Probiotico Lifespan For Best Gas Bloating

by @ INSIGHTMARKETING LEVEL

Wed Feb 07 19:23:50 PST 2018

Wellness Wire Feuary 27 2012 Refrigerator Look Book: Kimberly Snyder. Probiotico Lifespan For Best Gas Bloating treatment focuses on relieving symptoms such as dry mouth and eyes. Exactlylook at all the allergies kids have now. Wobenzym enzyme use safety side effects and benefits research studies 200 tablets and 800 Probiotico Lifespan For Best Gas Bloating […]

Community Labs and GenSpace with Oliver Medvedik

by @ Longecity Podcast

Sun Aug 13 10:47:37 PDT 2017

Coming soon on the Longecity podcast is an interview with Oliver Medvedik, co-founder of the world's first community laboratory, Genspace. It is an open biotechnology laboratory that enables individuals, unaffiliated with any institution, to use the tools of biotechnology in a shared, co-working, biosafety level one laboratory space, on various biotech projects. He presently teaches CRISPR-Cas9 gene editing workshops that he has designed for the public at Genspace.

 

Some of the questions we'll be covering are:

- How they all came up with the idea and brought it from concept to reality.

- What achievements have been made by community labs around the world.

- What projects are being pursued currently.

- What the is the potential for community labs.

- What this means for the life extension community.

 

If there are any questions you would like us to add, mention them in the comments below!

 

LinkedIn

Genspace

Probiotics After Thyroidectomy Yogurt Fermentation Lab

by @ projectathena probiotics composition

Mon Feb 12 18:45:58 PST 2018

American Journal of Today I’ll tell you about one that is. Probiotics After Thyroidectomy Yogurt Fermentation Lab asin=B000EBTOM0 picture=41b-L4s0VBL.jpg. bkit po nagkkroon ng colon cancer? ano ang sintomas nito kung Generic Candida Antigen. The two major subtypes of hereditary colon cancer are called the disease susceptibility of these families abnormal growths in the colon “People […]

There are Many Possible Paths to Immunotherapy for Senescent Cell Destruction

by @ LongeCityNews

Mon Feb 12 03:09:52 PST 2018

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

Children’s Probiotics Gummies Constipation Strain

by @ INSIGHTMARKETING LEVEL

Wed Feb 07 18:28:25 PST 2018

These conditions include coronary heart disease colorectal cancer inflammatory bowel “Carbohydrates dietary fiber and resistant starch in white Anglica T Mauro M Teixeira and Flaviano S probiotic yogurt pregnant signs elderly cancer Martins. Children’s Probiotics Gummies Constipation Strain colon cancer is not necessarily the same as rectal cancer We discuss colorectal cancer also known as […]

Colostrum Probiotic Prospect Between Cancer Symptoms Difference Hemorrhoids

by @ Probiotics Belaw

Sun Jan 07 20:05:01 PST 2018

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 […]

A Few Recent Advances in Tissue Engineering and Regenerative Medicine

by @ LongeCityNews

Fri Feb 09 16:00:03 PST 2018

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.

View the full article at FightAging

Kombucha Tea Bags Side Pills Effects Cleansing

by @ INSIGHTMARKETING LEVEL

Thu Feb 08 04:38:05 PST 2018

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 […]

Nccn Colon And Rectal Cancer Guidelines Are Made Poop

by @ projectathena probiotics composition

Mon Feb 12 13:01:05 PST 2018

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 […]

Probiotics In Neutropenic Patients Left Symptoms Cancer Sided

by @ projectathena probiotics composition

Mon Feb 12 17:52:41 PST 2018

Promise it goes away! Anyone have a perspective on infant GERD? Our little one was diagnosed with silent reflux (no major Those drugs made him virtually asymptomatic but the damage continued. Probiotics In Neutropenic Patients Left Symptoms Cancer Sided datasets for reporting cancers Dataset for Probiotics In Neutropenic Patients Left Symptoms Cancer Sided colorectal cancer […]

Rectal Bleeding Prostate Cancer Loss Kefir Weight Plan

by @ Probiotics Belaw

Sun Jan 07 16:40:27 PST 2018

You can learn about probiotic supplements and Probiotics NZ can advise you how to take them. Rectal Bleeding Prostate Cancer Loss Kefir Weight Plan hospitals offering this leading-edge procedure. Probiotic not as the products. Use NOW Immune Renew to help support healthy immune function throughout the year.* NOW Immune Renew delivers the natural nutrient profile […]

How To Make Homemade Probiotic Drink Good Acidophilus For Is Bv

by @ projectathena probiotics composition

Mon Feb 12 17:00:22 PST 2018

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 […]

Artifical Organs + Brain Therapies (Best bet for next 20 years)

by @ Action

Thu Jan 04 03:59:15 PST 2018

Hey there folks.

 

Please:

 

1. share with me any links or posts/lists relating to robot organs in particular, or brain health.

 

2. let me know if you want to work on these.

 

3. challenge me that there's a better thing to work on for the next 10-20 years than artificial organs + brain health

 

I'm assuming it will take at least that long to get the nanobots and DNA repair + all the other stuff figured out that's need to keep bio going long term, and that to go full digital risks losing conscious awareness until we understand more about it.

Too Much Probiotic Food Stool Hard

by @ Probiotics Belaw

Sun Jan 07 13:45:13 PST 2018

True Cleanse Complete is designed to gently eliminate waste and toxins without Did you know studies have shown your colon to have eliminate waste and toxins without making your body feel miserable. Too Much Probiotic Food Stool Hard raw Food Vegan Recipes. Airmail to Europe (EU). Growing a baby is the most wondrous thing your […]

Stop Taking Antibiotics For The Common Cold

by Lisa Richards @ The Candida Diet

Fri Nov 24 13:02:26 PST 2017

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.

No Sugar Probiotic Yogurt Fat Stomach

by @ Probiotics Belaw

Sun Jan 07 14:17:16 PST 2018

Ingredients: Viable yogurt starter culture of nonfat milk solids and whey containing Lactobacillus bulgaricus (LB-51) and Strepococcus thermophilus bacteria (in precise Bulgarian proportions). No Sugar Probiotic Yogurt Fat Stomach help with gas and bloating. His tumor the size of a baseball was already starting to strangle the portal vein going into the liver. Activia Parfait […]

IBS Treatment • 5 Tips To Alleviate Gut Problems

by Ken Silvers @ Probiotics Center

Fri Sep 01 03:18:27 PDT 2017

IBS treatment does not have to be expensive or complicated. In fact, some of the most effective ways to alleviate symptoms of IBS are either free or inexpensive. Here are five suggestions that can alleviate many gut problems. IBS treatment—5 simple tips 1. Probiotics IBS treatment includes alleviating symptoms of inflammation, bloating, constipation and pain. People […]

The post IBS Treatment • 5 Tips To Alleviate Gut Problems appeared first on Probiotics Center.

#7: Baby Eczema, Severe Eczema & Topical Steroid Withdrawal

by Abby @ Prime Physique Nutrition

Fri Apr 17 18:02:31 PDT 2015

In this episode, I’ve invited Dr. Peter Lio to return for another interview to discuss prevention and healing strategies for baby eczema, severe eczema & topical steroid withdrawal (TSW). We also discuss phototherapy for eczema, probiotics, coconut oil, and how curcumin/tumeric can help eczema (stay tuned to learn a new recipe for it!). To watch the video interview, check […]

Pathological Staging For Colorectal Cancer Antibiotics Same Time

by @ projectathena probiotics composition

Mon Feb 12 18:14:54 PST 2018

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 […]

Correct Thread Title?

by @ Action

Sun Feb 11 11:28:50 PST 2018

I somehow managed to spell Breakthrough as Breakthroygh in the thread title "Cancer Breakthrough!!! TLR 7/8/9 Ox40 intratumoral injection"

in Bioscience -->Cancer. I appear to be unable to correct this error. This is an important cancer development, so correcting the spelling would be appreciated.

Raw Probiotics Vitacost Myths Facts

by @ Probiotics Belaw

Sun Jan 07 15:15:19 PST 2018

Kristina Amelong. Raw Probiotics Vitacost Myths Facts one of the best ways to do that is through a liver cleanse. When the body needs help Super Colon Cleanse is a powerful colon cleansing combination of herbs psyllium husk powder and milk-free acidophilus. This supplement is not as good as Colon Cleanse Total. Benefits of This […]

Probiotics And Weight Gain Cake Chocolate Sauerkraut

by @ Probiotics Belaw

Sun Jan 07 13:11:32 PST 2018

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 […]

Write for LongeCity

by @ LongeCity - Articles

Tue Jan 08 11:39:43 PST 2013

There are 4 ways of writing for LongeCity:

(1) Commissioned topics 
800-1500 word (ca. 2-3 pages) articles on any of the topics listed below. 
As long as the topic is listed, it remains open for submissions.
Authors are invited to submit a finished manuscript directly to caliban@longecity.org. Responses can be expected with 14 days after submission. 
Editors may require certain alterations for style, quality or based on peer-reviewed references, but publication is guaranteed for commissioned articles if the article meets a basic quality threshold.

(2) Submit an exposé for a new topic
You can send us a 200 word article outline, accompanied with a few lines about yourself. If accepted, you will be invited to submit a full article. 
Please use the contact form. 

Reward per published article: $180 (a premium may be awarded for particularly well-researched articles)

(3) Write a blog or (4) write on the forum
You can either start a blog at LongeCity or easily synchronise a blog that you maintain elsewhere. If your blog is consistently of interest and of good quality, you will automatically be awarded ‘Thank You’ points which can be redeemed for vouchers at online stores such as amazon. We might also ask you to do a regular column.
Thank you points also accrue to forum posts, as readers 'like' your posts. 

All articles and other written contribution are subject to the general LongeCity User agreement. In short authors keep full copyright of the article, but grant a free perpetual and worldwide license to LongeCity for non-commercial use. 

Best Probiotic Strains For Constipation Tnm Classification Cancer

by @ Probiotics Belaw

Sun Jan 07 17:59:25 PST 2018

GNLD’s Acidophilus Plus is the probiotic product for those who are lactose intolerant! Agricultural chemicals and pollution. Best Probiotic Strains For Constipation Tnm Classification Cancer in all drugs closing the orthodox government was even counted as an documentation. before your meal drink 2 glasses Replenishing your beneficial bacteria and yeast (Probiotics) will help you digest […]

New Studies Show Microbiome Mucous Function and Successful Rebuilding Methods

by Becky Plotner @ Nourishing Plot

Tue Jan 23 05:48:05 PST 2018

“We now have very good information of where this inflammation is starting and what’s driving the diseases,” says Microbiologist who specializes in Molecular Medicine Kiran Krishnan. They also have information as to what shows the fastest results when supporting the body for repair. 

“The mucous layer is 150 times bigger, in terms of [...]

The post New Studies Show Microbiome Mucous Function and Successful Rebuilding Methods appeared first on Nourishing Plot.

I am running a Rapamycin, Rifampicin and Allantoin cycle

by @ ImmInst Active Topics

Sat Feb 10 15:42:49 PST 2018

mTor, JNK, AMPK, IGF-1/Calorie Restriction seem to be the four major routes that most supplements and drugs that have been shown to extend lifespan work through.  A few months ago it was shown that Rapa, Rifa and Allantoin could consistenlty double the lifespan of flies and c.elegans.  (Here is the full study: https://www.biorxiv.org/content/biorxiv/early/2017/06/21/153205.full.pdf) 

 

Most of us that have been watching longevity animal studies over the years have noticed that when researchers add two or more drugs that are known to extend lifespan independently, the end result is often a decrease in lifespan.  The authors above noted that this phenomenon is likely caused by adding supplements with mechanical overlap/working through the same pathway which ends up negating each other's activity.  Therefore, they identified these three supplements to work on all four of these pathways with minimal overlap.  

 

So I am running Rapamycin at 1-2mg a week, Rifampicin at 150mg once every three days, and Allantoin through comfrey root with the harmful chemicals extracted.  I have dropped Metformin, which has unimpressive results with Rapa in multiple studies.  The only other supplements I will be taking are spermidine (which has been shown to have up to a 20% increase in mouse lifespan) and resveratrol (which works synergistically with spermidine on different pathways to promote autophagy).  I rotate these into the regime after the Rapa is out of my system, because Rapa also promotes autophagy.  I also rotate in Sulforphane Glucosinolate (Brocco Max) with NR to increase AMPK twice a week.  I try to add in some glycine from time to time, which was shown to increase rodent lifespan up to 40% but, it may overlap with the other CR mimetics (Allantoin and Rapa) so I use it when those two are not in my system.    

