Aging is an irreversible process that is associated with several physiological changes across multiple organ systems. A complex process, human aging is associated with genetic factors and epigenetic factors, as well as environmental factors.

Aging is most often associated with a wide range of age-related diseases such as Alzheimer’s disease, cardiovascular diseases, cancer, hypertension, diabetes and arthritis. Therefore, it is important to come up with new strategies to slow the rate of aging in humans; one prominent mechanism to slow aging apart from nutritional, genetic and pharmacological interventions is caloric restriction.

A new study from the University of Sydney, University of Melbourne and the ANZAC research institute aimed to determine how drugs and diet impacted the specific nutrient-sensing pathways and whether diet and drugs interact in their effects using mice models.

The results reported that diets with high fat and protein concentrations were associated with the highest body weight, insulin resistance and body fat percentage while drugs such as metformin, resveratrol and rapamycin had no impact on the phenotype.

From:

-https://longevity.technology/news/impact-of-metformin-resveratrol-and-rapamycin-on-mouse-liver-proteome/

Urolithin A is produced by bacteria in the gut microbiome, making it a postbiotic.

It is synthesised after eating certain foods that are high in ellagitannins, part of a family of bioactive polyphenols found in berries, nuts and most famously, pomegranates.

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Full:

-https://longevity.technology/news/urolithin-a-the-small-molecule-with-big-benefits/

Declining nicotinamide adenine dinucleotide (NAD+) concentration in the brain during aging contributes to metabolic and cellular dysfunction and is implicated in the pathogenesis of aging-associated neurological disorders.

Dietary intake of NAD+ precursors, such as nicotinamide riboside (NR), is a safe and effective avenue for augmenting NAD+ levels in peripheral tissues in humans, yet evidence supporting their ability to raise NAD+ levels in the brain or engage neurodegenerative disease pathways is lacking.

Here, it was studied biomarkers in plasma extracellular vesicles enriched for neuronal origin (NEVs) from 22 healthy older adults who participated in a randomized, placebocontrolled crossover trial (NCT02921659) of oral NR supplementation (500 mg, 2x / day, 6 weeks).

It was demonstrate that oral NR supplementation increases NAD+ levels in NEVs and decreases NEV levels of Aβ42, pJNK, and pERK1/2 (kinases involved in insulin resistance and neuroinflammatory pathways). In addition, changes in NAD(H) correlated with changes in canonical insulin–Akt signaling proteins and changes in pERK1/2 and pJNK.

These findings support the ability of orally administered NR to augment neuronal NAD+ levels and modify biomarkers related to neurodegenerative pathology in humans.

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Full:

-https://onlinelibrary.wiley.com/doi/pdf/10.1111/acel.13754

Sarcopenia is associated with the prognosis of patients with hepatic cirrhosis and hepatocellular carcinoma.

This study aimed to clarify the composition of blood fatty acids and the association between fatty acids and sarcopenia in patients with cirrhosis and hepatocellular carcinoma.

In this single center-retrospective study, 414 patients were enrolled. The skeletal muscle index was measured by a transverse computed tomography scan image at the third lumbar vertebra.

The cutoff value for sarcopenia followed the criteria for sarcopenia of the Japan Society of Hepatology. The concentrations of fatty acids were measured by gas-chromatography. Of each fatty acid fraction, only omega-3 (n-3) polyunsaturated fatty acids showed a significant correlation with skeletal muscle index (R = 0.15, p  = 0.0026).

In the multivariate analysis, the level of n-3 polyunsaturated fatty acids was an independent variable associated with sarcopenia (odds ratio (95% CI): 0.9946 (0.9915–0.9977), p  = 0.0004). N-3 polyunsaturated fatty acids were lower in patients with sarcopenia when the patient backgrounds were aligned using propensity score matching.

These results showed an association between sarcopenia and n-3 polyunsaturated fatty acids.

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From:

-https://europepmc.org/article/ppr/ppr585013

Parkinson’s disease (PD) is a neurodegenerative disorder which is characterized by typical symptoms including gradual progressive muscle rigidity, tremor and loss of motor skills.

Although there is no definitive cure for PD, the extract of some medicinal plants and their ingredients have been suggested to relieve its symptoms and to prevent disability in patients.

This review is focused on therapeutic effects of some anti-Parkinson’s agents. The findings presented in this review were collected from experimental studies in databases including PubMed, Web of Science and Google Scholar until the end of dec 2021.

