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Philadelphia, PA, USA / Moscow, Russia — Bioquark, Inc., (www.bioquark.com) a life sciences company focused on the development of novel bio-products for regeneration, disease reversion, and healthy aging, and Moscow based, Lakmus LLC, a diversified investment company with business interests in pharmacies, restaurants, and real estate, announced a multi-disciplinary research collaboration with the FSBI Zakusov Institute of Pharmacology, Russian Academy of Medical Sciences (http://www.academpharm.ru/), and the Pavlov Institute of Physiology of the Russian Academy of Sciences (http://www.infran.ru/), to jointly study the pharmacotherapeutic longevity enhancement properties of its combinatorial regenerative biologic candidates.

“We are very excited about this continued collaboration with Lakmus,” said Ira S. Pastor, CEO, Bioquark Inc. “The disciplined development of our combinatorial biologic candidates (Bioquantines) for healthy longevity enhancement, represents another important step in our continued evolution as a company focused on a broad range of therapeutic products and services in the regenerative healthcare space.”

Throughout the 20th century, natural products formed the basis for a majority of all pharmaceuticals, biologics, and consumer healthcare products used by patients around the globe, generating trillions of dollars of wealth. However, many scientists believe we have only touched the surface with what the natural world, and its range of organisms, which from a health and wellness perspective are much further advanced than human beings, has to teach us.

The integration of a complex set of newer research disciplines, including interkingdom signaling, semiochemical communication, and evolutionary biology, as well as significant recent activity in the areas of the microbiome, are highlighting a myriad of new ways that non-human bio-products can affect the human genome for positive transitions in health and wellness dynamics.

“Bioquark has spent several years studying the natural ability of many species to turn back biological time in order to maintain health, fitness, and survival, developing a broad understanding of the combinatorial biochemical approaches they use to control nested hierarchies of disease (i.e. gene, cell, tissue, organism, environment),” said Dr. Sergei Paylian, Founder, CSO, and President, Bioquark Inc. “This research initiative is one more step in the path in allowing humans to recapture these capabilities to effectively counter our unfortunate progression into aging, disease and degeneration.”

About Bioquark, Inc.

Bioquark Inc. is focused on the development of natural biologic based products, services, and technologies, with the goal of curing a wide range of diseases, as well as effecting complex regeneration. Bioquark is developing both biological pharmaceutical candidates, as well as products for the global consumer health and wellness market segments.

Bioquark Inc. (www.bioquark.com) Interview in MoneyWeek

bioquarklogo

Read whole story: http://moneyweek.com/who-wants-to-live-forever/

Philadelphia, PA, USA / Mexico City, Mexico — Bioquark, Inc., (www.bioquark.com) a life sciences company focused on the development of novel bioproducts for complex regeneration, disease reversion, and aging, and RegenerAge SAPI de CV, (www.regenerage.clinic/en/) a clinical company focused on translational therapeutic applications of a range of regenerative and rejuvenation healthcare interventions, have announced a collaboration to focus on novel combinatorial approaches in human disease and wellness. SGR-Especializada (http://www.sgr-especializada.com/), regulatory experts in the Latin American healthcare market, assisted in the relationship.

regenerage

“We are very excited about this collaboration with RegenerAge SAPI de CV,” said Ira S. Pastor, CEO, Bioquark Inc. “The natural synergy of our cellular and biologic to applications of regenerative and rejuvenative medicine will make for novel and transformational opportunities in a range of degenerative disorders.”

As we close in on $7 trillion in total annual health care expenditures around the globe ($1 trillion spent on pharmaceutical products; $200 billion on new R&D), we are simultaneously witnessing a paradoxical rise in the prevalence of all chronic degenerative diseases responsible for human suffering and death.

With the emergence of such trends including: personalization of medicine on an “n-of-1” basis, adaptive clinical design, globalization of health care training, compassionate use legislative initiatives for experimental therapies, wider acceptance of complementary medical technologies, and the growth of international medical travel, patients and clinicians are more than ever before, exploring the ability to access the therapies of tomorrow, today.

recovering patient

The estimate of the current market size for procedural medical travel, defined by medical travelers who travel across international borders for the purpose of receiving medical care, is in the range of US $40–55 billion.

Additionally, major clinical trial gaps currently exist across all therapeutic segments that are responsible for human suffering and death. Cancer is one prime example. As a leading cause of morbidity and mortality worldwide for many decades, today there are approximately 14 million new cases diagnosed each year, with over 8 million cancer related deaths annually. It is estimated that less than 5% of these patients, take the initiative to participate in any available clinical studies.

