feel much more ‘soft’ and relaxed. I do feel pretty weary and as the amazon B1, B5 and B12 have arrived and the B3 and D are due in a couple of days I hope that the supplements will restore my energy. I did an hour’s serious Pilates at 10.00 and 90 minutes of gentle Racketball at 12.00, which was interesting as it is taking me 15 minutes to persuade my left arm which doesn’t have the tremor, to play smoothly, whereas my right arm which does, was pretty cooperative! This may also be connected to the fact that my ketostix say I’m only barely in ketosis and I’m eating NO carbs, not much protein and LOTS of fat. The real question is whether on the Keto Diet my tremor will improve or not. Mentally I feel sharp, I’m sleeping well - 1am to 6am! Just trying to get back into ketosis
The video above with Eran Segal takes that further to demonstrate that different diets affect people in different ways, so that what may be good for one person would be bad for another due to the genetics of the individual and the genetics of their microbiome.
He shows a graph with two very different responses.
The red spikes in blood sugar are the result of the ‘wrong’ diet and the blue the result of the ‘good’ diet - but these could easily be the opposite way round for different individuals.
With the amount I used to eat it is surprising that I didn’t become obese and get T2 diabetes - but instead I got Parkinson’s Disease which is a trickier option to deal with but is surely linked to diet.
So - I’ve been on the Keto Diet for 4 weeks now and am enjoying it, now I’ve worked out things that I like that comply with carb avoidance. I’ve also now been off the Ropinirole and Sinemet for 8 days and that’s a bit more of a challenge. I hope that there is no trace of the 2 drugs in my system as the DAWS (Dopamine Agonist Withdrawal Syndrome) is pretty tough - strong right hand tremor, feeling jittery and being pretty tired and certainly having trouble moving quickly - so I have some anxiety as to whether these symptoms will worsen if there is more to come, so to speak! I went for a 15km bike ride and picked up some Movicol to replace the Fybogel I’ve been using having just noticed that it contained Aspartame, to my astonishment. On the plus side, I then played Racketball for 90 minutes, which was interesting as I now find that every time I play I have to re-train my left arm to hit the ball smoothly without twitching but the right arm which has the tremor is fairly good from the outset. My main difficulty on court is trying to motivate myself to move fast enough to retrieve the ball. This is incredibly frustrating as I used to be extremely fast around a Squash court and now I’m being outclassed by very ordinary players (Oh the humiliation!;-(). Nevertheless, the process of playing with both arms improves both my physical and mental fitness immensely.
In the search for clues as to the origin - and treatment - of my Parkinson’s Disease I would be very interested to know if any other PD sufferers have had the following features in their personal history:
* An ability to eat enormous amounts while remaining slim
* Alopecia
* Severe perspiration when exercising
* Reynaud’s syndrome
* Total inability to play a dropshot in their chosen sport
* Dreadful handwriting with a biro, much improved by using an italic fountain pen
* Shoulder problems eg Rotator Cuff and torn long biceps and supraspinatus
I’d also love to hear how others have got on with Keto Diet and with coming off Ropinirole and Sinemet
I look forward to hearing from you. Best regards, Phil
Hi 2 bats. I too really like your outlook on life, and that you spend UK winters in NZ! I can recommend the NZ summers and lifestyle for anyone, particularly with PD, as it is relaxed and easy-going. And I too feel I had 'pre PD' for many years, even during teenage years, but no doctor is interested in going back that far. I've now officially diagnosed for 3 years and been on Sinemet for a couple of years, and can slowly feel myself reducing in physical capacity. I've always been uncontrollably sugar-addicted. So your recommendation about the Keto diet came as a symphony orchestra to my ears, especially as my diabetic daughter has been recommending it for a while. I've downloaded Colin Potter's material (thank you Colin) and we're away, me more seriously than my husband, but he's also enjoying it. Thank you - for your post, and your take on things, great - please keep possting.
1 month in and I’m finally in ketosis to about 6mmol/L - and I finally have some energy - my right arm tremor is finally improving after getting worse since 4th July when I took my last dose of Ropinirole and Sinemet. Looks like the light at the end of the tunnel is not an oncoming train!!!
I am able to monitor changes to my strength by using STRAVA which is a cycling/running app. Several times a week I cycle the 5 miles/ 8km to the squash club and back, which involves a climb up a 6% hill. My changing times for the hill clearly showed a reduction in ability after starting Keto, but yesterday I found my time had at last improved - not to the full pre-Keto level, but noticeably, tallying with my ability to stay in the middle gear on the front chainring for the first time without having to drop to the lowest ratio due to fatigue. This was after a session where it took a little less time to ‘re-educate’ my left arm to play smoothly and after 30 minutes I quite suddenly began to time the Racketball strokes properly for the first time since I dropped the Ropinirole and the Sinemet. I also felt that I was moving better on court. I think the medication is finally out of my system after 12 days! It was horrible in the DAWS phase, but I’m pretty confident that the symptoms are improving gradually.
