[HN Gopher] Nanoparticle-remodeled gut microbiota slows neurodeg...
___________________________________________________________________
Nanoparticle-remodeled gut microbiota slows neurodegeneration via
gut-brain axis
Author : bookofjoe
Score : 102 points
Date : 2023-11-10 20:29 UTC (1 days ago)
(HTM) web link (www.nature.com)
(TXT) w3m dump (www.nature.com)
| pfd1986 wrote:
| In mice.
| scns wrote:
| Yes but we have to start somewhere.
| stavros wrote:
| Which is stronger evidence for humans than "in nowhere".
| flappyeagle wrote:
| This is the stupidest glib reply format on par with "citation
| needed" and "tell me you're [thing] without telling me you're
| [thing]"
|
| Animal models are used in research. Is this news to you? Do you
| think people don't know that?
| calf wrote:
| "In mice" is one of those shorthand sayings that
| scientists/professors themselves coined, it's not as
| dismissive as you're making it out.
|
| In this context of social media it's very useful as a
| reminder.
| l8_to_catch_up wrote:
| And not just any mice; specially bred mice.
|
| So it's not even generalizable to all mice, much less humans.
|
| More studies are needed.
| andriesm wrote:
| Ib my younger days I used to get all excitef about new
| scientific breakthroughs. After decades I know better and apply
| the heuristic of disregard whenever I come across the hidden
| punch-line "In mice".
|
| It really is a very good metric for preventing you to get
| sucked into hype that will 99.99 percent of the time result in
| exactly zero real world impact 10 years later.
| pella wrote:
| Another option for people is to have a fecal microbiota
| transplant.
|
| https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10019775/ Fecal
| microbiota transplantation in Parkinson's disease--A randomized
| repeat-dose, placebo-controlled clinical pilot study
|
| _" Conclusions: Subjects with Parkinson's disease tolerated
| multi-dose-FMT, and experienced increased diversity of the
| intestinal microbiome that was associated with reduction in
| constipation and improved gut transit and intestinal motility.
| Fecal microbiota transplantation administration improved
| subjective motor and non-motor symptoms."_
| bboygravity wrote:
| The good ol shitswap.
| account-5 wrote:
| A good ol' turdtrade.
| Etheryte wrote:
| A poop-loop, if you will.
| OscarTheGrinch wrote:
| ))><((
| falcor84 wrote:
| Wait, what? As far as I understand, there's a donor and a
| receiver - I don't see any reason for this to loop back.
| dartos wrote:
| Yet
| LinuxBender wrote:
| Maybe I'm too chicken to receive someone elses poo but I took
| what I consider to be the more scientifically controlled middle
| ground, mixing large amounts of probiotics with MCT oil and
| using it rectally. 36 strains, about 2 trillion CFU. To my
| surprise I have found several doctors that love this idea and
| one that also does it. It's not as diverse and that is exactly
| why I do it. I know what cultures I am getting and what
| benefits each one has.
|
| Or maybe I have discovered a fetish.
| andai wrote:
| Fascinating, hadn't heard of MCT nor rectal administration of
| probiotics (save for FMT).
|
| Do you get them in pills and then mix it with coconut oil or
| what? (Or does it need to be pure MCT)
| LinuxBender wrote:
| I open the capsules and mix them. I've tried to get the
| company to sell me a bag or can of the probiotics but they
| won't do it. Not a big deal though, it doesn't take long to
| open them. I just use the large containers of coconut MCT
| oil. If there is something that would be better for the
| bacteria and for the large intestine cells I would love to
| know.
| andai wrote:
| Heh they're probably scared you'll start selling the ass
| formula!
| LinuxBender wrote:
| Hurry up and trademark that.
| yellow_lead wrote:
| Whats your benefit from this? Do you credit it with any GI
| improvements?
| LinuxBender wrote:
| Benefits:
|
| - Bypass the stomach acid, preserving more bacteria
|
| - Keep the bacteria out of the small intestine _mostly_ to
| avoid SIBO and avoid having to chase the probiotics with
| Betaine hcl, Ginger root, digestive enzymes, etc... to keep
| the small intestine clear which can trigger inflammation.
| Also not having to pre-coat the small intestine with
| cranberry molecules to cover any section that is missing
| the mucous layer.
|
| - Feed the colon and large intestine cells MCT oil without
| having to consume it.
