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  1. Does anyone else eat natto, the fermented soybean product which is quite popular in Japan? It is the richest food source of vitamin K2 (menaquinone-7 or MK-7) with 1 mg (1000 mcg) of K2 per 100g natto. That is about 20x higher than the next highest source, certain cheeses like Gouda. Unlike vitamin K1 which is found primarily in leafy greens, there is virtually no vitamin K2 in regular fruits and vegetables. Why should we care about vitamin K2 you ask? First and foremost because it has been shown to be protective against osteoporosis [1-2], a concern for CR practitioners. From [2], a study of 244 postmenopausal women supplemented with 180mcg/day of Vitamin K2 (MK-7) for three years: MK-7 intake significantly improved vitamin K status and decreased the age-related decline in BMC and BMD at the lumbar spine and femoral neck, but not at the total hip. Bone strength was also favorably affected by MK-7. MK-7 significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the vertebrae. CONCLUSIONS: MK-7 supplements may help postmenopausal women to prevent bone loss. Another significant benefit of Vitamin K2 is for cardiovascular health. Vitamin K2 seems to prevent artery calcification (aka hardening of the arteries) [3-5], which happens when calcium circulating in the blood is turned into a crust in the arteries. In study [5] the same group of researchers from [2] measured arterial calcification in the same 244 postmenopausal women on 180mcg/day of K2 for three years, and found multiple markers of arterial stiffness improved with K2 supplementation, concluding: Long-term use of MK-7 supplements improves arterial stiffness in healthy postmenopausal women, especially in women having a high arterial stiffness. But those were studies of direct supplementation of vitamin K2 (MK-7), rather than getting it from food. Does eating natto actually raise serum MK-7 levels? Thankfully the answer is yes, according to [6]: erum MK-7 level with the frequency of dietary natto intake were examined in 134 healthy adults (85 men and 39 women) without and with occasional (a few times per month), and frequent (a few times per week) dietary intake of regular natto including MK-7 (775 micrograms/100 g). Serum MK-7 and gamma-carboxylated osteocalcin concentrations in men with the occasional or frequent dietary intake of natto were significantly higher than those without any intake. So where to get natto? I buy my natto in frozen form at my local asian market, for about $2.50 for four styrofoam containers each of which contains about 50g of natto. Here is what the package of four look like: I eat half of a container's worth of natto per day (cost ~ $0.30/day). That 25g of natto per day provides about 250mcg of Vitamin K2 (MK-7), which is about 30% more than the dose shown to improve bone health [2] and reduce arterial stiffness [5] in postmenopausal women. What's natto like you ask? There is no getting around the fact that it looks pretty gross, and has a very slimy texture. As a result, many people can't stomach it, but I actually enjoy the taste, especially when mixed into the serving of other legumes and starches I eat. Below is a photo of natto in the styrofoam container. Pretty appetizing, huh?! The chopsticks in the photo are helpful for scale: For those of you who would be too grossed out by natto to eat it, there are supplements available. In fact I take one of these* to increase my K2 beyond what I get from natto - adding an extra 100mcg MK-7 per day for $0.09. But I'm always in favor of getting nutrients from food sources when practical. This is one of the rare cases where the natural food source is price competitive with supplement sources. So for me natto is a good choice. Does anyone else eat natto? If not, you might consider giving it a try! [Note: This post does not address Natto's brain health benefits. For discussion of that, see this post further down this thread.] --Dean *Note - I've updated my supplement regime to this vegan NOW Foods brand K2 supplement, to make sure I'm getting K2 in MK-7 form, rather than (mostly) MK-4 per my previous supplement. --------- [1] J Bone Miner Metab. 2014 Mar;32(2):142-50. doi: 10.1007/s00774-013-0472-7. Epub 2013 May 24. Low-dose vitamin K2 (MK-4) supplementation for 12 months improves bone metabolism and prevents forearm bone loss in postmenopausal Japanese women. Koitaya N(1), Sekiguchi M, Tousen Y, Nishide Y, Morita A, Yamauchi J, Gando Y, Miyachi M, Aoki M, Komatsu M, Watanabe F, Morishita K, Ishimi Y. Author information: (1)Department of Food Function and Labeling, National Institute of Health and Nutrition, 1-23-1 Toyama, Shinjyuku-ku, Tokyo, Japan. Menaquinone-4 (MK-4) administered at a pharmacological dosage of 45 mg/day has been used for the treatment of osteoporosis in Japan. However, it is not known whether a lower dose of MK-4 supplementation is beneficial for bone health in healthy postmenopausal women. The aim of this study was to examine the long-term effects of 1.5-mg daily supplementation of MK-4 on the various markers of bone turnover and bone mineral density (BMD). The study was performed as a randomized, double-blind, placebo-controlled trial. The participants (aged 50-65 years) were randomly assigned to one of two groups according to the MK-4 dose received: the placebo-control group (n = 24) and the 1.5-mg MK-4 group (n = 24). The baseline concentrations of undercarboxylated osteocalcin (ucOC) were high in both groups (>5.1 ng/ml). After 6 and 12 months, the serum ucOC concentrations were significantly lower in the MK-4 group than in the control group. In the control group, there was no significant change in serum pentosidine concentrations. However, in the MK-4 group, the concentration of pentosidine at 6 and 12 months was significantly lower than that at baseline. The forearm BMD was significantly lower after 12 months than at 6 months in the control group. However, there was no significant decrease in BMD in the MK-4 group during the study period. These results suggest that low-dose MK-4 supplementation for 6-12 months improved bone quality in the postmenopausal Japanese women by decreasing the serum ucOC and pentosidine concentrations, without any substantial adverse effects. PMID: 23702931 ------------ [2] Osteoporos Int. 2013 Sep;24(9):2499-507. doi: 10.1007/s00198-013-2325-6. Epub 2013 Mar 23. Three-year low-dose menaquinone-7 supplementation helps decrease bone loss in healthy postmenopausal women. Knapen MH(1), Drummen NE, Smit E, Vermeer C, Theuwissen E. Author information: (1)VitaK, Maastricht University, Oxfordlaan 70, 6229 EV, Maastricht, The Netherlands. We have investigated whether low-dose vitamin K2 supplements (menaquinone-7, MK-7) could beneficially affect bone health. Next to an improved vitamin K status, MK-7 supplementation significantly decreased the age-related decline in bone mineral density and bone strength. Low-dose MK-7 supplements may therefore help postmenopausal women prevent bone loss.INTRODUCTION: Despite contradictory data on vitamin K supplementation and bone health, the European Food Safety Authorities (EFSA) accepted the health claim on vitamin K's role in maintenance of normal bone. In line with EFSA's opinion, we showed that 3-year high-dose vitamin K1 (phylloquinone) and K2 (short-chain menaquinone-4) supplementation improved bone health after menopause. Because of the longer half-life and greater potency of the long-chain MK-7, we have extended these investigations by measuring the effect of low-dose MK-7 supplementation on bone health. METHODS: Healthy postmenopausal women (n = 244) received for 3 years placebo or MK-7 (180 μg MK-7/day) capsules. Bone mineral density of lumbar spine, total hip, and femoral neck was measured by DXA; bone strength indices of the femoral neck were calculated. Vertebral fracture assessment was performed by DXA and used as measure for vertebral fractures. Circulating uncarboxylated osteocalcin (ucOC) and carboxylated OC (cOC) were measured; the ucOC/cOC ratio served as marker of vitamin K status. Measurements occurred at baseline and after 1, 2, and 3 years of treatment. RESULTS: MK-7 intake significantly improved vitamin K status and decreased the age-related decline in BMC and BMD at the lumbar spine and femoral neck, but not at the total hip. Bone strength was also favorably affected by MK-7. MK-7 significantly decreased the loss in vertebral height of the lower thoracic region at the mid-site of the vertebrae. CONCLUSIONS: MK-7 supplements may help postmenopausal women to prevent bone loss. Whether these results can be extrapolated to other populations, e.g., children and men, needs further investigation. PMID: 23525894 ----------- [3] Acta Physiol Hung. 2010 Sep;97(3):256-66. doi: 10.1556/APhysiol.97.2010.3.2. Vitamin K and vascular calcifications. Fodor D(1), Albu A, Poantă L, Porojan M. Author information: (1)University of Medicine and Pharmacy, 2nd Internal Medicine, Clinic Iuliu Hatieganu, Cluj-Napoca, Romania. dfodor@umfcluj.ro The role of vitamin K in the synthesis of some coagulation factors is well known. The implication of vitamin K in vascular health was demonstrated in many surveys and studies conducted over the past years on the vitamin K-dependent proteins non-involved in coagulation processes. The vitamin K-dependent matrix Gla protein is a potent inhibitor of the arterial calcification, and may become a non-invasive biochemical marker for vascular calcification. Vitamin K(2) is considered to be more important for vascular system, if compared to vitamin K(1). This paper is reviewing the data from recent literature on the involvement of vitamin K and vitamin K-dependent proteins in cardiovascular health. PMID: 20843764 ---------------- [4] Nutrients. 2015 Aug 18;7(8):6991-7011. doi: 10.3390/nu7085318. High-Dose Menaquinone-7 Supplementation Reduces Cardiovascular Calcification in a Murine Model of Extraosseous Calcification. Scheiber D(1), Veulemans V(2), Horn P(3), Chatrou ML(4), Potthoff SA(5), Kelm M(6,)(7), Schurgers LJ(8), Westenfeld R(9). Author information: (1)Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. daniel.scheiber@med.uni-duesseldorf.de. (2)Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. verena.veulemanns@med.uni-duesseldorf.de. (3)Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. patrick.horn@med.uni-duesseldorf.de. (4)Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht 6229 ER, The Netherlands. m.chatrou@maastrichtuniversity.nl. (5)Department of Nephrology, University Duesseldorf, Medical Faculty, Duesseldorf 40225, Germany. sebastian.potthoff@med.uni-duesseldorf.de. (6)Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. malte.kelm@med.uni-duesseldorf.de. (7)Cardiovascular Research Institute Duesseldorf, University Duesseldorf, Medical Faculty, Duesseldorf 40225, Germany. malte.kelm@med.uni-duesseldorf.de. (8)Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht 6229 ER, The Netherlands. l.schurgers@maastrichtuniversity.nl. (9)Division of Cardiology, Pulmonology, and Vascular Medicine, Medical Faculty, University Duesseldorf, Duesseldorf 40225, Germany. ralf.westenfeld@med.uni-duesseldorf.de. Cardiovascular calcification is prevalent in the aging population and in patients with chronic kidney disease (CKD) and diabetes mellitus, giving rise to substantial morbidity and mortality. Vitamin K-dependent matrix Gla-protein (MGP) is an important inhibitor of calcification. The aim of this study was to evaluate the impact of high-dose menaquinone-7 (MK-7) supplementation (100 µg/g diet) on the development of extraosseous calcification in a murine model. Calcification was induced by 5/6 nephrectomy combined with high phosphate diet in rats. Sham operated animals served as controls. Animals received high or low MK-7 diets for 12 weeks. We assessed vital parameters, serum chemistry, creatinine clearance, and cardiac function. CKD provoked increased aortic (1.3 fold; p < 0.05) and myocardial (2.4 fold; p < 0.05) calcification in line with increased alkaline phosphatase levels (2.2 fold; p < 0.01). MK-7 supplementation inhibited cardiovascular calcification and decreased aortic alkaline phosphatase tissue concentrations. Furthermore, MK-7 supplementation increased aortic MGP messenger ribonucleic acid (mRNA) expression (10-fold; p < 0.05). CKD-induced arterial hypertension with secondary myocardial hypertrophy and increased elastic fiber breaking points in the arterial tunica media did not change with MK-7 supplementation. Our results show that high-dose MK-7 supplementation inhibits the development of cardiovascular calcification. The protective effect of MK-7 may be related to the inhibition of secondary mineralization of damaged vascular structures. PMCID: PMC4555157 PMID: 26295257 ------------- [5] Thromb Haemost. 2015 May;113(5):1135-44. doi: 10.1160/TH14-08-0675. Epub 2015 Feb 19. Menaquinone-7 supplementation improves arterial stiffness in healthy postmenopausal women. A double-blind randomised clinical trial. Knapen MH, Braam LA, Drummen NE, Bekers O, Hoeks AP, Vermeer C(1). Author information: (1)Cees Vermeer, PhD, VitaK, Maastricht University, Biopartner Center Maastricht, Oxfordlaan 70, 6229 EV Maastricht, The Netherlands, Tel: +31 43 388 5865, Fax: +31 43 388 5889, E-mail: c.vermeer@vitak.com. Observational data suggest a link between menaquinone (MK, vitamin K2) intake and cardiovascular (CV) health. However, MK intervention trials with vascular endpoints are lacking. We investigated long-term effects of MK-7 (180 µg MenaQ7/day) supplementation on arterial stiffness in a double-blind, placebo-controlled trial. Healthy postmenopausal women (n=244) received either placebo (n=124) or MK-7 (n=120) for three years. Indices of local carotid stiffness (intima-media thickness IMT, Diameter end-diastole and Distension) were measured by echotracking. Regional aortic stiffness (carotid-femoral and carotid-radial Pulse Wave Velocity, cfPWV and crPWV, respectively) was measured using mechanotransducers. Circulating desphospho-uncarboxylated