{"id":3044,"date":"2026-05-23T23:42:40","date_gmt":"2026-05-24T03:42:40","guid":{"rendered":"https:\/\/haidut.me\/?p=3044"},"modified":"2026-05-23T23:42:40","modified_gmt":"2026-05-24T03:42:40","slug":"vitamin-b3-can-prevent-treat-fatty-liver-masld-nafld-nash","status":"publish","type":"post","link":"https:\/\/haidut.me\/?p=3044","title":{"rendered":"Vitamin B3 can prevent\/treat fatty liver (MASLD\/NAFLD\/NASH)"},"content":{"rendered":"<p>Metabolic-associated fatty liver disease (MASLD) affects roughly\u00a0<strong>30% of the global population<\/strong>\u00a0\u2014 billions of people. Mainstream medicine has no effective targeted therapies, offering only lifestyle advice (weight loss, exercise) that most patients cannot sustain. I have written extensively about\u00a0<strong>niacinamide (vitamin B3)<\/strong>\u00a0as a metabolic therapy, primarily focusing on its role as an\u00a0<strong>NAD+ precursor<\/strong>\u00a0that supports mitochondrial electron flow, oxidative phosphorylation, and overall energy metabolism. Now, researchers have discovered that\u00a0<strong>niacin (another form of vitamin B3)<\/strong>\u00a0directly inhibits a specific genetic driver of fatty liver disease \u2014\u00a0<strong>microRNA-93 (miR-93)<\/strong>\u00a0\u2014 which then restores\u00a0<strong>SIRT1<\/strong>\u00a0activity. This is a perfect example of the dual mechanism I have always emphasized: B3 works both by\u00a0<strong>boosting NAD+\/energy metabolism<\/strong>\u00a0and by\u00a0<strong>directly inhibiting pathological signaling pathways<\/strong>.<\/p>\n<p class=\"ds-markdown-paragraph\">As the study below demonstrates, researchers from UNIST and other institutions identified\u00a0<strong>microRNA-93 (miR-93)<\/strong>\u00a0as a central regulator of MASLD. Levels of miR-93 are\u00a0<strong>unusually high<\/strong>\u00a0in both human patients and animal models with fatty liver disease. MiR-93 drives fat buildup, inflammation, and scarring in the liver by\u00a0<strong>suppressing SIRT1<\/strong>\u00a0\u2014 a gene that plays a key role in fat metabolism. When the researchers used gene editing to stop miR-93 production, mice showed significantly less fat accumulation, improved insulin sensitivity, and better liver function.<\/p>\n<p class=\"ds-markdown-paragraph\">The team then screened\u00a0<strong>150 FDA-approved drugs<\/strong>\u00a0to see if any could reduce miR-93 levels.\u00a0<strong>Niacin (vitamin B3)<\/strong>\u00a0stood out as the most effective option. In mice treated with niacin, miR-93 levels dropped sharply, SIRT1 activity increased, and normal fat-processing pathways were restored.<\/p>\n<p class=\"ds-markdown-paragraph\">This finding is significant for two reasons that align perfectly with what I have been saying for years:<\/p>\n<ol start=\"1\">\n<li>\n<p class=\"ds-markdown-paragraph\"><strong>NAD+ and SIRT1:<\/strong>\u00a0Niacin (like niacinamide) is converted to NAD+. SIRT1 is a NAD+-dependent deacetylase that regulates metabolism, inflammation, and aging. By increasing NAD+, vitamin B3 directly activates SIRT1. The study shows that B3 also works by\u00a0<strong>lowering miR-93<\/strong>, which then\u00a0<strong>derepresses SIRT1<\/strong>. So B3 attacks the problem from two directions: increasing SIRT1 activity directly (via NAD+) and removing the inhibitor (miR-93) that suppresses SIRT1 expression.<\/p>\n<\/li>\n<li>\n<p class=\"ds-markdown-paragraph\"><strong>The specific enzyme target:<\/strong>\u00a0The study identifies\u00a0<strong>miR-93<\/strong>\u00a0as the key pathogenic microRNA. This is not an enzyme in the traditional sense, but a non-coding RNA that regulates gene expression. Vitamin B3 inhibits miR-93 levels, which is a novel mechanism that mainstream research has not previously appreciated. I have discussed how B3 inhibits other pathological pathways (e.g., PARP1 overactivation, NF-\u03baB), and this adds miR-93 to the list.<\/p>\n<\/li>\n<\/ol>\n<p class=\"ds-markdown-paragraph\">The study used\u00a0<strong>niacin<\/strong>\u00a0(nicotinic acid), which is one form of vitamin B3. I have generally recommended\u00a0<strong>niacinamide<\/strong>\u00a0(nicotinamide) because it does not cause the painful &#8220;niacin flush&#8221; associated with nicotinic acid. However, both forms are converted to NAD+ and likely share the ability to lower miR-93 (though this would need to be confirmed for niacinamide specifically). The human-equivalent dose is not explicitly stated in the press release, but based on the mouse studies and the fact that niacin is already used clinically for hyperlipidemia at doses of\u00a0<strong>500\u20132,000 mg per day<\/strong>, the effective human dose for fatty liver disease is likely in the same range. I have consistently recommended\u00a0<strong>500\u20131,500 mg of niacinamide daily<\/strong>\u00a0for metabolic support.