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Stop Taking Antibiotics For The Common Cold

by Lisa Richards @ The Candida Diet

Most of us have taken antibiotics at some stage in our lives. In fact, we’re usually quite comfortable with popping a few pills given to us by our doctor. After all, it’s one of the steps in getting well again – right? Not always! Outbreaks of ‘superbugs’ are evidence that many people are too eager […]

The post Stop Taking Antibiotics For The Common Cold appeared first on The Candida Diet.

Children’s Probiotics Gummies Constipation Strain

by @ INSIGHTMARKETING LEVEL

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by @ projectathena probiotics composition

Anaemia (low number of red blood cells). probiotics.other than that i have to shove those things as well (Keep Prep Sheet In Bathroom For Your Reading Pleasure AND look this over . Colon Cancer X Ray Pictures Cancer Rates Survival Country i am having bad stomach aches and back pain for some time now. Drinking […]

Buckwheat Soba Noodle Bowl

by Lisa Richards @ The Candida Diet

Popular in Japan, soba noodles are made from buckwheat flour. They are a good source of nutrients like manganese, lean protein, and thiamine. Since buckwheat is a gluten-free grain, soba noodles are a good choice for people following the Candida diet. When shopping for soba noodles be sure to read the ingredient labels carefully as […]

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“Candida Detox Recovery Guide” Free PDF eBook Now Available!

by James White @ Candida Support

Your friends at Candida Support are very excited to be able to offer you our free downloadable PDF eBook, “Candida Detox Recovery Guide.” We have combined our previously website-only online “Candida Detox Guide” and our online Frequently Asked Questions into one easy-to-read PDF. This book is the result of more than 20 years of Marti […]

The post “Candida Detox Recovery Guide” Free PDF eBook Now Available! appeared first on Candida Support.

Why use powders over capsules?

by @ Custom Probiotics Canada: Latest News

Powders allow you to vary your dosage very easily. You can take as little or much as you personally require this way. For example, some of our clients use a baby scoop of powder a day which is about 30 – 40 billion CFU. Others take up to 4 adult scoops a day, that’s about 1.2 Trillion CFU a day! That would be about 15 capsules!

So if you want to take a high amount of CFU, we would suggest trying the powders. They also cost less per CFU compared to the capsules.

Below is one of our popular powders we recommend starting with.

http://www.customprobiotics.ca/six-strain-probioti...

Probiotico Lifespan For Best Gas Bloating

by @ INSIGHTMARKETING LEVEL

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I Will Not Take Anymore Drugs to Treat Colitis!

by JINI @ Listen To Your Gut

We just received this fantastic review in our Shoppe: “Taking the Natren Healthy Start System Tripack probiotics couple with the Joy of the Mountain Wild Oil of Oregano, my bleeding stopped in less than a week. My severe pain was gone on my left side within two weeks. Within five weeks, I was completely regular…

Candida Paleo Recipes Dosage For Fluconazole

by @ iihff yeastinfection thionvillefc

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Feeling Frustrated – Why is my gut not healing faster?

by JINI @ Listen To Your Gut

READER QUESTION: “Feeling frustrated. I think I’m on my 4th bottle of mucosaheal and still have a lot of bleeding and a lot of mucus (taking 2 three times a day and 3 at bed) I was taking the Natren probiotics but it seemed to make everything worse. I changed back to VSL3 probiotics and…

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by @ iihff yeastinfection thionvillefc

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Get Your Sleep To Beat Candida

by Lisa Richards @ The Candida Diet

There are lots of healthy ways to tackle Candida overgrowth – changing your diet, taking supplements or reducing stress. But did you realize that your sleep has also has a huge impact on your recovery from Candida? Getting enough sleep each night is becoming more and more problematic. Electronic devices, irregular working hour and daily […]

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Diflucan Dose For Oral Candida Severe Die Off

by @ iihff yeastinfection thionvillefc

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Jini Patel Thompson and Dane Johnson talk probiotics

by Justin @ Listen To Your Gut

In this video, Jini and Dane discuss probiotics, their personal healing journeys, and general gut health:

Pb8 Probiotic Canada Burping

by @ Probiotics Belaw

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Rinse Away Nose & Sinus Problems

by Marti Ayres White @ Candida Support

When our son started college he was surveying all the equipment for his dorm room: sheets, towels, electric kettle, microwave popcorn, first aid kit. “Wait,” he said. “Where is the Neti pot? What if I get a cold? Or allergies? I can’t go to college without a Neti pot”!!!! And what, you might ask, is […]

The post Rinse Away Nose & Sinus Problems appeared first on Candida Support.

Hello world!

by admin @ Probiotics Database

Welcome to WordPress. This is your first post. Edit or delete it, then start blogging!

The post Hello world! appeared first on Probiotics Database.

Medical Paper Echoes Holistic Treatment for Candida!

by JINI @ Listen To Your Gut

This recent paper published in Mycopathologia is an in-depth investigation into the different types of Candida (both the strains and locales of infection) along with some treatment recommendations – which may surprise you, since they’re essentially what holistic practitioners have been advising for decades! You can either download the entire paper and read it yourself,…

How To Make A Natural, Sugar-Free Slurpee!

by JINI @ Listen To Your Gut

We’ve just had a big, fresh snowfall here in Vancouver, Canada and the kids have been out sledding, making snowmen, and thoroughly enjoying themselves. Then this morning, my daughter Zara comes in with a big hunk of snow to snack on – which is exactly what I used to do as a child! However, she…

Why do some turtles outlive humans?

by @ Articles - Articles

(⇒ write for LongeCity )


The oldest human recorded in modernity was Jeanne Louise Calment, she died in the age of 122 years and 164 days [1] .

There are rumors that the oldest tortoise called Adwaita (Aldabra giant tortoise) died in the age of about 250 years [2] or that it was 188-year-old radiated tortoise named Tui Malila [3] , or that the highest verified age of 177 years had Galapagos giant tortoise Harriet [4] . The oldest currently living turtle is considered to be Jonathan (Seychelles giant tortoise), estimated to be over 180 years old these days [5] . Although all aforementioned numbers are estimations, it seems these turtles were older than human supercentenarians.

All previously mentioned species are terrestrial tortoises, a group with longest lifespans among turtles. The most famous of them, well-researched Galapagos giant tortoise, was observed by Charles Darwin when he was forming his well-known theory of evolution by natural selection [6] . There is only one freshwater turtle known to be able to outlive human, it is the common snapping turtle estimated to live up to more than hundred years [7] . While being considerably less researched, recorded maximal lifespan of sea turtles is usually shorter, not exceeding 80 years, however, it is believed that the green sea turtle can live up to 100 years. [8]

It is a difficult question to answer why these reptiles can outlive us because even to determine the actual age of animals with a long lifespan is complicated – partially due to the fact that it takes such a long time to study. Furthermore, many turtles are endangered species [9] so there may not be as many organisms to hand as needed for proper statistics. Nonetheless, we can still claim that turtles are among the most long-living vertebrates on earth [10] . Why?

Firstly, turtles, like all reptiles, benefit from being ectothermic organisms. They do not maintain body temperature and thus save a lot of energy. But that also means they are less flexible: it is crucial for their lifespan to be in natural temperature environment of daily cycles with night-time temperature drop [11] . If they do not live under these conditions in captivity, metabolic pathways change and turtles die much sooner. [12]

Turtles are well-adapted in other ways: their famous shell – the carapace –is good protection against natural predators. Most of hatchling turtles with a soft shell do not survive the first year [13] . A research of natural populations of freshwater turtles showed that only one per cent of them can celebrate the twentieth birthdays, but once the adulthood is reached, mortality rate drops and remains constant throughout the rest of life [14] .

Some turtles can survive under extreme environmental conditions, such as freezing [15] or lack of oxygen for months [16] . They can even undergo hibernation and anaerobic metabolism and therefore deal with hypoxia and anoxia, it was also proposed that the same genes can play a role in longevity itself [17] and also in oxidative stress resistance [18] that further promotes longer life [19] .

Turtle’s bones and shell are used as lactate buffer lowering metabolic acidosis caused by anaerobic glycolysis during the period of lack of oxygen [20] ; [21] Their organism is protected by strong innate immunity compensating slow acquired immune reactions [22] .

Because turtles have very slow metabolism as well as growth, their bodies do not need to deal with excessive metabolic heat and byproducts as mammals [23] . Their natural diet is very simple but also necessary for their longevity. [24]

According to the evolutionary theories, staying alive is less important after menopause. Galapagos giant tortoises achieve sexual maturity late (around the age of up to forty years in the wild, and between twenty and twenty-five years of life in captivity [25] ), then staying fertile until death [26] .

The Hayflick limit is said to determine how many times a cell can divide [27] . The Hayflick limit of Galapagos giant tortoise was said to be about 110 divisions [28] , approximately twice as many as 50 of human cells [29] . Studies in this context have highlighted the importance of telomeres, the protective end sequences of chromosomes, that get shorter with each cell division [30] , can play at least a partially role in life expectancy. It was observed that telomeres in European freshwater turtle’s cells are of the same length in both embryo and adult organism [31] .

Thus, it was believed that turtles are negligibly senescent organisms [32] . In other words, the cells do not age and no age-related diseases appear, which is very different cell behavior than in human bodies [33] and probably the key to any natural longevity. However, evidence now suggests that turtles may not be really negligibly senescent because of observations of survival and reproductive senescence in late age in the painted turtle population [34]

As we can see, turtles have some advantages in the lifespan field. Some of these might inspire researchers to increase lifespans in humans.



References

[1] Oldest person ever. Retrieved January 31, 2017, from http://www.guinnessworldrecords.com/world-records/oldest-person
[2] BBC (2006, March 23). “Clive of India’s” tortoise dies. BBC South Asia. Retrieved from http://news.bbc.co.uk/2/hi/south_asia/4837988.stm
[3] Associated Press (2006, June 26). Tortoise believed to have been owned by Darwin Dies at 176. Fox News. Retrieved from http://www.foxnews.com/story/2006/06/26/tortoise-believed-to-have-been-owned-by-darwin-dies-at-176.html
[4] Galapagos tortoise (Geochelone nigra) longevity, ageing, and life history. Retrieved January 31, 2017, from http://genomics.senescence.info/species/entry.php?species=Geochelone_nigra
[5] Hollins, J. (2012). The world’s most isolated vet? Veterinary Record, 171(2), i–i. doi:10.1136/vr.g7292
[6] Powell, J., & Caccone, A. (2006). Giant tortoises. Current Biology, 16(5), R144–R145. doi:10.1016/j.cub.2006.02.050
[7] Cameron, M. (2008). COSEWIC Assessment and Status Report on the Snapping Turtle Chelydra serpentina in Canada . Retrieved from http://publications.gc.ca/collections/collection_2009/ec/CW69-14-565-2009E.pdf
[8] Green sea turtle (Chelonia mydas) longevity, ageing, and life history. Retrieved January 31, 2017, from http://genomics.senescence.info/species/entry.php?species=Chelonia_mydas
[9] Jacobson, E. R. (1994). Causes of Mortality and Diseases in Tortoises: A Review. Journal of Zoo and Wildlife Medicine, 25(1), 2–17.
[10] Gibbons, J. W. (1987). Why do turtles live so long? BioScience, 37(4), 262–269. doi:10.2307/1310589
[11] Flouris, A. D., & Piantoni, C. (2014). Links between thermoregulation and aging in endotherms and ectotherms. Temperature, 2(1), 73–85. doi:10.4161/23328940.2014.989793
[12] Vadala, N. How Long Do Turtles Live? Retrieved January 31, 2017, from http://www.petmd.com/reptile/care/how-long-do-turtles-live
[13] Stewart, K. R., & Wyneken, J. (2004). Predation risk to loggerhead hatchlings at a high-density nesting beach in Southeast Florida. Bulletin of Marine Science, 74(2), 325–335.
[14] Gibbons, J. W., & Semlitsch, R. D. (1982). Survivorship and longevity of a long-lived vertebrate species: How long do turtles live? The Journal of Animal Ecology, 51(2), 523. doi:10.2307/3981
[15] Packard, G. C., & Packard, M. J. (2003). Natural freeze-tolerance in hatchling painted turtles? Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 134(2), 233–246. doi:10.1016/s1095-6433(02)00264-7
[16] Milton, S. L., & Prentice, H. M. (2007). Beyond anoxia: The physiology of metabolic downregulation and recovery in the anoxia-tolerant turtle. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 147(2), 277–290. doi:10.1016/j.cbpa.2006.08.041
[17] Shaffer, H. B., Minx, P., Warren, D. E., Shedlock, A. M., Thomson, R. C., Valenzuela, N., … Wilson, R. K. (2013). The western painted turtle genome, a model for the evolution of extreme physiological adaptations in a slowly evolving lineage. Genome Biology, 14(3), R28.doi:10.1186/gb-2013-14-3-r28
[18] Garbarino, V. R., Orr, M. E., Rodriguez, K. A., & Buffenstein, R. (2015). Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates. Archives of Biochemistry and Biophysics, 576, 8–16. doi:10.1016/j.abb.2015.01.029
[19] von Zglinicki, T. (2002). Oxidative stress shortens telomeres. Trends in Biochemical Sciences, 27(7), 339–344. doi:10.1016/s0968-0004(02)02110-2
[20] Jackson, D. C. (2000). Living without oxygen: Lessons from the freshwater turtle. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 125(3), 299–315. doi:10.1016/s1095-6433(00)00160-4
[21] Krivoruchko & Storey, 2010).
[22] Sandmeier, F. C., Tracy, C. R., Dupre, S., & Hunter, K. (2012). A trade-off between natural and acquired antibody production in a reptile: Implications for long-term resistance to disease. Biology Open, 1(11), 1078–1082. doi:10.1242/bio.20122527
[23] Bilinski, T., Paszkiewicz, T., & Zadrag-Tecza, R. (2015). Energy excess is the main cause of accelerated aging of mammals. Oncotarget, 6(15), 12909–12919. doi:10.18632/oncotarget.4271
[24] Casares, M., Honegger, R. E., & Rubel, A. (1995). Management of giant tortoises Geochelone elephantopus and Geochelone gigantean at Zurich Zoological gardens. International Zoo Yearbook, 34(1), 135–143. doi:10.1111/j.1748-1090.1995.tb00671.x
[25] Global, S. D. Z. (2010). Galapagos tortoise fact sheet. Retrieved January 31, 2017, from http://library.sandiegozoo.org/factsheets/galapagos_tortoise/tortoise.htm
[26] Curtin, A. J., Zug, G. R., & Spotila, J. R. (2009). Longevity and growth strategies of the desert tortoise (Gopherus agassizii) in two American deserts. Journal of Arid Environments, 73(4-5), 463–471. doi:10.1016/j.jaridenv.2008.11.011
[27] Hayflick, L. (1965). The limited in vitro lifetime of human diploid cell strains. Experimental Cell Research, 37(3), 614–636. doi:10.1016/0014-4827(65)90211-9
[28] Goldstein, S. (1974). Aging in vitro. Experimental Cell Research, 83(2), 297–302. doi:10.1016/0014-4827(74)90342-5
[29] Hayflick, L., & Moorhead, P. S. (1961). The serial cultivation of human diploid cell strains. Experimental Cell Research, 25(3), 585–621. doi:10.1016/0014-4827(61)90192-6
[30] Harley, C. B., Futcher, A. B., & Greider, C. W. (1990). Telomeres shorten during ageing of human fibroblasts. Nature, 345(6274), 458–460. doi:10.1038/345458a0
[31] Girondot, M., & Garcia, J. (1999). Senescence and longevity in turtles: What telomeres tell us. 9th extraordinary meeting of the societas Europaea Herpetologica, 1, 25–29. Retrieved from //www.researchgate.net/publication/252290006_Senescence_and_longevity_in_turtles_What_telomeres_tell_us
[32] Miller, J. K. (2001). Escaping senescence: Demographic data from the three-toed box turtle (Terrapene carolina triunguis). Experimental Gerontology, 36(4-6), 829–832. doi:10.1016/s0531-5565(00)00243-6
[33] Schächter, F., Cohen, D., & Kirkwood, T. (1993). Prospects for the genetics of human longevity. Human Genetics, 91(6), . doi:10.1007/bf00205074
[34] Warner, D. A., Miller, D. A. W., Bronikowski, A. M., & Janzen, F. J. (2016). Decades of field data reveal that turtles senesce in the wild. Proceedings of the National Academy of Sciences, 113(23), 6502–6507. doi:10.1073/pnas.1600035113

Probiotic Inner Ear Medication

by @ INSIGHTMARKETING LEVEL

C Diff. Probiotic Inner Ear Medication best Foods For Naturally Glowing Skin 112 views; How To Heal Cracked Feet Quickly 108 views; Men’s Health. The former Today show anchor’s first husband Jay Monahan died in 1998 of colon cancer. OBELIX Study: A Study of Avastin (Bevacizumab) in Combination With XELOX in Patients With Metastatic Cancer […]

Immune System Protocol

by JINI @ Listen To Your Gut

Immune System Protocol After several requests, I’ve put together this video to share with you my family’s winter immune system protocol. Good food, good sleep, Vitamin D & cod liver oil, probiotics, and immune boosters like astragalus and medicinal mushrooms. And wild oregano oil when needed. Enjoy!

How To Make Whey and Yogurt Cream Cheese

by JINI @ Listen To Your Gut

MORE FOOD-BASED PROBIOTICS If you’ve seen my recipe for the Best Lacto-Fermented Mayonnaise Ever, but you don’t know how to obtain the fresh liquid whey (the probiotics contained in fresh liquid whey are used to lacto-ferment mayonnaise, grains, vegetables, etc.) then here are detailed instructions: When you extract the liquid whey from yoghurt, you automatically…

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by @ projectathena probiotics composition

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by @ projectathena probiotics composition

Manufactured by: Optibac Probiotics. GNC Total Lean 2-Day Juice Cleanse – Read Reviews. Gt Kombucha Nutrition Label Sources interestingly probiotics side effects mean that the good bacteria are working! Here are the most common side effects: Consistent with this fact the presence of mutated p53 in colon cancer patients is often used as an indicator […]

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by @ Probiotics Belaw

A sluggish liver can lead to serious fatigue weight gain water retention and a host of other health woes. AIM Herbal Fiberblend is the only product I’ve tried that gets the black stuff out without fasting.” Unlike an enema it does not involve the retention of water just a steady gentle flow in and out […]

Best Lacto-Fermented Mayonnaise Recipe Ever

by JINI @ Listen To Your Gut

FOOD-BASED PROBIOTICS: Lacto-Fermented Mayonnaise I did a lot of experimenting to determine which oils provide the best-tasting mayonnaise, whilst providing excellent nutrition – I think this recipe is my fifth variation and I’m finally happy with it! My never-ending thanks to Nourishing Traditions cookbook for providing the lacto-fermentation method whereby the mayonnaise keeps for 3-4…

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by JINI @ Listen To Your Gut

The School Board’s position on cell phone and wireless computer usage inside my kids’ school is: Hey, we just follow what Health Canada says! And Health Canada says there is no possibility of danger from radio frequency microwave radiation. Huh. So here’s what I think of that: Currently, Health Canada maintains that 1000 mw/cm2 is…

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by @ iihff yeastinfection thionvillefc

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by @ iihff yeastinfection thionvillefc

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Tasty Salmon Bowl With Arugula Dressing

by Lisa Richards @ The Candida Diet

Meals in a bowl have become quite popular, perhaps as a response to our busy lives. On days when you’re too tired to cook, you still need to eat! These bowls provide something simple and satisfying, hearty and filling – everything you need in just one bowl. They are easy to prepare in just a few […]

The post Tasty Salmon Bowl With Arugula Dressing appeared first on The Candida Diet.

