Category Archives: Articles

This could be the beginning of More Years and Less Tears – Basis by Elysium Health

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Time will prove the validity of this supplement, but time is ticking. I submit to you the first major commercial anti-aging supplement to be introduced by anti-aging research scientist since the inception of this blog.

Link to the product here.

BASIS BY ELYSIUM

Science has enabled us to focus on the cellular level to achieve optimal health, beyond what can be accomplished with diet and exercise. Basis is designed to optimize NAD+ levels and sirtuin function in our cells to support our most critical metabolic processes like cellular detoxification, DNA repair and energy production.

Background

Basis exemplifies Elysium’s focus on providing direct access
to scientific breakthroughs in health.

The encapsulation of 35 years of research in a bottle.

For decades, scientists have been searching for answers to what internal mechanisms lead to ongoing health as well as health decline. This led to the discovery of a critical coenzyme called NAD+, which controls cellular communication, and sirtuin proteins, which play a key role in our long-term health. Sirtuin proteins require NAD+ to function, and our NAD+ levels naturally decline over time, leading to a decline in cellular health. With a focus on NAD+ and sirtuins, we can help to sustain their function over time and support the health of the building blocks of our body — our cells. This is the purpose of Basis.

Formulation

Basis contains two novel compounds that support
the production of NAD+ and the activation of sirtuins.

“NAD is one of the most compelling bits of chemistry related to aging. Its presence in the body is directly correlated with the passage of time.”

FAST COMPANY, 2015

  • Nicotinamide RibosideNR
  • PterostilbenePT

Nicotinamide Riboside Pterostilbene

The most direct precursor to NAD+. It is the most readily usable and effective building block for creating more NAD+ inside the cell. NAD+ plays a crucial role in regulating core metabolic functions including cell function, DNA repair and energy production. NAD+ supplies decline naturally with age, thus reducing a cell’s ability to function optimally and potentially impacting baseline health.

Specifications

Learn more about Basis, designed for long-term use
in adults from our 20s onward.

Instructions Take two capsules every morning with or without food. Each jar contains a 30-day supply.
Lead Scientist Dr. Lenny Guarente, Elysium Co-Founder, Leads Science of Aging Lab at MIT.
Purity Assessment Basis undergoes rigorous third party testing to confirm its content accurately reflects the ingredients listed on our label. Two capsules of Basis in our current lot contain 109% of promised quantity of NR, 112% of promised quantity of Pterostilbene.
Analysis Through our established laboratory model, Basis meets standard measures of safety and tolerability.
Both primary ingredients in Basis are GRAS (generally recognized as safe) under intended conditions of use by qualified experts.
Feedback Subtle changes in overall feeling of well-being, sleep quality, energy consistency, cognitive function, and skin health are often reported within 4-16 weeks of starting. Note that cellular health may not always manifest results at the surface.
Dietary Basis is vegetarian, vegan, gluten-free, nut-free, and contains no artificial colors or flavors.
See ingredient information here.
Production Basis is created in the United States in adherence with the FDA’s Good Manufacturing Practices.

Research

Review the scientific research that led to Basis
and how it can impact our cellular health.

  • Cellular DetoxificationCD
  • DNA RepairDR
  • Circadian Rhythm & SleepCRS
  • Protein FoldingPF
  • Mitochondrial Health & EnergyMHE
  • CognitionC
  • All Research Papers

Questions?

Visit our help center for more information.

Give us a call.

Our customer care team can answer your questions and help you place an order Monday through Friday, 9am – 5pm EST.

1 (888) 220-6436

Email us.

We would love to hear from you and will get back to your questions or feedback as soon as possible.

CARE@ELYSIUMHEALTH.COM

 

One’s ability to identify different smells may impact longevity

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Original Article Here Via EurekaAlert!

