Aging in a natural process is getting old.
Biologically, the process may also be characterized by ceased dividing (cellular senescence) of single cells within an organism.
Skin aging is one of most visible process which occurs constantly in our skin organ
Theories of aging
What causes aging? This question has been asked throughout human history, but it doesn't seem to get any answer but raises many more unanswered questions. While many theories try to answer the question by relating aging to tear and wear of the body, others deal with how the organs and systems in the body develop and deteriorate over time, etc.
1. Somatic mutation theory
In this theory, aging is due to our inherited genes that come directly from our parents. Since conception occurred, our body cells continue to divide and replication themselves. Since division and replication are a lifelong precess at some point, for whatever reason, if cells division and replication can process incorrectly, leading to mutation of the incorrect copy of DNA. Although the cause of this incorrect process is unknown, researchers found that exposures to toxins, radiation or ultraviolet light, artificial ingredients, unhealthy lifestyle, etc. can increase the risk of cells mutation and the cells copied incorrectly can mutate themselves, leading to accumulation of incorrect gene cells that trigger a chain reaction of an auto-catalytic nature in producing more and more incorrect gene cell, until it finally is brought under controlled, this processes can lead to aging. As an organism, the immune system tries to destroy or scavenge these mutated genes but at some points, it is overwhelming, leading to chronic age-related diseases.
2. Error catastrophe theory
The error catastrophe of aging was originally proposed by Leslie Orgel in 1963. Our body's immune system helps to maintain the structural integrity of DNA not only for cell survival but also for the transfer of correct genetic information to the daughter cells. Error catastrophe indicated that alterations DNA and the incorrect placement of amino acids in protein synthesis could result in a progressive degradation aging as a result of these abnormal protein are no longer functioning as chemical passengers or signalers.
3. Protein glycosylation
Protein glycosylation is a result of the chemical reaction of glucose with various proteins, including enzymes, elastin, and collagen in the blood. The cross-linked protein glycosylation leads to cell-to-cell adhesion causing stiffness and rigidity of individual cells, reducing the cells' function in taking nutrients and expelling waste.
If the cross-link protein glycosylation occurs in the elastin and collagen, it will cause brittle skin, causing aging, but if it happens in the organs it will be more serious and sometimes life-threatening.
4. The neuroendocrine theory
First proposed by Professor Vladimir Dilman and Ward Dean MD, this theory postulates on wear and tear of the neuroendocrine system. In the neuroendocrine system, the master pituitary gland secrets hormones to direct other glands in secreting their hormones and works conjunction with the hypothalamus glands to form a command post in the nervous system in closely directing the function of most of the body functions.
but as we age, the hypothalamus loses its ability as a hormone regulator as its receptors which uptake other gland hormones become less sensitive to them, including sex hormones, DHEA, serotonin, melatonin, etc.
As for cortisol, a hormone secreted by the adrenal glands due to stress, is produced with abundance as we age.
5. Immune system decline theory
As we age, our immune system is weakening which causes us to become vulnerable to dangerous pathogens, including microbial and viral invasion. Within the immune system, the thymus glands which play an important role in helping the formation of the immune system scavenger reduce the function of the immune system further that allow irregular cell growth cause of aging spots, tumors, cancer, infection, inflammation, and the onset of chronic illness.
6. Genetic programming theory
Genetic programming theory propose that aging is programmed as the cells cycle in our body are also genetic program since their inception. the explanation is that all the cells are undergoing a certain time in the division over the said amount of time before dying, leading to the conclusion that people with the long live genetic program live longer than others who do not.
The theory also emphasizes that genetic diseases as a result of genetic programming diminished life span, regardless of external and internal influences.
Further refinement of the programmed senescence theory was developed by Bernard Strehler, who proposed that as cells are program to perform specific functions within the organism that cause them to lose some of the ability to duplicate their genetic information, leading to aging.
7. Hayflick limit
The Hayflick limit (or Hayflick Phenomena) theory was discovered by Leonard Hayflick and a biologist in 1966. In vitro study, the number of times a fibroblast diploid cell will divide before it stops. The discovery is conferring a major hypothesis if the cell division can prolong in an infinite matter without conditions that cause damage to the cells, then the organism can liver forever.
Exceptions:
Stem cells
Since stem cells can continue to regenerate new cells for the entire lifespan of the organism, without limit, thus constitute a notable exception to the Hayflick limit theory.
Cancer cells
Cancer cells in the biological aspect, have found a way around the limit by becoming a group of immortalized cells produced from cell division that has no limit as to how many times this immortalized cell division might take place.
