Aaqgs-Scientific-Technology Theories of Aging

Aaqgs -Scientific-Technology & relevance to theories of Aging?

Aalan-semantics is used. Science explains the why of the world (nouns) and processes (verbs) we find.  Technology answers (why not) that enables us to novel uses of the processes as well as their control and creation of brand new applications. Philosophically, fixed-wing planes is unnatural way of flying, helicopters an unnatural way of hovering, rockets unnatural way to escape planetary gravity, most of nano-technology unnatural as are quantum processes outside nano-regions.

With science we seek to develop understanding, modifying our theories in light of newer organisms encountered. With technology, we seek to limit our theories to perhaps unnatural idealization that can still be manipulated to yield solutions to life extension! Following analogy from civil engineering is very apt – we know that modeling reinforced concrete by linearly elastic material is clearly wrong, yet the approximation leads to conservative designs that can be checked and accepted without magic and those that can be abandoned in limiting structures like thin shells.

Fundamental to science is unlimited increase in application till regions are encountered where it does not apply , delimit the boundaries and explain why it does not apply.

Why important?

We have no reliably known ways of life-extension or even ways of measuring the extensions from procedures!

organization generalities?

Consider fats being evil in Diabetes and heart troubles. Turns out, all fats are not equally bad, by the theory 2000-2010. You can specialize fats to unsaturated (mono, poly), and saturated (fully, Trans). By that theory, all saturated were bad and all unsaturated better, mono being the best and full being the better. Latest finding is mono, poly and fully saturated are equally good. Trans fat are always bad. What most people don’t know is that any unsaturated fat, reused after cool and reheating becomes trans-fat BECOMES MUCH WORSE THAN SATURATED! Saturated can be temperature cycled without trans-fat. Never reuse non-butters (vegetable oils or hydrogenated fats)  for frying, unless the remnant are discarded! You are unintentionally damaging, not being nice!

In general , absent testable filters, gross divisions may be worse than not-knowledgeable!

Why difficult?

No agreed ways of measuring the extensions or pain! The hormesis effect is another problem.

Common assumption?

1.       All believe that aging is NOT programmed into cells, unlike telomere hypothesis (telomeres shorten every division till cell death after 40-50 divides), but is instead accumulation of junk.

2.       There is no magic gene to fix and arrest aging. However there are two groups of theories – cmall number of aging genes and large number of genes. The engineering is easier if there are only a few, and some worm models have just 1 gene. In any case, we assert only a few important genes whose fixing will give us enough time to fix others. This is my understanding of the generalized dynamic Kurzweil model.

Glycation theory

Some research supports the hypothesis that cross-linking contributes to aging. Cross-linking of the skin protein collagen, for example, has proven at least partly responsible for wrinkling and other age-related dermal changes. Cross-linking of proteins in the lens of the eye is also believed to play a role in age-related cataract formation. Researchers speculate that cross-linking of proteins in the walls of arteries or the filtering systems of the kidney account for at least some of the atherosclerosis (hardening of the arteries) and age-related decline in kidney function observed in older adults. Another study conducted at the Bjorksten Institute in Wisconsin treated brain tissue from young animals with known cross-linkinducing compounds. That brain tissue soon looked quite similar to older brain tissue, with its naturally cross-linked brain proteins, adding evidence in support of this theory of aging. Recently, scientists have found evidence that glycation contributes to the formation of beta-amyloid, the protein that clumps together in the brains of Alzheimer’s patients.

Studies done in China and in the United Kingdom on the molecule carnosine are provocative. Carnosine occurs in very low concentrations in the brain and other tissues. In the laboratory, carnosine has been shown to delay the senescence or aging of human cells called fibroblasts. Carnosine works by preventing cross-linking of proteins. The more recent Chinese studies suggest carnosine might be of benefit in delaying the formation of cataracts, in which crosslinking is thought to play a part.

