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Visceral fat and cognitive decline

Visceral fat and cognitive decline

Kuo, Vksceral, Jones, RN, Milberg, High-quality ingredients, Tennstedt, Visceral fat and cognitive decline, Talbot, Cognotive, Morris, JN, et al. The use, distribution Viscerak reproduction in other decoine is permitted, provided the original author s and the copyright Visceral fat and cognitive decline s are credited and that the original publication in this journal Guarana for athletic performance cited, in accordance with accepted academic practice. He is also a servant leader who has dedicated his adult life to serving multiple communities through Rotary International and other notable causes. Expert Rev Proteomics. Following these findings, the NTU LKCMedicine scientists are now looking at how excess visceral fat across Asian ethnicities contributes to traits related to one's metabolism, such as insulin resistance, that are a result of a combination of factors, including genes, lifestyle, and the environment. These affected brain cortices correspond to the sites that show atrophy in the early stage of mild cognitive impairment McDonald et al.

Visceral fat and cognitive decline -

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Recent Blog Articles. Flowers, chocolates, organ donation — are you in? Cognition and regional adiposity in studies included in the systematic review: the table is ordered by fat depots from the newest to the oldest publication.

Twelve articles reported on the association between VAT and SAT and different brain changes 41 , 52 — 54 , 59 , 62 , 73 — The association between different brain compartments and regional fat depots can be found in Table 4. All the papers have used structural brain measures via brain MRI 41 , 52 — 54 , 59 , 62 , 73 — 78 , while only one study used also functional measures via functional MRI fMRI to assess degree of connectivity eigenvector centrality, EC This study showed that high VAT was associated with lower cerebellar structure gray matter density as well as lower degree of connectivity of the cerebellum with other brain regions in younger subjects; no associations were found in older individuals These results suggest that the relationship of increased VAT with reduced gray matter density and reduced connectivity in the cerebellum, which is involved in cognitive function, are age-dependent Structural measures have shown that higher VAT and SAT were associated with smaller total brain volume Moreover, elevated VAT was correlated with cortical thinning especially with lower hippocampal volume 54 but not with gray matter and white matter volumes 54 , Similarly, higher VAT was linked to smaller temporal lobe and the volume of several other sub-compartments of the brain Six studies 52 , 54 , 59 , 62 , 77 , 78 have assessed the associations between VAT and White Matter Hyperintensities WMH which has been recognized as a risk factor for cognitive impairment and dementia Among them, two have found a significant positive association, namely, associations of high VAT with greater volumes of WMH 62 , Similar associations were observed for higher VAT and greater vascular brain injury 52 , or lower brain connectivity fractional anisotropy [FA] , a measure of white matter integrity Higher VAT was associated with higher damage in a brain network implicated in cognitive decline 53 , suggesting that VAT is associated with accelerated brain aging In contrast to this relatively broad evidence linking VAT with lower brain volumes and pathologies, two studies found associations of higher VAT with thicker cortex in the posterior cingulate gyrus 75 , and with greater left cuneus volume Table 4.

Brain changes and regional adiposity in studies included in the systematic review. The relationship of VAT with dementia pathology has been examined in two studies 55 , Individuals with higher VAT metabolism, a marker of higher VAT dysfunction assessed through PET-CT, compared with individuals with low VAT metabolism, exhibited significantly higher cerebral Aβ burden Those findings suggest that VAT dysfunction could contribute to AD development.

In a second study, using brain 18 F-fluorodeoxyglucose FDG PET as a neurodegenerative biomarker for AD, computing the PALZ score a global index of AD-related hypometabolism, no significant correlation between VAT and the risk of AD pathology was found In the present study, we have identified seven studies examining the relationships of cognition and fatty liver or NAFLD 60 , 67 — In the past literature, we have identified three previous systematic review and meta-analyses 87 — 89 of observational studies, providing a comprehensive evaluation of the relationship between NAFLD and the risk of dementia or cognitive impairment.