|
| - Anecdotally I feed better for several days after doing
| this. I can do faster power-walks for longer. _I do not run
| to protect my cartilage._
|
| - The only GI improvement that I can _feel_ is the lack of
| discomfort from taking large amounts of probiotics orally.
|
| - Very large amounts taken orally can result in small
| amounts making it past the intestine cell junctions and
| triggering a small immune response which may have both
| positive and negative ramifications but that's a much
| bigger topic.
|
| - Less likely to disturb the mucous layer.
|
| Drawbacks:
|
| - To be useful requires a large amount of bacteria and that
| requires a large amount of MCT oil and getting into
| positions to get it up into the large intestine. Well ...
| it has to come out some time and being liquid one must stay
| near the restroom. _There 's no holding it in._ Some kind
| of paste injector tube would be better, probably something
| similar in form factor and design as the vaginal yeast
| infection treatments perhaps. If this were a product I
| would buy it even though it would be harder to get it into
| the large intestine.
|
| - The first few hours after can feel _weird_ as the body
| has to adjust.
| rokkitmensch wrote:
| Have you attempted to mechanically stopper yourself
| during this process to increase the treatment duration?
| LinuxBender wrote:
| I have not. Just guessing but I think it might have to be
| custom made or uncomfortably tight. Maybe others have
| done this. The doctor I know that does this makes these
| little frozen things in a custom freezer tray meant for
| enemas.
| rokkitmensch wrote:
| Check Amazon, there are a zillion shapes and materials to
| explore.
| shepardrtc wrote:
| Wouldn't the oil just lube it up so it would eventually
| get shot out like a bottle rocket?
| LinuxBender wrote:
| Another challenge with this is that the formula I use has
| prebiotics so it's just a matter of time before gas
| builds up and things could get painful. I will likely
| just stick with my method of staying near the restroom.
| InSteady wrote:
| Do you mind sharing how you decided which 36 strains to
| include and what they are? Bonus points for links to studies
| (or articles with good references).
|
| :)
| LinuxBender wrote:
| I plan to add a health section to my awful blog. That is
| where I would be linking to the list of cultures and links
| to the benefits and risks for each one. If you want to read
| up on which formula I am currently using ahead of time it
| is here [1] and if you mouse over the images one of them
| lists which strains they use. I alternate between them and
| a couple of other blends. Most of the strains have some
| studies on nih.gov which is best searched using google with
| "site:nih.gov probiotic culture_name benefits"
|
| [1] - https://www.amazon.com/NewRhythm-Probiotics-
| Digestive-Prebio...
| thenerdhead wrote:
| Have you done actual GI / microbiome tests before and after
| to see any cause/effect? Sounds a bit extreme when you could
| just follow the 4 K's of Kefir, Kombucha, Kimchi, and Kraut
| over a long period of time.
| LinuxBender wrote:
| _Have you done actual GI / microbiome tests_
|
| I have not. I can not find any labs that I can trust and
| that have not been hacked on a regular basis.
|
| _Sounds a bit extreme_
|
| It may be. I reset my gut bacteria some years ago and use
| this to improve the overall gut-scape. The 4 K's are great
| but my personal preference is to use this method that if
| for no other reason it is banned by WADA. If they consider
| it cheating then I like it that much more.
| thenerdhead wrote:
| https://humanmicrobiome.info/testing/
| Aurornis wrote:
| There are online communities of people attempting FMT on
| themselves. I remember seeing them even cite an online source
| of FMT supplies from some sketchy company operating
| internationally to avoid regulations. Others used very
| understanding family members or friends as sources.
|
| I haven't followed the topic for a long time, but I distinctly
| remember how many people were disappointed with the results of
| their self administered FMT. This is probably because they had
| unreasonable expectations about their health conditions being
| caused by the microbiome. The only real success stories were
| from people who had C. Diff and treated it with a combination
| of antibiotics and FMT.
|
| However, there were a lot of negative stories. Some people had
| major bowel problems for a while. One person even died, though
| it was speculated that it was due to some of the microbiome
| altering antibiotics he was experimenting with.
|
| Interesting research topic, but please don't DIY it.
| andai wrote:
| The guy who died wasn't DIYing it.
|
| > The first person known to die as a result of a fecal
| transplant is a 73-year-old man who developed a fatal
| infection with antibiotic-resistant bacteria that were in the
| donor's stool sample.
|
| > News of the man's death surfaced in June; he was one of two
| patients in separate clinical trials who became ill after
| receiving fecal transplants from the same donor
|
| https://www.livescience.com/fecal-transplant-death.html
| lambdaba wrote:
| Using gold nanoparticles.
