Parkinson’s disease ‘may start in gut’
bbc.co.uk
bbc.co.uk
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'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.
He said it all started from this book: http://brainhealthbook.com/why-isnt-my-brain-working
"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.
Doesn't that invalidate his claim if he had retracted it?
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.
https://www.amazon.com/Still-Thyroid-Symptoms-Tests-Normal/d...
https://www.amazon.com/dp/B00D8N6HBM/ref=dp-kindle-redirect?...
Edit: Hackaday had an article about a simple EMG recently
https://hackaday.com/2016/11/20/emg-tutorial-lets-you-listen...
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
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.
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?)
(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.
This is the best link I could find right now. But there are lots of good studies on this. http://mobile.nutraingredients-usa.com/Research/Vitamin-K2-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.
wow
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.
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.
I hope that helps.
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....
When I was young this disease shaped my perception of old age.
Got my self tested (23andme) 5 years ago and luckily I don't seem to have any predispositions for it.
> but it looks like any treatment
> based on this will still be
> quite some way off
I came away with the opposite impression. Wouldn't you just need a targetted antibiotic?Problem 2- can you actually make an antibiotic specifically target one bacteria only?
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.
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.
Apparently delirium is a common side effect of whatever they do in hospitals. I came across this link last month:
"Delirium: A Surprising Side Effect of Hospital Stays -- Often misdiagnosed as dementia, it can cause hallucinations and delusions" - http://www.nextavenue.org/delirium-a-surprising-side-effect-...
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.
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.
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.
https://en.wikipedia.org/wiki/Medium-chain_triglyceride#Medi... https://en.wikipedia.org/wiki/Fatty_acid_metabolism#Fatty_ac...
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.)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.
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.
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.
https://www.broadinstitute.org/hmp/human-microbiome-project https://www.mskcc.org/research-areas/topics/microbiome-infla... http://humanfoodproject.com/americangut/
Right now, the information is very scattered and siloed, and very difficult to survey.
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.
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.
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.
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
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.
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?)...
Recovery is unlikely at this stage, but even preventing the disease from progressing further would be quite something.
> The bacteria can break down fibre into short-chain fatty acids.
This doesn't make any sence. Fibre(fiber) is composed by carbohydrates bounded in a different way of the sugar that is used to sweeten.
Perhaps bacteria can eat fibre and produce fatty acids, but fibre is not made of fatty acids.
This is probably an error in the press article. Do someone with access to the research paper to understand what this means?
> Short-chain fatty acids (SCFAs), the end products of fermentation of dietary fibers by the anaerobic intestinal microbiota ...
So yes, SCFAs are end products of the process. You are right.
Technically they are breaking down fibre into SCFAs but it didn't say they were made of them.
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 had to search for the pathway to produce butyric acid (4 carbons). The main path is apparently splitting the glucose in pyruvate and adding a carbon to it, so it's not a direct break down. But there is an additional pathway, with glutaric acid, that perhaps may qualify, but I'm not convinced. https://en.wikipedia.org/wiki/Butyric_acid http://mbio.asm.org/content/5/2/e00889-14/F1.expansion.html
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.
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)...
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.
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.
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.
Some other supporting causes may be things like overuse of antibiotics in meat production and lack of fermented food in diet.
http://www.bbc.com/future/story/20151118-can-you-be-too-clea...
Another lifestyle example could be the prevalence of C-section births in more developed countries:
- Gut Bacteria are involved
- Inflammation is involved
- The brain works on glucose
- The brain can also work on Ketones
- 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.
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.
Stop making offensive and untrue claims.
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 day has come
http://goaskalice.columbia.edu/answered-questions/it-true-ea...
"the evidence that connects artificial sweeteners to “insulin spiking” is limited"
http://www.goaskalice.columbia.edu/answered-questions/diet-s...
It's also interesting that insulin resistance is reversible by simply eating less carbs. But clearly, diabetes has nothing to do with carbs :-)
Edit: I applaud the downvoter of this comment.
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.
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.
Source: parent of type 1 diabetic
What about if I was to start injecting large amounts of insulin regularly?
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.
To be clear:
> glucose building up in the bloodstream with no real way to utilize it
===
Inability to process carbs and sugar. Maybe your description is more accurate.
Its generally assumed that processing carbs is the act of digestion. You're using the word processed in the wrong situation here.
EDIT: Also you can still process carbs, you just can't utilize glucose in the blood as a diabetic.
But... If you have points to the contrary of what the person has said, please raise them instead of guessing at their motive.
Here is a very small scale study done in regard to this...
https://www.charliefoundation.org/ketogenic-therapy/therapie...
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.
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).
http://www.ted.com/talks/peter_attia_what_if_we_re_wrong_abo...
https://www.youtube.com/watch?v=nhzV-J1h0do
Also:
http://eatingacademy.com/nutrition/the-great-medical-disconn...
Enjoy!
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.
"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. "
https://www.reddit.com/r/Nootropics/comments/4c0nuz/im_inter...
Impressively wrong
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.
pubmed - human microbiome
year count
2017 27
2016 5464
2015 5544
2014 4283
2013 2993
2012 2064
2011 1405
2010 910
2009 679
2008 520
2007 392
2006 290
2005 245
2004 160
2003 135
2002 118
2001 74
2000 78
1999 57
1998 57
1997 54
1996 35
1995 30
1994 17
1993 18
1992 23
1991 24
1990 24
1989 25
1988 27
1987 14
1986 11
1985 20
1984 10
1983 10
1982 8
1981 9
1980 10
1979 13
1978 11
1977 7
1976 10
1975 3
1974 2
1972 1
1971 3
1970 2
1969 2
1968 2
1967 2
1966 3
1965 2
1964 2
1963 3
1961 2
1958 1
1956 1For 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 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.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.
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.