Intermittent fasting protects the brain| Lifespan Research Institute

Date Posted: December 6, 2022

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Intermittent Fasting Protects Mice from Brain Injury

Scientists from Singapore have found that intermittent fasting alleviates damage incurred by chronic cerebral hypoperfusion, the impaired blood flow to the brain that is thought to be a cause of age-related dementia [1].

Why intermittent fasting?

Back in the early days of geroscience, caloric restriction was the first intervention to substantially increase lifespan in lab animals, and now, many decades later, it remains one of the most powerful anti-aging interventions available. However, it is hard to maintain the required level of caloric restriction (35-40%) in humans. Recently, intermittent fasting has emerged as another version of dietary restriction, with one influential study suggesting that it promotes longevity in mice [2]. Another one found that intermittent fasting improves long-term memory and neurogenesis [3].

Many intermittent fasting regimens have been proposed, such as “day in, day out” and one meal a day, but the most popular is probably 16/8, in which daily food intake is restricted to an eight-hour window. This regimen is relatively easy to maintain, and one thorough review found it to be beneficial, including for humans [4].

Robust protection

In this new study, the researchers investigated whether intermittent fasting (IF) can help with chronic cerebral hypoperfusion (CCH), which is basically impaired blood flow to the brain. CCH is thought to contribute to age-related cognitive decline and dementia by increasing oxidative stress, inflammation, and matrix metalloproteinases.

The researchers developed a mouse model of CCH by artificially occluding the carotid artery. Two-month-old mice were put on a 16/8 IF diet, while the control group ate throughout the day. It is important to note that the mice’s diet was relatively healthy, with 58% carbohydrate, 24% protein, and 18% fat. After another four months, CCH was induced by carotid artery stenosis for either 15 or 30 days.

The IF group exhibited lower body weight and a significant increase in blood ketones, which supports the claim that 16/8 IF induces ketosis. The researchers then tested how IF affected various types of CCH-induced damage. One of the hallmarks of CCH is increased microvascular leakage, which was attenuated by IF very significantly, almost to the level of healthy controls.

The researchers then measured the permeability of the blood-brain barrier (BBB), which safeguards the brain from various pathogens. BBB permeability increased significantly in the non-IF CCH group, but intermittent fasting prevented this increase almost completely. IF also partially rescued levels of tight junction proteins reduced by CCH. Tight junctions are protein structures that “glue” cells together to decrease permeability.

Results were highly promising in neuronal pathologies as well. IF attenuated CCH-induced decreases in white matter integrity and almost completely protected hippocampal neurons from death. Cleaved caspase-3, a marker of cellular death, was significantly increased by the 30-day perturbation in non-IF animals but not in the IF group.

Matrix metalloproteinases (MMPs) are enzymes that degrade the cellular matrix, an important component of the blood-brain barrier. They are indispensable for healthy remodeling of the matrix, but their overexpression can be harmful, and in the brain, this has been linked to both vascular and neuronal pathologies. In this study, IF robustly protected against the increase in MMP levels induced by CCH.

IF helps the healthy brain

One of the mechanisms by which CCH damages the brain is oxidative stress. The levels of two major antioxidants, glutathione and superoxide dismutase, were not significantly changed by CCH in non-IF animals. However, they were greatly increased by IF in all groups, including healthy controls. In other words, even though antioxidant levels were not negatively affected by the injury, they were positively affected by IF, which might have helped to alleviate CCH-induced damage.

Interestingly, a similar tendency was evident in some other measurements, where IF led to beneficial changes even in non-injured controls. This included vascular leakage, BBB permeability, white matter integrity, and cortex levels of tight junction proteins. These results suggest that IF benefits even a healthy brain.

Conclusion

This study investigated some interesting aspects of the effect intermittent fasting has on the brain. Like many previous studies, it showed that IF, and its popular 16/8 form in particular, confer health benefits. IF robustly protected from damage induced to the brain by chronic cerebral hypoperfusion, a condition that might cause age-related dementia. However, this study would be hard to recreate in humans, because it involved long-term IF prior to CCH onset, which cannot be predicted in humans. On the other hand, IF is probably not popular enough yet to allow for an epidemiological study, so we will have to do with mouse data for now.

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Literature

[1] Rajeev, V., Fann, D. Y., Dinh, Q. N., Kim, H. A., De Silva, T. M., Jo, D. G., … & Arumugam, T. V. (2022). Intermittent Fasting Attenuates Hallmark Vascular and Neuronal Pathologies in a Mouse Model of Vascular Cognitive Impairment. International Journal of Biological Sciences, 18(16), 6052-6067.

