Today’s column addresses questions from our recent ASCRS Eyes on Fire lecture.
Proteomic science is changing the way many gerontologists think
about inflammation, the aging process and degenerative diseases. The
term proteomics was coined as an analogy to genomics, the study of
genes. Understanding the structure and function of each protein and the
complexities of protein-protein interactions is becoming critical to
the development of effective diagnostics, disease treatments and more
importantly, degenerative disease prevention including eye disease.
Our bodies are designed to replace our cells one at a time through a
fairly simply process of deterioration and growth. This brilliant
process is dependent on intact DNA and messenger RNA (mRNA), good
nutritional status, protein-protein interaction and regular aerobic
exercise, which is now suggested to help control the inflammation
associated with aging and most degenerative disease.
The proteins that control inflammation are called cytokines
(messenger molecules) and they regulate every aspect of our biology by
turning on and off the metabolic pathways in each tissue and cell in
our body. Each tissue has its own specific cytokines, but they
cross-react to coordinate growth or deterioration throughout our whole
body. The new word for skeletal muscle released cytokines associated
with aerobic exercise is myokine.
Science now suggests that good nutrition and physical exercise can
create a moment-to-moment chemical balance between growth
and deterioration within our muscles. These signals are then sent to
the rest of our body via a series of interleukin proteins including
interleukin-6 (IL-6) and interleudin-10 (IL-10), which are activated by
the physical stress associated with regular aerobic
exercise.
The inflammatory process associated with increased levels of stress
activated pro-inflammatory proteins causes most cells in our bodies
to deteriorate and fall apart after relatively short life spans. The
good news is that this allows the human body to adapt to new
environmental circumstances and it eliminates older cells that more
easily become malignant. All forms of aerobic exercise produce
pro-inflammatory proteins in logarithmic proportion to both the
duration and intensity of exercise.
The master proteins for growth and repair, including
anti-inflammatory IL-10, are produced in response to the level of
pro-inflammatory proteins, including IL-6. This is our body’s brilliant
mechanism for balancing growth and deterioration. If adequate
antioxidants are available and enough of the protein growth signals are
sent at once, they overwhelm the pro-inflammatory signals that activate
cellular and tissue atrophy, and our bodies turn on specific metabolic
processes to protect and build up the muscles, heart, capillaries,
tendons, bones, joints, brain and eyes.
Inflammatory protein levels peak right after strenuous exercise.
This peak signals the anti-inflammatory proteins to start cellular and
tissue repair. Il-10 protein levels, as an example, peak an hour or so
later and stay at fairly high levels for hours after hard exercise. And
this happens at any age.
Not all deterioration is good however, and not all IL-6 triggers
the production of IL-10. When we are sedentary, or only pretend to sort
of exercise, there is a constant slow release of pro-inflammatory
proteins, but not enough to switch on the growth and repair
anti-inflammatory proteins.
Unfortunately, the aging process also causes a slow release
of pro-inflammatory proteins that are below the level required to turn
on, or stimulate, growth and repair proteins. Thereby explaining the
silent inflammatory process associated with aging and also explaining
why aerobic exercise becomes even more important after the age of 50.
Ellen Troyer, MT MA - Biosyntrx Chief Research Officer