Jason Actualization

In order to optimize sexual performance in real life (i.e., erection quality) the optimal weekly view duration of porn expressed as a percent, rounded to the nearest whole number, is 0%. I have a high libido and, as such, the advice I would offer myself and others in a similar position, is the following: Ideally, absent the opportunity to be intimate with someone else, you would either abstain altogether or use your imagination while masturbating, visualizing yourself performing the act. Often times I will simply recall sexual memories of mine that I am particularly fond of. The goal (speaking merely for myself) was always to make memories, not fap to fantasies (these are inversely proportional, i.e., as the former increases, the latter will decrease until it reaches zero).

100%. Confidence is a master key to myriad doors which gatekeep many favorable experiences a man can have assuming he gains entry.

The belief itself has absolutely zero bearing unless it actually deters one from doing it in the first place. Unless I'm speaking or chewing, I'm mewing, but my initial motivation was purely to improve my breathing, and fortunately now it's something I just do unconsciously competently. 100%, this is the take home message that I believe everyone should leave with.

They have 2x the antioxidants of cultivated blueberries. I was born and raised in the state of Maine which produces something crazy like 99% of the blueberries in the U.S. If you ever get a chance to eat Wyman's wild blueberries, you will be sold haha. Eating foods that greatly enhance your antioxidant status such as wild blueberries is the #1 actionable step you can take to prevent cardiovascular and cerebrovascular disease. Unparalleled antioxidants which have been shown to not only prevent the progression of, but actually reverse plaque build up in arteries (PMID: 15158307). It is the #1 health hack that I universally recommend to folks.

For overall health/wellness: 1. Pomegranates (or 100% juice) 2. Blueberries (ideally wild) 3. Currants 4. Cranberries 5. Sweet Potatoes

I still maintain that you are severely B12 deficient regardless of what your labs say (i.e., the fact that you are within the "normal" reference range). Once you hit a four digit B12 level (i.e., 1000 pg/mL) come back and describe your new life experience. Until and only then would I wish to revisit the drawing board. For now, you have a gameplan my friend, you just need to execute. B12 deficiencies take years to manifest, and months to mend, possibly less if your doctor would actually sign off on you getting an intramuscular shot.

Do you have specific numbers you could share? Given this, I would be most concerned about your free testosterone. Unfortunately, what constitutes "normal" is a derivative of population-based data built around a Bell curve with a 95% confidence interval. This doesn't necessarily translate to what would make you specifically, feel normal, or better yet, optimal.

It's great man, and I love aesthetics too. I don't want to burst your bubble, but mewing honestly won't improve your jawline if you are beyond adolescence. That said, hopefully I can still convince you to do it nevertheless. Here's my take on it: mewing is nothing more than the correct tongue posture, and if you're not already doing it, then absolutely learn/practice until you become unconsciously competent. The #1 benefit to mewing is actually that it will prevent your tongue from collapsing your airway while you sleep, preventing sleep apnea which is arguably the most insidious health condition humans are currently contending with. It also greatly promotes nasal breathing.

Potassium and phosphorus do not cauterize. This is demonstrably false. Calves fed pasteurized milk do not die prematurely. Honestly my friend, the majority of these claims are not well-founded and most closely resemble lunacy in my estimation. That said, I do appreciate your take home message of defaulting to more ancestral ways and I'd like to echo that, while encouraging folks to also embrace and integrate the best of modernity (i.e., pasteurization, low temperature pressure cooking, water distillation, refrigeration, zinc-based sunscreens, polarized UV400 sunglasses, spot supplementation such as chelated magnesium, etc.) and to realize that you can actually leverage such to experience better health than would have been possible at any point in recorded human history.

Just ran the numbers, yes this checks out. The drop is not as drastic as I had assumed. A FFMI north of 25 is very impressive in my book, 28 (as a natural) is absolute top shelf, elite genetic superiority. Girls appreciate a developed male physique, but the concern in my estimation are the health-compromising and ego-driven lengths that guys will go to in order to achieve and supersede such, i.e., steroids, neurotic behavioral patterns in terms of training and nutrition, etc. It ends up devolving into a cock measuring contest and at some point you are in fact only impressing other guys. Confidence is the king at the end of the day, and one does not need an impressive physique to solidify that, albeit I do still believe the pursuit of building a "better" body offers immense carryover value into other areas of life.

