Category: Ageing, Longevity and disease.

Scientific and medical journal publications and studies in ageing and longevity.

Health Hacker Australia > The Science > Ageing, Longevity and disease.
Diluting blood plasma rejuvenates tissue and reverses aging – Neuroscience News

Diluting blood plasma rejuvenates tissue and reverses aging – Neuroscience News

Summary: Diluting the blood plasma of older mice has a stronger rejuvenating effect on the brain, liver, and muscles than transplanting the blood of younger mice.

Source: UC Berkeley

In 2005, University of California, Berkeley, researchers made the surprising discovery that making conjoined twins out of young and old mice — such that they share blood and organs — can rejuvenate tissues and reverse the signs of aging in the old mice. The finding sparked a flurry of research into whether a youngster’s blood might contain special proteins or molecules that could serve as a “fountain of youth” for mice and humans alike.

But a new study by the same team shows that similar age-reversing effects can be achieved by simply diluting the blood plasma of old mice — no young blood needed.

https://neurosciencenews.com/blood-plasma-aging-16541/

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases

In recent years, natural products, which originate from plants, animals, and fungi, together with their bioactive compounds have been intensively explored and studied for their therapeutic potentials for various diseases such as cardiovascular, diabetes, hypertension, reproductive, cancer, and neurodegenerative diseases. Neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis are characterized by the progressive dysfunction and loss of neuronal structure and function that resulted in the neuronal cell death. Since the multifactorial pathological mechanisms are associated with neurodegeneration, targeting multiple mechanisms of actions and neuroprotection approach, which involves preventing cell death and restoring the function to damaged neurons, could be promising strategies for the prevention and therapeutic of neurodegenerative diseases. Natural products have emerged as potential neuroprotective agents for the treatment of neurodegenerative diseases. This review focused on the therapeutic potential of natural products and their bioactive compounds to exert a neuroprotective effect on the pathologies of neurodegenerative diseases.

https://www.hindawi.com/journals/ecam/2020/6565396/?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity – He – – Aging Cell – Wiley Online Library

Inhibition of USP7 activity selectively eliminates senescent cells in part via restoration of p53 activity – He – – Aging Cell – Wiley Online Library

“The accumulation of senescent cells (SnCs) is a causal factor of various age‐related diseases as well as some of the side effects of chemotherapy. Pharmacological elimination of SnCs (senolysis) has the potential to be developed into novel therapeutic strategies to treat these diseases and pathological conditions. Here we show that ubiquitin‐specific peptidase 7 (USP7) is a novel target for senolysis because inhibition of USP7 with an inhibitor or genetic depletion of USP7 by RNA interference induces apoptosis selectively in SnCs. The senolytic activity of USP7 inhibitors is likely attributable in part to the promotion of the human homolog of mouse double minute 2 (MDM2) ubiquitination and degradation by the ubiquitin–proteasome system. This degradation increases the levels of p53, which in turn induces the pro‐apoptotic proteins PUMA, NOXA, and FAS and inhibits the interaction of BCL‐XL and BAK to selectively induce apoptosis in SnCs. Further, we show that treatment with a USP7 inhibitor can effectively eliminate SnCs and suppress the senescence‐associated secretory phenotype (SASP) induced by doxorubicin in mice. These findings suggest that small molecule USP7 inhibitors are novel senolytics that can be exploited to reduce chemotherapy‐induced toxicities and treat age‐related diseases.”

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13117?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

The effects of resveratrol on lipid profiles and liver enzymes

The effects of resveratrol on lipid profiles and liver enzymes

This meta-analysis demonstrated that resveratrol supplementation among patients with MetS and related disorders significantly reduced total cholesterol and increased GGT concentrations, but did not affect triglycerides, LDL-, HDL-cholesterol, ALT, and AST concentrations. This data suggests that resveratrol may have a potential cardio-protective effect in patients with MetS and related disorders

https://link.springer.com/article/10.1186/s12944-020-1198-x?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Reproductive Aging Process Reversed in Mice | Technology Networks

Reproductive Aging Process Reversed in Mice | Technology Networks

Dr. David Sinclair posted this morning on reversing the effects of aging on reproductive viability.

https://www.linkedin.com/posts/sinclairda_our-research-teams-just-published-a-promising-activity-6633781677380423680-fXys

https://www.technologynetworks.com/cell-science/news/reproductive-aging-process-reversed-in-mice-330636

Atg11 is required for initiation of glucose starvation-induced autophagy

Atg11 is required for initiation of glucose starvation-induced autophagy

“How energy deprivation induces macroautophagy/autophagy is not fully understood. Here, we show that Atg11, a receptor protein for cargo recognition in selective autophagy, is required for the initiation of glucose starvation-induced autophagy.”

https://www.tandfonline.com/doi/full/10.1080/15548627.2020.1719724?af=R&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Mitophagy and DNA damage signaling in human aging

Mitophagy and DNA damage signaling in human aging

Highlights

•DNA damage regulates mitophagy induction and mitochondrial homeostasis.

•Nuclear-mitochondrial signaling modulates aging and age-associated disorders.

•Combinatorial approaches targeting DNA repair and mitophagy could promote healthy aging.

Mitophagy and DNA damage signaling in human aging – ScienceDirect
Education and age-related decline in cognitive performance

Education and age-related decline in cognitive performance

Highlights

•Association of education and change in cognitive performance is negligible.

•Articles included in meta-analysis displayed high unexplained heterogeneity.

•Theories of cognitive aging need to be updated with regards to this association.

Education and age-related decline in cognitive performance: Systematic review and meta-analysis of longitudinal cohort studies – ScienceDirect
Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism – ScienceDirect

Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism – ScienceDirect

Extension of lifespan and amelioration of aging-associated phenotypes have been targets of many studies. Some of the established methods of increasing lifespan including dietary restriction and genetic manipulation are difficult to apply to humans, and their side effects are hard to predict. For that reason, it is important to discover compounds that can mimic the anti-aging actions or induce lifespan extension through different metabolisms within the cell. Here we summarize the recent studies to test various types of compounds and materials using budding yeast that show potential anti-aging effects.

