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 live 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 effect 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
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 1950s and 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 cell in body such as endocrine glands, leading to decreasing of hormone secretion, resulting in aging and Kupffer cell in liver can cause endotoxins accumulated in the blood, leading to more free radicals that weakening the immune system, etc.
