My Dad was recently diagnosed. Very early stage. This is very interesting news.
My take is that Parkinson's is a little like cancer in that it likely has multiple root causes that can injure the same part of the brain (substantia niagra) and cause the disease.
My research for his case led me to vitamin k2 deficiency as a possible cause / complicating factor. There are some genetic models and mouse trials that show k2 as a modality. He had his gallbladder removed about a year before symptoms started. He also has kidney stones. K2 is fat soluble, only acquired through diet, and affects calcium regulation. Oddly connected to his history/symptoms. So hard to help debug stuff like this.
He's on a supplement now. We don't have a great way to measure if it's working. The symptoms have such natural variance day to day.
I worked with a guy who has Parkinson's. He was _obsessed_ with nutrition and always said the same thing about it being related to his gut. I don't think I've ever seen someone eat as natural and health as this guy.
I'm obviously not a doctor and don't know, but from what I saw, he barely shook at all. He swore that when he went off his diet he would start shaking again. He also said his doctor couldn't believe how well he did on his own.
Is there a general overview of the scientific claims made in this book somewhere? It sounds somewhat promising, but the table of contents doesn't exactly inspire confidence that the information is accurate. Additionally, I can't find any reviews online about this that don't look like shills for the book itself.
"Having read his book in full [“Why Do I Still Have Thyroid Symptoms? When My Lab Tests are Normal"], visited one of his practitioners, and assembled the above lists of fraud indicators, I can solidly claim that Dr. Kharrazian is a quack." -- Dr. Christopher S. Baird
But note: Dr Baird deleted this article shortly after it was written in 2013.
Deletion doesn't necessarily mean retraction. As far as I know, only a retraction strictly means retraction.
The article makes plenty of factual claims that remain factual whether the article is published or merely preserved.
Like:
"autism is caused by genetic mutations, not “vaccines” or “leaky gut” as [Kharrazian] states on p.327 and 409."
And sure enough: [“Why Do I Still Have Thyroid Symptoms? When My Lab Tests are Normal“] searchable at Amazon does indeed have the claim that autism might be a result of immune system reaction to vaccine. Sure sounds like a quack.
I'll be honest, I'm a layman and don't know. There are loads of Amazon reviews, but I agree not the best source and could be shills. I read the book and not too much seems crazy or out there.
I'm very sorry about your father's diagnosis. A few years ago I came across this spoon invention which seemed to be very helpful to those that are dealing with the shaking symptoms:
Would it help to record the tremor intensity while tracing a smoothly moving dot with his finger on a cell phone screen? And/or record the tremor while holding the phone and tracing along a line with a corner of the phone. I bet you could get pretty good at-the-moment measurement of the tremor. Combine that with graphing and a rolling average, and you might have a pretty clear picture.
I bet you could homebrew an electromyograph pretty easily. It probably wouldn't be particularly accurate, but you could probably achieve enough precision to provide repeatability and measure day-to-day variance.
Edit: Hackaday had an article about a simple EMG recently
Interestingly he does not have the classic tremor symptom. For those who do, that might make for a good thing to track. He doesn't really have any symptoms that could be quantitatively measured, especially over the short term.
my dad's brother has Parkinsons and it is very disheartening but I make sure to visit him and take him to lunch each time I visit relatives. He still has mobility but he also is losing his sight. The annoying part is just how frustrating to him it can be when he wants to move and his body gets "stuck". He has to tell him self to stop, stand, and then move. It works a bit, then repeats.
as for it being a bacteria, after my personal experience with bacteria problems I wouldn't be surprised. I was on Cipro for an unrelated infection and this stuff killed all the bacteria in my gut, or at least the good stuff. What moved in made my life miserable for months till they could id it and flush it out.
still I am curious if it is, can it be related to pets? they bring along bacteria we don't handle well. diet would be a little odd to me so I figure it has to be environmental
>can it be related to pets? they bring along bacteria we don't handle well
wouldn't that have killed the human race long go? I think it is other way around - the much lesser exposure to pets in modern society seems to correlate with the rise of auto-immune and immune related diseases.
It could be the case. But in order to find out, the best way would be to correlate both conditions with medical reports of a large number of patients.
A platform like [1] could help in sorting this out.
(Question: Does anybody know other/better platforms for this purpose? Does anybody have positive experience in doing this kind of research using such platform?)
The best platforms for this sort of research in the US are internal proprietary toolkits of health insurance companies, auditing companies, and law firms. The profit motives of the US health care system don't currently incentivize putting these platforms to use for science, they are mostly used for (re-) billing.
(Source: Worked for an auditing/law firm company deep on their platform once. Have friends still in health insurance/auditing/law firms.)
As for an anecdotal positive experience, one of my friends working for a health insurance company did find a correlation in lack of remissions of a very specific form of cancer and the use of a prescription drug by datamining health insurance records and helped publish that as a cure for that very specific cancer.