“We look forward to working closely with Bioquark Inc. on this exciting initiative,” said Dr. Joel Osorio, Chief of Clinical Development RegenerAge SAPI de CV. “The ability to merge cellular and biologic approaches represents the next step in achieving comprehensive regeneration and disease reversion events in a range of chronic diseases responsible for human suffering and death.”

bioquarklogo

About Bioquark, Inc.
Bioquark Inc. is focused on the development of natural biologic based products, services, and technologies, with the goal of curing a wide range of diseases, as well as effecting complex regeneration. Bioquark is developing both biological pharmaceutical candidates, as well as products for the global consumer health and wellness market segments.

About RegenerAge SAPI de CV

RegenerAge SAPI de CV is a novel clinical company focused on translational therapeutic applications, as well as expedited, experimental access for “no option” patients, to a novel range of regenerative and reparative biomedical products and services, with the goal of reducing human degeneration, suffering, and death.

“He is not here; He has risen,” — Matthew 28:6

As billions of Christians around the world are getting ready to celebrate the Easter festival and holiday, we take pause to appreciate the awe inspiring phenomena of resurrection.

crypt

In religious and mythological contexts, in both Western and Eastern societies, well known and less common names appear, such as Attis, Dionysus, Ganesha, Krishna, Lemminkainen, Odin, Osiris, Persephone, Quetzalcoatl, and Tammuz, all of whom were reborn again in the spark of the divine.

In the natural world, other names emerge, which are more ancient and less familiar, but equally fascinating, such as Deinococcus radiodurans, Turritopsis nutricula, and Milnesium tardigradum, all of whose abilities to rise from the ashes of death, or turn back time to start life again, are only beginning to be fully appreciated by the scientific world.

deinoccous

In the current era, from an information technology centric angle, proponents of a technological singularity and transhumanism, are placing bets on artificial intelligence, virtual reality, wearable devices, and other non-biological methods to create a future connecting humans to the digital world.

This Silicon Valley, “electronic resurrection” model has caused extensive deliberation, and various factions to form, from those minds that feel we should slow down and understand the deeper implications of a post-biologic state (Elon Musk, Steven Hawking, Bill Gates, the Vatican), to those that are steaming full speed ahead (Ray Kurzweil / Google) betting that humans will shortly be able to “transcend the limitations of biology”.

transhumangirl

However, deferring an in-depth Skynet / Matrix discussion for now, is this debate clouding other possibilities that we have forgotten about, or may not have even yet fully considered?

Today, we find ourselves at an interesting point in history where the disciplines of regenerative sciences, evolutionary medicine, and complex systems biology, are converging to give us an understanding of the cycle of life and death, orders of magnitude more complex than only a few years ago.

In addition to the aforementioned species that are capable of biologic reanimation and turning back time, we show no less respect for those who possess other superhuman capabilities, such as magnetoreception, electrosensing, infrared imaging, and ultrasound detection, all of which nature has been optimizing over hundreds of millions of years, and which provide important clues to the untapped possibilities that currently exist in direct biological interfaces with the physical fabric of the universe.

jellyfish2

The biologic information processing occurring in related aneural organisms and multicellular colony aggregators, is no less fascinating, and potentially challenges the notion of the brain as the sole repository of long-term encoded information.

Additionally, studies on memory following the destruction all, or significant parts of the brain, in regenerative organisms such as planarians, amphibians, metamorphic insects, and small hibernating mammals, have wide ranging implications for our understanding of consciousness, as well as to the centuries long debate between the materialists and dualists, as to whether we should focus our attention “in here”, or “out there”.

I am not opposed to studying either path, but I feel that we have the potential to learn a lot more about the topic of “out there” in the very near future.

coolbrain

The study of brain death in human beings, and the application of novel tools for neuro-regeneration and neuro-reanimation, for the first time offer us amazing opportunities to start from a clean slate, and answer questions that have long remained unanswered, as well as uncover a knowledge set previously thought unreachable.

Aside from a myriad of applications towards the range of degenerative CNS indications, as well as disorders of consciousness, such work will allow us to open a new chapter related to many other esoteric topics that have baffled the scientific community for years, and fallen into the realm of obscure curiosities.

connection

From the well documented phenomena of terminal lucidity in end stage Alzheimer’s patients, to the mysteries of induced savant syndrome, to more arcane topics, such as the thousands of cases of children who claim to remember previous lives, by studying death, and subsequently the “biotechnological resurrection” of life, we can for the first time peak through the window, and offer a whole new knowledge base related to our place, and our interaction, with the very structure of reality.