Evolutionaary Senesense

Much experimental evidence exists to support the basic premises of the evolutionary senescence theory of aging. Natural selection, because it operates via reproduction, can have little effect on later life. In the wild, predation and accidents guarantee that there are always more younger individuals reproducing than older ones. Genes and mutations that have harmful effects but appear only after reproduction is over do not affect reproductive success and therefore can be passed on to future generations. In 1952, Peter Medawar proposed that the inability of natural selection to influence late-life traits could mean that genes with detrimental latelife effects could continue to be passed from generation to generation. This theory is called the mutation accumulation theory. A few years later, George Williams extrapolated on this idea by formulating the theory of “antagonistic pleiotropy.”

 Antagonistic pleiotropy means that some genes that increase the odds of successful reproduction early in life may have deleterious effects later in life. Because the gene’s harmful effects do not appear until after reproduction is over, they cannot be eliminated through natural selection. An example of antagonistic pleiotropy in humans is p53, a gene that directs damaged cells to stop reproducing or die. The gene helps prevent cancer in younger people, but may be partly responsible for aging by impairing the body’s ability to renew deteriorating tissues. Because of antagonistic pleiotropy, it is likely that tinkering with genes to improve late-life fitness could have a detrimental effect on health at younger ages.

Mitochondria theories

Oxidative free radicals are one of the toxic byproducts of normal cell metabolism. Natural substances within our cells called antioxidants sop up and neutralize these dangerous free radicals. But those that escape this cleanup process can damage DNA, proteins, and mitochondria. This damage, called oxidative damage, accumulates over time. Some fruit fly studies suggest that oxidative damage is one of the direct causes of aging. Proponents of the free-radical hypothesis of aging note that free radicals can cause DNA damage, the cross-linking of proteins, and the formation of age pigments. Oxidative damage contributes to many age-related diseases, such as cancer, heart disease, diabetes, and Alzheimer’s disease. Many scientists focus on the ­specific effects of free ­radicals on mitochondria, the tiny powerhouses of our cells that transform energy into useful forms. More than 90 percent of the cell’s free radicals are produced in the mitochondria, so they are at particular risk of damage. Oxidative free radicals, unless quickly neutralized by antioxidants, can cause considerable damage to the membranes of mitochondria and to mitochondrial DNA. Scientists studied the connection among mitochondria, oxidative stress, and aging in fruit flies by housing the flies in an environment of 100 percent oxygen. The elevated oxygen levels cause the mitochondrial membranes to crimp in swirled patterns, which in turn decreases the lifesapan.

From my point, this theory has wings because supplement reduction of deficits caused, and existence of 100 times better coQ10 in mitoq which simply take take coQ10 into the mitochondrial. There is something to research niagen into mitochondrial thus boosting its strength in creatinf NAD+, which can be explored by wittig reactions on niagen!

THE NEUROENDOCRINE HYPOTHESIS

The neuroendocrine system refers to the complex connections between the brain and nervous system and our endocrine glands, which produce hormones. The hypothalamus, a structure at the base of the brain, stimulates and inhibits the pituitary gland, often called the “master gland,” which in turn regulates the glands of the body (ovaries, testes, adrenal glands, thyroid) and how and when they release their hormones into our circulation. As we age, this system becomes less functional, and this can lead to high blood pressure, impaired sugar metabolism, and sleep abnormalities. The effects that the various hormones our different glands produce have on different facets of aging have been studied extensively. 

Reactive oxidation?

A flood of recent evidence has pinpointed this effect to one area: the insulin/IGF-1 hormonal pathway. IGF stands for insulinlike growth factor, a substance activated by growth hormone. Single-gene mutations in fruit flies and the roundworm C. elegans, widely studied by aging researchers, have recently been tied to the insulin/IGF-1 pathway. In 2002, a study by French researchers published electronically in Nature showed a similar effect in mice. In all the laboratory organisms studied, mutations that reduce the amount of circulating IGF extend life. In many cases, however, the long-lived mutants have defects that could potentially affect their ability to survive in the wild, possibly making the IGF-1 pathway’s relationship to aging an example of antagonistic pleiotropy.

