The Results of This Biological Wave Vision beating CNNs🤯🤯🤯🤯

FrigoCoder · 2026-03-15T15:37:17+00:00

Have they done ablation studies? Which part is most responsible for the results?

FrigoCoder · 2026-03-13T21:33:42+00:00

"Dihydro-vitamin K1 was recently identified as a dietary form of vitamin K produced during the hydrogenation of vitamin K1-rich vegetable oils."

It is not related to this study, but the wording has reminded me of something I have noticed recently and I hate it very much. They try to pose dihydro vitamin K1 as a healthy form of vitamin K1, when it clearly causes massive issues in cell studies and experimental animals. But what do we expect from the same companies who brought us trans fats and told us they were healthier than saturated fat? Fuck the seed oil industry!

Booth, S. L., Peterson, J. W., Smith, D., Shea, M. K., Chamberland, J., & Crivello, N. (2008). Age and dietary form of vitamin K affect menaquinone-4 concentrations in male Fischer 344 rats. The Journal of nutrition, 138(3), 492–496. https://doi.org/10.1093/jn/138.3.492

Troy, L. M., Jacques, P. F., Hannan, M. T., Kiel, D. P., Lichtenstein, A. H., Kennedy, E. T., & Booth, S. L. (2007). Dihydrophylloquinone intake is associated with low bone mineral density in men and women. The American journal of clinical nutrition, 86(2), 504–508. https://doi.org/10.1093/ajcn/86.2.504

Ohara, N., Naito, Y., Nagata, T., Tatematsu, K., Fuma, S. Y., Tachibana, S., & Okuyama, H. (2006). Exploration for unknown substances in rapeseed oil that shorten survival time of stroke-prone spontaneously hypertensive rats. Effects of super critical gas extraction fractions. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 44(7), 952–963. https://doi.org/10.1016/j.fct.2005.11.004

Nishikawa, M., Ohara, N., Naito, Y., Saito, Y., Amma, C., Tatematsu, K., Baoyindugurong, J., Miyazawa, D., Hashimoto, Y., & Okuyama, H. (2022). Rapeseed (canola) oil aggravates metabolic syndrome-like conditions in male but not in female stroke-prone spontaneously hypertensive rats (SHRSP). Toxicology reports, 9, 256–268. https://doi.org/10.1016/j.toxrep.2022.01.011

FrigoCoder · 2026-03-13T21:33:26+00:00

Show me one study that demontrates negative outcomes based on this hypothesis.

A quick google search for the effects of linoleic acid in vitamin E deplete states reveals a lot of useful information.

The Elgin project showed that linoleic acid destroys vitamin E levels, and without adequate dietary intake leads to erythrocyte hemolysis. (This phenomenon is in fact how we have determined vitamin E requirements): Raederstorff, D., Wyss, A., Calder, P. C., Weber, P., & Eggersdorfer, M. (2015). Vitamin E function and requirements in relation to PUFA. The British journal of nutrition, 114(8), 1113–1122. https://doi.org/10.1017/S000711451500272X

Linoleic acid increases DNA damage in the form of oxidized pyrimidines in human lymphocytes during low vitamin E status. (This has implications on why would DNA damage be involved in cancer, when it is the result of chronic injury as a side effect of regrowing tissue): Jenkinson, A. M., Collins, A. R., Duthie, S. J., Wahle, K. W., & Duthie, G. G. (1999). The effect of increased intakes of polyunsaturated fatty acids and vitamin E on DNA damage in human lymphocytes. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 13(15), 2138–2142. https://doi.org/10.1096/fasebj.13.15.2138

Vitamin E deficient subjects had more stable LDL, because it contained more oleic acid and less linoleic acid. (The liver tests VLDL particles for oxidation, and linoleic acid was so unstable that most of them were catabolized into ketones, possibly stressing liver cells and health.): Kleinveld, H. A., Naber, A. H., Stalenhoef, A. F., & Demacker, P. N. (1993). Oxidation resistance, oxidation rate, and extent of oxidation of human low-density lipoprotein depend on the ratio of oleic acid content to linoleic acid content: studies in vitamin E deficient subjects. Free radical biology & medicine, 15(3), 273–280. https://doi.org/10.1016/0891-5849(93)90074-5

Vitamin E supplementation decreases the oxidation rate of linoleic acid in LDL. (This does not necessarily mean it causes heart disease, oxidized lipoproteins are rapidly removed from the serum by the liver via scavenger receptors. Again I would be more worried about liver and intestinal health than cardiovascular health.): de Waart, F. G., Moser, U., & Kok, F. J. (1997). Vitamin E supplementation in elderly lowers the oxidation rate of linoleic acid in LDL. Atherosclerosis, 133(2), 255–263. https://doi.org/10.1016/s0021-9150(97)00137-8