But given the way the industries are incentivized and fight among each other and fail to cooperate, I fear I have plenty more negative anecdotes than positive ones of things researched on top of these walled garden platforms.
The US Department of Veterans Affairs has extensive longitudinal data on tens of thousands of Parkinson's patients. They do research as well as treatment.
Sorry, I don't know the details (this was essentially picked up in a party conversation) and I'm afraid to ask because I'm assuming it was work done under an NDA given the way the project had been described to me. I don't know exactly how proprietary things were and if it would be socially/legally appropriate to ask at this point because that was under that friend's previous employment. Once again, the binds of our for-profit health system incentivizing against public disclosures and (data) scientists getting public credit for their work.
Could be! Vitamin k2 is involved in calcium use throughout body and there's a good study of how k2 supplements significantly reduced osteoporosis over 2-3 years. Bone mineralization takes a while...
Last year, there was an interesting story about a woman who could smell a certain odour that seemed to be given off by people with Parkinson's (primarily her husband).
"We had them wear a t-shirt for a day then retrieved the t-shirts, bagged them and coded them.
"Her job was to tell us who had Parkinson's and who didn't.
"Her accuracy was 11 out of 12. We were quite impressed."
Dr Kunath adds: "She got the six Parkinson's but then she was adamant one of the 'control' subjects had Parkinson's.
"But he was in our control group so he didn't have Parkinson's.
"According to him and according to us as well he didn't have Parkinson's.
"But eight months later he informed me that he had been diagnosed with Parkinson's.
Not GP but ketones have a fairly distinct and strong aroma. That said, if it were ketones, they'd probably be too distinguishable for this story to be uniquely news-worthy.. it's probably a less identifiable smell than ketones, whatever it is..
Interesting you mention this, as I've reached a similar (albeit very preliminary) conclusion while researching a medication I've been forced on top by the so-called state govt 'chief health officer'.
It has wrecked my life, and I'm fairly convinced it is causing prolonged ketoacidosis. It's also likely that it's exposing me to greatly increased risk of Parkinson's disease, which killed my grandfather and is currently in the process of killing my uncle.
But enough of that sob story. One of the theorised causes of Parkinson's and diseases in the same class is the endogenous formation of persistent prions. Prions are proteins that are 'defective' and fold abnormally.
Your body will likely destroying/metabolise prions in fairly short order; a good thing because newly synthesised proteins (mostly from amino acid metabolism) 'learn' how to fold themselves from other proteins. If they happen to learn from a "prion", one that's likely avoided being metabolised for an abnormally long time, this behaviour can spread and proteins begin to behave abnormally, in some cases forming plaques on vein and arterial structures in the body.
This is obviously bad. It's arguably worse for someone in ketosis, as their brain is burning proteins for fuel door to depleted glyco-something (sorry, the name escapes me, it's the sugar your brain uses for energy). So now some of these prions migrate to various synapses (presumably the most energy hungry ones) and behind to form plaques on these synaptic structures.
In addition, my recent (totally amateur) theory is that ketosis increases the rate of prion occurrence. In ketosis, you're metabolising unusually high levels of amino acids/proteins. So more risk of a bad or incomplete enzymatic reaction. In many cases this metabolism occurs in red blood cells, where amino acids capture, and are broken apart by, hydrogen atoms (ions?).
So now you're entire system is under more oxidative stress, you're burning proteins and synthesising new ones at a high rate, is difficult to stay hydrated due to all these hydrogen atoms going missing, and one of the byproducts of some AA hydrogenation is ultimately acetone (paint striper). Also the metabolites are highly acidic, which unbalances your plasma pH levels and further interferes with normal metabolic processes. Interestingly is not necessarily unbalanced towards 'acid', as one might expect. The reasons are still unclear to me, but I'm guessing it's something like "homeostasis gone mad".
And acetone is what dogs can be trained to detect: to try and rid your body of the excess acetone, you start respiring (exhaling) acetone, with its trademark "over ripe fruit" smell.
Proteins don't usually "learn" how to fold from other proteins, their structure is usually determined by their amino acid sequence. In vivo there are chaperone proteins that help proteins fold into their natural structures by preventing premature aggregate folds, but still their final fold is a result of their amino acid sequence. Less commonly, there are some rare chaperones that cause specific folding that wouldn't otherwise occur, but these are the exception and not the rule. However you are right that prions are an exception here, prions are uniquely misfolded proteins that are amyloid-prone and cause their otherwise normal folded structure to refold into another prion form, leading to a chain reaction of refolding into the prion form for that particular protein. As far as I know there is still a lot of research to be done in order to verify the theories regarding prions.
It doesn't make sense to say newly synthesised proteins arises mostly from amino acid metabolism, metabolism involves both catabolism (breakdown) and anabolism (synthesis). Amino acid degradation results in glucose via gluconeogenesis or cellular energy (ATP), whereas amino acid synthesis is of course what is used for proteins, as proteins are made of amino acids. So yeah, doesn't really make sense. Perhaps you meant to say that newly synthesised protein uses amino acids of which are most often sourced from proteolysis?
