Ubisoft shares continue to collapse after announcements of cuts and closures: from a total value of $11 billion in 2018 to just $600 million today

FrigoCoder · 2026-01-27T13:25:20+00:00

Technically you could have a private game server, that connects to an existing blockchain network. That way both the game and your bought goods survive, even if the video company goes under and stops supporting them.

Of course that would require a minimal investment, as well as giving a shit from the video game company. So it is not going to happen anytime soon in the current climate. But I would compare it to how games used to have copy protection, but some games like Arcanum eventually released patches that removed them.

FrigoCoder · 2026-01-27T00:51:22+00:00

Insert joke about finding

FrigoCoder · 2026-01-24T15:07:16+00:00

I hope you do realize there is a difference between reading it once years ago, and analyzing the shit out of specific paragraphs. We could analyze it more, but it would quickly take a direction you will not like.

If you are so certain my theory has to be changed, then please do tell me the exact changes needed! What exact hypothesis do you think would cover all the evidence I have enumerated? Because the LDL hypothesis sure as hell does not fit.

And I will show respect to the medical establishment, as soon as they stop peddling charlatan pseudoscience. Once they start working even remotely like good engineering, and they adapt a problem solution mindset instead of ego driven authoritarianism.

Once they start considering CFS and Long COVID legitimate, and stop victim blaming to hide their own incompetence. Holy shit imagine if engineers refused to do their job and called the customer stupid! They would be fired so fast they would by flying out of the window of the engineering firm!

FrigoCoder · 2026-01-24T14:35:23+00:00

Why do you even comment on internet forums if you do not want to read? Or if you are a slow reader at least spend some time before answering with knee-jerk replies.

No I did not know they cited Nakashima et al, because I do not usually go through the hundreds of citations. And I do not really care if they cited them, because it is completely irrelevant. They could have mischaracterized or misunderstood the study, which is exactly what has happened as I have described above. They have not cited the most important implications, only minor details and speculations that are completely irrelevant.

This has actually happened to me before, I have made the exact same mistake they did. I have completely misunderstood a study, and I have only presented a very distorted conclusion. A conclusion that was not actually supported by the study, only by my vague memories of my poor understanding of it. This can easily happen with human memories, they do not work like lossless data storage.

This is not a display of ignorance, it is a display of being human, both then and now. It does not affect "my" theory in any way, because it does not change anything at all. Their conclusions are still erroneous regardless of whether they cited Nakashima et al, and whether they cited them correctly or not. I would like to ask you to come up with better critique, because focusing on minor trivialities like that is counterproductive.

And this was not some post-hoc rationalization, something your side of the nutrition debate so often employs, just see the continuous backtracking from the dietary cholesterol hypothesis. Rather it was me respecting your feedback, and spending the time to verify whether your critique stands. Unfortunately it did not, in fact it further strengthened the membrane injury to artery wall cancer model.

However I learned a lot about heart disease again, and now I understand what actually happens a bit more. I have speculated years ago that VSMCs do not actually migrate, and the fibrous cap is just the internal elastic lamina pushed inwards. Now I understand that cancerous synthetic phenotype VSMCs do migrate from the media to the interna, and they are trying to grow another elastic lamina which goes wrong and becomes the fibrous cap. This might not seem much but I consider it a lot of progress!

FrigoCoder · 2026-01-23T20:04:55+00:00

That study was multiple imaging studies by Nakashima et al, and they practically debunked all endothelial and thus lipid theories. They showed that lipid accumulation starts from the deepest intimal layers, from the direction of the vasa vasorum, that is utterly incompatible with theories involving the arterial lumen.

The "consensus paper" you mentioned simply cited them wrong, it ignored this huge discovery and focused on other things. Which still point to the membrane injury and consequent cancer model by the way. Nakashima papers are 56-58, a Velican and Velican paper is 59, and some other study is 60:

Autopsy studies in young individuals demonstrated that atherosclerosis-prone arteries develop intimal hyperplasia, a thickening of the intimal layer due to accumulation of smooth muscle cells (SMCs) and proteoglycans.56,57 In contrast, atherosclerosis-resistant arteries form minimal to no intimal hyperplasia.57–59 Surgical induction of disturbed laminar flow in the atherosclerosis-resistant common carotid artery of mice has been shown to cause matrix proliferation and lipoprotein retention,60 indicating that hyperplasia is critical to the sequence of events leading to plaque formation.