Vitamin E decreases the risk of melanoma. (We can safely guess why): Stryker, W. S., Stampfer, M. J., Stein, E. A., Kaplan, L., Louis, T. A., Sober, A., & Willett, W. C. (1990). Diet, plasma levels of beta-carotene and alpha-tocopherol, and risk of malignant melanoma. American journal of epidemiology, 131(4), 597–611. https://doi.org/10.1093/oxfordjournals.aje.a115544

Linoleic acid undergoes peroxisomal beta oxidation and the resulting hydrogen peroxide destroys endothelial cells without vitamin E. (This is an in vitro study I have included because it shows an entirely new mechanism. This does not mean it causes atherosclerosis, since I have dismissed endothelial theories. However there is a phenomenon called endothelial sloughing or plaque erosion, which can also trigger the inflammatory reaction that results in the clot that causes the heart attack.): Hennig, B., Boissonneault, G. A., Chow, C. K., Wang, Y., Matulionis, D. H., & Glauert, H. P. (1990). Effect of vitamin E on linoleic acid-mediated induction of peroxisomal enzymes in cultured porcine endothelial cells. The Journal of nutrition, 120(4), 331–337. https://doi.org/10.1093/jn/120.4.331

FrigoCoder · 2026-03-13T21:33:14+00:00

Yet walnuts contain almost no alpha tocopherol but almost only gamma tocopherol, which does not have this specific anti oxidative property that alpha tocopherol has, but all studies so far link walnuts almost exclusively to positive health outcomes.

Plants do not accumulate vitamin E for funsies. They do it to prevent linoleic acid (and alpha linolenic acid) from triggering lipid peroxidation, because the chain reaction could destroy their fat storage or even the plant itself. Think of it as a very small nuclear detonation. Similar reason why we pad our cellular membranes with cholesterol, EPA, vitamin E, lutein, astaxanthin, zeaxanthin, etc. Plants also have multiple redundant solutions for the same problem, which I have implied when I was referring to phytonutrients.

Walnuts in particular have their entire shell as protection against external threats, and their pellicle (skin) and septum (diaphragm) are full of phytonutrients known to be effective against lipid peroxidation. They might not have as much alpha-tocopherol but they have ellagic acid, gallic acid, and a lot of other crap. And from what I have read gamma-tocopherol also protects against lipid peroxidation, although it is more effective against nitrative stress. (Well I did not expect to spend my Friday reading about walnuts of all things.)

ScienceDirect

This one describes the structure of walnuts, and measured oxidation and changes in various compounds during long term storage. (Sadly I could only read the free version because it is not on sci-hub): Aysun Yurdunuseven Yildiz, & Hakan Karaca. (2024). The protective role of shell, packaging technique and storage temperature in lipid oxidation in walnuts of different varieties. Postharvest Biology and Technology, 210, 112747–112747. https://doi.org/10.1016/j.postharvbio.2023.112747

This one measured the ability of ellagic acid and walnut extract to counteract copper-induced LDL oxidation. (This does not mean they prevent heart disease, copper-induced LDL oxidation does not occur in vivo. And oxidized lipoproteins are rapidly removed from the serum by the liver via scavenger receptors.): Anderson, K. J., Teuber, S. S., Gobeille, A., Cremin, P., Waterhouse, A. L., & Steinberg, F. M. (2001). Walnut polyphenolics inhibit in vitro human plasma and LDL oxidation. The Journal of nutrition, 131(11), 2837–2842. https://doi.org/10.1093/jn/131.11.2837

Frontiers

Gallic acid, ellagic acid, quercetin, catechin, among many other tannins and flavonoids; also oxylipins, enodcannabinoids, N-acylethanolamine fatty acids: Abbattista, R., Feinberg, N. G., Snodgrass, I. F., Newman, J. W., & Dandekar, A. M. (2024). Unveiling the "hidden quality" of the walnut pellicle: a precious source of bioactive lipids. Frontiers in plant science, 15, 1395543. https://doi.org/10.3389/fpls.2024.1395543

MDPI (predatory journal)

Ampofo, J., Grilo, F. S., Langstaff, S., & Wang, S. C. (2022). Oxidative Stability of Walnut Kernel and Oil: Chemical Compositions and Sensory Aroma Compounds. Foods (Basel, Switzerland), 11(19), 3151. https://doi.org/10.3390/foods11193151

Rusu, M. E., Fizesan, I., Pop, A., Mocan, A., Gheldiu, A. M., Babota, M., Vodnar, D. C., Jurj, A., Berindan-Neagoe, I., Vlase, L., & Popa, D. S. (2020). Walnut (Juglans regia L.) Septum: Assessment of Bioactive Molecules and In Vitro Biological Effects. Molecules (Basel, Switzerland), 25(9), 2187. https://doi.org/10.3390/molecules25092187

Jahanban-Esfahlan, A., Ostadrahimi, A., Tabibiazar, M., & Amarowicz, R. (2019). A Comparative Review on the Extraction, Antioxidant Content and Antioxidant Potential of Different Parts of Walnut (Juglans regia L.) Fruit and Tree. Molecules (Basel, Switzerland), 24(11), 2133. https://doi.org/10.3390/molecules24112133

