Spend this much time in nature weekly to boost your health

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In 2018, more than 318.2 million people visited U.S. national parks, logging more than 1.4 billion recreation visitor hours.1 Their popularity hints at humans’ inherent desire to spend time in natural spaces, and research backs up the benefits, showing that greater exposure to parks and other “green” spaces is associated with better health and well-being.2

Taking time to explore national parks is a worthy endeavor to get in your nature fix, but even better may be taking time to explore the natural world on a daily or weekly basis. Is there a magic number when it comes to the ideal amount of time to spend in nature to maximize its benefits to your health?

120 minutes a week in nature is ideal for health and well-being

A study published in Scientific Reports explored the associations between contact with nature in the last seven days and self-reported health and well-being.3 Data from 19,806 participants were included, revealing that, compared to no nature contact, spending 120 minutes or more in nature during the previous week was associated with a greater likelihood of good health or high well-being.

There were decreasing returns with nature exposure beyond 120 minutes, and the association flattened out and even dropped between 200 and 300 minutes per week.

“We tentatively suggest, therefore, that 120 minutes contact with nature per week may reflect a kind of ‘threshold,’ below which there is insufficient contact to produce significant benefits to health and well-being, but above which such benefits become manifest,” the researchers said.4

It didn’t matter how the 120 minutes was achieved; multiple shorter visits had the same effect as fewer, longer visits, as long as they added up to 120 minutes, and the benefits held true across different populations, including older adults and people with long-term health issues. Lead study author Matthew White, of the University of Exeter Medical School, said in a news release:5

“It’s well known that getting outdoors in nature can be good for people’s health and wellbeing but until now we’ve not been able to say how much is enough.

The majority of nature visits in this research took place within just two miles of home so even visiting local urban greenspaces seems to be a good thing. Two hours a week is hopefully a realistic target for many people, especially given that it can be spread over an entire week to get the benefit.”

Health benefits of nature depend on the dose

The researchers of the featured study even suggested that, with further research, weekly nature guidelines could be developed similar to those given for physical activity. In fact, the study found that getting recommended levels of nature exposure weekly could result in a similar magnitude of health gains as achieving recommended levels of physical activity.6

Indeed, past research also shows that the health benefits of nature experiences depend on the dose. Among people in an urban environment, long visits to green spaces were associated with lower rates of depression and high blood pressure, while more frequent visits were linked to greater social cohesion, which is associated with physical and mental well-being. The study further revealed:7

“The results here suggest that nature experiences in urban green spaces may be having a considerable impact on population health, and that these benefits could be higher if more people were engaged in nature experiences.

Specifically, our results suggest that up to a further 7% of depression cases and 9% of high blood pressure cases could be prevented if all city residents were to visit green spaces at least once a week for an average duration of 30 minutes or more.”

More frequent and longer visits to green spaces were also associated with physical activity, which can further boost health. Visiting natural settings may help to facilitate exercise, as you can easily spend time walking, hiking or cycling trails.

How nature can improve your health

Spending time in nature carries an impressive potential to boost your health. One meta-analysis of 103 observational and 40 interventional studies investigating about 100 health outcomes revealed that spending more time in green spaces is associated with decreased:8

Salivary cortisol (a marker of stress)

Heart rate

Diastolic blood pressure

Preterm birth

Type 2 diabetes

All-cause mortality

Cardiovascular mortality

Further, increased nature exposure reduced the incidence of stroke, high blood pressure, asthma and coronary heart disease, while good self-reported health increased.

According to the study, “For several nonpooled health outcomes, between 66.7% and 100% of studies showed health-denoting associations with increased greenspace exposure including neurological and cancer-related outcomes, and respiratory mortality.”9

Delving even deeper into nature’s connection to health, some research suggests that green spaces with the highest levels of plants, butterflies and birds, otherwise known as species richness or biodiversity, may further enhance psychological health.10 On the other hand, the opposite also holds true in that living in an urban environment might negatively affect mental health.

City living is linked to mood and anxiety disorders, as well as increased incidence of schizophrenia, and it could be that lack of access to green spaces is one reason why.11

Doctors handing out ‘green prescriptions’

One of the goals of quantifying the optimal “dose” of nature is so doctors can advise their patients on how to get the most benefits of outdoor time. They could even hand out “green prescriptions.” The authors of the meta-analysis noted:12

“Green prescriptions involving greenspace use may have substantial benefits. Our findings should encourage practitioners and policymakers to give due regard to how they can create, maintain, and improve existing accessible greenspaces in deprived areas.

Furthermore the development of strategies and interventions for the utilisation of such greenspaces by those who stand to benefit the most.”

It’s an idea that’s catching on. One partnership project between NHS Shetland and the U.K.’s Royal Society for the Protection of Birds allows general practitioners to prescribe nature as part of their patients’ treatment.

The Nature Prescriptions program “recognizes the benefits of nature on reducing blood pressure, reducing anxiety and increasing happiness as well as the growing disconnection with nature throughout society.”13 The program includes a schedule of seasonal activities designed to encourage more time in nature, which include such activities as:14

Counting the birds in your garden

Stepping outside and being still for three minutes, just listening

Getting out “whatever the weather” and feeling the exhilaration of wind and rain on your face

Making a birdbath

Looking for tracks and signs of animals

Planting some bulbs

Are you getting enough nature time?

As scientists continue to reaffirm the benefits of spending time in nature, many Americans struggle with getting enough outdoor time. In a report commissioned by Velux, a window manufacturing company, it’s revealed that 25 percent of Americans hardly ever go outside.15,16

“We are increasingly turning into a generation of indoor people where the only time we get daylight and fresh air midweek is on the commute to work or school,” Peter Foldbjerg, the head of daylight energy and indoor climate at Velux, a window manufacturing company, said in a statement.17

In another survey of 11,817 U.S. adults and children, 25% of adults reported spending less than two hours in nature each week.18 “The relationship of Americans and nature is changing,” the Nature of Americans report found, adding:19

“Adults and children alike spend evermore time indoors, participation in activities like hunting and fishing is stagnant or declining, and shifts in social expectations treat engagement with nature as a mere amenity.

