Found this in Reason’s newsletter. Be sure to sign up to receive it. Fight Aging! Newsletter
Lots to chew on here.
Tables in the paper include lifestyle and chemical interventions to slow aging.
biology-14-00017-v4.pdf (357.0 KB)
Excerpts:
“ Our analysis highlights the intricate interplay between various factors contributing to immunosenescence, including the senescence-associated secretory phenotype (SASP), chronic activation of innate immune sensors, gut microbiome dysbiosis, and metabolic inflammation. Understanding these interconnected processes is crucial for developing targeted interventions to maintain immune function in aging populations.”
“Several factors contribute to metabolic inflammation in aging as follows:
Adipose tissue dysfunction: with age, there is an increase in visceral adiposity and a decline in the function of subcutaneous adipose tissue. Senescent adipocytes and infiltrating immune cells in adipose tissue produce pro-inflammatory cytokines, contributing to systemic inflammation”
Insulin resistance: age-related insulin resistance leads to hyperglycemia and elevated free fatty acids, which can activate inflammatory pathways through oxidative stress and ER stress mechanisms
Mitochondrial dysfunction: aging is associated with a decline in mitochondrial function, leading to increased production of reactive oxygen species (ROS) and activation of inflammatory pathways such as NF-κB
Altered nutrient sensing: dysregulation of nutrient-sensing pathways, including mTOR and AMPK, can lead to impaired autophagy and increased cellular stress, contributing to inflammation
The interplay between metabolic inflammation and immunosenescence creates a vicious cycle that accelerates age-related decline. For example, pro-inflammatory cytokines produced by adipose tissue can impair T cell function and promote the accumulation of senescent immune cells
Interventions targeting metabolic inflammation, such as caloric restriction, exercise, and pharmacological approaches (e.g., metformin), have shown promise in reducing inflammaging and improving healthspan in preclinical models. These strategies aim to restore metabolic homeostasis and reduce the chronic activation of inflammatory pathways.
In conclusion, inflammaging is driven by multiple interconnected molecular mechanisms, including the SASP, chronic activation of innate immune sensors, gut microbiome dysbiosis, and metabolic inflammation. Understanding these drivers and their consequences is crucial for developing targeted interventions to promote healthy aging and reduce the burden of age-related diseases. Future research should focus on integrating these various aspects of inflammaging to develop comprehensive strategies for maintaining immune health and overall well-being in older adults.“
“Emerging research has identified several promising molecular targets for intervention, including the modulation of NF-κB and mTOR pathways, targeting the SASP, activating sirtuins, and regulating AMPK signaling. Additionally, lifestyle interventions such as regular physical activity, a Mediterranean-style diet, stress management, and adequate sleep have shown potential in mitigating aspects of immunosenescence.“
I haven’t found anything new here but it is helpful to be reminded of the complexity of the problem we are trying to solve. Get the basics right before launching into extreme measures. Be patient and focus on slow and steady progress, unless you are out of time already.