Recent studies on anti-aging compounds with Saccharomyces cerevisiae as a model organism – ScienceDirect
SIRT6 Finding the gas pedal on a slow sirtuin

SIRT6 Finding the gas pedal on a slow sirtuin

“The class III histone deacetylase sirtuin 6 (SIRT6) modulates numerous functions in the cell by deacetylating histone lysine residues. Interestingly, SIRT6’s efficiency in in vitro experiments is far greater against substrates carrying long-chain fatty acyl modifications such as myristoylated lysine compared with acetylated counterparts, but the deacetylase activity can be stimulated by fatty acids and small-molecule allosteric modulators. A new study helps to explain this puzzling activation using a novel activator, thorough kinetic investigation, and mutagenesis studies. These data help elucidate the molecular requirements for activation of SIRT6 and provide a foundation for development of activators for therapeutic purposes.”

http://m.jbc.org/content/295/5/1400.full

Mitochondria Found Independently Living in Blood | | LEAF

Mitochondria Found Independently Living in Blood | | LEAF

“The research team has published a new study, which shows that aside from the usual mitochondrial populations living inside our cells, there are also wandering mitochondria floating around in our bloodstreams. From time to time, mitochondria are found outside the cells, but only in the context of debris within platelets, so what are these intrepid mitochondria doing out there alone in the bloodstream?

https://www.leafscience.org/mitochondria-found-independently-living-in-blood/

Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging: Cell Stem Cell

Fasting Activates Fatty Acid Oxidation to Enhance Intestinal Stem Cell Function during Homeostasis and Aging: Cell Stem Cell

Highlights
• Fasting induces fatty acid oxidation (FAO) in intestinal stem and progenitor cells
• Aging reduces ISC numbers and function, correlating with decreased FAO
• PPAR/CPT1a-mediated FAO augments ISC function in aging and during regeneration
• PPARδ agonists boost and restore ISC and progenitor function in young and old age

https://www.cell.com/cell-stem-cell/fulltext/S1934-5909(18)30163-2

Kynurenine pathway, NAD+ synthesis, and mitochondrial function: Targeting tryptophan metabolism to promote longevity and healthspan – ScienceDirect

Kynurenine pathway, NAD+ synthesis, and mitochondrial function: Targeting tryptophan metabolism to promote longevity and healthspan – ScienceDirect

Highlights
• The kynurenine pathway has recently been identified as a promising target to increase healthy longevity.

• Targeted inhibition of kynurenine pathway activity may alleviate several pathological conditions and promote healthspan.

• Changes to the production and recycling of NAD+ is a likely mediator of the beneficial effects of kynurenine pathway interventions.

• Mitochondrial function and dynamics represent NAD+-dependent processes downstream of kynurenine metabolism that may mediate benefits during aging.

https://www.sciencedirect.com/science/article/pii/S053155651930765X

Aging and Caloric Restriction Modulate the DNA Methylation Profile of the Ribosomal RNA Locus in Human and Rat Liver

Aging and Caloric Restriction Modulate the DNA Methylation Profile of the Ribosomal RNA Locus in Human and Rat Liver

“We confirm previous findings, showing age-related hypermethylation, and describe, for the first time, that this gain in methylation also occurs in human hepatocytes. Furthermore, we show that age-related hypermethylation is enhanced in livers of rat upon CR at two and 10 months, and that at two months a trend towards the reduction of rRNA expression occurs. Collectively, our results suggest that CR modulates age-related regulation of methylation at the rDNA locus, thus providing an epigenetic readout of the pro-longevity effects of CR.”

https://www.mdpi.com/2072-6643/12/2/277

Understanding oxidants and antioxidants: Classical team with new players

Understanding oxidants and antioxidants: Classical team with new players

We talk about antioxidants a lot. Much of our longevity supplements are in fact antioxidants but, what are antioxidants and what is oxidisation and, furthermore, why do we care about it?

https://onlinelibrary.wiley.com/doi/abs/10.1111/jfbc.13145?af=R&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound&sid=researcher

Oncotarget | From rapalogs to anti-aging formula

Oncotarget | From rapalogs to anti-aging formula

Inhibitors of mTOR, including clinically available rapalogs such as rapamycin (Sirolimus) and Everolimus, are gerosuppressants, which suppress cellular senescence. Rapamycin slows aging and extends life span in a variety of species from worm to mammals. Rapalogs can prevent age-related diseases, including cancer, atherosclerosis, obesity, neurodegeneration and retinopathy and potentially rejuvenate stem cells, immunity and metabolism. Here, I further suggest how rapamycin can be combined with metformin, inhibitors of angiotensin II signaling (Losartan, Lisinopril), statins (simvastatin, atorvastatin), propranolol, aspirin and a PDE5 inhibitor. Rational combinations of these drugs with physical exercise and an anti-aging diet (Koschei formula) can maximize their anti-aging effects and decrease side effects.

http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=18033&path%5B%5D=57761

Metformin mediates cardioprotection against aging‐induced ischemic necroptosis – Li – – Aging Cell – Wiley Online Library

Metformin mediates cardioprotection against aging‐induced ischemic necroptosis – Li – – Aging Cell – Wiley Online Library

“Notably, metformin treatment disrupted p62‐RIP1‐RIP3 complexes and effectively repressed I/R‐induced necroptosis in aged hearts, ultimately reducing mortality in this model. These findings highlight previously unknown mechanisms of aging‐related myocardial ischemic vulnerability: p62‐necrosome‐dependent necroptosis. Metformin acts as a cardioprotective agent that inhibits this unfavorable chain mechanism of aging‐related I/R susceptibility.”

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13096?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

Resveralogues: From Novel Ageing Mechanisms to New Therapies? – Abstract – Gerontology – Karger Publishers

Resveralogues: From Novel Ageing Mechanisms to New Therapies? – Abstract – Gerontology – Karger Publishers

“For much of the 20th century the ageing process was thought to be the result of the interplay of many different biological processes, each with relatively small effects on organismal lifespan. However, this model is no longer tenable. Rather it seems a few biological mechanisms, including nutrient sensing, telomere attrition and cellular senescence, mediate large effects on health and longevity. Biogerontology may have suffered from initial delusions of complexity. However, we argue that it is premature to assume either that the list of biological processes influencing lifespan is now comprehensive or that these mechanisms act independently of each other.”

https://www.karger.com/Article/Abstract/504845

IJMS | Free Full-Text | BCL-xL, a Mitochondrial Protein Involved in Successful Aging: From C. elegans to Human Centenarians

IJMS | Free Full-Text | BCL-xL, a Mitochondrial Protein Involved in Successful Aging: From C. elegans to Human Centenarians

“B-Cell Lymphoma-extra-large (BCL-xL) is involved in longevity and successful aging, which indicates a role for BCL-xL in cell survival pathway regulation. Beyond its well described role as an inhibitor of apoptosis by preventing cytochrome c release, BCL-xL has also been related, indirectly, to autophagy and senescence pathways.”

https://www.mdpi.com/1422-0067/21/2/418?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis – ScienceDirect

NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis – ScienceDirect

Highlights
• NAD+ plays an important protective role in some age-related degenerative disease states.

• NAD+ can improve mitochondrial function and maintain sufficient levels of ATP.

• NAD+ can influences DNA repair, and immune and longevity processes.

• Raising NAD+ levels can balance energy needs with supply and protect against oxidative damage and inflammation.

• Further clinical trials are necessary to validate NAD+ therapy in ageing and disease.

https://www.sciencedirect.com/science/article/pii/S0531556519307582

Zinc transporters maintain longevity by influencing insulin/IGF‐1 activity in Caenorhabditis elegans – Novakovic – – FEBS Letters – Wiley Online Library

Zinc transporters maintain longevity by influencing insulin/IGF‐1 activity in Caenorhabditis elegans – Novakovic – – FEBS Letters – Wiley Online Library

“Adequate dietary intake of essential metals such as zinc is important for maintaining homeostasis. Abnormal zinc intake in Caenorhabditis elegans has been shown to increase or decrease normal lifespan by influencing the insulin/IGF‐1 pathway. Distribution of zinc is achieved by a family of highly conserved zinc transport proteins (ZIPT in C. elegans). This study investigated the role of the zipt family of genes and show that depletion of individual zipt genes results in a decreased lifespan”

https://febs.onlinelibrary.wiley.com/doi/abs/10.1002/1873-3468.13725

The somatic mutation landscape of the human body | Genome Biology | Full Text

The somatic mutation landscape of the human body | Genome Biology | Full Text

“Somatic mutations in healthy tissues contribute to aging, neurodegeneration, and cancer initiation, yet they remain largely uncharacterized.”

https://genomebiology.biomedcentral.com/articles/10.1186/s13059-019-1919-5

Biologists identify pathways that extend lifespan by 500%

Biologists identify pathways that extend lifespan by 500%

“Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.