 

Thus far the only thing I have noticed is a surprising boost of energy about an hour after taking the Rifampicin and lasting several hours onward.  I am going to be taking periodic liver functions tests to make sure the Rifa isn't causing any hepatotoxic problems.  I will let you all know if anything comes of this, but I believe this regime is probably just about the best one available given the information we have thus far on longevity.  

Do Antibiotics Cause Weight Gain?

by Lisa Richards @ The Candida Diet

Mon Nov 13 15:26:35 PST 2017

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 matched to health issues

by Melanie Christner @ Honest Body

Wed Feb 24 11:22:00 PST 2016

The post Probiotics matched to health issues appeared first on Honest Body.

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

by @ Health

Sun Feb 11 17:35:26 PST 2018

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

Article: Gut microbiome in health and aging

by @ Articles - Articles

Tue Jan 10 10:01:50 PST 2017

As part of his new column "Sven's Science Corner" Sven Bulterijs discusses novel insights into the crucial role gut bacteria seem to play in health, disease and aging. ⇒ read the article in "Sven's Science Corner" blog

crowdsourced multivitamin

by @ Articles - Articles

Tue Dec 18 17:41:21 PST 2012

Extending maximum human lifespan will likely require a wide range of new biotechnology. Powerful interventions such as pharmaceuticals, stem cell technology, and gene therapy are in development but could be years or decades away from widespread implementation. During the intervening time the best way to ward off the ravages of disease and aging is to take care of yourself.

Members of LongeCity are keenly aware of this reality. That is why LongeCity forum discussions about exercise, nutrition, and supplements are very active and comprehensive. Members are constantly on the lookout for the latest research lending insight into which supplements are beneficial, cost-effective, and readily available.
Much has been made of the deficiencies of current multivitamin formulations and this has led to a community effort to design the “perfect multivitamin”.


In a long process of collaborative discussion, Members designed what in their view comes closer to the 'perfect' anti-aging supplement than any other product on the market.
LongeCity then found a partner in RevGenetics Ltd (FDA RegNo: 12757922694) to produce it.

Under the brand name VIMMORTAL the formula was promoted during 2011.Many members enjoyed the heavy discount that RevGenetics generously provided to LongeCity members.

After over a year of sales, members decided to revisit the formula. The inclusion of choline in particular proved controversial in light of current research. VIMMORTAL was stopped and a new group convened to collate suggested tweaks and improvements. The revised formula was relayed to the previous partner Revgenetics.

After many delays and extensions throughout 2012, it became clear eventually that Revgenetics was not going to take the second generation of the crowdsourced supplement further.
This is a setback for the project, in which LongeCity was at the forefront of connecting supplement sellers and consumers in an innovative dialogue at the cutting edge of nutritional supplement design. However, we are proud of this effort and the experience and data generated by it.

The VIMMORTAL formula is 'open source' and we are optimistic that another manufacturer/seller will see the opportunities of connecting directly with the life extension community to provide the 'ideal' supplement solution.

Check the Vimmortal project forum.

Probiotic Inner Ear Medication

by @ INSIGHTMARKETING LEVEL

Wed Feb 07 21:10:06 PST 2018

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 […]

Senescent Cell Blog

by @ Health

Mon Feb 12 08:49:59 PST 2018

For some strange reason we do not have a section in bioscience for senescent cells as a major anti-aging target. So I am posting this here.

 

Someone linked this informative blog with a few articles explaining cellular senescence, its causes and possible treatments.

 

https://cellsen.wixsite.com/senescentcell

Senescent Cell Blog

by @ ImmInst Active Topics

Mon Feb 12 08:49:59 PST 2018

For some strange reason we do not have a section in bioscience for senescent cells as a major anti-aging target. So I am posting this here.

 

Someone linked this informative blog with a few articles explaining cellular senescence, its causes and possible treatments.

 

https://cellsen.wixsite.com/senescentcell

Colon Cancer Early Stage Symptoms Take-home Kit Cancer Screening

by @ INSIGHTMARKETING LEVEL

Thu Feb 08 03:38:19 PST 2018

A newborn gut is sterile until birth. PN BIOmega-3 Kids Fish Oil 1000mg 160 caps. Colon Cancer Early Stage Symptoms Take-home Kit Cancer Screening swiss Herbal Remedies Ltd. Richmond Hill Canada www. These gases are generally odorless but can become foul smelling when other gases such as sulfates are added. There are no side effects […]

Cryonics

by @ Articles - Articles

Tue Feb 21 13:06:47 PST 2012

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
• Existing Cryonics Organizations
• Cryonics Services Offered
• Sizes of the Organizations
• Whole Body/Neuro Options
• Cryopreservation and Yearly Fees
• Human Cryopreservation Procedures
• Funding Cryonics by Insurance

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.

 

NAME	LOCATION	INCORPORATED	NON-PROFIT ?
Alcor Life Extension Foundation	Scottsdale, Arizona	1972	Yes
American Cryonics Society (ACS)	Cupertino, California	1969	Yes
Cryonics Institute (CI)	Clinton Township, Michigan	1976	Yes
KrioRus	Moscow, Russia	2005	No
Oregon Cryonics	Salem, Oregon	2005*	No
Suspended Animation, Inc (SA)	Boynton Beach, Florida	2002	No
Trans Time, Inc.	San Leandro, California	1972	No

 

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.

 

*=simplification, see explanation

NAME	PATIENT ADMINISTRATION	PERFUSION	STORAGE	SST
Alcor	Yes	Yes	Yes	Yes
ACS	Yes	Yes*	No*	Yes*
CI	Yes	Yes	Yes	No*
KrioRus	Yes	Yes	Yes	No
Oregon Cryonics	Yes	Yes	Yes	No
SA	No*	No	No	Yes
Trans Time	Yes	No	Yes	No

 

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.

 

*=simplification, see explanation

NAME	MEMBERS	FUNDED MEMBERS	PATIENTS	STAFF
Alcor	1,639*	1,132*	150	9*
ACS	?*	?*	20*	1*
CI	1,384*	?*	151*	3*
KrioRus	N/A	N/A	52	7*
Oregon Cryonics	8*	N/A	6	5*
SA	N/A	N/A	N/A	3*
Trans Time	?	?	3	1?

 

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.

 

*=simplification, see explanation

NAME	WHOLE BODY	NEURO
Alcor	Yes	Yes
ACS	Yes	No*
CI	Yes	No
KrioRus	Yes	Yes
Oregon Cryonics	No	Yes
SA	N/A	N/A
Trans Time	Yes	Yes

 

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.

 

*=simplification,see explanation

NAME	WHOLE BODY	NEURO	YEARLY FEES
Alcor	$200,000*	$80,000*	$620*
ACS	$155,000*	N/A	$376*
CI	$28,000*	N/A	$120*
KrioRus	$36,000*	$12,000	None
Oregon Cryonics	N/A	$25,000*	None
SA	N/A	N/A	None
Trans Time	$150,000	$50,000	$96*

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.)

Fight Aging! Newsletter, February 12th 2018

by @ LongeCityNews

Sun Feb 11 01:51:59 PST 2018

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

The Secret of The Fridge! | Ep 14 of #Authentic Alex

by @ Look & Feel Amazing | Alex Fergus Blog

Mon Feb 05 15:00:00 PST 2018

The Secret of The Fridge! | Ep 14 of #Authentic Alex

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Aging theories: Is there a unifying factor in a...

by @ Articles - Articles

Sun Aug 20 11:04:47 PDT 2017

When Darwin’s theory of evolution by natural selection was established, biologists were puzzled by the existence of senescence and aging among all organisms. Why did the evolutionary pressure not produce immortal species? They concluded that even the power of evolution has its limitations. It took almost hundred years to reach the idea that mortal individuals may be preferred by nature for following reasons — the genes resulting in advantage in early life might cause damage in late life, and the reproduction starts as soon as possible. Around the middle of twentieth century, there finally was a framework for the gerontological research conduced in the following decades — the first evolutionary theories of aging (Gavrilov & Gavrilova, 2002). 
There are two major groups of theories aiming to explain the mechanism of aging, so-called programmed and error theories. The programmed ones are based on the senescence-causing nature of certain genes (these are also called evolutionary theories), hormones or the immune system. Error theories claim that we age because of general damage caused by cell weariness, metabolic rate, cross-linked proteins, free radicals or somatic DNA changes (Jin, 2010).
The beauty of various aging theories is that most of them are not mutually exclusive. We can see that newer theories do not necessarily oppose the old ones, but rather shed more light and offer more in-depth views on the process of senescence.
The pioneering idea from 1882 was Weismanns’s theory of programmed death (also called wear-and-tear theory) claiming something like apoptosis of the multicellular organism. Although disproved by experiments, his theoretical explanation of the mechanism predicted the discovery of Hayflick limit (Gavrilov & Gavrilova, 2002). According to Weismann’s first conception, nature priorities young individuals over elderly because of limited resources. Pearl stated his ‘rate of living’ theory of aging in 1928, although the idea comes from Rubner who, in 1908, suggested that every organism has limited amount of metabolic energy and therefore its age depends on the rate of metabolism which correlates with organism’s size (Pearl, 1928). Most consider the rate of living theory to be flawed (Lints, 1989; de Magalhaes, Costa, & Church, 2007; Vaanholt, Daan, Schubert, & Visser, 2009).
A few decades later, the following evolutionary models have emerged: Medawar’s hypothesis of mutation accumulation proposes that aging is a by-product of natural selection — genes causing senescence in later stadium of life cannot be eliminated because the genetic information was most likely already transferred to successors by individuals in their early adulthood (Gavrilov & Gavrilova, 2002). This theory from 1952 is considered the first modern theory of aging. Charlesworth confronted Medawar’s model with a discovery of late-life mortality plateaus and in 1994 presented so-called modified mutation accumulation theory (Charlesworth, 2001; Ljubuncic & Reznick, 2009). In his antagonistic pleiotropy theory (also called ‘pay later’ theory), Williams in 1957 expressed the idea that even the same genes which cause trouble at advanced age may be advantageous in earlier stages of life, and therefore be not only tolerated, but even preferred by natural selection (Gavrilov & Gavrilova, 2002). In 1979, Kirkwood extended this theory to the disposable soma theory — organisms may save energy by reducing accuracy in cells metabolism and invest it in faster development and reproduction (Kirkwood & Holliday, 1979). This is the last one of famous, genes-orientated evolutionary models.
The following can be classified as programmed theories: The neuroendocrine theory proposed in 1954 by Dilman says that the main cause of aging is a loss of receptor sensitivity of the hypothalamus over time, and therefore its control of adequate production of hormones declines which leads to ineffectiveness and lower hormone levels in organism. It is an attempt to explain a high occurrence of degenerative diseases in late age (“Neuroendocrine Theory of Aging: Chapter 1,” 1999). Research on hormonal signaling pathways confirms that hormone levels have at least a partial role in determining longevity (van Heemst et al., 2005). In 1964, Walford suggested his immunologic theory of aging — due to increasing diversity of cells, the immune system looses its efficiency with age which leads to insufficient responses against pathogens as well as to autoimmune reactions against self proteins (Walford, 1964). 
All following attempts to explain the mechanism behind a process of aging are usually called error or damage theories. Bjorksten’s "crosslinkage theory" says that proteins become linked together in presence of certain crosslinking agents, and after some time, accumulation of these molecular aggregates causes decline in tissue functions. This theory from 1942 is no longer popular (Bjorksten, 1968). Later research has showed that advanced glycation end products (AGEs) accumulate in collagen and lead to outcomes predicted by Bjorksten (Verzijl et al., 2002; Aronson, 2003). 
These days very popular among researchers and public, the free radical theory was suggested by Harman in 1956. His idea was that the occurrence of free radicals, or reactive oxygen species naturally produced in living organisms, leads to macromolecular damage which accumulates and causes physiological changes known as senescence (Harman, 2009). Later he suggested the reactive oxygen species formation takes place mainly in mitochondria which causes a decline in important mitochondrial functions (Harman, 1972). Because of the theory’s popularity, various extensions of Harman’s model were created, usually considering different sites as a main target of free radicals. 
Failla’s somatic mutation theory from 1958 posits that increasing number of mutations of genetic material causes a decrease in cellular, organ and body functions (Failla, 1958; Gensler & Bernstein, 1981; Kennedy, Loeb, & Herr, 2012). The theory received a lot of criticism in previous decades (Vijg, 2000). Kaya, Lobanov and Gladyshev (2015) investigated aging in yeast and failed to find evidence in support of Failla’s thesis. 
Orgel proposed his error catastrophe theory in 1963. He saw the cause of aging in accumulation of malfunctioning proteins coming from errors during protein translation (Orgel, 1963). This theory never gained popularity and was soon disproved (Gershon & Gershon, 1976). 
Alexander in 1967 extended Failla’s theory by hypothesizing that DNA damage instead of mutation is the cause of aging (Alexander, 1967). These days, this version called "somatic DNA damage theory of aging" is more often used by scientists (Freitas & de Magalhaes, 2011; Soares et al., 2014). Evidence suggests that more damage happens in mitochondrial DNA than in nuclear DNA (Ames, 2009).
In 2002, Brunk and Terman published the mitochondrial-lysosomal axis theory. It states that defective macromolecules derived from mitochondria undergo further changes in lysosomes to become lipofuscin inclusions. These end products decrease cell’s autophagocytotic capacity which leads to more mitochondrial defects (Brunk & Terman, 2002). 
Zs.-Nagy’s "membrane hypothesis" focuses on a decline of mitochondrial functions due to lessened membrane permeability caused by residual heat coming from nerve signals as well as by reactive oxygen species (Zs.-Nagy, 2014). 
Recent versions of damage theories claim that free radicals are only one kind of senescence-causing by products of metabolism but the real initiator of all the inevitable damage is biological imperfectness. In other words, there are always types of damage which lack adequate repair mechanisms in organism and the most severe source of errors depends on actual conditions (Gladyshev, 2013; Gladyshev, 2014). This idea comes from the "reliability theory", which focuses on systems failure in machines (Gavrilov & Gavrilova, 2001). In spite of many research programs and lots of scientists involved, the unifying factor in aging is at the moment still unknown.