In a recent study of older adults, those with a reduced ability to identify certain odors had an increased risk of dying during an average follow-up of 4 years. The mortality rate was 45% in participants with the lowest scores on a 40-item smell test, compared with 18% of participants with the highest scores.

The study included 1169 Medicare beneficiaries who scratched and sniffed individuals odorant strips and chose the best answer from 4 items listed as multiple-choice.

“The increased risk of death increased progressively with worse performance in the smell identification test and was highest in those with the worst smelling ability, even after adjusting for medical burden and dementia,” said Dr. Davangere Devanand, lead author of the Annals of Neurology study. “This was a study of older adults–the question that remains is whether young to middle-aged adults with impaired smell identification ability are at high risk as they grow older.”

###

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

World’s Fittest OAP? | 95-year-old Sprinter Charles Eugster

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Dr. João Pedro Magalhães SPOTLIGHT

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Bio From His Personal Website Here  – His Lab Can Be Found Here  – His Twitter Here

In Addition to this spotlight, permanent links can now be found on our links page.

Dr. João Pedro Magalhães

I am originally from Porto in Portugal but have lived in Belgium and in Boston in the US, and I’m also of Spanish ancestry. Professionally, and following training at Harvard Medical School, I am now a Senior Lecturer (equivalent to an Associate Professor) at the University of Liverpool in England. My lab studies aging and longevity, in particular at the genetic level. As detailed on my senescence.info website dedicated to the biology of aging, I would ultimately like my work to help people live longer, healthier lives by contributing to retard, stop or reverse human aging. I have published dozens of scientific papers, including in top journals (e.g.,Nature– and Cell-family journals), and have given over 100 invited talks, including a TEDx talk. My research and I have been widely featured in scientific outlets (Science, Scientific American,New Scientist, etc.) and in the popular press (BBC, CNN, the Washington Post, the Financial Times and many others). I am also an advisor/consultant for various organizations, including nonprofit foundations and biotech companies. My academic work is further described on my lab’s website. I live in Heswall, Wirral, United Kingdom.

I think the human condition is only the beginning of the extraordinary journey of the mind through the universe. Technologies like genetic engineering, stem cells, cybernetics, and nanotechnology will allow us to ‘hack’ biology and evolve beyond our current human limits. As such, I am a so-called “transhumanist” in that I defend that humankind stands a better chance of survival if we understand and employ technology rather than if we try to ban it. I’m also an atheist with a life philosophy merging humanism, utilitarianism, and objectivism. May the dreams of today become the future.

Music is one of the greatest joys in my life. I started to play guitar in high school and in 1999 made a symphonic metal demo-album entitled The Legend of Hrothgar. All my songs are available for download in MP3 format.

I’m also an amateur stand-up comedian. You can find some of my older humor attempts in my news satire and cartoons sections, though nowadays I tend to use more Facebook and Twitter for this.

Among my other hobbies, I must highlight science fiction and football.

Please browse around my website to learn more about me, follow me on Twitter for the latest news, or skim through the FAQs. I am always open to suggestions, ideas, and criticisms, so please feel free to contact me.

How Old Are You, Really? Biological Age Is Harder to Pin Down Than You Think

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

BY  ON JAN 24, 2016

Original Article Here

In less than a month, I’ll be leaving my roaring 20s behind.

Like anyone crossing into a new decade of life, it feels surreal. I don’t look 30. I don’t feel 30. My health is better than it’s ever been. I tell my doctors I’m hitting the big 3-0 simply because that’s what the calendar — my only yardstick for the passage of time — is telling me.

how-old-are-you-really-31But what if there’s a better measure for age? A number that reflects how well your body is functioning as a whole, that predicts how rapidly you’re aging, that informs physicians when to expect medical issues, that aids the search for anti-aging therapies?

That number is a person’s biological age.

Scientists are increasingly making the distinction between your chronological age — the number of years that you’ve lived — and your biological age.