“Despite the discovery in C. elegans of cellular pathways that govern aging, it hasn’t been clear how these pathways interact,” said Hermann Haller, M.D., president of the MDI Biological Laboratory. “By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly aging population.””

https://phys.org/news/2020-01-biological-scientists-pathways-lifespan.html

Fad or Future Podcast | Hosted by Joey Thurman

Fad or Future Podcast | Hosted by Joey Thurman

“I’ve been talking about the benefits of “stressed plants” a lot of late. And that’s because of xenohormesis. I believe that when we eat plants that have been stressed, our bodies pick up on those chemical cues and allows us to get the stress benefits. That is, our own hormesis benefits. This is one of the reasons why I believe organic foods are better for us. More here from my discussion with Joey Thurman”

David A Sinclair

Full link here:

https://www.fadorfuture.com/

3 Ways We May Be Able To Reverse Aging, From A Microbiologist

3 Ways We May Be Able To Reverse Aging, From A Microbiologist

“Organic foods aren’t held with gloves. They’re a little bit more stressed out. The more stressed out your food is the brighter colors they’ll have because they’re producing these colors as a defense,” Sinclair explains.

Those bright colors, he adds, are indicators that the food has produced “xenohormesis molecules,” which activate our sirtuins that give our bodies an extra boost for longevity.

https://www.mindbodygreen.com/articles/3-easy-hacks-for-longevity-from-an-aging-microbiologist

Fisetin | | LEAF

Fisetin | | LEAF

“Fisetin, like many plant polyphenols, is known to have antioxidant properties and demonstrates the specific biological activity of protecting functional macromolecules against stress, resulting in a benefit to cellular cytoprotection. It is also known to have anti-inflammatory, chemopreventive, and chemotherapeutic properties.

Finally, more recently, it has also shown promise as a senolytic, a compound that encourages aged or damaged senescent cells to destroy themselves rather than lingering in the body and contributing to the chronic, age-related inflammation known as “inflammaging”, which is associated with a wide range of age-related diseases.

Since fisetin has a good safety profile, Mayo Clinic followed these mouse studies by launching three trials to see if the compound is effective for humans.”

Human Clinical Trials with Fisetin:

Fisetin | | LEAF

Centenarians: An excellent example of resilience for successful ageing – ScienceDirect

Centenarians: An excellent example of resilience for successful ageing – ScienceDirect

Highlights
• Centenarians maintain intrinsic capacity longer than individuals who display ordinary aging.

• Resilience is a determinant of health, and centenarians maintain it longer.

• Centenarians have specific genetic features.

https://www.sciencedirect.com/science/article/abs/pii/S0047637419302040

l-Theanine attenuates liver aging by inhibiting advanced glycation end products in d-galactose-induced rats and reversing an imbalance of oxidative stress and inflammation – ScienceDirect

l-Theanine attenuates liver aging by inhibiting advanced glycation end products in d-galactose-induced rats and reversing an imbalance of oxidative stress and inflammation – ScienceDirect

Highlights
• Tea-derived l-theanine inhibited AGE production in d-galactose-induced aging rats.

• l-Theanine increased FoxO1 expression and antioxidative enzymes in aged livers.

• l-Theanine could reduce oxygen free radicals and maintain the redox balance.

• l-Theanine supplementation could protect against age-related liver damage.

https://www.sciencedirect.com/science/article/pii/S0531556519306643

CoQ 10 enhances PGC1α and increases expression of mitochondrial antioxidant proteins in chronically ischemic swine myocardium | SpringerLink

CoQ 10 enhances PGC1α and increases expression of mitochondrial antioxidant proteins in chronically ischemic swine myocardium | SpringerLink

“Four weeks of dietary CoQ10 in HM pigs enhances active, nuclear-bound PGC1α and increases the expression of ETC proteins within mitochondria of HM tissue.”

https://link.springer.com/article/10.1186/s12986-019-0418-8?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Muscle wasting disease linked to defective mitochondrial energy and NAD+ biosynthesis pathways – Science Mission

Muscle wasting disease linked to defective mitochondrial energy and NAD+ biosynthesis pathways – Science Mission

“Moreover, results showed that sarcopenia was also associated with reduced levels of enzymes involved in the recycling of NAD+, which acts as a metabolic sensor in the cell and regulates energy production pathways.”

http://sciencemission.com/site/index.php?page=news&type=view&id=health-science%2Fmuscle-wasting-disease&filter=8%2C9%2C10%2C11%2C12%2C13%2C14%2C16%2C17%2C18%2C19%2C20%2C27

Mitochondrial Haplogroups and Lifespan in a Population Isolate – ScienceDirect

Mitochondrial Haplogroups and Lifespan in a Population Isolate – ScienceDirect

“The lifespan-lengthening association was apparent in both sexes but only after the age of 60. Our results provide further support for the role of mitochondrial genetics in lengthening human lifespan.”

https://www.sciencedirect.com/science/article/abs/pii/S1567724919301047

Calorie restriction mimetics: Can you have your cake and eat it, too? – ScienceDirect

Calorie restriction mimetics: Can you have your cake and eat it, too? – ScienceDirect

Highlights
• We review the literature pertaining to calorie restriction mimetics (CRM).

• We discuss history, definitions, and applications of CRM.

• We discuss the concept of upstream and downstream targeting.

• We review the leading candidates for developing CRM.

• We suggest where the field is heading.

https://www.sciencedirect.com/science/article/pii/S1568163714001275

Age and life expectancy clocks based on machine learning analysis of mouse frailty | bioRxiv

Age and life expectancy clocks based on machine learning analysis of mouse frailty | bioRxiv

“The identification of genes and interventions that slow or reverse aging is hampered by the lack of non-invasive metrics that can predict life expectancy of pre-clinical models. Frailty Indices (FIs) in mice are composite measures of health that are cost-effective and non-invasive, but whether they can accurately predict health and lifespan is not known. Here, mouse FIs were scored longitudinally until death and machine learning was employed to develop two clocks. ”

https://www.biorxiv.org/content/10.1101/2019.12.20.884452v1

AMPK Activation of Flavonoids from Psidium guajava Leaves in L6 Rat Myoblast Cells and L02 Human Hepatic Cells

AMPK Activation of Flavonoids from Psidium guajava Leaves in L6 Rat Myoblast Cells and L02 Human Hepatic Cells

“The findings demonstrated that quercetin and its glycosides from Psidium guajava leaves exhibited significant AMPK activity and were likely responsible for the antidiabetic effect of Psidium guajava leaves”

https://www.hindawi.com/journals/ecam/2019/9209043/?utm_source=researcher_app&utm_medium=referral&utm_campaign=resr_mrkt_researcher_inbound

The State of Ageing in 2019: Adding life to our years | Centre for Ageing Better

The State of Ageing in 2019: Adding life to our years | Centre for Ageing Better

How prepared is society for our longer lives? Our new report, ‘The State of Ageing in 2019’, uses publicly available data to give a snapshot of what life is like for people aged 65 and older today. It also investigates the prospects for people currently in their 50s and 60s looking across four crucial areas: work and finances, housing, health and communities.

