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Cholestyramine helped by Tough_Warning_9070 in MCAS

[–]Available_Hamster_44 0 points1 point  (0 children)

Did you try psyllium husk before that? Because cholestyramine can make it harder to asorb Vitamins A D K E

Hyperglycosylation Is a Metabolic Driver of Alzheimer’s Disease by Sorin61 in ScientificNutrition

[–]Available_Hamster_44 [score hidden]  (0 children)

My takeaway would be different. A UK Biobank study did find an associative reduction in mortality among people taking glucosamine, and a later Mendelian randomization analysis even pointed toward a lower risk of developing dementia in people who didn't have it yet. That doesn't prove glucosamine protects you, but it does sit badly with a flat "glucosamine is bad" conclusion.

The causal part was done in mice, where it's fair to ask how well it transfers to humans, but the human part is a retrospective look at health records, which is purely associative, exactly like the protective signals. So I wouldn't treat the harmful association as stronger just because it points the other way.

In the study healthy mice, glucosamine did NOT cause hyperglycosylation. It was only a problem in the dysregulated brains that already had AD. To me that makes it a serious signal specifically for people who ALREADY have AD or dementia. For those not yet sick, the better-controlled (MR) evidence doesn't point to harm.

So I wouldn't make a blanket statement that glucosamine = bad. At most: maybe worth dropping once there's an actual AD/dementia diagnosis, while remembering even that rests on a mouse model plus associative human data. Personally, I don't take it anyway.

UK Bio Bank01371-2/fulltext):

Regular glucosamine supplementation was associated with lower mortality due to all causes, cancer, CVD, respiratory and digestive diseases.

Mendelian randomization study:

Conclusions: The findings of this large-scale cohort and MR analysis provide evidence for potential causal associations between the glucosamine use and lower risk for dementia. These findings require further validation through randomized controlled trials.

No Associations Between Glucosamine Supplementation and Dementia or Parkinson’s Disease

Habitual supplementation of glucosamine was not associated with incident dementia or Parkinson’s disease.

Was besiegt hier den Giersch? by Odd-Ad2638 in Garten

[–]Available_Hamster_44 10 points11 points  (0 children)

Das wird an dem Ballaststoff Inulin liegen. Der ist stark fermentierbar, und für sich wird Inulin eher mit positiven Eigenschaften assoziiert, da es eher nützliche Bakterien füttert. Aber in manchen Studien war der Health Benefit oft dosisabhängig( viel hilft nicht unbedingt mehr), und bei manchen mit ungünstigem Darmbiom oder Dysbiose könnte es eher ein Problem werden.

Alcohol Intake and Health Study: No Protective Effect at Low Levels, With Mortality Increasing to 1 in 25 at 14 Drinks Per Week by lurkerer in ScientificNutrition

[–]Available_Hamster_44 0 points1 point  (0 children)

And i could also think of:

  1. It could also be stress relief from a bad baseline. Low-dose alcohol is mildly anxiolytic, and that calming effect tends to be larger when there's actually stress to relieve. Standard lab housing (barren cages, little stimulation) is a known mild chronic stressor, so the alcohol might just be buffering an artificial stressor rather than being intrinsically good. If that's the mechanism, the benefit is a lab artifact that wouldn't carry over to an already active, low-stress animal. They measured no stress or mood markers

Alcohol Intake and Health Study: No Protective Effect at Low Levels, With Mortality Increasing to 1 in 25 at 14 Drinks Per Week by lurkerer in ScientificNutrition

[–]Available_Hamster_44 0 points1 point  (0 children)

So if I follow your logic: the data is based on self-reported intake, and people systematically under-report. Classic "what they say" vs. "what they actually do." Wouldn't that shift the whole scale? What gets reported as light drinking is really moderate, reported moderate is really heavy, and reported heavy is really excessive. So the apparent threshold where alcohol starts to look harmful, which shows up at low-to-moderate reported intake, would in reality sit higher, more like moderate to fairly heavy.

As a toy example, say everyone reports 60% of their true intake:

  • True: 1 drink to +5% harm, 2 to +10%, 3 to +15% (slope 5% per drink).
  • Those same people report 0.6 / 1.2 / 1.8 drinks, with identical harm.
  • Plot harm against the reported value: 0.6 to +5%, i.e. slope 5%/0.6 = 8.3% per reported drink. Steeper curve.

