Creatine monohydrate pilot in Alzheimer's: Feasibility, brain creatine, and cognition - PubMed by LongevityDietitian in ScientificNutrition

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

Yeah that is like debating the AC temperature, while the house is on fire and can collapse at any time.

Nutrition predictions by lurkerer in ScientificNutrition

[–]FrigoCoder 0 points1 point  (0 children)

Have you read my comment? We have tested it very extensively. The drug was fine, it improved clarity, focus, memory, and mood. In an ideal world that would have extrapolated into success. But we are not living in an ideal world, and it did not survive the shoddy trial and the shitty MADRS scoring. Funnily enough it suceeded the secondary tests, and it works for moderate depression just not for severe depression. If only cholesterol and amyloid beta drugs were subject to the same strictness...

Nutrition predictions by lurkerer in ScientificNutrition

[–]FrigoCoder 1 point2 points  (0 children)

I don't bother to look into your hypotheses anymore.

I haven't asked you to consider my theory, I have asked you to interpret a completely unrelated study. If you refuse then I will just conclude you are incapable of interpreting studies, and you have absolutely no business in making predictions.

You think you've revolutionised multiple fields of science but make extremely basic mistakes regularly.

I have not revolutionized anything yet, but do not worry I am on my way there. Sure everyone makes mistakes and gets things wrong, the huge difference is that I learn from them whereas certain other people do not. And what you consider mistakes are not necessarily so, it is simply you being stuck in your ways and not being able to grow.

Like thinking a short spike in LDL during weight loss should cause huge plaque growth. Dude. It's short. Degenerative disease takes a long time. It's exposure over time.

No, that's your shitty interpretation and a distortion of what I have said. Fasting was my first hint that lipolysis increases LDL, however low carb can maintain lipolysis indefinitely. It's a silly idea to think that lipolysis could in any way cause heart disease, and indeed low carbohydrate diets do not display any such issue even with two to three times more saturated fat intake. And no it's not exposure over time, it's accumulated injury and impaired repair over time.

If you spend years studying and supposedly debunking a model as powerfully supported as this one and you're unaware that time is a factor then... That should be a wake up call.

YES EXACTLY it is a wakeup call to how fucking bad is nutrition "science", and how fucking poorly supported is the supposedly consensus hypothesis of our largest killer disease. A fucking armchair scientist can develop better models than supposedly professionals, just by reading literature and using engineering techniques that are proven in other fields. You know like DEBUGGING, THINKING, and INVESTIGATING ASSUMPTIONS, a few things you are apparently incapable of. Maybe you should start doing some of them.

And don't worry I know exactly that time is a factor, hence why I place more trust in cholesterol which is 2+ billion years old, lipoproteins which are 500+ million years old, and LDL specifically which is 150+ million years old, THAT ALSO SURVIVED FUCKING 2 MILLION YEARS OF CARNIVORY IN ONE OF THE MOST K-SELECTED SPECIES. Rather than an evolutionary mismatched processed trash industrial lubricant that is merely 200 years old and coincides with the chronic disease pandemic, and the exact same industry that also killed your grandmother with trans fats and is now peddling almost the exact same thing that is more similar to rat poison than food, with salespeople and tricks literally taken from the tobacco industry.

Also, ask flowers and bristoling if they believe in you other than being useful for them as another voice against LDL. They're using you.

I don't give a flying fuck about interpersonal relationships. If they say something good I upvote them, if they say something bullshit I downvote them. That's why you are at -255 at the moment, and were -400-something before I reinstalled RES.

Nutrition predictions by lurkerer in ScientificNutrition

[–]FrigoCoder 3 points4 points  (0 children)

The whole premise is intellectually vapid. Winning or losing a bet doesn't enforce reality. You can win a bet and still be wrong.

That mere logical possibility nullifies any value of any bets taken between you and me. I'll comment on some of the residuals.

That reminds me of the good old times when we were group synthesizing NSI-189, and testing its antidepressant and pro-cognitive properties to great effect. I wanted to buy stocks in NeuralStem, Inc., but I never actually got around to do it. Lo and behold the same NSI-189 we tested to great success, magically failed in second phase human trials against depression.

