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10 New Biohacks for Peak Aging: Neurofeedback & Chill 🧠

Andrew Hill, PhD

On my weekly Neurofeedback & Chill livestream I run a training session on my own brain, take questions, then walk through whatever has been moving in the research. This week the theme was aging. Ten new findings hit the literature in the past several weeks, some of them with effect sizes large enough to change how I think about intervention timing. Here is the substance, with my read on what each finding actually means.

While I talked, I trained two protocols on myself. I want to start there, because the mechanics tell you a lot about how this work operates.

What does a real neurofeedback session look like?

I ran a C4-A2 montage first, then switched to PZ-A1. On the C4 site I set a 4-7 Hz inhibit and an 11.75 to 14.75 Hz reward. That reward band is SMR, sensorimotor rhythm, a low-frequency beta over the sensory strip. SMR supports staying still, falling asleep, staying asleep, and resisting impulsivity. Cats produce it when they hold motionless while tracking prey, focused and physically calm at the same time. Strong SMR ability sits at the opposite end from the fidgetiness and unstable attention you see in ADHD.

The ADHD-sleep overlap is worth naming here. Martin Arns and the Brain Clinics group in Utrecht have modeled part of ADHD as a sleep-regulation problem, with SMR alterations and changes in sleep spindles (spindles are the same rhythm as SMR, just expressed during sleep) and shifts in sleep architecture (Arns & Kenemans, 2014). If you want the deeper mechanism, I covered it in SMR Neurofeedback: Train Sleep, Focus, and Self-Control.

For the second half I moved to PZ-A1 with a 4-7 Hz inhibit and an alpha reward from 7 to 10 Hz. That is alpha one, the idling alpha. A strong, healthy alpha in that range lets me turn down rumination, threat sensitivity, and over-evaluation. When I am tired it also speeds processing slightly. More on what alpha is doing in Decoding Alpha Waves: Your Brain's Idle and Its Brakes.

The training itself is mostly involuntary. The computer measures my brain moment to moment, rewards a half-second of movement in the right direction with a beep and gameplay, and stops when the brain drifts the wrong way. The brain prefers the game running, so it figures out which bursts of activity keep it going and makes more of them. This taps basic associative learning that every brain already does. I demonstrated the one piece you can drive on purpose: active concentration suppresses theta. I dropped my theta about 25% across 30 seconds by concentrating, then let it climb back the moment I relaxed.

A few questions from the audience are worth keeping, because they come up constantly.

Does neurofeedback work for all brains?

In my experience, when 20 short sessions produce no change, the answer is usually that the wrong protocol was applied, not that the brain is unresponsive. Neurofeedback is not magical and selective. It taps associative learning, the same process that works on non-verbal people, people in comas, animals, annoyed teenagers, and skeptical executives. The field discovered it on cats, which are famously bad at following instructions. The right approach is iterative, more like a personal trainer than a doctor: run a protocol, learn from the after-effects, adjust, build the change over a few months until the brain holds the practice on its own. Worth being honest that non-response is real, with something like 15 to 30% of people not showing the expected gains, so good practitioners build in re-mapping and off-ramps.

What is the youngest age for neurofeedback?

The field generally says four, because that is when most kids are verbal enough to report what they notice and have enough behavioral control. Some practitioners work with much younger children when there is a clear reason. For infants, the case is usually seizures, where you record long enough to find the focus and then train SMR. Whether the child is six months or nine months matters little, because the learning is involuntary.

The placement question matters at home. To find a site like T6, you learn the adjacent landmarks and triangulate. The whole system is the 10-20 system because every location sits 10 or 20 percent away from its neighbors. Find T4 above the preauricular notch and O2 at the back, then split the difference. Photographing your head and getting a placement checked is the practical fix.

How big is the blood pressure effect on dementia?

This one published in Nature and it is the largest of the ten. Researchers ran two groups, one with active interventions targeting a systolic blood pressure of 120, the other usual care. The trial was designed to run longer and stopped early because the trajectory had already separated. Lowering systolic blood pressure below 120 reduced all-cause dementia risk by about 15% (He et al., 2025).

That is a striking number. Most of what we have in aging modifies symptoms rather than the disease trajectory. This looked like genuine trajectory modification, and it covered all-cause dementia, not one diagnosis. If your blood pressure runs high, this is a real lever. The relationship between vascular health and brain decline also sits inside The Critical Aging Window: Why Your Brain Starts Aging at 44, Not 70.