Excellent. We have a fellow member on this forum, namely ZenAlex, with a 292 ng/L level, giving rise to a host of problems, exercise intolerance among them. Glad to see your levels being appreciably higher, although personally and in advocating for others, I suggest striving for for 1000 minimum.

Bingo. The external validity of most studies is quite poor, i.e., one cannot, in confidence, blindly extrapolate the findings of that study to daily living. Arriving at truth mandates the scrutiny and synthesis of many studies until a self-consistent picture emerges.

The one major problem here is that FFMI doesn't translate across different body fat percentages, i.e., a 28.4 FFMI at 15% will drop drastically once that person reaches single digit body fat, but yes, great physiques are indeed possible naturally. In terms of modern fitness influencers, a great example of what's possible naturally with top 10% genetics is Jesse James West. But yes, you are correct, genetics are a primary factor, so much so that people with elite genetics will exceed the physique, naturally, of someone with poor genetics who is on gear. I have been training for over a decade, and while rare, there are literally guys bigger than me who have never stepped foot in a fitness facility, lol. What's possible is all relative to your starting stats. Ronnie Coleman looked absolutely insane as a natural lifter (his mom probably has more muscle than every man on this forum, myself included, lol).

Glad you supplement, that's great. I'd be curious to know the exact number since the reference range for B12 is notoriously low/suboptimal. Sure, the diet may not be worsening your situation, but it would all be relative to what your diet consisted of back then. As for testosterone and SHGB, I would be concerned on several levels in terms of optimizing these, but not least ensuring you're getting enough zinc in your diet, especially relative to copper.

I'm curious if you happen to know what your total and free testosterone is, as well as SHGB? Do you have a recent vitamin B12 level as well?

Lol, yes I recognize that, great discussion nevertheless. But where is alcohol found in nature in appreciable/toxic amounts in whole food? Glucose, unlike alcohol, neither poses hepatotoxic concerns, nor in any way deleterious in healthy individuals who maintain physiologically sound blood sugar levels (glucose is not what's causing insulin resistance, but excess fructose is certainly contributory). Perhaps I should rephrase and say that the brain's need for glucose is why gluconeogenesis exists. Glucose is absolutely essential at the end of the day, no matter how keto adapted one is. I still maintain that glucose is the preferred energy source, but perhaps that is less granularly able to be elucidated than is the necessity of glucose. At rest, yes, but for example, to meet the demands of a weight training session, anaerobic glycolysis will demand the use of carbohydrates (glycogen) stored in the muscles. My preference is to consume a carbohydrate rich diet (200+ grams daily) with enough dietary fat to optimize my endocrine system (1g/kg) and by doing this, in concert with infrequent meals (2 per day without snacking in between) I consider myself extremely metabolically flexible. The keto/carnivore folks who submit that the Randle cycle is my enemy (because I co-consume plentiful amounts of both carbohydrates and fats) are also the same folks who fail to appreciate the importance of energy balance. They actually believe that calories are entirely irrelevant, which is, quite frankly, beyond me to cognize their contention.

Yeah, their reasoning doesn't resonate with me. The bottom line is that the brain can utilize ketones when glucose is in short supply, but it prefers glucose as evidenced by the fact that, when both are readily available, the brain burns glucose. The brain's preference for glucose is why gluconeogenesis even exists. Throughout human history a reliable carbohydrate source was not always available and so we needed a backup fuel supply. Having a generator (ketosis) kick in when the electricity goes out (carbohydrates are scarce) is useful, but not the optimal way to power your home long-term after the electricity (carbs) comes back. Even a FULLY keto-adapted person needs 30-40 grams of glucose for the brain per day. I hope folks really let that land, because while sure, you can omit such consumption exogenously, and burn through a lot of amino acids instead, but then your protein requirements greatly increase (carbohydrates are protein-sparing). Carbohydrates are not causing the human health crisis we currently face. Unfortunately they have been erroneously demonized. Perhaps these folks no longer exist, but if there any remaining keto proponents who submit that the brain does not need glucose, here is the test they need to run: inject a traditionally fatal amount of rapid-acting insulin. If they are fully adapted to ketones and their brain no longer requires glucose, they should observe no ill effects whatsoever as they should be immune to the blood glucose drop.

