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Posted: November 30, 2016 at 5:43 am

If you lived on another planet and everything you knew about humans came from mainstream media, youd be absolutelyshocked to find out a couple of facts:

1) Female humans do not die or crawl into caves to disappear at age 40 while male humans live much longer, active lives.

2) As female humans age, they tend to develop lines on their faces where facial movements occur, as well as looser skin, darker spots from the sun, gray or white hair, and other features that distinguish them from teenagers as they progress throughout their lifetimes. This is NOT only true for men.

Thankfully, most people have the ability to see a variety offemales face-to-face to disprove those laughable media myths of women disappearing with age or perpetual teenage faces and bodies. Unfortunately, that ability to see reality hasnt put a dent in the anti-aging industries that sell extreme appearance anxiety for record profits each year. But still, thats what we want to focus on here: reality. Most notably, we want to emphasize how shockingly different reality looks from the ever-present and powerful media world, and how that impacts real, aging people.Once we recognize the effects of the anti-female-aging phenomenon that what were buying into by the billions, we can fight back.

One of several awesome graphs from Vulture. See the rest by clicking the image.

From local or national nightly news to childrens cartoons, people over 40 are drastically underrepresented in all forms of media, despite the fact that they make up the majority of the population.A whopping62 percent of the female population of the U.S. is over 40. But get this:Older men appear as much as 10 times more frequently than older women in media (1). Even when film depictions of relationships feature older men, their girlfriends and wives are most often decades younger (for more evidence, see this cool pieceon how leading men age, but their ladies do not, including graphs documenting age differences). We could probably call this the Liam Neeson/Olivia Wilde phenomenon (see right side of graph). Men in all forms of media are featured well into their 70s while women tend to start becoming invisible in media right around age 40. Academics even have a name for this egregious level of under-representation: symbolic annihilation. Unfortunately, the effects of that annihilation on womens body image, feelings of self-worth and bank accounts arent so symbolic.

With an extremely low number of women over 40 represented in media at all, the WAY theyre represented becomes especially important. And once again, the news isnt good. Headline #1: Older Women are Portrayed in Negative Ways Much More Often than Men. Think of the wise, funny, intelligent, sexy image represented by men in media well into their 50s, 60s and even later Harrison Ford, Sean Connery, Richard Gere, Tom Cruise, Liam Neeson, Pierce Brosnan, Denzel Washington, Mel Gibson, Clint Eastwood it isnt hard to think of a list of examples from past or present. Trying to come up with female equivalents is much more difficult. Its rare to think of really positive portrayals of women over 40 NOT the neurotic, crazy, evil, out-of-touch-with-reality characters that are most prominent. Betty White is one notable exception to this rule, as a truly funny, relatable, positive character in her many roles who isnt simply the butt of jokes or the domineering mother-in-law.

Studies show the vast majority of any older mom, grandma, aunt, boss, teacher, queen or extraneous female character over 40 in any media fits a negative stereotype (2). And that sucks. The largest segment of the population is not seeing themselves represented, and when they do, its in negative ways*. Whats more, that information is only about white women. We dont have any accurate information about how older women from other races are represented. Why? Because there arent enough examples to generate any significant findings. One study examined 835TV characters and found only four African American characters over the age of 60. Im no math whiz, but 4 out of 835 is a sad statistic. Interestingly, the most popular older woman of color in media happens to be played by a 42-year-old black man, Tyler Perry, as the much-loved Madea.

Vogues Age Issue, where perfectly normal signs of aging are not welcomed!

But aside from the monster oversight in under-representing and misrepresenting older women, mainstream media knows exactly what it is doing when it comes to that huge,money-packing demographic. Excellent business decision #1: Convince women their value entirely depends on their appearance, and that aging is the worst thing that could happen to their appearance. And dont forget, older women areTHE WORST gross cougars, not hot, totally out of touch with the real world, neurotic OR age-defying wonders! Then, convince them its possible to entirely stop aging and look 15 years younger with these products. Since people over age 50own 70 percent of the total net worth of American households (4), targeting this powerful demographic is a strategic move especially considering that women over 40 influence 80 percent of the purchasing decisions in the U.S. (5). I dont know if youve noticed, but the age-old fountain of youth, which has long been fabled to stop the aging process entirely, has been discovered! Its being marketed and sold to women in the U.S. and raking in billions for several different industries each year. You can see it in countless magazines, billboards, commercials, TV shows or movies you know, the 50+ year-old women with zero signs of aging. No lines or wrinkles, tight skin all over, no signs of silver hair sparkling through their thick, flowing brunette and blonde heads of hair. We rarely see an older woman in media, but when we do, she generally fits that description. These women have obviously partaken of the fountain of youth, but what did the trick?! Weve discovered it!

Medias totally normal-appearing ageless older women are the product of two tricks: cosmetic procedures and digital alteration. Whether we like it or not, we start to look different as we age. For men, those changes are most often** depicted as looking distinguished and arent something for men to be ashamed of. For women, those changes are to be immediately stopped, reversed and hidden at all costs. Seriously, ALL costs financially, time-wise and health-wise. Because youre worth it.

Lets talk about Botox, baby. Plastic surgery is the most profitable industry in the U.S., and Botox is the No. 1 cosmetic treatment. Several million people haveBotulinum Toxin injected into their facial muscles in order to paralyze them and conceal the appearance of wrinkles, which must be repeated every 3-6 months. About 92 percent of those who get Botox are women. The next most popular procedures were all also for anti-aging, including soft tissue fillers, hyaluronic acid and chemical peels.

While watching The Bachelorette a few years ago (I know, I know, not the greatest choice), my beautiful, 27-year-old friend proclaimed that she had the forehead of a 90-year-old woman. What prompted that (extremely untrue) declaration? Emily, the beautiful bachelorette, who is our same age, has a perfectly smooth, line-less face. So does every other woman on TV, in movies or in magazines. Lineless and expression-free starts to look normal and ideal, while real-life, expression-ful(?) faces look abnormal and sub-par. Yikes.Thats why, in just the last 15 or so years,there has been a 446 percent increase in cosmetic procedures in the U.S., which raked in $12 billion in 2010 alone. The American Academy of Plastic Surgeons called laser de-wrinkling procedures recession proof. Its a little startling that in the toughest economic times in decades, women are still sacrificing thousands of dollars for painful and temporary procedures to prevent the appearance of aging.

That brings us to the other fountain of youth trick: Digital Alteration. If a woman isnt outrageously gorgeous, thinand young-looking for her age, shes almost always either Photoshopped to look that way or is completely invisible in mainstream media. This DOES have an effect. These pervasive, nearly inescapably and strikingly consistent images of young-looking older women create not just a new ideal for female beauty, but a new normal for us.

Our Photoshop Phoniness Hall of Shamesheds some light on the extreme abnormality of those images by pairing before-and-after alteration shots. A couple of epic age-defying examples are Faith Hill on the cover of Redbook and Twiggy in Olays eye cream ads.

Faith Hill on the July 2007 Redbook cover. Right arm? Suddenly appeared on the cover. Left arm? Cut down by at least 1/3 of its original size. Wrinkles, normal complexion or any other signs of life on her face? Erased. Back? Sliced out almost entirely. Enough said.

A 2009 Oil of Olay eye cream ad featuring Twiggy one of the worlds biggest modeling/fashion icons for more than a decade, now shes relegated to the unglamorous realm of photoshopping disasters for beauty industries lies. Straight-up lies. Amazingly, this ad was banned by the UKs advertising watchdog after more than 700 complaints were gathered for a campaign against airbrushing in ads by the Liberal Democrat MP Jo Swinson. The ad was deemed to be misleading. Um yep!

These arent two freak accidents these are daily deliberate decisions by media powerholders who profit from female anxiety about our faces and bodies. Keep in mind thatOlay, the anti-aging skin care brand owned by Procter & Gamble, spent more than ANY OTHER COMPANY in the U.S. on advertising in 2011. Thats more than any company in any industry. They and many other companies claim to sell the keys to the fountain of youth at every drug store in the nation, but the only real solution to aginglies in the hands of their photo editors. Ever noticed the stark difference in the way mens faces are portrayed compared to womens faces in mass media whether its the cover of GQ or a Chanel ad? Heres an extremely telling example we pieced together, featuring about as comparable of a pairing as you could ever find: similar age, both major celebrities, both in ads for the same company from the same year. Just one major difference: one is a human face and one is a cartoon.

Wonder why you never see women with gray hair featured positively in any sort of mainstream media? Because gray hair doesnt make anyone any money. A very telling example from the must-read The Beauty Myth by Naomi Wolf is of afashion magazine in the 90s that featured a spread of beautiful gray-haired older women in all the latest fashions. Despite positive feedback from readers, one of the magazines main advertisers, Clairol, threatened to pull all its advertising support if gray-haired women were ever featured positively again. Thus, no gray-haired women are everfeatured positively in any magazine that depends on beauty advertising dollars (hint: all of them).

One scary fact is that those great lengths women are going to in order to achieve a youthful ideal are not limited to surgical procedures and magic creams they also include disordered eating of all types. Our friend Michelle Konstantinovsky at HelloGiggles reported ona study from the University of North Carolina School of Medicine, whichfound that in their sample of 1,900 women 50 and older, more than 60 percent of womensaid their body weight or shape negatively affected their lives and 13 percent admitted to having an eating disorder. We agree withMichelle in saying duh to the surprising new finding that older women also suffer from disordered eating.

But enough with the depressing stuff already. Lets get to some solutions!

What can be done to break these body image issues? Importantly but not surprisingly, the researcher agrees with everything we preach at Beauty Redefined:The lead researchers main solution isto help women get themselves out of this appearance focus. She recommends instead of looking for flaws, women work on focusing on something positive about themselves a characteristic that will endure long after their looks fade. Easier said than done, right? We can helpyou start with this list of totally doable strategies, including going on a media fast, complimenting others on more than their looks, shutting down negative thoughts, and many more. Please choose even just one, and start right now to change the way you perceive your own face and body. This isnt an individual fight with individual effects. The way we feel about ourselves and treat our bodies has real influence on those around us, even if we arent aware of it.

Please consider your influence on the reality of the girls, women, boys and men in your life.

What would happen if confident, happy, beautiful women decided to forego painful and expensive anti-aging procedures, breast lifts and enhancements, liposuction, all-over hair removal or tanning regimens? How could that change the way their daughters, students, friends, nieces and coworkers perceived themselves and their own flawed, lined, real faces?How could simply owning (and treating kindly and speaking nicely about) our so-called imperfect bodies affect not only our own lives, but those over whom we have influence? Is it possible to slowly but deliberately change the perception of these flaws as something to shame, hide and fix at any cost to something acceptable and embraceable in all their human, womanly real-ness? We say yes.

Yes, maybe every 30- to 80-year-old woman on TV or movies has a wrinkle-free, perfectly stiffand lifted face that appears ageless. The pressure to Photoshop ourselves into hopeful conformity with beauty ideals is intense, and backlash against female aging is unbelievable. At 29, I frankly dont yet grasp the real pain and anxiety that accompanies aging and its effects on female faces and bodies that become invisible and worthless in some ways to a society that prizes youthful beauty above all else. But at any age, embracing your own beautiful reality and owning it for the others in your life is the epitome of redefining beauty. Media will continue to symbolically annihilate women who dont fit money-making beauty ideals, but WE do not have to annihilate our own faces and bodies to fit those unreal standards. What we COULD annihilate is our allegiance to the idea that women have to look young forever, and that women who dont look young forever arent worthwhile or beautiful. I promise that will be much more empowering and less painful.Let the anti-anti-aging annihilation begin!

*Theres a wonderful organization called Invisible Women that is working to fight against the under-representation and misrepresentation of older women in media through a documentary and education outreach.

**This may start to change as media capitalize on sparking mens insecurities as well as womens but its rare. Key example: Those mens hair color commercials with the little girls convincing Dad to dye his hair and beard in order to get back in the dating game. Ugh. We dont endorse this tactic. Evening the playing field by bringing down both men and women with body shame and appearance focus helps no one.

The rest is here:

Utah Healthcare Provider – Let’s Live Better | Revere Health

Posted: November 28, 2016 at 6:42 am

At Revere Health, we value the health of our patients above all else. As the largest independent multi-specialty physician group in Utah, our integrated system gives patients the best in quality, communication, coordination and innovation. Founded in 1960 in Provo, Revere Health has grown to include over 100 locations and suites in 40 cities throughout Utah, Arizona and Nevada.

Our family practices and 29 medical specialties allow us the opportunity to offer you and your family complete healthcare at any stage of life. Our world-class physicians are proud to offer specialized healthcare services that in some cases are unavailable elsewhere. We take pride in providing care to your family as well as Olympic and collegiate athletes.

As one of two Accountable Care Organizations accredited by Medicare in Utah, Revere Health offers a unique, patient-oriented approach to healthcare. We strive to keep medical costs at a minimum while providing the utmost in quality healthcare.

Revere Health: lets live better.

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Utah Healthcare Provider - Let's Live Better | Revere Health

Fight Aging! Reports from the front line in the fight …

Posted: at 6:42 am

Hunter-Gatherer Data Used to Evaluate the Effects of Exercise on Long-Term Health


To what degree does regular exercise beyond the recommended minimum of 30 minutes a day improve long-term health and life expectancy? This and related questions on the shape of the dose-response curve for aerobic exercise remain open for debate. It is clear that being sedentary has a cost in terms of health and life expectancy, and the balance of evidence to date suggests that the 80/20 point for benefits due to exercise is found somewhere higher than the generally recommended level. Yet it is unclear as to whether professional athletes, who tend to live longer than the general population, live longer because of the high levels of exercise or because they also tend to be more robust individuals who would have enjoyed greater longevity regardless of profession. While it remains to put good numbers to much of the dose-response curve for exercise, this study of the Hadza people adds to the evidence for additional benefits to accrue to those who go beyond 30 minutes a day:

The Hadza live a very different kind of lifestyle - and a very active one, engaging in significantly more physical activity than what is recommended by U.S. government standards. They also have extremely low risk of cardiovascular disease. Researchers have spent several years studying the lifestyle of the Hadza. "Our overall research program is trying to understand why physical activity and exercise improve health today, and one arm of that research program aims to reconstruct what physical activity patterns were like during the evolution of our physiology. The overarching hypothesis is that our bodies evolved within a highly active context, and that explains why physical activity seems to improve physiological health today."

The U.S. Department of Health and Human Services recommends that people engage in 150 minutes per week of moderate intensity activity - about 30 minutes a day, five times a week - or about 75 minutes per week of vigorous intensity activity, or an equivalent combination of the two. However, few Americans achieve those levels. The Hadza, on the other hand, meet those weekly recommendations in a mere two days, engaging in about 75 minutes per day of moderate-to-vigorous physical activity, or MVPA. Furthermore, and consistent with the literature identifying aerobic activity as a key element necessary to a healthy lifestyle, researchers' health screenings of Hadza people have shown that the population has extremely low risk for heart disease. "They have very low levels of hypertension. In the U.S., the majority of our population over the age of 60 has hypertension. In the Hadza, it's 20 to 25 percent, and in terms of blood lipid levels, there's virtually no evidence that the Hadza people have any kind of blood lipid levels that would put them at risk for cardiovascular disease."

While physical activity may not be entirely responsible for the low risk levels - diet and other factors may also play a role - exercise does seem to be important, which is significant because humans' physical activity levels have drastically declined as we have transitioned from hunting and gathering to farming to the Industrial Revolution to where we are today. "Over the last couple of centuries, we've become more and more sedentary, and the big shift seems to have occurred in the middle of the last century, when people's work lives became more sedentary. In the U.S., we tend to see big drop-offs in physical activity levels when people age. In the Hadza, we don't see that. We see pretty static physical activity levels with age. This gives us a window into what physical activity levels were we like for quite a while during our evolutionary history, and, not surprisingly, it's more than we do now. Perhaps surprisingly, it's a whole lot more than we do now. Going forward, this helps us model the types of physical activity we want to be looking at when we explore our physiological evolution. When we ask what kinds of physical activity levels would have driven the evolution of our cardiovascular system and the evolution of our neurobiology and our musculoskeletal system, the answer is not likely 30 minutes a day of walking on a treadmill. It's more like 75-plus minutes a day."