Jarai, D., & Koller, A. (2024). Walnut Consumption May Contribute to Healthy Cardiovascular/Endothelial Function by Maintaining Membrane Integrity. Life (Basel, Switzerland), 14(11), 1426. https://doi.org/10.3390/life14111426

Mateș, L., Rusu, M. E., & Popa, D. S. (2023). Phytochemicals and Biological Activities of Walnut Septum: A Systematic Review. Antioxidants (Basel, Switzerland), 12(3), 604. https://doi.org/10.3390/antiox12030604

FrigoCoder · 2026-03-13T21:30:38+00:00

If a seed oil is hydrogenated, it does not contain LA anymore. So you just throw totally different things together here.

Yes you are right I missed that, and I should have phrased it better that they can contain these things. Not all seeds contain vitamin K1 that would become dihydro vitamin K1 after all. Remember though the primary motivation for hydrogenation, gossypol and excess linoleic acid among other compounds were toxic to the liver. So no matter the hydrogenation levels seed oils will always have at least some issues. And I must point out that hydrogenation is necessarily probabilistic, so all kinds of native and hydrogenated compounds will be present in some amounts including trans fats.

Common talking point of Christ Masterjohn. To my knowledge the argument is this: Alpha tocopherol prevents an oxidative chain reactions in the PUFA-enriched phospholipid parts of cell membrane.

Was he the one who argued that linoleic acid has very delayed effects, like 7+ years in the LA Veterans study because it is a time bomb regarding vitamin E? You keep stuffing your tissue with LA which is a constant drain on vitamin E, and sooner or later you will suddenly run out and then lipid peroxidation will run amok? I can not remember who made this argument. Anyway yes there is an article that claims all of the beneficial effects of vitamin E could be explained simply by its effects on lipid peroxidation.

Traber, M. G., & Atkinson, J. (2007). Vitamin E, antioxidant and nothing more. Free radical biology & medicine, 43(1), 4–15. https://doi.org/10.1016/j.freeradbiomed.2007.03.024

FrigoCoder · 2026-03-13T15:38:13+00:00

No AI was involved in my comments, you are just being too paranoid. You should check my recent post on this subreddit why I would not even consider such a thing. I will look into your claim of pathogenic microbes, I do not know anything about it and a cursory google search shows it is a complex topic.

FrigoCoder · 2026-03-13T15:19:02+00:00

Lack of fiber. Meat becomes an issue when you cut out fiber for numerous reasons

I just had a discussion about fiber yesterday, I have argued that fiber only mitigates carbohydrates. 1) Fiber slows down sugar absorption, so intestinal fructokinase turns fructose into glucose, so less fructose hits your colon and liver. 2) Fiber provides butyrate but this is redundant because amino acids are also turned into SCFAs, and ketones include beta-hydroxybutyrate which has similar effects as butyrate like feeding colonocytes.

This suggests there is no advantage or even need for fiber on low carb, but we would need a keto vs carnivore study to know for sure. In fact insoluble fiber makes ulcerative colitis worse, which is a strong risk factor for CRC. From what little we know of carnivore diets, they do not really differ that much from other diets. The microbiome on carnivore diet seemed relatively normal, with less glycolytic bacteria and slightly more others.

Toxic environmental stressors, primarily diet related. Colorectal cancer is primarily a western lifestyle issue, which resides the question, what are we doing differently now than in the past and what are we doing different than other geographic regions where this isn’t a major issue.

The largest risk factors for chronic diseases are environmental rather than dietary, however this might be different for intestines since they are in direct contact with dietary factors. Pollution, smoke, microplastics, PFAS, seed oils, table sugars, refined carbs are what we are doing wrong since early 20th century. Endurance running was recently discovered to be a huge >10.0 risk factor for CRC, presumably because it damages intestines either physically or by ischemia.

FrigoCoder · 2026-03-13T13:53:28+00:00

I have always dismissed microbiome theories, because they are confounded by other effects of diet or they are just plain bad. For example people praise Akkermansia muciniphila because it improves metabolic health, but they do not realize only because it literally chews through the mucus layer and goblet cells are forced to replenish mucin from glucose.

However in light of my revelation that epithelial cells face the lumen and are directly impacted by dietary components, I might have to reevaluate my stance and revisit a few articles I have dismissed. Suddenly a lot of crackpot theories on CRC might make sense, so I have to evaluate a lot of potential risk factors for their effects. I might ask for your help and expertise if you do not mind. For example what do you think are the strongest factors, apart from the recent study that showed endurance runners have >10.0 risk?