References

• Alexander, P. (1967). The role of DNA lesions in the processes leading to ageing in mice. Symp Soc Exp Biol, 21, 29-50.
• Ames, B. (1989). Endogenous Oxidative DNA Damage, Aging, and Cancer. Free Radical Research Communications, 7(3-6), 121-128. http://dx.doi.org/10.3109/10715768909087933
• Aronson, D. (2003). Cross-linking of glycated collagen in the pathogenesis of arterial and myocardial stiffening of aging and diabetes. Journal Of Hypertension, 21(1), 3-12. http://dx.doi.org/10.1097/01.hjh.0000042892.24999.92
• Bjorksten, J. (1968). The Crosslinkage Theory of Aging. Journal Of The American Geriatrics Society, 16(4), 408-427. http://dx.doi.org/10.1111/j.1532-5415.1968.tb02821.x
• Brunk, U., & Terman, A. (2002). The mitochondrial-lysosomal axis theory of aging. European Journal Of Biochemistry, 269(8), 1996-2002. http://dx.doi.org/10.1046/j.1432-1033.2002.02869.x
• Charlesworth, B. (2001). Patterns of Age-specific Means and Genetic Variances of Mortality Rates Predicted by the Mutation-Accumulation Theory of Ageing. Journal Of Theoretical Biology, 210(1), 47-65. http://dx.doi.org/10.1006/jtbi.2001.2296
• De Grey, A. (1997). A proposed refinement of the mitochondrial free radical theory of aging. Bioessays, 19(2), 161-166. http://dx.doi.org/10.1002/bies.950190211
• Dean, W. (1999). Neuroendocrine Theory of Aging: Chapter 1. Warddeanmd.com. Retrieved 30 March 2017, from http://warddeanmd.com/articles/neuroendocrine-theory-of-aging-chapter-1/
• Failla, G. (1958). The Aging Process and Cancerogenesis. Annals Of The New York Academy Of Sciences, 71(6 Genetic Conce), 1124-1140. http://dx.doi.org/10.1111/j.1749-6632.1958.tb46828.x
• Freitas, A., & de Magalhães, J. (2011). A review and appraisal of the DNA damage theory of ageing. Mutation Research/Reviews In Mutation Research, 728(1-2), 12-22. http://dx.doi.org/10.1016/j.mrrev.2011.05.001
• Gavrilov, L., & Gavrilova, N. (2001). The Reliability Theory of Aging and Longevity. Journal Of Theoretical Biology, 213(4), 527-545. http://dx.doi.org/10.1006/jtbi.2001.2430
• Gavrilov, L., & Gavrilova, N. (2002). Evolutionary Theories of Aging and Longevity. The Scientific World JOURNAL, 2, 339-356. http://dx.doi.org/10.1100/tsw.2002.
• Gensler, H., & Bernstein, H. (1981). DNA Damage as the Primary Cause of Aging. The Quarterly Review Of Biology, 56(3), 279-303. http://dx.doi.org/10.1086/412317
• Gershon, D., & Gershon, H. (1976). An Evaluation of the ‘Error Catastrophe’ Theory of Ageing in the Light of Recent Experimental Results. Gerontology, 22(3), 212-219. http://dx.doi.org/10.1159/000212136
• Gladyshev, V. (2013). The origin of aging: imperfectness-driven non-random damage defines the aging process and control of lifespan. Trends In Genetics, 29(9), 506-512. http://dx.doi.org/10.1016/j.tig.2013.05.004
• Gladyshev, V. (2014). The Free Radical Theory of Aging Is Dead. Long Live the Damage Theory!. Antioxidants & Redox Signaling, 20(4), 727-731. http://dx.doi.org/10.1089/ars.2013.5228
• Harman, D. (1972). The Biologic Clock: The Mitochondria?. Journal Of The American Geriatrics Society, 20(4), 145-147. http://dx.doi.org/10.1111/j.1532-5415.1972.tb00787.x
• Harman, D. (2009). Origin and evolution of the free radical theory of aging: a brief personal history, 1954–2009. Biogerontology, 10(6), 773-781. http://dx.doi.org/10.1007/s10522-009-9234-2
• Jin, K. (2010). Modern Biological Theories of Aging. Aging and Disease, 1(2), 72-74.
• Kaya, A., Lobanov, A., & Gladyshev, V. (2015). Evidence that mutation accumulation does not cause aging inSaccharomyces cerevisiae. Aging Cell, 14(3), 366-371. http://dx.doi.org/10.1111/acel.12290
• Kennedy, S., Loeb, L., & Herr, A. (2012). Somatic mutations in aging, cancer and neurodegeneration. Mechanisms Of Ageing And Development, 133(4), 118-126. http://dx.doi.org/10.1016/j.mad.2011.10.009
• Kirkwood, T., & Holliday, R. (1979). The Evolution of Ageing and Longevity. Proceedings Of The Royal Society B: Biological Sciences, 205(1161), 531-546. http://dx.doi.org/10.1098/rspb.1979.0083
• Lints, F. (1989). The Rate of Living Theory Revisited. Gerontology, 35(1), 36-57. http://dx.doi.org/10.1159/000212998
• Ljubuncic, P., & Reznick, A. (2009). The Evolutionary Theories of Aging Revisited – A Mini-Review. Gerontology, 55(2), 205-216. http://dx.doi.org/10.1159/000200772
• Magalhaes, J., Costa, J., & Church, G. (2007). An Analysis of the Relationship Between Metabolism, Developmental Schedules, and Longevity Using Phylogenetic Independent Contrasts. The Journals Of Gerontology Series A: Biological Sciences And Medical Sciences, 62(2), 149-160. http://dx.doi.org/10.1093/gerona/62.2.149
• Muller, F., Lustgarten, M., Jang, Y., Richardson, A., & Van Remmen, H. (2007). Trends in oxidative aging theories. Free Radical Biology And Medicine, 43(4), 477-503. http://dx.doi.org/10.1016/j.freeradbiomed.2007.03.034
• Orgel, L. (1963). The Maintenance of the Accuracy of Protein Synthesis and its Relevance to Ageing. Proceedings Of The National Academy Of Sciences, 49(4), 517-521. http://dx.doi.org/10.1073/pnas.49.4.517
• Soares, J., Cortinhas, A., Bento, T., Leitão, J., Collins, A., Gaivã, I., & Mota, M. (2014). Aging and DNA damage in humans: a meta-analysis study. Aging, 6(6), 432-439. http://dx.doi.org/10.18632/aging.100667
• Vaanholt, L., Daan, S., Schubert, K., & Visser, G. (2009). Metabolism and Aging: Effects of Cold Exposure on Metabolic Rate, Body Composition, and Longevity in Mice. Physiological And Biochemical Zoology, 82(4), 314-324. http://dx.doi.org/10.1086/589727
• Van Heemst, D., Beekman, M., Mooijaart, S., Heijmans, B., Brandt, B., & Zwaan, B. et al. (2005). Reduced insulin/IGF-1 signalling and human longevity. Aging Cell, 4(2), 79-85. http://dx.doi.org/10.1111/j.1474-9728.2005.00148.x
• Verzijl, N., DeGroot, J., Zaken, C., Braun-Benjamin, O., Maroudas, A., & Bank, R. et al. (2002). Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: A possible mechanism through which age is a risk factor for osteoarthritis. Arthritis & Rheumatism, 46(1), 114-123. http://dx.doi.org/10.1002/1529-0131(200201)46:1<114::aid-art10025>3.0.co;2-p
• Vijg, J. (2000). Somatic mutations and aging: a re-evaluation. Mutation Research/Fundamental And Molecular Mechanisms Of Mutagenesis, 447(1), 117-135. http://dx.doi.org/10.1016/s0027-5107(99)00202-x
• Walford, R. (1964). The Immunologic Theory of Aging. The Gerontologist, 4(4), 195-197. http://dx.doi.org/10.1093/geront/4.4.195
• Zs.-Nagy, I. (2014). Aging of Cell Membranes: Facts and Theories. Aging, 62-85. http://dx.doi.org/10.1159/000358900

The above is a short perspective by Vit Zemanek. Continue the discussion and analysis on LongeCity's long-running AGING THEORIES forum.

Community Testing of Aging Bio-Markers

by @ Action

Wed Feb 07 15:58:56 PST 2018

Legitimate bio-marker testing is important to our community to help determine what current approaches are the best for slowing aging

 

It is 2018, and I can't believe how many anecdotal placebo-driven reports populate the LongeCity forum. Here is one egregious recent example if you want to chuckle: http://www.longecity.org/forum/topic/99447-hello-everybody-im-the-longest-continuous-user-of-hgh-in-human-history/

 

There was a budgeted effort to promote legitimate bio-marker testing last year, but it required members to pay for their first test, before embarking on an anti-aging regimen, where at the conclusion of the regimen time period, LongeCity would pay for a second test.

 

I am proposing a simpler approach. Here is the outline:

 

1. LongeCity pays for a standard aging-biomarker test. The most cost effective, easy to implement, and robust test available today is probably DNA methylation. LongeCity has a current relationship with Osiris Green and their test is the cheapest on the market, however, the standard deviation on their test is +/- 5 years. I have spoken with ZYMO and they will offer their test "at cost" for an effort such as this. ZYMO is HIPPA compliant and their standard deviation is only +/- 1.7 years.

 

2. We aim to offer this as a member benefit and to engage other communities such as the calorie restriction society.

 

3. Test subjects can opt to remain anonymous.

 

4. A simple questionnaire accompanies each test. This would ask each subject to rank their general approaches to life extension. Supplements, Diet, Exercise, Other. Depending upon the response, we could drill down further into regimens, but I would want to keep it simple at first to ensure a larger response.

 

5. We aim to complete the study before the end of Summer 2018, and present findings at RAADFest in September.

 

6. Stretch goal: Have a small number of people do DNA methylation testing at 3 different times of day. It is currently unknown if there is inter-day variability in DNA methylation.

 

7. Perhaps work in conjunction with newly formed OpenCures to complete and promote the study.

 

8. If successful, continue with testing on an annual or semi-annual basis. preferably with the same study participants.

 

Drawbacks/Objections

 

1. There are already a lot of groups (example: patients like me) that share test data, and there are many studies involving aging bio-markers. However, I am unsure that there are any studies that have easily accessible data AND focus upon longevity activists.

 

2. It is unlikely that a small study of a few dozen people will produce statistically valid results. To me, that is okay. We WILL learn something and I am certain there will be incredible marketing and community-building opportunities with such a study.

 

3. Cost. 5-10K, maybe higher if we can get some other groups to promote the study or if we can use other crowd-funding platforms. With 10K we could test between 50 and 75 people.

 

Leadership: I would be lead organizer and promoter.