[2] Mitchell, S. J., Bernier, M., Mattison, J. A., Aon, M. A., Kaiser, T. A., Anson, R. M., … & de Cabo, R. (2019). Daily fasting improves health and survival in male mice independent of diet composition and calories. Cell Metabolism, 29(1), 221-228.

[3] Dias, G. P., Murphy, T., Stangl, D., Ahmet, S., Morisse, B., Nix, A., … & Thuret, S. (2021). Intermittent fasting enhances long-term memory consolidation, adult hippocampal neurogenesis, and expression of longevity gene Klotho. Molecular psychiatry, 26(11), 6365-6379.

[4] De Cabo, R., & Mattson, M. P. (2019). Effects of intermittent fasting on health, aging, and disease. New England Journal of Medicine, 381(26), 2541-2551.

Date Posted: December 6, 2022

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Turn Biotechnologies Changes Paradigm in Skin Rejuvenation

Turn Biotechnologies has unveiled data at four industry conferences suggesting that a single ERA treatment may be more effective than combination therapies used today. Biomarker analysis demonstrates ERA’s regenerative impact on fibroblast proliferation, collagen VII production, and the eTurna™ lipid-based delivery platform proves groundbreakingly effective at reaching targeted tissue. The company plans to present updated data during a January webinar.

MOUNTAIN VIEW, California, Dec. 6, 2022 – Turn Biotechnologies, a cell rejuvenation company developing novel mRNA medicines to cure untreatable, age-related conditions, released preliminary data that show its therapies rejuvenate skin cells more effectively and safely than existing treatments.

The company’s ERA™ (Epigenetic Reprogramming of Aging) treatment, precisely transported using Turn Bio’s proprietary eTurna™ lipid-based delivery platform, reversed the hallmarks of aging in human skin – something never before achieved. The treatment simultaneously increased fibroblasts and collagen VII to restore the production of collagen and elastin, and reduced inflammation markers, oxidative stress, senescence, and MMPs, proteins responsible for skin degradation versus those untreated.

Preclinical data were presented to dermatologists and industry KOLs attending four global conferences in the past five weeks: Global Aesthetics Conference in Miami; Cosmetic Surgery Forum in Nashville, Tennessee; Beauty Through Science in New York City, and The Longevity Summit in San Francisco, California.

“The data suggest we may be close to redefining the care dermatologists can provide their patients,” said Jill Waibel, a board-certified dermatologist and respected regenerative medicine researcher who presented findings at the Global Aesthetics Conference. “The potential to improve the quality of patients’ skin – its elasticity and its ability to heal – could change the future of regenerative medicine.”

Hema Sundaram, a board-certified dermatologist and noted researcher in regenerative medicine and cell science, presented the data at Cosmetic Surgery Forum.

“This early research suggests that ERA could significantly improve the balance between key biomarkers of cell aging and cell youthfulness,” she said. “From an evidence-based perspective, this carries more weight as a rejuvenation strategy than efforts to improve a single biomarker. Research of this type may open the door to a new paradigm of dermatologic care.”

Data were also presented during sessions of the Beauty Through Science conference and the Longevity Summit.

“We believe this promises to be a game-changer for dermatologists, plastic surgeons and their patients,” said Turn Bio CEO Anja Krammer. “The true breakthrough of combining our mRNA-based ERA therapy with our eTurna lipid delivery system, for the first time shows reversal from the effects of aging and offers an ability to improve the overall quality of the skin.”

Turn Bio executives have committed to releasing additional data during a January webinar. Details will be announced in coming weeks.

Image of a cross-section of human skin that was treated with ERA, showing Collagen VII expressed at the dermal-epidermal junction (in red). The cell nuclei are stained with DAPI (blue).

About Turn Biotechnologies

Turn Bio is a pre-clinical-stage company focused on repairing tissue at the cellular level and developing transformative drug delivery systems. The company’s proprietary mRNA platform technology, ERA™ (Epigenetic Reprogramming of Aging), restores optimal gene expression by combatting the effects of aging in the epigenome. This restores cells’ ability to prevent or treat disease and heal or regenerate tissue. It will help to fight incurable chronic diseases. Its eTurna™ Delivery Platform uses unique formulations to precisely deliver cargo to specific organs, tissues, and cell types.