These trends pose a nationwide problem, since overwhelming evidence shows the physical, psychological, and social wellbeing of humans depends on contact with nature.”

The report described a significant gap between Americans’ interest in nature and their efforts and ability to pursue that interest. While numerous factors are contributing to an increasing disconnect between Americans and nature, the report highlighted five of the most prominent:20

  1. Physical places, or a built environment, generally discourage contact with the natural world.
  2. Competing priorities for time, attention and money prevent contact with nature from becoming routine and habitual.
  3. Declining direct dependence on the natural world for livelihoods and subsistence allows Americans to orient their lives to other things.
  4. New technologies, especially electronic media, distract and captivate.
  5. Shifting expectations about what “good” contact to nature ought to be mean adults are generally satisfied with the relatively little time they spend outdoors in nature.

How to make nature part of your daily life

The good news is that it may require only 120 minutes a week to reap the many benefits that nature has to offer, and this is an amount that should be achievable for most people. Further, you needn’t spend two hours at one time; if you break it up into daily increments, that’s only about 17 minutes a day.

Taking time to walk outdoors during your lunch break, tend to your garden after work or walk your dog in the morning can all increase your exposure to beneficial green spaces. Try to make a habit of getting outdoors as much as possible; meal times, family gatherings and washing your dog are all opportunities to be outdoors.

Combining your workouts with nature by doing them outdoors is another good idea, and even talking a longer walk outdoors when you have time can be incredibly beneficial.

In one study, people who took a 90-minute walk in nature reported lower levels of rumination and had reduced neural activity in an area of the brain (the subgenual prefrontal cortex) linked to risk of mental illness such as depression than people who took a comparable walk in the city.21

As it stands, more than 50% of people live in urban areas, and this is expected to increase to 70% by 2050,22 which means making a conscious effort to increase access to green spaces will become ever more important — as will taking the time to use such spaces.

The Nature of Americans report suggested “transformative action” to achieve this, including the recommendations that follow to help connect Americans with nature:23

Emphasize regular, recurrent and routine engagement with nature, the outdoors and wildlife.

For adults and children, promote nature not only as a place for experiences, but also as a place for involvement and care.

Assure adults and children that time in nature can be (and even ought to be) social.

Provide socially safe and satisfying places outdoors, especially for urban and minority adults and children.

Work to lower the perceived costs of participation in recreational activities.

Promote experiences in nature that match Americans’ multidimensional values of nature.

Broaden programming to include a range of outcomes.

For adults, promote conservation efforts as a way to improve their overall community and quality of life.

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Spikenard may boost memory and cognitive function

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Spikenard (Nardostachys jatamansi), also known as jatamansi,1 is an herb originating from the Himalayas.2 It’s commonly used as an essential oil, which is added to perfumes due to its sweet, balsamic and woody scent.3 But aside from its aroma, spikenard contains more healthful components that you can benefit from. To learn more about spikenard’s health benefits and uses, continue reading.

What is spikenard?

For centuries, spikenard has been used in medicine to treat numerous conditions, both physical and aesthetic. Its popularity as a therapeutic agent is widely known throughout the world, with the herb having been used in Indian, Greek, Egyptian, Arabic and Roman medicine. In fact, legend says that spikenard was the expensive ointment referenced in the Bible,4 when Mary Magdalene5 anointed Jesus’ feet.

The spikenard plant typically grows in mountainous regions, between 1,200 and 3,000 meters (almost 4,000 to 10,000 feet) above sea level.6

It is easily recognizable by its rosy or pale pink flowers and its rhizomes that are covered in tail-like brown fibers.7 These rhizomes, which are commonly hydrodistilled to make an essential oil, are the main parts of the spikenard plant that are used in Ayurvedic medicine.8 But because of difficulties in cultivating it at such high altitudes, its rarity and its environment, spikenard has been deemed as an endangered plant.9

While the name “spikenard” is often associated with Nardostachys jatamansi, it actually shares the same name with the Aralia racemosa, the American counterpart of this Indian herb. They do, however, offer different uses, with American spikenard being primarily used for easing coughs, asthma and arthritis.10

Help boost your brain function and get other benefits from spikenard

Spikenard is mainly utilized for its benefits for neurological and mental conditions, such as epilepsy, insomnia and mental weakness. In modern times it’s also been used to treat disorders of the cardiovascular system.11 Numerous studies have focused on the neuroprotective characteristics12 of this herb, with it being used as an alternative treatment for minimizing symptoms and slowing down the development of both Alzheimer’s13 and Parkinson’s disease.14

Its ability to help alleviate the symptoms of both these diseases is due to its high concentration of sesquiterpenes. These are natural chemicals that can penetrate the blood-brain barrier and help fight numerous neurological symptoms.15

But aside from this, spikenard can actually have an effect on a wide range of bodily functions. Some of these health benefits include:

  • Hepatoprotective — In a 2000 study from the Journal of Ethnopharmacology, researchers found that spikenard extract may have hepatoprotective properties. Rats were pretreated with 800 milligrams per kilogram of the extract, which protected their liver from damage after they were exposed to thioacetamide, a hepatotoxic compound.16
  • May improve learning and memory — In a 2006 animal study from the Journal of Medicinal Food, young mice were given doses of spikenard extract for eight successive days. The extracts improved their learning and memory and also reversed diazepam-induced amnesia.17
  • Helps in stress management — A 2009 study from the Indian Journal of Biochemistry and Biophysics showed that the antioxidant properties of spikenard helped curb stress in rats by reversing the elevation in lipid peroxidation and nitric oxide levels in the stomach and the catalase activity in the brain.18
  • May assist with depression — The effects of electron beam radiation has been linked to DNA damage and depression. In a 2013 animal study from the International Journal of Research in Ayurveda and Pharmacy, spikenard ethanolic root extract reduced the risk of depression caused by radiation.19 Additionally, a 1994 animal study showed that spikenard extracts caused significant increase in serotonin, GABA and taurine.20
  • Aids in managing diabetes A 2018 study from the Journal of Medicinal Food showed that spikenard extract helped increase insulin sensitivity and inhibit glucose production in the diabetic control group of mice.21

Other uses of spikenard

While spikenard’s aroma is extremely pleasurable, its uses are not limited to deodorizing. Because of the impressive components of spikenard, you can use the oil or extract in numerous ways, particularly for these conditions:

  • Heart palpitations, convulsions and hysteria — Spikenard oil has both anticonvulsive and anti-arrhythmic activities, which help in reducing heart palpitations and hysteria symptoms.22
  • Premature graying of hair — Spikenard essential oil is used as a hair tonic, promoting hair growth and blackening of hair. It has also been found to improve hair luster.23
  • Painful menstruation and constipation — Spikenard extracts has antispasmodic and stimulant properties, which may help alleviate dysmenorrhea and regulate urination and digestion.24

Tips on growing spikenard

If you want to grow your own spikenard, note that this plant may be extremely picky due to the climate and altitude it’s commonly found in. To start, make sure that you have soil rich in carbon and organic nitrogen. At lower altitudes, spikenard prefers a terrain that has a slight tilt. Locate an area that has moist soil and is partially exposed to sunlight. It’s best that you use a litter treatment with manure to boost the organic content of the soil.

To ensure that you’re getting the spikenard roots that have the highest levels of active compounds, harvest after they become mature, usually in September or October in higher altitudes.25

What is spikenard essential oil and how can you use it?

Spikenard essential oil, which has been used for a variety of applications for hundreds of years, has been used in religious rites. In funerals over 2,000 years ago, it was used to anoint the bodies of the departed, alongside myrrh oil and other oils.26 Today, some of spikenard essential oil’s uses include:

  • Hair growth — The nardin, jatamansic acid and nardal terpenoids found in spikenard essential oil may have a positive effect on hair growth activity.27
  • Skin care — Spikenard oil may be used to help alleviate eczema, skin inflammation, psoriasis and sores.28
  • Wound healing — In a 2017 study from Biochimie Open, spikenard essential oil was found to contain cytotoxic and antiproliferative properties, which promoted anti-inflammatory and tissue remodeling effects on wounds.29

Contraindications for spikenard oil use

While there are no proven side effects caused by spikenard, it is suggested that you seek the opinion of a health care practitioner to see if this herb is recommended for you and whether it will interfere with any medications that you may be taking. For topical application, dilute the essential oil in a carrier oil and test on a small patch of skin to check if it causes an allergic reaction to avoid irritation and scarring.

Breastfeeding mothers should steer clear of this herb because of the possible repercussions it can cause. Spikenard oil use is also highly discouraged for pregnant women because of its supposed effect on menstruation. While it may improve menstrual cycles, spikenard may cause dangerous effects during pregnancy.30

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Cellular Senescence in Mesenchymal Stem Cells

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Cellular senescence is a cause of aging. Cells become senescent in response to a variety of circumstances: damage, a toxic environment, reaching the Hayflick limit on replication, and so forth. In all cell populations, older individuals exhibit increasing numbers of senescent cells, perhaps largely due to the progressive decline of the immune system and its growing failure to clear out unwanted or harmful cells. Lingering senescent cells secrete a potent mix of signals that rouse the immune system into a state of chronic inflammation, and degrade tissue function and structure. The more of them there are, the worse the outcome.

Mesenchymal stem cells (MSCs) are located in specific areas of tissues, called “niches“, and are characterized as being in a state of relative quietness, from which they can exit under the proper conditions to obtain the proliferative potential necessary for tissue regeneration. MSCs have sustained interest among researchers by contributing to tissue homeostasis and modulating inflammatory response, all activities accomplished primarily by the secretion of cytokines and growth factors, because their paracrine action is the main mechanism explaining their effects, regardless of source.

Senescence is defined as a mechanism for limiting the regenerative potential of stem cells. It is now evident that senescent cells secrete dozens of molecules, for which the terms “senescence-associated secretory phenotype (SASP)” and “senescence-messaging secretome (SMS) factors” have been proposed. The secreted factors contribute to cellular proliferative arrest through autocrine/paracrine pathways as well as in vivo and in vitro. SMS factors released by senescent cells play a key role in cellular senescence and physiological aging by activation of cytoplasmic signalling circuitry.

The population of mesenchymal stem cells, also known as mesenchymal stromal cells, contributes directly to the homeostatic maintenance of organs; hence, their senescence could be very deleterious for human bodily functions. The milestone in MSC investigation will be discovering senescence markers to determine the quality of the in vitro cells for cell-based therapies. Researchers have proposed TRAIL receptor CD264 as the first cellular senescence mesenchymal marker in bone marrow-derived MSCs, because it has the same expression profile of p21 during culture passage.

Link: https://doi.org/10.4252/wjsc.v11.i6.337

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Dysfunctional Stem Cells Contribute to Impaired Fracture Repair in Old Age

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Stem cells perform the vital function of supporting surrounding tissue by providing new daughter somatic cells to make up losses and take their place to maintain tissue function. This stem cell activity declines with age, however, due to a combination of intrinsic damage to these cell populations, and increasing inactivity. The latter is an evolved reaction to rising levels of damage, one that serves to reduce cancer risk in earlier old age, but at the cost of a lengthy decline into incapacity. Pick near any dysfunction of aging and it is likely that loss of stem cell activity is to some degree contributing to the outcome.