matrix Gla-protein (dp-ucMGP) as well as acute phase markers Interleukin-6 (IL-6), high-sensitive C-reactive protein (hsCRP), tumour necrosis factor-α (TNF-α) and markers for endothelial dysfunction Vascular Cell Adhesion Molecule (VCAM), E-selectin, and Advanced Glycation Endproducts (AGEs) were measured. At baseline dp-ucMGP was associated with IMT, Diameter, cfPWV and with the mean z-scores of acute phase markers (APMscore) and of markers for endothelial dysfunction (EDFscore). After three year MK-7 supplementation cfPWV and the Stiffness Index βsignificantly decreased in the total group, whereas distension, compliance, distensibility, Young's Modulus, and the local carotid PWV (cPWV) improved in women having a baseline Stiffness Index β above the median of 10.8. MK-7 decreased dp-ucMGP by 50 % compared to placebo, but did not influence the markers for acute phase and endothelial dysfunction. In conclusion, long-term use of MK-7 supplements improves arterial stiffness in healthy postmenopausal women, especially in women having a high arterial stiffness. PMID: 25694037 ---------- [6] J Bone Miner Metab. 2000;18(4):216-22. Intake of fermented soybean (natto) increases circulating vitamin K2 (menaquinone-7) and gamma-carboxylated osteocalcin concentration in normal individuals. Tsukamoto Y(1), Ichise H, Kakuda H, Yamaguchi M. Author information: (1)Central Research Institute, Mitsukan Group Co., Ltd., Aichi, Japan. Changes in circulating vitamin K2 (menaquinone-7, MK-7) and gamma-carboxylated osteocalcin concentrations in normal individuals with the intake of fermented soybeans (natto) were investigated. Eight male volunteers were given sequentially fermented soybeans (natto) containing three different contents of MK-7 at an interval of 7 days as follows: regular natto including 775 micrograms/100 g (MK-7 x 1) or reinforced natto containing 1298 micrograms/100 g (MK-7 x 1.5) or 1765 micrograms/100 g (MK-7 x 2). Subsequently, it was found that serum MK-7 and gamma-carboxylated osteocalcin concentrations were significantly elevated following the start of dietary intake of MK-7 (1298 or 1765 micrograms/100 g). Serum undercarboxylated osteocalcin concentrations were significantly decreased by dietary MK-7 (1765 micrograms/100 g) supplementation. Moreover, the changes in serum MK-7 level with the frequency of dietary natto intake were examined in 134 healthy adults (85 men and 39 women) without and with occasional (a few times per month), and frequent (a few times per week) dietary intake of regular natto including MK-7 (775 micrograms/100 g). Serum MK-7 and gamma-carboxylated osteocalcin concentrations in men with the occasional or frequent dietary intake of natto were significantly higher than those without any intake. The present study suggests that intake of fermented soybean (natto) increases serum levels of MK-7 and gamma-carboxylated osteocalcin in normal individuals. PMID: 10874601
  2. All, This new study [1] (science press coverage) appears like it might be a significant breakthrough in the treatment of Alzheimer's disease. Researchers appear to have discovered a small molecule that at least in rodents is safe, crosses the blood-brain barrier, and is effective at breaking up beta amyloid plaques, thought to play an important role in the neuronal death associated with Alzheimer's disease. From the article linked above: The Korean scientists, led by YoungSoo Kim of the Brain Science Institute at the Korea Institute of Science and Technology (KIST) in Seoul, investigated the ability of EPPS [4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid] to attach to amyloid-beta clumps and convert them into simpler, smaller molecules. Through a series of experiments, they found that EPPS could break apart plaque in a living mammal. They also found the molecule could be added to drinking water yet still travel in the blood to the brain and cross the blood-brain barrier, which otherwise prevents foreign material from entering the brain. EPPS could penetrate the barrier because it is a relatively small molecule, Kim said. The scientists found that doses between 30 and 100 milligrams per kilogram of body weight per day were effective in breaking up the amyloid beta. Further tests demonstrated that EPPS appears to have no toxic effects in mice up to 2,000 mg/kg per day. From the full text, not only did mice treated with EPPS show a reduction in beta amyloid plaques in their hippocampus and other brain areas in a dose dependent manner, they also showed less cognitive impairment relative to control mice using several measures of cognitive performance. The lead author is quite optimistic about this compound's potential: "I strongly believe these drug candidates [based on EPPS] will halt the neurodegeneration and rescue patients from death," Kim said. Here's hoping human trials prove that he's right! --Dean ------ [1] Nat Commun. 2015 Dec 8;6:8997. doi: 10.1038/ncomms9997. EPPS rescues hippocampus-dependent cognitive deficits in APP/PS1 mice by disaggregation of amyloid-β oligomers and plaques. Kim HY(1,)(2,)(3), Kim HV(1,)(2), Jo S(4), Lee CJ(4), Choi SY(1), Kim DJ(1), Kim Y(1,)(2). Full text: http://www.nature.com.sci-hub.io/ncomms/2015/151208/ncomms9997/abs/ncomms9997.html Alzheimer's disease (AD) is characterized by the transition of amyloid-β (Aβ) monomers into toxic oligomers and plaques. Given that Aβ abnormality typically precedes the development of clinical symptoms, an agent capable of disaggregating existing Aβ aggregates may be advantageous. Here we report that a small molecule, 4-(2-hydroxyethyl)-1-piperazinepropanesulphonic acid (EPPS), binds to Aβ aggregates and converts them into monomers. The oral administration of EPPS substantially reduces hippocampus-dependent behavioural deficits, brain Aβ oligomer and plaque deposits, glial γ-aminobutyric acid (GABA) release and brain inflammation in an Aβ-overexpressing, APP/PS1 transgenic mouse model when initiated after the development of severe AD-like phenotypes. The ability of EPPS to rescue Aβ aggregation and behavioural deficits provides strong support for the view that the accumulation of Aβ is an important mechanism underlying AD. PMCID: PMC4686862 PMID: 26646366
  3. On the thread about cranberries, Rodney got us talking about prunes, and how they may be good for maintaining bone health via increased IGF-1, which is a double-edged sword. This is pretty well-known among knowledgeable CR practitioners, but I thought it worth highlighting, particularly since I came across this interesting discussion & video on the potential tradeoff between "performance" and longevity with respect to IGF-1. It discusses (and gives citations) for many of the benefits of IGF-1, including muscle repair/preservation as well as long-term cognitive health. Interestingly, it doesn't mention helping maintain bone health as another benefit of the anabolic effects of IGF-1. But on the downside, it talks about increased cancer risk and the widely-observed reduced longevity (in humans and animals) associated with higher levels of IGF-1. Here is the summary paragraph: There you have it. It’s a trade-off when it comes to growth hormone and IGF-1. More of it enhances muscle and neuronal growth while simultaneously preventing atrophy. Less of it will increase the expression of stress resistance genes and extend your lifespan. Which do you prefer, having better muscle and cognitive performance or living longer? Overall, it seems like a good primer for anyone who wants to learn about the pros and cons of the reduced IGF-1 often associated with practicing CR. --Dean