The company is completing pre-clinical research on tailored therapies targeting indications in dermatology and immunology, and developing therapies for ophthalmology, osteo-arthritis, and the muscular system. For more information, see www.turn.bio.

For more information, contact:

Jim Martinez, rightstorygroup jim@rightstorygroup.com or (312) 543-9026

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Date Posted: December 5, 2022

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Finding Interventions That Truly Impact Aging

Researchers publishing in Nature Communications have determined that interventions that extend lifespan in mice may not have significant effects on the processes of aging.

Improvement is not the same as slowing decline

The researchers begin this paper by noting that previous studies have outlined a broad variety of dietary, environmental, and genetic factors that are associated with lifespan [1]. The researchers contend that this fact has had an influence on modern models of aging, including the Hallmarks of Aging. However, lifespan is often controlled by specific pathologies of old age. It is possible for an intervention to extend lifespan by preventing specific causes of death while having no real effect on any of the various aspects of aging.

Therefore, the researchers argue that how long organisms live is, counterintuitively, not a very good endpoint for analyzing how much the organisms are aging. They point out that the vast majority of laboratory mice die of cancer [2] and hold that interventions known to extend lifespan in these mice, such as intermittent fasting, are doing so by delaying cancer [3].

The researchers also note that an intervention that improves a phenotype of aging may not be doing so by directly impacting its decline as such. They choose as their example a theoretical intervention that broadly increases the number of neurons in the brain. While such an intervention would be extremely welcome for many, many reasons, it may not be addressing the underlying mechanisms causing the decline of neurons with aging.

in order to tell the difference between an intervention that provides baseline improvement and interventions that impact aging, the researchers use a simple test: does it improve the old more than the young?

A phenotypic look at aging

This paper contains an in-depth analysis of phenotypic aging over time in mice, including specific aspects of reactions, heart function, immune function, metabolism, fat mass, and blood contents. Some of these changes can be detected early in life, while others only show up in middle-aged and older mice.

They also note the effects of some hallmarks of aging: on the molecular level, genomic instability, cellular senescence, deregulated nutrient sensing, and altered intercellular communication appear to accelerate only at older ages, while loss of proteostasis and mitochondrial dysfunction appear to decline more gradually. Cell proliferation immediately dropped shortly after birth to a steady level.

The researchers gathered this data in the service of the next phase of their experiment: determining if fundamental interventions known to extend lifespan have age-dependent effects.

Reversing age-related phenotypes in the young

For their first experiment, the researchers examined the effects of phenotypic aging on mice that were engineered to have a growth hormone deficiency. These mice live longer than unaltered mice. 35 age-sensitive phenotypes were unaffected, 18 age-sensitive phenotypes were accelerated, and 38 age-sensitive phenotypes were improved. However, only five of these age-sensitive phenotypes were found to be significantly improved in a way that correlated with the age of the animals; in the other cases, young animals were helped approximately as much as old animals were. A similar analysis in human beings with related mutations found very few statistically significant observations, most of which related to body fat.

On the other hand, mTOR deficiency did seem to have more age-dependent effects. Here, 42 age-dependent phenotypes were unaffected, 14 age-dependent phenotypes were accelerated, and of the 56 age-dependent phenotypes improved, 22 were improved in an age-related manner. Unfortunately, in human beings with related mutations, there were also relatively few statistically significant observations.

Intermittent fasting, an intervention known to improve mouse lifespan, did not affect 48 age-related phenotypes, accelerated 11 of them, and improved 42, 20 of which were improved in an age-related manner.

Conclusion

The first logical question that can be asked in response to this line of research is “Does it matter?” After all, if an intervention extends lifespan and improves health, whether or not it has effects that are truly representative of reversed aging seems to be an academic question at best. Vanishingly few people would refuse a healthspan-extending intervention on the grounds that it does not truly impact aging as such. It may also be the case that some repeatable interventions will be able to stave off individual aspects of aging indefinitely, despite having similar effects on the young as the old.

However, there are good reasons for this sort of research. Coupled with deep learning, epigenetic clocks, and other analytic tools, this approach can be used to determine which interventions provide simple health benefits and which impact the processes of aging themselves.

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Literature

[1] Tacutu, R., Thornton, D., Johnson, E., Budovsky, A., Barardo, D., Craig, T., … & De Magalhães, J. P. (2018). Human ageing genomic resources: new and updated databases. Nucleic acids research, 46(D1), D1083-D1090.

[2] Pettan-Brewer, C., & M. Treuting, P. (2011). Practical pathology of aging mice. Pathobiology of Aging & Age-related Diseases, 1(1), 7202.

