How does healthy life become possible through programmed cell death?

The Answer

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9.2.10-Healthy life is possible only through programmed cell death

Fatal diseases occur if the programmed cell death mechanism in the living being is disrupted.

The programmed cell death mechanism is also in charge of eliminating harmful cells and preventing diseases. The safe destruction of aging, lost, over-produced, irregularly developed or genetically damaged cells for the organism takes place with programmed cell death. The programmed cell death signaling mechanism is integrated into the cell signaling network that regulates responses to all cell factors, from cell death to growth, and from development to stress responses. Programmed cell death is a mechanism that eliminates unwanted, damaged or abnormal cells and maintains normal tissue and organ development and function. Thus, programmed cell death is a necessary mechanism for normal organism function and survival. Acting upon this fact, it can be said, ‘The way of life is through death’. For, balanced cell growth and cell death are features of healthy organisms. Fatal diseases occur if the programmed cell death mechanism in the living being is disrupted.1

The mechanism of programmed death that is balanced in healthy individuals is impaired only in diseases.*

Being healthy or maintaining health depends only on the balanced operation of the programmed death mechanism in the living being (Figure 3).

Aging cells in tissues where cell production and destruction are rapid, such as skin, intestinal epithelium and blood, are also killed by programmed cell death; they are cleared from the body without causing inflammation by accumulating in the body and place is made available for new cells. Elimination of harmful cells in the organism occurs as follows: Virus-infected cells are eliminated by cytotoxic T cells; immune system cells are eliminated by cellular immune systems; cells with DNA damage are eliminated by p53; cancer cells are eliminated by chemotherapy agents.

Figure 3. Both unbalanced increase and decrease in the number of cells cause diseases.

The destruction of harmful cells whose structures are disrupted in the living beings is carried out by programmed cell death actively at every stage of life. The continuation of life is ensured in this way. For example, cancer cells always occur in the human body. Therefore, it is always possible to get cancer. However, under normal conditions, the programmed cell death mechanism destroys cancer cells whose structures are disrupted and prevents cancer. If programmed cell death mechanism is not operated regularly and if disrupted cells are not destroyed, we will get cancer.

The destruction of harmful cells whose structures are disrupted in the living beings is carried out by programmed cell death actively at every stage of life. The continuation of life is ensured in this way.

Healthy nutrition and environmental factors are effective in the operation of the death program. However, no matter how favorable the conditions are, no living being can escape death. It is based on the will of the Creator, who decides when the death program is to be operated and when the living being is to be killed.

*For instance, neurodegenerative diseases (Alzheimer, Huntington, Parkinson, etc.), hematologic diseases (aplastic anemia, Fanconi anemia, Hodgkin’s disease, etc.), autoimmune diseases (fulminant hepatitis, insulin-dependent diabetes, multiple sclerosis, rheumatoid arthritis, etc.), toxin-related diseases (alcohol-induced hepatitis, sepsis, pulmonary fibrosis, etc.), ischemic diseases (kidney infarction, myocardial infarction, stroke, etc.), bacterial and viral infections (AIDS, Ebola virus, etc.), etc. occur due to the excessive increase of programmed death.Cancer, leukemia, lymphoma, sarcoma, premalignant diseases, autoimmune diseases, atherosclerosis, osteoporosis, Wilson’s disease and various viral infections, Down syndrome, early aging, etc. occurdue to the inadequacy of programmed death mechanism in living beings.
1.Milisavet al.,Apoptosis, 2017, 22, 265–283.

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