toasty7718

I see you've provided me with over 60 sources cited by authors of a paper entitled "Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis" This is a screen-snip from a paper by James J DiNicolantonio and James H O'Keefe. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196963/ For starters, let's just examine the competing interests of the authors: "Competing interests: JD is the author of The Salt Fix and Superfuel and operates the website thesaltfix.com. JHO has an ownership interest in CardioTabs, a nutraceutical company" @Leo Gura so I suppose supplement is the easy way to make $$$, especially if you have mechanistic outcome data to back up your claims interesting ... I appreciate the evidence that you've given me from these two authors to support your proposition, but on first glance what I notice is an over abundance of mechanistic speculation. Why need mechanistic speculation when we have meta-analyses of prospective cohort studies showing that those with higher intakes or blood levels of linoleic acid have lower all-cause mortality, CVD incidence and mortality, stroke, and cancer mortality? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326588/ Let's examine some of the sources these unbiased authors cite, shall we Source (2) states: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334131/ "Our findings suggest that adipose tissue LA has increased substantially in the United States over the last half century, and, to our knowledge, for the first time demonstrate that this increase is highly correlated with increased dietary LA intake over the same period ... Because LA is in involved in numerous physiologic and pathophysiologic processes, these changes have potentially significant implications for public health. These findings call for further research into the consequences, positive or negative, of such a major shift in the adipose tissue concentration of a single bioactive FA occurring over a relatively short period of time in the United States." Even the authors of that paper conclude that based purely on the increase of linoleic acid in adipose tissue requires further research to see if it has positive or negative health effects. Given the meta-analysis and epidemiologic studies that I've provided, all this paper does is prove my point even further They say with source (4) Linoleic acid serum concentrations (as opposed to per cent of fatty acids) are higher in patients with CAD https://pubmed.ncbi.nlm.nih.gov/8472362/ An interesting finding for sure, but how do we link it as being causal? What we need is an RCT that shows that increasing linoleic acid serum concentrations increased CAD compared to a control group, not looking at CAD and seeing that they have higher concentrations of it, you know? That's much better at determining causality. For source (3) they state linoleic acid in adipose tissue and platelets positively associates with CAD, whereas EPA and DHA in platelets are inversely correlated with CAD Another interesting finding. Again - correlation does not equate to causation. Also - this is a small sample size of 226 patients. Preferably, we want to have a large group of people to see if the effects are repeatable. Let's examine more robust studies - more specifically, meta-analyses preferably Just a side note: when it comes to correlation not equating to causation, an example I like to use is the fact that countries that smoke more live longer, or the fact that those who own lighters are more likely to have lung cancer, or the fact that some foods raise blood pressure so therefore they're bad. You know what else raises blood pressure? Exercise! Having sex! So we can't rule out something raising blood pressure short-term as being bad. https://www.sciencedirect.com/science/article/pii/S000291652200778X This is a systematic review and meta-analysis of prospective cohort studies to examine associations between LA intake and mortality (including, but not limited to CVD) It pooled together 38 studies with 44 prospective cohorts and included 811,069 participants (a far-cry from the 226 you mentioned earlier) To summarize, the authors finish the article by saying "In prospective cohort studies, higher LA intake, assessed by dietary surveys or biomarkers, was associated with a modestly lower risk of mortality from all causes, CVD, and cancer. These data support the potential long-term benefits of PUFA intake in lowering the risk of CVD and premature death." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/ This study was written by a whopping 59 PhD holding authors (I counted it, by the way) This is a harmonized, de nova, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries that looked at the circulating and adipose tissue LA biomarkers with total CVD and subtypes. Heterogeneity was explored by age, sex, race, diabetes, stain use, aspirin use, omega-3 levels, among others. In the prospective cohort studies ranging from 2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659, and higher levels of LA were significantly associated with lower risks of total CVD and its subtypes They conclude by saying higher in vivo circulating and tissue levels of LA were associated with lower risk of major cardiovascular events. So - let's leave the reader with a choice. A study pool of hundreds of patients undergoing coronary angiography without heterogeneity taken into account vs. two meta-analyses of