I had to triple check the date because I was pretty sure that this was known before. Maybe it is simply the confirmation aspect of it?
Edit:
> Our findings reveal for the first time, that Alzheimer’s symptoms can be transferred to a healthy young organism via the gut microbiota, *confirming a causal role* of gut microbiota in Alzheimer’s disease ...
> One early event in AD is an increase in circulating glucocorticoids
You could sum up Alzheimer's as:
Diet/Lifestyle + a congenital form of Cushing's syndrome and you have increasing glucocorticoids which imply downregulation of the PVN, less progesterone and low levels of Prolactin reducing oligodendrocyte reducing myelin sheaths. Add in APOE e4 without choline in the diet and you have accumulation of lipids to round it all out.
There is a reason why Omega 3 + B+D vitamins are talked about as preventative as they all reduce inflamation.
"You could sum up Alzheimer's as: Diet/Lifestyle + a congenital form of Cushing's syndrome and you have increasing glucocorticoids which imply downregulation of the PVN, less progesterone and low levels of Prolactin reducing oligodendrocyte reducing myelin sheaths. Add in APOE e4 without choline in the diet and you have accumulation of lipids to round it all out."
Unfortunately, the parent commenter is making huge leaps of logic and exaggerating the results of various studies. The Reddit source they linked to is from a telehealth medical provider who has invented a new condition and named it after himself. Skimming his writings gives strong pseudoscience / alternative medicine vibes.
For example, Cushing's syndrome is a disorder of extreme excess cortisol. The incidence is estimated to be somewhere between 1 in 100,000 and 1 in 26,000. In other words, it's an extremely rare condition. Suggesting that a congenital form of Cushing's syndrome is behind Alzheimer's wouldn't make sense.
There's a trend in alternative medicine to take a large collection of studies, reduce them to overly simplistic this-causes-that links, then to string them all together to generate misleading conclusions.
In this case, the comment is trying to claim that lifestyle factors combined with an extremely rare 1-in-100,000 condition from birth results in a set of hormonal changes that lead to damage to the insulating layer around your nerves. It's extreme speculation, not indicative of the actual science.
In general, be wary of anyone who claims to have solved complex medical conditions like Alzheimers that are still elusive to actual researchers. I hope it goes without saying that a random Hacker News commenter hasn't figured out what countless researchers have been working on for decades.
I agree with Auromis. The reported research is interesting, and yet is not yet ready for application to human health. It's tempting to leap to conclusions. The top poster takes this too far.
I hope that NIH funds a lot more Alzheimer's research looking for microbial causes, and also, that the technology for understanding gut microbiome continues to develop.
Cushing syndrome is and overarching term that encompases Cushing disease, subclinical Cushing syndrome, paraneoplastic Cushing's disease, and other tumors. subclinical Cushing's was more what I was referring to when I wrote 'congenital form of Cushing's syndrome'. You don't honestly think I was talking about something that is a 1-in-100,000 condition when talking about Alzheimer's do you?
As you want to be pedantic 'Subclinical Hypercortisolism' would be the much more accurate terminology.
I refuse to copy/paste ChatGPT but it breaks it down well enough to help you target specific slices of the statement to google yourself and do your own analysis of the accuracy of the claims.
This shouldn’t come across as “lmgtfy” and also nothing ChatGPT says can be taken as fact, but I do think it provided some helpful restructuring of the original.
I think its probably (mildly) overly pessimistic about some less-supported claims, and it may be worth reviewing the latest work on those claims first.
I personally feel that pregnenolone supplementation had a noticeably negative affect on my mental health. High prolactin would also be somewhat miserable but it makes slightly more sense that it could be better for alzheimer incidence rate. Drugs to lower prolactin, like cabergoline, have profound effects on the brain: https://news.ycombinator.com/item?id=33186046
Wow. When someone is so well versed in a topic that everyone else has to use the world's most popular and advanced artificial intelligence to understand what they have just said. Bravo.
Haha I tossed together that sentance before running to a meeting. I simply know the topic to such detail and intimately that I didn't think to make it simpler. If I had known it was going to be tossed at ChatGPT I would have fleshed it out more. The key thing that ChatGPT missed in its summary was that the entire PVN is often downregulated in Alzheimer's. This is where you get all of the other comorbidities that don't make sense and are red herrings such as thyroid issues and leads to a direct pathway to the reduction of myelin sheaths which is a crucial requirement before dementia.