As for red blood cells, they don't have any mitochondria, so they only metabolise glucose and other sugars (and anaerobically at that, due to their function of carrying oxygen). They certainly don't metabolise amino acids or proteins, so I'm not sure where you got that idea from.
Yeah I oversimplified protein 'chaperoning' for brevity's sake. As for prion recruitment of other proteins leading to amyloid plaque formation in the brain, I concede it's an open question. But my money would be on 'yes' to this hypotheses, given recent studies that have been coming out (except for a particular German one that concluded the opposite based on a mouse model of PD).
I'm probably on the wrong end of the metabolic semantics here; I was specifically referring to hydrolysis (or is the correct term hydrogenation?) occurring in red-blood cells. If this is not considered part of normal metabolic processed then mea culpa. The particular (pro)drug I mentioned (likely) relies on this mechanism to cleave/dissolve a covalent bond between the two constituents of the prodrug, to produce a 'time-release' effect: the constituents being l-lysine and dexamfetamine/dextroamphetamine ('lisdexamfetamine').
For example, here's one of the few serious studies I've been able to find on its metabolism (i.e. not a single dose study that concludes 'yes, this leads to amphetamine in the blood'): http://www.tandfonline.com/doi/full/10.3109/21556660.2013.77... . There was another (better) one somewhere on pubmed, but I can't seem to find it atm (although it was also an in vitro study). I also found this, more general paper, quite interesting (although I'm guessing it's outdated?): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142344/
I admit, my understanding of the process by which amino-acids are synthesised in to proteins in vivo is not the best. I'm actually a little hazy on how I first arrived at the notion that an over-abundance of l-lysine could disrupt the Krebs-cycle. I probably came up with it during one of my long treks across Wikipedia, so it's very likely wrong....
I watched my great grandfather lose everything to Parkinson's. I really hope this leads to a treatment that stops the progression of symptoms and fast.
My father suffered from the disease and passed away in October. Awful disease. This is great news, but it looks like any treatment based on this will still be quite some way off.
I also got the impression that the damage was done over years. Killing the bad bacteria now might not be enough to cure an existing case of Parkinsons.
Yes, in the form of a bacteriophage. They're well known, but limited normally because they are very species specific. But if you needed to kill exactly one type of bacteria, they'd be the tool to reach for.
Best i can tell, the problem is not just that they are picky eaters but that they also keep mutating. thus you can't just mix a batch and shelve it for later usage.
I am so sorry for your loss. My uncle passed away from Parkinsons 20 years ago, when he was fully incapacitated and incapable of doing anything. As difficult as it is to witness, I cannot imagine the pain of the experience.
I never researched too much, mostly watched what happened to M.J.Fox. I thought PD was mostly affecting motor controls on non life critical muscles (limbs). What are the other effects ?
PD is bad enough on its own without dementia. My mother has had the early onset variety since her mid-thirties, and while her cognitive function has clearly declined, she's no where near dementia. On its own, the disease is like prison. You slowly become trapped in your own body and lose the ability to have an impact on the world around you. The treatments and medication cause diskinesia (the violent/uncontrollable tremors associated with the disease) and the wrong dose (for that day/time), or the wrong setting on the implant they put into the motor cortex to stimulate it, is as bad as no treatment at all. Depression is a common co-morbidity.
Parkinsonism is watching yourself die with full knowledge of what's happening to you and a complete inability to do anything about it. My mother had polio as a child as well, so she's trying to learn to walk for the third time.
There is no fate I find more horrifying on a personal level. None.
Adding to this, dementia might be a "side" effect of the medication for the muscles' rigidity. It's hard to explain but eventually there comes a time when you need to opt between not being able to move or take the medication and start having more and more frequent surreal visions.
My grandfather survived a few cancer appearances but during the last surgery to remove some cancer lumps he woke up as a completely new person. It seems the anesthesia triggered the first signs of Parkinson's and dementia exactly at the same time. He was pretty "normal" before the surgery but after it he couldn't walk and thought the hospital staff attacked him with dogs during the night. Fortunately (?) he didn't last long after that day but still had time to be kicked off from his home by my grandmother who couldn't handle the dementia.
Sorry for the rant, I'm obviously not over it, will never be. Dementia is the worst thing I've ever witnessed.
If you're lucky they'll feed you coconut oil (short saturated fatty acids are easily burned in the cells for energy) and the dementia will pass. If you're not lucky they'll give you "anti-psychotic" drugs to sedate you, or other interventions that ruin the metabolism. Many treatments have the side effect of ensuring the patient will never recover.