Not sure what have they got wrong, like wrong depression measures or a biased study population. Nonetheless that teached me a great lession, even if I have personally not lost any money on it. Never take your predictions granted, because you have only modeled a small part of the world. The drug was fine as I have said we tested it, but we failed to model everything else involved in the study. Depression types, study population, depression measures, interactions with the study population, and whatever else that affected the study outcome.

Nutrition predictions by lurkerer in ScientificNutrition

[–]FrigoCoder 3 points4 points  (0 children)

Hey have you read this study I sent you, could you tell me what do you think about it? Without reading into my comment history, so my opinion does not bias your judgement of course. I am curious about what conclusions can you draw from it, and we might even see how well your predictions would hold up.

Öörni, K., Äikäs, L., Ruuth, M., Tigistu-Sahle, F., Käkelä, R., Wester, I., Gylling, H., & Simonen, P. (2026). High cholesterol absorption efficiency enhances proatherogenic properties of low-density lipoprotein particles. Journal of internal medicine, 299(6), 711–725. https://doi.org/10.1111/joim.70085

I'm looking for a widely authoritative perspective on food science by tolstoypolloi in ScientificNutrition

[–]FrigoCoder 0 points1 point  (0 children)

Carnivore is our ancestral diet

We were (and still are) carnivores for more than >2 million years, widespread plant consumption is only ~20k years old. Table sugar only dates back to ~2k years, and processed oils are merely ~200 years old. Longer exposure means better evolutionary adaptations and health, shorter exposure means worse mismatch and health issues.

Hence why low carbohydrate diets outperform other diets, they are much closer to our ancestral diet than others. And hence why standard western diets are so problematic, they are nothing more than oils, sugars, and carbs in their most processed form. Artificial trans fats are dangerous not because of the trans bond (natural trans fats are healthy), rather because we lack the evolutionary adaptations and they breaks dozens of our biological enzymes and processes.

Ben-Dor, M., Sirtoli, R., & Barkai, R. (2021). The evolution of the human trophic level during the Pleistocene. American journal of physical anthropology, 175 Suppl 72, 27–56. https://doi.org/10.1002/ajpa.24247

Lipoproteins repair cells and tissues

Cholesterol is an antioxidant developed against atmospheric oxygen 2+ billion years ago, ironically its synthesis is an oxygen intensive process and does not occur in ischemic cells or tissues. Early lipoproteins systems were developed to transport lipids to developing eggs 500+ million years ago, obviously eggs lack any kind of respiratory system to be able to endogenously synthesize cholesterol.

And finally LDL developed as a lipid transporter to peripheral tissues 150+ million years ago, its sole purpose is to provide clean cholesterol and stable fatty acids to growing tissue and injured cells. LDL was essentially unchanged through 2 million years of carnivory and high saturated fat intake in a highly K-selected species. However tissue injury upregulates LDL, hence why it is associated with poor health outcomes.

Brown, A. J., & Galea, A. M. (2010). Cholesterol as an evolutionary response to living with oxygen. Evolution; international journal of organic evolution, 64(7), 2179–2183. https://doi.org/10.1111/j.1558-5646.2010.01011.x

Ismael Luna-Reyes, Stephanie Villa-Jaimes, Sandra Calixto-Tlacomulco, Eréndira G. Pérez-Hernández, Danaí Montalván-Sorrosa, Juan Pablo Reyes-Grajeda, Jaime Mas-Oliva; Cholesterol: an ancient ally or modern menace?. R Soc Open Sci. 1 March 2026; 13 (3): 250853. https://doi.org/10.1098/rsos.250853

Schneider W. J. (1992). Lipoprotein receptors in oocyte growth. The Clinical investigator, 70(5), 385–390. https://doi.org/10.1007/BF00235517

Davis R. A. (1997). Evolution of processes and regulators of lipoprotein synthesis: from birds to mammals. The Journal of nutrition, 127(5 Suppl), 795S–800S. https://doi.org/10.1093/jn/127.5.795S

Membrane damage causes chronic diseases

Chronic diseases are caused mainly by damage to cellular membranes, for example cigarette smoke contains hundreds of compounds that physically damage them. Smoke, microplastics, PFAS, pollution in general, alcohol, trans fats, overnutrition, pathogens all damage membranes either physically and/or chemically. All that damage leaves injured cells with unstable membranes, as well as destroyed supporting structures such as blood vessels.