The State of Ageing in 2019: Adding life to our years

https://www.ageing-better.org.uk/publications/state-of-ageing-2019

Senescent cell turnover slows with age providing an explanation for the Gompertz law | Nature Communications

Senescent cell turnover slows with age providing an explanation for the Gompertz law | Nature Communications

“A causal factor in mammalian aging is the accumulation of senescent cells (SnCs). SnCs cause chronic inflammation, and removing SnCs decelerates aging in mice. Despite their importance, turnover rates of SnCs are unknown, and their connection to aging dynamics is unclear. Here we use longitudinal SnC measurements and induction experiments to show that SnCs turn over rapidly in young mice, with a half-life of days, but slow their own removal rate to a half-life of weeks in old mice.”

https://www.nature.com/articles/s41467-019-13192-4

Consumption of chili pepper cuts down the risk of death from a heart or cerebral attack

Consumption of chili pepper cuts down the risk of death from a heart or cerebral attack

“Chili pepper is a common ingredient in Italians kitchens, and over the centuries, it has been praised for its supposed therapeutic virtues. Now, an Italian study shows that people who consume it on a regular basis have an all-cause mortality risk 23 percent lower than those who do not consume it.”

https://medicalxpress.com/news/2019-12-consumption-chili-pepper-death-heart.html

Alcohol extract from Vernonia anthelmintica willd (L.) seed counteracts stress-induced murine hair follicle growth inhibition

Alcohol extract from Vernonia anthelmintica willd (L.) seed counteracts stress-induced murine hair follicle growth inhibition

Background: Vernonia anthelmintica (L.) willd is a traditional urgur herb in China for a long history. Its alcohol extract (AVE) has been proved to promote hair follicle growth in C57BL/6 mice. We conducted this study to investigate the hair-growth effects of AVE in stressed mice and its possible mechanism of action

Results: Our results showed that AVE counteract murine hair follicle growth inhibition caused by chronic restraint stress via inducing the conversion of telogen to anagen and inhibiting catagen premature, increasing bulb keratinocytes and bulge stem cells proliferation, promoting melanogenesis, and reducing the numbers of substance P and calcitonin gene-related peptide nerve fibers. Furthermore, AVE also counteracted murine hair follicle growth inhibition caused by substance P in organ culture. Conclusion: These results suggest that AVE counteract stress-induced hair follicle growth inhibition in C57BL/6 mice in vivo and in vitro, and may be an effective new candidate for treatment of stress-induced hair loss.

https://bmccomplementalternmed.biomedcentral.com/track/pdf/10.1186/s12906-019-2744-9

Rapamycin persistently improves cardiac function in aged, male and female mice, even following cessation of treatment – Quarles – – Aging Cell – Wiley Online Library

Rapamycin persistently improves cardiac function in aged, male and female mice, even following cessation of treatment – Quarles – – Aging Cell – Wiley Online Library

“In this report, we demonstrate that the rapamycin‐dependent improvement of diastolic function is highly persistent, while decreases in both cardiac hypertrophy and passive stiffness are substantially persistent 8 weeks after cessation of an 8‐week treatment of rapamycin in both male and female 22‐ to 24‐month‐old C57BL/6NIA mice.”

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13086

Effects of dairy consumption on SIRT1 and mitochondrial biogenesis in adipocytes and muscle cells. – PubMed – NCBI

Effects of dairy consumption on SIRT1 and mitochondrial biogenesis in adipocytes and muscle cells. – PubMed – NCBI

“These data indicate that dairy consumption leads to systemic effects, which may promote mitochondrial biogenesis in key target tissues such as muscle and adipose tissue both by direct activation of SIRT1 as well as by SIRT1-independent pathways.”

Notice the word dairy is used, not milk. see our previous post on milkand its mTor activation and AMPK suppression.

https://www.ncbi.nlm.nih.gov/pubmed/22185590

High glucose augments ROS generation regulates mitochondrial dysfunction and apoptosis via stress signalling cascades in keratinocytes. – PubMed – NCBI

High glucose augments ROS generation regulates mitochondrial dysfunction and apoptosis via stress signalling cascades in keratinocytes. – PubMed – NCBI

“Mitochondria are fascinating structures of the cellular compartments that generate energy to run the cells. However, inherent disorders of mitochondria due to diabetes can cause major disruption of metabolism that produces huge amount of reactive oxygen species (ROS). Here we study the elevated level of ROS provoked by high glucose (HG) environment triggered mitochondrial dysfunction, inflammatory response and apoptosis via stress signalling pathway in keratinocytes. Our results demonstrated that elevated glucose level in keratinoctes, increase the accumulations of ROS and decrease in cellular antioxidant capacities.”

High glucose augments ROS generation regulates mitochondrial dysfunction and apoptosis via stress signalling cascades in keratinocytes. – PubMed – NCBI
Frontiers | Intense physical exercise induces an anti-inflammatory change in IgG N-glycosylation profile | Physiology

Frontiers | Intense physical exercise induces an anti-inflammatory change in IgG N-glycosylation profile | Physiology

“Observed changes show the potential of intense physical exercise to reduce levels of systemic basal inflammation as well as the potential for IgG N-glycosylation to serve as a sensitive longitudinal systemic inflammation marker.”

https://www.frontiersin.org/articles/10.3389/fphys.2019.01522/abstract

Mechanisms of Calorie Restriction: A Review of Genes Required for the Life-Extending and Tumor-Inhibiting Effects of Calorie Restriction

Mechanisms of Calorie Restriction: A Review of Genes Required for the Life-Extending and Tumor-Inhibiting Effects of Calorie Restriction

” We reviewed and discussed underlying mechanisms of CR from an aspect of CR genes. It should be stressed that the isoform specificity of FoxO transcription factors for longevity becomes apparent under CR conditions but not AL conditions. Npy and FoxO1 both play pleiotropic roles in aging and related disorders, depending on the nutritional state. As briefly described in Section 1 and Section 2, the life-extending effects of CR and reduced IGF-1 signaling are also sexually dimorphic. Genes associated with regulation of the aging process should be investigated carefully in a context-dependent manner, i.e., abilities of physiological adaptation for individuals against environmental challenges, particularly food shortage. “

https://www.mdpi.com/2072-6643/11/12/3068/htm

Protein intake and transitions between frailty states and to death in very old adults: the Newcastle 85+ study

Protein intake and transitions between frailty states and to death in very old adults: the Newcastle 85+ study

“High protein intake, partly mediated by energy intake, may delay incident frailty in very old adults. Frailty prevention strategies in this age group should consider adequate provision of protein and energy.”