Link: https://uanews.arizona.edu/story/modern-huntergatherers-show-value-exercise


Cellular senescence is one of the root causes of aging, and there are at present serious, well-funded efforts underway to produce rejuvenation therapies based on the selective destruction of senescent cells in old tissues. This progress is welcome, but it could have started a long time ago. It has taken many years of advocacy and the shoestring production of technology demonstrations to finally convince the broader community of scientists and funding institutions that the evidence has long merited serious investment in treatments to clear senescent cells. This is what it is, and now we must look to the future, for all that it has been a long, uphill battle. Cellular senescence is today having its time in the sun. Many research groups are linking the mechanisms of senescence to other aspects of aging; senescent cells are showing up in many more research papers than in past years, now that there is more of a scientific and financial incentive to search carefully for their influence. I think that declaring cellular senescence to be the causal nexus of aging, as one research group did, is going overboard a little, as there are, after all, other independent causes of aging, forms of metabolic waste and damage that would cause death and disease even if cellular senescence did not exist. Nonetheless, it is gratify to watch the spreading realization that cellular senescence plays a role in many areas of health and biology associated with aging. The advent of therapies that can remove senescent cells promises to produce sweeping beneficial effects on aging and disease.

There is a set of fairly well established threads of research that link aging with visceral fat tissue and immune dysfunction in the form of chronic inflammation. Visceral fat produces an accelerated pace of aging by generating greater chronic inflammation, producing an hostile tissue environment of inappropriate signals that attract immune cells and then cause those cells to become dysfunctional. The more fat there is the more inflammation it creates. This is thought to be the primary mechanism by which obesity increases the risk and severity of age-related disease. All of the common age-related diseases are accelerated in their progression by higher levels of chronic inflammation. The material difference between a lot of fat and a normal amount of fat is well demonstrated by a study in which researchers produced life extension in mice through surgical removal of visceral fat, but there is a mountain of data on human health to show that people who are overweight will suffer a shorter life expectancy and more age-related illness, and that this effect scales by the amount of excess fat tissue. How do senescent cells fit into this picture? One of the characteristic features of senescent cells is that they produce greater levels of chronic inflammation via the secretion of signal molecules such as cytokines. Of late, researchers have shown that senescent cells are found in the immune system, as in other cell populations. Given this, it should not be a surprise to find that cellular senescence can be implicated in the way in which visceral fat accelerates aging: their presence in visceral fat tissue and the immune cells interacting with that tissue fits right in with the broader picture of inflammation and bad cellular behavior.

Obesity accelerates T cell senescence in murine visceral adipose tissue

Visceral obesity is associated with chronic low-grade inflammation in visceral adipose tissue (VAT) and a sustained whole-body proinflammatory state, which may underlie metabolic and cardiovascular diseases. VAT inflammation associated with obesity involves a complex network of responses of immune cell components, including acquired immune cells such as various subsets of T cells and B cells and innate immune cells such as macrophages. Among these cells, CD4+ T cells have been recognized as a central regulator of chronic VAT inflammation. The number of CD4+ T cells in VAT increases as the tissue expands in obesity. Factors that drive CD4+ T cell expansion and into proinflammatory effectors in VAT during the development of high-fat diet-induced (HFD-induced) obesity may include MHC class II-associated antigens, possibly self-peptides, because the T cell receptor (TCR) repertoire of CD4+ T cells in VAT is limited, and deficiency of MHC class II protects mice from high fat diet (HFD)-induced VAT inflammation and insulin resistance. However, the obesity-associated immune background underlying chronic inflammation in VAT remains elusive.

Significant changes occur in the overall T cell populations with age. In CD4+ T cells, proportions of naive (CD44loCD62Lhi) cells sharply decline in ontogeny, with an age-dependent increase in cells of the memory phenotype (CD44hiCD62Llo). Among CD44hiCD4+ T cells, a unique population expressing programmed cell death 1 (PD-1) and CD153 actually increases with age in mice. The CD153+PD-1+CD44hiCD4+ T cell population shows compromised proliferation and regular T cell cytokine production on T cell receptor (TCR) stimulation but secretes large amounts of proinflammatory cytokines, such as osteopontin. These CD4+ T cells also show signatures of cell senescence, including a marked increase in senescence-related gene expression and nuclear heterochromatin foci, and are termed senescence-associated T cells (SA-T cells). Notably, the age-dependent development of SA-T cells, which may include autoreactive cells, is dependent on B cells. As such, the increase in SA-T cells is suggested to be involved in part in immune aging phenotypes such as impaired acquired immune capacity, increased proinflammatory traits, and high risk for autoimmunity.

In the present study, we demonstrate that CD153+PD-1+CD44hiCD4+ T cells are remarkably increased and preferentially accumulated in the VAT of HFD-fed mice in a B cell-dependent manner and that these CD4+ T cells show functional and genetic features strongly resembling SA-T cells that increase in secondary lymphoid tissues with age. We also indicate that the CD153+PD-1+CD44hiCD4+ T cells play a crucial role in inducing chronic VAT inflammation and metabolic disorder via secretion of large amounts of osteopontin. We demonstrated that adoptive transfer of CD153+PD-1+CD44hiCD4+ T cells, but not other CD4+ T cells, from HFD-fed spleens into VAT of ND-fed mice recapitulates the features of VAT inflammation, including a striking increase in CD11chiCD206lo macrophages and expression of proinflammatory cytokine genes. It is noteworthy that CD153+PD-1+CD4+ T cells in VAT of HFD-fed mice show features indistinguishable from those of CD153+ SA-T cells, which gradually increase systemically with age. The age-dependent increase in CD153+ SA-T cells may partly underlie the immune aging, including a reduction in acquired immunity and an increase in the inflammatory trait and autoimmunity risk. Obesity is also associated with diminished resistance against infection, chronic low-grade inflammation, and a greater susceptibility to autoimmunity. It has been suggested that the increase in CD153+ SA-T cells in chronological aging and systemic autoimmunity is attributable to a robust, homeostatic T cell proliferation, but the precise mechanism underlying the accumulation of these T cells in VAT of HFD-fed mice remains to be investigated. Nonetheless, it is an intriguing possibility that the predisposition often associated with obesity may partly be a systemic manifestation of the premature increase in CD153+ SA-T cells in VAT, since adipose tissues can constitute up to 50% to 60% of total BW in severe obesity.


Both birds and bats have great longevity for their size in comparison to mammalian species that do not fly, which has led researchers to theorize that the metabolic demands of flight lead to the evolution of cell structures that are more resistant to the damage of aging. Energy metabolism revolves around the mitochondria, the power plants of the cells, and so this in turn points to an important role for mitochondrial function and damage to mitochondria in determining aging and longevity, both across species and in individuals. There are good correlations between mitochondrial composition, the degree to which mitochondrial structures can resist oxidative damage, and mammalian life span, for example. Researchers here take a more reductionist approach to the question of why bats are exceptionally long-lived, and begin by mapping the RNA of a bat species:

Of all mammals, bats possess some of the most unique and peculiar adaptations that render them as excellent models to investigate the mechanisms of extended longevity and potentially halted senescence. They are considered the 'Methusalehs' among mammals due to their exceptional and surprising longevity given their body size and metabolic rate. Typically mammals that are small have a high metabolic rate (e.g. shrews) and do not live for a long time. However, despite their small size and high metabolic rate bats can live for an exceptionally long time, with the oldest recorded Brandt's bat (wild caught as an adult) ever recaptured being more than 41 years old with a body weight of 7 grams. Indeed, to get a positive correlation between longevity and body size in mammals, bats must be removed from the analyses. By comparing the ratio of expected longevity to that predicted from the 'non-bat placental mammal' regression line (longevity quotient - LQ) only 19 species of mammals are longer lived than man, one of these species being the naked mole rat and the other 18 are bats. This suggests that bats have some underlying mechanisms that may explain their exceptional longevity.

MicroRNA (miRNA) are a subset of short endogenous non-coding RNA that play a significant role in post-transcriptional regulation, via repression of translation. Since the first miRNA was discovered in 1993, a multitude of miRNA have subsequently been identified, and implicated in the regulation of the vast majority of biological pathways including cell cycle regulation, metabolism, tumorigenesis, as well as immune response. However, the role of miRNA regulation in mammalian ageing and the onset of age-related diseases has only recently been established. In mammals, various miRNA have been shown to be differentially expressed during ageing, most of which appear to be generally tissue-specific. In addition to tissue-specific ageing, it is increasingly evident that many miRNA regulate gene expressions in well-known ageing pathways, most notably in the p53 tumor suppressor pathway and insulin-like growth factor signaling pathway.

Despite being the second largest order of mammals (~1200 species), there is a scarcity of genomic and transcriptomic bat resources. To date, only five well-annotated bat genomes are publically available. Phylogenomic studies of bat genomes and other mammalian species reveal that a number of genes are under positive selection in bats. These genic adaptations have been correlated with traits such as echolocation, powered flight, hibernation, immunity and longevity. For example, specific non-synonymous mutations in GHR and IGF1R, key ageing-related genes, were detected in several long-lived vespertilionid bats (M. brandtii, M. lucifugus and Eptesicus fuscus), while a large proportion of genes involved in DNA repair (RAD50, KU80, MDM2, etc.) and the NF-B pathway (c-REL and ATM2, etc.) were reported to be under positive or divergent selection in M. davidii and P. alecto. These results suggest bats may better detect and repair DNA damage. Intriguingly, positive selection was also detected in mitochondrial-encoded and nuclear-encoded oxidative phosphorylation genes in bats, which may explain their efficient energy metabolism necessary for flight. Apart from comparative genome analysis, only a small number of transcriptomic studies on bats using have been carried out, focused primarily on the characteristics of hibernation, immunity, echolocation and phylogeny. However, the molecular mechanisms of adaptations affecting longevity are still far from understood, especially with respect to gene regulation.

In the present study, we sequenced six small RNA libraries from whole blood sampled from wild-caught greater mouse-eared bats (Myotis myotis) and for the first time made genome-wide comparisons of both miRNomes and mRNA transcriptomes between bat and non-bat mammalian species (human, pig and cow). The profiling of the M. myotis blood miRNome showed a large number of bat-specific miRNA involved in regulating important pathways related to immunity, tumorigenesis and ageing. Comparative analyses of both miRNomes and transcriptomes also revealed distinctive longevity mechanisms in bats. Several up-regulated miRNA possibly act as tumor suppressors. Gene Ontology (GO) enrichment analysis of differentially expressed protein-coding genes showed that up-regulated genes in bats compared to other mammals were mainly involved in mitotic cell cycle and DNA damage repair pathways while a high number of down-regulated genes were enriched in mitochondrial metabolism. The results and data presented here show unique regulatory mechanisms for protection against tumorigenesis, reduced oxidative stress, and robust DNA repair systems, likely contribute to the extraordinary longevity of bats.

Link: http://dx.doi.org/10.1186/s12864-016-3227-8


Very few genetic variants robustly correlate with longevity across different study populations, and those that do, such as variants of APOE and FOXO3A, have small effects, only visible in the mortality statistics of large numbers of people. This indicates that the genetics of longevity, the way in which variations in metabolism and the response to high levels of age-related cell and tissue damage in later life can produce modestly different mortality rates, is a matter of many thousands of tiny, interacting contributions, very sensitive to environmental factors. It appears ever less likely that there will be any easy, small number of genetic changes that can be made to humans in order to produce significant lengthening of life. Thus the study of genetics and longevity isn't the place to be looking for cost-effective ways to produce radical life extension of decades and more. This paper is one of many recent illustrations of this point; none of the described problems would be anywhere near as much of a challenge if there was a large genetic effect on aging and longevity with simple, narrow origins there to be found. That would stand out from the data much more readily.

The results of many genome-wide association studies (GWAS) of complex traits suffer from a lack of replication. Differences in population genetic structures among study populations are considered to be possible contributors to this problem. One aspect of population structure - the differences in genetic frequencies among subgroups of individuals comprising the population - was traditionally linked with the effects of population stratification. Another one - the presence of linkage disequilibrium (LD) in many parts of the human genome including those that contain causal single-nucleotide polymorphisms (SNPs) - was actively exploited in GWAS of complex traits. Methods of fine mapping following the "discovery" phase are used for evaluating causal SNPs. One could expect that the non-replication problem due to differences in LD patterns among study populations in GWAS would disappear if the detected marker SNP is a causal one, i.e., if it contributes to the variability of a trait. It turns out that the differences in LD levels around a functional SNP may still contribute to the non-replication problem.

The estimated associations in this case depend on whether the detected functional SNP is in LD with another functional SNP, the effects of these SNPs on the trait in the absence of LD (pure effects), and on the level of LD between corresponding SNP loci. This property has important consequences for interpretation of the results of genetic analyses of complex traits. In the presence of LD the estimated effects of a causal SNP may be spurious and may incorrectly characterize the biological relationships between the SNP and the trait. In contrast the pure effect of a given causal SNP estimated in the absence of LD with other such SNPs may correctly characterize the biological connections between the SNP and the trait. Therefore, for example, performing genetic analyses of African populations (that have lower levels of LD patterns for many SNP pairs than populations of European origin) has the potential to reduce bias in the estimated effects of functional SNPs on a trait caused by the presence of LD between functional loci. This condition is, however, not sufficient because of the possible presence of hidden gene/gene interaction effects, gene/environment correlations, and gene/environment interaction effects.

Human lifespan and many other aging, health and longevity related traits are multifactorial phenotypes, that is, they are affected by many genetic and non-genetic factors. The relationships between genes and these phenotypes have special features that distinguish them from other complex traits, influence methods of their genetic analyses, and affect the interpretation of the research results. The genetic variants that influence aging, health, and longevity related traits generate age dependent changes in the population genetic structure, i.e., changes in the frequencies of genetic variants and in the levels of linkage disequilibrium (LD) among them. This feature has important implications for studies focused on the replication of GWAS research findings: independent populations involved in such studies often have different genetic structures, due in part to the differences in the population age distribution at the time of biospecimen collection. As a result, the frequencies of the genetic variants associated with these traits and their LD patterns may differ even if the genetic structures in the corresponding population cohorts were the same at birth.

Detecting statistically significant associations of genetic variants with complex traits is not the end of the genetic analyses. One reason is that the relationship between a detected marker SNP and the complex trait of interest is not, necessarily, a causal one. More often these relationships serve as proxies for the real effect of some unobserved causal SNPs (due to linkage disequilibrium (LD) between the marker and causal SNPs), and, hence, do not have a direct biological effect on the phenotype. To generate insights about the biological mechanisms responsible for the trait's variability one has to identify the causal SNPs responsible for the association signal. To identify such SNPs a number of efficient fine-mapping procedures have been recommended. The main limitation of existing methods is that they seek to identify a single causal variant which is independent of (not in LD with) other causal variants. Since this is not sufficiently realistic, a new approach that allows for efficient detection of multiple causal variants has been proposed. The case where two or more causal SNPs are in LD creates additional problems for interpretation of the results of genetic association studies.

In this paper we show that the estimates of the effects of a causal SNP on lifespan depend on the genetic structure of the population under study (e.g., the level of LD of the SNP with other causal SNPs). Genetic association studies of this trait using data from populations with different LD levels are likely to produce different results. We show that differences in population genetic structures can explain why genetic variants favorable for longevity in one population appear as harmful risk factors in another population. Population structure may also be responsible for the age-specific effects of genetic variants on mortality risk. Differences in genetic structures in distinct populations may be responsible for the low level of replicability of GWAS of human aging, health, and longevity related traits.

Link: http://dx.doi.org/10.3389/fgene.2016.00188


I stumbled upon an interesting open access paper a few days ago, linked below, in which the authors present their view of immunosenescence, the age-related failure of the immune system, as being in part a process wherein some cells of the adaptive immune system change their characteristics and function to become more like innate immune system cells. It makes for interesting reading, though it is worth bearing in mind that the immune system as a whole is fantastically complex, and in many ways still a dark and unmapped forest. It is easy to theorize unopposed when there is such a lot of empty space remaining on the map, making it hard to argue concretely about the relative importance of various mechanisms and observations. This poor understanding of the intricacies of the immune system is why autoimmune diseases and immune aging are largely lacking in effective treatments, and why the best of the prospective cures are those that sidestep the entire question of specific causes and mechanisms in face of the Gordian strategy of destroying the entire immune system in order to start over with new stem cells and immune cells.