[3] Blackwell, B. N., Bucci, T. J., Hart, R. W., & Turturro, A. (1995). Longevity, body weight, and neoplasia in ad libitum-fed and diet-restricted C57BL6 mice fed NIH-31 open formula diet. Toxicologic pathology, 23(5), 570-582.

Date Posted: December 5, 2022

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BioAge Announces Positive Results Against Muscle Atrophy

BioAge Labs has concluded a Phase 1b study in which human volunteers undergoing 10 days of bed rest were shown to have their related muscle atrophy significantly attenuated by BGE-105.

RICHMOND, Calif.–(BUSINESS WIRE)–BioAge Labs, Inc. (“BioAge”), a clinical-stage biotechnology company developing therapeutics that target the molecular causes of aging to extend healthy human lifespan, today announced positive Phase 1b clinical data for BGE-105, a highly selective, potent, orally available small-molecule agonist of the apelin receptor APJ. BGE-105 treatment resulted in statistically significant prevention of muscle atrophy relative to placebo in healthy volunteers aged 65 or older after 10 days of strict bed rest.

Muscle atrophy—loss of muscle mass and strength—is a universal feature of human aging that increases the risk of multiple morbidities, shortens lifespan, and diminishes quality of life. Hospitalization and periods of forced inactivity greatly accelerate this loss in older people.

“The data from this Phase 1b study provide clinical validation of BioAge’s AI-driven discovery platform and demonstrate the power of our human-first approach to identify medically relevant drug targets,” said Kristen Fortney, PhD, CEO and co-founder of BioAge. “Our analysis of BioAge’s human aging cohorts revealed that the apelin pathway is a strong predictor of healthy longevity and muscle function, and now this has translated directly into our clinical finding that apelin pathway activation with BGE-105 improves muscle physiology in older adults. Today’s announcement is a milestone in BioAge’s mission to create a pipeline of drugs that treat disease and extend healthy lifespan by targeting the mechanisms of aging.”

BioAge’s analysis of proprietary human biobanks showed that apelin pathway activity, which declines with age, is positively associated with longevity, mobility, and cognitive function. Apelin, the natural ligand of APJ, is secreted by skeletal muscle in response to exercise and regulates multiple aspects of muscle metabolism, growth, and repair. BGE-105 binds APJ and activates apelin signaling. In April 2021, BioAge entered into an exclusive worldwide license agreement with Amgen, Inc. to develop and commercialize BGE-105 for all indications.

Study design and results

The double-blind, placebo-controlled trial evaluated the safety and pharmacodynamics of BGE-105. Twenty-one volunteers underwent 10 days of bed rest while receiving infusions of BGE-105 or placebo.

Volunteers on placebo (n=10) exhibited muscle atrophy, reflected by statistically significant reductions in thigh circumference and ultrasound measurement of vastus lateralis muscle dimensions (cross sectional area and thickness) and muscle quality (fatty degeneration).

Treatment with BGE-105 (n=11) significantly ameliorated muscle atrophy relative to placebo:

Muscle dimensions: Volunteers receiving BGE-105 showed a 100% improvement in thigh circumference (p < 0.001) relative to placebo-treated volunteers, and ultrasound measurements showed a 58% improvement in vastus lateralis cross-sectional area (p < 0.05) and a 73% improvement in vastus lateralis thickness (p < 0.01).

Muscle quality: Ultrasound echo density measurements revealed that the Goutallier grade, an index that quantifies fatty degeneration in muscle, worsened in 8 of 10 volunteers on placebo vs. only 1 of 11 volunteers receiving BGE-105 (p < 0.005).

Muscle protein synthesis: Proteomic analysis of muscle microbiopsy samples revealed that bed rest decreased production of muscle proteins, and this effect was significantly ameliorated by BGE-105 (p < 0.005). The higher rate of muscle protein synthesis in the drug vs. placebo group provides a potential mechanistic basis for BGE-105’s protective effect on muscle dimensions.

The drug was well tolerated in the study, consistent with prior phase 1 trials conducted by Amgen showing that oral or intravenous BGE-105 was safe and well-tolerated in 198 subjects.

“Older men and women lose substantial muscle mass during periods of immobilization and bed rest, often with devastating consequences,” said William Evans, PhD, Adjunct Professor at UC-Berkeley and Duke University. “Based on the promising data from this Phase 1b study, BGE-105 should be investigated for the treatment of a wide range of age-related syndromes driven by loss of muscle, including acute myopathies in hospitalized patients as well as chronic medical conditions that are common among millions of older people but lack effective therapies, representing an enormous unmet clinical need.”