I’m seeing my Neurologist and the PD Nurse for my annual check-up on the 19th July - that’s going to be an interesting conversation as all that usually happens is that they strongly recommend upping the dosage... I have a mind to keep my Keto Diet and drug elimination a dark secret initially;-)). I think I’ll start by asking what they think about hypothetically going on a Keto Diet and giving up the meds!
Hey 2bats, Great to hear about such success! Thanks. I LOVE the idea of getting rid of “medications”. Drugs! But, I question whether or not it is necessary to go as extreme is Keto. I agree sugar is BAD! But it has been my understanding that fruits (natural unprocessed sugars) are Good? Since reading your posting a week ago I have stopped all forms of processed sugar. (Not easy as I was addicted to Mt. Dew Kick, energy drinks), usually around 4 or 5 per day. And I switched from ice cream to plain yogurt with my own added fruit for my midnight snack.
And from my research, there is a difference between simple and complex carbs, the general opinion is that simple carbs, White rice, white flour etc., bad... Brown rice, whole wheat flour etc. complex carbs, good.
I feel like I would be missing some good nutrition by being so restrictive with my fruits. AND breads and cereals, I like to bake bread. (100% stone ground whole wheat bread). VERY difficult to give up!
I HOPE the main necessary thing we get from your experience is Sugar is BAD! So if we cut out ALL processed sugars, (and simple carbs) we live? :+)
Cycled to the racketball club and back and achieved a slight improvement in time to climb the 60m hill. Took videos showing the quadriceps stretch that I do to de-tension my back muscles, much easier to do now the muscles are not super tense. Also videos of my progress in an hour from almost unable to time hitting the ball with either arm to moderately competent albeit still slow round the court. I’d say this was the equivalent of John Pepper’s “fast walking”. Then off to see the neurologist who commented that my tremor was ‘cosmetic’ and that it was more relevant that I was ‘slow’. It is true, but I had become slow in the year since I saw him - that and the excruciating back pain were why I decided to go on the Keto Diet and gradually come off the meds in the first place! I apparently did that at the right rate and he confirmed that I will have cleared both the Ropinirole and the Sinemet from my system by now. He kindly agreed to set me up with a good range of blood tests (including PSA I’m happy to say) and we parted amicably for another year. I’m of course hoping that I will have made some more progress on getting my life back in the next 12 months
I’m looking forward to seeing the excellent Parkinson’s Disease Nurse in November before we fly south to Australia and New Zealand for the Winter.
If anyone out there has any thoughts on methods to minimise the tremor I’m all ears!
Got to stop now as I’m due back at the club for another Racketball game - it’s all go...
Update on 27.07.2018
Yesterday I cycled 8km to the club played Racketball for an hour went out for Keto Diet lunch of salmon and then cycled 8km home in reasonable time bearing in mind it was 34degC! Got home, caught up on more Keto research - Dom D’agostino videos - and then went back to the club for another 45 minutes of Racketball just to see if I could! And I could - although with the heat I did feel pretty bushed:). I did get offered a third game an hour later, but had the senses to decline.
I played another hour today - without the bike ride - and felt pretty good. I should explain that I’m now taking B1, B3, B5, B12, C, Magnesium, D3, EPO, E, C8 MCT and I’ve just started taking Copaiba Oil which is rumoured to be good for the tremor. By one of those weird coincidences one of my Racketball mates happens to be in the pharmaceutical industry and his area of expertise is Parkinson’s Disease and dopamine. He actually reckoned I had Parkinson’s Disease a couple of years before my diagnosis. He was I think quite surprised that I am functioning so well after almost a month of ZERO MEDS, so I’m pretty confident that the Keto Diet is the main reason for being in good shape apart from the tremor. I still have some back pain when I wake - it starts as something like cramp in the muscles round the left hip and then migrates to the right lumbar region. I’ve taken to wearing knee pads when I’m playing Racketball so that I can quickly ‘take a knee’ to stretch the quadriceps in between rallies to get the back pain to back off, I would love to try some proper CBD/THC as I feel pretty sure it would help enormously - but with the current regime that may be a few months away. I’m considering being a health-tourist in Amsterdam so that I would at least know whether it does work!
I’d love to hear your feedback, Best regards, Phil 2bats
Did a 42km ride yesterday and felt totally exhausted, so much so that I almost quit, but I made it home and the slow time for the final Hedgerley Lane hill turned out to be slightly better than my slowest time on the first climb after starting the Keto Diet. I felt pretty wrecked this morning but gradually improved and played a 40 minute solo practice racketball to a reasonable standard. I was concerned that i had overdone the exhaustion on the bike and with Ketones at about 8mmol/L I felt that the stress of the ‘Keto Flu’ might trigger either a collapse or more optimistically a breakthrough!