As you might know, the immune system of most higher animals is two-layered. The layer that evolved first, and which remains the entirety of the immune system in lower animals such as insects, is known as the innate immune system. It reacts quickly, generates inflammation, and reacts in the same, predictable way to every threat. It has no memory and does not reconfigure its operations in response to circumstances and history. Later in evolutionary history, a second layer known as the adaptive immune system came into being, a more sophisticated set of functions resting on top of the existing innate mechanisms. The innate immune system reacts to intruders, and then the adaptive immune system records the nature of the threat and responds in its own manner, augmenting the attack. As the name suggests, the adaptive immune system maintains a memory and adjusts its operations in order to more aggressively destroy pathogens that it has encountered in the past. As anyone in the field will tell you, however, this high level picture of cleanly divided dualism is overly simplistic, however. There are numerous grey areas and incompletely understood complexities at the border between the two sides of the immune system.

Given that the adaptive immune system can adapt, its failure with aging is in large part a matter of acquired misconfiguration. There is only a small influx of new immune cells in adults, and this puts an effective limit on the number of immune cells that is supported at any one time. The inevitable problem in a space-limited system that keeps a continual record of history is that it runs out of space: evolutionary pressures produced the trade-off of a system that works very well out of the gate in young people, but fails sometime in later life. An old adaptive immune system is burdened with too many cells devoted to memory and too few cells devoted to attacking new threats. That is on top of the progressive failures that occur due to the the growing burden of the molecular damage that accompanies aging: persistent metabolic waste products such as cross-links and lipofuscin, mitochondrial damage, diminished stem cell activity, and so forth. The innate immune system has its own problems that arise from this damage, but is less prone of the issue of misconfiguration.

Understanding exactly how aging progressively harms the intricate choreography of the immune response is a massive project, and nowhere near completion. It is possible to judge how far along researchers are in this work by the side effect of the quality of therapies for autoimmune disease, which are malfunctions in immune configuration, and largely incurable at the present time. From a practical point of view, and as mentioned above, the best prospects for effective treatments in the near future involve destroying and recreating the immune system. That works around our comparative ignorance by removing all of the problems that researchers don't understand in addition to ones that they do. Destroying the immune system can only be done with chemotherapy at the moment, which no-one would undergo unless there was no choice in the matter given that it has significant negative effects on long-term health, but once new methods of selective immune cell destruction are developed, lacking side-effects, then we can start to talk about treating immune aging by rebooting the immune system.

Convergence of Innate and Adaptive Immunity during Human Aging

Aging is associated with a general decline in immune function, contributing to a higher risk of infection, cancer, and autoimmune diseases in the elderly. Such faulty immune responses are the result of a profound remodeling of the immune system that occurs with age, generally termed as immunosenescence. While the number of nave T cells emerging from the thymus progressively decreases with age as a result of thymic involution, the memory T cell pool expands and exhibits significant changes in the phenotype and function of antigen-experienced T cells, particularly evident in the CD8+ T cell compartment. Chronic immune activation due to persistent viral infections, such as cytomegalovirus (CMV) and Epstein-Barr virus (EBV), is one of the main drivers contributing to the accumulation of highly differentiated antigen-specific CD8+ T lymphocytes that have characteristics of replicative senescence. In combination with the depletion of the peripheral pool of nave T cells, the accumulation of these terminally differentiated T cells with age skews the immune repertoire and has been implicated in the impaired immune responses to new antigens and vaccination in the elderly

Natural killer cells and CD8+ T lymphocytes are the two major cell lineages with constitutive cytotoxic activity and have a crucial role in the recognition and killing of abnormal cells. However, the paradigm for the recognition of target cells is fundamentally different between these two cell types: conventional CD8+ T cells rely on the T cell receptor (TCR) to recognize specific peptides presented by major histocompatibility complex class-I (MHC-I) molecules, whereas NK cells use a repertoire of germ line-encoded receptors to detect "missing self" or "altered-self" antigens and directly kill abnormal cells, without prior sensitization. Besides antigen specificity, the development of immunological memory is conventionally another distinctive feature between NK and T cells, categorizing them into distinct arms of the immune system and the innate and adaptive immune system, respectively.

Nevertheless, accumulating evidence supports the existence of NK cell memory, as well as evidence for TCR-independent responses mediated by CD8+ T lymphocytes, suggesting that the conventional limits between the innate and adaptive arms of the immune system may be not as distinct as first thought. NK and T lymphocytes have a common origin from a lymphoid progenitor cell in the bone marrow, and recent comparative proteomic and transcriptomic studies have demonstrated a remarkably close proximity between effector CD8+ T lymphocytes and NK cells, reiterating an evolutionary ancestry and shared biology between the two cell lineages.

An increasing body of literature reveals the existence of subsets of T cells with features that bridge innate and adaptive immunity. These cells typically co-express a TCR and NK cell lineage markers, distinguishing them from NK cells and other innate lymphoid cells, which lack the expression of a TCR or somatically rearranged receptors. Functionally, innate-like T cells respond to TCR ligation but are also able to respond rapidly to danger signals and pro-inflammatory cytokines, independently of TCR stimulation, resembling innate cells. Recently, subsets of conventional CD8+ T cells expressing NK cell markers and intraepithelial T cells have been included in this vaguely defined group of innate-like T cells. Despite the similarities in phenotype and function, there are clear differences in ontogeny and tissue distribution between them.

In this review, we will discuss recent evidence that aging is associated with the expansion of a subset of conventional CD8+ T cells with phenotypic, functional, and transcriptomic features that resemble NK cells. Such innate-like CD8+ T cells have the characteristics of terminally differentiated T cells, and the acquisition of functional NK receptors is most likely part of a general reprograming of the CD8+ T cell compartment during human aging, to ensure broad and rapid effector functions. We propose that innate-like CD8+ T cells share important features with other innate-like T cells; however, fundamental differences in origin and development separate them from truly innate cells. Interestingly, these cells are also differentially affected by aging, suggesting distinct roles in immune responses at different times of life. Evidence indicates that chronological aging is associated with accumulation of cells combining features of both the innate and adaptive arms of the immune system, most likely to compensate for functional defects of conventional NK and CD8+ T cells with age. We propose that senescent CD8+ T cells should not be seen as a dysfunctional population but instead a functionally distinct subset, which uses recently acquired NK cell machinery to maintain rapid effector functions throughout life. Contrary to the classic paradigm that peripheral TCR ligation is essential for T cell activation, this subset of highly differentiated T cells has impaired TCR responsiveness and may be non-specifically activated by inflammatory cytokines or after ligation of innate receptors. The switch to an innate mode of function may shed light on the mechanisms that allow highly differentiated CD8+ T cells to maintain functionality, despite the loss of TCR signal functions.

Our understanding of the physiological significance of the expression of NKRs on T cells is still incomplete, and the identification of the molecular mechanisms and the transcriptional regulators underpinning the development of innate features in T cells is essential. Most importantly, it will be important to understand how the intersection between innate and adaptive immune features may be manipulated to enhance immune function and to use this information to develop new approaches to improve immunity in the elderly.


There are many possible answers to the question of why women have a longer life expectancy than men, but no real consensus on which of the candidate mechanisms are the important ones. It is interesting to note that, in an age in which rejuvenation therapies are starting to arrive, the research community has a better idea of how to bring aging under medical control, and thus make natural variations in longevity irrelevant, than of how to definitively determine the mechanisms causing those natural variations between groups of humans. Fully understanding our biochemistry is a massive undertaking, far greater in scope than merely wrestling degenerative aging into submission by addressing its root causes. Biology is enormously complex, and working with statistical demographic data or evolutionary theory doesn't tend to produce firm answers, only helping to narrow down the directions for further inquiry.

People worldwide are living longer, healthier lives. A new study of mortality patterns in humans, monkeys and apes suggests that the last few generations of humans have enjoyed the biggest life expectancy boost in primate history. The gains are partly due to advances in medicine and public health that have increased the odds of survival for human infants and reduced the death toll from childhood illness. Yet males still lag behind females - not just in humans but across the primate family tree, the researchers find. "The male disadvantage has deep evolutionary roots."

An international team compiled records of births and deaths for more than a million people worldwide, from the 18th century to the present. The data included people in post-industrial societies such as Sweden and Japan, people born in pre-industrial times, and modern hunter-gatherers, who provide a baseline for how long people might have lived before supermarkets and modern medicine. The researchers combined these measurements with similar data for six species of wild primates that have been studied continuously for three to five decades, including sifaka lemurs, muriqui monkeys, capuchins, baboons, chimpanzees and gorillas. The data confirm a growing body of research suggesting that humans are making more rapid and dramatic gains than ever before seen in the primate family tree. For example, in the last 200 years life expectancy in Sweden has jumped from the mid-30s to over 80, meaning that a baby born today can hope to live more than twice as long as one born in the early 19th century. The data show that today's longest-lived human populations have a similar 40- to 50-year advantage over people who live traditional lifestyles, such as the Hadza hunter-gatherers of Tanzania and the Ach people of Paraguay.

In contrast, these modern hunter-gatherers - the best lens we have into the lives of early humans - live on average just 10 to 20 years longer than wild primates such as muriquis or chimpanzees, from which human ancestors diverged millions of years ago. "We've made a bigger journey in lengthening our lifespan over the last few hundred years than we did over millions of years of evolutionary history." One indicator of healthcare improvement is infant mortality, which strikes fewer than 3 in 1000 babies born in Sweden or Japan today. But it was more than 40 times higher for those born two centuries ago, and is still high among hunter-gatherers and wild primates.

The researchers also studied lifespan equality, a measure similar to income equality that indicates whether longevity is distributed evenly across society, or only enjoyed by a few. They found that, for both humans and wild primates, every gain in average lifespan is accompanied by a gain in lifespan equality. That is, for a population to be very long-lived, everyone must benefit more or less equally, with fewer individuals left behind. The researchers were surprised to find that the longevity of human males has yet to catch up with females, and the improvements in males aren't spread as evenly. A girl born in Sweden in the early 1800s could expect to outlive her male counterparts by an average of three to four years. Two hundred years later, despite Swedes adding 45 years to their average lifespan, the gulf that separates the sexes has barely budged. The life expectancy gender gap isn't just true for humans. Females outlived males in almost every wild primate population they looked at.

Link: https://today.duke.edu/2016/11/life-expectancy-grows-men-still-lagging


In the field of tissue engineering, this is the era of organoids. Researchers are limited in the size of tissue they can produce because of the lack of a robust method of generating the blood vessel networks needed to support large tissue sections, but are otherwise making significant progress in the generation of functional organ tissue. Initially this is producing the greatest benefit for further research and development, allowing tests to be conducted in living tissue at a much faster pace and lower cost. For many tissue types, however, organoids also offer the possibility of benefits realized through transplantation, as in many cases they are capable of integrating with existing organ tissue to improve its function.

Scientists report using human pluripotent stem cells to grow human intestinal tissues that have functioning nerves in a laboratory. The paper puts medical science a step closer to using human pluripotent stem cells (which can become any cell type in the body) for regenerative medicine and growing patient-specific human intestine for transplant. "One day this technology will allow us to grow a section of healthy intestine for transplant into a patient, but the ability to use it now to test and ask countless new questions will help human health to the greatest extent." This ability starts with being able to model and study intestinal disorders in functioning, three-dimensional human organ tissue with genetically-specific patient cells. The technology will also allow researchers to test new therapeutics in functioning lab-engineered human intestine before clinical trials in patients.

Researchers started out by subjecting human pluripotent stem cells to a biochemical bath that triggers their formation into human intestinal tissue in a petri dish. The process was essentially the same as that used in a 2010 study, which reported the first-ever generation of three-dimensional human intestinal organoids in a laboratory. Intestinal tissues from the initial study lacked an enteric nervous system, which is critical to the movement of waste through the digestive tract and the absorption of nutrients. The gastrointestinal tract contains the second largest number of nerves in the human body. When these nerves fail to work properly it hinders the contraction of intestinal muscles. To engineer a nervous system for the intestinal organoids already growing in one petri dish, researchers generated embryonic-stage nerve cells called neural crest cells in a separate dish. The neural crest cells were manipulated to form precursor cells for enteric nerves. The challenge at this stage was identifying how and when to incorporate the neural crest cells into the developing intestine. "We tried a few different approaches largely based on the hypothesis that, if you put the right cells together at the right time in the petri dish, they'll know what do to. It was a long shot, but it worked." The appropriate mix caused enteric nerve precursor cells and intestines to grow together in a manner resembling developing fetal intestine.

A key test for the engineered intestines and nerves was transplanting them into a living organism - in this case laboratory mice with suppressed immune systems. This allowed researchers to see how well the tissues grow and function. Study data show the tissues work and are structured in a manner remarkably similar to natural human intestine. They grow robustly, process nutrients and demonstrate peristalsis - series of wave-like muscle contractions that in the body move food through the digestive tract.

Link: https://www.cincinnatichildrens.org/news/release/2016/hirschsprungs-intestinal-nerve-disorder


The first rejuvenation therapies to work well enough to merit the name will be based on the SENS vision: that aging is at root caused by a few classes of accumulated cell and tissue damage, and biotechnologies that either repair that damage or render it irrelevant will as a result produce rejuvenation. Until very recently, no medical technology could achieve this goal, and few research groups were even aiming for that outcome. We are in the midst of a grand transition, however, in which the research and development community is finally turning its attention to the causes of aging, understanding that this is the only way to effectively treat and cure age-related disease. Age-related diseases are age-related precisely because they are caused by the same processes of damage that cause aging: the only distinctions between aging and disease are the names given to various collections of symptoms. All of frailty, disease, weakness, pain, and suffering in aging is the result of accumulated damage at the level of cells and protein machinery inside those cells. Once the medical community becomes firmly set on the goal of repairing that damage, we'll be well on the way to controlling and managing aging as a chronic condition - preventing it from causing harm to the patient by periodically repairing and removing its causes before they rise to the level of producing symptoms and dysfunction. The therapies of the future will be very different from the therapies of the past.

The full rejuvenation toolkit of the next few decades will consist of a range of different treatments, each targeting a different type of molecular damage in cells and tissues. In this post, I'll take a look at the likely order of arrival of some of these therapies, based on what is presently going on in research, funding, and for-profit development. This is an update to a similar post written four years ago, now become somewhat dated given recent advances in the field. Circumstances change, and considerable progress has been made in some lines of research and development.

1) Clearance of Senescent Cells

It didn't take much of a crystal ball four years ago to put senescent cell clearance in first place, the most likely therapy to arrive first. All of the pieces of the puzzle were largely in place at that time: the demonstration of benefits in mice; potential means of clearance; interested research groups. Only comparatively minor details needed filling in. Four years later no crystal ball is required at all, given that Everon Biosciences, Oisin Biotechnologies, SIWA Therapeutics, and UNITY Biotechnology are all forging ahead with various different approaches to the selective destruction of senescent cells. No doubt many groups within established Big Pharma entities are also taking a stab at this, more quietly, and with less press attention. UNITY Biotechnology has raised more than $100 million to date, demonstrating that there is broad enthusiasm for this approach to the treatment of aging and age-related disease.

With the additional attention and funding for this field, more methods of selective cell destruction have been established, and there is now a greater and more detailed understanding of the ways in which senescent cells cause harm, contributing to the aging process. Senolytic drugs that induce apoptosis have been discovered; senescent cells are primed to enter the programmed cell death process of apoptosis, and so a small nudge to all cells via a drug treatment kills many senescent cells but very few normal cells. Researchers have established that senescent cells exist in the immune system, and may be important in immune aging. Similarly, the immune cells involved in the progression of atherosclerosis are also senescent, and removing them slows the progression of that condition. Other research has shown that removing senescent cells from the lungs restores lost tissue elasticity and improves lung function. Beyond these specific details, senescent cells clearly contribute to chronic inflammation in aging, and that drives the progression of near all common age-related conditions. The less inflammation the better. These effects are caused by the signals secreted by senescent cells: that their harm is based on signaling explains how a small number of these cells, perhaps 1% by number in an aged organ, can cause such widespread havoc.