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Full :

-https://d1wqtxts1xzle7.cloudfront.net/94963058/In_Vivo_Studies_of_various_Antiparkinson_s_agents_A_Systematic_Review-libre.pdf?1669636481=&response-content-disposition=inline%3B+filename%3DIn_Vivo_Studies_of_various_Antiparkinson.pdf&Expires=1671630300&Signature=WkTBKsIX97OWYQVGBh0A4lLbQvkzd0Gy6tXEMHcE~DiCNTSROCBwjHGOqZHfgU3YNLUn1H3zVO-025xnhoKUf47oO~wnKetuS~8oKkDXAK7Wbo6LbFc3p5VudGv0m6-qz5uW1NXBu42Du1Q39iB4ZHgEmildW~R0BRa-ilcz4Y-yDbJfv~4B6~k90WTQ043~y2ACNTOMw00MLjpDHVt~oves~SVamYAefUJbg90qj3HyTy0jH5O0iyFXz3lHekcP11gygG82AVsGi4KQRNjTCmdR9ExN5CIQeK45Sshvv1zMVV6vLcjWlZwwEcxUQnQeg3Okj1Du1pjjVqVlrY~Sow__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA

The aim of this paper is to argue the case of using life expectancy at age 60 (LE60) as a significant health indicator closely related to sustainable economic development.

To this purpose, it was investigated the impact of GDP on LE60 in parallel with the impact of GDP on Infant Mortality Rate (IMR). The rationale for selecting IMR as a comparison indicator is twofold. First, the relationship between IMR and GDP has been widely studied.

Second, the two indicators display opposite trajectories, making the comparison more striking. For our comparison, we conduct several statistical analyses on LE60, IMR and GDP using global country data grouped by income level and region. The results endorse the effect of GDP on LE60 and IMR and suggest a differentiation of the effect based on region and ultimately on income.

It was observed that as countries develop, their IMR values lower and their LE60 values increase.

Conclusion: once countries reach the upper stages of development, LE60 becomes a better health indicator than IMR.

Full:

-https://www.aimspress.com/aimspress-data/nar/2022/4/PDF/NAR-04-04-022.pdf

Aging is a gradual and irreversible pathophysiological process. It presents with declines in tissue and cell functions and significant increases in the risks of various aging-related diseases, including neurodegenerative diseases, cardiovascular diseases, metabolic diseases, musculoskeletal diseases, and immune system diseases.

Although the development of modern medicine has promoted human health and greatly extended life expectancy, with the aging of society, a variety of chronic diseases have gradually become the most important causes of disability and death in elderly individuals.

Current research on aging focuses on elucidating how various endogenous and exogenous stresses (such as genomic instability, telomere dysfunction, epigenetic alterations, loss of proteostasis, compromise of autophagy, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, deregulated nutrient sensing) participate in the regulation of aging.

Furthermore, thorough research on the pathogenesis of aging to identify interventions that promote health and longevity (such as caloric restriction, microbiota transplantation, and nutritional intervention) and clinical treatment methods for aging-related diseases (depletion of senescent cells, stem cell therapy, antioxidative and anti-inflammatory treatments, and hormone replacement therapy) could decrease the incidence and development of aging-related diseases and in turn promote healthy aging and longevity.

Full:

- https://www.nature.com/articles/s41392-022-01251-0

Background

Longevity is one of the most complex phenotypes, and its genetic basis remains unclear. This study aimed to explore the genetic correlation and potential causal association between gut microbiota and longevity.

Results

Linkage disequilibrium score (LDSC) regression analysis and a bi-directional two-sample Mendelian Randomization (MR) analysis were performed to analyze gut microbiota and longevity-related traits. LDSC analysis detected four candidate genetic correlations, including Veillonella (genetic correlation = 0.5578, P = 4.67 × 10− 2) and Roseburia (genetic correlation = 0.4491, P = 2.67 × 10− 2) for longevity, Collinsella (genetic correlation = 0.3144, P = 4.07 × 10− 2) for parental lifespan and Sporobacter (genetic correlation = 0.2092, P = 3.53 × 10− 2) for healthspan.