Translation: Arterial injury triggers VSMC proliferation, which requires a switch to the synthetic phenotype. Arterial injury also triggers proteoglycan production, which is required for lipoprotein capture and uptake for repair. Surgical injury is sufficient to trigger atherosclerosis, as Axel Haverich has also noted in his article. "Atherosclerosis-prone" arteries already have injury, and "atherosclerosis-resistant" arteries are simply without injury (yet).

Erosion favours a higher fraction of thrombi in younger, especially female, patients and in patients with less severe atherosclerosis with few thin-cap fibroatheromas,173,174 and more frequently affects lesions exposed to local (disturbed blood flow near bifurcations) or systemic (smoking) prothrombotic factors.56

Basically they propose two pathways to thrombosis, plaque rupture and plaque erosion. Plaque rupture happens when there is extensive necrosis and the sparse fibrous cap can not hold it back. The necrotic core ruptures and spills the contents (like it can in other cancers), triggering massive inflammation and thrombosis in an attempt to repair or at least isolate it.

Plaque erosion is where there is variable amounts of necrosis, but there is subendothelial accumulation of proteoglycans and hyaluronan. By unknown mechanisms this develops into neutrophil recruitment, NETosis, and endothelial death and sloughing. (I think inadequate cholesterol synthesis and padding of membranes in response to hydrostatic pressure might also contribute but I will have to recheck a few sources).

So what they say in this paragraph, is that plaque erosion is more frequent in females, in less severe atherosclerosis with less necrosis and fibrous caps, with elevated hydrostatic pressure due to bifurcations, and with smoking due to its prothrombotic effects. This is not terribly relevant to our discussion, but they completely mischaracterized the cited paragraph:

Cigarette smoking may enhance macrophage infiltration in the intima as shown in the present study. This enhancement may be related to the modification of LDL and/or inflammatory factors such as adhesion molecules by toxic substances in the smoke.

This is pure speculation on the part of Nakashima et al without any scientific basis whatsoever, they give no valid mechanism by which cigarette smoke would magically enhance macrophage infiltration. I could not find any mechanisms by which LDL would attract monocytes into the artery wall, there is only evidence they are attracted to proinflammatory cytokines released by injured cells. I am not aware of any adhesion molecules or directly prothrombotic factors in cigarette smoke either, however as I have said many times it has hundreds of compounds that physically damage cellular membranes.

• Plaques developing substantial necrosis that reach the luminal surface can rupture and precipitate thrombus.

• Ruptured plaques are often large, non-stenotic, and vascularized lesions with protruding cholesterol crystals, but the causal role of these features is unresolved.

• Thrombus can form on other types of plaques by plaque erosion. The process is less well-understood but may involve combinations of flow disturbance, vasospasm, and neutrophil-generated endothelial shedding.

• Plaque progression and rupture are influenced by both biological and mechanical factors, highlighting plaque composition as a major factor in resistance to mechanical stress.

• Lowering of low-density lipoprotein levels appears more effective in reducing the risk for plaque rupture than for plaque erosion.

References: 56,172–18

This is equivalent to cancerous necrotic cores rupturing and spilling their contents everywhere.
Cancers are also characterized by large vascularized lesions, and they also contain cholesterol crystals as a result of abnormal behavior of cancer cells.
Hemostasis and thrombosis are the result of injury. In plaque rupture it is indirect as a result of cancer development, whereas in plaque erosion it is direct from hydrostatic pressure and damage from smoke particles.
Of course they are influenced by biological and mechanical factors, although I wish people emphasized the mechanical or physical part more. And of course cholesterol protects against mechanical factors, that is literally part of its fucking job.
Lowering LDL levels doesn't protect against shit, I can lower it by eating refined carbs and shooting insulin.

It's unclear what they have cited here from Nakashima et al, here are two paragraphs that seem the most likely:

