A 10-ingredient powder blend targeting the core mechanisms of Post-Acute COVID Vaccination Syndrome — mitochondrial dysfunction, vascular impairment, oxidative stress, and immune dysregulation.
All ingredients are combined into a single pre-measured powder. Two scoops daily, taken with water, for 90 days. No separate pills or complex schedules.
For each ingredient: what it does at a cellular level, why it is relevant to PACVS, and what the clinical evidence shows.
Glutamine is the most abundant free amino acid in the body and the primary fuel source for rapidly dividing immune cells (lymphocytes, macrophages) and intestinal epithelial cells. It is conditionally essential during illness, when endogenous synthesis cannot meet demand.
In post-viral states, glutamine depletion impairs gut barrier integrity, allowing bacterial products to translocate into circulation and amplify systemic inflammation. Glutamine also feeds the TCA cycle via alpha-ketoglutarate and serves as a precursor to glutathione — the body's primary antioxidant.
Glutamine depletion is well-documented in critical illness, major surgery, and post-viral syndromes. Supplementation at 0.2–0.5 g/kg/day reduces infection rates, shortens ICU stays, and improves nitrogen balance in multiple RCTs.
In post-COVID and ME/CFS cohorts, gut microbiome disruption and intestinal permeability are consistent findings. Restoring glutamine availability directly addresses this upstream driver of systemic inflammation.
The 14 g dose reflects established therapeutic use (approximately 0.2 g/kg for an adult) rather than the lower supplemental doses used in healthy populations.
Citrulline is converted to arginine in the kidney via the urea cycle, then used by nitric oxide synthase (NOS) to generate nitric oxide (NO). Unlike direct arginine supplementation, citrulline bypasses first-pass hepatic arginase catabolism, producing more sustained and meaningful elevations in plasma arginine and NO.
Nitric oxide is a vasodilator, anti-platelet, and anti-inflammatory signalling molecule produced by endothelial cells. Its depletion is a central feature of endothelial dysfunction — a hallmark of PACVS.
Citrulline supplementation at 3–6 g/day consistently improves NO bioavailability, reduces arterial stiffness, and improves exercise performance and recovery in clinical trials. Meta-analyses confirm efficacy across cardiovascular and fatigue endpoints.
Endothelial dysfunction and reduced NO production are documented in Long COVID and PACVS. Salivary nitric oxide — one of the trial's primary biomarkers — provides a non-invasive window on systemic NO status that citrulline supplementation is expected to raise.
Serine is a conditionally essential amino acid serving as the precursor to phosphatidylserine (a key neuronal membrane phospholipid), glycine, sphingolipids, and cysteine. It is central to one-carbon metabolism via the folate cycle, which underpins methylation reactions required for gene regulation, neurotransmitter synthesis, and DNA repair.
In the nervous system, serine is specifically required for the synthesis of myelin sphingolipids and for normal glial function. Serine deficiency produces progressive peripheral neuropathy and cognitive impairment.
Small fibre neuropathy and cognitive impairment are prevalent in PACVS cohorts. Serine supplementation has been studied in hereditary spastic paraplegia and ALS — neurological conditions sharing mechanistic overlap with post-viral neuropathy — with doses up to 15 g/day used safely.
Plasma serine levels are reduced in ME/CFS patients in some cohort studies, suggesting impaired synthesis or excess catabolism. At 4 g/day, this protocol uses a conservative therapeutic dose with a well-established safety profile.
Arginine is the direct substrate for nitric oxide synthase and provides the guanidino group for creatine synthesis. It also participates in the urea cycle for nitrogen disposal and modulates T-cell and macrophage function. When combined with citrulline, the two amino acids create a sustained NO-generation cycle: citrulline raises systemic arginine availability, while arginine provides the immediate NOS substrate.
A 2021 RCT (Tosato et al., European Review for Medical and Pharmacological Sciences) combined L-arginine (1.66 g × 3/day) with vitamin C in Long COVID patients — demonstrating significant reductions in fatigue, dyspnoea, and improved 6-minute walk distance versus placebo over 4 weeks.
This is direct RCT evidence for the arginine-vitamin C combination in a post-acute COVID phenotype, providing the strongest available clinical anchor for this protocol's NO-pathway approach.
Phosphocreatine is the body's fastest ATP regeneration system, replenishing ATP from ADP in under one second without requiring mitochondrial involvement. In cells with impaired mitochondrial function — a core feature of PACVS — the phosphocreatine system provides an alternative energy pathway for muscle contraction and neuronal activity.
Beyond acute energy buffering, creatine supports mitochondrial biogenesis, reduces lactate accumulation, and has well-documented neuroprotective effects by maintaining neuronal energy homeostasis.
Creatine monohydrate has one of the most extensive safety and efficacy profiles in nutritional supplementation. Hundreds of trials confirm improved exercise performance, reduced fatigue, and cognitive benefit across healthy and clinical populations.
In post-exertional malaise — the central disabling feature of ME/CFS and PACVS — creatine supplementation is particularly rational because PEM is mechanistically linked to a crash in mitochondrial ATP output. 5 g/day is the standard maintenance dose across the literature.