Successful fracture healing requires the simultaneous regeneration of both the bone and vasculature; mesenchymal stem cells (MSCs) are directed to replace the bone tissue, while endothelial progenitor cells (EPCs) form the new vasculature that supplies blood to the fracture site. In the elderly, the healing process is slowed, partly due to decreased regenerative function of these stem and progenitor cells.

MSCs from older individuals are impaired with regard to cell number, proliferative capacity, ability to migrate, and osteochondrogenic differentiation potential. The proliferation, migration and function of EPCs are also compromised with advanced age. Although the reasons for cellular dysfunction with age are complex and multidimensional, reduced expression of growth factors, accumulation of oxidative damage from reactive oxygen species, and altered signaling of the Sirtuin-1 pathway are contributing factors to aging at the cellular level of both MSCs and EPCs.

Because of these geriatric-specific issues, effective treatment for fracture repair may require new therapeutic techniques to restore cellular function. The causes of cellular aging and the concomitant decline in functionality are wide-ranging, but provide some intriguing indications of potential targets for speeding fracture healing in older individuals. In the future, cell therapies that supplement the inadequate native cellular response with MSCs or endothelial colony forming cells (ECFCs); bone anabolic pharmacological agents, particularly in combination with strategies to localize their delivery to the bone fracture; drugs that reduce oxidative stress, cellular senescence, or activate SIRT1; and/or physical therapeutics may prove effective in promoting fracture healing in the elderly.

Advanced age is the primary risk factor for a fracture, due to the low bone mass and inferior bone quality associated with aging; a better understanding of the dysfunctional behavior of the aging cell will provide a foundation for new treatments to decrease healing time and reduce the development of complications during the extended recovery from fracture healing in the elderly.

Link: https://doi.org/10.4252/wjsc.v11.i6.281

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Tired of Insomnia? Helpful Herbs and Sleep Hygiene

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Tired of Insomnia? Helpful Herbs and Sleep Hygiene
Ashley Wyckoff, Bachelor of Science

Insomnia affects approximately 24 million people, or 10% of the U.S. adult population.1,2 Symptoms of insomnia go beyond just trouble falling asleep; people who experience sleep disturbances also tend to have low energy, fatigue, difficulty concentrating and emotional changes.

Since sleep disturbance is such a prevailing problem, there are many options on the market for those affected by insomnia. The good news is there are herbs that have been clinically shown to help. Plus, lifestyle habits can play a role. Get some sleep with these lifestyle hacks and clinically studied herbs!

As with many health conditions, it is important to get to the root cause. Stress, improper sleep hygiene and circadian rhythm imbalance can all cause insomnia. Poor mental health can not only cause one to not be able to fall asleep, but also for the little sleep that one gets to not be replenishing.3 One’s “sleep hygiene” comprises the customs and routines a person has that influences their sleep.4 A circadian rhythm is one’s sleep/wake cycle that can be disturbed by travel, daylight savings and change in routine.3

The Best Herbs for Sleep

Honokiol is a polyphenol found in magnolia bark, leaves and seed cones. It has been found to promote the GABAA receptor, allowing the neurotransmitter to better bind to their active sites.5 The GABAA receptor is fast-acting and results in sedation and reduced stress.6,7

Lemon balm is an herb that is part of the mint family.8 It can help support GABA levels by inhibiting the enzyme that normally degrades it.9

Chamomile is a flower commonly used in herbal infusions. It has been shown to have many benefits due to the high amounts of bioactive components, flavonoids and terpenoids in it. One compound in particular, apigenin, works in the central nervous system to reduce stimulation.10

Ashwagandha is an herb that has been used for thousands of years. It is an adaptogen which allows you to adapt better to stress.11

How to Improve Sleep Hygiene and Circadian Rhythm

Avoid stimulants at night: Stimulants such as caffeine, alcohol and even the blue light from electronics can make it more difficult to fall and stay asleep. Alcohol, while it can help some people fall asleep, typically results in waking up in the middle of the night. Electronics’ bright lights can cause your body to not produce the melatonin it should at night.12,13

Sleep environment: Make your sleep environment as relaxing as possible. Make sure your room is dark, quiet and comfortable. Try to avoid watching TV, eating or doing other activities in bed. This helps train your body to correlate being in bed to sleeping.14

Yoga/exercise: Exercising regularly can help improve sleep quality and has been shown to support mood.12,15 Yoga can also be a relaxing activity to do before bed or to help your body wake up in the morning.

Keep a sleep/wake routine: It is important to keep a schedule by going to bed and waking up at consistent times, even on the weekend. This helps keep your circadian rhythms in balance. It can also help to have the same routine every night.12

Insomnia comes with more problems than just feeling tired. Inadequate amounts of sleep can lead to depression, cognitive impairment and other illnesses.3,15 However, that does not mean there is nothing to help. Finding the cause of your sleep disturbance and then implementing better sleep hygiene could help you improve your sleep. Stress-reducing herbs can also help you to relax and have higher quality sleep.

About the Author: Ashley Wyckoff, BS, is a product operation specialist at Life Extension headquarters in South Florida. She holds a Bachelor of Science in Biology from the University of Florida. In her spare time, she enjoys hiking, reading and yoga to keep her mind and body healthy. She believes in equal access to quality healthcare and it is her goal to make it a reality.