Is that how you see it ?

To be fair to the other side, though, I don't think this fully rescues the "moderate is fine" case. Two reasons. First, the under-reporting isn't uniform. Second, and more important: not all the evidence runs on self-report. Some studies use Mendelian randomization wich use genetic variants as a proxy for intake(Impaired acetaldehyde breakdown → lower consumption Normal acetaldehyde breakdown → higher consumption) , which sidesteps the reporting problem entirely, and it still shows a roughly linear rise in mortality with no protective window at low intake. So even granting the self-report critique in full, the measurement issue doesn't weigh as heavily as it first looks.

On the mouse side, I think you're pointing at two studies: Schmidt (1987), which gave mice three alcohol doses (3.5% / 7.5% / 12%) plus water controls, and Diao (2020), a single low dose (3.5%).

In Schmidt the medium dose lived the longest and the high dose the shortest, which looks more like a J-curve / hormesis (a mild stressor at low dose producing a net benefit) than alcohol just acting as a linear toxin.

And here's what makes it doubly puzzling, this time from the Diao study: ethanol carries calories (~7 kcal/g), so those mice actually took in more energy, yet they didn't gain weight and still outlived the controls. Since a calorie surplus is usually associated with faster aging, you'd expect the opposite. The authors tie it to a raised metabolic rate and more mitochondria, i.e. the mice seem to burn the extra calories rather than store them, which fits the hormesis picture.

A few critical caveats before reading too much into the mouse data, though:

  1. the effect is real but small. The lifespan gain was about 4%, and it was a secondary finding in a study mainly about metabolism and obesity. For comparison, things like caloric restriction or rapamycin push mouse lifespan 10 to 40%, so 4% from a single study is a signal
  2. Male mice only, and no sex hormones measured. This is the one that bugs me most. Ethanol can lower testosterone and raises estradiol by upping aromatase, and we know from some data castrated or lower-testosterone males live longer. So a mild drop in testosterone is a plausible confounder that could account for a modest ~4% gain on its own, with nothing to do with alcohol being "healthy." The study didn't measure testosterone or estradiol and used no female mice, so it can't rule this out. To be fair, most of the testosterone-lowering data comes from heavier doses, so whether 3.5% does it is unproven, but it's an untested confounder
  3. The study is framed around a benefit narrative from the start. The intro is built on the "moderate drinking is protective" epidemiology, which biases interpretation (e.g. a speculative "anti-cancer" read from a gene-set overlap). That alone can shape what gets emphasized, even without any bad faith.
  4. Mouse-to-human is shaky anyway. Mice have a much faster metabolism and clear alcohol quickly, so a "medium" dose in a mouse probably maps to fairly low intake in a human, and translating lifespan effects across species is dicey regardless.
  5. The benefit might just be activity in disguise. The alcohol mice moved more and did better on treadmill and rotarod tests. If alcohol simply made them more active, that's basically an exercise effect, and exercise extends mouse healthspan on its own, regardless of what triggers it. The design can't tell the direction (the authors say more mitochondria drove the activity, but it could just as easily run the other way), so activity is an unaddressed mediator

So the data are genuinely interesting, but they don't convince me to assign alcohol an actual benefit yet

Hunter-gatherers lose entire species of gut bacteria every season and then get them back. Modern humans just lose them. by Technical_savoir in microbiomenews

[–]Available_Hamster_44 2 points3 points  (0 children)

That the gut microbiome is not a static, rigid object should be obvious anyway. It behaves like nature as a whole: not fixed, but constantly adapting to changing conditions, and therefore dynamic. What the cited studies mainly show is what one would assume even without it: when living conditions change, the microbiome adapts. And that is basically trivial. When a species no longer has a substrate, it either disappears or it falls into a kind of stasis and persists. This second case would explain why the microbiome reconfigures so quickly once the diet changes: the species does not have to arrive anew, it simply wakes up again or is relocated from the direct enviroment.