To be honest, is seems more likely the 'delirium' is actually mild psychosis brought on by excess dopamine in the PDF in particular. Many Parkinson's medicines treat some of the cognitive deficits it can cause with stuff like L-Dopa and other 'pro dopamine' drugs. Given the brain is progressively becoming more 'dysfunctional', some abnormal brain functionality + excess synaptic dopamine is probably psychosis waiting to happen.
However, I'd personal take the intermittent low level psychosis any day if it meant retaining my brain, retaining 'me', for just a bit longer.
Also yeah, as stated elsewhere: Parkinson's + anti-psychotic meds == dangerous and egregious medical malpractice. Anti-psychotics are basically an anti-cute for Parkinson's, given the generally work by attenuating dopamine prevalence in various synaptic clefts.
My thinking is that delirium is probably a symptom of impaired metabolism and/or malnourishment and/or insulin resistance. When a person's mitochondria can't make enough ATP to keep them going, sometimes they become delirious/psychotic [1].
Coconut oil is useful because of its high proportion of medium chain triglicerides. Longer fatty acids have to be transported with carnitine to be metabolized in the mitochondria.
The alcoholic brain tends to be insulin resistant, and uses acetate (a breakdown product of ethanol) as fuel, because glucose isn't available, or isn't can't be delivered to the mitochondria in sufficient quantity.
[1]
Thus, without careful assessment and history, delirium can easily be confused
with a number of psychiatric disorders or long term organic brain syndromes,
because many of the signs and symptoms of delirium are conditions also present
in dementia, depression, and psychosis.
- https://en.wikipedia.org/wiki/Delirium (IMHO, doctors distinguish between "delirium" and "psychosis" because they don't realize they have similar etiologies.)
The dementia pre-treatment was an aid to my diagnosis. Hallucinations, wild mood swings, forgetfulness, not recognizing familiar people and places, the whole nine yards, are part and parcel of the whole affair. And then you string a few "good days" together and feel like things might be sort of normal, or at least manageable, again. Then yoink!
Parkinson's kinda sucks that way: I'd say about a third of the people I know with the diagnosis re people I would have been able to point to from across the street and say, "that fellow has Parkinson's." The rest have a presentation that doesn't look much like the textbook, but we have a few things in common if you look deeply enough. Frankly, though, there's a lot of diagnosis by elimination and medication.
>I really hope this leads to a treatment that stops the progression of symptoms and fast.
it seems that it is just one among several paths to Parkinson's. Not being a doctor, just from googling, it seems that Parkinson's - specifically those protein clumps in the brain cells - is a result of inflammation, ie. immune system reaction. Some gut bacteria (or its by-product), as in this study, seems to be a trigger for such reaction. Looking into the spread of Parkinson's around the world - many places/localitites with high rates are completely different from each other - confirms to me that there are possibly many different triggers for such immune system reaction, one of them seems to be pesticides for example.
There is need for research into what is happening in the gut, what the microbiome looks like and how it is influenced by food and stress.
This research money can either come by government funding (ideal for basic research) or by private funding (focused, to produce top medicines).
As it looks now, the private funding may not work because any remedy in the form of a medicine, would be applied a couple of times and that's it. There may not be enough money to make.
I would like to see what folk medicine traditions from around the world thought of and how they treated the stomach. They might not have known about bacteria, but given enough time some of them might have established some cause and effect of symptoms and treatments (typically herbal). We might learn from them hints to speed up or microbiome research.
Right now, the information is very scattered and siloed, and very difficult to survey.
To those familiar with various skin conditions, this may not be a big surprise
Skin conditions such as seborrheic dermatitis disproportionately affect those with HIV or Parkinson's and those skin conditions themselves have been liked to gut health, although not widely received in the medical community.
Seeing as how many skin ailments are linked to those with early or long term use to antibiotics (e.g. childhood ear infections, antibiotic use as infants), and Parkinson's patients are disproportionately affected by them, this is an even greater reminder that gut flora health is something not to be taken lightly.
So how do you go about actually fixing it? I've had that condition in a minor form for pretty much my entire life, getting worse when I was a teenager. I've gone to many derms and they all end up just giving me some form of corticosteroids.
I've tried vegan diets, various supplements, probiotics, natrual paths, salt baths, oatmeal baths and on and on, and it doesn't do much other than treat symptoms. I haven't tried to fix it any further because it's just a minor annoyance in my life, but I'm all ears if there is something that explains it better and some measurement that I can use to help understand it.
I would say first and foremost, avoid all uses of topical steroids and topical antifungals. And do not use antibiotics "just in case" (this is common for routine dental surgeries, but unnecessary). I do know from enough anecdotal evidence and reading published literature that those are only stopgaps and will eventually make your symptoms worse.
Unfortunately, I'm not a doctor and I don't exactly know either. All I know is that there are serious links to diseases like IBS, Crohn's, dementia, Parkinson's, seb/atopic dermatitis, etc. that many have known to be associated with gut that is being only proven in recent years.
