toasty7718

Dude. Absolutely. I've not met many people who've shared the same experiences I've had with early childhood. But the best way I can articulate it is is almost as if my early childhood (age 0-5) was a psychedelic dream that you gradually forget as you get older. Funnily enough, it was through smoking DMT that my memories from this era of my life were reignited. Imagination was reality. If I imagined something, then it would materialize before me. I would go into my own mind and play these types of games ... it was almost as if I visited an "astral plain," or something like that. I saw reality as it was, but my imagination was so intense that the room around me was subject to influence from it. Another thing that brings back memories is the breath-hold portion of the WHM, which feels a bit like DMT.

Martin W. Ball, PhD. He was an adjunct professor at the university of Ashland, Oregon teaching religious studies. His entheological paradigm framework is turquoise in it's values and interpretation of reality. Highly recommend checking him out. Note: the signature of my profile is an excerpt from one of his poems entitled "my love."

AI. I've been using various chat GPT prompts to deepen my learning and it's been amazing. Try asking it for that specifically and it will tailor it to you. There's a definite reason why Kahn Academy is embracing AI. I'm pretty sure if you can get an open AI software app on your phone you can talk to it and it responds in a tts voice, which will be practice articulating your points. Albert Einstein once said something along the lines of if you can't explain something simply, then you don't understand it deeply.

Just finished listening to this, it's amazing. Here's a few of my favorite excerpts "A huge part of psychological health is realizing that when I die, life doesn't end. My life in this form ends, but life continues. I get to be here, part of this whole game of life for a little while, and like what a fucking miracle that there's experience as opposed to no experience. There could just be nothing. As soon as I realized like, I got to see a tree, I got to see a sunset, I got to see color, I got to hear sound, as opposed to just nothingness … the mindset of "what's in it for me I need more" is a fucking mental illness. The realization that existence exists and I'm apart of it for a little while is awakeness, and then I would totally choose to incarnate just to have experience at all, even a little bit of it as opposed to nothing. " "Before, when I reflected on last year, what do I do this year, what to do this coming year on January 1st, etc., whatever it is, I'm always reflecting in light of thinking I can do it over differently next year. When people are on their deathbed, that doesn't happen. There's a deeper type of reflection. I've been on so many death beds with people, Daniel's parents were awesome to take him to assisted living homes and could have that experience. He's never met old people who spent their time wishing they had fixed themselves more and their "if I could do it over again" wasn't a narcissistic focus. That just never happened. What was really meaningful was always the ways they express love to people and the ways they offered things. It will outlast them and the ways that they appreciated life. "

Personally, I'd go easy on the maple syrup and honey

Here's some recipe ideas with tempeh (one of my personal favorites) Tempeh Three table spoon lemon juice One tablespoon white miso Two tablespoons of olive oil Two tablespoons of water Cut tempeh in quarters and sliver it and salte in olive oil for five minute on very low and turn and five minutes more and take it out and cut up some onion and put it in the olive oil and throw the tempeh in and throw the sauce on top Tempeh bacon Sliver the tempeh from the rectangle package and cut it in really thin pieces and marinate it in tamari or shoyu instead of soy sauce, marinate in this and sesame oil and dry it they get crispy Steam tempeh and put it in salad Boil tofu for five minutes Tofu salad red onion pickle capers celery Dates with dark chocolate inside, preferably baking chocolate

The developed world has borne witness to diseases whose primary cause is that of over-consumption. While the causes of disease are multifactorial in nature, with each individual case involving thousands of complex mechanisms interacting with each other, the vast majority of health experts have determined that auto-immue diseases like cardiovascular disease and cancer show similar causal pathways of deterioration, like with apoB for CVD. The ratio between macronutrients and micronutrients has changed with the advent of industrial processing mechanisms, and human genetics are ill-equipped to handle the modern nutrient surplus. Modern processing mechanisms have sacrificed essential micronutrients, like fiber, vitamins, enzymes, minerals, for more palatable, macronutrient options like basic-carbohydrates and saturated fats with a higher caloric density. To do so, you must find the derivative of a highly-hybridized part of a plant or animal product and extract the parts that evolution has developed reward-circuitry pathways for. All forms of ultra-processed foods are elaborate combinations of fat, sugar, and salt. There wasn’t an abundance of fat, sugar, or salt in an evolutionary environment. The infrequency in which our ancestors had ready access to a food high in fat, sugar or salt, produced a strong dopaminergic and opioid-like response as incentive to find more of it. In addition to nourishment, dopaminergic responses to certain micronutrients doubled as a survival-necessity in times of scarce famine. TLDR; Nutrient surplus is genetically maladaptive in the wake of ready access to ultra-processed food in the twenty-first century.

Veganism is a luxury of the 21st century. what are you implying by saying this?

Nate's channel is an amazing yellow, glad other people on this forum know about him

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?