| polskibus wrote:
| What's chiral Au? Can we get it OTC?
| gilleain wrote:
| Interesting. So 'chiral' is another word for 'handedness' -
| your hands are chiral, in that you can't rotate your left hand
| in such a way that it looks like your right hand (yes I know
| what the Greek word for 'hand' is).
|
| So I assumed that these would be gold atoms with a chiral
| molecule around them - the ligand, that is. However, from a
| quick search it appears that there are these gold nanoparticles
| that are chiral shapes. In other words, the structure of the
| particle is chiral, not the molecule itself.
|
| In any case, I doubt you can get them over the counter any time
| soon, but who knows.
|
| edit: Here is a nice looking review that is free to read :
| https://www.nature.com/articles/s44222-022-00014-4
|
| Seems like there are a variety of different techniques but
| Figure 2d in that review shows an image referencing - 'Lee,
| H.-E. et al. Amino-acid- and peptide-directed synthesis of
| chiral plasmonic gold nanoparticles. Nature 556, 360-365
| (2018)'
| xchip wrote:
| 'slows' is click-baity, we should mention the two numbers
| (average and std)
| xitrium wrote:
| The last thing I read about the link between amyloid-b
| accumulation and Alzheimer's was that the entire field was full
| of fake data ( https://www.science.org/content/blog-post/faked-
| beta-amyloid... ). In particular, even treatments that directly
| reduce amyloid-b in the brain did not restore cognitive
| abilities.
|
| At least this paper tests both cognitive abilities as well as
| "amyloid-b pathologies." I'm not at all an expert in this field
| but gold nanoparticles sounds like something you'd see on a late
| night infomercial, lol.
| Etheryte wrote:
| Don't worry, it's not just this field, roughly 70% of medical
| studies are fake or severely flawed [0].
|
| [0] https://news.ycombinator.com/item?id=37572394
| mft_ wrote:
| That may or may not be the case, but you're rather detracting
| from the original comment, either deliberately or not.
|
| The issue in the Alzheimer's world is the possibility that
| _the very disease mechanism concept underlying the vast
| majority of research and interventional trials into which
| countless multiple billions have been poured, is incorrect_.
|
| Within that space, this is orders of magnitude more
| fundamental and serious than a flip aside that lots of trials
| have problems, so who cares about another?
| epistasis wrote:
| > the very disease mechanism concept underlying the vast
| majority of research and interventional trials into which
| countless multiple billions have been poured, is incorrect.
|
| Not "is incorrect," but _might be_ incorrect. And we almost
| certainly won 't know it is correct until we actually have
| a therapy.
|
| Those pursuing cures could have waited until there was more
| solid science, but they and their funders took on the risk,
| knowing full well that the amyloid hypothesis is not
| proven.
|
| This is not some indictment of science, this is normal risk
| taking for a problem that hugely affects society.
| smolder wrote:
| > Not "is incorrect," but might be incorrect.
|
| That's why the part you quoted is preceded by "the
| possibility that".
| epistasis wrote:
| But the entire framing of the comment is that the amyloid
| hypothesis is taken as fact and not possibility, when in
| fact _the core research question_ is whether it is true
| or not.
|
| It is the best possible explanation so far, but four
| decades of research have not reached a definitive
| conclusion.
|
| An open problem is not a problem for science, that's the
| fundamental focus of science. The problem is people
| misrepresenting what science is and what it aims to do.
| InSteady wrote:
| Ah, the game of telephone.
|
| >For more than 150 trials, Carlisle got access to anonymized
| individual participant data (IPD). By studying the IPD
| spreadsheets, he judged that 44% of these trials contained
| _at least_ some flawed data: impossible statistics, incorrect
| calculations or duplicated numbers or figures, for instance.
| And in 26% of the papers had problems that were so widespread
| that the trial was impossible to trust, he judged -- either
| because the authors were incompetent, or because they had
| faked the data.
|
| Firstly, this is only from one journal, _Anesthesiology._
| Second, the phrase "at least" indicates that while 44% had
| some amount of (presumably) flawed data, only 26% of the
| studies were bad enough to be judged fake or severely flawed
| by this one (admittedly esteemed) researcher in the field of
| anesthesiology. It's important to be skeptical and do your
| homework when you hear sweeping and/or shocking results. It's
| also important to read carefully, especially with science
| journalism because it is written for clicks and broad
| audiences, not to reduce ambiguity and adhere to strict
| standards of accuracy.