However, the studies included in our review include only the ones that have assessed liver fat and NAFLD with imaging technique. In most of the studies, higher severity of NAFLD was associated with increased risk of cognitive impairment 60 , 67 — 71 ; in some cases, cardiovascular disease attenuated this relationship Strong associations between NAFLD and worsening of cognition in patients meeting the criteria for vascular dementia was found Five studies have reported the association between structural brain changes and fatty liver 41 , 67 , 79 , 80 , Among them only one used a noninvasive functional measure, pseudo-Continuous Arterial Spin Labeling pCASL measuring cerebral blood flow CBF The results are reported in Table 4.

Hepatic fat depots were significantly associated with smaller total cerebral brain volume 79 as well as smaller cingulate gyri and hippocampal volumes NAFLD was associated with a smaller total cerebral volume even after adjustment for VAT, pointing to a relationship between NAFLD and brain aging In this study, no significant associations were observed between NAFLD and hippocampal and WMH volumes, nor with covert brain infarcts small ischemic cerebral lesions here assessed by abnormal signal intensity Conversely, NAFLD was significantly associated with the presence of WMHs, even after adjusting for cardiometabolic risk factors 82 in another study.

In NAFLD patients with lower cognitive score, the volumes of brain gray and white matter were significantly reduced compared to NAFLD patients with higher cognitive score However, no comparison between the NAFLD patients and the control group without NAFLD volumes was done Finally, higher liver fat shown by lower liver attenuation on abdominal CT was associated with decreased total-CBF and gray matter-CBF and this association remained after adjustment for cardiovascular risk factors One study assessed NAFLD and AD-related neuropathology via PET-CT Prevalent NAFLD was not associated with Aβ or tau PET, the main two pathologies characterizing AD We found only one study investigating associations of NAFLD and dementia risk Moderate-to-severe NAFLD was found to be associated with dementia and AD risk, especially with vascular dementia Moreover, participants with vascular dementia and NAFLD had worse neuropsychological outcomes than participants without NAFLD Higher epicardial adipose tissue EAT has been associated with poorer cognitive functioning in two studies 64 , Pericardial adipose tissue PAT has been associated with lower hippocampal white matter but not hippocampal gray matter One study examined associations of pancreatic fat with regional brain volume.

Albeit in all analyses higher pancreatic fat was associated with lower hippocampal, cingulate gyri and temporal lobe volumes, none of these associations reached statistical significance To our knowledge, no studies examining relationships of kidney fat depots with cognition or brain changes have been done.

A few studies have explored inflammatory markers as possible factors linking fat depots, brain changes and cognition. Cannavale et al. Indeed, plasma C-reactive protein CRP and Interleukin-6 IL-6 concentrations mediated the relationship between higher VAT and lower attentional inhibitory control, suggesting that systemic inflammation could play a role in the deleterious effects of VAT on cognition Higher levels of SAT and VAT were associated with worsening cognitive function in men even after controlling for metabolic disorders, adipocytokines adiponectin, IL-6, tumor necrosis factor α [TNF-α], and plasminogen activator inhibitor-1[PAI-1] , and sex hormone levels estradiol and testosterone Conversely, there was no association between adiposity and cognitive change in women However, in another study where higher VAT was associated with lower cognitive functioning, estradiol level attenuated the negative consequences of VAT on cognition in women Similar results were found for moderate-to- severe NAFLD, which was associated with increased serum levels of multiple cytokines, i.

Higher VAT and hepatic fat remained significantly associated with WMH 62 , 82 , decreased total-CBF and GM-CBF 79 and smaller brain volumes 41 , 80 after adjustment for cardiovascular risk factors. Similarly, VAT was found to be significantly associated with reduced cognitive scores, after adjustment for cardiovascular risk factors, and for MRI-detected vascular brain injury In several studies 60 , 68 , 69 , 71 the association between NAFLD and cognitive impairment varied across the cognitive tests when adjusting for cardiovascular risk factors and diseases.

