So how are things coming along with the Open Cures project? (If this is new to you, please do follow that link to see what this is all about).

I should preface this post by noting that my work on any given project tends to take place in waves, and the past couple of months have been a trough of comparatively low activity for Open Cures. The earlier part of this year was a crest in which planning was accomplished, discussions held, an email group and web site site up, posts and articles written, and a few thousand dollars expended to test the waters for paid writing of protocol documents, largely through contractors with life science backgrounds met via the oDesk marketplace. A start, in other words, for something that I anticipate will run at a more modest rate for a number of years.

You never get as far as you'd like in any given period of time, of course, and the rest of the world rarely cooperates by conforming to initial expectations. Since the last update posted here, work on finding reliable authors and writing has proceeded at a slow but steady pace. I'm comfortable with my ability to source these folk now - there are a surprisingly large number of life science graduates and researchers offering their services on the global market for distance work. So the focus has been on establishing high quality baseline documents as examples, templates to help future writers toe the line, and similar issues. One of the slowdowns here has been a matter of dealing with the questions that bedevil the setup for any process: what exactly do we want the results to look like, what is the best way to obtain them, how does it all fall into place in detail.

From an operations perspective, I've shifted most of the ongoing publishing into the Open Cures Wiki: if I'd decided to do that at the outset it would have saved some time in setting up the website, but such is life. I'm presently within striking distance of finishing up the LysoSENS bacterial discovery protocol: a final and rewritten draft is in hand, just not yet posted, and the author will be fixing up the outline to conform with it. A protocol outline for the synthesis of SkQ1, the targeted mitochondrial antioxidant, was completed and posted last month and is awaiting expansion into a full document. There's a nice backlog of other items to be reworked into the final template, and a nice list of research results that I'd like to produce protocols to describe.

I had hoped that the LysoSENS bacterial discovery would prove to be a useful overture to the DIYbio community - it's an interesting project with bacteria and various chemical synthesis activities, well suited as a hobbyist project but one which can assist real, significant research. Watching and interacting with the DIYbio community has led me to think that I'm too early, however, and that they are not going to be particularly receptive any time soon for a range of reasons. Firstly, the movers and shakers are focused on growth and technology over specific projects; they are a small community still, and the most important things for them right now involve producing low-cost and open versions of common technologies (such as OpenPCR), and building shared laboratory spaces to help grow and solidify local groups (such as BioCurious).

Secondly, most of these folk are either disinterested or hostile towards engineered longevity and human rejuvenation as long-term goals. I would guess that this stems in part from the fact that this describes the population in general, and there's no particular reason that a selection of entrepreneurial life science folk should be any different, and in part from the plant biotech / third world farming assistance / environmentalist roots of a fair-sized fraction of the community. They have a tendency to look down on things that they can argue do not primarily help the poor and disadvantaged first; environmentalist hostility towards human longevity is well known and widespread.

Thirdly, the DIYbio community is somewhere between scared and terrified of the possibility of hostile government regulation arriving before they have a large enough community and mindshare to effectively resist it - so there is considerable self-censorship, caution, and opposition to any proposed work with animals, animal cells, or indeed anything that might touch on the heavy regulation that attends professional life science research on the medical side. Similarly, you won't win many friends by having the declared goal of working around the FDA as is the case for Open Cures - and for much the same reasons.

So, in short, I'm thinking that it's too early to expect useful allies there. That community needs to become larger, have listened to what the longevity advocacy community has to say for longer, and Open Cures needs more than just an idea and a website to demonstrate its solidity and useful nature. A nice library of protocols would be a good start, and that's underway at a modest, side-project sort of pace.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Via EurekAlert!: "Research into differentiation has led to a variety of breakthroughs as stem cell researchers harvest cells from one part of the body and genetically adapt them to fulfill a specialized role. However, if the implanted cells are too much like the cells of the targeted area they may not have the plasticity to engraft and repair the injured tissue. ... Stem cell differentiation and transplantation has been shown to improve function in conditions including degenerative diseases and blood supply disorders. However, the survival rate of transplanted cells in patients limits their overall effectiveness, which is a barrier to clinical use. ... To overcome this issue [researchers] explored de-differentiation, a process that reverts specialized, differentiated cells back to a more primitive cell. The team focused their research on multipotent stem cells, (MSCs) which can be altered into a variety of cell types through differentiation. Bone marrow MSCs have the potential to differentiate into each of the three basic types of lineage cells which form bone (osteocytes), cartilage (chondrocytes) and fat tissue (adipocytes). The team first differentiated bone marrow MSCs towards a neuronal lineage, but then removed the differentiation conditions, allowing the cell to revert back to a form with more basic cellular characteristics. Following this process the team recorded increased cell survival rates following transplants. In an animal model de-differentiated cells were found to be more effective in improving cognitive functions and in aiding recovery from strokes, compared to un-manipulated stem cells both in living specimens and in laboratory experiments."

Link: http://www.eurekalert.org/pub_releases/2011-11/w-rsc110111.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

An interesting open access review paper - the full thing is in PDF format only: "The development of materials and technologies for the assembly of cells and/or vesicles is a key for the next generation of tissue engineering. Since the introduction of the tissue engineering concept in 1993, various types of scaffolds have been developed for the regeneration of connective tissues in vitro and in vivo. Cartilage, bone and skin have been successfully regenerated in vitro, and these regenerated tissues have been applied clinically. However, organs such as the liver and pancreas constitute numerous cell types, contain small amounts of extracellular matrix, and are highly vascularized. Therefore, organ engineering will require the assembly of cells and/or vesicles. In particular, adhesion between cells/vesicles will be required for regeneration of organs in vitro. ... adhesive materials and technologies will work as 'glues' for assembling various kinds of cells. The adhesive materials should be degraded when cells themselves biosynthesize cell adhesion molecules ... Although integration of newly developed materials and technologies will be required for the regeneration of organs in vitro, this will ultimately lead to the creation of three-dimensionally engineered organs with functions similar to those of natural organs."