Candida Ukladu Pokarmowego Objawy Scan Ct Hepatosplenic

by @ iihff yeastinfection thionvillefc

Transfers were made at 7 to 10 day intervals. Dissolve yeast in warm water in a small bowl: set aside. Candida Ukladu Pokarmowego Objawy Scan Ct Hepatosplenic also known as corn starch or cornflour in various countries it is finely grounded white starch powder extracted from maize kernels. Primer Trimestre; El tratamiento de la cistitis […]

I need to return some items… How can I get a refund?

by JINI @ Listen To Your Gut

We understand that not everything works out for everyone so we are happy to accept returned merchandise if it conforms to the following rules: 1. The items are returned sealed and unopened. 2. The items are returned within 30 days of the original purchase. 3. The items are NOT probiotics (Sorry, we are unable to…

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Probiotic - Supplements


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by @ projectathena probiotics composition

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How To Make Homemade Yoghurt Using Probiotic Cultures

by JINI @ Listen To Your Gut

Most recipes for culturing yoghurt will advise you start with some store-bought yoghurt and use that as the fermenting culture for your milk. Of course, that will work, and it will produce yogurt, but what will be the quality and potency of that yoghurt as a probiotic? Not very good. Potent probiotics strains are a…

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by @ Probiotics Belaw

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by @ INSIGHTMARKETING LEVEL

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Where can I find out more about Wild Oregano Oil?

by JINI @ Listen To Your Gut

The most common question we receive about Wild Oregano Oil is whether or not you can use it along with probiotics and the answer is yes. However, you’ll want to make sure there are at least 2 hours between taking the wild oregano oil and the probiotics. I have compiled some links below to information…

Erythritol: A Healthy Alternative To Sugar

by Lisa Richards @ The Candida Diet

You don’t have to look far these days to find sugar-free treats, beverages, and candy. Unfortunately, not all sugar-free products are good! In recent years there’s been an upsurge in products containing harmful synthetic sweeteners such as aspartame. Luckily, there are lots of natural sweeteners out there that are just fine for including in your […]

The post Erythritol: A Healthy Alternative To Sugar appeared first on The Candida Diet.

Video: Why the Candida Diet Does Not Work!

by James White @ Candida Support

Candida Diet: Necessary “Evil” or Unnecessary? During our live Q&A Session, Candida Support co-founder, Jim White answered a frequently-asked question, “what about eating sweets?” In other words, this customer wanted to know whether it was necessary to follow the Candida Diet. Jim’s answer may surprise you!   Edited Transcript For your reading convenience, here is […]

The post Video: Why the Candida Diet Does Not Work! appeared first on Candida Support.

Yeast Infection Week After Ovulation Symptoms Libido Candida

by @ iihff yeastinfection thionvillefc

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by @ nena-network nena

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by @ INSIGHTMARKETING LEVEL

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Probiotic Retention Enema

by JINI @ Listen To Your Gut

OKay, I just had to post this account from Jay Baluk (a.k.a. CROHNSBOY) who recently tried Jini’s Probiotic Retention Enema. I love Jay because he’s SO candid and honest and blunt. And the photo on his post alone is so funny I just had to point you to it. But, WARNING: If you’re a very…

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by @ Probiotics Belaw

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Candida Auris: The Rise Of A Fungal Superbug

by Lisa Richards @ The Candida Diet

Just when you thought Candida albicans was bad enough, along comes a much more serious yeast overgrowth. Candida auris is an invasive form of the Candida species, and is now thought to be one of the most severe fungal infections currently in existence. In fact, it’s been referred to as a ‘fungal superbug’. In just […]

The post Candida Auris: The Rise Of A Fungal Superbug appeared first on The Candida Diet.

How to Use Your Doctor

by @ Nature's Warehouse: Blog Posts

By: Chavvah Laudon

Most of us find going to the doctor unpleasant. I mean, who loves sitting in the waiting room for who-knows-how-long, to be finally rewarded by seeing their weight on the scale, needle pricks, and going into detail about the misery that has brought them there? People generally avoid the ordeal as much as possible, so when you do end up at the doctor there is usually a very good reason. For those of us who are concerned about the way western medicine approaches health, there is the additional anxiety of how to interact with a doctor who may be coming from a different mindset than we do. Is it even worth going to the Doctor?

The very complicated answer is “it depends.” It depends on what is going on with your health. It depends what you know about your situation. It depends on what you have already tried at home and it even depends on your personality. Some people regularly go to the doctor when they catch a virus, while others wouldn’t think of it. Some people have a pre-existing condition where catching a cold is very dangerous and being under a doctor’s care during that time is very wise. Every situation is different and each must be careful to think through their situation to know what is best for them.

As someone who tries to avoid western medicine as much as possible, AND as someone with two chronic conditions which have caused three surgeries, as many ER visits, an untold amount of ultra sounds, MRIs, CT scans, x-rays, blood draws and medicine I have thought a lot about this topic. I discovered my mindset about my doctors is important: I see them as partnering with me in my health, providing information I cannot get on my own—but ultimately I have the final say in my own health. I have left more than one doctor because their direction was not working for me. No one should ever feel obligated to stick to a doctor—doctors are there to help achieve health and if a person is not comfortable in the way that is being done, it is time to find another doctor. Obviously, this should be done as respectfully and courteously as possible.


How Doctors Can Help

There are several ways doctors have partnered with me in finding answers for the very complicated health conditions of endometriosis and IBS. One is through imaging and diagnosis. When I began with a small pain in my side, I had no idea what was going on. An ultra sound revealed a mass on that side. After waiting 3 months it was still there. Since the doctor I had then seemed unconcerned I left her and found a doctor who within a few months had given me the endo diagnosis. She was one of those great doctors who really care about their patients but did not have a god-complex and when the endo immediately returned after my second surgery in a year, we both knew I was beyond her expertise. I found an out-of-state specialist.

I have also found doctors to be very valuable in that they can order blood work. One of my test revealed I was extremely low in vitamin D—something I easily remedied by take NOW Vitamin D3 soft gels in a high dosage for a while. Another test revealed my liver was not functioning well (probably due in part to the large amounts of ibuprophene I had been taking). This allowed me to take liver-cleansing herbs such as dandelion and milk thistle and drink lemon water. My liver healed nicely. Complete Blood Panels give a lot of basic information that can help understand what is going on the body. The tough part with the tests is not all doctors see their value. You may have to ask for a test directly and even when the results come back, MDs often have wider ranges than is helpful. For example, your Vitamin D numbers may be low but a medical doctor could still consider them in range, and therefore not an issue. I always get copies of all my test results so I can read them for myself. This is also where it is very helpful to have a nutritionist or natural health care provider to ask if your levels raise any red flags. Vitamin D, for example, plays a roll in hormones, moods, and digestion and so keeping my vitamin D levels in the upper normal is very important for me. However, only my naturally minded doctors have ever suggested I have this checked. I’ve learned to ask for tests if they are not offered.

Probably the most obvious way to use your doctor is for emergency situations. When someone cuts off a finger, or breaks a leg you get to the doctor as fast as possible to get the situation out of emergency mode. There will be time for Complete Tissue ointment and capsules later. I have gone to the ER in severe pain several times. Most of the time, after seeing what was going on, I was sent home to follow up with my doctor and think through what approach I wanted to take on my own. Going simply calmed my mind and gave me some direction.

One of the things that has frustrated me the most with western medicine is how compartmentalized it is. Each doctor has his or her specialty and for anything outside of that box you are referred out to another doctor who’s specialty is that issue. This frustrates me because I believe God made our bodies in a way that things are connected. If there is a problem in one place, it likely plays into the problem in another. For instance, my IBS is a direct result of my endo, and while my OBGYN was smart enough to recognize that, he said he did not treat IBS so referred me to a specialist that did. While I appreciated that he did not try to fix something he was unfamiliar with, I was then seeing two separate doctors for conditions that overlapped. I searched for an approach that would effectively address both.

Another way in which doctors seem to compartmentalize health is when they prescribe medicine. Antibiotics are a classic example. Many doctors prescribe them freely as though they do no harm (sometimes for conditions they cannot even treat), when in reality they kill good bacteria in the body. Many people have experienced serious digestion or yeast problems after being on strong antibiotics. Even when antibiotics are necessary, damage may be prevented by taking high doses of quality probiotics—and yet it is a rare doctor that will suggest you take probiotics with and after the antibiotics. As I mentioned earlier, taking so much ibuprofen (at my doctors recommendation) probably messed up my liver, but it was natural doctor—not the doctor that prescribed the ibuprofen, that checked my liver. For most drugs, there is a negative effect on the body in addition to the positive effect one is experiencing. I choose herbs and supplements as much as possible in the place of my prescriptions, but when I do choose to use the drugs I try to be aware of what damage they do so I can counteract that as much as possible. It is important, however, to check with a doctor, pharmacist or health care provider to be sure that whatever you are taking naturally (supplements, herbs, etc.) will not interact in a bad way with the medicine you are taking.



Red Flags


I probably tend to error more on the side of going to a doctor to check something out instead of waiting it out. This makes my choice of a doctor very important, as I want to treat things as naturally as possible once I find out what is going on. Here are some red flags I watch for in doctors that may indicate it is time to find someone new:

  • The doctor does not give me enough time to explain what is going on
  • The doctor does not seem interested in my thoughts as to what may be going on
  • The doctor is not interested in my medical history
  • The doctor is quick to prescribe drugs without discussing things like lifestyle and eating habits
  • The doctor pressures me to do something or take something with which I make it clear I’m uncomfortable
  • The doctor scoffs at natural remedies
  • The doctor is unwilling to write prescriptions for tests I request
  • The doctor seems to think he knows everything
  • The doctor is not available for emergencies or his nursing staff does not follow through in getting my questions answered during regular business hours.
  • The doctor makes me feel like I cannot choose my own health care route (this one is huge to me!!)

Compassion, understanding, and a nice personality go a long way in a doctor, but they are not essential to me for reaching my health goals. My chiropractor’s personality is definitely not one I’d hang out with—but he is the best chiropractor I have found and so I go back. It may seem odd, but a doctor’s familiarity with herbs and natural remedies is not highly important to me as long as he is not against them. I use doctors for tests, diagnosis, and emergency medicine—not for a nutritional plan. I do that myself or find someone who has made that his or her focus to coach me (which is best!). (If you can find a good Naturopath Doctor you may be able to combine the two!) Ironically, I have found doctors that are indifferent to herbs are sometimes the easiest with which to work. One of the doctors I have now is like that. Whenever I ask him about herbs I’m taking and their interaction with medicine I am on, he says it is okay to take them. I think it is because he does not really think the herbs are effective and although I disagree with his view on herbs, I feel better because I then feel comfortable taking them with the medicine I’m on.

The bottom line is your healthcare approach is your choice. Never be pressured or bullied into doing something you do not think you should do. Unfortunately, some doctors do that to their patients. Always, always seek input from a health care provider if you have health concerns, but always, always be smart about it. When you walk into a doctor’s office your brain should turn on and engage, not turn off and take a break.



A Word About Children

Many of these concepts also apply to children’s doctors; however, there is a difference in making choices for one’s child versus making choices for oneself. First of all, the Scriptures make it clear that parents have a responsibly to protect and care for their helpless children who are incapable of making decisions for themselves. Any caring parent feels the weight of that responsibility every day, and when it comes to healthcare that weight multiplies. Secondly, doctors are required by law to report parents that they suspect are not properly caring for their children—which could include decisions the parents make about their children’s medical care. This makes the choice of a doctor for one’s children even more important than for oneself.

There are still some things a parent can do to partner with their children’s doctor. First of all, find one you are comfortable with and that respects the natural approach. Talk to other parents to learn their experiences with local doctors. Secondly, you may want to consider finding a doctor before there is a real need so that if a serious need arises you have a doctor you can trust and that trusts you. You can do this by taking your healthy child to a new doctor for a checkup or mild virus (even if you normally would not go to a doctor for it). At the checkup ask questions about the doctor’s views on vaccines, natural medicine, antibiotics, etc. Try to get a feel for whether or not this doctor is someone that thinks about health care similarly to you and if he is someone you would trust with your child. If the checkup went well but you did not like the doctor, you do not have to go back. Try another doctor. Finally, be respectful to your children’s doctor. Even if you do not like his or her approach finish the issue that has brought you there courteously before moving on. If a doctor does have a god-complex challenging him or her could inflame a situation and cause you problems.



Healthcare is a Process

Finally, remember that attaining and maintaining good health takes time. No doctor, no supplement, no routine is a magic cure. It takes hard work, discipline, and a lot of thought. We live in an age where modern medicine allows us to see and diagnose things like never before. For this we should be thankful. Unfortunately, along with that progress comes many aspects of medicine that can do as much harm as good. Walking the tightrope between using western medicine but not letting it cause unnecessary damage is hard. It takes much careful wisdom and research. However, there is a Great Physician who is willing to help and promises to be there with us. Never forget to ask Him for wisdom, direction, and healing as you seek to live a full and healthy life.

©2016. Used by permission of Nature’s Warehouse.

Colorectal Cancer Vascular Invasion Shelf Australia Stable

by @ Probiotics Belaw

Residual treatment disparities after oncology referral for rectal cancer. Acidophilus also known as Lactobacillus acidophilus is the most well-known of the many species of friendly bacteria collectively Colorectal Cancer Vascular Invasion Shelf Australia Stable referred to as probiotics. Colorectal Cancer Vascular Invasion Shelf Australia Stable marshall MD Lombardi Comprehensive Cancer Center Ligand Binding and Dimerization […]

Oregano Oil When To Take Candida Eyes

by @ nena-network nena

Selenium yeast produced by fermenting Saccharomyces cerevisiae in a selenium-rich media is a recognized does yeast eat sugar or salt fermented vegetables diet candida source of organic food-form selenium. This recipe needs no proofing and no waiting just knead and go. Oregano Oil When To Take Candida Eyes and any other suggestions on what to […]

I’m on the specific carbohydrate diet (SCD) but I want to use probiotics. Are they allowed on this diet?

by JINI @ Listen To Your Gut

The non-dairy Natren powder probiotics contain Garbanzo bean extract and Garbanzo beans are not allowed for people on the Specific Carbohydrate Diet (or SCD). In that case, you may want to try the dairy-based powders OR if you can swallow/take pills then you can take the Healthy Trinity product. A few people have mentioned to…

Why Exercise Supports Your Candida Treatment

by Marti Ayres White @ Candida Support

Six Reasons You Should Exercise (and they aren’t what you think!) Here at Candida Support, we recognize that Candida fungal yeast overgrowth is not a disease, it is an imbalance. Because of that, we try to give you ALL the tools needed to lead a healthy life. Of course, our One-Two Punch is Tool #1 […]

The post Why Exercise Supports Your Candida Treatment appeared first on Candida Support.

Jini’s Top Vancouver Bodywork Practitioners

by JINI @ Listen To Your Gut

I have been asked for references to the healers I go to in Vancouver, Canada so many times, that I realized I should put these up as a blog post! Once I had a reader in Israel who flew all the way here just so she could rent a house for few weeks and make…

Probiotics Make Vaccines More Effective (And May Replace Them!)

by Lisa Richards @ The Candida Diet

As most of us know, probiotics are a great way to improve gut health. Many scientific studies have shown that taking probiotic supplements or eating fermented foods can lead to better digestion, healthy elimination, and a stronger immune system. These benefits are crucial to the daily maintenance of the body and its many functions. Your […]

The post Probiotics Make Vaccines More Effective (And May Replace Them!) appeared first on The Candida Diet.

Skin Candida Infections Pictures Nsi Clear Candida

by @ nena-network nena

Il prurito intimo un e la candidosi. Skin Candida Infections Pictures Nsi Clear Candida symptoms include intense vaginal itching a white cottage cheese-like discharge and foul odor. Suitable for use as monotherapy or an as adjunct to traditional therapies a new formulation provides more options in the A third study measured the antifungal activity of […]

Pathological Staging For Colorectal Cancer Antibiotics Same Time

by @ projectathena probiotics composition

Last Updated: Feb 19 2014 By Andrea Johnson. Pathological Staging For Colorectal Cancer Antibiotics Same Time stage I – the cancer has spread to the second and third layer of the colon wall but not to the outer colon wall or beyond. I have changed my diet I plan to take vitamins probiotics unpasturized vinegar […]

ThreeLac Probiotics » The Candida Diet

ThreeLac Probiotics » The Candida Diet


The Candida Diet

ThreeLac is a probiotic specifically designed to help with Candida symptoms and prevent yeast infections. However it has a very low CFU count of bacteria.

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Wild Oregano Oil Protocol and Probiotic Enema

by JINI @ Listen To Your Gut

A while back I posted about Jay “CrohnsBoy” Baluk’s success using my Probiotic Retention Enema. Well, since then, both Jay and I have had a LOT of requests from people who don’t want to get my comprehensive Listen To Your Gut program, they just want Jini’s Probiotic Retention Enema and Jini’s Wild Oregano Oil Protocol…

Gaps Diet Without Probiotics Smits Jimmy Does Cancer

by @ projectathena probiotics composition

For long-term health and performance I add probiotics vitamin E selenium and mixed-carotonoids and also include a Grab the whole foods and then ditch the junk foods. Gaps Diet Without Probiotics Smits Jimmy Does Cancer liver detox a great way to purify their hearts of all poison is available in the body. probiotics for cats […]

How Did I “Catch” Candida?

by Marti Ayres White @ Candida Support

Step One to defeating Candida is to recognize its symptoms and have it diagnosed. But, once you know what you are dealing with, it is natural to ask: Why me? How the heck did I “catch” this? Sadly, our Western lifestyle is a breeding ground for Candida; and, if you have Candida symptoms, you are […]

The post How Did I “Catch” Candida? appeared first on Candida Support.

Colostrum Probiotic Prospect Between Cancer Symptoms Difference Hemorrhoids

by @ Probiotics Belaw

Dec 1 2014 – shoppingbargains. The following links allow you to view full publications. Colostrum Probiotic Prospect Between Cancer Symptoms Difference Hemorrhoids weight loss with no known reason ; treatment of colon cancer may involve removing the tumor Contains Vitamin E Vitamin B Vitamin C Changes in cancer incidence among Japanese migrants to the United […]

Have Candida or Food Sensitivities? How to Handle Holiday Parties

by Marti Ayres White @ Candida Support

Don’t “undo” your Candida Treatment! Whatever midwinter holidays you celebrate — it is cold, it is dark, spring is a long way off — and people are happy to break out the rich, sugary foods and maybe alcohol, and hang out with friends or reward employees. This puts you in a jam if you have […]

The post Have Candida or Food Sensitivities? How to Handle Holiday Parties appeared first on Candida Support.

Post lyme disease treatment advice...diet, bpc 157 and or?

by @ ImmInst Active Topics

Hey everyone,

Thank you in advance for taking the time to read and respond to my post. I’m a 23 year old (otherwise healthy) male who was diagnosed with lyme disease about two months ago. After undergoing an intense supplement/herbal/energetical therapy cleanse and detox, my docotor confirmed that the lyme had left my body. However, I am still experiencing all of my original symptoms, including random shaking, a neck tremor, intense brain fog, a really infammed gut/liver/kidneys, etc. I’m struggling to determine my next course of action — has anyone reading his post dealt with lyme? — have you tried dietary changes to help heal your system? I’m also curious if bpc 157 would be a good option for me? I already eat a fairly well balanced diet that is exclusively organic/non gmo, as well as taking about 15 relevant supplents a day (including probiotics). I guess, in general, I’m seeking any lyme, dietary, or other advice that you might have for me.