Decided to record weight - 69.5kg, waist - 84cm, right thigh 48cm, left thigh 46cm, R biceps 33cm, L biceps 32, R forearm 28, L forearm 27. My weight prior to all this was 72kg, so I’ve stabilised at a 2.5kg loss of weight. Getting fed up with being told I need to gain weight by people who are obese! I’m smack in the middle of the green Body Mass Index...
Still on the Keto Diet - still have no strength and no energy. Also reliant on laxatives to function... Tremor is irritating but manageable although typing is tedious. Fell off my bike today, fortunately at low speed but I’ll be sporting some impressive scabs on my face for a fortnight I think. Taking all the vitamins recommended, but would appreciate suggestions for regaining strength on Keto diet please!
Hi 2Bats - Congratulations on fighting so hard. That, I think is key.
-
I do have two suggestions for you to consider. First, there is strong evidence that the reason a keto diet is helpful is simply because it increases the production of NAD+ in the body. NAD+ is necessary for every cellular function in your body and the amount of NAD+ your body produces declines drastically with age and with disease. Here is a study that investigated the possible reasons why a keto diet is helpful for neuro protection:
Second, there is an enormous amount of research on exercise and PD, and clearly any exercise is better than no exercise, BUT there is only one study to date that tried to look at exercise in a truly "double blind" type study and that one report said that running on a treadmill 4 times a week for 30 minutes at 80% max heart rate STOPPED THE PROGRESSION OF PD,
and what to me is even more amazing is that a second study examined bad alpha-synuclein build up in mice and found that mice that ran had less build up in their brains. If you read my post you will see that I am a believer in the theory that alpha-synuclein is the one common "bad boy" in most PD cases. So here you have two studies. One shows it stopped PD progression and the other helps explain why.
-
What does all this mean?
-
Niagen boosts NAD+ dramatically and running on a treadmill may halt progression so instead of eating a keto diet and biking why not try taking Niagen and running. What have you got to lose from trying?
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Joe in NY
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PS If you click on a person's name or avatar you see all their posts and replies.
Hi Kia, Any brand is fine so long as the bottle says - licensed by Chromadex. That is the only way to be sure you are getting NR and not NAM. Unfortunately it is not cheap.
Hi Joe, many thanks for the suggestions. Sadly running is not an option as I have a full fusion of the left ankle - so I can cycle and scuttle round a Squash court, but running is extremely difficult! Feeling more lively today, so I’m off to the club on the bike to assess. Could be the extra Thiamine I’m now taking. Cheers, Phil
Still on the Keto Diet - still have no strength and no energy. Also reliant on laxatives to function... Tremor is irritating but manageable although typing is tedious. i.e. the same as last update. I’m nearly 9 weeks in ketosis and 6 weeks on zero meds. I’m taking Thiamin and CoQ10 plus all recommended vitamins but wondering how long it’ll take to get my strength back and whether I’ll succeed in reversing my Parkinson’s. On the plus side my back is running 4/10 instead of 8/10 for pain and I do feel good on the Keto Diet and generally positive. Also I’ve noticed a big improvement in my vision to the point where I can see nearly perfectly without my glasses - I’ve bought a couple of pairs off Glasses Direct and the -1.0 diopter correction on both eyes with no cylindrical correction at all is all I now need. In other news my 35% BMI brother has lost 7kgs in a fortnight on a lax version of the Keto Diet i.e. indulging in the odd carb... I’m still riding the bike to the squash club and back and playing solo with two rackets for an hour, plus the 10 miles in the saddle which definitely helps.
For those PWP concerned about Mercury Amalgam in their fillings, it would appear not to be a major risk and I think I would only go for removal when they fail. Here’s the research kindly provided by the BDA:
BDA Parkinsons Disease MERCURY AMALGAM 2018:
Database: Ovid MEDLINE(R) and Epub Ahead of Print, In-Process & Other Non-Indexed Citations, Daily, and Versions(R) <1946 to August 03, 2018>
Cariccio, Veronica Lanza. IRCCS Centro Neurolesi "Bonino Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124, Messina, Italy.
Sama, Annalisa. IRCCS Centro Neurolesi "Bonino Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124, Messina, Italy.
Bramanti, Placido. IRCCS Centro Neurolesi "Bonino Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124, Messina, Italy.
Mazzon, Emanuela. IRCCS Centro Neurolesi "Bonino Pulejo", Via Provinciale Palermo, Contrada Casazza, 98124, Messina, Italy. emazzon.irccs@gmail.com.
