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Found 7 results

  1. Dean Pomerleau

    Latest Bloodwork

    Hi everyone, I just got my annual suite of blood tests done via the Male Anti-Aging Ultimate w/Free (Direct) Testosterone offered by Private MD Labs. As you can see from the link, the test is pretty comprehensive and it doesn't require a doctor's referral. The cost was $300 (with 15% coupon code) and the blood/urine collection is done at your local LabCorp office. I highly recommend there service (although see my next post for an alternative service that looks promising). Here is a link to the (big) table of results. The latest results are in the column all the way to the right. I'm overall pretty pleased with the results. I continue to show the hallmarks of human CR (e.g. see here and here for results from Luigi Fontana study of fellow CRONies), including: Low IGF-1 Low Insulin Low Total/Free Testosterone Low White Blood Cell Count High MCV/MCH Low C Reactive Protein (inflammation) Borderline low Thyroid hormone (Free T4) Good fasting glucose / HBA1c Great cholesterol levels If you look at the 3 columns immediately prior to the latest round, you'll notice troublingly high liver markers (Alkaline Phosphatase, AST and ALT) from earlier this year. In fact, three months ago (3/18/15) my AST and ALT were 8x the upper reference range! As you might imagine, I was quite concerned, as was my GP and the gastroenterologist he referred me to. I had an abdominal ultrasound, and all my organs (liver, kidney, gallbladder, pancreas) looked good - which was a relief. Most relevant, there was no sign of fatty liver, liver cysts/tumors or other liver abnormalities. They were planning to do a liver biopsy, but before that, I decided to try cutting out (Saigon) cinnamon (a known liver toxin due to naturally occuring coumarin) along with a few other unusual foods that I had been consuming and thought might have an impact on the liver. I retested a couple weeks later before the biopsy, and thankfully my elevated liver markers had cleared up. I strongly suspect it was the cinnamon. Three months later, my liver markers look better than they have in years (all within the normal reference range). The other thing that I find interesting in these results is that I continue to show the biomarkers of 'serious' CR despite vigorously exercising a lot (~4.5h/day) - and eating enough to maintain my weight. I haven't been tracking calories for a while, but I'm clearly eating many more than most CRONies to maintain my weight (120lbs, 18.0 BMI) with all that exercise. In fact, my current biomarkers compare favorably with my results from 2/21/13, when I was much more severely CRed (112lbs, 16.8 BMI) and exercising minimally (30-60min / day). My testosterone and IGF-1 were lower back then, but as many people thought (including me), they were too low. I find this very interesting. It seems to suggest that either: These biomarkers aren't very good at discriminating "genuine" CR (i.e. relatively sedentary lifestyle with low calorie intake) from "exercise-induced" CR (like I'm doing now), or that Perhaps "exercise-induced" CR will have a similar effect on human health/longevity as "genuine" CR. As another data point, I spoke with Paul McGlothin recently and learned that he too exercises quite a bit (~2.5h/day) these days, although not as much as I do. Why do I exercise so much you ask? I enjoy it, I have lots of free time (I'm semi-retired) and I feel really good - better than I have in a long time. I consider myself to be in quite good shape for my age (almost 51). My resting heart rate is 40 BPM. A few weeks ago, I ran a 5K and won the 18+ age group (3rd overall), with a time of 20:40, which I thought was pretty respectable. I'm curious if others (I'm thinking of you Michael Rae :) ) believe I'm likely to be undermining my prospects for health and longevity with this regime, relative to "genuine" CR. --Dean
  2. BrianMDelaney

    Theranos

    Check out the prices here: http://www.theranos.com/test-menu?ref=for_providers Backstory: http://www.wired.com/2014/02/elizabeth-holmes-theranos/?cid=18964974 If this pans out, it will revolutionize medicine -- and will certainly make our citizen science projects more doable! If anyone is near Palo Alto, s/he could even give it a spin! Brian