Link: http://dx.doi.org/10.1088/1468-6996/12/6/064703

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

At any given time a whole bunch of cells in your body need to be destroyed before they cause harm - cells that are past the productive stage of their life cycle and have become senescent, cells that are damaged and malfunctioning, and so forth. The majority of these cells are indeed destroyed, either by the immune system or through self-destruction mechanisms that evolved to trigger when vital cellular processes begin to run ragged. But this protective culling fails with age, and the accumulation of cells that should have been destroyed but were not is one of the driving forces of degenerative aging.

This fact is reflected in the proposed apoptoSENS research program, one of the seven branches of the Strategies for Engineered Negligible Senescence. Where the body isn't keeping up with cells that should be destroyed, appropriate forms of biotechnology can could be developed to perform this necessary work - and thereby remove and reverse this contribution to aging. The first array of therapies will probably look much like the targeted cell killing strategies under development in the cancer research community: using bacteria, viruses, nanoparticles, or the patient's own immune system to selectively seek out and destroy cells based on their surface markers.

I see that recent research adds weight to proposals for therapies that will eliminate senescent cells:

Scientists at the Mayo Clinic, in the US, devised a way to kill all senescent cells in [mice genetically engineered to age more rapidly than normal, and therefore accumulate senescent cells more rapidly than normal]. ... when they were given a drug, the senescent cells would die. The researchers looked at three symptoms of old age: formation of cataracts in the eye; the wasting away of muscle tissue; and the loss of fat deposits under the skin, which keep it smooth. Researchers said the onset of these symptoms was "dramatically delayed" when the animals were treated with the drug. When it was given after the mice had been allowed to age, there was an improvement in muscle function.

[The study] suggests if you get rid of senescent cells you can improve [physical traits] associated with ageing and improve quality of life in aged humans.

The caveat here is that these are not normal mice. Animals that suffer accelerated aging are used for the standard cost effectiveness reasons: the researchers were already working with the breed, effects will be easier to find, and can be found in a shorter period of time. Now that the researchers have an effect and a mechanism by which they can reliably destroy senescent cells, the next step is to repeat the study in ordinary mice and see what happens - which will of course take a few years if they want to evaluate the effects on life span as well as health, risk of age-related disease, and so forth.

Here's a link to the research paper and a little detail on how the authors are clearing out senescent cells:

Senescent cells accumulate in various tissues and organs with ageing and have been hypothesized to disrupt tissue structure and function because of the components they secrete. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16Ink4a, to design a novel transgene, INK-ATTAC, for inducible elimination of p16Ink4a-positive senescent cells upon administration of a drug.

The mice used were BubR1 mutants, and you can find an interesting article on that topic at the laboratory website.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

In response to a news item posted yesterday, a commenter asks:

The fact that rejuvenation in mice seems to have been ten years away for around eight years now does not fill me with confidence. I understand of course that those estimates were for a scenario in which SENS had been adequately funded, and that it hasn't come remotely close. ... I want to know how far we are from actually achieving our goals given that funding is likely to continue to be inadequate. Fifteen years? Twenty? Fifty?

Which is a fair question. For reference, the fully funded SENS scenario called for a budget of $100 million per year over ten years the last time I checked, those funds spread between work on the seven categories of repair biotechnology required to prevent and reverse the degenerations of aging. That scenario is proposed to give a fifty-fifty shot at mouse rejuvenation by the end of the ten year period. As the clock keeps ticking without funding at that level materializing, one would expect the cost estimates to fall somewhat over time even if no-one is working on SENS: the cost of research and development in biotechnology is falling across the board, and in addition researchers benefit from a steady rate of progress throughout the fundamental life sciences. Some things that were obscure will become clear and some things that were hard will become easier because of progress in related areas of the broader field.

If SENS work stopped tomorrow and someone were to return to the drawing board ten years from now and run the numbers again, would rejuvenation in mice still be ten years and $100 million? Quite possibly yes on the ten years, and no on the $100 million - I think the cost would be significantly lower. But that doesn't mean it would take less time: as I've argued in the past there is a certain lower limit in the time taken for human endeavors. Organization of large projects, large-scale fundraising, and sequential tasks that depend upon one another can't be brought down below a certain minimum length of time for so long as there are humans in the decision loop. From this perspective, spending tens of millions of dollars on research in a few years is just as large and complex an undertaking as raising venture capital and starting a company - you can't expect to get much of anywhere without it taking a few years, no matter how good your tools and ideas are.

So watching estimated future costs ticking down is one form of progress - but not the one we want to see. The trouble with the question in the comment that I quoted above is that research funded at very low levels is inherently unpredictable:

I would say that the principal cause of uncertainty for the timeline leading to rejuvenation biotechnology - ways to repair and reverse the cellular and molecular damage that causes aging - is the fact that we lack a large, well-funded, well-supported research community at this time. Only comparatively small initiatives exist now, such as the SENS Foundation, and the actions, choices, and happenstance of individuals have large effects on the future timeline leading to the desired solid research community. That future community will be large enough that individual choices don't tend to have much of an effect on its progress one way or another, but here and now the element of chance is significant.

If funding of $100 million per year results in a big enough research group to allow for an averaging of the risks and reasonable predictions for a decade of work, then $1 million a year (the 2010 budget of the SENS Foundation) is far removed from predictability. If that continues for ten or twenty years, who can say what will result - certainly not fully implemented SENS, but my point is that no prediction of the actual resulting science and technology can be reasonable at these levels of funding.

