scholarly journals What the future held: Childhood psychosocial adversity is associated with health deterioration through adulthood in a cohort of British women

2014 ◽  
Author(s):  
Daniel Nettle
Keyword(s):  
Adult Life ◽  
Reproductive Period ◽  
Dependent Manner ◽  
Inflammatory Biomarker ◽  
Individual Level ◽  
Physical Decline ◽  
Reactive Protein ◽  
Simple Index ◽  
Age Related ◽  
Psychosocial Adversity

Childhood psychosocial adversity is associated with accelerated onset of reproductive effort in women. Adaptive explanations for this phenomenon are built on the assumption that greater childhood psychosocial adversity is statistically associated with having a shorter period of healthy adult life during which reproduction will be possible. However, this critical assumption is never actually tested using individual-level longitudinal data. In this study, I revisit a large, longitudinally-studied cohort of British women. In an earlier paper, we showed that a simple index of psychosocial adversity in the first seven years of life predicted age at first pregnancy in a dose-dependent manner. Here, I show that the same index of adversity also predicts accelerated deterioration of health across the potentially reproductive period, and increased levels of the inflammatory biomarker c-reactive protein at age 44-46. These associations are robust to controlling for adult socioeconomic position, and do not appear to be solely a consequence of accelerated reproductive schedule. I argue that childhood psychosocial adversity may cause latent somatic damage that will, in adulthood, accelerate age-related physical decline. This provides a compelling adaptive rationale for the accelerated reproductive schedules observed in women who experience childhood psychosocial adversity.

scholarly journals What the future held: Childhood psychosocial adversity is associated with health deterioration through adulthood in a cohort of British women

2014 ◽  
Author(s):  
Daniel Nettle
Keyword(s):  
Adult Life ◽  
Reproductive Period ◽  
Dependent Manner ◽  
Inflammatory Biomarker ◽  
Individual Level ◽  
Physical Decline ◽  
Reactive Protein ◽  
Simple Index ◽  
Age Related ◽  
Psychosocial Adversity

Childhood psychosocial adversity is associated with accelerated onset of reproductive effort in women. Adaptive explanations for this phenomenon are built on the assumption that greater childhood psychosocial adversity is statistically associated with having a shorter period of healthy adult life during which reproduction will be possible. However, this critical assumption is never actually tested using individual-level longitudinal data. In this study, I revisit a large, longitudinally-studied cohort of British women. In an earlier paper, we showed that a simple index of psychosocial adversity in the first seven years of life predicted age at first pregnancy in a dose-dependent manner. Here, I show that the same index of adversity also predicts accelerated deterioration of health across the potentially reproductive period, and increased levels of the inflammatory biomarker c-reactive protein at age 44-46. These associations are robust to controlling for adult socioeconomic position, and do not appear to be solely a consequence of accelerated reproductive schedule. I argue that childhood psychosocial adversity may cause latent somatic damage that will, in adulthood, accelerate age-related physical decline. This provides a compelling adaptive rationale for the accelerated reproductive schedules observed in women who experience childhood psychosocial adversity.

scholarly journals What the future held: Childhood psychosocial adversity is associated with health deterioration through adulthood in a cohort of British women

2014 ◽  
Author(s):  
Daniel Nettle
Keyword(s):  
Adult Life ◽  
Reproductive Period ◽  
Dependent Manner ◽  
Inflammatory Biomarker ◽  
Individual Level ◽  
Physical Decline ◽  
Reactive Protein ◽  
Simple Index ◽  
Age Related ◽  
Psychosocial Adversity

Childhood psychosocial adversity is associated with accelerated onset of reproductive effort in women. Adaptive explanations for this phenomenon are built on the assumption that greater childhood psychosocial adversity is statistically associated with having a shorter period of healthy adult life during which reproduction will be possible. However, this critical assumption is never actually tested using individual-level longitudinal data. In this study, we revisit a large, longitudinally studied cohort of British women. In an earlier study, we showed that a simple index of psychosocial adversity in the first seven years of life predicted age at first pregnancy in a dose-dependent manner. Here, we show that the same index of adversity predicts accelerated deterioration of health across the potentially reproductive period, and increased levels of the inflammatory biomarker c-reactive protein at age 44. These associations are robust to controlling for adult socioeconomic position, and do not appear to be a consequence of accelerated reproductive strategy, smoking, or BMI. We argue that childhood psychosocial adversity may lead to the lasting embedding of somatic damage that accelerates age-related physical decline. This provides a compelling adaptive rationale for the accelerated reproductive schedules observed in women who experience childhood psychosocial adversity.