Indeed, the NAFLD-cognitive function association was either attenuated 60 , 71 or disappeared 68 , 69 , 71 when adjusting for these factors. Based on the current available literature, the findings indicate that different regional fat depots are likely associated with increased risk of cognitive impairment and dementia 36 , 41 , 52 — Specifically, VAT 52 , 54 , 57 , 61 , 63 , EAT 64 , 65 and liver fat through NAFLD 60 , 67 — 71 , 79 were associated with cognitive impairment.

Moreover, regional fat was linked to different brain changes 41 , 52 — 63 , 73 — 78 , with a relatively consistent association of different fat depots with cortical volume 41 , 54 , 59 , 73 , 76 , 78 — 80 , and with white matter disease 62 , 74 , Both lower cortical volume and white matter disease have been linked to cognitive decline, AD and dementia 90 , Interestingly, higher VAT, but not the other regional fat depots, was associated with amyloid β, a core neuropathological feature of AD 55 , This could be explained by the excessive secretion of leptin by high VAT, which in turn could inhibit the transport of Amyloid-β precursor protein and promote the fabrication of amyloid β Finally, one of the studies has shown that greater severity of NAFLD was associated with higher risk of dementia 66 , while among women higher SAT and thigh fat with lower likelihood of dementia Overall, results from this systematic review suggest that different regional fat depots may lead to different neurobiological alterations and ultimately to different cognitive-related outcomes and dementia.

Exploring potential mechanisms underlying the inter-relationships of regional adiposity- brain changes - cognition could lead to targeted and personalized treatments for cognitive-related outcomes. The findings of associations of different regional fat depots with lower cognitive scores are concordant with previous research indicating that adiposity assessed by BMI is associated with cognitive impairment and risk of dementia Central adiposity is a core feature of the metabolic syndrome 94 and has been associated with cognitive decline, dementia and neuropathology 94 , 95 , especially in old age Yet, the metabolic syndrome has been associated with NAFLD and pancreatic fat independently of central obesity and insulin resistance 34 , Also, accumulation of VAT was found to be the best predictor for metabolic syndrome in women while it was a poor predictor for men compared to SAT One possibility is that the impaired vascular function resulting from the different conditions of the metabolic syndrome could lead to brain changes that could then lead to cognitive impairment Another core feature of the metabolic syndrome is insulin resistance which also has been linked to cognitive decline and dementia VAT rather than SAT is more strongly associated with insulin resistance and NAFLD has also been closely linked to insulin resistance , showing that different fat compartments may be associated with differential metabolic risk.

Although both VAT and fatty liver have been shown to be related to impaired cognition and both are determinants of insulin resistance, their impact is different due to the different roles played by adipokines and hepatokines, respectively Those results imply the importance of assessing regional adiposity rather than central adiposity to understand the specific contribution of excess adiposity to cognition.

Therefore, further studies should be done on regional fat depots to better understand the mechanism underlying the association between adiposity, metabolic syndrome, cognition, and brain changes. Investigation of regional fat in metabolically healthy obese population may shed light into these discrepancies 27 , In the present review, we have gathered data showing that regional fat depots are associated with deleterious brain changes.

Regional fat depots including VAT, SAT and fatty liver were associated with smaller cerebral volumes 78 — Fatty liver and VAT but not SAT were significantly associated with smaller hippocampal volume 41 , 54 , 59 which is one of the first regions affected by AD Those results are concordant with recent evidence from our group showing associations of higher BMI with thinning of the middle temporal gyrus Overall, the present review indicates that different fat depots can affect different parts of the brain suggesting a potential role of different regional fat depots in brain atrophy and pathology, targeting those fats could then prevent deleterious impact on the brain.