  1. United States Census Bureau. QuickFacts: United States. Table. https://www.census.gov/quickfacts/fact/table/US/PST045218. Accessed 7/10/2019.
  2. Medscape online. News & Perspectives page. What is the prevalence of insomnia? https://www.medscape.com/answers/1187829-70532/what-is-the-prevalence-of-insomnia. Accessed 7/10/2019.
  3. Mayo Clinic. Insomnia. Symptoms & causes. https://www.mayoclinic.org/diseases-conditions/insomnia/symptoms-causes/syc-20355167. Last updated 10/15/2016. Accessed 7/10/2019.
  4. Yang, Chien-Ming et al. “Maladaptive sleep hygiene practices in good sleepers and patients with insomnia.” J Health Psychol. 2010;15(1):147-55.
  5. Alexeev, Mikhail et al. “The natural products magnolol and honokiol are positive allosteric modulators of both synaptic and extra-synaptic GABA(A) receptors.” Neuropharmacology vol. 62,8 (2012): 2507-14. doi:10.1016/j.neuropharm.2012.03.002
  6. Hasler, Gregor et al. “Effect of acute psychological stress on prefrontal GABA concentration determined by proton magnetic resonance spectroscopy.” The American journal of psychiatry vol. 167,10 (2010): 1226-31. doi:10.1176/appi.ajp.2010.09070994
  7. Nutt, D. GABAA Receptors: Subtypes, Regional Distribution, and Function. Journal of Clinical Sleep Medicine. 2006;2(suppl 2): S7-S11.
  8. Najafian, S. Storage conditions affect the essential oil composition of cultivated Balm Mint Herb (Lamiaceae) in Iran. Industrial Crops and Products. 2014;52:575-81.
  9. Weeks, BS. Formulations of dietary supplements and herbal-extracts for relaxation and anxiolytic action: Relarian. Med Sci Monitor. 2009;15(11):Ra256-62.
  10. Srivastava, Janmejai K et al. “Chamomile: A herbal medicine of the past with bright future.” Molecular medicine reports vol. 3,6 (2010): 895-901. doi:10.3892/mmr.2010.377
  11. Kaushik, Mahesh K et al. “Triethylene glycol, an active component of Ashwagandha (Withania somnifera) leaves, is responsible for sleep induction.” PloS one vol. 12,2 e0172508. 16 Feb. 2017, doi:10.1371/journal.pone.0172508
  12. Irish, Leah A et al. “The role of sleep hygiene in promoting public health: A review of empirical evidence.” Sleep medicine reviews vol. 22 (2015): 23-36. doi:10.1016/j.smrv.2014.10.001
  13. National Sleep Foundation. Sleep Problems, Sleep Routine, Sleep Tools & Tips, The Science of Sleep. Why Electronics May Stimulate You Before Bed. https://www.sleepfoundation.org/articles/why-electronics-may-stimulate-you-bed. Copyright 2019. Accessed 7/11/2019.
  14. National Sleep Foundation. Sleep Hygiene. https://www.sleepfoundation.org/articles/sleep-hygiene. Copyright 2019. Accessed 7/11/2019.
  15. Fortier-Brochu, Émilie et al. Insomnia and daytime cognitive performance: a meta-analysis. Sleep Med Rev. 2012;16(1):83-94.

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Fibrates as a Potential Class of Senolytic Therapy to Clear Senescent Cells

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Accumulation of senescent cells with age is one of the causes of aging. In recent years, the broader scientific community has become convinced of this point, and thus funding is now directed towards many varied investigations of cellular senescence and what to do about it. A young industry has emerged, made up of biotech companies focused on the selective destruction of senescent cells, mostly using small molecule drugs. Since these drugs operate through different mechanisms, tend to be tissue specific, only clear a fraction of senescent cells that varies by tissue, and will thus probably be more effective when combined together, research continues to find ever more senolytic compounds.

Senescent cells are created constantly, either in response to damage or a toxic local environment, or more commonly as the result of a somatic cell reaching the Hayflick limit on cell replication. Senescence is an irreversible state in which cell replication shuts down, and a potent mix of inflammatory signals is secreted. This can be useful in the short term, such as during wound healing, or to put a halt to potentially cancerous cells. Near all senescent cells either self-destruct or are destroyed by the immune system quite quickly. It is the tiny minority to linger that contribute to the aging process, such as by generating an environment of chronic inflammation.

The open access paper here is representative of numerous projects presently underway in the research and development communities, performing screening of small molecules from established databases in search of new senolytics. Some of these searches are more informed by prior investigation of plausible mechanisms than others, but at the end of the day the output is compounds that are then evaluated in detail for their ability to selectively destroy senescent cells. The best of the compounds noted here, fenofibrate, is on a par with navitoclax for selectivity, which is about at the lower level of what might be tolerable as a human therapy. The more off-target cells that are destroyed, the worse the side-effects. This is a starting point, however: other compounds in this category will no doubt be better, or might be engineered to be better.

Fibrates as drugs with senolytic and autophagic activity for osteoarthritis therapy

Increasing evidence about the molecular mechanisms of ageing suggests that many chronic diseases such as osteoarthritis (OA) are associated with the hallmarks of ageing, including cellular senescence and defective autophagy. Accumulation of senescent cells in tissues contributes to age-related diseases. Articular cartilage of patients with OA shows features of senescence. Senescence-associated secretory phenotype (SASP) factors released from chondrocytes, such as pro-inflammatory cytokines and extracellular matrix degrading enzymes, have been identified as major mediators contributing to the development and progression of OA. Similarly, intra-articular injection of senescent cells in mice results in OA-like pathology.

Cartilage ageing can be modified by selective elimination of senescent chondrocytes to prevent the detrimental microenvironment changes occurring in joint dysfunction. A major step into the translation of senolytic treatments for OA was demonstrated by the beneficial effects of selective clearance of senescence chondrocytes using the Bcl-2 family inhibitor Navitoclax in animal models. The broad impact of senolytic treatment is also highlighted by the efficacy of dasatinib and quercetin combination in several models of age-related disease, which results in an extension of healthspan and lifespan in mice.