We are entering a very exciting era of discovery and exploration.

Reanimalogo

About the author

Ira S. Pastor is the Chief Executive Officer of Bioquark Inc. (www.bioquark.com), an innovative life sciences company focusing on developing novel biologic solutions for human regeneration, repair, and rejuvenation. He is also on the board of the Reanima Project (www.reanima.tech)

Since ancient times people have been searching for the secret of immortality. Their quest has always been, without exception, about a physical item: a fountain, an elixir, an Alchemist’s remedy, a chalice, a pill, an injection of stem cells or a vial containing gene-repairing material. It has never been about an abstract concept.

Our inability to find a physical cure for ageing is explained by a simple fact: We cannot find it because it does not exist. It will never exist.

Those who believe that someday some guy is going to discover a pill or a remedy and give it to people so that we will all live forever are, regrettably, deluded.

I should highlight here that I refer to a cure for the ageing process in general, and not a cure for a specific medical disease. Biotechnology and other physical therapies are useful in alleviating many diseases and ailments, but these therapies will not be the answer to the basic biological process of ageing.

In a paper I published in the journal Rejuvenation Research I outline some of the reasons why I think biotechnology will not solve the ageing problem. I criticise projects such as SENS (which are based upon physical repairs of our ageing tissues) as being essentially useless against ageing. The editor’s rebuttal (being weak and mostly irrelevant) proved and strengthened my point. There are insurmountable basic psychological, anatomical, biological and evolutionary reasons why physical therapies against ageing will not work and will be unusable by the general public. Some of these reasons include pleiotropy, non-compliance, topological properties of cellular networks, non-linearity, strategic logistics, polypharmacy and tolerance, etc. etc.

So, am I claiming that we are doomed to live a life of age-related pathology and degeneration, and never be able to shake off the aging curse? No, far from it. I am claiming that it is quite possible, even inevitable, that ageing will be eliminated but this will not be achieved through a physical intervention based on bio-medicine or bio-technology. Ageing will be eliminated through fundamental evolutionary and adaptation mechanisms, and this process will take place independently of whether we want it or not.

It works like this: We now age and die because we become unable to repair random background damage to our tissues. Resources necessary for this have been allocated by the evolutionary process to our germ cell DNA (in order to assure the survival of the species) and have been taken away from our bodily cells. Until now, our environment was so full of dangers that it was more thermodynamically advantageous for nature to maintain us up to a certain age, until we have progeny and then die, allowing our progeny to continue life.

However, this is now changing. Our environment is becoming increasingly more secure and protective. Our technology protects us against dangers such as infections, famine and accidents. We become increasingly embedded into the network of a global techno-cultural society which depends upon our intelligence in order to survive. There will come a time when biological resources spent to bring up children would be better spent in protecting us instead, because it would be more economical for nature to maintain an existing, well-embedded human, rather than allow it to die and create a new one who would then need more resources in order to re-engage with the techno-cultural network. Disturbing the network by taking away its constituents and trying to re-engage new inexperienced ones is not an ideal action and therefore it will not be selected by evolution.Alchemist complex

The message is clear: You have more chances of defying ageing if, instead of waiting for someone to discover a pill to make you live longer, you become a useful part of a wider network and engage with a technological society. The evolutionary process will then ensure that you live longer-as long as you are useful to the whole.

Further reading
http://ieet.org/index.php/IEET/more/kyriazis20121031
https://lifeboat.com/blog/2013/12/the-seven-fallacies-of-aging
https://lifeboat.com/blog/2013/04/the-life-extension-hubris-why-biotechnology-is-unlikely-to-be-the-answer-to-ageing
http://www.ncbi.nlm.nih.gov/pubmed/25072550
http://arxiv.org/abs/1402.6910

By Avi Roy, University of Buckingham and Anders Sandberg, University of Oxford

Men who are unemployed for more than two years show signs of faster ageing in their DNA, according to a study published today in the journal PLOS ONE.

Researchers at the University of Oulu, Finland and Imperial College, London arrived at this conclusion by studying blood samples collected from 5,620 men and women born in Northern Finland in 1966. The researchers measured the lengths of telomeres in their white blood cells, and compared them with the participants’ employment history for the prior three years, and found that extended unemployment (more than 500 days in three years) was associated with shorter telomere length.

Telomeres are repetitive DNA sequences at the ends of chromosomes, which protect the chromosomes from degrading. With every cell division, it appears that these telomeres get shorter. And the result of each shortening is that these cells degrade and age.

