A recent open access paper from a Spanish research group outlines yet another methodology to add to the growing list of ways to increase healthy life span in mice. Progress is signified by diversity these days; there are, I think, more than twenty different demonstrated methods of bringing about meaningful extension of life in mice as of today.

RasGrf1 deficiency delays aging in mice:

We observed that mice deficient for RasGrf1-/- display an increase in average and most importantly, in maximal lifespan (20% higher than controls). This was not due to the role of Ras in cancer because tumor-free survival was also enhanced in these animals.

Aged RasGrf1-/- displayed better motor coordination than control mice. Protection against oxidative stress was similarly preserved in old RasGrf1-/-. IGF-I levels were lower in RasGrf1-/- than in controls. Furthermore, SIRT1 expression was increased in RasGrf1-/- animals. Consistent with this, the blood metabolomic profiles of RasGrf1-deficient mice resembled those observed in calorie-restricted animals.

...

Our observations link Ras signaling to lifespan and suggest that RasGrf1 is an evolutionary conserved gene which could be targeted for the development of therapies to delay age-related processes.

The results are similar to those noted for PAPP-A knockout mice - both longer lives and less cancer. At this stage it's anyone's guess as to whether many of these methodologies in fact operate through the same thicket of connections and mechanisms in mammalian biochemistry. Time, and further research, will tell.

RasGrf1 was mentioned here last year in connection with the intriguing bi-maternal mice:

mice artificially produced with two sets of female genomes have an increased average lifespan of 28%. Moreover, these animals exhibit a smaller body size, a trait also observed in several other long-lived mouse models. One hypothesis is that alterations in the expression of paternally methylated imprinted genes are responsible for the life-extension of bi-maternal mice. Considering the similarities in postnatal growth retardation between mice with mutations in the Rasgrf1 imprinted gene and bi-maternal mice, Rasgrf1 is the most likely culprit for the low body weight and extended lifespan of bi-maternal mice.

This latest work adds weight to the supposition quoted above.

The modest goals of the mainstream longevity science community are outlined by one of its members in this article - to enable everyone to age as slowly as only some people presently do. No radical life extension or rejuvenation, as would be enabled by the damage repair approach to longevity science, but rather just a gentle slowing of aging, enabled by technologies that would probably not emerge in time to benefit those of us in middle age today. "It is the aging of our cells that causes us to develop most diseases, says Dr. Nir Barzilai, professor of medicine and genetics at the Albert Einstein College of Medicine in New York. 'We know this, paradoxically, because of the amazing success we have had in treating heart disease. We have been able to save people from heart attacks with stents and bypass surgery - only to find that within a year or two they develop Alzheimer's, diabetes or cancer at an alarming rate. Why? Because we have never treated the underlying aging of their cells. We have simply treated the disease manifestation.' So, explains Barzilai, if we can find the processes in the body that control aging and find a way to treat them, we will be able to protect people from the diseases of aging. Barzilai heads a unique longevity study of more than 500 people who have reached the age of 100. The LonGenity study is looking at the genetic makeup of centenarians to identify the biological markers that explain why they live so long and so well. Because the remarkable thing about these people is not simply that they live to the age of 100, it is that they live to 100 in pretty good health. Just why they live that long without getting sick and dying is what Barzilai wanted to find out."

Link: http://www2.macleans.ca/2011/03/17/living-like-a-centenarian/

Via EurekAlert!: "A gene therapy called NLX-P101 dramatically reduces movement impairment in Parkinson's patients, according to results of a Phase 2 study ... The approach introduces a gene into the brain to normalize chemical signaling. ... The study is the first successful randomized, double-blind clinical trial of a gene therapy for Parkinson's or any neurologic disorder ... Half of patients receiving gene therapy achieved dramatic symptom improvements, compared with just 14 percent in the control group. Overall, patients receiving gene therapy had a 23.1 percent improvement in motor score, compared to a 12.7 percent improvement in the control group. ... Improved motor control was seen at one month and continued virtually unchanged throughout the six-month study period. ... Gene therapy is the use of a gene to change the function of cells or organs to improve or prevent disease. To transfer genes into cells, an inert virus is used to deliver the gene into a target cell. In this case, the glutamic acid decarboxylase (GAD) gene was used because GAD makes a chemical called GABA, a major inhibitory neurotransmitter in the brain that helps 'quiet' excessive neuronal firing related to Parkinson's disease. ... In Parkinson's disease, not only do patients lose many dopamine-producing brain cells, but they also develop substantial reductions in the activity and amount of GABA in their brains. This causes a dysfunction in brain circuitry responsible for coordinating movement."