Interestingly, this ­evidence flies in the face of popular support for anti-aging treatments involving injections of growth hormone, which increases circulating IGF-1. Rather than prolonging life as some companies claim, such treatment may instead do the opposite. BE warned on trying ideas without lot of consulting!

THE GENOME MAINTENANCE HYPOTHESIS

Damage to our DNA happens thousands of times every day in every cell in our body throughout our lives. This damage can be caused by oxidative free radicals, mistakes in replication, or outside environmental factors such as radiation or toxins. Mutations or spontaneous changes in the structure of our genes that occur in our egg or sperm cells will be passed on to future generations, if those mutations are not so potentially disruptive as to be fatal to our offspring. Mutations that occur in the rest of the cells of the body will only affect that individual and cannot be passed on to future generations. Most of those body cell, or somatic, mutations will be corrected and eliminated, but some will not. Those will accumulate, eventually causing the cells to malfunction and die. This process, it has been suggested, is a crucial component in the aging process. This theory also encompasses a role for mitochondria, the cellular powerhouses, as important factors in aging. Mitochondria create damaging free radicals as a by-product of normal energy production. Somatic mutations in the DNA of the mitochondria accumulate with age, increasing free radical production, and are associated with an age-related decline in the functioning of mitochondria. Many scientists believe that mitochondrial aging is an important contributor to aging in general.

THE OXIDATIVE DAMAGE/ FREE RADICAL HYPOTHESIS

Oxidative free radicals are one of the toxic byproducts of normal cell metabolism. Natural substances within our cells called antioxidants sop up and neutralize these dangerous free radicals. But those that escape this cleanup process can damage DNA, proteins, and mitochondria. This damage, called oxidative damage, accumulates over time. Some fruit fly studies suggest that oxidative damage is one of the direct causes of aging. Proponents of the free-radical hypothesis of aging note that free radicals can cause DNA damage, the cross-linking of proteins, and the formation of age pigments. Oxidative damage contributes to many age-related diseases, such as cancer, heart disease, diabetes, and Alzheimer’s disease. Many scientists focus on the ­specific effects of free ­radicals on mitochondria, the tiny powerhouses of our cells that transform energy into useful forms. More than 90 percent of the cell’s free radicals are produced in the mitochondria, so they are at particular risk of damage. Oxidative free radicals, unless quickly neutralized by antioxidants, can cause considerable damage to the membranes of mitochondria and to mitochondrial DNA. Scientists studied the connection among mitochondria, oxidative stress, and aging in fruit flies by housing the flies in an environment of 100 percent oxygen. The elevated oxygen levels cause the mitochondrial membranes to crimp in swirled patterns, which in turn decreases the lifespan of the insects from two months to about a week. The injury caused by free radicals initiates a self-perpetuating cycle in which oxidative damage impairs mitochondrial function, which results in the generation of even greater amounts of free radicals.

However,  experiments attempting to reverse the effects of oxidative damage by feeding experimental animals dietary antioxidants, and other experiments that genetically increase oxidative damage, have not yielded conclusive results.

Technologically useless theories

THE RATE OF LIVING THEORY

THE REPLICATIVE SENESCENCE HYPOTHESIS

Excellent reference, heavily used, but requires interpretation. The reality may be complex importance driven combination of these. Setting my sights nly on painfree 10 years age-extension, the question is what theories and what what importance patterns stand out. I believe that mitrochondrial theories and free-radical theories stand out, there are tools NOW to help in the two goals, and I want them used on me and all religious theories are independent bullshit, hence irrelevant.

I believe that Aaqgs technology is possible within the constraints of physicians saying “most likely a waste” and the limited goal of 10 year life extension and sharply reduced pain to a life time of 90 to 100 years with Aaqgs-interpretation and exercise together with metformin, niagen, coQ10 and ECP with blood transfusion and raqpamycin in active continued research. It does not lead to IGF-1 or large number of anti-disease pills. We conservatively believe in GRAS (Generally recognized as safe) stamp of USA FDA, though unusual uses.