When cells are grown in a lab, their telomeres do indeed shorten each time the cells divide. This process can be used to find a cell’s “expiry date”, a prediction of when that cell will run out of telomeres and stop dividing. However, this does not seem to relate to the actual health of the cells.

In the new study, the researchers found that that on average, men who had been unemployed for more than two of the preceding three years were more than twice as likely to have short telomeres compared to men who were continuously employed. In women, there was no association between unemployment status and telomere length.

The researchers accounted for telomere length differences resulting from medical conditions, obesity, socio-economic status and early childhood environment.

Previous studies, noted by the study authors, have found a correlation between shorter telomeres and higher rates of age-related diseases like Type 2 diabetes and heart disease. The authors conclude that the reduction in these men’s telomeres may have been the result from the stress of long-term unemployment, adding to evidence of a direct connection between prolonged unemployment and poor health.

An abstract concept

Employment is something very abstract; an employed and unemployed body are apparently more or less the same. So it might seem surprising that such an abstract thing as employment can affect a body on the cellular level. But the same is true for how stimuli affect our brains: remote objects trigger electrochemical cascades in our visual system – and when we learn new things, gene expression in the brain changes. We are interactive creatures, with innumerable stimuli that are constantly shaping multiple processes in our bodies. In this sense, the hypothesis that employment experience has cellular effects is not surprising.

This was an association study, which means than under certain set of circumstances two variables are statistically linked. This study is therefore incapable of genuinely predicting whether unemployment is the cause, and short telomeres the effect. Perhaps the opposite is true: maybe people whose cells lose their telomeres also lose their jobs. More likely, an outside factor that shortens telomeres could have a limiting effect on success in the labour market. For example, such a factor might somehow contribute towards illness or pessimism.

Additionally, because the study was conducted in an isolated and genetically quite homogeneous population, the results of the study may be due to their genetic make-up as well as (or instead of) environmental effects.

In the end, we do not need a genetic study to know long-term unemployment is bad for people socially, medically and psychologically; there is plenty of evidence for that. Additionally, the bio-gerontology community (those who study the biological processes of ageing) recognises telomere attrition as one of the nine causes of the disease of ageing, including Type 2 diabetes and cardiovascular diseases.

Where this study does make a significant contribution is in recognising long-term, low-level stress as a major problem. In momentarily stressful situations, the instant fight-or-flight response stimulates us; but being under pressure for a long time with no relief wears us down. Prolonged stress is bad for memory and health, and could quite conceivably shorten telomeres – making an unemployed person significantly more unhealthy, with the effects persisting even after they get a job.

In the long run, what we really need to learn to slow or stop the ageing process is how to reduce or repair the damage done by stress.

The authors do not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article. They also have no relevant affiliations.

This article was originally published at The Conversation.
Read the original article.

By Avi Roy, University of Buckingham

In rich countries, more than 80% of the population today will survive past the age of 70. About 150 years ago, only 20% did. In all this while, though, only one person lived beyond the age of 120. This has led experts to believe that there may be a limit to how long humans can live.

Animals display an astounding variety of maximum lifespan ranging from mayflies and gastrotrichs, which live for 2 to 3 days, to giant tortoises and bowhead whales, which can live to 200 years. The record for the longest living animal belongs to the quahog clam, which can live for more than 400 years.

If we look beyond the animal kingdom, among plants the giant sequoia lives past 3000 years, and bristlecone pines reach 5000 years. The record for the longest living plant belongs to the Mediterranean tapeweed, which has been found in a flourishing colony estimated at 100,000 years old.

This jellyfish never dies. Michael W. May

Some animals like the hydra and a species of jellyfish may have found ways to cheat death, but further research is needed to validate this.

The natural laws of physics may dictate that most things must die. But that does not mean we cannot use nature’s templates to extend healthy human lifespan beyond 120 years.

Putting a lid on the can

Gerontologist Leonard Hayflick at the University of California thinks that humans have a definite expiry date. In 1961, he showed that human skin cells grown under laboratory conditions tend to divide approximately 50 times before becoming senescent, which means no longer able to divide. This phenomenon that any cell can multiply only a limited number of times is called the Hayflick limit.

Since then, Hayflick and others have successfully documented the Hayflick limits of cells from animals with varied life spans, including the long-lived Galapagos turtle (200 years) and the relatively short-lived laboratory mouse (3 years). The cells of a Galapagos turtle divide approximately 110 times before senescing, whereas mice cells become senescent within 15 divisions.