2) Immune System Destruction and Restoration

At the present time it is a challenge to pick second place. A number of fields are all equally close to realization, and happenstance in funding decisions, regulatory matters, or technical details yet to be uncovered will make the difference. The destruction and recreation of the immune system wins out because it is already possible, already demonstrated to be successful, and just missing one component part that would enable it to be used by ordinary, healthy, older people. At present researchers and clinicians use chemotherapy to destroy immune cells and the stem cells that create them. Repopulation of the immune system is carried out via cell transplants that are by now a safe and proven application of stem cell medicine, little different from the many varieties of first generation stem cell therapy. This approach has been used to cure people with multiple sclerosis, and has been attempted with varying degrees of success for a number of other autoimmune conditions for going on fifteen years now: there are researchers with a lot of experience in this type of therapy.

The catch here is that chemotherapy is a damaging experience. The cost of undergoing it is high, both immediately, and in terms of negative impact on later health and life expectancy, similar to that resulting from a life spent smoking. It only makes sense for people who are otherwise on their way to an early death or disability, as is the case for multiple sclerosis patients. However, there are a number of approaches very close to practical realization that will make chemotherapy obsolete for the selective destruction of immune cells and stem cells - approaches with minimal or no side-effects. A combined approach targeting c-kit and CD47 was demonstrated earlier this year, for example. Sophisticated cell targeting systems such as the gene therapy approach developed for senescent cell clearance by Oisin Biotechnologies could also be turned to stem cell or immune cell destruction, given suitable markers of cell chemistry. There are quite a few of these, any one of which would be good enough.

Replacing the chemotherapy with a safe, side-effect-free treatment would mean that the established programs for immune system restoration could immediately expand to become a useful, effective treatment for immunosenescence, the age-related failure of the immune system. This is in part a problem of configuration: a lifetime of exposure to persistent pathogens such as herpesviruses leaves too much of the immune system uselessly devoted to specific targets that it cannot effectively clear from the body, and too little left ready to fight new threats and destroy malfunctioning cells. Then there are various forms of autoimmunity that become prevalent in older people, not all of which are in any way fully understood - consider just how recently type 4 diabetes was discovered, for example. Clearing out the entire immune system, all of its memory and quirks, and restarting it fresh with a new supply of stem cells is a good approach to many of the issues in the aged immune system. Not all of them, but many of them, and considering the broad influence immune function has over many other aspects of health and tissue function, it seems a worthwhile goal.

3) Clearance of the First Few Types of Amyloid

There are about twenty different types of amyloid, misfolded proteins that form solid deposits. Not all are robustly associated with age-related dysfunction, but of those that are, some progress has been made towards effective therapies based on clearance. Last year, a clinical trial of transthyretin amyloid clearance produced good results. This type of amyloid is associated with heart disease, and is thought to be the primary cause of death in supercentenarians. This year researchers finally demonstrated clearance of amyloid- in humans, after a long series of failures. Amyloid- is one of the forms of metabolic waste that accumulates in Alzheimer's disease.

So these types of rejuvenation therapy already exist in the sense of prototypes and trial treatments. To the degree that they are effective and safe, everyone much over the age of 40 should be undergoing a course of treatment every few years. In practice, since both of the above mentioned therapies are tied up in the slow-moving edifice of Big Pharma regulatory capture, it will be a long time before they make it to the clinic in any way that is accessible to an ordinary individual. The most likely path to that goal is for other groups outside that system to reverse engineer the basic technology from the scientific publications, implement their own methodologies, and market it in other regulatory regions, making it available via medical tourism. This is how stem cell medicine progressed, and seems likely to be the way that any other very significant field will also move forward.

4) Clearance of Glucosepane Cross-Links

Clearance of cross-links in the extracellular matrix of tissues is, like senescent cell destruction, one of the most exciting of early rejuvenation therapies. It is a single target that influences a great many aspects of aging: if we look at just the cross-link-induced loss of elasticity in blood vessels alone, that has a major influence on mortality through hypertension and consequent impact on cardiovascular health. It is also a single target in the sense that near all persistent cross-links important to aging in humans so far appear to be based on one compound, glucosepane. Thus all that is needed is one drug candidate.

Four years ago, the situation for glucosepane clearance looked pretty bleak. The funding was minimal, and the tools for working with glucosepane in living tissues didn't exist. Researchers avoided the whole topic, as making any progress would require a lot of funding and effort to even get to the point of starting in earnest. The SENS Research Foundation and their allies have since made major inroads into this challenge, however. Last year, a method of cheaply and reliably synthesizing glucosepane was established, and now the road is open to anyone who wants to try their hand at drug discovery. That is now underway in the Spiegel Lab, among others, and I'd hope to see the first potential drug candidates emerge at some point in the next couple of years.

5) Thymic Rejuvenation to Increase the Supply of Immune Cells

Another possible approach to partially restore lost function in the aging immune system is to increase the pace at which new immune cells are created. This is a very slow pace indeed in older people, due in large part to the age-related decline of the thymus. The thymus acts as a nursery for the maturation of T cells, and its atrophy thus restricts the rate at which new cells enter circulation. There has been some progress towards engineering of replacement active thymus tissue, as well as methods of providing signal proteins that instruct the old thymus to regenerate and begin to act in a more youthful manner. Transplants of young thymus organs into old mice has demonstrated that this class of approach can produce a meaningful improvement in immune function, and thereby extend healthy life. This is one of a number of regenerative approaches that is on the verge, just waiting for someone to start a company or join the final two dots together and get moving.

6) Mitochondrial Repair

Mitochondria, the power plants of the cell, are herds of bacteria-like organelles that bear their own DNA. This DNA becomes damaged in the course of normal cellular processes, and certain forms of mitochondrial DNA damage - to the thirteen genes needed for oxidative phosphorylation - produce malfunctioning mitochondria that can overtake their cells, either by replicating more readily or being more resistant to quality control mechanisms. Such cells become dysfunctional exporters of harmful signals and oxidized proteins, something that contributes to the progression of atherosclerosis via increased amounts of oxidized lipids in the bloodstream, to pick one example. If we're lucky, a substantial proportion of these cells will become senescent as a result of their mutant mitochondria, and will thus be destroyed by senescent cell clearance therapies. Regardless of whether or not that is true, a method of either repairing or working around this type of damage is needed.

Most of the possible approaches may or may not work well, because of the replication advantage that damaged mitochondria have over normal mitochondria, and are still to be tested in practice rather than theory or demonstration: upregulation of existing repair mechanisms; delivery of extra functional mitochondrial DNA or whole mitochondria; and so forth. The SENS approach is somewhat more radical, involving gene therapy to introduce copies of the thirteen genes into the cell nucleus, altered to ensure that the proteins produced can migrate back to the mitochondria where they are needed. Mitochondria will thus have the necessary protein machinery for correct function regardless of the state of their DNA. This has been demonstrated for three of the thirteen genes of interest, numbers two and three just this year, and getting that far has taken the better part of ten years at a low level of funding. It is likely that things will go faster in the future, now that there is a for-profit company, Gensight Biologics working on the problem in addition to non-profit groups, but it is still the case that the bulk of the work remains to be done.

Will it be useful to have therapies that fix half the problem, moving six or seven genes to the cell nucleus? Will that reduce the impact on aging by half? Hard to say until it is done and demonstrated in mice. Halfway there is probably a target reached by 2020 or so at the present pace. Mitochondrial function appears from all the evidence to be an important aspect of aging, so it is to my eyes worth trying at the halfway point to see what the outcome is.

7) A Robust Cure for Cancer

Some might find it counterintuitive that a universal cure for cancer is not last in this list. We've all been educated to think of cancer as the greatest challenge for medical science, the problem to be solved last of all. Nonetheless, a more rapid arrival of a generally applicable cure for cancer looks to be the likely course of events, as the basis for a treatment that can in principle put a halt to all cancer at all stages of development is currently in the earliest stages of development. All cancers depend absolutely on the ability to continually lengthen telomeres, and so avoid the Hayflick limit on cell replication. Telomere lengthening occurs through the activity of telomerase or the less well understood alternative lengthening of telomeres (ALT) mechanisms: these two are a small set of targets for modern medicine, and researchers are working on the challenge. If telomerase and ALT can both be blocked, temporarily and either globally throughout the body or selectively in cancerous tissue, then cancer will wither and become controllable. This is too fundamental a part of cellular biochemistry for the rapid mutational evolution of cancer cells to work around, as they can for many of the standard approaches to cancer treatment at the present time. Stem cell populations will suffer while telomerase activity is blocked, as they require telomere lengthening for self-renewal, but that is a lesser problem when compared to cancer and one that the stem cell research community will become increasingly able to address in the years ahead.

8) Reversing Stem Cell Aging

The stem cell industry is massively funded, and is on a collision course with stem cell aging. Most of the conditions that one would want to use stem cell therapies to treat are age-related conditions. Researchers must thus ensure that the altered cellular environment, the damage of aging, doesn't prevent the treatments from working - that pristine cells can integrate and work well, not immediately die or decline in response to an age-damaged stem cell niche. On the whole, the research community isn't engaging aggressively with this goal, however. Possible reasons for this include the fact that most stem cell treatments, even without addressing issues of the aged tissue environment, represent a considerable improvement in the scope of what is possible to achieve through modern medicine. So the incentive to go further is perhaps not as strong as it might otherwise be.

Stem cell populations become damaged by age, falling into quiescence or declining in overall numbers. They should be replaced with new populations, but while simple in concept, and even achieved for some cell types, such as the blood stem cells that produce immune cells, this is easier said than done for the body as a whole. Every tissue type is its own special case. There are hundreds of types of cell in the body. Each supporting stem cell population has so far required specific methodologies to be developed, and specific behaviors and biochemistry to be laboriously mapped. It isn't even entirely clear that researchers have found all of the stem cell or stem-like cell populations of interest. There is an enormous amount of work to be done here, and at the moment the field is still largely in the phase of getting the basics, the maps, and the reliable therapeutic methods sorted out for a few of the better understood tissue types, bone marrow and muscles in particular. So this seems at the present time like a long-term prospect, despite the high levels of funding for this line of medical research and development.

9) Clearance of Other Amyloids, Aggregates, and Sundry Lysosomal Garbage

A good portion of aging is driven by the accumulation of waste products, either because they are hard for our biochemistry to break down, is the case for glucosepane cross-links and many of the components of lipofuscin that degrade lysosomal function in long-lived cells, or because clearance systems fail over time, as appears likely to be the case for the amyloid- involved in Alzheimer's disease. There are a lot of these compounds: a score of amyloids, any number of lipofuscin constituents, the altered tau that shows up in tauopathies, and so on and so forth. In many cases there isn't even a good defensible link between a specific waste compound and specific age-related diseases: the waste is one contribution buried in many contributions, and the research community won't start putting numbers to relative importance until it is possible to clear out these contributions one by one and observe the results.

A range of research groups are picking away at individual forms of waste, some with large amounts of funding, some with very little funding, but this is a similar situation to that I outlined above for stem cell aging. There is a huge amount of work to accomplish because there are many targets to address, and with few exceptions, such as amyloid-, it is unclear which of the targets are the most important. They will all have to be addressed, in some order, but there are only so many researchers and only so much funding. We can hope that as the first effective therapies make it into the clinic, most likely for the clearance of forms of amyloid, there will be a growing enthusiasm for work on ways to remove other types of metabolic waste.


The big question in the study of the comparative biology of regeneration is the degree to which mammals retain the mechanisms needed for the exceptional regeneration found in species such as zebrafish and salamanders. The individuals of these highly regenerative species are capable of regrowing fins, limbs, and major portions of internal organs. Has evolution removed this machinery from mammals, or only buried it, leaving it dormant and awaiting activation? This experiment, in which the molecular signals provided via transplanted extracellular matrix material from zebrafish are shown to enhance heart regeneration in mice, argues for the latter theory. The heart in mammals is among the least regenerative of tissues, and does not recover well from damage, but there is considerable room for improvement in the healing processes for all mammalian tissues. Zebrafish and other highly regenerative species heal without scars and without loss of function, something that cannot be said for mammals.

Many lower forms of life on earth exhibit an extraordinary ability to regenerate tissue, limbs, and even organs - a skill that is lost among humans and other mammals. Now, researchers have used the components of the cellular "scaffolding" of a zebrafish to regenerate heart tissues in mammals, specifically mice, as well as exhibiting promising results in human heart cells in vitro. The researchers found that a single administration of extracellular matrix (ECM) material from zebrafish hearts restored the function of the heart and regenerated adult mouse heart tissues after acute myocardial infarction. The study also found that the zebrafish ECM protected human cardiac myocytes - specialized cells that form heart muscle - from stresses.

ECM are the architectural foundations of tissues and organs; not only do they provide a "scaffolding" on which cells can grow and migrate, they assist in the signaling necessary for the organ to develop, grow, or regenerate. In mammals, the heart quickly loses the ability to regenerate after the organism is born, except for a brief period after birth. In lower animals, such as zebrafish, the heart retains that ability throughout their lives: up to 20 percent of a zebrafish's heart can be damaged or removed, and within days the heart's capacity has been fully restored. The researchers first separated the ECM from the cells so that the recipient heart would not reject the treatment. They did this by freezing the zebrafish cardiac tissue, causing the cell membranes to burst and allowing the researchers to retrieve the ECM, a process called decellularization. They then injected the ECM into the hearts of mice with damaged heart muscles and watched the hearts repair themselves. It is difficult to inject foreign cells into a body because the body will recognize them as foreign and reject them. That's not the case with ECM because it is composed of collagen, elastin, carbohydrates and signaling molecules and has no cell surface markers, DNA or RNA from the donor, and so the recipient is less likely to reject the treatment.

Restored function starts almost immediately, and healing is noticeable as early as five days after treatment; within a week, his team could see the heart beating more strongly than the hearts of the untreated animals. The researchers tested the effectiveness of ECM from normal zebrafish and from zebrafish with damaged hearts, in which the ECM had already begun the healing process. They found that while both types of ECM were effective in repairing damage to the mice hearts, the ECM obtained from the zebrafish hearts that were healing were even more potent in restoring heart function in the mice. The researchers are now working on a process to regenerate nerves in mammals using the same process and hope to expand the heart treatments to larger animals in a future study.

Link: http://www.news.pitt.edu/news/how-do-you-mend-broken-heart


Heterochronic parabiosis involves joining the circulatory systems of an old and a young mouse. This produces harmful effects on the young mouse and beneficial effects on the old mouse. There is considerable interest in the research community in identifying the molecular signals involved. So far theory has focused on delivery of beneficial signals from young blood to the old individual, but here researchers present evidence to suggest it may be more a matter of diluting detrimental signals present in the old blood. This has implications for efforts to build therapies based on transfusions of young blood: if dilution is the primary mechanism, those efforts will have little to no effect.

A new study found that tissue health and repair dramatically decline in young mice when half of their blood is replaced with blood from old mice. The study argues against the rejuvenating properties of young blood and points to old blood, or molecules within, as driving the aging process. "Our study suggests that young blood by itself will not work as effective medicine. It's more accurate to say that there are inhibitors in old blood that we need to target to reverse aging." In 2005, researchers found evidence for tissue rejuvenation in older mice when they are surgically joined to younger mice so that blood is exchanged between the two. Despite remaining questions about the mechanism underlying this rejuvenation, media coverage of the study fixated on the potential of young blood to reverse the aging process, and on comparisons to vampires, which was not the takeaway from the study. In the years since the 2005 study, scientists have spent millions to investigate the potential medical properties of youthful blood with enterprises emerging to infuse old people with young blood. "What we showed in 2005 was evidence that aging is reversible and is not set in stone. Under no circumstances were we saying that infusions of young blood into elderly is medicine."

While the experimental model used in the 2005 study found evidence that some aspects of aging may be reversed, the techniques used in the study do not allow scientists to precisely control the exchange of blood, which is necessary to dig deeper into blood's effect on aging. When two mice are sutured together, a technique called parabiosis, blood is not the only thing that is exchanged in this setup; organs are also shared, so old mice get access to younger lungs, thymus-immune system, heart, liver and kidneys. In surgical suturing it takes weeks to a month for the effects of blood to take place and the precise timing is not actually known. Nor is the precise amount of the exchanged blood. In the new study, researchers developed an experimental technique to exchange blood between mice without joining them so that scientists can control blood circulation and conduct precise measurements on how old mice respond to young blood, and vice versa. In the new system, mice are connected and disconnected at will, removing the influence of shared organs or of any adaptation to being joined. One of the more surprising discoveries of this study was the very quick onset of the effects of blood on the health and repair of multiple tissues, including muscle, liver and brain. The effects were seen around 24 hours after exchange.