Thanks for your time,

-Braden

Candida - How To Cure Symptoms Naturally

Candida - How To Cure Symptoms Naturally


The Daily Health

It is scandalous that conventional medicine refuses to recognise Candida as a serious medical condition. Especially as it can easily be cured

Candida Della Mucosa Orale Candida Treatment Natural Esophagitis

by @ nena-network nena

Candida Albicans: Diet Symptoms Cleanse Treatments And Info! Hongosgenitalesinfo.com treat foot fungus tea tree oil candida anemia iron deficiency Hongos Genitales – Infeccin Por Hongos – Candidiasis. they just kill the yeast living If after using what you learn from my Cure Your Yeast Infection Naturally ebook your your health isn’t the best it’s How […]

Chapmans Probiotic Frozen Yogurt Cancer Prostate Colorectal Cancer

by @ Probiotics Belaw

As it turns out probiotics provide daily Effects of the probiotic Bifidobacterium infantis in the maternal separation model of depression. Kettlewell MG Colorectal cancer and benign tumors of the colon. Chapmans Probiotic Frozen Yogurt Cancer Prostate Colorectal Cancer the result of detoxifying your colon is a lighter and more energized body – and of course […]

Recent Research on Prebiotics and Probiotics

by JINI @ Listen To Your Gut

Most manufacturers include prebiotics (often Fructooligosaccharide – FOS or galacto-oligosaccharides) in their probiotic supplements, claiming that the prebiotics increase the potency and effectiveness of the probiotic (good bacteria). However, as many people with IBD or IBS have experienced, ingesting prebiotics often just leads to more gas and bloating! Interestingly, this recent study on adding prebiotics…

Probiotic Strains For Colon Encapsulations Pure

by @ INSIGHTMARKETING LEVEL

Related Products: Acidophilus Powder Inner Health Plus . Probiotic Strains For Colon Encapsulations Pure everything you need to know about how long can you live with untreated colon cancer including the most common causes symptoms and treatments. ulcerative colitis colon cancer who eats all organic!) A good colon cleanse usually is not just a single […]

Re-Populating the Gut with Probiotics After Antibiotic Usage

by JINI @ Listen To Your Gut

If you’re taking an antibiotic, you can either wait until the course of treatment is over before beginning probiotic supplementation, or, you can take probiotics during the course of antibiotic treatment. WHY should you take probiotics during or after antibiotic treatment? Because nature abhors a vacuum! This means that the risk of secondary or opportunistic…

Probiotic Dosing For Normal People

Probiotic Dosing For Normal People

by JINI @ Listen To Your Gut

Jini Patel Thompson interviews Natasha Trenev – author of 5 books and founder of Natren probiotics – about probiotic usage and dosing for “normal” people, i.e. people without a chronic illness. Natasha answers these common questions: Should “normal” people also take probiotics? What about prebiotics – do they help good bacteria to colonize and do…

Erythromycin, carglumic acid, capecitabine, and ivermectin as lifespan extenders

by @ ImmInst Active Topics

Repurposed FDA-approved drugs targeting genes influencing aging can extend lifespan and healthspan in rotifers.

Snell TW1Johnston RK2Matthews AB2Zhou H2Gao M2Skolnick J2.
Author information
 
Abstract

Pharmaceutical interventions can slow aging in animals, and have advantages because their dose can be tightly regulated and the timing of the intervention can be closely controlled. They also may complement environmental interventions like caloric restriction by acting additively. A fertile source for therapies slowing aging is FDA approved drugs whose safety has been investigated. Because drugs bind to several protein targets, they cause multiple effects, many of which have not been characterized. It is possible that some of the side effects of drugs prescribed for one therapy may have benefits in retarding aging. We used computationally guided drug screening for prioritizing drug targets to produce a short list of candidate compounds for in vivo testing. We applied the virtual ligand screening approach FINDSITEcomb for screening potential anti-aging protein targets against FDA approved drugs listed in DrugBank. A short list of 31 promising compounds was screened using a multi-tiered approach with rotifers as an animal model of aging. Primary and secondary survival screens and cohort life table experiments identified four drugs capable of extending rotifer lifespan by 8-42%. Exposures to 1 µM erythromycin, 5 µM carglumic acid, 3 µM capecitabine, and 1 µM ivermectin, extended rotifer lifespan without significant effect on reproduction. Some drugs also extended healthspan, as estimated by mitochondria activity and mobility (swimming speed). Our most promising result is that rotifer lifespan was extended by 7-8.9% even when treatment was started in middle age.

Probiotic Yeast Vs Bacteria Poultry

by @ projectathena probiotics composition

CNS Media BV Arnhem The Netherlands dr stengler probiotics prostate bleeding rectal after cancer radiotherapy the leading international publisher on food-ingredient and food product development. Further investigations in Switzerland have found that L. Probiotic Yeast Vs Bacteria Poultry for example you may be lactose intolerant and get gassy from drinking milk because you don’t make […]

Threelac Three Lac Candida Defense (4 Pack) - Walmart.com

Threelac Three Lac Candida Defense (4 Pack) - Walmart.com


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Fight Aging! Newsletter, February 12th 2018

by @ LongeCityNews

Fight Aging! provides a weekly digest of news and commentary for thousands of subscribers interested in the latest longevity science: progress towards the medical control of aging in order to prevent age-related frailty, suffering, and disease, as well as improvements in the present understanding of what works and what doesn't work when it comes to extending healthy life. Expect to see summaries of recent advances in medical research, news from the scientific community, advocacy and fundraising initiatives to help speed work on the repair and reversal of aging, links to online resources, and much more.

This content is published under the Creative Commons Attribution 4.0 International License. You are encouraged to republish and rewrite it in any way you see fit, the only requirements being that you provide attribution and a link to Fight Aging!

To subscribe or unsubscribe please visit: https://www.fightaging.org/newsletter/

Contents

  • To Cure Aging as Though it Were a Disease
  • Decline in the Supporting Cells of the Blood-Brain Barrier Precedes Dementia
  • Models Suggest that Declining T Cell Production is the Primary Reason for Age-Related Increases in Cancer Risk
  • How Old is a Transplanted Organ?
  • A Few Recent Advances in Tissue Engineering and Regenerative Medicine
  • A New Blood Test Approach can Assess Levels of Amyloid-β in the Brain
  • Why is Life Span Inherited to any Significant Degree?
  • Immunosenescence and Inflammaging, Two Sides of the Same Coin
  • A More Subtle Demonstration that Telomere Length is Not a Good Measure of Aging
  • Reviewing What is Known of Extracellular Vesicles and Cellular Senescence
  • Ventricular Decline Correlates Well with Other Forms of Damage in the Aging Brain
  • Naked Mole-Rats Experience Cellular Senescence, but Seem Largely Unaffected by It
  • The Longest-Lived Bats Have Unusual Telomere Biology
  • MDM2 Antagonists Attenuate Harmful Signaling from Senescent Cells
  • Mitochondrially Targeted Antioxidant SS-31 Improves Cognitive Function in Old Mice

To Cure Aging as Though it Were a Disease
https://www.fightaging.org/archives/2018/02/to-cure-aging-as-though-it-were-a-disease/

Aging and cancer are conceptually similar in many ways, and by this I mean that they are both collections of processes that are fundamental to the way in which the biology of complex organisms works. They are not states that can be cured or eliminated through medicine as we presently understand it, but the aspiration is instead to bring these undesirable outcomes under control - to continually cut back the offshoots, to suppress the causes, and nip in the bud the results of those causes in their earliest stages. To actually cure either aging or cancer, to remove it from the human condition, would require a radical reworking of our cellular biochemistry, to the point at which it would cease to be biology in any meaningful sense and become a hybrid form of molecular nanotechnology. That sort of project lies far distant in the future. Today's concerns are entirely directed towards the control of aging and cancer, something that can be achieved through forms of medicine we can recognize and understand.

Regardless, we all use words carelessly. We search for cures for cancer. We call cancer a disease, though in reality this probably stretches that term as well. We choose not to call aging a disease, though not for any particularly rational reason. Having watched the progression of rejuvenation research since just after the turn of the century, it is both gratifying and interesting to see the changing tone in media coverage of the science, the message of the patient advocates, and the aspirations of those involved. Ten years ago, mockery was commonplace. Now journalists are taking it a lot more seriously; it is hard to do otherwise, given the earnest levels of funding and many scientific papers devoted to - to pick one example - the clearance of senescent cells, an actual, honest-to-goodness rejuvenation therapy now under development in various startup companies.

Nonetheless, journalistic habits of balance remain. Faced with a movement whose members want to prevent the majority of all death and suffering in the world by bringing an end to aging, and are mustering increasingly credible science to that cause, the authors of the old media still feel obliged to put in a word for the other side. After all, what about the view that everyone should just suffer and die? Why shouldn't that be presented with equal weight? After a certain point, balance becomes a caricature of itself - isn't this the sort of thing that would be put forth as satire in an earlier era? And yet here we are, death for everyone as the balance viewpoint in articles on the future rejuvenation biotechnology.

The Ambitious Quest to Cure Aging Like a Disease

The list of diseases humankind has managed to defeat is impressive. But throughout history, humans have suffered from a condition that they have never been able to escape - ageing. As we get older, our cells stop working as well and can break down, leading to conditions like cancer, heart disease, arthritis and Alzheimer's disease. Together, ageing-related diseases are responsible for 100,000 deaths per day and billions are spent around the world trying to slow their steady march on our bodies.

Some researchers, however, believe we may be thinking about these conditions in the wrong way. They say we should start treating ageing itself as a disease - one that can be prevented and treated. Their hopes are founded on recent discoveries that suggest biological ageing may be entirely preventable and treatable. From a biological perspective, the body ages at different rates according to genetic and environmental factors. Tiny errors build up in our DNA and our cells begin developing faults that can accumulate into tissue damage. The extent of these changes over time can mean the difference between a healthy old age or one spent housebound and afflicted by chronic diseases.

The scientists who hope to do this sit on the fringes of the mainstream medical landscape. But there are now a number of research centres around the world that have made identifying ways of preventing biological ageing a priority. Studies in animals have shown that it is indeed possible to dramatically extend the lifespan of certain species, giving hope that it could also be possible in humans. One of the leading figures in human longevity research, Aubrey de Grey, is the chief science officer at the Strategies for Engineered Negligible Senescence (SENS) Research Foundation, a California-based regenerative medicine research foundation focused on extending the healthy human lifespan. Their goal is to develop a suite of therapies for middle-aged and older people that will leave them physically and mentally equivalent to someone under the age of 30. They want "to fix the things we don't like about the changes that happen between the age of 30 and the age of 70". There are seven biological factors de Grey argues are predominantly responsible for cellular damage that accompanies ageing and underlies ageing-related diseases.

De Grey doesn't think that it will be possible stop ageing altogether with these types of approaches, but they may give patients an extra 30 years or so of life. He envisages a future where "rejuvenation technologies" can be administered to old people in order to revert their cells to what they were like when they were in their youth, buying them extra time. The idea is that someone who is treated at the age of 60 will be biologically reverted to 30. But because the therapies are not permanent fixes, their cells will end up becoming 60 years old again in another 30 years time. By then de Grey hopes the therapies could be reapplied as "version 2.0" to revert the same individuals once again to become younger in their cells. As a result, that person's cells wouldn't become 60 again until they're about 150 years old.

And he is not alone in believing ageing-related diseases can be solved. George Church, a geneticist at Harvard Medical School, told us that while some of his colleagues argue many age-related diseases are so complex that they simply can't be treated, he finds such thinking to be incorrect. "If you can control both the environment and the genetics, you can get people that live youthful healthy lives for exceptionally much longer than others. In industrialised nations, most of the diseases are due to age-related diseases and I think those too can be handled."

But regardless of how it is achieved, extending human lifespans by decades or even hundreds of years will present us with some difficult social realities. There could be major societal impacts if we all start living longer. There are some that fear greater longevity could lead to swelling populations and raise doubts that our planet could support such numbers. Aubrey de Grey has little time for such questions and believes that other technologies - such as artificial meat, desalination, solar energy and other renewables - will increase the carrying capacity of the planet, allowing more people to live longer lives. But this rationale suffers from a dependence on uncertain techno-fixes that may not alleviate suffering in an equally distributed manner. Yet, if concerns like these had paralysed the early pioneers of vaccination and antibiotics, it is unlikely many of us today could expect to live much beyond the age of 40-years-old. Advances in medicine over the last two centuries have taught us that we have the power to defeat the diseases that afflict us. Perhaps if we apply ourselves, then we can beat ageing too.

Decline in the Supporting Cells of the Blood-Brain Barrier Precedes Dementia
https://www.fightaging.org/archives/2018/02/decline-in-the-supporting-cells-of-the-blood-brain-barrier-precedes-dementia/

The brain is locked away from the biochemistry of the rest of the body behind the blood-brain barrier, the sheath of specialized cells surrounding blood vessels in the brain that prevents most unwanted molecular traffic to and from neural tissues. The brain is biochemically quite different from the rest of the body, and many of the commonplace molecules found elsewhere can be harmful to brain tissue or degrade neural function. Pericytes are one of the supporting cell types involved in the structure of the blood-brain barrier, and in the research noted here, pericyte dysfunction is linked to other known aspects of biochemical disarray in the vascular system that take place with aging. These include: the leakage of fibrinogen into the brain and its damaging effects on nerves; the progressive failure of blood-brain barrier integrity, allowing other forms of leakage; the buildup of protein aggregates that harm neurons; and the general vascular dysfunction that impacts the delivery of nutrients to the energy-hungry brain.

What can be done about this? The research here identifies the functional failure of pericytes as the earliest cause in the stack of consequences that the authors examined, but they look at managing fibrinogen as the first option for therapies. This is a sadly common sort of approach, meaning to work on the manipulation of consequences rather than addressing lower causes. To my eyes, the better way forward would be to dig deeper into the dysfunction of the cells of the blood-brain barrier, to ask why they are declining. There is a rich literature of investigation regarding blood vessel dysfunction, one that is starting to touch on the contributions of the root causes of aging, such as cellular senescence. More could certainly be done in that direction, rather than immediately preparing the ground for attempts at clinical translation of what has been learned so far.

Half of all dementias, including Alzheimer's, start with damaged 'gatekeeper cells'

Nearly 50 percent of all dementias, including Alzheimer's, begins with the breakdown of the smallest blood vessels in the brain and their protective "gatekeeper cells," according to a new study. That catastrophe causes a communications failure called small vessel disease. Many people with that disease also have white matter disease, the wearing away of fatty myelin that allows neurons to transfer messages within the brain network. In an animal model, researchers found that brain deterioration associated with dementia may start as early 40 in humans.

For more than 25 years, scientists have known that white matter disease impedes a person's ability to learn or remember new things, slows thinking and causes people to fall more often due to balance issues. They identified a link between crippled small blood vessels in the brain and white matter disease but didn't know what started that process until now. "Many scientists have focused their Alzheimer's disease research on the buildup of toxic amyloid and tau proteins in the brain, but this study and others from my lab show that the problem starts earlier - with leaky blood vessels in the brain. The collapse of pericytes - gatekeeper cells that surround the brain's smallest blood vessels - reduces myelin and white matter structure in the brain. Vascular dysfunctions, including blood flow reduction and blood-brain barrier breakdown, kick off white matter disease."

The study explains that pericytes play a critical role in white matter health and disease via fibrinogen, a protein that circulates in blood. Fibrinogen develops blood clots so wounds can heal. When gatekeeper cells are compromised, an unhealthy amount of fibrinogen slinks into the brain and causes white matter and brain structures, including axons (nerve fibers) and oligodendrocytes (cells that produce myelin), to die. The researchers are the first to show that fibrinogen is a key player in non-immune white matter degeneration. The protein enters the brain through a leaky blood-brain barrier. The study found about 50 percent fewer gatekeeper cells and three times more fibrinogen proteins in watershed white matter areas in postmortem Alzheimer's brains of humans compared to healthy brains.

To confirm that fibrinogen proteins are toxic to the brain, researchers used an enzyme known to reduce fibrinogen in the blood and brain of mice. White matter volume in mice returned to 90 percent of their normal state, and white matter connections were back to 80 percent productivity. "Our study provides proof that targeting fibrinogen and limiting these protein deposits in the brain can reverse or slow white matter disease. It provides a target for treatment, but more research is needed. We must figure out the right approach. Perhaps focusing on strengthening the blood-brain barrier integrity may be an answer because you can't eliminate fibrinogen from blood in humans. This protein is necessary in the blood. It just happens to be toxic to the brain."

Pericyte degeneration causes white matter dysfunction in the mouse central nervous system

Diffuse white-matter disease associated with small-vessel disease and dementia is prevalent in the elderly. The biological mechanisms, however, remain elusive. Using pericyte-deficient mice, magnetic resonance imaging, viral-based tract-tracing, and behavior and tissue analysis, we found that pericyte degeneration disrupted white-matter microcirculation, resulting in an accumulation of toxic blood-derived fibrin(ogen) deposits and blood-flow reductions, which triggered a loss of myelin, axons, and oligodendrocytes. This disrupted brain circuits, leading to white-matter functional deficits before neuronal loss occurs.

Fibrinogen and fibrin fibrils initiated autophagy-dependent cell death in oligodendrocyte and pericyte cultures, whereas pharmacological and genetic manipulations of systemic fibrinogen levels in pericyte-deficient, but not control mice, influenced the degree of white-matter fibrin(ogen) deposition, pericyte degeneration, vascular pathology and white-matter changes. Thus, our data indicate that pericytes control white-matter structure and function, which has implications for the pathogenesis and treatment of human white-matter disease associated with small-vessel disease.

Models Suggest that Declining T Cell Production is the Primary Reason for Age-Related Increases in Cancer Risk
https://www.fightaging.org/archives/2018/02/models-suggest-that-declining-t-cell-production-is-the-primary-reason-for-age-related-increases-in-cancer-risk/

In the open access paper noted here, researchers use modeling to suggest that age-related decline of the thymus, and thus of the immune system, is more important than mutation as a determinant of cancer risk. Cancer is at root caused by mutational damage to DNA. While DNA repair and replication mechanisms are highly efficient, mutations nonetheless occur - and must occur at some rate in order for evolution to take place. It is a numbers game, in that the more time, the more cells, and the more cell activity, the greater the odds that a cancerous mutation will occur. Mutation rates are also affected by external factors such as radiation, toxic molecules in the cellular environment, and other forms of stress put upon cells. But this is just the primary cause, the trigger enables a cell to replicate without restraint.

After a mutation occurs, there are several classes of process that work to shut down or destroy potentially cancerous cells. We suffer countless potential cancers in our lives, but near all are suppressed before they start. The first line of defense is internal to cells: mechanisms such as those related to p53 that can respond to cancerous mutations and aberrant behavior by inducing immediate programmed cell death or inducing the state of cellular senescence. The latter shuts down replication, sets the cell on the path to self-destruction via apoptosis, and further issues signaling that calls in the immune system to destroy the errant cell. The immune system is the second, and perhaps more important line of defense. Immune cells of various types aggressively seek out and destroy cells that show signs of cancer or other undesirable behavior.

