Standard Age determination

I have definite plan for indefinite life with great life extension to (?)first singularity. But how will one test my claims?

There is a population mean by age and a healthy and acceptable range around them. Missing the acceptable range marks you a patient, while healthy range implies very fit. A person can be classified as the highest range achieved without sickness. Thus a person may be less or more good than the standard for the age. One can thus determine the standard age from tests. None of the tests measure psychological age.

There are two methods, both NOT dependent on clocks but the fact that one is not only interested in life-extension but in Quality-of-life extension as well - not extending life in ICU! QoL extension has the added charm of application even without extension! QoL gives us one of two methods, discussed here - idea is to mark the QOL datas for an organism and compare it to a standard chart. The organism would be better than average or not. Matching to the standard chart gives us an age - works because standard charts ALWAYS decline with age after brief youth!

 (beta HCG) When you finally get pregnant, the doctor will monitor the health of your pregnancy by measuring your beta HCG ( also known as beta) levels. A pregnancy should be documented as early as possible. This is important, because appropriate care and precautions can then be taken at an early stage. The most sensitive, accurate and reliable pregnancy test is a blood test for the presence of beta HCG (human chorionic gonadotropin), often just called "beta". The HCG is produced by the embryo, and is the embryo's signal to the mother that pregnancy has occurred. Beta HCG levels vary according to the gestational age. In a non-pregnant woman, they are less than 10 mIU/ml. They are typically about 100 mIU/ml 14 days after ovulation in a healthy singleton pregnancy. They should double every 48- 72 hours in a healthy pregnancy.

 (CBC) A complete blood count (CBC) is a blood test used to evaluate your overall health and detect a wide range of disorders, including anemia, infection and leukemia. A complete blood count test measures several components and features of your blood, including: Red blood cells, which carry oxygen.

(CMP) A comprehensive metabolic panel is a blood test that measures your sugar (glucose) level, electrolyte and fluid balance, kidney function, and liver function. Glucose is a type of sugar your body uses for energy. Electrolytes keep your body's fluids in balance.

Cortisol is a steroid hormone, in the glucocorticoid class of hormones. When used as a medication, it is known as hydrocortisone.

It is produced in humans by the zona fasciculata of the adrenal cortex within the adrenal gland.^[1] It is released in response to stress and low blood-glucose concentration. It functions to increase blood sugar through gluconeogenesis, to suppress the immune system, and to aid in the metabolism of fat, protein, and carbohydrates.^[2] It also decreases bone formation

 (DHEA) Dehydroepiandrosterone is a hormone that comes from the adrenal gland. It is also made in the brain. DHEA leads to the production of androgens and estrogens (male and female sex hormones). DHEA levels in the body begin to decrease after age 30. Levels decrease more quickly in women. Lower DHEA levels are found in people with hormonal disorders, HIV/AIDS, Alzheimer's disease, heart disease, depression, diabetes, inflammation, immune disorders, and osteoporosis. Corticosteroids, birth control taken by mouth, and agents that treat psychiatric disorders may reduce DHEA levels.

DHEA-S (dehydroepiandrosterone sulfate) is a male hormone (androgen) that is made in the adrenal glands. The body turns it into testosterone. A test for DHEA-S checks the level of this hormone in the blood.

Testosterone affects sexual features and development. In men, it is made in large amounts by the testicles. In both men and women, testosterone is made in small amounts by the adrenal glands. In women, small amounts are made by the ovaries.

 Estradiol (E2), also spelled oestradiol, is a steroid, an estrogen, and the primary female sex hormone. It is named for and is important in the regulation of the estrous and menstrual female reproductive cycles. Estradiol is essential for the development and maintenance of female reproductive tissues such as the breasts, uterus, and vagina during puberty, adulthood, and pregnancy,^[7] but it also has important effects in many other tissues, including bone, fat, skin, liver, and the brain. While estrogen levels in men are lower compared to those in women, estrogens have essential functions in men, as well. It is found in most vertebrates and crustaceans, insects, fish, and other animal species.

An estrogen panel test measures the level of the most important estrogen hormones in a blood or urine sample. It measures estradiol, estriol, and estrone.