close to a million participants with sex, age, weight, habits, omega-3 intake, etc., taken into account and still finding that higher intake of PUFA contributes to lower risk of CVD. Your evidence is weak, suffice to say Source (5) doesn't contribute to your proposition either because it shows benefit of going on a weight loss high carb low fat diet, and one group high in MUFAs with beneficial effects of weight loss to lower risk factors of CVD https://pubmed.ncbi.nlm.nih.gov/9538963/ "MUFA-enriched hypocaloric diets potentiate the beneficial effects of weight loss to ameliorate cardiovascular risk factors in obese patients with type 2 diabetes." https://pubmed.ncbi.nlm.nih.gov/14739118/ From what I've seen, none of the studies they cited about oxidized LDL even make the slightest hint that oxidized LDL is caused by increased intake of PUFA, like seed oils. Also - measuring oxidized LDL is something that no cardiologist does because it's a meaningless metric. None of the studies they mentioned were adjusted against ApoB either because if it did, it would have no meaning. This paper touches on that and says that oxLDL should be compared with ApoB Viita, H., Närvänen, O., & Ylä-Herttuala, S. (1999). Different apolipoprotein B breakdown patterns in models of oxidized low density lipoprotein.. Life sciences, 65 8, 783-93 . https://doi.org/10.1016/S0024-3205(99)00305-7. "We suggest that in order to improve interpretation and comparison of results, data obtained with various models of oxidized LDL should be compared to the simplest and most reproducible models of 3 h and 18 h copper-oxidized LDL (apoB breakdown) and MDA-LDL (apoB aggregation) since different models of oxidized LDL have significant differences in apoB breakdown and aggregation patterns which may affect immunological and biological properties of oxidized LDL." To name some more of the studies they cited and the inconsistencies I see Sources (6), (53), (54), and (56) and models done on rodents, so I don't see any relevancy there in terms of human health-outcome data. Source 57 is funded by the National Cattleman's Beef Association, so it's best taken with a grain of salt. https://www.metabolismjournal.com/article/S0026-0495(00)97008-2/pdf I'm absolutely certain that more are sponsored by that, but... I don't feel like going through and picking out weak pieces of evidence. One of the sources concludes https://academic.oup.com/ajcn/article-abstract/75/2/221/4689295 "Increased ALA intakes decrease the estimated IHD risk to an extent similar to that found with increased LA intakes. Group nutritional education can effectively increase fish intake." This doesn't support their proposition either. RCTs like the LA Veterans study where they measured levels of linoleic acid in adipose tissue and the intervention group saw levels increase on the vegetable oil diet and a statistically significant reduction in heart disease. There's many more sources, but I don't really see a point in dismantling them all given the fact that a) the authors have a conflicting bias for their own supplement companies b) the first of the studies I mentioned were weak evidence c) the narrative just doesn't suddenly flip one day with nutrition science and foods are bad all of a sudden, you have to look at the totality of the evidence, and the totality of the evidence has leaned towards replacing SFA intake with PUFA intake to decrease risk of CVD d) correlation does not equate to causation e) the oxidized LDL hypothesis has no real bearing given the fact that the studies never compare it to ApoB (because if they did, it would expose it as a meaningless metric), and therefore no cardiologists use it f) there is much more robust evidence than mechanistic outcome data speculation g) the better evidence is in the form of a systematic review and meta-analysis of prospective cohort studies and / or RCTs with very large sample sizes (tens or hundreds of thousands of participants) of people with heterogeneity taken into account, written by authors with nuance and (preferably) without bias h) "USDA: moderate saturated fat AHA: moderate sat fat Canada: moderate sat fat UK: moderate sat fat Spain: moderate sat fat Australia: moderate sat fat China: moderate sat fat South Africa:moderate sat fat WHO:moderate sat fat" g) I'm getting tired of this TL,DR: the paper you took a screen snip of was written by two authors with conflicting biases for their own supplement companies and they rely mostly on mechanistic outcome data and speculation for their claims (and some of the sources even contradict their proposition). Why focus on that singular paper there is much more robust evidence in the form of a systematic reviews, meta-analysis, and prospective cohort studies which have hundreds of thousands of participants each? They examine the link between CVD with the intake of omega-6 and find that higher intake of linoleic acid decreases risk of CVD. At this point I really think you should concede on your proposition, but I find that unlikely to happen. I've debunked your pseduoscientific claims more than once and at this point I'm done with this debate. It takes me hours to compile the evidence (which don't get me wrong, I enjoy doing. It gives me an opportunity and reason to read into nutrition, which is something I'm interested in) I'll state again: misinformation kills people. What you're doing is a disservice to this whole forum.