The lesson to take away here is that we should view the SENS research program as a growth endeavor, and success in the long term goal of building a toolkit for human rejuvenation can only come through tremendous growth. These are still the early, formative years in a curve spanning decades. Present small scale work is accomplished to build the case beyond mere advocacy, to prove that the SENS vision leads to positive and useful results at every stage, and to attract greater levels of funding and support and greater numbers of researchers. Early outputs from SENS research will likely be technologies of use in producing therapies for end-stage age-related diseases, for example, or new science that contributes to these ends.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Making therapies that can work in older patients despite their frailty and damage is an important part of progress in stem cell medicine of all sorts: "Age alone no longer should be considered a defining factor when determining whether an older patient with blood cancer is a candidate for stem cell transplantation. That's the conclusion of the first study summarizing long-term outcomes from a series of prospective clinical trials of patients age 60 and over ... the five-year rates of overall and disease-progression-free survival among mini-transplant patients were 35 percent and 32 percent, respectively. Patients in three age groups - 60 to 64, 65 to 69 and 70 to 75 - had comparable survival rates, which suggested that age played a limited role in how patients tolerate the mini-transplant. ... Conventional transplants, which are generally not perfomed on people over age 60 or others who are medically unfit, use high doses of total-body irradiation and potent chemotherapy to eliminate leukemic cells. The intense treatment destroys the blood and immune system and is fatal unless the patient is rescued by infusion of donor bone marrow or stem cells isolated from peripheral blood. The mini-transplant, in contrast, relies on the ability of donor immune cells to target and destroy the cancer - without the need for high-dose chemotherapy and radiation. Instead, low-dose radiation and chemotherapy is used to suppress the immune system rather than destroy it. This helps the body accept the donor stem cells, which then go to work to attack cancer cells - called the graft-vs.-leukemia effect - and rebuild the immune system."

Link: http://www.eurekalert.org/pub_releases/2011-11/fhcr-anl102611.php

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Not having enough natural vitamin E and naturally-produced vitamin D in the body can predispose a person to dementia and cognitive decline.

In a recent Dutch study published in the Journal of Alzheimer’s Disease, it was found that not having enough vitamin E and vitamin D over the long term predisposed a person to cognitive decline and even the psychiatric disorder dementia.

Vitamin E and dementia

The study, which was undertaken by researchers from the Erasmus Medical Center, used questionnaires to track the diet of more than five thousand individual respondents.  The respondents were further tracked for an additional ten years.  Within this period of time, more than four hundred respondents were diagnosed with dementia while more than three hundred respondents developed Alzheimer’s disease.

After analyzing the combined data produced by the five thousand plus test subjects, it was found that an average intake of 18.5 mg of vitamin E reduced the chances of developing the psychiatric disease dementia than those who did not.  Individuals who had developed dementia had an average intake of only 9 mg of vitamin E per day.

According to the researchers, the connection between vitamin E intake and brain health is quite straightforward: the brain is an organ that is in constant metabolic activity.  Organic metabolism produces waste products, including free radicals.  If there are too many free radicals in the brain and too little anti-oxidants in the body, the brain tissue suffers directly from oxidative stress.  Vitamin E and other anti-oxidants can help reduce oxidative stress, which in turn promotes overall wellness and not just brain health.

Vitamin D and cognitive decline

In an unrelated study, researchers from UK’s University of Exeter discovered that individuals who had too little vitamin D were at risk for cognitive decline over the long term.  The study made use of data collected from more than 800 adults in the UK, who were above 50 in age.  Instead of questionnaires, the UK study used actual cognitive tests to measure cognitive stability and decline over a six year period.  They also tested the level of vitamin D present in the blood of the test subjects.

It was found that test subjects who had less than twenty-five nanomoles for every liter of blood had a 60% higher chance of cognitive decline.  According to David Llewellyn, lead researcher, a causal pathway between vitamin D deficiency and cognitive decline has finally been established with the help of their study, which means that cognitive decline can indeed be prevented by increasing the amount of vitamin D in the body.  And the easiest and most natural way to do this is to get direct sun exposure for at least ten minutes everyday.

In a  commentary produced by academics from the University of Auckland, it was said that it was high time that further examinations be performed to find out whether or not the public should be formally made aware of the benefits of vitamin D.

Natural or synthetic vitamin E

There are two main forms of vitamin E available in the market – synthetic vitamin E and natural vitamin E.  While some experts say that it’s basically the same, a study that had been published in the American Journal of Clinical Nutrition begs to differ.

According to the study, natural vitamin E was more bio-available than synthetic vitamin E.  Bio-availability is an important issue when it comes to supplements because it is the direct measurement of how much of a supplement is actually absorbed and used by the body. When there is low bio-availability, the benefits of a supplement are not maximized because only part of the dose is actually absorbed.

Other benefits of vitamin D and vitamin E

Vitamin D

1. Getting enough vitamin D can prevent advanced arthritic conditions from manifesting – you just have to be outdoors a few minutes everyday to keep your vitamin D levels up.  As one ages, the natural vitamin D production decreases, so you have to adjust your lifestyle to increase production during the golden years.

2. Healthy levels of vitamin D can help benefit the cardiac function by regulating blood pressure levels.

3. A link between vitamin D intake and reduction of the risk for multiple sclerosis has been established by numerous independent studies.

4. Vitamin D can help people with chronic pain.  People with fibromyalgia, arthritis and joint pain can also benefit from vitamin D intake.

Vitamin E

1. Vitamin E can keep older women healthy and free from common chronic, degenerative disease, says a study that has been published in the Journal of the AMA.

2. Vitamin E has been shown to slow down the growth of prostate cancer, according to a US study called the SELECT trial.

3. Vitamin E has natural anti-oxidant properties, which reduces oxidative stress and may also help reduce the occurrence of many types of cancer, including breast cancer and prostate cancer.