• Estradiol is the most common type of estrogen measured for nonpregnant women. The amount of estradiol in a woman's bloodvaries throughout her menstrual cycle. After menopause, it drops to a very low but constant level.
• Estriol levels are most often measured only during pregnancy. Estriol is produced in large amounts by the placenta. This is the tissue that links the fetus to the mother. Estriol can be found as early as the 9th week of pregnancy. The levels keep rising until delivery. Estriol can also be measured in urine.
• Estrone may be measured in women who have gone through menopause. It's done to find out their estrogen levels. It also may be measured in men or women who might have cancer of the ovaries , testicles , or adrenal glands .
• Both men and women make estrogen hormones. Estrogens are responsible for female sexual development and function, such as breast development and the menstrual cycle. In women, estrogens are made mainly in the ovaries and in the placenta during pregnancy. Small amounts are also made by the adrenal glands. In men, small amounts of estrogens are made by the adrenal glands and testicles.

 Homocysteine is a non-protein α-amino acid. It is a homologue of the amino acid cysteine, differing by an additional methylene bridge (-CH₂-). It is biosynthesized from methionine by the removal of its terminal C^ε methyl group. Homocysteine can be recycled into methionine or converted into cysteine with the aid of certain B-vitamins. A high level of homocysteine in the blood (hyperhomocysteinemia) makes a person more prone to endothelial cell injury, which leads to inflammation in the blood vessels, which in turn may lead to atherogenesis, which can result in ischemic injury.^[3] Hyperhomocysteinemia is therefore a possible risk factor for coronary artery disease. Coronary artery disease occurs when an atherosclerotic plaque blocks blood flow to the coronary arteries, which supply the heart with oxygenated blood. Hyperhomocysteinemia has been correlated with the occurrence of blood clots, heart attacks and strokes, though it is unclear whether hyperhomocysteinemia is an independent risk factor for these conditions.^{[citation needed]} Hyperhomoscyteinemia has also been associated with early pregnancy loss^[4] and with neural tube defects

(IGF-1) Insulin-Like Growth Factor 1 is a hormone that is similar in structure to insulin and works with Growth Hormone to reproduce and regenerate cells. Growth Hormone, made by the pituitary gland, stimulates the liver to produce IGF-1 and IGF-1 subsequently stimulates growth in cells throughout the body, leading to growth and development (as in the womb and through adolescence), strengthening of tissues (improving bone density, building muscle), and healing (skin, bones, gut lining, etc.), depending on what the body needs (R). IGF-1 is so crucial to development that if it is not present in adequate amounts during the time when a child is developing, a short stature may result. IGF-1 is commonly known to help build muscle or something to avoid when dealing with cancer. However, IGF-1 is also crucial in healing and tends to be low in those with chronic inflammation.

(FSH) Follicle-stimulating hormone (FSH) is a gonadotropin, a glycoprotein polypeptide hormone. FSH is synthesized and secreted by the gonadotropic cells of the anterior pituitary gland,^[1] and regulates the development, growth, pubertal maturation, and reproductive processes of the body. FSH and luteinizing hormone (LH) work together in the reproductive system.

(LH) Luteinizing hormone (LH) is an important hormone both men and women produce. This hormone is known as a gonadotropin, and it affects the sex organs in both men and women. For women, it affects ovaries, and in men, it affects the testes. LH plays a role in puberty, menstruation, and fertility. Knowing the amount of LH in your blood can indicate underlying problems associated with a variety of reproductive health issues. LH is a hormone that’s produced in the pituitary gland. The pituitary gland is located at the base of the brain, and it’s roughly the size of a pea. If you’re a woman, LH is an important part of your menstrual cycle. It works with follicle-stimulating hormone (FSH), which another gonadotropin made in the pituitary gland. FSH stimulates the ovarian follicle, causing an egg to grow. It also triggers the production of estrogen in the follicle.

A lipid panel is a blood test that measures lipids-fats and fatty substances used as a source of energy by your body. Lipids include cholesterol, triglycerides, high-density lipoprotein (HDL), and low-density lipoprotein (LDL).

Progesterone is an endogenous steroid and progestogen sex hormone involved in the menstrual cycle, pregnancy, and embryogenesis of humans and other species.^[11] It belongs to a group of steroid hormones called the progestogens,^[11] and is the major progestogen in the body. Progesterone is also a crucial metabolic intermediate in the production of other endogenous steroids, including the sex hormones and the corticosteroids, and plays an important role in brain function as a neurosteroid

(PSA) Prostate-specific antigen, is a protein produced by cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are usually reported as nanograms of PSA per milliliter (ng/mL) of blood. Blood levels of PSA can be elevated in men with prostate cancer. For this reason, measurement of PSA in the blood has been used as a screening test for prostate cancer.

