Eric Remensperger has been a practicing attorney for over 30 years, and casual biohacker until he discovered his Stage IV cancer and began an exploration of the science and treatment possibilities available to him. Learn about how he returned to health.
Episode Summary
This episode of Head First featured a guest I met through the biohacking community: a practicing attorney of more than 30 years who spent two decades chasing wellness before a stage IV prostate cancer diagnosis turned that hobby into a survival project. He pointed every tool he had collected at one question: how do you move your body out of a state that grows cancer and back into one that heals?
I want to walk through the science he engaged with, where the evidence is strong, where it is a working hypothesis, and where it is one man's extrapolation from his own reading. None of this is medical advice. It is a map of how a smart, motivated person navigated a confusing field, and what holds up when you look at the mechanisms.
What does a stage IV diagnosis look like when you think you are healthy?
My guest had spent 20 years eating clean, doing yoga, fasting, and reading everything in the wellness space. Then, at a conference, he had trouble urinating. A urologist found his PSA at 21. Reference range tops out around 4. The biopsy came back with all 12 sites positive, a Gleason score of 9, with spread to lymph nodes and bone.
The shock for him was the contradiction. Two decades of grass-fed beef, clean water, ocean air, and the disease was aggressive anyway. That contradiction is worth sitting with, because it points at something most prevention narratives skip. Prostate cancer is usually indolent. Most men our age carry precancerous cells and die with the disease, rather than from it. His was the aggressive version. The question that drove his research was why his took off.
Is cancer a genetic disease or a metabolic one?
He read 14 books in 21 days and landed on a fork in the road that the field has argued about for a century. One camp says cancer is a genetic disease, a DNA mutation that drives uncontrolled growth. The other, going back to Otto Warburg's Nobel Prize work, says it is a metabolic and mitochondrial problem first, and the DNA damage comes downstream.
Here is the mechanism Warburg described (Warburg, 1956). Healthy cells use oxygen to make ATP, burning glucose or ketones through oxidative phosphorylation in the mitochondria. Cancer cells lose the ability to respirate with oxygen efficiently. They become anaerobic and generate energy through fermentation of glucose, producing lactic acid. This is the Warburg effect, and it is well documented (Vander Heiden et al., 2009). The interpretive leap, the part that remains a working hypothesis, is whether the metabolic shift is the root cause or just an early step that produces DNA damage, fungal overgrowth, and the other features other theories point at (Seyfried & Shelton, 2010).
The mitochondrion is an organelle inside the cell that generates energy and heat. Cells vary in how many they carry. In cancer cells the mitochondria are functionally impaired, and energy production shifts toward fermentation in the cytoplasm. Whether you call this cause or consequence, the practical implication is the same: cancer cells are glucose-hungry. That is exactly how a PET scan finds them. You inject radio-labeled glucose, run the patient through the scanner, and look for where it concentrates. The tumors light up because they are sponges for sugar.
Why might fasting and ketosis matter for cancer metabolism?
If cancer cells depend heavily on glucose, lowering available glucose should pressure them more than it pressures healthy cells. That is the rationale behind ketogenic and fasting approaches in oncology research, and there is real signal for certain cancers, glioblastoma in particular (Seyfried et al., 2014).
My own prior frame on fasting and cancer was about starving the greediest cells first, robbing the fast-dividing tissue of fuel so it fails before healthy tissue does. The Warburg framing adds a second layer: you are also feeding your healthy cells a fuel source, ketones and fats, that cancer cells handle poorly.
He distinguished two levels of ketosis. Nutritional ketosis sits around 0.5 millimolar blood ketones. Therapeutic ketosis runs above 2. Because he had been on a paleo-style diet for years, he was already fat-adapted, so pushing into the higher range was easy. Someone coming off a high-carbohydrate diet might spend a month or two in the "keto flu" before the body learns to run on ketones. His first intervention after diagnosis was an eight-day water fast, which put him deep into ketosis at six or seven millimolar. If you want the background on the metabolic and cognitive side of this, I cover it in strategic fasting.