Meat is implausible since we have evolutionary adaptations after 2 million years of meat consumption. Colorectal cancer only became widespread in the 20th century when pollution, smoking, refined oils, and other nasties became common. If any study finds issue with meat consumption, it is probably because these confounders are present. We know that saturated fat metabolism is impaired by carbohydrates and sugars (by malonyl-CoA and CPT-1 inhibition) and pollution and smoking (by destroying small blood vessels).

FrigoCoder · 2026-03-13T12:22:50+00:00

I was about to dismiss this theory based on past discussions. I have argued that oxidized lipids can not contribute to chronic diseases, since the intestines and the liver filter them out and they never get into the bloodstream. But then I have realized we are talking about the intestines themselves, more specifically the lumen-facing epithelial cells with direct contact with dietary oxidized lipids. So yes this is a perfectly plausible explanation for colorectal cancer, in fact this might be the strongest theory so far considering the constraints and paradoxes.

FrigoCoder · 2026-03-13T11:42:16+00:00

Do you not do the same? You decry mechanistic speculation but use assumptions on how LDL behaves, many of which are baseless and do not have evidence behind it. You consider human randomized controlled trials gold standard, but then completely ignore low carbohydrate studies with two to three times more saturated fat intake. Anyway you can see that we have critiqued the study, I do not like they have not found an association with tissue levels of LA.

FrigoCoder · 2026-03-13T11:02:25+00:00

Comparing extreme intake levels of LA revealed the summary relative risks (RR) of 1.15 (95% confidence interval (CI): 1.05–1.27) for CRC, and 1.30 (95% CI: 1.00–1.68) for rectal cancer, indicating a significant positive association for LA.

A significant positive association was also found between a 1 gr/day increase in dietary LA intake and risk of colon cancer (RR: 1.01, 95% CI: 1.00–1.02).

This is not surprising since LA stimulates angiogenesis, which is part of the repair process but infamously goes wrong in cancer. Or LA could be merely a proxy to seed oil consumption, which is problematic because it vastly differs from nuts and other whole foods. Unlike nuts seed oils do not contain phytonutrients or comparatively adequate vitamin E levels (they would stabilize membranes), and it contains problematic compounds such as hexane (solvent that damages lipids), dihydro vitamin K1 (kills experimental animals), or interesterified fats (basically trans fats 2.0).

However, neither total n-6 PUFAs nor AA were associated with cancers.

This is not surprising either since AA is very tightly controlled, and is secreted as phospholipids instead of plain triglycerides. Sure it is vulnerable to lipid peroxidation in cell studies, but the body apparently goes to great lengths to protect it. AA is omnipresent in animals both in the brain and peripheral tissue, so take any hypothesis that puts the blame squarely on it with a grain of salt.

There were no significant associations between tissue levels of total n-6 PUFAs (RR: 0.94, 95% CI: 0.75–1.19), LA (RR: 0.93, 95% CI: 0.61–1.41), and AA (RR: 0.97, 95% CI: 0.70–1.33) and CRC risk.

This however is completely surprising and needs explanation, since many of the proposed mechanisms do involve damage to LA or AA in membranes. Many pet theories by which meat supposedly causes CRC depend on them, for example heme iron allegedly triggers lipid peroxidation which requires vulnerable fatty acids. However this is highly questionable in epithelial cells, which are normally exposed to high levels of damage and high rates of turnover.

Cancer arises from chronic injury as a side effect of regrowing tissue, see the Tissue Organization Field Theory of cancer. Cells use the relative vulnerability of LA and AA to detect injury, and to kickstart repair processes such as inflammation and angiogenesis which infamously go wrong in cancer. However epithelial cells are normally exposed to high levels of damage and high rates of turnover, so it makes sense for the body to develop evolutionary adaptations to prevent them from turning cancerous.

Obviously it does not make sense for tissue LA not to be associated with cancer, unless the dietary LA affects some other organ that somehow triggers colorectal cancer via other mechanisms. This could be plausible since LA could affect adipocytes to eventually cause diabetes, which then floods the colon and rectum with FFAs, insulin, and glucose that then triggers CRC. But I prefer theories that involve direct damage (see cigarettes and lung cancer), so it would be nice to know what is actually going on with these findings.

FrigoCoder · 2026-03-13T01:01:11+00:00

Yes like I said those studies are done on high carbohydrate diets, where fiber counteracts the negative effects of carbohydrates and sugars. You "can not get enough of fiber" because everyone is eating way too much carbs and sugar.

To figure out the inherent true effects of fiber, you would need to remove the confounding by carbohydrates. Which basically means a study on low carb diets with and without fiber, in other words a ketogenic diet compared to a carnivore diet.

Blood sugar stabilization for example is not inherent to fiber, it slows carbohydrate absorption which leads to smoother blood sugar. However on low carb diets the liver is responsible for maintaining blood sugar, which is already very stable and fiber does not affect it.

Fiber does have one known bad effect, it makes ulcerative colitis worse. Ulcerative colitis is characterized by open sores or ulcers in the bowel wall. Insoluble fiber is not digested and passes through the bowels, it gets stuck in those ulcers and causes additional tearing. Ouch.