That's interesting. what evidence do you have for your proposition about seed oils and heart disease?

jason I'm going to ask you again, What evidence for you have for this proposition?

I see, The seamless logic of ecological associations between the use of surgical interventions, like coronary artery bypass grafting, does explain at an epidemiological level the risk for CVD mortality going down, so we can't rule PUFA intake exclusively because there's an abundance of confounding factors. That's a logical fallacy on my part So for that reason, the intake of PUFAs and lowering of CVD mortality at a population wide scale isn't robust enough. I should specify that in terms of large scale RCTs, we don't really have large scale outcome trials on the effects of PUFA intake and CVD risk. Given the bulk of the evidence that has been accumulated over the past century, health experts have ruled that performing such an RCT to be unethical because it would mean upping the intake of SFA. The best evidence we currently have in terms of RCTs are trials that were completed decades ago. When it comes down to the observational evidence, what we find is that higher intake of PUFAs and MUFAs reduces CVD risk. This is a prospective cohort study done analyzing the intake of saturated fats, unsaturated fats, and carbs with CVD risk. It has a total of 127,536 participants and their diets were assessed by food frequency questionnaire every four years. It followed them for up to 30 years, and they found that higher intake of PUFAs and unrefined carbohydrates was associated with lower risk of CVD https://www.sciencedirect.com/science/article/pii/S0735109715046914 "During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of [PUFAs] and carbohydrates from whole grains were significantly associated with a lower risk of CHD [...] Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk." That's just observational evidence, is it not? How accurate even are FFQs? In truth, not very accurate. There are a multitude of pitfalls that come with self-reporting, so for that very reason, researches have resorted to measuring biomarkers (more on that later) Increasing your intake of saturated fat past a certain threshold increases your circulating levels of LDL cholesterol and ApoB. This is a study from the World Health Organization analyzing the effect of modifying of of SFA intake with MUFAs, PUFAs, and carbs, and here are the results they found: https://apps.who.int/iris/bitstream/handle/10665/246104/9789241565349-eng.pdf There was a 0.058 mmol/L change in LDL cholesterol per 1% of energy replaced when you replace calories from PUFAs with calories from SFAs, as compared with 0.019 mmol/L and 0.012 mmol/L with replacement with carbs and MUFAs, respectively. But do keep in mind that LDL cholesterol is a surrogate marker for atherogenic lipoproteins, and a much better metric would be apolipoprotein B (ApoB). The atherogenic lipoprotein molecules all have one molecule tag of ApoB. This includes: LDL, VLDL, Lp(a), chylomicron remnant particles, and IDL. And as such, what this table shows is that replacement of PUFAs with SFA marks a 10.3 mg/dL increase of ApoB particles in the blood. And as I've already noted before, ApoB increases risk for CVD and shortens life-span: https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext](https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext "In conclusion, our evaluation of apoB using outcomes in first-degree relatives identified that higher apoB is detrimental to lifespan and increases the risk of coronary heart disease and type 2 diabetes. Lifestyle and pharmacological approaches to lowering ApoB should have widespread beneficial effects, including preventing common diseases and prolonging life." But when it comes to self reporting, it is well known that for large groups of people it reasonably helpful. Not so much for small groups of people in an RCT. Therein lies the reason why researchers have started using biomarkers instead of FFQs. This group of researches sought to evaluate how circulating levels of omega 6 fatty acids relate to the incidence of CVD, and it pooled together thirty studies from across the world. and their results are as follows: https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.118.038908 "In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659 participants. Higher levels of [Omega-6] were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke" So basically to summarize this, the links between increased PUFA consumption, CVD mortality, and the use of surgical interventions to deal with CVD are hypothesis generating pieces of evidence in of themselves, and much more robust evidence is needed to raise certainty in the domain of omega 6 rich seed oils and CVD risk. The preponderance of the evidence suggests that replacing SFA intake with PUFAs lowers your ApoB and decreases your risk of heart disease.