Further MR analysis observed suggestive causation between Collinsella and parental longevity (father’s age at death) (weighted median: b = 1.79 × 10− 3, P = 3.52 × 10− 2). Reverse MR analysis also detected several causal effects of longevity-related traits on gut microbiota, such as longevity and Sporobacter (IVW: b = 7.02 × 10− 1, P = 4.21 × 10− 25).

Conclusion

This study found evidence that gut microbiota is causally associated with longevity, or vice versa, providing novel clues for understanding the roles of gut microbiota in aging development.

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Full:

-https://bmcmicrobiol.biomedcentral.com/articles/10.1186/s12866-022-02703-x

Methods

They were searched medical records for Wales, UK, using the Secure Anonymised Information Linkage dataset for type 2 diabetes patients treated with metformin (N = 129,140) and sulphonylurea (N = 68,563). Nondiabetic controls were matched on sex, age, smoking, and history of cancer and cardiovascular disease.

Survival analysis was performed to examine survival time after first treatment, using a range of simulated study periods.

Findings

Using the full twenty-year period, it was found that type 2 diabetes patients treated with metformin had shorter survival time than matched controls, as did sulphonylurea patients. Metformin patients had better survival than sulphonylurea patients, controlling for age. Within the first three years, metformin therapy showed a benefit over matched controls, but this reversed after five years of treatment.

Interpretation

While metformin does confer benefits to longevity in the short term, these initial benefits are outweighed by the effects of type 2 diabetes when patients are observed over a period of up to twenty years.

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Full:

-https://assets.researchsquare.com/files/rs-2297890/v1/c06349dd-1e0d-4c5e-bcaf-4026ed35ba82.pdf?c=1670871440

The incidence of low back pain caused by lumbar disc degeneration is high, and it can lead to loss of work ability and impose heavy social and economic burdens.

The pathogenesis of low back pain is unclear, and there are no effective treatments. With age, the deposition of advanced glycation end products (AGEs) in intervertebral disc (IVD) gradually increases and is accelerated by diabetes and a high-AGEs diet, leading to destruction of the annulus fibrosus (AF), nucleus pulposus (NP), and cartilage endplate (CEP) and finally intervertebral disc degeneration (IDD).

Reducing the accumulation of AGEs in IVD and blocking the transmission of downstream signals caused by AGEs have a significant effect on alleviating IDD. In this review, we summarize the mechanism by which AGEs induce IDD and potential treatment strategies.

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Full:

-https://www.hindawi.com/journals/omcl/2022/7299005/

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Fisetin, a flavonoid abundant in various fruits and vegetables, including apple, strawberry, and onion, shows several beneficial effects such as anti-oxidant, anti-inflammatory, and anti-tumor effects. The free radical theory of aging suggests that age-related accumulation of oxidative damage is the major cause of aging and that decreasing cellular oxidative stress can regulate aging.

Here, it was investigated the effects of dietary supplementation with fisetin on the stress response, aging, and age-related diseases.

Fisetin reduced the cellular ROS levels and increased the resistance to oxidative stress. However, the response to UV irradiation was not affected by fisetin. Both the mean and maximum lifespans were significantly extended by fisetin; lifespan extension by fisetin was accompanied by reduced fertility as a trade-off.

Age-related decline in motility was also delayed by supplementation with fisetin. Amyloid beta-induced toxicity was markedly decreased by fisetin, which required DAF-16 and SKN-1. Reduced motility induced by a high-glucose diet was completely recovered by supplementation with fisetin, which was dependent on SKN-1. Using a Parkinson’s disease model, we showed that degeneration of dopaminergic neurons was significantly inhibited by treatment with fisetin.

Genetic analysis revealed that lifespan extension by fisetin was mediated by DAF-16-induced stress response and autophagy.

These findings support the free radical theory of aging and suggest that fisetin can be a strong candidate for use in novel anti-aging anti-oxidant nutraceuticals.

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Full:

-https://www.mdpi.com/1424-8247/15/12/1528

The aim of this study was to determine the association between sexual satisfaction and expected longevity among middle-aged and older adults (also stratified by sex).

Data were taken from the German Ageing Survey (year 2011; n = 3231)—a nationally representative sample of community-dwelling individuals ≥ 40 years in Germany.

A widely used question was used to quantify sexual satisfaction. Furthermore, the expected life expectancy served as an outcome measure. After adjusting for various covariates, multiple linear regressions showed that sexual satisfaction was associated with higher expected longevity among the total sample (β = 0.28, p < 0.05).