Brain small vessel disease which includes higher WMHs, and lacunar infarcts may lead to cognitive impairment and dementia In the present review, different regional fat depots have also been associated with higher WMHs 62 , 77 , In addition to its associations with cognitive impairment and AD 86 , WMH is prevalent in individuals with insulin resistance, metabolic syndrome and T2D , all conditions accompanied by high adiposity Furthermore, adiposity is associated with chronic low-grade systemic inflammation, which increases proinflammatory cytokine secretion Pro-inflammatory cytokines have been linked to greater volumes of WMHs which in turn are linked to cognitive impairment.

As suggested by one of the studies reviewed, mechanisms by which VAT exerts a negative influence on cognitive function includes systemic inflammation Therefore, disentangling factors secreted by different fat depots affecting systemic inflammation may shed light into their role in cognitive decline and dementia.

Indeed, different fat depots release different secreted factors, some of which cross readily the blood brain barrier BBB and may cause damage, ultimately leading to cognitive decline 56 , 63 , For example, pro-inflammatory factors such as leptin, IL-6, TNF-α , which are secreted by adipocytes can cross the BBB and lead to neuroinflammation, which plays a role in cognitive impairment and AD Conversely, anti-inflammatory adipocytokines such as Adiponectin , Interleukin 10 IL , , and Apelin , are associated with less adiposity and are related to cognition and AD.

Neuroinflammation likely causes synaptic remodeling and neurodegeneration resulting in disruption of cognitive functioning possibly resulting from damage brain regions subserving cognition such as the hippocampus Targeting these factors could be an efficacious way to prevent or delay later cognitive decline and AD.

Other factors, such as proteins are secreted from different fat depots, and may explain the role of peripheral fats in the brain. For example, Amylin, a hormone synthesized and co-secreted with insulin by pancreatic β-cells, is elevated in obesity and may share similar pathophysiology with Amyloid-β, characteristic of AD neuropathology Also, Glucagon-like peptide-1 GLP-1 , a gut released hormone, which can protect pancreatic β-cells from apoptosis and induce insulin secretion, is attracting attention as a possible link between metabolic syndrome and brain impairment , Additional factors, secreted by hepatocytes, the most common cells in the liver, are found to be related to cognition such as plasminogen activator inhibitor 1 PAI-1 , and fetuin , Indeed, in the presence of elevated fatty acids , circulating fetuin-A can induce insulin resistance and inflammatory signaling which may cause damage to the brain leading to cognitive impairment , Therefore, identifying novel factors altered due to excess fat in different abdominal regions and associated with cerebrovascular pathology, neuropathology, and impaired cognitive functioning is crucial for developing fat-specific interventions.

Potential mechanisms underlying the inter-relationships of adiposity- brain changes — cognition and therapeutic modalities, is presented in Figure 2. Figure 2. Potential mechanisms underlying the adiposity- brain changes - cognition inter-relationships and therapeutic modalities. A Adiposity is commonly used to describe excess body fat or obesity.

Different fat depots can be found in the body independently of central obesity. Subcutaneous adiposity refers to the accumulation of fat underneath the skin, in the adipose tissue layer. Visceral adiposity refers to the accumulation of fat in the abdominal cavity, specifically around the organs such as the liver, pancreas, and intestines.

Ectopic fat refers to the accumulation of fat in areas where it is not normally found, such as the liver, muscle, and pancreas. Both types of fat are associated with increased risk of metabolic disorders such as insulin resistance, type 2 diabetes, and cardiovascular disease.

Understanding the association of adiposity, brain changes and cognitive abilities would provide key insights into the mechanisms by which adiposity impacts cognitive health and to possible treatments.

Lifestyle interventions, such as specific diets and physical activity may diminish accumulation of fat depots. B Adiposity is associated with chronic low-grade systemic inflammation. Different fat depots can release different proinflammatory cytokines, hormones and enzymes some of which cross readily the blood brain barrier BBB and may cause damage ultimately leading to cognitive decline.