Bingo on the latter, but what makes you so sure of the former?

I agree with your overall position. For longevity, nothing beats low intensity steady state cardio, i.e., walking. My philosophy is to prioritize food first. I believe that when one's diet is truly dialed in, exercise nearly becomes obsolete to maximize one's health (which is not to be conflated with physical fitness, as these are separate entities that, at their extremes, are indeed at odds with one another).

The candle that burns twice as bright burns for half as long. Extreme activity is at odds with longevity, yes.

Bingo. Ketosis is a starvation response my friends, and, while useful, is not something to strive for just for the sake of being in that state of "fat-burning" which, when energy is equated, offers no unique benefits other than perhaps satiety, but I would maintain that becoming metabolically healthy and flexible with at minimum, a moderate carbohydrate intake (at least 150g bare daily for men) will reign supreme.

Woah, that is shocking. Sinclair always struck me as a nice enough lad, thanks linking this!

You make a good point. For me, I sleep and exercise to be a high testosterone man which renders a qualitative experience that I'm partial to. I do not do these things for the sake of themselves, but rather, the life experience they afford me. I agree, I would not see the point in that. Personally, I love sleeping like a rock and waking up as hard as one, lol. I also love picking up heavy things and putting them down. For the average person though, exercise is quite overrated and I believe nutrition is far more important for quality and duration of live. The healthiest form of exercise is honestly just walking.

