Smart Economy

Do palm trees hold the key to immortality?

 

Recent review reveals unique cellular structure and function that may contribute to their long life-span

		IMAGE:Detail of a single vascular bundle from a transverse section of the mature stem, embedded in celloidin and stained with safranin and fast green. It shows the result of sustained... Click here for more information.

For centuries, humans have been exploring, researching, and, in some cases, discovering how to stave off life-threatening diseases, increase life spans, and obtain immortality.  Biologists, doctors, spiritual gurus, and even explorers have pursued these quests—one of the most well-known examples being the legendary search by Ponce de León for the "Fountain of Youth." Yet the key to longevity may not lie in a miraculous essence of water, but rather in the structure and function of cells within a plant—and not a special, mysterious, rare plant, but one that we may think of as being quite commonplace, even ordinary: the palm.  

As an honors botany student at the University of Leeds, P. Barry Tomlinson wrote a prize-winning essay during his final year titled, "The Span of Life."  Fifty years later, Tomlinson (now a Distinguished Professor at The Kampong Garden of the National Tropical Botanical Garden, Miami, FL) teamed up with graduate student Brett Huggett (Harvard University, MA) to write a review paper exploring the idea that palms may be the longest-lived tree, and whether this might be due to genetic underpinnings.  Having retained his essay in his personal files, Tomlinson found that it provided an excellent literature background for working on the question of cell longevity in relation to palms.  Together, Tomlinson and Huggett published their review in the December issue of the American Journal of Botany (http://www.amjbot.org/content/99/12/1891.full.pdf+html).

A component of an organism's life span that biologists have been particularly interested in is whether longevity is genetically determined and adaptive. For botanists, discovering genetic links to increasing crop production and the reproductive lifespan of plants, especially long-lived ones such as trees, would be invaluable. 

In their paper, Tomlinson and Huggett emphasize that in many respects, an organisms' life span, or longevity, is determined by the period of time in which its cells remain functionally metabolically active.  In this respect, plants and animals differ drastically, and it has to do with how they are organized—plants are able to continually develop new organs and tissues, whereas animals have a fixed body plan and are not able to regenerate senescing organs.  Thus, plants can potentially live longer than animals.

"The difference in potential cell longevity in plants versus animals is a significant point," states Tomlinson. "It is important to recognize that plants, which are so often neglected in modern biological research, can be informative of basic cell biological features in a way that impacts human concern at a fundamental level."

The authors focused their review on palm trees because palms have living cells that may be sustained throughout an individual palm's lifetime, and thus, they argue, may have some of the longest living cells in an organism.  As a comparison, in most long-lived trees, or lignophytes, the main part, or trunk, of the tree is almost entirely composed of dead, woody, xylem tissues, and in a sense is essentially a supportive skeleton of the tree with only an inner ring of actively dividing cells.  For example, the skeleton of Pinus longaeva may be up to 3000 years old, but the active living tissues can only live less than a century.

In contrast, the trunks of palms consist of cells that individually live for a long time, indeed for the entire life of an individual.

Which brings up the question of just how long can a palm tree live? The authors point out that palm age is difficult to determine, primarily because palms do not have secondary growth and therefore do not put down annual or seasonal growth rings that can easily be measured.  However, age can be quite accurately assessed based on rate of leaf production and/or visible scars on the trunk from fallen leaves.  Accordingly, the authors found that several species of palm have been estimated to live as long as 100 and even up to 740 years.  The important connection here is that while the "skeleton" of the palm may not be as old as a pine, the individual cells in its trunk lived, or were metabolically active, as long as, or longer than those of the pine's. 

Most plants, in addition to increasing in height as they age, also increase in girth, putting down secondary vascular tissue in layers both on the inner and outer sides of the cambium as they grow.  However, palms do not have secondary growth, and there is no addition of secondary vascular tissue.  Instead, stem tissues are laid down in a series of interconnected vascular bundles—thus, not only is the base of the palm the oldest and the top the youngest, but these tissues from old to young, from base to top, must also remain active in order to provide support and transport water and nutrients throughout the tree. 

		IMAGE:This shows Sabal causiarum, native to Puerto Rico, planted in 1932 at the Montgomery Botanical Center, Coral Gables Florida and in the prime of its long life (estimated height, 20... Click here for more information.

Indeed, the authors illustrate this by reviewing evidence of sustained primary growth in two types of palms, the coconut and the sago palm. These species represent the spectrum in tissue organization from one where cells are relatively uniform and provide both hydraulic and mechanical functions (the coconut) to one where these functions are sharply divided with the inner cells functioning mainly for transporting water and nutrients and the outer ones for mechanical support (the sago palm).  This represents a progression in specialization of the vascular tissues.

