Jason Actualization

Haha, and to think that one or more fellow attendees of these retreats must volunteer to sound the gong at that time every morning. The hearts of a lion, they have. That is my usual/natural wake up time, and even I didn't volunteer, lol: shame on me.

Which furthermore means that most people also lack the training to evaluate the currently prevailing paradigm, yes? That said, indeed, I am asking that people trust me, which I take extremely seriously and assume with great responsibility. I wouldn't be disseminating these ideas if I didn't have full confidence in them, and if this were not a hill I would be willing to die on. If I had unlimited resources, I would facilitate the following: Study 1: Quantify the concentration of lipid oxidation products present in the 1. industrial seed oils at the point of consumer acquisition (i.e., Mazola/corn oil on the shelf of Walmart) and 2. industrial seed oils used in fast food chains (i.e., the corn oil present in a deep fryer at Burger King). Since my hypothesis is that the consumption of lipid oxidation products in the amounts quantified will promote nearly every disease that has been named, but not least, atherosclerosis, the second study I would propose would never pass an ethics board to be done in humans. As such: Study 2: In primates, chimpanzees for example, have 2 groups that are fed weight-adjusted amounts of the previously quantified lipid oxidation products corresponding with the average daily American intake, and 1 group that serves as the control, with nothing added to their feed. Monitor all 3 groups for plaque formation/progression via CT angiography. Yes, and I will record an apology video titled "I Was Wrong" that I will post publicly and link to in a new thread on this forum, specifically in the "Health, Fitness, Nutrition, Supplements" subsection. For that to happen, I would need to intercept evidence of one or more of the following: 1. Industrial seed oil consumption lowers rates of LDL oxidation (which is universally acknowledged as necessary for LDL to be atherosclerotic) 2. Humans directly fed oxidized cholesterol do not develop atherosclerosis, ideally those with the lowest possible ApoB. 3. Humans directly fed oxidized phytosterols do not develop atherosclerosis, ideally those with the lowest possible ApoB. 4. Eliminating them entirely from someone's diet worsens their health (yes, that means that by and large, they will no longer be consuming processed foods, but that's the entire point, i.e., that these oils embody the epitome of ultra processing) What would you need to encounter Michael, in order to to begin advising others to never ingest industrial seed oils again? That's right, it's not a matter of lowering cholesterol, but rather, rendering it less susceptible to oxidation. There is actually no known mechanism by which saturated fat increases cholesterol. What actually happens has to do with decreased phytosterol intake when one transitions from a more plant-based, to a more animal-based diet, which just happens to correlate with an increased saturated fat intake. This can be appreciated upon considering the fact that saturated fat-rich, yet phytosterol-containing, coconut oil, does not affect one's lipid panel in the way that would be otherwise predict based merely on its saturated fat content (i.e., relative to the saturated fat-rich butter which is nearly devoid phytosterols). By consuming an appreciable amount of phytosterols, you actually artificially lower your cholesterol, and saturated fat simply restores it to a physiologic level.

I hope you develop an appetite for a slice of humble pie over the next decade, because that's what's on the menu. You will one day be thoroughly disgusted by the depth and breadth of human havoc downstream of these industrial oils increasingly inundating the modern food supply chain, and this moment in history will be seen for the clown act that it effectively is (i.e., the mainstream misunderstanding of cholesterol, the widespread dispensation of cholesterol-lowering medications, the demonization of saturated fat and the abominable advocacy of "heart-healthy" "vegetable" oils. Hold on to your hat my friend.

