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All, We've talked quite a bit around here lately about the optimal BMI for longevity, most notably in this thread about the Optimal Late-Life BMI for Longevity, and this one called Will Serious CR Beat a Healthy Obesity-Avoiding Diet & Lifestyle , and this one called Relationship between BMI and Disease, Longevity, and finally this one called Body Mass Index and All-Cause Mortality. In general, it appears (to my interpretation) that it doesn't pay to be very thin when it comes to longevity, and may in fact be counterproductive, particularly as someone gets into their senior years. Being average weight or even overweight does not appear to adversely impact longevity in older folks, in fact if anything the evidence points the other way - being a heavy senior appears associated with increased longevity. But what about cognitive health? It would be pretty tragic to live an especially long time, but lose your marbles along the way. Three recent studies that came across my radar shed some light on the issue of BMI and cognitive health. The first  looks pretty bad for chubby folks. It found being overweight was associated with a reduction in the volume of several important brain areas. The researchers did structural MRI scans of the brains of 203 relatively young men and women (mean age 32, range 18-50). They ranged in BMI from 18.5 to 46.4. They all self-reported being healthy, and were not receiving any pharmacological treatments. They processed the MRI scans to estimate cortical thickness and surface area, both globally and on a per-region basis. Overall they didn't find a correlation between any of the global brain anatomy measures and BMI: There was no association between BMI and global measures of average cortical thickness, total surface area or average LGI [Local gyrification index - a measure of how folded the cortex is. DP]. But in two brain areas there was a difference between obese folks and people who were either thin or simply overweight: Post-hoc contrasts revealed that while lean (BMI < 25) and overweight subjects (25 ≤ BMI < 30) did not significantly differ in the thickness of the right vmPFC or left LOC (p = 0.29 and p = 0.34, respectively), obese subjects (BMI ≥ 30) had significantly thinner cortices in these clusters, compared to both lean (p < 0.0001 in both clusters) and overweight subjects (p < 0.0001 in both clusters). The ventromedial prefrontal cortex (vmPFC) is at the front of the brain, above the eyebrows and is involved in executive function and decision-making. The LOC (lateral occipital cortex) is at the back of the brain, and is involved in vision processing and object recognition. The scatter plots for the cortical thickness in those two brain areas as a function of BMI look pretty scattered to me. It seems difficult to put too much stock in their results, especially below a BMI of 30, where the plots look pretty random, at least to my eyes: My dubiousness about the result is bolstered by the fact that this cortical thinning effect was discovered in post-hoc analysis. In other words, the researchers were fishing for differences in brain anatomy as a function of BMI, after the main effect they were looking for (cortical changes across the whole brain varying with BMI) didn't pan out. After undoubtedly looking at many regions, these two showed up with statistically significant variations as a function of BMI. There is always the danger with this sort of post-hoc approach of finding spurious correlations if you look hard enough at enough different variables. But other studies have found variations in the vmPFC related to obesity. In fact, these authors and others have speculated that the direction of causality may be reserved for the vmPFC. Rather than obesity causing brain shrinking in the vmPFC, having a smaller vmPFC may predispose someone to gaining weight. Why? Because the vmPFC is critical for good decision-making, and the thought is that a smaller vmPFC may result in poor impulse control, and therefore overeating and weight gain. In a separate new study by the same authors  (popular press coverage), this time looking at white matter (axons between brain areas) rather than grey matter (neuronal cell bodies and dendrites), the authors did find a more widespread difference between the brains of obese/overweight people and thin people. This time they scanned the brains of over 500 people aged 20 to 87. Basically, when it came to white matter volume, the brains of overweight (avg BMI 27.1) or obese (avg BMI 33.5) folks looked about 10 years older than the lean (normal weight) folks (avg BMI 22.7). Here are the curves for white matter volume as a function of age: As you can see, everyone's white matter volume declines past age 40, but the overweight/obese folks appear to never reach the same peak volume as the normal weight folks and start to decline earlier than the normal weight folks as well. As a result, past middle age the overweight/obese folks' brains looked about 10 years older than the thin folks in terms of white matter volume. The impact of BMI on white matter volume appeared to be independent of exercise, income or education. Interestingly, the authors also found that "a previous diagnosis of elevated cholesterol" was associated with reduced white matter volume, independent of age and BMI. But perhaps most surprisingly, despite the reduced white matter volume in