8. The telomerase theory
The telomerase theory is a continuation of support to the Hayflick limit (or Hayflick Phenomena) theory involved in telomeres and telomerase. Telomeres are the structure at the end of the chromosome. As each time the cell divides, its telomeres are shortened, and at certain length, the cell stops division and goes into senescence.
The experiment shows, the cell senescence can be reversed by controlling the genes of telomerase autocatalytic nature, which in turn, promotes the forever cell division capacity
9. The free radical theory
A free radical is any atom or molecule that has a single unpaired electron in an outer shell and is highly reactive to react with other cells, which in turn, causes oxidative damage to the enzymes, other proteins, unsaturated fatty acids, phospholipids, DNA, and RNA, etc., leading to aging of the organisms, as a result of widespread damage due to set of a chain reaction auto-catalytically after attacking the lipid bilayers of the cell walls.
10. Other theories
a. Rate of living and lifespan
The rate of living is defined that a bigger organism, the longer it lives with humans is one of the exceptions due to its slower rate of metabolism and lower rate of free radical activity, leading to low levels of age lipid pigment, resulting in a longer life span. Experiments show that there are 100,000 free radicals hit every day in rats, comparing 10, 000 in humans.
b. Caloric restriction
The caloric restriction hypothesis suggested in a study of young rats showed that if a rat is put into a restricted diet and given necessary nutrients, it lives longer than those allowed to eat freely. With the result also the same in the old rat, the theory also suggests eating less may cause fewer toxins in the body that affects the immune system and reduces the risk of hormone change, leading to free radicals caused by aging.
c. Age spots
Age spots are mainly composed of lipofuscin and lip pigment caused by the reaction of free radicals and peroxidation, leading to the formation of age spots, as a result of oxygen species interacting with autophagocytic degradation occurring inside the lysosomes.
d. Protein oxidation
Protein oxidation can affect protein function in normal and pathological processes as a result of postranslation protein being alter by reduce oxygen species (ROS) cause of damage to an enzyme, leading to dysfunction of its role and resulting in aging.
e. Fast track of aging
The theory suggests that there are many diseases and syndromes which can contribute to a faster track to aging.
* Hutchison-Gilford syndrome
It is an extremely rare genetic condition wherein symptoms resembling aspects of aging are manifested at an early age. Those born with progeria typically live to thirteen years, although many have been known to live into their late teens and early twenties and rare individuals may even reach their forties due to gene mutation.
*Werner syndrome
It is Adult progeria, a disorder that causes the appearance of premature aging. The syndrome does not develop until they reach puberty and is caused by autosomal recessive disorder due to altering gene on chromosome 8.
f. Altered genes
Alter genes are the work of Friedman and Johnson 1988 " .... the effect of elevated expression of SIR2 in yeast appears to be conserved in C. elegans (Tissenbaum & Guarente 2001) and Drosophila (Rogina & Helfand 2004), and mutations in genes encoding components of the target of rapamycin (TOR) pathway also extend the lifespan in all four organisms... "
"... It was originally suspected that extension of lifespan by reduced IIS might turn out to be a worm peculiarity. This was because mutations in genes in the IIS pathway can also cause the worms to enter a type of developmental arrest (dauer), normally seen only in response to low food or crowding (Riddle & Albert 1997). Dauer larvae are long-lived, and the long life of IIS mutant adult worms could therefore have been a result of re-expression in the adult of the genes that make the Dauer larva long lived...."
g. Free radical connection
Free radical is any atom or molecule that has a single unpaired electron in an outer shell and accumulation of free radical damage over time can cause aging. The theory is first proposed by Denham Harman in the 1950s and in the 1970s extended the idea to implicate mitochondrial production of reactive oxygen species into the 1970s. A study showed that nutant strains of the roundworm that are more susceptible to free radicals have shortened lifespans, and those with less susceptibility have longer lifespans
If free radical causes damage to the DNA repaired enzymes, it can increase the risk of unrepaired DNA damage, leading protein synthesis incorrectly. In fact, free radicals can inflict damage to all cells in the body such as endocrine glands, leading to decreasing in hormone secretion, resulting in aging and Kupffer cell in the liver, causing endotoxins to accumulate in the blood, leading to more free radicals attacks the immune system, etc.
10. Hormone depletion
The researchers found that if a decrease or absence of the pituitary gland hormones mice is given enough amount of pituitary hormones, it lives longer than a control group of normal mice as it stimulates the production of growth and other hormones such as prolactin, adrenocorticotropic hormone, thyroid-stimulating hormone, etc.
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Kyle J. Norton, Master of Nutrition
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, healthblogs, selfgrowth, best before it's news, the Karate GB Daily, etc.,.
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Some articles have been used as references in medical research, such as the international journal Pharma and Bio Science, ISSN 0975-6299.
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