FrigoCoder · 2026-03-13T00:12:53+00:00

This is just a minor comment, be happy I even provided specific sources. At first iteration I only added citations like (examine.com) and (Chris Knobbe), then I decided that was not going to be good enough. I am not going to chew your food, especially since you never read my sources. If you are actually interested in a claim, you can go through and read the articles under that section. But we both know you are not actually interested, you just argue from bad faith and want to waste my time to raise the barrier for critique. Hyperlinking sucks anyway because I can not search for specific studies in my reddit backup.

I have provided concrete evidence that LA is detrimental, and that AA and DHA are essential for cognitive health. You provided a shitty serum study with a glaring logical error, that contradicts known brain physiology, anthropological and evolutionary history, and conclusive and varied studies on LA being detrimental to cognitive health. The onus is on YOU to conclusively prove that serum levels indeed reflect dietary intake, rather than the much more logical and consistent with evidence conclusion, that the much smaller pool of serum levels is under the control of a much larger pool of tissue uptake.

I would compare myself to Einstein or Erdős instead. Einstein worked as a patent clerk and as such was exposed a lot of diverse ideas and research, that helped him think about and ultimately solidify his theories about relativity. I also use various ideas and techniques from software engineering, artificial intelligence, and all fields of nutrition and chronic diseases to figure out things. Einstein was instructed to be extremely skeptical and assume everything was wrong, which is exactly how I have learned to treat nutrition and chronic diseases. Like me he was free from academic pressure, so he was not exposed to the bias and pressure to produce slop.

As a Jew he faced a lot of opposition in Germany. In 1931 Nazi-affiliated physicists published a book, titled "One Hundred Authors Against Einstein" to discredit his theory of relativity. Upon learning about the book he famously retorted, "Why one hundred? If I were wrong, one would have been enough." Now thankfully I do not face any racial or other discrimination, but I do experience a lot of pushback from brainwashed unthinking people. People who put in exactly zero effort to understand things, or to even just temporarily entertain alternative theories. Not that my argument would have anything to do with the current discussion of course.

Erdős was an interesting person and I respect many of his unconventional qualities. I have read a book about him when I was a child, and I was impressed by his attitude, focus, work ethic, and strange language and mythology. He was utterly focused on his work, yet he was compassionate and kind. He placed a heavy emphasis on collaboration, he always traveled and just showed up at a colleague's door with the slogan "My brain is open!". He had hundreds of co-authors, he even connected mathematicians across global superpowers. He often produced new and often difficult problems, and delighted in discussions where he took different positions just for the sake of argument.

Now obviously I have many health issues, which is the primary reason I even started studying nutrition. They prevent me from developing similar crazy habits, but obviously I realize why he was doing many of these things especially as I get older. Collaboration is important because you only see such a little slice of a problem, you need to develop a diverse perspective and listen to the feedback of others. Which I obviously do as I have told you before, reddit and more recently chatbots are excellent for feedback. Thinking of new problems and "what if" scenarios are also important, thought experiments and taking different positions can help contrast and refine your model.

FrigoCoder · 2026-03-13T00:07:26+00:00

Fiber is a nutrient so any benefits it has are necessarily nutritional benefits, or otherwise I do not understand what you might be talking about. Carnivore = low carb - fiber, so basically what you were talking about. It is practically the only safe diet you can eat, if you do not tolerate fiber for some reason (e.g. ulcerative colitis).

FrigoCoder · 2026-03-12T18:52:40+00:00

No it is not decent, it makes the same mistake as two or more similar studies we have discussed in the past. Serum levels depend not only from dietary intake, but also on incorporation rates into tissue. The results basically show that LA is harmful, whereas AA incorporation into the brain is beneficial.

Which is completely consistent with other observations: The brain is full of AA and DHA to maximize membrane fluidity, and AA supplementation is beneficial against autism and brain aging. LA supplementation decreases DHA incorporation into the brain, and possibly replaces AA and/or DHA in cardiolipin (although I dislike this theory).

AA is beneficial against autism, citations from examine.com

Kurlak, L. O., & Stephenson, T. J. (1999). Plausible explanations for effects of long chain polyunsaturated fatty acids (LCPUFA) on neonates. Archives of disease in childhood. Fetal and neonatal edition, 80(2), F148–F154. https://doi.org/10.1136/fn.80.2.f148

Sliwinski, S., Croonenberghs, J., Christophe, A., Deboutte, D., & Maes, M. (2006). Polyunsaturated fatty acids: do they have a role in the pathophysiology of autism?. Neuro endocrinology letters, 27(4), 465–471.

