Ryan is a former fitness model and gym owner turned writer, speaker, and biohacker. He's a mental and physical performance specialist with a degree in Food Science & Human Nutrition from Clemson University. An avid hunter, you'll often find him in the woods.
Episode Summary
On a recent episode of my Head First podcast, I sat down with a performance-focused biohacker and nutrition specialist who works as the lead product person at a supplement company. He trained as a food scientist, ran a strength gym, and now spends his days testing interventions on himself and reporting what holds up. We hooked his brain up to a QEEG twice in two days, once clean and once on his company's flagship nootropic stack, and the difference was large enough to talk about. Here is what the conversation covered and what the brain data showed.
How does CILTEP actually work in the brain?
The stack he sells is a CILTEP formula, which stands for chemically induced long-term potentiation. Five ingredients, all disclosed on the label in full amounts. I respect that. The industry habit of hiding doses behind a proprietary blend is a way of selling you less than you think you are buying.
The two heavy hitters are artichoke extract and forskolin. Artichoke extract is a PDE4 inhibitor. PDE4 is a phosphodiesterase enzyme that breaks down cyclic AMP (cAMP). Block the enzyme and cAMP stops getting cleared as fast, so it accumulates. Forskolin pushes from the other direction by directly raising cAMP production. You get elevated cAMP from two angles at once.
Why does that matter for cognition? Cyclic AMP is one of the intracellular signals that drives long-term potentiation, the cellular process behind learning and memory. The role of cAMP and PDE4 in synaptic plasticity and memory is well-established in animal work (Barad et al., 1998). Stronger LTP means tighter encoding of whatever you take in, which feeds better consolidation and better recall later. The company has run small recall tests with memory athletes who improved on the stack. That is suggestive, not a controlled trial, and I will say so plainly.
The other three ingredients support the experience rather than drive it. Acetyl-L-carnitine handles the early-version problem where users crashed around noon. Phenylalanine gives a small push down the dopamine synthesis pathway for motivation. B6 sits in as a cofactor so a rate-limiting nutrient deficiency does not blunt the rest.
If you want the broader picture on chemically tuning learning and memory, I cover the encoding-consolidation-retrieval pipeline in Biohacking Memory and the substrate that LTP depends on in Biohacking Plasticity.
Does CILTEP stack with caffeine?
Caffeine is also broken down by phosphodiesterase, so the question comes up often. My guest does not report feeling more caffeinated on the stack, and I would not expect a dramatic potentiation here. They work alongside each other rather than amplifying each other in any way you would feel. He takes his with bulletproof-style coffee, using ghee instead of butter because the residual dairy proteins in regular butter flare an inflammatory skin response for him. The ghee gets clarified past most of that protein.
What did the QEEG show on a single dose?
This was the part I wanted to see for myself. A QEEG compares one person's brain to a normative database and produces statistical maps of how unusual each pattern is. If you want the full walkthrough of the method, I wrote QEEG Brain Mapping: What It Is, What It Shows, and What to Expect.
Day one, no caffeine and no stack. His brain was clean. No anxiety markers, no sleep disruption, no head-injury signatures. His resting alpha ran two to three standard deviations above age and sex norms, eyes open and eyes closed. Excess alpha at rest tends to track with inattention, getting stuck in neutral, a slightly spacey quality, the kind of pattern that would have collected an ADD label twenty or thirty years ago. He recognized himself in it immediately, and his wife, listening in, laughed.
Day two, identical resting baseline, this time with the stack in his system. The excess alpha dropped by roughly a full standard deviation. To put that in context: when neurofeedback moves a brain, which is one of the few interventions the research associates with lasting EEG change, I expect to see roughly one to two standard deviations over about three months of aggressive training. He got a one-dose shift in the same direction equivalent to a month or two of hard work, except this is a state change, not a trait change.
That distinction matters completely. A supplement gives you a state. It lifts while it is in your system and fades when it clears. Neurofeedback is learning, so it builds a trait, a new resting baseline that holds. I dig into how alpha functions as both your brain's idle and its brakes in Decoding Alpha Waves, and into why the QEEG profile is so useful for predicting day-to-day function in Biohacking with EEG Phenotypes.
A QEEG result like his does something beyond the numbers. It validates. When you see inattention show up as a measurable resting pattern, the framing shifts from "I am lazy" to "my brain is tuned to do some things well and others less well." Nobody asks a person with a broken leg why they are not sprinting. We do ask that of inattention, because the brain pattern is invisible until you map it.
Could CILTEP and neurofeedback work together?
This is extrapolation, so flag it as such. Neurofeedback is fundamentally a learning process, and learning runs on long-term potentiation. CILTEP raises cAMP and supports LTP through PDE4 inhibition. There is a plausible case that pairing the two could accelerate training gains, because you would be reinforcing the same cellular mechanism the feedback is trying to recruit. I have not tested it formally. I have noticed across the brain maps I read that people who exercise hard or do vigorous yoga alongside brain training tend to change faster, which fits the same theme. The company has trials underway, with an 18-month to two-year timeline even on a fast study, and a PDE4 specialist reading the data.
If you are weighing neurofeedback itself, start with Does Neurofeedback Work for ADHD? and the inattention-relevant protocol in SMR Neurofeedback.
What does fat-adapted, minimal-carb eating actually do?
