Susan what you've done is extraordinary🙌 I want to say that plainly before anything else — NED in April 2025, a tumour that shrank significantly before surgery, and all of it achieved through an approach you largely researched, reasoned through, and implemented yourself. Fasting, ketogenic periods, fenbendazole, exercise, weight loss, statins, vitamin D, a clean whole-foods diet, intermittent fasting — these are not random choices. You assembled a genuinely sophisticated multi-mechanism strategy, and your body gave you the clearest possible answer: it worked. As someone who has been a survivor of stage 4 cancer for over twenty years myself, I don't say this lightly. That result is the one that matters. Truly amazing and you need to give yourself huge credit for that!

Now to your questions, because they are genuinely good ones and the confusion you're feeling is completely understandable as the science here is real, layered, and sometimes seems to point in opposite directions at once.

The mitochondria question is probably the most important one to untangle. Think of it this way: the mitochondria is the battleground, not inherently a friend or a foe. It's a remarkably adaptable organelle, and that's precisely what makes it so central to this whole story. In ER-positive breast cancer, particularly in tamoxifen-resistant or aromatase-inhibitor-resistant cells, and especially in cancer stem cell, tumour cells can upregulate (switch on) mitochondrial fatty acid oxidation (essentially burning fat through the OXPHOS pathway) as a way of surviving treatment and evading the stresses we throw at them. So in that context, yes, the cancer is hijacking the mitochondria and using it as its engine. But -and this is the critical flip side - we can also turn that same machinery against the cancer by deliberately overloading it. Agents like atovaquone, bezafibrate, and DCA all stress or disrupt mitochondrial function in ways that push cancer cells past their tolerance threshold. So it's not that the mitochondria is a weapon for cancer or a weapon for us, it's both, depending on context. The question is who gets to use it first, and how strategically.

Your metformin question is one I get asked a lot, and it's a really important one to get right, because the standard explanation, "it lowers blood sugar", is technically true but almost completely misses why it matters in cancer. Metformin's primary anti-cancer mechanism isn't about glucose at all. It acts on Complex I of the mitochondrial electron transport chain, which means it inhibits OXPHOS regardless of what fuel the cell is trying to burn — glucose or fat. It also activates AMPK, which suppresses mTOR signalling and reduces IGF-1 — and that IGF-1 axis is particularly significant in ER+ breast cancer, where insulin and growth factor signalling feeds into oestrogen receptor pathways. The glucose-lowering effect people talk about is essentially a downstream consequence of these mitochondrial actions, not the mechanism itself. There's an additional strategic layer too: if you block glucose, cancer cells will tend to pivot toward fat - and that's exactly when you want a complementary agent targeting fat metabolism (bezafibrate, statins) already in place. You're not just blocking one fuel; you're creating conditions where both escape routes are narrowed simultaneously. Most cancers are 'metabolically flexible' - they can switch, so the goal is to close off that flexibility, not simply remove one fuel source. This is the whole premise of my Metro Map.

Fenbendazole and ivermectin are operating on entirely different nodes, which is why they remain relevant even when the primary driver is mitochondrial/fat-based. Fenbendazole doesn't primarily target fuel supply, it disrupts microtubule polymerisation (tubulin binding), which interferes with cell division at a structural level, and it also suppresses GLUT1 and GLUT3 glucose transporter expression and can trigger ferroptosis and apoptosis through separate pathways. So it's actually hitting glucose metabolism and structural integrity simultaneously. Ivermectin targets the Wnt/β-catenin signalling pathway and cancer stem cells, inhibits PAK1, and has OXPHOS inhibitory activity of its own. Neither of these is a single-mechanism drug — they're both what I'd call 'multi-node' agents, which is precisely why they've attracted so much interest in the repurposing space. The logic of the Metro Map framework, which I developed is to try to make sense of exactly this kind of complexity, is that you don't stake everything on one fuel blockade — you attack multiple nodes simultaneously: fuel, proliferation, stemness, structural vulnerability, signalling. That's what you've instinctively been doing.

On diet: I want to validate what you're already doing, because I think it's genuinely well-calibrated. Your observation about body fat and androgen-to-oestrogen conversion is exactly right - adipose tissue is a significant source of oestrogen production after menopause through aromatase activity, so reducing total body fat is directly anti-oestrogenic, not just generally healthy. That alone is a meaningful therapeutic intervention. For ER+ breast cancer, the evidence supports keeping insulin and IGF-1 low, which means whole foods, minimal processed carbohydrates, and avoiding blood sugar spikes — not necessarily strict ketogenic eating indefinitely, which can be hard to sustain and may not always be necessary at the maintenance stage. Adequate protein matters too, especially post-chemotherapy, to protect muscle mass. Sarcopenia is a real risk that people don't talk about enough. The Mediterranean-style whole-food approach, with periods of more structured fasting or carbohydrate restriction as you're doing, is probably the most evidence-backed long-term model for your situation. Your one-main-meal rhythm, the intermittent three-day fasts every four months, these are not random choices either. They're keeping insulin low, triggering autophagy, and giving your body regular metabolic resets. I wouldn't change a thing.

The confusion you're feeling about the sea of information is real and completely valid — this science is genuinely complex, and different researchers are often looking at different cancer populations, different cell types, different stages of disease. Seyfried's contribution, which this post was exploring, is in restoring the mitochondria and metabolism to their proper place at the centre of the conversation - that framing matters. But the full picture is more granular than any single theory, which is why applying it to any individual cancer requires mapping the specific metabolic and signalling characteristics of that cancer type. That's the work my Metro Map approach was built to do: to give people a structured way to navigate the complexity rather than drowning in it.

But here's what I keep coming back to when I read your comment. You navigated it. Imperfectly, with uncertainty, in a sea of contradictory information — and you got to NED. Your body gave you the answer. That's not nothing. That's everything. Congratulations!