4. Vitamin E when applied topically can help lighten scars by improving the production of new skin and the formation of collagen, an important component in the skin that makes it resistant to physical stresses and also makes it supple.

400 IU of natural vitamin E per day is recommended for women over the age forty for general wellness and possible cancer prevention.

Sources:
nutraingredients.com
vitamins-nutrition.org
longevity.about.com
heartdisease.about.com
ms.about.com
arthritis.about.com
nutrition.about.com
prostatecancer.about.com
breastcancer.about.com
adam.about.com
altmedicine.about.com
longevity.about.com

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A study published in the February issue of the Chest revealed that vitamin D deficiency is linked to a higher risk of interstitial lung disease.

The Lungs

The principal function of the lungs is to transport the oxygen acquired through breathing to the blood streams and to release carbon dioxide back to the atmosphere. The whole process of respiration is accomplished by tiny specialized cells called alveoli or the air sacs. In the process of breathing, air passes through the nose then travels through the nasopharynx, larynx, trachea and through the branches of the bronchial tubes before finally reaching the aveoli. The diaphragm, on the other hand, is important in driving air to the lungs.

Pulmonary Health Risks

The increasingly deteriorating conditions of the environment make it even harder to keep the lungs healthy. Though the lungs are naturally capable of filtering the air that we breathe, they may not be able to filter toxic materials in the air that may affect our health. This results to lung problems that can be life threatening. Lung cancer, for example, has a high prevalence rate in the United States and other parts of the world.

The number one cause of lung damage is smoking. Numerous studies had found out that smoking can dramatically increase the risk of developing lung cancer and other pulmonary disorders. A single stick of cigarette can contain hundreds of toxins and harmful materials that can directly harm the lungs and other vital organs of the body. Indeed, smoking is bad for the health. Other factors and bad habits can also result to an increased risk of developing lung disease. Inhaling aerosols like paint and deodorants can result to serious damage of the lungs. Vehicles like trucks and cars release toxic fumes that can damage the lungs when inhaled. The lack of sufficient nutrition can also lead to certain lung problems.  A study published in the February issue of the Chest revealed that vitamin D deficiency can increase the risk of interstitial lung disease, a health condition associated with inflammation of the tissues surrounding the air sacs.

Interstitial Lung Disease

The air sacs found in the inner lining of the lungs plays a very important role in extracting oxygen from the air and are supported by a thin lining of tissue. When this tissue becomes inflamed, the function of the air sacs is affected. This health condition of the lungs is called interstitial lung disease. ILD is not limited to certain portions of the lungs but the inflammation can spread all throughout the lungs. Unlike pneumonia, the inflammation of the lungs in interstitial lung disease is not caused by infection but by other factors including the misdirected response of the immune system to infection and toxins like silica dusts and asbestos. Other cases of ILD are idiopathic or with no definite cause.

The first symptom of ILD is difficulty in breathing due to the reduced amounts of circulating oxygen in the body followed by frequent coughing. The condition can be mistakenly diagnosed as pneumonia. Health examinations to conclude ILD include blood tests to rule out infection, imaging studies like CT scans and chest x-rays, PFT or pulmonary function tests and biopsy. Though all these tests are not required in order to determine ILD, some cases may need more examinations that others.

Vitamin D Deficiency and Lung Health

In a study conducted by a team of researchers from the University of Cincinnati College of Medicine, results revealed that vitamin D deficiency can affect the proper function of the lungs. The researchers observed that patients with interstitial lung disease or ILD are mostly deficient in vitamin D especially in patients with connective tissue disease or CTD. They gathered a group of 67 patients with CTD-ILD and 51 patients with other types of ILD and found that the prevalence of vitamin D insufficiency and deficiency is 69 percent and 38 percent, respectively.  Vitamin D plays an important role in maintaining healthy lung function. And aside from keeping the respiratory system in tip-top shape, vitamin D also plays an essential role in other body functions.

Health Benefits of Vitamin D

United States laws require the fortification of all milk brands with vitamin D. So drinking one to two glasses of milk a day can supply the body with its needed dosage of vitamin D to maintain and promote better health. Other rich sources of vitamin D are cream, butter, and other dairy products. Some oysters and fish are also rich sources of vitamin D.

The efficient absorption of calcium in the bones need the assistance of vitamin D. Vitamin D deficiency is commonly associated with rickets in children and osteoporosis in older adults. Too much vitamin D can also have adverse effects to the body since it results to the excessive absorption of calcium which can accumulate in vital organs like the heart and lungs. Muscle weakness, vomiting and the appearance of kidney stones are also linked to too much vitamin D.

Infants and children aged 0 to 13 years need 5 micrograms of vitamin D a day; this recommended daily intake of vitamin D is relatively consistent up to the age of 50 with an increase to 10 micrograms for people 51 years and older.

Natural Ways to Promote Lung Health

Frequent exercise, proper nutrition and avoiding harmful habits are keys to keeping the lungs healthy. Even if the person exercise frequently and is receiving sufficient nutrition, smoking can keep his risk of developing lung disease high compared to sedentary and malnourished non-smokers. It has been well established that smoking can lead to numerous health conditions like lung cancer and other types of cancer. Smoking can also weaken the immune system and make the person more susceptible to infection.

Medical experts advise regular check-ups for the early diagnosis of a lung disorder. Taking the stairs instead of using the lift will also give the lungs a healthy workout if there’s no time to go to the gym. Second hand smoke can damage the lungs more than cigarette does to the actual smoker. So try to stay away from smoky areas and always make it a point to take the non-smokers area in bars and restaurants. Certain household products may also release toxic fumes when used. Make it a habit to always check the labels of household cleaning products before buying or using them.