Emerging Role of C/EBPβ and Epigenetic DNA Methylation in Ageing: Trends in Genetics

Emerging Role of C/EBPβ and Epigenetic DNA Methylation in Ageing: Trends in Genetics

“Ageing is closely associated with and influenced by energy metabolism, and C/EBPβ is emerging as a key regulator of energy metabolism and longevity.”

https://www.cell.com/trends/genetics/fulltext/S0168-9525(19)30245-8?dgcid=raven_jbs_aip_email

How to Slow Aging (and even reverse it) – Veritasium – YouTube

How to Slow Aging (and even reverse it) – Veritasium – YouTube

Scientists like Prof Sinclair have evidence of speeding up, slowing, and even reversing aging.

12 Ways To Upgrade Your Lifespan & Healthspan IQ

12 Ways To Upgrade Your Lifespan & Healthspan IQ

The amount of time we live is called lifespan. The length of time that a person is healthy and functional—not just alive—is called healthspan. Scientific understanding in these areas is advancing rapidly. Below are 12 things the collective thinks will help on your journey to a longer healthier you. 

1. BOOST NAD+ LEVELS

2. POWER UP WITH ATP

3. CREATE FIT MITOCHONDRIA

4. ACTIVATE AMPK

5. CALORIE RESTRICTION AND CALORIE RESTRICTION MIMETICS

6. EXERCISE AND EXERCISE MIMETICS

7. BODY CLOCK 

8. FOLLOW A HEALTHY AGING EXPERT

12 Ways To Upgrade Your Lifespan & Healthspan IQ

Mitochondria: Exploring 5 Lifestyle Habits to Benefit Cell Health

Mitochondria: Exploring 5 Lifestyle Habits to Benefit Cell Health

In each of our cells are small energy generators called mitochondria. The health of our mitochondria determines the amount of adenosine triphosphate (ATP) they can produce from the calories we eat and oxygen we consume. Without robust mitochondria, cells cannot do as much work as they’re capable of and we need them to do so we can stay healthy. To achieve higher levels of performance we must optimize our mitochondria, the powerhouse of our cells, to produce energy. Cell function isn’t always the first place biohackers and nootropics enthusiasts start because it is challenging to notice a subjective boost in our mitochondrial function. Whether we can detect enhanced mitochondria subjectively or not, the science is pretty clear that healthy mitochondria play a role in supporting all indicators of cognition, physical performance, and aging. In a series of comprehensive posts, we will introduce scientifically-backed lifestyle changes and nootropics that up-regulate your mitochondrial function. In our last post, we went over how to use light and temperature to boost mitochondria. Now let’s tackle 5 more lifestyle habits we can implement to achieve healthier mitochondria.

Mitochondria: Exploring 5 Lifestyle Habits to Benefit Cell Health

Frontiers | Physiological and Epigenetic Features of Yoyo Dieting and Weight Control | Genetics

Frontiers | Physiological and Epigenetic Features of Yoyo Dieting and Weight Control | Genetics

“Most individuals fail in maintaining their weight loss due to weight cycling, often referred to as Yoyo dieting. Weight regain often starts within the first year, and the pre-intervention weight is reached or even surpassed in the subsequent 2 to 5 years (Anderson et al., 2001; Weiss et al., 2007). Lean individuals that were voluntarily overfed with 50% additional calories for 3 days showed decreased pre-meal hunger and increased post-meal satiety (Cornier et al., 2004). In obese individuals that underwent weight loss, overfeeding did not diminish hunger or increase satiety. This absence of compensatory changes in hunger and satiety upon overfeeding likely contributes to an increased propensity for weight regain in obese individuals that undergo weight loss (Cornier et al., 2004). Overall, only 11% of the individuals with early-onset weight re-gain can achieve a subsequent body weight loss within that first year (Wing and Phelan, 2005).”

https://www.frontiersin.org/articles/10.3389/fgene.2019.01015/full?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Maf1‐dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan – Shetty – – Aging Cell – Wiley Online Library

Maf1‐dependent transcriptional regulation of tRNAs prevents genomic instability and is associated with extended lifespan – Shetty – – Aging Cell – Wiley Online Library

Fundamental cellular mechanisms such as nutrient sensing, DNA damage response pathways, and cell cycle regulation influence the aging process. Studies have shown that the nutrient sensory kinase, mTOR (TOR in yeast), regulates lifespan in response to nutrient availability. The mTOR kinase forms two distinct protein complexes: TORC1 and TORC2. TORC1, which is inhibited by rapamycin, regulates cell growth, proliferation, and metabolism. It is well established that TORC1 promotes protein translation via phosphorylation of ribosomal protein S6 kinase and the eIF4E‐binding protein (BP; Zoncu, Efeyan, & Sabatini, 2011). The TORC2 branch is less studied; however, TORC2 also plays important roles in metabolism, cell survival, and proliferation (Zoncu et al., 2011). Although the involvement of the TORC1 pathway in lifespan regulation is conserved among many species (i.e., TORC1 inhibition extends lifespan), it is still unclear how this pathway affects multiple downstream stress and damage response mechanisms.

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13068?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

Measuring biological aging in humans: A quest – Ferrucci – – Aging Cell – Wiley Online Library

Measuring biological aging in humans: A quest – Ferrucci – – Aging Cell – Wiley Online Library

“The global population of individuals over the age of 65 is growing at an unprecedented rate and is expected to reach 1.6 billion by 2050. Most older individuals are affected by multiple chronic diseases, leading to complex drug treatments and increased risk of physical and cognitive disability. Improving or preserving the health and quality of life of these individuals is challenging due to a lack of well‐established clinical guidelines. Physicians are often forced to engage in cycles of “trial and error” that are centered on palliative treatment of symptoms rather than the root cause, often resulting in dubious outcomes. Recently, geroscience challenged this view, proposing that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging. In fact, strong correlations have recently been revealed between health dimensions and phenotypes that are typical of aging, especially with autophagy, mitochondrial function, cellular senescence, and DNA methylation. Current research focuses on measuring the pace of aging to identify individuals who are “aging faster” to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging. Understanding how the underlying biological mechanisms of aging connect to and impact longitudinal changes in health trajectories offers a unique opportunity to identify resilience mechanisms, their dynamic changes, and their impact on stress responses. Harnessing how to evoke and control resilience mechanisms in individuals with successful aging could lead to writing a new chapter in human medicine.”

https://onlinelibrary.wiley.com/doi/full/10.1111/acel.13080?utm_campaign=RESR_MRKT_Researcher_inbound&af=R&utm_medium=referral&utm_source=researcher_app

Comparative Effectiveness of Three Exercise Types to Treat Clinical Depression in Older Adults

Comparative Effectiveness of Three Exercise Types to Treat Clinical Depression in Older Adults

A Systematic Review and Network Meta-Analysis of Randomised Controlled Trials – ScienceDirect

Highlights

•Older adults can benefit from either aerobic, resistance, or mind-body exercise.

•Exercise is a therapeutic ally to pharmacological treatment of clinical depression.