scholarly journals Fear and C-reactive protein cosynergize annual pulse increases in healthy adults

2014 ◽  
Vol 112 (5) ◽  
pp. E467-E471 ◽  
Author(s):  
Shani Shenhar-Tsarfaty ◽  
Nadav Yayon ◽  
Nir Waiskopf ◽  
Itzhak Shapira ◽  
Sharon Toker ◽  
...  
Keyword(s):  
Health Risks ◽  
Hierarchical Regression ◽  
C Reactive Protein ◽  
Partial Least Squares Analysis ◽  
Inflammatory Biomarker ◽  
Reactive Protein ◽  
Exposed Population ◽  
Age Related ◽  
All Cause Mortality

Recent international terror outbreaks notably involve long-term mental health risks to the exposed population, but whether physical health risks are also anticipated has remained unknown. Here, we report fear of terror-induced annual increases in resting heart rate (pulse), a notable risk factor of all-cause mortality. Partial least squares analysis based on 325 measured parameters successfully predicted annual pulse increases, inverse to the expected age-related pulse decline, in approximately 4.1% of a cohort of 17,380 apparently healthy active Israeli adults. Nonbiased hierarchical regression analysis among 27 of those parameters identified pertinent fear of terror combined with the inflammatory biomarker C-reactive protein as prominent coregulators of the observed annual pulse increases. In comparison, basal pulse primarily depended on general physiological parameters and reduced cholinergic control over anxiety and inflammation, together indicating that consistent exposure to terror threats ignites fear-induced exacerbation of preexisting neuro-immune risks of all-cause mortality.

Homocysteine and C-Reactive Protein Levels Are Associated With Frailty in Older Spaniards: The Toledo Study for Healthy Aging

2019 ◽  
Vol 75 (8) ◽  
pp. 1488-1494 ◽  
Author(s):  
Nuria Álvarez-Sánchez ◽  
Ana Isabel Álvarez-Ríos ◽  
Juan Miguel Guerrero ◽  
Francisco José García-García ◽  
Leocadio Rodríguez-Mañas ◽  
...  
Keyword(s):  
Physical Activity ◽  
Healthy Aging ◽  
High Sensitivity ◽  
Inflammation Markers ◽  
C Reactive Protein ◽  
Physical Decline ◽  
Protein Levels ◽  
Reactive Protein ◽  
Risk Of Death ◽  
Age Related

Abstract High-sensitivity C-reactive protein (hsCRP) and homocysteine (Hcy) are inflammation markers but are also related to cardiovascular diseases, disability, or higher risk of death. Although inflammation is considered to be associated with frailty, data regarding the association between hsCRP or Hcy and frailty are controversial or scarce, especially with respect to their association with prefrailty. Thus, our objective was to study the association of hsCRP and Hcy with prefrailty and frailty in 1,211 Spanish men and women aged 65–98 years from the Toledo Study for Healthy Aging (TSHA) cohort, classified according to Fried’s criteria. Hcy was independently associated with frailty (odds ratio [OR] = 1.06; 95% confidence interval [CI]: 1.01–1.12), whereas hsCRP was independently associated with both prefrailty (OR = 1.03; 95% CI: 1.01–1.06) and frailty (OR = 1.07; 95% CI: 1.02–1.12). Furthermore, both markers were positively correlated with the number of Fried’s criteria that were met and were independently associated with the criteria of exhaustion (Hcy: OR = 1.03, 95% CI: 1.00–1.06), weakness (hsCRP: OR = 1.03, 95% CI: 1.01–1.05), and low physical activity (hsCRP: OR = 1.04, 95% CI: 1.02–1.06). Thus, our results highlight the importance of inflammation in age-related physical decline and, in particular, its association with fatigue, low strength, and decreased physical activity.

scholarly journals Age-Related Neuroprotection by Dietary Restriction Requires OXR1-Mediated Retromer Function

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 562-562
Author(s):  
Sudipta Bar ◽  
George Brownridge ◽  
Jennifer Beck ◽  
Rachel Brem ◽  
Hugo Bellen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dietary Restriction ◽  
Disease Diagnosis ◽  
Lifespan Extension ◽  
Dependent Manner ◽  
Physical Decline ◽  
Protein Levels ◽  
Age Related ◽  
Multiple Species