Sources
medicinenet.com
eurekalert.org
medicinenet.com
nlm.nih.gov
ods.od.nih.gov
rd.com

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A study conducted by a team of researchers from Clemson University in South Carolina found that raspberries have protective effects against cancer.

Raspberries belong to the rose family and are classified as a bramble fruit like blackberry. Its fragrant scent and sweet taste makes it an appetizing ingredient to pastries, sweets and certain dishes. Though raspberries are available in limited supply and are primarily grown in California from June through October, the red berry can be bought fresh or in preserved form at any supermarket. And aside from its succulent and delicious taste, raspberries are also rich sources of an antioxidant called ellagic acid. This nutrient belongs to the group of phytonutrients called tannins and is considered as responsible for the various health benefits of other berries.

The growing interest of different scientific bodies in raspberry roots from its potential in fighting cancer through its antioxidant content. A preliminary study conducted by a team of researchers from the Clemson University, South Carolina observed that raspberry extracts can effectively kill breast, colon and stomach cancer cells by up to 90 percent.

Raspberries Kill Cancer Cells

A study from CU in South Carolina observed how certain cancer cells react to raspberry extract and found that the substance can effectively destroy breast, colon and stomach cancer cells by 90 percent. For years, raspberry has been thought to be a rich source of antioxidants. The new study aims to determine whether there is more to raspberry than its antioxidant content. With their findings, researchers are saying that other substances are also responsible for the raspberry extract’s efficacy in eliminating cancer cells.

The researchers used a popular US variety of raspberries called Meeker red raspberries in their study. They compared their results with the effects of vitamin C, or ascorbic acid, which is a stronger antioxidant. They found that raspberries are eight times more effective in killing cancer cells. Thus, they concluded that other substances in raspberry are helping in destroying cancer cells, and for their next study, the researchers will further investigate on what these substances are.

A related study on the use of raspberry in fighting cancer published in the American Association for Cancer Research found that the anthocyanins from black raspberry can efficiently inhibit the growth of esophageal cancer cells and stimulate them to die through apoptosis. The ellagic acid extracted from raspberry has received greater attention than its other nutrient content. Studies have shown that the nutrient can effectively prevent certain cancers like breast, esophagus, lung, bladder and skin cancer.

Raspberries and its Variety of Health Benefits

With more data providing evidence on the various health benefits of raspberries, people have more reason to have a serving or so on a regular basis. Though nutrients extracted from raspberries are widely available as food supplements, the study that showed that there are other compounds in raspberries that can potentially help in protecting the body from certain cancers suggests eating fresh raspberries instead in order to fully take advantage of everything that this red berry has to offer.

Raspberry is rich in phytonutrients that has anticarcinogenic, antimicrobial and antioxidant properties. As a plain antioxidant, raspberry contains ellagic acid that helps prevent the damage caused by free radicals to cells and cell membranes. Raspberry’s flavonoid content is also as well-researched as its ellagic acid content. Studies have found that the flavonoids in raspberry do not only offer antioxidant protection but they can also prevent the growth of certain bacteria and fungi in the body. Candida albicans, for example, is the primary culprit for the development of vaginal infections and a contributor of irritable bowel syndrome.

Compared to other berries, raspberry contains 50 percent more antioxidants than strawberries, 300 percent more than kiwis and 10 times more than what tomatoes can offer. This information is according to a study conducted by researchers from Netherlands and which was published in an issue of the health journal BioFactors. And like the other studies on raspberries, this is primarily due to its high ellagitanin content.

Raspberries are also packed with different vitamins and minerals that help promote overall health. These are excellent sources of vitamin C and manganese which are two of the most powerful antioxidants that help protect the cells from oxidative damage. Raspberry is also rich in copper, potassium, magnesium, niacin, folate, riboflavin, vitamin B complex and dietary fiber. In addition to this, health professionals are recommending raspberry as a natural alternative to processed sugar in sating people’s craving for sweets, especially to those with diabetic conditions.

A study published in an issue of The Archives of Ophthalmology showed that eating raspberries can help promote eye health. Researchers found that eating 3 or more servings of the red berry a day can significantly reduce the risk of developing ARMD or age-related macular degeneration by more than 30 percent; ARMD is the primary cause of vision loss in older people.

Selecting and Storing Your Berries

Raspberries are highly perishable and it can only be stored for up to 2 days even when kept in the fridge. So always make it a point to purchase only what you can consume for the period. This is also the reason why most people opt to buy preserved raspberries or raspberry food supplements. But since raspberry has a lot more to offer when eaten fresh, it is recommended that you add fresh raspberry to your shopping list. A study published in the Journal of Agricultural and Food Chemistry found that processed foods like canned goods, baby foods, cereals and bread containing raspberries have almost undetectable amounts of anthocyanins and other antioxidants.

Before storing the fruit in your fridge, make sure to remove any molded fruits and other foods may affect the freshness of your berries. Also, pick out any wilted or spoiled raspberry to prevent it from contaminating the others. Since raspberries are often pre-packed, you will likely find spoiled pieces packed together with the fresh ones. And always keep them inside the fridge since putting them in room temperature or exposing them to sunlight will cause the raspberry to become spoiled even before you get the time to eat them. But if you want to keep them longer, raspberries can last for about a year inside the freezer. But make sure to store them in a single layer.

