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Deep-dive into the science behind peptides and protocols.
Specialized pro-resolving mediators (SPMs) β resolvins, protectins, and maresins β are enzymatically synthesized from EPA and DHA to actively terminate inflammation. Their deficiency drives chronic inflammatory disease.
Glycine plays a dual role: inhibitory neurotransmitter in the brainstem and obligatory NMDA co-agonist in the SCN. The result is peripheral vasodilation, lower core body temperature, and measurably deeper slow-wave sleep.
ACTH(4-10) is a seven-amino-acid fragment of adrenocorticotropic hormone stripped of its steroidogenic activity but retaining potent effects on central melanocortin receptors β modulating attention, memory consolidation, and neurotrophic signaling.
The Na+/K+-ATPase consumes nearly a third of the body's resting energy budget to maintain the ion gradients that make life possible. Its decline drives neuronal hyperexcitability, arrhythmia, and cognitive aging.
Resolution of inflammation is not passive decayβit's an active biochemical program driven by specialized pro-resolving mediators (SPMs) synthesized from EPA and DHA. Here's what the science shows.
CD38 is the dominant consumer of NAD+ in aging tissues, and its activity rises sharply with inflammaging and senescent cell accumulation β making it a central enzymatic axis linking metabolic decline to cellular aging.
PGC-1Ξ± is the transcriptional coactivator that builds mitochondria, enables oxidative metabolism, and powers brown fat thermogenesis. Its age-related decline is a central driver of metabolic inflexibility.
MMP-1 and MMP-9 are zinc-dependent enzymes that UV radiation activates within hours of sun exposure, cleaving type I and type III collagen and accelerating dermal aging. Understanding TIMP regulators and copper peptide modulation reveals why some interventions reverse photoaging while others fail.
Matrikines are peptide fragments liberated from collagen, elastin, and laminin during extracellular matrix turnover. Unlike growth factors, they directly instruct fibroblasts to remodel tissue β making them a foundational target in dermal aging therapy.
Orexin neurons in the lateral hypothalamus act as the brain's master arousal switch. Understanding their pathological hyperactivity reframes chronic insomnia as a disorder of excessive wakefulness rather than sedative deficiency.