Moreover, there is evidence of continued metabolic activity in several types of tissues present in the stems of palms, including vascular tissue, fibers, ground tissue, and starch storage.  Since the vascular tissues in palms are nonrenewable, they must function indefinitely, and Tomlinson and Huggett point out that sieve tubes and their companion cells are remarkable examples of cell longevity as they maintain a long-distance transport function without replacement throughout the life of the stem, which could be for centuries.

Despite several unique characteristics of palms, including the ability to sustain metabolically active cells in the absence of secondary tissues, seemingly indefinitely, unlike conventional trees, in which metabolically active cells are relatively short-lived, the authors do not conclude that the extended life span of palms is genetically determined.

"We are not saying that palms have the secret of eternal youth, and indeed claim no special chemical features which allows cells in certain organisms to retain fully differentiated cells with an indefinite lifespan," states Tomlinson. "Rather, we emphasize the distinctive developmental features of palm stems compared with those in conventional trees."

Tomlinson indicates that this reflects the neglect of the teaching of palm structure in modern biology courses. "This paper raises incompletely understood aspects of the structure and development of palms, emphasizing great diversity in these features," he concludes. "This approach needs elaborating in much greater detail, difficult though the subject is in terms of conventional approaches to plant anatomy."

###

Tomlinson, P. Barry and Brett A. Huggett. 2012. Cell longevity and sustained primary growth in palm stems. American Journal of Botany 99(12): 1891-1902. DOI: 10.3732/ajb.1200089

The full article in the link mentioned is available for no charge for 30 days following the date of this summary at http://www.amjbot.org/content/99/12/1891.full.pdf+html. After this date, reporters may contact Richard Hund at ajb@botany.org for a copy of the article.

The Botanical Society of America (www.botany.org) is a non-profit membership society with a mission to promote botany, the field of basic science dealing with the study and inquiry into the form, function, development, diversity, reproduction, evolution, and uses of plants and their interactions within the biosphere. It has published the American Journal of Botany (www.amjbot.org) for nearly 100 years. In 2009, the Special Libraries Association named the American Journal of Botany one of the Top 10 Most Influential Journals of the Century in the field of Biology and Medicine.

For further information, please contact the AJB staff at ajb@botany.org.

