Peak 90: Cognitive Performance & Longevity - Reno, NV

Your Brain Is Running Below Capacity. We Find Out Why

A 90-day, measurement-first protocol for high-performing adults who refuse to accept "normal" as their ceiling.

Somewhere along the way, the 2 PM crash became normal. Forgetting why you walked into a room became a joke you make about yourself. You told yourself it was just age, just stress, just life.

Underneath a vague sense that you're not as sharp as you used to be are specific, measurable biological systems, and in most patients, more than one is malfunctioning at once. We don't guess which one. We test for it, we name it, and we build a staged clinical protocol around what we actually find in you.

"The 2 PM wall isn't a willpower failure, and it isn't just age. It's biology, and biology can be measured. We don't guess which system is failing. We test for it, name it, and build a staged protocol around what we actually find in you."

Clinical Note: Peak 90 is a performance-and-longevity protocol layered alongside appropriate care, not a replacement for treatment of a diagnosed psychiatric or medical condition, and not a cure, guarantee, or promise to reverse aging. No individual outcome can be promised in advance. If you are in crisis or having thoughts of harming yourself, call or text 988, call 911, or go to the nearest emergency department.

The Problem is

Illustration of a translucent human brain with glowing neural connections inside a rounded square frame on a light background.

Decline Starts Earlier Than You Think

Measurable cognitive decline does not begin at 65, or even 50. Longitudinal research finds specific aspects already detectable in healthy adults in their 20s and 30s, because the brain's maintenance systems lose ground to daily wear years before anyone calls it "aging." The fog you manage with coffee is the earliest, most reversible chapter of that trajectory.

The Approach:

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Measured, Named, Sequenced

We test for the specific drivers active in you, assign your allostatic phase before any other decision, and build a staged plan around what we find. Brain measurement is repeated at Day 45 and Day 90, so progress is confirmed, not assumed.

This Is Not a

Icon of an intravenous (IV) bag with a diagonal prohibition symbol overlay, indicating no IV or infusion.

Supplement Stack, Not a Guarantee

Not a fixed menu, not a cure, and not a wellness trend. The specific modality, formulation, and sequence in your case are built from your own labs, brain measurement, and allostatic phenotype. If your evaluation doesn't support an intervention, it isn't part of your plan.

Cognitive Decline Has Up To Seven Measurable Drivers

Before we talk about treatment, we look for which of these are active in you, because the right intervention depends entirely on the answer.

1

Mitochondrial Energy Failure

The prefrontal cortex alone uses roughly a fifth of the body's energy. When mitochondrial efficiency falls from oxidative stress, cortisol, or nutrient depletion, ATP production drops before you consciously feel tired. This is the biology of the 2 PM wall.

2

HPA-Axis Dysregulation

Chronic stress drives a staged cortisol-failure pattern. Elevated cortisol suppresses BDNF, shrinks hippocampal volume over time, and blocks prefrontal function, capping focus regardless of effort.

3

Neuroinflammation & Kynurenine Shunting

Systemic inflammation diverts tryptophan away from serotonin and melatonin into neurotoxic kynurenine metabolites, producing serotonin deficiency, suppressed BDNF, and the specific fog-and-disconnection many people describe but can't name.

4

BH4 Cofactor Depletion

A single nutrient-cofactor deficiency can blunt production of dopamine, serotonin, norepinephrine, and nitric oxide at once, a mechanism conventional evaluation rarely screens for.

5

Microglial Activation

Chronically activated microglia sustain a cytokine environment that independently degrades barrier integrity, BDNF, and monoamine cofactor status, compounding the cascade rather than just overlapping with it.

6

Synaptic & Myelin Degradation

The scaffolding that anchors the connections between brain cells degrades under oxidative stress and reduced growth-factor signaling. Working memory, learning speed, and word-finding all suffer, even when a standard brain scan looks normal.

7

Sleep Architecture & Glymphatic Failure

Deep, slow-wave sleep is when the brain physically clears metabolic waste, including beta-amyloid, at roughly double the waking rate. Fragmented or shallow sleep is a missed maintenance window that compounds over years.