  4. All, The benefits of yoga has been discussed on various threads lately, so I figured it was time to consolidate the discussions into a single master thread, particularly since there is a new study I wanted to post (see below). First we saw in this thread that yoga beats both walking and a mediterranean diet for CVD risk reduction. Then we saw in this post by Cloud that 12 weeks of yoga reduces inflammatory markers in recovering cancer patients. Now, a new study [1] (popular press story) found that 12 weeks of yoga beat out the "gold standard" memory training technique in people with mild cognitive impairment. The yoga group had lower depression scores, and improved verbal and visuospatial memory compared with memory training. While the study was small, its effects were pretty impressive, and were accompanied by changes in brain region connectivity as measured by FMRI brain scans. With all this evidence of benefit, it seems like a good idea to start practicing yoga, and consider having the next CR Conference at a yoga center like Saul suggests - maybe Sthira and Saul can teach the rest of us! --Dean ---------- [1] J Alzheimers Dis. 2016 Apr 5;52(2):673-84. doi: 10.3233/JAD-150653. Changes in Neural Connectivity and Memory Following a Yoga Intervention for Older Adults: A Pilot Study. Eyre HA(1,)(2), Acevedo B(1), Yang H(1), Siddarth P(1), Van Dyk K(1), Ercoli L(1), Leaver AM(3), Cyr NS(1), Narr K(3), Baune BT(2), Khalsa DS(4), Lavretsky H(1). Author information: (1)Semel Institute for Neuroscience and Human Behavior, UCLA, Los Angeles, CA, USA. (2)Discipline of Psychiatry, University of Adelaide, Adelaide, South Australia, Australia. (3)Ahmanson-Lovelace Brain Mapping Center, Department of Neurology, UCLA, Los Angeles, CA, USA. (4)Alzheimer's Research and Prevention Foundation, Tucson, AZ, USA. BACKGROUND: No study has explored the effect of yoga on cognitive decline and resting-state functional connectivity. OBJECTIVES: This study explored the relationship between performance on memory tests and resting-state functional connectivity before and after a yoga intervention versus active control for subjects with mild cognitive impairment (MCI). METHODS: Participants ( ≥ 55 y) with MCI were randomized to receive a yoga intervention or active "gold-standard" control (i.e., memory enhancement training (MET)) for 12 weeks. Resting-state functional magnetic resonance imaging was used to map correlations between brain networks and memory performance changes over time. Default mode networks (DMN), language and superior parietal networks were chosen as networks of interest to analyze the association with changes in verbal and visuospatial memory performance. RESULTS: Fourteen yoga and 11 MET participants completed the study. The yoga group demonstrated a statistically significant improvement in depression and visuospatial memory. We observed improved verbal memory performance correlated with increased connectivity between the DMN and frontal medial cortex, pregenual anterior cingulate cortex, right middle frontal cortex, posterior cingulate cortex, and left lateral occipital cortex. Improved verbal memory performance positively correlated with increased connectivity between the language processing network and the left inferior frontal gyrus. Improved visuospatial memory performance correlated inversely with connectivity between the superior parietal network and the medial parietal cortex. CONCLUSION: Yoga may be as effective as MET in improving functional connectivity in relation to verbal memory performance. These findings should be confirmed in larger prospective studies. PMID: 27060939
  5. All, I found this interesting. University of Pittsburgh (yeah!) researchers have found [1] (press release) that cognition tends to decline much more rapidly in elderly folks who test positive for chronic, seemingly harmless viral infections, such as cytomegalovirus, toxoplasma gondii (the virus that makes rats love cats, and humans take risks!), and various herpes simplex viruses. The lead author said: “It’s possible that these viruses, which can linger in the body long after acute infection, are triggering some neurotoxic effects.” The smart folks over at Fight Aging! observe: A good deal of evidence from past years supports the theory that CMV accelerates immune system aging, causing the immune system to devote ever more of its limited capacity to uselessly fighting CMV rather than productively carrying out its other tasks. Our immune response is incapable of clearing CMV from the body, and the virus lingers to return in force again and again regardless of the effort devoted to battle it. Chronic infections with these three viruses is surprisingly common. T. gondii infection rates are around 22% of the general population. And between 50 and 80% of people are infected with cytomegalovirus by age 40! I wonder if chronic elevation of WBC, as a sign of chronic infection, is associated with accelerated cognitive decline... I suspect it probably is. For CRers whose WBC count remains unusually high, it might be worth getting tested for chronic viral infections, including the three listed above. --Dean ------------ [1] Alzheimer Dis Assoc Disord. 2015 Dec 24. [Epub ahead of print] Temporal Cognitive Decline Associated With Exposure to Infectious Agents in a Population-based, Aging Cohort. Nimgaonkar VL(1), Yolken RH, Wang T, Chung-Chou HC, McClain L, McDade E, Snitz BE, Ganguli M. Author information: (1)Departments of *Psychiatry ∥Medicine ¶Neurology, University of Pittsburgh School of Medicine Departments of †Human Genetics §Biostatistics #Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA ‡Department of Pediatrics, Stanley Division of Neurovirology, Johns Hopkins University School of Medicine, Baltimore, MD. BACKGROUND: Numerous cross-sectional studies have related exposure to neurotropic infectious agents with cognitive dysfunction in older adults, however, the temporal sequence is uncertain. METHODS: In a representative, well-characterized, population-based aging cohort, we determined whether the temporal trajectories of multiple cognitive domains are associated with exposure to cytomegalovirus (CMV), Herpes Simplex virus, type 1 (HSV-1), Herpes Simplex virus, type 2 (HSV-2), or Toxoplasma gondii (TOX). Complex attention, executive functions, memory, language, and visuospatial function were assessed annually for 5 years among consenting individuals. Study entry IgG antibody titers indexing exposure to each infectious agent were examined in relation to slopes of subsequent temporal cognitive decline using multiple linear regressions adjusted for potential confounders. RESULTS: The IgG levels for HSV-2 were significantly associated with baseline cognitive domain scores (N=1022 participants). Further, the IgG levels for HSV-2, TOX, and CMV, but not HSV-1 were significantly associated with greater temporal cognitive decline that varied by type of infection. CONCLUSIONS: Exposure to CMV, HSV-2, or TOX is associated with cognitive deterioration in older individuals, independent of general age-related variables. An increased understanding of the role of infectious agents in cognitive decline may lead to new methods for its prevention and treatment. PMID: 26710257