The Hayflick limit gained more support when Elizabeth Blackburn and colleagues discovered the ticking clock of the cell in the form of telomeres. Telomeres are repetitive DNA sequence at the end of chromosomes which protects the chromosomes from degrading. With every cell division, it seemed these telomeres get shorter. The result of each shortening was that these cells were more likely to become senescent.

Other scientists used census data and complex modelling methods to come to the same conclusion: that maximum human lifespan may be around 120 years. But no one has yet determined whether we can change the human Hayflick limit to become more like long-lived organisms such as the bowhead whales or the giant tortoise.

What gives more hope is that no one has actually proved that the Hayflick limit actually limits the lifespan of an organism. Correlation is not causation. For instance, despite having a very small Hayflick limit, mouse cells typically divide indefinitely when grown in standard laboratory conditions. They behave as if they have no Hayflick limit at all when grown in the concentration of oxygen that they experience in the living animal (3–5% versus 20%). They make enough telomerase, an enzyme that replaces degraded telomeres with new ones. So it might be that currently the Hayflick “limit” is more a the Hayflick “clock”, giving readout of the age of the cell rather than driving the cell to death.

The trouble with limits

Happy last few days? It doesn’t have to end this way. ptimat

The Hayflick limit may represent an organism’s maximal lifespan, but what is it that actually kills us in the end? To test the Hayflick limit’s ability to predict our mortality we can take cell samples from young and old people and grow them in the lab. If the Hayflick limit is the culprit, a 60-year-old person’s cells should divide far fewer times than a 20-year-old’s cells.

But this experiment fails time after time. The 60-year-old’s skin cells still divide approximately 50 times – just as many as the young person’s cells. But what about the telomeres: aren’t they the inbuilt biological clock? Well, it’s complicated.

When cells are grown in a lab their telomeres do indeed shorten with every cell division and can be used to find the cell’s “expiry date”. Unfortunately, this does not seem to relate to actual health of the cells.

It is true that as we get older our telomeres shorten, but only for certain cells and only during certain time. Most importantly, trusty lab mice have telomeres that are five times longer than ours but their lives are 40 times shorter. That is why the relationship between telomere length and lifespan is unclear.

Apparently using the Hayflick limit and telomere length to judge maximum human lifespan is akin to understanding the demise of the Roman empire by studying the material properties of the Colosseum. Rome did not fall because the Colosseum degraded; quite the opposite in fact, the Colosseum degraded because the Roman Empire fell.

Within the human body, most cells do not simply senesce. They are repaired, cleaned or replaced by stem cells. Your skin degrades as you age because your body cannot carry out its normal functions of repair and regeneration.

To infinity and beyond

If we could maintain our body’s ability to repair and regenerate itself, could we substantially increase our lifespans? This question is, unfortunately, vastly under-researched for us to be able to answer confidently. Most institutes on ageing promote research that delays onset of the diseases of ageing and not research that targets human life extension.

Those that look at extension study how diets like calorie restriction affect human health or the health impacts of molecules like resveratrol derived from red wine. Other research tries to understand the mechanisms underlying the beneficial effects of certain diets and foods with hopes of synthesising drugs that do the same. The tacit understanding in the field of gerontology seems to be that, if we can keep a person healthy longer, we may be able to modestly improve lifespan.

Living long and having good health are not mutually exclusive. On the contrary, you cannot have a long life without good health. Currently most ageing research is concentrated on improving “health”, not lifespan. If we are going to live substantially longer, we need to engineer our way out of the current 120-year-barrier.

Avi Roy does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

Read the original article.

By Avi Roy, University of Buckingham

I want to live longer and help others do the same. I assumed the most effective way to do that is by understanding the science of aging and then engineering solutions to extend human lifespan. That is why I became a biomedical researcher and over the past several years I have pursued this goal almost single-mindedly.

When a 2004 study showed that reducing the calorie intake in mice extended their life by 42%, I enthusiastically embraced the results and even put myself on a calorie restricted diet. But, subsequently, a 2012 study showed that long-term calorie restriction may not have the promised benefits. On the contrary, fewer calories without the required nutrients might actually cause harm.

Calorie restriction is not the first such “promising” route that eventually did not live up to the promise, and it will not be the last. Antioxidants showed promise in holding back diseases caused by aging, but now we know that antioxidant supplements are more likely to shorten your life.

Earlier in May, researchers showed that reducing a protein called NF-kB in mouse brains modestly improved their lifespan. I am not holding out for this result either. Before too long, I’m sure there will be reports of severe side effects of manipulating levels of NF-kB.