We disagreed productively on exogenous ketones. He takes brain octane (a beta-hydroxybutyrate precursor) in his coffee. My skepticism: if you swallow a ketone product without having burned through your glycogen, you get the anti-inflammatory and brain-fuel effects of circulating ketones, but you are in a different whole-body metabolic state than endogenous ketosis produces. He agreed the fasting-driven state is the real target and uses the exogenous stuff mostly for the anti-inflammatory benefit.
How can too many nutrients accelerate cancer? The hormesis problem
This was the most important exchange in the episode, and it connects directly to the aging work I teach.
Before his diagnosis, he made a daily shake packed with every nutrient he could find: maca, natto, frozen chicken liver, dozens of powders. The preparation took hours each week. His own theory now is that by flooding his system with constant nutrients every single day, he never let his body run autophagy, the intracellular cleanup process that recycles dead and damaged cellular components. He fed the cancer cells alongside the healthy ones, and suppressed his body's own quality-control signal.
The mechanism here is hormesis. There is a study showing oral antioxidant supplementation can increase mortality, and the reason is elegant (Bjelakovic et al., 2007). When a mitochondrion is damaged, it leaks free radicals. The cell reads that stream of free radicals as a signal that the mitochondrion is broken, and triggers it to self-destruct through mitophagy. That free-radical "damage signal" is how the cell keeps its energy machinery clean (Ristow & Schmeisser, 2011). Flood the system with oral antioxidants and you mute the signal. Broken mitochondria do not get told to self-destruct, they accumulate, and the total free-radical load eventually climbs higher than it would have without any supplementation at all.
My read was that his nutrient mega-dosing did something similar: it hijacked and suppressed the hormetic danger signal across his body. He agreed, and he reorganized his entire approach around pulsing rather than constant input. Nibble and flow. Build tension, then release it. He varies what he eats day to day and leans on fasting to keep ketones up.
This is the same principle that governs healthy aging. The failures I study in gerontology happen when the regulatory range, the signaling capacity of a system, gets exceeded and stops varying. The body handles huge spikes of insulin or cortisol fine, as long as they come back down. A cortisol spike in the morning wakes you up. Cortisol that goes up and stays up tracks with hippocampal damage and with depression (Sapolsky, 2000). The damage is in the loss of variability, not the spike itself. Static systems are dead systems. If you want the broader picture on why this matters across the lifespan, see the critical aging window.
What does the autonomic nervous system have to do with it?
He also went deep into Wilhelm Reich's work, which sits well outside mainstream science and which I would file under speculative. The piece worth flagging is Reich's clinical observation that cancer patients showed an autonomic nervous system stuck in contraction, in sympathetic dominance, without the normal ebb and flow into parasympathetic recovery. That maps onto something measurable: cancer patients often show reduced autonomic flexibility, measurable as lower heart rate variability.
Whatever you make of the framework, the testable claim is about variability again. A nervous system that only contracts, that never cycles back to recovery, has lost its regulatory range. That is the same failure mode I described for cortisol and for nutrients. The body needs the swing.
What therapies did he actually use, and which are mechanistically plausible?
His self-described "chemotherapy" was oxidative stress, deployed as a hormetic signal rather than as a constant assault. The logic: if a therapy is toxic to cancer cells but tolerated by healthy ones, and it pushes oxygenation, it earns a place. His tools:
- Hyperbaric oxygen. Drives oxygen into tissues, including the nooks and crannies that normal circulation reaches poorly. He met a man with glioblastoma whose only protocol change, after surgery and a ketogenic diet, was adding hyperbaric oxygen, and whose follow-up thermal imaging came back clear. A single case, mechanistically coherent given the Warburg framing.
- Ozone therapy (rectal insufflation) and high-dose vitamin C (which generates hydrogen peroxide), both used as oxidative stressors.
- Intermittent hypoxia-hyperoxia training, alternating low and high oxygen during exercise to open capillaries.
He also tried things that did not stick. Coffee enemas were a logistical struggle. Some caustic chlorine-based compounds he bought, he never had the nerve to use. He takes B17 (laetrile) only in its natural form as apricot kernels, and the conventional concern there is cyanide content.