It’s not just an academic curiosity. A 2015 study, which comprehensively analyzed the function of multiple body systems of nearly 1,000 young adults, found that a 38-year-old’s biological clock can read anywhere from a spritely 20 to a feeble 60.

Even more frightening is this: although none of the participants had overt health issues, some were aging three times faster than expected.

Most people think aging happens only later in life, but — not to be macabre — our life expectancy clocks are constantly ticking down, said first author Dan Belsky, a researcher at the Duke University Center for Aging.

If we want to prevent age-related disease, we’re going to have to start treatments young, he explained. The problem is: what is “young”? How do we tell a person’s true biological age?

It’s a surprisingly hard question to answer.

Belsky took the clinical route, repeatedly giving their participants the ultimate full body workup over multiple years.

His team measured the function of the liver, kidney, heart and immune system. They tracked metabolic rate, cholesterol levels, aerobic fitness and lung function. They measured memory, reasoning and creativity. They even looked at the length of telomeres — protective “caps” at the end of chromosomes that safeguard our DNA and chip away with age.

Using these data, the team was able to construct a monster algorithm that calculates a person’s biological age and predicts the pace of deterioration.

The study made waves, and for good reason: for the first time, scientists are able to quantify aging in a younger population before the first hint of diabetes, Alzheimer’s or other age-related diseases appears. Imagine if your biological age is 10 years older than what you expected, said Belsky. It’s like a tap on the shoulder, letting you know that you need to exercise, to try caloric restriction and take better care of yourself.

Yet Belsky stresses that his study is proof-of-concept only. It took years and a fortune, he laughed. For a test for biological age to go mainstream, we need “better, faster and cheaper” markers and methods.

The dream is to take a sample of your skin or blood and tell you what your biological age is, much like a saliva sample sent to 23andMe can tell you (among other things) what kind of earwax you have.

While researchers still disagree on what constitutes a good marker, recent advances have yielded a group of candidates.

All are related to molecular processes that correlate with aging.

how-old-are-you-really-2

Chromosomes are capped with repeating nucleotide sequences called telomeres that get shorter over time.

Discovered in the 1980s, telomeres are extra ATCG bits that trail off the end of chromosomes. Every time a cell divides, telomeres get chopped shorter, until they reach a critical length and prohibit the cell from dividing further. Subsequent population-wide studies found correlationsbetween telomere length, disease and mortality, further increasing its worth as a marker for biological age.

 

 

Backed by decades of research and a Nobel Prize, telomere length — a measure in Belsky’s study — is perhaps the leading candidate.

Scientists and investors alike have taken notice.

In 2010, Elizabeth Blackburn, one of the discoverers of telomeres, started a company in Menlo Park, California that provides analyses of telomere length from a person’s saliva sample. Life Length, a startup based in Madrid, claims to calculate a person’s biological age by the median length of their telomeres — if you’re willing to shell out $395 a pop.

Geron, another Silicon Valley company initially backed by Blackburn’s protégé, Carol Grieder, promised substantial clinical benefits of its telomere tests before abruptly switching gears. It now focuses on cancer therapies, and Grieder has long left her role as advisor to the company.

Geron’s switch away from telomere-based aging assays is telling. Telomere tests are fast, easy and cheap, but there’s one problem — they don’t particularly reflect age accurately when it comes to each individual person.

Honestly, the value of such tests is their “cocktail party” appeal, said Jerry Shay, a biologist at the Texas Southern Medical Center and advisor to Life Length. The variation in telomere length among people of the same age is huge, he explains. Besides, longer is not always better — recent studies have revealed a tradeoff between long telomeres and a higher risk of cancer.

Despite these caveats, telomere length still remains a highly valuable marker. “There’s going to be a huge amount of heterogeneity in any marker,” said Grieber. Telomeres are just part of the puzzle — the question is, what other markers can help complete the puzzle?

how-old-are-you-really-1

Human red blood cells.

Eline Slagboom, a molecular epidemiologist at Leiden University in the Netherlands, has her money on blood.