Personally, I have reduced my intake of carbs (even "healthy" carbs) to a minimum. I eat a small serving of carbs when I'm eating other food, but never a small serving of carbs by itself. I rarely eat anything with yeast or sugar, which is a dealbreaker for most people.
I drink kefir and kombucha in small amounts and I take copious servings of probiotics. Right now I'm taking synthol and garden of life but I'll switch to a different set in a few months.
I also consume a lot of natto, kimchi (you can make this at home), and organic unfiltered apple cider vinegar.
I apply a very small amount of sea salt and water and keep it on everyday and clean my face with ACV for a few minutes each morning and evening.
Same like you. Have tried a lot of things. I am certain it has to do with my diet.
I tried switching it and change it occasionally but could never nail what affected the it.
Lots of people also say it has to do with stress but not to my personal experience. It's not that I don't get stressed, it's just that I've seen it come out bad in calm periods of my life as well.
Another factor that I think affects it is weather. I find .y condition to improve greatly when I'm in a dry area like a desert.
I also started taking curcumin pills and I think that it also help.
The problem with seborrheic dermatitis is that its right on the edge between not bad enough to make you want to change your life significantly and annoying enough to make you suffer
This is especially interesting, since coffee is moderately protective for Parkinson's.
Does that mean the coffee may be working at the gut level rather than its caffeine working in the brain? On second thought, coffee definitely works on the gut in normal people, if you know what I mean.
Interesting. Might the effect be due to coffee's acidity? When you drink coffee, the environment in your stomach becomes more acidic, which would (just speculating) make it more effective at destroying/metabolising any mal-folded amino-acid metabolites/proteins (i.e. prions, scary stuff).
Pharmacokinetics does not seem to be particularly well understood currently, but we do seem to be finding it's much more important than we thought. That, and whatever you call the 'study of metabolism' (metabolomics?)...
Mother in law has had it for about 15 years (so has lived longer than expected). Currently has implanted electrodes in the brain, which fixes some issues and leads to others.
Recovery is unlikely at this stage, but even preventing the disease from progressing further would be quite something.
Short chain fatty acids can be things like acetic acid, propionic acid, butyric acid. The fermentation process takes in fiber and puts out these guys, so while fiber isn't an SCFA polymer, I don't think this statement is inaccurate (i.e. I don't have the metabolic pathways off hand but these could be direct breakdown products given the shortness of the carbon chains - acetic acid almost certainly is.)
The main path for glucose involves splitting it in two 3 carbon molecules, mainly pyruvate https://en.wikipedia.org/wiki/Glycolysis From this it's easy to make acetic acid (2 carbons), like the acetic acid in vinegar. And , I guess it's also not very difficult to make propionic acid (3 carbons).
I can accept that they say that fiber or glucose is "break down" to acetic acid, propionic acid, but I think it's misleading. (And the usual definition of fatty acid starts at 4 carbons https://en.wikipedia.org/wiki/Fatty_acid )
I think they're using it colloquially: you can "break down" trees in to paper, even though the paper technically requires reassembly and further processing from the most deconstructed tree step.
But it is a phrase that the average layperson would take as "simpler things made from the raw ingredients by the processors", rather than a direct deconstruction pathway.
It's a common problem when technical language collides with a common term or phrase, because most articles will mean the common one and send pendants in to a fit.
I think this is the crux of the issue. If one ascribed to the prion hypothesis, than ketogenic metabolism would almost certainly have to be related to higher probability of prion formation, and more survivable conditions in vivo.
Another common way some AAs are metabolised is by hydrogenation is red blood cells. So I think this eats up a hydrogen ion at the very least, leading to greater intra-cellular oxidisation and a messed up blood plasma pH, increasing the occurrence of abnormal enzymatic reactions. The metabolites you mentioned are present in much larger quantities on low carbs, due to increased synthesis and use of proteins for energy, including for the brain...
Oh and at least a few of those metabolites sometimes ultimately metabolise to acetone, especially if normal metabolism disrupted by wonky pH balance.
Anion gap in soft tissue cells may also explain 'twitches': spontaneous muscular activation due to soft tissue cell hyper-natremia (unbalanced towards sodium).
Crazily, excess acetone restoration is one theory that explains spontaneous human combustion (acetone is quite volatile and flammable)...
There is related work on dementia as well, wish I could find it. Something to do with increasing dietary ketones (using oils) to make up for glucose processing issues in people who were long term pre-diabetic.
It was a dinner conversation, where a guy was reasoning that some degenerative and autoimmune diseases were related to tissue starvation as a result of inhibited glucose processing, and he was using ketones (with some perceived success) to treat symptoms of his own auto-immune disorder.
It's not evidence or confirmation in any way, but for any biohackers out there it's something to play with.
Just to provide the counter-point: also possible that increased protein metabolism and synthesis (the defining feature of ketogenic diets) increases the likely hood of long -lived prions: proteins that fold abnormally, which can be learned by other newly synthesised proteins leading to these "mutant proteins" forming plaques on the brain (which is now burning protein for energy due to depletion of glucose).
