Category Archives: Longevity

Reversing Age-Related Impairment and Immunity

July 31, 2020

While the average life-expectancy for humans continues to increase, a longer life span has been tied to an uptick in age-related disease and impairment across the globe. As a result of a declining immune system, the growing elderly population is more prone to infectious diseases – including influenza and COVID-19. Additionally, this group is commonly affected by age-related frailty, which has a significant negative impact on quality of life. The high level of care and involvement required to maintain the health of these patients has the potential to bear a growing burden on the healthcare system which is part of the reason underlying research efforts in the field of human longevity.

The current body of knowledge suggests the role of chronic low-grade inflammation in the biological aging process and development of age-related diseases; scientific evidence implicates that the presence of inflammation in the body accelerates aging. Hoping to uncover more information about additional factors that may contribute to an accelerated process and potential methods of reversing them, a team of researchers from the Department for BioMedical Research at the University of Bern conducted a study with findings published in Nature Metabolism.

Age-Related Frailty and Immunity

Under Bernese guidance, Dr. Mario Noti and Dr. Alexander Eggel aimed to identify new approaches to improving health-span in an ever-increasing aging population by focusing on adipose tissue eosinophils (ATEs) present in humans and mice. These immune cells found in visceral adipose tissue, otherwise known as belly fat, play an essential role in regulating inflammation and could be used to reverse aging processes; these cells are important in the control of obesity-related inflammation and metabolic disease as they are responsible for maintaining local immune homeostasis. Increasing age is tied to a decrease in eosinophils in adipose tissue and an increase in pro-inflammatory macrophages – turning belly fat into a source of pro-inflammatory activity.

Role of Eosinophils in Chronic Inflammation

The study’s authors demonstrated that visceral adipose tissue contributed to the development of chronic low-grade inflammation. They found that ATEs undergo major age-related changes in distribution and function associated with impaired adipose tissue homeostasis and systemic low-grade inflammation in human subjects as well as mice. However, exposure to a young systemic environment  was able to partially restore ATE distribution in aged subjects by reducing adipose tissue inflammation.

“In different experimental approaches, we were able to show that transfers of eosinophils from young mice into aged recipients resolved not only local but also systemic low-grade inflammation,” the researchers told ScienceDaily. ”In these experiments, we observed that transferred eosinophils were selectively homing into adipose tissue.”

Using an adoptive transfer or eosinophils from young mice to aged subjects, researchers were able to restore ATE distribution and sufficiently mitigate age-related local and systemic low-grade inflammation. As a result of the transfer, youthful systemic environments were restored and systemic rejuvenation took place in aged mice. Changes were both physical – assessed by endurance and grip strength tests – and immune-related – manifested in improved vaccination responses.

Dr. Noti and Dr. Eggel’s findings support the critical function of adipose tissue as a source contributing to accelerated aging and uncover the new role of eosinophils in sustaining adipose tissue homeostasis and thus, promoting healthy aging.

Because the age-related changes in adipose immune cell distribution were confirmed in human subjects, the latest study may have significant positive implications for the anti-aging medicine field when translated into clinical practice. Age-related frailty and immune decline may be halted and potentially even reversed as a result of this novel cell-based therapeutic approach.

“Our results indicate that the biological processes of aging and the associated functional impairments are more plastic than previously assumed,” Dr. Noti stated. “A future direction of our research will be to now leverage the gained knowledge for the establishment of targeted therapeutic approaches to promote and sustain healthy aging in humans,” his research partner Dr. Eggel concluded.

 

Inflammaging: Chronic Inflammation and Healthy Aging

July 9, 2020

In recent years, the scientific community has been increasingly focused on a rarely recognized yet widely prevalent condition that contributes to an array of diseases, including cardiometabolic diseases, arthritis, Alzheimer’s, and depression. Chronic inflammation, although it may progress slowly, is the root cause of most chronic diseases and poses a significant threat to public health and longevity.

Trending in many medical specialities chronic, low-grade inflammation associated with changes in stem cell structure and deterioration is being referred to as “inflammaging”. The condition, which often results from an accumulation of health risk factors such as environmental causes, dietary habits, UV exposure, and sleep patterns, is linked to a number of age-related diseases – including diabetes, cardiovascular disease, and cancer. To delay and support healthy aging while protecting the body from illness, medical experts continue to investigate the prominent role of chronic inflammation and its implications on the development of anti-aging therapies.

Causes of Chronic Inflammation

Current literature has identified several underlying molecular causes of the phenomenon of inflammaging. The condition stems from a failure of the immune system to mitigate responses to illness or injury; factors can include the body’s failure to eliminate bacterium or fungus, exposure to a toxic substance, or the presence of an autoimmune condition. With age, immune responses tend to become less well-regulated and thus, may result in consistently elevated levels of inflammatory agents such as C-reactive protein, chemokines, interleukin-6 (IL-6), and tumor necrosis factor-a.

Further, inflammaging can have a direct impact on skin health and vitality. Chronic oxidative stress can cause accelerated tissue damage, weakening skin structure and leading to the breakdown of elastin and collagen, ultimately impairing the skin’s barrier function. This contributes to the development of many unwanted dermatologic symptoms – wrinkles, hyperpigmentation, uneven skin tone, and textural changes.