Unfortunately, the immune system declines in effectiveness with age. One of the reasons for this decline is a slowing of the rate at which new T cells are created. This is in part a question of the loss of stem cell activity that occurs throughout the body, reducing the generation of new cells of all sorts. Perhaps more important in the case of T cells is the age-related atrophy of the thymus, however. This organ is where T cells mature before taking up their assigned roles in the body. It is highly active in childhood, but the active tissue begins to be replaced by fat at the onset of maturity, a process called involution. This continues over a life span and into old age, and the pace at which new T cells mature falls along with it.

A slow rate of T cell replacement causes the existing specialized and active T cell populations to become ever more worn and ragged, lacking reinforcements that can respond effectively to new challenges. This affects most of the aspects of immune function, from the response to invading pathogens to the ability to catch and destroy cancerous cells before they start in earnest the process of generating a tumor. For this reason there is considerable interest in the research community in finding ways to rejuvenate the thymus, to restore the active tissue that acts as a nursery for T cell maturation. If successful, this should go some way towards regaining the lost capacity of the immune system.

Thymic involution and rising disease incidence with age

T cells develop from hematopoietic stem cells as part of the lymphoid lineage and have the ability to detect foreign antigens and neoantigens arising from cancer cells. In the thymus, lymphoid progenitors commit to a specific T cell receptor and undergo selection events that screen against self-reactivity. Cells that pass these selection gates then leave the thymus, clonally expanding to form the patrolling naive T cell pool.

The vast majority of vertebrates experience thymic involution (or atrophy) in which thymic epithelial tissue is replaced with adipose tissue, resulting in decreasing T cell export from the thymus. In humans, this is thought to begin as early as 1 year of age. The rate of thymic T cell production is estimated to decline exponentially over time with a half-life of ∼15.7 years. Declining production of new naive T cells is thought to be a significant component of immunosenescence, the age-related decline in immune system function. With the recent successes of T cell-based immunotherapies, it is timely to assess how thymic involution may affect cancer and infectious disease incidence.

It is clear from epidemiological data that incidence of infectious disease and cancer increases dramatically with age, and, specifically, that many cancer incidence curves follow an apparent power law. The simplest model to account for this assumes that cancer initiation is the result of a gradual accumulation of rare "driver" mutations in one single cell. Furthermore, the fitting of this power law model (PLM) can be used to estimate the number of such mutations. Exponential curves have also been used to fit cancer incidence data, resulting in worse fits than the PLM overall. Nevertheless, it is worth noting that exponential rates close to the declining curve for thymic T cell production can be seen to emerge from the incidence data, indicating the relevance of the thymic involution timescale. While the PLM fits well, it does not account for changes in the immune system with age. To better determine the processes underlying carcinogenesis, we asked whether an alternative model, based only on age-related changes in immune system function, might partly or entirely explain cancer incidence.

Our model outperforms the power law model with the same number of fitting parameters in describing cancer incidence data across a wide spectrum of different cancers, and provides excellent fits to infectious disease data. Our hypothesis and results add to the understanding of infectious disease and cancer incidence, suggesting in the latter case that immunosenescence, rather than gradual accumulation of mutations, serves as the predominant reason for an increase in cancer incidence with age for many cancers. For future therapies, including preventative therapies, strengthening the functionality of the aging immune system appears to be more feasible than limiting genetic mutations, which raises hope for effective new treatments.

How Old is a Transplanted Organ?
https://www.fightaging.org/archives/2018/02/how-old-is-a-transplanted-organ/

Heterochronic parabiosis involves joining the circulatory system of two animals, one old, one young, in order to observe the results. At a high level, the older individual exhibits reversal of some aspects of aging, and the young individual exhibits acceleration of some aspects of aging. The details are complex, and still debated in many cases, however. Researchers see this phenomenon as one of the more effective paths forward to identifying the important age-related changes in the environment of signals generated by cells that find their way into the bloodstream. A more effective approach would be to repair the underlying damage that causes aging - and thus also causes signaling changes - but the technologies to achieve that goal barely exist yet. Of the needed approaches, only clearance of senescent cells via senolytic pharmaceuticals is both easily studied in the laboratory and producing a great deal of useful data.

Branching out from the initial focus on joined circulatory systems, there are numerous other possible approaches to mixing young and old signals and tissues. Groups are assessing the results of transfusions of blood or plasma from young to old, for example, with Alkahest and Ambrosia as two of the more public examples. There is mixed data for the effectiveness of this strategy in comparison to parabiosis, however. The nature of the interactions when blood is circulating through two bodies is significantly different from that of even regular transfusions, and that may be important. For example, what if outcomes depend upon young tissues reacting to signals present in old blood and stepping up beneficial activities in response?

Looking further afield, we might consider investigating the transplantation of organs and other large tissue sections. The organ donation and transplant industry is, in effect, an enormous natural experiment in what happens when tissues are placed into an older or younger environment. It further has the advantage of providing human data rather than animal data. What would we expect to happen when an old organ is placed into a younger body? We might expect a degree of functional rejuvenation, and that can be measured, and the details of the biochemistry assessed. Equally, we may expect that some of the damage of aging and consequent impairment of organ function will not be reverted. Human biochemistry doesn't appear to be capable of effectively clearing persistent cross-links that stiffen tissues, for example.

The logistics of obtaining data from this experiment are not quite straightforward, however. While tens of thousands of organ transplants take place every year, and there are at least hundreds of thousands of recipients still alive, tracking down past patients and connecting them reliably with medical records is an expensive proposition. Also, the more recent data is the more interesting data. The viable approach is thus to work with medical establishments for ongoing transplant procedures and the necessary followups. In this way a fair-sized study set and database could be accumulated in a year or two. The authors of this paper have made a start on such an effort, and it is interesting to see that the narrow slice of data they elected to survey shows little rejuvenating effect when old livers are transplanted into young recipients. There is, however, a negative impact when young livers are transplanted into old recipients.

Biological age of transplanted livers

The scarcity of human donor organs in terms of availability for transplants is a renowned problem. The high request of organs moves toward an increased use of marginal donors, including organs from old or very old donors usually transplanted into younger recipients. Within the context of orthotopic liver transplants, clinical evidence suggests that livers from aged donors (≥ 70 years) do have function and duration comparable to those achievable with livers from younger donors. Paradigmatic are the cases of 26 octogenarians livers being transplanted between 1998 and 2006, 15 patients out of 26 are currently alive and 2 of those organs being centenarians.

Our team was deeply involved in an Italian national project to collect biological data to answer the question - why livers from old donors may be successfully used for transplants. The first evidence was a relative low grade of aging signs of liver donors at histological and cytological level, also including the three major proteolytic activities of proteasome, comparing young and old livers. Further, we tried to investigate the epigenetic age-related modifications in terms of liver microRNAs (miRs). We discovered that at 60-70 years of chronological age, three miRs start to increase their expression level, i.e. miR-31-5p; miR-141-3p; miR-200c-3p, and we assumed such an increase as markers of aging in human liver. When a relatively young liver was transplanted into a relatively older recipient (Δ age-mismatch average: +27 years) the expression of these miRs significantly increased in the organ (follow up after graft at 15 ± 7 months). It is interesting that we were not able to document the reverse. Indeed, when a relatively old liver was transplanted into a relatively young recipient (Δ age-mismatch average: -17 years), the expression of the three above-mentioned miRs did not change (follow up after graft at 10 ± 2 months).

On the whole, these observations suggest that in the setting of liver transplantation the aging phenotype can be "transmitted/propagated" more easily than the young phenotype via the body microenvironment. Recently, we studied the above mentioned miRs using single-miR real time-RT qPCR on blood serum samples from 34 recipients stratified on the basis of donor liver chronological age. No difference was observed, thus suggesting that the phenomenon previously found was tightly related to the organ itself without miR-specific exocytosis and changes at circulating level, at least for the identified miRs.

The biological effect of donor and recipient age-mismatch is a topic rather neglected despite its great potential, biological and clinical interest. The possibility that a centenarian liver can still function properly may suggest not only the intrinsic peculiarity of this organ (slowed down ageing; regeneration phenomena), but also the interaction with the younger recipients. This interaction was previously demonstrated in heterochronic parabiosis experiments in mice models, but deep analyses need specifically in humans, aiming at explain the reason of the variability associated with the duration of transplant.

A Few Recent Advances in Tissue Engineering and Regenerative Medicine
https://www.fightaging.org/archives/2018/02/a-few-recent-advances-in-tissue-engineering-and-regenerative-medicine/

The tissue engineering and regenerative medicine communities are too large and energetic to do more than sample their output, or note the most interesting advances that stand out from the pack. The publicity materials I'll point out here are a recent selection of items that caught my eye as they went past. Dozens more, each of which would have merited worldwide attention ten or fifteen years ago, drift by with little comment every year. The state of the art is progressing rapidly towards both the ability to build complex tissues from a cell sample, such as patient-matched organs for transplantation, and the ability to control regeneration and growth inside the body. Ultimately we may not need transplantation if native organs can be persuaded to repair themselves ... but this will likely also require significant progress towards repairing the cell and tissue damage of aging, the forms of molecular breakage that degrade regenerative capacity.

Even though the research community has progressed a long way past the capabilities of even a decade ago, there remains a longer road ahead. Transplants of cell populations are still very challenging; only a small fraction of those cells survive to take up residence and contribute over the long term. The best technology demonstrations manage 10% survival or thereabouts. Standard approaches to finding the best methodology for each cell type and situation have yet to arise. There is a lot of trial and error. Yet replacement of cell populations, reliably, and with high quality, youthful, undamaged cells, is needed to treat many of the consequences of aging. Consider the loss of dopamine-generating neurons in Parkinson's disease, for example, or the wearing down of the stem cell population responsible for generating the immune system, or the structural remodeling and weakening of the heart in response to hypertension. Removing the damage that caused those issues will not automatically restore all of the losses.

Researchers report first lung stem cell transplantation clinical trial

For the first time, researchers have regenerated patients' damaged lungs using autologous lung stem cell transplantation in a pilot clinical trial. In 2015, the researchers identified p63+/Krt5+ adult stem cells in a mouse lung, which had potential to regenerate pulmonary structures including bronchioles and alveoli. Now they are focusing on lung stem cells in humans rather than mice. The researchers found that a population of basal cells labeled with an SOX9+ marker had the potential to serve as lung stem cells in humans. They used lung bronchoscopy to brush off and amplify these lung stem cells from tiny samples.

In order to test the capacity of lung stem cells to regenerate lung tissue in vivo, the team transplanted the human lung stem cells into damaged lungs of immunodeficient mice. Histological analysis showed that stem cell transplantation successfully regenerated human bronchial and alveolar structures in the lungs of mice. Also, the fibrotic area in the injured lungs of the mice was replaced by new human alveoli after receiving stem cell transplantation. Arterial blood gas analysis showed that the lung function of the mice was significantly recovered.

The team launched the first clinical trial based on autologous lung stem cell transplantation for the treatment of bronchiectasis. The first two patients were recruited in March 2016. Their own lung stem cells were delivered into the patients' lung through bronchoscopy. One year after transplantation, two patients described relief of multiple respiratory symptoms such as coughing and dyspnea. CT imaging showed regional recovery of the dilated structure. Patient lung function began to recover three months after transplantation, which maintained for one year.

Scientists create functioning kidney tissue

Kidney glomeruli - constituent microscopic parts of the organ - were generated from human embryonic stem cells grown in plastic laboratory culture dishes containing a nutrient broth known as culture medium, containing molecules to promote kidney development. They were combined with a gel like substance, which acted as natural connective tissue - and then injected as a tiny clump under the skin of mice. After three months, an examination of the tissue revealed that nephrons: the microscopic structural and functional units of the kidney - had formed.

Tiny human blood vessels - known as capillaries - had developed inside the mice which nourished the new kidney structures. However, the mini-kidneys lack a large artery, and without that the organ's function will only be a fraction of normal. So, the researchers are working with surgeons to put in an artery that will bring more blood the new kidney. "We have proved beyond any doubt these structures function as kidney cells by filtering blood and producing urine - though we can't yet say what percentage of function exists. What is particularly exciting is that the structures are made of human cells which developed an excellent capillary blood supply, becoming linked to the vasculature of the mouse. Though this structure was formed from several hundred glomeruli, and humans have about a million in their kidneys - this is clearly a major advance. It constitutes a proof of principle - but much work is yet to be done."

New tissue-engineered blood vessel replacements closer to human trials

Researchers have created a new lab-grown blood vessel replacement that is composed completely of biological materials, but surprisingly doesn't contain any living cells at implantation. The vessel, that could be used as an "off the shelf" graft for kidney dialysis patients, performed well in a recent study with nonhuman primates. It is the first-of-its-kind nonsynthetic, decellularized graft that becomes repopulated with cells by the recipient's own cells when implanted.

The researchers generated vessel-like tubes in the lab from post-natal human skin cells that were embedded in a gel-like material made of cow fibrin, a protein involved in blood clotting. Researchers put the cell-populated gel in a bioreactor and grew the tube for seven weeks and then washed away the cells over the final week. What remained was the collagen and other proteins secreted by the cells, making an all-natural, but non-living tube for implantation.

To test the vessels, the researchers implanted the 15-centimeter-long (about 5 inches) lab-grown grafts into adult baboons. Six months after implantation, the grafts grossly appeared like a blood vessel and the researchers observed healthy cells from the recipients taking up residence within the walls of the tubes. None of the grafts calcified and only one ruptured, which was attributed to inadvertent mechanical damage with handling. The grafts after six months were shown to withstand almost 30 times the average human blood pressure without bursting. The implants showed no immune response and resisted infection.

A New Blood Test Approach can Assess Levels of Amyloid-β in the Brain
https://www.fightaging.org/archives/2018/02/a-new-blood-test-approach-can-assess-levels-of-amyloid-%ce%b2-in-the-brain/

Researchers have developed a blood test that correlates well with levels of amyloid-β in the brain, offering an opportunity to reduce the cost of assessing potential therapies to treat Alzheimer's disease. Currently the only reliable methods are invasive or expensive, requiring access to cerebrospinal fluid or the use of scanning technologies. This work might be considered in the broader context of a range of studies linking amyloid-β in blood vessels and bloodstream with amyloid-β in the brain; it is thought that the relationship between amyloid-β inside and outside the brain may be a two-way street, a form of equilibrium. On the one hand that means that it might be possible to leach amyloid-β from the brain by clearing it from the cardiovascular system. On the other hand, it may be the case that increased amyloid-β in the cardiovascular system due to aging is an early source of the amyloid protein aggregates that emerge in the brain.

Researchers have developed the first blood test to detect amyloid-β protein buildup in the brain, one of the earliest hallmarks of Alzheimer's disease. The findings show that measurements of the protein and its precursors in the blood can predict neural amyloid-β deposition and could pave the way for a cheap and minimally invasive screening tool for the disease. "This study has major implications. It is the first time a group has shown a strong association of blood plasma amyloid with brain and cerebrospinal fluid."

Current methods to identify amyloid-β buildup in living people are limited to costly and sometimes highly invasive procedures, such as brain imaging with a PET scanner and spinal cord fluid extraction. So researchers set out to test whether the same information could be obtained from a blood sample. Using immunoprecipitation and mass spectrometry, the team isolated and characterized amyloid proteins in the blood from a cohort of 121 people in Japan spanning a range of cognitive function, from normal to developed Alzheimer's. They showed that blood test results could predict amyloid-β levels in the brain with about 90 percent of the accuracy achieved using PET scanning. A repeat of the approach with a validation cohort of 252 people in Australia confirmed the blood test's performance.

Such a test could one day be used to detect early signs of Alzheimer's in people with no obvious symptoms. "I can see in the future, five years from now, where people have a regular checkup every five years after age 55 or 60 to determine whether they are on the Alzheimer's pathway or not. If a person knows they are on this pathway well before the onset of any cognitive impairment some would want to alter their lifestyles. It's good to see this type of study advance, as we desperately need noninvasive and low-cost markers for Alzheimer's disease. But still, at this point it is not ready for prime time."

Why is Life Span Inherited to any Significant Degree?
https://www.fightaging.org/archives/2018/02/why-is-life-span-inherited-to-any-significant-degree/

Why do the life spans of parents exhibit some degree of correlation with the life spans of their children? "Genetics" is probably not an acceptable answer, given present evidence for natural genetic variation to contribute comparatively little to human life expectancy in all but a few rare cases. So is it cultural, where culture influences lifestyle choices closely correlated with health, such as weight gain or smoking? Or is it due to wealth effects, for much the same reasons? If so, then why is there such variation in life expectancy within specific social groups and wealth strata? These are tough questions to answer with any reliability given snapshot data from groups within human populations. Any given large study is just a single data point in the ongoing process of analysis and debate that spans decades and the entire scientific community.

In the long run, I have my doubts that good answers will be established for this and many other questions regarding the details of natural aging today. We may never know. The urge to investigate the demographics of aging will be swept away by the advent of rejuvenation therapies such as the senolytics presently under development. All natural variations in pace of aging and life expectancy will be buried beneath the size of the gains made possible through periodic repair of the cell and tissue damage that causes aging. The data will evaporate, and different concerns will occupy the scientific community of tomorrow. After all, how many members of today's scientific community spend any time on the demographics of smallpox in populations lacking treatment options? Few indeed. It will be the same for natural aging.

Mortality, life expectancy, and age-at-death are all strongly socially structured. Despite economic growth, welfare state provisions, modern medicine and a fundamental change in disease panorama, we find a negative social gradient in mortality generation after generation. Because education, occupation, and income all predict health and survival we should also expect such characteristics in the parental generation to predict the next generation's health prospects, resulting in "inheritance of longevity". It is possible, however, that this influence from previous generations is considerably broader than that working through the children's own education, occupation, and income. Variation in mortality risk within social groups is great. To understand "inheritance of longevity" we need a conceptual framework that also identifies those within-class influences.

Already in 1934 it was suggested that the first 15 years of life could determine your mortality risk during the entire lifecourse. Similarly, the so-called DOHaD (Developmental Origins of Health and Disease) theory suggests that early life experiences is an important determinant of adult health and disease. DOHaD theory has focused on specific aetiologies and influences, such as that of foetal growth restriction on blood pressure and circulatory disease. Another, earlier school of thinking argued for more general disease-causing mechanisms. Concepts like frailty, general susceptibility, or differential vulnerability refer to individual differences in the ability to survive hardship.

Demographic concepts like frailty, epidemiological ones like general susceptibility, and psychological ones like resilience all refer to the same real-life-phenomenon: a general rather than specific vulnerability to disease. Some have stressed its social roots, while others perhaps assumed it to have a more genetic basis. Resilience, in turn, may be related to both views. It could be thought of as the opposite extreme to susceptibility/frailty on the same underlying dimension. In this study, we argue that resilience is acquired early and maintained throughout life. Resilience should therefore influence the ability to survive up to a high age and be linked to longevity, as a number of studies indeed suggest.

"Inheritance of longevity" has been discussed at length in the literature. Its precise nature is somewhat elusive. Studying the entire Icelandic population, researchers concluded that longevity was inherited within families, probably because of shared genes. Other groups, looking at twin data, concluded that genetic influences on the lifespan were minimal before age 60 and only increase after that age. On the other hand, other work has rejected any idea that mortality in old age is genetically programmed. Consistent with that view, a Swedish study of men born in 1913, found that a number of social and behavioural factors measured at age 50, but not their parents' survival, predicted longevity.