Abstract
Neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis are characterized by a chronic and selective process of neuronal cell death. Although the causes of neurodegenerative diseases remain still unknown, it is now a well-established idea that more factors, such as genetic, endogenous, and environmental, are involved. Among environmental causes, the accumulation of mercury, a heavy metal considered a toxic agent, was largely studied as a probable factor involved in neurodegenerative disease course. Mercury exists in three main forms: elemental mercury, inorganic mercury, and organic mercury (methylmercury and ethylmercury). Sources of elemental mercury can be natural (volcanic emission) or anthropogenic (coal-fired electric utilities, waste combustion, hazardous-waste incinerators, and gold extraction). Moreover, mercury is still used as an antiseptic, as a medical preservative, and as a fungicide. Dental amalgam can emit mercury vapor. Mercury vapor, being highly volatile and lipid soluble, can cross the blood-brain barrier and the lipid cell membranes and can be accumulated into the cells in its inorganic forms. Also, methylmercury can pass through blood-brain and placental barriers, causing serious damage in the central nervous system. This review describes the toxic effects of mercury in cell cultures, in animal models, and in patients with neurodegenerative diseases. In vitro experiments showed that mercury exposure was principally involved in oxidative stress and apoptotic processes. Moreover, motor and cognitive impairment and neural loss have been confirmed in various studies performed in animal models. Finally, observational studies on patients with neurodegenerative diseases showed discordant data about a possible mercury involvement.
Publication Type
Journal Article. Review.
Year of Publication
2018
<2>
Unique Identifier
2725805
Title
Epidemiologic study on the association between body burden mercury level and idiopathic Parkinson's disease.
Source
Neuroepidemiology. 8(3):128-41, 1989.
VI 1
Status
MEDLINE
Authors
Ngim CH; Devathasan G.
Authors Full Name
Ngim, C H; Devathasan, G.
Institution
Ngim, C H. Department of Community, Occupational and Family Medicine, National University of Singapore.
Abstract
A case-control study was conducted among the multiethnic population of Singapore to test the hypothesis that a high level of body burden mercury is associated with an increased risk of Parkinson's disease (PD). Selected factors investigated that could contribute to the body burden of mercury included dietary fish intake, ethnic over-the-counter medications, occupational exposures and possession of dental amalgam fillings. Detailed interviews were completed in 54 cases of idiopathic PD and 95 hospital-based controls, matched for age, sex and ethnicity, between July 1985 and July 1987. After adjusting for potential confounding factors, including dietary fish intake, medications, smoking and alcohol consumption, there was clear monotonic dose-response association between PD and blood mercury levels. The odds ratios (OR) and 95% confidence intervals (CI) for the approximate subject tertiles based upon blood mercury levels were 8.5 (CI = 2.2-33.2) and 9.4 (CI = 2.5-35.9), relative to the tertile with lowest blood mercury levels (less than 5.8 ng Hg/ml). Similar associations were revealed using scalp hair and urinary mercury levels. However, only the comparisons between the highest and lowest tertiles were statistically different from unity (p less than 0.05). When the body burden mercury indicators were mutually adjusted in addition to the four confounding factors, blood and urinary mercury levels showed ORs of 21.00 and 18.65, respectively. These ORs were statistically different from unity (p less than 0.05, 2-sided test). After adjustment, scalp hair mercury was shown to be a poor predictor of PD risk.
Publication Type
Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
1989
<3>
Unique Identifier
27906991
Title
Association between History of Dental Amalgam Fillings and Risk of Parkinson's Disease: A Population-Based Retrospective Cohort Study in Taiwan.
Source
PLoS ONE [Electronic Resource]. 11(12):e0166552, 2016.
VI 1
Status
MEDLINE
Authors
Hsu YC; Chang CW; Lee HL; Chuang CC; Chiu HC; Li WY; Horng JT; Fu E.
Hsu, Yung-Chuang. Department of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan.
Chang, Cheng-Wei. Department of Information Management, Hsing Wu University, New Taipei City, Taiwan.
Lee, Hsin-Lin. Department of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan.
Chuang, Chuan-Chung. Department of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan.
Chiu, Hsien-Chung. Department of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan.
Li, Wan-Yun. Department of Computer Science and Information Engineering, National Central University, Chungli, Taiwan.
Horng, Jorng-Tzong. Department of Computer Science and Information Engineering, National Central University, Chungli, Taiwan.
Horng, Jorng-Tzong. Population-Health and Clinical Informatics Research Group, Department of Biomedical Informatics, Asia University Taiwan, Taichung, Taiwan.
Fu, Earl. Department of Dentistry, Tri-Service General Hospital and National Defense Medical Center, Taipei, Taiwan.
Abstract
The impact of dental amalgam on the development of Parkinson's disease (PD) is still uncertain, although a positive association between dental amalgam and PD has been found in a few case-control studies. The patients with amalgam fillings restored between 2000 and 2008 were identified by using the National Health Insurance Research Database (NHIRD) in Taiwan. The same number of patients who had no new amalgam filling restored was matched by sex, age, and treatment date. Both cohorts were followed up from the treatment date until the date of diagnosis of PD, death, or the end of the year 2008. The individuals who received amalgam fillings had a significantly higher risk of PD afterward (adjusted hazard ratio [HR]=1.583, 95% confidence interval [CI]=1.122-2.234, p=0.0089) than those who did not. In the individuals who received amalgam fillings, being diagnosed with diabetes or hyperlipidemia demonstrated a significantly lower HR of PD occurrence than in the patients without diabetes or hyperlipidemia (HR=0.449, 95% CI=0.254-0.794, p=0.0059; HR=0.445, 95% CI=0.260-0.763, p=0.0032) after adjusting for comorbidities and Charlson-Deyo Comorbidity Index (CCI) scores. Meanwhile, hypertension increased the hazard risk of PD (HR=1.645, 95% CI=1.098-2.464, p=0.0159). The patients exposed to dental amalgam fillings were 1.583 times more likely to have PD afterward compared to their non-exposed counterparts after adjusting for comorbidities and CCI scores.