Increased linoleic acid consumptions marks the most significant change in CVD mortality over the last 100 years https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5268076/

Yea, too much of anything can be problematic

You still haven't given me any evidence for this proposition

I'm sorry, I don't understand. Can you provide a proposition to this statement?

Maybe do what Peter Santenello does & document what it's really like around the world and have one of the locals show you around for a 40+ minute video? His channel motto is something like "showing you the world the media doesn't show" or something like that.

Daniel Schmactenberger was homeschooled That speaks enough volume

Yes, I would agree with the fact that interpretation and extrapolation of scientific data is a major source of where disagreement and argument in the field of medicine, but could you provide me of an example of how you view studies through a "nuanced" lens? I think that would clear up the air some because, aside from the health effects you got from the diet you're on now, it would give me some insight into why you came to the conclusions you did. I'm not entirely sure what you mean by this. I would assume you're using this as an argument to as to why saturated fat doesn't actually contribute to CVD and the studies done on it are correlational, right? Using this type of wishful thinking to justify a preconceived notion for a dietary pattern is a sophisticaed form of mental gymnastics and has no bearing for people who actually want accurate data to influence choices about their health. Don't just take my word for it, here's an epidemiological study examining just that by some researchers from Oxford. https://academic.oup.com/aje/article-abstract/95/1/26/167903?redirectedFrom=fulltext&login=false "The hearts and aortae of 50 Masai men were collected at autopsy. These pastoral people are exceptionally active and fit and they consume diets of milk and meat. The intake of animal fat exceeds that of American men. Measurements of the aorta showed extensive atherosclerosis with lipid infiltration and fibrous changes but very few complicated lesions. The coronary arteries showed intimal thickening by atherosclerosis which equaled that of old U.S. men. The Maasai vessels enlarge with age to more than compensate for this disease. It is speculated that the Maasai are protected from their atherosclerosis by physical fitness which causes their coronary vessels to be capacious." The fact that Maasai don't seem to develop heart disease despite their high saturated fat intake can be explained by the multitude of confounding factors, such as their remarkably high physical fitness levels, infant mortality rates that exceed over 50%, enviornment, etc.. If you were to take a group of infants and kill the weakest half of them and only selected for the most physically fit and capable and raised them their whole lives getting 8+ hours of extensive physical activity everyday, then of course you wouldn't see the same trends of death and disease develop. Promoting an ancestral diet high in SFA because the Maasai don't die of heart disease is inadvertently promoting infanticide if you want to see the similar results they do. This phenomenon is known as survivorship bias. Their enviornment shares virtually no resemblance to our modernized and industrial western one, so how would this have any bearing on our choices for optimal health? We have much better data on the relationship between CVD and SFA intake than hunter gatherer populations with survivorship bias. And as the researches noted, the Maasai of Africa are not immune to atherosclerosis. That's precisely the thing that the world's leading researchers into death, diet, and disease have been doing for the past half-century. Yet all the conclusions they come to seem to be at odds with what you're saying, do they not? Across the world, the dietary recommendations are all pretty much identical to each other about 95% of the time and they have been for the past half century. (Side note: the 95% is a rough estimate I've heard before so don't take my word on it exactly) Here's an example of such: 1. Eat a Variety of Foods 2. Maintain Ideal Weight 3. Avoid Too Much Fat, Saturated Fat, and Cholesterol 4. Eat Foods with Adequate Starch and Fiber 5. Avoid Too Much Sugar 6. Avoid Too Much Sodium 7. If You Drink Alcohol, Do So in Moderation Pretty sound advice, right? Most health experts would agree with this advice, even despite the fact that these were the dietary guidelines from 1980 (43 years ago) https://www.dietaryguidelines.gov/about-dietary-guidelines/previous-editions/1980-dietary-guidelines-americans Point is - people who have been studying nutrition throughout their whole academic and medical careers near universally come to the same conclusions, and they've been doing so since longer than most of us have been alive. I'm curious to know what makes the way in which you interpret studies in a "nuanced lens" is somehow the better way and renders all the doctors, professionals, and health-experts wrong. Also - how would the interpretation of these studies be nuanced if you're using personal anecdotes and experiences intermingled with it? That's not to say that personal experience is not important in the slightest, but that does render your viewpoint very biased given how your own experience differs drastically from what the studies say? And again, you never actually answered my question regarding how you know with absolute certainty that cutting out PUFAs cured your autism and chronic diseases and this is the ONLY way to do so. How do you take into account other factors, like a possible allergy / intolerance to foods or nutrients found in those foods, like fiber? I'd be more than happy to provide you with resources about fiber intolerance and how to cure it. It's actually a very common occurrence among those who adopt a carnivore-style diet to have some form of messed up gut microbiome or a lacking of a specific type of amino acid, for example, and when they cut this out they feel better and more energized. This food intolerance or fucked up gut microbiome can be cured by working with a skilled healthcare practitioner and has been demonstrated repeatedly through a multitude of studies, but that's a topic for another time You're entitled to your own opinion, but you're not entitled to your own facts my friend.