Abstract Dietary restriction (DR) is the most robust method to delay aging and the onset of neurogenerative disorders across multiple species, though the mechanisms behind this phenomenon remain unknown. To elucidate how DR mediates lifespan extension, we analyzed natural genetic variants that associate with increased longevity under DR conditions in the Drosophila Genetic Reference Panel. We found that neuronal expression of the fly homolog of human Oxidation Resistance 1 (OXR1) is necessary for DR-mediated lifespan extension. Neuronal knockdown of OXR1 also accelerated visual decline but not physical decline, arguing for a specific role of OXR1 in neuronal signaling. Further, we find that overexpression of the TLDc domain from human OXR1 is sufficient for lifespan extension in a diet-dependent manner. Studies from the Accelerating Medicines Partnership - Alzheimer's Disease network show that patients with reduced OXR1 protein levels are more prone to Alzheimer's disease diagnosis, and we find that overexpression of human OXR1 is protective in animal and cell Alzheimer's models. In seeking the mechanism by which OXR1 protects against age-related neuronal decline, we discovered that it provides a necessary function in regulating the neuronal retromer complex, which is essential for the recycling of transmembrane receptors and for maintenance of autophagy. We further discovered that OXR1 deficiency can be rescued by genetic or pharmacological enhancement of retromer function, and that this enhancement extends lifespan and healthspan. Understanding how OXR1 operates could help uncover novel mechanisms to slow neurodegeneration including Alzheimer's disease.

scholarly journals Dietary restriction improves proteostasis and increases life span through endoplasmic reticulum hormesis

2019 ◽  
Vol 116 (35) ◽  
pp. 17383-17392 ◽  
Author(s):  
Latika Matai ◽  
Gautam Chandra Sarkar ◽  
Manish Chamoli ◽  
Yasir Malik ◽  
Shashi Shekhar Kumar ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Life Span ◽  
Dietary Restriction ◽  
Adult Life ◽  
Dependent Manner ◽  
Adult Life Span ◽  
Unfolded Protein ◽  
Age Related ◽  
Protein Response ◽  
Polyglutamine Aggregation

Unfolded protein response (UPR) of the endoplasmic reticulum (UPRER) helps maintain proteostasis in the cell. The ability to mount an effective UPRER to external stress (iUPRER) decreases with age and is linked to the pathophysiology of multiple age-related disorders. Here, we show that a transient pharmacological ER stress, imposed early in development on Caenorhabditis elegans, enhances proteostasis, prevents iUPRER decline with age, and increases adult life span. Importantly, dietary restriction (DR), that has a conserved positive effect on life span, employs this mechanism of ER hormesis for longevity assurance. We found that only the IRE-1–XBP-1 branch of UPRER is required for the longevity effects, resulting in increased ER-associated degradation (ERAD) gene expression and degradation of ER resident proteins during DR. Further, both ER hormesis and DR protect against polyglutamine aggregation in an IRE-1–dependent manner. We show that the DR-specific FOXA transcription factor PHA-4 transcriptionally regulates the genes required for ER homeostasis and is required for ER preconditioning-induced life span extension. Finally, we show that ER hormesis improves proteostasis and viability in a mammalian cellular model of neurodegenerative disease. Together, our study identifies a mechanism by which DR offers its benefits and opens the possibility of using ER-targeted pharmacological interventions to mimic the prolongevity effects of DR.

scholarly journals Dendranthema zawadskii var. lucidum (Nakai) J.H. Park Extract Inhibits Cellular Senescence in Human Dermal Fibroblasts and Aging-Related Inflammation in Rats

Processes ◽  
2021 ◽  
Vol 9 (5) ◽  
pp. 801
Author(s):  
Jehun Choi ◽  
Gwi-Yeong Jang ◽  
Jeonghoon Lee ◽  
Hae-Young Chung ◽  
Hyung-Jun Noh ◽  
...  
Keyword(s):  
Cellular Senescence ◽  
Cell Cycle Progression ◽  
Inflammatory Responses ◽  
Dermal Fibroblast ◽  
Dermal Fibroblasts ◽  
Dependent Manner ◽  
Aged Rats ◽  
Age Related ◽  
Dendranthema Zawadskii ◽  
Beta Galactosidase