Link: http://www.eurekalert.org/pub_releases/2011-03/nyph-gtr031411.php

Via EurekAlert!: "A gene therapy called NLX-P101 dramatically reduces movement impairment in Parkinson's patients, according to results of a Phase 2 study ... The approach introduces a gene into the brain to normalize chemical signaling. ... The study is the first successful randomized, double-blind clinical trial of a gene therapy for Parkinson's or any neurologic disorder ... Half of patients receiving gene therapy achieved dramatic symptom improvements, compared with just 14 percent in the control group. Overall, patients receiving gene therapy had a 23.1 percent improvement in motor score, compared to a 12.7 percent improvement in the control group. ... Improved motor control was seen at one month and continued virtually unchanged throughout the six-month study period. ... Gene therapy is the use of a gene to change the function of cells or organs to improve or prevent disease. To transfer genes into cells, an inert virus is used to deliver the gene into a target cell. In this case, the glutamic acid decarboxylase (GAD) gene was used because GAD makes a chemical called GABA, a major inhibitory neurotransmitter in the brain that helps 'quiet' excessive neuronal firing related to Parkinson's disease. ... In Parkinson's disease, not only do patients lose many dopamine-producing brain cells, but they also develop substantial reductions in the activity and amount of GABA in their brains. This causes a dysfunction in brain circuitry responsible for coordinating movement."

Link: http://www.eurekalert.org/pub_releases/2011-03/nyph-gtr031411.php

A recent early stage trial demonstrated that first generation autologous stem cell transplants should be beneficial even if provided long after a serious damage has occurred. Large numbers of transplanted stem cells, grown over a period of weeks from a patient's own cells, can spur the body to heal injuries that would normally linger:

Heart Damage Improves, Reverses After Stem Cell Injections in a Preliminary Human Trial:

Researchers have shown for the first time that stem cells injected into enlarged hearts reduced heart size, reduced scar tissue and improved function to injured heart areas ... while this research is in the early stages, the findings are promising for the more than five million Americans who have enlarged hearts due to damage sustained from heart attacks. These patients can suffer premature death, have major disability and experience frequent hospitalizations. Options for treatment are limited to lifelong medications and major medical interventions, such as heart transplantation

...

Using catheters, researchers injected stem cells derived from the patient's own bone marrow into the hearts of eight men (average age 57) with chronically enlarged, low-functioning hearts.

"The injections first improved function in the damaged area of the heart and then led to a reduction in the size of the heart. This was associated with a reduction in scar size. The effects lasted for a year after the injections, which was the full duration of the study,"

...

"This therapy improved even old cardiac injuries. [Some] of the patients had damage to their hearts from heart attacks as long as 11 years before treatment."

This is generally good news for people who presently bear injuries and damage - or expect to suffer damage in the years between now and when stem cell medicine is in its prime. The most plausible future outcome looks to be that even the early stage and comparatively crude transplant therapies will provide significant benefits above and beyond any present form of medicine.

Of course, they would arrive far more rapidly and be far less costly in a world absent the FDA - but there is always medical tourism. A range of stem cell therapies that are presently forbidden from commercial development in the US have been available for several years elsewhere in the world:

The FDA forbids the development of new medical technologies long past the point at which any sane person would consider them a good risk, and in the process makes these technologies vastly more expensive. Medical tourism is a sane response to heavy-handed and unaccountable government employees: "Gregg Victor is one of the 1.5 million Americans who traveled abroad to get medical treatments last year. ... More than a few were pursuing new stem-cell-based treatments unavailable in the States ... 'I am not waiting for the FDA to rule to get treatments,' says Gregg Victor, who chose her clinic in Germany after spending a year and a half looking into stem cell treatments available all over the world. ... Jordan happened upon TheraVitae, a Bangkok-headquartered biotechnology company that markets 'VesCell stem cell treatments' via licensing agreements with four clinics in Thailand ... Thai doctors injected 25 million of his own stem cells into Jordan's heart. Twenty thousand miles, 22 days, a cardiac arrest and $43,000 later, he came home to his wife with an ejection fraction between 30% and 35%. Even Jordan's doctor had to admit he was happy with the results." Results are mixed, much as you'd expect. Caveat emptor, and do your research - but a great many people are materially benefiting from technologies still forbidden by their own governments.

Researchers recently demonstrated that increased cellular housekeeping could slow neurodegeneration, and here a different group show the same outcome: "Cells, which employ a process called autophagy to clean up and reuse protein debris leftover from biological processes, were the original recyclers. A team of scientists [have] linked a molecule that stimulates autophagy with the reduction of one of Alzheimer's disease's major hallmarks, amyloid peptide. Their finding suggests a mechanism that could be used to eliminate built-up proteins in diseases such as Alzheimer's, Down syndrome, Huntingdon's and <a href="http://en.wikipedia.org/wiki/Beta_amylo&quot; the="The" molecule,="molecule," called="called" smer28,="SMER28," spurs="spurs" autophagy,="autophagy," which="which" in="in" turn="turn" eliminates="eliminates" unwanted="unwanted" materials="materials" such="such" as="as" amyloid-beta, the protein aggregates that cause Alzheimer's plaques. Increasing autophagy, either through a drug or a natural process such as diet, could improve the outcome for people with neurodegenerative diseases ... The researchers [tested] various compounds for their ability to reduce the buildup of amyloid-beta by exposing cultured cells to compounds known to activate autophagy. They then compared the effect of these compounds by removing growth factors from the culture medium, a well-established stimulant of autophagy known as 'starvation.' The researchers found that SMER28 was the most effective compound, and focused their studies on it to characterize the cellular components involved in this phenomenon. They compared the effect of SMER28 on amyloid-beta formation using normal cells or cells where the expression of genes known to be involved in autophagy was reduced or abolished. They found that three important autophagic players were involved, and one of them was essential for SMER28's effect."