And there might be a runaway/tipping point somewhere here: some amino acids have acidic metabolites and also need to capture hydrogen ions from red blood cells to metabolise/synthesise protein. Some of these metabolites also cause acetone build up in body, which starts to be expelled via lungs.
So combo of high rates of protein synthesis, abnormal blood plasma pH balance and increases cell oxidisation and anion gap == greater rate of prion formation and survival.
This is just a personal hypothesis, no real evidence to back it up. Just suggesting caution should be exercised here. PD is a horrible disease, I wouldn't wish it on my worst enemy.
It's important to discuss. There is a lot of stuff out there that screams snakeoil about MCT and coconut oil products, and it can have the effect of both discouraging legit research and duping the dupable.
If there were only a way to test medical hypothesis like hacking on code. Maybe a platform to crowdsource data for experiments then control for factors and double blind it.
not to reply to own thread on theme, but want to also add ketogenic diet was also used for treating "epilepsy," now known as a general class of seizure disorders, which are related to many issues, among them brain lesions. I have zero medical background, and if you are searching on this stuff, my point is that beyond the political stuff, there is something up with sugar.
A silbing comment mentions some causes such as over-cleanliness and c-section, but other more detrimental effects may be lack of breast milk in infancy and antibiotics use (particularly as a toddler/infant).
Some other supporting causes may be things like overuse of antibiotics in meat production and lack of fermented food in diet.
I'm not sure if it has differentiation, but lifestyle factors could have an impact. If, for example, in more developed countries there's a great emphasis on (especially) childhood cleanliness, it may be affecting the development of "good" bacteria:
From the map I linked above, developed countries seem to have high rates. Parkinson's doesn't seem to discriminate there, so is there any other thing interesting by country? Spurious and sounds silly, but spicy foods, maybe?
- Cinnamon seems to help in mice trials (and also has anti-inflammatory properties).
- Could diabetes be analogous to Parkinson's? Diabetics generally have lost the ability to process carbs (usually by eating too many); could Parkinsons be caused by people being very dopamine focused and wearing their brains out?
I wonder if diet can change the type of bacteria in the gut, the inflammation in the body, have a neuroprotective effect on the brain?
Sounds like I'd try a ketogenic diet which has known neuroprotective effects, changes the bateria in your gut and reduces inflammation.
> Diabetics generally have lost the ability to process carbs (usually by eating too many)
That's an outrageous misrepresentation of diabetes (all types).
Diabetics process carbs exactly like everyone else. The body breaks them down and throws the sugars into the bloodstream in the perfectly normal way.
The lack of insulin (generally Type 1) or the resistance to insulin present (generally Type 2), means the cells struggle to process the glucose, leading to uncontrolled rise in glucose levels to dangerous levels.
The body has a poor 'over-limit' response to glucose and tries rather inefficiently to dump the excess in urine which has limited success. As a consequence lots of short-term and long-term damage to the body results - some of which is still being discovered.
Causes of diabetes have multiple possible elements, including none, one or more of : genetics, environmental [e.g. infection] and lifestyle.
"eating too many [carbs]" is a myth and intended to be derisive and offensively stereotype diabetics as being wholly responsible for their condition - just dressed up as a more socially acceptable victim-blame than saying they're receiving God's punishment for having sugar in their coffee.
Science has conclusively proven diabetes is not some simple response to over-indulgence in carbohydrate.
I'm sorry for upsetting you but from my research eating high sugar/carb diets (without exercise) causes insulin resistance in the majority of people. There are some groups that are more susceptible to this of course.
I'm not blaming anyone or even thinking about that; I've just done a lot of research and listened to a lot of interesting studies about the gut biome, western diet, insulin resistance, weight training, HIIT, noticing how I feel if I eat lots of sugar and carbs, and trying to eat a more health diet.
Maybe I'll be proved to be wrong, I'm just giving an opinion based on some research I've done.
Also by process I've definitely used the wrong word there. I definitely mean utilise.
That doesn't disprove anything I've said; it says diabetes is probably caused by eating too much which spikes blood glucose which causes diabetes. What you are saying with your pithy comment is really great but what I've said is eating sugar and processed carbs spikes blood sugar, over time it leads to resistance to the insulin your body produces. If you eat too much your body (even some fats or protein) produce an insulin spike. If you spike your insulin 20 times per day with soda you will almost certainly at some point become diabetic. You simply won't be able to eat enough fat or protein let alone veggies to do this so we are back to my original point...
Every time I hear it, it is offensive. Let me explain why.
It's often quoted in the context of a relatively young person who has died and people discussing the young and sudden death as 'well, they were diabetic, so they died because they just kept eating donuts and didn't stop when they were told'. That brings no comfort to the family and it is often completely untrue. Most diabetics do try very hard to deal with their condition responsibly but simply stopping eating carbohydrate is not really a 'cure' or answer to the condition. Some may chose to deal with it, in part, by doing this because they feel that helps them specifically. But that is not the case for everyone.