Take it easy

Looking at the data I have come to the conclusion that “doing nothing” may be the best option in most cases. This may not be as pessimistic as it sounds and it is definitely not to say that research in fighting aging must not be carried out.

When I say “do nothing”, I am assuming that you do not smoke or drink too much alcohol, and have access to medical care in case of injury. Such measures are bound to increase your lifespan.

But currently, not intervening in the aging process is more likely to help you live longer than trying any of the methods I’ve mentioned, not by a few months but by many years. Trying any of those interventions may actually cause harm, and will do so for the foreseeable future.

Lesson from the past

The chart below shows the survival rates – the percentage of the population that lives to a certain age – for men in England and Wales from 1860 to 2010.

In the 1860s, more than 20% of children died at birth or soon after. On average, men’s health started to decline around the age of 30, and only about 20% of the population survived for more than 70 years.

By 1910, child mortality decreased, thanks to improvements in hygiene and better medical care. This meant more men lived past the age of 50. Circle A shows this reduction in childhood mortality between 1860 and 2010. But, as can be seen from Circle D, the gain towards the end was not significant. This is because only 30% of males passed the age of 70.

Fifty years later, after the discovery of penicillin and invention of more vaccines, 90% of English and Welsh men lived until 50, and more than half survived to 70. Arrow B marks this trend.

Today almost 80% of men live to the age of 70. Four times as many men reach 70 now than in 1860.

What accounts for the change? Between 1860 and 1960, the significant increase in survival rate was due to medical intervention. Since 1960, the survival curve has improved mainly due to reduction in smoking.

This trend is similar in many rich countries, including the US. Druin Burch, a physician and writer, says in his book Taking the Medicine, that eliminating smoking would provide more benefits than being able to cure people of every possible type of cancer.

Age gracefully

Many experts believe that human lifespan might actually have an upper limit of 125 years. The average may not increase much beyond 90. If we are to agree with them, this leaves little room for improvement.

But we have never concentrated on maximising human lifespan before. Most people believe human lifespan is finite, so all drugs being manufactured today are targeted towards certain age-related diseases such as diabetes and hypertension. They are not designed to extend human lifespan.

If this bleak outlook is indeed true, we should not practise naive interventionism because it is unlikely to help. As Nassim Nicholas Taleb describes in his book Antifragile, naive interventionism occurs when we try to fix a single thing, but end up disturbing a complex system.

In case of extending human lifespan, those naive interventions would include calorie restriction, antioxidant supplements or manipulating the protein NF-kB, as mentioned earlier. They also include the current obsession with replacing fat in foods with sugar, the health benefits of drinking red wine, or the use ofsurgery or supplements to “fight” aging. This latter industry has grown in the past decade from being non-existent to an estimated worth of $88 billion today.

If intervening in the aging process with current biomedical science has any positive effect at all, it will be far too small to worry about. It’s far more likely to harm us.

That is why I have decided to do nothing and follow a simple rule: unless I meet with an accident, or suffer from a terminal disease, I will not add anything to my life with the explicit purpose of extending it. To do anything else would most likely do more harm than good.

Avi Roy does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.

The Conversation

This article was originally published at The Conversation.
Read the original article.

As leaders of calorie restriction research and practice, Meredith Averill and I often participate in media events. A recent news conference covered rapidly evolving aspects of calorie restriction research that anyone could benefit from, whether they choose to follow a low-calorie lifestyle or not. Therefore, we thought it appropriate to share the details of the event with the Lifeboat Foundation audience.

The conference was hosted by the American Federation of Aging Research (AFAR). AFAR is a forward-looking organization that provides financial support for early- and mid-career scientists who are developing careers in the study of aging.

This conference, entitled “You are What you Don’t Eat!” presented two world-famous CR scientists, Drs. Luigi Fontana and Donald Ingram. After an introduction from AFAR’s board member, Dr. Jack Watters, both scientists shared many profound insights that could extend healthy lifespan for millions of people.

Dr. Fontana first reminded us how important calorie restriction research is for the health and financial viability of the health care system: “Cardiovascular disease (CVD), cancer, stroke and diabetes account for nearly 70% of the deaths in the United States and Europe. About 80% of adults over 65 years of age have at least one chronic disease, and 50% have two or more of these chronic diseases that accelerate the aging process1 .” The point he makes is that health care systems, especially with our rapidly aging population cannot sustain this large number of people with disease.

