A 22-year-old student teacher in Illinois sent a private Snapchat message to her boyfriend and two roommates. A student had walked up to her laptop and deleted her lesson plan mid-class. frustrated, she typed something like "should I shoot him" with a gun emoji. venting. four people. private group chat. An hour later, police walked into her school and arrested her. here's what happened in between. Snapchat's AI scanned the private message. flagged it as a potential threat. automatically reported it to the FBI. the FBI forwarded it to local law enforcement. deputies arrived at the school within the hour. she cooperated immediately. handed over her phone. when shown the message she said: "oh yes. okay. yeah. i'm realizing that was a bad joke. i did not mean it at all serious at all." police determined she was not a threat. school officials determined she was not a threat. prosecutors reviewed and issued a disorderly conduct charge. she was released the next morning. she lost her student teaching placement. This means: Snapchat scans private messages. Not just public posts or stories. private group chats between you and your closest contacts. automated AI. no human reviewed it first, got flagged and reported. Snapchat AI → FBI → local police → school → arrest. in under an hour. Snapchat's privacy policy says it may share your information with law enforcement when it believes there is a risk of harm. the definition of "risk of harm" is determined by an algorithm. you are not told when a message is flagged. you are not told when a report is filed. you find out when the police arrive. the message was private. it wasn't.

Okay hCG masterclass for the people. Exogenous androgens whether its just TRT or full on blasts will shut down your HPG axis we all know this. This means no signal to your testicles to keep making testosterone as there's plenty in the system. Most people think hCG is only use to "keep your balls big" or just to "preserve fertility" and it's not quite that simple although both do occur. hCG is made up of 2 parts, an alpha and beta subunits. The alpha subunit is exactly the same for hCG, FSH, LH and TSH. The beta subunit is what allows allows it to be specific for the LH receptors in the Leydig cells and prevents its breakdown. Small caveat hCG can technically bind to the TSH receptor due to the same alpha receptor. However, the binding is incredibly weak - like 1/4000th of actual TSH. Unless you're taking doses of 5000iu+ in one go this isn't at all a problem. Endogenous LH has zero cross reactivity with the TSH receptor and hCG has zero cross reactivity with FSH receptor. Once hCG binds to the LH receptors in the Leydig cells it activates cAMP, PKA blah blah intracellular mechanisms. The aim of the game is to express the Steroidogenic Actue Regulatory (StAR) protein. This is what allows the cells to produce testosterone. But that's not where it starts. The first step is to force cholesterol into the mitochondria and create pregnenolone - the mother hormone. It is pregnenolone that then gets converted into progesterone or DHEA, the latter then eventually becomes your testosterone. The progesterone has a massive role in regulating your CNS. The binding of hCG to the LH receptors is also what leads to synthesis of aromatase enzyme. It's famously known that AIs do not work to block the aromatase in your testes, but why? The concentration of testosterone in your bloodstream is much much lower than the concentration in your testes. The AIs have no problem saturating aromatase in fat and muscle. But they are simply outcompeted when it comes to the testes. Especially when you consider how little of your oral dose will get to your testes in the first place. Now onto the fertility side of things. Your intratesticular testosterone (ITT) levels need to be like 100x higher than that in your bloodstream for sperm production. hCG allows this to take place and your Leydig cells pump out testosterone into the interstitial space. A hCG only protocol prioritises raw sperm yield over optimal quality because of the lack of FSH. ITT prevents the death of sperm getting them through the first couple of phases giving you a viable sperm count. FSH is what allows phase 3 to take place which is essentially quality control - building the head and tails of the sperm properly. But hCG has no FSH activity and therefore no Sertoli cell activation so sperm counts are good but sperm quality isnt the best. But usually still enough for most men to be fertile (you can always do a sperm analysis to check if curious). So if there's no FSH how do any sperm make it alive? The testicles are separated into 2 main compartments. The interstitial space where your Leydig cells are, and the seminiferous tubules where the Sertoli cells and Germ cells are. Normally FSH stimulates Sertoli cells which produce Androgen Binding Protein (ABP) which traps testosterone inside the tubules. Without endogenous FSH or exogenous hMG, ABP production is zero. However, because ITT is so high, some of this testosterone will still make it through. And although its not bound in the tubules by ABP, enough diffuses through to bind to the androgen receptors on Sertoli cells and get the absolute bare minimum nursing required to keep some sperm alive. The downside is that after a decade or more of zero FSH activity, your tubules will develop fibrosis and scarring which is permanent. hMG or coming off is the only way around this but most people dont actually care about that which is fine. Another benefit of taking hCG is that whilst it has zero FSH activity, just the act having high ITT levels will protect the tubules for longer compared to having no LH and FSH. Luckily, if you don't take hCG for years and years, theres no scarring or fibrosis that takes place. Your Leydig cells can stay dormant for a long long time waiting for the signal to turn back on. Because Leydig cells will still involute, the longer they are in this state the longer the revival takes. It's not all sunshine and rainbows though. Over decades, a lack of hCG or LH will and subsequent lack of neurosteroids like pregnenolone and progesterone, your CNS will likely suffer due to the protective nature of these hormones. How much this translates in reality though we simply don't know. Might not be noticeable for some, might be quite bad for others. Now onto dosing. Endogenous LH has a half life of 20-30m and is released every 60-90minutes. hCG has a half life of 24-36 hours. Bolus dosing like 250-500iu three times a week is the standard, and its fine for almost everyone. If you truly wanted to optimise though, you would go for daily dosing to try and mimic endogenous LH as much as possible. 125iu EOD produces ITT around 25% below baseline. 250iu EID produces ITT around 7% below baseline. 500iu EOD produces ITT around 25% above baseline. - this can drive massive aromatisation too. 100iu daily produces ITT around 12% below baseline. 150iu daily produces ITT around exactly baseline. 200iu daily produces ITT around 12% above baseline. 250iu daily prodcues ITTaround 25% above baseline. Fertility protocols usually prescribe 1000-3000iu hCG 2-3 times a week to drive massive ITT concentrations and wake up the cells. Sperm life cycles are 74 days so usually a minimum of 3 months is required to get some functional sperm. In actual fertility protocols you're also usually prescribed hMG for more viable sperm. Onto Leydig cell desnesitisation. Massive doses of 1000iu+ push cells into overdrive. This not only results in massive aromatisation but produces reactive oxygen species (ROS) and subsequent internalisation of the LH receptors to protect itself. To balance out the ROS you can take antioxidants like NAC. Injectable glutathione can also help (dont inject into your balls please). Last but not least I'll talk about the 'shooting strings' phenomenon. Many people report that their ejaculate is more stringy and kinda dense. Now while this may seem cool, it doesn't mean you have super sperm. Your seminal vesicles produce 3/4s of your ejaculate volume and contain semenogelin - the protein causing the gel-like structure. Your prostate produces the rest of the volume providing zinc and PSA which breaks down semenogelin to liquify it as much as possible. If your hCG dose is a bit high, too much ITT can result in too much semenogelin and not enough PSA to match, resulting in ejaculate thats more stringy and less liquidy. This can trap sperm as its very thick. Not saying your sperm won't get to where they need to go, because higher ITT also means more sperm overall. Adding in hMG ofc will also help the quality of the sperm and help the PSA production. Bonus points if you actually read all of this. If there's any other topics you want me to break down like this mention it below and I'll consider it.