Link: http://www.eurekalert.org/pub_releases/2011-03/ru-mts031611.php

The present generation of therapies for rheumatoid arthritis are based on TNF inhibition - a fairly crude manipulation of the immune system when considered in the grand scheme of what is possible, but one that is getting better. From Technology Review: "A new protein engineered to inhibit molecules that cause inflammation not only reduces symptoms of rheumatoid arthritis in mice but also may have potential to reverse the disease's course. Researchers hope the findings will point toward a new therapy for this crippling and difficult-to-treat disease, which occurs when the immune system attacks the body's own joints. Even medications that are most successful in halting joint inflammation are effective in only about half of the patients who try them. ... The new synthetic protein [appears] to target TNF in a far more specific fashion and could be produced at a small fraction of the cost [of present TNF inhibitors]. ... a protein called progranulin binds to TNF receptors and that administering the protein to mice with rheumatoid arthritis reduced or even eliminated their symptoms. Then they determined which fragments of progranulin were responsible for binding to TNF and combined those fragments to engineer a protein that works even better to suppress disease. Mice with mild arthritis appeared to be disease-free after several weeks of regular injections of the modified progranulin."

Link: http://technologyreview.com/biomedicine/35091/

The Global Forum for Longevity is an industry-sponsored forum taking place later this month; fairly mainstream, no talk of radical life extension or other forms of futurism that might lead to intellectual discomfort for some. I mention it because it is a symptom of the growing interest in biogerontology on the part of the vast insurance industries of the world - which should not be a surprising phenomenon. To find people likely to pay close attention to the future of longevity science, you want to look amongst the folk who stand to gain or lose a great deal of money due to changes in human life spans. Life insurance, pensions, and other forms of making money through managing statistical risks on life expectancy data are, taken together, a very big business indeed.

So here an insurance conglomerate is, as many of them are, sponsoring an event to help spread knowledge through the system: from scientists to actuaries to risk managers and other decision makers in the food chain. Building bridges and forming communities is in and of itself a form of risk management in the long term: it is a way to lower the likelihood of unpleasant surprises by trying to better understand what the scientific community believes are likely outcomes for longevity science over the decades ahead.

Some quotes from the conference site:

We are living in an era of radical change. Longevity offers us all an opportunity to make more ambitious life choices and look to the future with renewed hope. This is why it is vitally important that we move quickly to meet the challenges which it poses for our society.

Drawing on its expertise as an insurer, AXA is playing its part by creating a space to convene an exchange between decision-makers and experts working to ensure this phenomenon is better defined and fully grasped: the Global Forum for Longevity.

...

Our conviction as an insurer and observer of demographic and societal changes worldwide, is that longevity is not a fate to be endured but instead an opportunity. We need to respond quickly in order to meet the challenges which it poses to our society.

"Challenges." One thing to bear in mind here is that the big insurance groups are inextricably tied in to the unsustainable pension promises made by politicians past and present in many countries around the world - unsustainable even with modest increases in longevity, never mind what is likely to result from the biotechnology revolution. So there is a certain amount of long term public relations work being undertaken by various parties so as to avoid becoming the sacrificial goat in the end when the system of entitlements collapses. You can make your own decision as to how much of the motivation behind this conference falls into that bucket versus the knowledge transfer aims discussed above.

Empires end when an entrenched elite can spend from the public purse and take on debt without immediate consequence or forethought, destroying the value of their currency in the process. Assuming (perhaps optimistically) that present economic empires survive the next couple of decades, a combination of foolish promises and increasing human longevity will be the rock that sinks them.

Nanotechnology can be used to build assemblies of designed molecules that seek out specific cells - such as cancer cells - but an alternative approach to targeted therapies is to build machinery large enough to be controlled from outside the body, such as the microcarriers demonstrated here: "Soon, drug delivery that precisely targets cancerous cells without exposing the healthy surrounding tissue to the medication's toxic effects will no longer be an oncologist's dream but a medical reality ... sing a magnetic resonance imaging (MRI) system, [researchers] successfully guided microcarriers loaded with a dose of anti-cancer drug through the bloodstream of a living rabbit, right up to a targeted area in the liver, where the drug was successfully administered. This is a medical first that will help improve chemoembolization, a current treatment for liver cancer. ... The therapeutic magnetic microcarriers (TMMCs) [are made] from biodegradable polymer, [measure] 50 micrometers in diameter - just under the breadth of a hair - [and] encapsulate a dose of a therapeutic agent (in this case, doxorubicin) as well as magnetic nanoparticles. Essentially tiny magnets, the nanoparticles are what allow the upgraded MRI system to guide the microcarriers through the blood vessels to the targeted organ. During the experiments, the TMMCs injected into the bloodstream were guided through the hepatic artery to the targeted part of the liver where the drug was progressively released."

