Hey Warriors 🙂, I’ve been a bit quieter lately as we’ve been working behind the scenes on something important: My mum completed the Astron Health multi-omic analysis, and the results have finally arrived. Next week we meet Astron’s integrative oncologist to go through the full interpretation — but I want to share the key insights now, because this is something that can empower every person in this community. ⭐ What Astron Revealed About My Mum’s Cancer Her tumour is not random. It runs on specific biological pathways — almost like an engine with identifiable components. The major drivers they identified were: 🔥 FGFR2 → MAPK (Main Growth Engine) 🔥 VEGF / Angiogenesis (Blood Supply) 🔥 MMP15 (Invasion + Tissue Breakdown) 🔥 WNT Signalling (Stem-Cell Survival + Recurrence) 🔥 FANCA Mutation (DNA-Repair Weakness → ROS Sensitivity) And important update: ➡️ CTCs were only 2, which is very low and extremely reassuring. ⭐ This Report Was NOT Essential — But It Was Incredibly Helpful I want to make something clear to everyone: You do NOT need expensive molecular testing to build an effective, multi-pathway protocol. Over the past 1.5 years, I created my mum’s protocol by studying: - cancer signalling pathways - metabolic vulnerabilities - invasion markers - angiogenesis mechanisms - mitochondrial weaknesses - stem-cell biology And what shocked me was this: The Astron findings matched almost exactly what I had already built through research alone. This is HUGE for this community. It proves that: ✔ you can learn what drives your cancer ✔ you can build precision strategies without testing ✔ you can target the actual pathways behind the disease ✔ you do NOT need to shoot in the dark The report confirmed the work — it didn’t create it. ⭐ The One Pathway We Had Not Fully Targeted: RAS → MAPK Astron’s report highlighted one important component: Atorvastatin This inhibits RAS prenylation, which is the top upstream switch that activates the MAPK pathway — the main engine of her tumour.

Hi everyone, I noticed some people have commented that they’re struggling to get their GKI below 2 and/or maintain it. So I thought I’d share some tips. I am day 6 into a 14 day fast. This time I am experimenting with a tea fast of matcha, dandelion root and graviola leaves - they all have very promising data indicating evoking of apoptosis in colorectal cancer cells (and other cancer cells too). They may prevent cancer cells using autolytic cell cannibalism to their advantage (whereby they eat surrounding cells in fermentation-driven stress situations) and give this advantage to T-Cells and NK cells to eat the cancer cells instead. Also, they may reduce glutamine’s capacity to be transported and converted to glutamate. Anyway, I have been able to maintain a GKI of 0.3-0.7 when I am in my “pulse” phase with the following strategies: 1. Fasting for 48 hours - sometimes dry, sometimes water-only and sometimes fat-only - they all have produced similar results, but dry fasting is king! 2. Don’t measure ketones and blood glucose within 2 hours of exercising or waking up and be disheartened - your glucose will be naturally higher as it’s the first fuel source drawn on for anaerobic activity (but ketones will eventually be used over time) and due to the “dawn effect” 3. Gluconeogenesis from protein can increase your blood glucose levels, as well as muscle cannibalism during fasting, so drop your protein intake and/or lift weights to prevent this (disregard the short blood glucose increase - this will stop once you’re fully depleted of glycogen). But don’t overdo it - aim to maintain rather than grow because hypertrophy will stimulate mTOR signalling and throw off autophagy. 4. Don’t only rely on ketone supplements and huge amounts of fat - teach your body to use its own fat because it is not just ketones but the metabolic process of ketogenesis that is effective in metabolic therapy. Also, if you eat a lot of fat and take a lot of ketone supplements, this may drive down your blood glucose reading but your insulin could still be high (which we can’t measure regularly and hyperinsulinemia is a driver of tumour growth). 5. If safe to do so, consider fasting to evoke deeper ketosis. For example, in the first day of fasting my GKI was 4.1. On the second day it was 3.2. Then on the third day, it drove down to 0.7 and has been 0.5-0.7 on days 4, 5 and 6. If you are worried about undesired weight loss or feel unwell when fasting, fat fasting is more gentle and won’t block autophagy as fat has zero impact on insulin. This includes bullet proof coffee, e.g. a little butter and MCT oil but NOT cream. 6. Monitor your GKI more closely after you break the fast - you should not go above 2 unless you’re eating too much protein or (like me) have a mindless, carb-addict relapse! 7. Get over the uncomfortable feeling that comes with going from being jacked to skinny as fuck. I totally get it because I used to be so muscular and with each fast I end up looking like I’ve just come out of a labour camp by the end. But at the end of the day, the longer you can go (safely of course and under medical monitoring or at least with a supportive friend or family member) the better your GKI outcome will be.

Hey guys, just wondering if anyone has had problems with liver dysfunction during their treatment. Dad has been on fenbendazole (222mg, 6 days a week) and ivermectin (1mg/kg) for six weeks with no issues. Started pembrolizumab/carboplatin 10 days ago and today had a blood test showing liver dysfunction with ALT around 1000, up from 40 2 weeks prior. The doctors are thinking it's autoimmune from the pembro, and treating as such. Anyone had liver function go off to that degree with fenben? Thanks

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