Researchers define key events early in the process of cellular aging

Studies bring unprecedented clarity to aging process and provide paradigm for studying how genes and environment -- including calorie restriction -- may influence lifespan SEATTLE – For the first time, scientists at Fred Hutchinson Cancer Research Center have defined key events that take place early in the process of cellular aging. Together the discoveries, made through a series of experiments in yeast, bring unprecedented clarity to the complex cascade of events that comprise the aging process and pave the way to understanding how genetics and environmental factors like diet interact to influence lifespan, aging and age-related diseases such as cancer and neurodegenerative disorders. The findings, including unexpected results that link aspects of aging and lifespan to a mechanism cells use to store nutrients, are described in the Nov. 21 issue of Nature by co-authors Daniel Gottschling, Ph.D., a member of the Hutchinson Center's Basic Sciences Division, and Adam Hughes, Ph.D., a postdoctoral fellow in the Gottschling Lab. The researchers found the acidity of a structure in yeast cells known as the vacuole is critical to aging and the functioning of mitochondria – the power plants of the cell. They also describe a novel mechanism, which may have parallels in human cells, by which calorie restriction extends lifespan. The work began with Hughes and Gottschling searching for the source of age-related damage in mitochondria. "Normally, mitochondria are beautiful, long tubes, but as cells get older, the mitochondria become fragmented and chunky," said Gottschling, also an affiliate professor in the Department of Genome Sciences at the University of Washington. "The changes in shape seen in aging yeast cells are also observed in certain human cells, such as neurons and pancreatic cells, and those changes have been associated with a number of age-related diseases in humans." What causes mitochondria to become distorted and dysfunctional as cells age had long been a mystery, but Gottschling and Hughes have discovered that specific changes in the vacuole lead directly to its malfunctioning. The vacuole – and its counterpart in humans and other organisms, the lysosome – has two main jobs: degrading proteins and storing molecular building blocks for the cell. To perform those jobs, the interior of the vacuole must be highly acidic. Hughes and Gottschling found that the vacuole becomes less acidic relatively early in the yeast cell's lifespan and, critically, that the drop in acidity hinders the vacuole's ability to store certain nutrients. This, in turn, disrupts the mitochondria's energy source, causing them to break down. Conversely, when Hughes prevented the drop in vacuolar acidity, the mitochondria's function and shape were preserved and the yeast cells lived longer. "Until now, the vacuole's role in breaking down proteins was thought to be of primary importance. We were surprised to learn it was the storage function, not protein degradation, that appears to cause mitochondrial dysfunction in aging yeast cells," Hughes said. The unexpected discovery prompted Hughes and Gottschling to investigate the effects of calorie restriction, which is known to extend the lifespan of yeast, worms, flies and mammals, on vacuolar acidity. They found that calorie restriction – that is, limiting the raw material cells need – delays aging at least in part by boosting the acidity of the vacuole. "Now that we have preliminary evidence in yeast of how calorie restriction extends lifespan, our hope is that it can be translated to higher organisms like humans," Hughes said. Given the similarities in the fundamental biology of yeast and human cells, the researchers' newly defined link between what cells "eat" and how they age could shed valuable light on the events that lead to age-related disorders in humans. "There has been a lot in the scientific literature and the general media lately about how what you eat affects the aging process, but it has been incredibly confusing. Now we have a new paradigm for understanding how genetics and environment interact to influence lifespan, aging and age-related diseases. That's what I'm really excited about," Gottschling said. Gottschling and Hughes speculate that if the vacuole's declining acidity limits its ability to store certain nutrients and metabolites, they may build up in the cell, flooding the mitochondria. Overwhelmed, the mitochondria use up all their energy – essentially burning out their motors – taking in the surplus. With no power left to import the proteins they need to maintain their elegant shape and execute their regular duties, the mitochondria literally break down. Gottschling and his colleagues are now investigating this hypothesis in detail. They are also exploring what triggers the initial drop in the vacuole's acidity. The latter research question is of particular interest because the researchers found that even though vacuolar acidity drops as mother yeast cells age, the acidity in the vacuoles of their newborn daughter cells is normal. This corresponds to previous findings in the field that all daughter yeast cells have the same potential lifespan, regardless of the age of their mothers. The resetting of the daughter's vacuolar acidity is the earliest event yet observed in cellular rejuvenation, a phenomenon in which age-related defects are seemingly erased in an organism's offspring. This could help explain how the act of cell division itself contributes to aging. These results are just the newest chapter in a "decade-old interest," according to Gottschling. He and his colleagues have made several landmark discoveries in the past 10 years, including finding that aging yeast cells exhibit the same genomic instability seen in human cancer cells and proving that mitochondrial dysfunction causes that instability. Gottschling's team also has developed innovative tools to leverage the power of yeast as a model organism, including a technique called the Mother Enrichment Program that makes experiments more efficient by enabling researchers to generate large populations of aging yeast cells. "It's worth using yeast to study complex things like aging because a lot of person-years of research have gone into understanding the fundamentals. The genetic and cell-biology tools available for studying yeast are unparalleled," Gottschling said. "Having the proper tools is like having new glasses; you can see things you never could before, and once you start to see new things, you can dissect them to understand how they work." In addition to the latest eye-popping technology, the researchers relied on sheer tenacity – with a little help from motion-sickness pills – in pursuit of their discoveries. Some of the painstaking experiments required Hughes to delicately manipulate individual yeast cells as they divided every two hours for days at a time. For another series of experiments that lasted several months, Hughes took Dramamine to ward off the queasiness that came with inspecting brightly colored yeast cells as they streaked across his microscope's field of view. "There were definitely tough points, but it was worth it when we knew the story as a whole. Showing that the change in vacuolar acidity was real and that it mattered – that it affected lifespan – made the grueling experiments worthwhile," Hughes said. Gottschling is an elected member of the National Academy of Sciences, the American Academy of Arts & Sciences, the Washington State Academy of Sciences and the American Academy of Microbiology. ### This research was funded by grants from the National Institutes of Health, the Helen Hay Whitney Foundation, a University of Washington's Genetic Approaches to Aging Training Grant and the Glenn Foundation for Medical Research. Preliminary support, including for the development of technologies used in this research, was provided by the Hutchinson Center's Hartwell Innovation Fund. Editor's note: To obtain an embargoed copy of the Nature paper, "An early-age increase in vacuolar pH limits mitochondrial function and lifespan in yeast," please contact press@nature.com. Once the paper is published electronically, the abstract (available to everyone) and full text (available only to subscribers) can be retrieved by visiting http://dx.doi.org/10.1038/nature11654 Image available upon request: A color image showing vacuolar acidity in a population of cells is available upon request Public release date: 21-Nov-2012 Contact: Kristen Woodward kwoodwar@fhcrc.org 206-667-5095 Fred Hutchinson Cancer Research Center

New discoveries in cell aging

[N.B....Fullerenes (Hydrated Fullerenes Hy-C60) likely regulate/prevent protein aggregation and protein mis-folding--WD]

New discoveries in cell aging

A group of researchers led by the Institute of Biotechnology and
Biomedicine (IBB) and Universitat Autònoma de Barcelona (UAB) have achieved to
quantify with precision the effect of protein aggregation on cell aging
processes using as models the Escherichia coli bacteria and the molecule which
triggers Alzheimer's disease. Scientists demonstrated that the effect can be
predicted before it occurs. Protein aggregation is related to several diseases,
including neurodegenerative diseases.