With the new experimental setup, the research team repeated the experiments from 2005. In each test, blood was exchanged between an old mouse and a young mouse until each mouse had half its blood from the other. The researchers then tested various indicators of aging in each mouse, such as liver cell growth as well as liver fibrosis and adiposity (fat), brain cell development in the region that is needed for learning and memory, muscle strength and muscle tissue repair. In many of these experiments, older mice that received younger blood saw either slight or no significant improvements compared to old mice with old blood. Young mice that received older blood, however, saw large declines in most of these tissues or organs. The most telling data was found when researchers tested blood's impact on new neuron production in the area of the brain where memory and learning are formed. In these experiments, older mice showed no significant improvement in brain neuron stem cells after receiving younger blood, but younger mice that received older blood saw a more than twofold drop in brain cell development compared to normal young mice. The researchers think that many benefits seen in old mice after receiving young blood might be due to the young blood diluting the concentration of inhibitors in the old blood.

Link: http://news.berkeley.edu/2016/11/22/young-blood-does-not-reverse-aging-in-old-mice-uc-berkeley-study-finds/


Cryonics is the low-temperature preservation of at least the brain following death, leaving open the possibility of restoration to life in a future in which molecular nanotechnology and total control of cellular biochemistry are mature industries. As individuals, each of us is the data of the mind, no more, no less, and that data is stored in the form of fine physical structures, most likely those of the synapses connecting neurons. If that structure is preserved sufficiently well, then the individual is not yet gone - only ceased for the moment. Early cryopreservations involved straight freezing to liquid nitrogen temperatures, and this likely caused great damage to the structures of the brain due to ice crystal formation. Modern cryopreservations use cryoprotectants and staged cooling to achieve vitrification of tissues with minimal ice crystal formation. There the degree of damage is much reduced, contingent on sufficient perfusion of cryoprotectant and the quality of the other aspects of the process. These technologies are also under development by groups in the organ transplantation and tissue engineering communities: reversible vitrification of organs would solve a great many logistical problems. From the present state of the science, that goal isn't very far distant. Proof of concept vitrification, thawing, and transplantation of mammalian organs has taken place in the laboratory. Even without present reversibility, however, the merits of cryonics stand: people who are preserved are not dead and gone, just dead, with a chance to return. A chance of unknown size, yes, but that is a big improvement over the grave and certain oblivion.

Cryonics suffers from being a small industry. People encountering the concept for the first time tend look at it askance because it is a small community and thus not the usual end of life choice. Then they make up reasons in their own minds as to why it won't work, or is stupid, or illogical, or otherwise wrong, simply because it is not the norm. It takes multiple exposures to a topic for most people to come around and actually engage with what is known rather than with their own knee-jerk reaction to the topic. In the normal run of things, however, few people actually encounter the ideas of cryonics; it doesn't get all that much press, and since it is such a small industry and surrounding community, few people encounter those involved as they make their way through life. Thus public awareness and understanding of the long-standing cryonics industry seems to advance by a series of infrequent great leaps rather than ongoing incremental gains, each such leap driven by the high-profile cryopreservation of a sympathetic or noted individual that attracts a short-lived mob of press attention. First there is a flood of commentary from those who know next to nothing of cryonics and are quick to condemn it for being different, then a following wave of more thoughtful commentary, for and against, and finally some few of the many people who read the coverage choose to dig further, peruse some of the mountain of literature written on cryonics over the past 40 years, and conclude that cryonics does make sense and is a good idea. So the community of supporters and those signed up as members of a cryonics organization grows a little.

The latest leap forward was spurred by the cryopreservation of a terminally ill young lady in the UK, unusual for its surrounding legal case regarding consent and self-determination. The UK has a cryonics support organization, as is the case for many countries, but like most parts of the world lacks a cryonics provider. This may be why so much of the initial commentary has been from those fairly new to the idea, and has been unusually hostile in tone when compared to the media attention of the past five years or so. Being the UK, there is also a considerable focus on regulation, since the bias over there, in the media at least, is very much towards the idea that nothing must ever happen without government involvement - all that is not explicitly allowed is forbidden, any new endeavor must be quickly regulated by a new government office, and so forth. Sadly the US has been heading in that direction quite energetically since the turn of the century; it has been a sad thing to watch taking place. Cultural differences aside, many cryopreservations are carried out under difficult circumstances, and this was one of them. The ideal preservation takes place at the cryonics provider location, or very close by, within a known window of time, and cooldown is rapid following death so as to minimize damage. Departures from that ideal have a cost, both monetary and in the quality of the preservation, but the people involved here by all accounts did the best possible under the circumstances, hampered by the existing regulatory environment that prevents near every possible approach that could make things easier, cheaper, and more reliable.

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Best Anti Aging Products | timetospa

Posted: at 6:41 am

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Posted: November 26, 2016 at 6:42 am

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Aging of wine – Wikipedia

Posted: November 24, 2016 at 10:41 pm

The aging of wine is potentially able to improve the quality of wine. This distinguishes wine from most other consumable goods. While wine is perishable and capable of deteriorating, complex chemical reactions involving a wine's sugars, acids and phenolic compounds (such as tannins) can alter the aroma, color, mouthfeel and taste of the wine in a way that may be more pleasing to the taster. The ability of a wine to age is influenced by many factors including grape variety, vintage, viticultural practices, wine region and winemaking style. The condition that the wine is kept in after bottling can also influence how well a wine ages and may require significant time and financial investment.[1][2] The quality of an aged wine varies significantly bottle-by-bottle, depending on the conditions under which it was stored, and the condition of the bottle and cork, and thus it is said that rather than good old vintages, there are good old bottles. There is a significant mystique around the aging of wine, as its chemistry was not understood for a long time, and old wines are often sold for extraordinary prices. However, the vast majority of wine is not aged, and even wine that is aged is rarely aged for long; it is estimated that 90% of wine is meant to be consumed within a year of production, and 99% of wine within 5 years.[3]

The Ancient Greeks and Romans were aware of the potential of aged wines. In Greece, early examples of dried "straw wines" were noted for their ability to age due to their high sugar contents. These wines were stored in sealed earthenware amphorae and kept for many years. In Rome, the most sought after winesFalernian and Surrentinewere prized for their ability to age for decades. In the Book of Luke, it is noted that "old wine" was valued over "new wine" (Luke 5:39). The Greek physician Galen wrote that the "taste" of aged wine was desirable and that this could be accomplished by heating or smoking the wine, though, in Galen's opinion, these artificially aged wines were not as healthy to consume as naturally aged wines.[4]

Following the Fall of the Roman Empire, appreciation for aged wine was virtually non-existent. Most of the wines produced in northern Europe were light bodied, pale in color and with low alcohol. These wines did not have much aging potential and barely lasted a few months before they rapidly deteriorated into vinegar. The older a wine got the cheaper its price became as merchants eagerly sought to rid themselves of aging wine. By the 16th century, sweeter and more alcoholic wines (like Malmsey and Sack) were being made in the Mediterranean and gaining attention for their aging ability. Similarly, Riesling from Germany with its combination of acidity and sugar were also demonstrating their ability to age. In the 17th century, two innovations occurred that radically changed the wine industry's view on aging. One was the development of the cork and bottle which allowed producers to package and store wine in a virtually air-tight environment. The second was the growing popularity of fortifying wines such as Port, Madeira and Sherries. The added alcohol was found to act as a preservative, allowing wines to survive long sea voyages to England, The Americas and the East Indies. The English, in particular, were growing in their appreciation of aged wines like Port and Claret from Bordeaux. Demand for matured wines had a pronounced effect on the wine trade. For producers, the cost and space of storing barrels or bottles of wine was prohibitive so a merchant class evolved with warehouses and the finances to facilitate aging wines for a longer period of time. In regions like Bordeaux, Oporto and Burgundy, this situation dramatically increased the balance of power towards the merchant classes.[4]

There is a widespread misconception that wine always improves with age,[3] or that wine improves with extended aging, or that aging potential is an indicator of good wine. Some authorities state that more wine is consumed too old than too young.[5] Aging changes wine, but does not categorically improve it or worsen it. Fruitness deteriorates rapidly, decreasing markedly after only 6 months in the bottle.[5] Due to the cost of storage, it is not economical to age cheap wines, but many varieties of wine do not benefit from aging, regardless of the quality. Experts vary on precise numbers, but typically state that only 510% of wine improves after 1 year, and only 1% improves after 510 years.[3][5]

In general, wines with a low pH (such as Pinot Noir and Sangiovese) have a greater capability of aging. With red wines, a high level of flavor compounds, such as phenolics (most notably tannins), will increase the likelihood that a wine will be able to age. Wines with high levels of phenols include Cabernet Sauvignon, Nebbiolo and Syrah.[4] The white wines with the longest aging potential tend to be those with a high amount of extract and acidity. The acidity in white wines, acting as a preservative, has a role similar to that of tannins in red wines. The process of making white wines, which includes little to no skin contact, means that white wines have a significantly lower amount of phenolic compounds, though barrel fermentation and oak aging can impart some phenols. Similarly, the minimal skin contact with ros wine limits their aging potential.[1][2][5]

After aging at the winery most wood-aged Ports, Sherries, Vins doux naturels, Vins de liqueur, basic level Ice wines and sparkling wines are bottled when the producer feels that they are ready to be consumed. These wines are ready to drink upon release and will not benefit much from aging. Vintage Ports and other bottled-aged Ports & Sherries will benefit from some additional aging.[4]

Champagne and other sparkling wines are infrequently aged, and frequently have no vintage year (no vintage, NV), but vintage champagne may be aged.[4] Aged champagne has traditionally been a peculiarly British affectation, and thus has been referred to as le got anglais "the English taste",[6] though this term also refers to a level of champagne sweetness. In principle champagne has aging potential, due to the acidity, and aged champagne has increased in popularity in the United States since the 1996 vintage.[7] A few French winemakers have advocated aging champagne, most notably Ren Collard (19212009).[8] In 2009, a 184-year-old bottle of Perrier-Jout was opened and tasted, still drinkable, with notes of "truffles and caramel", according to the experts.[9]

A guideline provided by Master of Wine Jancis Robinson[5]

A guideline provided by Master of Wine Jancis Robinson. Note that vintage, wine region and winemaking style can influence a wine's aging potential so Robinson's suggestion of years are very rough estimates of the most common examples of these wines.[5]

The ratio of sugars, acids and phenolics to water is a key determination of how well a wine can age. The less water in the grapes prior to harvest, the more likely the resulting wine will have some aging potential. Grape variety, climate, vintage and viticultural practice come into play here. Grape varieties with thicker skins, from a dry growing season where little irrigation was used and yields were kept low will have less water and a higher ratio of sugar, acids and phenolics. The process of making Eisweins, where water is removed from the grape during pressing as frozen ice crystals, has a similar effect of decreasing the amount of water and increasing aging potential.[2][5]

In winemaking, the duration of maceration or skin contact will influence how much phenolic compounds are leached from skins into the wine. Pigmented tannins, anthocyanins, colloids, tannin-polysaccharides and tannin-proteins not only influence a wine's resulting color but also act as preservatives. During fermentation adjustment to a wine's acid levels can be made with wines with lower pH having more aging potential. Exposure to oak either during fermentation or after (during barrel aging) will introduce more phenolic compounds to the wines. Prior to bottling, excessive fining or filtering of the wine could strip the wine of some phenolic solids and may lessen a wine's ability to age.[1][4]

The storage condition of the bottled wine will influence a wine's aging. Vibrations and heat fluctuations can hasten a wine's deterioration and cause adverse effect on the wines. In general, a wine has a greater potential to develop complexity and more aromatic bouquet if it is allowed to age slowly in a relatively cool environment. The lower the temperature, the more slowly a wine develops.[4] On average, the rate of chemical reactions in wine double with each 18F (8C) increase in temperature. Wine expert Karen MacNeil, recommends keeping wine intended for aging in a cool area with a constant temperature around 55F (13C). Wine can be stored at temperatures as high as 69F (20C) without long term negative effect. Professor Cornelius Ough of the University of California, Davis believes that wine could be exposed to temperatures as high as 120F (49C) for a few hours and not be damaged. However, most experts believe that extreme temperature fluctuations (such as repeated transferring a wine from a warm room to a cool refrigerator) would be detrimental to the wine. The ultra-violet rays of direct sunlight should also be avoided because of the free radicals that can develop in the wine and result in premature oxidation.[2][12]

Wines packaged in large format bottles, such as magnums and 3 liter Jeroboams, seem to age more slowly than wines packaged in regular 750 ml bottles or half bottles. This may be because of the greater proportion of oxygen exposed to the wine during the bottle process. The advent of alternative wine closures to cork, such as screw caps and synthetic corks have opened up recent discussions on the aging potential of wines sealed with these alternative closures. Currently there are no conclusive results and the topic is the subject of ongoing research.[1][4]

One of the short-term aging needs of wine is a period where the wine is considered "sick" due to the trauma and volatility of the bottling experience. During bottling the wine is exposed to some oxygen which causes a domino effect of chemical reactions with various components of the wine. The time it takes for the wine to settle down and have the oxygen fully dissolve and integrate with the wine is considered its period of "bottle shock". During this time the wine could taste drastically different from how it did prior to bottling or how it will taste after the wine has settled. While many modern bottling lines try to treat the wine as gently as possible and utilize inert gases to minimize the amount of oxygen exposure, all wine goes through some period of bottle shock. The length of this period will vary with each individual wine.[2][5]

The transfer of off-flavours in the cork used to bottle a wine during prolonged aging can be detrimental to the quality of the bottle. The formation of cork taint is a complex process which may result from a wide range of factors ranging from the growing conditions of the cork oak, the processing of the cork into stoppers, or the molds growing on the cork itself.[1][2]

During the course of aging, a wine may slip into a "dumb phase" where its aromas and flavors are very muted. In Bordeaux this phase is called the age ingrat or "difficult age" and is likened to a teenager going through adolescence. The cause or length of time that this "dumb phase" will last is not yet fully understood and seems to vary from bottle to bottle.[12]

As red wine ages, the harsh tannins of its youth gradually give way to a softer mouthfeel. An inky dark color will eventually lose its depth of color and begin to appear orange at the edges, and then later eventually turning brown. These changes occur due to the complex chemical reactions of the phenolic compounds of the wine. In processes that begin during fermentation and continue after bottling, these compounds bind together and aggregate. Eventually these particles reach a certain size where they are too large to stay suspended in the solution and precipitate out. The presence of visible sediment in a bottle will usually indicate a mature wine. The resulting wine, with this loss of tannins and pigment, will have a paler color and taste softer, less astringent. The sediment, while harmless, can have an unpleasant taste and is often separated from the wine by decanting.[5]

During the aging process, the perception of a wine's acidity may change even though the total measurable amount of acidity is more or less constant throughout a wine's life. This is due to the esterification of the acids, combining with alcohols in complex array to form esters. In addition to making a wine taste less acidic, these esters introduce a range of possible aromas. Eventually the wine may age to a point where other components of the wine (such as a tannins and fruit) are less noticeable themselves, which will then bring back a heightened perception of wine acidity. Other chemical processes that occur during aging include the hydrolysis of flavor precursors which detach themselves from glucose molecules and introduce new flavor notes in the older wine and aldehydes become oxidized. The interaction of certain phenolics develop what is known as tertiary aromas which are different from the primary aromas that are derived from the grape and during fermentation.[2][4]

As a wine starts to mature, its bouquet will become more developed and multi-layered. While a taster may be able to pick out a few fruit notes in a young wine, a more complex wine will have several distinct fruit, floral, earthy, mineral and oak derived notes. The lingering finish of a wine will lengthen. Eventually the wine will reach a point of maturity, when it is said to be at its "peak". This is the point when the wine has the maximum amount of complexity, most pleasing mouthfeel and softening of tannins and has not yet started to decay. When this point will occur is not yet predictable and can vary from bottle to bottle. If a wine is aged for too long, it will start to descend into decrepitude where the fruit tastes hollow and weak while the wine's acidity becomes dominant.[4]