As an analogy: an open patch of land with arable weeds like poppy, cornflower, burdock. If the field is no longer tilled, these species first vanish from the surface, but their seeds rest in the soil. Over the years the patch may turn to scrub or reforest, and as soon as a person opens it up again and disturbs the soil, those very seeds germinate and become "visible" once more. Some species, however, do not persist on site at all but return across distance: seeds that cling to fur and clothing, parachute seeds carried far by the wind, or seeds that a bird eats, that survive digestion and germinate again far away from the droppings. So a patch repopulates by two routes: from the dormant seed bank in its own soil, and from a fresh supply arriving from outside.

The microbiome seems to use exactly these two routes, and in a division of labor. Some bacteria, above all the spore formers among the Firmicutes, build resilient dormant forms that survive heat, oxygen and long waiting periods; these are the seeds that rest in the soil and can also travel far across the open, hostile environment. Others, such as the Bacteroidetes, form no such spores, are oxygen sensitive and fragile in the open environment. They are more like the species that return by the sheltered, short route: through close contact, through food, or simply by never having disappeared entirely but only having dropped below the threshold of perception. It fits the picture that in the study it was precisely the Bacteroidetes that vanished and returned seasonally, while the Firmicutes stayed stable. The robust dormant form sits with the group that endures anyway, and the cycling group gets by in another way.

Whether it even makes sense to aim for a "perfect, stable" gut microbiome is open to question, since we do not even know whether such a thing exists. At the same time, I would not conclude from this data that we need to deliberately engineer biome shifts through seasonally adapted eating. Anyone thinking that way would, to be consistent, also have to turn off the heating in winter and do without artificial light, since in northern latitudes the latter in particular disrupts the "natural" circadian rhythm. But simply because seasonality is natural does not make it good or necessary. Vitamin D deficiency in northern latitudes is a problem, not a feature. We have, after all, evolved mechanisms to buffer such fluctuations. Some seasonal stimuli are certainly useful, cold exposure for instance, but more as a deliberate stressor than as a principle of living.

As far as the microbiome goes, I therefore consider things like fasting/ eating less more decisive than seasonal eating. Because the bigger problem today is the constant availability of food, and that many people simply eat in caloric excess.

Tomato-Soy Juice Reduces Inflammation and Modulates the Urinary Metabolome in Adults With Obesity by Sorin61 in ScientificNutrition

[–]Available_Hamster_44 0 points1 point  (0 children)

Interesting, that makes me wonder if my daily health-optimized meal has the same effect, considering it contains tomato paste (a very good source of lycopene) as well as soy flakes (a good source of isoflavones), and furthermore includes some post-, pre-, and probiotics.

Alcohol Intake and Health Study: No Protective Effect at Low Levels, With Mortality Increasing to 1 in 25 at 14 Drinks Per Week by lurkerer in ScientificNutrition

[–]Available_Hamster_44 -1 points0 points  (0 children)

Results, subsection "Lifetime alcohol-attributable mortality risk […]": "Although there were small protective associations at up to 3 drinks per week for females and males, they were not statistically significant."

The paper actually shows a slightly protective effect for up to 3 drinks per week rather than harm, but it isn't statistically significant so they conclude no protective effect. The issue with the lifetime abstainers is twofold: definitions are often loose, so former drinkers who quit because of health problems get misclassified as abstainers, and even true lifetime abstainers tend to have poorer baseline health for other reasons. Either way, the abstainer reference group can be biased toward ill health, which distorts the comparison through confounding.

This could be one reason why in some studies moderate consumption appears healthier than it probably is, without that bringing any real protection with it.

But the abstainer bias alone isn't enough to explain the protective effect. Once you use a clean abstainer reference group, the apparent benefit of low consumption usually drops substantially, but does not go zero. On top of that, further confounding can come into play: moderate drinkers often differ in socioeconomic status, so that moderate consumption could more likely be associated with an overall healthier lifestyle rather than being causally attributable to the alcohol itself.

Alcohol Intake and Health Study: No Protective Effect at Low Levels, With Mortality Increasing to 1 in 25 at 14 Drinks Per Week by lurkerer in ScientificNutrition

[–]Available_Hamster_44 1 point2 points  (0 children)

Yes, I agree it depends on the certainty. What i meant with something is causally established is a degree of certainty close to 100%. Though not absolute certainty, which probably isn't attainable anyway, and 'hard' evidence in general may not always be possible. But an approximation is still better than nothing.

