Today is the day I launch N1 Health. I built it from scratch. Been thinking about this for a long time. I’ve spent over a decade working in healthcare and looking at blood results. Literally thousands of them. And every single one is after the fact. The person is already ill. In a bed on the ward. On multiple meds. Cancer has even hit my own family. Blood is one of the best and easiest ways to get a quick insight into what’s actually going on inside your body. You shouldn’t have to get sick before anyone (including you) takes a look. But the private testing market is honestly a mess. Bloated panels. Hundreds of tests that are literally the same thing with one or two markers swapped. Insane markups. So people either buy the most expensive one to be safe or they buy nothing at all. I got tired of it. I knew I could do it better myself. So I did. A small number of profiles and panels that actually measure everything you need. Then a selection of add-ons so you can personalise it any way you want. Finger prick is available where it actually works well. Where it doesn’t, we don’t sell it. Prices are not the cheapest you will find anywhere. But they are fair. And they've been set so you can do it again and again and again. One blood test is a snapshot. Three is a trend. The more you track, the better you can take control. I also put everything I know on the site for free. The Body Guide and the Biomarker Guide. Over 150,000 words. And I'm not done yet. No paywall. No account. No email. Read them and then go buy your test somewhere else? Genuinely fine by me. The whole point is you know more about your own body than you did yesterday. UK only for the testing. But the guides are for everyone. It’s your N=1. Let's start. Bismillah.

hCG indirectly can raise prolactin through estrogen (e2). When you take hCG you don’t just increase testicular testosterone. Once hCG binds LH receptors on your Leydig cells they create more aromatase enzyme as well as testosterone. More aromatase means more e2. That e2 then goes into your bloodstream and has two mechanisms to increase prolactin. 1. It goes inside the prolactin cells (lactotrophs) in the pituitary and tells them to make more prolactin. 2. It goes to your hypothalamus and tells it to make less dopamine. Dopamine is what puts the brakes on prolactin. Less dopamine means more prolactin and vice versa. (Side note: the reason breast tissue produces milk is not because the prolactin cells are there, they just have prolactin receptors) Another little known fact is that the pituitary itself also has aromatase enzyme so it can convert testosterone to e2 locally. And you wouldn’t see this in a blood test since it’s not happening in the serum but at the tissue level. But if hCG is causing your prolactin to increase it’s likely because of your e2. Increase frequency of injections and lower overall weekly dose to lower e2 and subsequently lower prolactin. And stop gooning too.

Bioslacking

This is exactly it. I genuinely could not agree more. I mean why else are we here? Why else are any of us even trying to optimise our health and our lives? Not just to be the best version of ourselves for our kids. But to pass this on to our kids. There is nothing more important than our children. Nothing. Not by a long shot. And it’s one of the few things in life you never truly understand until you become a parent. And I truly hope and pray everyone gets to experience it. You look into their eyes and they stare back at you. And you just KNOW there is nothing on this earth you would not do for them. And by far the most important thing you can do for them is the one that most people overlook. It is to be healthy and pass on that health. Health is wealth. And not only that. But generational health is the ultimate generational wealth. If you cannot find it within yourself to do it for you. Fine. Don’t. Then do it for them. Those that you brought into this world. Those that you are wholly responsible for. Those that you owe your best efforts to forever. Your children are the ultimate proof of work. And they are watching every single thing that you do. I pray Allah makes us all the parents our children deserve, and lets us live to see them grow up healthy and strong 🤲🏼

Never thought I would see this in the UK

It’s American week at Lidl

And this

I’m sure some of my American friends grew up on this

My wife let me go to the store on an empty stomach and there’s Halloween snacks and treats everywhere

One of the reasons I love doing deep dives into certain topics is the fact that you’re guaranteed to find something new every time. In the preg for ITT deep dives I discovered the Peritubular myoid cells. I literally had no idea these cells exist and most people don’t either. I mean sure they’re not the most important or coolest cells out there. But they play their part. There’s so much about the human body we still actually don’t know at all, and even more than we just don’t understand.