•Pooled NMA evidence demonstrates high compliance and tolerance of exercise.

•There is opportunity for patients to select their preferred type(s) of exercise.

•Clinicians should facilitate exercise prescription based on patient preference.

Comparative Effectiveness of Three Exercise Types to Treat Clinical Depression in Older Adults: A Systematic Review and Network Meta-Analysis of Randomised Controlled Trials – ScienceDirect

Dietary inflammatory index and mortality

Dietary inflammatory index and mortality

“Higher Dietary Inflammatory Index (DII®) scores are associated with increased morbidity and mortality. However, little is known about the effects of DII on mortality in Mediterranean countries. Therefore, in the present study, we aimed to investigate the potential association between DII scores and overall, cancer and cardiovascular disease (CVD) mortality in people living in a Mediterranean area.”

“Higher DII scores were associated with a significantly higher mortality risk, whereas the association with cause‐specific mortality was less clear. These findings highlight the potential importance of diet in modulating inflammation and preventing death. ”

Dietary inflammatory index and mortality: a cohort longitudinal study in a Mediterranean area – Veronese – – Journal of Human Nutrition and Dietetics – Wiley Online Library

Distinct DNA methylation targets by aging and chronic inflammation

Distinct DNA methylation targets by aging and chronic inflammation

a pilot study using gastric mucosa infected with Helicobacter pylori

” Aberrant DNA methylation is induced by aging and chronic inflammation in normal tissues. The induction by inflammation is widely recognized as acceleration of age-related methylation. However, few studies addressed target genomic regions and the responsible factors in a genome-wide manner. Here, we analyzed methylation targets by aging and inflammation, taking advantage of the potent methylation induction in human gastric mucosa by Helicobacter pylori infection-triggered inflammation. “

Alzheimer’s drug candidates reverse broader aging, study shows — ScienceDaily

Alzheimer’s drug candidates reverse broader aging, study shows — ScienceDaily

” In mouse models of Alzheimer’s disease, the investigational drug candidates known as CMS121 and J147 improve memory and slow the degeneration of brain cells. Now, researchers have shown how these compounds can also slow aging in healthy older mice, blocking the damage to brain cells that normally occurs during aging and restoring the levels of specific molecules to those seen in younger brains.”

https://www.sciencedaily.com/releases/2019/12/191210134028.htm

Skin Rejuvenation by Low-Level Light Therapy

Skin Rejuvenation by Low-Level Light Therapy

Risk-Benefit Analysis

Forever Healthy Foundation gGmbH

Amalienbadstraße 41

D-76227 Karlsruhe, Germany

Low-level light therapy (LLLT) is the use of low incident levels of photon energy at a particular wavelength, targeting tissue to achieve a clinically useful local or systemic effect without the creation of heat (athermal) or damage (atraumatic) (Calderhead & Tanaka, 2017). LLLT has shown dramatic effects when used for wound healing, pain management, and various musculoskeletal conditions.

This review focuses on its potential use in skin rejuvenation. It has been shown that upon exposure to light, chromophores in the skin (mitochondrial cytochrome C, melanin, and protoporphyrins) absorb photons which lead to downstream alterations in physiology such as changes in cell proliferation, differentiation, migration, inflammatory mediators, and collagen production. It is supposed that these photobiomodulative effects have beneficial effects on the skin, leading to a more youthful appearance through increased collagen and elastin production, and a reduction in age spots and wrinkles. 

Key Questions 

This analysis seeks to answer the following questions:

  • Which benefits with regard to skin rejuvenation result from LLLT? 
  • Which risks are involved in using LLLT for skin rejuvenation (general and method-specific)?
  • What are the potential risk mitigation strategies?
  • Which method/device or combination of methods/devices is most effective for skin rejuvenation using LLLT?
  • Which of the available devices/methods are safe for use? 
  • What is the best therapeutic protocol available at the moment?  

https://brain.forever-healthy.org/display/EN/Skin+Rejuvenation+by+Low-Level+Light+Therapy

Fisetin Senolytic Therapy

Fisetin Senolytic Therapy

Risk-Benefit Analysis

Forever Healthy Foundation gGmbH

Amalienbadstraße 41

D-76227 Karlsruhe, Germany

Senolytics are agents that selectively induce apoptosis of senescent cells. Fisetin is a flavonoid polyphenol found in many types of fruits and vegetables (Arai et al., 2000) that is believed to act as a senolytic in addition to its numerous other known benefits. Although natural senolytics are less potent, compared to the targeted senolytics, they have lower toxicity and are thus, likely to be more readily translatable to clinical medicine. This RBA focuses on the risks and benefits of using fisetin as a senolytic rather than its more common use as a supplement.

Key Questions 

This RBA seeks to answer the following questions:

  • Which health and/or longevity benefits result from the use of fisetin as a senolytic? 
  • Which risks are involved in the use of fisetin as a senolytic (general and method-specific)?
  • What are the potential risk mitigation strategies?
  • Which method or combination of methods of using fisetin as a senolytic are most effective?
  • Which of the available methods are safe for use?
  • What is the best therapeutic protocol available at the moment?  

https://brain.forever-healthy.org/display/EN/Fisetin+Senolytic+Therapy

NAD+ Restoration Therapy

NAD+ Restoration Therapy

Risk-Benefit Analysis

Forever Healthy Foundation gGmbH

Amalienbadstraße 41

D-76227 Karlsruhe, Germany

NAD+ is a pyridine nucleotide found in all living cells. It plays an important role in energy metabolism and is a substrate for several enzymes (including those involved in DNA repair). NAD+ levels may decline markedly with age (Massudi et al., 2012Clement et al., 2019Zhu et al., 2011) and restoring those levels to a youthful state is believed to have beneficial effects on health and longevity. 

Key Questions 

This analysis seeks to answer the following questions:

  • Which health and/or longevity benefits result from raising NAD+ levels in humans? 
  • Which risks are involved in raising NAD+ levels (general and method-specific)?
  • What are the potential risk mitigation strategies?
  • Which method or combination of methods is most effective in raising NAD+ levels?
  • Which of the available methods are safe for use? 
  • What is the best therapeutic protocol available at the moment?  

https://brain.forever-healthy.org/display/EN/NAD+Restoration+Therapy

Probiotic bacteria as modulators of cellular senescence: emerging concepts and opportunities

Probiotic bacteria as modulators of cellular senescence: emerging concepts and opportunities

Probiotic bacteria are increasingly gaining importance in human nutrition owing to their multifaceted health beneficial effects. Studies have also shown that probiotic supplementation is useful in mitigating age-associated oxi-inflammatory stress, immunosenescence, and gut dysbiosis thereby promoting health and longevity. However, our current understanding of the process of aging suggests a strong interrelationship between the accumulation of senescent cells and the development of aging phenotype, including the predisposition to age-related disorders. The present review studies the documented pro-longevity effects of probiotics and highlights how these beneficial attributes of probiotics could be related to the mitigation of cellular senescence.

https://www.tandfonline.com/doi/full/10.1080/19490976.2019.1697148?af=R&utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Nicotinamide mononucleotide ameliorates the depression-like behaviors and is associated with attenuating the disruption of mitochondrial bioenergetic… – PubMed – NCBI