Link: http://www.eurekalert.org/pub_releases/2011-03/pm-wf-031511.php

Because veterinary medicine is less (oppressively) regulated than human medicine, animals are benefiting from stem cell therapies that are safe enough for human use but nonetheless still illegal to commercially develop in the US: "In a very unusual breakthrough, a stem cell treatment for racehorses is ready to be tried ... on you. British scientists pioneered a technique in horses where an individuals' own stem cells are grown outside the body, then injected into the damaged tendon. There will be a clinical trial in the UK in which 24 human patients will undergo this radical new stem cell treatment for similar tendon injuries. We'll tell you about the proven benefits in racehorses so you'll understand the possible benefits in people. The test subjects who join the clinical trial will be in the unique position of enjoying a medical procedure that is years behind the veterinary equivalent. If human beings have the same barely believable 80% recovery rate, this will be a leap forward for sports medicine. ... The reason animals can get commercial drugs and treatments faster than people in the US and other Western countries is simple: there is enormous oversight in human medical research. Veterinary research is comparably simple. According to the FDA, bringing a new drug to market for humans requires pre-clinical laboratory tests, animal tests, and human clinical trials. Each one of those steps costs money, lots and lots of it. Approval for veterinary drugs is simpler, requiring a single study that proves the drug is safe and effective. Because of regulatory difference, progress on animal medical research can move very quickly compared to human research."

Link: http://singularityhub.com/2011/03/10/uk-stem-cell-company-cures-race-horse-tendons-humans-next/

I notice that Science Progress has thoughtfully posted an overview of a book that, like so many, passed beneath my distracted field of vision. It's a good overview, and in reading it I'm struck by just how greatly modern fields of intellectual study have devolved into the title of this post - efforts to find smart ways to say profoundly stupid things. This isn't the aim and goal at the outset, of course, but with postmodernism leading the way, there is a well defined sort of style that accompanies the ability of a community of intellectuals to cut themselves off from rationality and evidence in order to build castles in the sky. Up becomes down and left becomes right, and all sorts of nonsense rises to rule the roost. The end result is a core of stupidity well wrapped by a tremendous expenditure of earnest intellectual effort: a sort of Emperor's new clothes situation wherein few parties involved have any incentive to point out the obvious.

Outside of theology and the worst reaches of postmodernism, this disconnect from reality is perhaps most evident in modern macroeconomics - largely an effort to convince the world against all the evidence that up is down and black is white - and the various fields of ethics, such as bioethics. The bioethics community in particular long ago lost its way.

But back to some examples from that Science Progress piece:

When I say that here, too, Agar builds his argument on an appeal to nature, I have in mind his foundational premise regarding what he calls "species relativism." The "relativism" part of that label might at first sound like a rejection of anything resembling an appeal to nature. But Agar holds that there is something good, something worth preserving, about the way members of our species typically or naturally find happiness. As he puts it, "Experiences typical of the ways in which humans live and love are the particular focus of my species-relativism" (pg.15).

So for an enhancement to count as moderate on Agar's account, it has to be "relative" to our species. As distinct from a radical or "purported" enhancement, a moderate one has to enhance a way of being that is typical of homo sapiens.

...

He argues that, while it is indeed reasonable to want more of "a recognizably human life," it is not reasonable to want a form of life without the sorts of experiences that are typical for members of our species. As he says, there are some Galapagos tortoises that live up to 150 years, and they no doubt enjoy experiences that are pleasurable for members of their species, but no human being would trade our "distinctively human varieties of pleasure" for distinctively tortoise varieties of pleasure. Because, however, he grants the respect in which that example is unfair - becoming a tortoise would entail diminished cognition and radical life extension would not - he needs to say more.

He begins by suggesting that de Grey's "Strategies for Engineered Negligible Senescence" (SENS) might create an obsessive fear of death, which might come to completely dominate the lives of those who adopted such strategies. Agar worries that, because negligibly senescent people would have more years of life to lose if they failed in one of their projects, they would have a strong reason not to take any risks at all (pg. 116). Indeed, at this point he invokes the concern that later in the book he will call its central theme: the concern about alienation, about becoming separated from the kinds of, here, risky experiences that constitute human lives as we know them. According to Agar, de Grey's ambition to radically extend our lives "is likely to alienate us from the things and people who currently give our lives meaning" (pg. 122).

Agar allows that there may appear to be a way around the obsessive fear of death that SENS could bring about. To get around the risks associated with going out into the real world, he allows, negligibly senescent people could use technologies to have virtual experiences instead. But the problem with that strategy, he says, is that it fails to appreciate the extent to which human beings want "direct" contact with the "real" world. It fails to appreciate that "We think differently about these kinds of indirect contact [with the real world] than we do about 'being there.'" No one, he suggests, thinks that "seeing a Discovery Channel documentary filmed on Mount Everest substitutes for actually climbing it" (pg. 123).

Castles in the sky, and straw ones at that. I would hope that little needs to be said in response to this sort of thing - it is so self-evidently hollow, a gut feel trying to cover itself in words and failing, that it falls apart at a glance.

A study conducted by researchers from the Ohio State University found that selenium can reduce specific markers that increase the risk of prostate cancer.