Cellular senescence and autophagy are not only essential for homeostasis but are potential therapeutic targets for age-related diseases. We aim to test this therapeutic hypothesis in preclinical models of OA, where senescence and autophagy play a relevant role. A novel cell-based dual imaging screening assay was developed to identify both senotherapeutics, able to either suppress markers of senescence (senomorphics) or to induce apoptosis of senescent cells (senolytics), and autophagy modulators.

Senotherapeutic molecules with pro-autophagic activity were identified. Fenofibrate (FN), a PPARα agonist used for dyslipidaemias in humans, reduced the number of senescent cells via apoptosis, increased autophagic flux, and protected against cartilage degradation. FN reduced both senescence and inflammation and increased autophagy in both ageing human and OA chondrocytes whereas PPARα knockdown conferred the opposite effect. Moreover, PPARα expression was reduced through both ageing and OA in mice and also in blood and cartilage from knees of OA patients.

Remarkably, in a retrospective study, fibrate treatment improved OA clinical conditions in human patients from the Osteoarthritis Initiative (OAI) Cohort. Blood from the PROspective Osteoarthritis Cohort of A Coruña (PROCOAC) and human cartilage from non-OA and knee OA patients were employed. Levels of PPARα were lower in OA patients compared to non-OA controls. The potential efficacy of PPARα agonists was also evaluated using the Osteoarthritis Initiative (OAI) Cohort. In this cohort, there were 35 fibrate users and 3322 participants not taking fibrates in the selected sample. Using a genetic matching, 35 fibrate users were matched to 35 participants in the control group. Interestingly, the results indicate that fibrate use by time interaction was associated with a statistically significant improvement of self-reported Western Ontario McMaster Osteoarthritis Index (WOMAC) function and WOMAC total scores. There was also a trend towards a decrease in WOMAC pain score. The results suggest that the fibrate use, when compared with non-use, was associated with a yearly decrease in WOMAC.

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Chromatin Stress Promotes Longevity in Yeast. Flies, and Nematodes

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Researchers here report on the finding that modest impairment of the histones responsible for packaging nuclear DNA into chromatin leads to slowed aging in short-lived laboratory species. This adds to the sizable number of existing forms of stress that can somewhat slow aging via hormetic processes, such as heat, lack of nutrients, and so forth. A little damage induces greater cellular maintenance activities, which on balance leads to more efficient, less damaged cells and tissues over the long term. Unfortunately, effects on life span are very much smaller in long-lived species such as our own, when compared with effects in short-lived species such as flies, worms, and mice.

In the nucleus of cells, DNA wraps itself around histone proteins forming a ‘beads-on-a-string’ structure called chromatin. Other proteins bind along chromatin and the structure folds further into more complicated configurations. Everything involving DNA would have to deal with this chromatin structure. For example, when a particular gene is expressed, certain enzymes interact with the chromatin structure to negotiate access to the gene and translate it into proteins. When chromatin stress happens, disruption of the chromatin structure can lead to unwanted changes in gene expression, such as expression of genes when they are not supposed to or lack of gene expression when it should occur.

In this study, researchers worked in the lab with the yeast Saccharomyces cerevisiae to investigate how the dosage of histone genes would affect longevity. They expected that yeast genetically engineered to carry fewer copies of certain histone genes than normal or control yeast would have chromatin changes that would result in the yeast living less than controls. “Unexpectedly, we found that yeast with fewer copies of histone genes lived longer than the controls.” Yeast with a moderately low dose of histone genes showed a moderate reduction of histone gene expression and significant chromatin stress. Their response to chromatin disruption was changes in the activation of a number of genes that eventually promoted longevity.

“We have identified a previously unrecognized and unexpected form of stress that triggers a response that benefits the organism. The mechanism underlying the chromatin stress response generated by moderate reduction of histone dosage is different from the one triggered by histone overexpression we had previously described, as shown by their different profiles of protein expression responses.” The researchers found that chromatin stress also occurs in other organisms such as the laboratory worm C. elegans, the fruit fly, and mouse embryonic stem cells, and in yeast and C. elegans the chromatin stress response promotes longevity. “Our findings suggest that the chromatin stress response may also be present in other organisms. If present in humans, it would offer new possibilities to intervene in the aging process.”

Link: https://www.bcm.edu/news/molecular-and-human-genetics/novel-form-of-stress-longevity

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A Mainstream View of the Longevity Industry

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This popular science article from the AARP is representative of the sort of outsider’s view of the longevity industry that is presently dominant. On the one hand, it is good that the media and advocacy organizations such as AARP are finally talking seriously about treating aging as a medical condition. On the other hand, the author looks at two of the most popular areas of development, mTOR inhibitors and senolytics, in a way that makes them seem more or less equivalent, and then further adds diet and exercise as another equivalent strategy. This will be continuing issue, I fear. People, as a rule, don’t think about size of effect and quality of therapy when discussing present initiatives.

These strategies are in fact very different, and the differences are important. Clearance of senescent cells via senolytic treatments is a radically different and better class of therapy than mTOR inhibition. Senolytics remove a cause of aging in one treatment, improving all aspects of health in later life in consequence, while mTOR inhibitors must be taken continually and only encourage the aging metabolism into a state that is somewhat more resistant to the underlying damage that causes aging. Tackling underlying causes will always be more effective than trying to cope with those causes without repairing them.

“We’ve reached the perfect storm in aging science,” says physician Nir Barzilai. “Everything is happening. We have the foundation from decades of animal studies. We’re ready to move on to people.” The ultimate goal: to put the brakes on aging itself – preventing the pileup of chronic health problems, dementia and frailty that slam most of us late in life. “I want 85 to be the new 65,” says Joan Mannick, the chief medical officer and cofounder of resTORbio.