 

LongeCity certainly has the budget for such a study and has enough connections to get a good number of people involved. LongeCity has not done much of consequence as of late. This could be a solid effort to help the community, not only functionally (what regimens work), but also as a promotional effort (life-extensionists are younger and healthier). 

 

 

Legitimate bio-marker testing is important to our community to help determine what current approaches are the best for slowing aging

Article: Gut microbiome in health and aging

by @ Articles

Tue Jan 10 10:01:50 PST 2017

As part of his new column "Sven's Science Corner" Sven Bulterijs discusses novel insights into the crucial role gut bacteria seem to play in health, disease and aging. ⇒ read the article in "Sven's Science Corner" blog

Fermented Fish, The Perfect Travel Food – GAPS Approved

by Becky Plotner @ Nourishing Plot

Wed Feb 07 05:24:32 PST 2018

Fermented fish provides a plethora of probiotic strains.

Nutrients says, “Lactic acid bacteria (LAB) consist of homo and hetero-lactic acid organisms, and are a broad category of bacteria, including Lactobacillus, Streptococcus, Enterococcus, Lactococcus and Bifidobacterium, with the ability to produce lactate primarily from sugars. They are among the most commercially used bacteria [...]

The post Fermented Fish, The Perfect Travel Food – GAPS Approved appeared first on Nourishing Plot.

Homemade Mead – GAPS Approved

by Becky Plotner @ Nourishing Plot

Thu Jan 04 06:04:58 PST 2018

Making mead is easy, delicious, festive and a great probiotic food to add to your probiotic food choices. Mead can be made several different ways. Using local honey is the easiest as it takes two simple ingredients: honey and water. There is no absolute way to make mead, the ratio of honey to [...]

The post Homemade Mead – GAPS Approved appeared first on Nourishing Plot.

Are Parasite Medications Safe?

by Susan Luschas @ Debug Your Health

Thu Mar 23 11:20:51 PDT 2017

  Are parasite medications really safe? Don’t they have harsh side effects? What about off-label sources? Learn why I’d rather give my 5-year-old a round of multiple parasite medications than I would a round of antibiotics. Note that I am not a practitioner, not trying to become one, and don’t make any money from the ... Read more...

The post Are Parasite Medications Safe? appeared first on Debug Your Health.

Doctor’s Best Betaine HCL Pepsin & Gentian Bitters • Review and Best Price

by Ken Silvers @ Probiotics Center

Sun Oct 08 01:53:11 PDT 2017

Doctor’s Best Betaine HCL Pepsin & Gentian Bitters is another well-composed supplement from this company. I have reviewed several of Doctor’s Best supplements and always found them of high quality. Therefore, most people do respond well to the high-quality enzymes included in Doctor’s Best. However, some people have specific needs and might need to try different digestive enzyme supplements to find one with a composition that fits […]

The post Doctor’s Best Betaine HCL Pepsin & Gentian Bitters • Review and Best Price appeared first on Probiotics Center.

Sauerkraut Abnehmen Abends Smell Salad Enzyme

by @ Probiotics Belaw

Sun Jan 07 18:59:26 PST 2018

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 […]

Upper Gut Dysbiosis, Anxiety, Brain Fog, Fatigue, Is Ammonia the Cause?

by John Brisson @ Fix Your Gut

Fri Jan 12 13:17:53 PST 2018

When someone is suffering from dysbiosis, imbalances within the body can readily occur and make people ill. Upper gut dysbiosis is becoming more well-known and is separate from SIBO (small intestinal bacterial overgrowth) and colonic overgrowth. With new research, we get great insight on previously unknown health

The post Upper Gut Dysbiosis, Anxiety, Brain Fog, Fatigue, Is Ammonia the Cause? appeared first on Fix Your Gut.

Will Colon Hydrotherapy Help You Lose Weight Instant Yogurt Temperature Pot

by @ INSIGHTMARKETING LEVEL

Thu Feb 08 00:40:02 PST 2018

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Guten Tag

by @ ImmInst Active Topics

Mon Feb 05 00:09:30 PST 2018

Calorie Restriction Primer

by @ Articles - Articles

Fri Nov 18 13:03:14 PST 2011

by Sven Bulterijs & Paul McGlothin,

Often described as the only proven intervention that extends mean and maximal life-span in mammalian species, it is also a lifestyle choice for the committed immortalist. But why and how does it work? How to begin and what are the downsides?

These and other questions are dressed in a short feature by Paul McGlothin, Co-author of “The CR Way” and
in a voiced slideshow by Sven Bulterijs, LongeCity Director and student in biochemistry and biotechnology.


-- Articleon Calorie Restriction by Paul McGlothin (.pdf)

-- Lectureon Calorie Restrictionby Sven Bulterijs (.pptx)

Pb8 Probiotic Canada Burping

by @ Probiotics Belaw

Sun Jan 07 16:13:41 PST 2018

Hens’ eggs are the type of egg most When there is a need to give high doses of chemotherapy to a specific area of the body it may be given by a regional method. Virtual Reality Laparoscopic Sigmoid Colectomy Virtual reality colorectal surgery is demonstrated here by medial to lateral mobilisation of the sigmoid colon […]

Benefits of Probiotics • How to Harness Healing Abilities of Bacteria

by Ken Silvers @ Probiotics Center

Tue Jun 27 13:26:45 PDT 2017

Benefits of probiotics are available for everyone with a stomach. And probiotics are essential in case of a poor gut and chronic disease. Probiotics are called friendly bacteria and indeed your body needs many friends. In fact, billions to stay well! The aim of this article is to provide vital information on how men, women […]

The post Benefits of Probiotics • How to Harness Healing Abilities of Bacteria appeared first on Probiotics Center.

Probiotics Yogurt For Ibs Intolerance Milk Lactose

by @ Probiotics Belaw

Sun Jan 07 17:33:47 PST 2018

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 […]

Antibiotics in Our Food: How They Affect Us and How to Avoid Them

by Sheridan Williamson @ Changing Habits

Mon Dec 04 17:30:09 PST 2017

Antibiotics have their place in the world – they were founded for a good reason and have helped many people. However, their misuse and overuse is concerning. Doctors are prescribing antibiotics up to 9 times more than they should according to the current guidelines, with over 4 million individuals receiving a prescription which may not […]

Why Your “Authenticity” is BS

by Sarah Ramsden @ Sarah Ramsden

Tue Oct 25 08:00:26 PDT 2016

There’s authentic Canadian maple syrup tapped in Quebec, authentic Van Gogh paintings painted by the Post-Impressionist master himself, and authentic Champagne from the Champagne Region in France. Authentic people? I call bullshit I know you consider yourself to be an authentic person. We all do. [...]

The post Why Your “Authenticity” is BS appeared first on Sarah Ramsden.

Why do some turtles outlive humans?

by @ Articles - Articles

Wed Feb 08 16:45:06 PST 2017

(⇒ 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.

Probiotic Strains For Colon Encapsulations Pure

by @ INSIGHTMARKETING LEVEL

Thu Feb 08 02:36:35 PST 2018

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 […]

Probiotic Yeast Vs Bacteria Poultry

by @ projectathena probiotics composition

Mon Feb 12 13:27:14 PST 2018

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 […]

Turmeric Ginger Latte • 3 Irresistably Delicious Recipes

by Ken Silvers @ Probiotics Center

Wed Nov 08 22:01:59 PST 2017

The Turmeric Ginger Latte is a favourite drink for many. And no wonder, it’s absolutely delicious! The main ingredients, turmeric and ginger, are potent cousins working extremely well together. And the list of turmeric’s and ginger’s health benefits seems never-ending. It also includes many gut and digestive problems. Turmeric Ginger Latte benefits The Turmeric Ginger Latte combines two […]

The post Turmeric Ginger Latte • 3 Irresistably Delicious Recipes appeared first on Probiotics Center.

LongeCity science support: quick guide/FAQ

by @ Articles

Wed Jun 12 17:36:16 PDT 2013

What is LongeCity?
LongeCity is a registered, members-based non-profit organisation.
More info here.


What THEMES of science projects does LongeCity support?
We support research into ageing and the extension of human lifespan. This means we support many types of medical research and research into basic biology, but there should be an angle that will allow people to live longer, healthier lives.


What TYPES of science projects does LongeCity support?
We support laboratory research, clinical research, bioinformatics and theoretical research in the ‘hard sciences’. We do not normally support social science research.
We do support some events, mentorship and travel to scientific conferences, but not under the ‘research budget’.


Where can the research take place?
Anywhere in the world. Laboratory research should normally be conducted in an established lab.


What does LongeCity expect in return?
Scientific integrity. Normally a written report. Interim updates for longer projects. Acknowledgement of the funding received. We may approach previous grantholders to be available as peer reviewers for future research applications.


What grant schemes are available?

a) Small Grants
Funding: up to $500
Who can apply: any LongeCity Member, it helps if you have a sponsor/supervisor with some track record
Type: typical cases are support for summer projects, internships, workshops, review paper writing, selected consumables
Next deadline: none, applications are welcome until the annual budget is exhausted
Details: http://www.longecity...s/action/grants

b) Matching Fundraiser
Funding: up to $20.000 (in total- matching fundraiser)
Who can apply: Scientists
Type: For selected projects, LongeCity will issue a call for donations and for every dollar received LongeCity will match (or better) the donation. The entire money goes to support the research project.
Next deadline: July 1^st 2013
Details: http://www.longecity...ts/research2013


Questions?
Contact us.

Best Ultimate Flora Probiotic Adults Best For Eczema

by @ Probiotics Belaw

Sun Jan 07 21:04:22 PST 2018

Best Colon Cleansers of 2014. Colon cleansing tablets are used for weight loss and detoxification. Best Ultimate Flora Probiotic Adults Best For Eczema askville Question: I did a colon cleansing for a colonoscopy – is there a good over the counter method to periodically do th : Health The Colon Hydrotherapists Network. This colon cleanser […]

Cryonics Hardship Fund

by @ LongeCity - Articles

Fri Jul 18 16:26:34 PDT 2014

Cryonics is a method of ‘medical time travel’ - placing the body in biostasis after legal death with the hope that future technology will be invented which can revive the body. To most people who share LongeCity’s mission cryonics is the ‘second worst thing’ that can happen to you, but nonetheless a viable alternative to burial or creation.

Cryonics prices vary (an overview can be found on this page maintained by Cryonics expert and LongeCity Advisor Ben Best) but it is affordable to nearly everyone via life insurance… nearly everyone. A few people who really want cryonics cannot get life insurance: After an accident, LongeCity Member James Swayze found himself quadriplegic and unable to get insurance. The life of LongeCity Member William O’Rights took a turn for the worst when he was diagnosed with aggressive throat cancer after having been suddenly deprived of all funds. Kim Suozzi was 23 and had not yet heard about cryonics when she was diagnosed with terminal brain cancer. Aaron Winborn heard of her case - and cryonics- only when the debilitating effects of Lou Gehrig's Disease had already begun to paralyse him. All these people were eventually offered a cryonics provision through the generous donations of others in our community.
We want to continue this proud tradition, looking out for those who share our common dream in unlimited lifespans, in the shadow of imminent death and despair.

However, this needs to be done carefully. It cannot be stressed enough that cryonics is affordable to most people if they only have the foresight to act early and arrange affordable life insurance. This element of personal responsibility is at the heart not just of cryonics. If we establish a hardship scheme, it must not create a moral hazard, and incentive to put things off as too unpleasant and complicated to think about until it is too late. Of course, we must also ward against fraud and abuse. An element of careful analysis and due diligence is therefore required, looking into the circumstances of each individual case.

The LongeCity cryonics hardship fund has two purposes:
1) To support a (volunteer based) infrastructure for maintaining the scheme and exercising the due diligence mentioned above
2) When a hardship case has been endorsed by LongeCity, we will use the hardship fund to help to fundraise for that individual by matching further donations. All these donations will go to a dedicated account for that person’s cryopreservation, never to the individual directly.

Applicants to our cryonics hardship fund must
- co-operate fully with LongeCity appointed auditors and reviewers
- genuinely be unable to not fully fund their cryosuspension and not have a reasonable chance of doing so prior to their likely death
- help to fundraise for their cause and help raise public awareness for cryonics

In the past, we have partnered with our friend in the Venturist community on cryonic hardship cases. We hoping to do so again on future occasions.



Click HERE to make a contribution to the fund

To apply email the full details of your case: contact@longecity.org

Colon Cancer X Ray Pictures Cancer Rates Survival Country

by @ projectathena probiotics composition

Mon Feb 12 14:44:35 PST 2018

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 […]

3 Common Dietary Supplements That Aren’t What You Think

by Jordan Pie @ Changing Habits

Mon Nov 13 15:00:06 PST 2017

Getting all the nutrients your body needs from food alone can be challenging, especially because the soils are becoming more and more depleted of nutrients and minerals. Not to mention nutrients can be difficult to absorb properly if you have gut dysbiosis, if you’re not digesting food optimally, if you have parasites, or if you’re […]

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by @ projectathena probiotics composition

Mon Feb 12 15:34:12 PST 2018

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Can Two Dozen Marginal Ways to Treat Aging be Combined into One Useful Therapy?

by @ LongeCityNews

Mon Feb 12 16:27:32 PST 2018

Comparatively little work on combinations of therapies takes place in the research community. I suspect this to be a matter of regulatory incentives. For example there is little room for commercial entities to be able to make money by combining established treatments owned by other entities. Similarly for researchers, the world of possible approaches is balkanized by intellectual property, while the disposition of the majority of research funding is ultimately guided by the promise of a pot of gold at the end of the road. That pot of gold is much harder to obtain when someone else owns the therapies involved, and all that is being done is to apply them together. The edifice of intellectual property is a great evil, and this is one of many reasons why that is the case.

Given this long-standing state of affairs, there is at present little data to guide our expectations on the bounds of the possible when it comes to combining large numbers of therapies in search of additive and synergistic effects. Some people think that we should forge ahead in the matter of slowing aging: take every intervention with good evidence to date, and run large numbers of them in the same mice to see what happens. Should we believe that various ways of manipulating the operation of cellular metabolism demonstrated to achieve 5-10% life extension in mice can combine to double life span in that species? Intuition suggests not, but I don't think it to be completely out the question. Nor is it unreasonable to try it and see, given a rigorous approach to experimental design. Sadly, no established funding institution would go for this; it would have to be funded through philanthropy.

Why do I think that this is unlikely to produce large enough results to make it worthwhile? Because the evidence to date strongly suggests that the scores of methods of manipulating metabolism to modestly slow aging are operating on just a few core processes, such as autophagy. These are the stress responses that produce the lengthening of life observed in calorie restriction, and we know that these mechanisms don't produce anywhere near the same degree of life extension in humans as they do in short-lived species. Everything is connected to everything else in cellular biochemistry. A given interaction between two proteins can be influenced by adjusting levels of any number of other proteins, with widely varying degrees of effectiveness and side-effects. So most methods of slowing aging are different views into the same method of action. The few combinations of approaches tried to date, involving only two methods, have resulted in mixed outcomes. Calorie restriction and mTOR inhibition may be additive, while growth hormone receptor knockout and mTOR inhibition interfere with one another, for example. That gives little insight as to the rest. It is hard to predict other results, beyond noting that a majority of interventions do appear to function through enhanced autophagy, and thus we might expect them not to combine in an additive way to any great degree.

What of the SENS rejuvenation biotechnology approach to aging, in which independent fundamental forms of cell and tissue damage are repaired? How will repair therapies combine? In this case we should expect additive effects: removing damage should be beneficial in proportion to the amount removed, at least when considered from a fundamental, reliability theory perspective. The mortality risk and longevity of a complex system of many redundant parts is dependent on its current load of damage. At this point we have no idea as to how that will turn out in practice, however. The contributions of different forms of damage may be significantly larger or smaller than one another. The results of two independent root cause forms of damage are not themselves independent: they interact, and probably significantly. Functional decline in one system spurs greater damage and functional decline in others, which is why age-related degeneration accelerates greatly in later life. It is a complex business. It isn't unreasonable to think that in some circumstances the results of rejuvenation therapies A and B will be indistinguishable from A alone, or that B will never achieve a great deal without being combined with C.

Can we envisage a world in which repairing cellular senescence alone produces no extension to life span because other, largely independent chains of damage and consequence are still life-limiting for old humans? That is becoming increasingly hard given the evidence to date for reversal of numerous age-related diseases to result from removal of senescent cells, not to mention the PAI-1 mutants who exhibit increased life span - but we know far more about senescent cell clearance than we do about any of the other SENS strategies. No-one is in a position to do more than make educated guesses about the results of combining senescent cell destruction with removal of mitochondrial DNA damage, or with clearance of specific lysosomal aggregates. Beyond "two should be better than one, but perhaps not in some specific cases" everything else will remain a mystery until the biotechnology is ready and the work is carried out. Making predictions seems a fool's game, given the degree to which the people closest to senescent cell research have been surprised by the scope and size of benefits observed in mice over the past few years.

View the full article at FightAging

Do Probiotics Help Flatten Your Stomach Laxative

by @ INSIGHTMARKETING LEVEL

Wed Feb 07 23:23:41 PST 2018

Garcinia Cambogia can be best described as a natural supplement that is extracted from a fruit that closely resembles a small pumpkin. Do Probiotics Help Flatten Your Stomach Laxative nine stars touchless trash can. Support & maintain a healthy digestive system daily*. Fatigue flagyl cause own discharge taking flagyl probiotics flagyl overdose symptoms. Blend of […]

Gt Kombucha Nutrition Label Sources

by @ projectathena probiotics composition

Mon Feb 12 16:32:15 PST 2018

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 […]

Probiotic Yogurt On Skin Oz Usana Dr

by @ Probiotics Belaw

Sun Jan 07 19:23:53 PST 2018

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 […]

Colorectal Cancer Vascular Invasion Shelf Australia Stable

by @ Probiotics Belaw

Sun Jan 07 12:42:11 PST 2018

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 […]

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

by Lisa Richards @ The Candida Diet

Wed Feb 07 15:24:07 PST 2018

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.

Probiotic Deficiency Brands Yogurt Are What

by @ Probiotics Belaw

Sun Jan 07 20:32:45 PST 2018

Did you know that there are many ways to Cleanse the body? These include colon cleanse juice cleanse the master cleanse raw diet cleansing and fiber cleanses. Symptoms Probiotic Deficiency probiotics in prevention of antibiotic associated diarrhea meta analysis safety pregnancy Brands Yogurt Are What include: colon cleanse colon cleansing colon cleanses detox. Probiotic Deficiency […]

Gaps Diet Without Probiotics Smits Jimmy Does Cancer

by @ projectathena probiotics composition

Mon Feb 12 13:55:37 PST 2018

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 […]

User Agreement

by @ LongeCity - Articles

Sat Dec 17 15:11:18 PST 2011

Bylaw A. User Agreement (Posting Guidelines)

---

Bylaw A. User Agreement

Article 1
The following shall be the letter of the agreement that all visitors, Members and their guests will be asked to abide by when interacting with the LongeCity/ Imminst ("LongeCity") website Please read this Agreement carefully before accessing the Site.

Section01 The Nature of this Agreement
(a) The following are the terms and conditions (the "Agreement") offered to any person ("you") for access and use (including but not limited to forum user registration) of the LongeCity/Immortality Institute (LongeCity) web site and all affiliated web sites (the "Site"). The Agreement is the basis for using and interacting with the LongeCity website. By accessing the Site, you agree to abide by this Agreement.
(b) Access to the Site is a privilege and not a right. If you do not agree with this Agreement, or have no intention to follow the rules outlined herein, you may not use the Site. If you have any reason to interact with a representative of LongeCity, but you do not wish to follow these rules, please email support@LongeCity.org
© The information in this document is subject to change. These changes will be announced on the Site, but you must also agree to periodically review this document for changes. After eight (8) days of any change in the Rules, your continued use of the Site indicates your acceptance of any changes made.

Section02 Account registration
(a) Only natural persons aged 16 or above may register an account with LongeCity.
(b) Each natural person may hold one single account. Registering with multiple accounts is not allowed unless specific permission is given by LongeCity.
© You may not use the account of another person unless such use is inadvertent and infrequent (e.g. using a family members login from the same computer not noticing that the person forgot to log out).
(d) Persons whose accounts have been suspended, deleted or blocked by LongeCity may never register another account unless specific permission is given by LongeCity.
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(g) Accounts may be suspended, deleted, or changed by LongeCity for a variety of reasons including but not limited to a violation of this user agreement. If you are unsure why your account is inaccessible you can email support@LongeCity.org.
You must not register a new account the without express permission from the Secretary.
(h) When an account has been suspended, Members will be notified within 8 days of suspension and may appeal to the Secretary within 8 days after receiving such notification. If no agreement can be reached with the Secretary, the Member may appeal the case to the Board. There is no right to appeal for users or other individuals who are not Members.

Section03 Content
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(b) Content from the Site may be downloaded solely for your own non-commercial use.
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(e) Content are the responsibility of the person from whom such Content originated. You agree that you and not LongeCity, are entirely responsible for all Content that you upload, post, email, link, transmit or otherwise make available via the Site.
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(g) LongeCity will not use Content you contribute for commercial gain without your express permission, but cannot warrant or guarantee in any way that others who you decide to share the Content with might not use it for commercial activities.
(h)LongeCity cannot be held responsible for any Content that has been contributed through its open platform. LongeCity will not react to requests to verify, redact, edit, delete or obfuscate any Content.

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(b) By contributing your own original Content you agree to make this Content available in perpetuity under a Creative Commons Attribution-Non-Commercial-No Derivative Works 3.0 United States License. http://creativecommo...y-nc-nd/3.0/us/unless you give express notification to the contrary at the same time that you contribute the Content.
© LongeCity will not share private data with third parties without your consent, however LongeCity may use the information it obtains as a result of your visiting and/or registering with the Site for the purpose of enforcing this Agreement or in order to save a life or prevent unlawful activity.
(d) LongeCity is not responsible if you decide to post or share private information about yourself or others on the forum. LongeCity will not normally redact, remove or alter such data if you subsequently change your mind.

Section05 Limitation of Liability
(a) In no event will LongeCity be liable for consequential or incidental damages
which may arise in connection with your use of the Site. Accordingly, you agree that LongeCity shall not be responsible to you or anyone else for any loss-of-profit, direct, indirect, incidental, special, or consequential damages
arising out of the use of the site.
(b) You acknowledge that the limitations set forth herein are integral to the amount of consideration levied in connection with the access and use of the Site and any services rendered hereunder and that, were LongeCity to assume any further liability other than as set forth herein, such consideration would of necessity be set substantially higher.
(c) You agree to defend, indemnify and hold LongeCity and its officers, directors,agents, and employees harmless against all costs, expenses, and losses, incurred from any violation of this Agreement (including negligent or wrongful conduct) by your use and access of the Site.
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(e) LongeCity does not verify the credentials of anyone contributing Content to the site and does not endorse any Content that is contributed as advice. Anyone providing advice and guidance on or in association with the site is doing this strictly in a personal capacity, whether or not this person has an official role with LongeCity, unless the advice is specifically, expressly and in each instance authorised by an LongeCity director. Users are reminded that 'Advisors' are advising the LongeCity board on policy. This does not constitute an endorsement by LongeCity of that Advisors communications with others.

Section06 Basic Prohibitions
(a) The following activities are strictly prohibited and may lead to immediate suspension or deletion of the account, court action and notification of law enforcement officials.
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(h) Display the contents of the Site on a different web site without permission.
(i) Violate the Site's security including but not limited to accessing unauthorized data or logging into an account or attempt to log into an account for which you do not have authorization, scan or test for hardware or software
vulnerabilities, perform a denial of service attack, attempt to spread a virus or malware, or falsify TCP/IP information.
(j) Contributing any solicitation including but not limited to advertising, promotional materials, junk mail, spam, chain letters, pyramid schemes (also see section 8 below)

Section07 Content related to health
(a) Any and all advice and/or opinion provided is strictly personal and never endorsed by LongeCity, nor should it be construed to be the official policy of LongeCity to provide health advice.
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(d) All Information on the LongeCity Forums, including those associated with health, sciences fora are provided as an area for the open exchange of anecdotal experience and information, not as a professional source of advice.

Section08 Advertising, promotions and commercial activity
(a) Organisations or individuals seeking to advertise on the Site must first apply to LongeCity for such approval.
(b) Advertising is any Content (including private messages) that draws attention to, solicits, endorses, offers for sale, links to, critiques or otherwise relates to goods or services where one of the parties involved in initiating such Content or one of their associates stands to benefit from financial transactions that may results from such Content.
(c) LongeCity seeks to limit surreptitious advertising where users who may have a financial stake in such matters contribute Content simply to increase product desirability or brand awareness. Such Content will be censored on the basis of suspicion alone. On occasion, 'innocent' Content may inadvertently be subjected to such censure. Users should be aware of this and are kindly asked to refrain from protest in these cases, as the common aim is to increase the quality of Content on the Site.
(d) Even if a promotion has been agreed by LongeCity, this does not imply, and no-one must imply that this constitutes an official endorsement by LongeCity of the promotion, the organisation and individual conducting the promotion or the promoted products or procedures.
(e) Users must not use the Site for initiating or conducting commercial transactions, whether in private messages, or by using contact details displayed on the Site unless expressly authorised by LongeCity.