obese/overweight folks relative to lean folks, they saw no difference in cognitive scores (on the Cattell test - "used to capture fluid intelligence by measuring abstract reasoning ability") between the chubby and the lean folks: The authors say: Although previous studies have linked white matter integrity, processing speed and fluid intelligence (Kievit et al., 2016) our results suggest that BMI does not additional influence the age and brain structure relationship with cognition. In other words, despite having less white matter, the heavier folks didn't suffer any faster cognitive decline than the thin folks, at least as measured by this test of "fluid intelligence" in a snapshot of people at various ages. The authors again point to the possibility of reverse causality (less white matter → weight gain), but it seems harder to argue in this case, where the white matter shrinkage/deficit was global rather than confined to decision-making parts of the brain like they saw in . Despite minor doubts about the arrow of causality, and despite a lack of cognitive deficits in the heavier folks, it seems to me like a no-brainer to prefer potentially preserving white matter by staying lean (avg BMI ~23) relative to becoming overweight (BMI >25) or obese (BMI > 30). So these two studies (weakly) suggest it's better to be lean than overweight/obese for brain health. But what about the other end of the scale? That's where study  comes in. In this one, a different set of researchers did PET brain imaging on 280 healthy older people (mean age 73, range 62-90) with normal cognitive function. More on demographics: Subjects were roughly average for the American population in terms of prevalence for antihypertensive use (58%) and statin use (44%), but had less diabetes mellitus type 2 (9%) and active smoking (4%).d Here was the distribution of BMIs: Body-Mass Index 26.9 (16–41) - Underweight (BMI <18.5) 2.5% (n=7) - Normal (BMI 18.5–24.9) 31.8% (n = 89) - Overweight (BMI 25–29.9) 41.4% (n = 116) - Obese (BMI >30) 24.3% (n = 68) What they did was correlate BMI with PiB retention, which is a surrogate for brain amyloid concentration, an early marker for increased risk of cognitive impairment / alzheimer disease. What they found that was being on the thin end of the BMI spectrum (i.e. < 25) was associated with an increased PiB retention, i.e. increased risk of future cognitive decline. This association was seen across the board, but was only significant in APOE4 carriers (i.e. those with a genetic tendency to develop cognitive impairment / alzheimer's disease). Here are the scatter plots of data from APOE4 carriers (green) and non-carriers (blue): As you can see, once again there was a pretty wide scatter, and the blue points have only a very modest downward slope (i.e. reduced risk of cognitive decline) with increasing BMI. In short, it appears if you know you are an APOE4 carrier (or if you don't know that you aren't an APOE4 carrier) it looks like it may be a good idea to avoid being thin late in life. But once again it is hard to know if being thin causes cognitive decline in APOE4 carriers, or that being an APOE4 carrier causes weight loss later in life. When taken together, the upshot of these three studies of BMI & cognitive health seems to point to a similar conclusion as we've seen for BMI & longevity. Namely that a middle-of-the-road BMI (i.e. 23-25) in one's elder years appears associated with the maximum chance of keeping one's marbles intact with age. --Dean ------------  Int J Obes (Lond). 2016 Jul;40(7):1177-82. doi: 10.1038/ijo.2016.42. Epub 2016 Mar 22. Increased body mass index is associated with specific regional alterations in brain structure. Medic N(1,)(2), Ziauddeen H(1,)(2,)(3), Ersche KD(1), Farooqi IS(2), Bullmore ET(1,)(4), Nathan PJ(1,)(5), Ronan L(1), Fletcher PC(1,)(2,)(3). Author information: (1)Department of Psychiatry, University of Cambridge, Cambridge, UK. (2)Wellcome Trust-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, UK. (3)Cambridgeshire and Peterborough NHS Foundation Trust, University of Cambridge, Cambridge, UK. (4)Medicines Discovery and Development, GlaxoSmithKline, Clinical Unit Cambridge, Cambridge, UK. (5)School of Psychological Sciences, Monash University, Melbourne, Victoria, Australia. Full text: http://sci-hub.cc/10.1038/ijo.2016.42 BACKGROUND: Although obesity is associated with structural changes in brain grey matter, findings have been inconsistent and the precise nature of these changes is unclear. Inconsistencies may partly be due to the use of different volumetric morphometry methods, and the inclusion of participants with comorbidities that exert independent effects on brain structure. The latter concern is particularly critical when sample sizes are modest. The purpose of the current study was to examine the relationship between cortical grey matter and body mass index (BMI), in healthy participants, excluding confounding comorbidities and using a large sample size. SUBJECTS: A total of 202 self-reported healthy volunteers were studied using surface-based morphometry, which permits the measurement of cortical thickness, surface area and cortical folding, independent of each other. RESULTS: Although increasing BMI was not associated with global cortical changes, a more precise, region-based analysis revealed significant thinning of the cortex in two areas: left lateral occipital cortex (LOC) and right