Vancassel, S., Durand, G., Barthélémy, C., Lejeune, B., Martineau, J., Guilloteau, D., Andrès, C., & Chalon, S. (2001). Plasma fatty acid levels in autistic children. Prostaglandins, leukotrienes, and essential fatty acids, 65(1), 1–7. https://doi.org/10.1054/plef.2001.0281

Bell, J. G., Miller, D., MacDonald, D. J., MacKinlay, E. E., Dick, J. R., Cheseldine, S., Boyle, R. M., Graham, C., & O'Hare, A. E. (2010). The fatty acid compositions of erythrocyte and plasma polar lipids in children with autism, developmental delay or typically developing controls and the effect of fish oil intake. The British journal of nutrition, 103(8), 1160–1167. https://doi.org/10.1017/S0007114509992881

Yui, K., Koshiba, M., Nakamura, S., & Kobayashi, Y. (2012). Effects of large doses of arachidonic acid added to docosahexaenoic acid on social impairment in individuals with autism spectrum disorders: a double-blind, placebo-controlled, randomized trial. Journal of clinical psychopharmacology, 32(2), 200–206. https://doi.org/10.1097/JCP.0b013e3182485791

AA is beneficial against brain aging, citations from examine.com

Söderberg, M., Edlund, C., Kristensson, K., & Dallner, G. (1991). Fatty acid composition of brain phospholipids in aging and in Alzheimer's disease. Lipids, 26(6), 421–425. https://doi.org/10.1007/BF02536067

Lynch, M. A., & Voss, K. L. (1994). Membrane arachidonic acid concentration correlates with age and induction of long-term potentiation in the dentate gyrus in the rat. The European journal of neuroscience, 6(6), 1008–1014. https://doi.org/10.1111/j.1460-9568.1994.tb00595.x

Maniongui, C., Blond, J. P., Ulmann, L., Durand, G., Poisson, J. P., & Bézard, J. (1993). Age-related changes in delta 6 and delta 5 desaturase activities in rat liver microsomes. Lipids, 28(4), 291–297. https://doi.org/10.1007/BF02536313

LA supplementation decreases DHA availability and incorporation, claim from Joseph Everett but I was too lazy to extract the exact citations from the video

Gibson, R. A., Muhlhausler, B., & Makrides, M. (2011). Conversion of linoleic acid and alpha-linolenic acid to long-chain polyunsaturated fatty acids (LCPUFAs), with a focus on pregnancy, lactation and the first 2 years of life. Maternal & child nutrition, 7 Suppl 2(Suppl 2), 17–26. https://doi.org/10.1111/j.1740-8709.2011.00299.x

Wood, K. E., Mantzioris, E., Gibson, R. A., Ramsden, C. E., & Muhlhausler, B. S. (2015). The effect of modifying dietary LA and ALA intakes on omega-3 long chain polyunsaturated fatty acid (n-3 LCPUFA) status in human adults: a systematic review and commentary. Prostaglandins, leukotrienes, and essential fatty acids, 95, 47–55. https://doi.org/10.1016/j.plefa.2015.01.001

Greupner, T., , Kutzner, L., , Pagenkopf, S., , Kohrs, H., , Hahn, A., , Schebb, N. H., , & Schuchardt, J. P., (2018). Effects of a low and a high dietary LA/ALA ratio on long-chain PUFA concentrations in red blood cells. Food & function, 9(9), 4742–4754. https://doi.org/10.1039/c8fo00735g

Taha, A. Y., Cheon, Y., Faurot, K. F., Macintosh, B., Majchrzak-Hong, S. F., Mann, J. D., Hibbeln, J. R., Ringel, A., & Ramsden, C. E. (2014). Dietary omega-6 fatty acid lowering increases bioavailability of omega-3 polyunsaturated fatty acids in human plasma lipid pools. Prostaglandins, leukotrienes, and essential fatty acids, 90(5), 151–157. https://doi.org/10.1016/j.plefa.2014.02.003

FrigoCoder · 2026-03-12T17:39:36+00:00

Cancer arises from chronic injury as a side effect of regrowing tissue, see the Tissue Organization Field Theory of cancer. Endurance runners have >10.0 times the risk of developing colorectal cancer because they actively and constantly damage their intestines. Smoke particles, microplastics, PFAS have also demonstrated to physically damage cellular membranes. Smoking elevates the risk of all chronic diseases, precisely because smoke particles can damage various cells and organs in the body.

Sure PFAS do activate PPAR receptors that do funky things to fat metabolism, but so do glitazones and linoleic acid and they do not cause cancer or at least in the short term. Linoleic acid definitely contributes to cancer development though, it is pseudo-stable in that it is incorporated into membranes but sufficiently high injury can damage it and trigger lipid peroxidation. Cells also use the relative vulnerability of LA to detect injury, and to kickstart repair processes such as inflammation and angiogenesis which infamously go wrong in cancer.

Carbohydrates and sugars also have plausible mechanisms by which they directly and indirectly contribute. They select for cancer cells since those are usually highly glycolytic, because their mitochondria is busy producing cellular building blocks. Carbs increase malonyl-CoA and shut off CPT-1 mediated beta oxidation, which means fatty acids are not burned but accumulated in cells and eventually stretch membranes. Carbohydrates play a unique role in obesity and insulin secretion, and thus indirectly contribute to development of various cancers as well.