Meanwhile, his CR studies – many done in conjunction with the CR Society Intl. – show that those following a serious CR diet exhibit less risk of cardiovascular disease, cancer, stroke, and diabetes – all chronic diseases that people in Western societies are so prone to. Drawing parallels with animal studies, Fontana points out that CR mice are found to live much longer and in better health. When they die, autopsies show no sign of a chronic condition. Dr. Fontana says the same is possible for people. He hailed the healthiest old people as “escapers:” people who live to 100 and contract no chronic disease.

Against that backdrop, Dr. Fontana explained that his human CR studies have looked carefully at various markers in human calorie restrictors – T3, IGF-I, insulin, glucose, correlating them to successful CR, established in animal studies. This has given him a battery of indicators that can used by anyone to judge the effectiveness of a CR regimen. These are the core of the CR Way biomarkers that we recommend for testing and tracking by anyone following a CR diet. Fontana’s presentation underlines the reality that living free of chronic disease is attainable for humans.

Dr. Ingram presented valuable research results. He discussed many aspects of his productive CR research career, including his search for a CR mimetic. He has looked at some well known candidates such at Metformin (producing no difference in life span extension in his studies), 2 d-oxyglucose, (proving to be unusable because of dangerous side effects in the heart). And a promising possibility: avocado-derived mannoheptulose. Highly recommended by The CR Way, avocados have a profound glucose/insulin-lowering effect, according to Dr. Ingram. He attributes this to mannoheptulose, a sugar that’s rare in the human diet and that reduces glycolysis via hexokinase inhibition.

Bioavailability of avocado-derived mannoheptulose in dogs

Gary Davenport1, Stefan Massimino1, Michael Hayek1, Michael Ceddia1, John Burr1, Chyon-Hwa Yeh1, Lijuan Li1, George Roth2 and Donald Ingram3

1 Procter & Gamble, Lewisburg, OH
2 Geroscience, Pylesville, MD
3 Pennington Biomedical Research Center, Baton Rouge, LA

The FASEB Journal: The Journal of the Federation of the Societies for Experimental Biology, now on their Web site: http://www.fasebj.org/cgi/content/meeting_abstract/24/1_MeetingAbstracts/725.3, accessed April 1, 2011

Mannoheptulose (MH) is a 7-carbon sugar found in avocados and other natural sources that acts to reduce glycolysis via hexokinase inhibition. It has been proposed as a calorie restriction (CR) mimetic that delivers anti-aging and health-promoting benefits of CR without reducing food intake. Three studies were conducted to evaluate MH bioavailability when fed to dogs as an avocado extract (AvX) based on MH levels in urine (Study 1) and plasma (Study 2 & 3). In Study 1, Labrador Retrievers (LR; n=15) and Fox Terriers (n=15) were fed AvX-containing diets formulated to deliver 0, 2 or 5 mg MH/kg BW. All dogs were subjected to 24-hour quantitative urine collections. A dose-dependent increase (p<0.05) in urinary MH occurred with increasing dietary MH. In Study 2, LR (n=6) were fed AvX-containing diets once daily to deliver 0, 1 or 2 mg MH/kg BW. Sequential blood samples were collected before and after feeding through 12 hr and at 24-hr post-feeding. Plasma MH increased (P<0.05) with both MH diets compared to control. Peak MH occurred 6–8 hr post-feeding and returned to non-detectable levels by 24 hr. In Study 3, similar MH results were observed for LR (n=10) fed AvX-containing diets twice daily to provide 0 or 2 mg MH/kg BW. Peak MH occurred within 2–4 hr of MH consumption and returned to non-detectable levels by 24 hr.

Mannoheptulose, fed as an avocado extract, is biologically available in dogs based on its appearance in plasma and urine.

Dr. Ingram shared some additional successful research2 on the neuroprotective effects of blueberries. He and his colleagues found that mice that were injected with a blueberry extract were protected against neurodegeneration induced by a toxic substance.

The growing interest in phytonutrients for health and longevity was reinforced by Dr. Fontana, who reported a current experiment gauging the effects of a cocktail of polyphenol extracts.

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On behalf of everyone interested in longevity, we asked the scientists to tell us where they think the next important areas of their research should be. Dr. Fontana wants to turn his attention to CR and cancer, noting that many unknowns continue to make preventing cancer’s occurrence – even predicting its likelihood – difficult. He reminded us that “cancer is the second leading cause of death in many developed countries,” accounting for approximately one-fourth of all deaths. Among women, aged 40 to 79, and among men aged, 60 to 79, cancer is the leading cause of death in the U.S. The lifetime probability of developing cancer is 46% for men and 38% for women2 . Furthermore, many of the processes of cancer mirror processes of aging, so this research will do double duty.