Blood provides oxygen vital nutrients to every tissue in our body and in turn receives their waste products. We’ve known for years that the levels of some types of waste go up with age and correlate with declining organ function, said Slagboom.

For example, a 2011 study from Tony Wyss-Coray and Saul Villeda, then at Stanford University, found that injecting a young mouse with blood collected from an aged mouse throttles its brain function. Subsequent studies also showed negative effects of old blood on the liver and heart of younger recipients.

There’s a wealth of information hidden in blood, said Slagboom. Her team is running a massive study of 3,500 people aged between 40 to 110, looking at molecules in the blood that associate with age-related diseases, including cardiovascular health, dementia, diabetes and depression.

Slagboom and others’ efforts have already led to several pro-aging candidates.

Surprisingly, many are linked to the body’s immune function, which goes into overdrive with age. One candidate, with the unwieldy name of alpha1-acid-glycoprotein, is known to increase with age and independently predicts a higher risk for mortality. Another, B2M (beta-2-microglobulin), floods the body in old age and disrupts learning and memory.

Without a doubt, the race for identifying pro-aging (and pro-youth) factors is heating up.

Earlier last year, Wyss-Coray snapped up $50 million to fund his startup Alkahest, which hopes to reverse brain deficits by inhibiting pro-aging factors that accumulate with age. Although focuses on developing blood-based therapies, it’s not hard to imagine that the slew of pro-youth and pro-aging factors it uncovers could be used to measure a person’s biological age.*

In the end, no single factor — telomere, alpha1-acid-glycoprotein, B2M or other harder to measure markers such as DNA and protein damage — can paint a complete picture of a person’s true age. It’ll take multiple factors and a lot of trial and error.

But the stakes are sky high; for startups in the game of measuring biological age, literally so.

Objective age-related markers could push the anti-aging field into a whole new era, said Luigi Fontana at Washington University. They give us a way to test promising anti-aging drugs such as rapamycin andmetformin using short-term clinical trials. Instead of decades, we could be looking at months.

I can’t stress this enough, said Fontana. Knowing someone’s biological age is “very, very important.”


* Disclosure: The author works as a postdoctoral researcher with Dr. Saul Villeda, an advisor to Alkahest, at UCSF to study pro-youth factors in young blood.

Image Credit: sergign/Shutterstock.comunderworld/Shutterstock.comAJC ajcann.wordpress.com/FlickrCC; MdougM/Wikimedia Commons

Gene thought to suppress cancer may actually promote spread of colorectal cancer

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Original Source Here Via EurekAlert!

UNIVERSITY OF MISSOURI-COLUMBIA

COLUMBIA, Mo. (Jan. 4, 2016) – A gene that is known to suppress the growth and spread of many types of cancer has the opposite effect in some forms of colorectal cancer, University of Missouri School of Medicine researchers have found. It is a finding that may lay the foundation for new colorectal cancer treatments.

IMAGE

IMAGE: UNIVERSITY OF MISSOURI SCHOOL OF MEDICINE RESEARCHER SHARAD KHARE, PH.D., FOUND THAT A GENE THAT IS KNOWN TO SUPPRESS THE GROWTH AND SPREAD OF MANY TYPES OF CANCER HAS THE… view more CREDIT: JUSTIN KELLEY/MU

“The gene known as Sprouty2 has previously been shown to protect against metastasis, or the spreading of cancer to other parts of the body, in breast, prostate and liver cancer,” said Sharad Khare, Ph.D., associate professor of research in the MU School of Medicine’s Division of Gastroenterology and Hepatology and lead author of the study. “However, our recent molecular studies found that this gene may actually help promote metastasis instead of suppress it.”