Plans for advancement to Phase 2

BioAge plans to proceed with a Phase 2 trial of BGE-105 to prevent adverse outcomes in older patients under mechanical ventilation in the intensive care unit (ICU). The study will assess the ability of BGE-105 to prevent two conditions: ICU diaphragmatic atrophy and critical illness myopathy, a broad weakening of the muscles due to disuse under prolonged bed rest. These conditions, which affect millions of patients every year, are both associated with poor clinical outcomes and substantially increased mortality. No effective treatments are currently available, representing a high unmet medical need. The Phase 2 trial is anticipated to begin in 2023. The company will also continue to develop the drug for chronic conditions related to muscle aging.

About BioAge Labs, Inc.

BioAge is a clinical-stage biotechnology company developing a pipeline of therapies to extend healthy lifespan by targeting the molecular causes of aging. BioAge uses its discovery platform, which combines quantitative analysis of proprietary longitudinal human samples with detailed health records, to map the key molecular pathways that impact healthy human aging. By targeting the mechanisms of aging with a large, mechanistically diverse portfolio of drugs, BioAge is unlocking opportunities to treat or prevent age-related disease in entirely new ways. BioAge has multiple programs targeting muscle, immune, and brain aging, including the clinical-stage apelin receptor agonist BGE-105 and a differentiated CNS-penetrant NLRP3 inhibitor. Investors include Andreessen Horowitz, Kaiser Foundation Hospitals, Caffeinated Capital, Khosla Ventures, and others.

Contacts

PR: Chris Patil, media@bioagelabs.com IR: Daniel Ferry, daniel@lifesciadvisors.com BD: Peng Leong, partnering@bioagelabs.com Web: https://bioagelabs.com

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Date Posted: December 2, 2022

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Rapamycin, not Dietary Restriction, Fights Infection in Mice

A meta-analysis published in GeroScience has shown that the well-studied drug rapamycin has positive effects on infection in mice, but dietary restriction seems to worsen the problem.

Aging, immunity, and interventions

This paper begins with the well-known information that aging impairs the immune system, harming its effectiveness against infectious diseases [1] while causing systemic inflammation (inflammaging) [2]. Interestingly, while both rapamycin and dietary restriction are thoroughly documented interventions against aging, high-dose rapamycin is used in clinical settings as an immunosuppressant [3], and there is prior evidence that dietary restriction impedes immune function against pathogens [4].

This line of research has been explored many times in the past. Therefore, these researchers performed a study of studies, a true meta-analysis, in order to determine whether dietary restriction and rapamycin are helpful or harmful against infection.

Counterintuitive results

While it is clear that not all of these studies agreed with each other, the researchers note that the standard Black 6 mouse and a standard 40% dietary restriction rate were common throughout. By thoroughly comparing these various studies, the researchers found that dietary restriction slightly but significantly increased the risk of pathogen infection, while rapamycin treatment significantly decreased it, particularly in secondary infections. There did not seem to be evidence of publication bias, and the type of pathogen did not seem to matter either. However, the researchers do note that the sex of the mice, a frequent confounding factor, was not reported enough to be used as part of the meta-analysis.

The researchers note several aspects of these findings. Caloric restriction has been previously reported to youthen the immune system, such as by protecting T-lymphocytes from oxidative damage [5]. However, it decreases leptin, which has been shown to reduce the effectiveness of natural killer cells [6]. Rapamycin, on the other hand, increases the population of T regulatory cells [7] and improves immune memory [8], which could explain its effectiveness against secondary infections.

Conclusion

This meta-analysis serves as a sharp reminder that while systemic immune overactivation is a key part of age-related diseases, underactivation has its own obvious problems as well. Treatments to fight inflammaging need to allow the immune system to perform its original, core function. Furthermore, while these studies were done on mice rather than people, practitioners of caloric restriction might also want to keep these results in mind.

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Literature

[1] Gavazzi, G., & Krause, K. H. (2002). Ageing and infection. The Lancet infectious diseases, 2(11), 659-666.

[2] Baylis, D., Bartlett, D. B., Patel, H. P., & Roberts, H. C. (2013). Understanding how we age: insights into inflammaging. Longevity & healthspan, 2(1), 1-8.

[3] Saunders, R. N., Metcalfe, M. S., & Nicholson, M. L. (2001). Rapamycin in transplantation: a review of the evidence. Kidney international, 59(1), 3-16.