The need is enormous. In a decade, nearly 1 in 5 Americans will be 65 or older. Three out of 4 will have two or more serious health conditions. At least 1 in 4 can expect memory lapses and fuzzy thinking, while 1 in 10 will develop dementia. “Right now doctors play whack-a-mole with chronic diseases in older adults. You treat one, another pops up. The goal instead is to tackle aging itself, the major risk factor for almost every major disease. Our society, our drug companies and medical profession aren’t addressing all this suffering that happens as people grow old. But the older people in my life are beloved to me. If we can do something about aging, we shouldn’t ignore it.”

Older people who took the mTOR inhibitor RAD001, a similar drug to resTORbo’s RTB101, had a stronger response to a flu vaccine. Their immune systems looked younger, with fewer exhausted T cells – a depressingly common feature of aging called immunosenescence. “This was the first evidence that if you target a pathway in humans, you may actually impact how we age.” The results of a trial of RTB101 were particularly strong for people 85 and older; they had 67 percent fewer infections. That’s good news, because – in part due to an age-related weakening of the immune system – respiratory infections are the fourth-leading reason older U.S. adults wind up in the hospital and their eighth-leading cause of death.

Alas, there’s more going wrong in older cells than on-the-fritz mTOR. Among these issues: inflammation; out-of-whack metabolism; inactive stem cells that can’t repair body tissues; damage from stress, environmental toxins and free radicals; reduced “quality control,” which can’t eliminate rogue cells. These glitches boost the risk for everything from heart disease and stroke to diabetes, osteoarthritis, Alzheimer’s disease, Parkinson’s and cancer. If these and other cellular issues are the underlying causes of so many diseases, preventing cells from succumbing to them as they age is a key to preventing disease. That’s why resTORbio, other biotech start-ups and university aging labs across the U.S. are launching an unprecedented number of human clinical trials with experimental compounds aimed at these mechanisms.

One big target: senescent cells that refuse to die, instead glomming up in joints and other body tissues. They pump out dozens of inflammatory compounds and other chemicals that contribute to age-related diseases. In a raft of mouse studies, clearing out these senescent cells boosted health – easing arthritis pain, improving kidney and lung function, increasing fitness, extending life and even making fur thicker. In January, the first-ever human study of a treatment to kill senescent cells in the lungs was published. Fourteen people with the fatal lung disease idiopathic pulmonary fibrosis took a mix of the drugs dasatinib and quercetin for three weeks. The verdict: The drug combo was safe, triggered just one serious side effect (pneumonia), and seemed to improve study volunteers’ basic ability to stand up and walk. There were also hints it may have reduced senescent-cell activity, but the researchers say bigger, longer studies are needed.

Right now, simply staying healthy into our 80s, 90s and beyond is a lot like hitting the lottery jackpot. In a survey of 55,000 Americans age 65-plus, just 48 percent rated their health as very good or excellent. No wonder drugstores, the internet, and human history are littered with unproven rejuvenation come-ons. Meanwhile, as researchers slowly test these more legitimate drugs, what can we do today if we wish to retain good health longer? That answer has been with us all along. Not smoking, eating healthy, getting exercise, managing stress and sleep.

Link: https://www.aarp.org/health/drugs-supplements/info-2019/pill-drug-aging.html

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Notes on the 2019 Ending Age-Related Diseases Conference in New York

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I recently attended the second Ending Age-Related Diseases conference in New York, hosted by the Life Extension Advocacy Foundation (LEAF). The mix of attendees was much the same as last year: an even split between scientists, entrepreneurs, investors, patient advocates, and interested onlookers, all focused on the treatment of aging as a medical condition. The presentations were similarly a mix of scientists talking about their research programs, entrepreneurs presenting on the data produced by their companies, and investors discussing the state of the industry.

For my part, I have already presented several times this year on the work taking place at Repair Biotechnologies, while we were raising our seed round. So rather talk again on a familiar topic, I chose instead to discuss the terrible state of clinical translation in the life science industry – the institutional, widespread, ongoing failure to develop promising research programs into therapies. This is particularly the case for the treatment of aging, given that translational research in gerontology was actively suppressed by leading scientists for much of the last 40 years. This was an overreaction to the “anti-aging” industry of fraud, supplements, and false hope established in the 1970s, and probably set us back decades.

Even now there is a great gulf between academia and industry, into which projects vanish. This gulf is built of many factors: scientists rarely have good connections to the people who could carry forward their projects; academic funding tends to stop once projects get close to the point at which they could be translated; universities do far too little to nurture new companies, and instead focus on being toll collectors; most investors sit around waiting for companies to form and come to them, rather than devoting their resources to helping companies form; and so forth. The result is that the research community is littered with credible projects in a dormant state, just waiting for someone to champion their development.

A number of fellow entrepreneurs in the longevity industry presented their latest data at the conference. Doug Ethell of Leucadia Therapeutics noted the proof of principle of his thesis on the roots of Alzheimer’s disease, data obtained in ferrets. Partially occluding the cribriform plate in the skull, to mimic the process of ossification that occurs with age in humans, blocks drainage of cerebrospinal fluid, thus allowing amyloid and other molecular waste to build up in the brain and cause neurodegeneration and cognitive decline.

Greg Fahy of Intervene Immune presented quite a lot of data on what six to twelve months of treatment with growth hormone and DHEA does to the thymus and measures of immune system composition in older individuals. It makes for a compelling story, given their evidence for thymic regrowth and improvement in the immune system, for all that I remain dubious about growth hormone as a mode of treatment for aging. There is a lot of evidence to suggest that it isn’t such a great plan. But perhaps undergoing a year of such treatment to have a somewhat larger, somewhat more active thymus going forward is a sensible trade-off, should these results hold up in larger patient groups.