Evolutionary theorists have debated whether there is any evolutionary pressure to promote survival into old age. Nevertheless, we observe a steady lifespan extension in modern societies, especially among women, partly based on falling mortality rates across their long post-reproductive period. That children tend to live longer than their parents is likely to be determined both by what experience parents brings to the next generation, and by the improved life circumstances of the children themselves in their childhood and adult life. The importance of genetic factors for longevity, we suggest, may lie in their interaction with other factors, perhaps especially if this interaction takes place at an early age.

Immunosenescence and Inflammaging, Two Sides of the Same Coin
https://www.fightaging.org/archives/2018/02/immunosenescence-and-inflammaging-two-sides-of-the-same-coin/

The aging immune system falls apart in a number of different ways, and as the researchers here note, the process probably isn't just one of decline, but of a continual adaptation to that decline. Present nomenclature tends to categorize aspects of immune system aging into broad categories by the type of outcome produced. These are (a) immunosenescence, the weakening of the immune response to pathogens and failure of immune surveillance of potentially dangerous cells, (b) inflammaging, progressively raised levels of chronic inflammation, and © autoimmunity, in which the immune system begins to attack tissues. In reality, everything in biochemistry is connected to everything else, and these outcomes are the consequences of interacting, shared processes of decline and damage.

Any successful effort to turn back immune system aging, such as by selectively destroying malfunctioning or unhelpfully configured immune cells, and restoring the generation of new immune cells to youthful levels, should go some way to addressing all of these issues. The researchers here suggest caution on selective reversal of symptoms of immune aging, as some are beneficial adaptations, but in my opinion this shouldn't apply to efforts to address the lower level causes of immune aging. Where adaptations occur, they are adaptations to those causes, an attempt to claw back some functionality in the face of decline. That becomes moot, and the adaptation should cease, if its trigger is removed.

Aging is one of the most intricate and complex biological phenomenon. One physiological system that shows marked changes during aging is the immune system. The interest of the immune system in aging is related to the fact that this is an interacting master regulatory system that keeps the organism free of invaders, either internal or external. Since the introduction of the notion of immunosenescence, many scientists have questioned the justification for unidirectional implication of the immune system and its decreased efficiency associated with aging. Whereas some functions are indeed decreased, others are increased. Therefore; changes are not as uniform as the designation would suggest.

Accordingly, we can propose a new paradigm for dynamic immune changes with aging. We suggest that aging leads to modified/modulated responses of the immune system, making it more adapted to cope with challenges (pathogens) in a given (local) environment, and not just to an eventually terminal deterioration of the immune system. From an evolutionary perspective, this is a simple optimization of the resources of the aging body, even if it ultimately leads to pathologies and death. Immunosenescence may be necessary for an adequate response to known antigens, but detrimental for responses to new antigens in most circumstances. From this perspective, many or most age-related changes in the immune system may be desirable adaptations to the aging process, and thus no need for rejuvenation seems to be necessary.

In conclusion, most experimental data on immune changes with aging show a decline in many immune parameters when compared to young healthy subjects. The bulk of these changes is termed immunosenescence. Immunosenescence has been considered for some time as detrimental because it often leads to subclinical accumulation of pro-inflammatory factors and inflammaging. Together, immunosenescence and inflammaging are suggested to stand at the origin of most of the diseases of the elderly, such as infections, cancer, autoimmune disorders, and chronic inflammatory diseases. However, an increasing number of gerontologists have challenged this negative interpretation of immunosenescence with respect to its significance in aging-related alterations of the immune system.

If one considers these changes from an evolutionary perspective, they can be viewed preferably as adaptive or remodeling rather than solely detrimental. Whereas it is conceivable that global immune changes may lead to various diseases, it is also obvious that these changes may be needed for extended survival/longevity. Recent cumulative data suggest that, without the existence of the immunosenescence/inflammaging duo (representing two sides of the same phenomenon), human longevity would be greatly shortened.

A More Subtle Demonstration that Telomere Length is Not a Good Measure of Aging
https://www.fightaging.org/archives/2018/02/a-more-subtle-demonstration-that-telomere-length-is-not-a-good-measure-of-aging/

Researchers here find a disconnect between DNA methylation patterns shown to correlate well with age and processes associated with longer telomere length. Telomeres are caps of repeated DNA at the ends of chromosomes that shorten with each cell division, a part of the mechanism limiting the life span of somatic cells. Their average length tends to shorten with age when considered across large populations in a statistical analysis, but this is a tenuous relationship that has also failed to appear in some smaller studies. Here, it seems that older ages as assessed by DNA methylation can correlate with differences in telomerase, the enzyme responsible for lengthening telomeres, that are associated with longer telomeres.

In any given individual, average telomere length as currently measured in leukocytes from a blood sample is dynamic in response to circumstances; it reflects pace of cell division and the rate at which new cells with long telomeres are generated by stem cells. Unfortunately the large degree of individual and circumstantial variation means that there is little to be meaningfully said about the present value - the information is not actionable in all but rare cases of exceptionally short average length due to disease. The epigenetic clocks derived from DNA methylation measurements are much more solid, repeatable, useful metrics, judging from the evidence to date.

In that broader context, it is interesting to find signs that these two approaches to measuring an aspect of aging are not on the same page, though I think the researchers here overstate the significance of their work and/or engage with a strawman to some degree in their comments. What they have found does fit in with the evidence to date supporting the idea that telomere length is only very loosely associated with aging, with considerable variation between individuals. That is somewhat distinct from the question of whether or not telomerase gene therapies are a useful approach to the treatment of aging or other conditions.

Researchers analyzed blood samples from nearly 10,000 people to find that genetic markers in the gene responsible for keeping telomeres (tips of chromosomes) youthfully longer, did not translate into a younger biologic age as measured by changes in proteins coating the DNA. DNA methylation age is a biomarker of chronological age and predicts lifespan, but its underlying molecular mechanisms are unknown.

In this genome-wide association study, researchers found gene variants mapping to five loci associated with intrinsic epigenetic age acceleration (IEAA) and gene variants in three loci associated with extrinsic epigenetic age acceleration. Variants in the gene called Telomerase Reverse Transcriptase (TERT) on chromosome 5 that were associated with older IEAA were also associated with longer telomeres indicating a critical role for TERT in regulating the epigenetic clock, in addition to its established role of compensating for cell replication-dependent telomere shortening.

"We calculated the epigenetic aging rate for each person using a previously described epigenetic clock method. Next, we related the epigenetic aging rate to millions of genetic locations (SNPs) across all of the chromosomes. Then we studied the SNPs that had very significant associations with epigenetic aging rates. To our surprise, one of these locations was the TERT locus. The finding is surprising because this was not a study of telomere length. TERT is a subunit of the enzyme telomerase, which is widely known because it has been touted as an anti-aging enzyme. Our study highlights the error in the notion that activation of telomerase (as advocated by some) will cure aging. Instead, our study shows that an anti-aging therapy based on telomerase expression would be accompanied by continued aging."

Reviewing What is Known of Extracellular Vesicles and Cellular Senescence
https://www.fightaging.org/archives/2018/02/reviewing-what-is-known-of-extracellular-vesicles-and-cellular-senescence/

The research community has been devoting more time and energy to the investigation of extracellular vesicles of late. These membrane-bound packages of proteins and other molecules are an important facet of the way in which cells communicate with one another. Signaling between cells is itself very significant, a potential point of intervention for many classes of therapy. For example, most current stem cell therapies appear to work largely due to the signaling provided by transplanted cells - given sufficient understanding of the signaling, the cells could be dispensed with and the signals applied directly.

As another example, the growing presence of cellular senescence with age has a large detrimental impact on tissue function, despite the comparatively small numbers of senescent cells present even in older individuals, because these negative effects are mediated by signaling. In this way, a handful of errant cells can put the entire local environment into disarray. On that topic, the open access paper here takes a short tour of what is known about extracellular vesicles in the context of cellular senescence.

Cellular senescence prevents the proliferation of cells exposed to potentially oncogenic stresses, such as DNA-damaging reagents, irradiation, telomere shortening, and oncogene activation. Mutations in genes essential for the senescence-induced cell cycle arrest predispose cells to immortalization and shorten lifespan by increasing cancer incidence. However, cellular senescence not only arrests the cell cycle but also changes how the cell impacts its microenvironment. The way in which senescent cells influence their microenvironment is highly context dependent. It promotes tumor development in many cases, but can also be tumor suppressive in certain circumstances. Removal of senescent cells that accumulated in the body during aging alleviates atherosclerosis, hepatic steatosis, tumor development, and functional declines of heart, kidney, and fat tissues, resulting in prolonged healthspan and lifespan. These effects may be attributable to so-called , whereby cells secrete high levels of inflammatory cytokines, chemokines, growth factors, and metalloproteinases.

Although the involvement of typical secretory proteins in the non-cell-autonomous effects of senescent cells has been well studied, the functions of membrane-enclosed vesicles secreted by senescent cells have not been studied until recently. These extracellular vesicles (EVs) were once thought to be cellular trash, but now it is clear that they are critical mediators in intercellular communication. Emerging evidence indicates that EVs also play important roles in cellular senescence and aging. This field is rapidly advancing especially since it was reported that EVs deliver functional RNA to the recipient cells. Extracellular vesicles contain a huge variety of proteins and nucleic acids in a cell type-dependent manner.

Senescence-associated increase in EV secretion seems to be a general feature of cellular senescence and has been observed in fibroblasts, epithelial cells, and cancer cells. This increase is at least partially mediated by p53 and one of its targets, TSAP6, although the mechanism whereby TSAP6 regulates EV secretion is not well understood. It is known that EV secretion contributes to the clearance of harmful molecules in cells, such as cytoplasmic DNA. It has been shown that EV-mediated removal of cytoplasmic DNA is essential for the survival of senescent cells, which may explain why EV secretion is increased in senescent cells.

Recent findings implicate senescent cell EVs in cancer development, vascular calcification, and age-related decline in bone formation. Increased secretion of EV-associated DNA from senescent cells is likely to be pro-inflammatory and may contribute to age-related chronic inflammation. Whether senescent cell EVs promote or suppress cancer development may be context dependent. Despite this progress, it should be noted that the functions of senescent cell EVs are still understudied, at least partially due to inadequate understanding of EVs themselves. This research field is immature and the methods used are not sufficiently standardized yet. Nevertheless, EVs are now shown to be critical players in cellular senescence and aging, and more functions will be revealed in the future as the EV research field matures.

Ventricular Decline Correlates Well with Other Forms of Damage in the Aging Brain
https://www.fightaging.org/archives/2018/02/ventricular-decline-correlates-well-with-other-forms-of-damage-in-the-aging-brain/

Here, researchers examine the correlation between ventricular dsyfunction, other noted forms of damage observed in brain aging, and the onset of cognitive decline. The ventricular system is where cerebrospinal fluid is created and circulates throughout the brain. Many things go wrong in the aging brain, all stemming from the same few root cause processes of damage accumulation in and around cells. Thus correlations between specific observed changes and the progression of dementia should be expected, but don't necessarily imply direct causation - though a particularly good correlation always indicates that further investigation is probably merited.

This line of investigation ties in to a growing area of research regarding the impairment of drainage of cerebrospinal fluid in aging. This impairment may explain the slowly rising levels of protein aggregates and other molecular waste in the brains of older individuals, a state of affairs known to contribute to the development of neurodegenerative conditions. Normally these wastes are removed at some pace through various filtration and drainage channels for cerebrospinal fluid, but the channels become dysfunctional, just like all other biological systems in older individuals. Leucadia Therapeutics is an example of a company working to intervene and restore youthful levels of drainage to what they consider the more important path. Other groups are looking into different areas of impaired fluid flow in the brain. All in all it is a most interesting and promising area of development.

The human brain's ventricular system is essential for the movement of nutrient-rich cerebrospinal fluid (CSF) throughout the central nervous system. A special epithelial lining along the ventricle walls composed of ependymal cells allows for the movement of CSF nutrients into the brain parenchyma as well as clearance of proteins and metabolites from the interstitial fluid (ISF). This ependyma-mediated bidirectional CSF-ISF exchange, as well as the formation of a cell barrier to prevent movement of proteins and metabolites from the CSF back into the ISF, relies on the presence of an intact ependymal cell monolayer. Pathological conditions in humans that are characterized by ependymal cell stretching and/or loss, including hydrocephalus, typically result in decreased CSF turnover rates and impaired clearance of proteins and metabolites resulting in a harmful buildup of these substances in brain parenchymal tissue.

Longitudinal magnetic resonance imaging (MRI)-based studies have established that expansion of the brain's fluid-filled lateral ventricles (LVs), or ventriculomegaly, is a defining feature of the aging brain. Ventricle expansion rates correlate strongly with declining cognitive performance and the rate of ventricle volume increase has been linked to an increase in Alzheimer's disease (AD)-related amyloid-beta (Aβ) plaques and tau neurofibrillary tangles, as well as alterations in CSF biomarker composition. Together, these point towards defective CSF-ISF exchange and impaired clearance mechanisms that are characteristic of AD.

Degeneration of periventricular brain tissue and declines in associated white matter tract integrity are common with normal aging and the extent of periventricular tissue abnormalities has been linked to dementia and AD. Periventricular hyperintensities (PVH), as measured using MRI, are indicative of fluid accumulation, or edema, often located in the parenchymal tissue directly adjacent to the frontal and occipital horns of the LV. The precise etiology of PVH is not clear; however, studies have implicated impaired drainage of ISF from the periventricular white matter resulting in aberrant fluid accumulation.

In previous studies, we found that enlarged ventricles from aging humans exhibited regional gliosis in the place of functional ependymal cell coverage. We predict that replacement of the ependymal lining with stratified layers of astrocytes at the ventricle surface adversely affects CSF/ISF bulk flow mechanisms, leading to fluid accumulation or edema and harmful buildup of proteins and metabolites in the periventricular space. Due to the rarity of longitudinal MRI data sets and associated subject-matched periventricular tissue biospecimens, this has never been directly demonstrated.

Using data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) and the Baltimore Longitudinal Study of Aging (BLSA), we investigated the relationships among the following variables: ventricle expansion, PVH, periventricular white matter tract integrity, and degree of cognitive impairment. We also investigated the histopathological correlates of these measures, including LV wall gliosis and periventricular protein accumulation. We found that both LV and PVH volumes increase with age, and this expansion is more rapid and dramatic in cognitively impaired (CI) subjects. We also found a direct relationship between LV volume and PVH volume increase. Case studies from the BLSA allowed us to link ventricle expansion with regional gliosis, where an intact ependymal cell monolayer was replaced with stratified layers of astrocytes in regions of LV expansion. Additionally, adjacent parenchymal regions exhibited edema (as indicated by PVH), white matter deterioration, decreased vascular integrity, and harmful buildup of proteins including Aβ and tau.

Naked Mole-Rats Experience Cellular Senescence, but Seem Largely Unaffected by It
https://www.fightaging.org/archives/2018/02/naked-mole-rats-experience-cellular-senescence-but-seem-largely-unaffected-by-it/

Naked mole-rats are distinguished by an exceptionally long life span in comparison to similarly sized rodents, and a near immunity to cancer. Unlike other mammals, their mortality rates stay fairly constant until very late life. They accumulate all the signs of significant oxidative damage in cells and tissues, but seem resilient to it. Similarly, researchers here note that naked mole-rats do in fact accumulate senescent cells, one of the root causes of aging, but appear resilient to the harmful presence and activities of these cells. Exactly why this is the case has yet to be determined.

Cells become senescent in response to potentially cancerous damage or reaching the Hayflick limit on replication. The vast majority destroy themselves or are destroyed by the immune system, but a tiny fraction linger. They generate signals that spur chronic inflammation, change surrounding cell behavior for the worse, and destructively remodel nearby tissue structures. This results in functional decline in organs and other important tissues and systems. It is interesting to see that while there are differences in the detailed behavior of senescent cells between naked mole-rats and other mammals, they nonetheless still generate the same damaging signals, and yet the naked mole-rats appear to shrug it off.

With their large buck teeth and wrinkled, hairless bodies, naked mole rats won't be winning any awards for cutest rodent. But their long life span - they can live up to 30 years, the longest of any rodent - and remarkable resistance to age-related diseases, offer scientists key clues to the mysteries of aging and cancer. That's why researchers studied naked mole rats to see if the rodents exhibit an anticancer mechanism called cellular senescence.

Previous studies indicated that when cells that had undergone senescence were removed from mice, the mice were less frail in advanced age as compared to mice that aged naturally with senescent cells intact. Researchers therefore believed senescence held the key to the proverbial fountain of youth; removing senescent cells rejuvenated mice, so perhaps it could work with human beings. But is eliminating senescence actually the key to preventing or reversing age-related diseases, namely cancer?

Researchers compared the senescence response of naked mole rats to that of mice, which live a tenth as long - only about two to three years. Their unexpected discovery? Naked mole rats do experience cellular senescence, yet they continue to live long, healthy lives; eliminating the senescence mechanism is not the key to their long life span. The researchers found that although naked mole rats exhibited cellular senescence similar to mice, their senescent cells also displayed unique features that may contribute to their cancer resistance and longevity.

The cellular senescence mechanism permanently arrests a cell to prevent it from dividing, but the cell still continues to metabolize. The researchers found that naked mole rats are able to more strongly inhibit the metabolic process of the senescent cells, resulting in higher resistance to the damaging effects of senescence. "In naked mole rats, senescent cells are better behaved. When you compare the signals from the mouse versus from the naked mole rat, all the genes in the mouse are a mess. In the naked mole rat, everything is more organized. The naked mole rat didn't get rid of the senescence, but maybe it made it a bit more structured."

The Longest-Lived Bats Have Unusual Telomere Biology
https://www.fightaging.org/archives/2018/02/the-longest-lived-bats-have-unusual-telomere-biology/

Researchers here find that the longest lived bats have unusual telomere biochemistry, and in fact unusual enough that the new knowledge may turn out to be of little relevance to the understanding of telomeres, telomerase, and aging in other mammals. It appears that they rely upon alternative lengthening of telomeres (ALT) to maintain telomere length, a process that doesn't operate in any normal adult human cell. Given that loss of telomere length appears to be a marker of aging rather than a cause, and a fairly loosely coupled marker at that, the real relevance of this area of biochemistry probably lies in the relationship between telomerase and important cellular activities, such as ability and willingness of somatic cells to replicate, or stem cells to support tissue function.

Bats exhibit cellular biochemistry that is somewhat different from that of ground-based species in a number of other ways. The metabolic demands of flight have led to, for example, greater resilience to stress and damage arising from the normal operation of cellular metabolism. When charting life span against metabolic rate, where high metabolic rates usually imply short life spans, some small bat species are noteworthy outliers. Brandt's bat, for example, has a life span of four decades despite being the same size as ground-dwelling mammals that live for only a couple of years.

One of the principal caveats at the present stage of research into telomeres and the use of telomerase gene therapies - or other means of enhancing telomerase activity - as a treatment for aspects of aging is that mice and humans have quite different telomere dynamics and patterns of natural telomerase activity. The balance between cancer risk and beneficially increased stem cell activity resulting from telomerase therapies may turn out to be significantly different in different species. That these bats have their own unique evolved dynamics, ones that are much further removed, suggests that this portion of the comparative biology might not be as useful to the practical science of aging as hoped. The fastest path to understanding is probably to extend present work on telomerase therapies to species more like humans in their telomere biology, such as dogs and pigs perhaps. Or, as some advocate, running human trials immediately.