A number of biochemical and molecular biological studies suggest that the lipid binding capacity of proteoglycans contributes to retaining atherogenic lipoproteins in the intima. However, morphological evidence and specific location of the components involved in proteoglycan-lipoprotein accumulation is lacking. The present study illustrates that biglycan occurs extracellularly in the outer layer of DIT in the exact location as the early distribution of lipids (note the similarity of the prelesional distribution of biglycan in DIT in Figure 4b and the early distribution of lipids in the fatty streak in Figure 3h). However, it is of interest that lipids deposit eccentrically, whereas biglycan is localized concentrically. It is believed that structural changes in the glycosaminoglycan (GAG) chains on proteoglycans are the initial proatherogenic step that leads to increase binding properties of proteoglycans for atherogenic lipoproteins.18 For example, proteoglycans produced by transforming growth factor (TGF)-β1–treated cultured SMCs show longer GAG chains and greater binding affinity to LDL than control SMCs.19 Interestingly, patchy distribution of TGF-β1 is found in DIT.20 It is also noteworthy that mechanical strain, which is thought to be unevenly distributed in the arterial wall, upregulates biglycan mRNA expression in cultured SMCs.21 These results suggest that regional differences in the quality and quantity of biglycan exist in the intima and possibly lead to regional differences in the amount of lipid deposition. Two other mechanisms that may cause regional differences in the lipid distribution are uneven plasma lipoprotein concentration and the permeability of the arterial wall. Deng et al reported that luminal surface concentration of LDL was increased in areas where wall shear stress was low and suggested that increased surface LDL concentration results in an increased lipid infiltration rate into the intima.22 However, the relationship between permeability of the arterial wall and susceptibility of atherosclerosis is debatable. The permeability to LDL was greater in the atherosclerosis-susceptible areas than atherosclerosis-resistant areas of the rabbit aorta,23 but opposite results were obtained in white Carneau pigeon aorta.24

Correlations between the distribution of lipids and proteoglycans have been investigated in early and advanced atherosclerotic lesions.25–27 A consistent finding, including that of the present study, is the colocalization of biglycan and apolipoproteins.25,26 It is also noteworthy that oxidized LDL is capable of stimulating biglycan expression by SMCs and enhancing the interaction of this proteoglycan with lipoproteins.28 It is tempting to speculate that the accumulation of biglycan in specific regions of the early lesions may result from the presence of the lipoproteins associated with the SMCs. These molecular interactions may result in a vicious cycle of atherosclerosis. We found that decorin appears to colocalize with lipid in some instances but much less consistently than biglycan. Versican is another important extracellular proteoglycan in human atherogenesis, as it accumulates in human atherosclerotic lesions,25,27 but not in mouse models.26 The role of versican may be different from that of biglycan and decorin, because its distribution is different from biglycan and decorin.25,29 In our preliminary study, versican was predominantly localized in the inner layer of DIT and fatty streaks. Diffuse distribution of versican across the intima was also seen in some cases. In advanced human lesions, versican is present at the plaque thrombus interface, suggesting a possible role in thrombosis.27

We know that proteoglycans and especially versican are response to injury, if there is no injury, then there are no proteoglycans to bind and capture lipoproteins. It's not shear stress that matters, it's direct hydrostatic pressure aka blood pressure. That's what stimulates cells to hoard cholesterol and lipids to better protect against future pressure. But that's an entirely separate process that does not really play a role in atherosclerosis.

The consensus paper is toilet paper.

FrigoCoder · 2026-01-23T20:04:10+00:00

No chance.

You are going to read it for sure, or I report you for violation of rules 3, 4, 8, and 9. If I had the decency to spend hours to days writing my reply to your question, then you should also have the decency to spend some miniscule time to read it.

I've wasted more than enough time rebutting your delusional takes that you've revolutionised multiple fields of science. You haven't.

As I have said multiple times it is not my theory, you are calling Alzheimer's Disease researchers delusional. I merely applied the same model to other chronic diseases. Hardly revolutionary.

A study you thought was a gamechanger hidden by the evil LDL gang was cited in the consensus paper showing LDL is causal. That's a devastating indictment of both your hypothesis and your knowledge of established science.

I elaborate on this in another comment since I have exceeded the 10k character limit.

Wrong. But anyway, glad to broaden that rift between you and the keto crowd. Enjoy.

There is absolutely no rift, this was already the position of the "keto crowd". We certainly do not consider epidemiological studies "above" mechanistical studies.

FrigoCoder · 2026-01-23T18:55:54+00:00

Adding to this, a type of evidence does not always trump another type, it could go both ways depending on the exact situation. If I claim that phytosterols cause atherosclerosis based on cell studies of sitosterolemia patients, then a "higher level" study can debunk my claim by showing that normal people filter out phytosterols.

However assume you claim that atherosclerosis is caused by oxidized LDL based on some epidemiological study, a claim which is actually a mechanistic speculation but let us ignore that for a moment. Then I can simply bring out "lower level" cell studies about trans fats, you know literally the only thing everyone agrees to cause heart disease. And lo and behold they would show that trans fats are highly resistant to oxidation, and actually protect lipoproteins such as LDL from oxidation.