The Dreaded Prostate Cancer

The average age of prostate cancer diagnosis is 67 years old.  This is according to the National Cancer Institute Surveillance and Epidemiology and End Results Center; this is based on the incidence of prostate cancer in the United States from 2003 to 2007. Based on the same data, more than 16 percent of men will be diagnosed with prostate cancer in their lifetime. In the United States alone, it is estimated that more than 210,000 men will be diagnosed of prostate cancer and over 32,000 will die of the dreaded condition.

There are no assured means of preventing prostate cancer. But making smart choices in the foods that you eat and avoiding the risk factors associated with it can help in preventing the disease. Like other types of cancer, prostate cancer starts when cells begin to behave abnormally. It is clear that this behavior of the cells is caused by the mutation of the genes but researchers are still trying to better understand what causes and what triggers the mutation.

Lowering the risk of prostate cancer will take a little more than just diet modification. Taking bigger steps like changing your lifestyle and avoiding cancer-inducing habits may help in reducing your risk. Studies show that lifestyle intervention is the best approach in preventing prostate cancer and other diseases for people with heightened risk.

Natural Ways to Lower Your Risk

The nutritional guidelines for preventing prostate cancer is yet to be established. But so far, studies show that specific eating habits are linked to a lowered risk of developing the disease. Eating a variety of fruits and vegetables can supply the body with essential nutrients that helps in preventing different kinds of cancer.  Food sources rich in cancer-fighting substances like folate, vitamin B complex and diindolylmethane, which is found in cruciferous vegetables like kale, cabbage and broccoli, are well-recommended.  Sensible eating means balancing your calorie intake according to your body’s requirement.

The incidence of prostate cancer varies in different countries. Studies show that the highest rate appears in populations with the highest intake of fat. Foods rich in saturated fats, like those found in red meats, can increase the risk of developing prostate cancer. Eating whole-grain foods like whole-wheat breads and brown rice while limiting the consumption of refined sugar and white flour can also help in preventing the disease.

Eating foods rich in omega-3 fatty acids is also linked to a lower risk of developing prostate cancer. Omega-3 is found in salmon, mackerel, herrings and other cold-water fishes. Although there are mixed scientific evidence regarding the potency of omega-3 in lowering the risk of developing cancer, adding foods rich in the nutrient into your daily diet offers other health benefits like the prevention of cardiovascular disease.

Soybean products and other legumes are rich in phytoestogens, an enzyme found in plants that act like estrogen in the body. These chemicals can help reduce the risk of prostate cancer. A good evidence for this is the low incidence of prostate cancer in Asian countries where soybeans and soybean products are popular food choices.

Green tea contains various antioxidants like polyphenols that has been found to lower the risk of developing cancer. Vitamin D, on the other hand, has also showed strong potential in lowering the risk of developing prostate cancer. Foods rich in vitamin D are egg yolks, and fish liver oil. Exposing the skin to the sun for a few minutes a day will also trigger the production of vitamin D in the body.

The high incidence of prostate cancer drives state and privately-funded studies to determine better ways to prevent the disease. Researchers are also looking at the potency of some nutrients in fighting prostate cancer risk. A study conducted by researchers from the Ohio State University found that the supplementation of selenium can lower the levels of prostate cancer markers such as prostate specific antigen (PSA) and help in reducing the risk of the disease.

Selenium to Lower the Risk of Prostate Cancer

A study published in the Nutrition Research journal showed that selenium glycinate can improve the activities of plasma enzymes and reduce the levels of prostate cancer markers. The researchers from the Ohio State University said that the regular supplementation of selenium in a group of 30 middle-aged Americans resulted to a reduced risk of developing prostate cancer. They added that their study contradicts the popular notion that selenium cannot improve the activity of blood glutathione peroxides and lower the risk of prostate cancer.

Head researcher Dr Robert DiSilvestro of the Department of Human Nutrition and his co-authors said that if selenium has the ability to lower prostate-specific antigens in study participants, it can also lower the risk of prostate cancer.  This could be better achieved by introducing the nutrient in daily diet. They used a certain form of selenium called selenium glycinate which has not been used in previous studies. The researchers added that selenium glycinate has significantly high bioactivity.

The researchers reported that the supplementation of selenium raised the levels of erythrocyte and plasma activities in study participants. They also found that cancer risk marker serum PSA was lowered by selenium glycinate. But they added that the reduction in prostate cancer markers does not necessarily mean a lower risk of developing the disease.

Health Benefits of Selenium

Selenium is a mineral present in the soil and which appears in small amounts in some foods and in water. The nutrient plays an important role in metabolism and recent studies show that selenium has strong antioxidant properties. Although there are some evidences suggesting that high levels of selenium can increase the risk of skin cancer, regulated levels of the nutrient can result to a lower risk of developing various diseases. Population studies show that selenium deficiency is rare in healthy people.

The Recommended Dietary Intake of selenium for adults and children aged 14 years and above is 55 to 70 micrograms in a day. For the prevention of prostate cancer, men can take as much as 200 micrograms a day. But the threshold for selenium intake should be no more than 400 micrograms; anything beyond this is considered an overdose. Selenium has been used as a treatment for asthma, infertility and arthritis. But more importantly, selenium can act as an antioxidant which neutralizes cancer-causing free radicals and at the same time improve the potency of other antioxidants.