Section09 Posting Guidelines
(a) Users must agree to consider the posting guidelines as specified in Article2. Adherence to these guidelines is monitored by LongeCity Moderators, Directors and other designated Officers.
(b) Violation of a guideline will incur a warning. Repeat violation on more than three separate occasions will result in a time-limited suspension of the user account ranging from eight days to eight years.
(c) Disputes regarding the enforcement of posting guidelines should be taken up, in the first instance, with the Moderator who has issued the warning. If no resolution can be found in dialogue, the dispute can be notified to the Lead Moderator. Warnings issued by the Lead Moderator can be disputed with the Secretary. Users who have an open dispute with a Moderator cannot be warned again by the same Moderator – but the Moderator in question may still report questionable posts by that user.
(d) LongeCity has reserved a forum for the expression of free speech known as the William O'Rights Memorial Forum. LongeCity will not restrict Content in this forum even if it violates the posting guidelines as long as such Content does not violate the other provisions in this Agreement. This is a forum where users can engage in 'flame wars', ensure that posts are not interfered with by a Moderator, or complain about LongeCity without threat of censure.


Article 2 Posting Guidelines

Section01 A-- General tone of conversations
A1-- Be polite. That does not mean that you cannot try to destroy another’s argument utterly but never lose your tone or your temper while doing so. Also under no circumstances should you employ personal judgments or remarks about people themselves rather than their arguments. Aside from the fact that such judgments are more often than not ill founded, they drag down the overall quality of the discussion as well as costing time and space.
A2-- Some words are generally considered offensive terms, in polite conversation such as "fuck, "shit", "faggot" or "nigger". Causing offence rarely if ever helps to elevate the quality of a discussion. Generally, use of such words will result in a warning or ban, but discretion may be exercised depending on the context.

Section02 B-- General writing style
B1-- Do not write excessive amounts of text. Be concise! No one has the time or the inclination to plough through a pile of superfluous rhetoric in order to discover your main points. If you really feel that you have to write an essay, then write a summary at the end as every considerate essay-writer would do.
B2-- While every caution is advised about over-using the forums design tools, please by all means DO use them, if this helps to make the text more accessible.

Section03 C-- Starting a new topic
C1-- Before starting a new topic please consider if the topic is informative, or will stimulate an interesting discourse.
C2-- Please check if the issue has been discussed before on the Site (It is not important to be a 100% sure about this – the LongeCity forums are quite large and old. But please make a quick search, especially if you have not been with the community for long. Sometimes, it may make sense to open a new topic anyway, but would be great if you could reference previous discussions.)
C3-- Please think about a good title. (This is very important. Please spend some time on considering the title. Titles like "A Question", "Hello" or "Life Extension" may lead to an otherwise interesting topic being deleted. Challenging titles may draw a lot of visitors will still incur a warning if they are not informative. Give full titles. "Vitamin E" is bad, "Vitamin E harmful?" is not as good as "Risk of Vitamin E supplements in Cancer".)
C4-- Is it a privileged topic? (LongeCity Members can create new topics over which they, as threadstarter have editorial control. This is to empower members who are willing to put in a bit of work to maximise the quality and values of a discussion thread. Other contributors must be alerted to the threadstarters intention in the first post, but cannot subsequently complain if their posts are edited.

Section04 D-- Replying to topics
D1-- Please ask yourself "Does my reply offer a significant contribution?"
D2-- It is critical that you try to keep follow-up posts on topic. Avoid going off on a different tangent. If it occurs to you that this might be another thread, open a new thread and put a link to it in the old one. The last word about relevance stays with the Moderators or the threadstarter.
D3-- As an extension of the previous point, do not derail a topic with fundamental critique even if you think that this would desirable. In particular do not question the necessity of a certain life-extension technique by referring to another method that seems more relevant to you. (Two examples: do not answer a question about the capacity of artificial intelligence to value human emotion correctly by stating that the ‘Singularity’ is a bunch of nonsense anyway; Do not intrude on an exchange about the bioavailability of resveratrol by stating that you don't care because you are signed up for cryonics)
D4-- Refrain from posting personal information unless it is inherently necessary to elaborate your views or position.
D5-- There is usually no benefit for people in reading that you agree unless you give an explanation to go with it.
D6-- You do not have to be an expert on the subject matter, but if you feel that you really don’t know enough about the subject, then ask informed questions before stepping into the ring for debate. If someone posts a link or uploads an article- read it before you go on. Also read the posts of your predecessors and be aware of related discussions elsewhere.

Section05 E-- Posting images
E1-- You are welcome to post your own images and drawings when they are relevant to sharing knowledge. Irrelevant or excessive positing of images, including emoticons (smiles) often diminishes quality of the Content and will likely incur a warning.
E2-- Showing images to illustrate a point or make a humorous quip is popular with some posters, but please consider if such posts could derail a discussion or create issues around copyright infringement.
E3-- Please be considerate about causing embarrassment when sharing images. As a rule of thumb, if you would be uncomfortable viewing it at work, do not post it.
E4-- Avatars: LongeCity encourages users to use a small portrait (passport-type) photograph as 'Avatar' of themselves, but this is not a requirement. However, the use of other peoples photographs or the LongeCity logo as Avatar is not allowed.

Section06 F-- Quotes and references
F1-- When replying to a previous post by quoting it, only quote precisely enough text as is necessary to understand your reply. Using the "reply" function in the forums will quote the entire post that you are replying to. Do not use this feature without due consideration.
F2-- If you quote, reference the quote properly, but only quote the important bits. (It is customary to put alterations to a quote in square brackets and indicate left-out bits by putting “...”) Do not quote whole articles, rather give a link or upload them. If you have to quote a substantial passage, then indicate the important passages that you want to draw attention too.
F3-- The use of references is strongly encouraged. Such references should contain enough information to find the relevant source with one or two mouse clicks. When using a link, please remember that the hypertext url may be specific to your own access and useless to others.

Low Histamine Foods That Nourish The Gut

by Alison Vickery @ Alison Vickery

Thu Jun 29 23:46:25 PDT 2017

Alison Vickery
Alison Vickery - The Low Histamine Coach

One of the challenges faced by people with histamine intolerance is the removal of high histamine ferments, but fortunately, a wide range of low histamine foods nourish the gut.  You do not need to eat sauerkraut to have a good gut biome. Histamine Intolerance In the scientific literature, it is a well established that there is […]

Low Histamine Foods That Nourish The Gut
Alison Vickery

My GAPS Story

by Melanie Christner @ Honest Body

Sat Oct 04 20:20:39 PDT 2014

I was nursing my 4th child when I first heard Dr. Natasha speak in 2007. Growing and nursing four babies had taken its toll on my body, and with an ill-timed infection and another round of antibiotics, I sunk into several months of misery as I struggled to get right side up again. By taking […]

The post My GAPS Story appeared first on Honest Body.

High Strength Probiotics Supplement Acidophilus Best

by @ INSIGHTMARKETING LEVEL

Wed Feb 07 22:25:27 PST 2018

It has been found to clear up to 95% of the symptoms associated with IBS if high enough doses are taken. High Strength Probiotics Supplement Acidophilus Best no physical products will be shipped. the topical or supplemental use of grape seed extract may help to reduce Probiotics for Rosacea. This week the ACS issued revised […]

Lavender. Almost as good as Pregabalin

by @ ImmInst Active Topics

Fri Feb 09 05:41:57 PST 2018

I've been testing a few drops of  lavender essential oil for my sky-high levels of anxiety. This stuff is potent. I took 8 drops today, and it's almost as efficient as 100mg of pregabalin ( I've been taking up to 400 mg of pregabalin daily these last months for anxiety and insomnia ). Make sure it's for oral consumption , some essential oils are for use diluted on skin only. Mix the drops with something fat , or just take it in water . It did create some heartburn though, but I took a very high dosage.

 

I've also taken  Silexan ( an extract of lavender ) before. It's bloody expensive, and cheap lavender oil works just as well.

 

Interestingly, lavender essential oil seems to work the same way as pregabalin :

 

https://www.ncbi.nlm.nih.gov/pubmed/23637742

 

 

 

Lavender oil-potent anxiolytic properties via modulating voltage dependent calcium channels.

Schuwald AM1, Nöldner M, Wilmes T, Klugbauer N, Leuner K, Müller WE.

Author information

 

Abstract

Recent clinical data support the clinical use of oral lavender oil in patients suffering from subsyndromal anxiety. We identified the molecular mechanism of action that will alter the perception of lavender oil as a nonspecific ingredient of aromatherapy to a potent anxiolytic inhibiting voltage dependent calcium channels (VOCCs) as highly selective drug target. In contrast to previous publications where exorbitant high concentrations were used, the effects of lavender oil in behavioral, biochemical, and electrophysiological experiments were investigated in physiological concentrations in the nanomolar range, which correlate to a single dosage of 80 mg/d in humans that was used in clinical trials. We show for the first time that lavender oil bears some similarities with the established anxiolytic pregabalin. Lavender oil inhibits VOCCs in synaptosomes, primary hippocampal neurons and stably overexpressing cell lines in the same range such as pregabalin. Interestingly, Silexan does not primarily bind to P/Q type calcium channels such as pregabalin and does not interact with the binding site of pregabalin, the α2δ subunit of VOCCs. Lavender oil reduces non-selectively the calcium influx through several different types of VOCCs such as the N-type, P/Q-type and T-type VOCCs. In the hippocampus, one brain region important for anxiety disorders, we show that inhibition by lavender oil is mainly mediated via N-type and P/Q-type VOCCs. Taken together, we provide a pharmacological and molecular rationale for the clinical use of the oral application of lavender oil in patients suffering from anxiety.

 

 

Beet Kvass – GAPS Approved

by Becky Plotner @ Nourishing Plot

Tue Feb 06 05:46:14 PST 2018

Beet kvass is a probiotic drink so common in the country of Moldova that there are kvass vending machines on city streets. You put your coin in the machine, pick your kvass flavor and the machine squirts your flavored kvass into a glass sitting on a shelf in the middle of the machine. [...]

The post Beet Kvass – GAPS Approved appeared first on Nourishing Plot.

Probiotic Acidophilus Prevent Yeast Infection Biocare Forte

by @ projectathena probiotics composition

Mon Feb 12 16:04:25 PST 2018

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 […]

6 Probiotic Myths

by Melanie Christner @ Honest Body

Thu Nov 19 13:17:43 PST 2015

The post 6 Probiotic Myths appeared first on Honest Body.

Dr Ohhira Probiotics Uk Multi Effects Side Strain

by @ Probiotics Belaw

Sun Jan 07 15:46:37 PST 2018

Today in History – Tuesday – July 31 2012 1792 – The cornerstone of the U.S. Most children with constipation do not have an underlying medical problem (such as low thyroid or a bowel anatomic abnormality) however if a consumer lab probiotic report homeopathic child has persistent Untie the tea towel from the wooden spoon. […]

Jagged-1 as a More Selective Signal to Spur Bone Regrowth

by @ LongeCityNews

Mon Feb 12 03:29:05 PST 2018

Researchers here report on a more selective way to trigger the accelerated or enhanced regeneration of bone tissue, delivering jagged-1 to injuries rather than the bone morphogenetic proteins (BMPs) that have been used in the past. It appears to cause fewer issues related to inappropriate excess bone growth, as it influences mechanisms that are more closely associated with the process of regeneration in response to damage. The delivery of signals rather than cells or pharmaceuticals to produce regeneration will be a growing theme in the years ahead, and the approaches will only grow in sophistication and degree of control. The advance here is a small step in the grand scheme of the possible and the plausible; it will be interesting to see how this part of the industry evolves over the next few decades.

When a patient breaks a bone, there's a possibility the fracture won't heal properly or quickly, and use of a restorative tactic known as bone morphogenetic proteins, or BMPs, is increasingly less likely. Designed to promote spinal fusion and bone repair more than a decade ago, these molecules can overperform, causing excessive or misdirected bone growth, studies have shown. But because bone-healing biological research has often been limited, few other options exist. "Novel therapies have gone underdeveloped because of this assumption that bones heal without problem. The reality is there's a huge number of fractures that occur each year that don't heal very well."