I will say this again Jason. I won't believe what you say until you provide better evidence than "it makes me feel good." the people on this forum are also smarter than that.

I'd be considered an adult if I was Jewish

@Princess Arabia absolutely. that's why nuance is such an important thing in the realm of data-analyzation

Okay, From what it seems to me, you're very passionate about your beliefs and you seem to be dead-set in your personal anecdotes for the diet you're preaching. That's fine. What I'm mostly worried about is you preaching this diet to the people on the forum and saying that it is the way to best way to eat and that this will reverse their chronic diseases. I understand why you're coming from this place given your own experience, but based on the evidence done on MILLIONS of people, the epidemiology of this diet seems to result in unfavorable health outcomes. Not to mention it demonizes many food groups and will most likely lead to an eating disorder for most people. For someone who isn't very well versed in nutrition, they might see your posts and start eating in a way that will, worst case scenario, have their risk of CVD and cancer increase drastically. Or, they could see the short-term benefits that you've seen, I'm not denying that. But do remember, misinformation kills people. Let's start with your claims: If everyone told you that smoking cigarettes was highly addictive and hazardous to your health yet when you smoked a pack a day you felt happier, more clear, more energized, and well-rounded, would you still continue smoking cigarettes despite what the evidence says? This is wrong on so many levels. I don't even know where to begin. First off, this is just a blatant appeal to nature fallacy. Might I remind you of a little thing called Antagonistic Pleiotropy? This is the biological phenomenon wherein an individual's genes will favor and select for traits that prioritize short-term survival and reproductive success over long-term survival. As you know, genetics are a tricky and counter-intuitive thing. Many things effect whether genes are turned on and turned off, so you can't just boil things down to genetics, enviornment and diet play a huge part in it. It's very individualized. Each one of us has a unique biology - even identical twins! Identical twins who grew up in a different environments will have different genetics. With that in mind, this is the reason behind how eating an ancestral diet will result in long-term detrimental health outcomes. TLDR: we shouldn't look to the amount of polyunsaturated fat our ancestors ate, we need something more robust. This is where human outcome data comes into the mix of things I'll link here some meta-analysis studies done regarding polyunsaturated fat intake and oxidation / chronic disease. I'm well aware that me and your views differ drastically when it comes to the hierarchy of evidence, but I'm mostly doing this in case others want to see it for themselves. On one hand we have close to half a million participants health outcome data (more on that later), and then we have you and your anecdotal experience. I'm not dismissing your own experience by any means, what I'm trying to get across is the fact that the epidemiology of what your preaching seems to be in direct contradiction. This is also blatantly wrong on so many levels. Here are the two studies that many people who share your beliefs about saturated fat might cite. It's also why the Time Magazine Issue titled "Eat Butter" came out an generated a media firestorm. https://pubmed.ncbi.nlm.nih.gov/24723079/[https://pubmed.ncbi.nlm.nih.gov/20071 https://pubmed.ncbi.nlm.nih.gov/20071648/ These studies looked at people who eating varying amounts of saturated fat and they found they had similar rates of CVD. It's hard to see through this type of study because of many confounding factors (the people on the low saturated fat group may have been eating other things that contributed to that outcome). Here's a study done to clarify the findings of the previous one. Harvard researchers told people to limit their SFA intake and replace it with PUFAs and MUFAs from nuts and seeds, and what they found was that they had lower rates of CHD risk. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4593072/ "Higher intakes of polyunsaturated fatty acids (PUFAs) and carbohydrates from whole grains were significantly associated with lower risk of CHD" They also had a group that ate refined grains and what they found is that their risk remained the same. So, we can conclude that the previous two studies linked above weren't robust enough and when SFA is replaced with healthier forms of fat, risk of CVD goes down. But that's CVD risk, what about oxidative stress? I'd assume by oxidative stress you're also inferring that this leads to atherosclerosis like you said in previous posts, but there simply isn't enough evidence to say with absolute certainty that this is the case yet. What we need is a multitude of repeated RCTs and human outcome data before we can say something like that for sure. The best metric we have currently is ApoB, which I will cover