There’s a new geoscientific concept surrounding aging and diseases. We talk about inflammaging in this article, so keep reading to find out more.
In this article:
- What Is Geroscience?
- What Is Inflammaging?
- What Is Metaflammation?
- What Is the Link Between Aging, Age-Related Diseases, and Inflammaging?
- What New Biomarkers Can You Apply to Metabolic Diseases?
Understanding Inflammaging and Its Role in Age-Related Diseases
What Is Geroscience?
Geroscience is a research field that offers a new perspective in understanding age-related diseases. Unlike other perspectives, geroscience attempts to tie together the molecular relationship between aging and age-related chronic diseases.
Geroscience researchers believe that there are seven interconnected pillars of aging:
- Regeneration of stem cells
- Macromolecular damage
These pillars don’t operate on their own, but they influence and modulate one another. Researchers believe these pillars aren’t just aging mechanisms, but may also be responsible for the development of age-related chronic diseases and metabolic disorders such as:
- Metabolic syndrome
- Type 2 diabetes
- Cardiovascular diseases
Rather than treating these age-related diseases individually, geroscience researchers believe that you can counteract age-related diseases together by focusing on the seven pillars of aging.
If there’s one central point of convergence among the seven pillars of aging, it would be inflammation. If there’s something wrong with one of the pillars, it usually triggers an inflammatory response which, in turn, will affect the other pillars in one way or another.
What Is Inflammaging?
Inflammaging is a specific type of chronic inflammation. It’s often characterized as a sterile inflammation which means it persists even if the body isn’t battling any infections.
Unlike infection-driven inflammation, inflammaging is low-grade. In it, inflammation is chronic and sustained by the following types of stimuli:
- Self (cell debris and molecules)
- Quasi-self (gut microbiota)
- Non-self (pathogens)
A small number of damaged receptors triggers this type of inflammation. It picks up on the stimuli and activates the innate immune response.
Here are other cellular and molecular mechanisms that may trigger inflammaging:
- Cellular senescence – a state wherein cells are stable but are no longer dividing and entering the cell cycle
- Mitochondrial dysfunction – a state wherein the mitochondria in cells can’t produce enough energy
- Defective autophagy – the inability to clear out damaged cells
- Defective mitophagy – the inability to shut down the mitochondria of damaged cells
- Inflammasome activation – activation of a multiprotein intracellular complex that detects pathogens and sterile stressors
- Dysregulated ubiquitin-proteasome system – the inability to clear damaged proteins
- Activation of DNA damage response – causes the body to repair, kill, or senescent cells with damaged DNA
What Is Metaflammation?
Metaflammation is another type of inflammatory response. It refers to metabolic inflammation, and it’s usually caused by an excess of nutrients.
This type of inflammation is seen in metabolic diseases such as obesity and type 2 diabetes. Metaflammation can proceed or become a contributing factor to inflammaging.
It’s also possible for inflammaging to contribute to metaflammation. In fact, metaflammation and inflammaging share common molecular mechanisms.
For instance, gut microbiota plays a vital role in both types of inflammation. It can trigger metaflammation and inflammaging by:
- Releasing inflammatory products
- Contributing to circadian rhythms
- Regulating crosstalk between organs and systems
Gut microbiota connects diet, metabolism, and the innate immune response. It digests food so that you can gain nutrients from them.
On top of that, it also evolves as you age. Your gut microbiota will respond to your dietary habits and energy requirements.
It adjusts to your unique immune and metabolic needs, so it can affect your overall health. Its immune response to diseases, as well as its age-related evolution, may lead to systemic inflammaging.
What Is the Link Between Aging, Age-Related Diseases, and Inflammaging?
The aging and disease model proposed by the geroscience researches isn’t unidirectional. Geroscience researchers argue that chronic diseases aren’t just the result of inflammaging and aging, but these diseases can also accelerate the aging process.
They also believe that you can view these diseases as evidence of accelerated aging. In their multidirectional model, aging and inflammaging can lead to age-related diseases and vice-versa.
What New Biomarkers Can You Apply to Metabolic Diseases?
Biomarkers are important because they help diagnose diseases. If the same mechanisms contribute to both aging and age-related diseases, you can also use similar biomarkers to assess metabolic diseases.
Geroscience researchers believe the following biomarkers of biological age are also applicable to metabolic diseases:
- DNA methylation – refers to any alterations of the chromatin structure or epigenetic signature in DNA
- Glycomics – a comprehensive study of sugar levels in organisms.
- Metabolomics – the examination of the levels of metabolites in cells. Metabolites are any substance that contributes to metabolism.
- Lipidomics – the assessment of cellular lipid pathways or networks in an organism
These biomarkers can help determine an individual’s trajectory between healthy and unhealthy metabolic aging. The researchers believe it’s best to integrate these new biomarkers with traditional biochemical and hormonal parameters for better diagnosis and treatment of metabolic diseases.
Want to know how to avoid inflammaging? Watch this video below and learn more about it!
This new perspective offered by geroscience allows us to view aging and age-related diseases in a more holistic manner. Talk to an integrative health specialist today to learn more about this and how it could impact the treatment of age-related diseases.
What are your thoughts about this new perspective? Let us know in the comments section below.