For more than three years, Khare studied Sprouty2 in cancer cell models, mouse models and human biopsy samples. Using different molecular methods, the researchers found that the gene functions differently in colorectal cancer than in other types of cancers. Sprouty2 is known to block molecular circuits to prevent cancer cells from growing and spreading to other parts of the body. However, the researchers found that in colorectal cancer, Sprouty2 may increase the metastatic ability of cancer cells instead of suppress it. Khare believes this occurs when the gene is up-regulated, or supercharged.

Cancer deaths attributed to colorectal cancer are mainly due to tumor recurrence and metastasis to other organs. Excluding skin cancers, colorectal cancer is the third most common cancer diagnosed in both men and women in the United States, according to the American Cancer Society. It’s estimated that the lifetime risk of developing colorectal cancer is about 1 in 20.

“This finding is a very significant step in our understanding of metastasis in colorectal cancer, but it’s important to note that we believe this phenomenon may occur in only a subset of colorectal cancer patients,” Khare said. “We don’t yet know why this is the case, but we hope to determine if there is a correlation between the up-regulation of this gene and the life expectancy of patients with colorectal cancer. Future studies will help us understand who may be at risk, and ultimately, if personalized treatments can be planned to target this gene.”

###

The study, “Atypical Role of Sprouty in Colorectal Cancer: Sprouty Repression Inhibits Epithelial-mesenchymal Transition,” recently was published in the cancer research journalOncogene. Research reported in this publication was supported by the National Institutes of Health under award numbers CA150081 and DC010387, Veterans Affairs Merit Award 1171590, the MU Research Board Award and MU School of Medicine Bridge funding. The content is solely the responsibility of the authors and does not necessarily represent the official views of the funding agencies.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

valentinarr via Getty Images

BILLIONAIRE PETER THIEL INVESTS IN THE WAR ON AGING

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Via Popular Science – Original Link Here

valentinarr via Getty Images

valentinarr via Getty Images

Earlier this year, Breakout Labs, the subsidiary organization created by PayPal co-and billionaire-investor Peter Thiel, announced a few select biotechnology startups that would receiving funding to further their ideas. Breakout Labs’ mission is to invest in companies that are looking to make “radical scientific advances” mainstream, essentially boosting the best underfunded inventions to the tune of up to $350,000 (plus consultation help from Breakout Labs).

Well, Breakout Labs is at again, announcing funding ventures for the second time this year. This time, the ideas range from adhesives that mimic the skin of geckos, low-cost sensors that can tell if food has gone bad, metals that repel water, and a mission to fight aging. The overarching trend in this announcement is funding advances in microstructure: three companies use mechanical innovation on a nanoscale to seemingly change the property of the material.

CyteGen

Google’s Calico Lab made headlines in 2013, when the company announced it was going to “cure death.” Now, Thiel is investing in a similar mission. CyteGen tackles aging from the perspective that aging is a holistic process, not specific deterioration of body parts.

“There is an assumption that aging necessarily brings the kind of physical and mental decline that results in Parkinson’s, Alzheimer’s, and other diseases. Evidence indicates otherwise, which is what spurred us to launch CyteGen,” said George Ugras, co-founder and president of CyteGen.

While CyteGen has held their cards close in regards to technique, the team members from eight universities will focus on neurodegenerative diseases. The name, CyteGen, is a close parallel to the field of cytogenetics, which looks at chromosomal structure in individual cells.

Study finds calorie restriction lowers some risk factors for age-related diseases

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

 

Original Article Here

A National Institutes of Health-supported study provides some of the first clues about the impact of sustained calorie restriction in adults. Results from a two-year clinical trial show calorie restriction in normal-weight and moderately overweight people did not have some metabolic effects found in laboratory animal studies. However, the researchers found calorie restriction modified risk factors for age-related diseases and influenced indicators associated with longer life span, such as blood pressure, cholesterol, and insulin resistance. The study was reported in the September, 2015 issue of Journal of Gerontology: Medical Sciences.