later. Anyways, here are the effects of high polyunsaturated fat diets and CVD risk: This epidemiological study analyzed 521,120 individuals and here were their findings: https://pubmed.ncbi.nlm.nih.gov/33853582/ "Consumption of butter and margarine was associated with higher total and cardiometabolic mortality. Replacing butter and margarine with canola oil, corn oil, or olive oil was related to lower total and cardiometabolic mortality. Our findings support shifting the intake from solid fats to non-hydrogenated vegetable oils for cardiometabolic health and longevity." Finally, a Cochrane systematic review, a HIGHLY respected medicine journal that pooled together all available randomized clinical trials done on this topic. It had to meet certain criteria of course, like having to be compared with a higher saturated fat intake, intending to reduce SFA intake or include MUFAs or PUFAs, lasting at least 2 years. Here were their results. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD011737.pub3/full "Replacing the energy from saturated fat with polyunsaturated fat or carbohydrate appear to be useful strategies, while effects of replacement with monounsaturated fat are unclear. The reduction in combined cardiovascular events resulting from reducing saturated fat did not alter by study duration, sex or baseline level of cardiovascular risk, but greater reduction in saturated fat caused greater reductions in cardiovascular events." But this is epidemiology. Isn't this inaccurate? No. https://pubmed.ncbi.nlm.nih.gov/34308960/ "Comparing both bodies of evidence from Cohort Studies, the difference in the results was also small (RRR: 0.92; 95% CI: 0.88, 0.96). Our findings suggest that bodies of evidence from randomized control trials and cohort studies are often quantitatively concordant. Prospective systematic reviews in nutrition research should include, whenever possible, bodies of evidence from randomized control trials and cohort studies on dietary intake and biomarkers of intake to provide the whole picture for an investigated diet-disease association." https://www.ncbi.nlm.nih.gov/pmc/articles/instance/8803500/bin/nmab095fig1.jpg What about ApoB as a metric for CVD? What is ApoB? ApoB is a marker of atherogenic lipoprotein particles in our bloodstream. Here's a study from the lancet that shows high levels of ApoB increases risk for CVD and life-span. They got their data from the UK Biobank and it has approximately 500,000 participants. To verify their hypothesis, they replicated the estimates from the UK Biobank using mendelian-randomization (a type of study that analyzes the genetic predisposition of participants). https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext "In conclusion, our evaluation of apoB using outcomes in first-degree relatives identified that higher apoB is detrimental to lifespan and increases the risk of coronary heart disease and type 2 diabetes. Lifestyle and pharmacological approaches to lowering apoB should have widespread beneficial effects, including preventing common diseases and prolonging life." So how do PUFAs and MUFAs contribute to the lowering of APoB? This is a review done on eighty-seven studies. Here is what they found https://pubmed.ncbi.nlm.nih.gov/27821191/ "Replacement of carbohydrate by MUFA, not SFA, decreased plasma apoB. Moreover, dietary enriching with n-3 fatty acids [PUFAS] (FA) (from fish: 1·1-1·7 g/d or supplementation: 3·2-3·4 g/d EPA/DHA or 4 g/d EPA), psyllium (about 8-20 g/d), phytosterols (about 2-4 g/d) or nuts (30-75 g/d) also decreased plasma apoB, mostly in hyperlipidaemic subjects" I'll leave you with some of principles regarding SFA: - It's a dose-dependent response, dose matters, there's a threshold effect associated with it - What you replace it with also matters - Source matters. Fish, dark chocolate, olive oil are high in SFA and the health outcomes are overwhelmingly positive. The same can't be said for something like margarine or butter. But even that's not to mention saturated fat is surface level. We want to analyze the health effects of foods over the macros and micro. My goal here is to give others on this forum a more evidentially-based approach to their health that will, in all likelihoods, result in favorable health outcomes based on the evidence that we have. This brings us back to your anecdote. I have no doubts about how you feel healthier and happier after removing PUFAs from your diet, but how exactly would you know that that was the ONE and ONLY thing that caused you to reverse your eosinophilic esophagitis? What if you have a microbiome that doesn't respond well to fiber, for example? Point is, the way you're presenting your argument for everyone changing their diet because you got individual gains in a way that can have a multitude of confounding factors and goes against what the overwhelming majority of the studies say is ignorant at best and fatal at worst. I really think you should approach this topic with more nuance and less absolute certainty. I'll state again: misinformation kills people my friend. What you're doing isn't a favor, it's a disservice.

