Aging Research Article & Low Insulin IGF-1 Extends Life?

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Wrote:Since you bring it up, there is a lot of literature out there whichdiscusses the impact of insulin on longevity. And clearly, the Atkinsdiet is one where little insulin is produced. There are also studiesout there showing that body fat may be the actual life spandeterminant (as indicated by GM mice studies). Wrote:What about genetically obese mice (ob/ob) that are reduced to a normal levelof body fat (via caloric restriction)? This is the longest lived breed in aCR situation, so clearly it's not related to body fat if the more body fatthe mice retain while on CR, the longer they live...Nonetheless, reduced insulin levels are associated with both CR and theAtkins diet.Hi ALL:This is an interesting article on aging research which relates to some of the recent discussions here.Short Link:http://tinyurl.com/r63pLong Link to Kenyon "I Want to Live Forever"http://www.newscientist.com/opinion/opinterview.jsp;jsessionid=IBBMJFCDEKFB?id=ns24171

Interesting, this scientist is promoting aging research & a target pill mimic to slow aging, but she does not practice calorie restriction. She does practice a low insulin type diet to slow aging damage.Excerpts from this article:But for now, caloric restriction seems the one proven way to extendlifespan. Is that why you've virtually given up carbohydrates?That's not necessarily why I do it. I do it because it makes me feel greatand keeps me slender. And I don't feel really tired after a meal. But Ithink if I wanted to eat in a way that extended lifespan this is how I woulddo it. In fact, I stopped eating carbohydrates the day we found that puttingsugar on the worms' food shortened their lifespans.How does it work?I eat a diet that keeps my insulin levels low. So, for example, at breakfastI have bacon and eggs with tomatoes and avocados. It's bit like the Atkinsdiet. I don't actually know if I eat fewer calories, but I feel great and Iweigh what I did in high school. I certainly wouldn't want to be hungry allthe time, but I'm not, I'm never hungry. I tried caloric restriction justfor two days but I couldn't stand it, being hungry all the time.What don't you eat?I don't eat sweets, bread, pasta, potatoes or rice. I actually do eat lotsof carbohydrates, just not starchy ones, the ones that turn into sugarquickly in your body. I eat lots of vegetables and salads, and lots of fishand nuts, cheese, eggs and meat. People are now studying these low-carbdiets like Atkins and the zone diet scientifically.How do you know it's doing you any good?My blood profile is off the scale. Apparently triglycerides are very goodindicators of your insulin and glucose levels. Anything below 200[milligrams per decilitre] is good, and mine is 30! And my "good"cholesterol (HDL) is 86 [mg/dl], which is fabulous.

This is why this scientist thinks Insulin ( & IGF-1) is so important...What are genes like this doing?But you have a single hormone receptor, the IGF-1/insulin receptor, and a transcription factor commanding between 50 and 100 genes that directly affect the ageing process. It's like an orchestra conductor coordinating the flutes and the cellos and the French horns. That's how you get these big effects on lifespan.End of Excerpt xxxxxxxxxxxxxxIn light of this new article it might be interesting to study furthermethods to mimic through food selections or quantity-timing of meals ways toreduce insulin response and levels circulating between meals. Many here aredoing "crON Lite" versions of mild calorie restriction, so using these othermethods of food selection, number-timing of meals, may be very beneficialtoo.Has anybody done any research or dietary changes based on these ideas?

Here is part of a post related to these matters I did at CRSociety last month.I start wondering if the "Insulin Index" might be an important factorrelated to longevity??? Dairy proteins (see yogurt on the graph, linkbelow) & some other high-protein sources can boost insulin response. I findit interesting that some "breakfast cereals" were found to have the lowestinsulin response in general.Maybe we should eat some All Bran Cereal, Pasta, Muesli, Eggs, Lentils,Peanuts, and I'll add Chana Dal? Maybe there are very good carbs some don'teat here in fear or concern of other problems, those dang evil Zone killercarbs, yet the "insulin response" may be far more important than these otherconcerns? Oh well, back to my veggies & fasting too? :-)Do we figure Insulin Load the same way as Glycemic Load? :-)http://venus.nildram.co.uk/veganmc/insulin.htmOn average the snack foods produced the highest food group IS, followed bybakery products, carbohydrate-rich foods, fruit, protein rich foods and thenbreakfast cereals respectively (see figure). The researchers foundsignificant variations in foods of the same food group, so food group aloneis not a good predictor of insulin or glucose scores. Furthermore, at thefood group level, variations are not as dramatic as between specific foods,so that generalisation about food groups and insulin or glucose scores areinaccurate.The researchers did find that jellybeans (made of sugar and animal protein)produced the highest mean IS, whereas peanuts (an oily legume) had thelowest IS. The reference food, white bread, consistently had the highestglucose and insulin responses, and had a higher insulin score than most ofthe other foods. On average fish produced twice as much insulin secretion asdid the equivalent portion of eggs. Amongst the few fruits examined, orangesand apples produced significantly lower scores than grapes and bananas,despite similar carbohydrate content. Potatoes had significantly higherscores than all of the other carbohydrate-rich foods. White and brown ricehave similar scores, as do white and brown pasta. Despite containing similaramounts of carbohydrate, jellybeans induced double the insulin secretion asany of the four fruits.Tim T. Protein Reference:1: Mutat Res. 1993 Dec;295(4-6):165-79. Related Articles, LinksProtein restriction (PR) and caloric restriction (CR) compared: effects onDNA damage, carcinogenesis, and oxidative damage.Youngman LD.Division of Biochemistry and Molecular Biology, University of California atBerkeley 94720.Protein restriction (PR) and caloric restriction (CR) similarly impinge uponvarious physiological factors that can significantly inhibit the growth ofDNA-damaged tissue and, therefore, carcinogenesis. Whether this effect islargely, or only in part, due to simple inhibition of body weight gain isexamined. Among their many other health-improving effects, PR and CR delaythe onset of puberty. It has been suggested that animals have developedmechanisms to cope with lean periods and that, when food is limited,resources are diverted from those physiological functions that offer nobenefit for immediate survival (e.g., reproductive capacity) to therebysupport an increase in the maintenance functions that prolong life. PR hasalso been shown to affect numerous other varied mechanisms that can affectcarcinogenesis, including gene expression and metabolism of xenobiotics. Theeffects of PR on initiational and promotional growth of DNA-damaged tissueis also discussed. PR also seems to boost antioxidant defenses and inhibitthe accumulation of oxidative damage (as does CR). Protein restrictedanimals have been shown to accumulate more calories, but develop fewerpreneoplastic lesions and tumors than their high-protein counterparts. Thisobservation seems quite counter to most ideas about dietary restrictions andCR. Despite the fact that both PR and CR induce many beneficialphysiological effects in common, it is possible that PR is the more feasibleoption for human consideration. The levels of PR likely to improve healthwithout negative side effects are discussed.Publication Types:ReviewReview, TutorialPMID: 7507555 [PubMed - indexed for MEDLINE].