  3. All, Over on the Body-mass index and all-cause mortality thread, TomB posted the following, asking about what we might learn from the lifestyle and biomarkers of the very old in order to optimize our own diets and lifestyles. TomB said (my emphasis): [Note: the blue highlights above will factor into the discussions below] That other Michael (i.e. Mike Lustgarten hereafter referred to as 'Mike' to avoid confusion) and I have had several debates on this subject before on the CR Facebook forum. Namely, Mike likes to look at the characteristics (e.g. BMI, or selenium level) of very long-lived people (i.e. who've made it into their 90s or 100s), declare "they must be doing something right!" and target those same biomarker levels, diet characteristics and/or lifestyle practices for himself, and advocate others do the same to maximize their chance of living a long time. But as I've tried to point out to him on several occasions (relatively unsuccessfully it would seem), this approach to diet and lifestyle optimization is naive and fraught with problems. Here are the reasons why. It all boils down to one overarching observation - we're not like very old people. But just how we are unlike them, and why it matters, will take some unpacking. Freakishly good gene combinations - Perhaps the most common way for people these days to reach a very ripe old age is to have freakishly good genes. This allows them to avoid the major killers, like heart disease and cancer, often despite bad diet and lifestyle habits. Think of this as the George Burns effect. Actor George Burns lived to 100 despite smoking 10-15 cigars per day for 70 years (ref). Don't try that at home sports fans! The same thing is happening when you hear on TV about the latest 110 year old who attributes their longevity to "eating two strips of bacon per day" or "drinking whisky". In short, just because someone with freakishly good genes got away with a bad habit and lived to a ripe old age, doesn't mean you could, or should, try to emulate them, since most of us have crappy, run-of-the-mill gene combos, by definition, which means emulating such behavior would kill us quick. Survivor bias - In addition to a few folks with freakishly good genes, in any large population, there will also be a few folks with average genes who get lucky, and live to a ripe old age, avoiding the major killers. In fact, they might have bad genes or lifestyle habits that would on average shorten lifespan, but because they got lucky, they lived a long time. Here are a couple great examples of survivor bias (and/or other explanations discussed below) from the study Tom posted above (PMID:25446984), and that I've highlighted in blue. Notice above in that study the people who lived a very long time, into their 90s and 100s, had significantly lower levels of calcium and iron than did middle-aged controls. What gives? Isn't calcium supposed to be good for bones and iron important for avoiding anemia-complications and having a healthy immune system? Those benefits of Ca and Fe may hold true for middle-aged folks, and even the average senior. But at the same time, calcium can calcify arteries, and iron can cause oxidative damage, both of which can exacerbate the major killers - heart disease and cancer. So if you are one of those very rare individuals with either good genes and/or very good luck, you can get away with keeping Ca and Fe on the low (deficient) side, and avoid Ca and Fe deficiency-related maladies that would kill off the average person early - like a hip fracture from weak bones or a respiratory infection from a weak immune system. If you get lucky and escape those downsides of low Ca and Fe, then you are golden because keeping them low will help you avoid heart disease and cancer and hence live a long time. But if you're like the average person, low Ca and/or Fe will lead to broken bones and/or infections that will cut your life short on average. In other words, low Ca and/or low Fe will harm most people, and only benefit a lucky few. Another good example here is directly related to immunity - namely white blood cell (WBC) count. Several studies (discussed in http://dx.doi.org/10.1371/journal.pone.0127550) have found that that oldest of the old have low WBC. This is great for them, since it enabled them to avoid the major diseases of aging, which are triggered by inflammation. But they very well may have gotten luck or had good genes, enabling them to avoid infections that would normally have killed an average person with such a low WBC. In short, it doesn't necessarily pay for the average person to try to emulate the blood chemistry profile of the very old. Late Life / Near Death Changes - It's not just good genes or survivor bias (i.e. freakish luck) that sets the oldest of the old apart from the rest of us, and which makes them poor models to emulate. Why? Because biomarkers change drastically later in life, and especially when you are approaching death, which centenarians almost invariably are. So their blood chemistry levels when they are old aren't necessarily reflective of what got them to a ripe old age. Serum cholesterol is a great example of this. For various reasons, ranging from intestinal parasites to cancer, serum cholesterol tends to drop precipitously as people get sick and approach death. This can result in several misleading observations. First, old people with the highest cholesterol often live longer (i.e. have a lower mortality rate) than old people with low cholesterol, due to reverse causality. That is, the folks with low cholesterol are low because they've got a disease that will soon kill them. This observation (i.e. mortality risk is lowest in elderly folks with high cholesterol) is often pointed to by saturated fat apologists who like to claim keeping cholesterol from getting too low is critical for health and that low cholesterol is as bad or worse than high cholesterol. Bogus argument. Conversely, the oldest of the old, e.g. centenarians or supercentenarians, who are almost invariably within a year or two of death, may exhibit freakishly low cholesterol, for the same "reverse causality" reason - i.e. they are close to death causing low cholesterol. In both cases, the cholesterol level these old or freakishly old folks exhibit when they get to their ripe old age tells us nothing about what cholesterol level is best to get you to old age. For that we can look at longitudinal studies, that show low cholesterol in middle age is associated with improved longevity, for obvious reasons. That's why, BTW, studies of the freakishly old often look at their offspring or (younger) siblings as well, to see what characteristics people with similar genes had when they were younger, to avoid these late life changes/biases. In summary, looking at the blood chemistry, diet and/or lifestyle of very old people and trying to emulate them is fraught with difficulty, and therefore ill-advised. This is unfortunate, since it makes us much more reliant on longitudinal studies in people and intervention studies in animals, which have their own pitfalls, as we are all well-aware. --Dean
  4. Zeta

    Extreme blood values

    It looks like I've developed mild -- maybe not so mild... pancytopenia. I'm wondering whether my CR, which really isn't extreme these days, might be part of the explanation? Has anyone on CR ever had white blood cell counts as low as mine (see below)? As for anemia, that also could be CR, secondary to CR-induced low testosterone. After reflecting on the recent Longo paper, I think I'm going to try a "4:2" diet (not 5:2, because the irregularity of the 2, then 3 days of feasting makes me nervous -- I could also call my diet "2:1": 2 days of feasting, 1 of quasi-fasting). I think Michael's right that there's no evid. in Longo's work that any kind of fasting that doesn't also reduce energy-intake overall will slow aging, but, at this point, I'm just trying to get some food-restriction benefits, while not feeling so weak.... Name --------------- me -------- units ------- reference range Albumin. ----------- 42 ---------- g/L --------- 36-45 Antitrypsin. -------- 1.1 --------- g/L ---------- 0.9-1.9 Orosomucoid ------ 0.3* ------- g/L ---------- 0.5-1.2 Haptoglobin ------ <0,05* ------ g/L ---------- 0.2-1.9 IgG ----------------- 7.5 ---------- g/L ---------- 7-15 IgA ------------------ 2.7 --------- g/L ----------- 0.9-4.5 IgM ----------------- 1.2 ---------- g/L ---------- 0.3-2.1 (Got tired of writing in the units here -- but just look at the ref. range.) Leukocytes -------- 2.1* -------- 3.5-8.8 Erythrocytes ------ 3.8* ----- 4.2-5.7 Hb ------------------ 121* ----- 134-170 EFV ---------------- 0.37* ----- 0.39-0.50 MCH -------------- 32 -------- 27-33 MCV --------------- 97 ------- 82-98 MCHC ------------- 328 -------- 317-357 Thrombocyte ----- 127* ----- 145-348 Neutrophils ------- 1.1* ------ 1.7-7.5 Esonphil. ---------- 0.00 -------- 0.0-0.6 Basophil. ---------- 0.00 ----- 0.0-0.2 Lymphocytes ----- 0.8* ----- 1.1-4.8 Monocytes -------- 0.20 ----- 0.1-1.0 Reticulocyte -------- 64 -------- 26-124 Rtc-MCH ---------- 33 ------- 24-36 The low haptoglobin with normal reticulocyte count was a head-scratcher for the doctors. Bone marrow biopsy yielded no signs of cancer.
