{"id":3022,"date":"2026-05-23T18:42:55","date_gmt":"2026-05-23T22:42:55","guid":{"rendered":"https:\/\/haidut.me\/?p=3022"},"modified":"2026-05-23T18:42:55","modified_gmt":"2026-05-23T22:42:55","slug":"a-constipation-drug-can-treat-kidney-disease-likely-by-lowering-endotoxin-lps","status":"publish","type":"post","link":"https:\/\/haidut.me\/?p=3022","title":{"rendered":"A constipation drug can treat kidney disease, likely by lowering endotoxin\/LPS"},"content":{"rendered":"<p>Chronic kidney disease (CKD) is conventionally managed with blood pressure control, protein restriction, and phosphate binders. Constipation \u2014 which affects the majority of CKD patients \u2014 is rarely treated as a primary intervention. Ray Peat has repeatedly stated that\u00a0<strong>endotoxin (LPS)<\/strong>\u00a0from intestinal bacteria is a major driver of systemic inflammation, fibrosis, and organ damage, including kidney disease. He has long recommended simple interventions like\u00a0<strong>carrot salad<\/strong>\u00a0to reduce constipation and lower endotoxin absorption. Now, a randomized clinical trial has confirmed that treating constipation directly slows kidney decline \u2014 but the researchers misinterpreted the mechanism.<\/p>\n<p class=\"ds-markdown-paragraph\">As the study below demonstrates, the constipation drug\u00a0<strong>lubiprostone<\/strong>\u00a0significantly slowed the decline of kidney function (eGFR) in patients with moderate CKD over 24 weeks. The higher dose (16 mcg) outperformed the lower dose (8 mcg), which outperformed placebo. The researchers observed changes in gut bacteria and increased levels of\u00a0<strong>spermidine<\/strong>, which they attribute to mitochondrial protection.<\/p>\n<p class=\"ds-markdown-paragraph\"><strong>However, from the bioenergetic perspective, the primary mechanism is almost certainly endotoxin reduction.<\/strong>\u00a0Constipation increases gut transit time, which allows Gram-negative bacteria to proliferate and release large quantities of\u00a0<strong>lipopolysaccharide (LPS)<\/strong>. LPS absorbed from the gut circulates to the kidneys, where it triggers inflammation, oxidative stress, fibrosis, and mitochondrial dysfunction. By relieving constipation, lubiprostone reduces LPS load, thereby lowering the inflammatory burden on the kidneys. The observed increase in spermidine may be a secondary or parallel effect \u2014 but the core intervention is simply\u00a0<strong>keeping the gut moving<\/strong>.<\/p>\n<p class=\"ds-markdown-paragraph\">This explains why Ray Peat recommended\u00a0<strong>carrot salad<\/strong>\u00a0(fiber that binds endotoxin) and other pro-motility agents for kidney protection. The drug industry has now accidentally validated what Peat has said for decades:\u00a0<strong>treat constipation, lower endotoxin, protect the kidneys.<\/strong>\u00a0The human-equivalent doses are already provided in the article as the clinical doses used (8 mcg and 16 mcg daily), since this was a human trial \u2014 no animal-to-human conversion is needed.<\/p>\n<p class=\"ds-markdown-paragraph\">Once again, a simple intervention targeting gut motility outperforms complex pharmaceutical approaches by addressing the root issue: endotoxin-driven inflammation.<\/p>\n<p><a href=\"https:\/\/doi.org\/10.1126\/sciadv.adw3934\">https:\/\/doi.org\/10.1126\/sciadv.adw3934<\/a><\/p>\n<p><a href=\"https:\/\/www.earth.com\/news\/common-constipation-drug-lubiprostone-may-also-protect-failing-kidneys\/\">https:\/\/www.earth.com\/news\/common-constipation-drug-lubiprostone-may-also-protect-failing-kidneys\/<\/a><\/p>\n<div class=\"ds-message _63c77b1\">\n<div class=\"ds-markdown\">\n<p class=\"ds-markdown-paragraph\">&#8220;Some received a placebo. Others took <strong>8 micrograms or 16 micrograms of lubiprostone<\/strong>\u00a0daily for 24 weeks&#8230; The primary measure was\u00a0<strong>estimated glomerular filtration rate (eGFR)<\/strong>. In moderate kidney disease, that number falls year over year.&#8221;<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;Patients on placebo did what the research predicted. Their <strong>eGFR drifted downward<\/strong>\u00a0over the six-month window. The\u00a0<strong>lubiprostone groups did not<\/strong>\u00a0\u2013 or did so more slowly.\u00a0<strong>Higher doses held kidney function steadier.<\/strong>\u00a0The\u00a0<strong>16 microgram group outperformed the 8 microgram group<\/strong>, which in turn outperformed placebo.&#8221;<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;When the gut microbiome falls out of balance, <strong>inflammation tends to rise<\/strong>\u00a0and bacterial byproducts that should leave the body start to build up instead.&#8221;<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;The mechanism is where the work gets strange&#8230; the drug had <strong>reshaped which bacteria were thriving<\/strong>\u00a0in patients&#8217; guts&#8230;\u00a0<strong>Spermidine<\/strong>\u00a0has drawn attention in aging research for its effects on\u00a0<strong>mitochondria<\/strong>\u00a0\u2013 the tiny structures inside cells that turn nutrients into usable energy. Kidney cells&#8230; are\u00a0<strong>particularly sensitive to mitochondrial decline<\/strong>.&#8221;<\/p>\n<p class=\"ds-markdown-paragraph\">&#8220;Going in, the researchers had a different prediction. They expected lubiprostone to lower <strong>uremic toxins<\/strong>&#8230;\u00a0<strong>That is not what happened.<\/strong>\u00a0Uremic toxin levels held roughly steady throughout. The <span style=\"text-decoration: underline; color: #ff0000;\"><strong>kidney benefit traveled through a\u00a0different route entirely: gut bacteria changes and mitochondrial support, not detoxification<\/strong><\/span>.&#8221;<\/p>\n<\/div>\n<\/div>\n","protected":false},"excerpt":{"rendered":"<p>Chronic kidney disease (CKD) is conventionally managed with blood pressure control, protein restriction, and phosphate binders. Constipation&#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":[1353,285,9,12,1379,10,106,77],"class_list":["post-3022","post","type-post","status-publish","format-standard","hentry","category-science","tag-ckd","tag-diabetes","tag-endotoxin","tag-inflammation","tag-kidney","tag-lps","tag-microbiome","tag-mitochondria","wpcat-2-id"],"_links":{"self":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/3022","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=3022"}],"version-history":[{"count":1,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/3022\/revisions"}],"predecessor-version":[{"id":3023,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/3022\/revisions\/3023"}],"wp:attachment":[{"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=3022"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=3022"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=3022"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}