[4] Speakman, J. R., & Mitchell, S. E. (2011). Caloric restriction. Molecular aspects of medicine, 32(3), 159-221.

[5] González, O. A., Tobia, C., Ebersole, J. L., & Novak, M. J. (2012). Caloric restriction and chronic inflammatory diseases. Oral diseases, 18(1), 16-31.

[6] Clinthorne, J. F., Adams, D. J., Fenton, J. I., Ritz, B. W., & Gardner, E. M. (2010). Short-term re-feeding of previously energy-restricted C57BL/6 male mice restores body weight and body fat and attenuates the decline in natural killer cell function after primary influenza infection. The Journal of nutrition, 140(8), 1495-1501.

[7] Canivet, C., Menasria, R., Rhéaume, C., Piret, J., & Boivin, G. (2015). Valacyclovir combined with artesunate or rapamycin improves the outcome of herpes simplex virus encephalitis in mice compared to antiviral therapy alone. Antiviral research, 123, 105-113.

[8] Keating, R., Hertz, T., Wehenkel, M., Harris, T. L., Edwards, B. A., McClaren, J. L., … & McGargill, M. A. (2013). The kinase mTOR modulates the antibody response to provide cross-protective immunity to lethal infection with influenza virus. Nature immunology, 14(12), 1266-1276.

Date Posted: December 2, 2022

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Polyphenols Help Reduce Visceral Fat

Pitching two variants of the Mediterranean diet against each other in a randomized controlled trial, scientists have found that the plant-oriented one, which contained more polyphenols, was more effective for weight loss [1].

Beyond the Med diet

A healthy diet is one of the most powerful anti-aging interventions available today, but the question of which diet is the healthiest is very much open, due to the sheer number of factors involved. The Mediterranean diet, rich in olive oil, vegetables, legumes, fish, and nuts, is probably the most evidence-based of all. Numerous epidemiological studies, and a handful of interventional studies, have linked the Mediterranean diet to various positive health outcomes, including decreased overall mortality along with a lower incidence of cardiovascular diseases and cancer [2].

Now, scientists want to dig deeper and understand which of the many ingredients of the Mediterranean diet make it healthy. In this new paper, the researchers used an interesting study design to elucidate the role of polyphenols, a class of phytochemicals known for their antioxidant and anti-inflammatory properties [3]. Polyphenols are abundant in berries, nuts, vegetables, tea, coffee, and many other plant products.

Double the polyphenols

This group has been studying polyphenols for years, and its previous studies have all linked polyphenols to better cardiometabolic outcomes. For this new randomized controlled trial called DIRECT-PLUS, 294 participants were divided into three groups. The control group ate according to Healthy Dietary Guidelines, while the two study groups were put on a generic Mediterranean diet (MED) and on a more plant-oriented Mediterranean diet (MED-green). Patients in all groups were also put on an identical physical activity regimen.

The two study groups were isocaloric (providing identical numbers of calories), but participants in the MED-green group also consumed 3-4 cups of green tea and one green shake with Wolffia globosa (a strain of duckweed also known as Mankai) a day. These alterations effectively doubled the amount of polyphenols (from 440 mg/day for MED to 800 mg/day for MED-green).

The participants’ mean age was 51 and their mean BMI was 31, indicating obesity. 36% were prediabetic, and another 11% were diabetic. The main endpoint of the trial was weight loss, but it was measured in a more sophisticated way than just putting people on a scale. Instead, MRI technology was used to quantify abdominal adipose tissues. Unfortunately, the trial was lopsided regarding sex, as 88% of the participants were male.

The best diet for the worst type of fat

Following the 18-month trial period, mean weight loss in the control group was negligible, despite patients being physically active. The two study groups, on the other hand, showed substantial weight loss. Although it was bigger in the MED-green group (3.9% vs 2.7% in the MED group), this difference did not reach statistical significance. Results for waist circumference were largely similar.

Importantly, the MED-green diet was proved to be much more effective in reducing the amount of visceral fat, which is considered more harmful than subcutaneous fat [4]. Here, the difference between the two MED diets was evident and statistically significant: the mean visceral fat reduction was 14% in the MED-green group and only 6% in the MED group.

Component analysis

The researchers went to great lengths to establish the effects of particular dietary components. According to their calculations, higher consumption of green tea, walnuts, and dietary fiber, as well as reduced red meat consumption, were all significantly associated with greater visceral fat loss when adjusted for age and sex. However, further adjustments for weight loss and reduction in waist circumference complicated the picture, with only increased dietary fiber consumption remaining statistically significant.

