tag:blogger.com,1999:blog-8859456735165996893.post3980162661456211955..comments2024-03-28T02:36:04.078-07:00Comments on Health Correlator: Ketosis, methylglyoxal, and accelerated aging: Probably more fiction than factNed Kockhttp://www.blogger.com/profile/02755560885749335053noreply@blogger.comBlogger6125tag:blogger.com,1999:blog-8859456735165996893.post-44159350740581602742011-03-30T13:44:22.135-07:002011-03-30T13:44:22.135-07:00Interestingly, ketoacidosis often happens together...Interestingly, ketoacidosis often happens together with hyperglycemia, so at least part of the damage associated with ketoacidosis is likely to be caused by high blood sugar levels. Ketosis, on the other hand, is not associated with hyperglycemia.viagra onlinehttp://www.iservepharmacy.com/noreply@blogger.comtag:blogger.com,1999:blog-8859456735165996893.post-27329011799714203722010-07-27T16:08:11.593-07:002010-07-27T16:08:11.593-07:00It seems you MG is in hyperglycemia as well: "...It seems you MG is in hyperglycemia as well: "Methylglyoxal (MG) is a highly reactive dicarbonyl metabolite formed during glucose, protein and fatty acid metabolism. MG levels are elevated in hyperglycemia and other conditions. An excess of MG formation can increase ROS production and cause oxidative stress. MG reacts with proteins, DNA and other biomolecules, and is a major precursor of advanced glycation end products (AGEs). AGEs are also associated with the aging process and age-related diseases such as cardiovascular complications of diabetes, neurodegenerative diseases and connective tissue disorders. AGEs also increase oxidative stress." <br />Abstract <br />http://is.gd/dNbu2<br />Fulltext<br />http://is.gd/dNbDE<br /><br />Can a normal person go hyperglycemic on a ketogenic, high protein diet?rickhttps://www.blogger.com/profile/09851778022532692163noreply@blogger.comtag:blogger.com,1999:blog-8859456735165996893.post-34322999611062306362010-03-19T05:47:54.948-07:002010-03-19T05:47:54.948-07:00Thanks ET. Yes, and ketoacidosis is also strongly ...Thanks ET. Yes, and ketoacidosis is also strongly associated with very high glucose levels. Impaired glucose metabolism is the main contributor to the formation of AGEs. This makes it difficult to differentiate the negative effects of ketoacidosis from those caused by elevated glucose levels.Ned Kockhttps://www.blogger.com/profile/02755560885749335053noreply@blogger.comtag:blogger.com,1999:blog-8859456735165996893.post-30364974710975744822010-03-17T09:51:33.023-07:002010-03-17T09:51:33.023-07:00Found this doing a search on methylglyoxal. Ketoa...Found this doing a search on methylglyoxal. Ketoacidosis does increase it, not ketosis.<br /><br />The 2-oxoaldehyde methylglyoxal (MeG) is the precursor to a number of the known advanced glycation endproducts (AGE) implicated in the development of diabetic complications. Other 2-oxoaldehydes that are important in AGE formation, such as glyoxal, glucosone, deoxyglucosone, xylosone and deoxyxylosone, are produced by nonenzymatic reactions. By contrast, MeG is produced by both enzymatic and nonenzymatic processes, most of which appear to be enhanced in diabetes. MeG may be a major precursor to formation of AGE, and rates of production of MeG depend upon physiological conditions such as hyperglycemia and ketoacidosis. MeG is also unique compared to the other 2-oxoaldehydes in its complex metabolism. At least four pathways contribute to detoxification of MeG: (1) aldose reductase, a member of the aldo–keto reductase superfamily, catalyzes the NADPH-dependent reduction of a wide range of aldehydes. MeG is the best of the known physiological aldehyde substrates of aldose reductase. The distribution of aldose reductase in human tissue is restricted; there is little expression in liver; (2) the ubiquitous and highly active glyoxalase system converts MeG into -lactate. However, this system depends upon the availability of glutathione; activity is severely limited by conditions of oxidative stress that impact levels of glutathione; (3) betaine aldehyde dehydrogenase, also known as ALDH9, is able to catalyze the oxidation of MeG to pyruvate, although less efficiently than with its substrate betaine aldehyde; (4) the long-known but not widely studied 2-oxoaldehyde dehydrogenases (2-ODHs) catalyze the oxidation of MeG to pyruvate, primarily in liver. There are two NADP-dependent 2-ODHs in human liver. Both of these require an activating amine. The physiological activator is unknown.Ed Terryhttps://www.blogger.com/profile/07891923598027174669noreply@blogger.comtag:blogger.com,1999:blog-8859456735165996893.post-19954988374590277522010-03-17T01:19:44.395-07:002010-03-17T01:19:44.395-07:00I agree. By the way, De Grey has a minor co-author...I agree. By the way, De Grey has a minor co-author in his book, Ending Aging. That co-author is an active member of the calorie restriction society. The book has many references to calorie restriction. It usually refers to it as the ONLY proven method to delay aging. Oh well …Ned Kockhttps://www.blogger.com/profile/02755560885749335053noreply@blogger.comtag:blogger.com,1999:blog-8859456735165996893.post-5415939480431123552010-03-16T03:05:15.437-07:002010-03-16T03:05:15.437-07:00Saw De Grey on TED. He looks miserable on caloric ...Saw De Grey on TED. He looks miserable on caloric restriction. Believe a low carb + IF diet could do him a lot of good.Mikihttps://www.blogger.com/profile/01336665212024168702noreply@blogger.com