Experiment ledger
Research leads and active tests are separated so curiosity does not blur into action. This is documentation of one person's decision process, not medical advice, prescribing, coaching, or sourcing guidance.
Under construction. Coming soon.
LDN keeps coming up as a possible immune, inflammation, pain, mood, and recovery lever.
The possible upside is not direct muscle growth. The interesting angle is whether reducing inflammatory drag could improve recovery quality, pain tolerance, sleep stability, training consistency, and how well the rest of the stack feels.
A peptide studied around innate repair signaling, small fiber neuropathy, nerve repair markers, and inflammatory tissue stress.
This maps to recovery, pain sensitivity, nerve health, and longevity-adjacent tissue repair. If there is a useful signal, I would expect it to show up as better resilience under training stress, less inflammatory drag, or improved recovery capacity rather than direct hypertrophy.
A very short thymic peptide bioregulator from the Khavinson research line, discussed around immune aging, T-cell signaling, and gene-expression changes.
This is mostly a longevity and immune-resilience idea. The possible upside would be less about immediate gym performance and more about keeping immune function, inflammation, and recovery capacity from becoming limiting factors over time.
A mitochondria-targeted peptide studied as a cardiolipin-directed repair signal, with some of the cleaner human evidence among mitochondrial candidates.
This is the repair-lane candidate. The angle is whether better mitochondrial membrane function could translate into less fatigue friction, better training tolerance, cleaner recovery, and more resilient energy production over time.
NAD+ sits upstream of cellular energy metabolism, redox balance, DNA-repair signaling, and several longevity-adjacent pathways.
This is the substrate-tank idea. The possible upside is not a stimulant effect, but better support for energy production, recovery capacity, metabolic health, and the systems that become more expensive to maintain with age and training stress.
A nicotinamide N-methyltransferase inhibitor discussed as a way to reduce NAD+ drain and shift metabolic signaling, mostly from preclinical obesity and metabolism work.
This is the NAD+ efficiency-multiplier idea. If the mechanism matters, the relevant outcomes would be body composition, metabolic flexibility, nutrient partitioning, and keeping energy metabolism cleaner while training hard.
A mitochondrial-derived peptide studied around exercise signaling, skeletal muscle metabolism, insulin sensitivity, and metabolic stress adaptation.
This maps to the performance-longevity overlap: glucose handling, metabolic flexibility, endurance signaling, body composition, and recovery capacity. The useful question is whether it can support training adaptation rather than simply feel like an acute performance boost.
A synthetic estrogen-related receptor agonist studied as an exercise-mimetic compound in preclinical models of endurance signaling and metabolic syndrome.
This is the most experimental performance-metabolism idea in the stack. The draw is oxidative capacity, fatty-acid use, endurance signaling, and body-composition leverage, but the current signal is still mainly animal and mechanistic research.