I mean, I understood most of it from just hobbyist-level interest in anabolic steroids. Many of those (testosterone, nandrolone, masteron, trenbolone, trestolone) also interact with prolactin and there’s occasional discussion about pregnenolone as well.
So I was able to validate at a surface level that ChatGPT at least didn't completely mangle the meaning, intention, and facts.
But the truth is that the GP shouldnt be viewed as being “so well versed in the topic”. Most of these hormones (even pregnenolone) havent been studied well enough to understand the full effects of manipulating them in otherwise “healthy-ish” people. We know their most powerful effects in niche, extreme situations - so if someone has a true medical issue/emergency related to them we know to raise/lower them to get certain desired effects.
But we really don’t know the vast majority of the effects that subtle changes in these hormones might have. Supplementing pregnenolone seems to cause temporary depression in many of the folks I’ve talked with in the bodybuilding community - myself included (until supplementation is ceased). For me that effect greatly outweighs its potential contribution to Alzheimer’s later in life.
For those that are curious and not well verse in research level biology, what kind of food, drink and lifestyle will help maintain a gut biome that prevent Alzheimer
Fatty fish, most nuts (that don't have high omega-6, which is inflammatory), fruits high in antioxidants like berries and dark fruit in general, colorful vegetable, cooking with olive/avocado/sunflower oil, *kefir* which is the champion of all good microbiota inducers
As for avoiding: red meat (high in omega-6), gluten (chickpea, rice, lentil pasta instead of wheat), cooking with hydrogenated oils, preservatives, processed food, refined sugar
The lists could be much longer. Look up anti-inflammatory diet aka mediterranean diet. What I will say is adhering to this diet has done as much for my inflammatory condition as all the medication. With some foods I feel their effect right away (pork, too much sugar), with some it sneaks up as I let it slip for a few days. So I stand by it.
Red meat is not necessarily high in omega 6, and on the contrary grass fed meat can be high in omega 3. Also the debate is still out on whether or not omega 6 is inflammatory or not, and even omega 6 rich nuts are probably health promoting in typical quantities. From my understanding gluten is probably fine for those that don’t have a sensitivity. I think you should caveat your claims about diet since we don’t totally know to an absolute manner yet.
Fair enough, I'll rephrase it this way: most large mammal meat causes inflammation for me and my partner, whereas chicken, turkey, fish, rabbit, etc are all fine (and I should say I used to basically eat meat with carbs). As far as omega fatty acids are concerned, I believe one shouldn't let their omega-6 and omega-9 levels be much higher than omega-3. Gluten is associated with all sorts of issues that I think we will be learning more about in the next few years. There are plenty of alternatives so that one is easy for me. I can still make pasta (chickpea, lentil, brown rice), and use tortillas (almond, chickpea, cassava).
Exactly this, I get regular blood work. On top of that, I can feel the inflammation. It is pressure, or warmth. It's a very obvious bodily reaction. Now of course for the average immune system the effects would be more subtle, but could still be noticed in energy levels, focus/attention, etc. And even if not noticeable, low-grade inflammation long term is one of the main factors of age-related decline.
Among inflammatory substances, alcohol is the elephant in the room. Cutting out alcohol is the lowest hanging fruit in this garden. Unfortunately, people convince themselves that it is perfectly healthy when consumed in small quantities every day. Anybody who monitors their health/fitness parameters with a smart watch will notice how damaging alcohol is.
I'm a fermentation freak so I have to highlight how uncooked fermented foods like sauerkraut and the aforementioned kefir play into anti-inflammation [0].
yes. I had to heal my gut and kimchi and sauerkraut plus the occasional Kefir are great. I also take from time to time zinc L-carnosine and L-glutamine, great for the gut as well.
If we're focusing on effects of diet on immune systems, especially those not functioning nominally, it is quite readily available information now. Was not so half a decade ago. The immune system is affected strongly by gut microbiota health, therefore it is a solid base to assume the same applies dietary considerations apply for Alzheimer's.
I'm going to plug a health model rapidly gaining mainstream acceptance by healthcare providers: https://en.wikipedia.org/wiki/Biopsychosocial_model?wprov=sf...
It posits that all factors of life are important for overall good health. The TL;DR is that one needs to consider diet, exercise, socialization, hobbies, etc in addition to whatever medication regimen is helping.