Dr. Fontana believes that by looking at CR, which has been shown to reduce cancer incidence and rate of metastasis in animal and human studies3, better ways will be found to predict the likelihood of cancer as well as to prevent it.

This line of study will also help determine potential aging markers, a recurring theme for both presenters. Dr. Ingram declared in his answer to our question: Rate-of- aging markers need to be established and validated. Future projects need to focus on this work. Further, he called on the gerontological community to work hard on building consensus on these biomarkers, so that they can be used by researchers, healthcare professionals, and longevists.

We are heartened to know that forward-thinking organizations like AFAR are facilitating the work of talented scientists who will likely make it possible ultimately for all to live in good health longer.

The hope of the CR Society Intl. and The CR Way is that the work of these scientists will be fully appreciated and that government and other funders will respond with the support that is needed to pursue research that helps us all live longer, disease-free lives and ultimately makes a big difference in the financial viability of health care.

Thanks to the Lifeboat Foundation for inviting me to share this information.

Paul McGlothin,

Vice President Research, The CR Society International

Co-author, The CR Way

Executive Director, The CR Way Longevity Center

[email protected]

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1 Modulating Human Aging and Age-Associated Diseases

Luigi Fontana, M.D., Ph.D.

Biochimica Biophysica Acta. 2009 Oct;1790(10):1133–8. Epub 2009 Feb 10.

Population aging is progressing rapidly in many industrialized countries. The United States population aged 65 and over is expected to double in size within the next 25 years. In sedentary people eating Western diets aging is associated with the development of serious chronic diseases, including type 2 diabetes mellitus, cancer and cardiovascular diseases. About 80 percent of adults over 65 years of age have at least one chronic disease, and 50 percent have at least two chronic diseases. These chronic diseases are the most important cause of illness and mortality burden, and they have become the leading driver of health care costs, constituting an important burden for our society.

Data from epidemiological studies and clinical trials indicate that many age-associated chronic diseases can be prevented, and even reversed, with the implementation of healthy lifestyle interventions. Several recent studies suggest that more drastic interventions (i.e. calorie restriction without malnutrition and moderate protein restriction with adequate nutrition) may have additional beneficial effects on several metabolic and hormonal factors that are implicated in the biology of aging itself. Additional studies are needed to understand the complex interactions of factors that regulate aging and age-associated chronic disease.

PMID: 19364477

2A blueberry-enriched diet provides cellular protection against oxidative stress and reduces a kainate-induced learning impairment in rats.

Duffy KB, Spangler EL, Devan BD, Guo Z, Bowker JL, Janas AM, Hagepanos A, Minor RK, DeCabo R, Mouton PR, Shukitt-Hale B, Joseph JA, Ingram DK.

Laboratory of Experimental Gerontology, Intramural Research Program, National Institute on Aging, National Institutes of Health, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.

Neurobiology of Aging. 2008 Nov;29(11):1680–9. Epub 2007 May 23.

Young male Fischer-344 rats were fed a diet containing 2% blueberry (BB) extract or control diet for at least 8 weeks and then received bilateral hippocampal injections of kainic acid (KA 200 ng/0.5 microl) or phosphate buffered saline (PBS). One week later rats were trained in one-way active footshock avoidance in a straight runway followed the next day by training in a footshock motivated 14-unit T-maze with documented sensitivity to hippocampal glutamatergic manipulations. Based on analyses of several performance variables, KA-treated rats exhibited clearly impaired learning performance; however, the BB diet significantly reduced this impairment. Supporting the behavioral findings, stereological assessment of CA1 pyramidal neurons documented greater neuronal loss in KA-treated controls compared to KA-treated rats on the BB diet.

In an in vitro experiment, FaO cells grown in medium supplemented with serum from BB-fed rats had enhanced viability after exposure to hydrogen peroxide. These findings suggest that BB supplementation may protect against neurodegeneration and cognitive impairment mediated by excitotoxicity and oxidative stress.

3 Calories and carcinogenesis: lessons learned from 30 years of calorie restriction research.
Hursting SD, Smith SM, Lashinger LM, Harvey AE, Perkins SN.
Carcinogenesis. 2010 Jan;31(1):83–9. Epub 2009 Dec 7.

Calorie restriction (CR) is arguably the most potent, broadly acting dietary regimen for suppressing the carcinogenesis process, and many of the key studies in this field have been published in Carcinogenesis. Translation of the knowledge gained from CR research in animal models to cancer prevention strategies in humans is urgently needed given the worldwide obesity epidemic and the established link between obesity and increased risk of many cancers.

PMID: 19969554

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