Does bmi predict all 11 food addiction criteria?
We tested whether BMI links to all 11 parts of our food addiction quiz equally. It doesn't, and one result ran opposite to our own prediction.
Where beauty meets biology
We tested whether BMI links to all 11 parts of our food addiction quiz equally. It doesn't, and one result ran opposite to our own prediction.
Understand what body composition really measures, why BMI is limited, and how waist‑to‑height ratio, body...
That sudden 4pm carb craving after a proper lunch isn’t a lack of willpower. It’s...
How long does barrier repair actually take? Evidence-based timeline from days to weeks, with age-adjusted...
When trusted skincare products suddenly sting, or persistent tightness resists every expensive moisturiser, you're experiencing whispers before the shout - early warnings of a compromised skin barrier.
From the calcium trap that silences your skin's own repair alarm, to the NHE1 proton pump quietly declining with age – this deep dive explains what's actually happening at a cellular level, and what to do about it.
Your skin is home to over a trillion microorganisms and they aren't just passengers. In this deep dive we unpack the astonishing biology of your skin microbiome: how commensal bacteria manufacture ceramides, maintain the acid mantle, regulate dangerous enzymes, and train your immune system. We explore what happens when that ecosystem collapses (dysbiosis, eczema, neurogenic inflammation), how perimenopause triggers a 60% loss of your microbial workforce, and what the latest clinical evidence says about rebuilding it.
Beauty sleep isn't just aspirational wellness. Your skin cells contain molecular clocks running 24-hour repair schedules whether you respect them or not. Learn to align your habits with biology's non-negotiable schedule.
The beauty industry frequently stamps "28-day skin reset" on skin products, but full epidermal turnover in healthy adult skin takes 40 to 56 days, and that's before accounting for age or hormonal change. In this deep dive we unpack the real biology of barrier repair: how hard water and S. aureus trigger a cytokine loop that actively blocks healing, and why oestrogen decline during perimenopause shifts the biological clock to four to eight weeks of recovery. We then look at what the evidence actually supports and why working with your skin's own intelligence will always outperform rushing it.
The metabolic convergence point where glucose, fatty acid, and amino acid catabolism each deliver a two-carbon acetyl unit.
A biomimetic neuro-modulatory peptide that reduces expression lines by competing with the SNARE complex, offering a non-invasive alternative to botulinum toxin.
The dynamically maintained acidic pH environment of the stratum corneum. Controls ceramide processing, desquamation timing, antimicrobial defence, and microbiome composition simultaneously.
The enzyme that converts sphingomyelin to ceramide via the sphingomyelinase pathway. Active in both lamellar body secretion and UV-induced keratinocyte stress signalling.
A chronic inflammatory disease of the pilosebaceous unit producing follicular hyperkeratinisation, seborrhoea, C. acnes phylotype dysbiosis, and immune activation.
Adipocytes are energy‑storing endocrine cells that release fatty acids and adipokines to regulate metabolism, inflammation, and whole‑body metabolic health.
The hypothalamic neuropeptide that drives sustained food-seeking by blocking and actively suppressing melanocortin-4 receptor activity.
The molecular building blocks from which every structural and functional protein in the skin is assembled. Collagen, elastin, keratin, and filaggrin are all amino acid sequences.
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.
Progressive genetic hair loss where follicles gradually miniaturise, shortening growth phases and producing finer, thinner hairs.
Endogenous peptides that defend against microbes yet can drive inflammation, acting as antimicrobial, immunomodulatory, and microbiome‑shaping signals.
The terminal pro-inflammatory omega-6 fatty acid, produced from DGLA. Feeds the eicosanoid pathways that drive vasodilation, immune cell recruitment, and inflammatory skin conditions.
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.
A family of cationic antimicrobial proteins with distinct roles in baseline defence, inducible microbiome‑responsive immunity, and broad‑spectrum pathogen control.
Beta-hydroxybutyrate (BHB) is the predominant ketone body produced by the liver during states of carbohydrate restriction, fasting, caloric deficit, or sustained aerobic exercise.
Water‑soluble B vitamin serving as a covalent cofactor for carboxylase enzymes in fatty‑acid, amino‑acid, and glucose metabolism; its skin, hair, and nail effects appear only in true deficiency.
Liquid component of blood containing platelets and proteins, separated and concentrated during PRP and iPRF treatments.
The pattern of recurrent postprandial glucose spikes, prolonged hyperglycaemia, and insulin dysregulation that characterises dietary glycaemic load excess and insulin resistance.
Butyrate is a four-carbon short-chain fatty acid with roles as a gut barrier protector, epigenetic immune regulator, and a contributor to keratinocyte differentiation.
A sustained energy deficit in which caloric intake falls below the body's metabolic requirements. The body responds through conserved survival mechanisms.
The mitochondrial outer‑membrane enzyme that controls fatty‑acid entry via carnitine transport and is inhibited by malonyl‑CoA to regulate fat oxidation.
The transition phase of the hair cycle, lasting two to three weeks, during which the follicle's inferior segment undergoes controlled apoptotic regression.
Catecholamines are a class of monoamine compounds — principally adrenaline (epinephrine), noradrenaline (norepinephrine), and dopamine.
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.
Ceramide subtype providing structural support within the skin barrier's lipid matrix, contributing to overall barrier integrity.
Ceramide subtype that helps anchor the barrier's crucial long periodicity phase structure alongside Ceramide EOS.
Critical ceramide subtype comprising about 10% of total ceramides, essential for forming the barrier's most important structural element.
Most abundant ceramide subtype in skin, primarily responsible for the barrier's hydration-retention function.
Family of lipids comprising 50% of your skin barrier, essential for retaining moisture and defending against environmental damage.