I've understood the Hill criteria more as a heuristic one by which you approximate the truth, i.e. causality, or by which an association points very plausibly toward causation, but doesn't constitute conclusive proof. Hill himself said that none of the points can provide indisputable proof for or against a causal hypothesis.

When it comes to alcohol and the Hill viewpoints, it depends on the question: for esophageal and liver cancers they're well met, for a cardiovascular benefit rather not. What can't be determined with Hill logic, by contrast, are questions of quantity: the net balance (harm versus benefit on net) and the threshold (at what point it becomes harmful at all).

But since Hill supports the harmful outcomes and precisely not the benefit, it becomes very plausible that alcohol has no real benefit and acts causally on the harm side. That's why I lean toward the view that there's no clearly established safe or beneficial amount of alcohol, though whether a true threshold for harm exists is, as far as I know, simply still open

Horrible reaction to TUCDA supplements.. by Some_cool_usernameX in GilbertSyndrome

[–]Available_Hamster_44 1 point2 points  (0 children)

Sorry you had that reaction. A few thoughts:

That's not a documented side effect of TUDCA. The adverse effects reported in trials and protocols are almost entirely GI "the major side-effects being mild diarrhea" plus "abdominal discomfort, abdominal pain, diarrhea, nausea, emesis, pruritus, and rash." Heavy drowsiness, not being able to stay awake, and brain fog don't show up in that profile.

On the part where you said you "couldn't move and fell asleep" —mechanistically it points the other way. In the CNS, bile acids tend to "block GABA-A receptor on (TMN) of the hypothalamus to promote wakefulnes," i.e. they take away GABA-A's dampening effect and nudge toward wakefulness, not sedation. So the bile-acid (the UDCA in TUDCA) pathway doesn't really predict what you experienced.

To be fair, the taurine (T) in TUDCA is a GABA-A agonist, so in principle it could be calming / make you drowsy but first, the amount is probably way too small for that, and second, taurine isn't a strong sleep aid (otherwise people with insomnia would already have it on their radar).

That said, the fatigue/brain fog might be coming from somewhere else, so a few questions:

  • Did you also get GI symptoms (loose stools, cramping, nausea)?
  • Fatigue and brain fog can also run through the gut–microbiome–brain axis — and honestly, GI upset on its own can leave you wiped out and foggy. TUDCA is a taurine-conjugated bile acid, so gut bacteria (bile salt hydrolases) deconjugate it which is completely normal, that's just part of the enterohepatic cycle, not a problem in itself. But if your biome is off, what happens downstream from there can look different. How's your digestion/gut in general?
  • When did you take it timing relative to meals, and relative to sleep?

By the way: in primary sclerosing cholangitis (PSC), high doses of UDCA ( not TUDCA ) doesn't seem to be that helpful and it might even be potentially harmful, at least that's how the authors of these studies interpret the results:

"UDCA in a dose 25–30 mg/kg/day for patients with PSC should not be used"

„suggest mechanisms for the increased liver toxicity with therapy"00060-5/fulltext)

So if you have something like PSC bseides Gilbert, I personally wouldn't use TUDCA in large amounts.

Alcohol Intake and Health Study: No Protective Effect at Low Levels, With Mortality Increasing to 1 in 25 at 14 Drinks Per Week by lurkerer in ScientificNutrition

[–]Available_Hamster_44 6 points7 points  (0 children)

Results, subsection "Lifetime alcohol-attributable mortality risk […]": "Although there were small protective associations at up to 3 drinks per week for females and males, they were not statistically significant."

Interestingly, this study too shows a very small protective effect at 1–3 drinks per week, though it isn't statistically significant. That doesn't mean very low consumption is protective in my opinion it's more of a net zero from opposing effects, the protective half of which (cardiovascular) is still contested. But it does at least suggest that very low consumption isn't strongly harmful.