This is impossible to say if you do not know your genetics. For example, being a FUT2 non-secretor will change everything about what you eat. Trust me, I am a FUT2 non-secretor. So in my case I need to eat a lot of seaweed and mushrooms which are both high in fucose (not fructose!).
Generalizing but it seems that harmful microbiota prefers glucose but leaves behind bad metabolic byproducts. Whereas beneficial microbiota leaves behind lactic acid? So maybe lactofermented foods will help.
I've been on a journey of hyper-optimisation of my nutrition for various goals (sport performance, health, intellectual performance, etc). Mediterranean diet seem to be the GOAT in most cases
"... something as simple as taking fish oils had reduced dementia risk by 9%. This is equivalent to the risk reduction found from quitting smoking. However, the effect is not the same without B vitamins."
So yeah. My summary simply illuminates the pathway/reason why as well as why there are so many confusing comorbidities.
Every kind of food processing has trade offs including cooking which destroys vitamin C among other things.
White rice was historically missing thiamine (B1) found in brown/hole which was killing off a surprisingly large number of people in Asia as it became popular. Now days foods are often fortified with various things to cover the most common and severe issues, but that’s probably not enough on its own.
In terms of highly processed foods you run into various additives. There’s a long list of minimally studied additives/dyes/preservatives/etc being used only for them to later be recalled and replaced with some other poorly studied substances. Ignorance may be a legal defense for Nabisco adding X to their products, but it’s not going to protect your health.
So, the advice is basically to have the absolute minimum amount of processing steps which is a surprisingly useful heuristic alongside having a varied diet including lots of different plants.
Industrial processing. As a simple rule, the longer the list of ingredients on the food label, the more processed. The ingredients aren't something you'd normally think of as food? More processed.
Another way I've heard it stated: "single ingredient foods." And as you prepare them, try to keep them that way.
For example, adding a ton of butter to potatoes makes them 10x less healthy. More or less, calorically they become fries. Fries taste great but they should be an occasional treat, not a staple.
Keep in mind that if you buy a bunch of "let's pretend it's not processed" "healthy" foods and use them to cook a meal, you're a) creating an ultra-processed meal, and b) it now has a long list of ingredients, you're just not writing it down.
I take it you interpret "save money" to mean keep yourself barely fed, clothed and housed, and otherwise consuming the bare minimum so that you can maximize the amount you put away?
If not, you might want to loosen your interpretation of words in other domains, too.
> You could sum up Alzheimer's as: Diet/Lifestyle + a congenital form of Cushing's syndrome and you have increasing glucocorticoids which imply downregulation of the PVN,
Between weight loss, inhibiting addictive behavior, lowering the risk of major cardiovascular events such as stroke, heart attack, and potentially derisking for Alzheimer’s, we should be pumping GLP-1 agonists out like a wartime effort. Likely contributor to fixing 70+ years of socioeconomic configuration that gave us Western Disease and the trimmings that come with it.
Japan researchers have know about this for years. I don't know if Japan makes a big deal about publishing their findings but I watched a documentary several years ago which that went into very specific detail about the relationship between specific gut bacteria and Alzheimers. No disrespect to King's College - perhaps there is no overlap but this is more of an advancement than it is a breakthrough.
No way this was known before. There may be certain correlations but you have to realize this research effort is different. In controlled experiments if you as the experimenter can "cause" something to happen then you've skipped past the correlation != causation mantra that every Tom, Dick and Jane keeps chanting without fully understanding. At this point you've found causation.
Causal evidence of Alzheimer's? I don't think that's ever been known. The worst case scenario after finding this is that they find out that there's multiple causative sources of Alzheimer's.
Microbiome researcher here. As usual, when a microbiome paper reaches HN, I emerge to urge caution.
You should be extremely skeptical of the larger conclusions drawn from this paper. The biology of Alzheimer's disease (AD) is poorly understood, and the contribution of dietary and microbiome factors are extremely unclear. I think you should treat the evidence from this paper (and shared in this thread) as more like "fails to converge" than "I will use this data to update my priors".
I want to note, first, that the researchers should be commended on clearly communicating their procedures, crafting a well written paper, and doing some nice experiments (in figure 4 particularly). The main criticisms I have relate to the conclusions drawn, and then echoed in this HN thread.