Unavoidable, yes. The immune system will not inherently identify them as foreign and mount an attack unless/until they become oxidized, so their presence alone is necessary but insufficient. The oxidation can occur both prior and subsequent to entry into the subendothelial space. To be crystal clear here, the fact that these lipoproteins contain ApoB has absolutely nothing to do with the pathophysiology. The only reason ApoB correlates so favorably with CVD is because it is contained within the lipoproteins that are the most prone to oxidation. Oxidized lipoproteins (or other oxidized things) do not need to enter the subendothelial space to initiate plaque formation, they can simply adhere to the endothelium and initiate it. Oxidized lipoproteins and, for example, red blood cells, etc., are seen as foreign objects and are attacked by the immune system, and that response is responsible for the inflammation and plaque development. I believe we should set our sights on ascertaining what makes the particle more prone to oxidation, not to entering the subendothelial space. It happens in both locations: the initiation of atherosclerosis requires oxidation to occur inside the subendothelial space, and the progression will occur within the circulation (once plaque forms, these particles are no longer traversing said plaque to enter the subendothelial space). Right, so technically CVD is actually caused by our immune system defending itself in response to the oxidative stress. Again, ApoB has nothing to do with this process, it’s actually an innocent bystander, but I see what you’re saying and believe that’s correct, yes. Yes, I find it obnoxious that every 33 seconds in America alone, someone drops dead of this disease. I will preface what I’m about to suggest by acknowledging its seemingly radical nature, and too I will start by agreeing that it’s not 100% avoidable (without the right information). That said, I honestly believe that this is the easiest disease to prevent and reverse with the right understanding of it. They don’t have to be in order to be atherogenic. Great point, I see OxLDL in the serum as simply a surrogate for the overall oxidative stress in ones body, which is more insightful than any other cholesterol test currently available, in my estimation. Whether they enter the subendothelial space or just adhere to the endothelium makes zero difference. After the initial plaque formation, newly oxidized lipoproteins no longer even come in contact with the endothelium, they merely bind to the plaque already there and cause it to thicken. ApoB is a red herring and LP(a), while useful, is simply another lipoprotein that is more susceptible to oxidizing. The strategy still is to lead lives that render more oxidation-resistant lipoproteins. Highly recommended man, this is the top health tip I give to everyone. It can reverse plaque, yes. In the 2004 study cited before, the control group had their carotid intima-media thickness (IMT) increase by 9% after 1 year, whereas the intervention arm entailing PJ consumption, resulted in a significant IMT reduction, by up to 30%, after 1 year. What do you hypothesize the cause to be in this case? I should be clear too and say that the cause of heart disease is the defense mechanism employed by our own immune system (chronic inflammation) but what elicits the mounting of that response is the imbalance of oxidative stress relative to antioxidant activity. I'm not sure about this one. Yes, artificially lowering cholesterol is not without consequence, and my greatest concern are the cerebrovascular conditions that can arise in time. They are rich sources of easily oxidizable phytosterols and they also contain ancestrally inconsistent amounts of linoleic acid which increase LDL susceptibility to oxidation. And this is where we face the fork in the road and may have differing epistemic assumptions. This may very well be the most important point I’ve ever made on this forum because it cuts to the core of our base assumptions. There is a lot of talk about valuing the human outcome studies and disregarding, or at best, putting on the backburner, mechanistic data. Here is the problem: if human outcomes are the truthful territory we wish to explore, the human outcome data is a misleading map that is at best, incomplete, and at worst, entirely erroneous. So, while I agree wholeheartedly that actual human outcomes are what we actually care about and are the ultimate arbiter dictating what constitutes a healthy lifestyle, the problem is that the data pertaining to such has led us astray. When we see whether or not linoleic acid increases LDL susceptibility to oxidation, it not only does so, but it happens every single time. It’s very black and white. If mechanistic studies are black and white portraits, human outcome studies are nebulous water paintings that elicit different moods and feelings for different folks depending on how they happen to view and interpret such. Mechanistic studies corroborate with one another, but human outcome studies do not. The problem is that the direction that human outcome studies point to is something people cannot unsee. They aren’t able to scratch the entirety of that data set and construct an entirely new understanding from ground zero, this time, being sure to lay down merely solid bricks, but never broken ones. I am personally convinced that these oils are in fact the primary driver of heart disease. Unfortunately, you would be hard-pressed to find a person, let alone a cohort of folks with an adipose linoleic acid (LA) level below 10%. These people are becoming increasingly rare due to the landscape of the modern food supply chain. I wish we had data comparing people who have single digit LA levels in their adipose to people with 20%+. This, in my estimation, is absolutely vital to getting human health back on track (i.e., subtracting the seed oil). Definitely my friend. At the end of the day, the only aspect, as far I know, regarding your practical takeaways, that I disagree with, is the caution you exert pertaining to saturated fat intake. But honestly, even though I prefer a higher saturated fat intake, so long as people are not consuming excess PUFA, I am perfectly fine with that (i.e., we agree that monounsaturated fats are innocuous). Could you explain how ApoB exactly it causes CVD progression? Absolutely not, oxidation is necessary for atherogenic activity, ApoB is a transport protein that is not implicated in the causal pathway. That said, the ApoB number indicates the total number of potentially atherogenic particles, the higher the number the higher the risk, all else equal. But the optimal strategy then is not to bottom this out at all cost, in my strong opinion. I'd like to read this research if you don't mind taking the time to cite them for me. I would prefer to be selective with the research findings I integrate into my understanding, emphasizing and opting for the quality and replicability of a sniper rifle, as opposed to the magnitude and chaos of Oppenheimer’s atom bomb. The fastest way to end this debate would be to conduct a RCT wherein one arm of the trial is fed fresh cholesterol, and the other is fed oxidized cholesterol. The confusion would clear very quickly. That said, I'm confident enough in this causal pathway that I don't need to see this (admittedly) highly unethical study transpire in order to satisfy my curiosity, but nevertheless I do recognize how impactful it would be in advancing our understanding of CVDD. That said, I recognize not everyone will find my train of thought equally compelling/convincing, and so I must rest my case.

How do you mean? Ideally you'd sleep even more, closer to 1/3 of it (for the vast majority of people, myself included). Sleep is the cornerstone of enhancing the quality and quantity of one's life. When I'm sleeping this well, I feel on top of the world: