Controlling inflammation can have huge implications when it comes to the treatment of numerous diseases. Efforts to understand and control inflammation are complex and ongoing. Interestingly, breaking research discovered how macrophages play a role in turning mitochondria into chemical-producing and toxic promoters of inflammation.
Inflammation is the way the body tries to protect itself against harmful stimuli and is an essential part of the immune system. Severe inflammation is an aspect of many aging-related diseases, and the lifelong accumulation of molecular damage resultant from chronic inflammation has been suggested to serve as a major contributor to the process of aging.
Mitochondria are present in nearly all cell types and generate the major part of the cells' adenosine triphosphate (ATP), the primary source of the cells' chemical energy. They are responsible for generating the energy that the cells need to conduct their work. As many as 30% of all cancers employ mitochondria, the powerhouses inside cells, to create an environment that is conducive to tumor growth.
Macrophages are white blood cells that are “biological dustbins” that engulf and digest foreign substances and cellular debris, destroy pathogens, stimulate the immune system to action when needed, and promote inflammation when the body needs it to help prevent further damage. When the time comes for the inflammatory response to end, they normally switch and suppress inflammation and help to repair damaged tissue.
However, the inflammatory response can instead go awry and cause diseases and damage to healthy tissue during diseases such as arthritis, inflammatory bowel disease, septic shock, periodontitis, and some cancers. They must be tightly controlled.
Telomere shortening can be accelerated with Inflammation and stress and are therefore makes us age faster. This is not necessarily apparent on the outside of the body, but these factors can significantly shorten the life of a person.
Telomeres act as a biological clock governing the life of cells. This theory is known as the telomere theory of aging. But there is an enzyme capable of reversing the process of synthesizing new telomeric DNA sequences: it is telomerase.
The inflammatory process is dependent upon intercellular communication mediated by biomolecules such as cytokines, C-reactive protein, and other acute phase reactants. Epitalon is a peptide that has been observed to play a role in the regulation of these molecules & thus counteract against the inflammatory response.
Studies have shown that short telomeres are associated with a higher risk of age-related diseases and a shorter life expectancy.
Foods have a direct effect on inflammation!
- olive oil.
- green leafy vegetables, such as spinach, kale, and collards.
- nuts like almonds and walnuts.
- fatty fish like salmon, mackerel, tuna, and sardines.
- fruits such as strawberries, blueberries, cherries, and oranges.
Try to avoid or limit these foods as much as possible:
- refined carbohydrates, such as white bread and pastries
- French fries and other fried foods
- soda and other sugar-sweetened beverages
- red meat (burgers, steaks) and processed meat (hot dogs, sausage)
- margarine, shortening, and lard
A swiftly-growing new area of specialty study is immuno-metabolism that looks at what exists between the metabolic responses and the immune system and creates a better understanding of the complexities of inflammation. The end goal is to design therapeutic approaches that should assist in the treatment of diseases that are difficult to manage.
Anisimov VN, Khavinson VK, Provinciali M, Alimova IN, Baturin DA, Popovich IG, et al. Inhibitory effect of the peptide epitalon on the development of spontaneous mammary tumours in HER-2/neu transgenic mice. Int J Cancer. 2002 Sep 1;101(1):7-10.
Kossoy G, Zandbank J, Tendler E, Anisimov V, Khavinson V, Popovich I, et al. Epitalon and colon carcinogenesis in rats: proliferative activity & apoptosis in colon tumors & mucosa. Int J Mol Med. 2003 Oct;12(4):473-7.
Owen JA, Punt J, Stranford SA. Immunology. 7th ed. New York: W.H. Freeman & Company; (c) 2013.