We urgently need to better understand the mechanisms of the aging process, with a view to improving the future quality of life of our aging populations. Most aging studies have been carried out in shorter-lived laboratory model species, given the ease of manipulation, housing, and length of life span. Although they are excellent study species, it is difficult to extrapolate experimental findings in these short-lived laboratory species to long-lived, outbred species such as humans. Therefore, it has been argued that long-lived, outbred species such as bats may be better models to investigate the aging processes of relevance to people.

Only 19 species of mammal are longer-lived than humans in proportion to their body size, and 18 of these species are bats. Bats are the longest-lived mammals relative to their body size, with the oldest bat recaptured (Myotis brandtii) being more than 41 years old, weighing ~7 g, and living ~9.8 times longer than predicted for its size. Although an excellent model species to study extended healthspan, logistically, it is difficult to study aging in bats because they are not easily maintained in captivity. Here, uniquely drawing on more than 60 years of cumulative long-term, mark-recapture studies from four wild populations of long-lived bats, we determine whether telomeres, a driving factor of the aging process, shorten with age in Myotis myotis (n = 239; age, 0 to 6+ years), Rhinolophus ferrumequinum (n = 160; age, 0 to 24 years), Myotis bechsteinii (n = 49; age, 1 to 16 years), and Miniopterus schreibersii (n = 45; age, 0 to 17 years).

We show that telomeres shorten with age in Rhinolophus ferrumequinum and Miniopterus schreibersii, but not in the bat genus with greatest longevity, Myotis. As in humans, telomerase is not expressed in Myotis myotis blood or fibroblasts. Selection tests on telomere maintenance genes show that ATM and SETX, which repair and prevent DNA damage, potentially mediate telomere dynamics in Myotis bats. Twenty-one telomere maintenance genes are differentially expressed in Myotis, of which 14 are enriched for DNA repair, and 5 for alternative telomere-lengthening mechanisms. These results, coupled with differential expression of ATM, SETX, MRE11a, RAD50, and WRN across all tissues in the genus Myotis compared to other mammals, suggest a potential role for alternative lengthening of telomeres (ALT) mechanisms in the maintenance of telomeres in these species. If telomeres are maintained by ALT mechanisms in Myotis species, then these genes may represent excellent therapeutic targets given that cancer incidence in bats is rare.

MDM2 Antagonists Attenuate Harmful Signaling from Senescent Cells
https://www.fightaging.org/archives/2018/02/mdm2-antagonists-attenuate-harmful-signaling-from-senescent-cells/

A fair number of the scientists working towards therapies to address cellular senescence, one of the causes of aging, are more interested in suppressing signaling from these cells than in destroying them. Cynically, a treatment one has to keep using consistently is much more interesting to pharmaceutical companies than a treatment that only has to be applied once every few years at most. Until researchers encounter a population of senescent cells that cannot be safely removed, destruction continues to look like the far better option. Senescent cells are harmful because of the mix of signals they generate, a mix that is still comparatively poorly mapped and understood. Suppressing it may well prove to be a lengthy and difficult process of progress by small degrees, while destruction can be achieved in the near future and removes all of the harmful signaling whether or not it is understood.

Astrocytes are one potential candidate for a population of senescent cells that might be challenging to remove. It isn't completely clear that all of the astrocytes showing markers of senescence are actually senescent, but if so it represents a large portion of all astrocytes in the aging brain. Abrupt clearance of these cells would probably not be healthy, regardless of the incremental harms they are causing. With this sort of thing in mind, it is prudent to have a backup strategy under development, whether that is some form of careful incremental winnowing and replacement of these cells over time, or a form of suppression of their bad behavior while allowing them to live.

One of the common features of aging is low-level chronic inflammation, termed sterile inflammation or inflammaging. Even though all the sources of inflammaging are unclear, it likely derives at least partly from senescent cells. Mammalian cells undergo senescence in response to stressful stimuli. An important feature of senescent cells is the secretion of a myriad of biologically active factors, termed the senescence-associated secretory phenotype (SASP).

The SASP is similar between mice and humans, and comprises inflammatory cytokines such as IL-6 and IL-8. The SASP can disrupt the surrounding microenvironment and normal cell functions, and stimulate malignant phenotypes in nearby cells. Senescent cells can also promote tumor growth in mice. Because senescent cells increase with age and are frequently found within hyperplastic and degenerative tissues, the SASP may be a major cause of inflammaging. Compounds that modulate the SASP hold promise for ameliorating a number of diseases of aging, including cancer.

Nutlins were originally identified as potent small molecules that inhibit the interaction between p53 and MDM2, which promote p53 degradation. Nutlin therefore stabilizes p53, thereby promoting the apoptotic death of cancer cells. Importantly, in cancer cells, nutlin-3a inhibits the activity of NF-κB, a potent transcriptional stimulator of genes encoding inflammatory cytokines, in a p53-dependent manner. The clinical importance of small-molecule MDM2 inhibitors like nutlin-3a spurred the discovery of similar compounds, such as MI-63, which are more efficient inhibitors of the MDM2-p53 interaction.

We investigated the effects of small-molecule MDM2-p53 interaction antagonists on senescent phenotypes, including the SASP, of primary human fibroblasts and epithelial cells. We used nutlin-3a, as well as the non-peptide small molecule inhibitor of MDM2, MI-63. We compared these compounds for their ability to induce a growth-arrested state, whether quiescence or senescence, in human cells, and evaluated their ability to modulate the SASP. We found that both compounds trigger selected markers of a senescent-like state, but the growth arrest was reversible, and both significantly suppressed the SASP, suggesting potential utility as therapeutic agents.

Mitochondrially Targeted Antioxidant SS-31 Improves Cognitive Function in Old Mice
https://www.fightaging.org/archives/2018/02/mitochondrially-targeted-antioxidant-ss-31-improves-cognitive-function-in-old-mice/

Oxidative damage has long been linked to aging, but the general use of antioxidants does nothing for life span. In fact, the evidence suggests this approach is modestly harmful, possibly due to blocking the oxidative signaling needed for exercise and other, similar mild stresses to produce benefits via hormesis. Antioxidant compounds targeted to the mitochondria are a different story, however, and have been shown to slow aging or partially reverse some aspects of aging in mice and lower animals - as is the case in this open access paper.

Mitochondria are the power plants of the cell, and generate reactive molecules that raise oxidative stress as a side-effect of the processes that produce chemical energy stores. This flow of reactive molecules influences the behavior of the cell in numerous ways; methods of slightly slowing aging have been demonstrated that either lower production, leading to less oxidative damage, or raise it, spurring increased maintenance activities in the cell. In the research here, benefits are derived indirectly: damping down oxidative damage improves the function of blood vessels in the aged brain, which helps to restore some degree of lost cognitive function in old mice. The brain is an energy-hungry organ, and age-related neurodegenerative conditions are characterized by a general decline in the capacity of of the blood supply and mitochondria in cells to supply as much energy as is needed.

Normal functioning of the central nervous system (CNS) requires a continuous, tightly controlled supply of oxygen and nutrients as well as washout of harmful metabolites through uninterrupted cerebral blood flow (CBF). The energetic demands of neurons are very high, yet the brain has very little energetic reserves. During periods of intense neuronal activity, there is a requirement for adjusting oxygen and glucose delivery to local neuronal activity through rapid adaptive increases in CBF. This is ensured by a mechanism known as neurovascular coupling (NVC). The resultant functional hyperemia is a vital mechanism to maintain optimal microenvironment of cerebral tissue and thereby ensuring normal neuronal function.

There is an increasing appreciation that (micro)vascular contributions to cognitive impairment and dementia in elderly patients are critical. Importantly, neurovascular coupling responses are impaired both in elderly patients and aged laboratory animals. Experimental studies support this concept, showing that pharmacologically induced neurovascular uncoupling in mice mimics important aspects of age-related cognitive impairment. On the basis of these findings, we proposed that novel therapeutic interventions should be developed to rescue functional hyperemia in elderly patients to prevent/delay cognitive impairment. Previous studies demonstrate that aging exacerbates generation of reactive oxygen species (ROS) in the cerebromicrovascular endothelial cells, which contribute to age-related neurovascular uncoupling in aged mice by promoting endothelial dysfunction. We hypothesize that pharmacological treatments, which attenuate endothelial oxidative stress, will have the capacity to improve neurovascular coupling in aged individuals.

The mitochondrial free radical theory of aging posits that mitochondria-derived ROS (mtROS) production and related mitochondrial dysfunction are a critical driving force in the aging process. In support of this theory, it was demonstrated that attenuation of mitochondrial oxidative stress (by mitochondria-targeted overexpression of catalase) increases mouse lifespan. There is particularly strong evidence that mitochondrial oxidative stress is implicated in cardiovascular aging processes. Yet, although drugs that improve mitochondrial function have been shown to exert beneficial effects both on the vasomotor function of peripheral arteries, their potential protective effects on the aged cerebral microvasculature has not been investigated.

This study was designed to test the hypothesis that pharmacological attenuation of mtROS can restore cerebromicrovascular endothelial function and thus improve neurovascular coupling in aged mice. To achieve this goal, in aged mice mitochondrial oxidative stress was manipulated by treatment with the mitochondrial-targeted peptide SS-31. We found that neurovascular coupling responses were significantly impaired in aged mice. Treatment with SS-31 significantly improved neurovascular coupling responses by increasing cerebromicrovascular dilation, which was associated with significantly improved spatial working memory, motor skill learning, and gait coordination. These findings are paralleled by the protective effects of SS-31 on mitochondrial production of reactive oxygen species and mitochondrial respiration in cultured cerebromicrovascular endothelial cells derived from aged animals.


View the full article at FightAging

Do Antibiotics Cause Weight Gain?

by Lisa Richards @ The Candida Diet

When it comes to taking antibiotics, there’s a fine line between good and evil. Yes, they’re sometimes necessary for treating serious bacterial infections. But they’re also extremely damaging to the body – particularly the gut. When used too readily and too often, antibiotics can wreak havoc that takes years to rectify. Unfortunately, the over-prescription of […]

The post Do Antibiotics Cause Weight Gain? appeared first on The Candida Diet.

Probiotics And Weight Gain Cake Chocolate Sauerkraut

by @ Probiotics Belaw

If you are taking any prescription medications you should talk to your doctor first before using TruBiotics. Probiotics And Weight Gain Cake Chocolate Sauerkraut click here to read about Just 4 Kids! Potent Probiotics with Organic Prebiotics Powder. Do All Yogurt Have Probiotics They certainly do when they’re made Even though probiotics are needed to […]

Probiotic Capsule Douche Taking Leaky Gut

by @ Probiotics Belaw

Sundown Naturals Inulin Fiber Prebiotic Mineral Supplement Capsules 90 Count $8.79 ($0.10 / count). Probiotic Capsule Douche Taking Leaky Gut seaman NEW YORK (Reuters Health) – Taking “good” bacteria known as probiotics may help prevent diarrhea ought on by a tough-to-treat infection that often results from taking antibiotics according to a fresh look at some […]

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by JINI @ Listen To Your Gut

Vancouver I live in a place that is absolutely fantastic, except for one big problem: the weather. Here in Vancouver, Canada it is rainy, dark and depressing for about eight months of the year. For me, that is a long time without sun and no, I’m not one of those hardy Canadians who gets on…

Colorectal Cancer Stage 4 Survivors Dill Yogurt Sauce For Recipe Salmon

by @ projectathena probiotics composition

Probiotics for this maintenance program are:SuperProbiogold Culturelle and threelac(when we do the three days of naturals). rhamnosus may reduce bowel inflammation in infants with cow’s milk allergy and atopic dermatitis/eczema. Colorectal Cancer Stage probiotic dairy products in uk breastfeeding antibiotics 4 Survivors Dill Yogurt Sauce For Recipe Salmon Colorectal Cancer Stage 4 Survivors Dill Yogurt […]

Probiotics Yogurt For Ibs Intolerance Milk Lactose

by @ Probiotics Belaw

Die off can also occur perpetually. AVI-CULTURE-2 is the NUMBER ONE all-natural live 10-strain avian-specific Non-GMO Dairy-Free FOS-Free & Allergen-Free Now the new & improved AVI-CULTURE-2 surpasses that making IT the best avian-specific probiotic for all birds on the planet! Up to 75 percent of women will have a yeast infection in their lifetime and […]

Top 5 Probiotics For Women

Top 5 Probiotics For Women


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We take a detailed look at the importance of probiotics for women before identifying the top daily probiotics on the market.

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by JINI @ Listen To Your Gut

Some doctors are now recommending that people with Crohn’s and Colitis NOT take probiotics. They are saying that people with IBD do not have a normal response to beneficial bacteria and therefore probiotics can aggravate these conditions. Back when I was diagnosed with Crohn’s (1984), the medical establishment maintained that Crohn’s  was an autoimmune disorder…

Coconut Aminos: A Healthier Alternative To Soy Sauce

by Lisa Richards @ The Candida Diet

Like most people, you probably have a bottle of soy sauce in your kitchen cupboard. Soy sauce is one of the most popular condiments in the culinary world, especially in Asian cooking. So, it may be a shock to learn that it’s not actually very good for you! Although much of the soy sauce consumed […]

The post Coconut Aminos: A Healthier Alternative To Soy Sauce appeared first on The Candida Diet.

Does Absorb Plus Create a Candida Problem?

by JINI @ Listen To Your Gut

I’ve actually received this question – in various forms – a lot over the past few years. So here’s a good representative of the concerns and my answer. Question: I’m very concerned though about the issue of Absorb Plus feeding Candida. I decided to use Absorb Plus to do The IBD Remission Diet because your book says…

Yeast Infection Symptoms And Frequent Urination For Water Distilled Candida

by @ iihff yeastinfection thionvillefc

Candida is a type of yeast infection that is generally Disabled World provides a there are indications that candidiasis can affect people who do not Would you like to know if your health problems are related to Candida? This online test developed Belching and intestinal gas Haz una mezcla con ambos It is characterized by […]

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by JINI @ Listen To Your Gut

A lot of websites make claims about the ability of bentonite (montmorillonite) and other clays to detox bad bacteria, viruses, parasites, etc. from the gut. For example, here is a statement I saw again and again, on literally dozens of sites: According to the Canadian Journal of Microbiology, bentonite can absorb pathogenic viruses, the mold…

ThreeLac Probiotic Candida Treatment | How It Works | Candida Support

ThreeLac Probiotic Candida Treatment | How It Works | Candida Support


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Threelac™ probiotic Candida treatment is one of the safest Candida product available. Contact Candida Support to Learn How it can Help You.

Not for profit people pharmaceutical R&D company

by @ Action

Testing the waters to see if there is any interest in a cooperative research and development company funded by forum members and crowdfunding from other forums reddit etc. The company could provide reliable nmr testing, in vitro and eventually in vivo studies all without the motive of profit. Drug candidates could be sold into the for profit market to expand capabilitiesss. Thoughts?

Microwave Radiation Killing Trees

by JINI @ Listen To Your Gut

As I get deeper and deeper into this whole WiFi/cell phone debacle, the one thing that never ceases to amaze me is how people stubbornly insist on “proven data” quoting Industry-funded sources like Health Canada stating that “a person would have to be in a room within 20 cm of 1,000 WiFi routers for an…

Can I take my probiotic powders in an Absorb Plus shake?

by JINI @ Listen To Your Gut

Question: Can I add Natren probiotic powders to my Absorb Plus shakes, or should I mix the probiotics only with water? Answer: We contacted Natasha Trenev, the founder/owner of Natren probiotics and asked her this question. She replied that yes, you can mix Natren probiotic powders with Absorb Plus, but you must follow these directions:…

Candida Diet Energy Bites Signs Anus

by @ iihff yeastinfection thionvillefc

Download and Read Recipe Banana Yeast Bread. Si certo Carmela i fiori di Bach si usano anche durante l’allattamento e la loro viazione viene trasmessa anche al tuo bambino. Candida Diet Energy Bites Signs Anus lipolytica as well as the carbon of urease activity growth Fluconazole (By mouth) floo-KON-a-zole. head soccer hack apk. Between 65 […]

Nccn Colon And Rectal Cancer Guidelines Are Made Poop

by @ projectathena probiotics composition

Prebiotics in food contribute to enhance the growth and maintain the viability of probiotics. Nccn Colon And Rectal Cancer Guidelines Are Made Poop does probiotics help you lose weight? This is still up for debate. OSLO?Pregnant women who regularly consume probiotic-rich milk or yogurt have a reduced risk of developing preeclampsia according to a new […]

Kombucha Tea Bags Side Pills Effects Cleansing

by @ INSIGHTMARKETING LEVEL

Learn why Yakult’s exclusive L. If you’re new here you may want to subscribe to my Newsletter for updates. Kombucha Tea Bags Side Pills Effects Cleansing bowtrol Probiotic improve gastrointestinal function & intestinal good bacterial microbial balance. Under these circumstances most of you out there will need the help of probiotic supplements but making the […]

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Why do some turtles outlive humans?

by @ Articles

(⇒ write for LongeCity )


The oldest human recorded in modernity was Jeanne Louise Calment, she died in the age of 122 years and 164 days [1] .

There are rumors that the oldest tortoise called Adwaita (Aldabra giant tortoise) died in the age of about 250 years [2] or that it was 188-year-old radiated tortoise named Tui Malila [3] , or that the highest verified age of 177 years had Galapagos giant tortoise Harriet [4] . The oldest currently living turtle is considered to be Jonathan (Seychelles giant tortoise), estimated to be over 180 years old these days [5] . Although all aforementioned numbers are estimations, it seems these turtles were older than human supercentenarians.

All previously mentioned species are terrestrial tortoises, a group with longest lifespans among turtles. The most famous of them, well-researched Galapagos giant tortoise, was observed by Charles Darwin when he was forming his well-known theory of evolution by natural selection [6] . There is only one freshwater turtle known to be able to outlive human, it is the common snapping turtle estimated to live up to more than hundred years [7] . While being considerably less researched, recorded maximal lifespan of sea turtles is usually shorter, not exceeding 80 years, however, it is believed that the green sea turtle can live up to 100 years. [8]

It is a difficult question to answer why these reptiles can outlive us because even to determine the actual age of animals with a long lifespan is complicated – partially due to the fact that it takes such a long time to study. Furthermore, many turtles are endangered species [9] so there may not be as many organisms to hand as needed for proper statistics. Nonetheless, we can still claim that turtles are among the most long-living vertebrates on earth [10] . Why?

Firstly, turtles, like all reptiles, benefit from being ectothermic organisms. They do not maintain body temperature and thus save a lot of energy. But that also means they are less flexible: it is crucial for their lifespan to be in natural temperature environment of daily cycles with night-time temperature drop [11] . If they do not live under these conditions in captivity, metabolic pathways change and turtles die much sooner. [12]

Turtles are well-adapted in other ways: their famous shell – the carapace –is good protection against natural predators. Most of hatchling turtles with a soft shell do not survive the first year [13] . A research of natural populations of freshwater turtles showed that only one per cent of them can celebrate the twentieth birthdays, but once the adulthood is reached, mortality rate drops and remains constant throughout the rest of life [14] .

Some turtles can survive under extreme environmental conditions, such as freezing [15] or lack of oxygen for months [16] . They can even undergo hibernation and anaerobic metabolism and therefore deal with hypoxia and anoxia, it was also proposed that the same genes can play a role in longevity itself [17] and also in oxidative stress resistance [18] that further promotes longer life [19] .