The natural esterification that takes place in wines and other alcoholic beverages during the aging process is an example of acid-catalysed esterification. Over time, the acidity of the acetic acid and tannins in an aging wine will catalytically protonate other organic acids (including acetic acid itself), encouraging ethanol to react as a nucleophile. As a result, ethyl acetate the ester of ethanol and acetic acidis the most abundant ester in wines. Other combinations of organic alcohols (such as phenol-containing compounds) and organic acids lead to a variety of different esters in wines, contributing to their different flavours, smells and tastes. Of course, when compared to sulfuric acid conditions, the acid conditions in a wine are mild, so yield is low (often in tenths or hundredths of a percentage point by volume) and take years for ester to accumulate.[1]

Coates Law of Maturity is a principle used in wine tasting relating to the aging ability of wine. Developed by the British Master of Wine, Clive Coates, the principle states that a wine will remain at its peak (or optimal) drinking quality for a duration of time that is equal to the time of maturation required to reach its optimal quality. During the evolution (aging) of a wine certain flavors, aromas and textures appear and fade. Rather than developing and fading in unison, these traits each operate on a unique evolutionary path and time line. The principle allows for the subjectivity of individual tastes because it follows the logic that positive traits that appeal to one particular wine taster will continue to persist along the principle's guideline while for another taster these traits might not be positive and therefore not applicable to the guideline. Wine expert Tom Stevenson has noted that there is logic in Coates' principle and that he has yet to encounter an anomaly or wine that debunks it.[13]

An example of the principle in practice would be a wine that someone acquires when it is 9 years of age, but finds it dull. A year later the drinker finds this wine very pleasing in texture, aroma and mouthfeel. Under the Coates Law of Maturity the wine will continue to be drunk at an optimal maturation for that drinker until it has reached 20 years of age at which time those positive traits that the drinker perceives will start to fade.[13]

There is a long history of using artificial means to try to accelerate the natural aging process. In Ancient Rome a smoke chamber known as a fumarium was used to enhance the flavor of wine through artificial aging. Amphorae were placed in the chamber, which was built on top of a heated hearth, in order to impart a smoky flavor in the wine that also seemed to sharpen the acidity. The wine would sometimes come out of the fumarium with a paler color just like aged wine.[14] Modern winemaking techniques like micro-oxygenation can have the side effect of artificially aging the wine. In the production of Madeira and rancio wines, the wines are deliberately exposed to excessive temperatures to accelerate the maturation of the wine. Other techniques used to artificially age wine (with inconclusive results on their effectiveness) include shaking the wine, exposing it to radiation, magnetism or ultra-sonic waves.[4] More recently, experiments with artificial aging through high-voltage electricity have produced results above the remaining techniques, as assessed by a panel of wine tasters.[15] Other artificial wine-aging gadgets include the "Clef du Vin", which is a metallic object that is dipped into wine and purportedly ages the wine one year for every second of dipping. The product has received mixed reviews from wine commentators.[16]

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Holism – Wikipedia

Posted: November 23, 2016 at 1:41 pm

Holism (from Greek holos "all, whole, entire") is the idea that systems (physical, biological, chemical, social, economic, mental, linguistic, etc.) and their properties should be viewed as wholes, not as collections of parts. This often includes the view that systems function as wholes and that their functioning cannot be fully understood solely in terms of their component parts.[1][2]

The term Holism was coined by J C Smuts in Holism and Evolution.[3][4] It was Smuts' opinion that Holism is a concept that represents all of the wholes in the universe, and it is a factor because the wholes it denotes are the real factors in the universe. Further, it was his opinion that Holism also denoted a theory of the universe in the same vein as Materialism and Spiritualism; that the ultimate reality in the universe is neither matter nor spirit but wholes as defined in Holism and Evolution. While he offered these different definitions, Smuts clearly stated his opinion that its primary and proper use was to denote the totality of wholes which operate as real factors and give to reality its dynamic evolutionary creative character.[3]:120121 Aside from the idea that the whole is greater than the sum of its parts, the editor[who?] has been unable to identify authoritative secondary sources corroborating Smuts' definitions. When elaborations for the mental, personal and social categories are provided[clarification needed], and a case is made that Holism is a bonafide monistic ontology, we[clarification needed] can revisit the vision of Holism that Smuts held.

After identifying the need for reform in the fundamental concepts of matter, life and mind (chapter 1) Smuts examines the reformed concepts (as of 1926) of space and time (chapter 2), matter (chapter 3) and biology (chapter 4) and concludes that the close approach to each other of the concepts of matter, life and mind, and the partial overflow of each other's domain, implies that there is a fundamental principle (Holism) of which they are the progressive outcome.[3]:86 Chapters 5 and 6 provide the general concept, functions and categories of Holism; chapters 7 and 8 address Holism with respect to Mechanism and Darwinism, chapters 9-11 make a start towards demonstrating the concepts and functions of Holism for the metaphysical categories (mind, personality, ideals) and the book concludes with a chapter that argues for the universal ubiquity of Holism and its place as a monistic ontology.

The following is an overview of Smuts' opinions regarding the general concept, functions, and categories of Holism; like the definition of Holism, other than the idea that the whole is greater than the sum of its parts, the editor is unaware of any authoritative secondary sources corroborating Smuts' opinions.

Wholes are composites which have an internal structure, function or character which clearly differentiates them from mechanical additions, aggregates, and constructions, such as science assumes on the mechanical hypothesis.[3]:106 The concept of structure is not confined to the physical domain (e.g. chemical, biological and artifacts); it also applies to the metaphysical domain (e.g. mental structures, properties, attributes, values, ideals, etc.)[3]:161

The field of a whole is not something different and additional to it, it is the continuation of the whole beyond its sensible contours of experience.[3]:113 The field characterizes a whole as a unified and synthesised event in the system of Relativity, that includes not only its present but also its pastand also its future potentialities.[3]:89 As such, the concept of field entails both activity and structure.[3]:115

Darwins theory of organic descent placed primary emphasis on the role of natural selection but there would be nothing to select if not for variation. Variations that are the result of mutations in the biological sense and variations that are the result of individually acquired modifications in the personal sense are attributed by Smuts to Holism; further it was his opinion that because variations appear in complexes and not singly, evolution is more than the outcome of individual selections, it is holistic.[3]:190192

The whole exhibits a discernible regulatory function as it relates to cooperation and coordination of the structure and activity of parts, and to the selection and deselection of variations. The result is a balanced correlation of organs and functions. The activities of the parts are directed to central ends; co-operation and unified action instead of the separate mechanical activities of the parts.[3]:125

It is the intermingling of fields which is creative or causal in nature. This is seen in matter, where if not for its dynamic structural creative character matter could not have been the mother of the universe. This function, or factor of creativity is even more marked in biology where the protoplasm of the cell is vitally active in an ongoing process of creative change where parts are continually being destroyed and replaced by new protoplasm. With minds the regulatory function of Holism acquires consciousness and freedom, demonstrating a creative power of the most far-reaching character. Holism is not only creative but self-creative, and its final structures are far more holistic than its initial structures.[3]:18, 37, 6768, 8889

As it relates to causality Smuts makes reference to Whitehead, and indirectly Spinoza; the Whitehead premise is that organic mechanism is a fundamental process which realizes and actualizes individual syntheses or unities. Holism (the factor) exemplifies this same idea while emphasizing the holistic character of the process. The whole completely transforms the concept of Causality; results are not directly a function of causes. The whole absorbs and integrates the cause into its own activity; results appear as the consequence of the activity of the whole.[3]:121124,126 Note that this material relating to Whiteheads influence as it relates to causality was added in the second edition and, of course, will not be found in reprints of the first edition; nor is it included in the most recent Holst edition. It is the second edition of Holism and Evolution (1927) that provides the most recent and definitive treatment by Smuts.

The fundamental holistic characters as a unity of parts which is so close and intense as to be more than the sum of its parts; which not only gives a particular conformation or structure to the parts, but so relates and determines them in their synthesis that their functions are altered; the synthesis affects and determines the parts, so that they function towards the whole; and the whole and the parts, therefore reciprocally influence and determine each other, and appear more or less to merge their individual characters: the whole is in the parts and the parts are in the whole, and this synthesis of whole and parts is reflected in the holistic character of the functions of the parts as well as of the whole.[3]:88

A rough and provisional summary of the progressive grading of wholes that comprise Holism is as follows:[3]:109

In philosophy, any doctrine that emphasizes the priority of a whole over its parts is holism. Some suggest that such a definition owes its origins to a non-holistic view of language and places it in the reductivist camp. Alternately, a 'holistic' definition of holism denies the necessity of a division between the function of separate parts and the workings of the 'whole'. It suggests that the key recognizable characteristic of a concept of holism is a sense of the fundamental truth of any particular experience. This exists in contradistinction to what is perceived as the reductivist reliance on inductive method as the key to verification of its concept of how the parts function within the whole.

In the philosophy of language this becomes the claim, called semantic holism, that the meaning of an individual word or sentence can only be understood in terms of its relations to a larger body of language, even a whole theory or a whole language. In the philosophy of mind, a mental state may be identified only in terms of its relations with others. This is often referred to as "content holism" or "holism of the mental". This notion involves the philosophies of such figures as Frege, Wittgenstein, and Quine.[5]

Epistemological and confirmation holism are mainstream ideas in contemporary philosophy.

Ontological holism was espoused by David Bohm in his theory[6] on The Implicate Order.

Hegel rejected "the fundamentally atomistic conception of the object," (Stern, 38) arguing that "individual objects exist as manifestations of indivisible substance-universals, which cannot be reduced to a set of properties or attributes; he therefore holds that the object should be treated as an ontologically primary whole." (Stern, 40) In direct opposition to Kant, therefore, "Hegel insists that the unity we find in our experience of the world is not constructed by us out of a plurality of intuitions." (Stern, 40) In "his ontological scheme a concrete individual is not reducible to a plurality of sensible properties, but rather exemplifies a substance universal." (Stern, 41) His point is that it is "a mistake to treat an organic substance like blood as nothing more than a compound of unchanging chemical elements, that can be separated and united without being fundamentally altered." (Stern, 103) In Hegel's view, a substance like blood is thus "more of an organic unity and cannot be understood as just an external composition of the sort of distinct substances that were discussed at the level of chemistry." (Stern, 103) Thus in Hegel's view, blood is blood and cannot be successfully reduced to what we consider are its component parts; we must view it as a whole substance entire unto itself. This is most certainly a fundamentally holistic view.[7]

[Editors note:work in progress, moving references to Hegel to a common section] Hegel[8][9] and Edmund Husserl.[10][11]

The concept of holism played a pivotal role in Baruch Spinoza's philosophy[12][13]

There are several newer methods in agricultural science such as permaculture and holistic planned grazing that integrate ecology and social sciences with food production. Organic farming is sometimes considered a holistic approach.

In the latter half of the 20th century, holism led to systems thinking and its derivatives, like the sciences of chaos and complexity. Systems in biology, psychology, or sociology are frequently so complex that their behavior is, or appears, "new" or "emergent": it cannot be deduced from the properties of the elements alone.

Holism has thus been used as a catchword. This contributed to the resistance encountered by the scientific interpretation of holism, which insists that there are ontological reasons that prevent reductive models in principle from providing efficient algorithms for prediction of system behavior in certain classes of systems.[citation needed]

Scientific holism holds that the behavior of a system cannot be perfectly predicted, no matter how much data is available. Natural systems can produce surprisingly unexpected behavior, and it is suspected that behavior of such systems might be computationally irreducible, which means it would not be possible to even approximate the system state without a full simulation of all the events occurring in the system. Key properties of the higher level behavior of certain classes of systems may be mediated by rare "surprises" in the behavior of their elements due to the principle of interconnectivity, thus evading predictions except by brute force simulation.

Complexity theory (also called "science of complexity") is a contemporary heir of systems thinking. It comprises both computational and holistic, relational approaches towards understanding complex adaptive systems and, especially in the latter, its methods can be seen as the polar opposite to reductive methods. General theories of complexity have been proposed, and numerous complexity institutes and departments have sprung up around the world. The Santa Fe Institute is arguably the most famous of them.

Holistic thinking is often applied to ecology, combining biological, chemical, physical, economic, ethical, and political insights. The complexity grows with the area, so that it is necessary to reduce the characteristic of the view in other ways, for example to a specific time of duration.

John Muir, Scots born early American conservationist,[15] wrote "When we try to pick out anything by itself we find it hitched to everything else in the Universe".

More information is to be found in the field of systems ecology, a cross-disciplinary field influenced by general systems theory.

In primary care the term "holistic," has been used to describe approaches that take into account social considerations and other intuitive judgements.[16] The term holism, and so-called approaches, appear in psychosomatic medicine in the 1970s, when they were considered one possible way to conceptualize psychosomatic phenomena. Instead of charting one-way causal links from psyche to soma, or vice versa, it aimed at a systemic model, where multiple biological, psychological and social factors were seen as interlinked.[17]

Other, alternative approaches in the 1970s were psychosomatic and somatopsychic approaches, which concentrated on causal links only from psyche to soma, or from soma to psyche, respectively.[17] At present it is commonplace in psychosomatic medicine to state that psyche and soma cannot really be separated for practical or theoretical purposes.[citation needed] A disturbance on any levelsomatic, psychic, or socialwill radiate to all the other levels, too. In this sense, psychosomatic thinking is similar to the biopsychosocial model of medicine.[citation needed]

Many alternative medicine practitioners claim a holistic approach to healing.

A lively debate has run since the end of the 19th century regarding the functional organization of the brain. The holistic tradition (e.g., Pierre Marie) maintained that the brain was a homogeneous organ with no specific subparts whereas the localizationists (e.g., Paul Broca) argued that the brain was organized in functionally distinct cortical areas which were each specialized to process a given type of information or implement specific mental operations. The controversy was epitomized with the existence of a language area in the brain, nowadays known as the Broca's area.[18]

Architecture is often argued by design academics and those practicing in design to be a holistic enterprise.[19] Used in this context, holism tends to imply an all-inclusive design perspective. This trait is considered exclusive to architecture, distinct from other professions involved in design projects.

A holistic brand (also holistic branding) is considering the entire brand or image of the company. For example, a universal brand image across all countries, including everything from advertising styles to the stationery the company has made, to the company colours.

With roots in Schumpeter, the evolutionary approach might be considered the holist theory in economics. They share certain language from the biological evolutionary approach. They take into account how the innovation system evolves over time. Knowledge and know-how, know-who, know-what and know-why are part of the whole business economics. Knowledge can also be tacit, as described by Michael Polanyi. These models are open, and consider that it is hard to predict exactly the impact of a policy measure. They are also less mathematical.

The Taxonomy of Educational Objectives identifies many levels of cognitive functioning, which can be used to create a more holistic education. In authentic assessment, rather than using computers to score multiple choice tests, a standards based assessment uses trained scorers to score open-response items using holistic scoring methods.[20] In projects such as the North Carolina Writing Project, scorers are instructed not to count errors, or count numbers of points or supporting statements. The scorer is instead instructed to judge holistically whether "as a whole" is it more a "2" or a "3". Critics question whether such a process can be as objective as computer scoring, and the degree to which such scoring methods can result in different scores from different scorers.

A major holist movement in the early twentieth century was gestalt psychology. The claim was that perception is not an aggregation of atomic sense data but a field, in which there is a figure and a ground. Background has holistic effects on the perceived figure. Gestalt psychologists included Wolfgang Koehler, Max Wertheimer, Kurt Koffka. Koehler claimed the perceptual fields corresponded to electrical fields in the brain. Karl Lashley did experiments with gold foil pieces inserted in monkey brains purporting to show that such fields did not exist. However, many of the perceptual illusions and visual phenomena exhibited by the gestaltists were taken over (often without credit) by later perceptual psychologists. Gestalt psychology had influence on Fritz Perls' gestalt therapy, although some old-line gestaltists opposed the association with counter-cultural and New Age trends later associated with gestalt therapy. Gestalt theory was also influential on phenomenology. Aron Gurwitsch wrote on the role of the field of consciousness in gestalt theory in relation to phenomenology. Maurice Merleau-Ponty made much use of holistic psychologists such as work of Kurt Goldstein in his "Phenomenology of Perception."