For example, pro-inflammatory factors such as leptin, secreted by adipocytes, can cross the BBB and lead to neuroinflammation, which plays a major role in cognitive impairment and AD. Conversely, anti-inflammatory adipocytokines such as adiponectin, are associated with less adiposity and are related to better cognitive functioning and lower AD risk.

Treatment targeting enhancing protective factors released from adipocytes and diminishing inflammatory factors secreted from fats could be an efficacious way to prevent brain damage and ultimately support healthy cognition.

C Initial evidence suggests that different fat depots affect a plethora of brain pathologies including cortical volume, the cerebral vasculature, primarily white matter hyperintensities, and neuroinflammation. These pathologies contribute to cognitive impairment and as treatments addressing the neurobiology of cognition evolve, cognitive health may be maintained in spite of accumulation of fat deposits and their respective secreted factors.

Finally, sex differences should be taken into consideration as they may also contribute to the fat-brain-cognition axis. Women have overall more fat mass than men. Those differences in regional fat depots may lead to different consequences on cognition.

Higher levels of VAT were associated with worsening cognitive function in men after adjustment for metabolic disorders, adipocytokines, and sex hormone levels Conversely, there was no association between adiposity and cognitive changes in women Furthermore, while VAT exacerbates the association between aging and poorer brain network covariance in both men and women, estradiol reduces the negative association in women These findings highlight the need to account for sex differences in the investigation of relationships of regional adiposity with brain and cognition.

This review provides evidence for the association of different regional fat depots, cognition, and brain changes. However, this study had several limitations. First, the initial intention of our group was to conduct a meta-analysis on regional adiposity and cognition.

But, due to the limited number of studies and the variability in methodologies the meta-analysis could not be conclusive as it carried high heterogeneity. The studies have different designs, sample sizes, and cognitive tests as well as different ways of assessing regional fat depots to quantify adiposity, adding complexity to the interpretation of results.

Indeed, quantification of the degree of adipose tissues is different in each of the studies, as some quantify by fat volume and others by surface or percentage of fat in the different regions, making it difficult to directly compare the studies.

Further prospective studies are needed to establish the relationship between regional fat depots with brain changes and cognition with similar methodologies.

Only three studies in this review had longitudinal cognitive decline 56 , 60 , Considering that the duration of exposure to adiposity may affect the onset and the severity of cognitive impairment, the lack of longitudinal data for regional adiposity is a significant limitation in the field.

All studies were observational studies and not clinical trials therefore no causation can be inferred. In some studies, there were no associations between regional fat and cognition. However, many of these studies included relatively young individuals e. In such young ages the range of cognitive functioning is relatively narrow, possibly contributing to the lack of associations.

It is important to note that the literature on fat and cognition may suffer from selection bias since older adults with cognitive impairment are less likely to participate in research.

Finally, this review focuses specifically on body fat composition, rather than on general body composition, and does not discuss muscle mass and function which are strongly associated with cognitive decline and dementia risk 18 — This review of 33 studies indicates that different regional fat depots may affect cognition and different regions of the brain.

Regional fat depots, especially VAT and hepatic fat, have been associated with cognitive decline, cortical thinning and WMHs. Regional fat depots, rather than central obesity, may better explicate the association between adiposity and brain and may open horizons for new personalized fat-reducing treatments for prevention of cognitive decline.

EB, SG, and MB conceived the presented idea and have made a substantial contribution to the concept and design of the manuscript. EB carried out the literature search from electronic databases, drafted the manuscript, and provided the tables.

SG participated with EB to the full-text screening of the articles from the literature search, read and approved the manuscript. MB revised critically the manuscript and approved the version to be published. All authors contributed to the article and approved the submitted version.

This work was funded by National Institutes of Health grants RAG, AG, and AG to MB. The authors thank Marina Nissim Milan Italy Funding. The authors are also grateful for the generosity of the LeRoy Schecter Foundation.