The research, published recently in the Journal of Molecular Biology, provides an
extremely reliable system with which to model and quantify the effect of
protein aggregation on the viability, division and aging of cells. It also aids
in further understanding the natural evolution of proteins. According to
Salvador Ventura, researcher at IBB and director of the research project, "it
will serve to develop computer approximations to predict the effects
aggregation has on cell aging, as well as to search for molecules that act as
natural chaperones, highly conserved proteins which are present also in humans
and which have the ability to reduce this effect in the bacteria".

Although it is widely accepted that bad folding and aggregation of proteins reduces the
cell's ability to survive and reproduce, the damage caused had not been
previously measured experimentally as precisely as it was in this research.

In previous studies scientists had verified that the expression of the Alzheimer's AB42
peptide in bacteria induces the process of protein aggregation. Now they have
demonstrated that this effect is coded in the protein aggregation sequence and
that it depends on intrinsic properties, not on a direct response from within
the cell. This makes it possible to predict the effect. Scientists also
demonstrated that damage caused to the bacteria is controlled by molecular
chaperones, which reduce the tendency of proteins to aggregate and favour cell
survival.

In addition to researchers from IBB and the UAB Department of Biochemistry and Molecular
Biology, participating in the project were scientists from the Biophysics Unit
at CSIC-UPV, the University of the Basque Country, the Institute for
Bioengineering of Catalonia and the Barcelona Centre for International Health
Research.

 

Johns Hopkins scientists link DNA 'end-caps' or Telomere length to diabetes risk

New role for short telomeres

New evidence has emerged from studies in mice that short telomeres or "caps" at the ends of chromosomes may predispose people to age-related diabetes, according to Johns Hopkins scientists.

Telomeres are repetitive sequences of DNA that protect the ends of chromosomes, and they normally shorten with age, much like the caps that protect the end of shoelaces. As telomeres shorten, cells lose the ability to divide normally and eventually die. Telomere shortening has been linked to cancer, lung disease, and other age-related illnesses. Diabetes, also a disease of aging, affects as many as one in four adults over the age of 60.

The Johns Hopkins research, described in the March 10 issue of PLoS One, arose from scientist Mary Armanios' observation that diabetes seems to occur more often in patients with dyskeratosis congenita, a rare, inherited disease caused by short telomeres. Patients with dyskeratosis congenita often have premature hair graying and are prone to develop early organ failure.

"Dyskeratosis congenita is a disease that essentially makes people age prematurely. We knew that the incidence of diabetes increases with age, so we thought there may be a link between telomeres and diabetes," says Armanios, assistant professor of oncology at the Johns Hopkins Kimmel Cancer Center.

Armanios studied mice with short telomeres and their insulin-producing beta cells. Human diabetics lack sufficient insulin production and have cells resistant to its efficient use, causing disruption to the regulation of sugar levels in the blood.

Armanios found that despite the presence of plentiful, healthy-looking beta cells in the mice, they had higher blood sugar levels and secreted half as much insulin as the controls. "This mimics early stages of diabetes in humans where cells have trouble secreting insulin in response to sugar stimulus," says Armanios.

"Many of the steps of insulin secretion in these mice, from mitochondrial energy production to calcium signaling, functioned at half their normal levels," says Armanios.

In beta cells from mice with short telomeres, they found disregulation of p16, a gene linked to aging and diabetes. No such mistakes were found in the controls.

In addition, many of the gene pathways essential for insulin secretion in beta cells, including pathways that control calcium signaling, were altered in beta cells from mice with short telomeres.

Armanios says that some studies have suggested that diabetic patients may have short telomeres, but it was not clear whether this contributes to diabetes risk or is a consequence of the disease.

"Age is the most important risk factor for diabetes, and we also know that family heredity plays a very important role. Telomere length is an inherited factor and may make people more prone to develop diabetes," says Armanios.