  5. Hi all, Quite while back, on the old email-based CR list, Michael Rae asked about web-based tools for tracking one's health data, and particularly one's bloodwork. Given how unwieldy and ugly my current method is (just a big HTML table - see this post), I went looking for a better alternative, along the lines of what Michael was looking for. I came across the service called WellnessFX. It looks pretty cool, and I'm wondering if anyone else has used this service. Hear are some of its features: A free account allows you to put in your data from prior tests. The have all the standard (and many non-standard) tests to choose from. Unfortunately, the process appears to require entering one item at a time - very tedious, but doable. Once you've uploaded your data (or gotten a blood test via them - see below), you can see tables and graphs of your data over time, which is pretty cool. See image at the bottom of this post for an example. Paying members get blood testing services, ordered through LabCorp or Quest, without a doctor's referral. Like the service I use (Private MD Labs). Their "Performance Package" appears to include almost all of the tests that the "Male Ultimate Anti-Aging with Free Testosterone" test from Private MD Labs that I use, plus a few more. Its somewhat more expensive though - although there appears to be a $100 coupon code available on-line that brings the cost down to the same ballpark (~$400). You can also order a custom panel of tests that you choose a la carte, although the price isn't specified for the individual tests - you have to ask them explicitly for the cost of the custom tests you want. They also offer (for a fee) consultations with physicians, registered dietitians and nutritionists about your results. They got a very good review from the website "Cool Tools". Here is another positive review. They comply with the US HIPAA regulations. Here is their privacy policy. I can't say that I've read or understand it all. Has anyone looked into WellnessFX, and/or used their service? --Dean Here is an example of the WellnessFX data visualization tools: If the image doesn't show up, here is a link to it.
  6. Here is another study posted by Al Pater that particularly interested me, both because it focused on inflammation (now understood to be an important contributor to all of the major chronic diseases of aging) and because it focused on CR vs. exercise vs. both. It compared the effects of one-year of a calorie restricted diet, aerobic exercise (without calorie restriction) or both exercise and calorie restriction on biomarkers of inflammation in overweight/obese postmenopausal women. The results can be summarized as follows: The diet-only group and the diet+exercise group lost close to the same amount of weight (8.5% vs 10.5%, respectively). The exercise-only group lost much less on average (2.5%), although there were some women in the exercise-only group who lost > 5% (see below). "There were no significant differences between the diet and diet+exercise groups or between the exercise[-only] and control groups, in any inflammatory biomarker." Virtually everyone* in the study who lost >5% of body weight saw a significant reduction in hr-CRP, an important marker of inflammation, independent of whether they lost weight via diet-alone, exercise-alone, or diet+exercise. So by my reading, it looks like its either the weight/fat loss or possibly the energy deficit, rather than simply eating fewer calories, that determines the benefits, at least when it comes to biomarkers of inflammation in this population. In particular, the women who lost nearly 10% of their bodyweight saw a dramatic (and equivalent) improvement in biomarkers of inflammation whether they achieved this weight loss via a large calorie deficit, or via a more modest calorie deficit "topped off" with exercise. --Dean * Except for two outliers with very high hr-CRP who were excluded ------------------------ [1] Effects of a caloric restriction weight loss diet and exercise on inflammatory biomarkers in overweight/obese postmenopausal women: a randomized controlled trial. Imayama I, Ulrich CM, Alfano CM, Wang C, Xiao L, Wener MH, Campbell KL, Duggan C, Foster-Schubert KE, Kong A, Mason CE, Wang CY, Blackburn GL, Bain CE, Thompson HJ, McTiernan A. Cancer Res. 2012 May 1;72(9):2314-26. doi: 10.1158/0008-5472.CAN-11-3092. PMID:22549948 Free PMC Article http://cancerres.aacrjournals.org/content/72/9/2314.long http://cancerres.aacrjournals.org/content/72/9/2314.full.pdf+html Abtract Obese and sedentary persons have increased risk for cancer; inflammation is a hypothesized mechanism. We examined the effects of a caloric restriction weight loss diet and exercise on inflammatory biomarkers in 439 women. Overweight and obese postmenopausal women were randomized to 1-year: caloric restriction diet (goal of 10% weight loss, N = 118), aerobic exercise (225 min/wk of moderate-to-vigorous activity, N = 117), combined diet + exercise (N = 117), or control (N = 87). Baseline and 1-year high-sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA), interleukin-6 (IL-6), leukocyte, and neutrophil levels were measured by investigators blind to group. Inflammatory biomarker changes were compared using generalized estimating equations. Models were adjusted for baseline body mass index (BMI), race/ethnicity, and age. Four hundred and thirty-eight (N = 1 in diet + exercise group was excluded) were analyzed. Relative to controls, hs-CRP decreased by geometric mean (95% confidence interval, P value): 0.92 mg/L (0.53-1.31, P < 0.001) in the diet and 0.87 mg/L (0.51-1.23, P < 0.0001) in the diet + exercise groups. IL-6 decreased by 0.34 pg/mL (0.13-0.55, P = 0.001) in the diet and 0.32 pg/mL (0.15-0.49, P < 0.001) in the diet + exercise groups. Neutrophil counts decreased by 0.31 × 10(9)/L (0.09-0.54, P = 0.006) in the diet and 0.30 × 10(9)/L (0.09-0.50, P = 0.005) in the diet + exercise groups. Diet and diet + exercise participants with 5% or more weight loss reduced inflammatory biomarkers (hs-CRP, SAA, and IL-6) compared with controls. The diet and diet + exercise groups reduced hs-CRP in all subgroups of baseline BMI, waist circumference, CRP level, and fasting glucose. Our findings indicate that a caloric restriction weight loss diet with or without exercise reduces biomarkers of inflammation in postmenopausal women, with potential clinical significance for cancer risk reduction.
  7. Since Michael Rae posted a link on the official CR Society blog to the this series of three papers [1][2][3] from the same study on Protein Restriction (PR) vs. Calorie Restriction (CR) which James Cain posted in last week's weekly research updates (thanks James for this service!), I figured I'd take a look to see what the hubbub is about. While it was relatively short term (3 months), it appears to be a very well-conducted and informative study. They first had a 14-day baseline period where they fed the mice ad lib a standard mice chow diet of 20% protein, 70% carbs and 10% fat (by energy). Then, when the mice reached 20 weeks of age (early adulthood in humans), they were put on the various diets. One had 24-hour ad lib access to the same baseline diet (24AL) and one group had 12-hour ad lib access to the same baseline diet (12AL), during the normal time mice eat (at night). So right off the bat this is interesting because it investigates some degree of time-restricted feeding (although over the course of the study the 24AL mice gained more weight and fat than the 12AL mice, and not much is made in the papers about differences between these two groups). In addition, there were 5 different groups of of CR mice with 0, 10, 20, 30 and 40% lower food intake than their own individual intake measured over the 14-day baseline period. There were also three levels of protein restriction, down from the baseline 20% to 16, 14 and 12% protein, which matched the quantity of protein consumed by the 20, 30 and 40% CR mice. The diet of the protein-restricted mice was supplemented with extra carbs to bring their total calorie intake up to their individual calorie intake during the ad lib baseline period. In other words, the protein-restricted mice were eating their AL level of calories, but getting a reduced quantity of protein to matched the amount of protein in the three most restricted CR groups. So it was a pretty cool design. Like the 12AL controls, the CR and PR groups were fed during the 12-hour dark period, although the mice in the CR groups (being hungrier) probably scarfed down their food faster than the 12AL and the PR groups, which were getting fed an ad lib quantity of food, meaning the CR mice ate during a narrower time window than the other groups... They followed this protocol for three months and then sacrificed the mice and measured a boatload of biomarkers reported in these three papers. Long story short, they found that compared with the 12AL control mice, the CR mice exhibited all the usual hallmarks of effective CR, including reduced body weight, fat mass and organ weight (except for digestive system weight, which was increased!), lower leptin, tumor necrosis factor-alpha, and IGF-1, improved glucose tolerance and insulin sensitivity, lower "investment in reproduction" (measured via urine protein markers) and lower body temperature. Interestingly, if anything the authors observed an improvement in bone health of the CR mice relative to the 12AL controls, which was nice to see. They said: [O]ur results offer no evidence that three months of CR, even at the 40% level, had a negative effect on bone composition or mechanics. In fact one could conclude that there was a beneficial effect of