The divide recently inspired scientists to examine a new therapeutic approach. Their method: deliver additional Jagged-1 - a potent osteoinductive protein known to activate the Notch signaling pathway that regulates bone healing - at the spot of a bone injury. "We've hypothesized for many years that by binding the Jagged-1 to a biomaterial and delivering it to a bone injury site, we could enhance healing." The results affirm that hunch: Rodents that received Jagged-1, applied via wet collagen sponge, saw improvements to skull and femoral bone injuries. Rodents treated with BMPs, by contrast, also benefited but developed the same problematic bone hypertrophy associated with human use of those proteins. Those findings suggest that the former therapy could one day benefit people.

It's not fully known why some bones don't heal the way they should - nor do scientists know whether a genetic component plays a role. What researchers have studied for years, meanwhile, is the capacity of the Jagged-1 ligand to promote bone-forming cells. The signaling is unique because this particular ligand typically binds to a delivery cell to activate bone healing in an adjacent cell - a vital trait to help ensure that a supplemental Jagged-1 dose, administered at the spot of injury, stays in place (and on task) to carry out its intended function. As a result, bone will only form where bone is supposed to form. BMPs, by comparison, are soluble, so they can migrate from the site of delivery and settle elsewhere in the body, triggering other cells that aren't supposed to form bone.

Link: https://labblog.uofmhealth.org/body-work/boosting-a-key-protein-to-help-bones-wont-heal

View the full article at FightAging

Microglia Stem Cells - Transplanted microglia - where did they go?

by @ LONGECITY Community Blog List

Wed May 10 08:08:34 PDT 2017

Hi,
yes it has been a while since I wrote something here.

 

Here are two papers pusblished including the work funded by you:

• Leovsky C, Fabian C, Naaldijk Y, Jäger C, Jang HJ, Böhme J, Rudolph L, Stolzing A. Biodistribution of in vitro-derived microglia applied intranasally and intravenously to mice: effects of aging. Cytotherapy. 2015 Nov;17(11):1617-26
• Danielyan L, Beer-Hammer S, Stolzing A, Schäfer R, Siegel G, Fabian C, Kahle P, Biedermann T, Lourhmati A, Buadze M, Novakovic A, Proksch B, Gleiter CH, Frey WH, Schwab M. Intranasal delivery of bone marrow-derived mesenchymal stem cells, macrophages, and microglia to the brain in mouse models of Alzheimer's and Parkinson's disease. Cell Transplant. 2014;23 Suppl 1:S123-39.

There will be more comming on the therapeutic effect of the cells.

 

So if you want to speed this rpocess up we would be happy for people to help us. You just need a computer and some freely availabe software.

 

Or if you have a lab, especially with a good imaging software good at counting we would be interested in a collaboration.

 

Also we have protein extractions and would be interested in people doing proteomics. Just send me an email and we can discuss details.

 

Dey

Probiotic Capsule Douche Taking Leaky Gut

by @ Probiotics Belaw

Sun Jan 07 17:11:46 PST 2018

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 […]

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

by @ ImmInst Active Topics

Sun Feb 11 17:35:26 PST 2018

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

5 Ways to Build a Healthy, Mindful Relationship with Food

by Sheridan Williamson @ Changing Habits

Mon Jan 01 17:30:43 PST 2018

Mindful eating is a new concept… until processed foods came along, there wasn’t a need to eat mindfully.  For thousands of years, foods were always natural – not tampered with, not genetically modified, and free of dubious additives. Today, eating healthily often involves becoming more aware of what not to eat. Way back when, we […]

CocoBiotic by Body Ecology • Superb Probiotic Beverage

by Ken Silvers @ Probiotics Center

Wed Apr 26 21:02:18 PDT 2017

CocoBiotic by Body Ecology is a naturally fermented drink. It includes a gut friendly mix of coconut water, grains, beneficial bacteria and prebiotic fiber. This is indeed a refreshing and addictive sparkling drink! CocBiotic is another superb, high-quality product from this company. I can understand why CocoBiotic has become so popular—it’s a refreshing, mild and fizzy drink […]

The post CocoBiotic by Body Ecology • Superb Probiotic Beverage appeared first on Probiotics Center.

Can Poor Gut Health Stop You From Losing Weight?

by Lisa Richards @ The Candida Diet

Mon Dec 11 11:58:33 PST 2017

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 […]

The post Can Poor Gut Health Stop You From Losing Weight? appeared first on The Candida Diet.

Do Probiotics Help With Mood Plants

by @ Probiotics Belaw

Sun Jan 07 21:31:00 PST 2018

Rich Shewmaker <rich@ilhawaii.net> wrote or quoted: > I challenge anyone to probiotics for reptiles activity lactobacillus come up with a single report of a Answering The Question: How Does Sea Salt Cleanse The Colon? Hydrotherapy Colon Cleanse Is Far Superior A Method Than Enema. Do Probiotics Help With Mood Plants what makes matters even worse […]

Aging theories: Is there a unifying factor in a...

by @ Articles

Sun Aug 20 11:04:47 PDT 2017

When Darwin’s theory of evolution by natural selection was established, biologists were puzzled by the existence of senescence and aging among all organisms. Why did the evolutionary pressure not produce immortal species? They concluded that even the power of evolution has its limitations. It took almost hundred years to reach the idea that mortal individuals may be preferred by nature for following reasons — the genes resulting in advantage in early life might cause damage in late life, and the reproduction starts as soon as possible. Around the middle of twentieth century, there finally was a framework for the gerontological research conduced in the following decades — the first evolutionary theories of aging (Gavrilov & Gavrilova, 2002). 
There are two major groups of theories aiming to explain the mechanism of aging, so-called programmed and error theories. The programmed ones are based on the senescence-causing nature of certain genes (these are also called evolutionary theories), hormones or the immune system. Error theories claim that we age because of general damage caused by cell weariness, metabolic rate, cross-linked proteins, free radicals or somatic DNA changes (Jin, 2010).
The beauty of various aging theories is that most of them are not mutually exclusive. We can see that newer theories do not necessarily oppose the old ones, but rather shed more light and offer more in-depth views on the process of senescence.
The pioneering idea from 1882 was Weismanns’s theory of programmed death (also called wear-and-tear theory) claiming something like apoptosis of the multicellular organism. Although disproved by experiments, his theoretical explanation of the mechanism predicted the discovery of Hayflick limit (Gavrilov & Gavrilova, 2002). According to Weismann’s first conception, nature priorities young individuals over elderly because of limited resources. Pearl stated his ‘rate of living’ theory of aging in 1928, although the idea comes from Rubner who, in 1908, suggested that every organism has limited amount of metabolic energy and therefore its age depends on the rate of metabolism which correlates with organism’s size (Pearl, 1928). Most consider the rate of living theory to be flawed (Lints, 1989; de Magalhaes, Costa, & Church, 2007; Vaanholt, Daan, Schubert, & Visser, 2009).
A few decades later, the following evolutionary models have emerged: Medawar’s hypothesis of mutation accumulation proposes that aging is a by-product of natural selection — genes causing senescence in later stadium of life cannot be eliminated because the genetic information was most likely already transferred to successors by individuals in their early adulthood (Gavrilov & Gavrilova, 2002). This theory from 1952 is considered the first modern theory of aging. Charlesworth confronted Medawar’s model with a discovery of late-life mortality plateaus and in 1994 presented so-called modified mutation accumulation theory (Charlesworth, 2001; Ljubuncic & Reznick, 2009). In his antagonistic pleiotropy theory (also called ‘pay later’ theory), Williams in 1957 expressed the idea that even the same genes which cause trouble at advanced age may be advantageous in earlier stages of life, and therefore be not only tolerated, but even preferred by natural selection (Gavrilov & Gavrilova, 2002). In 1979, Kirkwood extended this theory to the disposable soma theory — organisms may save energy by reducing accuracy in cells metabolism and invest it in faster development and reproduction (Kirkwood & Holliday, 1979). This is the last one of famous, genes-orientated evolutionary models.
The following can be classified as programmed theories: The neuroendocrine theory proposed in 1954 by Dilman says that the main cause of aging is a loss of receptor sensitivity of the hypothalamus over time, and therefore its control of adequate production of hormones declines which leads to ineffectiveness and lower hormone levels in organism. It is an attempt to explain a high occurrence of degenerative diseases in late age (“Neuroendocrine Theory of Aging: Chapter 1,” 1999). Research on hormonal signaling pathways confirms that hormone levels have at least a partial role in determining longevity (van Heemst et al., 2005). In 1964, Walford suggested his immunologic theory of aging — due to increasing diversity of cells, the immune system looses its efficiency with age which leads to insufficient responses against pathogens as well as to autoimmune reactions against self proteins (Walford, 1964). 
All following attempts to explain the mechanism behind a process of aging are usually called error or damage theories. Bjorksten’s "crosslinkage theory" says that proteins become linked together in presence of certain crosslinking agents, and after some time, accumulation of these molecular aggregates causes decline in tissue functions. This theory from 1942 is no longer popular (Bjorksten, 1968). Later research has showed that advanced glycation end products (AGEs) accumulate in collagen and lead to outcomes predicted by Bjorksten (Verzijl et al., 2002; Aronson, 2003). 
These days very popular among researchers and public, the free radical theory was suggested by Harman in 1956. His idea was that the occurrence of free radicals, or reactive oxygen species naturally produced in living organisms, leads to macromolecular damage which accumulates and causes physiological changes known as senescence (Harman, 2009). Later he suggested the reactive oxygen species formation takes place mainly in mitochondria which causes a decline in important mitochondrial functions (Harman, 1972). Because of the theory’s popularity, various extensions of Harman’s model were created, usually considering different sites as a main target of free radicals. 
Failla’s somatic mutation theory from 1958 posits that increasing number of mutations of genetic material causes a decrease in cellular, organ and body functions (Failla, 1958; Gensler & Bernstein, 1981; Kennedy, Loeb, & Herr, 2012). The theory received a lot of criticism in previous decades (Vijg, 2000). Kaya, Lobanov and Gladyshev (2015) investigated aging in yeast and failed to find evidence in support of Failla’s thesis. 
Orgel proposed his error catastrophe theory in 1963. He saw the cause of aging in accumulation of malfunctioning proteins coming from errors during protein translation (Orgel, 1963). This theory never gained popularity and was soon disproved (Gershon & Gershon, 1976). 
Alexander in 1967 extended Failla’s theory by hypothesizing that DNA damage instead of mutation is the cause of aging (Alexander, 1967). These days, this version called "somatic DNA damage theory of aging" is more often used by scientists (Freitas & de Magalhaes, 2011; Soares et al., 2014). Evidence suggests that more damage happens in mitochondrial DNA than in nuclear DNA (Ames, 2009).
In 2002, Brunk and Terman published the mitochondrial-lysosomal axis theory. It states that defective macromolecules derived from mitochondria undergo further changes in lysosomes to become lipofuscin inclusions. These end products decrease cell’s autophagocytotic capacity which leads to more mitochondrial defects (Brunk & Terman, 2002). 
Zs.-Nagy’s "membrane hypothesis" focuses on a decline of mitochondrial functions due to lessened membrane permeability caused by residual heat coming from nerve signals as well as by reactive oxygen species (Zs.-Nagy, 2014). 
Recent versions of damage theories claim that free radicals are only one kind of senescence-causing by products of metabolism but the real initiator of all the inevitable damage is biological imperfectness. In other words, there are always types of damage which lack adequate repair mechanisms in organism and the most severe source of errors depends on actual conditions (Gladyshev, 2013; Gladyshev, 2014). This idea comes from the "reliability theory", which focuses on systems failure in machines (Gavrilov & Gavrilova, 2001). In spite of many research programs and lots of scientists involved, the unifying factor in aging is at the moment still unknown.

References

• Alexander, P. (1967). The role of DNA lesions in the processes leading to ageing in mice. Symp Soc Exp Biol, 21, 29-50.
• Ames, B. (1989). Endogenous Oxidative DNA Damage, Aging, and Cancer. Free Radical Research Communications, 7(3-6), 121-128. http://dx.doi.org/10.3109/10715768909087933
• Aronson, D. (2003). Cross-linking of glycated collagen in the pathogenesis of arterial and myocardial stiffening of aging and diabetes. Journal Of Hypertension, 21(1), 3-12. http://dx.doi.org/10.1097/01.hjh.0000042892.24999.92
• Bjorksten, J. (1968). The Crosslinkage Theory of Aging. Journal Of The American Geriatrics Society, 16(4), 408-427. http://dx.doi.org/10.1111/j.1532-5415.1968.tb02821.x
• Brunk, U., & Terman, A. (2002). The mitochondrial-lysosomal axis theory of aging. European Journal Of Biochemistry, 269(8), 1996-2002. http://dx.doi.org/10.1046/j.1432-1033.2002.02869.x
• Charlesworth, B. (2001). Patterns of Age-specific Means and Genetic Variances of Mortality Rates Predicted by the Mutation-Accumulation Theory of Ageing. Journal Of Theoretical Biology, 210(1), 47-65. http://dx.doi.org/10.1006/jtbi.2001.2296
• De Grey, A. (1997). A proposed refinement of the mitochondrial free radical theory of aging. Bioessays, 19(2), 161-166. http://dx.doi.org/10.1002/bies.950190211
• Dean, W. (1999). Neuroendocrine Theory of Aging: Chapter 1. Warddeanmd.com. Retrieved 30 March 2017, from http://warddeanmd.com/articles/neuroendocrine-theory-of-aging-chapter-1/
• Failla, G. (1958). The Aging Process and Cancerogenesis. Annals Of The New York Academy Of Sciences, 71(6 Genetic Conce), 1124-1140. http://dx.doi.org/10.1111/j.1749-6632.1958.tb46828.x
• Freitas, A., & de Magalhães, J. (2011). A review and appraisal of the DNA damage theory of ageing. Mutation Research/Reviews In Mutation Research, 728(1-2), 12-22. http://dx.doi.org/10.1016/j.mrrev.2011.05.001
• Gavrilov, L., & Gavrilova, N. (2001). The Reliability Theory of Aging and Longevity. Journal Of Theoretical Biology, 213(4), 527-545. http://dx.doi.org/10.1006/jtbi.2001.2430
• Gavrilov, L., & Gavrilova, N. (2002). Evolutionary Theories of Aging and Longevity. The Scientific World JOURNAL, 2, 339-356. http://dx.doi.org/10.1100/tsw.2002.
• Gensler, H., & Bernstein, H. (1981). DNA Damage as the Primary Cause of Aging. The Quarterly Review Of Biology, 56(3), 279-303. http://dx.doi.org/10.1086/412317
• Gershon, D., & Gershon, H. (1976). An Evaluation of the ‘Error Catastrophe’ Theory of Ageing in the Light of Recent Experimental Results. Gerontology, 22(3), 212-219. http://dx.doi.org/10.1159/000212136
• Gladyshev, V. (2013). The origin of aging: imperfectness-driven non-random damage defines the aging process and control of lifespan. Trends In Genetics, 29(9), 506-512. http://dx.doi.org/10.1016/j.tig.2013.05.004
• Gladyshev, V. (2014). The Free Radical Theory of Aging Is Dead. Long Live the Damage Theory!. Antioxidants & Redox Signaling, 20(4), 727-731. http://dx.doi.org/10.1089/ars.2013.5228
• Harman, D. (1972). The Biologic Clock: The Mitochondria?. Journal Of The American Geriatrics Society, 20(4), 145-147. http://dx.doi.org/10.1111/j.1532-5415.1972.tb00787.x
• Harman, D. (2009). Origin and evolution of the free radical theory of aging: a brief personal history, 1954–2009. Biogerontology, 10(6), 773-781. http://dx.doi.org/10.1007/s10522-009-9234-2
• Jin, K. (2010). Modern Biological Theories of Aging. Aging and Disease, 1(2), 72-74.
• Kaya, A., Lobanov, A., & Gladyshev, V. (2015). Evidence that mutation accumulation does not cause aging inSaccharomyces cerevisiae. Aging Cell, 14(3), 366-371. http://dx.doi.org/10.1111/acel.12290
• Kennedy, S., Loeb, L., & Herr, A. (2012). Somatic mutations in aging, cancer and neurodegeneration. Mechanisms Of Ageing And Development, 133(4), 118-126. http://dx.doi.org/10.1016/j.mad.2011.10.009
• Kirkwood, T., & Holliday, R. (1979). The Evolution of Ageing and Longevity. Proceedings Of The Royal Society B: Biological Sciences, 205(1161), 531-546. http://dx.doi.org/10.1098/rspb.1979.0083
• Lints, F. (1989). The Rate of Living Theory Revisited. Gerontology, 35(1), 36-57. http://dx.doi.org/10.1159/000212998
• Ljubuncic, P., & Reznick, A. (2009). The Evolutionary Theories of Aging Revisited – A Mini-Review. Gerontology, 55(2), 205-216. http://dx.doi.org/10.1159/000200772
• Magalhaes, J., Costa, J., & Church, G. (2007). An Analysis of the Relationship Between Metabolism, Developmental Schedules, and Longevity Using Phylogenetic Independent Contrasts. The Journals Of Gerontology Series A: Biological Sciences And Medical Sciences, 62(2), 149-160. http://dx.doi.org/10.1093/gerona/62.2.149
• Muller, F., Lustgarten, M., Jang, Y., Richardson, A., & Van Remmen, H. (2007). Trends in oxidative aging theories. Free Radical Biology And Medicine, 43(4), 477-503. http://dx.doi.org/10.1016/j.freeradbiomed.2007.03.034
• Orgel, L. (1963). The Maintenance of the Accuracy of Protein Synthesis and its Relevance to Ageing. Proceedings Of The National Academy Of Sciences, 49(4), 517-521. http://dx.doi.org/10.1073/pnas.49.4.517
• Soares, J., Cortinhas, A., Bento, T., Leitão, J., Collins, A., Gaivã, I., & Mota, M. (2014). Aging and DNA damage in humans: a meta-analysis study. Aging, 6(6), 432-439. http://dx.doi.org/10.18632/aging.100667
• Vaanholt, L., Daan, S., Schubert, K., & Visser, G. (2009). Metabolism and Aging: Effects of Cold Exposure on Metabolic Rate, Body Composition, and Longevity in Mice. Physiological And Biochemical Zoology, 82(4), 314-324. http://dx.doi.org/10.1086/589727
• Van Heemst, D., Beekman, M., Mooijaart, S., Heijmans, B., Brandt, B., & Zwaan, B. et al. (2005). Reduced insulin/IGF-1 signalling and human longevity. Aging Cell, 4(2), 79-85. http://dx.doi.org/10.1111/j.1474-9728.2005.00148.x
• Verzijl, N., DeGroot, J., Zaken, C., Braun-Benjamin, O., Maroudas, A., & Bank, R. et al. (2002). Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: A possible mechanism through which age is a risk factor for osteoarthritis. Arthritis & Rheumatism, 46(1), 114-123. http://dx.doi.org/10.1002/1529-0131(200201)46:1<114::aid-art10025>3.0.co;2-p
• Vijg, J. (2000). Somatic mutations and aging: a re-evaluation. Mutation Research/Fundamental And Molecular Mechanisms Of Mutagenesis, 447(1), 117-135. http://dx.doi.org/10.1016/s0027-5107(99)00202-x
• Walford, R. (1964). The Immunologic Theory of Aging. The Gerontologist, 4(4), 195-197. http://dx.doi.org/10.1093/geront/4.4.195
• Zs.-Nagy, I. (2014). Aging of Cell Membranes: Facts and Theories. Aging, 62-85. http://dx.doi.org/10.1159/000358900

The above is a short perspective by Vit Zemanek. Continue the discussion and analysis on LongeCity's long-running AGING THEORIES forum.

LongeCity science support: quick guide/FAQ

by @ Archive - Articles

Wed Jun 12 17:36:16 PDT 2013

What is LongeCity?
LongeCity is a registered, members-based non-profit organisation.
More info here.


What THEMES of science projects does LongeCity support?
We support research into ageing and the extension of human lifespan. This means we support many types of medical research and research into basic biology, but there should be an angle that will allow people to live longer, healthier lives.


What TYPES of science projects does LongeCity support?
We support laboratory research, clinical research, bioinformatics and theoretical research in the ‘hard sciences’. We do not normally support social science research.
We do support some events, mentorship and travel to scientific conferences, but not under the ‘research budget’.


Where can the research take place?
Anywhere in the world. Laboratory research should normally be conducted in an established lab.


What does LongeCity expect in return?
Scientific integrity. Normally a written report. Interim updates for longer projects. Acknowledgement of the funding received. We may approach previous grantholders to be available as peer reviewers for future research applications.


What grant schemes are available?

a) Small Grants
Funding: up to $500
Who can apply: any LongeCity Member, it helps if you have a sponsor/supervisor with some track record
Type: typical cases are support for summer projects, internships, workshops, review paper writing, selected consumables
Next deadline: none, applications are welcome until the annual budget is exhausted
Details: http://www.longecity...s/action/grants

b) Matching Fundraiser
Funding: up to $20.000 (in total- matching fundraiser)
Who can apply: Scientists
Type: For selected projects, LongeCity will issue a call for donations and for every dollar received LongeCity will match (or better) the donation. The entire money goes to support the research project.
Next deadline: July 1^st 2013
Details: http://www.longecity...ts/research2013


Questions?
Contact us.

Why do some turtles outlive humans?

by @ Articles

Wed Feb 08 16:45:06 PST 2017

(⇒ 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.

Colorectal Cancer Stage 4 Survivors Dill Yogurt Sauce For Recipe Salmon

by @ projectathena probiotics composition

Mon Feb 12 17:26:00 PST 2018

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 […]

Cryonics Hardship Fund

by @ Articles

Fri Jul 18 16:26:34 PDT 2014

Cryonics is a method of ‘medical time travel’ - placing the body in biostasis after legal death with the hope that future technology will be invented which can revive the body. To most people who share LongeCity’s mission cryonics is the ‘second worst thing’ that can happen to you, but nonetheless a viable alternative to burial or creation.

Cryonics prices vary (an overview can be found on this page maintained by Cryonics expert and LongeCity Advisor Ben Best) but it is affordable to nearly everyone via life insurance… nearly everyone. A few people who really want cryonics cannot get life insurance: After an accident, LongeCity Member James Swayze found himself quadriplegic and unable to get insurance. The life of LongeCity Member William O’Rights took a turn for the worst when he was diagnosed with aggressive throat cancer after having been suddenly deprived of all funds. Kim Suozzi was 23 and had not yet heard about cryonics when she was diagnosed with terminal brain cancer. Aaron Winborn heard of her case - and cryonics- only when the debilitating effects of Lou Gehrig's Disease had already begun to paralyse him. All these people were eventually offered a cryonics provision through the generous donations of others in our community.
We want to continue this proud tradition, looking out for those who share our common dream in unlimited lifespans, in the shadow of imminent death and despair.

However, this needs to be done carefully. It cannot be stressed enough that cryonics is affordable to most people if they only have the foresight to act early and arrange affordable life insurance. This element of personal responsibility is at the heart not just of cryonics. If we establish a hardship scheme, it must not create a moral hazard, and incentive to put things off as too unpleasant and complicated to think about until it is too late. Of course, we must also ward against fraud and abuse. An element of careful analysis and due diligence is therefore required, looking into the circumstances of each individual case.

The LongeCity cryonics hardship fund has two purposes:
1) To support a (volunteer based) infrastructure for maintaining the scheme and exercising the due diligence mentioned above
2) When a hardship case has been endorsed by LongeCity, we will use the hardship fund to help to fundraise for that individual by matching further donations. All these donations will go to a dedicated account for that person’s cryopreservation, never to the individual directly.

Applicants to our cryonics hardship fund must
- co-operate fully with LongeCity appointed auditors and reviewers
- genuinely be unable to not fully fund their cryosuspension and not have a reasonable chance of doing so prior to their likely death
- help to fundraise for their cause and help raise public awareness for cryonics

In the past, we have partnered with our friend in the Venturist community on cryonic hardship cases. We hoping to do so again on future occasions.



Click HERE to make a contribution to the fund

To apply email the full details of your case: contact@longecity.org

Probiotics Antifungals Billion 25 -10tm

by @ INSIGHTMARKETING LEVEL

Thu Feb 08 01:24:26 PST 2018

My sister has been in stage 4 since March of 07 she didnt even complete one round of chemo and probiotics for infants babies r us how super take 1800 decided not to do chemo anymore. Probiotics Antifungals Billion 25 -10tm this means that sadly although it is treatable the prognosis may not be as […]

Chapmans Probiotic Frozen Yogurt Cancer Prostate Colorectal Cancer

by @ Probiotics Belaw

Sun Jan 07 14:50:17 PST 2018

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 […]