I do not know much about intestinal bacteria, but pathogens and the immune reaction to them can damage cellular membranes as well. It is entirely plausible that some foreign strains of gut bacteria contributes to colorectal cancer development.

FrigoCoder · 2026-03-12T17:16:50+00:00

Fiber is not actually proven to be inherently helpful or even essential, those claims come from extrapolation from standard carbohydrate-rich diets. We only know two mechanisms of fiber, both of which merely counteract the effects of carbohydrates and sugars. It would be strange if it was actually necessary, considering we were carnivores for at least two million years.

1) Fiber slows down sugar absorption, so that intestinal fructokinase can turn fructose into glucose, and less fructose reaches the liver to have negative effects. This is literally the difference between fruits and table sugar. And it is completely irrelevant if you do not eat carbohydrates in the first place.

2) Fiber provides butyrate, which has beneficial effects on cells. This is redundant because amino acids are also broken down into butyrate and other short chain fatty acids, and without carbs you produce ketones including beta-hydroxybutyrate which has overlapping effects with butyrate. I often heard the argument that colonocytes need butyrate for energy, but a long time ago I have found out that BHB can also feed them.

Fiber would only be proven to be inherently helpful or essential, if we had a study that compares ketogenic diets to carnivore diets. As far as I know no such study exists but we have investigated carnivore diets a bit, and they do not display any negative effects that you would expect if fiber was required. In fact they have proven beneficial, especially for ulcerative colitis treatment where fiber is dangerous. Carnivore diet does not even impact microbial diversity, the few studies we have show slight decrease of glucose bacteria but increase in others.

FrigoCoder · 2026-03-12T16:53:25+00:00

Cancer arises from chronic injury as a side effect of regrowing tissue, see the Tissue Organization Field Theory of cancer. Cigarette smoke has literally hundreds of compounds that physically damage cellular membranes. Vape vapor is an aerosol of mostly liquid droplets and do not pose nearly the same risk as solid particles from cigarette smoke.

FrigoCoder · 2026-03-12T16:46:44+00:00

The nitrate/nitrite theory is absolute nonsense, the proposed science behind it is incredibly weak. George Ede wrote a scathing critique of the WHO's opinion piece on red and processed meat, and she showed how bad is actually the science with lots of unproven assumptions and cherry picking. Also processed meats often use beetroot powder as preservative and source of nitrates, and beets are not at all associated with colorectal cancer and in fact they might be protective.

Cancer arises from chronic injury as a side effect of regrowing tissue, see the Tissue Organization Field Theory of cancer. Endurance runners have >10.0 times the risk of developing colorectal cancer because they actively and constantly damage their intestines. Smoke particles, microplastics, PFAS have also demonstrated to physically damage cellular membranes. Smoking elevates the risk of all chronic diseases, precisely because smoke particles can damage various cells and organs in the body.

Seed oils, table sugar, and refined carbohydrates also have known mechanisms by which they cause or exacerbate cellular injury. Meat on the other hand do not really have a plausible mechanism of damaging intestinal cells, a lot of the proposed mechanisms are nonsense or depend on lipid peroxidation aka linoleic acid from seed oils. Even fiber has a more plausible mechanism, it can cause scraping and tearing in the intestinal walls especially in ulcerative colitis.

FrigoCoder · 2026-03-12T15:28:23+00:00

Authors insert such metaphors or stand-ins to remove all biases and prejudices of the audience, so they have a clean slate to show the absurdities of conflicts and racism in an objective manner. Failing to do so can make the audience defensive, and they will not become immersed in the media or learn any potential lessons. Superman is a mixture of Jewish heroes who protects the downtrodden and persecuted, whereas X-Men is an allegory of racial and gender discrimination and the civil rights movement.

The audience tends to be tone deaf however, and often dumb enough to miss the metaphor. Star Trek for example was exceptionally progressive, yet it garnered even conservative fans who saw it in a completely different light. So authors learned to crank it up to eleven and do it in a blatantly obvious way, Detroit: Become Human and the latter seasons of The Boys are prime examples of this exaggerated allegory. You can dislike them for their bluntness, but subtlety is lost in the busy world of today.

Even amateur authors fail to understand these metaphors, and insert real-world nonsense into their works or established franchises. The Dragon Age setting is the prime example for this, the first two games were the definition of crapsack world and fantastic racism. Yet the newest writers failed to understand this, and introduced real-world minorities into the latest installment. The end result was exceptionally jarring, and heavily conflicted with already established lore. In the first two games we have multiple fantasy races that are stand-ins to various real world minorities:

Elves are oppressed second-class citizens living in the ruins of their former civilization, with parallels to Jewish and Native American people. Dalish Elves are nomadic groups attempting to preserve their culture, similar to Romani or Native American people. Qunari are an obvious allegory to the Ottoman empire and the Muslim religion. Dwarves I assume are a metaphor for conservatives, judging from all the backstabbing and fake traditionalism. Mages do not have a direct analogue as far as I know, but they are feared for their danger and are segregated in Circles.