Publication Type
Journal Article.
Year of Publication
2016
<4>
Unique Identifier
21712780
Title
Monitoring of selenium in oral cavity argyria - a clinical and microscopic study.
Source
Neuroendocrinology Letters. 32(3):286-91, 2011.
VI 1
Status
MEDLINE
Authors
Venclikova Z; Benada O; Joska L.
Authors Full Name
Venclikova, Zora; Benada, Oldrich; Joska, Ludek.
Institution
Venclikova, Zora. Institute of Dental Research, 1st Faculty of Medicine of the Charles University, General Teaching Hospital in Prague, Prague, Czech Republic.
Abstract
OBJECTIVE: Argyria is generally classified as localized or generalized condition. Distinct pigmentation of the oral mucosa in the vicinity of amalgam fillings is often referred to as amalgam tattoos. Pigmented areas can also be associated with silver-containing corrosion products of dental alloys used for prosthetic restorations. Silver-containing electron dense particles (Ag-EDPs) are frequently found in pigmented areas. We attempted to correlate results of the elemental composition of Ag-EDPs with excerpts from health profiles of our study paticipants.
DESIGN/SETTING: Eight patients with diagnosed signs of localized argyria were investigated in this study. Biopsies from distinctly pigmented gingival areas were subjected to histological examination, electron microscopy and x-ray microanalysis.
RESULTS: Elemental composition of Ag-EDPs determined by x-ray microanalysis showed mainly silver in combination with sulfur or selenium or a combination of both chalcogens. Elemental analyzes results of Ag-EDPs were analyzed along with excerpts from the patient's clinical records. Two patients with low or undetectable selenium in the Ag-EDPs suffered from autoimmune thyroiditis, Parkinson's disease, bronchial asthma, and allergies to molds, pollen and dust.
CONCLUSIONS: We suggest that selenium in Ag-EDPs is a product of the detoxification process for Ag(+) ions in gingival tissue and that it may reflect the availability of endogenous selenium for physiological processes in the human body. Its presence or absence might thus be used as another marker of a patient's health status.
Publication Type
Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2011
<5>
Unique Identifier
21508427
Title
Hospital admissions for neurological and renal diseases among dentists and dental assistants occupationally exposed to mercury.
Thygesen, Lau Caspar. National Institute of Public Health, University of Southern Denmark, Oster Farimagsgade 5 A, 2nd floor, DK-1353 Copenhagen K, Denmark. lct@niph.dk
Abstract
OBJECTIVES: For many years an amalgam containing metallic mercury, which has been associated with neurological and renal diseases, has been used in dentistry. In this nationwide study we compared hospital admissions due to neurological and renal diseases among dentists and dental assistants to admissions in controls.
METHODS: This register-based cohort study included all Danish workers employed in dental clinics, general practitioners' clinics or lawyers' offices between 1964 and 2006. We compared dentists with general practitioners and lawyers, and dental assistants with medical secretaries, nurses and legal secretaries. We also compared dentists and dental assistants employed during periods with high occupational mercury exposure with dentists and dental assistants employed during periods with less mercury exposure. We followed all subjects in a nationwide register of hospital admissions. We analysed risk of neurological diseases, Parkinson's disease and renal diseases using a Cox regression model.
RESULTS: The cohort consisted of 122,481 workers including 5371 dentists and 33,858 dental assistants. For neurological diseases, no association was observed for dental assistants, while for dentists an increasing risk for periods with less mercury exposure was observed. Among dental assistants, a negative association between employment length and risk of neurological disease was observed. Admissions for renal disease among dental assistants were increased during periods with less mercury exposure compared with controls. For dentists a non-significant increased risk was observed between employment length and renal disease risk.
CONCLUSIONS: Our nationwide study does not indicate that occupational exposure to mercury increases the risk of hospital admissions for neurological, Parkinson's or renal diseases.
Publication Type
Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2011
<6>
Unique Identifier
17539227
Title
Accessing and restoring root caries: a case report.
Source
Journal of the Tennessee Dental Association. 87(2):20-2; quiz 23-4, 2007.
VI 1
Status
MEDLINE
Authors
Turner EW; Shook LW; Lackey M.
Authors Full Name
Turner, E W; Shook, Larry W; Lackey, Mark.
Institution
Turner, E W. Expanded Function Program at the University of Tennessee, College of Dentistry, USA.