Withing the MED-green group, higher consumption of Mankai was significantly associated with greater visceral fat loss, improved cardiovascular outcomes, and better lipid profiles. Higher walnut consumption and lower red meat consumption seemed to help as well. Most importantly, higher plasma polyphenol levels were significantly associated with visceral fat loss in all models, showing a direct contribution by polyphenols.

Urolithin A is a compound produced by human endogenous bacteria from polyphenols. It is thought to possess health benefits and has been an increasingly popular supplement. Direct urolithin supplementation can overcome limitations of endogenous production such as variability in gut microbiota [5]. In this study, urine urolithin A levels showed a robust association with visceral fat reduction and were themselves associated with increased consumption of walnuts and Mankai.

Conclusion

The Mediterranean diet and polyphenols receive a lot of praise, but proper interventional studies are still rare. The results of this randomized controlled trial confirm the importance of polyphenol consumption and hint at “greener” variants of the Mediterranean diet being more effective for weight loss – especially when it comes to the dreaded visceral fat. Since many aspects of aging are sex-dependent, the disproportionate number of men in this study could have limited the generalizability of the results. On the other hand, visceral fat is thought to be more harmful in men [6].

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Literature

[1] Zelicha, H., Kloting, N., Kaplan, A., Yaskolka Meir, A., Rinott, E., Tsaban, G., … & Shai, I. (2022). The effect of high-polyphenol Mediterranean diet on visceral adiposity: the DIRECT PLUS randomized controlled trial. BMC medicine, 20(1), 1-11.

[2] Martinez-Gonzalez, M. A., & Martin-Calvo, N. (2016). Mediterranean diet and life expectancy; beyond olive oil, fruits and vegetables. Current opinion in clinical nutrition and metabolic care, 19(6), 401.

[3] Cory, H., Passarelli, S., Szeto, J., Tamez, M., & Mattei, J. (2018). The role of polyphenols in human health and food systems: A mini-review. Frontiers in nutrition, 5, 87.

[4] Stefan, N. (2020). Causes, consequences, and treatment of metabolically unhealthy fat distribution. The lancet Diabetes & endocrinology, 8(7), 616-627.

[5] Singh, A., D’Amico, D., Andreux, P. A., Dunngalvin, G., Kern, T., Blanco-Bose, W., … & Rinsch, C. (2022). Direct supplementation with Urolithin A overcomes limitations of dietary exposure and gut microbiome variability in healthy adults to achieve consistent levels across the population. European journal of clinical nutrition, 76(2), 297-308.

[6] Kouli, G. M., Panagiotakos, D. B., Kyrou, I., Georgousopoulou, E. N., Chrysohoou, C., Tsigos, C., … & Pitsavos, C. (2017). Visceral adiposity index and 10-year cardiovascular disease incidence: the ATTICA study. Nutrition, metabolism and cardiovascular diseases, 27(10), 881-889.

Date Posted: December 1, 2022

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De-Aging Movie Stars Won’t Solve Aging

In the fifth installment of the popular Indiana Jones franchise, Harrison Ford will reportedly be “de-aged” by means of computer graphics, presumably to make him kicking Nazi butt at least somewhat believable. A regular person would react to this piece of showbiz gossip with a chuckle and quickly scroll further down their feed. For a longevity enthusiast, however, this raises a bunch of important questions.

A blind eye to the problem

Aging is perhaps the biggest problem people are refusing to face. In a sense, facing death is easier: as the saying goes, you will not be there when it happens. Aging, on the other hand, is a slow decline accompanied by frailty, excruciating disease, and losing people who are dear to you. Fear of death can be alleviated by a belief in an afterlife, but aging is inescapable. Without a full suite of life-extending medical interventions, it will happen to you, just like it happened to Harrison Ford. The CGI-tweaked picture might gloss over the ugly truth, but it cannot change it.

Language also has filters that obfuscate the truth about aging. Take “healthy aging”, a term that has been gaining popularity despite being an oxymoron. Aging is an umbrella term that describes the loss of function that the human body experiences with the passage of time. How can loss of function be healthy? The idea of “healthy aging” makes people complacent by suggesting that if they just do this therapy or follow that diet, they will somehow be okay. Well, they won’t.

