The Hidden Secrets and Truth of Skin Aging, You Probably Don't Know

By Kyle J, Norton

Skin aging is one of most visible process which occurs constantly in our skin organ.

According to the Clinical Centre of Nis, certain plant extracts may have the ability to scavenge free radicals, to protect the skin matrix through the inhibition of enzymatic degradation, or to promote collagen synthesis in the skin, affected skin elasticity and tightness(a). 

Other suggested that free radicals induced domino effects in production of reactive oxygen species, can react with DNA, proteins, and fatty acids, causing oxidative damage and impairment of antioxidant system, leading injuries damage regulation pathways of skin, including wrinkles, roughness, appearance of fine lines, lack of elasticity, and de- or hyperpigmentation marks(b).

The degradation of the epidermal and dermal layers of the extracellular matrix (ECM), the non-cellular component present within all tissues and organs, such as UV Exposure, decline of lysosomal/endosomal cathepsin K, S and V activity(c) 

Some environmental factors may also have strong implication on skin aging in induced visible signs such as irregular dryness, dark/light pigmentation, sallowness, severe atrophy, telangiectases, premalignant lesions, laxity, leathery appearance and deep wrinkling, through re modification of the surface of skin and the physical properties in facilitated skin aging.

Certain chemical ingredients, such as aloin, ginsenoside, curcumin, epicatechin, asiaticoside, ziyuglycoside I, magnolol, gallic acid, hydroxychavicol, hydroxycinnamic acids, hydroxybenzoic acids, etc. derived from herbs have been found to be intergraded into some cosmetic products in treating premature aging(d).

Theories of aging
What cause aging? The question that has been asked throughout the human history, but it doesn’t seem to get any answer.
Many theories try to answer the question by related aging to tear and wear of the body, others deal with how the organs and systems in the body develop and deteriorate overtime, etc.

1. Somatic mutation theory
In this theory, aging is due to our inherited genes that come directly from our parents. Since the conception occurred, our body cells continue to divide and replication themselves. Since the division and replication are a life long precess at some point, for what ever reason, if cells division and replication can process incorrectly, leading to mutation of incorrect copy of DNA. Although the cause of this incorrect process are unknown, but researchers found that exposures to toxins, radiation or ultraviolet light, artificial ingredients, unhealthy life style, 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 fincorrect 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 scavenger these mutated genes but at some points, it is over whelming, leading chronic age related diseases.

2. Error catastrophe theory
The error catastrophe of aging, originally proposed by Leslie Orgel in 1963. Our body 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 chemical reaction of glucose with vary proteins, including enzyme, 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, aging, but 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 neuroendocrine system, the master pituitary gland secrets hormones to direct other glands in secreting their hormones and works conjunction with the hypothalamus glands form a command post in the nervous system in closely direct the function of most of the body functions.
but as we age, the hypothalamus loses its ability as a hormone regulator as its receptors of 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 that cause us become vulnerable to the dangerous pathogens, including microbial and viral invasion. Within the immune system, the thymus glands which play an important role in helping formation of the immune system scavenger that reduces the function of immune system further that allow irregular cell growth cause of aging spot, tumors, cancer, infection, inflammation and 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 certain time in division over the a said amount of time before dying, leading to conclusion that people with the long live genetic program live longer than others who do not.
The theory also emphasizes the genetic diseases as a result of genetic programing diminished life span, regardless external and internal influence.
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 discovered by Leonard Hayflick and a biologist in 1966. In vitro study, the number of times a fibroblast diploid cells will divide before it stops. The discover is conferring a major hypothesis if the cell division can prolong in a infinite matter without conditions which cause damage of the cells, then 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 constituting a notable exception to the Hayflick limit theory.
Cancer cells
Cancer cell in biological aspect, have found a way around the limit by becoming a group of immortalized cells produced from cell division that have no limit as to how many times this immortalized cell division might take place.

8. The telomerase theory
The tolomerrase 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 is shortened, 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 highly reactive to react with other cell, which in turn, causes oxidative damage to the enzymes, other protein, unsaturated fatty acid, phospho-lipids, 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
Rate of living is defined that a bigger organism, the longer it lives with human is one of the exception due to its slower rate of metabolism and lower rate of free radical activity, leading to low levels of age lipid pigment, resulting in longer life span. Experiment show that there 100,000 free radicals hit everyday in rat, comparing 10, 000 in human.
b. Caloric restriction
Caloric restriction hypothesis suggested in a study of young rat showed that if a rat is put into restricted diet with given of necessary nutrients, it lives longer than those were allowed to eat freely. With the result also the same in the old rat, the theory also suggest eating less may cause less toxins in the body that affects the immune system and reduces the risk of hormone change, leading to free radicals cause of aging.
c. Age spots
Age spots are mainly composed of lipofuscin and lipopigment caused by reaction of free radical and peroxidation, leading to the formation of age spot, as a result of oxygen species interact with autophagocytic degradation occurring inside the lysosomes.
d. Protein oxidation
Protein oxidation cay 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 enzyme, leading to dysfunction of its role resulting in aging.
e. Fast track of aging
The theory suggest that there are many of diseases and syndromes of which can contribute to 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 genes mutation.
*Werner syndrome
It is Adult progeria, an disorder causes the appearance of premature aging. The syndrome does not develop until they reach puberty is caused by autosomal recessive disorder due to alter 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. Theory is first proposed by Denham Harman in the 1950sand in the 1970s extended the idea to implicate mitochondrial production of reactive oxygen species into the 1970s. 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 celsl in body such as endocrine glands, leading to decreasing of hormone secretion, resulting in aging and Kupffer cell in liver, causing endotoxins accumulated in the blood, leading to more free radicals attacks the immune system, etc.

10. Hormone depletion
The researchers found that if an 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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 References
(a) Skin ageing: natural weapons and strategies by Binic I1, Lazarevic V, Ljubenovic M, Mojsa J, Sokolovic D.(PubMed)
(b) Phytoconstituents as photoprotective novel cosmetic formulations by Saraf S1, Kaur CD.(PubMed)
(c) Differential expression of cathepsins K, S and V between young and aged Caucasian women skin epidermis by Sage J1, De Quéral D2, Leblanc-Noblesse E2, Kurfurst R2, Schnebert S2, Perrier E2, Nizard C2, Lalmanach G3, Lecaille F4.(PubMed)
(d) Bioactive compounds from natural resources against skin aging by Mukherjee PK1, Maity N, Nema NK, Sarkar BK.(PubMed)