Abstract
Adequate access to root caries can be problematic. The inability to view, isolate, and access the entire lesion may result in residual caries, poor adaptation of the restoration, and defective margins. Minor periodontal procedures, ranging from a mini-flap involving only one tooth, to conventional flap surgery can provide increased visibility and access to these troublesome areas. Through utilization of this technique, excellent preparations and restorations can be achieved. Restorative materials with a high potential for fluoride release as well as uptake should be highly considered in cases of root caries. The selection of a conventional or resin-modified glass ionomer provides several advantages. Most notably are the ability of these restoratives to chemically bond to tooth structure, and to provide significant fluoride release and uptake. These properties are not present in amalgam, composites, or compomers. Additionally, the material itself is relatively easy to use and provides an effective zone of caries inhibition around the margins of the restoration. Glass ionomers are not as sensitive to moisture as conventional resin composites or compomers, and, as a result, may provide a better bond to tooth structure and margination in areas where moisture control is troublesome. Finally, the polymerization shrinkage of these materials is not as great as resin composites, which should also improve marginal integrity. Clinical studies have demonstrated longevity of ten years or greater as well as success in xerostomic patients. Management of xerostomic patients should be directed toward finding satisfactory methods to relieve dryness. Some prescription medications are available, but should only be recommended after consultation with the primary care physician. Oral moisturizers are also available as are saliva substitutes. Caution should be used when recommending saliva substitutes due to the fact that some commercial products have been demonstrated to have a pH below the demineralization point of enamel. Products of this nature should be avoided. In the last few decades, the age of the patient population has increased and individuals have a greater tendency to maintain their natural dentition throughout their entire life. Gingival recession and subsequent root exposure has become more prevalent in the adult population. Additionally, the use of prescription medications that impact the flow and consistency of saliva is widespread. As a result of these phenomena, it has been predicted that root caries will become more prevalent. When preventive measures prove to be ineffective and restorations must be placed, access, visibility, and appropriate material selection are paramount. A combined minor periodontal surgery and restorative procedure is relatively simple, and when done properly, can provide excellent and affordable dentistry in these problematic areas.
Publication Type
Case Reports. Journal Article.
Year of Publication
2007
<7>
Unique Identifier
16448848
Title
Mercury amalgam dental fillings: an epidemiologic assessment. [Review] [61 refs]
Source
International Journal of Hygiene & Environmental Health. 209(4):309-16, 2006 Jul.
VI 1
Status
MEDLINE
Authors
Bates MN.
Authors Full Name
Bates, Michael N.
Institution
Bates, Michael N. Division of Environmental Health Sciences, School of Public Health, 140 Warren Hall, University of California, Berkeley, CA 94720-7360, USA. m_bates@berkeley.edu
Abstract
Dental amalgam fillings containing approximately 50% mercury have been used for almost 200 years and have been controversial for almost the same time. Allegations of effects caused by amalgams have involved many diseases. Recent evidence that small amounts of mercury are continuously released from amalgam fillings has fuelled the controversy. This is a comprehensive review of the epidemiologic evidence for the safety of dental amalgam fillings, with an emphasis on methodological issues and identifying gaps in the literature. Studies show little evidence of effects on general chronic disease incidence or mortality. Limited evidence exists for an association with multiple sclerosis, but few studies on either Alzheimer's or Parkinson's diseases. The preponderance of evidence suggests no renal effects and that ill-defined symptom complexes, including chronic fatigue syndrome, are not caused by amalgams. There is little direct evidence that can be used to assess reproductive hazards. Overall, few relevant epidemiologic studies are available. Most prior assessments of possible amalgam health effects have been based on comparisons of dental mercury exposures with occupational exposures causing harm. However, the amalgam-exposed population contains a broader, possibly more susceptible, spectrum of people. Common limitations of population-based studies of dental amalgam effects include inadequate longitudinal exposure assessment and negative confounding by better access to dental care in higher socioeconomic groups. Better designed studies are needed, particularly for investigation of neurodegenerative diseases and effects on infants and children. [References: 61]
Publication Type
Journal Article. Research Support, Non-U.S. Gov't. Review.
Year of Publication
2006
<8>
Unique Identifier
15155698
Title
Health effects of dental amalgam exposure: a retrospective cohort study.
Source
International Journal of Epidemiology. 33(4):894-902, 2004 Aug.
VI 1
Status
MEDLINE
Authors
Bates MN; Fawcett J; Garrett N; Cutress T; Kjellstrom T.
Bates, Michael N. Institute of Environmental Science and Research Ltd. (ESR), PO Box 50-348, Porirua, New Zealand. m_bates@uclink.berkeley.edu
Abstract
BACKGROUND: Whether dental amalgam fillings (containing mercury) are hazardous is a long-standing issue, with few epidemiological investigations. Allegations have particularly involved nervous system disorders, such as multiple sclerosis, Alzheimer's disease, and chronic fatigue syndrome. This retrospective cohort study, the largest of its kind, contained people in the New Zealand Defence Force (NZDF) between 1977 and 1997. The NZDF has its own dental service, providing all personnel with regular and consistent treatment. Comprehensive treatment records are maintained and archived.