| svnt wrote:
| I didn't go look up the quote but based on your version
| here it sounds like roughly half (44%) had some kind of
| suboptimality, and of those roughly a quarter (26%) had
| serious problems preventing them from being relied on.
|
| That means 11% of the total papers should be discarded,
| which means 89% of the papers can be used.
| InSteady wrote:
| As per usual, science reporting fails to use precise
| language. It can be interpreted either way, although I
| think your interpretation is the slightly larger leap
| based on phrasing. In any case, it is far below the 70%
| (and not directed broadly at all scientific research)
| that GP states.
| instagraham wrote:
| It's hard to discern discourse in a field one is unfamiliar in,
| I'd tried with the Alzheimer's fiasco. Here's my tuppence:
|
| The plaques are known to be linked to Alzheimer's, the
| debunking of one paper that messed with its figures does not
| detract from the whole body of research. The inefficacy of
| plaque-targeting treatments may not be proof that the plaques
| are not causal in nature, only that their damage is not
| reversible/fully understood.
| epistasis wrote:
| In a massive field, one researcher does not constitute "full of
| faked data," despite how concerning it is.
|
| The problem is viewing individual papers as the unit of truth
| in science. The "self-correcting" nature of science will
| actually reject entire papers, and entire directions of
| inquiry. Including, maybe, a casual relationship between beta
| amyloid and AD, but maybe not.
|
| The other key part of science is holding everything in a state
| of uncertainty. There's some "facts" but mostly just hints and
| clues. And with Alzheimer's disease in particular we are trying
| to make progress with completely inadequate vision; we really
| can't even measure so much of what we want to measure. Feynman
| said it back in the 1960s, too, physicists have failed to
| deliver the tools to biologists to really measure what needs to
| be measured. There have been advancements, and DNA sequencing
| technology in the past decade has been turned into the most
| clever sorts of information theoretic microscopy by combining
| DNA sequences with many other biochemical processes. But we as
| a species still can not measure a lot of the things we'd like
| to measure.
| SubiculumCode wrote:
| A most eloquent response that needed to be said.
| brnaftr361 wrote:
| But he's correct, amyloid plaque theory was founded on bad
| data. Amyloid plaques as causal agents is unclear, but it was
| made to appear clear by poisoned data, and many studies
| conducted afterwards, in good faith, assumed that the
| information and conclusions were sound. However it doesn't
| appear to be the case, and instead something along the
| amyloid beta pathway is more likely to be the true causal
| factor, and plaques an association. It has spawned something
| of a wild goose chase in Alzheimer's research and treatment.
| epistasis wrote:
| The faked data is not foundational to the field, if we are
| to believe the article linked from that comment.
|
| > But my impression is that a lot of labs that were
| interested in the general idea of beta-amyloid oligomers
| just took the earlier papers as validation for that
| interest, and kept on doing their own research into the
| area without really jumping directly onto the _56 story
| itself. The bewildering nature of the amyloid-oligomer
| situation in live cells has given everyone plenty of
| opportunities for that! The expressions in the literature
| about the failure to find_ 56 (as in the Selkoe lab's
| papers) did not de-validate the general idea for anyone -
| indeed, Selkoe's lab has been working on amyloid oligomers
| the whole time and continues to do so. Just not Lesne's
| oligomer.
|
| And
|
| > Did the _56 Work Lead to Clinical Trials? That's a
| question that many have been asking since this scandal
| broke a few days ago. And the answer is that no, I have
| been unable to find a clinical trial that specifically
| targeted the AB_ 56 oligomer itself (I'll be glad to be
| corrected on this point, though).
| xitrium wrote:
| I appreciate your commitment to modernist capital-S Science
| here :) I'm familiar with how the field ought to work but
| after working in Andrew Gelman's lab for some years, also
| with how it can fail us. Here I think the researcher in
| question has had a much larger impact than you are allowing
| for. Here's a choice quote:
|
| > Every single disease-modifying trial of Alzheimer's has
| failed.
|
| > The huge majority of those have addressed the amyloid
| hypothesis, of course, from all sorts of angles. Even the
| truest believers are starting to wonder. Dennis Selkoe's
| entire career has been devoted to the subject, and he's
| quoted in the Science article as saying that if the trials
| that are already in progress also fail, then "the A-beta
| hypothesis is very much under duress". Yep.
