All cellular functions and cell survival begins and ends with proper mitochondrial function.
There are many things that can impact your mitochondrial function - and one of the main factors is what you choose to eat.
WHAT ARE MITOCHONDRIA, AND HOW ARE THEY RELATED TO AGING?
The main purpose of the mitochondria is to produce energy for the cell from dietary inputs. This is done via what’s known as ‘cellular respiration’. Aging reduces this ability of the mitochondria. Reactive oxygen species (ROS,) or free radicals, are a normal byproduct of energy production.
However, these are very damaging molecules if not managed properly. As we age, the amount of ROS exceeds the cell’s management ability - and oxidative stress and cell damage results.
HOW AGING AFFECTS THE BODY
Some tissues are very energy intensive. One of these tissues is skeletal muscle. Aging then, is particularly harmful to the function, form and abilities of skeletal muscle. This is because the mitochondria become dysfunctional and there are far too many oxidants around and way too few antioxidants.
Similar to the effects of aging are the effects of a high fat diet.
Therefore, if you eat a HFD and you are aging, you might be in trouble.
Being sedentary and eating a HFD is causative of mitochondrial exhaustion.
This creates massive damage to your body and brain. This is true of your muscle as well.
Obesity and Type 2 Diabetes actually cause a slow-down in cellular respiratory function (energy production) and will increase the mitochondrial ROS production. This causes an increase in loss of functional muscle. This also enhances all effects of aging.
HOW DIET CAN REVERSE AGING
AMPK and TOR are major upstream regulators of mitochondrial metabolism. These molecules are essential with regard to how dietary restriction induces longevity and weight loss. TOR (target of rapamycin) is activated by certain amino acids such as leucine. This gene induces protein synthesis and is stimulated by energy availability.
When TOR is activated, it causes a reduction of autophagy/mitophagy - the clean up of damaged mitochondria. Insulin and high levels of glucose also stimulate the release of TOR; TOR basically stops the maintenance of good and functional mitochondria. This is pro-aging.
AMPK as stated is very important to healthspan. This regulator senses stress and energy levels; it responds accordingly. If in a low nutrient situation it will activate metabolic processes and produce ATP. It will inhibit biosynthesis and control the change from catabolism to anabolism. AMPK is activated in low energy states; when energy stores are depleted. This is sensed through tiny increases in the AMP/ADP:ATP ratios.
When AMPK is turned on, it restores cellular energy by inhibiting energy-intensive process such as protein synthesis, glycogen synthesis and fatty acid synthesis. Also, energy-producing reactions are stimulated. These include glucose uptake, glycolysis and fatty acid B-oxidation. In multiple species, activation of AMPK is known to extend life and improve health.
Activated AMPK also inhibits TOR. Inhibition of TOR will likewise activate AMPK. AMPK activation always increase autophagy/mitophagy and promotes cellular cleanup of damaged structures. This is opposite to TOR; stimulation of TOR reduces autophagy/mitophagy.
AMPK also participates in a positive feedback loop with SIRT1 and SIRT3. This is through an increase in the NAD+:NADH ratio and sirtuin activation. This of course results in deacetylation of mitochondrial proteins involved in metabolism and lifespan.
HOW INTERMITTENT FASTING CAN HELP REVERSE AGING
Calorie restriction is essentially a 20-40% reduction in caloric intake, but without malnutrition.
This slows aging and expands healthspan.
This is an intervention that is conserved in all species. This method uses nutrient-sensing pathways that are common to most forms of life.
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