Nicotinamide mononucleotide ameliorates the depression-like behaviors and is associated with attenuating the disruption of mitochondrial bioenergetic… – PubMed – NCBI

https://www.ncbi.nlm.nih.gov/pubmed/31818774/

Brain-age in midlife is associated with accelerated biological aging and cognitive decline in a longitudinal birth cohort | Molecular Psychiatry

Brain-age in midlife is associated with accelerated biological aging and cognitive decline in a longitudinal birth cohort | Molecular Psychiatry

https://www.nature.com/articles/s41380-019-0626-7?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus

Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus

Milk exosomal miRNAs: potential drivers of AMPK-to-mTORC1 switching in β-cell de-differentiation of type 2 diabetes mellitus

“Persistent milk miRNA signaling adds a new perspective to the pathogenesis of T2DM and explains the protective role of breastfeeding but the diabetogenic effect of continued milk miRNA signaling by persistent consumption of pasteurized cow’s milk.”

http://link.springer.com/article/10.1186/s12986-019-0412-1?utm_source=researcher_app&utm_medium=referral&utm_campaign=RESR_MRKT_Researcher_inbound

Oxidative stress, inflammatory cytokines and body composition of master athletes: The interplay

Oxidative stress, inflammatory cytokines and body composition of master athletes: The interplay

Oxidative stress, inflammatory cytokines and body composition of master athletes: The interplay

https://link.researcher-app.com/Phic

– via Researcher (@ResearcherApp)

Oxidative stress, inflammatory cytokines and body composition of master athletes: The interplay

Oxidative stress, inflammatory cytokines and body composition of master athletes: The interplay

Oxidative stress, inflammatory cytokines and body composition of master athletes: The interplay

https://link.researcher-app.com/Phic

– via Researcher (@ResearcherApp)

The influence of metformin on IGF-1 levels in humans: A systematic review and meta-analysis

The influence of metformin on IGF-1 levels in humans: A systematic review and meta-analysis

We found in children, intervention duration <12 weeks yielded significant reductions in IGF-1, whilst paradoxically, in participants >18 years old, metformin intake significantly increased IGF-1. We suggest that caution be taken when interpreting the findings of this review, particularly given the discordant supplementation practices between children and adults.

https://www.sciencedirect.com/science/article/abs/pii/S104366181932081X?dgcid=rss_sd_all&utm_campaign=RESR_MRKT_Researcher_inbound&utm_medium=referral&utm_source=researcher_app

Identification of a key protein linked to ageing

Identification of a key protein linked to ageing

“These studies demonstrate an important link between the [pathological] accelerated ageing process and normal aging, and also expose the CSB protein as a key factor against cellular ageing” concludes Dr. Ricchetti.

https://medicalxpress.com/news/2019-12-identification-key-protein-linked-ageing.html

Specific features in the pineal g… preview & related info | Mendeley

Specific features in the pineal g… preview & related info | Mendeley

“Analysis of these data demonstrates that pineal peptides (epithalamin and epithalon) have a more pronounced geroprotective effect on the thymus as compared with those of the thymus peptides (thymalin and thymogen) on the pineal gland.”

https://www.mendeley.com/catalogue/specific-features-pineal-glandthymus-relationships-during-aging/

Telomerization as a method of obt… preview & related info | Mendeley

Telomerization as a method of obt… preview & related info | Mendeley

“The expression of this gene led to the appearance of telomerase activity in the fibroblasts, elongation of telomeres (to the size characteristic of the embryonic cells), and immortalization.”

https://www.mendeley.com/catalogue/telomerization-method-obtaining-immortal-human-cells-preserving-normal-properties/

Telomere dynamics in human cells … preview & related info | Mendeley

Telomere dynamics in human cells … preview & related info | Mendeley

“While these results reveal some heterogeneity in the reprogramming process with respect to telomere length, human somatic cells reprogrammed to pluripotency generally displayed elongated telomeres that suggest that they will not age prematurely when isolated from subjects of essentially any age.”

https://www.mendeley.com/catalogue/telomere-dynamics-human-cells-reprogrammed-pluripotency/

Epigenetics of aging and disease: a brief overview. – PubMed – NCBI

Epigenetics of aging and disease: a brief overview. – PubMed – NCBI

“Aging is an important risk factor for several human diseases such as cancer, cardiovascular disease and neurodegenerative disorders, resulting from a combination of genetic and environmental factors (e.g., diet, smoking, obesity and stress), which, at molecular level, cause changes in gene expression underlying the decline of physiological function. Epigenetics, which include mechanisms regulating gene expression independently of changes to DNA sequence, regulate gene expression by modulating the structure of chromatin or by regulating the binding of transcriptional machinery to DNA. Several studies showed that an impairment of epigenetic mechanisms promotes alteration of gene expression underlying several aging-related diseases. Alteration of these mechanisms is also linked with changes of gene expression that occurs during aging processes of different tissues. In this review, we will outline the potential role of epigenetics in the onset of two age-related pathologies, cancer and cardiovascular diseases.”

https://www.ncbi.nlm.nih.gov/pubmed/31811572?dopt=Abstract

Chronic inflammation in the etiology of disease across the life span. – PubMed – NCBI

Chronic inflammation in the etiology of disease across the life span. – PubMed – NCBI

Although intermittent increases in inflammation are critical for survival during physical injury and infection, recent research has revealed that certain social, environmental and lifestyle factors can promote systemic chronic inflammation (SCI) that can, in turn, lead to several diseases that collectively represent the leading causes of disability and mortality worldwide, such as cardiovascular disease, cancer, diabetes mellitus, chronic kidney disease, non-alcoholic fatty liver disease and autoimmune and neurodegenerative disorders. In the present Perspective we describe the multi-level mechanisms underlying SCI and several risk factors that promote this health-damaging phenotype, including infections, physical inactivity, poor diet, environmental and industrial toxicants and psychological stress. Furthermore, we suggest potential strategies for advancing the early diagnosis, prevention and treatment of SCI.

https://www.ncbi.nlm.nih.gov/pubmed/31806905?dopt=Abstract

The SMART App: an interactive web application for comprehensive DNA methylation analysis and visualization | Epigenetics & Chromatin | Full Text

The SMART App: an interactive web application for comprehensive DNA methylation analysis and visualization | Epigenetics & Chromatin | Full Text

“The SMART App serves as a new approach for users, especially wet-bench scientists with no programming background, to analyze the scientific big data and facilitate data mining. The SMART App is available at http://www.bioinfo-zs.com/smartapp.&#8221;

https://epigeneticsandchromatin.biomedcentral.com/articles/10.1186/s13072-019-0316-3

Growth Hormone DHEA Metformin In Aging Clinical Study

Growth Hormone DHEA Metformin In Aging Clinical Study

“A new clinical trial found that a combination of Growth Hormone, DHEA & Metformin helped to restore the size of the thymus gland and reverse biological age (epigenetic age via the GrimAge test).”