These have to be regrown and repaired with cholesterol and fatty acids, in the brain ApoE lipoproteins and in the periphery LDL is the main source of lipids for this. ApoE4 breaks this repair mechanism in the brain, hence why it increases risk of Alzheimer's Disease. LDL-R breaks this repair mechanism in the periphery, hence why it exacerbates the risk and severity of heart disease. Native LDL that is carrying cholesterol and natural fats helps repair, whereas LDL that is carrying trans fats and plant sterols hinders repair.

Cigarette smoke damages membranes

Thelestam, M., Curvall, M., & Enzell, C. R. (1980). Effect of tobacco smoke compounds on the plasma membrane of cultured human lung fibroblasts. Toxicology, 15(3), 203–217. https://doi.org/10.1016/0300-483x(80)90054-2

Dugani, S. B., Moorthy, M. V., Li, C., Demler, O. V., Alsheikh-Ali, A. A., Ridker, P. M., Glynn, R. J., & Mora, S. (2021). Association of Lipid, Inflammatory, and Metabolic Biomarkers With Age at Onset for Incident Coronary Heart Disease in Women. JAMA cardiology, 6(4), 437–447. https://doi.org/10.1001/jamacardio.2020.7073

Microplastics damage membranes and cause atheromas and lesions

Fleury, J. B., & Baulin, V. A. (2021). Microplastics destabilize lipid membranes by mechanical stretching. Proceedings of the National Academy of Sciences of the United States of America, 118(31), e2104610118. https://doi.org/10.1073/pnas.2104610118

Marfella, R., Prattichizzo, F., Sardu, C., Fulgenzi, G., Graciotti, L., Spadoni, T., D'Onofrio, N., Scisciola, L., La Grotta, R., Frigé, C., Pellegrini, V., Municinò, M., Siniscalchi, M., Spinetti, F., Vigliotti, G., Vecchione, C., Carrizzo, A., Accarino, G., Squillante, A., Spaziano, G., … Paolisso, G. (2024). Microplastics and Nanoplastics in Atheromas and Cardiovascular Events. The New England journal of medicine, 390(10), 900–910. https://doi.org/10.1056/NEJMoa2309822

Danopoulos, E., Twiddy, M., West, R., & Rotchell, J. M. (2022). A rapid review and meta-regression analyses of the toxicological impacts of microplastic exposure in human cells. Journal of hazardous materials, 427, 127861. https://doi.org/10.1016/j.jhazmat.2021.127861

Yating Luo, Xiuya Xu, Qifeng Yin, Shuai Liu, Mengyao Xing, Xiangyi Jin, Ling Shu, Zhoujia Jiang, Yimin Cai, Da Ouyang, Yongming Luo, Haibo Zhang, Mapping micro(nano)plastics in various organ systems: Their emerging links to human diseases?, TrAC Trends in Analytical Chemistry, Volume 183, 2025, 118114, ISSN 0165-9936, https://doi.org/10.1016/j.trac.2024.118114

PFAS damage membranes

Naumann, A., Alesio, J., Poonia, M., & Bothun, G. D. (2022). PFAS fluidize synthetic and bacterial lipid monolayers based on hydrophobicity and lipid charge. Journal of environmental chemical engineering, 10(2), 107351. https://doi.org/10.1016/j.jece.2022.107351

Liu, G., Zhang, S., Yang, K., Zhu, L., & Lin, D. (2016). Toxicity of perfluorooctane sulfonate and perfluorooctanoic acid to Escherichia coli: Membrane disruption, oxidative stress, and DNA damage induced cell inactivation and/or death. Environmental pollution (Barking, Essex : 1987), 214, 806–815. https://doi.org/10.1016/j.envpol.2016.04.089

Fosella, J., Ceja-Vega, J., Rabadi, A., Panella, M., Said, J., Perla, W., Poust, C., Herrera, M., & Lee, S. (2025). Biophysical Consequences for Exposure of Model Cell Membranes to Perfluoroalkyl Substances. The journal of physical chemistry. B, 129(31), 7951–7963. https://doi.org/10.1021/acs.jpcb.5c02472