ventromedial prefrontal cortex (vmPFC). An analogous region-based analysis failed to find an association between BMI and regional surface area or folding. Participants' age was also found to be negatively associated with cortical thickness of several brain regions; however, there was no overlap between the age- and BMI-related effects on cortical thinning. CONCLUSIONS: Our data suggest that the key effect of increasing BMI on cortical grey matter is a focal thinning in the left LOC and right vmPFC. Consistent implications of the latter region in reward valuation, and goal control of decision and action suggest a possible shift in these processes with increasing BMI. DOI: 10.1038/ijo.2016.42 PMCID: PMC4936515 [Available on 2017-01-01] PMID: 27089992 ------------  Neurobiology of Aging (2016), Obesity associated with increased brain-age from mid-life Ronan, L., Alexander-Bloch, A.F, Wagstyl, K., Farooqi, S., Brayne, C., Tyler, L.K, Cam-CAN, Fletcher, P.C, Free full text: http://www.neurobiologyofaging.org/article/S0197-4580(16)30140-3/pdf Abstract Common mechanisms in aging and obesity are hypothesized to increase susceptibility to neurodegeneration, however direct evidence in support of this hypothesis is lacking. We therefore performed a cross-sectional analysis of MRI-based brain structure on a population-based cohort of healthy adults. Study participants were originally part of the Cambridge Centre for Ageing and Neuroscience (Cam-CAN) and included 527 individuals aged 20 – 87 years. Cortical reconstruction techniques were used to generate measures of whole brain cerebral white matter volume, cortical thickness and surface area. Results indicated that cerebral white matter volume in overweight and obese individuals was associated with a greater degree of atrophy, with maximal effects in middle-age corresponding to an estimated increase of brain-age of 10 years. There were no similar BMI-related changes in cortical parameters. This study suggests that at a population level, obesity may increase the risk of neurodegeneration. Keywords obesity; white matter volume; structural MRI; population-based PMID: Not available doi: 10.1016/j.neurobiolaging.2016.07.010. -----------  J Alzheimers Dis. 2016 Jun 18;53(3):1097-105. doi: 10.3233/JAD-150987. Lower Late-Life Body-Mass Index is Associated with Higher Cortical Amyloid Burden in Clinically Normal Elderly. Hsu DC(1,)(2,)(3), Mormino EC(4), Schultz AP(4), Amariglio RE(4,)(2), Donovan NJ(1,)(2,)(5), Rentz DM(4,)(2,)(5), Johnson KA(4,)(6,)(2), Sperling RA(4,)(2), Marshall GA(4,)(2); Harvard Aging Brain Study. Author information: (1)Department of Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. (2)Department of Neurology, Center for Alzheimer Research and Treatment, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. (3)Department of Psychiatry, Mercy Medical Group, Sacramento, CA, USA. (4)Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. (5)Department of Psychiatry, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. (6)Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Full text: available on request BACKGROUND: Lower body-mass index (BMI) in late life has been associated with an increased risk of dementia, and weight loss has been associated with more rapid decline in Alzheimer's disease (AD) dementia. OBJECTIVE: To explore the association between BMI and cortical amyloid burden in clinically normal (CN) elderly at risk for AD dementia. METHODS: Cross-sectional analyses were completed using baseline data from the Harvard Aging Brain Study, consisting of 280 community-dwelling CN older adults aged 62-90. Assessments included medical histories and physical exam, Pittsburgh compound B (PiB) positron emission tomography (PET) amyloid imaging, and apolipoprotein E ɛ4 (APOE4) genotyping. For the primary analysis, a general linear regression model was used to evaluate the association of BMI with PiB retention. Covariates included age, sex, years of education, and APOE4 carrier status. Secondary analyses were performed for BMI subdivisions (normal, overweight, obese), APOE4 carriers, and BMI×APOE4 interaction. RESULTS: In the primary analysis, greater PiB retention was associated with lower BMI (β = -0.14, p = 0.02). In the secondary analyses, APOE4 carrier status (β= -0.27, p = 0.02) and normal BMI (β= -0.25, p = 0.01), as opposed to overweight or obese BMI, were associated with greater PiB retention. The BMI×APOE4 interaction was also significant (β= -0.14, p = 0.04). CONCLUSIONS: This finding offers new insight into the role of BMI at the preclinical stage of AD, wherein lower BMI late in life is associated with greater cortical amyloid burden. Future studies are needed to elucidate the mechanism behind this association, especially in those with lower BMI who are APOE4 carriers. DOI: 10.3233/JAD-150987 PMCID: PMC4976009 PMID: 27340843