(SHBG) Sex hormone-binding globulin or sex steroid-binding globulin (SSBG) is a glycoprotein that binds to the two sex hormones: androgen and estrogen. Other steroid hormones such as progesterone, cortisol, and other corticosteroids are bound by transcortin. SHBG is found in all vertebrates apart from birds. These hormones are estrogen; dihydrotestosterone (DHT), and testosterone. SHBGcarries these three hormones throughout your blood. lthough SHBG binds 3 hormones, the hormone that's critical in this test is testosterone. ... The level ofSHBG in your blood changes because of factors such as sex and age. test measures the level of sex hormone binding globulin (SHBG) in your blood. SHBG is a protein made by your liver. It binds tightly to 3 sex hormones found in both men and women. These hormones are estrogen; dihydrotestosterone (DHT), and testosterone. SHBG carries these three hormones throughout your blood. Although SHBG binds 3 hormones, the hormone that's critical in this test is testosterone. SHBG controls the amount of testosterone that your body tissues can use. Too little testosterone in men and too much testosterone in women can cause problems. The level of SHBG in your blood changes because of factors such as sex and age. It can also change because of obesity, liver disease, and hyperthyroidism

A lesser fraction is albumin bound and a small proportion exists as free hormone. Historically, only thefree testosterone was thought to be the biologically active.Testosterone is the major androgenic hormone. ... Most circulating testosterone is bound to sex hormone-binding globulin (SHBG), which in men also is calledtestosterone-binding globulin. A lesser fraction is albumin bound and a small proportion exists as free hormone.

(D 25) Known as the sunshine vitamin, vitamin D is produced by the body in response to skin being exposed to sunlight. It is also occurs naturally in a few foods -- including some fish, fish liver oils, and egg yolks -- and in fortified dairy and grain products. Vitamin D is essential for strong bones, because it helps the body use calcium from the diet. Traditionally, vitamin D deficiency has been associated with rickets, a disease in which the bone tissue doesn't properly mineralize, leading to soft bones and skeletal deformities. But increasingly, research is revealing the importance of vitamin D in protecting against a host of health problems.

A thyroid panel is used to evaluate thyroid function and/or help diagnose hypothyroidism and hyperthyroidism due to various thyroid disorders. The paneltypically includes tests for: Thyroid-stimulating hormone (TSH) Free thyroxine (free T4) Total or free triiodothyronine (total or free T3)

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.

The Arya protocol

The protocol is designed to measure the effectiveness of avariety of products/prayers to scientifically measure any improvements evenwhen the benefits are measurable but they have a random sparse distribution. Can aging claims be statistically tested? First prove yourself they can’t then enjoy my claim of yes! It is widely said that age-extension properties of coQ10 are suspected but not proven! Well, either yes or no, with arya-test I can find in 2 years, not the sixty it has been there!

Consider a protocol for improving the age. Or pain management over a number of patients who can reliability measures their pain on a pain-scale, but can suffer from many diseases at the same time, some not even known! Or someone who claims that proper prayer to his deo reduces the impact of earthquakes. One might dismiss such arguments but it is far better there be a scientific proof against. Such an activity provides provable, as opposed to instinctive, arguments against certain cult-extremes of Christianity, in fact any religion.

Because of the general applicability of the protocol, it is separated away, but be confidentially applied and approved by various grant givers.

This is the protocol itself, first stated in generality, and then applied to the proposal. Two running examples are aging and pain management. The claim-argument under examination is that P increases age and Q reduces pain. Our job is define a statistical double blind scheme such that participants age.i for I in 1..n-age is given, and one concludes from that the membership in P scheme that it improved the expected age. Similarly, from j in 1..n-pain, one can conclude the people treated under Q. Note that numbering is not random!

… the test

The useful ness of prayer can be ascertained by image-idol in many places. The argument then becomes magical properties of the idol only. Perhaps challenging prayer is a bad idea.

Aging test

Almost all physicians consider it pseudo-science; I am not one! But respect physicians 100% in acute medicine and only 50% in chronic medicine. There is an explanation in my weltanschauung why the standard dose-response methods fail in chronic diseases.

