{"id":1768,"date":"2022-03-30T13:17:11","date_gmt":"2022-03-30T17:17:11","guid":{"rendered":"http:\/\/haidut.me\/?p=1768"},"modified":"2022-03-30T13:17:11","modified_gmt":"2022-03-30T17:17:11","slug":"aging-and-disease-are-the-same-process-driven-by-low-metabolism","status":"publish","type":"post","link":"https:\/\/haidut.me\/?p=1768","title":{"rendered":"Aging and disease are the same process, driven by low metabolism"},"content":{"rendered":"<p>I am posting about this mostly due to its &#8220;told you so&#8221; factor &#8211; i.e. more and more professionals in the medical and research fields are starting to realize that the super-specialized approach to treating chronic diseases has not produced any substantial results. In addition, the correlation between age and chronic diseases has pushed scientists to explore the connection between the two issues and a consensus has started to form that there is nothing &#8220;natural&#8221; about aging, just as there is nothing &#8220;natural&#8221; about developing say cancer, diabetes or a neurological disease. In fact, as the researchers have started to realize, chronic diseases share all of their features with aging and can be viewed as nothing more than premature aging of specific organ\/tissue. More importantly, scientists have started to realize that the common cause underpinning both aging and diseases is mitochondrial hypofunction\/dysfunction, which is another way of saying that both aging and diseases are driven by low metabolism. Let&#8217;s hope this sentiment and approach that has already established itself in certain research circles takes over the more practical fields (such as medicine) as well.<\/p>\n<p><a href=\"https:\/\/universityofcalifornia.edu\/news\/fight-diseases-aging-scientist-makes-aging-itself-target\">https:\/\/universityofcalifornia.edu\/news\/fight-diseases-aging-scientist-makes-aging-itself-target<\/a><\/p>\n<p>&#8220;&#8230;\u201c<span style=\"text-decoration: underline;\"><strong>If we could pause, delay or even reverse aging, we would make a significant impact against numerous diseases<\/strong><\/span>,\u201d said Guo, professor of neurology, molecular and medical pharmacology at the\u00a0<a href=\"https:\/\/medschool.ucla.edu\/\">David Geffen School of Medicine at UCLA<\/a>. \u201cI want to create a higher quality of life over a healthy life span, rather than just prolonging life.\u201d Her particular approach to her research is inspired by her compassion for her patients who have Alzheimer\u2019s and Parkinson\u2019s diseases and other brain degenerative disorders, and from the discoveries she has made in her research lab. The percentage of people with Alzheimer&#8217;s doubles every five years after the age of 65, so Guo believes that <span style=\"text-decoration: underline;\"><strong>intervening in the aging process could be the path to reducing the disease\u2019s massive impact. Slowing aging could also help combat a range of other diseases and conditions, including Parkinson\u2019s disease, heart disease, cancer and osteoporosis, as well as the increased vulnerability to infection that occurs with aging<\/strong><\/span>.&#8221;<\/p>\n<p>&#8220;&#8230;<strong><span style=\"text-decoration: underline;\">There\u2019s now a body of research indicating that damaged mitochondria contribute to premature aging, and their implications for human health stretch beyond one illness.<\/span> \u201cDysfunctional mitochondria are associated with not only Parkinson\u2019s disease, but also other neurodegenerative diseases, cancer, diabetes and heart disease<\/strong>,\u201d Guo said. \u201cSo we asked, \u2018Is it possible for us to reverse this damaged mitochondrial signature?\u2019\u201d Mitochondria have their own genetic materials \u2014 distinct from those in the cell\u2019s nucleus \u2014 and exploring mitochondrial DNA has become a signature of Guo\u2019s research. In one of her recent studies, a collaboration with Caltech researchers, Guo and her colleagues <span style=\"text-decoration: underline;\"><strong>discovered how to reverse up to 95% of the damage to mitochondrial DNA in animals<\/strong><\/span>.&#8221;<\/p>\n","protected":false},"excerpt":{"rendered":"<p>I am posting about this mostly due to its &#8220;told you so&#8221; factor &#8211; i.e. more and&#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":[101,62,97,77,883],"class_list":["post-1768","post","type-post","status-publish","format-standard","hentry","category-science","tag-aging","tag-disease","tag-metabolism","tag-mitochondria","tag-oxphos","wpcat-2-id"],"_links":{"self":[{"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/1768","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=1768"}],"version-history":[{"count":1,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/1768\/revisions"}],"predecessor-version":[{"id":1769,"href":"https:\/\/haidut.me\/index.php?rest_route=\/wp\/v2\/posts\/1768\/revisions\/1769"}],"wp:attachment":[{"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=1768"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=1768"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/haidut.me\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=1768"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}