Can transcranial stimulation give months of pain relief?

A study this April found that 20 minutes of transcranial direct current stimulation (tDCS) for five consecutive days produced pain relief lasting three months versus sham. tDCS sends a small current between an anode and a cathode. Placement decides the effect: the anode site becomes more likely to fire, the cathode site less. For chronic pain they were almost certainly inhibiting frontal regions involved in the pain experience. A durable effect from a single week of stimulation is worth taking seriously for chronic pain.

What is the UTSA neurofeedback program doing for anxiety and PTSD?

The University of Texas at San Antonio is running a neurofeedback program inside its counseling training, with Mark Jones involved, making real impact on anxiety and PTSD. The framing matters as much as the tool: trauma changes the brain, and a physiological perspective informs the therapy itself. Adding neurofeedback can accelerate psychotherapy for anxiety and trauma. I cover the evidence base in Neurofeedback for Anxiety: What the Research Shows.

What does the AP2A1 protein finding mean for cellular aging?

A March paper identified a protein, AP2A1, tied to cellular senescence. When suppressed in cell lines, it reversed senescence and promoted rejuvenation. AP2A1 interacts with integrin and appears involved in how the cellular matrix and collagen degrade. We have long treated collagen breakdown as a feature of aging. This suggests it may be partly causal: reverse the matrix aging and the cell rejuvenates. Same pattern as blood pressure, an ancillary mechanism that turns out to drive more than we assumed.

Does cold exposure actually slow cellular aging?

University of Ottawa researchers reported in April that daily cold-water immersion produced anti-aging benefits at the cellular level. Healthy young men did one hour at 14°C (57°F) for seven straight days. There was an early dip in autophagy and cellular cleanup for a day or two, then an increased rate of repair, with faster recovery.

One caveat I always flag: if you are training for hypertrophy or strength, do not cold plunge right after the weight room. Cold immersion after resistance work measurably reduces muscle protein synthesis and blunts strength and size gains (Roberts et al., 2015). Separate the two by days. For an athlete already adapted, cold exposure is a tool for recovering from heavy load, useful for ultramarathoners and multi-day events.

Is there a safer senolytic drug?

UT Health San Antonio published in March on a drug that selectively clears senescent (zombie) cells from the liver. It degrades two proteins that build up, BCL-XL and BCL-2, reduced fatty liver and scar tissue, and inhibited liver cancer development with fewer toxic side effects than other senolytics. The overlap between anti-senescence and cancer biology keeps showing up.

Does 4:3 intermittent fasting beat calorie counting?

University of Colorado researchers published in April comparing a 4:3 fasting model (eat freely four days, intense caloric restriction three days, a cyclic approach) against traditional daily calorie restriction. Over a year, the 4:3 group lost about 7.6% of body weight versus about 5% for standard restriction (Catenacci et al., 2016). For the mechanism behind time-restricted eating, see Strategic Fasting: Time-Restricted Eating for Metabolic and Cognitive Health.

Do ketone esters improve working memory?

A March study found that ketone ester ingestion increased working memory regardless of metabolic syndrome status. This fits older work on insulin resistance in the brain, sometimes called type 3 diabetes, where the ketone pathways are spared while glucose metabolism falters. Going into ketosis or a paleo/primal mode early can recover some function before too much is lost. The metabolic status did not change the working-memory benefit, which is the interesting part. Blood glucose also dropped after ketone consumption, but appetite suppression only appeared in metabolically healthy people. Those with insulin resistance got no appetite effect.

One honest note on ketones and prevention. The acute working-memory result is real; the prevention story is not settled. More on the metabolic side at Biohacking Brain Fog: Restoring Mental Clarity.

What did the rapamycin study show?

A January study on rapamycin (the compound is named for Rapa Nui, Easter Island, where it was first found in the soil) found that commercially prepared versions differ substantially from compounded pharmacy versions, which appear lower quality. Blood levels also peaked about two days after dosing, underscoring a long response curve. If you need rapamycin for cancer or autoimmune or anti-aging reasons, get your levels monitored routinely, the way you would with lithium, which works well until it builds up and turns toxic.