Most stressed adults over 40 are running measurable dysfunction in several of these systems at once. Correcting one while ignoring the others is why standalone supplements and generic interventions plateau.

Three Allostatic Phenotypes, Three Starting Points

Starting a high-performing patient and a burned-out patient on the same protocol is a mistake. Your cortisol pattern determines your entry point, and phase assignment happens before any other decision.

Reactive

High output, driven, still performing but brittle: night crashes, early insomnia, a steep morning cortisol peak with evening bleed-through. Priority: HPA-axis normalization and autonomic calming first, before anything activating.

Dysregulated

Tired but wired: afternoon fatigue with no ability to wind down, coffee-dependent mornings, a flattened cortisol curve with no real rhythm left. Priority: hormonal-substrate restoration and sleep-architecture repair alongside early mitochondrial support.

Exhausted

No morning energy, heavy fatigue from the moment of waking, anhedonia, constant fog, a flat or absent cortisol curve. Priority: nothing stimulating until the cortisol floor is restored. The slowest, most carefully sequenced entry of the three.

Placing a neuroplasticity intervention into an Exhausted patient before restoring the cortisol floor is like fertilizing a plant with no root system.

How We Find Your Drivers

Comprehensive
Baseline Labs

Comprehensive baseline labs, not a standard panel

An HPA-axis cortisol curve, DHEA-S, inflammatory markers, the kynurenine-pathway ratio that reveals active neuroinflammatory shunting, serum BDNF, thyroid and hormonal substrate, and genetic markers relevant to lipid and cognitive risk, all measured before a single intervention is chosen.

The Modalities We Use

Every intervention is selected because it matches a specific, measured driver in you, not because it's on a fixed menu. Formulation, dose, and sequencing are built individually from your evaluation.

  • IV Nutrient Therapy (IVNT)

    Nutrient and cofactor infusions to correct mitochondrial substrate deficits and supply the raw material the brain needs to generate ATP.

  • Mitochondrial Support

    Targeted compounds to restore cellular energy production at its source, rather than masking fatigue with stimulants.

  • Hormone Optimization

    Cortisol, DHEA, thyroid, and related neurosteroid and hormonal substrate corrected where lab work confirms a deficit relevant to your presentation and phase.

  • Targeted Neuropeptide Therapy

    Regulatory peptides to support neuroplasticity substrate, cognitive processing, and emotional-regulation circuitry, matched to your active driver and allostatic phase.

  • Growth-Hormone Axis Support

    Where a confirmed sleep-architecture or recovery deficit is present, targeted secretagogue support for pulsatile growth-hormone release, tissue repair, and slow-wave sleep restoration.

  • Neuroinflammation-Targeted Therapy

    Combined IV and oral support to reduce microglial activation and neuroinflammatory burden, used when labs confirm the driver is active.

  • Sleep-Architecture Restoration

    Targeted intervention to restore deep, slow-wave sleep and circadian rhythm, distinct from and more precise than general sleep hygiene.

  • Photobiomodulation & Neuromodulatory Devices

    Non-invasive light-based and autonomic-modulating adjuncts to directly support ATP production and autonomic recovery.

A Staged Protocol, Not A Grab Bag

You are never handed every modality at once. Care is built in sequence, because the sequence itself is part of what makes it work.

Phase 1

Substrate Correction

Foundational nutrient, mitochondrial, and HPA-axis correction, informed directly by your labs and your allostatic phenotype. You cannot build meaningful neuroplasticity work on top of an unaddressed deficiency.

Phase 2

Driver-Targeted Normalization

HPA-axis, hormonal, and sleep-architecture normalization, prioritized according to your dominant driver pattern and allostatic phase, using the modalities matched specifically to what your evaluation found.

Phase 3

Neuroplasticity & Cognitive-Performance Priming

Once foundational systems are stabilized, BDNF-supportive and cognitive-performance-targeted interventions are layered in.

Reassessment, Not Assumption

Brain Gauge, WAVi EEG, and relevant labs are repeated at Day 45 and Day 90. Progression to the next phase, and the definition of success, is gated on real, measured change, not a calendar date or how a given day feels.