1. The behavioral analysis was not conducted in a blinded way - the researchers doing the behavioral analyses knew if the rats were AD or non-AD groups. From supplement "The experimenter was
blinded to the FMT human donor but not to the rat group." The degree to which rodent behavior reflects human behavior is unclear (I would argue very little) but you should definitely be skeptical of measures with significant subjectivity done without blinding.
2. The paper has many materially important assertions not backed by the data.
> However, at phylum level, Alzheimer’s patients had a higher abundance of Bacteroidetes (Fig. 1C) reported to comprise many pro-inflammatory species
A phylum is an extremely diverse group of microbes - the phylum Bacteroidetes contains microbes that likely diverged hundreds of millions of years ago (from their LCA). Claiming that an entire phylum is "pro-inflammatory" is not even wrong. The different Bacteroidetes found in humans can be "pro-inflammatory" or "anti-inflammatory" depending on a truly staggering number of factors (diet, what other microbes are there, host immune status, host epithelial integrity). To claim that it's clear that AD patients have more of a "bad phylum" exemplifies the strong claim X weak evidence of this paper.
> ...and a lower abundance of the phyla Firmicutes and Verruocomicrobiota, reported to produce beneficial metabolites.
Ahh yes, the beneficial metabolites of my favorite Firmicutes - Clostridium botulinum (most toxic metabolite known to man), Clostridium difficile (kills >20,000/year in the US), etc... Again, you can't paint with this broad a brush and have the conclusion mean anything.
> Importantly, a positive correlation was observed between the abundance of the health-associated SCFA producer Coprococcus and the MMSE score, and inverse correlations were detected between the abundance of the disease-associated pathobionts Desulfovibrio, Dialister and the MMSE score, supporting a microbiome signature for cognitive performance in Alzheimer’s disease.
Desulfovirbio has evidence of potential linkage to AD (a quick google found correlational, but no causal evidence). On the other hand, a quick google showed that other groups disagree about Dialister - Vogt et al 2017 (PMID: 29051531) find that Dialister is reduced in AD patients and the less Dialister you have, the worse your symptoms! Again, claims stronger (and in this willfully ignoring) than evidence.
3. The main data from this paper is generated in a standard fecal transplant experiment. In short, feces from AD patients is given to some rats, and feces from healthy donors (HD) is given to other rats. Figure 2-4 rely on this setup. These are not independent verifications or tests of the hypothesis "Do AD bacteria --> AD?". Any systematic difference between the feces with the AD label and the HD label could be causal for the results the authors see. This is a major confounder in all microbiome work. Behavioral changes associated with AD are going to change food intake and bowel habit, which in turn will substantially change microbial characteristics of the gut. Other than the microbes, there are a huge number of human derived proteins, metabolites, signaling molecules, viruses, etc in the stool. The researchers don't eliminate these, and their data would be consistent with this as an explanation just as much as the microbes. Even the best studies cannot create a design that blocks every confounder, but FMT paradigm suffers from a really large number of them and the authors don't address this. There are some experiments you can do - for example, you could culture the individual microbes you believe to be responsible for the AD pathology, introduce them into rats, and show the _microbe alone_ is enough to cause the disease (this resolves the last confounder cited). The authors don't do this. There are many other considerations in designing FMT experiments that I could quibble with (like why not germ-free animals - that is the standard rather than the microbiota depletion they do), but the main point is: any systematic difference in AD vs HD feces could cause the differences in rat physiology they observe.
4. Figure 2 is an excellent example of a broader phenomenon in microbiome papers: statistically significant results with extremely small effect sizes. Consider 2D-I. The authors show (for instance) that the mean water content of stool differs significantly in their AD- vs. HD-colonized rats. The effect size is maybe ~12%. Everything in 2G-I is smaller than this. Do we think that losing 12% of the water from feces is a part of the physiological cascade that leads to AD? While this could be true (or this could be evidence of some other underlying change being caused by the AD microbes) the effects are extremely small. I think it's much more likely that some other systematic difference in the feces (as outlined in 3) is causal for these small-scale changes seen.
This is similar to the data in Figure 3. Consider 3B - the AD microbiota induces a (significant) ~0.23% change in the "discrimination index". What size is that effect? It might be large, but considering there is no comparison to differences in whatever the human equivalent of this index is (if it even exists) I am going to guess it's more on the 'too small to be meaningful' side.
> These observations were further corroborated by correlating the clinical human donor profile to the Alzheimer’s behavioral readouts of the recipient rats.