<\/p>\n<p>The researchers explicitly note that niacin is a &#8220;well-established and safe medication&#8221; and that repurposing it for MASLD has &#8220;high translational clinical relevance.&#8221; This is exactly the kind of cheap, safe, off-patent intervention that the pharmaceutical industry ignores because it cannot be patented. Once again, vitamin B3 proves to be one of the most powerful metabolic therapies available.<\/p>\n<p><a href=\"http:\/\/dx.doi.org\/10.1016\/j.metabol.2025.156266\">http:\/\/dx.doi.org\/10.1016\/j.metabol.2025.156266<\/a><\/p>\n<p><a href=\"https:\/\/www.sciencedaily.com\/releases\/2026\/03\/260324080203.htm\">https:\/\/www.sciencedaily.com\/releases\/2026\/03\/260324080203.htm<\/a><\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;&#8230;Researchers have identified <strong>microRNA-93 (miR-93)<\/strong>\u00a0as a key genetic driver of fatty liver disease and discovered that\u00a0<strong>vitamin B3 can effectively shut it down<\/strong>. This finding suggests a safe, widely available vitamin could become a powerful new treatment.<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;&#8230;The researchers discovered that levels of miR-93 are <strong>unusually high<\/strong>\u00a0in both people with fatty liver disease and in animal models. Their analysis showed that miR-93 drives fat buildup, inflammation, and scarring in the liver by\u00a0<strong>suppressing SIRT1<\/strong>, a gene that plays a key role in managing fat metabolism inside liver cells.<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;&#8230;To better understand its role, the team used gene editing to stop the production of miR-93 in mice. These animals showed <strong>significantly less fat accumulation<\/strong>\u00a0in the liver, along with\u00a0<strong>improved insulin sensitivity<\/strong>\u00a0and better overall liver function.<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;&#8230;The researchers then screened <strong>150 FDA-approved drugs<\/strong>\u00a0to see if any could reduce miR-93 levels.\u00a0<strong>Niacin (vitamin B3) stood out as the most effective option<\/strong>. In mice treated with niacin,\u00a0<strong>miR-93 levels dropped sharply<\/strong>, while\u00a0<strong>SIRT1 activity increased<\/strong>. This helped restore normal fat-processing pathways in the liver and improved overall lipid balance.<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;&#8230;The research team explained, &#8216;This study precisely elucidates the molecular origin of MASLD and demonstrates the potential for <strong>repurposing an already approved vitamin compound<\/strong>\u00a0to modulate this pathway, which has high translational clinical relevance.&#8217;<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;&#8230;They added, &#8216;Given that <strong>niacin is a well-established and safe medication<\/strong>\u00a0used to treat hyperlipidemia, it holds promise as a candidate for combination therapies targeting miRNA pathways in MASLD.&#8217;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>Metabolic-associated fatty liver disease (MASLD) affects roughly\u00a030% of the global population\u00a0\u2014 billions of people. Mainstream medicine has&#8230;<\/p>\n","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[2],"tags":[862,2234,61,2233,70,59,67,68],"class_list":["post-3044","post","type-post","status-publish","format-standard","hentry","category-science","tag-b3","tag-fatty","tag-liver","tag-masld","tag-nad","tag-nafld","tag-niacinamide","tag-nicotinamide","wpcat-2-id"],"_links":{"self":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/3044","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=3044"}],"version-history":[{"count":1,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/3044\/revisions"}],"predecessor-version":[{"id":3045,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/3044\/revisions\/3045"}],"wp:attachment":[{"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=3044"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=3044"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=3044"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}