Acid mantle
BiologicalProcessThe dynamically maintained acidic pH environment of the stratum corneum. Controls ceramide processing, desquamation timing, antimicrobial defence, and microbiome composition simultaneously.
39 entities in this category
The dynamically maintained acidic pH environment of the stratum corneum. Controls ceramide processing, desquamation timing, antimicrobial defence, and microbiome composition simultaneously.
The cell's master energy sensor: a heterotrimeric kinase that detects rising AMP:ATP ratios and systematically switches metabolism from anabolic to catabolic programmes.
Active hair growth phase lasting 2-7 years; normally 85-90% of your follicles are in this growth-producing state.
The mitochondrial pathway that breaks down fatty acids into acetyl‑CoA, increasing acetyl‑CoA/CoA ratios that suppress PDH and shift fuel use toward fat.
The pattern of recurrent postprandial glucose spikes, prolonged hyperglycaemia, and insulin dysregulation that characterises dietary glycaemic load excess and insulin resistance.
A sustained energy deficit in which caloric intake falls below the body's metabolic requirements. The body responds through conserved survival mechanisms.
The transition phase of the hair cycle, lasting two to three weeks, during which the follicle's inferior segment undergoes controlled apoptotic regression.
Protective when transient and clearable; damaging when accumulated. UV drives both stress-induced senescence in fibroblasts and impairs the immune surveillance that clears senescent cells.
The endogenous 24-hour biological programme that coordinates physiological timing across virtually every organ, tissue, and cell type.
The pH-regulated enzymatic programme that sheds corneocytes from the stratum corneum surface at a rate matched exactly to keratinocyte production from below.
The depth-stratified calcium concentration system that coordinates keratinocyte proliferation, terminal differentiation, lamellar body secretion, and cornified envelope formation in epidermal layers.
Phenomenon where hunger hormone levels spike after stopping GLP-1 medications, sometimes exceeding pre-treatment levels.
Stopping GLP-1 medication (tirzepatide or semaglutide), which typically leads to appetite signal changes and potential weight regain.
Non‑enzymatic binding of sugars to proteins, forming AGEs that accumulate, cross‑link structural proteins, and drive inflammatory and oxidative damage via RAGE.
Skin dullness, yellowing, stiffness, and slowed repair caused by long‑term AGE buildup, producing a pattern distinct from chronological ageing or UV damage.
The community of gut microorganisms that modulates immune signalling, inflammation, and microbial metabolites with downstream effects on skin barrier function and disease risk.
The bidirectional communication system linking gut microbiota, immune signalling, and microbial metabolites to skin inflammation, barrier function, and disease susceptibility.
A framework of twelve interconnected biological processes - organised into Primary, Antagonistic, and Integrative tiers - that collectively produce the structural decline of ageing tissue.
Dietary pattern of elevated sugar and processed food intake that leads to increased blood glucose and potential skin effects.
The body’s central stress‑response system, driving CRH→ACTH→cortisol signalling systemically and via a parallel cutaneous HPA axis that regulates skin immunity, barrier function, and repair.
The ileal brake is a physiological feedback mechanism by which unabsorbed nutrients in the small intestine triggers the release of satiety hormones that suppress appetite.
Chronic low-grade sterile inflammation accumulating with age through senescence, cGAS-STING, and NF-κB amplification — impairing tissue repair and driving structural skin ageing.
The PI3K–AKT signalling pathway triggered by insulin receptor activation that drives glucose uptake, suppresses hepatic glucose output, and restrains adipose lipolysis.
The coordinated, one-way molecular programme by which a basal keratinocyte progresses through the epidermal layers to produce the structural and biochemical components of the skin barrier.
The calcium-triggered exocytosis event at the stratum granulosum–stratum corneum interface that delivers ceramide precursors, enzymes, and antimicrobial peptides into the extracellular space.
The biological process by which skin cells produce ceramides, cholesterol, and fatty acids - the structural lipid building blocks of the stratum corneum's protective barrier.
Metabolic adaptation is the physiological reduction in resting energy expenditure that exceeds what would be predicted from changes in body weight and composition alone during caloric restriction.
The process by which metabolic inflexibility depletes cellular NAD⁺, stalling SIRT1 deacetylase activity and progressively dampening the molecular circadian clock.
The progressive reduction in oestrogen that begins in the early 40s and accelerates through perimenopause into menopause, driving simultaneous changes across the dermis, epidermis, and skin barrier.
Oxidative phosphorylation generates the bulk of cellular ATP in mitochondria, coupling oxygen use to energy production while also producing ROS, a process central to tissue function and ageing.