Thanks to Marina Nissim for her generosity. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Panuganti, KK, Nguyen, M, Kshirsagar, RK, and Doerr, C. Obesity nursing In:. StatPearls : StatPearls Publishing Google Scholar. Luchsinger, JA, and Gustafson, DR. Curr Opin Clin Nutr Metab Care. doi: PubMed Abstract CrossRef Full Text Google Scholar. Gustafson, DR, and Luchsinger, JA.

Alzheimers Res Ther. Ravona-Springer, R, Schnaider-Beeri, M, and Goldbourt, U. Body weight variability in midlife and risk for dementia in old age. Pedditizi, E, Peters, R, and Beckett, N. Age Ageing. Fitzpatrick, S, Gilbert, S, and Serpell, L.

Systematic review: are overweight and obese individuals impaired on behavioural tasks of executive functioning? Neuropsychol Rev. Coppin, G, Nolan-Poupart, S, Jones-Gotman, M, and Small, DM.

Working memory and reward association learning impairments in obesity. Cournot, MCMJ, Marquie, JC, Ansiau, D, Martinaud, C, Fonds, H, Ferrieres, J, et al. Relation between body mass index and cognitive function in healthy middle-aged men and women.

Beeri, MS, Tirosh, A, Lin, HM, Golan, S, Boccara, E, Sano, M, et al. Stability in BMI over time is associated with a better cognitive trajectory in older adults.

Alzheimers Dement. Gustafson, D, Rothenberg, E, Blennow, K, Steen, B, and Skoog, I. An year follow-up of overweight and risk of Alzheimer disease. Arch Intern Med. West, RK, Ravona-Springer, R, Heymann, A, Schmeidler, J, Leroith, D, Koifman, K, et al.

Waist circumference is correlated with poorer cognition in elderly type 2 diabetes women. Obesity, diabetes and cognitive deficit: the Framingham heart study. Neurobiol Aging. Kuo, HK, Jones, RN, Milberg, WP, Tennstedt, S, Talbot, L, Morris, JN, et al.

Cognitive function in normal-weight, overweight, and obese older adults: an analysis of the advanced cognitive training for independent and vital elderly cohort. J Am Geriatr Soc. Wotton, CJ, and Goldacre, MJ.

In one study, overweight adults were found to have lower scores on tests of cognitive function than adults of normal weight. The difference in scores was most pronounced in tests of executive function, which includes tasks such as planning, organizing, and multitasking.

Another study found that obese adults were more likely to experience declines in cognitive function over time than adults of normal weight. This study also found that the longer someone was obese, the greater their risk of cognitive decline.

These studies suggest that obesity may have a negative impact on brain health and cognitive function. This is yet another reason to take steps to maintain a healthy weight. Making even small changes in these areas can have a big impact on your health.

So if you are concerned about belly fat and brain function, make a plan to start reducing abdominal obesity today. Recently, there have been a number of new non-surgical options for reducing belly fat.

These include:. These procedures are typically less invasive than surgery and carry a lower risk of complications. They can be an effective option for people who are not candidates for surgery or who do not want to undergo a major procedure.

These procedures are typically done by a qualified physician. If you are considering any of these options, be sure to consult with a doctor to see if they are right for you. There are a number of surgical interventions that can be used to reduce obesity.

The most common is gastric bypass surgery, which involves making changes to the digestive system to limit the amount of food that can be consumed. Other types of surgery include gastric banding, which involves placing a band around the stomach to limit its size, and gastric sleeve surgery, which involves removing a portion of the stomach.

Surgical interventions for obesity are typically only recommended for people who are severely obese and have not been able to lose weight through other means. Surgery is a major procedure and carries with it a number of risk factors, so it should not be undertaken lightly.

There are a number of risks associated with surgical interventions for obesity, including:. Before undergoing any type of surgery, it is important to speak with your doctor about the risk factors and benefits.