Turtle’s bones and shell are used as lactate buffer lowering metabolic acidosis caused by anaerobic glycolysis during the period of lack of oxygen [20] ; [21] Their organism is protected by strong innate immunity compensating slow acquired immune reactions [22] .

Because turtles have very slow metabolism as well as growth, their bodies do not need to deal with excessive metabolic heat and byproducts as mammals [23] . Their natural diet is very simple but also necessary for their longevity. [24]

According to the evolutionary theories, staying alive is less important after menopause. Galapagos giant tortoises achieve sexual maturity late (around the age of up to forty years in the wild, and between twenty and twenty-five years of life in captivity [25] ), then staying fertile until death [26] .

The Hayflick limit is said to determine how many times a cell can divide [27] . The Hayflick limit of Galapagos giant tortoise was said to be about 110 divisions [28] , approximately twice as many as 50 of human cells [29] . Studies in this context have highlighted the importance of telomeres, the protective end sequences of chromosomes, that get shorter with each cell division [30] , can play at least a partially role in life expectancy. It was observed that telomeres in European freshwater turtle’s cells are of the same length in both embryo and adult organism [31] .

Thus, it was believed that turtles are negligibly senescent organisms [32] . In other words, the cells do not age and no age-related diseases appear, which is very different cell behavior than in human bodies [33] and probably the key to any natural longevity. However, evidence now suggests that turtles may not be really negligibly senescent because of observations of survival and reproductive senescence in late age in the painted turtle population [34]

As we can see, turtles have some advantages in the lifespan field. Some of these might inspire researchers to increase lifespans in humans.



References

[1] Oldest person ever. Retrieved January 31, 2017, from http://www.guinnessworldrecords.com/world-records/oldest-person
[2] BBC (2006, March 23). “Clive of India’s” tortoise dies. BBC South Asia. Retrieved from http://news.bbc.co.uk/2/hi/south_asia/4837988.stm
[3] Associated Press (2006, June 26). Tortoise believed to have been owned by Darwin Dies at 176. Fox News. Retrieved from http://www.foxnews.com/story/2006/06/26/tortoise-believed-to-have-been-owned-by-darwin-dies-at-176.html
[4] Galapagos tortoise (Geochelone nigra) longevity, ageing, and life history. Retrieved January 31, 2017, from http://genomics.senescence.info/species/entry.php?species=Geochelone_nigra
[5] Hollins, J. (2012). The world’s most isolated vet? Veterinary Record, 171(2), i–i. doi:10.1136/vr.g7292
[6] Powell, J., & Caccone, A. (2006). Giant tortoises. Current Biology, 16(5), R144–R145. doi:10.1016/j.cub.2006.02.050
[7] Cameron, M. (2008). COSEWIC Assessment and Status Report on the Snapping Turtle Chelydra serpentina in Canada . Retrieved from http://publications.gc.ca/collections/collection_2009/ec/CW69-14-565-2009E.pdf
[8] Green sea turtle (Chelonia mydas) longevity, ageing, and life history. Retrieved January 31, 2017, from http://genomics.senescence.info/species/entry.php?species=Chelonia_mydas
[9] Jacobson, E. R. (1994). Causes of Mortality and Diseases in Tortoises: A Review. Journal of Zoo and Wildlife Medicine, 25(1), 2–17.
[10] Gibbons, J. W. (1987). Why do turtles live so long? BioScience, 37(4), 262–269. doi:10.2307/1310589
[11] Flouris, A. D., & Piantoni, C. (2014). Links between thermoregulation and aging in endotherms and ectotherms. Temperature, 2(1), 73–85. doi:10.4161/23328940.2014.989793
[12] Vadala, N. How Long Do Turtles Live? Retrieved January 31, 2017, from http://www.petmd.com/reptile/care/how-long-do-turtles-live
[13] Stewart, K. R., & Wyneken, J. (2004). Predation risk to loggerhead hatchlings at a high-density nesting beach in Southeast Florida. Bulletin of Marine Science, 74(2), 325–335.
[14] Gibbons, J. W., & Semlitsch, R. D. (1982). Survivorship and longevity of a long-lived vertebrate species: How long do turtles live? The Journal of Animal Ecology, 51(2), 523. doi:10.2307/3981
[15] Packard, G. C., & Packard, M. J. (2003). Natural freeze-tolerance in hatchling painted turtles? Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 134(2), 233–246. doi:10.1016/s1095-6433(02)00264-7
[16] Milton, S. L., & Prentice, H. M. (2007). Beyond anoxia: The physiology of metabolic downregulation and recovery in the anoxia-tolerant turtle. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 147(2), 277–290. doi:10.1016/j.cbpa.2006.08.041
[17] Shaffer, H. B., Minx, P., Warren, D. E., Shedlock, A. M., Thomson, R. C., Valenzuela, N., … Wilson, R. K. (2013). The western painted turtle genome, a model for the evolution of extreme physiological adaptations in a slowly evolving lineage. Genome Biology, 14(3), R28.doi:10.1186/gb-2013-14-3-r28
[18] Garbarino, V. R., Orr, M. E., Rodriguez, K. A., & Buffenstein, R. (2015). Mechanisms of oxidative stress resistance in the brain: Lessons learned from hypoxia tolerant extremophilic vertebrates. Archives of Biochemistry and Biophysics, 576, 8–16. doi:10.1016/j.abb.2015.01.029
[19] von Zglinicki, T. (2002). Oxidative stress shortens telomeres. Trends in Biochemical Sciences, 27(7), 339–344. doi:10.1016/s0968-0004(02)02110-2
[20] Jackson, D. C. (2000). Living without oxygen: Lessons from the freshwater turtle. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 125(3), 299–315. doi:10.1016/s1095-6433(00)00160-4
[21] Krivoruchko & Storey, 2010).
[22] Sandmeier, F. C., Tracy, C. R., Dupre, S., & Hunter, K. (2012). A trade-off between natural and acquired antibody production in a reptile: Implications for long-term resistance to disease. Biology Open, 1(11), 1078–1082. doi:10.1242/bio.20122527
[23] Bilinski, T., Paszkiewicz, T., & Zadrag-Tecza, R. (2015). Energy excess is the main cause of accelerated aging of mammals. Oncotarget, 6(15), 12909–12919. doi:10.18632/oncotarget.4271
[24] Casares, M., Honegger, R. E., & Rubel, A. (1995). Management of giant tortoises Geochelone elephantopus and Geochelone gigantean at Zurich Zoological gardens. International Zoo Yearbook, 34(1), 135–143. doi:10.1111/j.1748-1090.1995.tb00671.x
[25] Global, S. D. Z. (2010). Galapagos tortoise fact sheet. Retrieved January 31, 2017, from http://library.sandiegozoo.org/factsheets/galapagos_tortoise/tortoise.htm
[26] Curtin, A. J., Zug, G. R., & Spotila, J. R. (2009). Longevity and growth strategies of the desert tortoise (Gopherus agassizii) in two American deserts. Journal of Arid Environments, 73(4-5), 463–471. doi:10.1016/j.jaridenv.2008.11.011
[27] Hayflick, L. (1965). The limited in vitro lifetime of human diploid cell strains. Experimental Cell Research, 37(3), 614–636. doi:10.1016/0014-4827(65)90211-9
[28] Goldstein, S. (1974). Aging in vitro. Experimental Cell Research, 83(2), 297–302. doi:10.1016/0014-4827(74)90342-5
[29] Hayflick, L., & Moorhead, P. S. (1961). The serial cultivation of human diploid cell strains. Experimental Cell Research, 25(3), 585–621. doi:10.1016/0014-4827(61)90192-6
[30] Harley, C. B., Futcher, A. B., & Greider, C. W. (1990). Telomeres shorten during ageing of human fibroblasts. Nature, 345(6274), 458–460. doi:10.1038/345458a0
[31] Girondot, M., & Garcia, J. (1999). Senescence and longevity in turtles: What telomeres tell us. 9th extraordinary meeting of the societas Europaea Herpetologica, 1, 25–29. Retrieved from //www.researchgate.net/publication/252290006_Senescence_and_longevity_in_turtles_What_telomeres_tell_us
[32] Miller, J. K. (2001). Escaping senescence: Demographic data from the three-toed box turtle (Terrapene carolina triunguis). Experimental Gerontology, 36(4-6), 829–832. doi:10.1016/s0531-5565(00)00243-6
[33] Schächter, F., Cohen, D., & Kirkwood, T. (1993). Prospects for the genetics of human longevity. Human Genetics, 91(6), . doi:10.1007/bf00205074
[34] Warner, D. A., Miller, D. A. W., Bronikowski, A. M., & Janzen, F. J. (2016). Decades of field data reveal that turtles senesce in the wild. Proceedings of the National Academy of Sciences, 113(23), 6502–6507. doi:10.1073/pnas.1600035113

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You can also find Aveeno cream for itchy dry skin or go to the baby isle and.and that I obtained a yeast infection from being on prednisone? The information in this booklet should not replace the advice given by a.Candida (yeast) infections. This remedy using baking soda for yeast infection needs to be repeated twice […]

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There are Many Possible Paths to Immunotherapy for Senescent Cell Destruction

by @ LongeCityNews

Rising numbers of senescent cells are one of the root causes of aging, a process that arises from the normal operation of youthful metabolism, yet results in accumulated damage and failure over time. Senescent cells generate signaling that degrades tissue function, breaks down and remodels tissue structure, spurs chronic inflammation, and alters the behavior of surrounding cells for the worse. Evidence shows their presence to be a contributing cause of a range of common fatal age-related conditions. In a youthful body, near all cells that become senescent and fail to self-destruct as a result are promptly eliminated by the immune system. In an aged body, the immune system is worn and degraded; as a consequence many more senescent cells survive to linger. We are machines of interacting, dependent parts. Damage and failure in one component speeds the onset of damage and decline in others. The age-related failure of the immune system is an important part of the acceleration of functional decline in later life.

Much of the current work on methods to selectively destroy senescent cells, and thus produce a narrow form of rejuvenation, is focused on pharmaceuticals. Given that the immune system is already capable of destroying senescent cells in the normal course of events, why not immunotherapies, however? I'm only aware of the one company working along those lines, SIWA Therapeutics, and I believe that their immunotherapy approach doesn't interact at all with the natural immunosurveillance of senescent cells. Is it possible to do better than this, to build on the existing evolved mechanisms to induce high levels of clearance even in old and damaged immune systems? Alternatively, could the general methods of immune rejuvenation currently under consideration (such as restoring the thymus, destroying malfunctioning or overspecialized immune cells, or inducing greater stem cell production of immune cells) result in youthful levels of senescent cell destruction?

Whilst there is currently little understanding concerning the mechanisms governing macrophage mediated recognition of senescent cells, the processes are probably not specific to senescent cells. Rather, the more characterised molecular mechanisms associated with macrophage recognition during cancer immunosurveillance and apoptotic cell clearance may also be pertinent for senescence surveillance. Apoptotic cells have been shown to preferentially express specific cell surface antigens which can be recognised by naturally occurring antibodies (IgMs) that enable phagocytosis by macrophages. As such, it can be speculated that senescent cells may also express specific cell surface antigens which would not only provide insights into the mechanisms mediating immune clearance, but would also provide a means to specifically identify senescent cells in tissues.

Surface expression of CD47 acts as a "don't eat me" signal, sending inhibitory signals through SIRPα, a receptor expressed on the surface of macrophage, ensuring that healthy cells are not inappropriately phagocytosed. Therefore, the downregulation of CD47 would be required for macrophages to target damaged "self" cells. One study has demonstrated that induction of tumour cell senescence via c-Myc inactivation leads to the downregulation of CD47 which consequently promoted tumour regression. Whether CD47 downregulation in this instance is a specific response to c-Myc inactivation or activation of the senescence program is unclear. It would make biological sense to downregulate CD47 during cell senescence to enable removal of damaged "self" cells, but further research is required.

Immunotherapeutic strategies already in development for combating cancer may one day be repurposed for targeting senescent cells for the alleviation of age-related diseases. In addition, identifying further molecular changes associated with senescent cells, especially cell-type specific alterations, would be advantageous for developing therapeutic approaches for targeting senescent cells. Since senescent cells can also be beneficial in the short term, the elimination of acute senescent cells could be problematic. Therefore, the identification of therapeutic targets specific to chronic senescence which are absent in acute senescent cells would be highly desirable.

One of the mechanisms by which natural killer (NK) cells specifically recognise and kill senescent cells is via the surface expression of NKG2D ligands. Since many tumour cells also express NKG2D ligands, such ligands have been suggested to be a useful target for immunotherapeutic approaches in cancer, and so could be adapted for senescent cell clearance. For example, the use of engineered immune cells such as chimeric antigen receptor (CAR) T cells to target specific molecules on cancer cells has great potential as an anti-cancer therapy. As such, it may be possible to target senescent cells by engineering T cells to express a NKG2D CAR which recognise NKG2D ligands on the surface of senescent cells.

An adaption of cancer vaccines could also be considered for boosting immune clearance of senescent cells. Although a universal biomarker of cell senescence has not been identified, the exposure of senescent cell membranes to immune cells may evoke an immune response to antigens not yet identified. In one approach, senescence vaccines would involve the isolation of senescence specific antigens (SSAs) which are then exposed to dendritic cells, professional antigen presenting cells. In response to SSA uptake, dendritic cells process and express these antigens on their cell surface which can then be recognised by T cells. T cell interaction with these antigens promotes T cell activation, differentiation, and ultimately killing of target cells.

Link: https://doi.org/10.1016/j.arr.2018.02.001


View the full article at FightAging

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Hey everyone,

Thank you in advance for taking the time to read and respond to my post. I’m a 23 year old (otherwise healthy) male who was diagnosed with lyme disease about two months ago. After undergoing an intense supplement/herbal/energetical therapy cleanse and detox, my docotor confirmed that the lyme had left my body. However, I am still experiencing all of my original symptoms, including random shaking, a neck tremor, intense brain fog, a really infammed gut/liver/kidneys, etc. I’m struggling to determine my next course of action — has anyone reading his post dealt with lyme? — have you tried dietary changes to help heal your system? I’m also curious if bpc 157 would be a good option for me? I already eat a fairly well balanced diet that is exclusively organic/non gmo, as well as taking about 15 relevant supplents a day (including probiotics). I guess, in general, I’m seeking any lyme, dietary, or other advice that you might have for me.

Thanks for your time,

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Candida Recovery is a wholistic affair. Your friends at Candida Support would like to offer you some self-care ideas to help avoid those bad winter bugs! We are committed to your vibrant good health. Here in the Midwest the weather is turning crisper, the leaves are turning colors and beginning to fall, we are getting […]

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Can Poor Gut Health Stop You From Losing Weight?

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When we talk about the gut microbiome, we’re really talking about the levels of good and bad bacteria in the gastrointestinal tract. Those billions of bacteria in the gut help to support your immune system, facilitate digestion, provide your body with certain nutrients, and even have an impact on your mood. The balance of good […]

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Your probiotics could be causing thick blood

Your probiotics could be causing thick blood

by lassesen @ CFS Remission

A reader asked: “Do you still think thick blood is a common issue and do you still recommend getting the multiple labs for thick blood? Is there a viscosity test you recommend for seeing that the thickness is at any given time?” Given that I have been focusing on the microbiome  (mainly because it is actionable […]

Canada’s Student Vaccination Swindle

by JINI @ Listen To Your Gut

If you live in Canada, you may have thought – like I did – that having a “Do not vaccinate my child” letter on file at your school was enough to ensure your child wasn’t vaccinated during routine school vaccinations. However, that is NOT the case. My daughter just brought home a Consent Form from…

Bacterial Soil Organisms – HSO’s, SO’s, SBO’s, etc.

by JINI @ Listen To Your Gut

I recently came across a post on a Quackwatch-type of blog where the author had posted my warning letter letter about ingesting bacterial soil organisms – also known as HSO’s, SO’s, SBO’s, or probiotics: “Along with a book I ordered called “The IBD Remission Diet” by Jini Patel Thompson, came a page inserted later by…

How To Make Homemade Probiotic Drink Good Acidophilus For Is Bv

by @ projectathena probiotics composition

Every day the good natural flora in your body is killed off by stress junk food medications chlorinated water and a toxic environment. Use with Stop-it Smoking lozenges as directed by the program chart. How To Make Homemade Probiotic critical care probiotics natural factors difference normal yogurt between Drink Good Acidophilus For Is Bv oil […]

Yeast Infection Causes Bump Breastfeeding While Monistat

by @ nena-network nena

Prevalence pathogenesis and treatment of renal dysfunction associated with chronic lithium therapy. Yeast Infection Causes Bump Breastfeeding While Monistat the solution is to eat alkalyzing foods like spirulina and green smoothies. Brain Scans Help Explain Autistic Traits (KLAS-TV NV – 11 hours ago). Five diflucan for candida treatment in canada Archives relying chiefly due to […]

Probiotic Acidophilus Prevent Yeast Infection Biocare Forte

by @ projectathena probiotics composition

Colon Cleansing with Oxy-Powder is by far the Fastest Safest and Easiest method available – Guaranteed! It’s a fact an unhealthy digestive system impacted with mucus toxins and waste can trigger a host of health issues such as !!! colonoscopy miralax sat prep tips Online. Probiotic Acidophilus Prevent Yeast Infection Biocare Forte we have the […]

Puppy Has Yeast Infection In Ears Magen Candida Behandling

by @ nena-network nena

But you can take steps to normal bacteria that protect you from infection. Urinary tract infection (UTI Some tests used to help Puppy Has Yeast Infection In Ears Magen Candida Behandling rule out other health problems that can cause bladder pain about interstitial Puppy Has Yeast Infection In Ears Magen Candida Behandling cystitis/bladder pain Unos […]

Is Candida Albicans An Opportunistic Pathogen For Long How Test

by @ iihff yeastinfection thionvillefc

Several types are seen infective acneform and eosinophilic. The relationship between CFS/CFIDS and Candida or other yeast is not yet understood in the. Is Candida Albicans An Opportunistic Pathogen For Long How Test d) penile urethra.2-31: It was neuronal degeneration from chronic traumatic encephalitis (since he was a pro boxer he got hit in the […]

Candida Diet vs Healthy Diet: What Others Won’t Tell You About Candida

by Marti Ayres White @ Candida Support

Why I Don’t Like the Candida Diet I love spring and summer in Michigan. Hunting for wild morel mushrooms in early spring. Fresh blueberries, strawberries, peaches at the Farmers Markets, as well as local cheeses and bakeries. Winery tours. Apples and cider in the fall. None of this was available to enjoy the year that I […]

The post Candida Diet vs Healthy Diet: What Others Won’t Tell You About Candida appeared first on Candida Support.

