Parkinson’s disease ‘may start in gut’ • Hacker News Board

Re: Parkinson’s disease ‘may start in gut’

#131

Post by natdempk » Sat, Dec 03, 2016, 1:57 AM UTC

tshadley wrote: post #124

natdempk wrote: post #117

Earlier quoted context omitted.

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.

A rather fascinating article on Dr. Kharrazian was saved by the internet archive here: https://web.archive.org/web/20130924001750/http://scienceque... "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 B…

Thanks, this is the type of thing I was looking for. Doesn't inspire confidence in his book about the brain.

Re: Parkinson’s disease ‘may start in gut’

#132

Post by fatdog » Sat, Dec 03, 2016, 3:22 AM UTC

spangry wrote: post #118

fatdog wrote: post #39

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 (wi…

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…

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.

Re: Parkinson’s disease ‘may start in gut’

#133

Post by spangry » Sat, Dec 03, 2016, 4:48 AM UTC

pizza wrote: post #127

spangry wrote: post #113

Earlier quoted context omitted.

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…

PDF? Do you mean PFC?

Sorry, damn phone spell check. Yeah I meant PFC.

Re: Parkinson’s disease ‘may start in gut’

#134

Post by rhinoceraptor » Sat, Dec 03, 2016, 4:07 PM UTC

pascalmemories wrote: post #83

mankyd wrote: post #54

Earlier quoted context omitted.

I am curious. Did you really find his claim "offensive"? Or was it simply incorrect and over simplified?

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 th…

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.

Re: Parkinson’s disease ‘may start in gut’

#135

Post by apinstein » Sun, Dec 04, 2016, 4:44 AM UTC

sgt101 wrote: post #46

apinstein wrote: post #33

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…

My father has Parkinson's and has severe osteoporosis, I wonder if there is a connection.

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...

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...

Re: Parkinson’s disease ‘may start in gut’

#136

Post by apinstein » Sun, Dec 04, 2016, 4:46 AM UTC

NPMaxwell wrote: post #52

apinstein wrote: post #33

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…

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.

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.

Re: Parkinson’s disease ‘may start in gut’

#137

Post by apinstein » Sun, Dec 04, 2016, 4:46 AM UTC

NPMaxwell wrote: post #52

apinstein wrote: post #33

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…

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.

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.

Re: Parkinson’s disease ‘may start in gut’

#138

Post by cdsx » Mon, Dec 05, 2016, 4:06 AM UTC

spangry wrote: post #110

trendia wrote: post #40

Earlier quoted context omitted.

If it's ketones, then it would be easy to train a dog to detect it.

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…

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.

I hope that helps.

Re: Parkinson’s disease ‘may start in gut’

#139

Post by spangry » Tue, Dec 06, 2016, 8:10 PM UTC

cdsx wrote: post #138

spangry wrote: post #110

Earlier quoted context omitted.

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…

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…

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....