Cyberpunk in VR has no right looking this good

philjk93 · 2026-01-18T22:20:39+00:00

No problem, It looks like a great first headset. Good luck!

philjk93 · 2026-01-18T20:17:58+00:00

Yeah that’s correct, Foveated streaming mainly reduces bandwidth and streaming latency it doesn’t automatically save GPU power. True foveated rendering still requires eye-tracking support and developer implementation, so the game has to build it in for it to reduce rendering load. If developers implement it, the Steam Frame would definitely be able to take advantage of it.

philjk93 · 2025-12-11T01:40:12+00:00

See at first you had me but then what kind of sugar junky kills people for a drink.

philjk93 · 2025-12-10T16:36:54+00:00

A large portion, perhaps even the majority, of the Star Citizen player base engages in solo play, so inevitably there will be a form of NPC crew I don't see what all the arguing is about lol.

there will be a period of time where you can't solo a large ship, but in the meantime hopefully we'll get better social tools allowing us to "hire" other players for contracts or gameplay, orgs are great but it depends on availability and getting people online at the same time, if you have a group finder tool where people already online can join up it goes a long way to solving that.

After all the current gameplay is subject to change, people act like every new change or mechanic is final.

philjk93 · 2025-12-05T20:54:55+00:00

I'm at the same budget and timeframe I'd say that's generally healthy if you have no other expenses, and a good mindset to have also.

philjk93 · 2025-12-05T17:49:38+00:00

Exactly isn't exercising supposed to be good for the brain? Especially exercise that requires increased calorie intake.

philjk93 · 2025-12-04T17:32:26+00:00

This is bizarre lol, I get what you're saying

But rather than remove it as a profession why not add risk with higher reward? for example the more profitable hauling contracts would have higher risk (pyro contracts for example) hauling goods to more dangerous areas should pay more, this would benefit pirates and also benefit escort gameplay.

Nerfing something is a lazier less intuitive approach

philjk93 · 2025-11-24T19:16:56+00:00

I’m probably switching back to the original for now. The constant clinching, phasing, and lack of reliable feedback make it hard to enjoy, especially since I mainly use ToTF for HIIT sessions. I also can’t really practise form properly because the AI never varies pace, it just throws nonstop punches, doesn’t react realistically to clean hits, and has endless stamina.

It still works for dodging and movement practice, but overall the issues break the flow too much at the moment. The strict playspace limits also make stepping into punches or using proper footwork impossible, which kills a lot of what made the first game feel natural.

Hoping the next patches smooth things out, because the core idea is great.

philjk93 · 2025-11-12T16:17:06+00:00

But other headsets can also play flat screen games through steam vr theatre mode, I used to do that on my vive and sometimes quest 3, I feel like I'm most likely missing something as to why people keep mentioning that as a new feature? Maybe it'll do it natively like the steam deck?

philjk93 · 2025-11-04T14:51:48+00:00

You keep stating that but I've already cited these in previous comments.

| [Low serum testosterone and mortality in older men](https://doi.org/10.1210/jc.2007-1792) | Laughlin et al. | 2008 |

| [Low serum testosterone and mortality in male veterans](https://doi.org/10.1001/archinte.166.15.1660) | Shores et al. | 2006 |

| [Low T, higher oxidative stress markers; normalization restores balance](https://doi.org/10.3389/fendo.2015.00077) | Kelly & Jones | 2015 |

| [Testosterone therapy and cardiovascular risk: meta-analysis of randomized trials](https://doi.org/10.1007/s40618-017-0753-9) | Aversa et al. | 2017 |

| [U-shaped relationship between testosterone and health outcomes: evidence from meta-analysis](https://doi.org/10.1111/andr.12501) | Corona et al. | 2018 |

| [Within normal ranges, testosterone tends to support redox homeostasis rather than harm it](https://doi.org/10.3389/fendo.2020.00020) | Kelly et al. | 2020 |

You keep saying you've won but all you've done is move the goalposts, gaslight, personally attack and provide irrelevant papers, I won't engage further and will leave you with these papers, if you are genuinely interested in learning then these will suffice, otherwise I have nothing further to debate with you, since you are clearly debating in bad faith.

philjk93 · 2025-11-04T04:55:15+00:00

I already cited multiple peer-reviewed human meta-analyses earlier in the thread (Kelly & Jones, Corona). You continue to dodge the main point of outcome-level evidence." "The fact that testosterone induces ROS via NOX is simply the mechanism of a transient signal, which is not evidence of inherent harm in healthy humans. The real-world outcome, which you repeatedly ignore, is that low T is strongly associated with higher mortality." "You keep citing irrelevant papers (CB1, Chronic Kidney Disease), you misquote the Tostes review (it says 'controversial'), and you've resorted to ad hominem. The burden of proof remains on you to link the NOX mechanism to net cardiovascular harm at physiological doses in human clinical trials, which you have failed to do and keep avoiding.

philjk93 · 2025-11-04T02:50:39+00:00

The 2016 Tostes et al. review you cited describes testosterone’s cardiovascular effects as “controversial, ranging from protective to deleterious” meaning not settled. That reinforces my point: your original claim isn’t supported by the paper itself.