METHODS: Yearly dental treatment histories, including amalgam filling placements, were compiled from individual records. To minimize amalgam exposure misclassification the cohort was restricted to people who, at NZDF entry, were aged <26 years and had all their posterior teeth. The cohort was linked with morbidity records. Data were analysed with a proportional hazards model, using a time-varying exposure unit of 100 amalgam surface-years.
RESULTS: The final cohort contained 20 000 people, 84% males. Associations with medical diagnostic categories, particularly disorders of the nervous system and kidney, were examined. Of conditions allegedly associated with amalgam, multiple sclerosis had an adjusted hazard ratio (HR) of 1.24 (95% CI: 0.99, 1.53, P = 0.06), but there was no association with chronic fatigue syndrome (HR = 0.98, 95% CI: 0.94, 1.03), or kidney diseases. There were insufficient cases for investigation of Alzheimer's or Parkinson's diseases.
CONCLUSIONS: Results were generally reassuring, and provide only limited evidence of an association between amalgam and disease. Further follow-up of the cohort will permit investigation of diseases more common in the elderly.
Publication Type
Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
2004
<9>
Unique Identifier
8628466
Title
Possible environmental, occupational, and other etiologic factors for Parkinson's disease: a case-control study in Germany.
Seidler, A; Hellenbrand, W; Robra, B P; Vieregge, P; Nischan, P; Joerg, J; Oertel, W H; Ulm, G; Schneider, E.
Institution
Seidler, A. Department of Epidemiology and Social Medicine, Hannover Medical University, Germany.
Abstract
In a case-control study, we investigated the possible etiologic relevance to Parkinson's disease (PD) of rural factors such as farming activity, pesticide exposures, well-water drinking, and animal contacts; toxicologic exposures such as wood preservatives, heavy metals, and solvents; general anesthesia; head trauma; and differences in the intrauterine environment. We recruited 380 patients in nine German clinics, 379 neighborhood control subjects, and 376 regional control subjects in the largest case-control study investigating such factors and collected data in structured personal interviews using conditional logistic regression to control for educational status and cigarette smoking. The latter was strongly inversely associated with PD. There were significantly elevated odds ratios (OR) for pesticide use, in particular, for organochlorines and alkylated phosphates, but no association was present between PD and other rural factors. A significantly elevated OR was present for exposure to wood preservatives. Subjective assessment by the probands indicated that exposure to some heavy metals, solvents, exhaust fumes, and carbon monoxide was significantly more frequent among patients than control subjects, but this was not confirmed by a parallel assessment of job histories according to a job exposure matrix. Patients had undergone general anesthesia and suffered severe head trauma more often than control subjects, but a dose-response gradient was not present. Patients reported a significantly larger number of amalgam-filled teeth before their illness than control subjects. The frequency of premature births and birth order did not differ between patients and control subjects. Patients reported significantly more relatives affected with PD than control subjects. These results support a role for environmental and genetic factors in the etiology of PD.
Publication Type
Comparative Study. Journal Article. Research Support, Non-U.S. Gov't.
Year of Publication
1996
<10>
Unique Identifier
1292449
Title
Side-effects: mercury contribution to body burden from dental amalgam. [Review] [6 refs]
Source
Advances in Dental Research. 6:110-3, 1992 Sep.
VI 1
Status
MEDLINE
Authors
Reinhardt JW.
Authors Full Name
Reinhardt, J W.
Institution
Reinhardt, J W. Department of Operative Dentistry, University of Iowa College of Dentistry, Iowa City 52242.
Local Messages
THIS JOURNAL IS AVAILABLE IN THE BDA LIBRARY, TO REQUEST THIS ARTICLE FROM THE LIBRARY GO TO: bda.org/library/journals-ar...
Abstract
The purpose of this paper is to examine and report on studies that relate mercury levels in human tissues to the presence of dental amalgams, giving special attention to autopsy studies. Until recently, there have been few published studies examining the relationship between dental amalgams and tissue mercury levels. Improved and highly sensitive tissue analysis techniques have made it possible to measure elements in the concentration range of parts per billion. The fact that mercury can be absorbed and reach toxic levels in human tissues makes any and all exposure to that element of scientific interest. Dental amalgams have long been believed to be of little significance as contributors to the overall body burden of mercury, because the elemental form of mercury is rapidly consumed in the setting reaction of the restoration. Studies showing measurable elemental mercury vapor release from dental amalgams have raised renewed concern about amalgam safety. Mercury vapor absorption occurs through the lungs, with about 80% of the inhaled vapor being absorbed by the lungs and rapidly entering the bloodstream. Following distribution by blood circulation, mercury can enter and remain in certain tissues for longer periods of time, since the half-life of excretion is prolonged. Two of the primary target organs of concern are the central nervous system and kidneys. [References: 6]
The more I read, the more I’m convinced that my PD was caused by my diet. Watching a video of JJ Virgin on what not to eat - specifically apple juice - I was reminded that about 30 or so years ago I gave up milk and substituted apple juice in everything, mistakenly thinking it was healthier - duh! So for around 3 or more decades I subjected my body to a daily diet of almost neat fructose. I never put on weight, possibly due to very high exercise levels, but I did get Parkinson’s Disease... Did anyone else make that sort of dietary error?