They test 50 different metadata correlations, don't correct for multiple hypotheses, and find one correlation at p<0.05 and one at p<0.08. This does not match the tone of that sentence.
5. Quoting from the paper: "Rats colonized with faecal material from Alzheimer’s donors exhibited no change in locomotor parameters in the Open Field Test (Supplementary Fig. 6A), no change in anxiety-related behaviours in the Elevated Plus Maze (EPM) (Supplementary Fig. 6B), or in antidepressant-like behaviour in the Forced Swim test (FST) (Supplementary Fig. 6C), indicating no specific effects of the Alzheimer’s human gut microbiota on comorbid features of Alzheimer’s disease in rats."
So clearly whatever the effect of the microbiota is, it's not enough to trigger these measures of pathology. Does that suggest that the microbiota causes only some AD features? If you read their abstract "Our findings reveal for the first time, that Alzheimer’s symptoms can be transferred to a healthy young organism via the gut microbiota, confirming a causal role of gut microbiota in Alzheimer’s disease" they certainly don't qualify the result this way.
6. Figure 4 - there are some nice experiments here. They show differences in neuronal survival conditioned on AD or HD feces. There are microbial metabolites that affect neuronal survival that are certainly not linked to AD causally (e.g. the short chain fatty acids). Evaluate this in the context of point 3 above: the authors show differences in neuronal survival, but whether that is due to changes in AD patients microbiome that are _caused_ by the disease (e.g. they eat weird and get weird microbes that don't make short chain fatty acids) rather than _casual for_ the disease cannot be evaluated from this data.
7. Figure 5 has no evidence of microbial cause. The authors show that serum from AD patients injected into rats caused reduced neurogenesis. As outlined in point 3 above - this could be (and seems much more liekly to be) from any of the human-derived factors floating in the blood. They try to address this by saying "gut microbiota composition explains up to 58% of the variance of individual plasma metabolites" and citing a paper (PMID: 36151114) but this is a very misleading citation. First, the authors of the cited paper corrected that figure to 46%. Second, that figure is for a SINGLE metabolite, not the whole plasma metabolome. Quoting from the cited paper "We detected the largest variance explained (46%) for an uncharacterized common metabolite with the provisional identifier X-11850.". The gut microbiome makes a lot of chemicals, but your body makes many many more. The idea that gut-derived metabolites are the predominant thing in the bloodstream is...not correct. The authors similarly try to suggest with figure 6 that because the AD-transplanted rats show a different plasma metabolome, that means the serum injection experiment points to the microbes. This is not causal evidence, and it isn't a test of what they say it is.
It's a bit sad that this comment is in the lower half of the thread, while the comments in the higher half are at the same time: clearly uninformed on the topic and still making strong statements.
Hey thanks for this info, all of which I'm sure is super insightful for people who understand this level of detail.
What would you say the average person in the street should eat in terms of supplements, vitamins and food in general to maintain excellent microbiome based on your learnings?
Thanks for that great write-up. I wonder if there are microbiome studies with actually large effect sizes in diseases which we do not typically associate with infectious factors (e.g. diabetes).
Doesn't look very impressive. Lots of overlap in the scatter graphs, and no mention of whether they corrected for multiple comparisons. Overall it looks like the typical breathless press release clickbait that HN users seem to constantly post here.
They did correct for multiple testing - "P-values were multiple-test corrected
using the Benjamini-Hochberg False Discovery Rate (FDR) procedure and a cutoff of 0.1 was applied to select the differentially abundant genera". However, they used Wilcoxon test which has unacceptably high FDR [1].
I certainly hope they are going to replicate while knocking out one species of gut biota each time. Would be super helpful right?
Edit: Experiemental design
we establish indvidual colonies of each of the biota detected in our earlier work, we then recombine them in the ratios found in the original work and replicate the previous results.
We then creation combinations lacking a single organism from our mix and look for replication.
Finally we vary the percentages of the biota in our origianal mix and look to see if that affects our ability to replicate.
except our bodies already kinda do that on their own
how would killing species of gut biota would helpful? helpful for whom to accomplish what??
we're headed to a future in which you have to take special pills so that the food doesn't kill you. like the glysophate and GMOs but applied against ALL life, including humans. if this is too far fetched for you then I also hope we don't get there.
> except our bodies already kinda do that on their own
> how would killing species of gut biota would helpful? helpful for whom to accomplish what??