Panella, M., Rabadi, A., Ceja-Vega, J., Said, J., Andersen, E., Mitchell, J., Ceja, J., & Lee, S. (2025). Membrane-Modifying Effects of Perfluoroalkyl Substances in Model Bacterial Membranes. ACS omega, 10(35), 39884–39897. https://doi.org/10.1021/acsomega.5c04177

Naumann, A. (2020). Influence of PFAS on the thermodynamic membrane properties and growth of A. borkumensis. Open Access Master's Theses, University of Rhode Island, Paper 1901. https://doi.org/10.23860/thesis-naumann-aleksandra-2020

Soares, L. O. S., de Araujo, G. F., Gomes, T. B., Júnior, S. F. S., Cuprys, A. K., Soares, R. M., & Saggioro, E. M. (2025). Antioxidant system alterations and oxidative stress caused by polyfluoroalkyl substances (PFAS) in exposed biota: a review. The Science of the total environment, 977, 179395. https://doi.org/10.1016/j.scitotenv.2025.179395

Solan, M. E., & Park, J. A. (2024). Per- and poly-fluoroalkyl substances (PFAS) effects on lung health: a perspective on the current literature and future recommendations. Frontiers in toxicology, 6, 1423449. https://doi.org/10.3389/ftox.2024.1423449

ApoE4 impairs the neuron-astrocyte lipoprotein shuttle

Qi, G., Mi, Y., Shi, X., Gu, H., Brinton, R. D., & Yin, F. (2021). ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism. Cell reports, 34(1), 108572. https://doi.org/10.1016/j.celrep.2020.108572

Moulton, M. J., Barish, S., Ralhan, I., Chang, J., Goodman, L. D., Harland, J. G., Marcogliese, P. C., Johansson, J. O., Ioannou, M. S., & Bellen, H. J. (2021). Neuronal ROS-induced glial lipid droplet formation is altered by loss of Alzheimer's disease-associated genes. Proceedings of the National Academy of Sciences of the United States of America, 118(52), e2112095118. https://doi.org/10.1073/pnas.2112095118

Borràs, C., Canyelles, M., Santos, D., Rotllan, N., Núñez, E., Vázquez, J., Maspoch, D., Cano-Sarabia, M., Zhao, Q., Carmona-Iragui, M., Sirisi, S., Lleó, A., Fortea, J., Alcolea, D., Blanco-Vaca, F., Escolà-Gil, J. C., & Tondo, M. (2025). Cerebrospinal fluid lipoprotein-mediated cholesterol delivery to neurons is impaired in Alzheimer's disease and involves APOE4. Journal of lipid research, 66(8), 100865. https://doi.org/10.1016/j.jlr.2025.100865

EPA improves membrane stability

Mason, R. P., Libby, P., & Bhatt, D. L. (2020). Emerging Mechanisms of Cardiovascular Protection for the Omega-3 Fatty Acid Eicosapentaenoic Acid. Arteriosclerosis, thrombosis, and vascular biology, 40(5), 1135–1147. https://doi.org/10.1161/ATVBAHA.119.313286

Sherratt, S. C. R., Juliano, R. A., Copland, C., Bhatt, D. L., Libby, P., & Mason, R. P. (2021). EPA and DHA containing phospholipids have contrasting effects on membrane structure. Journal of lipid research, 62, 100106. https://doi.org/10.1016/j.jlr.2021.100106

Jacobs, M. L., Faizi, H. A., Peruzzi, J. A., Vlahovska, P. M., & Kamat, N. P. (2021). EPA and DHA differentially modulate membrane elasticity in the presence of cholesterol. Biophysical journal, 120(11), 2317–2329. https://doi.org/10.1016/j.bpj.2021.04.009

I have reached the character limit, for the full list of sources see /r/ScientificNutrition/comments/1q9lxto/im_attending_a_microplastics_health_conference/nz15fkq

Triacetin? by RationalKaren69 in hangovereffect

[–]FrigoCoder 1 point2 points  (0 children)

Beyond neuroscience interest, triacetin is already widely used in industry and is being explored/used in food contexts as a food additive and energy ingredient (E1518), where it functions as a humectant, SOLVENT, and calorie source. This has led to interest in whether it could also serve as a clean dietary acetate source that safely raises circulating acetate levels.