Alfred Adler believed that the individual (an integrated whole expressed through a self-consistent unity of thinking, feeling, and action, moving toward an unconscious, fictional final goal), must be understood within the larger wholes of society, from the groups to which he belongs (starting with his face-to-face relationships), to the larger whole of mankind. The recognition of our social embeddedness and the need for developing an interest in the welfare of others, as well as a respect for nature, is at the heart of Adler's philosophy of living and principles of psychotherapy.

Edgar Morin, the French philosopher and sociologist, can be considered a holist based on the transdisciplinary nature of his work.

Mel Levine, M.D., author of A Mind at a Time,[21] and co-founder (with Charles R. Schwab) of the not-for-profit organization All Kinds of Minds, can be considered a holist based on his view of the 'whole child' as a product of many systems and his work supporting the educational needs of children through the management of a child's educational profile as a whole rather than isolated weaknesses in that profile.

There is an ongoing dispute as to whether anthropology is intrinsically holistic. Supporters of this concept consider anthropology holistic in two senses. First, it is concerned with all human beings across times and places, and with all dimensions of humanity (evolutionary, biophysical, sociopolitical, economic, cultural, psychological, etc.) Further, many academic programs following this approach take a "four-field" approach to anthropology that encompasses physical anthropology, archeology, linguistics, and cultural anthropology or social anthropology.[22]

Some leading anthropologists disagree, and consider anthropological holism to be an artifact from 19th century social evolutionary thought that inappropriately imposes scientific positivism upon cultural anthropology.[23]

The term "holism" is additionally used within social and cultural anthropology to refer to an analysis of a society as a whole which refuses to break society into component parts. One definition says: "as a methodological ideal, holism implies ... that one does not permit oneself to believe that our own established institutional boundaries (e.g. between politics, sexuality, religion, economics) necessarily may be found also in foreign societies."[24]

mile Durkheim developed a concept of holism which he set as opposite to the notion that a society was nothing more than a simple collection of individuals. In more recent times, Louis Dumont[25] has contrasted "holism" to "individualism" as two different forms of societies. According to him, modern humans live in an individualist society, whereas ancient Greek society, for example, could be qualified as "holistic", because the individual found identity in the whole society. Thus, the individual was ready to sacrifice himself or herself for his or her community, as his or her life without the polis had no sense whatsoever.

The French Protestant missionary Maurice Leenhardt coined the term "cosmomorphism" to indicate the state of perfect symbiosis with the surrounding environment which characterized the culture of the Melanesians of New Caledonia. For these people, an isolated individual is totally indeterminate, indistinct, and featureless until he can find his position within the natural and social world in which he is inserted. The confines between the self and the world are annulled to the point that the material body itself is no guarantee of the sort of recognition of identity which is typical of our own culture.[26][27]

Holistic concepts are strongly represented within the thoughts expressed within Logos (per Heraclitus), Panentheism and Pantheism.[citation needed]

In theological anthropology, which belongs to theology and not to anthropology, holism is the belief that body, soul and spirit are not separate components of a person, but rather facets of a united whole.[28]

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Alzheimer’s Disease Living & Managing – WebMD

Posted: November 19, 2016 at 5:41 pm

Living with Alzheimer's disease means caring for the patient -- and caring for the caregiver. Here's how to manage both of those essential tasks.

If you're an Alzheimer's caregiver, you have to take care of yourself, too. Learn why -- and how.

When you're a caregiver for a person withAlzheimer's disease, one of your main goals is to help your loved one do as much he can on his own. Use this checklist to help you help him with daily care.

Here are the basic principles of daily care for a person with Alzheimer's disease.

People with Alzheimer's disease eventually need help with very personal tasks. Here's an overview.

It's not always easy to communicate with a person who has Alzheimer's disease. Here are some tips.

People with Alzheimer's disease can act strangely. Here's how to deal with it.

Alzheimer's diseaseoften begins withmemory loss. But as the disease gets worse, it can cause many other mental, emotional, and physical problems. Here are some ways to deal with the problems that your loved one with Alzheimer'smay face.

The doctor says it's Alzheimer's. How do you handle news like that? To cope, click here.

Life goes on. So can a person with Alzheimer's disease. Here are some tips for daily living with Alzheimer's.

A person with Alzheimer's disease needs both physical and mental care. Here's where to learn about the options for counseling for Alzheimers.

Eating a balanced diet is even more important for person with Alzheimer's. Here are some nutrition tips.

For as long as possible, it's important for a person with Alzheimer's to stay active. Here are some do's and don'ts.

If youre caring for someone withdementiaorAlzheimer's disease, you may have noticed big changes in how they act in the late afternoon or early evening. Doctors call it sundowning, or sundown syndrome.

People with Alzheimers disease go through many changes, andsleep problems are often some of the most noticeable.

Sometimes, people with Alzheimers disease lash out for no clear reason. Aggression may be a symptom of Alzheimers disease itself. If your loved one becomes aggressive, its important to remember that she isnt doing it on purpose. There are also things you can do to make her feel better and keep outbursts from happening.

SomeAlzheimers treatments involvemedications. Others are non-medical Alzheimers therapies like art, music, and more. The goal of an Alzheimers therapy is to help the person maintain a better quality of life.

Most people knowAlzheimer's diseaseaffects the memory. But the symptoms can be physical as well as mental.

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Alzheimer's Disease Living & Managing - WebMD

Caring for Someone With Alzheimer’s Disease

Posted: November 17, 2016 at 9:42 am

Is it Alzheimer's?

Is it forgetfulness, a "senior moment," or Alzheimer's disease (AD)? The following slides are designed to present some signs of Alzheimer's disease. About 1 in 3 people over the age of 65 that die have either Alzheimer's disease or another type of dementia. Over 5 million people in the U.S. currently have Alzheimer's disease.

In early Alzheimer's, memory loss, especially of short-term memories, becomes noticeable. Forgotten recent conversations and repeated similar questions become more frequent. A change in speech, such as not remembering common words, becomes more noticeable in people with Alzheimer's disease. Although this may happen occasionally with people, such memory problems become more frequent and progressively worse in Alzheimer's disease patients.

Mood swings, poor judgment, and changes in appearance (poor hygiene, wearing soiled clothing), and confusion about previously commonly-performed tasks are some of the behavior changes seen in Alzheimers disease patients, especially as the disease progresses.

If there are signs of Alzheimer's in a person, that person should be evaluated by their physician when symptoms first arise. The doctor can help distinguish Alzheimer's disease from other treatable health problems like thyroid problems or electrolyte imbalances that may cause similar symptoms.

Diagnosis of Alzheimer's disease is based on clinical criteria; there is no definitive test currently available for Alzheimer's disease. Mental status tests can help evaluate the patients mental and memory function. Other blood tests, brain scans (CT, MRI, PET, or SPECT), electroencephalograms (EEGs), and others are used to determine if there are other causes (metabolic, stroke, brain tumor) that could be causing the Alzheimer's disease symptoms.

Alzheimer's disease results in brain nerve cells dying; this cell loss throughout the brain is eventually visualized in brain scans as enlarged ventricles and smaller (shrinking) areas of brain tissue. The result is disrupted cellular communication that is evidenced by the person's decline in memory, speech, comprehension, and other changes.

Alzheimer's disease is progressive, but its progression varies from patient to patient. The average survival time varies from about 3 to 9 years; some patients survive about 20 years with a slow progression of symptoms.

Alzheimer's progression leads to changes that affect daily life. Patients develop increasing difficulties such as balancing a checkbook or getting lost easily. Progression can result in the inability to recognize loved ones, loss of language skills, and physical problems such as loss of balance or incontinence.

As mentioned above, progressive loss of mental and physical abilities occurs with Alzheimer's patients. A difficult task is convincing such a patient that it is no longer safe for them to drive. Many patients may not understand their progressive decline so they may resist this effort. Your loved one may benefit from discussions and plans for alternate transportation; if not, involve the patients doctor to help. If the patient still insists on driving, you may need to contact the Department of Motor Vehicles to assess the person's driving abilities.

Exercise should be encouraged for people with Alzheimer's because it improves muscle strength, coordination, and may improve mood and reduce anxiety. However, the person should not be stressed to avoid making symptoms worse. Walking, gardening, or visiting a museum or park are examples of mild-to-moderate exercise activities that may help improve strength and reduce anxiety.

There is no medical cure or way to stop progressive nerve cell damage in Alzheimer's patients. However, some medications (Aricept, Exelon, Razadyne, Namenda XR) may help slow the progression of the disease, treat symptoms (neuroleptic agents, antidepressants), and allow the patient to be relatively independent longer.

An Alzheimer's disease patient's caregiver is a difficult job that needs to strike a balance between trying to maximize the patient's independence and providing assistance and assuming responsibility for tasks the patient can no longer do. For example, the patient may have difficulty remembering tasks, so the caregiver can leave notes or other reminders to aid the patient in tasks the patient can still do.

As Alzheimer's disease progresses, the challenges to be a caretaker also progress. Early Alzheimer's disease patients may cooperate well with caregivers because they still may have an understanding of the disease process. As Alzheimer's disease progresses, many patients may develop depression, anxiety, resentment, and paranoia. Caretakers may become exposed to belligerent or even violent behaviors. It may be difficult for some caretakers to realize that Alzheimer's disease is the cause of this change; violent behavior should cause a caregiver to immediately notify the patient's doctor.

Sundown syndrome (also termed sundowning) is a condition that may occur in about 20% of Alzheimer's disease patients that results in anxiety, agitation, and/or confusion at the end of the day when the sun goes down. The cause is not known but may be related to disorientation, mental or physical exhaustion, anxiety, and paranoia as light dims and shadows appear. It may be reduced by keeping the home well lit starting in the afternoon, having the patient view TV programs that occupy their interest, and providing a comfortable sleeping area with nightlights.

Alzheimer's patients may eventually have difficulty remembering names, even those of close family members. One good aid is a photo album with the family member's name listed under their picture. Some patients will no longer recognize family members. Although this is difficult for some family members to accept, it may be helpful to remind them that Alzheimer's disease is causing this situation and it is not caused by the patient.

Alzheimer's disease caregivers need to understand they can be affected by the intense demands of their job. About 1 in 3 Alzheimer's disease caregivers develops symptoms of depression. About 60% of caretakers rate the emotional stress of Alzheimer's disease caregiving as high or very high. Signs of caregiver stress include sadness, anger, mood swings, headaches, back pain, and difficulty sleeping and concentrating.

An Alzheimer's disease caregiver has a difficult job; they need to be careful not to burnout. Caregivers need to make time for themselves every day to both relax and to get some physical exercise. Caregivers can find local support groups. Groups can be located through the Alzheimer's Association Helpline (800-272-3900).

Be prepared. While the Alzheimer's disease patient is still able to make good judgments, the patient should, with a loved one present if necessary, contact an attorney to draw up legal documents (advance directives). These documents can designate the patient's medical treatments, end-of-life care, and designate a person to make decisions (medical, financial) when the Alzheimer's disease patient can no longer make decisions for themselves.

The desire of many Alzheimer's disease patients is to stay at home for as long as they can. This time can be extended with careful daily planning and with a home health aide that can assist the person in daily activities like personal hygiene, meal preparation, or transportation. The local Alzheimer's support groups can help caregivers find home health aide organizations.

Some Alzheimer's disease patients with more advanced symptoms need more care than can be provided at home. Assisted living facilities (ALF) may be the next step in care where housing, meals, activities, and other amenities are provided. Other Alzheimer's disease patients may need a special care unit that has 24-hour nursing supervision of patients with dementia.

As Alzheimer's disease progresses, the symptoms may become more severe. The person may not be able to talk, walk, or recognize anyone. Some patients become bedridden and even lose the ability to swallow. Such patients have reached the end-stages of Alzheimer's disease and may benefit from hospice care. Hospice care usually provides nursing care and around-the-clock pain relief and comfort to the terminally ill.

Because children may become upset, afraid, or confused about the Alzheimer's disease progression in a family member, it is important to try to explain how the family member has an illness that is causing these changes and actions. Changes within their brain are the cause and their loved one cannot control these changes. The Alzheimer's Association offers videos and suggestions to help children and teens to understand the effect of Alzheimer's disease on a family member.

To date, there is no definitive way proven to prevent Alzheimer's disease. However, researchers are investigating the effects of mental and physical fitness, diet, and environment on Alzheimer's disease development. Current studies suggest a heart-healthy diet (a diet rich in fish, nuts, vegetables, fruit, and grains) may help protect the brain from Alzheimer's disease and other problems. Similar studies suggest that people who exercise regularly decrease their risk of developing Alzheimer's disease.



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Caring for Someone With Alzheimer's Disease

Vital Cell, 180 capsules | Tango Advanced Nutrition

Posted: November 15, 2016 at 3:41 pm

What is the recommended daily dose of Vital Cell?

We recommend Vital Cell as a general daily herbal supplement that can be combined with your daily vitamin and mineral supplements. The recommended daily dose of Vital Cell is 1-2 capsules, 2-3 times per day. Each bottle contains 180 capsules and is a one-month supply at 6 capsules per day.

How much Vital Cell can I safely take in a day?

You can take up to 12 capsules of Vital Cell per day and expect to get additional benefit sooner. However, for most people 6 capsules is very effective at promoting circulatory and immune health.

How do I know Vital Cell is working for me?

You should expect gradual improvements in your overall health with regular use of Vital Cell. By promoting circulatory and immune system health you should feel better throughout the day and night. You should also note positive changes in the quality of your blood in blood tests taken at least 30 days after starting Vital Cell.

Do I have to take Vital Cell forever?

Individual circumstances will determine how quickly your circulatory and immune health will improve when taking Vital Cell. Issues involving circulatory and immune system function may be long-standing and may determine how soon you notice positive changes, and how long you may need or wish to take the formula.

When positive changes in circulation and immune function occur, you can lower your dose gradually by one capsule at a time every 4-5 days and expect to see continued benefits. The reason for this is that, as with all true health-promoting supplements, Vital Cell provides restorative results.

However, as a daily supplement, best results for most people will occur when taking 6 capsules per day.

When should I take Vital Cell?

The most important consideration in taking Vital Cell is to take it daily and consistently. Convenience makes regular use possible, so including Vital Cell in your regular supplement routine is a good idea. You can take Vital Cell with or away from meals. Morning and early evening are the best times to take the formula to spread out its benefits over a 24-hour period. Some men and women take Vital Cell about 1 hour before bedtime to make sure they have beneficial nutrients working while they are sleeping.

Can I take Vital Cell with other supplements?

Yes, you can take Vital Cell with, and at the same time, as you take other dietary supplements.

I take over-the-counter/prescriptive medicines for better circulation. Can I take Vital Cell with them?

You can take Vital Cell while using medicines for your circulation or any other condition. However, you should always take Vital Cell or any other supplement at least 2 hours away from any medication to reduce any possible risk of interaction.

As a special precaution, you should not take Vital Cell if you are on the drastic blood thinning medication warfarin/coumadin.

You should also exercise caution when taking aspirin, plavix or other blood-thinning medication while also using Vital Cell.

If you have any questions about using Vital Cell or any other supplement while you are using medications of any type, ask your doctor or pharmacist for advice.

Can I combine Vital Cell with some of your other products like OsteoPhase, CardioPhase, or Herbal Boost?

Yes, you can take Vital Cell with OsteoPhase for bone health. We suggest that you take 1 capsule of Vital Cell for each 2 capsules of OsteoPhase.

You can also take Vital Cell and CardioPhase together. We suggest starting at a lower dose of each formula than that recommended on the bottle, as there is some overlap in function between the supplements. You can increase the doses of each by one capsule per day until you feel the effect that you are trying to achieve.

As noted above, you do not need to take Vital Cell and Herbal Boost together for circulatory health. For quick restoration, we suggests you take Herbal Boost for 3-4 months then switch to Vital Cell as your daily circulation and immune system supplement.

You can also call one of our product specialists if you have questions about how best to combine our formulas. The toll-free number for product questions is 1-866-778-2646, ext. 2.