The most appropriate response to which, would seem to be "YIKES" and yet nobody is ringing the alarm bell amidst the rampant use of drugs that indiscriminately lower such. Once you appreciate the necessity and sufficiency of oxidative stress in promoting heart disease, it becomes apparent that targeting a lower cholesterol is profoundly inadequate and introduces adjacent consequences approximating the drool dribbling down to the lip and chin of a demented resident in an aged care facility. Here are the keys to the kingdom my friends, (if you never want to develop heart disease, dementia, or any of the thousands of so-called "diseases" that are downstream of the upstream oxidative stress) listed in descending order of importance, at least in my estimation, although I personally go out of my way to satisfy each of the following: 1. AVOID AT ALL COSTS notable pro oxidants such as: industrial seed oils, (corn, canola, cottonseed, soybean, sunflower, safflower, ricebran and grapeseed) smoking of any sort but most notably cigarettes, alcohol ingestion, exposure to air pollution, toxic heavy metals, pesticides/herbicides, excess UV exposure and radiation, for example emitted via medical procedures such as X-rays. 2. Get more antioxidants in your system (you may prefer nuts, seeds, and leafy greens, but I prefer pomegranate juice or wild blueberries in concert with vitamin C and E supplementation). If you do opt for supplementation, please just ensure your formulation offers not merely alpha-tocopherol, but too, gamma-tocopherol in your vitamin E supplement. 500mg of Vitamin C in supplement form is all you need to take at a time, twice a day if possible. 3. Be metabolically healthy (assess your fasting insulin and/or A1c in concert with your HDL and triglycerides to put your finger on the pulse of this). The reason that poor glucose control so greatly correlates with the modern diseases of civilization is that advanced glycation end products (AGEs) often undergo further oxidative modification. Excess iron can also introduce undesired amounts of oxidation, so ensuring that your ferritin does not creep too high is furthermore prudent, as is offloading such via whole blood donations as deemed appropriate. 4. Consume, if possible, 9x more (combined) saturated and monounsaturated fat relative to polyunsaturated fat (PUFA). Given that most folks here tend to lean plant-based, I would recommend prioritizing monounsaturated fat sources that are low in PUFA, such as macadamia nuts, to accomplish this. Now, as you read this, if you found yourself nodding in agreement while reading the first three points, but cringing your nose at the prospect of prioritizing saturated and monounsaturated fats relative to polyunsaturated fats, I leave with the following to ponder: Consider that the chemistry doesn't lie, is infallibly reproducible, valid, and more fundamental than are human outcome trials. Consider that a higher saturated and mono fat to poly fat ratio has the same outcome as the first three points that you were nodding to, in that it reduces overall oxidative stress. When the chemistry asserts that 2+2 = 4, question the pharma-funded human outcome data that says it "should" equal 5. Do not outsource the arithmetic, plug and chug the numbers for yourself and see if it makes sense what we've been told about saturated fat and cholesterol. I hope this reasoning resonates with you my friend.

Has your TG:HDL ratio been that high historically? At ~3 it is certainly fair, but lower would be even better (2 or even below 1 for example).

To anyone reading this, I would just honestly ask you to explore the possibility that the mainstream medical establishment has committed a cognitive blunder with ramifications spanning far and wide. Ask yourself if it really makes sense that we are artificially lowering our cholesterol below physiologic levels via the addition of a drug, which will almost certainly stifle the amount of cholesterol your brain needs to thrive, and your body needs to be hormonally optimized. Consider the oddity of the fact that our LDL target is continually decreasing, and the possibility that the oxidative modification of such, is perhaps the necessary, rate-limiting step for atherosclerotic development and progression, which we should be targeting. Consider the migration from a sole fixation on LDL, to now ApoB, as opposed to starting over from scratch, and building back our model from the ground up. We need a model that reconciles the fact that atherosclerosis rapidly progresses in rabbits who are fed pure, oxidized cholesterol, null and void of ApoB, LDL, or any lipoprotein for that matter. I recognize that this would be inhumane, but I often genuinely wonder how folks would interpret a study like this, replicated in humans, assuming it did indeed elicit rapid atherosclerotic activity as I predict it would. Could they finally relinquish their ties to the prevailing LDL/ApoB paradigm? Honestly, what is it going to take to see the truth? Take care friends.