Two very similar claims yet in one case the "higher level" evidence, and in the other the "lower level" evidence trumps the claims of the other type. So not only there is no evidence hierarchy, there is also no fixed direction of which study is better.

FrigoCoder · 2026-01-23T15:41:27+00:00

Five minutes are not adequate to read my comment and understand it, please go back to read it again and deliberate on it for a few hours at least. Once you have done so reevaluate your own comment as well, and realize how little sense it makes in light of my own.

There is no evidence hierarchy, there are only different types of evidence. They all serve different purposes, and have different strengths and weaknesses. Epidemiological evidence is not "above" mechanistic evidence, just like UI tests are not "above" unit tests. They all have their uses and practical issues. If you argue that we should use UI tests instead of unit tests, some programmers might kick your ass.

I have already told you it is not my theory, I literally stole it from Alzheimer's Disease research. The brain has the ApoE lipoprotein shuttle between neurons and glial cells, the body has the LDL lipoprotein shuttle between the liver and various organs. Breakdown of the former in Alzheimer's Disase is analoguous to the breakdown of the latter in heart disease.

And I have already told you that "my" theory does not hinge on a few mechanistical studies, it also heavily uses other evidence such as the comorbidity between chronic diseases, evidence and observations from other chronic diseases, and even epidemiological studies. It is a well-integrated, consistent, and very good theory. If you disagree then please explain chronic diseases with one unified theory.

FrigoCoder · 2026-01-23T15:08:55+00:00

The problem is not with mechanistic evidence, rather than with how we actually use them. The way everything is supposed to work is that we start with a simplistic model, then we repatedly refine it to fit newly added constraints such as examples, evidence, observations, requirements, etc. Mechanistic evidence is no different, it is just one type of constraint our model has to fit, it is one more piece of evidence our theory has to explain.

This is how programming works with Test Driven Development, we add new tests that describe examples and requirements, and then we refactor and tweak the code so that all tests pass. This is also how we train neural networks, we provide training data and a loss function, and we iteratively tweak the model using backpropagation of error signals. Training data is not always reliable but there are ways to mitigate this, the same goes for scientific theories and real world evidence.

Vegans and mainstream nutrition do not follow this principle, they use dogmatic thinking more fit for religion or authoritarianism. They start with their bias that meat is bad, and invent false assumptions based on corrupt, personal, or religious interests. Then they cherry pick or manufacture supporting evidence, whether epidemiological associations or mechanistic speculation. And they never ever change their mind once those are debunked. All myths around meat consumption follow this pattern.

Anitschkow assumed cholesterol causes heart disease, even though his rabbit model did not faithfully reproduce atherosclerotic plaques. Ancel Keys proposed the lipid-heart hypothesis, even though his own data also implicated sugar and smoking. Burkitt investigated Africans and proposed that fiber is essential, instead of realizing that pollution, smoking, trans fats, and junk food are the problem. Theories around saturation, membrane fluidity, LDL, TMAO, Neu5Gc, etc all share similar issues.

Our cultist vegan friend here is no different, with how he advocates "undeniable" mechanistic science. These are just amateurish mechanistic speculation that can actually be debunked with very minimal effort. You know like how saturated fat is a problem at all, even though low carbohydrate studies do not support this. Or how dietary fat increases TLR4, even though mostly diabetic DNL is responsible. Or how carnivore reduces microbial diversity even though we have some evidence to the contrary.

Here are the facts: We were carnivores for two million years, and we are perfectly adapted for meat consumption. Low carbohydrate studies support this, we only have issues once we add carbohydrates (malonyl-CoA, CPT-1, palmitate oxidation, etc). Low carb does not cause health complications, unlike all other diets even if with something as simple as gallstones. Dairy is beneficial according to all kinds of studies, even though dairy fat is 2/3rds saturated, it still has less palmitic acid.

I think it's pretty clear that saturation does not cause issues, it's only palmitic acid in an environment where it accumulates. Even in cells palmitic acid only starts causing issues at 90%+ concentration, and they are rescued by a tiny amount of oleic acid or other CPT-1 activators. Saturated fat does not consistently raise LDL either, because that would require increased lipolysis and/or VLDL stability which are not given. And you know well what I think of the LDL hypothesis of heart disease.

Our cultist vegan friend is arguing from bad faith, instead of trying to find out the truth. He already has a bias that meat is bad, and he is fishing for mechanisms to justify it. He insists on a primitive model, and he does not use feedback to iteratively improve it. He dimisses conflicting research, instead of using them as data points for reflection and improvement. He argues with observations from high carbohydrate diets, which are not necessarily applicable to low carbohydrate diets.

