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Longevity, Antiaging, Fountain of Youth, whatever you want to call it!

Would you like to have your organs function for a longer time and stay healthy? It’s a substitute for the term “longevity” because we don’t know how long we might live and no way to predict it. But we don’t know we have ways to enhance the viability of all organs with good data to support our recommendations for the treatments

There has been for years, physicians and patients looking for the “fountain of Youth”. There has been little interest in the government or institutions in looking for an answer until recently. People., in general, are very sceptic of anything that might increase longevity only because they know nothing about it and don’t care to learn. Much research has been done on medications such as Rapamycin, exosomes, NAD and TA 65. Plaque-x is also used to decreases the plaque in the arteries. I used TA 65 about 6 years ago. Had my telomere lengths measured before and after treatment and the length was increased by 25% which translated that I was 5 years biological younger than when I started. I would first like to go into detail how the medications work and how they are administered.

1. Exosomes are derived from mesenchymal stem cells obtained from amniotic fluid at the time of a woman’s Caesarian section. Within the stem cells from the fetus are small vesicles called Exosomes, the “work horse” of the stem cell. They demonstrate extensive tissue regeneration, repair and are anti-inflammatory. They are concentrated in over 300 billion per 1 ml. We lose every day over 300 million cells through the process of cell division. After the cell divides about 30 times, the telomeres on the end of the chromosome become frayed and the cell become senescent (dies). These exosomes will regenerate the senescent cells back to functioning which will in turn affect all organs to live longer thereby being more functional for a longer period of time. There is no DNA in the exosomes, only, RNA so absolutely no side effects. They are given intravenously every 1 to 3 months. There are other sources of exosomes that work just as well but I limited the discussion to one source for the sake of too much information.

2. Rapamycin is a drug used to prevent rejection of an organ after transplant. It decreases mTor that can cause rejection of the organ. Those patients that require the drug to prevent rejection will be taking 4-6 mg daily while the method to decrease mTor to increase longevity is only 2-6 mg a week. At that dose there are no side effects. It has been calculated that rapamycin slows geroconversion by approximately 3-fold [6]. By doing so, rapamycin slows development and aging, reproduction and menopause, and hyperfunction and functional decline. The mechanistic target of rapamycin (mTOR) is a nutrient and growth factor responsive kinase that modulates lifespan in species from yeast to mice (Johnson et al., 2013b). mTOR exists in two complexes within cells, mTOR complex I (mTORC1) and mTOR complex 2 (mTORC2) (Laplante and Sabatini, 2012).

a. Abundant evidence suggests that mTORC1 is the primary mTOR complex involved in regulating longevity: mutations that reduce the activity of mTORC1 have been shown to extend lifespan in yeast (Kaeberlein et al., 2005; Powers et al., 2006), nematode worms (Jia et al., 2004; Vellai et al., 2003), fruit flies (Kapahi et al., 2004), and mice (Lamming et al., 2012), as has deletion of the mTORC1 substrate ribosomal S6 kinase (Fabrizio et al., 2004; Fabrizio et al., 2001; Kapahi et al., 2004; Pan et al., 2007; Selman et al., 2009).

b. Consistent with these genetic data, treatment with the mTORC1 inhibitor rapamycin has also been found to increase lifespan in yeast (Medvedik et al., 2007; Powers et al., 2006), worms (Robida-Stubbs et al., 2012), fruit flies (Bjedov et al., 2010), and mice (Harrison et al., 2009).

c. The following are the specific cardinal concepts NOT ACCEPTED by conventional medicine:

i. Aging in humans is programmed.

ii. mTOR is driving programmed aging.

iii. Aging is the fundamental cause of most Age-related diseases

iv. Aging is a treatable condition.

v. Physicians should treat aging to increase health span in older people.

d. Too much mTOR activation is associated with a large number of human diseases, including cancer, obesity, acne, type 2 diabetes, depression, and neurodegeneration [2, 10].

e. mTOR is associated with cancer and indeed, it increases angiogenesis (via HIF-1a), a process through which new blood vessels form from pre-existing vessels, helping tumors grow [7].

f. Increased mTOR promotes Th1 and Th17 immunity, possibly leading to increased intestinal inflammation [11], among other issues. It increases Th17 cells by increasing another protein called hypoxia-induced factor (HIF)-1α [12].

g. A reduction in mTOR improved insulin sensitivity in muscle cells, possibly by increasing the process of breaking down sugar (glycolysis) [13, 14].

h. When T cells (CD4 and CD8) are stimulated, they rapidly reproduce [14].

i. The rapid production of T Cells requires energy. Activation of mTOR allows the T Cells to rapidly expand by shifting how they get energy. Instead of getting energy from the mitochondria (via oxidative phosphorylation), they get it primarily from breaking glucose down (glycolysis) [14].

j. When you prevent this process of glucose breakdown, T cells realize that they don’t have what it takes to rapidly expand and fight pathogens. So instead, they turn into Treg cells, which dials the immune system down [14].