Based on this work, Armanios says that telomere length could serve as a biomarker for development of diabetes. Armanios and her colleagues are planning to conduct research to examine whether telomere length can predict the risk of diabetes prospectively.

###

The research was funded by the National Institutes of Health, a Ruth L. Kirschstein Award, the Maryland Stem Cell Research Fund, Sidney Kimmel Foundation, Doris Duke Charitable Foundation, the Swedish Research Council and the Family Erling-Persson Foundation.

Participants in the research included Nini Guo, Erin M. Parry, Frant Kembou, Naudia Lauder, Mehboob A. Hussain from Johns Hopkins; and Luo-Sheng Li and Per-Olof Berggren from the Karolinska Institutet in Sweden.

Walking for 40 minutes three times a week can make you smarter

 

Walking at one’s own pace for 40 minutes three times a week can enhance the connectivity of important brain circuits, combat declines in brain function associated with aging, and increase performance on cognitive tasks, researchers have found.

The new study used fMRI to determine whether aerobic activity increased connectivity in the default mode network (DMN), which dominates brain activity when a person is least engaged with the outside world, and in the fronto-executive network, which aids in the performance of complex tasks. Previous studies found that a loss of coordination in the DMN is a common symptom of aging and in extreme cases can be a marker of disease.

“Almost nothing in the brain gets done by one area — it’s more of a circuit,” said University of Illinois psychology professor and Beckman Institute Director Art Kramer, who led the study with kinesiology and community health professor Edward McAuley and doctoral student Michelle Voss. “These networks can become more or less connected. In general, as we get older, they become less connected, so we were interested in the effects of fitness on connectivity of brain networks that show the most dysfunction with age.”

The study, in Frontiers in Aging Neuroscience, followed 65 adults, aged 59 to 80, who joined a walking group or stretching and toning group for a year. All of the participants were sedentary before the study, reporting less than two episodes of physical activity lasting 30 minutes or more in the previous six months. The researchers also measured brain activity in 32 younger (18- to 35-year-old) adults.

The paper, “Plasticity of Brain Networks in a Randomized Intervention Trial of Exercise Training in Older Adults,” is available online.

More info: University of Illinois news

New longevity protein discovered

Jefferson scientists identify a new protein involved in longevity

(PHILADELPHIA) Researchers in the Department of Biochemistry and Molecular Biology at Thomas Jefferson University have found that the level of a single protein in the tiny roundworm C. elegans determines how long it lives.

 

Worms born without this protein, called arrestin, lived about one-third longer than normal, while worms that had triple the amount of arrestin lived one-third less.

 

The research also showed that arrestin interacts with several other proteins within cells to regulate longevity. The human version of one of these proteins is PTEN, a well-known tumor suppressor. The study, to be published in the online edition of the Journal of Biological Chemistry, was chosen by the journal as the "Paper of the Week" – considered in the top one percent of published articles.

Because most proteins in worms have human counterparts, these findings may have relevance to human biology and the understanding of cancer development, said Jeffrey L. Benovic, Ph.D., professor and chair of the department.

"The links we have found in worms suggest the same kind of interactions occur in mammals although human biology is certainly more complicated. We have much work to do to sort out these pathways, but that is our goal," said Dr. Benovic.

Researchers use the roundworm as a model because it offers a simple system to study the function of genes and proteins that are relevant to human biology. The worm, for example, has one arrestin gene, whereas humans have four. Worms only have 302 neurons compared to the 100 billion or so in the human brain. In addition, their short lifespan of two to three weeks allows for timely observation of effects on longevity.

Dr. Benovic and the study's first author, Aimee Palmitessa, Ph.D., a postdoctoral research fellow, studied signaling pathways activated by G protein-coupled receptors. These receptors bind to all kinds of hormones, sensory stimuli (such as light, odorants and tastants), neurotransmitters, etc., which then activate a cascade of signals inside the cell. They regulate many physiological processes and are the target for about half of the drugs currently on the market.

"When it comes to receptors, worms are actually more complex," said Dr. Benovic. "Humans have about 800 different kinds of G protein-coupled receptors while the worm has about 1,800. It relies upon these receptors to respond to sensory stimuli as well as various neurotransmitters and hormones."

Arrestins were initially found to turn off the activation of G protein-coupled receptors inside cells. "Their name comes from the fact that they arrest the activity of receptors, so the worm offers a good way to study how its single arrestin protein interacts with protein receptors," says Dr. Benovic. Two of the four arrestins that humans have are devoted to regulating receptors that respond to visual stimuli while the other two regulate most other receptors.