Sources
nutraingredients.com
webmd.com
webmd.com
mayoclinic.com
seer.cancer.gov

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A study published in the Journal of Nutrition showed that the antioxidants in pecans can lower the risk of heart disease.

Heart Disease

Heart disease is a term used to refer to a variety of health conditions that involves the heart. It is often interchanged with cardiovascular disease which is commonly used to define the condition involving the narrowing of the blood vessels that can lead to chest pains, heart attack and stroke. Unlike cancer and other chronic diseases wherein the causes remain to be unclear, the causes of heart diseases are well-established and the condition can be prevented by making healthy lifestyle choices.

Most diseases are caused by the damage caused by the accumulation of fatty plaques in the arteries. The arteries are responsible for carrying nutrients and oxygen to different parts of the body. In order to properly perform these tasks, the arteries need to stay strong and flexible. Aging and poor, unhealthy habits can put too much pressure in the arteries and make the walls stiff, weak and thick with fatty plaques. This disorder will lead to the insufficient distribution of blood in organs and tissues. Because of this, nutrition and oxygenation are compromised.

Atherosclerosis, or the hardening of the arteries caused by deposition of fatty plaques, is the most common cardiovascular disease. The other heart conditions are heart arrhythmia, or abnormal heart rhythms, cardiomyopathy or the enlargement and thickening of the heart muscle, heart infection and valvular heart diseases.

Although heart diseases are caused by different factors, studies show that they are primarily due to unhealthy diet and habits, and lack of exercise.

The Risk Factors of Heart Disease

Getting older increases the risk of heart disease. The heart and blood vessels become more at risk of damage. Men are also more at risk of developing the disease than women although a woman’s risk is increased after menopause. Certain heart diseases are also caused by genetic factors. The condition can run in the family and some individuals can be more inclined of developing the condition than others.

Smoking has always been proven to be bad for the health. Nicotine in tobacco can constrict the blood vessels, making blood flow difficult resulting to an increase in blood pressure, while its carbon monoxide content can damage the lining and make them more at risk of damage. Population studies show that the incidence of heart disease is higher in smokers than in non-smokers.

A diet rich in sodium and harmful fats can lead to the development of heart disease. Hypertension, or chronically high blood pressure, can cause the blood vessels to become thick and hard. The accumulation of cholesterol plaques on the walls of the arteries can inhibit the healthy flow of blood and cause serious complications. The other risk factors of heart disease are obesity and diabetes – two health conditions that share similar risk factors: the lack of exercise, poor eating habits and high stress levels.

The risk factors of developing heart disease can be countered by healthy lifestyle choices. Eating the right kinds of food, for example, will supply the body with the nutrients needed to maintain a healthy heart and prevent damage. A study conducted by researchers from Loma Linda University School of Public Health found that the antioxidants in pecans can contribute in the prevention of heart disease.

Pecans Against Heart Disease

The study published in the Journal of Nutrition showed that pecans contain potent antioxidants flavan-3-ol and gamma-tocopherol that helps in lowering the risk of heart disease. The researchers said that these compounds can double the amount of antioxidants in the blood plasma and inhibit the oxidation of LDL cholesterol by more than 30 percent. Head researcher Dr Ella Haddad said that the consumption of pecans can improve the levels of antioxidants in the body and added that antioxidants are needed in order to prevent diseases like cancer and heart disease.

The researchers explained in their study that pecan is a good source of various kinds of vitamin E, especially in the form of tocopherols. This is in addition to its phenolic content which also has antioxidant properties. Formation of plaque on the surface of the blood vessels is primarily due to the high concentration of oxidized LDL cholesterol in the blood. The antioxidants in pecan can help in lowering oxidized LDL cholesterol levels by preventing oxidation. The researchers said that the bioactive content of pecans like flavan-3-ol monomers and gamma-tocopherol exhibit strong antioxidant action in vitro but it has not been established whether this is the case in the human body. The study aimed to investigate and measure the antioxidant effects of pecans after ingestion.

Blood and urine samples were taken from 16 study participants. Prior to these, they were randomly assigned three meals with pecans blended with water, whole pecans and a control meal with equivalent nutritional content. And in between each treatment was one week of washout period.  Study participants who ate meals with whole and blended pecans doubled their gamma-tocopherol blood levels after eight hours. The researchers also observed that the oxidation of LDL cholesterol was reduced by 33 percent after 3 hours. The researchers concluded that their findings are another addition to the health benefits of pecans in preventing various diseases and that the antioxidants in pecans can be absorbed and used by the body.

Natural Ways to Lower Heart Disease Risk

Eating foods rich in dietary fiber and antioxidants, low in sodium and LDL cholesterol, and regular exercise are a few of the lifestyle choices you can make in order to lower your risk of developing heart disease. Dietary fiber helps prevent the absorption of cholesterol.

A high sodium diet can make the blood thicker and increase blood pressure. It has also been linked to a higher risk of developing cardiovascular disease. According to the American Heart Association, the recommended sodium consumption should not be greater than 2,300 milligrams or approximately 1 teaspoon a day. For those with existing heart conditions, only 1500 milligrams of sodium is recommended. Avoiding foods and processed products that are rich in sodium as well as carefully avoiding the use of condiments that are sodium-rich can help in reducing your sodium intake.

