一項重大的醫學突破表明，每日服用降膽固醇藥片可能很快就會成為歷史。科學家利用 CRISPR 基因編輯技術，關閉了肝臟中負責產生過量膽固醇的基因。只要一次注射，人體膽固醇的調節機制就被永久性地改變了。
在早期的人體試驗中，低密度脂蛋白膽固醇（「壞」膽固醇）水平下降了約 50%，三酸甘油酯水平下降了超過 55%。與需要每日服用的他汀類藥物或其他藥物不同，這種療法似乎具有持久性，有可能使患者無需終身服藥。這種改變發生在肝細胞內的基因層面。
這種方法針對的是高膽固醇的根本原因，而不是只控制症狀。透過編輯驅動膽固醇過度生成的基因，肝臟無需持續幹預即可自然地維持更健康的血脂水平。研究人員認為，這可以顯著降低高風險族群的心臟病和中風風險。
這項技術的意義遠不止於膽固醇。類似的基因編輯策略未來或許可以應用於高血壓、2 型糖尿病和遺傳性心血管疾病等疾病的治療。醫學或許正在從慢性治療模式轉向永久性的生物學解決方案。
儘管長期安全性和更大規模的試驗仍在進行中，但專家表示，這標誌著預防醫學的轉捩點。未來，一次性療法將取代數十年的每日服藥，這可能會重新定義醫療保健、醫療成本以及疾病的根源治療方式。
#基因編輯 #CRISPR #膽固醇 #醫學突破 #未來醫學
A major medical breakthrough suggests daily cholesterol pills may soon be a thing of the past. Scientists used CRISPR gene-editing technology to switch off a single
gene in the liver responsible for producing excess cholesterol. With just one injection, the body’s cholesterol regulation was permanently altered.
In early human trials, LDL (“bad”) cholesterol levels dropped by around 50%, while triglycerides fell by more than 55%. Unlike statins or other medications that require daily use, this treatment appears to be long-lasting, potentially eliminating the need for lifelong drug therapy. The change happens at the genetic level inside liver cells.
This approach targets the root cause of high cholesterol rather than managing symptoms. By editing the gene that drives overproduction, the liver naturally maintains healthier lipid levels without ongoing intervention. Researchers believe this could dramatically reduce heart attack and stroke risk in high-risk patients.
The implications extend far beyond cholesterol. Similar gene-editing strategies could one day be applied to conditions like hypertension, type 2 diabetes, and inherited cardiovascular disorders. Medicine may be shifting from chronic treatment models toward permanent biological fixes.
While long-term safety and wider trials are still underway, experts say this marks a turning point in preventive medicine. A future where one-time therapies replace decades of daily pills could redefine healthcare, costs, and how diseases are treated at their source.