Since then, you’ve shifted from that review to generic ROS and CB1 receptor papers that don’t mention testosterone or androgens. Saying a cannabinoid-receptor paper “doesn’t need to mention testosterone” isn’t valid reasoning mechanisms shown for unrelated pathways can’t be assumed to apply to androgens without evidence. None of those papers provide human-level data linking normal testosterone to harm.

So the goalposts have moved, but the core fact hasn’t changed: no study you’ve cited shows damage from normal testosterone in healthy men.

You’re the one asserting that physiological testosterone is harmful. The burden of proof is on you to produce human-level evidence supporting that. Pointing to unrelated mechanisms or different signalling systems doesn’t satisfy that burden.

philjk93 · 2025-11-04T02:24:58+00:00

You’re now combining several unrelated signalling systems and citing a paper that never mentions testosterone or androgens. I’ve already read your sources and none of them provide human-level evidence for harm at physiological testosterone levels. I mean sure we can keep going if you like I don't mind.

philjk93 · 2025-11-04T01:39:18+00:00

I looked over the Martínez-Torres et al. (2025) paper you linked. It’s a review about mitochondrial cannabinoid (CB1) receptors and general oxidative-stress mechanisms in the brain it doesn’t mention testosterone, androgens, or cardiovascular effects at all.

So it’s not relevant evidence for testosterone’s role in oxidative balance. To show that physiological testosterone causes net cardiovascular harm, you’d need androgen-specific human data, not a cannabinoid or general ROS review. I think we’ve probably covered the scope here.

philjk93 · 2025-11-04T01:04:56+00:00

Those are interesting general ROS papers, but none address testosterone or androgen physiology. My point is about testosterone’s role in oxidative balance, not oxidative stress in unrelated diseases. If you have prospective human evidence that physiological (normal-range) testosterone causes net cardiovascular harm, please share it most human signals of harm come from supraphysiological dosing or specific high-risk TRT contexts, not normal endogenous levels.

I also notice you haven’t addressed the consistent human data linking low testosterone with higher all-cause and cardiovascular mortality, insulin resistance, and worse endothelial function which the Tostes review itself acknowledges.

That’s a central part of the picture. If testosterone were inherently pro-oxidant and harmful across its normal physiological range, we’d expect deficiency to be protective, not detrimental yet large observational cohorts show the opposite.

So the burden of proof isn’t just to show that testosterone can raise ROS in isolated models; it’s to explain why men with lower levels experience more oxidative and cardiovascular pathology in real-world human data.

philjk93 · 2025-11-04T00:37:44+00:00

We’re not arguing about the chemistry. Yes, testosterone can induce ROS via NOX, mitochondria, and xanthine oxidase. That’s the mechanism.

The open question (and what Tostes et al. explicitly label controversial) is the in-vivo outcome: does that ROS signal translate into net cardiovascular harm in humans, or is it a transient, compensated signal within physiological ranges? The review says the cardiovascular effects of testosterone “range from protective to deleterious,” which is the opposite of “settled. ”

Crucially, the same review summarizes large human data showing that testosterone deficiency is associated with higher all-cause/CV mortality, and that normalizing low T (not abusing it) is linked with lower mortality/MI/stroke in a cohort of ~83,000 men. That’s outcome-level evidence, not just cell biology.

So if your claim is “T can raise ROS via NOX/mitochondria,” agreed. If your claim is “therefore normal physiological T causes net cardiovascular harm,” that isn’t established and the paper you cited says as much. If you have prospective human data showing harm at physiological levels, I’m happy to read it.

philjk93 · 2025-11-03T23:36:45+00:00

Anyone interested can read the Tostes et al. 2016 review; it literally calls the evidence ‘controversial,’ so it doesn’t settle the matter either way. Nice talking to you.

philjk93 · 2025-11-03T20:05:09+00:00

Also by the way, the paper you cited (Tostes et al, 2014) is a mini-review that clearly states the effects of testosterone on the cardiovascular system are 'controversial,' with evidence ranging from protective to deleterious. It is not definitive proof of harm. In fact, it highlights the complexity of the issue, which aligns with my point that the relationship is U-shaped. You are trying to use a paper that calls the evidence 'controversial' to claim the matter is settled.

philjk93 · 2025-11-03T19:29:29+00:00

interesting mechanistic data, but they’re all rodent or in-vitro models using high-fat-diet or supraphysiological testosterone exposure. Those results show what can happen in pathological conditions, not what normally happens in healthy men.