3. NAD (Nicotinamide adenine dinucleotide). It is a coenzyme that is present in all living cells derived from vitamin B3. Nicotinamide adenine dinucleotide exists in two forms, an oxidized and reduced form abbreviated as NAD+ and NADH respectively. It is therefore safe for us to say that NADH is a reduced form of NAD+. IV NAD is a crucial coenzyme in metabolism. NAD is used for:

a. Anti-aging

b. Mitochondrial issues

c. Fatigue (CFS)

d. Alcohol or substance abuse

e. Energy production

f. Mental acuity (focus)

g. Jet lag

h. Brain restoration

i. Mood balance

j. Nicotinamide adenine dinucleotide (NAD (+)) is a classical coenzyme mediating many redox reactions. NAD (+) also plays an important role in the regulation of NAD (+)-consuming enzymes, including sirtuins, poly-ADP-ribose polymerases (PARPs), and CD38/157 ectoenzymes.

i. NAD (+) biosynthesis, particularly mediated by nicotinamide phosphoribosyl transferase (NAMPT), and SIRT1 function together to regulate metabolism and circadian rhythm. NAD (+) levels decline during the aging process and may be an Achilles' heel, causing defects in nuclear and mitochondrial functions and resulting in many age-associated pathologies. Restoring NAD (+) by supplementing NAD (+) intermediates can dramatically ameliorate these age-associated functional defects, counteracting many diseases of aging, including neurodegenerative diseases.

ii. Thus, the combination of sirtuin activation and NAD (+) intermediate supplementation may be an effective antiaging intervention, providing hope to aging societies worldwide.

4. TA 65: TA-65 is a dietary supplement based on an improved formulation of a small molecule telomerase activator that was discovered in a systematic screening of natural product extracts from traditional Chinese medicines. This study summarizes the findings on telomere length (TL) changes from a randomized, double blind, placebo-controlled study of TA-65 over a 1-year period. The study was conducted on 97 relatively healthy cytomegalovirus-positive subjects aged 53-87 years old. Subjects taking the low dose of TA-65 (250 U) significantly increased TL over the 12 months period, as compared to the placebo group (530 ± 180 bp; p = 0.005), whereas subjects in the placebo group significantly lost TL (290 ± 100 bp; p = 0.01).

a. The high dose of TA-65 (1000 U) showed a trend of improvements in TL compared with that of the placebo group; however, the improvements did not reach statistical significance.

b. TL changes in the low-dose group were similar for both median and 20th percentile TLs. The findings suggest that TA-65 can lengthen telomeres in a statistically and possibly clinically significant manner.

5. Metformin: Metformin also, inhibits the inflammatory pathway and increases AMPK activation, which inhibits mTOR, a primary target for cell aging modulation. Inflammation, apoptosis, autophagy, cell survival, and protein synthesis are all affected by these mechanisms and are all linked to accelerated aging.

6. Thymic Regeneration, Immune restoration and Insulin Mitigation, reveals a pathway for restoring thymic function and possibly slowing or reversing aging. In the study, researchers used a protocol intended to regenerate the thymus with the use of high, metformin, and DHEA. The results showed participants shed 2 years off their biological age according to the GrimAge predictor model (a method of analyzing a subject’s DNA to track a person’s biological age vs their chronological age). In addition, MRI studies revealed highly significant evidence of thymic regeneration, with restoration of functional thymic mass. Furthermore, favorable changes in immune cell proliferation of previously exhausted cells were demonstrated. Underactive immune systems, especially in older people, leave them at risk for age-related diseases, especially infections and cancers.

7. Plaque-x: Plaque-x is used to remove plaque from the arteries. Unfortunately, there is no good way to determine how much plaque one has without having a coronary arteriogram that insurance won’t pay for unless you have angina or a heart attack, then it’s too late. We use indicators that one my need the plaques if one has a positive calcium score, elevated lipids not responding to diet or hormone therapy, strong family history of high cholesterol or LDL or strong family history of heart disease especially early heart attacked or stents. It’s obvious that if one has plaques developing, longevity may be delayed because of the consequences of plaque causing heart disease, dementia, kidney failure, or failure of other organs.

8. Mediterranean diet is the preferred diet which is low in carbohydrates and saturated fat.

9. Exercise of course will improve the cardiovascular system, help in weight loss and decrease fat mass.

10. Weight loss has been shown to be very beneficial in longevity, especially if one is below their idea weight. There’s no question that it can shorten your lifespan, and by large numbers. If you can get the weight off before there’s major damage done to your organs, that will tremendously prolong your life.” Losing weight, even just 5 to 10 percent of excess weight, can add years to your life. Not only will you live longer, but also, you’ll feel better and deal with fewer health complications.

11. Intermittent fasting

12. Reduce stress

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