Anyone who said a cancer patient died because they brought it upon themselves would rightfully expect to be ostracized (or worse) but, for some bizarre reason, people are happy to unquestioningly accept the point for diabetes, but not cancer (another disease with complex reasons behind it).
Addressing some other comments, insulin resistance can be a natural condition due to genetic factors and occur in the absence of excessive carbohydrate consumption. It can also develop in type 1 diabetes as a reaction to the artificial insulin introduced to control the condition (GM 'human' insulins can help but sometimes switching to Bovine/Pork insulins helps - again, it's complex and not well understood). Low carbohydrate consumption may mask the condition, but the person is still insulin resistant/diabetic regardless of whether they eat carbohydrate or not. Diabetes is not cure-able (yet - there are pioneering attempts).
I know diabetics devastated with guilt that they've somehow caused their diabetes and are responsible because someone told them it is because - based on no evidence at all - they eat too much sugar.
Perpetrating this myth and forcing guilt upon diabetics is potentially psychologically damaging, especially to a group know to have a higher propensity to depression because of the condition.
My final point on the matter, some diabetics have a form which is virtually impossible to manage manually and the only avenue for treatment is to use the new insulin pump technology which can combine continuous glucose monitoring with ultra-fine insulin control (complex time slot/insulin sensitivity/carbohydrate dosage calculations) in order to control the condition. This is showing excellent results but does come with considerable costs - although these are a small fraction of the cost of amputations, blindness or organ failure which can otherwise result.
I see where you're coming from, but I don't think any low carb advocates are making a moral judgement against diabetics. It's not just diabetics who have suffered from the wrongheaded diet advice that's been given for the past 40 years.
Yes, a low carb diet is not a cure to diabetes, any more than a low peanut diet is a cure for peanut allergies. But I think the idea that people can eat whatever they want and use more and more insulin has lead to a lot of unnecessary human suffering.
Could diabetes be analogous to Parkinson's? Diabetics
generally have lost the ability to process carbs (usually
by eating too many);
No.
I'm assuming you are talking about type 2, which has nothing to do with the ability to process carbs but instead resistance to insulin. This is caused by so many different factors like genes, medications, stress, smoking, high intake of certain types of fats, lack of exercise, white rice, pollution, etc.
You can't be talking about type 1 because you'd be absurdly wrong if you were.
Hes pointing out that what you said was factually incorrect. Diabetics don't lose the ability to process carbs at all.
Carbs are broken down along with proteins and fats. What Type 2 diabetes entails is glucose building up in the bloodstream with no real way to utilize it due to insulin resistance.
Yeah I'm with you on this. If someone assumes by one word you mean another word, and by using the other word, you're wrong, well, I think their logic is flawed.
I feel like your post is a is a rhetorical bait-and-switch: Only the first two points seem to be related to the article, the rest are from elsewhere and chosen ahead of time to guide the user towards a particular conclusion.
I think it's up to the reader to draw which ever conclusions they wish. I don't think this person is writing with any other purpose other than to share an opinion.
But... If you have points to the contrary of what the person has said, please raise them instead of guessing at their motive.
Sounds like a study should be done on the diets of those with Parkinson's compared to the "average" diet. There's a chance for too much or too little of something that could make a difference.
I would also like to see a comprehensive study of the immune systems of those with and without, perhaps these people have little protection against these gut bacteria.
The most interesting cases would be those with the right conditions for Parkinson's yet do not have it. I think those cases would be very revealing.
It's also interesting that these bacteria are transferable across species. What if these bacteria are found in common meats from aanimal? When preparing an animal to remove it's meat, I imagine there's an off chance the gut is split in removal - which they probably just hose down the animal as not to waste the meat. Or perhaps the bacteria has the ability to spread in the host?
This research has definitely opened up new avenues to look for root cause and possible prevention.
Perhaps they have, but this new research may give more incentive to look much harder. If there is a link, I would imagine that it would not be trivial - otherwise as you say it would probably have been found.
I never know what people mean by "carbs". Are they typically referring to refined foods like white bread, white rice, etc? Or are they actually talking about the macronutrient?
When it comes to the macronutrient, high-carb populations eating whole foods are among the healthiests in the world (look at the blue zones, adventists studies, okinawans, etc).
Sorry that we got sidelined with carbs and diabetes on this, it's pretty off topic. My fault for being inaccurate probably. Please watch this, especially if you have been downvoting me:
> Diabetics generally have lost the ability to process carbs (usually by eating too many);
This is very wrong, but the stuff in the parenthesis is even more so.
Please do not mix type 1 and type 2 diabetes. While it could be argued that type 2 is improved by diet, the amount of carbs eaten by type 1 diabetics is completely and utterly irrelevant, there's no correlation between that and them developing the disease.
