toasty7718

https://pubmed.ncbi.nlm.nih.gov/24871675/ This is the Adventist health study 2, a prospective cohort study with a large sample pool that followed different dietary groups for long periods of time, including vegans "Non-vegetarian diets were compared to vegetarian dietary patterns (i.e., vegan and lacto-ovo-vegetarian) on selected health outcomes. Vegetarian diets confer protection against cardiovascular diseases, cardiometabolic risk factors, some cancers and total mortality. Compared to lacto-ovo-vegetarian diets, vegan diets seem to offer additional protection for obesity, hypertension, type-2 diabetes, and cardiovascular mortality"

What evidence do you have for this claim dude?

Let me give you a choice. Diet A covers all your base nutrients Diet B covers almost all nutrients but you need supplements. Intensive long term research says that this diet decreases your risk for auto immune diseases and makes you live longer. Which diet would you choose?

I think what's he's referring to is if you aren't sourcing your protein sources intelligently from a variety of plants then you can end up with low levels of a specific amino acid.

I wouldn't look down on someone for eating for eating an animal product if their body just can't go with plants, like Leo for example. If our goal is to minimize suffering, then it should apply to the person also. There are people who have an easier time being with animal products than without them. But it's also important to remember that many people who go onto a carnivore diet do so out of desperation, and so with an elimination diet their gut microbiome isn't in such a constant state of inflammation, so therefore they feel better in the short term. This is an issue that can be addressed by working with a functional medicine doctor or naturopathic doctor who is willing to incrementally uptake your fiber intake to get your microbiome used to fiber. The long term benefits outweigh the short term costs. Having a complete nutrient profile is also of concern, like EPA/DHA, certain amino acids, and vitamin b12 (among others). Aside from that, I don't see any ethical considerations that justify killing an animal without necessity for survival. But if someone just isn't ready to make the full transition to veganism or isn't in a place to because of their environment or health issues that stem from it, then I would say ethically source animal products to only the minimum degree that supports you and hold right to ethical lines you draw. I would be more than happy if somebody struggling to go vegan just ate farm-fresh eggs from the farmer's market to get by yet refused to eat eggs from restaurants and their friend's house, or something along those lines. This also means not automatically going to something like red meat, a kill product. If I do xyz then I automatically should do xyz because it's black & white is dangerous thinking. "Humane slaughter" is an oxymoron. Would you want to be at the other end of that? This brings in the pie slice theorem of ethics—imagine if you cut the pie and the other got to choose which slice they got. As humanity becomes more and more conscious, our circle of concern will grow. This is a hallmark of stage green thinking. As humanity progressed, the differences that the we saw in other sentient beings (like women, black people, other tribes, etc.) don't matter because they experience as much as we do and they have deserve negative rights. Empathy is the progressive expanding of understanding that things that are seemingly different from us have so much more similarities with us than we can ever imagine. This circle of concern will eventually expand to all animals and eventually all sentient beings as humanity progresses their level of consciousness.

Your claims mean absolutely nothing at this point dude.

Great post. I agree with everything you said. Beef, eggs, chicken and fish are entirely optional though, you can do just fine without them

I agree with the fact that the Standard American Diet is problematic because our biology isn't designed to digest ultra-processed foods. I also agree with the fact that community - more specifically, connection - is also an inherent part of our biology. But determining the health value of food based on the fact that indigenous peoples consume them and have a seemingly longer life-expectancy doesn't hold much relevancy when determining the long-term impacts the food has. We have much more robust evidence stating the contrary in large groups of people studied in our modern world and with heterogeneity taken into account. Virtually every single dietary guidelines report across the world agrees that butter and margarine increase your risk for CVD. How do you account for the fact that indigenous populations have an infant mortality rate of ~50%? I can almost all but guarantee you that if you took a small sample of our population and killed the weakest half and only selected for the strongest and most fit then you would see similar results. Especially when you add other causational factors - like the fact that their gut microbiome more diverse than our's, they consume more than 100 grams of fiber per day, and they get 8+ hours of physical activity every day.

What evidence do you have for this proposition?

Meditations by Marcus Aurelius

I love this bread

"Dr." Eric Berg is a con-artist who sells more problems than solutions, I'm glad YouTube is finally pulling the plug on his channel. there's a reason why he never accepts any of the debates that he is invited to, especially on medical twitter. I'm not sure how I feel about YouTube censoring every anti-science video though. YouTube hasn't exactly been known to be the best company ever with good values and morals. I can easily see some abuse to happen with that.

& sorry if I got a bit heated at times, I'm just passionate about evidence-based nutrition and find it appalling when people give health advice that has been demonstrated time and time again to result in detrimental health outcomes.

I mean it shows that it's possible. I'll grant it's possible that you're right; that's trivially true. What's the evidence that the claim is actually true? The body of the cake is that it doesn't actually demonstrate your claim, it just shows that it's theoretically possible. yeah, take care man, wish you the best. just don't be surprised when you start to develop CVD in your mid to late 30s

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.