Inventor of the Basque Cheesecake Plans to Retire. His Secret: He Prefers Chocolate

Santiago Rivera is widely credited with creating the “burnt” cheesecake in the 1980s, though he doesn’t love the spinoffs it has spawned. Decades later, he’s preparing to hand over his kitchen to his children.

The New York Times

Eli Lilly is preparing a phase 2 trial for VERVE-102, a one-time gene editor acquired from Verve Therapeutics. The highest dose cut LDL cholesterol by 62% in patients, a reduction sustained for up to 18 months across 35 participants.

The treatment permanently switches off PCSK9, a cholesterol-producing gene, using base editing that flips a single DNA letter without breaking the double helix.

#news #health #medicine #cholesterol #GeneTherapy #GeneEditing

One thing can ‘reverse’ high cholesterol damage without the need for statins, study finds

https://fed.brid.gy/r/https://www.mirror.co.uk/news/health/one-thing-can-reverse-high-37210063

One infusion. One time. Possibly forever. A breakthrough gene-editing treatment just slashed LDL "bad" cholesterol by up to 62% — and the results are holding 18 months later. Published in the New England Journal of Medicine, the small study of 35 patients could reshape how we fight heart disease, which kills 800,000 Americans annually. No daily pills. No repeat treatments. Just one shot. Experts call it potentially "game-changing." Larger trials are next — but the early signs are extraordinary. The future of heart health may have just arrived. #HeartDisease #GeneTherapy #MedicalBreakthrough #Cholesterol #Health #Science #Medicine #NEJM #Innovation #Healthcare https://www.nytimes.com/2026/05/25/health/cholesterol-ldl-gene-therapy.html?unlocked_article_code=1.lVA.l-ru.p7FYphe9x4Tx&smid=nytcore-android-share
One-and-Done Heart Disease Prevention? Scientists Show It May Be Possible.

A single infusion of an experimental gene-editing drug seemed to reduce LDL long-term in a small trial. The results may point to something “curative,” one expert said.

The New York Times

Game Changer for Cholesterol and Cardiovascular Diseases?

In Vivo Base Editing of PCSK9 with VERVE-102 for Hypercholesterolemia

In a small study, an experimental gene-editing treatment dramatically lowered #cholesterol levels, perhaps permanently, after just one infusion, scientists reported on Monday. If confirmed in larger studies, researchers hope the findings may lead to a one-and-done way to prevent heart disease in large numbers of people. The study, published in The New England Journal of Medicine, was an interim analysis of 35 patients in a trial that will involve as many as 85 participants.

https://www.nejm.org/doi/full/10.1056/NEJMoa2601283

A tiny (five people, the BBC said) trial of a gene-editing fix for bad cholesterol could be revolutionary, if it turns out to be safe. And, if it is safe, could the same method be used for the tragedies of psychoses, autism, even for the controllable but expensive and dangerous asthma? https://www.edgen.tech/news/post/lillys-gene-editor-cuts-bad-cholesterol-62-in-a-one-time-dose
#DNA #cholesterol
Lilly's gene editor cuts bad cholesterol 62% in a one-time dose

Eli Lilly’s investigational base editor, VERVE-102, reduced “bad” cholesterol by up to 62% with a single dose in a clinical trial, a result that could challenge the multi-billion dollar market for chr...

Edgen

Researchers Identify Liver Protein HELZ2 That Regulates Blood Cholesterol Production

📰 Original title: Scientists discover hidden liver switch that cuts harmful cholesterol

🤖 IA: It's not clickbait ✅
👥 Users: It's not clickbait ✅

View full AI summary: https://en.killbait.com/researchers-identify-liver-protein-helz2-that-regulates-blood-cholesterol-production.html?utm_source=mastodon_world&utm_medium=social&utm_campaign=killbait.mastodon_world

#health #cholesterol #liverprotein #cardiov...