I'll just preface by offering you my appreciation. As a fellow healthcare worker, I appreciate you man, and I hope the following expression of a number of different points of concern and contention that I offer, are well-received. At the end of the day, my hope is that someday soon we will all arrive at a satisfactory understanding of the cardiovascular disease underpinnings, so that we can best inform our, and our patients', daily actions to never need to deal with its consequences. Fair enough, I was just curious if you had any ideas of your own that may diverge from the mainstream understanding. Nevertheless, given the non-trivial number of times that the target LDL-C has been modified, (as depicted below) i.e., systematically lowered, my skepticism grows. In my paradigm however, it's unsurprising that said target has needed to be lowered, because as we lead lives that increasingly facilitate oxidation, most notably high PUFA intake by way of increased "vegetable" oil consumption, the percent of circulation Apo-B-containing lipoproteins that becomes oxidized, also increases. Metabolic disorders also factor into this, because uncontrolled blood glucose levels facilitate glycation, the products of which undergo oxidative modification. The paradigm I'm operating within would explain why both diabetics and those who smoke (and thus introduce themselves to oxidative stress) cigarettes are both at a much greater risk of heart disease, independent of Apo-B-containing lipoprotein concentrations. How does the lipid hypothesis reconcile these two observations, i.e., that those who smoke and have poorly controlled blood sugar have a greater ASCVD risk? What do you predict would happen if you fed human beings (with the lowest Apo-B on the entire planet) oxidized cholesterol that was devoid of any Apo-B-containing lipoproteins, i.e., just pure cholesterol that had been pre-oxidized prior to consumption? My concern is that this, to me, still illustrates a misunderstanding of the root cause of heart disease, and results in us combatting such with a bazooka which invariably introduces adjacent consequences, not least the deprivation of cholesterol cerebrally and the cerebrovascular diseases that could give rise to. I would rather enter the scene with a sniper rifle and address the root cause here, which I would submit is the oxidative modification of Apo-B-containing lipoproteins, and other things in actual circulation (i.e., in the luminal space) such as phytosterols and red blood cells. I believe Apo-B is simply a proxy for the amount of oxidizable lipoproteins, but that the rate-limiting step remains oxidative modification. Would you, rather submit that the rate-limiting step is the migration of Apo-B-containing lipoproteins into the endothelium? Once a plaque has formed and continues to grow, how are Apo-B-containing lipoproteins still able to traverse the endothelium? Gotcha. When you said "trapped lipoproteins" my concern was that you were unaware of reverse cholesterol transport. HDL is an important piece of the puzzle, I would agree. So painting with broad strokes, you would agree that net plaque deposition occurs when the rate of build up exceeds that of removal? Are you of the mindset that Apo-B is necessary (but necessarily sufficient) for atherosclerosis to ensue, and that if, hypothetically, we had none in circulation, plaque formation would be an impossibility? Lastly, I'm not sure that I understand your notion of "supraphysiological levels of Apo-B particles" as that would seem to suggest that modern humans are behaving in a way that renders higher Apo-B-containing particles in circulation than would otherwise be physiologically plausible. If so, could you please detail what that/those specific behavior(s) is/are, and if possible, what a physiologic amount of Apo-B in circulation would be? Thank you.

Thanks for explaining, I really want to better understand your position/paradigm. So you would submit that unoxidized Apo-B-containing lipoproteins can accumulate in the endothelium at a sufficient rate to cause plaque formation in and of themselves, and that the primary driver of that is the amount in circulation? Are you under the impression that the oxidation of these Apo-B-containing lipoproteins is inevitable, and that they truly are trapped in some inescapable sense? Do you see the atherogenic process as unidirectional, i.e., merely plaque deposition, or do you see it bidirectionally as being a certain rate of deposition, and a certain rate of removal, the net of these two processes, being what we macroscopically appreciate?

Could someone kindly articulate how ApoB, a mere transport protein, itself causes plaque formation?

Absolutely, necessitating nasal breathing by way of mouth taping has honestly been one of the highest impact decisions I've ever made on my day to day quality of life (I was a habitual mouth breather as well). 3M micropore tape effectively tops everything on the market in my opinion, and it's the most cost-effective.

I think you'll find this video I just released extremely useful, both in equipping you with not only a far more effective, but also affordable (1/60th the expense) method to enhance your nasal breathing:

Regarding Aubrey, my suspicion is that he was engaging in extended water-only fasting, a practice that necessitates electrolyte incorporation. For anyone nourishing themselves at least once every 24 hours, assuming an intelligently orchestrated intake, (i.e., ensuring micronutrient sufficiency from any and all angles) the fact that distilled water is absent minerals/electrolytes is entirely moot in my estimation. Water distillation emulates the water cycle, in fact superiorly, because it eliminates the unfortunate modern element that is air pollution, and the inevitable micro and nanoplastics therein. For anyone currently on the fence in their contemplation of whether or not to drink distilled water, I have just released this video offering an examination of my own reasoning in the hopes that it resonates with you.

The prospect of an IRL meetup with you all is attractive, indeed, we need to make this happen. @Schizophonia - would you like to arm wrestle me? We could also compare grip strength, engage in any relative strength showdown (i.e., max chins, dips, etc.) or opt for a day game manifesto (I have an early bedtime, lol) frame battling it out for who can pull and close the hottest woman in field, same day. I don't have a fighting background, but I'd be game to hop in the ring with you.

Not specifically/directly for sleep, no.

Good question, I personally don't pay any mind to that aspect of it. Here are some things I do to maintain sleep regularity: 1. After sunset I wear blue light blocking glasses and a red headlamp (I turn off all artificial lights in my living space). 2. I don't set an alarm to go to bed (except perhaps a time or two per year to catch an early flight). 3. I take a warm/hot shower a couple hours before my usual bedtime. 4. I use a 100% cotton sleep mask, Mack's 33 NRR earplugs, a nasal dilator, and 3M micropore tape (to necessitate nasal breathing) while sleeping. Sleep is such a superpower once you get things dialed man.