That applies to diabetes as well, I happen to believe that reducing sugar concentrations with insulin after a certain age replace one poison for another and brings death closer. Fact of immediate benefit from insulin is noticeable, long term evil effects are not! I consider alternative medicine to have valuable suggestions there, particularly of supplements. They should be exposed to the physician who can then indicate contraindication or more common unproved status, unlikely benefit comment. Using the term “complementary medicine” and “arya protocol”, I believe that many complementary medicine procedures can be placed “beyond proved” to “statistically sound” methods, which are NOT known as mechanism of working to enable it for chronic medicine, but enough statistical proof exists against thug-claimers.

I am very interested in state of my parents, especially welfare in the last stage. That being so, I demand methods that

1.       Do not interfere with their medical care

2.       Improve their life

3.       Extend their age by 10 years

4.       Do not open me to thugs. Robust Age Extension has been age-old wish and criminal abuse is the oldest profession (religions are ALWAYS criminal!).

5.       Extensions of normal research, particularly challenge able and discard able. I do not claim infallibility but do claim strong reasonable belief! Challenge on reasoning is accepted when references are common trusted empirical.

With these filters (5 is science, though challenge able versions require science!), I have concluded

1.       Metformin and Niagen should be used and proved for age extension
2.       Reservatrol and other oxidants are considered too delicate for commercial use
3.       Blood transfusion and rapamycin can be tested within the expected 10 year extension
4.       There is certain chance of better life and rare chance to first singularity
5.       The Kurzweil approach to life-extension is fundamentally flawed in absence of known interactions on materials input particularly with questions on purity!
6.       Aging tests can and will be employed on them and my family!

Feeling better

CoQ10 and ECP are in that category. I have started on CoQ10 and can anecdotally reports works very well and has hooked me. Best way is get supply from US and pay 60% taxes of GST and Customs (handled by carrier DHL after several photo updates). ECP machine awaits my doing  outpatient-ECP and then use my somewhat strange beneficial diet (bad if soyabeen-allergic or anti-convinced, japs seem to handle it well).

More tests

Parbiosis with clone? Transfusion grand kids? Crisis of transfusion to ancestors? … I am rearing to become an author and test scientist (Not mad but within ethics).

Aaqgs-aging

http://aaqg-arunarya.blogspot.in/2017/08/aaqgs-aging.html why this link?

What is inevitable aging?

Aging is NOT fighting mortal diseases. It is to lead to indefinite life which is NOT immortality. You have to understand these two statements very well if ever you wish to criticize Aaqgs-aging in sane manner; all other critics are considered stupid henceforth forever ignored mother fuckers. Any one can be aaqgs-purged by developing the argument to violate any of these two; or others.

The single most important concept is self-funded-trajectory. No government should spend money on unseen benefits; however the benefits are those appropriate for a government. In fact, I strongly suggest patent activity for the government, with the benefits going to funders, funding decisions allowing in non-discriminatory buy-ins at various stages and non-discriminatory availability of government patents to all fee-paying users.

By this token, the Nixon war on cancer should not have been launched. NASA would not have been launched either. Rocket science is in fact self-funding trajectory of ICBM development that would leave us about now, while reused first stage would have needed no shuttle and done in 2000’s. Americans would be talking of going to moon now!

The self-funding-trajectory to indefinite-life-research would be fight against cancer. The stupidest thing that can happen to aging development is entry of a government or bigger subhuman – the professional politician. As law has learned the hard way trying to manage Boston mayoralty administration, the professional managers are no better or worse; just a different profession! Best that can be done by politicians is to leave all self-funded-trajectory alone! War-against-cancer and NASA are monuments to government folly.

Good afternoon to all.. today I thank god.. my mother has already been out of therapy.. it has already happened in a room... that big is my God.. ALWAYS TRUST MY LORD.. my creator .. for God nothing is impossible...

That’s you, lady, my parents are in same boat. You pray to non-existent God, I don’t, but get my solace from deep search in medical world, result

http://aaqg-arunarya.blogspot.in/2017/08/more-on-niagen.html

http://aaqg-arunarya.blogspot.in/2017/07/aging-aaquantum-approach.html

and many more. Neither link search, nor write-up are motivated by profit, but love for my parents. Question I ask is, how  to provide pain free years and more 10 yrs. Both possible, try on self-first. My experiences might benefit you too. Mind you, I am NOT a moral person by your experience perhaps, but definitely non-violent and non-criminal.

