Medical Bulletin 17/January/2026

Childhood obesity explodes globally—8.5% obese, 14.8% overweight from 2000-2023—with China's 7-18-year-olds hitting 9.6%. Screens rule sedentary habits, with over 70% of kids blasting past WHO's strict 2-hour daily recreational limit, fueling fat via mindless snacking, junk food ads, blue-light sleep disruption, and zero calorie burn.

Every extra screen hour spiked visceral fat area by 2.9% (P=0.009), body fat mass index by 10.9%, body fat percentage by 46.9%, and dropped protective HDL-cholesterol by 1.4%. Kids crossing 2+ hours/day showed massive fat surges and 14.5% worse fitness scores.

Cardiorespiratory endurance explained a whopping 66.6% of screen time's visceral fat link, 67.5% for fat mass index, 65.1% for body fat percentage, and 22.6% for HDL-C. Prolonged sitting tanks energy expenditure and cardiovascular power, but building endurance through sports or runs dramatically cuts these obesity drivers.

This urgent wake-up call demands screen caps at 2 hours max, plus active play mandates. Simple shifts—less Netflix, more shuttle runs—could slash hidden belly fat, boost heart health, and dodge lifelong diabetes risk, positioning fitness as kids' ultimate screen-time shield.

REFERENCE: Zhang J. (2026). The association of screen time with childhood obesity and metabolic status: a mediation analysis of cardiorespiratory fitness. Frontiers in Endocrinology. https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2025.1719372/full

Scientists Discover Novel Hidden Diabetes Type in Newborn Infants

One sneaky gene mutation silently destroys newborn insulin factories—while simultaneously scrambling their developing brains.

University of Exeter Medical School and Belgium's Université Libre de Bruxelles just cracked open a medical mystery: TMEM167A gene mutations cause a brand-new form of neonatal diabetes. Published in The Journal of Clinical Investigation, their landmark study of 6 infants proves this single DNA defect triggers BOTH skyrocketing blood sugar AND devastating brain problems like epilepsy and microcephaly—before babies even hit 6 months old.

The crisis: Neonatal diabetes strikes ~1 in 100,000 newborns (far earlier than Type 1). Over 85% trace to genetic causes. These 6 cases stood out—kids had diabetes PLUS neurological red flags. Researchers sequenced every child's DNA and found identical TMEM167A mutations across all patients.

Lab work:

1. Skin → Stem cells: Converted patient skin cells into insulin-producing pancreatic beta cells

2. CRISPR attack: Gene-edited TMEM167A out of these lab-grown beta cells

3. Disaster unfolded: Mutant cells STOPPED secreting insulin → toxic stress exploded inside → self-destruct pathways activated → complete beta cell death

Key findings that rewrite diabetes science:

• TMEM167A = "guardian gene" for insulin secretion AND neuron survival

• Mutations hit pancreas + brain hardest (spares most other tissues)

• Stem cell models PERFECTLY recreated patient cell failure

• Dr. Elisa de Franco: "These DNA changes decode TMEM167A's vital role"

• Professor Miriam Cnop: "Lab beta cells = diabetes cure testing ground"

With 589M adults diabetic worldwide, TMEM167A stress pathways could unlock Type 1/2 treatments too.

This isn't just rare baby diabetes—it's a roadmap showing exactly how insulin factories fail under genetic attack. Future CRISPR therapies could rescue newborn pancreases while guiding common diabetes fixes. One tiny gene mutation unlocks massive metabolic secrets for everyone from fragile infants to aging adults.

REFERENCE: Enrico Virgilio, Sylvia Tielens, Georgia Bonfield, et. al.; Recessive TMEM167A variants cause neonatal diabetes, microcephaly, and epilepsy syndrome. Journal of Clinical Investigation, 2025; 135 (22) DOI: 10.1172/JCI195756

Y Chromosome Loss Strongly Associated with Elevated Cardiovascular Disease Risk: Study

Men lose their Y chromosome as they age—and it could be silently triggering heart attacks. Researchers tracking over 5,000 healthy men aged 65+ uncovered a shocking link: blood cells missing the Y chromosome (LOY) dramatically boost heart attack risk.

Published in JACC, this prospective study from a major prevention trial followed participants for 8.4 years, proving LOY acts as an independent warning signal for coronary disaster in aging males without prior heart disease.

As men age, some white blood cells mysteriously lose their Y chromosome—the male sex chromosome. Previously tied to smoking, cancer, and early death, LOY was unclear in healthy hearts. This study asked: does it predict heart attacks specifically?

Researchers analyzed genetic and clinical data from 5,000+ healthy older men in a prevention trial. They measured LOY levels in blood at baseline, then tracked major events (heart attacks, strokes) over 8.4 years. Stats adjusted for smoking, cholesterol, blood pressure, diabetes—everything known. For backup, they cross-checked 190,000+ middle-aged men from a massive biobank.

Findings:

• Nearly 10% suffered major heart events during follow-up

• Each LOY increase = 14% higher heart attack risk

• Men with highest LOY = 68% greater heart attack odds vs. no LOY

• NO stroke link—LOY targets coronary arteries specifically

• Biobank confirmed: even modest LOY raises heart attack risk

Why coronary arteries, not strokes? LOY belongs to clonal haematopoiesis—blood cells mutate with age, pumping out inflammation that clogs heart arteries. Stroke vessels seem more resistant.

Heart disease kills most men globally. LOY offers a simple blood test to spot high-risk guys early, beyond cholesterol checks. While observational (no causality proven), findings held across huge datasets of mostly White males.

This breakthrough reframes aging men's hearts—not just pipes clogging, but blood cells rebelling. Future tests could catch silent LOY before the first chest pain, guiding statins or lifestyle for the invisible chromosome threat lurking in every older man's blood.

REFERENCE: Hussain, S, Bjurling, J, Yu, C. et al. Loss of Y Chromosome and Major Cardiovascular Events in a Prospective Study of Older Men. JACC. 2026 Jan, 87 (1) 36–45.https://doi.org/10.1016/j.jacc.2025.10.069