Calorie restriction is a reduction in without deprivation of essential nutrients. It has been shown to increase longevity and delay the progression of a number of age-related diseases in multiple animal studies. Called Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy (CALERIE), the randomized trial was funded by the National Institute on Aging (NIA) and the National Institute of Diabetes and Digestive and Kidney Diseases, both part of NIH. It was conducted at Washington University in St. Louis, Louisiana State University’s Pennington Biomedical Research Institute in Baton Rouge, and Tufts University in Boston. The study coordinating center was at Duke University in Durham, North Carolina.

CALERIE was designed to test the effects of on resting metabolic rate (after adjusting for ) and body temperature, which are diminished in many laboratory animal studies and have been proposed to contribute to its effects on longevity.

“The study found that this calorie restriction intervention did not produce significant effects on the pre-specified primary metabolic endpoints, but it did modify several for age-related diseases. It is encouraging to find positive effects when we test interventions that might affect diseases and declines associated with advancing age,” notes NIA Director Richard J. Hodes, M.D. “However, we need to learn much more about the health consequences of this type of intervention in healthy people before considering dietary recommendations. In the meantime, we do know that exercise and maintaining a healthy weight and diet can contribute to healthy aging.”

In laboratory animals, calorie restriction’s favorable effects on have generally been found when it is begun in youth or early middle age. An equivalent trial in people would take decades. However, shorter trials can determine feasibility, safety and effects on quality of life, disease risk factors, predictors of life span and effects on mechanisms influenced by calorie restriction in laboratory animal studies. CALERIE was a two-year randomized controlled trial in 218 young and middle-aged healthy normal-weight and moderately overweight men and women to measure these outcomes in a calorie restriction group, compared with a control group who maintained their regular diets.

The calorie restriction participants were given weight targets of 15.5 percent weight loss in the first year, followed by weight stability over the second year. This target was the weight loss expected to be achieved by reducing calorie intake by 25 percent below one’s regular intake at the start of the study. The calorie restriction group lost an average of 10 percent of their body weight in the first year, and maintained this weight over the second year. Though weight loss fell short of the target, it is the largest sustained weight loss reported in any dietary trial in non-obese people. The participants achieved substantially less calorie restriction (12 percent) than the trial’s 25-percent goal, but maintained calorie restriction over the entire two-year period. The control group’s weight and calorie intake were stable over the period. The study found a temporary effect on resting metabolic rate, which was not significant at the end of the study, and no on body temperature.

Although the expected metabolic effects were not found, calorie restriction significantly lowered several predictors of cardiovascular disease compared to the control group, decreasing average blood pressure by 4 percent and total cholesterol by 6 percent. Levels of HDL (“good”) cholesterol were increased. Calorie restriction caused a 47-percent reduction in levels of C-reactive protein, an inflammatory factor linked to cardiovascular disease. It also markedly decreased insulin resistance, which is an indicator of diabetes risk. T3, a marker of thyroid hormone activity, decreased in the calorie restriction group by more than 20 percent, while remaining within the normal range. This is of interest since some studies suggest that lower thyroid activity may be associated with longer life span.

The study also assessed calorie restriction’s effects on mood (particularly hunger-related symptoms) and found no adverse effects. No increased risk of serious adverse clinical events was reported. However, a few participants developed transient anemia and greater-than-expected decreases in bone density given their degree of weight loss, reinforcing the importance of clinical monitoring during calorie restriction.

“The CALERIE results are quite intriguing. They show that this degree of sustained calorie restriction can influence disease risk factors and possible predictors of longevity in healthy, non-obese people. It will be important to learn how calorie restriction at this level affects these factors despite the lack of the predicted metabolic effects,” said Evan Hadley, M.D, director of NIA’s Division of Geriatrics and Clinical Gerontology and an author of the paper. “Since this group already had low risk factor levels at the start of the study, it’s important to find out whether these further reductions would yield additional long-term benefits. It also would be useful to discover if calorie restriction over longer periods has additional effects on predictors of health in old age, and compare its effects with exercise-induced weight loss.”