On hormones, he used androgen deprivation therapy to drop testosterone to near zero. The footnote worth knowing: the research supports cycling off ADT. The studies show intermittent ADT is not inferior to continuous therapy for some patients, which to him meant there was no reason to spend the rest of his life testosterone-deprived when his body could use intermittent windows of normal hormone function (Crook et al., 2012). His testosterone has since recovered and his PSA dropped to the low single digits, down dramatically from 21.
Does breathing actually oxygenate your tissues?
This surprised me and changed how I think about my own yoga practice. The intuition is that breathing hard floods you with oxygen. The Patrick McKeown framing he described flips that. Hyperventilation actually tightens the bond between oxygen and hemoglobin, making it harder to release oxygen into the tissues. The release depends on carbon dioxide, the Bohr effect. You need enough CO2 in your system for the oxygen to unload where it is needed.
That is why a trained endurance athlete breathes slowly and nasally rather than gasping. It is why the ujjayi breath in yoga, the slow nasal breath with a faint sound, generates so much heat and lets you hold demanding poses while barely breathing audibly. The sound is a feedback signal: if the breath is smooth, the energy is smooth; if it is ragged, you are struggling. I do ashtanga, and this gave me a new hypothesis for why a long, slow, nasal breath during a hard practice leaves me pouring sweat in an unheated room. We are generating heat and possibly improving oxygen offloading into tissue. McKeown's practical suggestion is to keep the mouth closed at night, even taping it, so you nasal-breathe through sleep. My guest found that consistent nasal-breathing practice during yoga eventually opened up airways that a deviated septum had partly blocked.
Why does taking charge of your own health research matter?
The through-line of his platform, and of my work at Peak Brain, is the same. Even the best physician can give you a tiny slice of attention. Evidence-based medicine produces findings that are valid at the population level, across a hundred or a thousand subjects, and then often break down for the individual who does not sit in the middle two-thirds of the bell curve. That gap is where self-directed research lives.
I made the same point I make about brain training. Practitioners in neurofeedback hold three or four genuinely different models of how the training works, and they all get results. The same is true across cancer therapies: ketogenic, hyperbaric, oxidative. They appear to work through different doors. This is a blind-men-and-the-elephant situation, and the honest position is to say where you have context and where you do not. The ability to say "I don't know" is a feature of doing this well.
For people who want to avoid cancer rather than treat it, the foundational moves overlap heavily with anti-aging: ketogenic eating, fasting, oxygenation, exercise, and managing inflammation. He puts curcumin and sulforaphane high on his list. Curcumin absorbs poorly on its own, so he pairs it with fat (brain octane) rather than relying only on black pepper. That detail matters for anyone on prescription drugs, because piperine in black pepper inhibits the same liver enzymes that metabolize many medications, and you can drive your drug levels up without changing your dose (Bhardwaj et al., 2002). If you take that route, have your physician check your medication levels.
The shift in perspective
The part that lands hardest is a reframe about time. He described the diagnosis as the best thing that happened to him, a sentiment I have heard from others who have faced terminal illness. We live as if there is always a tomorrow, and that false sense of unlimited time lets us spend years on things outside our real priorities. A terminal diagnosis collapses that. Priorities snap into focus. There is a meditation practice built around living a single year as if it were your last, and the point is that you can access some of that clarity without waiting for the disease. Gratitude has measurable effects on wellbeing, and his version of it extends even to the cancer itself.
His PSA is now in the low single digits, his bone cancer is gone, his lymph nodes are functioning normally, and his prostate returned to normal size. He is 60 and in remission. From the gerontology data, the trajectory of your health markers from 60 to 70, weight, oxygenation, hormone levels, skin elasticity, predicts the next two or three decades. The work in front of him is holding those gains through that window.
If you want to see how the same agency-first, mechanism-first philosophy applies to the brain, start with QEEG brain mapping and biohacking sleep, which is the single highest-leverage lever most people are ignoring.
References
- Ristow (2011). Pulmonary hypertension in sickle cell disease. doi:10.1056/NEJMc1109130