In this study, Dr. Palmitessa deleted the single arrestin gene in worms to see what would happen, and found, to her surprise, that these worms lived significantly longer. She also found that over-expressing arrestin in worms shortened their lifespan. "A little less arrestin is good – at least for worms," Dr. Benovic reported.

This isn't the first discovery made regarding longevity in worms. Researchers have already found that activity of the insulin-like growth factor-1 (IGF-1) receptor can influence longevity in worms – a finding that has also been replicated in fruit flies, mice, and humans. Like arrestin, a little less IGF-1 receptor activity is good, Dr. Benovic explained. Further research has shown that caloric restriction can also reduce IGF-1 receptor activation and, conversely, over-expression of the IGF-1 receptor is found in some human cancers.

In this study, Dr. Benovic and Dr. Palmitessa dug a little deeper and found that in the worms, arrestin interacted with two other proteins that play a critical role in its ability to regulate longevity. One of those proteins is the tumor suppressor PTEN; mutations in PTEN are involved in a number of different cancers.

Dr. Benovic said the connection between human arrestin and PTEN is not clear.

 

"We don't know at this point if human arrestins regulate PTEN function or if anything happens to arrestin levels during the development of cancer," he said. "Do increasing levels turn off more PTEN, thus promoting cancer, or do levels decrease and allow PTEN to be more active?

"If it turns out to be the first scenario – that increasing amounts of arrestin turn off the tumor suppressor activity of PTEN, then it may be possible to selectively inhibit that process," he says. "We have some interesting work ahead."

###

Walter Derzko, The Opportunity Clinic, Smart Economy 

What does aging, inflammatory disease, cancer, genes. omega-3-fatty acids and telomeres have in common?

Scientists identify first genetic variant linked to biological aging in humans

 

Discovery has important implications for the understanding of cancer and age associated diseases

 

Scientists announced today (7 Feb) they have identified for the first time definitive variants associated with biological ageing in humans. The team analyzed more than 500,000 genetic variations across the entire human genome to identify the variants which are located near a gene called TERC.

 

The study in Nature Genetics published today by researchers from the University of Leicester and King's College London, working with University of Groningen in the Netherlands,

 

Researchers explained that there are two forms of ageing – chronological ageing i.e. how old you are in years and biological ageing whereby the cells of some individuals are older (or younger) than suggested by their actual age.

 "There is accumulating evidence that the risk of age-associated diseases including heart disease and some types of cancers are more closely related to biological rather than chronological age.

 

 

"What we studied are structures called telomeres which are parts of one's chromosomes. Individuals are born with telomeres of certain length and in many cells telomeres shorten as the cells divide and age.

 

Telomere length is therefore considered a marker of biological ageing.

 

"In this study what we found was that those individuals carrying a particular genetic variant had shorter telomeres i.e. looked biologically older. Given the association of shorter telomeres with age-associated diseases, the finding raises the question whether individuals carrying the variant are at greater risk of developing such diseases"

Professor Tim Spector from King's College London and director of the TwinsUK study, who co-led this project, added:

"The variants identified lies near a gene called TERC which is already known to play an important role in maintaining telomere length. What our study suggests is that some people are genetically programmed to age at a faster rate. The effect was quite considerable in those with the variant, equivalent to between 3-4 years of 'biological aging" as measured by telomere length loss. Alternatively genetically susceptible people may age even faster when exposed to proven 'bad' environments for telomeres like smoking, obesity or lack of exercise – and end up several years biologically older or succumbing to more age-related diseases. "

 

The paper, will be published online in Nature Genetics on 07 February 2010. To view the paper, please visit http://www.nature.com/naturegenetics/

 

The GOOD NEWS ?

Telomere length can be controlled and unravelling delayed  by consuming more omega-3-fatty acid (but not Omega-6 or Omega-9) or drinking tea made from the herb Rhodiola Rosea or taking the Rodiola capsules.

 

Washington Post recently offered the following story:

 

Omega-3s may help people live longer; maybe people can lose weight on their own

 

By Adapted from voices.washingtonpost.com/checkup Tuesday, January 26, 2010

 

Fighting aging

Do omega-3 fatty acids help stave off aging?  A new study suggests the answer may be yes.

Previous research has shown that heart disease patients who get a lot of omega-3 fatty acids in their diets do better than those who don't.  So Ramin Farzaneh-Far of the University of California at San Francisco and colleagues looked at structures known as telomeres, which are the ends of chromosomes and which have been linked to aging.  Every time a cell divides, these structures get a little shorter.  Evidence has been accumulating that the faster telomeres unravel, the shorter people may live.