Explore further: Low-calorie diet may not prolong life: study (Update)

More information: Ravussin, E., et al., A 2-Year Randomized Controlled Trial of Human Caloric Restriction: Feasibility and Effects on Predictors of Health Span and Longevity. J Gerontol A Biol Sci Med Sci (2015) 70 (9): 1097-1104. DOI: 10.1093/gerona/glv057

Cute! How to Age Gracefully

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Interview with Dr. Sushmita Roy: Predicting Cell-Type Specific Mammalian Regulatory Networks

Jonathon Fulkerson
Follow me

Jonathon Fulkerson

Undergraduate at The University of Southern Indiana + More Years Less Tears + Your NeXt Computer
After 15+ years as an IT professional. Jonathon decided to return to school in hopes of one day troubleshooting the most universal problem effecting all. Death, pain, and suffering by aging. As an undergraduate he is currently performing research in Dr. Richard Bennetts lab at the University of Southern Indiana, as well as volunteering for various organizations including the Buck Institute for research on Aging.
Jonathon Fulkerson
Follow me

Latest posts by Jonathon Fulkerson (see all)

Interview with Dr. Sushmita Roy: Predicting Cell-Type Specific Mammalian Regulatory Networks

Research Background

Dr. Sushmita Roy

Sushmita Roy is an Assistant Professor in the Biostatistics and Medical Informatics Department at the University of Wisconsin, Madison.  She received her B.S. in Computer Engineering at the University of Pune, India. She received her Ph.D. in Computer Science in 2009 from the University of New Mexico and did a post-doctorate at the Broad Institute of MIT and Harvard. She is a recipient of the 2014 Alfred P. Sloan Foundation Fellowship and an NSF CAREER award.

It’s not just genes that make us who we are. The way that genes are regulated and turned on or off (also called epigenetics), rather than the DNA sequence of the genes themselves, is also very important. Dr. Roy’s lab focuses on the development and application of statistical computational methods to identify the gene regulation networks which drive cellular functions by integrating different types of genome-wide datasets. In her seminar at the Buck Institute, she first explained why mammalian gene regulation is complex:

  • There are thousands of transcription factors with unknown binding specificity
  • Gene expression is regulated by the interplay of transcription factors and chromatin (chromatin is the combination or complex of DNA and proteins that make up the contents of the nucleus of a cell)
  • Regulatory DNA elements are not necessarily next to the gene
  • 3D organization of the genome also plays a role in gene expression.

She also introduced three projects from her lab:

  • Gene regulatory network which controls host response to different strains of influenza infections
  • Examining chromatin state model to help identify epigenetic barriers in cellular reprogramming
  • Predicting target genes of candidate enhancers (regulatory sequence elements).

SAGE sat down with Dr. Roy to ask a few more questions…


Q: Could you summarize your research to the general public using non-scientific words?

SR: I am interested in understanding how cells know what to do when. So basically more complicated organisms have different types of cells, and each cell has different types of functions. One of the ways that cells are able to do a particular specialized function is by expressing the right type of genes or the right set of genes. I am interested in developing computational methods to try to understand the molecular circuitry of cells that determine what genes must be expressed when and where. Specifically, we want to know: what is the underlying gene network in a particular cell type? How does the network change between different cell types or different environmental conditions?

Q: Can you tell us a little more about how chromatin state plays a role in gene expression?

SR: When I say the chromatin state, I mean that you should think of DNA as not just a string of letters. DNA is wrapped around histone proteins, and this is how the DNA is packaged inside the nucleus of a cell. These histones get modified bio-chemically, which in turn influences the accessibility of the associated DNA to other important proteins that activate genes (e.g. transcription factor proteins). In particular, some modifications make the DNA more conducive to activate expression while some modifications make the DNA less open and conducive to expression. Expression of a gene in turn is controlled by the set of transcription factors that are bound to the gene’s promoter. We are still figuring out the interplay between chromatin state and transcription factors. As more datasets from multiple cell types become available, we hope to get a better understanding of the relative importance of chromatin state, chromatin modifying enzymes and transcription factors in specifying gene expression levels.