Thanks Kia, did you make the same sort of dietary errors that I did? I used to eat at least double the amount of sugar and carbs tha my friends ate, confident that constant exercise would keeep me slim
I used to start my day with a huge amount of carbohydrates and orange juice and also during the day with proteins which were worse than sugar. I deprived myself from eating fat because of the fat stigma that wrongly imposed to our society.I have always been a gym goer and like you said it caused me to be OBVIOUSLY fit and healthy.I have told several times and say it again that the Ketogenic diet is the sloution to the PD problems and also PD prevention.
Sounds just like me! I’m reading Nina Teicholz’s book ‘’The Big Fat Lie’ which so clearly shows what ludicrous health advice we have been forcefed throughout our entire lives. Ancel Keys was presidential in his duplicity
How is it going on no meds. Has it caused any problems with no motor things. I am desperate to stop as get really bad side effects which have got worse over the 5 years I have been taking it. But I am worried it has damaged my nervous system. I get levodopa induced dystonia in my throat neck mouth jaw chest stomach and bladder. When kicking in and kicking out. Sinemet causes it but also stops it. It causes swallowing, choking and talking problems I can't eat or drink. I can't breathe properly and have over active and retension in bladder.
I know that if I was able to get through the difficult bit that it would all stop but it gets so bad when I can't breathe or swallow properly I get really panicy. The neurologist thinks it is the condition but I know it isn't as it gets worse the more Sinemet I take.
How long were you on the diet before you were able to begin to reduce your meds? Do you have to check daily to make sure you’re in Ketosis ? Thank you!!
I started the Keto Diet and took 1 month to taper linearly to zero from 16mg of Ropinirole and 16 Sinemet, It took a week to get into ketosis and I’ve been there ever since, around 0.5-4.0mmol/L. I check only once a day now - if it goes low I skip lunch and it goes up to 4.0! I still feel a bit jumpy and the tremor persists - BUT I do think that my symptoms are reducing on the Keto Diet although I’m thinking it’ll take 6 months...
Keep up the Keto and especially look at dietdoctor.com which is excellent - a really, really good information source.
Good Luck Connie - it’s worth the fight! Best regards, Phil 2bats
I have seen an article to comment that these things start off in early childhood, even before you are born, meaning, there is developmental factor at play.
One observation I've made is that it seems people who eat meats, fats,carbs etc don't seem to get PD, while many of us who eat healthy, do.
I go on many cruises and see seemingly normal healthy people heap mile high piles of fatty food on their plates, while I'm limping along with toast, and an egg white omelet !
I’ve just been on a couple of short cruises and saw the same thing, but reckon most of the passengers were actually quite ill. Almost all were overweight and probably diabetic or pre-diabetic and with bad skin and many aches and pains. Yes, they were eating a lot of fats, but also, unlike me, massive amounts of inflammatory carbs so very definitely not on Keto Diets!
When you’ve converted to a ketogenic diet, you really notice what an awful diet the average human lives on - and the results are all around you, waddling to the buffet to load up with what I now regard as POISON... Boy did I eat a lot of cheese instead of sweet desserts, but I stayed in ketosis!
My theory is that the western high carb diet predominantly causes obesity and Type 2 diabetes but there is a skinny minority ~1% maybe, who get Parkinson’s Disease instead. I hope to prove that my Parkinson’s Disease can be reversed by the Keto or LCHF Diet as can diabetes.
I agree with you re 'food hoarders' on cruises as being unhealthy looking, and probably quite sick, but it's not fair to people who ate healthy most of their lives and get PD. I'd rather have diabetes, and hypertension. Their more fixable.
Cholesterol is nearly all good except for the little particles. Your brain needs it. The cholesterol scare is all the legacy of Ancel Keys and his henchmen!
Hi 2bats. This is Colin Potter. I've just come across this post. I'd be really interested to learn how you're doing now. Can you email, please, at colin.potter@fight-parkinsons.org
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Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
) I got banned because I wrote a post claiming a "partial cure" for my illness. I then got banned here for a few days for making the same claim and ultimately I realized if I used the words "alternative therapy" and told people never to try something without first consulting a doctor then the mods would be happy.
“emergency room” PT 2 - amantadine, benadryl and tremor dominant prognosis
Spanning an octave - Sinemet does it again
Amantadine for tremor?
