Chronic inflammation and aging
We remind you that physiological aging and health are ensured by a normal catabolism/anabolism equilibrium.
The catabolic stage produces the energy necessary to support and overcome stressors. During this stage, energy is produced inside the cells starting from glucose and fatty acids.
Glucose can be found in food and endogenous sources.
More specifically, our organism is capable of producing carbohydrates also without food supply.
In fact, part of the sugars used as energy source come from tissue protein transformation.
Therefore, our lean protein mass is the substrate for the synthesis of the fuel necessary to combat the stressor and until this one is not overcome the lean mass will keep on supplying energy.
Talking about lean mass as energy substrate we refer to:
– skin proteins
– muscle proteins
– bone and cartilage proteins
– inner organ proteins
The continuous presence of stressors forces the organism to use its proteins accelerating the aging with wrinkles and skin spots, osteoporosis, arthrosis, mass force and muscular force loss, etc. and different pathologies of the organ.
That is why the lean mass of our organism is considered an important health and longevity index.
During the transformation of proteins in sugars we can observe the following processes:
– free radicals hyper production (oxidative stress increase)
– AGEs and ALEs hyper production (protein glycation increase)
– difficulty in eliminating the metabolic waste
The waste present in tissues stimulates the chronic inflammation processes producing the so called proinflammatory cytokines.
– IL 1
– TNF alfa
This sub acute chronic inflammation is the cause of premature aging and disease and is represented by the so called ‘inflammaging’.
In particular we know that proinflammatory cytokines are responsible for:
– indistinct and non-specific symptoms
– muscle lean mass destruction
– visceral fat mass increase (with overweight, obesity, diabetes, hypertension)
– premature skin aging
– cellulitis and edematous fibrosclerotic
– neuronal death
– reduced NGF and BDNF synthesis (neuron growth factors) with neuronal regeneration deficit
– neuritic plaque and neurofibrillary tangles sedimenting on neurons (responsible for Alzheimer and other dementias).
By GIORGIO CRUCITTI