Avoid foods rich in saturated and trans fats. These foods can increase the LDL cholesterol levels in your blood which is a strong risk factor of heart disease. Regular exercise also helps in keeping the heart healthy and strong while promoting the healthy flow of blood through the blood vessels.

Sources
nutraingredients.com
disabled-world.com
mayoclinic.com
mayoclinic.com

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In a recent post at Depressed Metabolism Aschwin de Wolf discusses arguments against cryonics - the low temperature storage of the deceased that aims to preserve the data contained in the brain. For example, what would be needed to make a rational, scientific case against cryonics?

What is striking about cryonics is that those who have taken serious efforts to understand the arguments in favor of its technical feasibility generally endorse the idea. Those who have not made cryonics arrangements usually give non-technical arguments (anxiety about the future, loss of family and friends, etc), lack funding or life insurance, or are (self-identified) procrastinators. In contrast, those who reject cryonics are almost invariably uninformed. They do not understand what happens to cells when they freeze, they are not aware of vitrification (solidification without ice formation), they think that brain cells "disappear" five minutes after cardiac arrest, they demand proof of suspended animation as a condition for endorsing cryonics, etc.

his does not mean that no serious arguments could be presented. [For example, it could be argued that] memory and identity are encoded in such a fragile and delicate manner that cerebral ischemia, ice formation or cryoprotectant toxicity irreversibly destroy it. Considering our limited understanding of the nature of consciousness, and the biochemical and molecular basis of memory, this cannot be ruled out.

Cryonics advocates can respond to such a challenge by producing an argument that pairs our current understanding of the neuroanatomical basis of identity and memory to a cryobiological argument in order to argue that existing cryonics procedures are expected to preserve it. An excellent, knowledgeable, response of this kind is offered in Mike Darwin's Does Personal Identity Survive Cryopreservation? Cryonics skeptics in turn could produce evidence that existing cryonics procedures fall short of this goal.

To my eyes, the weight of evidence presently favors low temperature vitrification being an adequate methodology to preserve the data of the brain. The practice could be greatly improved upon in many ways, such as by eliminating the toxicity of chemicals that must presently be used. There is always room for revolutionary improvement in any technology, but vitrification as it stands seems to be up to the bare essentials of the job: preserve the data sufficiently well for later restoration of a human mind.

Sadly most of the arguments made against cryonics are far from scientific and rational, and in this it is in a similar position to research into the biotechnologies of engineered human longevity. Most people argue against radical life extension from the gut, not the head, when they are first introduced to the concept. It is an instinctive rejection of anything that looks like change: one of the less helpful aspects of human nature at work. People are fiercely defensive of the norm, whatever the norm might happen to be, even when it involves ongoing preventable deaths on a massive, staggering scale.

The human death toll in the Year 2001 from all 227 nations on Earth was nearly 55 million people, of which about 52 million were not directly caused by human action, that is, not accidents, or suicides, or war. They were "natural" deaths.

Neurodegeneration has an inflammatory component, and some research groups use that as a starting point for treatment: "Neurodegenerative diseases like Alzheimer's and Parkinson's are partly attributable to brain inflammation. Researchers [now] demonstrate [that] a well-known family of enzymes can prevent the inflammation and thus constitute a potential target for drugs. Research suggests that microglial cells - the nerve system's primary immune cells - play a critical part in neurodegenerative diseases, such as Alzheimer's and Parkinson's. The over-activation of these cells in the brain can cause inflammation, resulting in neuronal death. Scientists [have] now found a way to prevent the activation of the microglia and consequently the inflammation they cause. The key is the blocking of enzymes called caspases, which the team has shown control microglial activation. ... By studying cell cultures and mice, the researchers show that certain caspases (3, 7 and 8) activate rather than kill microglial cells, which triggers an inflammatory reaction. Mice given caspase inhibitors displayed fewer activated microglia and less inflammation and cell death in the surrounding neurons."

Link: http://ki.se/ki/jsp/polopoly.jsp?d=130&a=118749&l=en&newsdep=130

An example of a class of stem cell medicine that involves manipulation of existing populations of cells in the body: "Circulating through the bloodstream of every human being is a rare and powerful type of cell, one that can actually create new blood vessels to bypass blockages that cause heart attacks and peripheral artery disease. Though everyone has these cells - called endothelial progenitor cells - they are often dysfunctional in people prone to vascular disease. Now researchers [have] discovered that a molecule - called Wnt1 - can improve the function of endothelial progenitor cells, increasing the blood flow to organs that previously had been cut off from the circulation. The finding could enhance clinical trials already testing these powerful cells in patients hospitalized with cardiac arrest. ... A number of studies in the past few years have suggested that genes that play an important role during early development and get 'turned off' during adulthood may also get 'turned on' or expressed again in response to injury, such as heart attack. [Researchers] found that one gene in particular, Wnt1, was expressed during development of blood vessels, shut off during adulthood and then re-expressed in angiosarcoma, a cancer of endothelial cells. ... treating these special cells with Wnt1 not only greatly increased their function but also their number. Next, [researchers] investigated what effect the protein would have on a mouse model of peripheral artery disease, an illness in humans caused by decreased blood flow to the extremities. They found that treating these animals with a single injection of the Wnt1 protein resulted in almost three fold increase in blood flow in the affected areas."