CR on bone mass in the current study. They report that in general the changes in biomarkers of the CR mice correlated most with changes in individual body weight (morphology changes), so the more weight the mice lost, the greater the biomarker changes they observed, (somewhat) independent of the level of CR they were subjected to. I found this interesting since it indirectly speaks to a question of interest to me, which is whether its the calories or the resulting weight loss (equivalent to net energy deficit?) that matters when it comes to CR benefits. In contrast to the beneficial biomarker changes seen in the CR mice, the mice fed the diets with ad lib calories but restricted protein didn't lose weight, and didn't exhibit any of the biomarker changes observed in the CR groups, at least to a statistically significant degree. In fact, by the end of the 3 months, the protein restricted mice weighed significantly more, and had significantly more fat mass than even the 12AL control mice! Further, the amount of weight gain and fat mass gain was proportional to the degree of protein restriction. On the surface, this extra weight & fat gain in the PR mice relative to controls seems surprising, since the PR groups of mice were given the same number of calories as they individually consumed during the AL baseline, and the 12AL mice had free access to food during the same 12-hour period as the PR mice. Here is how the authors explained this seeming paradox: As PR increased the animals became fatter over the three month manipulation period. Since the animals were provided with the same total calorie intake as during the baseline period and the same intake across the different PR groups, the most likely reason for this effect on fatness was that reducing the levels of protein in the diet reduced the specific dynamic action (SDA) of the diet, which is known to be greatest for the protein component [71]. Thus while gross energy intake remained constant the net metabolizable energy increased as the protein level declined. This would lead to surplus energy above requirements that the animals could deposit as fat. Since the extra fat in the 40PR group amounted to just over 1 g (39.5 kJ), this was equivalent to less than 0.3 kJ/day over the 90 day experiment and hence entirely consistent in magnitude with an alteration in the level of SDA. The unfamiliar (to me) term Specific Dynamic Action (SDA) is another name for a more familiar concept, the Thermic Effect of Food (TEF). In short, when food is metabolized, some of the energy is wasted as heat, rather than converted to useable energy. More energy is wasted as heat when metabolizing protein as compared with carbs (or fat). Since the PR mice were eating less protein and more carbs, they were getting more useable energy from their food, which resulted in weight and fat gain over the course of the study, even relative to ad lib fed controls (which also gained a lot of weight and fat, BTW). So the failure of this study to replicated the previous results (see this thread for some discussion) that PR can mimic many of the biomarker changes associated with CR is not as surprising as one might initially have thought. The discrepancy can be explained by the fact that the PR mice in this study gained a lot of weight and fat, and the negative effects of these gains were enough to trump and obviate any improvements in the measured biomarkers that might have otherwise been observed from protein restriction. The fact that the PR mice weren't worse off than the AL controls with respect to these biomarkers, despite being significantly fatter, might be interpreted as weak evidence in support of the health benefits of a low protein, high carb diet, but that would be a stretch. Instead, the major takeaway message from this one on the subject of protein restriction seems to be that becoming obese on a low protein, high (refined) carb diet is not a particularly good recipe for health or longevity. Not quite as informative a study as I'd originally hoped... --Dean ----------------------------- 1. Oncotarget. 2015 Jun 30;6(18):15902-30. The effects of graded levels of calorie restriction: I. impact of short term calorie and protein restriction on body composition in the C57BL/6 mouse. Mitchell SE1, Tang Z1, Kerbois C1, Delville C1, Konstantopedos P1, Bruel A1, Derous D1, Green C1, Aspden RM2,Goodyear SR2, Chen L3, Han JJ4, Wang Y5, Promislow DE6, Lusseau D1, Douglas A1, Speakman JR1,5. Author information AbstractFaced with reduced levels of food, animals must adjust to the consequences of the shortfall in energy. We explored how C57BL/6 mice withdrew energy from different body tissues during three months of food restriction at graded levels up to 40% (calorie restriction: CR). We compared this to the response to equivalent levels of protein restriction (PR) without a shortfall in calories. Under CR there was a dynamic change in body mass over 30 days and thereafter it stabilized. The time to reach stability was independent of the level of restriction. At the end of three months whole body dissections revealed differential utilization of the different tissues. Adipose tissue depots were the most significantly utilized tissue, and provided 55.8 to 60.9% of the total released energy. In comparison, reductions in the sizes of structural tissues contributed between 29.8 and 38.7% of the energy. The balance was made up by relatively small changes in the vital organs. The components of the alimentary tract grew slightly under restriction, particularly the stomach, and this was associated with a parallel increase in assimilation efficiency of the food (averaging 1.73%). None of the changes under CR were recapitulated by equivalent levels of PR. KEYWORDS:Gerotarget; body composition; calorie restriction; dietary restriction; food intake; protein restriction PMID: 26079539 [PubMed - in process] Free full text Similar articles Select item 260617452. Oncotarget. 2015 Jun 1. [Epub ahead of print] The effects of graded levels of calorie restriction: II. Impact of short term calorie and protein restriction on circulating hormone levels, glucose homeostasis and oxidative stress in male C57BL/6 mice. Mitchell SE1, Delville C1, Konstantopedos P1, Hurst J2, Derous D1, Green C1, Chen L3, Han JJ4, Wang Y5, Promislow DE6, Lusseau D1, Douglas A1, Speakman JR1,5. Author information AbstractLimiting food intake attenuates many of the deleterious effects of aging, impacting upon healthspan and leading to an increased lifespan. Whether it is the overall restriction of calories (calorie restriction: CR) or the incidental reduction in macronutrients such as protein (protein restriction: PR) that mediate these effects is unclear. The impact of 3 month CR or PR, (10 to 40%), on C57BL/6 mice was compared to controls fed ad libitum. Reductions in circulating leptin, tumor necrosis factor-α and insulin-like growth factor-1 (IGF-1) were relative to the level of CR and individually associated with morphological changes but remained unchanged following PR. Glucose tolerance and insulin sensitivity were improved following CR but not affected by PR. There was no indication that CR had an effect on oxidative damage, however CR lowered antioxidant activity. No biomarkers of oxidative stress were altered by PR. CR significantly reduced levels of major urinary proteins suggesting lowered investment in reproduction. Results here support the idea that reduced adipokine levels, improved insulin/IGF-1 signaling and reduced reproductive investment play important roles in the beneficial effects of CR while, in the short-term, attenuation of oxidative damage is not applicable. None of the positive effects were replicated with PR. KEYWORDS:adipokines; calorie restriction; glucose homeostasis; oxidative stress; protein restriction PMID: 26061745 [PubMed - as supplied by publisher] Free full text Similar articles Select item 262869563. Oncotarget. 2015 Jul 30;6(21):18314-37. The effects of graded levels of calorie restriction: III. Impact of short term calorie and protein restriction on mean daily body temperature and torpor use in the C57BL/6 mouse. Mitchell SE1, Delville C1, Konstantopedos P1, Derous D1, Green CL1, Chen L2, Han JD3, Wang Y4, Promislow DE5,Douglas A1, Lusseau D1, Speakman JR1,4. Author information AbstractA commonly observed response in mammals to calorie restriction (CR) is reduced body temperature (Tb). We explored how the Tb of male C57BL/6 mice responded to graded CR (10 to 40%), compared to the response to equivalent levels of protein restriction (PR) over 3 months. Under CR there was a dynamic change in daily Tb over the first 30-35 days, which stabilized thereafter until day 70 after which a further decline was noted. The time to reach stability was dependent on restriction level. Body mass negatively correlated with Tb under ad libitum feeding and positively correlated under CR. The average Tb over the last 20 days was significantly related to the levels of body fat, structural tissue, leptin and insulin-like growth factor-1. Some mice, particularly those under higher levels of CR, showed periods of daily torpor later in the restriction period. None of the changes in Tb under CR were recapitulated by equivalent levels of PR. We conclude that changes in Tb under CR are a response only to the shortfall in calorie intake. The linear relationship between average Tb and the level of restriction supports the idea that Tb changes are an integral aspect of the lifespan effect. KEYWORDS:Gerotarget; body temperature; calorie restriction; dietary restriction; protein restriction; torpor PMID: 26286956
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