Surgery should only be considered as a last resort after all other options have been exhausted. If you are considering surgery for obesity, make sure to consult with a qualified surgeon who has experience performing the procedure you are interested in.

At APEX Brain Centers , we administer cold laser treatment as a modality to improve brain function by reducing belly fat. This procedure is called laser lipolysis and it involves using a laser to break down body fat. This is a minimally invasive procedure that carries a lower risk of complications than surgery.

We use Zerona Z6 a non-invasive cold laser for fat loss because it is the only treatment FDA Market Cleared for overall body circumference reduction and has the greatest results for combined circumference reduction in the industry.

If you are interested in laser treatment for reducing belly fat, please contact us to schedule a consultation. We will be happy to discuss the procedure with you and answer any questions.

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Background: Viwceral emerging Ingredients for youthful skin suggesting that eecline fat may play a anr role in obesity-induced neurodegeneration, little qnd exists on the association between Protein intake and gut health fat and brain cortical thickness in Visceral fat and cognitive decline elderly. Purpose: We aimed to examine the association between abdominal fat and brain cortical thickness in a Korean elderly population. Areas of visceral fat and subcutaneous fat cm 2 were estimated from computed tomography scans. Regional cortical thicknesses mm were obtained by analyzing brain magnetic resonance images. Given the inverted U-shaped relationship between visceral fat area and global cortical thickness examined using a generalized additive modelvisceral fat area was categorized into quintiles, with the middle quintile being the reference group. A generalized linear model was built to explore brain regions associated with visceral fat.

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8 Ways to Lose Visceral Fat and Shrink Your Belly (Skinny Fat Solution) Body mass Viscwral BMI is the most Viscefal measure of decoine adiposity, but inconsistent results fognitive found since it is a global measurement. Fta does not represent regional fat distribution which Wheezing between sexes, race, and Vicseral. Fat-specific Viscsral therapies Type diabetes mental health lead Visceral fat and cognitive decline personalized improvement of cognition. The goal of this systematic review is to explore whether regional fat depots, rather than central obesity, should be used to understand the mechanism underlying the association between adiposity and brain. We included only studies that have assessed regional adiposity using imaging technics and excluded studies that were review articles, abstract only or letters to editor. Studies on children and adolescents, animal studies, and studies of patients with gastrointestinal diseases were excluded. PubMed, PsychInfo and web of science were used as electronic databases for literature search until November

Visceral fat and cognitive decline -

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Featured NBC News Now Nightly Films Stay Tuned Special Features Newsletters Podcasts Listen Now. More From NBC CNBC NBC. Panuganti, KK, Nguyen, M, Kshirsagar, RK, and Doerr, C. Obesity nursing In:. StatPearls : StatPearls Publishing Google Scholar.

Luchsinger, JA, and Gustafson, DR. Curr Opin Clin Nutr Metab Care. doi: PubMed Abstract CrossRef Full Text Google Scholar. Gustafson, DR, and Luchsinger, JA. Alzheimers Res Ther. Ravona-Springer, R, Schnaider-Beeri, M, and Goldbourt, U. Body weight variability in midlife and risk for dementia in old age.

Pedditizi, E, Peters, R, and Beckett, N. Age Ageing. Fitzpatrick, S, Gilbert, S, and Serpell, L. Systematic review: are overweight and obese individuals impaired on behavioural tasks of executive functioning?

Neuropsychol Rev. Coppin, G, Nolan-Poupart, S, Jones-Gotman, M, and Small, DM. Working memory and reward association learning impairments in obesity. Cournot, MCMJ, Marquie, JC, Ansiau, D, Martinaud, C, Fonds, H, Ferrieres, J, et al.

Relation between body mass index and cognitive function in healthy middle-aged men and women. Beeri, MS, Tirosh, A, Lin, HM, Golan, S, Boccara, E, Sano, M, et al. Stability in BMI over time is associated with a better cognitive trajectory in older adults. Alzheimers Dement. Gustafson, D, Rothenberg, E, Blennow, K, Steen, B, and Skoog, I.