Sources
naturalnews.com
ezinearticles.com
lifestyle.iloveindia.com
whfoods.com

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From the Guardian: "The human body has tremendous capacity to repair itself after disease or injury. Skin will grow over wounds, while cells in our blood supply are constantly being manufactured in our bone marrow. But there is a limit to the body's ability to replace lost tissue. Cartilage cells are notoriously poor at regrowing after injury, for example. As a result, accidents and illnesses - including cancers - often leave individuals with disfiguring wounds or life-threatening damage to tissue. The aim of Molly Stevens, a nanoscience researcher at Imperial College, London, and founder of the biotech firm Reprogen, is a simple but ambitious one. Working with a team of chemists, cell biologists, surgeons, material scientists and engineers, she is developing techniques that will help the body repair itself when it suffers damage. This is the science of regenerative medicine. ... One approach that we have had considerable success with involves taking quite straightforward materials including simple polymers and using them to boost bone growth in a person. We made them into gels that we could inject into bones. The key to this technique lies with the fact that our bones are covered in a layer of stem cells. We inject our material under that layer and that wakes up those stem cells. They start to multiply and produce lots of new bone."

View the Article Under Discussion: http://www.guardian.co.uk/technology/2010/may/16/bright-idea-get-body-grow-spare-parts

Read More Longevity Meme Commentary: http://www.longevitymeme.org/news/

According to a European study, calcium is good not only for the bones of postmenopausal women, but also for their hearts.

In a very recent study presented in the Annual Congress of European League Against Rheumatism, researchers discovered that low levels of calcium  translated not only to weaker, less dense bones for postmenopausal women but it also predisposed the latter to high blood pressure.

According to the researchers, women with low calcium levels were forty-three percent more prone to developing degenerative bone conditions such as osteoporosis.  The same percentage applies to a woman’s risk of eventually developing hypertension.  According to Maria Manara, one of the key researchers, their study establishes the coordinates that associate low intake of calcium with heart problems and bone problems.

Further benefits of getting enough calcium

The RDA for calcium is 990 to 1,000 mg per day for individuals between the ages of nineteen and fifty, according to the National Institutes of Health.  Doses exceeding 2,500 milligrams per day may interfere with the body’s ability to absorb other nutrients.

Here are some more reasons to love your calcium supplements and low-fat dairy products:

1. According to a study published in the American Journal of Epidimiology, taking calcium reduces one’s risk of dying from a sudden heart attack.

2. Taking calcium along with the mineral magnesium may help reduce the risk of males from dying of different causes, including heart problems and certain cancer.

3. Combined with vitamin D supplementation, calcium may also help prevent the onset of prostate cancer.  According to another study, the same potent combination can also help stop colorectal cancer in its tracks.  According to Emory University researchers, laboratory tests show that the two nutrients are capable of normalizing intestinal cells.  The study made use of 2,000 mg of calcium, combined with 800 international units of vitamin D.

4. Based on a study published in Obesity Reviews, regular intake of calcium may help in weight loss efforts. Studies show that calcium increases the amount of fat excretion.  According to Arne Astrup, a researcher from the University of Copenhagen, calcium may also prevent folks from regaining the weight they have already lost.  It was noted that people who had formerly low calcium levels will have enhanced benefits from calcium supplementation.

5. Enough calcium ensures that your muscles will contract and relax efficiently whenever you are on the move.  Calcium deficiency can cause problems like muscle pain and cramps.

6. Having problems with premenstrual syndrome?  Adding calcium to your daily supplementation may help improve the symptoms of PMS.

7. Sufficient calcium also ensures that your teeth will remain firmly anchored in your gums.

Sources:
nutraingredients.com
nutraingredients.com
nutraingredients.com
nutraingredients.com
vitamins-nutrition.org

Discuss this post in Frank Mangano’s forum!

The liver is likely to be one of the earliest human organs grown to order from a patient's stem cells: liver tissue is already far more capable of regeneration than the tissues of other organs, and researchers have been making good progress in recent years in coaxing stem cells to form live tissue. As of today, a press report is doing the rounds to claim that a Japanese group have managed to grow a small functional mass of liver tissue - calling it a liver is no doubt considerably overstating the case, given the small size. Details are somewhat light on the ground, but we'll no doubt hear more soon.

Japanese researchers grow stem cell liver:

Japanese researchers have created a functioning human liver from stem cells, a report says. ... A team of scientists transplanted induced pluripotent stem (iPS) cells into the body of a mouse, where it grew into a small, but working, human liver, the Yomiuri Shimbun said.

A team led by professor Hideki Taniguchi at Yokohama City University developed human iPS cells into "precursor cells", which they then transplanted into a mouse's head to take advantage of increased blood flow. The cells grew into a human liver 5 millimetres (0.2 inches) in size that was capable of generating human proteins and breaking down drugs, the Yomiuri reported.

An abstract of Taniguchi's research was delivered to regenerative medicine researchers ahead of an academic conference next week, but Taniguchi declined to comment to AFP before the meeting.

The liver is a good example of an organ where the real challenges will lie in generating suitable blood vessels throughout the liver tissue and then integrating it with a patient's vascular system - being able to reliably build a mass of liver tissue from stem cells is but the first step on the path. Not that this is unknown; you might take a look at one of the more recent publications from Hideki Taniguchi's team, for example:

Generation of functional human vascular network:

One of the major obstacles in regenerating thick, complex tissues such as the liver is their need for vascularization, which is essential to maintain cell viability during tissue growth and to induce structural organization. Herein, we have described a method to engineer a functional human vascular network.

...

Vascularization is the key challenge to organ generation. We successfully generated human vascular networks inside a matrix. Integration of parenchymal cells using our engineering technique should facilitate future efforts to reconstitute vascularized human organ systems in vitro.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Paul Lewis - Longevity
Longevity - Medicine for Life.