There is NO empirical solution but calorie restriction. Niagen and metformin imitate them. CoQ10 and ECP improve life. Ten years for me to try rapamycin and blood-transfusion on me. No one gets hurt, even I value my skin a lot.

Perhaps you can meet me next time in Ghaziabad, India.! In any case read and chase-link-read!

Why this link

A reader may wonder at the self-aggrandizement represented by including a link to self in the document. It is not so, the stories are copied verbatim by me to send and also by readers to keep the copy when examined.

But the story might (often) changes after the copied alternative! The latest copy can always be referenced from the link included with the article.

More on Niagen

(1 year later) Nad+ is the goal, NMN is 1step away, avoids NAMPT bottleneck, Niagen is two steps away - A form of Vitamin B3. But NMN is 1.5 times more expensive.

http://aaqg-arunarya.blogspot.in/2017/08/more-on-niagen.html why this link?

This is a patent protected nutraceutical, all its commercial forms are derived from chromadex niagen, and hence quality difference is from additional chemicals and interactions.

Niagen boosts NAD+. What's that?

xidative stress and decreased DNA damage repair in vertebrates increase with age also due to lowered cellular NAD+. NAD+ depletion may play a major role in the aging process at the cellular level by limiting (1) energy production, (2) DNA repair, and (3) genomic signaling. In this study, we hypothesize that it is not NAD+ as a cofactor in redox reactions and coenzyme in metabolic processes that has the ultimate role in aging, but rather the role of NAD+ in cellular signaling when used as substrate for sirtuins (SIRT1-7 in mammals) and PARPs [Poly(ADP-ribose) polymerases]. Both sirtuins and PARPs influence many transcription factors and can affect gene expression. As a signaling molecule, NAD+ is consumed in the reaction donating ADP-ribose and releasing nicotinamide (NAM) as a by-product. It seems that aging at the cellular level is associated with a decline of NAD+ and that NAD+ restoration can reverse phenotypes of aging by inducing cellular repair and stress resistance. Adequate intracellular NAD+ concentrations may be an important longevity assurance factor, while lowered cellular NAD+ concentration may negatively influence the life span.

What is the state of niagen as per FDA?

This 2015 determination is validated just a few days ago.

Why should anyone believe Niagen?

1.     Ultimate proof is empirical, a Japanese study started in 2016, how will anyone prove anti-aging?

2.     Cells have NaDH – NAD+ cycle. One can show empirically that NAD+ level FALL directly vary with age and tiredness correlated with age.

3.     Eating Niagen provably boosts the level of NAD+ by empirical standard measures.

4.     Anecdotally, consumers feel better. A dosage level of 250 mg has been set by informal studies (larger doses do not raise NAD+ SIGNIFICANTLY before fall to 250 mg level).

5.     It is very expensive, far more than coQ10. Cheapest reliable I could find was at amazon,  at Rs. 6913 (when link taken) per month! It is not likely to fall. I see a battle-royal on drug patents by 2020!

Some more references?

1.    Reversing Aging: Not as Crazy as You Think. TIME, 2013 Dec 19

What makes cells age? Wear and tear, yes. But biologically, says, Dr. David Sinclair, professor of genetics at Harvard Medical School, it’s lack of oxygen that signals cells that it’s their time to go. Without oxygen, the energy engines known as the mitochondria become less efficient at turning physiological fuel like glucose into the energy that the cells need to function. Eventually, they shut down…

2.  Niagen Nicotinamide Riboside New NDI Status from FDA

ChromaDex Lead Ingredient NIAGEN® Nicotinamide Riboside Receives New Dietary Ingredient (NDI) Status From the FDA

November 16, 2015

IRVINE, Calif., Nov. 16, 2015 (GLOBE NEWSWIRE) -- ChromaDex Corp. (OTCQX:CDXC), an innovator of proprietary health, wellness and nutritional ingredients that creates science-based solutions for dietary supplement, food and beverage, skin care, sports nutrition, and pharmaceutical products announced today it has received New Dietary Ingredient (NDI) status from the FDA for its patented and proprietary lead ingredient, NIAGEN^® nicotinamide riboside….