Pregnenolone for intratesticular testosterone (ITT) instead of hCG. Part 3. Preg has 21 carbons. Testosterone has 19. CYP17A1 cuts those 2 carbons off and HSD17B3 does the final step. Every route to an androgen runs through that CYP17A1 lyase step. So something in there has to be carrying the enzyme for it to work. Sertoli and germ cells aren't it, they have no CYP17A1. And Leydig cells need LH or hCG, which drives CYP17A1 transcription itself, not just cholesterol delivery. Exogenous test at a normal clinical dose drops Star, Cyp11a1 and Cyp17a1. But there's a 3rd cell nobody mentions in any of these conversations. Peritubular myoid cells. They form the actual wall of the tubule. They're like smooth muscle and they squeeze sperm along. They carry androgen receptors from fetal life onwards, earlier than Sertoli cells get them. If you knock the androgen receptor out of ONLY these cells in a mouse, it becomes infertile (Welsh 2009). Looking into these cells showed me something I didn't expect. They already have most of the parts needed. Landreh 2014 found human peritubular cells expressing StAR, CYP11A1, CYP17A1 and 3beta-HSD, AND measured them producing pregnenolone and progesterone. So the tubule wall isn't some useless one job thing. It runs the early steps for real. What's missing though is the last step. HSD17B3, the enzyme that turns androstenedione into testosterone, has never been reported in these cells. The same group's conclusion in 2022 was that they can make progesterone but most likely cannot make androgens. So it's not that nobody has looked at them. It’s that their ability stops one step short, and it’s an important step. Human testis have also been mapped and the atlas found HSD17B3 in Sertoli cells as well as Leydig (Guo 2018). But without CYP17A1 they have no substrate to feed it, so the parts are scattered across different cells. A 2025 paper found fetal Leydig cells and their neighbours each carrying INCOMPLETE sets of steroidogenic genes. This kinda suggests androgen output is a shared job rather than one cell doing it all. That reframes the whole picture imo. The question isn't which single cell can do it. It's whether a shut down testis can still assemble the chain between cells by working together. Which we don't know. The body often has systems that come together in disease/damaged states that otherwise never turn on. That being said, I still don't think preg works here convincingly. All good results in the old studies is maintenance started before or just as the testis shut down. Preg has NEVER restarted offline testis in the studies that tried it. A rat can keep full sperm production down to ~20% of normal ITT. In humans we don't know the number. Coviello 2004 showed ITT at serum equivalent levels (which is like 1-2% of normal), wasn't anywhere near enough. I would assume we need quite close to full ITT. ITT and fertility are not necessarily the same thing though in everyone (but that's another set of long posts for another time). Atrophied Leydig cell still have all the enzymes, just way less. Give it enough substrate (preg) and it might convert enough to saturate the tubules rnext door by diffusion, and not enough to show up in the bloods. It's plausible sure, but likely? I really don't think so. Could injecting megadosed pregn (especially with a long chain ester) change it? Maybe. Every rat result that worked used injection and every weak study is oral. And it was last tested in 1949. So all this has been to say In conclusion, at this point in time, hCG (+/- hMG) is the only thing with direct evidence for reliably holding ITT and sperm on TRT.

Pregnenolone for intratesticular testosterone (ITT) instead of hCG. Part 2. There's also lots of old data. Between 1942 and 1985 this was studied properly and then it stopped (once hCG came about). Leathem and Brent 1943 showed preg could MAINTAIN sperm production in rats with no pituitary. Masson 1946 found it could not RESTART it in already atrophied testis. Dvoskin 1949 tried 3mg then 20mg a day for 20 days. Saw nothing. He also compared injecting against oral. (As far as I know it's never been compared since) Harris and Bartke 1975 injected 2mg a day and got test and DHT in the fluid leaving the testis at intact levels, sperm production nearly fully maintained, with atrophied Leydig cells. A second paper that year used radiolabelled preg and pulled labelled testosterone back out of testicular tissue, while the prostate and seminal vesicles shrivelled like untreated rats. So it was converted in the testis but not elsewhere (which is interesting). Vreeburg 1976, 2mg for 30 days. Testicular testosterone dropped to about 30% compared to intact rats. Sperm count 23% of normal. But the sperm were FERTILE. Anthony 1984 later showed ABP maintained on preg alone, fertilising ability kept. Then Turner and Ewing 1985 ran a shorter version, same 2mg but 14 days not 30, and sperm production wasn't maintained, androgen inside the tubules only at 10-20% level of controls. They measured BOTH compartments and showed the fluid leaving the testis can read normal while the tubules are low. So preg keeps between 1/5 and 1/3 of the system running, and in one study that was enough for fertile sperm. But in a rat. Most of you knew a lot of that already but the foundation is needed. Now the compartments, because they matter for what comes next. The interstitial space is where Leydig cells are, connected to the bloodstream. The seminiferous tubules where Sertoli cells and sperm live is walled off behind the blood testis barrier. That means everything you measure in a blood test comes from the first compartment including 17OHP. So IF preg was being converted inside the tubule rather than by Leydig cells, you wouldn't see it in the bloods at all. That's a small possibility. Part 3 is the end of the story with a bit about a cell (almost) nobody knows about. Check QT.