My guest frames his diet around what he calls a minimal effective dose of carbohydrate. He runs mostly ketogenic with intermittent fasting, usually one meal a day in a roughly four-hour window in the early afternoon, and adds carbs when training demands them. The principle driving his carb timing: the harder and more frequently you train at high intensity, the greater your physiological need for glycogen replenishment. A CrossFit athlete training six days a week needs carbs more often than someone training twice a week.
His core target is time under the insulin curve. Carbohydrate, however clean, breaks down to glucose, glucose triggers an insulin spike to clear it, and the longer insulin stays elevated the more total exposure you accumulate. He wants to minimize that area under the curve daily, weekly, and across a lifetime. My own framing is insulin sensitivity. Biological signaling molecules need variability to stay meaningful. When insulin is chronically elevated, receptors downregulate and the system goes deaf to the signal, which is part of how metabolic regulation degrades. We arrive at the same practice from two different descriptions.
One specific recommendation he makes: skip carbs at breakfast. Morning is when cortisol peaks as part of the circadian rise that gets you out of bed, and that window favors growth hormone, glucagon, and the fat-mobilizing, muscle-preserving cascade. Drop carbohydrate into that window and you raise insulin while cortisol is high. Insulin and glucagon are inverse, so insulin suppresses glucagon and blocks the growth hormone release you would otherwise get. The practical result is fat storage and morning brain fog.
For more on these mechanisms, see Strategic Fasting on time-restricted eating, Biohacking Your Morning on circadian timing, and Biohacking Brain Fog.
Where did the conventional diet advice go wrong?
We both came up against the same wall. The 1970s and 80s anti-fat consensus was shaped by industry marketing more than science. The surfaced documentation showing sugar-industry-funded scientists steering blame toward fat in the late 1960s set the template for half a century of dietary guidance (Kearns et al., 2016). The studies that condemned fat did not control for sugar. Fat with sugar is genuinely bad for metabolic health. Sugar without fat is bad. Fat without sugar is fine. Academia lags the research because follow-up studies take years, and the programs are often funded by the same interests the new science challenges.
I made the parallel to my own field. The chemical imbalance theory of mental illness has no strong evidentiary basis, and reviews of the serotonin literature have not found consistent support for it (Moncrieff et al., 2023). The absolute level of a neurotransmitter tells you almost nothing without knowing receptor density, phosphorylation state, and the rest of the circuit. Both stories are cases of a tidy claim outliving the evidence.
What daily habits move performance more than supplements?
Most of what my guest does day to day is closer to life-hacking than biohacking, and that is the point. He optimizes for output and experience rather than collecting supplements as a to-do list.
His morning runs on a sequence. He drinks warm water with organic lemon juice, raw apple cider vinegar, a teaspoon of sea salt, and a dash of cayenne while his coffee brews. He calls it a detox drink, and I pushed back on that word, because you cannot accelerate the body's toxin clearance with a special drink. The ingredients still do real things. Warm water gently opens the digestive system, the salt supports blood pressure and adrenal function, lemon's D-limonene supports bile production, which matters on a high-fat diet because bile is how you actually metabolize the fat you eat.
He does breath work and sets an intention on his porch, then handles his single most important task before touching email. He frames it with a football analogy: average 3.4 yards per play and you keep getting first downs, you never punt, you keep scoring. That task on the legal pad is his 3.4 yards. He delays email to three to five scheduled checks so he is not living reactively from the moment he wakes. The same logic applies to the people I coach through brain training. I want to see the work happening, the focus on action rather than outcome.
I cover the neuroscience of building these into lasting routines in New Year, New Habits.
What about exercise and brain aging?
Movement and brain health are not separable. Exercise raises BDNF, brain-derived neurotrophic factor, which supports neurogenesis and the plasticity that learning depends on (Szuhany et al., 2015). Even a single bout of moderate exercise bumps brain activity in a way that primes learning.
The numbers matter here. I think about the floor of activity that keeps cardiovascular risk from climbing, and that risk is central to brain aging. Higher daily step counts track with lower mortality, with much of the benefit accruing as people move up toward several thousand steps a day (Paluch et al., 2022). You can be fully mentally engaged while your cardiovascular system is starving, and that combination accumulates real risk. Humans walked three to four miles a day for a hundred thousand years and have been sitting for about a hundred. Gene expression shifts with stress and environment, but the underlying hardware is the same. For why this compounds with age, see The Critical Aging Window.
The practical takeaways
A single dose of a PDE4-targeting nootropic produced a measurable, statistically clean QEEG shift in one person's resting alpha. That is a state change worth studying, and the company's trials will take years to confirm anything generalizable. Pairing a cAMP-supporting compound with neurofeedback to push toward a lasting trait change is a reasonable hypothesis worth testing directly.
For your own routine, the durable moves are the unglamorous ones. Protect your morning cortisol rhythm by keeping carbs out of breakfast. Time carbohydrate to actual training demand and keep your total insulin exposure low. Walk three to four miles a day. Do one meaningful task before you open your inbox. Map your brain before you guess at it, so you know whether you are training the right pattern. If you want to see what your own alpha and attention patterns look like, a QEEG is where I would start.
References
- Barad (1998). Rolipram, a type IV-specific phosphodiesterase inhibitor, facilitates the establishment of long-lasting long-term potentiation and improves memory. doi:10.1073/pnas.95.25.15020
- Kearns (2016). Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. doi:10.1001/jamainternmed.2016.5394