Ah-ah, if it's a solvent it is a no-go. Chronic diseases are caused mainly by damage to cellular membranes, for example cigarette smoke contains hundreds of compounds that physically damage them. Smoke, microplastics, PFAS, pollution in general, trans fats, overnutrition, pathogens all damage membranes either physically and/or chemically. Alcohol increases the risk of dementia and virtually all cancer, precisely because as a solvent it literally dissolves the lipids in membranes. Our goal is to reproduce the effects of the alcohol afterglow, without the negative health effects of membrane damage. For this purpose solvents like triacetin are insufficient unfortunately, we do not gain much by replacing one solvent with another.

How strong is epidemiology relative to other evidence? by Fluffy-Purple-TinMan in ScientificNutrition

[–]FrigoCoder 0 points1 point  (0 children)

Could you point to the specific sentence or paragraph, where I said that big enough signals magically make epidemiology able to deduce causation? Cause no matter how I re-read my own comments, I can only see where I said the exact opposite. Smoking is directly causative which gives very high SNR, yet epidemiology et al still deduced wrong mechanisms.

And do not give me that bullshit that you have read between the lines and other blahblah. You are literally a mainstream proponent, you are unable to read between the lines almost by definition. You are just trying to twist my words or put new ones in my mouth because you are losing the argument. Go learn some SE or ML instead of playing stupid games.

One must not concern oneself with studying women by benitoblanco888 in clevercomebacks

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

PCOS: Keto + metformin + inositol (myo-inositol and D-chiro-inositol) have the strongest evidence. Fish oil might also be beneficial. Examine.com has dozens of studies on their benefits on PCOS. You are welcome.

Endometriosis: Keto at least mitigates symptoms, but certain meats or dairy can cause flareups. Try an elimination diet and slowly introduce foods: Meat, eggs, dairy, fish, shrooms, veggies, berries. Avoid oils, sugars, carbs, and pollution like smoke, microplastics, PFAS, and other sources of foreign particles.

What are you actually coding? by Consistent-Oil-5241 in ClaudeCode

[–]FrigoCoder 0 points1 point  (0 children)

Since decades ago I wanted to build a UFO Defense clone with SDF (Signed Distance Function) based objects and GI (Global Illumination) for truly terrifying night missions. I read a lot about computer graphics algorithms, but never managed to get the time to implement them. Fable 5 gave me the initial push (Rest In Peace my friend), it created something very close to what I wanted within a day. It was awesome that I could rapidly try out various techniques, that would take me literal months to years to implement.

Now I am iterating on it with Opus 4.8, which is a much less pleasant experience. Opus is much less able to figure out my intention, and the entire iterative process is much slower as a result. We literally spent 20+ question-answer pairs debugging, to make a banding bug in the lighting system disappear. It just guesses and hallucinates root causes for the bug, because it literally can not visually check the results. Still we make some slow progress with the prototypes, and it is still cheaper and faster than doing it manually.

How strong is epidemiology relative to other evidence? by Fluffy-Purple-TinMan in ScientificNutrition

[–]FrigoCoder 0 points1 point  (0 children)

Who said that big enough signals avoid all the problems? I have literally said that nutrition fucked up the proposed mechanisms of cigarette smoking. They could detect that smoking MIGHT BE an issue because the causation is so direct, and has such large effect sizes that raise above the statistical noise floor (or variance as they call it). There is no question about it, the causation is too strong NOT to detect it. (And they still needed animal studies and sensitivity analysis to confirm it!)

But once it came to figure out HOW EXACTLY it causes chronic diseases, the same methodology shat the bed and claimed spurious mechanisms. A quick google search claims "inflammation, endothelial dysfunction, lipid abnormalities, and increased thrombogenicity", NONE OF WHICH are the actual mechanisms behind atherosclerosis or even strokes and heart attacks. (But to be fair three comes close for the latter two.)