Pregnenolone for intratesticular testosterone (ITT) instead of hCG. Part 1 of 3. The logic is simple, no LH means no preg from cholesterol so give preg and let them convert downstream. 17OHP (17-hydroxyprogesterone) sits in the middle of the pathway and is a marker for ITT production. On TRT it drops. With hCG it goes back up. But there's some problems in this situation. If preg did nothing, 17OHP stays low. If preg was converted somewhere other than the Leydig cells, 17OHP stays low. If you totally flood the body with preg, your adrenals can push it up 17OHP also isn't reliable everywhere. Amory 2008 showed it works well as an indicator of ITT when using hCG. But unstimulated i.e. natural men, it didn't correlate at all. Roth 2013 ran two markers at very low hCG doses and 17OHP showed nothing, but INSL3 tracked ITT fine (INSL3 wouldn't work for preg though since its downstream of LH pathway where hCG binds). A low result could basically fit every possible answer. So why is 17OHP the marker then? Pregnenolone can go down 2 routes to testosterone. Delta 4 is preg -> progesterone -> 17OHP -> androstenedione -> testosterone. Delta 5 is preg -> 17OHPreg (not the 17OHProg we measure) -> DHEA -> androstenedione or androstenediol -> test. CYP17A1 runs D5 way better than D4 (roughly 11x) and only 2-3% of 17OHP gets through to androstenedione compared to the D5 route. But that only applies to the final lyase step. The step before it works it's about the same on both (see image). A 3rd enzyme, 3beta-HSD, turns basically any D5 steroid into its D4 counterpart at any stage (not at equal rates though). So the 2 routes aren't completely separate. They're kind of a ladder and you can cross at any time. This is why 17OHP works. Its made off the D5 route by 3BHSD and then backs up, because our lyase is not good at clearing it. (The other exits are adrenal and only occur usually in disease). We see it in mice. Knock out cytochrome b5 in Leydig cells, lyase no longer works properly and 17OHP builds up 100x. It is spillover from a working Leydig cell. There's also where oral preg goes. A single 400mg dose tripled serum preg at 3h. But in a schizophrenia trial 500mg a day raised allopregnanolone about 5x and progesterone 4x, and DHEA-S by ~16%. It usually goes down the neurosteroid arm, not really the androgen arm (which is obvs what we want). Part 2 is the data. There's plenty of it. But it’s all old. Check QT.

D-Dimer of 27,558 ng/mL is crazy.

Monday. The day most people dread. It’s also the day everything is supposed to “start”. Diet starts Monday. Training starts Monday. Cardio starts Monday. Yada yada yada. It starts the second you make the decision that you’re going to start. But Monday is actually here. All the things you said were due on Monday need doing. Get to work.

World’s longest posts on the whole pregnenolone and testicular testosterone will be coming. Will probably need at least two parts.

Type 2 diabetes Hypertension Obesity NAFLD Arthritis (OA and joint pain) Depression/brain fog issues Hyperlipidaemia Fibromyalgia Neuropathy/nerve pain Sciatica Heart failure/disease Chronic kidney disease Macular degeneration (especially age related) Parkinson’s Alzheimer’s Chronic pain/fatigue Also literally any old person. Almost every chronic disease these days has some form of mito and/or inflammatory component. There’s very little that would not at the very least improve from either of these compounds or both.

High dose ss31 and kpv can help improve/fix a lot of problems for a lot of people