|
| And the original expose is quite interesting if you haven't
| read it yet
| https://www.science.org/content/article/potential-
| fabricatio...
| epistasis wrote:
| The hypothesis was under great duress even in 2004, when I
| took a protein structure course that spent a lot of time on
| prions and the beta amyloid. Many people have devoted their
| careers to chasing this down, only one as far as we know
| published impactful fake data.
|
| However, the particular faked data, despite lots of
| citations, has apparently not lead to any clinical trials:
|
| > Did the AB*56 Work Lead to Clinical Trials? That's a
| question that many have been asking since this scandal
| broke a few days ago. And the answer is that no, I have
| been unable to find a clinical trial that specifically
| targeted the AB*56 oligomer itself (I'll be glad to be
| corrected on this point, though).
| Aurornis wrote:
| > In particular, even treatments that directly reduce amyloid-b
| in the brain did not restore cognitive abilities.
|
| Correct, but this doesn't constitute "fake data". It could be
| that amyloid-b is a marker rather than a causative factor. Or
| it could be that amyloid-b related damage is downstream, and
| remove amyloid-b after the damage has been done won't remove
| the other damage.
|
| It's too quick to wave away an entire field because a single
| theory didn't pan out. Most medical research proceeds with a
| lot of dead ends before it is figured out.
| xitrium wrote:
| Very true, but it seems like you may not have seen the expose
| on this field in Science
| https://www.science.org/content/article/potential-
| fabricatio...
| fer wrote:
| Medicine isn't my field, but I wonder why the chirality, why
| gold, why microbiota as target, why those particular diseases?
|
| As in, I might be searching wrong, but I can't find previous
| research that would hint in this particular direction, and I
| think it's reasonable to be skeptical about any "random button
| pushing"-looking research showing positive results.
| epistasis wrote:
| Sometimes the only difference between random button pushing and
| science is if you write it down.
|
| Faff around and find out is the essence of the scientific
| method.
|
| That said, I never trust a paper that gets posted directly to
| HN much. But then, single papers are never to be trusted!
| InSteady wrote:
| I can't speak to chiral gold, but as for exploring the
| connection between microbiota and neurodegenerative diseases,
| this is a hot area of study. Take a sentence from the abstract:
|
| >The gut-brain axis has emerged as a therapeutic target in
| neurodegenerative diseases by modulating metabolic activity,
| neuroimmune functions and sensory neuronal signaling.
|
| You can pretty much formulate a few dozen google searches from
| various keywords in that sentence + "microbiome," "microbiota,"
| and/or "GI immune signaling," etc and come up with hundreds of
| papers. The GI tract is host to the majority of our immune
| system. Many of the molecules used for signaling (and all kinds
| of other tasks) come directly from the bacteria there, or else
| are dependent on bacterial metabolites as inputs.
|
| On a related note, I expect we will hear more about the
| metabolome in health and medicine research. As microbiome is
| the set of all microbes in the body, metabolome is the set of
| all metabolites (bacterial and endogenous) in the body. In this
| study, serum levels of an indole were found to be altered in
| Alzheimer's patients:
|
| >indole-3-acetic acid, which was lower in serum and
| cerebrospinal fluid of patients with AD compared with age-
| matched controls.
|
| In another study of MS patients, two other indoles, as well as
| butyrate, were found to be lower in serum concentration
| compared to healthy controls [1]:
|
| >Highlights - Gut microbiota and metabolites profiles of
| individuals with MS differ from healthy controls. Individuals
| with MS have reduced serum levels of indolepropionate.
| Individuals with MS have reduced serum levels of indolelactate
| and its producing bacteria. Individuals with MS have lower
| levels of species and genes involved in butyrate production.
|
| Indoles in particular may be an interesting avenue of research
| [2]:
|
| >What is the function of the indole in bacteria? Indole has
| recently been implicated as an important small molecule signal
| utilized by many bacteria to coordinate various forms of
| behavior. Indole plays a role in numerous bacterial processes,
| including: biofilm formation and maintenance, virulence factor
| production, antibiotic resistance and persister cell formation.
|
| [1] - https://www.cell.com/cell-reports-
| medicine/pdf/S2666-3791(21...
|
| [2] - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4175420/
| arrosenberg wrote:
| Something of an educated guess, but microbiota because there
| are current hypotheses that rely on the gut-brain interaction,
| gold probably because its inert, and chirality is most likely
| because their target requires specific kinetics.