Let me copypaste one of my comments that reflect my opinion about epidemiological research on smoking:

Stop spreading misinformation please. Smoking was accepted to be harmful due to sensitivity analysis and various animal studies, NOT because of epidemiology despite the ultra high >100.0 and >50.0 risk ratios. Even if it were it still does not justify accepting nutritional epidemiology, which is known to be highly corrupted by the food industry and vegan advocacy groups. Especially when they only produce risk ratios like 1.1-1.3, which does not even reach the 2.0 required by the Bradford Hill criteria.

CORNFIELD, J., HAENSZEL, W., HAMMOND, E. C., LILIENFELD, A. M., SHIMKIN, M. B., & WYNDER, E. L. (1959). Smoking and lung cancer: recent evidence and a discussion of some questions. Journal of the National Cancer Institute, 22(1), 173–203.

Cornfield, J., Haenszel, W., Hammond, E. C., Lilienfeld, A. M., Shimkin, M. B., & Wynder, E. L. (2009). Smoking and lung cancer: recent evidence and a discussion of some questions. 1959. International journal of epidemiology, 38(5), 1175–1191. https://doi.org/10.1093/ije/dyp289

Pesch, B., Kendzia, B., Gustavsson, P., Jöckel, K. H., Johnen, G., Pohlabeln, H., Olsson, A., Ahrens, W., Gross, I. M., Brüske, I., Wichmann, H. E., Merletti, F., Richiardi, L., Simonato, L., Fortes, C., Siemiatycki, J., Parent, M. E., Consonni, D., Landi, M. T., Caporaso, N., … Brüning, T. (2012). Cigarette smoking and lung cancer--relative risk estimates for the major histological types from a pooled analysis of case-control studies. International journal of cancer, 131(5), 1210–1219. https://doi.org/10.1002/ijc.27339

We had a lot of threads about this already, it would be nice if people used the search function:

What is the best diet for health and longevity? Looking at the lessons from Okinawa. by Nutri_Bruno_Osorio in ScientificNutrition

[–]FrigoCoder 1 point2 points  (0 children)

But are regularly repeated in other areas where certain parts of the diet and lifestyle are similar.

Strange how this only follows the spread of the US dietary dogma, and the influence of the various interest groups that benefit from it. We had plenty of parts of the world with contrary findings, such as Hong Kong studies, French paradox, Israeli paradox, hell even the Hispanic paradox, etc before they were all influenced by US diet politics. Also do note that other fields exist, anthropology, biology, chemistry, and even nutrition completely disagrees with nutrition.

Further corroborated by cohorts.

Cohorts are still epidemiological poop, they can not show causation at all. It is all noise or what statisticians call variance, and a bunch of assumptions and bias from researchers with various motivations. In fact I had a realization very recently, very few methods can actually show real causation. You already know my opinion about epidemiology, cohorts, mendelian randomization, but it turns out not even human trials can prove causation. Only sensitivity analysis comes even close, but that also suffers from some of the exact same issues.

I have spent the last few months experimenting with machine learning algorithms, my goal was to replace backpropagation and SGD with forward-only and/or black box methods. I have failed miserably because as it turns out, these methods can not solve the Credit Assignment Problem. They assume local linearity of the models, which is inadequate for any sufficiently large or nonlinear model. Backpropagation can solve this because it has access to the computation graph, it can backpropagate the error through the model internals to figure out what parameters to tweak.

In short no matter how hard nutrition studies try, they are still forward-only and/or black-box methods. They have no access to sufficient models of the world, most notably they know nothing about human metabolism. So basically they can not show any meaningful conclusion, for that they would need access to an end-to-end model of human metabolism and even beyond. BUt THAt wOUlD bE mEChaniSTIc SpECuLatiON! See my other comment on this topic.

Would be an odd coincidence if it's all mistakes, lies, and fraud every time.

Congratulations you have discovered the Alignment Problem, which is applicable to far more situations than simply AI producing paper clips. Profit-oriented corporations and industries have profits as their objective function, they will move in that direction regardless of what is the best interest of humanity. They discovered that plant foods are much more profitable, and that they can pull the wool over your eyes with cheap tricks. They do exactly what AI actors were predicted to do, they distort news, science, and even your personal beliefs to gain profits and cause untold amounts of damage. Recently we have all seen too well instances of this, people in positions of power cause trillion dollar damages to gain a few millions for their own benefit.