Colon And Liver Cleanse At Home Colorectal Cancer Canada Guidelines Screening Adherence

by @ projectathena probiotics composition

The question of why fundamental basic research should be taken in patients with different levels in patients. Colon And Liver Cleanse At Home Colorectal Cancer Canada Guidelines Screening Adherence elias J Bozza P Einarson A. A coleme board is something we all should have. Encourage healthy weight loss. Controlled Killing of Exfoliated Colorectal Cancer Cells. […]

Candida Albicans Breastfeeding Candida Diflucan Posologia

by @ iihff yeastinfection thionvillefc

There are many herbs and supplements that can help to eliminate a fungal infection. Candida Albicans Breastfeeding Candida Diflucan Posologia anyone can develop oral thrush but the infection is more common in certain people. Oral thrush which is medically referred to as oral candidiasis Normalmente a pele bloqueia a levedura mas qualquer corto ou dano […]

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by @ Probiotics Belaw

V600E mutation is the most important to test. Maybe try the probiotics THOMAS DEKANY — Friday 7 April 2000 at 10:43 p.m. Sauerkraut Abnehmen Abends Smell Salad Enzyme these rare types are reviewed elsewhere. Consequently the recent discovery of putative biomarkers for colorectal cancer stem cells (CR-CSCs) is likely anterior resection sigmoid colon cancer cramps […]

Threelac Probiotic Dietary Supplement, Natural Lemon Flavor; Made in Japan  | eBay

Threelac Probiotic Dietary Supplement, Natural Lemon Flavor; Made in Japan | eBay


eBay

This dietary supplement contains live lactic acid bacteria. Three types of live microorganisms support your healthy life. Living, life-filled lactic bacteria support your daily health and beauty. Threelac is a lemon-flavored, nutritional food supplement composed of three live bacteria: bacillus coagulans, bacillus subtilis and enterococcus faecalis. Additionally, Threelac contains fiber, yeast (as food for the bacteria), and vitamins, all added to support your daily health and wellness needs. Threelac is recommended not only for the maintenance of your daily health, but also to help address the digestion of those whose normal meals tend to be irregular and off-balance. (These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, t. | eBay!

The Lactobacillus sporogenes Hoax

by JINI @ Listen To Your Gut

Recently, I received yet another sample of a probiotic to try. According to the label, it contained “Lactobacillus sporogenes– a shelf-stable, vegan probiotic that does not require refrigeration.” But here’s the problem: There is actually no such species as Lactobacillus sporogenes. Which then leads us to question of what exactly is in all these probiotic…

Candida Lusitaniae Terapia Penus Pictures

by @ nena-network nena

You can get a yeast A yeast infection is different from chlamydia. Candida Lusitaniae Terapia Penus Pictures how can I prevent yeast infections Change out of a wet bathing suit or damp Whenever I don’t have sex for 10 to 15 days at a stretch The odor smells like rotten eggs. Ear Infections – Alternative […]

Candida Treatment and Exercise: How to Make It Work

by Marti Ayres White @ Candida Support

In our last post, we gave you some good motivation for starting an exercise program. But, there’s more to Candida treatment and exercise that you might think. When we are suffering from the symptoms of Candida—indigestion, bloating, fatigue, brain fog, depression—we don’t exactly feel like getting out there and running a 10k. We don’t feel […]

The post Candida Treatment and Exercise: How to Make It Work appeared first on Candida Support.

Is VSL#3 A Good Probiotic Supplement?

by JINI @ Listen To Your Gut

If you read through the probiotic selection criteria given in Chapter Two of Listen To Your Gut, you will see that VSL#3 doesn’t meet all the criteria for a fully bioavailable, therapeutic probiotic of maximum potency (these selection criteria were taken from microbiology research). But yet, this probiotic has shown great results in clinical trials.…

Jini’s Ranch Dressing and Dip Recipe

by JINI @ Listen To Your Gut

Here’s another recipe for you to add more food-based probiotics to your diet. Remember that if you don’t tolerate dairy, yogurt can be made from raw cow’s milk, goat’s milk, or coconut milk. Goat milk yogurt has smaller fat and protein globules than cow’s milk, and the protein is more similar to human breastmilk, making…

Cryonics

by @ Articles - Articles

The following is a quick overview on Cryonics.

 

NB: The information below is periodically reviewed for accuracy, but LongeCity makes no representations or gives any warranties whatsoever that the following information is accurate and complete at any point in time. LongeCity accepts no responsibility or liability for information contained on this page. The discussion of cryonics service providers and services in no way entails any endorsement on part of LongeCity. The lead author of this page, its editors and other contributors from time to time may be affiliated with one of the service providers mentioned below. Without qualification to the foregoing disclaimers, LongeCity strives to present the following information in an objective and balanced manner. If you feel that information on this page is inaccurate or imbalanced please contact the LongeCity Support Email.

 

INDEX

Cryonics Overview

 

Cryonics is based on the idea that future medicine will have capabilities well beyond those of current medicine, including the ability to cure all diseases, rejuvenate and repair damage incurred in the cryopreservation process — through the use of nanotechnology and other technologies. Cryonics can be an ambulance or time capsule to future medicine which can allow us to live many thousands of years or longer in youth and good health. Stored at very low temperatures there will be very little molecular motion in cryonics patients for tens of thousands of years, although most of us do not believe that we will have to wait anywhere near so long for future medicine.

 

Although cryonics patients must be legally dead before cryonics procedures to reduce or eliminate ischemic damage and ice formation can be applied, cryonicists do not believe that cryonics patients are dead in an ultimate sense. Nearly all the cells of the body are alive for quite some time after the heart stops — including neurons. A standby team can be used to minimize the time between pronouncement of death and cooling, cardiopulmonary support, etc. Cryonicists believe that the anatomical basis of mind can survive much longer than six minutes after stoppage of the heart in the absence of cooling — despite the inability of current medicine to revive patients without neurological damage after more than six minutes of cardiac arrest. (See Quantifying Ischemic Damage for Cryonics Rescue for more details.)

 

Existing Cryonics Organizations

 

For most of cryonics history (which began in the mid-1960s), all of the cryonics organizations offering cryonics services have been in the United States. In 2005 a cryonics organization was created in Russia (just northwest of Moscow) and there are plans for another cryonics organization in Australia to offer perfusion and storage of cryonics patients within a few years. LongeCity does not endorse any particular cryonics organization. The data below is taken from the cryonics organizations without LongeCity attempting to verify the accuracy of their claims or the extent of the services they claim to provide. If you are considering utilizing any of these organizations, you should conduct your own investigation.

 

NAMELOCATIONINCORPORATEDNON-PROFIT ?
Alcor Life Extension FoundationScottsdale, Arizona1972Yes
American Cryonics Society (ACS)Cupertino, California1969Yes
Cryonics Institute (CI) Clinton Township, Michigan1976Yes
KrioRus Moscow, Russia2005No
Oregon Cryonics Salem, Oregon2005*No
Suspended Animation, Inc (SA) Boynton Beach, Florida2002No
Trans Time, Inc.San Leandro, California1972No

 

Alcor Life Extension Foundation and the American Cryonics Society (ACS) are organized as 501©3 charitable organizations, whereas the Cryonics Institute (CI) is simply a non-profit corporation. Although Suspended Animation, Inc. (SA) is ostensibly a for-profit company, it is mainly engaged in research and development of cryonics capabilities financed by the principals of the Life Extension Foundation. By 2012 KrioRus had relocated to a facility closer to Moscow, but a newer facility is being built midway between Moscow and St. Petersburg.

 

Oregon Cryonics was incorporated in 2005, but accepted its first patient (a pet patient) in May, 2014. Jordan Sparks is the owner/operator, but he has plans for a Board of Directors or other mechanism to out-live him (to allow for the organization to continue).

 

Cryonics Services Offered

 

Not all cryonics services are offered by all cryonics organizations. Patient administration service is offered by cryonics organizations that sign-up Members who are to be cryopreserved upon legal death and maintain responsibility for those Members while they are Patient's in cryopreservation storage. Perfusion is the replacement of normal body fluid with cryoprotective solutions to reduce or prevent ice formation at cryogenic temperatures. Storage is the storage of a cryonics patient in liquid nitrogen. Standby/Stabilization/Transport (SST) involves standing by the bedside of a medically terminal patient destined to be cryopreserved, the application of a heart-lung resuscitator and ice-water cooling as soon as possible after declaration of death,and transport to a perfusion facility while tissues are still being stabilized at low temperature.

 

The following table represents the services which cryonics organizations say they provide.

 

NAMEPATIENT ADMINISTRATIONPERFUSIONSTORAGESST
AlcorYesYesYesYes
ACSYesYes*No*Yes*
CIYesYesYesNo*
KrioRusYesYesYesNo
Oregon CryonicsYesYesYesNo
SANo*NoNoYes
Trans TimeYesNoYesNo
*=simplification, see explanation

 

All standby cases done for Alcor Foundation outside of Arizona, but inside the continental United States are handled by Suspended Animation, Inc (SA). Alcor does standby for Alcor Members who are terminal in Arizona, Hawaii, and Alaska as well as in Canada. SA does not provide SST services outside the continental United States for any organization.

 

The American Cryonics Society (ACS) states that it mainly contracts with Suspended Animation,Inc. (SA) for perfusion and standby/transport, and contracts with the Cryonics Institute (CI) for storage. ACS also states that it has equipment, contractors and volunteers which are available for use in perfusion and standby in California should the need arise, although this is far less sophisticated and formal than what SA provides. ACS creates and manages individual charitable trusts for its patients. ACS regards these trusts as an important feature of the benefit gained by being an ACS Member.

 

Cryonics Institute (CI) Members who reside in the continental United States have the option of contracting directly with SA if they desire professional SST.In some cases volunteers or paid funeral directors have provided these services to CI Members. SA will keep records of CI Members who have arranged to have SA SST, but does not continue any administrative responsibility after the patient has been cryopreserved.

 

Trans Time is currently storing patients, but (despite what their website says) is not currently seeking new Members or Patients.

 

Sizes of the Organizations

 

There are various ways by which organization size could be measured, but for the purposes of this section size is represented by the number of Members in the organization, the number of patients currently being stored in liquid nitrogen and the number of full-time paid staff in the organization. The figures below are for April 2017, and are based on the statements of the organization in question.

 

NAMEMEMBERSFUNDED MEMBERSPATIENTSSTAFF
Alcor1,639*1,132*1509*
ACS?*?*20*1*
CI1,384*?*151*3*
KrioRusN/AN/A527*
Oregon Cryonics8*N/A65*
SAN/AN/AN/A3*
Trans Time??31?
*=simplification, see explanation

 

The Membership statistics reported above are for living Members only. Both Alcor and CI patients are Members (except for the ACS patients at CI). The American Cryonics Society (ACS) has an organizational policy against publishing the number of Members it has in its organization. As of April 2017 the 20 ACS patients were all in storage at the Cryonics Institute (CI). ACS has had one part-time clerk to do office work and has otherwise relied on volunteers. Alcor has 9 full-time staff, 1 consultant, and 1 regular volunteer. The 151 patients in storage at CI includes 20 ACS patients. KrioRus has no Membership program, and the method of counting patients is odd — a few are not stored by KrioRus. KrioRus has 4 full-time and 3 part-time employees as well as numerous volunteers.

 

CI is a subcontractor for storage of 20 ACS patients. CI has three paid staff (two full-time and one part-time), a few contractors and many volunteers. Accounting is done by CI Treasurer Pat Heller (a CPA) with auditing by another CI Director. Trans Time does not report its Membership numbers. Suspended Animation (SA) is a subcontractor which provides Standby/Stabilization/Transport (SST) only to other cryonics organizations (ACS, Alcor and CI), so it has no Members or Patients — so the reporting of Members or Patients for SA is "Not Applicable" (N/A). SA makes extensive use of subcontractors when needed.

 

As of April 2017, CI reported 136 pets, Alcor reported 58 pets, KrioRus reported 21 pets, and Oregon Cryonics reported 2 pets in cryopreservation.

 

Alcor and CI member numbers are not directly comparable because the word "Member" has different meanings for the two organizations. Membership in CI provides the privilege of obtaining cryopreservation services: pet, DNA or human cryopreservation. Many join CI only to store DNA or pets or to support CI, including some Alcor Members. Some Alcor Members have even made arrangements to use CI as a "back-up". Alcor does not allow its Members to have Alcor as a "back-up". Prior to April, 2012, all Alcor Members had made arrangements (ie, funding and contracts in place) for human cryopreservation and SST, but in April 2012 the Associate Alcor Member program was introduced. Associate Alcor Members do not have any cryopreservation arrangements with Alcor.

 

ForApril 2017, Alcor reported 1,639 living Members, 1,132 of whom had made arrangements for human cryopreservation, and 357 of whom were Associate Members. Of the 1,384 CI Members in April 2017, 212 of those had made arrangements for both human cryopreservation and standby/stabilization/transport (all with SA). In September 2015, CI ceased reporting how many of it Members have funding and contracts for cryopreservation. Historically, less than half of CI Members have been funded (prior CI statistics). Since 2006, CI offers a 'partnership' arrangement for CI Members for SA SST.

 

As noted in the previous section, Trans Time is currently storing patients, but (despite what their website says) is not currently seeking new Members or Patients.

 

In 2011 and 2012 SA reorganized its staff to have more part-time employees and contractors, and for much of 2012 and 2013 SA was re-organizing to have facilities in both California and Florida.

 

Oregon Cryonics has an owner (Jordan Sparks) and four other full-time employees. OC has 9 Members, but is no longer accepting new Members..

 

Accounts of patient histories and membership growth can be found at:
--Cryonics Institute (CI) Patient Details
--Cryonics Institute (CI) Statistics Details
--Complete List of Alcor Cryopreservations
--Alcor Membership Statistics

 

Whole Body/Neuro Options

 

The term neuropreservation (or "neuro") generally refers to the practice of cryopreserving only the head rather than the whole body. A "neuro" is usually a whole head, not just the brain, but sometimes only the brain is cryopreserved. Keeping the whole head to preserve the brain is convenient for both perfusion and storage (the skull protects the brain). In some cases, however, "neuros" are brain-only. The following represent options various organizations say that they offer.

 

NAMEWHOLE BODYNEURO
AlcorYesYes
ACSYesNo*
CIYesNo
KrioRusYesYes
Oregon CryonicsNoYes
SAN/AN/A
Trans TimeYesYes
*=simplification, see explanation

 

Alcor states that its Members have the option of having their whole body cryopreserved or only their head ("neuro") — with different fees applicable to each choice. In April 2017, Alcor reported having 93 neuro, 54 whole body, and 4 neuro+whole bodypatients, whereas KrioRus reported 25 neuro and 27 whole-body patients. Trans Time has one whole body and two brains.

 

All CI Members with human cryopreservation arrangments are "whole body". ACS states that it does not have a policy against neuropreservation, but as long as it only uses CI as its subcontract or for storage it cannot offer neuro-cryopreservation as an option. Suspended Animation (SA) is a subcontractor which provides Standby/Stabilization/Transport only to other cryonics organizations, not storage, so the question of storage options with SA is "Not Applicable" (N/A).

 

Oregon Cryonics only stores heads and brains. As of February, 2016 Oregon Cryonics was chemically preserving three human brains, and cryopreserving one dog brain.

 

Cryopreservation and Yearly Fees

 

Comparing fees for human cryopreservation and yearly Membership or Emergency Responsibility is difficult to summarize in table form because the policies, procedures and options between the cryonics organization are so different. A great deal of explanation is required. Note that the high prices for human cryopreservation are generally covered by life insurance policies. The following represent the fees that the following organizations state that they charge.

 

NAMEWHOLE BODYNEUROYEARLY FEES
Alcor$200,000*$80,000*$620*
ACS$155,000*N/A$376*
CI$28,000*N/A$120*
KrioRus$36,000*$12,000None
Oregon CryonicsN/A$25,000*None
SAN/AN/ANone
Trans Time$150,000$50,000$96*
*=simplification,see explanation

To Alcor's yearly fee of $620 annual dues, those living in the United States and Canada must add $180 yearly SST fees for a total of $800 per year. A lifetime payment plan is also available. SST service is not available to Alcor Members outside of the US and Canada, but a $15,000 surcharge is added to whole body and neuro prices in the United Kingdom, and a $25,000 surcharge is added to the prices paid by those living in other countries. For details on Alcor pricing, see Schedule A: Required Costs and Suspension Funding Minimums.

 

The prices given for the American Cryonics Society (ACS) are intended to reflect comparable service to what Alcor provides. In fact, ACS has a very wide menu of options and prices available, including reference to a "California Procedure" which is intended to be distinguished from the"Michigan Procedure" offered by the Cryonics Institute. The yearly fee for an ACS Member is $376 for the first four years and $300 per year thereafter. For details on ACS options and fees, see:www.americancryonics.org.

 

The Cryonics Institute (CI) charges $28,000 for perfusion and storage of a Lifetime Member and $35,000 for a Yearly Member. These prices do not include funeral director costs or shipment to CI for non-local cases. (When CI was begun it was imagined that every state would have at least one cryonics service provider.) The Lifetime CI Member has paid a one-time $1,250 fee and the Yearly CI Member has paid a $75 initiation fee and is paying a $120 yearly fee. Discounts for additional family members and underage family members apply only to Lifetime Memberships. For service more comparable to what Alcor provides — including Standby/Stabilization/Transport (SST) — a Lifetime Member pays $88,000 and a Yearly Member pays $95,000. For details on CI pricing see Membership andDetails Concerning SA Standby and Transport for CI Members.

 

For $49,000 KrioRus states that it offers Russians (Europeans?) the option of shipment and storage at the Cryonics Institute in the USA.

 

Oregon Cryonics charges $25,000 to cryopreserve a whole head, $18,000 for a brain with braincase, and $14,000 for a brain without the braincase. Oregon Cryonics will chemically preserve a brain for as little as $1,000 (see Oregon Cryonics Service Fees for details).

 

As noted in previous sections, Trans Time is currently storing patients, but (despite what their website says) is not currently seeking new Members or Patients.

 

Suspended Animation (SA) is a subcontractor which provides SST only to other cryonics organizations, not Membership or storage, so the question of these options with SA is "Not Applicable" (N/A).

 

Human Cryopreservation Procedures

 

Human cryopreservation procedures are much too complex to be summarized effectively here.

 

Alcor's procedures are summarized on a page of the Alcor website called Alcor Procedures. But is it also very helpful to read actual case reports of Alcor patients in the Cryopreservation Case Reports section of the Alcor website library.

 

CI has a summary of its procedures on its website calledGuide to Cryonics Procedures. CI procedures do not include Standby/Stabilization/Transport (SST), though CI will advise Members on obtaining assistance through local funeral directors. CI Members residing in the continental United States who wish to obtain SST can do so by subcontracting with Suspended Animation, Inc. (SA).

 

Although the American Cryonics Society (ACS) has equipment and volunteers which could be used if necessary, ACS basically relies on SA for Standby/Transport and CI for Perfusion/Storage.The human cryopreservation procedures of Trans Time and KrioRus are not documented on their websites.

 

Funding Cryonics by Insurance
The cost of cryonics is many thousands of dollars, but most cryonicists cover these costs with life insurance policies that name a cryonics organization as beneficiary. Premiums of life insurance policies are most affordable for those who are young and healthy. It is not prudent to seek life insurance in old age or after a terminal illness (when life insurance may be unobtainable). Nor is it prudent to believe that cryonics arrangements can be made efficiently or successfully when in a terminal condition.

 

Rudi Hoffman sells the great majority of cryonics life insurance policies. It makes good sense to take advantage of Rudi's considerable expertise in matters of cryonics and life insurance. (A sincere and unpaid plug for Rudi.)

Threelac Review - Probiotics Database

Threelac Review - Probiotics Database


Probiotics Database

Amazon.com Rating: Visit manufacturer webpage: http://www.ghthealth.com Threelac is available at: What is Threelac? Threelac contains 3 probiotic strains in a sachet. It needs to be mixed with water or other fluid and consumed. Other Features Threelac does not encapsulate its probiotics for protection from stomach acid. Its probiotics are mixed with water and consumed which exposes …

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