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Vital Cell, 180 capsules | Tango Advanced Nutrition

Nutrition in Cancer Care (PDQ)Patient Version – National …

Posted: November 6, 2016 at 5:50 am

Overview of Nutrition in Cancer Care Key Points

Nutrition is a process in which food is taken in and used by the body for growth, to keep the body healthy, and to replace tissue. Good nutrition is important for good health. Eating the right kinds of foods before, during, and after cancer treatment can help the patient feel better and stay stronger. A healthy diet includes eating and drinking enough of the foods and liquids that have the important nutrients (vitamins, minerals, protein, carbohydrates, fat, and water) the body needs.

When the body does not get or cannot absorb the nutrients needed for health, it causes a condition called malnutrition or malnourishment.

This summary is about nutrition in adults with cancer.

Nutrition therapy is used to help cancer patients get the nutrients they need to keep up their body weight and strength, keep body tissue healthy, and fight infection. Eating habits that are good for cancer patients can be very different from the usual healthy eating guidelines.

Healthy eating habits and good nutrition can help patients deal with the effects of cancer and its treatment. Some cancer treatments work better when the patient is well nourished and gets enough calories and protein in the diet. Patients who are well nourished may have a better prognosis (chance of recovery) and quality of life.

Some tumors make chemicals that change the way the body uses certain nutrients. The body's use of protein, carbohydrates, and fat may be affected, especially by tumors of the stomach or intestines. A patient may seem to be eating enough, but the body may not be able to absorb all the nutrients from the food.

For many patients, the effects of cancer and cancer treatments make it hard to eat well. Cancer treatments that affect nutrition include:

When the head, neck, esophagus, stomach, or intestines are affected by the cancer treatment, it is very hard to take in enough nutrients to stay healthy.

The side effects of cancer and cancer treatment that can affect eating include:

Cancer and cancer treatments may affect taste, smell, appetite, and the ability to eat enough food or absorb the nutrients from food. This can cause malnutrition (a condition caused by a lack of key nutrients). Malnutrition can cause the patient to be weak, tired, and unable to fight infections or get through cancer treatment. Malnutrition may be made worse if the cancer grows or spreads. Eating too little protein and calories is a very common problem for cancer patients. Having enough protein and calories is important for healing, fighting infection, and having enough energy.

Anorexia (the loss of appetite or desire to eat) is a common symptom in people with cancer. Anorexia may occur early in the disease or later, if the cancer grows or spreads. Some patients already have anorexia when they are diagnosed with cancer. Almost all patients who have advanced cancer will have anorexia. Anorexia is the most common cause of malnutrition in cancer patients.

Cachexia is a condition marked by a loss of appetite, weight loss, muscle loss, and general weakness. It is common in patients with tumors of the lung, pancreas, and upper gastrointestinal tract. It is important to watch for and treat cachexia early in cancer treatment because it is hard to correct.

Cancer patients may have anorexia and cachexia at the same time. Weight loss can be caused by eating fewer calories, using more calories, or both.

It is important that cancer symptoms and side effects that affect eating and cause weight loss are treated early. Both nutrition therapy and medicine can help the patient stay at a healthy weight. Medicine may be used for the following:

See the Nutrition Therapy in Cancer Care section and the Treatment of Symptoms section for more information.

Screening is used to look for nutrition risks in a patient who has no symptoms. This can help find out if the patient is likely to become malnourished, so that steps can be taken to prevent it.

Assessment checks the nutritional health of the patient and helps to decide if nutrition therapy is needed to correct a problem.

Screening and assessment may include questions about the following:

A physical exam is also done to check the body for general health and signs of disease. The doctor will look for loss of weight, fat, and muscle, and for fluid buildup in the body.

Early nutrition screening and assessment help find problems that may affect how well the patient's body can deal with the effects of cancer treatment. Patients who are underweight or malnourished may not be able to get through treatment as well as a well-nourished patient. Finding and treating nutrition problems early can help the patient gain weight or prevent weight loss, decrease problems with the treatment, and help recovery.

A nutrition support team will check the patient's nutritional health often during cancer treatment and recovery. The team may include the following specialists:

A patient whose religion doesn't allow eating certain foods may want to talk with a religious advisor about allowing those foods during cancer treatment and recovery.

The main goals of nutrition therapy for patients in active treatment and recovery are to provide nutrients that are missing, maintain nutritional health, and prevent problems. The health care team will use nutrition therapy to do the following:

Good nutrition continues to be important for patients who are in remission or whose cancer has been cured.

The goals of nutrition therapy for patients who have advanced cancer include the following:

See the Nutrition in Advanced Cancer section for more information.

It is best to take in food by mouth whenever possible. Some patients may not be able to take in enough food by mouth because of problems from cancer or cancer treatment. Medicine to increase appetite may be used.

A patient who is not able to take in enough food by mouth may be fed using enteral nutrition (through a tube inserted into the stomach or intestines) or parenteral nutrition (infused into the bloodstream). The nutrients are given in liquid formulas that have water, protein, fats, carbohydrates, vitamins, and/or minerals.

Nutrition support can improve a patient's quality of life during cancer treatment, but there are harms that should be considered before making the decision to use it. The patient and health care providers should discuss the harms and benefits of each type of nutrition support. (See the Nutrition in Advanced Cancer section below for more information on deciding whether to use nutrition support.)

Enteral nutrition is giving the patient nutrients in liquid form (formula) through a tube that is placed into the stomach or small intestine. The following types of feeding tubes may be used:

The type of formula used is based on the specific needs of the patient. There are formulas for patients who have special health conditions, such as diabetes. Formula may be given through the tube as a constant drip (continuous feeding) or 1 to 2 cups of formula can be given 3 to 6 times a day (bolus feeding).

Enteral nutrition is sometimes used when the patient is able to eat small amounts by mouth, but cannot eat enough for health. Nutrients given through a tube feeding add the calories and nutrients needed for health.

If enteral nutrition is to be part of the patient's care after leaving the hospital, the patient and caregiver will be trained to do the nutrition support care at home.

Parenteral nutrition is used when the patient cannot take food by mouth or by enteral feeding. Parenteral feeding does not use the stomach or intestines to digest food. Nutrients are given to the patient directly into the blood, through a catheter (thin tube) inserted into a vein. These nutrients include proteins, fats, vitamins, and minerals.

Parenteral nutrition is used only in patients who need nutrition support for five days or more.

A central venous catheter is placed beneath the skin and into a large vein in the upper chest. The catheter is put in place by a surgeon. This type of catheter is used for long-term parenteral feeding.

A peripheral venous catheter is placed into a vein in the arm. A peripheral venous catheter is put in place by trained medical staff. This type of catheter is usually used for short-term parenteral feeding.

The patient is checked often for infection or bleeding at the place where the catheter enters the body.

If parenteral nutrition is to be part of the patient's care after leaving the hospital, the patient and caregiver will be trained to do the nutrition support care at home.

Going off parenteral nutrition support needs to be done slowly and is supervised by a medical team. The parenteral feedings are decreased by small amounts over time until they can be stopped, or as the patient is changed over to enteral or oral feeding.

The body needs extra energy and nutrients to heal wounds, fight infection, and recover from surgery. If the patient is malnourished before surgery, it may cause problems during recovery, such as poor healing or infection. For these patients, nutrition care may begin before surgery.

Most cancer patients are treated with surgery. Surgery that removes all or part of certain organs can affect a patient's ability to eat and digest food. The following are nutrition problems caused by specific types of surgery:

All of these can affect the patient's ability to eat normally. Emotional stress about the surgery itself also may affect appetite.

Nutrition therapy can relieve or decrease the side effects of surgery and help cancer patients get the nutrients they need. Nutrition therapy may include the following:

It is common for patients to have pain, tiredness, and/or loss of appetite after surgery. For a short time, some patients may not be able to eat what they usually do because of these symptoms. Following certain tips about food may help. These include:

Chemotherapy affects fast-growing cells and is used to treat cancer because cancer cells grow and divide quickly. Healthy cells that normally grow and divide quickly may also be killed. These include cells in the mouth, digestive tract, and hair follicles.

Chemotherapy may cause side effects that cause problems with eating and digestion. When more than one anticancer drug is given, more side effects may occur or they may be more severe. The following side effects are common:

Patients who have side effects from chemotherapy may not be able to eat normally and get all the nutrients they need to restore healthy blood counts between treatments. Nutrition therapy can help relieve these side effects, help patients recover from chemotherapy, prevent delays in treatment, prevent weight loss, and maintain general health. Nutrition therapy may include the following:

Radiation therapy can kill cancer cells and healthy cells in the treatment area. The amount of damage depends on the following:

Radiation therapy to any part of the digestive system often has side effects that cause nutrition problems. Most of the side effects begin a few weeks after radiation therapy begins and go away a few weeks after it is finished. Some side effects can continue for months or years after treatment ends.

The following are some of the more common side effects:

Radiation therapy may also cause tiredness, which can lead to a decrease in appetite.

Nutrition therapy during radiation treatment can help the patient get enough protein and calories to get through treatment, prevent weight loss, help wound and skin healing, and maintain general health. Nutrition therapy may include the following:

Patients who receive high-dose radiation therapy to prepare for a bone marrow transplant may have many nutrition problems and should see a dietitian for nutrition support.

See the Stem Cell Transplant and Nutrition section for more information.

The side effects of biologic therapy are different for each patient and each type of biologic agent. The following nutrition problems are common:

The side effects of biologic therapy can cause weight loss and malnutrition if they are not treated. Nutrition therapy can help patients receiving biologic therapy get the nutrients they need to get through treatment, prevent weight loss, and maintain general health.

Chemotherapy, radiation therapy, and medicines used for a stem cell transplant may cause side effects that keep a patient from eating and digesting food as usual. Common side effects include the following:

Transplant patients have a very high risk of infection. High doses of chemotherapy or radiation therapy decrease the number of white blood cells, which fight infection. It is especially important that transplant patients avoid getting infections.

Patients who have a transplant need plenty of protein and calories to get through and recover from the treatment, prevent weight loss, fight infection, and maintain general health. It is also important to avoid infection from bacteria in food. Nutrition therapy during transplant treatment may include the following:

See the Low White Blood Cell Counts and Infections section for more information.

When side effects of cancer or cancer treatment affect normal eating, changes can be made to help the patient get the nutrients needed. Medicines may be given to increase appetite. Eating foods that are high in calories, protein, vitamins, and minerals is usually best. Meals should be planned to meet the patient's nutrition needs and tastes in food. The following are some of the more common symptoms caused by cancer and cancer treatment and ways to treat or control them.

Anorexia (the loss of appetite or desire to eat) is one of the most common problems for cancer patients. Eating in a calm, comfortable place and getting regular exercise may improve appetite. The following may help cancer patients who have a loss of appetite:

See the NCI website for Eating Hints: Before, During, and After Cancer Treatment, which has recipes such as Lactose-Free Double Chocolate Pudding, Banana Milkshake, and Fruit and Cream. For a free copy of this booklet, call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237).

Changes in how foods taste may be caused by radiation treatment, dental problems, mouth sores and infections, or some medicines. Many cancer patients who receive chemotherapy notice a bitter taste or other changes in their sense of taste. A sudden dislike for certain foods may occur. This can cause a loss of appetite, weight loss, and a decreased quality of life. Some or all of a normal sense of taste may return, but it may take up to a year after treatment ends. The following may help cancer patients who have taste changes:

Taking zinc sulfate tablets during radiation therapy to the head and neck may help a normal sense of taste come back faster after treatment.

Dry mouth is often caused by radiation therapy to the head and neck and by certain medicines. Dry mouth may affect speech, taste, and the ability to swallow or to use dentures or braces. There is also an increased risk of cavities and gum disease because less saliva is made to wash the teeth and gums.

The main treatment for dry mouth is drinking plenty of liquids. Other ways to help relieve dry mouth include the following:

See the Dry Mouth section of the PDQ summary on Oral Complications of Chemotherapy and Head/Neck Radiation for more information.

Mouth sores can be caused by chemotherapy and radiation therapy. These treatments affect fast-growing cells, such as cancer cells. Normal cells inside the mouth also grow quickly and may be damaged by these cancer treatments. Mouth sores can be painful and become infected or bleed and make it hard to eat. By choosing certain foods and taking good care of their mouths, patients can usually make eating easier. The following can help patients who have mouth sores and infections:

See the Oral Mucositis and Infection sections of the PDQ summary on Oral Complications of Chemotherapy and Head/Neck Radiation for more information on mouth sores and infections.

Nausea caused by cancer treatment can affect the amount and kinds of food eaten. The following may help cancer patients control nausea:

See the PDQ summary on Nausea and Vomiting for more information.

Diarrhea may be caused by cancer treatments, surgery on the stomach or intestines, or by emotional stress. Long-term diarrhea may lead to dehydration (lack of water in the body) or low levels of salt and potassium, which are important minerals needed by the body.

The following may help cancer patients control diarrhea:

See the Dehydration (Lack of Fluid) section for more information.

A low white blood cell count may be caused by radiation therapy, chemotherapy, or the cancer itself. Patients who have a low white blood cell count have an increased risk of infection. The following may help cancer patients prevent infections when white blood cell counts are low:

The body needs plenty of water to replace the fluids lost every day. Nausea, vomiting, and pain may keep the patient from drinking and eating enough to get the amount of water the body needs. Long-term diarrhea causes a loss of fluid from the body. One of the first signs of dehydration (lack of water in the body) is feeling very tired. The following may help cancer patients prevent dehydration:

It is very common for cancer patients to have constipation (fewer than three bowel movements a week). Constipation may be caused by the following:

Preventing and treating constipation is a part of cancer care.

To prevent constipation:

To treat constipation:

Good food sources of fiber include the following:

See the Constipation section of the PDQ summary on Gastrointestinal Complications for more information.

The goal of palliative care is to improve the quality of life of patients who have a serious or life-threatening disease. Palliative care is meant to prevent or treat symptoms, side effects, and psychological, social, and spiritual problems caused by a disease or its treatment.

Palliative care for patients with advanced cancer includes nutrition therapy (see the Treatment of Symptoms section) and/or drug therapy.

It is common for patients with advanced cancer to want less food. Patients usually prefer soft foods and clear liquids. Those who have problems swallowing may do better with thick liquids than with thin liquids. Patients often do not feel much hunger at all and may need very little food.

In patients with advanced cancer, most foods are allowed. During this time, eating can be focused on pleasure rather than getting enough nutrients. Patients usually cannot eat enough of any food that might cause a problem. However, some patients may need to stay on a special diet. For example, patients with cancer that affects the abdomen may need a soft diet to keep the bowel from getting blocked.

Answering the following questions may help to make decisions about using nutrition support:

Cancer patients and their caregivers have the right to make informed decisions. The healthcare team and a registered dietitian can explain the benefits and risks of using nutrition support for patients with advanced cancer. In most cases, there are more harms than benefits, especially with parenteral nutrition support. However, for someone who still has good quality of life but is unable to get enough food and water by mouth, enteral feedings may be best. The benefits and risks of enteral nutrition during advanced cancer include the following:


Cancer patients may be treated with a number of drugs. Taking certain foods and drugs together may decrease or change how well the drugs work or cause life-threatening side effects. The following table lists some of the food and drug interactions that may occur with certain anticancer drugs:

Talk with your doctor about possible food and drug interactions.

Taking some herbal supplements with certain foods and drugs may change how well cancer treatment works or cause life-threatening side effects. Talk with your doctor about how herbal supplements may affect your cancer treatment.

Everyone needs a healthy diet and exercise for good health and to help prevent disease. Cancer survivors have special health needs, especially because of the risks of late effects and the cancer coming back. Studies have shown that a healthy diet helps to prevent late effects such as obesity, heart disease, and metabolic syndrome. Researchers are also studying whether certain diet and exercise habits in cancer survivors can keep cancer from coming back or keep new cancers from forming.

Surveys show that many cancer survivors do not follow cancer prevention guidelines and have lifestyle behaviors that may increase their risk for late effects or make late effects worse. Education programs can help cancer survivors learn how to make behavior changes that keep them healthier. Programs that cover diet, exercise, and stress management are more likely to help cancer survivors make lasting changes.

The effects of diet and lifestyle on cancer continue to be studied.

The American Cancer Society and the American Institute for Cancer Research both have dietary guidelines that may help prevent cancer. Their guidelines are a lot alike and include the following:

Study results include the following:

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Nutrition in Cancer Care (PDQ)Patient Version - National ...