One would expect that when chromatin state changes, the associated gene expression levels also change. However we see that this is only partially true.

Q: What is the main challenge in your field right now? We know that the machine learning model involves using known data to make predictions of the unknown. Can you use your model to predict?

SR: A major challenge in the network community is the lack of good gold standards of a “correct” regulatory network that is large enough to get realistic estimates of how a method for network reconstruction works. Interpretation of results is also a challenge, again, due to the large number of unknowns. We can use our models to predict expression in a new condition provided we can measure the activity of some of the components of the network. The big picture would be to try to predict how a cell behaves in new perturbation – something that you’ve not measured.

Q: Which research project is the one you’re most excited about right now?

SR: All three of them are very exciting projects that ask pieces of a bigger question of building a predictive model of a cell’s expression profile. I’m very interested in delving deeper into the chromatin state and its connection to mRNA levels. That link is not very well understood, and I want to have a bigger picture of what it is. You can think of chromatin modifying enzymes also as potential regulators. I want to try to understand the connections among these different chromatin modifications and how that affects the structure and function of a regulatory network driving a particular process or a particular phenotype. That certainly is something that I want to spend more time on and understand more. Ultimately, I would like to gain a better understanding of transcriptional regulation as a function of the chromatin state, transcription factor occupancy, signaling networks and the organization of the genome and how network change impacts complex phenotypes.

Q: Are you planning to conduct studies that collaborate with aging research groups?

SR: Certainly if there is an area where I can add my expertise to. I would be certainly enthusiastic about working on aging, which I think is a very important problem. It would be very interesting to study the connection between diet and aging as well as aging and different diseases. So if approaches like mine can be used to try to address such problems, I would be enthusiastic to collaborate.

Q: Can you give postdocs advice for how to succeed in an academic career?

SR: You have to figure out what you want to do, what’s exciting to you and let that drive you. You need to ask yourself if you like research and if you’re driven by it. It’s also important to acquire skills that enable one to collaborate with a diverse set of scientists from different disciplines including from computational and biological areas.

I think having a good postdoc experience is also important. For me, my experience was great because I was working on what I wanted to do, and I was fortunate enough to meet people who were willing to support me. I am originally from India, and I was fortunate to have the opportunity to pursue higher education in the US. I always wanted to do something in medicine and biology, but I was a computer engineer. I really wanted to come back to biology, and I was fortunate to meet my PhD mentors in New Mexico to support my interdisciplinary focus of computer science and biology.   For my postdoc at the Broad Institute, I dived deeper into computational biology, and I was surrounded by computational scientists as well as experimentalists who were working in close collaboration with the computational scientists to address important questions in biology. That was a very useful and nurturing experience for me.

Q: As an international research scientist, what kind of difficulties or challenges have you faced, and how did you overcome them?

SR: When I came here, I came with uncertainties about funding, so that was bit of a worry initially. Making sure I had some way to support my education was important and once that was taken care of, I really enjoyed being here. I was also fortunate to have great advisors to support my PhD efforts. Overall, I’ve been around people who’ve been very supportive and encouraging mentors. I think I am pretty fortunate in having these kinds of people to help me understand how to be a scientist and researcher.

Q: What is the academic environment in India?

SR: It’s getting better but it’s not nearly as great as it is over here. There are some institutes with new PIs over there with a lot of energy, who have funded labs doing great work. But in general, we don’t have the resources and the infrastructure like the US. India is behind, but it’s getting better and better. Certainly having more funding and more support would help things to improve. The government is supporting, but I think there needs to be more.

For more on Dr. Roy’s work, check out the Roy lab website.