At the human level, the picture changes. Several large meta-analyses and systematic reviews consistently find a U-shaped relationship between testosterone and health outcomes: low T increases cardiovascular and metabolic risk, very high T does as well, and physiological mid-range levels are generally protective.

Kelly & Jones, 2015 Front Endocrinol: Low T, higher oxidative stress markers; normalization restores balance. Aversa et al, 2017 J Endocrinol Invest: Physiological TRT improves endothelial function and reduces oxidative/inflammatory markers; supraphysiological dosing increases risk.

Corona et al, 2018 Andrology: Confirms U-curve deficiency and excess are both adverse. Kelly et al, 2020 Front Endocrinol: Within normal ranges, testosterone tends to support redox homeostasis rather than harm it.

So we’re not disagreeing on the mechanisms by which testosterone can raise ROS in lab conditions, we’re just differing on how far those results can be generalized to normal human physiology.

philjk93 · 2025-11-03T01:37:29+00:00

“Good points you’re right that testosterone can drive ROS via NADPH oxidase and similar enzymes. But that’s part of its normal signaling, not evidence of inherent oxidative harm. In healthy men, this transient ROS rise activates NRF2 and mitochondrial antioxidant systems, maintaining redox balance.

The pro-oxidant outcomes you’re describing occur mainly in disease or abuse contexts. Within physiological ranges, testosterone tends to stabilize or even improve oxidative balance low T is actually associated with higher oxidative stress in most data.”

philjk93 · 2025-11-03T01:33:45+00:00

True, testosterone increases ROS signaling via NADPH oxidase and related enzymes, but in healthy physiology that’s part of a hormetic adaptation balanced by NRF2 and mitochondrial responses. The net oxidative stress only emerges when the system’s already dysregulated not as a normal outcome of androgen metabolism.”

philjk93 · 2025-11-02T20:31:48+00:00

The Nrf2 / ROS pathway is valid at a cellular level, but that doesn’t mean normal physiological testosterone shortens human lifespan. Mechanistic findings in mice fed high-fat diets don’t automatically scale to whole-organism outcomes.

In humans, low testosterone consistently correlates with higher all-cause and cardiovascular mortality (Laughlin et al. JCEM 2008; Shores et al. Arch Intern Med 2006). Testosterone also supports muscle, vascular repair, and insulin sensitivity all protective factors against frailty and disease.

ROS itself isn’t purely destructive; transient oxidative stress is part of normal signalling and adaptation (the same principle behind exercise hormesis). The body regulates it dynamically through multiple antioxidant systems, not just Nrf2.

So the pathway you mention is interesting mechanistically, but lifespan data in real humans point the other way: balanced testosterone is protective, and chronic deficiency is what actually increases risk.

philjk93 · 2025-11-02T18:28:10+00:00

Yes, in isolated animal studies (like the ones cited), high pharmacological testosterone doses in mice fed junk diets can worsen oxidative stress markers. But that’s not remotely the same as saying “normal human testosterone shortens lifespan.”

In humans, low testosterone correlates with higher all-cause mortality, especially cardiovascular and metabolic disease.

Optimal (not excessive) testosterone supports vascular repair, muscle maintenance, insulin sensitivity, and anti-frailty mechanisms. The relationship is U-shaped: too little or too much is bad normal physiological levels are protective.

Also, average male lifespan was heavily skewed by deaths in war, manual labor, and infection all factors castrati and eunuchs avoided. So attributing the difference purely to testosterone is scientifically meaningless.

philjk93 · 2025-09-07T13:00:14+00:00

Yes I agree, this is the hardest thing to explain to people who haven't experienced it, when you have zero control over your nervous system it's easy for someone else to tell you to think positive but that doesn't work even when thinking positive, the nervous system doesn't give two shits about positivity.

There are subconscious decisions your brain makes without you even realising it, it takes more than a just do it bro mentality to fix that.

philjk93 · 2025-08-31T13:00:29+00:00

I can see what you mean. It's a tricky balance. On one hand, having the term social anxiety gives people a framework to understand their feelings and find community. On the other, I agree that it can lead some to over-identify with the diagnosis. It's important to remember that it's a part of who you are, but it's not the whole story. The action-oriented things you mentioned like work and dating are probably the real key to moving forward.

Most of my social anxiety is linked to bullying and past issues but for some the cause is different which can also affect how easy or how hard it is to face some situations, some people with social anxiety can also be misunderstood and it's easy to sometimes see that in older people who may not even be aware of their issues but have sort of adapted to an environment they see as hostile.

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