I have my issues with the psychiatric system mostly due to the fact that I personally know many people who were fucked over by anti-depressants and anti-psychotics. That's a topic for another time though.

Can you provide a proposition to this statement and clarify it?

I watched the same interview. Great video, Martin ball is an amazing teacher

Offer me your evidence and explain why it's superior to mine

I set it to ignore his posts at this point. I agree with you all the way on this.

For the love of god, start giving us evidence for your bullshit propositions then we'll start to take you seriously.

This is amazing. Thank you so much!

Someone needs to lock this thread

Supplementing on Vitamin B and Vitamin B12 isn't a heroic effort lol some vegans may need to take more, like DHA, but generally all other nutrients are adequate from it.

Masculine energy is directed, looking to solve problems, warrior based & journeyed & competitive when added with more masculine energy. Feminine energy is beautiful, always in motion, with no straight lines (the essence of nature itself) and expanding when added with more feminine energy My belief is that these different types of archetypal energies respond in their own unique ways to states of consciousness that have massive energetic flows and releases (psychedelics, deep meditation, yoga, etc.) Most religious traditions are also patriarchal and created by men for men. With the releasing into the energy of psychedelics some women recount how it became highly sexual, where surrender allowed them to release into the divine energy of God. When it comes to sex, feminine energies usually release, open themselves up, and surrender, whereas masculine energies try to maintain energetic control and poise.