Senescence is the phenomenon by which physiological functions of organisms degenerate with time. Cellular senescence is marked by an inhibition of cell cycle progression. Beta-galactosidase accumulates in the lysosomes of aged cells. In this study, human dermal fibroblast cells (HDFs) were treated with 0.5 μM doxorubicin for 4 h to induce cellular senescence. Senescence-associated beta-galactosidase (SA-β-gal) activity was then measured 72 h after treatment with aerial parts of Dendranthema zawadskii var. lucidum (Nakai) J.H. Park (DZ) extract. Treatment with DZ extract significantly decreased SA-β-gal activity in a dose-dependent manner in HDFs. Additionally, DZ extract treatment reduced age-related oxidative stress and inflammation in the aortas of aged rats. The reactive oxygen species (ROS) levels in aortas of aged control rats were higher than those in young rats. However, DZ extract-fed aged rats showed significantly lower ROS levels than the aged control rats. When the aged rats were treated with DZ extract at either 0.2 or 1.0 mg∙kg−1∙day−1, NF-κB levels in aorta tissue decreased significantly compared to those in aorta tissue of the aged control rats without DZ treatment. In addition, DZ extract-fed aged rat aortas showed significant reductions in expression of iNOS and COX-2 induced by NF-κB translocation. Therefore, these results suggest that DZ effectively inhibited senescence-related NF-κB activation and inflammation. DZ extract may have a role in the prevention of the vascular inflammatory responses that occur during vascular aging.

scholarly journals Loss-of-function of p53 isoform Δ113p53 accelerates brain aging in zebrafish

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Ting Zhao ◽  
Shengfan Ye ◽  
Zimu Tang ◽  
Liwei Guo ◽  
Zhipeng Ma ◽  
...  
Keyword(s):  
Replicative Senescence ◽  
Brain Aging ◽  
Ventricular Zone ◽  
Human Fibroblasts ◽  
Cell Lineage ◽  
Lineage Tracing ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Antioxidant Genes ◽  
Age Related

AbstractReactive oxygen species (ROS) stress has been demonstrated as potentially critical for induction and maintenance of cellular senescence, and been considered as a contributing factor in aging and in various neurological disorders including Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS). In response to low-level ROS stress, the expression of Δ133p53, a human p53 isoform, is upregulated to promote cell survival and protect cells from senescence by enhancing the expression of antioxidant genes. In normal conditions, the basal expression of Δ133p53 prevents human fibroblasts, T lymphocytes, and astrocytes from replicative senescence. It has been also found that brain tissues from AD and ALS patients showed decreased Δ133p53 expression. However, it is uncharacterized if Δ133p53 plays a role in brain aging. Here, we report that zebrafish Δ113p53, an ortholog of human Δ133p53, mainly expressed in some of the radial glial cells along the telencephalon ventricular zone in a full-length p53-dependent manner. EDU-labeling and cell lineage tracing showed that Δ113p53-positive cells underwent cell proliferation to contribute to the neuron renewal process. Importantly, Δ113p53M/M mutant telencephalon possessed less proliferation cells and more senescent cells compared to wild-type (WT) zebrafish telencephalon since 9-months old, which was associated with decreased antioxidant genes expression and increased level of ROS in the mutant telencephalon. More interestingly, unlike the mutant fish at 5-months old with cognition ability, Δ113p53M/M zebrafish, but not WT zebrafish, lost their learning and memory ability at 19-months old. The results demonstrate that Δ113p53 protects the brain from aging by its antioxidant function. Our finding provides evidence at the organism level to show that depletion of Δ113p53/Δ133p53 may result in long-term ROS stress, and finally lead to age-related diseases, such as AD and ALS in humans.

scholarly journals Fecal Calprotectin, CRP and Leucocytes in IBD Patients: Comparison of Biomarkers With Biopsy Results

2020 ◽  
Author(s):  
Barry D Kyle ◽  
Terence A Agbor ◽  
Shajib Sharif ◽  
Usha Chauhan ◽  
John Marshall ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Fecal Calprotectin ◽  
Dependent Manner ◽  
Ascending Colon ◽  
C Reactive Protein ◽  
Concentration Dependent Manner ◽  
Reactive Protein ◽  
Inflammatory Bowel ◽  
Descending Colon ◽  
Active Inflammation

Abstract Background This study aimed to compare fecal calprotectin (FC) levels with other commonly used parameters as part of patient care during evaluation for inflammatory bowel disease (IBD). Methods We recruited adult IBD patients with ulcerative colitis (UC) and Crohn’s disease (CD) and compared the results of the patient’s biopsy results (i.e., inflamed versus noninflamed) for six sites (i.e., ileum, ascending colon, transverse colon, descending colon, sigmoid colon, rectum) with concentrations of C-reactive protein (CRP), total leucocytes and fecal calprotectin (FC). Results We found that FC was significantly elevated in a concentration-dependent manner that correlated with the number of active inflammation sites reported in biopsy. Although CRP and leucocyte measurements trended upwards in line with inflammation reported from biopsy, the results were highly variable and highlighted poor reliability of these biomarkers for indicating IBD inflammation. Conclusions These results strongly suggest that FC correlates best with biopsy reports and is a superior marker than CRP and leucocytes.

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