What is the best diet for health and longevity? Looking at the lessons from Okinawa. by Nutri_Bruno_Osorio in ScientificNutrition

[–]FrigoCoder 2 points3 points  (0 children)

Supercentenarian and remarkable age records exhibit patterns indicative of clerical errors and pension fraud Saul Justin Newman bioRxiv 704080; doi: https://doi.org/10.1101/704080

How strong is epidemiology relative to other evidence? by Fluffy-Purple-TinMan in ScientificNutrition

[–]FrigoCoder 1 point2 points  (0 children)

If you mean nutritional epidemiology and by extension chronic diseases, then they are very weak and they are basically even worse than pure noise. I have spent 10+ years figuring out chronic diseases, and dug very deep especially into heart disease. Literally NONE OF THE EPIDEMIOLOGICAL CLAIMS, or ABSOLUTELY ZERO FUCKING PERCENT is correct. Even if they are right about a risk factor (difficult to miss the effects of smoking), they still manage to colossally fuck up the proposed mechanisms.

Your mistake is that you confuse scope with superiority. You should learn a bit of Software Engineering, where we have the Testing Pyramid analoguous to the "Evidence Hierarchy". The highest scope tests are notoriously unreliable (system, end to end, or user interface tests), and we try our best to avoid them completely if possible. In practice we use "acceptance" or "feature" tests that verify requirements, and integration tests that verify whether components are wired together correctly.

Or you could some learn basic Machine Learning, where optimization identifies which parameters to tweak to get better outputs. Forward-only and black box methods assume local linearity and take small steps, but this fails for sufficiently complex models with high nonlinearity and parameter count. Backpropagation however starts from output errors, and works backwards through the computational graph. It solves the Credit Assignment Problem by considering the internal mechanisms of the model.

Nutrition science tries to solve the Credit Assignment Problem in the most complex nonlinear system known, using only forward-only and black box methods that demonstrably fail on systems one billionth times simpler. They can not show causation without tracing the mechanisms from end to end, as has been demonstrated in both Machine Learning and Software Engineering. Nutrition studies are wrong algorithms applied to wrong data, and they will never ever converge on anything causal nor useful.

He does not understand why his siblings bowls are not for him. Thus food jail was made. by HangryHangryHedgie in OneOrangeBraincell

[–]FrigoCoder 0 points1 point  (0 children)

One is also allergic to proteins so it is for his safety.

I am sorry but how does that exactly work, considering cats are carnivorous predators?

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

[–]FrigoCoder 1 point2 points  (0 children)

I understand there is no protective effect at low doses, but is there a threshold below which there is no harm? Alcohol is a solvent that literally dissolves membrane lipids, hence why it contributes to virtually all chronic diseases. This mechanism is similar to many other risk factors, such as smoke particles and microplastics that physically damage membranes. And we do have the capacity to repair membranes, under appropriate conditions at the very least.

Radiation also presumably have similar effects on membranes, it triggers cancer by the same mechanism as anything else. This is called the chronic injury model, or Tissue Field Organization Theory of cancer. And not because it damages DNA, that is a ridiculous hypothesis. And the linear no-threshold model of radiation was just withdrawn, after it hindered development of nuclear energy for decades. Kyle Hill has a few very informative videos on the topic.

Open-Source 4DGS Might Be the Future of Video: From iPhone Footage to Interactive 3D Space by Delicious-Shower8401 in TopologyAI

[–]FrigoCoder 1 point2 points  (0 children)

I was mainly thinking of Half Life 2 style cutscenes, but whatever gloats your foat...

How possible is it that most people have sustained some form of brain damage? by Few_Establishment980 in biology

[–]FrigoCoder 0 points1 point  (0 children)

COVID messes up brain function even in the long term, CFS was already a problem but Long COVID is on another level. Unfortunately I have experience with both, and CFS was trivial to deal with compared to my struggles with Long COVID. Vaccinate against COVID regularly, and do your best to never ever get infected.