  6. All, Here is an interesting article highlighting research that suggests silence (no not necessarily meditation, just quiet time) is good for the brain and cognition. Here are a couple passages I found most interesting: A 2013 study [1] on mice published in the journal Brain, Structure and Function used differed types of noise and silence and monitored the effect the sound and silence had on the brains of the mice. The silence was intended to be the control in the study but what they found was surprising. The scientists discovered that when the mice were exposed to two hours of silence per day they developed new cells in the hippocampus. The hippocampus is a region of the brain associated with memory, emotion and learning. The growth of new cells in the brain does not necessarily translate to tangible health benefits. However, in this instance, researcher Imke Kirste says that the cells appeared to become functioning neurons. “We saw that silence is really helping the new generated cells to differentiate into neurons, and integrate into the system.” In this sense silence can quite literally grow your brain. The 2013 study referenced is [1]. Here is a quote from the abstract: We used the standard noise level in the animal facility as baseline and compared this condition to white noise, pup calls, and silence. In addition, as patterned auditory stimulus without ethological relevance to mice we used piano music by Mozart (KV 448). All stimuli were transposed to the frequency range of C57BL/6 and hearing was objectified with acoustic evoked potentials.... [A]fter 7 days, only silence remained associated with increased numbers of [hippocampal] cells. Compared to controls at this stage, exposure to silence had generated significantly increased numbers of [hippocampal] neurons. and again quoting from the popular press article: A study that was published in 2002 in Psychological Science (Vol. 13, No. 9) examined the effects that the relocation of Munich’s airport had on children’s health and cognition. Gary W. Evans, a professor of human ecology at Cornell University notes that children who are exposed to noise develop a stress response that causes them to ignore the noise. What is of interest is that these children not only ignored harmful stimuli they also ignored stimuli that they should be paying attention to such as speech. “This study is among the strongest, probably the most definitive proof that noise – even at levels that do not produce any hearing damage – causes stress and is harmful to humans,” Evans says. Apparently, silence may be golden when it comes to brain health. --Dean ---------- [1] Brain Struct Funct. 2015 Mar;220(2):1221-8. doi: 10.1007/s00429-013-0679-3. Epub 2013 Dec 1. Is silence golden? Effects of auditory stimuli and their absence on adult hippocampal neurogenesis. Kirste I(1), Nicola Z, Kronenberg G, Walker TL, Liu RC, Kempermann G. Author information: (1)CRTD, DFG Research Center for Regenerative Therapies Dresden, Fetscherstraße 105, 01307, Dresden, Germany. We have previously hypothesized that the reason why physical activity increases precursor cell proliferation in adult neurogenesis is that movement serves as non-specific signal to evoke the alertness required to meet cognitive demands. Thereby a pool of immature neurons is generated that are potentially recruitable by subsequent cognitive stimuli. Along these lines, we here tested whether auditory stimuli might exert a similar non-specific effect on adult neurogenesis in mice. We used the standard noise level in the animal facility as baseline and compared this condition to white noise, pup calls, and silence. In addition, as patterned auditory stimulus without ethological relevance to mice we used piano music by Mozart (KV 448). All stimuli were transposed to the frequency range of C57BL/6 and hearing was objectified with acoustic evoked potentials. We found that except for white noise all stimuli, including silence, increased precursor cell proliferation (assessed 24 h after labeling with bromodeoxyuridine, BrdU). This could be explained by significant increases in BrdU-labeled Sox2-positive cells (type-1/2a). But after 7 days, only silence remained associated with increased numbers of BrdU-labeled cells. Compared to controls at this stage, exposure to silence had generated significantly increased numbers of BrdU/NeuN-labeled neurons. Our results indicate that the unnatural absence of auditory input as well as spectrotemporally rich albeit ethological irrelevant stimuli activate precursor cells-in the case of silence also leading to greater numbers of newborn immature neurons-whereas ambient and unstructured background auditory stimuli do not. PMCID: PMC4087081 PMID: 24292324
  7. Dean Pomerleau

    Nootropics

    I was surprised to find that a search of these forums turned up very little discussion of nootropics, or so-called "smart drugs", at least as far as I could find. Obviously cognitive performance and long-term brain health is an important consideration for everyone, but especially obsessive optimizers like us ☺. So I figured I'd start a thread to inquire if anyone has experimented with nootropics, and if so, which ones (if any) did you find beneficial. To kick off the discussion, I've never experimented with any nootropics myself, except for caffeine, which honestly I don't find has much of an observable effect on me (cognitive or otherwise), but I take it anyway (as coffee/tea, and as a B12-fortified mint) for other health reasons. But today I came across a new multi-nootropic supplement from someone I trust, respect and believe to be quite intelligent - Lincoln Cannon. Lincoln is the co-founder of the Mormon Transhumanism Association, a pretty cool longevity-focused organization to which I and many other non-Mormons belong. Lincoln is also responsible for formulating the New God Argument, which I find pretty compelling (see here for related discussion and here for science/philosophy heavyweights on the topic). But I digress... Thrivous, his new company (to which I have no affiliation), has developed a nootropic supplement called Clarity. Here is the Clarity label: Has anyone any personal experience, or done any research on any of these ingredients? Here is Lincoln's research on them, plus a couple others not included in this version of Clarity. They look reasonably beneficial (and harmless) based on the controlled studies Lincoln has compiled. The price is pretty reasonable - $25 for a month's supply. I'm forever interested in self-experimentation and lifestyle optimization, so I was thinking of conducting a single-blind, crossover trial on myself to see if I notice any difference between taking Clarity vs. a placebo. But if others have had bad experiences with these nootropics, or know of research that says they may be harmful, I'll obviously steer clear. Thanks! --Dean