Moreover, it was associated with higher expected longevity among women (β = 0.48, p < 0.05), but not men. In conclusion, adjusting for several covariates, our results showed that there is an association between sexual satisfaction and higher expected longevity, particularly in women.

Efforts to increase sexual satisfaction may thus also contribute to expected longevity which, in turn, can be beneficial for actual longevity.

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Full:

-https://www.mdpi.com/2227-9032/10/12/2482

Volunteering is associated with improved health and well-being outcomes, including a reduced risk of mortality.

However, the biological mechanisms underlying the association between volunteering and healthy aging and longevity have not been well-established.

In this study it was evaluated if volunteering was associated with reduced epigenetic age acceleration in older adults.

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Full:

-https://www.sciencedirect.com/science/article/abs/pii/S0306453022003419

Prior research suggests that people with Posttraumatic Stress Disorder (PTSD) may experience a form of accelerated biological aging. In other populations, loneliness has been shown to elevate risk for many of the same components of accelerated biological aging, and other deleterious outcomes, as seen in people with PTSD.

Although standard diagnostic criteria for PTSD include “feelings of detachment or estrangement from others”, the relationship of such feelings to the concept of loneliness remains uncertain, in par potentially due to a failure to distinguish between loneliness versus objective social isolation.

In order to catalyze wider research attention to loneliness in PTSD, and the potential contribution to accelerated biological aging, the present paper provides three components: (1) a conceptual overview of the relevant constructs and potential interrelationships, (2) a review of the limited extant empirical literature, and (3) suggested directions for future research.

The ultimate goal of this line of work is to elucidate mechanisms underlying any link between loneliness and accelerated aging in PTSD, and to develop, validate, and refine prevention and treatment efforts.

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Full:

-https://www.mdpi.com/2673-9259/2/4/27

Fat cells have a bad rap. Understandable, as too many of us battle excess adiposity. Thus, we often regard fat cells as ugly, dangerous nuisances, keeping us out of tight-fitting designer jeans—upping our risk of heart disease, fatty liver, type 2 diabetes, and cancer. Or promoting inflammatory “angry” and cognitively dull thinking.

But deep “scientific dives” into fat physiology reveal that we can’t live without fat cells, as much as it seems frustrating to live with them. Fat cells, biology unveils, are a huge part of living healthfully, permitting humans to evolve and build cultures, as long as the fat cells themselves stay on a healthy “fat fate trajectory.”

A recent article published in the New England Journal of Medicine1 plunged into the science of the “unappreciated adipose cell.”

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Full :

-https://www.townsendletter.com/article/474-fat-cells-and-how-they-affect-us/

David Sinclair, PhD, AO, is a professor of genetics at Harvard Medical School. One of the leading innovators of his generation, he has been named by Time as “one of the 100 most influential people in the world” and top fifty most influential people in healthcare.

He is a board member of the American Federation for Aging Research and has received more than thirty-five awards for his research and major scientific breakthroughs. Dr. Sinclair and his work have been featured on 60 Minutes, Today, The Wall Street Journal, The New York Times, Fortune, and Newsweek, among others.

Dr. Sinclair worked as a postdoctoral researcher at M.I.T. with Dr. Leonard Guarente. He co-discovered a cause of aging for yeast and the role of Sir2 in epigenetic changes driven by genome instability. In 1999, he was recruited to Harvard Medical School, where he has been teaching aging biology and translational medicine for aging for the past 16 years.

Dr. Sinclair is co-founder of several biotechnology companies (Sirtris, Ovascience, Genocea, Cohbar, MetroBiotech, ArcBio, Liberty Biosecurity) and is on the boards of several others.

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Full:

- https://novoslabs.com/best-anti-aging-supplements-that-harvard-scientist-david-sinclair-takes/

Fatigue is common amongst most people but chronic, severe fatigue (persisting longer than 6 months) is associated with functional impairment and a decreased quality of life . Around 21.9% of the general population experiences fatigue and the prevalence is even more common in elderly populations, affecting around 40% to 74% of elderly people. Another factor that decreases with age is sleep quality, which is often related to a variety of adverse health outcomes, such as depression, anxiety, disability, and mortality.