OP wasn't talking about practical uses, he was talking about further experimentation in which the researchers narrow down exactly which gut bacteria has the effect.
insert this.gif :-). One of the things that would be interesting would be to understand if a specific kind of bacteria in the gut was the cause or if it was a ratio of some sort. One could imagine an easy to use diagnostic test[1] that could help inform you if you needed to do something or not.
If this causality pans out (and it would if it was replicated several times) then this would go a long way to helping people figure out if they needed to do something to avoid "early onset Alzheimers" or even Alzheimers in general. An acquaintance had a fecal transplant (yeah it sounds yucky but it isn't really) which consisted of a course of broad spectrum anti-biotics followed by the introduction of a "non-Cdiff gut biome". It "cured" their issue completely and it hasn't returned.
[1] When the Microbiome project was a thing I submitted mine. The fecal test was pretty easy (if 'yucky' from a poopy sort of way).
Helpful to the host so another type can flourish. Certain classes of antibiotics will wipe out species then similar but harmful types will colonize the space and you end up with autoimmune disorders.
I wonder if simply taking antibiotics at some point, clearing everything out and repopulating the flora could help?
My guess is no - that something in the system is triggered by the fecal transplant but that gut flora isn't the main source, but it would be an interesting thing to look at. I'm not in this field and do not know how to mine this data or properly posit the question, but maybe something along the lines of: "How many people who have taken a strong antibiotic in the last 10 years get alzheimer's vs people who have not taken any antibiotics?" Seems like this data should be out there, right?
Maybe someone who works with this kind of data or research can weigh in. Can you imagine if the cure is that simple? Just take strong antibiotics at an early stage....!?!
Fecal transplants are used to repopulate the gut of someone when necessary - for example after strong antibiotics! You can use flora of someone living in your household, as you probably share a lot of flora by being in the same environement and sharing food.
Edit0: Not "you can use" as in "do this at home" but in the sense of "it's an option your healthcare provider might offer. I worded it odd.
N=1. I had various digestion problems, probably due to gut flora imbalances. After several years of trying to fix the problem with diet changes suggested by my doctor (more fiber), I traveled abroad and came home with a very nasty food borne illness.
After one Z-pack and several days of being "backed up", my gut was suddenly back to normal and has been fine since.
I wish it were that easy. I've had sibo for 3 years now, originally methane sibo, took 2 rounds of xifaxan and neomycin and 3 rounds of xifaxan alone and now still have hydrogen sibo. I've tried many other herbal treatments, done a ton of tests, tried probiotic loading to overcome it, but nothing seems to have really worked. Worst part is eating the same meal, for every meal, day in and day out because it's the only food that doesn't give me issues.
As someone who used to research neurogenesis in rats - there isn't great evidence that adult mammalian neurogenesis occurs in humans, so don't assume that this will translate to humans.
I have a cousin studying the gut microbiome's role in mood, and it seems to play a role. I wonder if there are companies that specialize in creating tailored probiotics to help individuals struggling with mental diseases.
> For the first time, researchers have found that Alzheimer’s symptoms can be transferred to a healthy young organism via the gut microbiota, confirming its role in the disease.
I just read “I Contain Multitudes” by Ed Yong where this topic was unsure as there’s only a handful confirmed links to things like depression, obesity, etc. Now it is confirmed for Alzheimer’s. This is extraordinary.
It's an interesting avenue, though a problem is that updates and interviews with Ed Yong post book appear to show they could only treat one thing - c diff effectively with fecal transplants and that is apparently temporary, with recent studies show it lasting possibly a year before another transplant is necessary, and that probiotics via food like yogurt/kefir cultures only last as long as you eat the food regularly, there is no way (yet) to permanently fix a broken (as in the same as someone who had regular, non highly processed diet for baseline versus people who had switched from their pre highly processed diet to the highly processed modern diet) microbiome. Here's his Fresh Air interview, https://www.npr.org/2016/08/18/490432969/eating-yogurt-is-no... but he's written a lot of stuff since then, too, for the Atlantic.
I know nothing about this but to me „highly processed“ seems like such a broad term that it seems unlikely that every form of processing is bad. Would be great if we could instead enumerated the handful worst offenders which would make it easier for people to see the causal relationship and adapt their behavior in a more fine-grained way
There are a lot of different studies and my comment was pretty short, but this is an explanation and evaluation of the generally used system for classifying food into ultra high processed versus not.
https://www.nature.com/articles/s41430-022-01099-1
Most studies involving human diet involve self reporting so that's why its important to understand the limitations of that classification system.