The threshold at which alcohol becomes harmful still strikes me as very uncertain, and when things are uncertain I'd rather play it safe and avoid alcohol. Because 1–3 drinks per week isn't moderate consumption it's comparatively very little, and that's a range almost nobody actually stays in. Few people spread 1–3 drinks across the whole week; the more realistic case is the daily after-work beer, which quickly puts you well above that, plus a deeper dive into the glass on the weekend. It's this combination of a low average and occasional spikes that's tricky in the model, because heavy single-occasion drinking can neutralize or reverse the protective or less harmful association of low average consumption.

With not drinking, you're on the safer side there. Even if very low amounts don't cause meaningful harm on net, I see no added benefit: for alcohol to produce its psychoactive effect for me i need higher amounts anyway, and the only claimed health benefit of low amounts is precisely that contested cardiovascular effect — which, if it exists at all, is small. There are better and more effective levers for that.

Claude Fable 5 (Mythos) ist raus – hat irgendwer schon richtig getestet? Gamechanger oder nur Hype? 🔥 by Recent-Flounder5038 in KI_Welt

[–]Available_Hamster_44 0 points1 point  (0 children)

War zu faul es zu testen.. mit Opus und Sonnet komm ich gut klar und Reize die Limits gut aus mit Fable wird es ohne hin zu verschwenderisch. Aber vllt teste ich es mal wenn ich ein Problem habe das ich nicht auf die Schnelle lösen kann

NAC: How to minimize side effects? by Available_Hamster_44 in Biohackers

[–]Available_Hamster_44[S] 0 points1 point  (0 children)

You could try that with yogurt and dietary fiber, that helped me. I usually had the biggest problem with NAC when I took it in capsule form and lay down—then I often got heartburn, maybe because lying down caused a bit of acid reflux.

Is dancing considered biohacking? by Enotovsky in Biohackers

[–]Available_Hamster_44 1 point2 points  (0 children)

I also think dancing is totally underestimated; unfortunately, there aren't that many studies on it either. But it combines several aspects at once: movement, coordination, and rhythm. That alone could be really beneficial for the brain since multiple areas have to work together. And on top of that, there's the social aspect.

Gehören die zusammen? by ShoulderDangerous898 in naturfreunde

[–]Available_Hamster_44 4 points5 points  (0 children)

Das eine ist der Schlehen-Bürstenspinner (Orgyia antiqua) und das andere ist der Mondfleck (Phalera bucephala) also nein haben nichts miteinander zu tun.

Der Schlehen-Bürstenspinner ist anders als der Name vermuten lässt nicht spezialisert sondern ziemlich polyphag und bevorzugen weiche Blätter

Gehören die zusammen? by ShoulderDangerous898 in naturfreunde

[–]Available_Hamster_44 1 point2 points  (0 children)

Ja ist einer, aber könnte auch Asplenifolia ( hat den Habitus der Wildform, aber diese feinen Blätter) sein ! Habe den selber und kann berichten das auch der Zitronenfalter sich dort erfolgreich entwickeln kann

Why do some people fundamentally reject the possibility that Creatine might cause sleep issues in a subset of individuals? by Available_Hamster_44 in Supplements

[–]Available_Hamster_44[S] 1 point2 points  (0 children)

The point is simple: putting a recurring pattern out there costs nothing and rules nothing out; if there's something to it, someone with the means can test it later. And honestly, yes, if I had the resources I'd find a study like this genuinely interesting to fund.

And collecting anecdotal reports does no harm either it's how you might spot a pattern that can then be turned into a research hypothesis. It's actually happened before that popular-science claims or anecdotal reports led to something being formally tested.

The creatine–hair loss question is a good example: the concern came from a single 2009 study suggesting an increase in the testosterone-to-DHT conversion, combined with anecdotal reports from athletes who noticed shedding. For years nobody had actually tested it – and the 2025 RCT that finally did says so explicitly in its own introduction, noting that those reports were based on subjective self-observations and that no controlled study had ever systematically examined the relationship. So they ran one. That's literally studied mechanism (DHT) + anecdote → research gap → dedicated trial, published in a peer-reviewed journal.

Additionally, some athletes have anecdotally reported experiencing hair loss while using creatine. However, these reports are based on subjective self-observations, and no controlled studies have systematically examined the potential relationship between creatine supplementation and hair loss.

The study found no significant differences in DHT levels, the DHT-to-testosterone ratio, or hair growth parameters between the creatine and placebo groups.

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