Researchers Identify Liver Protein HELZ2 That Regulates Blood Cholesterol Production

Researchers at UT Southwestern Medical Center have identified a previously unknown regulatory protein in the liver, called HELZ2, that plays a central role in controlling how much cholesterol is released into the bloodstream. The study, published in the journal Circulation, reveals that HELZ2 influences cholesterol levels by regulating the stability of APOB messenger RNA (mRNA), which contains the genetic instructions needed to produce apolipoprotein B (apoB). ApoB is a key structural component of lipoproteins such as LDL, which transport cholesterol and fats through the body and are strongly associated with cardiovascular disease when present in excess. The researchers found that when HELZ2 activity increases, it accelerates the breakdown of APOB mRNA inside liver cells. This leads to reduced production of apoB proteins and fewer cholesterol-carrying lipoproteins entering the bloodstream. In animal studies, mice with a gain-of-function mutation in HELZ2 showed lower levels of LDL cholesterol and triglycerides, as well as a reduced risk of atherosclerosis, the artery-clogging condition responsible for many heart attacks and strokes. However, this protective effect came with a trade-off: increased fat accumulation in the liver, suggesting a balance between circulating cholesterol and liver fat storage. Importantly, mice lacking the mutation showed the opposite effect, highlighting HELZ2 as a biological “dial” that shifts fat distribution between the bloodstream and the liver. Researchers believe this discovery could open a new therapeutic pathway for treating high cholesterol and fatty liver disease. Unlike statins, which reduce cholesterol after it is produced, targeting HELZ2 would intervene earlier in the process by controlling gene expression at the RNA level. This represents a potentially new class of treatments aimed at fine-tuning lipid metabolism and reducing cardiovascular risk while carefully managing liver health.

KillBait

Researchers Identify Liver Protein HELZ2 That Regulates Blood Cholesterol Production

📰 Original title: Scientists discover hidden liver switch that cuts harmful cholesterol

🤖 IA: It's not clickbait ✅
👥 Users: It's not clickbait ✅

View full AI summary: https://en.killbait.com/researchers-identify-liver-protein-helz2-that-regulates-blood-cholesterol-production.html?utm_source=mastodon_social&utm_medium=social&utm_campaign=killbait.mastodon_social

#health #cholesterol #liverprotein #cardi...

Researchers Identify Liver Protein HELZ2 That Regulates Blood Cholesterol Production

Researchers at UT Southwestern Medical Center have identified a previously unknown regulatory protein in the liver, called HELZ2, that plays a central role in controlling how much cholesterol is released into the bloodstream. The study, published in the journal Circulation, reveals that HELZ2 influences cholesterol levels by regulating the stability of APOB messenger RNA (mRNA), which contains the genetic instructions needed to produce apolipoprotein B (apoB). ApoB is a key structural component of lipoproteins such as LDL, which transport cholesterol and fats through the body and are strongly associated with cardiovascular disease when present in excess. The researchers found that when HELZ2 activity increases, it accelerates the breakdown of APOB mRNA inside liver cells. This leads to reduced production of apoB proteins and fewer cholesterol-carrying lipoproteins entering the bloodstream. In animal studies, mice with a gain-of-function mutation in HELZ2 showed lower levels of LDL cholesterol and triglycerides, as well as a reduced risk of atherosclerosis, the artery-clogging condition responsible for many heart attacks and strokes. However, this protective effect came with a trade-off: increased fat accumulation in the liver, suggesting a balance between circulating cholesterol and liver fat storage. Importantly, mice lacking the mutation showed the opposite effect, highlighting HELZ2 as a biological “dial” that shifts fat distribution between the bloodstream and the liver. Researchers believe this discovery could open a new therapeutic pathway for treating high cholesterol and fatty liver disease. Unlike statins, which reduce cholesterol after it is produced, targeting HELZ2 would intervene earlier in the process by controlling gene expression at the RNA level. This represents a potentially new class of treatments aimed at fine-tuning lipid metabolism and reducing cardiovascular risk while carefully managing liver health.

KillBait