➢ Link to study:

Fahy, G. M., Brooke, R. T., Watson, J. P., Good, Z., Vasanawala, S. S., Maecker, H., et al. (2019). Reversal of epigenetic aging and immunosenescent trends in humans. Aging Cell, 18(6), 421–12. http://doi.org/10.1111/acel.13028

https://highintensityhealth.com/growth-hormone-dhea-metformin-in-aging-clinical-study/

Watch “The Secret to Aging in Reverse Revealed by Harvard Professor | David Sinclair” on YouTube

Watch “The Secret to Aging in Reverse Revealed by Harvard Professor | David Sinclair” on YouTube

Diabetes drug has unexpected, broad implications for healthy aging

Diabetes drug has unexpected, broad implications for healthy aging

“Previously, the only biochemical that was known to be activated by metformin was the AMPK pathway, which Shaw discovered stalls cell growth and changes metabolism when nutrients are scarce, as can occur in cancer. But the scientists believed more pathways than AMPK might be involved.

The scientists developed a novel screening platform to examine kinases, the proteins that transfer phosphate groups, which are critical on/off switches in cells and can be rapidly flipped by metformin. Using this technology, the researchers were able to decode hundreds of regulatory “switch-flipping” events that could affect healthy aging.”

https://medicalxpress.com/news/2019-12-diabetes-drug-unexpected-broad-implications.html

Tools to eliminate senescent cells.

Tools to eliminate senescent cells.

“Ageing and many diseases are partly driven by the accumulation of damaged cells that no longer divide. It emerges that these senescent cells can be eradicated in mice using a drug that interferes with the activity of the protein FOXO4.

If cells incur too much damage, they undergo either a self-elimination process known as apoptosis or a self-disabling process called senescence. Senescent cells can be long-lived, and so accumulate in aged and damaged organs1. The elimination of senescent cells is known2,3,4,5,6 to increase healthy lifespan and reduce the severity of age-related diseases in mice. Writing in Cell, Baar et al.7 expand our understanding of this phenomenon. They report that senescent cells depend on the transcription factor forkhead box protein O4 (FOXO4) for their survival, and show in mouse models that both age-associated defects and tissue dysfunction caused by chemotherapy can be reversed by pharmacologically perturbing the function of this protein.

Senescent cells forcibly block their own capacity to proliferate while programming themselves to secrete signalling molecules — a phenomenon known as the senescence-associated secretory phenotype (SASP). It has been proposed8,9 that the normal function of the SASP is to restore tissue function in two ways: first, by stimulating less-damaged neighbouring cells to engage in tissue repair; and second, by attracting inflammatory cells to eliminate senescent cells and turn off SASP-mediated signals. However, this restorative process may fail when the extent, duration or frequency of damage exceeds repair capacity, or when reparative and inflammatory cells become unresponsive to the effects of the SASP. The end result is an aberrant accumulation of senescent cells that, contrary to their initial purpose, aggravate tissue dysfunction.” Serrano, M. Tools to eliminate senescent cells. Nature545, 294–295 (2017) doi:10.1038/nature22493

https://rdcu.be/bX5uQ

What is a stack and whats in one? – Opinion

What is a stack and whats in one? – Opinion

So you have a bunch of information on things that can help you live healthier and longer. What next?

Typically what a biohacker does is builds a stack. A stack is a collection of supplements that is aimed at a certain goal.

I’m going to give you some insight into my “pet rabbit” stack 😉 My rabbit is 104kgs and around 40 years old (Super Rabbit 😉 My rabbit is wanting to live healthier and longer as well as improve cognetive function and avoid cognitive decline. She wants to grow her hair and keep it a healthy colour and improve general health and fitness.

Firstly a dosing routine showing morning and evening dosing and which to take at what time of day for the desirable outcome.

Continue reading “What is a stack and whats in one? – Opinion”
Review of clinical studies of Polygonum multiflorum Thunb. (He Shou Wu) and its isolated bioactive compounds

Review of clinical studies of Polygonum multiflorum Thunb. (He Shou Wu) and its isolated bioactive compounds

Polygonum multiflorum Thunb. (PMT, Polygonaceae family, Figure 1)), well known as He shou wu in China and Fo-ti in North America,[5] is one of the most popular perennial Chinese traditional medicinal vine-like herbs, officially listed in the Chinese Pharmacopoeia.[6] Various parts of the plants were utilized for different medicinal purposes. The leaves [Figure 2a], root tuber [Figure 2b] and rhizomes [Figure 2c] of this plant have been used as tonic and anti-aging agents[7,8,9,10,11,12] whereas the stem [Figure 2d] is used to alleviate insomnia and even to have an antidiabetic therapeutic activity as well.[13,14,15]Figure 1Polygonum multiflorum ThunbFigure 2Photos of (a) leaves, (b) tuber roots, (c) underground rhizomes and (d) stem from Polygonum multiflorum ThunbLaboratory studies and clinical practice have demonstrated that PMT possesses various biological and therapeutic actions, including anti-tumor,[16,17] antibacterial,[18] anti-inflammatory,[13] anti-oxidant,[19,20,21] anti-HIV,[22] liver protection,[23,24] nephroprotection,[25] antidiabetic,[15,26] anti-alopecia,[27,28] and anti-atherosclerotic activities.[29,30] It has been also reported to exert preventive activity against neurodegenerative diseases,[31,32,33,34,35] cardiovascular diseases and to reduce hyperlipidemia as well.[36,37]

Review of clinical studies of Polygonum multiflorum Thunb. and its isolated bioactive compounds
Emodin-induced (HeShouWu) autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes. – PubMed – NCBI

Emodin-induced (HeShouWu) autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes. – PubMed – NCBI

Emodin significantly inhibited the viability of and induced apoptosis in L02 cells in a dose- and time-dependent manner. In addition, emodin increased the number of GFP-LC3 puncta in L02 cells and upregulated the expression of LC3B-II compared to those in control cells. Furthermore, emodin significantly decreased the expression of p-PI3K, p-AKT and p-mTOR in a dose-dependent manner compared to that in control cells without altering the expression of PI3K, AKT and mTOR. Notably, cotreatment with emodin and 3-methyladenine (3-MA) or rapamycin significantly increased and decreased the apoptosis rate of L02 cells, respectively, compared to that of cells treated with emodin alone.

Emodin-induced autophagy against cell apoptosis through the PI3K/AKT/mTOR pathway in human hepatocytes. – PubMed – NCBI
Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. – PubMed – NCBI

Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. – PubMed – NCBI

Nicotinamide adenine dinucleotide (NAD), the cell’s hydrogen carrier for redox enzymes, is well known for its role in redox reactions. More recently, it has emerged as a signaling molecule. By modulating NAD+-sensing enzymes, NAD+ controls hundreds of key processes from energy metabolism to cell survival, rising and falling depending on food intake, exercise, and the time of day. NAD+ levels steadily decline with age, resulting in altered metabolism and increased disease susceptibility. Restoration of NAD+ levels in old or diseased animals can promote health and extend lifespan, prompting a search for safe and efficacious NAD-boosting molecules that hold the promise of increasing the body’s resilience, not just to one disease, but to many, thereby extending healthy human lifespan.

Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence. – PubMed – NCBI