By: Paul Lewis

Here is the original post:
Paul Lewis - Longevity - Video

A human interest piece on research into the genetics and biochemistry of centenarians amongst the Ashkenazi Jewish population: "Irving Kahn is about to celebrate his 106th birthday. He still goes to work every day. Scientists are studying him and several hundred other Ashkenazim to find out what keeps them going. And going. And going. ... The world's oldest stockbroker, he first went to work on Wall Street in 1928. ... Still, a man who at 105 - he'll be 106 on December 19 - has never had a life-threatening disease, who takes no cholesterol or blood-pressure medications and can give himself a clean shave each morning (not to mention a 'serious sponge bath with vigorous rubbing all around'), invites certain questions. Is there something about his habits that predisposed a long and healthy life? (He smoked for years.) Is there something about his attitude? (He thinks maybe.) Is there something about his genes? (He thinks not.) And here he cuts me off. He's not interested in his longevity. But scientists are. ... Pharmaceutical companies and the National Institutes of Health are throwing money into longevity research. Major medical centers have built programs to satisfy the demand for data and, eventually, drugs. Irving himself agreed to have his blood taken and answer questions for the granddaddy of these studies, the Longevity Genes Project at Albert Einstein College of Medicine in the Bronx, which seeks to determine whether people who live healthily into their tenth or eleventh decade have something in common - and if so, whether it can be made available to everyone else."

Link: http://nymag.com/print/?/news/features/ashkenazi-jews-2011-11/

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The immune system falls apart with age in ways that are as much a matter of configuration as wear and tear - it is a machine in which the programming runs awry, leading it to do the wrong things at the wrong time, or just do nothing when it should be doing something. This activity leads to damage, which in turn accelerates aging: "Immune aging is associated with loss of critical immune functions, such as host protection from infection and malignancy. Unexpectedly, immunosenescence also renders the host susceptible to inflammation, which may translate into tissue-damaging disease as the senescent immune system loses its ability to maximize inflammatory protection while minimizing inflammatory injury. On the other hand, chronic inflammation associated with immune-mediated disease represents a profound stress factor for the immune system, affecting cellular turn-over, replication and exhaustion. Immune cell longevity is tightly connected to the functional integrity of telomeres which are regulated by cell multiplication, exposure to oxidative stress and DNA repair mechanisms. Lymphocytes are amongst the few cell types that can actively elongate telomeres through the action of telomerase. In patients with the autoimmune disease rheumatoid arthritis (RA), telomerase deficiency is associated with prematurity of immune aging. Patients with RA have other defects in DNA repair mechanisms, including the kinase Ataxia telangiectasia mutated (ATM), critically involved in the repair of DNA double strand breaks. ATM deficiency in RA shortens lymphocyte survival. Dynamics of telomeric length and structure are beginning to be understood and have distinct patterns in different autoimmune diseases, suggesting a multitude of molecular mechanisms defining the interface between chronic immune stimulation and progressive aging of the immune system."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22396899

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

With advancing age - and accumulating damage - the immune system moves into a state wherein it is constantly roused and on alert, exacting a toll on the integrity of tissue and cells through its signaling and activity, but also ineffective at actually tackling pathogens, senescent cells, precancerous cells, and other things that should be destroyed. So you have constant chronic inflammation and all its downsides with none of the compensatory immune activity boost that comes with short-term inflammation in the young. Researchers have given the name "inflammaging" to this progressive and increasingly harmful disarray of the immune system, and you'll find a few introductions to inflammaging as a concept back in the Fight Aging! archives.

Below is an open access paper that gives an overview of inflammaging and how it relates to some of the forms of cellular damage that cause aging. In this paper, the researchers paint a picture of inflammaging derived from root causes that involve mitochondrial damage and progressive failure of autophagy to clear out that damage, two line items that have been examined a fair number of times here in the past - under the Strategies for Engineered Negligible Senescence (SENS) viewpoint these two are amongst the fundamental, root causes of aging.

Inflammaging: disturbed interplay between autophagy and inflammasomes

In 2000, Franceschi et al. coined the term "inflammaging" in order to refer to a low-grade pro-inflammatory status appearing during the aging process. They emphasized the role of macrophages as well as cellular stress and genetic factors in the generation of the inflammaging condition. In addition, they hypothesized that this inflammatory environment could predispose the organism to the development of several age-related diseases. During recent years, this scenario has been confirmed by a plethora of experimental evidence. ... Interestingly, the aging process is simultaneously accompanied by both the features accelerating inflammaging and the counteracting, so-called anti-inflammaging characteristics. It seems that the balance between these opposite forces controls the outcome of the aging process, either leading to frailty and degenerative diseases or a healthy old age and longevity.

...

The aging process is associated with a decline in autophagic capacity which impairs cellular housekeeping, leading to protein aggregation and accumulation of dysfunctional mitochondria which provoke reactive oxygen species (ROS) production and oxidative stress.

Recent studies have clearly indicated that the ROS production induced by damaged mitochondria can stimulate intracellular danger-sensing multiprotein platforms called inflammasomes. [As a result of inflammasome activity, signaling molecules called] cytokines provoke inflammatory responses and accelerate the aging process by inhibiting autophagy.

There has been some good progress in recent years in pulling things together in the big picture - and the more that we see the mechanisms of SENS featured, the better to my eyes. That ways lies increased support for rejuvenation biotechnology that will actually work to reverse aging, rather than the present mainstream course of aiming to slow down aging just a little sometime in next few decades.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

The future of your health is a matter of chance and likelihood: you have the power to shape that statistical landscape through good lifestyle choices and strategies such as helping to fund research into rejuvenation biotechnology and signing up with a cryonics provider - but nothing is a certainty. You can shift your chances, shift your life expectancy (itself a statistical measure), but you can't entirely remove happenstance and sheer bad luck. You are far better off by making and following good plans, but bad end results are still possible.

For example, even someone who signs up to be cryopreserved and does a good job of managing the organization of his own cryosuspension at the end of life can still be cut short by bad luck:

Alcor member A-1088, Dennis Ross, was pronounced legally dead on Sunday October 30, 2011. A neurocryopreservation, Mr. Ross became Alcor's 108th patient. Alcor received emergency notification that a member in the St. Petersburg, Florida area had been rushed to the hospital on Friday, October 28th and was diagnosed with a massive intracerebral hemorrhagic stroke due to a ruptured brain aneurysm.