Source: diabetic brother from an early age.
> could Parkinsons be caused by people being very dopamine focused and wearing their brains out?
Unlikely. I have not seen any indications that dopamine is involved in any Parkinson mechanism at all.
look at CYP2D6 gene polymorphism and it's effect on enzymes and it's existence in many more parts of the body than at first expected, (brain, etc), here's someone smarter than me replying to my stabs in the dark on reddit;
"Enzymes are proteins that catalyze (speed up) reactions and consequently are involved in nearly every physiological process. You make a great point with the microbiota-brain interaction (also known as the gut-brain axis). We're starting to look at things like depression as a function of the gut-brain axis and consequently need to start looking to diet and antibiotics as a function of depression. "
Tldr: they showed certain gut bacteria are necessary for Parkinson's to progress (but not the sole cause) using an experiment with genetically identical mice.
More importantly, our understanding of parkinson's wasn't "Transformed", so much as, somebody ran a highly specific experiment on a substrain of mice that is not representative of humans, and tried to generalize their results.
My friend is a good Ayurvedic doctor. As per Ayurvedic diagnosis and treatment - root cause of most disorders point to improper digestion and accumulation of 'ama' (no English translation although some people say toxins for lack of better word). Practically all Ayurvedic treatments have diet guidelines to be followed with treatment.
I've seen some remarkable healing and recovery in people. But diagnosis and treatment is a specialized skill. Many modern Ayurvedic doctors also use allopathic diagnosis and reports in conjunction with pulse and other Ayurvedic diagnosis.
Has anyone noticed how quickly a new research direction gets connected to all the big diseases? It has only been a few years since microbiome research really became a thing. It is disconcertingly fad-like. From pubmed:
I know nothing about microbiome research. However, I don't think "fad-like" is a logical conclusion just because the amount of research is continuing to increase. This just seems more like typical human advancement and dissemination of knowledge.
For instance, I'm sure you'd find a similar trend with "computer", "solar energy" and "global warming". Someone discovers something and it takes a while for everyone to catch on. However, if the concept has legs, more and more research will take place until we understand the concept enough for it to become a part of every day life.
>"I don't think "fad-like" is a logical conclusion just because the amount of research is continuing to increase. This just seems more like typical human advancement and dissemination of knowledge."
I mean that the direction things are going it will eventually be discovered that "everything is correlated with everything else"... in hundreds of years. Why not just assume that to begin with? Take it as a first principle. Instead what we care about is measuring the quantitative relationships (what functional form, etc) between various factors.
Also, I just now looked at the paper. I cannot believe neuroscientists are still getting away with this. There is not a single scatter plot. Let's look at the highlights:
- Gut microbes promote a-synuclein-mediated motor deficits and brain pathology
- Depletion of gut bacteria reduces microglia activation
- SCFAs modulate microglia and enhance PD pathophysiology
- Human gut microbiota from PD patients induce enhanced motor dysfunction in mice
So I expect to see scatter plots of:
"# of gut microbes" (or "% pathogenic microbes") vs "motor deficits"
"a-synuclein levels" vs "motor deficits"
"# of Gut microbes" (or "% pathogenic microbes") vs "brain pathology"
"a-synuclein levels" vs "brain pathology"
"Gut bacteria levels" vs "microglia activation"
"SCFA levels" vs "microglia activity"
"SCFA levels" vs "PD pathophysiology"
"# of human PD microbes" (or "% human PD microbes") vs "motor dysfunction"
You can see the entire project was designed around seeing if there is a correlation, which we should already assume is true. Instead we should be looking at those scatter plots, so we can achieve the useful goal of discerning the relationship between various biological phenomena.
I don't think it's a fad, but a new causal link that's helping us understand the root cause of various ailments better.
We've found a new root cause and that's very important. What you're saying is akin to someone in the 19th century saying that the new germ theory "fad" is being applied as the root cause to various diseases/deaths.
>"We've found a new root cause and that's very important."
The problem is the next big thing to get a bunch of funding will also be a "root cause", and the next, and the next... Also, they will all be 100% correct in saying this medley of factors is related to parkinsons/cancer/etc. The trouble is, identifying "root causes" isn't what this research should be focused on. I explained more in my later post in this thread.
My take is that Parkinson's is a little like cancer in that it likely has multiple root causes that can injure the same part of the brain (substantia niagra) and cause the disease.
My research for his case led me to vitamin k2 deficiency as a possible cause / complicating factor. There are some genetic models and mouse trials that show k2 as a modality. He had his gallbladder removed about a year before symptoms started. He also has kidney stones. K2 is fat soluble, only acquired through diet, and affects calcium regulation. Oddly connected to his history/symptoms. So hard to help debug stuff like this.
He's on a supplement now. We don't have a great way to measure if it's working. The symptoms have such natural variance day to day.