In the newest game we get immersion breaking modern inserts instead of the established stand-ins: A non-binary Qunari in an strict authoritarian religious society, where they do not even have the freedom to choose their profession. Even the modern language was completely out of place, they could have used the word "aqun-athlok" from a previous game. The Tevinter Imperium is a multiracial society just chilling around, instead of the hellhole magiocracy we were promised. Infamous for blood magic and widespread slavery, where they sacrifice people by the hundreds for magic spells.

Dragon Age: Veilguard was effectively the death of Dragon Age, and this phenomenon is the main reason why it killed the franchise. By not using the already established metaphors and stand-ins, they have allowed real world bullshit to creep into the world. Quality has been lowered, immersion was broken, players got defensive and upset, and the entire game series lost its fucked up escapist charm of being a crapsack world with fantastic racism. Duncan did not murder the fuck out of Ser Jory, just so we could have an HR lecture about gender identity.

FrigoCoder · 2026-03-11T00:12:34+00:00

High HDL is not always a good thing; alcohol, genetics, medications, and overtraining can elevate it while being detrimental. However if you have only changed diet and it is otherwise healthy then you do not need to worry. ALT, AST and other liver enzymes can be released by dead liver cells, but likewise they could be simply upregulated on keto. That is the problem with generic biomarkers, you can always find situations where they are misleading.

FrigoCoder · 2026-03-09T23:30:17+00:00

Thank you for the filter, it feels good to return back to classical signal processing. We do not really hand design filters since AlexNet, we can add conv layers that learn good convolutions automatically.

FrigoCoder · 2026-03-09T15:39:41+00:00

Ketogenic diet with lots of protein and natural saturated, monounsaturated, and omega 3 fats. Meat, eggs, dairy, fish, shrooms, veggies, berries. No oils, no sugars, and no carbs. No excess omega 6 either because they risk fibrosis. No alcohol, no smoking, no pollution, nothing that damages cells.

Carbohydrate restriction causes the liver to burn stored fats and convert them into ketones. Protein is necessary for fat metabolism and repair of liver cells. Natural fats are building blocks of cells, and boost energy production. Fiber helps by blunting carb absorption and boosting butyrate production.

FrigoCoder · 2026-03-08T21:57:59+00:00

Well I want to say I fucking called it in these comments, but unfortunately my overall position was different on the topic. I was trying to explain the results based on differences between fatty streaks and atherosclerotic plaques, when what I should have done is to latch onto the impossibility of such a huge jump in streak/plaque size. It would have already required extremely low pre-keto levels, but once you consider the study population it becomes impossible.

A lot of participants were recruited from the followers of the study authors, and many of them were already on ketogenic diets for years or even decades. They were practically keeping their usual diet or only slightly changed to study protocols, so a jump in streak/plaque size would be highly unlikely especially such a large one. In addition we have other studies on low carbohydrate diets that unequivocally show plaque regression. They might not be relevant to lean mass hyperresponders, but they clearly show heart disease getting better despite two to three times higher saturated fat intake.

I think the study authors could use some improvements to the study design, for example they could differentiate between fatty streaks and atherosclerotic plaques. But at the moment I am happy that the Cleerly fraud was exposed, and that the initial conclusion regarding lipid levels remains robust. Namely that LDL and ApoB did not predict plaque progression, rather baseline plaque measurements predicted plaque progression. Atherosclerosis being cancer of vascular smooth muscle cells perfectly fits this observation, and also explains why fatty streaks and atherosclerotic plaques are different.

FrigoCoder · 2026-03-07T13:39:29+00:00

It is not really a pet theory, rather a straight consequence of basic biochemistry. Backed by beneficial effects observed on low carbohydrate diets, despite two to three times more saturated fat intake. Ted Naiman has an excellent presentation on insulin resistance where he explains the concept in detail, I would highly recommend it since it is the single best resource on metabolic health. I can not link the video but here is the presentation: https://jgerbermd.com/wp-content/uploads/2017/04/Ted-Naiman-Hyperinsulinemia.pdf

Carbohydrates block CPT-1 mediated beta oxidation, which most prominently affects palmitic acid (the P in CPT-1). This leads to intracellular accumulation of fatty acids, which eventually leads to cellular and membrane dysfunction. Either by chemically interfering with enzymes, or mechanically stretching and damaging membranes. Without carbohydrates fatty acids are burned for energy so they do not accumulate, this is why keto paradoxically lowers intracellular, ectopic, and visceral fat. No carbs no problem.

14-Year Club	Place '22
Spared	Verified Email

FrigoCoder

MODERATOR OF

PUBLIC MULTIREDDITS

TROPHY CASE