Link: http://news.unchealthcare.org/news/2011/march/wnt1

Here is some data for you to mull over today: the not so great odds that come with being male.

[The] disparity in mortality rates for males and females does not just occur in late adolescence/young adulthood. Males have a higher mortality rate at young ages (e.g. ages 1-4 the death rate for males is 12% higher than it is for females the same age) and older ages (e.g. ages 65-74 the death rate is 33% higher than it is for females that age). Considering the inequality in mortality rates between the genders across the lifespan makes it clear that it is not "nurture" alone that explains why males are more likely to die in every single age category, from the first year of life to age 85+.

The disparity between male and female life expectancy is well known and widely studied, but not definitively understood. What this means in practice is that there exists a very wide range of theories to explain some or all of the gender longevity gap:

Differing smoking rates, stem cell effectiveness, mitochondrial effectiveness, and the possible effects of hormones on the immune system are all on the list. [As well as the theory] that hormones influence the expression and activity of known longevity genes

Which is not to mention the raft of subtly different takes on evolutionary arguments to explain shorter male life spans, such as the debate over disposable soma theories as they apply to the genders.

On the one hand it is fascinating that we stand upon the verge of being able to repair aging, yet at the same time we cannot answer what appears to be a simple question about the nature of aging. On the other hand, this is an apt illustration that sometimes what appear to be simple questions are in fact very complex questions. In this case, the answer to why men and women exhibit different mortality rates and life expectancies must involve the summed interactions of all the systems of human biology, subject to the statistical blurring of a million different lifestyles lived concurrently by billions of people.

The path from epidemiology to clear vision of biological mechanisms is a long, tough trek - and in the end it will do no more for us than to make it easier to work on ways to change that biology. Which is all the more reason to place less of an emphasis on that and more of an emphasis on the path to repairing the forms of molecular damage that cause aging - which are already known and enumerated.

It is known that the hypoxic response at a cellular level is involved in the longevity induced by calorie restriction, and works like most forms of hormesis - by stimulating cells to greater housekeeping efforts. Here is an open access paper on the subject: "A mild reduction in mitochondrial respiration extends the life span of many species, including C. elegans. We recently showed that hypoxia-inducible factor 1 (HIF-1) is required for the acquisition of a long life span by mutants with reduced respiration in C. elegans. We suggested that increased levels of reactive oxygen species (ROS) produced in the respiration mutants increase HIF-1 activity and lead to this longevity. In this research perspective, we discuss our findings and recent advances regarding the roles of ROS and HIF-1 in aging, focusing on the longevity caused by reduced respiration. ... Many interesting questions remain unanswered. Which tissues and functional target genes are important in the regulation of aging by HIF-1? How can both up-regulation and down-regulation of HIF-1 promote longevity? What is the molecular mechanism by which mitochondrial ROS stimulates HIF-1 activity? ... Since many aging-regulatory processes are conserved between C. elegans and mammals, these studies may also provide insights into the regulatory mechanisms of aging in mammals, including humans. Moreover, in addition to aging, HIF-1 and mitochondrial impairment have been implicated in various human diseases such as cancer, diabetes, and neurodegenerative diseases. Thus, we believe that these future studies will help us better understand the pathophysiology of these diseases."

Link: http://www.impactaging.com/papers/v3/n3/full/100292.html

EurekAlert! passes on an advance in the technology of reprogramming cells: "In the past few months, a slew of papers have indicated that the therapeutic potential of a promising type of stem cell, called induced pluripotent stem (iPS) cells, might be limited by reprogramming errors and genomic instability. iPS cells are engineered by reprogramming fully differentiated adult cells, often skin cells, back to a primitive, embryonic-like state. Given these problems, a team of researchers [wondered] if there might be a better way to regenerate lost tissue to treat conditions like heart disease and stroke. ... they outline a method to obtain a new kind of stem cell they call 'induced conditional self-renewing progenitor (ICSP) cells.' ... It's amazingly cool that we can dial adult cells all the way back to embryonic-like stem cells, but there are a lot of issues that still need to be addressed before iPS cells can be used to treat patients. So we wondered... if we just want to treat a brain disease, do we really have to start with a skin cell, which has nothing to do with the brain, and push it all the way back to the point that it has potential to become anything? In this study, we developed ICSP cells using a cell from the organ we're already interested in - the nervous system, in this case - and pushed it back just enough so it continued to divide, giving us a quantity that we were able to apply efficiently, safely and effectively to treat stroke injury in a rodent model. ... the [reprogramming gene] used here is conditionally expressed. This means that ICSP cells can only produce [the gene] when the researchers add a compound called tetracycline to laboratory cultures. When tetracycline is removed, the cells cease dividing and start differentiating. Then, once transplanted into to an animal model, ICSP cells are no longer exposed to tetracycline and take their growth and differentiation cues from their new environment."

Link: http://www.eurekalert.org/pub_releases/2011-03/smri-ans030711.php