 

In the new study, the researchers examined the telomeres in white blood cells called leukocytes in 608 patients with heart disease.  Over five years, the telomeres of those who had the lowest levels of two omega-3 fatty acids known as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) shortened faster than those with the highest levels.

While more research is needed, the findings support the idea that omega-3 fatty acids may help people live longer.

Omega-3 fatty acids are found in oily fishes.  Scientists suspect these fatty acids may reduce inflammation, prevent blood clots, lower blood pressure and have other benefits.

 

Walter Derzko

Landmark research turns skin cells into brain cells without the intermediate pluripotent stem cell step

If Merlin the magician or Walt Disney were alive today they’d be proud. Just as sorcerers tried to turn lead into gold centuries ago, the journal Nature reported today that Stanford University researcher Marius Wernig has managed to directly turn skin cells from the tails of mice into neurons able to form connections crucial to brain function. It's a breakthrough worthy of a future Nobel prize.

 

Bloomberg reports:

 

"The work provides a more efficient way to make neurons from the skin of people with Alzheimer’s and Parkinson’s diseases than a method developed four years ago by Shinya Yamanaka of Kyoto University in Japan. Yamanaka’s breakthrough showed that skin cells from mice or humans could be made into stem cells and manipulated again to become any cell in the body.

Marius Wernig  identified 19 genes that are active in neurons and inserted them into skin cells taken from the tails of young mice. The team used a type of virus known as a lentivirus to carry the genes into the skin cells. After a month, a few of the skin cells showed signs of having turned into brain cells. The team then used a trial-and- error process to identify three genes from among the 19 that could do the job on their own. Using the three, Wernig’s team found that in just two weeks, 20 percent of the skin cells had morphed into neurons." 

“That means reprogramming doesn’t only go backward, but can occur in any direction,” Wernig said.“If you extrapolate from this, you could probably turn any cell in your body into any other cell if you just know the right factors. A year ago, I would not really have believed this was possible.”

 ...[...]...Before the cells have practical use, they’ll have to be shown to be true neurons, The question now is how these genetically engineered neurons stack up against real neurons in a real test-can they be used to repair the brains of mice that have experimentally induced Alzheimer's or Parkinson's disease, for example

 

This opens all sorts of fascinating possibilities and opportunities including personal cell banks,  rejuvination procedures and disease reversal,  cell growth lab services,  and extending human and animal  longevity.

 

Hydrated Fullerenes (HyFN's C60) that havebeen shown to prevent inflammatory diseases along with cell rejuvination therapy for people with extended diseases could be a powerful one two punch in extending health human life and longevity and reducing health care costs.

 

ETA: 7-10 years if fast tracked

 

Full Bloomberg story here

 

 

Walter Derzko

Smart Economy

Toronto

  

Author of the soon-to-be published book- Opportunity 45 Scenarios to Drive Your Business in Challenging Times,  published by J. Wiley and Sons

ISBN13: 978-0-470-73761-3

ISBN10: 0-470-73761-1

Contact us about the Opportunity Clinic workshop and to invite Walter Derzko as a keynote speaker at your next event 

How does nutrition affect healthy aging, longevity? The correct combination of proteins is decisive for healthy aging, not reducing the calories in our diet

from a press release from the Max Planck Institute for Biology of Ageing......

"A new study from the Max Planck Institute for Biology of Ageing could help us understand the positive effect of dietary restriction on healthy ageing. Previous evidence from different organisms (fruit flies and mice) have shown that dietary restriction increases longevity, but with a potential negative side effect of diminished fertility. So the female fruit fly reproduces less frequently with a reduced litter size on a low calorie diet, but its reproductive span lasts longer. This is the result of an evolutionary trait, as scientists believe: essential nutrients are diverted towards survival instead of reproduction. (Nature, December 3, 2009)

Researchers from the newly created Max Planck Institute for Biology of Ageing in Cologne have studied whether health benefits stem from a reduction in specific nutrients or calorie intake in general, by manipulating the diet of female fruit flies. The fruit flies were fed a diet of yeast, sugar and water, but with differing amounts of key nutrients, such as vitamins, lipids and amino acids. The scientists were able to show that longevity and fertility are affected by a combination of the type and amount of amino acids; whilst varying the amount of the other nutrients had little or no effect.

Furthermore, the researchers found out in previous studies that levels of a particular amino acid - methionine - were crucial to increasing lifespan without decreasing fertility. By carefully manipulating the balance of amino acids, both lifespan and fertility were maximised. For the first time, this indicates that it is possible to extend lifespan without wholesale dietary restriction and without lowering reproductive capacity.