Suspended Animation (SA) went to the hospital and began to prepare for a probable cryonics case. Through medical imaging on October 30, physicians determined the individual's brain damage was so extensive they declared him brain-dead. After the family decided to withdraw life support, SA performed field stabilization and attempted washout; however their success was limited due to the compromised blood flow of the brain. SA completed a neuroseparation before shipping the anatomical donation on dry ice to Alcor.

It's important to recognize that, despite best reasonable efforts, the possibility remains that we are going to be betrayed by our own biology in the end. The quote above is an unfortunate example of the type, in which the patient suffered a brain-damaging end of life incident that will greatly reduce the possibility of a good cryopreservation - and that despite high quality support from medical staff and everyone else involved in organizing the response. You'll recall that the point of cryonics is to preserve the fine structure of the brain, within which is the data that makes up the mind - keep that and none of the other damage matters in the long term. But the more neural damage that occurs prior to cooling, the worse the end result will be.

So the best preparation in the world can be sabotaged by the body breaking down in exactly the wrong way at the end of life. All we can do is strive to minimize the risks. In the case of cryonics, many of these late stage risks exist because Western legal systems make it impossible for people and services to collaborate in order to arrange the time and manner of death. Self-determination in end of life choices, and the ability to help people enact those choices, would make cryopreservation of the old and frail far less expensive and far less subject to risk of neural damage. This is just one of countless injustices and losses of freedom inherent in modern governance and law.

But back to the original point: the best we can do is to work to minimize risk. Risk cannot be removed entirely, and we all live in fragile bodies.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

A review paper on one of the trailing areas of tissue engineering - lungs present a harder and more complex challenge than many other organs: "End-stage lung disease is a major health care challenge. Lung transplantation remains the definitive treatment, yet rejection and donor organ shortage limit its broader clinical impact. Engineering bioartificial lung grafts from patient-derived cells could theoretically lead to alternative treatment strategies. Although many challenges on the way to clinical application remain, important early milestones toward translation have been met. Key endodermal progenitors can be derived from patients and expanded in vitro. Advanced culture conditions facilitate the formation of three-dimensional functional tissues from lineage-committed cells. Bioartificial grafts that provide gas exchange have been generated and transplanted into animal models. Looking ahead, current challenges in bioartificial lung engineering include creation of ideal scaffold materials, differentiation and expansion of lung-specific cell populations and full maturation of engineered constructs to provide graft longevity after implantation?in vivo. A multidisciplinary collaborative effort will not only bring us closer to the ultimate goal of engineering patient-derived lung grafts, but also generate a series of clinically valuable translational milestones such as airway grafts and disease models."

Link: http://www.ncbi.nlm.nih.gov/pubmed/22026560

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm

Cryonics industry figure Ben Best attended the fifth SENS conference that was held some weeks back in England, and his report can be read at Depressed Metabolism:

People who attend SENS conferences are the demographic that is the most receptive to cryonics of any identifiable group I have yet found. They are mostly scientists interested in intervening in the aging process.

...

great progress has been made in starting research programs on each of the SENS strategies, and by 2012 research on all the strategies is expected to be in progress.

...

In addition to my oral presentation on cryonics I also had a poster. Scientific conferences usually have poster sessions where scientists present research, reviews, or ideas in the form of a poster. Poster presenters stand by their posters at scheduled times to discuss their work on a one-to-one basis with individuals rather than to an audience. My poster dealt with challenging the concept of biological age and denying the possibility of a biomarker of aging that could determine biological age. I contended that biological age and biomarkers of aging assume a singular underlying aging process, which I denied on the grounds that aging is multiple forms of damage.

His view on biomarkers is an interesting one; you might look back in the Fight Aging! archives for a background on the search for biomarkers of aging - there are a good number of posts on the topic, and it's an area of research that has some importance to the future pace of progress. Absent good biomarkers, it's going to be hard to rapidly tell the difference between a working rejuvenation therapy and a non-working rejuvenation therapy - and time is in short supply.

I did want to draw you attention to a point from Best that I disagree with. He says:

I consider gene therapy to be an essential tool for the ultimate implementation of SENS, and a deficiency of SENS that there is so little attention paid to this technology. I don't see how SENS can be implemented by any means other than genetic re-programming. LysoSENS, for example, would require new genes to create new, more effective enzymes for the lysosomes. MitoSENS would require all mitochondrial proteins be made in the nucleus and imported into the mitochondria.

For mitochondrial repair, agreed, all of the most plausible paths look like gene therapy. The problem that MitoSENS seeks to solve is the accumulation of damage to mitochondrial DNA, and so that DNA either needs to be protected, repaired, or replaced. Fair enough. But I think there will be a wide range of other practical mechanisms for the delivery of necessary enzymes to lysosomes as a part of the LysoSENS program. Recent years have made it clear that biotechnologies other than gene therapy can target small molecules to specific cells and even specific portions of a cell, such as by hijacking normal protein targeting mechanisms or through carefully designed nanocarrier structures. I would agree that an ultimate implementation would be one that is always on - an unambigiously beneficial genetic change to allow lysosomes to digest what is presently indigestible and which will be passed on to future generations. But it seems far more likely that initial implementations will be periodic clinical treatments - injections and infusions - designed to flush the body's lysosomes with enzymes for a short period of time, and thereby clean them out. This would seem to be sufficient, given that we humans manage three decades of life at the outset without the obvious degenerations of aging starting to show up.

Source:
http://www.longevitymeme.org/newsletter/latest_rss_feed.cfm