F.A.Q.

Is this just for people with diagnosed cognitive decline or dementia?

No. Peak 90 is designed for high-functioning adults noticing a gap between their effort and their mental performance, often well before anything would show up on standard testing.

What if my labs already came back normal?

Standard panels rarely include the specific markers that reveal an active neuroinflammatory, HPA-axis, or mitochondrial driver. "Normal" on a standard panel and "no active biological driver" are not the same finding.

Do you use brain measurement for every patient?

Yes. Brain Gauge and WAVi EEG, administered together, are a standard part of the evaluation, and they are repeated at Day 45 and Day 90 to confirm the plan is actually working.

How is this different from a supplement regimen I could put together myself?

Peak 90 starts with objective measurement of your specific biology and allostatic phenotype, not a generic list. What you receive, and in what sequence, is determined by your labs, brain measurement, and phase, then re-evaluated against repeat testing.

Is this appropriate if I'm in crisis right now?

No. Peak Body and Mind is not an emergency service. If you are in immediate danger or having thoughts of harming yourself, call or text 988, call 911, or go to your nearest emergency department.

What happens after I request an evaluation?

You will complete comprehensive baseline labs, undergo Brain Gauge and WAVi EEG testing in-office, and review your results with your clinician. From there, we build your specific, staged plan together.

Josh Swigart Portrait

Josh Swigart, APRN, PMHNP-BC. Measurement-informed, biology-first psychiatry.

Josh Swigart, APRN, PMHNP-BC. Regenerative Psychiatry, Neuroplasticity, Cognitive Performance Medicine. KRI Fellow, A4M ABAAHP Fellow-in-Training, Triple Certified Peptide Therapy, Advanced IVNT Certified, Double Certified Neural Therapy, Koniver Method Clinician.

Josh Swigart Portrait

Stop managing the fog. Find out what's causing it.

The 2 PM crash, the word you can't find, the effort that no longer matches the output, these are measurable, and in most people more than one system is involved. Peak 90 tests for the drivers, names them, and builds a staged 90-day plan around what we actually find in you.

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References

[1] Salthouse TA (2009). When does age-related cognitive decline begin? Neurobiology of Aging, 30(4):507-514. PMID 19231028. Reconciles cross-sectional and longitudinal data, finding measurable age-related cognitive decline begins in healthy, educated adults in their 20s and 30s.

[2] Cai Y, Mok VCT, Markus HS (2026). Vascular dementia: World Stroke Organization fact sheet 2026. International Journal of Stroke, 21(2):152-163. PMID 41479247. 56.9 million people living with dementia worldwide in 2021, projected to exceed 137 million by 2050.

[3] Xie L, Kang H, Xu Q, et al. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156):373-377. PMID 24136970. Natural sleep produces a 60 percent increase in brain interstitial space, driving measurable clearance of beta-amyloid via the glymphatic system.

[4] Lim J, Dinges DF (2010). A meta-analysis of the impact of short-term sleep deprivation on cognition. Psychological Bulletin, 136(3):375-389. PMID 20438143. Across 70 studies, large effects on sustained attention and significant effects on working memory and processing speed.

[5] Miller AH, Raison CL (2016). The role of inflammation in depression. Nature Reviews Immunology, 16(1):22-34. PMID 26711676. Establishes the neuroinflammatory cascade, cytokine elevation, IDO activation, and kynurenine-pathway shunting behind the neuroinflammation driver.

[6] Zhu X, Zeng Q, Lei Y, Xu D (2026). Effects of Withania somnifera (Ashwagandha) on cognitive and physical function in adults: a systematic review and meta-analysis. Frontiers in Pharmacology, 17:1799467. PMID 42199854. Meta-analysis of 20 RCTs (1,249 participants) finding significant improvement in memory, attention, processing speed, and executive function with a targeted nutraceutical used in this protocol's HPA-support phase.

This page is educational and is not a diagnosis or a substitute for individualized medical advice. If you are in crisis, call or text 988, call 911, or go to your nearest emergency department.

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