| crdrost wrote:
| Alzheimer's is the most common form of dementia, affecting tens
| of millions of mostly elderly people, characterized by the
| brain getting "gummed up" by various mechanisms like reduced
| interconnectivity of your neurons, the formation of these
| plaques of a protein called amyloid beta on the brain tissue,
| tangles of a different protein called tau, and little "pearls"
| of a sort called vacuoles wrapping not sand grains but little
| lumps of hardened proteins. So there's a theme of proteins
| being where they're not supposed to be and misfolding and so
| on.
|
| There are several partial causes of these protein problems,
| including genetic factors, chronic high blood pressure, smoking
| history, depression history. One can alternatively characterize
| this as a sort of inflammatory response, which puts it in a
| bucket with Parkinson's and ALS and other things tied to
| oxidative stresses and long-term inflammation.
|
| I am not a physician but was trained as a physicist, part of
| where I know about this stuff comes from trying to research a
| speculative YouTube video that I never got around to making
| called "the biophysics of weight loss" where I would tell
| people that from a physics perspective, the scale in your
| bathroom lies, calories are necessary but not sufficient to
| understand the problem, feedback networks are complicated, and
| just in general tried to educate the public about basic physics
| from a direction that is not Newtonian mechanics. (So if you
| want to start with energy, what is the most frequent
| interaction with measured amounts of energy everyone has? It's
| either diet or the wattage ratings on electric bulbs, diet
| seemed more fun.)
|
| So where this gets interesting for me is, in trying to talk
| about the complex feedback loops and signaling and satiety
| around diet, diet and lifestyle factors do seem to affect these
| chronic levels of inflammation. Just a simple example, your
| blood has to maintain a strong homeostasis with respect to how
| much sugar is in there, too little and your cells don't have
| what they need, too much and bacteria could thrive inside of
| you. One mechanism the body uses is, if we detected the blood
| as too sugary, we dump this signaling molecule called insulin
| in there too. Muscle tissue will take up blood sugar without
| insulin, but fat cells need the insulin as a "key" to open a
| lock that lets sugar in for long-term storage as fat. But the
| fat cells have what we in computing would call backpressure--
| they don't just respond directly to insulin, they calibrate
| their response to what they can handle. If too much sugar is
| coming in and I can't store it, I reduce my sensitivity to the
| insulin, so that I take in less sugar for a given amount. If
| this happens chronically enough, you get a general insulin
| resistance, and that leads to high blood sugar, type-2
| diabetes.
|
| Well, elevated blood sugar does something else that is linked
| to Alzheimer's: the Maillard reaction. This is the crusty
| delicious browning that happens when we sear a steak, or bake
| bread. The natural sugars in the muscle and natural proteins in
| the flour are enough in either case, the formula is sugar plus
| protein plus heat equals denatured brown crusty proteins. You
| are warm enough on the inside that this does "sous vide" your
| proteins very slowly, it is part of aging. So if your blood
| sugar is high, you age faster. The term in the literature is
| "advanced glycation" if you want to read more about this.
|
| I don't have diet recommendations, I am just interested because
| I can ask prospective students "if we turned you into a hot
| dog, how far would it stretch" and other silly things like
| that. I will say, keto was originally invented to help with
| epileptics, and it does that by moving the brain off of sugars
| and to a fuel that the brain "prefers" (in the sense of having
| fewer barriers to letting it in) called ketone bodies.
| Intermittent fasting also does this on shorter timescales.
|
| Anyway, the story about the gut microbiome maybe playing into
| this is even more complicated, some people talk about "leaky
| gut," others say that that is crackpot, but the basic gist is
| that there is a theory that if you do not eat enough soluble
| and insoluble fiber, your gut microbiome (which needs to eat
| both to survive) essentially maybe eats you a little bit
| instead as it starves. And this causes you to be at war with
| your gut microbiome, and it means that the good bacteria that
| are not eating you are less able to crowd out the bad ones that
| want to eat you... And the claim is that this creates a
| constant chronic low-level inflammation, so there's that
| oxidative stress and early aging problem again, and so forth. I
| don't know that I believe this? But it does have me staying
| away from fruit juices, which are like fruit but you removed
| both the soluble and insoluble fiber.
| thenerdhead wrote:
| Read Ed Yong's book "I Contain Multitudes". This area has been
| more/less blocked for many decades and with recent innovations
| and pipelines we may be able to start finding causal patterns.
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