3.    Dose-Dependent Elevation of the Blood NAD+ Metabolome by NR

Dose-Dependent Elevation of the Blood NAD Metabolome by NR in Healthy Human Beings: Clinical Efficacy and Novel Diagnostic Biomarkers Abstract Nicotinamide riboside chloride (NR) is in wide use as an orally available NAD precursor vitamin. Here we conducted three experiments to determine the time and dose-dependent effects of NR on blood and liver NAD metabolomes in people and in mice, respectively. We report that human blood cell NAD+ can rise as much as 2.7-fold with a single dose of NR, that NR elevates mouse hepatic NAD+ with distinct and superior kinetics to those of Charles Brenner1 , Samuel AJ Trammell1 , Mark S Schmidt1 , Benjamin J Weidemann1 , Philip Redpath2 , Marie E Migaud2 , Frank Jaksch3 & Ryan W Dellinger3 University of Iowa, USA1; Queens University Belfast, Northern Ireland2 and ChromaDex, Inc, USA3 NAD+ Biosynthesis Study Design Phase: Day: -14 1 2 8 9 15 16 Visit: 1 2 3 4 5 6 7 2 Weeks Screening Treatment Period (3 Weeks) 7 Day Washout 7 Day Washout NAD metabolites undergo circadian oscillation(2,3). To eliminate circadian oscillation as an experimental confounder, we developed an oral gavage protocol in which male C57BL/6 mice were given single oral doses of NR at 185 mg/kg 20’, 1 hr, 2 hr, 4 hr, 6 hr, 8 hr and 12 hr prior to sacrifice, which was always performed at ~ 2 pm. In addition, mice were dosed with equimole amounts of NA, Nam and a control saline solution, and mice were sacrificed at 2 pm without gavage.

supplementationJ Neurosci. 2006 Aug 16;26(33):8484-91 (click to download)

4.   

Nature. 2004;429:771–776. doi: 10.1038/nature02583

Calorie restriction extends lifespan in organisms ranging from yeast to mammals¹. In yeast, the SIR2 gene mediates the life-extending effects of calorie restriction². Here we show that the mammalian SIR2orthologue, Sirt1 (sirtuin 1), activates a critical component of calorie restriction in mammals; that is, fat mobilization in white adipocytes. Upon food withdrawal Sirt1 protein binds to and represses genes controlled by the fat regulator PPAR-γ (peroxisome proliferator-activated receptor-γ), including genes mediating fat storage. Sirt1 represses PPAR-γ by docking with its cofactors NCoR (nuclear receptor co-repressor) and SMRT (silencing mediator of retinoid and thyroid hormone receptors). Mobilization of fatty acids from white adipocytes upon fasting is compromised in Sirt1^+/− mice. Repression of PPAR-γ by Sirt1 is also evident in 3T3-L1 adipocytes, where overexpression of Sirt1 attenuates adipogenesis, and RNA interference of Sirt1 enhances it. In differentiated fat cells, upregulation of Sirt1 triggers lipolysis and loss of fat. As a reduction in fat is sufficient to extend murine lifespan³, our results provide a possible molecular pathway connecting calorie restriction to life extension in mammals.​

5.    Rejuvenation Res. 2016 Mar 16. DOI: 10.1089/rej.2015.1767

Oxidative stress and decreased DNA damage repair in vertebrates increase with age also due to lowered cellular NAD+. NAD+ depletion may play a major role in the aging process at the cellular level by limiting (1) energy production, (2) DNA repair, and (3) genomic signaling. In this study, we hypothesize that it is not NAD+ as a cofactor in redox reactions and coenzyme in metabolic processes that has the ultimate role in aging, but rather the role of NAD+ in cellular signaling when used as substrate for sirtuins (SIRT1-7 in mammals) and PARPs [Poly(ADP-ribose) polymerases]. Both sirtuins and PARPs influence many transcription factors and can affect gene expression. As a signaling molecule, NAD+ is consumed in the reaction donating ADP-ribose and releasing nicotinamide (NAM) as a by-product. It seems that aging at the cellular level is associated with a decline of NAD+ and that NAD+ restoration can reverse phenotypes of aging by inducing cellular repair and stress resistance. Adequate intracellular NAD+ concentrations may be an important longevity assurance factor, while lowered cellular NAD+ concentration may negatively influence the life span.