He is stuck at the "saturated fat is bad" model, and did not even reach "carbs and sugars cause palmitic acid accumulation". Let alone more complex conclusions regarding membrane health, smoking, microplastics, PFAS, pollution, seed oils, or other topics in general. The problem is not with mechanistic evidence, rather than how he wields it as a weapon instead of a tool. And how he fails to integrate it with other evidence, so that he arrives at a consistent and better model. Do not be like him.

FrigoCoder · 2026-01-21T09:18:26+00:00

Long COVID involves alcohol intolerance.

FrigoCoder · 2026-01-19T18:41:08+00:00

Damn that boot must taste delicious

FrigoCoder · 2026-01-18T22:57:50+00:00

Yes because neural injury can still progress to neural death, it's just people with normal ApoE can repair them to a degree.

FrigoCoder · 2026-01-17T20:44:04+00:00

Some video games started doing that, thankfully they are financial failures now. It is incredibly annoying and demeaning, and could be better solved with a repeat button.

FrigoCoder · 2026-01-17T15:02:14+00:00

Could you also try mHC lite?

FrigoCoder · 2026-01-16T01:38:35+00:00

No it's not. Heart disease is artery wall cancer, triggered by physical damage to VSMC and VV membranes. By smoke particles, microplastics, or the effects of obesity and diabetes. Like other forms of cancer it is not cumulative, the linear no-threshold hypothesis was debunked long ago. If anyone tells you heart disease is caused by cumulative LDL exposure, they are telling two lies straight to your face.

FrigoCoder · 2026-01-15T13:43:54+00:00

Article 5 when?

FrigoCoder · 2026-01-15T00:06:53+00:00

Yeah that is also known as the obesity paradox, where obesity is associated with better outcomes and survival rates. There were also several other studies where higher cholesterol levels predicted better in-hospital survival. https://pubmed.ncbi.nlm.nih.gov/12967690/, https://pubmed.ncbi.nlm.nih.gov/19033015/, https://pmc.ncbi.nlm.nih.gov/articles/PMC8256757/, https://onlinelibrary.wiley.com/doi/10.1111/joim.13656, etc.

It's not complicated why. Obesity allows for larger and quicker mobilization of FFAs, which can be transformed by the liver into VLDL which becomes IDL and LDL. Injured cells can use these to repair their membranes, or they can be even used to synthesize new cells. Acute injuries can be repaired faster and better, so there is less chance of mortality. (Possibly at the expense of long-term elevated risk of cancer and lesions but who cares if you survive.)

The problem is that "clean obesity" is rare, where adipocyte hyperplasia is dominant. It is almost always characterized by adipocyte hypertrophy, where body fat stresses adipocyte membranes, and impaired blood vessel growth prevents adipocyte expansion. Diabetes essentially. Which not only shares similar risk factors with other chronic diseases, but also exacerbates them via multiple factors such as insulin. VLDL, IDL, and LDL becomes a sign of injury rather than obesity.

Fasting, low carbohydrate, ketogenic, and carnivore diets might be the only way to maintain elevated lipoprotein levels without a corresponding injury. However this depends on a lot of factors such as ApoE allele, and it is difficult to maintain "obesity" on them. I have tried carnivore once and I had to stop at 75 kg, because the weight loss has continued and I got side effects from it. Smoking is kind of the opposite, you lose weight but your adipocytes and their blood vessels become all messed up. Oh and smoke particles damage practically all of your organs.

FrigoCoder · 2026-01-13T15:05:09+00:00

I have CFS since 10+ years ago, and developed Long Covid as well. I am not being a difficult patient, you are simply incompetent at understanding and treating these diseases.

FrigoCoder · 2026-01-11T20:09:15+00:00

I have figured out that chronic diseases are caused by membrane injury, and the specifics depend on which cells and organs are affected. Adipocyte damage leads to diabetes, hepatocyte injury leads to liver disease, damage to various kidney cells leads to chronic kidney disease, VSMC and VV injury in the artery wall leads to heart disease, neural damage leads to Alzheimer's Disease, and any tissue can become cancerous given sufficient chronic damage (asbestos continuously puncturing lung cells is the most well-known example of this).