  8. Many of us have been conflicted over the long-chain omega-3 fatty acid DHA. On the one hand, it is known to be important for brain health. But on the other hand, Michael has long advocated keeping dietary intake of DHA and EPA low, especially for CR folks, since they are so easily damaged through peroxidation. Plus as I've pointed out, the primary natural food source of DHA/EPA is fatty fish, which pose a problem both for vegans, and for those who want to avoid ingesting heavy metals and pesticides which bioaccumulate in the fat of fish. As a result, people advocate getting one's omega-3s through alpha-linolenic acid (ALA) instead of DHA/EPA, by consuming flax seeds/oil, canola oil or walnuts. The problem with this approach is that the conversion of ALA into DHA/EPA is very limited, so it is not clear if one is getting sufficient DHA through this strategy. With this background, a new study [1] is quite exciting. It found that the combination of ALA and curcumin, one of the active compounds in the spice turmeric, increases the conversion of ALA into DHA, resulting in a 60% increase in the level of DHA in the hippocampal region of the brains of rats fed ALA+curcumin. Furthermore, feeding the combination of curcumin and ALA to rodents decreased their anxiety, suggesting that the DHA was having a beneficial behavioral effect in these rats. Here are the graphs from the full text showing the boosting of hippocampal DHA levels by ALA+curcumin (left) and the increase in time spent in the anxiety-provoking open arm of an elevated radial maze (right), illustrating reduced anxiety when rats were treated with ALA+curcumin: So despite Michael's flippant dismissal of curcumin in this post, in which he wrote: ... and you'll come up with a lot of rank nonsense ;) . Almost nothing that has been said about turmeric or curcumin has been validated in vivo, still less in normal mammals, and nearly nothing in humans — not even epidemiology: when you dig down into the few such studies on 'curries,' they aren't usually even on turmeric-based Indian curries but completely different spice blends from South Asia and the Pacific Islands. Sufficient quantities of curcumin (at levels too high to be obtained from turmeric) seem to lower TG, but (a) there are no long-term outcome studies, (b) the mechanism is unknown, and © CR people (even those on pretty high-carb diets) almost uniformly have very low TG. this study seems to provide strong, in vivo evidence in normal mammals that consuming curcumin may indeed be beneficial for DHA synthesis from ALA, for brain health and for reducing anxiety. The only thing I'm not certain about is dosing - i.e. whether or not the amount of curcumin in the diet of these rats (either 250 or 500 PPM) is reasonable or an unrealistic mega-dose. Perhaps Michael can help decipher the scaling, although I'm not holding my breath, considering how quiet Michael has been on these forums lately . --Dean --------- [1] Biochim Biophys Acta. 2015 May;1852(5):951-61. doi: 10.1016/j.bbadis.2014.12.005. Epub 2014 Dec 27. Curcumin boosts DHA in the brain: Implications for the prevention of anxiety disorders. Wu A(1), Noble EE(1), Tyagi E(1), Ying Z(1), Zhuang Y(1), Gomez-Pinilla F(2). Author information: (1)Department of Integrative Biology and Physiology, University of California at Los Angeles, 621 Charles E. Young Drive Los Angeles, CA 90095, USA. (2)Department of Integrative Biology and Physiology, University of California at Los Angeles, 621 Charles E. Young Drive Los Angeles, CA 90095, USA; Department of Neurosurgery, UCLA Brain Injury Research Center, David Geffen School of medicine at UCLA, Los Angeles, CA 90095, USA. Electronic address: fgomezpi@ucla.edu. Full text: http://www.sciencedirect.com.sci-hub.io/science/article/pii/S0925443914003779 Dietary deficiency of docosahexaenoic acid (C22:6 n-3; DHA) is linked to the neuropathology of several cognitive disorders, including anxiety. DHA, which is essential for brain development and protection, is primarily obtained through the diet or synthesized from dietary precursors, however the conversion efficiency is low. Curcumin (diferuloylmethane), which is a principal component of the spice turmeric, complements the action of DHA in the brain, and this study was performed to determine molecular mechanisms involved. We report that curcumin enhances the synthesis of DHA from its precursor, α-linolenic acid (C18:3 n-3; ALA) and elevates levels of enzymes involved in the synthesis of DHA such as FADS2 and elongase 2 in both liver and brain tissues. Furthermore, in vivo treatment with curcumin and ALA reduced anxiety-like behavior in rodents. Taken together, these data suggest that curcumin enhances DHA synthesis, resulting in elevated brain DHA content. These findings have important implications for human health and the prevention of cognitive disease, particularly for populations eating a plant-based diet or who do not consume fish, a primary source of DHA, since DHA is essential for brain function and its deficiency is implicated in many types of neurological disorders. Copyright © 2015 Elsevier B.V. All rights reserved. PMID: 25550171
  9. Ever since CR pioneer Roy Walford died of amyotrophic lateral sclerosis (ALS - or something resembling ALS), there has been some concern that CR may not protect against, and may in fact hasten, neurodegenerative diseases, particularly those involving dopaminergic neurons, like ALS, Parkinson's Disease (PD) and Multiple Sclerosis (MS). This new study [1] by Ingram et al posted by James in his latest weekly CR research update (thanks James!), suggests otherwise. It found that adult-onset CR in rats was protective against bradykinesia, a slowness of movement which is a hallmark of Parkinson's disease. They also found elevated levels of dopamine in an important brain region implicated in PD, the substantia nigra. This result supports an earlier, perhaps more germane finding from a study of primates done by Ingram's group in 2004 [2]. In [2], Ingram et al found that 30% CR for six months in adult male rhesus monkeys protected against a drop in dopamine level and dopamine neuron cell death when the (unfortunate ) monkeys were exposed to a neurotoxin that mimics Parkinson's Disease in primates. So overall that is more encouraging news for CR & brain health - on top of the finding of preserved white matter by CR I reported on earlier. In researching this post, I came across a review article [3] about a possible link between these three neurodegenerative diseases (PD, ALS & MS) and iodine. It observed that in regional population studies, long-term dietary iodine deficiency is associated with all three of these diseases, and may be explained by iodine deficiency interfering with dopamine and dopaminergic neurons. Whether this link holds up under scrutiny I'm not sure, but it is another possible reason to make sure one isn't deficient in iodine. Unfortunately, iodine is not well represented in the USDA (or any other) food database. For many people who consumed a low sodium diet, and in particular don't consume iodized salt, iodine deficiency is a real concern. That's why I supplement with the RDA (150mcg) of iodine per day. Note - high sodium processed foods typically do not contain iodine, so even the general population may be iodine deficient if they aren't eating foods with iodized salt. --Dean ---------- [1] Neurobiol Aging. 