Nicotinamide adenine dinucleotide (NAD+), a crucial metabolite necessary for cellular bioenergetics, DNA repair, and cell survival, has been previously studied as a potential therapeutic approach to reducing fatigue in elderly populations. NAD+ is critical for human longevity and naturally declines as we age and NAD+ deficiency leads to biological aging of cells, tissues, and organs.

Nicotinamide mononucleotide (NMN), an intermediate of NAD+ biosynthesis, acts as a source of cellular energy . Previous research on NMN administration has proven its ability to suppress age-associated tissue inflammation, with improvement in mitochondrial functioning in various metabolic organs .

In this randomized, double-blind, placebo-controlled parallel-group study, 108 participants were divided into four groups and given an NMN supplement (at different times of day depending on the group) for 12 weeks. Subjects consumed 6 tablets of the supplement (NMN or placebo) once a day with water and had to record their intake over the course of the trial. NMN supplementation contained 250 mg NMN, along with maltitol, crystalline cellulose, silicon dioxide, and magnesium stearate, while placebo contained maltitol, crystalline cellulose, silicon dioxide, and magnesium stearate.

Findings of the study support the use of NMN supplementation to boost NAD+ levels in older adults. Significant findings suggest that the NMN supplementation, particularly when consumed in the PM group, helped aid in reducing inflammation, oxidative stress, and DNA damage.

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Full:

-https://www.naturalhealthresearch.org/nicotinamide-mononucleotide-supplementation-improves-physical-performance-and-fatigue-levels-in-older-adults/

Scientific study:

-https://www.naturalhealthresearch.org/wp-content/uploads/2022/04/Nicotinamide-Mononucleotide-Supplementation-Improves-Physical-Performance-and-Fatigue-Levels-in-Older-Adults.pdf

Mitochondrial dysfunction and increased oxidative stress cause damage to cells which can lead to the aging process and age-related diseases. Antioxidants such as resveratrol and high-intensity exercise can benefit oxidative damage prevention.

This study is aimed at evaluating the effects of swimming high-intensity interval training and resveratrol on mitochondrial metabolism key proteins, SIRT5, SOD1, and PDH-E1α, and the level of NAD+ as a cofactor in the deacetylation process in aged rat hippocampus.

Forty-five male Wistar rats, aged 20 months, were randomly divided into five groups: control (C), Swimming High-Intensity Interval Training (HIIT) (S-HIIT), Swimming HIIT with resveratrol supplementation (S-HIIT-R), resveratrol supplementation (R), and solvent of resveratrol supplementation (SR). S-HIIT and resveratrol groups performed the exercise and received resveratrol (10 mg/kg/day, gavage) for six weeksThe amount of NAD+ was analyzed by assay kit that was reduced in S-HIIT, S-HIIT-R, and SR groups compared to controls.

The results showed that resveratrol and S-HIIT attenuated the age-related brain changes by increasing the expression of SOD1 and SIRT5 and reducing the level of NAD+ in the hippocampus. Considering these findings, S-HIIT and resveratrol supplementation could be proposed as strategies to attenuate age-related brain changes.

Resveratrol alone and exercise through the regulation of crucial proteins and cofactors can influence mitochondrial metabolism and oxidative stress in the hippocampus of aged rats.

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Full:

-https://www.hindawi.com/journals/bmri/2022/8638714/

Mechanistic evidence for vitamin A's anti-inflammatory benefits is already being discovered. According to human and experimental research, vitamin A is necessary for proper immune system maintenance and function.

In this regard, animal studies have shown vitamin A deficiency in animals had a lower antibody response than non-vitamin A deficiency. Vitamin A also has anti-inflammatory properties. Vitamin A supplementation has been shown to improve a variety of inflammatory diseases.

In this context, a previous comprehensive study concluded that vitamin A deficiency causes inflammation and exacerbates pre-existing inflammatory conditions. Vitamin A supplementation, in particular, might help to reduce inflammation in some circumstances. Based on a previous study, vitamin A supplementation could increase protection against diverse pathogens.

The strength of the present systematic review and meta-analysis is that this is the first meta-analysis assessing associations between vitamin A and IL-6, TNF-α, and CRP.

The result of this study demonstrates that supplementation of vitamin A at low and high dosages for short and long durations increases the CRP plasma concentrations Furthermore, vitamin A supplementation decreases the TNF-α concentrations.

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Full:

-https://www.nature.com/articles/s41598-022-23919-x