L-carnitine is the transporter that shuttles long-chain fatty acids across the inner mitochondrial membrane for beta-oxidation. Without adequate carnitine, fatty acids cannot enter the mitochondria and ATP production from lipids is impaired. The acetyl form (ALCAR) crosses the blood-brain barrier, acting additionally as an acetyl group donor for acetylcholine synthesis and neuronal metabolism.
ALCAR also reduces oxidative damage to mitochondrial membranes and supports the activity of complex I of the electron transport chain.
Carnitine deficiency is documented in ME/CFS and correlates with fatigue severity. ALCAR supplementation at 2–3 g/day has been studied in ME/CFS, HIV-associated neuropathy, fibromyalgia, and hepatic encephalopathy — with improvements in fatigue, pain, and cognitive function across multiple trials.
Impaired fat oxidation — measurable by reduced respiratory exchange ratio during exercise — is a documented feature of post-acute COVID syndrome. ALCAR directly addresses this metabolic impairment.
NAC is an acetylated cysteine derivative that serves as the primary precursor for glutathione synthesis. Cysteine is the rate-limiting substrate for glutathione, and NAC replenishes intracellular cysteine efficiently. Glutathione — the body's master antioxidant — neutralises reactive oxygen species, regenerates vitamin C and E, and detoxifies electrophilic compounds.
Beyond antioxidant function, NAC directly scavenges ROS, inhibits NF-κB inflammatory signalling, reduces platelet activation, and has mucolytic properties. It has a long record of clinical use and an excellent safety profile.
NAC has decades of clinical use — most prominently in acetaminophen overdose, COPD, and idiopathic pulmonary fibrosis. In the COVID context, NAC was proposed early as a therapeutic agent due to its ability to counter the cytokine storm and reduce oxidative stress.
Glutathione depletion and elevated oxidative stress are consistent findings in ME/CFS and Long COVID. Studies in these populations using 600 mg–2.4 g/day have reported improvements in fatigue and inflammatory markers. At 2.5 g/day, this protocol targets therapeutic rather than supplemental glutathione repletion.
Taurine is a sulfur-containing amino acid that is not incorporated into proteins but acts as a critical intracellular osmolyte and cytoprotective agent. It stabilises mitochondrial membranes, reduces electron transport chain ROS production, and modulates calcium ion handling in cardiac and skeletal muscle — relevant to the dysautonomia and cardiac symptoms in PACVS.
Taurine also conjugates bile acids, reduces inflammation via inhibition of neutrophil ROS production, and has direct anti-arrhythmic effects on cardiac conduction.
A 2023 study in Science (Singh et al.) demonstrated that taurine deficiency is a driver of the aging process across multiple species, and that taurine supplementation reversed markers of physiological aging including mitochondrial dysfunction and inflammation.
Clinical use of 3–6 g/day taurine is established in heart failure, where it improves cardiac output and reduces hospitalisation. At 1.5 g/day this protocol uses a conservative dose appropriate for a 90-day continuous protocol, targeting mitochondrial and cardiovascular support in PACVS.
Ascorbate is the primary water-soluble antioxidant in human plasma, scavenging ROS and regenerating vitamin E. It is an essential co-factor for two hydroxylation reactions required for L-carnitine biosynthesis — meaning that adequate vitamin C is a prerequisite for endogenous carnitine production and thus for efficient fat oxidation.
Vitamin C also drives collagen synthesis (via prolyl and lysyl hydroxylases), supports endothelial repair, and — at gram-level doses — augments the NO-producing effects of L-arginine by reducing oxidative inactivation of NO.
The Tosato et al. (2021) RCT combining L-arginine with vitamin C in Long COVID directly underpins this combination. Vitamin C deficiency was documented in hospitalised COVID patients and correlates with disease severity.
At 1 g/day, vitamin C exceeds the dose required for carnitine co-factor function and reaches the threshold at which plasma vitamin C becomes pharmacologically active as a vascular antioxidant — without the gastrointestinal tolerability concerns of higher doses.
NMN is a direct precursor to NAD⁺ (nicotinamide adenine dinucleotide), a molecule central to cellular energy metabolism, DNA repair, and gene regulation. NAD⁺ is required as an electron carrier in complex I and III of the mitochondrial electron transport chain and as a substrate for sirtuins — a family of deacylases that regulate inflammation, mitochondrial biogenesis, and stress response pathways.
NAD⁺ levels decline with age, illness, and oxidative stress. In post-viral illness, chronic immune activation and persistent oxidative stress deplete NAD⁺ rapidly through PARP activation (DNA repair) and CD38-mediated consumption.
Human trials by Yoshino et al. (2021, Science) confirmed that oral NMN raises NAD⁺ levels in blood, skeletal muscle, and peripheral blood mononuclear cells within weeks, with improvements in insulin sensitivity and muscle function in older women.
NAD⁺ depletion has been proposed as a key driver of Long COVID pathophysiology. At 250 mg/day, this protocol uses a dose consistent with the clinical trial literature — sufficient to raise NAD⁺ measurably while remaining within the dose range with established human safety data.
Be the first to hear when the VitalScan4PACVS self-funded pilot opens for participants and as results are published.
Register Your Interest →