2015 Oct 19. pii: S0197-4580(15)00495-9. doi: 10.1016/j.neurobiolaging.2015.10.006. [Epub ahead of print] Initiation of calorie restriction in middle-aged male rats attenuates aging-related motoric decline and bradykinesia without increased striatal dopamine. Salvatore MF(1), Terrebonne J(2), Fields V(3), Nodurft D(3), Runfalo C(2), Latimer B(3), Ingram DK(2). Aging-related bradykinesia affects ∼15% of those reaching age 65 and 50% of those reaching their 80s. Given this high risk and lack of pharmacologic therapeutics, noninvasive lifestyle strategies should be identified to diminish its risk and identify the neurobiological targets to reduce aging-related bradykinesia. Early-life, long-term calorie restriction (CR) attenuates aging-related bradykinesia in rodents. Here, we addressed whether CR initiation at middle age could attenuate aging-related bradykinesia and motoric decline measured as rotarod performance. A 30% CR regimen was implemented for 6 months duration in 12-month-old male Brown-Norway Fischer 344 F1 hybrid rats after establishing individual baseline locomotor activities. Locomotor capacity was assessed every 6 weeks thereafter. The ad libitum group exhibited predictably decreased locomotor activity, except movement speed, out to 18 months of age. In contrast, in the CR group, movement number and horizontal activity did not decrease during the 6-month trial, and aging-related decline in rotarod performance was attenuated. The response to CR was influenced by baseline locomotor activity. The lower the locomotor activity level at baseline, the greater the response to CR. Rats in the lower 50th percentile surpassed their baseline level of activity, whereas rats in the top 50th percentile decreased at 6 weeks and then returned to baseline by 12 weeks of CR. We hypothesized that nigrostriatal dopamine tissue content would be greater in the CR group and observed a modest increase only in substantia nigra with no group differences in striatum, nucleus accumbens, or ventral tegmental area. These results indicate that initiation of CR at middle age may reduce aging-related bradykinesia, and, furthermore, subjects with below average locomotor activity may increase baseline activity. Sustaining nigral dopamine neurotransmission may be one component of preserving locomotor capabilities during aging. Copyright © 2015 Elsevier Inc. All rights reserved. PMID: 26610387 ----------- [2] Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18171-6. Epub 2004 Dec 16. Caloric restriction increases neurotrophic factor levels and attenuates neurochemical and behavioral deficits in a primate model of Parkinson's disease. Maswood N(1), Young J, Tilmont E, Zhang Z, Gash DM, Gerhardt GA, Grondin R, Roth GS, Mattison J, Lane MA, Carson RE, Cohen RM, Mouton PR, Quigley C, Mattson MP, Ingram DK. Author information: (1)Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA. Comment in Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):17887-8. We report that a low-calorie diet can lessen the severity of neurochemical deficits and motor dysfunction in a primate model of Parkinson's disease. Adult male rhesus monkeys were maintained for 6 months on a reduced-calorie diet [30% caloric restriction (CR)] or an ad libitum control diet after which they were subjected to treatment with a neurotoxin to produce a hemiparkinson condition. After neurotoxin treatment, CR monkeys exhibited significantly higher levels of locomotor activity compared with control monkeys as well as higher levels of dopamine (DA) and DA metabolites in the striatal region. Increased survival of DA neurons in the substantia nigra and improved manual dexterity were noted but did not reach statistical significance. Levels of glial cell line-derived neurotrophic factor, which is known to promote the survival of DA neurons, were increased significantly in the caudate nucleus of CR monkeys, suggesting a role for glial cell line-derived neurotrophic factor in the anti-Parkinson's disease effect of the low-calorie diet. PMCID: PMC539733 PMID: 15604149 --------------- [3] Journal of Orthomolecular Medicine Vol. 14, 3rd Quarter 1999 Parkinson’s Disease, Multiple Sclerosis and Amyotrophic Lateral Sclerosis: The Iodine-Dopachrome-Glutamate Hypothesis Harold D. Foster Full text: http://orthomolecular.org/library/jom/1999/articles/1999-v14n03-p128.shtml Abstract Background. Globally, Parkinsonism, multiple sclerosis and amyotrophic lateral sclerosis mortalities tends to increase with latitude. These disorders also display a north-south gradient in the coterminous United States. This spatial distribution suggests their etiologies are significantly influenced by one or more geographical variables. Methods. Pearson’s correlation was used to compare mortalities, at the state scale, in the United States, from these three neurologic disorders and the spatial patterns of 81 other diseases and 219 environmental variables. Results. The resulting correlations suggest that mortality from Parkinsonism, multiple sclerosis and amyotrophic lateral sclerosis occurs most often in recently glaciated, iodine deficient regions, that were formerly marked by elevated goiter prevalence. Conclusions. Long-term iodine deficiency appears linked to abnormalities in the dopaminergic system that include an increased number of dopamine receptors. It is argued that this raises susceptibility to dopamine oxidation which, in turn, causes deficiencies of the antioxidant enzymes Cu/Zn superoxide dismutase, glutathione peroxidase and catalase. Dopamine deficiency also leads to elevated cytotoxic glutamate levels. Implications of the iodine-dopachrome-glutamate hypothesis, for treatment of these three neurologic disorders, are then discussed. Possible interventions include the use of levodopa, vitamin B3, Coenzyme Q10, various antioxidants, amino acids, iodine and glutamate antagonists. Key words: Parkinson’s disease, multiple sclerosis, amyotrophic lateral sclerosis, glaciation, iodine, goiter, dopamine, dopachrome, glutamate, oxidative stress.
