Aside from the EQ and Bass Enhancement sections what should I do in the rest? What's the best and most optimal settings for my current setup? As a side note there's an option to completely turn off DTS, Stereo Sound Enhancement and Reverberation if that helps.
Snapdragon 8 Elite Gen 5, 185Hz display, 9000mAh battery, 100W/120W fast charging. Pretty solid specs.
I now have two Alpine SPR-10TW tweeters installed in the front in the A pillars at the top and two Alpine S2-S10TW tweeters in the back right above the door handles. I also now have four Pioneer TS-Z65F coaxial speakers in the doors. The problem is that the sound is too harsh and bright and surprisingly the new Alpine S2-S10TW tweeters are way louder (and harsher for me personally) than the older Alpine SPR-10TW which I didn't expect at all.
Anyways I have 4 Infinity REF-6532EX speakers that were removed and basically replaced with the Pioneer ones. Should I put them back instead so that the sound becomes much warmer and more natural or will I lose alot in terms of sound quality? Because apparently the Pioneer TS-Z65F speakers are more dynamic and energetic in the mids than the Infinity ones so I don't want to sacrifice that good midrange.
This is just temporary though until I can buy 4 separate midrange woofers and install them in the car doors and avoid all that excess treble and highs. I've already increased the mids through my DSP (my headunit has a built in AKM AK7738 DSP) in order to compensate and balance the strong highs but the sound is still very bright and harsh. Should I switch back to the Infinity speakers?
I already have a JBL subwoofer with a built in amp in the back. I'm willing to put these speakers and tweeters in the front (tweeters specifically in the A pillers). Will this setup cause too much brightness or harshness?
This is a very long post but I had to really discuss it because I'm just sick of all the psychiatrists that I've been through throughout my life that gave me antipsychotics next to my antidepressant only to make my situation way worse and completely hopeless.
Apparently it's a very common practice to use an Atypical antipsychotic as an augmentation to antidepressants even if the patient already experiences Anhedonia and Apathy that was either there before he started the antidepressant or got worse after the addition of it (as is the case with alot of the SSRIs).
Now even though they argue that certain atypical antipsychotics such as Aripiprazole are not only Partial D2/D3 agonists with low intrinsic activity which therefore significantly reduce dopamine which would therefore worsen Anhedonia and Apathy (therefore becoming counterproductive) but they also argue that this usually comes with strong 5HT2A antagonism that supposedly helps reduce the side effects perceived from this significant dopaminergic reduction such as Akathisia. In reality that's not the case.
Cariprazine, Aripiprazole and Brexapiprazole are atypical antipsychotics that share the same function as D2/D3 partial agonists but with different intrinsic activities that are in the end very low compared to that of a full agonist and therefore act much more as stepped down antagonists rather than full and down to the throttle antagonists. This apparently reduces dopamine where dopamine is usually high such as in the Striatum and Nucleus Accumbens while the 5HT2A antagonism increases dopamine where dopamine is generally low such as in the Prefrontal Cortex.
Now this would be very beneficial in certain disorders where this is actually the case and that dopamine is very high or supersensitive in the Nucleus Accumbens and Striatum and is very low in the PFC such as in Schizophrenia therefore their use in conditions like these makes sense. Now why in hell would they be used in conditions that actually have low dopamine everywhere including the Striatum, Nucleus Accumbens and PFC and not just the latter? Most of those who're depressed are people who have low dopamine in those 3 areas hence why they already suffer from Anhedonia and Apathy. Why would I give them such drugs in the very first place?
To make matters worse they're rarely used alone and are mostly used as augmentations to antidepressants which ends up making the symptoms way worse because guess what? The most widely used antidepressants are SSRIs/SNRIs all of which at least inhibit 80% of the SERT and therefore end up overactivating the 5HT2A/C receptors which end up reducing dopamine and norepinephrine even further.
Now even if the strong 5HT2A antagonism from those Atypical Antipsychotics gets to reverse some of the SSRI/SNRI induced reduction in dopamine and norepinephrine in the PFC they mostly lack any strong 5HT2C antagonism/inverse agonism and therefore end up lowering dopamine even more in the Striatum and Nucleus Accumbens therefore not only causing Akathisia (very common when an Antipsychotic is added to an SSRI/SNRI) but also significantly worsen the Anhedonia and Apathy along with causing patients to significantly gain weight that can be very hard to lose afterwards if they ever decide to stop.
Finally multiple Meta Analysis studies confirm that Atypical Antipsychotics when used as augmentations in depression are generally not only less efficacious than placebo but also have very poor tolerability due to the many unwanted side effects that come with them. I'll leave the links down below for everyone to see and I really hope someone can prove me wrong or explain any misconceptions for me.
https://pmc.ncbi.nlm.nih.gov/articles/PMC4756722/
https://pmc.ncbi.nlm.nih.gov/articles/PMC7968624/
Basically all of the upcoming models will have a minimum of 185Hz. That probably means no more 2K phone screens and all of the upcoming will just be 1.5K. The 185Hz feels way too extreme especially for those who just want a budget or a mid tier option and aren't even into gaming.
The most useless epic weapon out there. Pretty sure the stolen stats don't make that much of a difference.
Has anyone tried Piribedil for depression (specifically for apathy/anhedonia) especially in Atypical Depression? It's supposedly a dopamine agonist but unlike Pramipexole and the rest of the dopamine agonist family it's also a very potent Alpha 2 antagonist which therefore increases norepinephrine which therefore increases dopamine in the PFC.
In fact this is very unique and quite different since nearly all of the available dopamine agonists are as selective as possible for the D2/D3 receptors which therefore significantly increases dopamine in the Striatum and Nucleus Accumbens at the expense of dopamine in the PFC therefore causing impulsivity and sleepiness/sleep attacks.
This extra Alpha 2 antagonism would basically make Piribedil pair really well with a SNRI/NRI for this very specific reason since it supposedly lifts the noradrenergic brakes off and allows the NRI component to work as strongly and effectively as possible. Also surprisingly those who respond pretty well to it are depressed people with low baseline dopamine or more specifically low dopamine metabolites (specifically the homovanilic acid or HVA metabolite) so I'm very curious about it especially since it's not used as commonly as Pramipexole or other dopamine agonists in general.
Hope everyone can share their full experience here. I've also attached the relevant and important links down below if anyone is interested in reading more about it.
https://en.wikipedia.org/wiki/Piribedil
https://www.gizmochina.com/2026/06/16/oneplus-16-185hz-display-bezels-under-1mm/
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It seems like it won't be pushing upwards towards 240Hz like it was previously reported. It'll probably be just like the Honor Win which basically maxes out at 185Hz. Still there are currently only 4 social media apps that support a refresh rate higher than 120Hz so I doubt this would be beneficial outside of gaming and in the regular day to day use apps.