As the effects of dietary restriction on lifespan is evolutionary conserved - observed in different organisms - researchers believe that the essential mechanisms apply to it as well. Even though the human genome has about four times the number of genes as the fruit fly genome, there are many similarities on a genetic level, allowing these results to be of significance for humans as well.

Walter Derzko

 

 

 

Author of the soon-to-be published book- Opportunity 45 Scenarios to Drive Your Business in Challenging Times,

published by J. Wiley and Sons

ISBN13: 978-0-470-73761-3

ISBN10: 0-470-73761-1

 

 

 

The Opportunity Clinic - 28 Tactics for Managing Your Business in a Recession Part 2 of 28 Innovation or Efficiency?

The Opportunity Clinic - 28 Tactics for  Managing Your Business (& surviving and thriving) in a Recession Part 2 of 28 Innovation or  Efficiency?

Entreperneurs must make many strategi choices. "Are we going to be innovative or efficient or possibly both vs our competition." is one of them. Firms that simultaneously engage in a high degree of both innovation and efficiency follow an approach that is often referred to in the academic business literature as an ambidextrous strategy.  Surprisingly, relatively few firms are able to balance these two approaches. Internal battles for resources often tip the scales in favor of efficiency over innovation, or vice versa. Management gurus frequently warn that simultaneously pursuing both can set the firm up for mediocre performance, yet the turbulent nature of today’s markets, cut-throat competition and despiration and anxiety from the recession create a renewed need for firms to reconsider this dual approach for longer-term success. Unfortunately, practical insights from empirical studies regarding performance benefits and implementation issues are still scant.  Perhaps this is one reason why few firms are successful in both efficiency and innovation.

 A paper called Innovation and efficiency: It is possible to have it all; this month in Business Horizons (2009) 52, 45—55 discusses the issue of an ambidextrous strategy.

From the Abstract

"In this article, the authors provide evidence—using a cross-industry survey of senior marketing managers in publicly-traded U.S. firms—that firms which successfully employ an ambidextrous strategy outperform those which overemphasize either efficiency or innovation. Furthermore, they highlight marketing’s role as an example of the often overlooked need for successful functional implementation. Finally, they provide useful methods for managers to answer three key questions: (1) Is my firm ambidextrous?; (2) Should my firm be ambidextrous?; and, if so (3) How can my firm become ambidextrous?"

 From the body of the article we find:

"Some management experts are now renewing the call for firms to break with tradition and become ambidextrous—leaders in both efficiency and innovation—to achieve competitive advantage. Two top academic management journals, Academy of Management Journal and Organization Science, recently dedicated special issues to the examination of ambidextrous organizations and how firms manage the balance between efficiency and innovation. Both special issues cite the importance for managers of understanding issues surrounding ambidextrous strategies.

Organizational inertia pushes firms down a particular path, making it harder to adapt to market changes, while short  term thinking crowds out longer-term goals. Home Depot, Dell, Airbus, Kodak, and Ford are just a few examples of companies that have recently found themselves falling behind competitors as a result of overemphasizing one goal over the other."

I wrote to the authors of the article to find out who these ambidextrous firms are and how they are fairing in the recession, compared to their non-ambidextrous competition. When I get a reply, I’ll let Smart Economy blog readers know

Source: Innovation and efficiency: It is possible to have it all; Business Horizons (2009) 52, 45—55 by Matthew Sarkees  and John Hulland

Walter Derzko, Smart Economy, Toronto

Author of the soon-to-be-released book: Hard Times Golden Opportunities.. about opportunity recognition in a recession/ depression featuring 45 opportunity scenarios.

Related posts in this series:

The Opportunity Clinic; 28 Tactics for managing your Business in a recession Part 6 of 28 What's in your Recession Playbook?

The Opportunity Clinic; 28 Tactics for Managing your Business in a Recession Part 5 of 28 Category Killer Innovation-India's $10 laptop

The Opportunity Clinic - 28 Tactics for Managing Your Business in a Recession Part 4 of 28 “Left Behind “Opportunities- Go Green & Go Slow

The Opportunity Clinic - 28 Tactics for Managing Your Business in a Recession Part 3 of 28 Design Opportunities- Hope or Nostalgia

The Opportunity Clinic - 28 Tactics for Managing Your Business in a Recession Part 2 of 28 Innovation or Efficiency?

The Opportunity Clinic - 28 Tactics for Managing Your Business (& surviving and thriving) in a Recession Part 1of 28

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Walter Derzko -"Changing the world, one idea at a time"©

Author of the soon-to-be-released book: Hard Times Golden Opportunities.. about opportunity recognition in a recession/ depression featuring 45 opportunity scenarios.

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