All I can say is that people are zombies when it comes to food choices... From : Diners ordered significantly more items when served by heavy wait staff with high body mass indexes (BMI; p < .001) compared with wait staff with low body mass indexes. Specifically, they were four times as likely to order desserts (p < .01),... In this popular press article on the study, the author says: “A fun, happy, heavy waiter, might lead a diner to say ‘What the heck’ and to cut loose a little.” --Dean -------------  The Waiter’s Weight - Does a Server’s BMI Relate to How Much Food Diners Order? Tim Döring1 Brian Wansink2⇑ 1Friedrich Schiller University Jena, Germany 2Cornell University, Ithaca, NY, USA Brian Wansink, Cornell University, 475 Warren Hall, Ithaca, NY 14853-7801, USA. Email: firstname.lastname@example.org http://eab.sagepub.com/content/early/2015/10/29/0013916515621108.abstract Abstract Does the weight of a server have an influence on how much food diners order in the high-involvement environment of a restaurant? If people are paying for a full meal, this has implications for consumers, restaurants, and public health. To investigate this, 497 interactions between diners and servers were observed in 60 different full-service restaurants. Diners ordered significantly more items when served by heavy wait staff with high body mass indexes (BMI; p < .001) compared with wait staff with low body mass indexes. Specifically, they were four times as likely to order desserts (p < .01), and they ordered 17.65% more alcoholic drinks (p < .01). These findings provide valuable evidence in recent lawsuits against weight discrimination, and it suggests to consumers who decide what they will and will not order at a restaurant—such as a salad appetizer, no dessert, and one drink—than to decide when the waiter arrives.
Dean Pomerleau posted a topic in General Health and LongevityAll, There is a new study  out this week getting lots of media attention with headlines like Study: Obesity more dangerous to health than lack of fitness and 'Fat but fit' counts for nothing scientists say. After reading the full text (via sci-hub.io) it appears this is a gross oversimplification, if not outright distortion of what the study really says. In the study, researchers looked at the aerobic fitness and weight of 1.3 million Swedish men at the time of their military conscription (mean age 18). Aerobic fitness was tested by seeing how long the men could keep pedalling on a stationary bike whose resistance was increased at a rate of 2.5 watts/min. The subjects were then followed for an average of 29 years (to around age 47 - so still relatively young), during which 44K of them died. They then compiled statistics about mortality rate as a function of both baseline weight and baseline aerobic fitness. The results of the entire study are nicely summarized in a single graph (don't you love it when that happens?!). Here it is: There are several interesting things that can be gleaned from this graph: Being more aerobically fit resulted in reduced mortality across all four BMI categories. There was virtually no difference in the mortality rate of men with low BMI (< 18.5) vs. normal BMI (18.5 - 25). The fact that the researchers did not correct for smoking would seem to make this lack of difference even more significant, since it is likely that the skinny group smoked more than the normal weight group, and so would be expected to have a higher mortality rate, based on many other studies. The most fit obese men were significantly more likely to die than the least fit normal or even overweight individuals. It is only the last of these three points which seem to have sparked all the media attention. But as you can see, the study has much more interesting information than just that, particularly for us CR practitioners - namely that when it comes to reducing mid-life mortality, being skinny isn't bad and being more aerobically fit is good. --Dean ---------  International Journal of Epidemiology, 2015, 1–10 doi: 10.1093/ije/dyv321 Aerobic fitness in late adolescence and the risk of early death: a prospective cohort study of 1.3 million Swedish men Gabriel Hogstrom, Anna Nordstrom and Peter Nordstrom Full text (via sci-hub.io): http://ije.oxfordjournals.org.sci-hub.io/content/early/2015/12/20/ije.dyv321.full Abstract Background: Fitness level and obesity have been associated with death in older populations. We investigated the relationship between aerobic fitness in late adolescence and early death, and whether a high fitness level can compensate the risk of being obese. Methods: The cohort comprised 1 317 713 Swedish men (mean age, 18 years) that conscripted between 1969 and 1996. Aerobic fitness was assessed by an electrically braked cycle test. All-cause and specific causes of death were tracked using national registers. Multivariable adjusted associations were tested using Cox regression models. Results: During a mean follow-up period of 29 years, 44 301 subjects died. Individuals in the highest fifth of aerobic fitness were at lower risk of death from any cause [hazard ratio (HR), 0.49; 95% confidence interval (CI), 0.47–0.51] in comparison with individuals in the lowest fifth, with the strongest association seen for death related to alcohol and narcotics abuse (HR, 0.20; 95% CI, 0.15–0.26). Similar risks were found for weight-adjusted aerobic fitness. Aerobic fitness was associated with a reduced risk of death from any cause in normalweight and overweight individuals, whereas the benefits were reduced in obese individuals (P< 0.001 for interaction). Furthermore, unfit normal-weight individuals had 30% lower risk of death from any cause (HR, 0.70; 95% CI, 0.53–0.92) than did fit obese individuals. Conclusions: Low aerobic fitness in late adolescence is associated with an increased risk of early death. Furthermore, the risk of early death was higher in fit obese individuals than in unfit normal-weight individuals. Key words: Fitness, obesity, death PMID: 26686843