There have been lots of studies showing a connection with microbiome changes, though some countries have been later than the USA in adopting more ultra high processed foods, allowing a more timely study, here is one about Spanish citizens and tried to guide the self reporting diet a bit more specifically about where to categorize their food intake.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8398738/
> The microbiome is not a panacea for our health problems. It doesn't explain them all in their entirety. I think it just shows how important microbes are in our lives and what a strong influence they have.
I'm optimistic. With the current AI wave and being able to process datasets once impossible to do, we can at least come up with findings (that we may not understand) but may help us to understand these diseases and life conditions through the lens of trillions of microbes.
I would bet that the root of both is diet. A diet that leads to Alzheimers will result in a certain kind of gut microbiota. I would guess that sugar and carbs generally, along with fiber, are the problem.
There's a lot of athletes and sportspeople that wouldn't mind an extra test to see if the carbs works out: especially as many of them really keep the fat levels down when athleting.
It's all of those things. Infectious disease increasingly seem to be behind or involved in most neurodegenerative, neurodevelopmental, chronic fatigue, severe psychiatric disorders.
Herpesviral reactivation specifically seems to be involved in everything a little, but my hunch is that this is often secondary to other immune system burden.
This is asking the wrong question: for example, there are antibiotics you are prescribed for IBS because generally they tend to have a balancing effect on the gut microbiome. I've done a course every year or two when things get unmanageable, since it's a good reset.
In this context, a treatment which reduced risk would likely be a combination of antibiotics and probiotics to try and shift the biome to a different one.
This is antibiotic marketing bs. There are antibiotic that harm pathogenic or prone-to-overgrowth bacteria harder than others, but they ALL lead to a state of dysbiosis and susceptibility to subsequent colonization/overgrowth/dysregulation
And this is the exact reason whymost of the time, GI problems come back or are replaced with different symptoms after antibiotics, and why we need more Fecal Microbiota Transplant research.
No, it isn't. The whole point of antibiotics for IBS treatment is that you already have an overgrowth, and you want to disrupt that and level the playing field.
This is literally the reason I've been on short course antibiotics (<1 week or a single 4 tab dose) at different points, because it eliminates the constant bloating and gives probiotics a chance to work.
The exact reason why overgrowth happens is because an opportunistic strain takes advantage of a dysbiotic state - even if you suppress it with antibiotics, your gut still lacks the robustness of composition necessary to be resilient. In fact, no antibiotic is selective enough to not impoverish your microbiome.
Probiotics might help, but a few or a few dozen non-gut-sourced strains simply cannot compare to the hundreds present in healthy stool. The effects on microbiota-dependent conditions are often weak to none.
tl;dr: Long-term harm that might happen to kill off whatever's harming you in the process, but don't count on it.
Long version: It depends on specific antibiotic- generally, they wipe a portion of the strains completely, suppress most of the rest, and give anything resistant the opportunity to grow out of control, a state which persists for weeks to months during which you're extra susceptible to external pathogens, food poisoning, etc. A healthy microbiome is resilient, and sadly if you don't have one, FMT is the only way to do it.
It really depends on what you mean by that. In terms of this article, the gut biome would have to be changed by that. There are definitely different things people do in preparation for anal sex that could change that environment but I'm not sure how much anal sex itself actually changes that. This doesn't account for STDs that have been known to involve the nervous system for a long time already.
Extremely unlikely and you'd have to be doing a threesome+. Gut bacteria are present throughout the entire digestive tract, and you can't really reach very far into the anus no matter what you've got.
If you look at the scatter graphs, it's not terribly impressive. Lots of overlap, and most of the results show no difference. The one that does show a large difference still has a lot of overlap in the scatter graph, and it seems to be some outliers that bring down the mean value.
It's kind of an extraordinary claim, which requires extraordinary evidence. This isn't that.
What interests me more is why HN users keep posting this study, and voting it to the top of the home page.
almost everyone on HN is interested in biology and especially biohacking but does not actually realise they have none of the necessary expertise to judge claims coming from that field; the level of discourse on these topics is sometimes worse than what I spot on reddit
Pish Posh! My understanding of C pointers makes me one of the smartest people in the world! Why else would I have cleared the hurdle at $COMPANY during a tremendous bull market!