An year follow-up of overweight and risk of Alzheimer disease. Arch Intern Med. West, RK, Ravona-Springer, R, Heymann, A, Schmeidler, J, Leroith, D, Koifman, K, et al. Waist circumference is correlated with poorer cognition in elderly type 2 diabetes women.

Obesity, diabetes and cognitive deficit: the Framingham heart study. Neurobiol Aging. Kuo, HK, Jones, RN, Milberg, WP, Tennstedt, S, Talbot, L, Morris, JN, et al. Cognitive function in normal-weight, overweight, and obese older adults: an analysis of the advanced cognitive training for independent and vital elderly cohort.

J Am Geriatr Soc. Wotton, CJ, and Goldacre, MJ. Age at obesity and association with subsequent dementia: record linkage study. Postgrad Med J. Cova, I, Clerici, F, Rossi, A, Cucumo, V, Ghiretti, R, Maggiore, L, et al. PLoS One. Johnson, DK, Wilkins, CH, and Morris, JC. Accelerated weight loss may precede diagnosis in Alzheimer disease.

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Oudbier, SJ, Goh, J, Looijaard, SMLM, Reijnierse, EM, Meskers, CGM, and Maier, AB. Pathophysiological mechanisms explaining the association between low skeletal muscle mass and cognitive function.

Yang, Y, Xiao, M, Leng, L, Jiang, S, Feng, L, Pan, G, et al. A systematic review and meta-analysis of the prevalence and correlation of mild cognitive impairment in sarcopenia. J Cachexia Sarcopenia Muscle.

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Association of non-alcoholic fatty liver disease with metabolic syndrome independently of central obesity and insulin resistance. Sci Rep. Kivipelto, M, Ngandu, T, Fratiglioni, L, Viitanen, M, Kåreholt, I, Winblad, B, et al. Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease.

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Adapted from a press release by Providence Southern California. The World Health Organization says we all need to boost mental health during these stressful times. Mental health has a critical effect on immune functioning.

But in a world where routines are limited, and fear and uncertainty abound, how do we cope? As these are not curable at this time, clinical trials and research are necessary to develop new and more effective ways of halting and even reversing cognitive decline in these diseases.

Find out more in this informative video. To give you the best possible experience, this site uses cookies and by continuing to use the site you agree that we can save them on your device. Skip to content. Home Blog Study finds abdominal body fat linked to brain shrinkage, possible dementia.

by Guest Author. The results from this large data set were contextualized down to individual examples when comparing two MRI scans in two participants from the study with the same age and sex: Examples of Higher Body Fat and Brain Volume Loss.

This figure shows two examples of coronal T1 weighted whole body MRI in two year-old women, one with a high level of both visceral fat and subcutaneous fat red border and the other with a normal amount of these types of fat blue border. There is corresponding increased brain atrophy in the person with high amounts of visceral and subcutaneous fat as evidenced by enlarged ventricles and widened sulci on the T1 brain MRI images.

Karen Miller Strange though it may seem, we can tone our brain tissue the same way we tone our muscles.

New research shows little risk Visceral fat and cognitive decline infection from prostate biopsies. Discrimination at Type diabetes mental health dat linked to high blood pressure. Visceraal fingers and declinf Poor circulation or Viscreal phenomenon? Previous research has linked excess body fat with a higher risk of cognitive decline. In the past, most studies have gauged body fat based on body mass index BMI. However, waist size may be a better way to predict possible cognitive impairment among older adults, according to a study in the Sept. Visceral fat and cognitive decline

Author: Katilar

5 thoughts on “Visceral fat and cognitive decline

  1. Ich meine, dass Sie nicht recht sind. Geben Sie wir werden es besprechen. Schreiben Sie mir in PM, wir werden reden.

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