A 109% lifespan extension in mice?

A February study delivered adeno-associated viruses encoding an inducible OSK system and extended the median remaining lifespan of elderly mice by 109% versus controls. OSK is part of the Yamanaka factor signaling involved in cellular reprogramming. The gene therapy targeted that pathway in aged mice and roughly doubled their remaining life.

We do not know if this translates to humans. Only about 10% of mouse studies translate cleanly. If it did, getting a compound like this in your mid-60s, with maybe 20 to 30 healthy years left, could in principle double that residual span. In senescence-knockout mouse work, old gray mice regrow brown fur. The plausible direction is an injection that rolls the clock back toward the point where senescence began.

Why I think everyone should get a brain map

A QEEG is non-invasive and gives you agency without diagnosis. Brain mapping is not diagnostically precise, so it does not function like reading a disease gene. It works more like a lipid panel: you see your triglycerides spiking and you ease off the ice cream. Learn to read your alpha peak frequency, your delta load, your beta power, and correlate them with how you feel, and you gain control over which interventions you choose. About 90% of the people I review maps with say some version of "I had no idea you could see that," because we are not taught about our brains the way we are taught about our waistlines. The brain is more changeable than the body. If you want to understand the process, start with QEEG Brain Mapping: What It Is, What It Shows, and What to Expect.

What about seizures and neurofeedback?

The field exists because of a seizure discovery. In the late 1960s, Barry Sterman at UCLA was testing how dangerous rocket fuel vapors were for NASA, exposing cats to monomethylhydrazine. Most of the cats seized within an hour. A subset did not, holding off much longer. Those cats had been in an earlier experiment where Sterman rewarded their SMR bursts, training the rhythm up. The SMR-trained cats had become seizure-resistant (Sterman et al., 1969).

In published case work, a participant with medication-resistant epilepsy then trained SMR with feedback and showed substantial seizure reduction over the training period. Sterman's later review across decades of literature found an average of roughly 50% seizure reduction, with a smaller subset achieving full control for at least the follow-up year (Sterman, 2000). Those are powerful effects. Joe Kamiya was discovering voluntary alpha control in Northern California around the same time, though SMR work shaped the field more.

A seizure is a coherent, high-amplitude, sharp delta event, an ictal spike that recruits neighboring tissue into the same wave in phase. In a tonic-clonic event it resonates between hemispheres and grows. The brain develops seizures most readily without injury in the hippocampus, precisely because that is one of the highest-plasticity regions. Plasticity is good until it tips into too much organization.

Epileptiform discharges interfere with speech, working memory, and attention even without overt seizures. Up to a third of people in some neurodevelopmental populations, autism among them, may have undiagnosed discharge activity. Every brain sits near the edge of seizure all the time and resists it successfully. Life is the balance at the edge of criticality: tip into chaos and you get a seizure, tip into total order and you get death. Staying alive is the constant work of dampening and shaping that activity while keeping it flexible enough to change.

A brain-healthy diet, briefly

The eating pattern I land on for aging is Mediterranean-leaning toward paleo/primal: moderate to high protein, lower fat, lower carbohydrate, heavy on colorful and above-ground vegetables and fruit, avoiding refined starches, excess oils, and sugars. A practical target is about a gram of protein per kilogram of body weight, women a bit under, men a bit over, with fat at roughly half the protein in grams and carbohydrate lower still, adding carbs around exercise to limit large insulin releases. Individual genetics matter; testing APOE variants can tell you how strict to be with sugars. The diet that works is the one you can sustain, because food carries hedonic, cultural, and ritual weight, not just nutrition.

That was the survey for the week. Pick whichever of these you want covered in depth and tell me in the comments, and I will build a longer piece on it. Until then, get your blood pressure under 120, and take care of those brains.

References

  1. Arns (2014). Neurofeedback in ADHD and insomnia: Vigilance stabilization through sleep spindles and circadian networks. doi:10.1016/j.neubiorev.2012.10.006
  2. Catenacci (2016). A randomized pilot study comparing zero-calorie alternate-day fasting to daily caloric restriction in adults with obesity. doi:10.1002/oby.21581
  3. Sterman (2000). Basic Concepts and Clinical Findings in the Treatment of Seizure Disorders with EEG Operant Conditioning. doi:10.1177/155005940003100111