Clearly I can learn any discipline by mucking about for a few afternoons. What is a billion years of natural selection to my towering intellect?
To be lovingly snarky: HN in aggregate is incredibly skeptical of academic research, claiming reproducibility crises everywhere, misalignment of incentives, brutal working environments whose results can't be trusted, only in mice, etc.
Unless it either confirms their existing beliefs, or is so technical that they don't understand it. Then the research must be ok :)
I concur; the graphs didn't show much difference to me (but I was on my phone so I couldn't be certain :-) The study seems impressive from the title, but reading it not so much. The Alzheimer's patients in the study are older, more male, and less educated than the controls, so it seems quite likely that they are eating worse which would explain the different microbiota. This could mess up the mice in multiple ways. (Seriously, the mice that receive Alzheimer's microbiota could have a stomach ache and do slightly worse on the tests.)
As for why there is so much interest on HN, I've noticed that Alzheimer's is one of the topics that is overly popular on HN, along with category theory, Lisp, and problems with Tesla, to name a few.
Not really weighing in one way or another, but I do not see scatter plots in the paper other than one PCA plot (which was not LDA... not sure why they chose PCA, so no strong reason to expect point separation there, though I do not know the diversity metric they are using so feel free to ignore my commentary).
Violin plots always look like they overlap. I think seaborn's split=True should be pushed a bit harder.
This field is littered with studies like this, measuring hundreds of different outcomes and then presenting the statistical noise as positive findings.
Are shady fecal transplant clinics a thing yet? Take these antibiotics for a week, then we’ll hose fecal matter from healthy, young, thin people into your intestines like a reverse enema. Move over sperm banks and blood banks, the poop bank is much easier. Only sorta joking.
I think that once you start having symptoms that it's too late because the bacteria has already spread outside your gut and at that point it'll be too difficult to put it back in check, it's passed the threshold
Analysis of gut microbiota composition by bacterial 16S rRNA gene sequencing in a subset of Alzheimer’s patients (Supplementary Fig. 1A–E) revealed no significant change in alpha and beta diversities between control subjects and Alzheimer’s patients (Supplementary Fig. 1B–D). However, at phylum level, Alzheimer’s patients had a higher abundance of Bacteroidetes (Fig. 1C) reported to comprise many pro-inflammatory species,53 and a lower abundance of the phyla Firmicutes and Verruocomicrobiota, reported to produce beneficial metabolites.54 At the genus level, Alzheimer’s patients had on average a significant reduction in the relative abundance of Clostridium sensu stricto 1 and the short chain fatty acid (SCFA) butyrate-producing genera Coprococcus, which is associated with healthy ageing in general55 (Fig. 1C). In addition, similar to a previous report using a transgenic mouse model of Alzheimer’s disease,56 the relative abundance of the pathobiont genera Desulfovibrio was significantly increased in Alzheimer’s patients compared to cognitively healthy control subjects
In addition, similar to a previous report using a transgenic mouse model of Alzheimer’s disease,56 the relative abundance of the pathobiont genera Desulfovibrio was significantly increased in Alzheimer’s patients compared to cognitively healthy control subjects
I believe there’s some benefit from boulardi yeast but I don’t know the reference except that it’s part of the bredeson protocol. Smells nice in a cleaning vinegar solution though.
Edit:
> Our findings reveal for the first time, that Alzheimer’s symptoms can be transferred to a healthy young organism via the gut microbiota, *confirming a causal role* of gut microbiota in Alzheimer’s disease ...
From: https://faculty.sites.uci.edu/kimgreen/bio/glucocorticoids-a...
Citing many papers
> One early event in AD is an increase in circulating glucocorticoids
You could sum up Alzheimer's as: Diet/Lifestyle + a congenital form of Cushing's syndrome and you have increasing glucocorticoids which imply downregulation of the PVN, less progesterone and low levels of Prolactin reducing oligodendrocyte reducing myelin sheaths. Add in APOE e4 without choline in the diet and you have accumulation of lipids to round it all out.
There is a reason why Omega 3 + B+D vitamins are talked about as preventative as they all reduce inflamation.
See this for example: https://www.grassrootshealth.net/two-nutrients-proven-stop-b...
Edit2: For the curious here is a larger brain dump on the topic with many more links when I had to untangle the pathway earlier this year while working on something else. https://www.reddit.com/r/DrWillPowers/comments/16ae4zy/alzhe...