  10. CR is known to improve spatial learning and memory in rodents on tasks like the Morris water maze. But it is a matter of some controversy as to whether this improvement is due to beneficial effects of CR on memory/cognition, or whether the lean CR rodents can just swim better [2][3]. James Cain posted this new study [1] which speaks to this issue a bit. Researchers found that short-term CR in young rats resulted in beneficial changes in the microstructure of synapses in their hippocampus, part of the brain known to be important for spatial learning. So that is nice to see! --Dean ---------------- [1] Hippocampus. 2015 Sep 19. doi: 10.1002/hipo.22533. [Epub ahead of print] Food restriction modifies ultrastructure of hippocampal synapses. Babits R1, Szőke B, Sótonyi P1, Rácz B1. Abstract Consumption of high-energy diets may compromise health and may also impair cognition; these impairments have been linked to tasks that require hippocampal function. Conversely, food restriction has been shown to improve certain aspects of hippocampal function, including spatial memory and memory persistence. These diet-dependent functional changes raise the possibility that the synaptic structure underlying hippocampal function is also affected. To examine how short-term food restriction (FR) alters the synaptic structure of the hippocampus, we used quantitative electron microscopy to analyze the organization of neuropil in the CA1 stratum radiatum of the hippocampus in young rats, consequent to reduced food. While four weeks of FR did not modify the density, size, or shape of postsynaptic spines, the synapses established by these spines were altered, displaying increased mean length, and more frequent perforations of postsynaptic densities. That the number of perforated synapses (believed to be an indicator of synaptic enhancement) increased, and that the CA1 spine population had on average significantly longer PSDs suggests that synaptic efficacy of axospinous synapses also increased in the CA1. Taken together, our ultrastructural data reveal previously unrecognized structural changes at hippocampal synapses as a function of food restriction, supporting a link between metabolic balance and synaptic plasticity. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc. KEYWORDS: CA1; dietary restriction; electron microscopy; memory; synaptic plasticity PMID: 26386363 -------------- [2] Physiol Behav. 2008 Feb 27;93(3):560-9. Epub 2007 Oct 30. Effects of chronic adult dietary restriction on spatial learning in the aged F344 x BN hybrid F1 rat. Fitting S(1), Booze RM, Gilbert CA, Mactutus CF. Author information: (1)Program in Behavioral Neuroscience, Department of Psychology, University of South Carolina, Columbia, SC 29208, USA. fitting@sc.edu <fitting@sc.edu> Dietary restriction (DR) has been shown to increase life span and reduce disease incidence across a variety of species. Recent research suggests that chronic adult DR may also alter age-related cognitive decline. The purpose of this study was twofold: (1) to examine the potential deficits in spatial learning ability in the aged F344 x BN hybrid F1 rat with specific attention to the contributory effects of motoric impairments and (2) to determine the influence of chronic adult DR on any such impairments. The Morris water maze (MWM) task was employed with a 1.8 m diameter tank, 10 cm2 escape platform, 28 degrees C water, and an automated collapsing central starting platform. Spatial learning impairments in the aged rats were evident on all dependent measures during training and the probe test. Motoric function, as reflected in measures of strength and locomotion demonstrated profound age-related performance impairments that were attenuated by chronic adult DR. The present data also replicate previous reports, indicating that DR attenuates the age-related impairments of performance in the MWM as indexed by the latency measure in acquisition, but critically was dissociated from any DR effect on measures of preference and, more critically, accuracy in the probe test. Collectively, the most parsimonious interpretation of DR effects on MWM performance would appear to be the preservation of motoric, and not cognitive, function. PMCID: PMC4041982 PMID: 18035382 ----------- [3] J Gerontol A Biol Sci Med Sci. 2009 Aug; 64A(8): 850–859. Published online 2009 May 6. doi: 10.1093/gerona/glp060 Influence of Calorie Restriction on Measures of Age-Related Cognitive Decline: Role of Increased Physical Activity Christy S. Carter,corresponding author1,2,3 Christiaan Leeuwenburgh,1 Michael Daniels,4 and Thomas C. Foster3 Abstract Controversy exists as to whether lifelong 40% calorie restriction (CR) enhances, has no effect on, or disrupts cognitive function during aging. Here, we report the effects of CR versus ad-lib feeding on cognitive function in male Brown Norway × Fisher344 rats across a range of ages (8–38 months), using two tasks that are differentially sensitive to age-related cognitive decline: object recognition and Morris water maze (MWM). All ages performed equally in object recognition, whereas, as a group, CR rats were impaired. In contrast, there was an age-related impairment in the MWM that was attenuated by CR as measured by time in proximity with and latency to reach the platform. Distance to the platform, a more sensitive measure, was not affected by CR. Finally, CR resulted in an overall increase in physical activity, one of several behavioral confounders to consider in the interpretation of cognitive outcomes in both tasks. PMCID: PMC2709546
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