Preventative Techniques 

As chronic inflammation is difficult to treat, employing adequate preventative measures is of utmost importance. Improving overall health by maintaining a balanced diet, regular physical activity, and consistent sleep patterns can be beneficial to supporting optimal functioning of stem cells in the body.

Highly processed foods contribute to the inflammatory response, increasing the risk of and worsening existing chronic inflammation. On the other hand, consuming a diet rich with anti-inflammatory foods – high in nutrient–dense vegetables, fruit, and unprocessed foods – can aid the body in regulating the immune response which becomes more challenging with age.

Additionally, experts emphasize the role of the gut microbiome in preventing chronic inflammation; research has found that the gut microbiota of elderly patients often has decreased diversity, leading to weakened barriers against bacteria and thus, increased risk and prevalence of chronic inflammation. To help maintain gut health it is recommended to increase the consumption of probiotic-rich foods – yogurt, kefir, and fermented products – and maintain a well-rounded diet.

Another important preventative measure to consider is the routine and careful use of sunscreen to protect the body against harmful UV exposure, which drives pro-inflammaging factors. To aid this, skincare products with the right ingredients can shield skin stem cells from the negative effects of environmental stressors and break the cycle of inflammaging.

While knowledge in the relatively novel field of inflammaging is continuously expanding, the role of chronic inflammation in the biological aging process and development of age-related disease has become well-known. Clinicians looking to gain a better understanding of current clinical evidence and strategies for targeting inflammatory activity are invited to attend the Inflammaging – Ways to Slow the Clock session taking place during our Longevity, Aging, and Immuno Competency Virtual Event.

Living in Disadvantaged Neighborhoods Increases Risk for Brain Atrophy

July 1, 2020

Continuous scientific efforts contribute to the emergence of new information revealing the intricate complexities of neurological functions and their surprising connection to a wide range of external factors. Protecting neurological function can be made possible through the growing identification of risk factors for neurodegeneration during the aging process and can help inform new preventative protocols for dementia and cognitive decline.

The latest data suggest an association between living in a disadvantaged neighborhood and developing brain atrophy, or experiencing a decrease in the number of brain cells or connections over time. Neighborhood disadvantage functions as a social determinant of health, reflecting the education, income, employment, and quality of housing within a particular geographic area. As brain atrophy typically predisposes individuals to dementia and cognitive decline, this finding has significant implications for protecting cognitive function as individuals age.

Impact of Neighborhood on Neurological Health

Examining the impact of neighborhood socioeconomic disadvantage on brain volume in a cognitively unimpaired population, researchers conducted a study of over 950 individuals without a history of cognitive impairment in Wisconsin. In their cross-sectional study, the research team evaluated participants living in the most socioeconomically disadvantaged neighborhoods using data from the Wisconsin Registry for Alzheimer’s Prevention and the Wisconsin Alzheimer’s Disease Research Center to assess T1-weighted structural MRI scans.

At the beginning of the trial, participants were not cognitively impaired based on the National Institute on Aging-Alzheimer’s Association diagnostic criteria, however, the cohort was enriched for Alzheimer’s disease risk based on a family history of dementia.

Led by Amy J.H. Kind, MD, PhD from the University of Wisconsin, researchers calculated total hippocampal volume by combining both left and right measurements and based total brain tissue volume measures on total white and gray matter volumes. Additionally, they computed both the Area Deprivation Index – a geospatially determined index of neighborhood-level disadvantage – and cardiovascular disease risk indices for each participant. Linear regression models were used to test the relationships between neighborhood disadvantage and hippocampal and total brain tissue volume – as assessed by magnetic resonance imaging.

Neighborhood Disadvantage Linked to Loss of Brain Volume

Earlier this year, the team published their findings online in JAMA Neurology which reveal that living in socioeconomically disadvantaged neighborhoods was associated with markedly decreased hippocampal and total brain tissue volume. Other middle-aged and older adults who lived in areas with lesser disadvantage experienced comparatively lower risks of both neurological outcomes. Researchers found that individuals living in the most disadvantaged neighborhoods experienced a mean of 7 years of age-related hippocampal atrophy.

Furthermore, they also noted that men living in these neighborhoods experienced a higher risk for brain atrophy than women, although the reasons for this correlation remain unknown.

Cardiovascular risk was found to mediate the association in the case of total cerebral volume, indicating that neighborhood-level disadvantage may be associated with the two neurological outcomes via distinct biological pathways.

However, investigators acknowledged potential limitations of the trial which included the “enriched risk study cohort” – including older participants and those with a family history of dementia. They note that this population “might be particularly vulnerable to the deleterious effects of neighborhood-level disadvantage on the hippocampus.” In addition, the study’s findings reveal associations and not causality due to its cross-sectional, observational nature and require further validation.

Different from the implications of individual-level socioeconomic status on neurological function, this is the first study to reveal a robust association between neighborhood-level disadvantage and hippocampal volume, according to researchers. The latest findings indicate that neighborhood disadvantage may be associated with brain tissue volume throughout the aging process even in the absence of clinical cognitive impairment.

These results may suggest new population markers to leverage in future research studies; neighborhood-level disadvantage could be considered in clinical decision-making or used to guide public health efforts that support healthy brain aging in such geographic areas.