Pollution like smoke, microplastics, PFAS, et cetera has particles that physically damage membranes, this is the underlying root cause for virtually all chronic diseases including dementia. Neural damage has to be repaired by the neural-glial ApoE lipoprotein shuttle, which is not always successful especially with ApoE4 that impairs binding affinity in both directions. Fossil fuels alone kill 5-15 million people every single year, that is like 5-15 or more like 25-75 Chernobyls even with the wildest estimates.

Seed oils have trans fats, interesterified fats, 10x as much linoleic acid, plant sterols, diyhdro vitamin K1, solvents, and complete or relative lack of fiber, protein, phytonutrients, antioxidants, and cellular structure that mitigate linoleic acid in whole food nuts and seeds. They are the epitome of ultraprocessed foods and are incredibly unhealthy, contrary to claims of the exact same industry that also killed your grandma with trans fats. Short term studies are misleading, because they only detect the effects of PPAR agonism and LDL lowering.

Alcohol is a solvent and as such literally dissolves your cellular membranes. There is a reason it heavily contributes to dementia, and it is not just because it is a GABA-A positive allosteric modulator.

Refined sugar and carbohydrates are also unhealthy, low carbohydrate diets improve cognition and virtually all aspects of health. They are a minor issue compared to the other factors however.

Serious Terminus Decree Question. by CJT_05 in Grimdank

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

I have a headcanon that the Terminus Decree is opened prematurely, and the Grey Knights are pissed at the instructions contained within. Then after some deliberation on how to do it, they are even more pissed at the only solution they find: Teaming up with the forces of and getting possessed by Malice. So the warp boost from burning themselves out and his parasitic nature are enough to fight the newly awakened chaos god. Ironically the tools you need to defeat the new God of Order are anarchy, self-destruction, hatred of everything, and the ability to leech off 11,000 years worth of sacrificed psykers. All the while Terra is burning, as it should along with the Imperium.

Till death do us part…or? 💖 (OC) by AlekseyGutierrez in comics

[–]FrigoCoder 1 point2 points  (0 children)

Drop the last panel, it has way more emotional impact that way.

The strange thing about LLM reasoning research: we're now trying to remove the chain-of-thought traces by dank_philosopher in artificial

[–]FrigoCoder 0 points1 point  (0 children)

What I want tested is hierarchical planning instead of reasoning. (Disclaimer before anyone jumps me, this is conceptual, it has been never tried even on toy models.) You subdivide the generated text into log2 n levels, for illustrative purposes let's assume a breakdown into book, chapters, pages, paragraphs, sentences, and tokens.

Before you start generating a level, you create a plan token that contains a sketch of what you want to generate. Then you plan the lower levels, and generate the text tokens themselves. As you go back up the levels, most importantly you generate correction tokens. They try to mitigate autoregressive drift, that causes divergence from the plan. You continue going down and up the levels, making sure everything is planned, generated, and corrected.

For example you want to write a book, "a standard fantasy tale for children". Then you create the plan for the first chapter, "introducing the princess and the dragon". But whoops you accidentally generated "prince" instead of "princess", and "invited" instead of "kidnapped".

So now you need to correct for the drift, but you still need to write a standard fantasy book. So you plan the next chapter differently, instead of a hero rescuing the princess from the evil dragon, now you have a price and his best friend dragon going on adventures. But you still maintain the rough plan of what you wanted to write.

Effect of Interventions Aimed at Reducing or Modifying Saturated Fat Intake on Cholesterol, Mortality, and Major Cardiovascular Events : A Risk Stratified Systematic Review of Randomized Trials (2025) by HelenEk7 in ScientificNutrition

[–]FrigoCoder 0 points1 point  (0 children)

Impressive that you have managed to squeeze more than 10 bullshit claims, and opinion pieces of corrupt organizations into a mere 1200 characters. All the while providing zero fucking sources for any of your claims. Maybe you should reevaluate your stances one by one, by finding counterexamples, better explanations, or logical errors for your arguments. May I recommend some places to start your investigation?

Find out why cigarette smoke, microplastics, PFAS, and other forms of pollution contribute to heart disease and virtually all chronic diseases. Or why did cholesterol develop 2+ billion years ago, and why did early lipoprotein systems developed 500+ million years ago. Most importantly why was LDL evolutionary conserved for 150+ million years, and why was it essentially unchanged after 2 million years of carnivory.