All About Aging, the Aging of Mitochondria.

These refer to the random occurrences of various natures which can cause damage to the key structures in the body, at a microscopic level.

An example of these is the free radicals, which are quite sensitive by-products of normal cellular respiration. These free radicals tend to cause random damage to key molecules like proteins, DNA as well as lipids. The cell membranes which are rich in unsaturated fatty acids are susceptible to free radicals as they are very sensitive and hence, reactive to minor intrusions. Mutagens, the chemicals which have the ability to react with DNA as well as change its genetic makeup, can destroy or disrupt the function of the genes. Certain chemicals like aldehydes, can tie together or cross-link cellular components, which lessens their ability to move as well as function. Though some substances that produce molecular damage originate in the environment, such as toxins or ultraviolet rays can be avoided. But many dangerous elements are a natural functioning part of the metabolism. Aging refers to a complex set of processes that involve a diverse set of conditions as well as reactions. Thus the aging process has always been very difficult to define. This is also the reason why there are multiple theories on the process of aging. The processes of aging can be divided into two types. One of them refers to the amassing of various degrees of damage to the cells and the other one, to the genetically programmed process of aging.

There are potentially damaging molecular occurrences taking place in the body’s cells all the time. The bulk of them does not cause long-lasting damage as the wound is fixed almost immediately by the reparation enzymes. A small number of lesions get passed over by the repair systems and these tend to stay damaged in the long run. Lesions that have not been repaired tend to accumulate and then they begin to have an effect on the vital cellular functions. As we get older, the accumulation of damage which has not been repaired grows, partly because the repair functions themselves have lower levels of efficiency and they can even be damaged themselves.

In the earlier days, there was a debate about the existence of aging clocks. Single-cell organisms as well as some of the more primitive species do not have any aging mechanisms. But there is now considerable evidence that more complex beings, like mammals, have multiple types of aging clocks. The majority of normal cells in the more developed organisms have a “clock.” What this means is that the cells can withstand only a finite number of divisions, unlike bacteria, which can grow indefinitely. Besides, there appears to be a “central clock” which is based in the brain. This clock controls the speed of both development as well as aging in the organism. Besides, there are other kinds of aging clocks, like menopause, which is the time when a woman’s reproductive functions shut down. These secondary clocks are, to as extent, reliant on the pace of the central as well as cellular clocks.

There is a big difference between biological clocks as well as regular clocks. The speed of biological clocks can vary by huge amounts between individuals and is even more diverse between different species. Various environmental events as well as factors can make the biological clock slow down or speed up. Stress, excessive eating as well as some insufficient levels of certain nutrients can increase the speed of the aging clock. Lowered stress levels, as well as certain therapies that renew certain brain structures, specifically the hypothalamus as well as the pituitary gland, can retard these clocks. In rodents, a low-calorie diet, if begun before sexual maturity has been shown to cause a massively increased lifespan. This attributes to the slowing of the biological clock. But this method of strict diet is not a viable alternative in humans because severely lowered levels of caloric intake when young can lead to brain damage. But it is possible that even a moderate limitation of caloric intake in adults can help in slowing the aging clock. Statistical studies of the population show that staying close to ideal body weight is quite effective in maintaining longevity in humans.

The majority of energy produced in the cells is done by the mitochondria, and cell function is dependent on it for providing energy to the rest of the system. Mitochondria are the main factor behind free radical damage. This mitochondrial fuel cycle produces free radicals as a common by-product. As free radical damage, as well as lower levels of energy production, are signs of aging it can be assumed that mitochondria play a vital role in the aging process.

Mitochondria are central to cellular function, and each cell has multiple copies of the mitochondria.

Additionally, mitochondria can even divide themselves in order to repair some kinds of free radical damage. Mitochondria have design flaws as well as certain vulnerabilities which makes them one of the weakest factors in the defense mechanisms of the anti-aging process.

DNA damage plays a big role in the process of aging as some of it cannot be fixed. There are some DNA lesions that can be repaired while others cannot. There are two parts of the cell which contain DNA – the nucleus as well as the mitochondria. The nucleus contains the bulk of the genetic material in its chromosomes, while the mitochondria also have a small but significant part of the cellular DNA. Free radical damage in DNA is more common in the mitochondria than in the nucleus. The DNA which is resident in the mitochondria is liable for up to 10 times the amount of damage than the nuclear DNA, as the majority of free radicals are formed in the mitochondria. This increased vulnerability of mitochondrial DNA is further increased as it is not as well protected by proteins.

Over time, the mitochondria’s ability to produce energy decreases. The first cellular system which slows down with age is the mitochondria, and this is also known as mitochondrial burnout. Cells show less metabolic activity which in turn leads to the lowered functionality of organs as well as a faster onset of degenerative diseases.

Stress has been a key accelerating force in mitochondrial burnout.

The by-products of stress include higher demands for energy making the mitochondria work harder, which can lead to a higher level of oxidative by-products and hence more free radicals. In an intensive stress situation, the mitochondrial membranes may get to the point where they leak, and this leakage is caused by free radical attacks which can interrupt the cell's energy as well as chemical balances. Severe oxidative damage tends to speed up the aging process as well as promote disease.

The primary role of the mitochondria as a power source as well as its vulnerability to free radical damage makes it an important target for anti-stress as well as anti-aging intercession. Some promising research on the prolonging of the lifespan has been done on the idea of inhibiting mitochondrial burnout. Acetyl-L-carnitine (ALC), coenzyme Q10 (CoQ10) as well as R-alpha lipoic acid (R-ALA) are important nutrients which have been proven to be active in mitochondria and can help to improve mitochondrial function.

Mitochondria contain ALC, a key part of the mechanism for transporting fatty acids. It can be produced by the body but its rate of production tends to drop with age. Taking ALC supplements will increase the use of fats by the mitochondria thereby producing more energy. ALC has been shown to be useful in the treatment of some diseases which affect the cardiovascular as well as nervous systems.

CoQ10 is an essential part of the mitochondrial fuel process besides being an antioxidant. CoQ10 can raise the rate as well as the efficiency of energy production besides providing protection for the mitochondria from free radicals. Though the body is able to produce its own stock of CoQ10 there are various reasons why the body will not produce enough CoQ10. Examples of the inhibitors include illness, age, malnutrition as well as a side effect of cholesterol-lowering drugs. CoQ10 is often referred to as a biomarker for aging since the body’s level of CoQ10 is directly related to degenerative diseases as well as aging. Taking CoQ10 supplements produces a modest increase in the life span of animals, while a significant number of CoQ10 studies on humans have shown that it can act as an effective healer for various different kinds of heart diseases. Hypertension, muscular atrophy besides lowered levels of immunity too can be helped by CoQ10.

R-alpha lipoic acid is an important part of the mitochondrial energy system besides being an antioxidant. Studies have shown that R-ALA supplements can reduce the number of free radicals in the mitochondria as well as increase energy production.

Despite the fact that ALC, CoQ10 as well as R-ALA have shown promise for protecting and revitalizing mitochondria further research is required in order to understand if these or any other substances can actually slow down the mitochondrial burnout in the long run.