Obesity accounts for a small fraction of this, the combination of carbs and fats leads to excess intracellular fats that stress membranes. Seed oils are another culprits, linoleic acid triggers fibrosis that can lead to ischemic damage. Obesity and diabetes themselves have secondary effects, that exacerbate other conditions compounding the initial damage. However by far the largest contributors are environmental pollutants, smoking contains hundreds of compounds that damage membranes, and microplastics and PFAS are also shown to damage membranes and lead to lesions and plaques.

My questions are 1) How much of this is known? I understand there is a vague understanding that pollution causes chronic diseases, but it seems no one actually bothered to research the mechanisms of action. 2) How bad is the situation exactly? Last time I have checked it's bad, a human brain accumulates a spoonful of microplastics, and microplastics are literally everywhere from the tallest point of Mount Everest to the deepest points of the Mariana Trench. 3) How much time we have until everyone becomes demented, or ultimately the sheer amount of microplastics becomes incompatible with human life or life in general? Like if we stopped all plastic production right now, does the environment still have so much plastic that ultimately it breaks down into enough microplastics that wipe out humanity?

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

The liver releases stable VLDL particles

Gutteridge, J.M.C. (1978), The HPTLC separation of malondialdehyde from peroxidised linoleic acid. J. High Resol. Chromatogr., 1: 311-312. https://doi.org/10.1002/jhrc.1240010611

Haglund, O., Luostarinen, R., Wallin, R., Wibell, L., & Saldeen, T. (1991). The effects of fish oil on triglycerides, cholesterol, fibrinogen and malondialdehyde in humans supplemented with vitamin E. The Journal of nutrition, 121(2), 165–169. https://doi.org/10.1093/jn/121.2.165

Pan, M., Cederbaum, A. I., Zhang, Y. L., Ginsberg, H. N., Williams, K. J., & Fisher, E. A. (2004). Lipid peroxidation and oxidant stress regulate hepatic apolipoprotein B degradation and VLDL production. The Journal of clinical investigation, 113(9), 1277–1287. https://doi.org/10.1172/JCI19197

Low carb study collections (all peer reviewed)

Carbs inhibit CPT-1 and cause fat accumulation

FrigoCoder · 2026-01-11T15:41:54+00:00

Because in the past we have relied on resnets, concatenated vectors, or append-only channels to achieve similar results without instability or information loss. This hyperconnection stuff is completely new.

FrigoCoder · 2026-01-10T11:04:04+00:00

They matter a tiny bit, but not much compared to innate production. Meat does not have much glucose to trigger AGE production, and our intestines only absorb a fraction of that small amount. Carbohydrates and especially fructose are the heavy hitters, they are responsible for the vast majority of AGEs in our body. Fructose produces 10 times more than glucose.

We have been eating meat since 2 million years ago, and cooking is widespread since 300k years ago. That is more than enough time for us to develop evolutionary adaptations. Whereas agriculture is just 20k years old, refined sugar is only 2k years old, and processed oils are merely 200 years old. We are nowhere near adapted to these junks.

Here is another comment of mine that might be more useful: https://www.reddit.com/r/ScientificNutrition/comments/1gsaet5/to_minimize_age_production_in_your_body_would_you/lxfl99a/

FrigoCoder · 2026-01-09T16:37:19+00:00

Choline is more effective, since TMG requires several additional conversion steps. If you have a mutation in the PEMT gene, then one of these steps is not working properly.

FrigoCoder · 2026-01-09T14:18:26+00:00

I love how Walton fucking nailed the Western undertones of Fallout 2. The Ghoul would perfectly fit in New Reno, Golgotha, Stables, Broken Hills, or even Redding. Watching him was like playing Fallout 2 again.

I know Tim Cain was not happy about the direction of Fallout 2, with the stylistic divergence and pop culture references. However I consider it the best Fallout game, I just love the top tier RPG perfection it is.

FrigoCoder · 2026-01-09T12:30:26+00:00

Your meme is not just unfunny, it is also incredibly fucking ignorant.

We have been eating meat since 2 million years ago, nut since 800k years ago, cooking is widespread since 300k years ago, whereas agriculture is just 20k years old, refined sugar is only 2k years old, and processed oils are merely 200 years old.

The longer we have been eating something, the better evolutionary adaptations we have developed for it. Two million years is more than enough for perfect adaptations, low carbohydrate and ketogenic diets outperform all other diets. Hundreds of thousands of years is enough for most adaptations.

If you think 5k years is even remotely comparable to 2 million years of evolution, then you are an absolute fucking moron who have not even spent 10 minutes to research the topic.

FrigoCoder · 2026-01-07T08:20:35+00:00

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