John Lewis of Entos Pharmaceuticals gave a great presentation on the lipid nanoparticle (LNP) platform used by Oisin Biotechnologies to destroy senescent cells and by OncoSenX to destroy cancer cells. This platform is one of the candidate technologies to power all of the next generation of gene therapies, ensuring that most implementations can just work, comparatively simply, and with far less effort than is presently required. The presentation included the final study results from the mouse lifespan study run by Oisin Biotechnologies in which LNPs were set to target cells that expressed p16, p53, or both p16 and p53. That last group lived significantly longer, and had their first death at the point at which half of the control group had died.

Kelsey Moody presented on LysoClear, one of the ever growing number of subsidiary companies generated by the Ichor Therapeutics team. The company is developing an approach to treat macular degeneration by using compounds derived from bacterial enzymes to break down molecular waste that builds up in the lysosome, impairing cell function. His emphasis was on the need to be careful, conservative, and methodical in preclinical development, using LysoClear development as an example of always proving each step before moving on, building on well-proven existing work.

From the scientific community, Maria Blasco discussed at length her work on telomeres and telomerase gene therapy in mouse models. Her group sees loss of telomere length in tissues as a significant contributing cause of aging, with wide-ranging downstream effects, rather than a marker of aging that results from loss of stem cell function. Amutha Boominathan presented on her work at the SENS Research Foundation, moving mitochondrial genes into the cell nucleus in order to prevent the consequences of damage to mitochondrial DNA. In principle this can stop inevitable mitochondrial DNA damage from causing aging. Morgan Levine discussed epigenetic clocks based on DNA methylation, and what lies ahead in getting them to be useful to speed up development of rejuvenation therapies. The clocks and the therapies must develop in parallel, and many different clocks will likely be needed. The biggest task ahead is to understand exactly what it is that these epigenetic clocks are measuring.

From the investment community, Joe Betts-Lacroix noted that of the 1000 or so biotech startups out there, maybe 70 or so are credibly involved in working on aging and longevity. This industry is in its very earliest stages. One of the worthies in our community is presently assembling a database of those aging-focused startups, which I hope will be made publicly available fairly soon. There is a lot more that our community needs to do in order to help newly arriving entrepreneurs and investors become knowledgeable and productive quickly, and a database of companies is a good idea in this context.

Both James Peyer of the newly founded Kronos BioVentures and Sree Kant of Life Biosciences discussed how to invest in longevity, given the nature of the industry and its present constraints and peculiarities. James Peyer, as always, brought a very interesting set of ideas to the conference, and Life Biosciences is itself a sensible strategic response to the twin challenges of (a) a lack of entrepreneurs and (b) researchers who really don’t want to leave academia. Life Biosciences wraps subsidiary companies around research teams, providing an environment that still feels like academia, and in which much of the trouble of running a company is abstracted away into the larger parent organization.

I have of course omitted mention of a number of other presentations and panels, and no offense is intended to the speakers. The above is really just a list of things that caught my attention, or that I happened to be there for rather than being caught up in meetings. All in all it was a good event, as was the case last year. The LEAF volunteers did a great job, and I encourage you to add this conference series to your 2020 agenda.

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Sabotaging a Mechanism of Decline in Age-Related Stem Cell Activity

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Stem cells are responsible for maintaining surrounding tissue function via generation of daughter cells to make up losses. Stem cell activity declines with age, and research of the past twenty years suggests that a sizable fraction of this decline is a reaction to rising levels of cell and tissue damage, rather than being due to intrinsic damage to the stem cells themselves. Thus researchers are searching for the signals that influence stem cell activity, with the intent of interfering in order to boost stem cell activity in old tissues. This seems a worse strategy than repairing the underlying damage that causes stem cell decline, but it is nonetheless a popular field of research, and there is plenty of evidence for it to be possible to produce some degree of benefits via this approach.

Researchers have discovered how regenerative capacity of intestinal epithelium declines when we age. Targeting of an enzyme that inhibits stem cell maintaining signaling rejuvenates the regenerative potential of an aged intestine. This finding may open ways to alleviate age-related gastrointestinal problems, reduce side-effects of cancer treatments, and reduce healthcare costs in the ageing society by promoting recovery.

The age-induced reduction in tissue renewal makes dosing of many common drugs challenging. Targeting of an inhibitor called Notum may provide a new way to increase the therapeutic window and to promote recovery in societies with the aging population. Researchers believe that in addition to direct targeting of Notum, lifestyle factors such as diet may also provide means to reduce Notum, and thus improve tissue renewal and repair.

Using organoid culture methods, researchers understood that poor function of tissue repairing stem cells in old intestine was due to aberrant signals from the neighboring cells, known as Paneth cells. “Modern techniques allowed us to examine tissue maintenance at a single cell level, and revealed which cell types contribute to the decline in tissue function. We were surprised to find that even young stem cells lost their capacity to renew tissue when placed next to old neighbors.”

Normally intestinal epithelium is renewed by stem cells that rely on activity of Wnt-signaling pathway. Surrounding cells produce molecules that activate this pathway. The study shows that during ageing, Paneth cells begin to express a secreted Wnt-inhibitor called Notum. Notum enzymatically inactivates Wnt-ligands in the stem cell niche, decreasing regenerative potential of intestinal stem cells. However, pharmacologic inhibition of Notum rejuvenated stem cell activity and promoted the recovery of old animals after treatment with a commonly used chemotherapeutic drug with severe side-effects in the gut.

Link: https://www.helsinki.fi/en/news/life-science-news/repair-of-aged-tissue-can-be-enhanced-by-inhibiting-signals-from-neighbouring-cells

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