Nobody is as good at whitewashing aging as the advertising industry. It uses a full arsenal of visual and verbal tools to weave a soothing narrative where ever-happy, ever-active slightly wrinkled people are having a blast with their well-earned retirement. Death and suffering are nowhere to be seen – that is, if you buy the advertised product, be it a drug, an insurance policy, or a house in Florida.

Sometimes, instead of masking the truth about aging, filters can do the opposite: bring the perspective of your own aging right in your face. The impact of such manipulation can be seen in this YouTube video, where the two young hosts of the podcast The Wineholics discuss their pretty faces being artificially aged by filters (created by Lifespan.io filmmaker Tim Maupin). Their sheer horror reeks of ageism but is also perfectly understandable. One of the hosts says something quite profound: “I think we need to define aging as a problem. If aging were defined as a problem today, in 20 years, maybe we would totally demolish it. We need to do anything not to age.”

It’s time to look at what we’ve been avoiding

This is something that we at Lifespan.io, along with other longevity advocates, have been saying for years. The world must see aging for what it is: a problem, and a huge one too. Interestingly, no one seems to object to labeling the economic aspects of aging, such as the rising cost of healthcare, a problem. But if you say that aging is bad because it causes disability and suffering, you may be accused of disparaging old people.

Refusing to normalize aging is not the same as disparaging the elderly. People who are battling aging deserve all the support and compassion in the world. Their old age does not make them less worthy; it is just a human condition that every person inevitably develops. Saying that cancer is horrible does not degrade cancer patients. Cancer is age-related, so why would we pretend there is nothing wrong with aging? Yes, we must be sensible and avoid hurting people’s feelings, but we also must look facts in the eye. Solving a problem starts with admitting its existence.

There is still, of course, the immensity of the problem. Aging is an extremely complex phenomenon, even if it is driven by a handful of underlying processes, and the science of aging is in its infancy. Recognizing a problem that might not be solved in your lifetime takes courage. It is tempting to keep our eyes shut and roll this over to the next generation, but it would be the wrong thing to do.

Solving aging might sound hopeless to some people, but like the hosts of The Wineholics, I believe in human ingenuity and perseverance. Humans are extremely good at cooperating and solving complex problems, when they put their minds to something. This is what I have been trying to do in my capacity as a science journalist at Lifespan.io: sway hearts and minds by showing that slowing and eventually stopping aging is crucial, moral, and possible, and I will not hesitate to use any pretext to talk about it, including a piece of gossip about Harrison Ford.

By the way, the filters that will be applied to his face can be put to better use – showcasing the effects of future anti-aging therapies.

Yes I will donate❤️

Date Posted: December 1, 2022

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Rejuvenation Roundup November 2022

The giving season is upon us once more! This month, we focus on November’s research, industry news, and ways that you can help hasten the defeat of aging.

LEAF News

Lifespan.io Presents at MIRAI 2.0 R&I Week 2022: At MIRAI 2.0 Research and Innovation Week 2022, Larisa Sheloukhova joined Swedish and Japanese researchers in discussing future-focused innovations related to aging.

Raising Awareness that Aging is a Problem Worth Solving: There has been plenty going on here at Lifespan.io, so we thought it was time to give you a little update on what’s been happening.

Lifespan News

Ground Coffee for Longevity: On this episode of Lifespan News, Ryan O’Shea discusses a new longitudinal study showing that drinking a few cups of coffee a day is associated with longer lifespans in human beings.

Olive Oil for Longevity: Olive oil is a popular diet component for people who seek to live longer. Olive oil is widely considered to be healthier than most other oils and fats, and for good reason, but some of its health benefits are exaggerated.

NMN and the FDA: On this episode of Lifespan News, Ryan O’Shea talks about a controversial decision by the Food and Drug Administration to restrict the sale of NMN as a supplement. NMN is popular among longevity enthusiasts and biohackers who take it for its potential, but as yet unproven, longevity benefits.

Exercise, Cancer, and Rapamycin: We discuss a new study revealing the effects of exercise on cancer and how rapamycin might actually reduce this benefit. Physical activity provides many health benefits, and it can even lower the risk of developing cancer. Now, scientists may have additional evidence of another benefit.

Interviews

Lou Hawthorne, NaNotics on Cleaning Blood with Nanoparticles: Lou Hawthorne is the founder and CEO of NaNotics, a biotech company that creates nanoparticles that can soak up harmful molecules in circulation. This paradigm-shifting technology can be used to fight cancer as well as various inflammatory disorders, such as sepsis, which kills more people than cancer does.

Dr. Matt Kaeberlein on WormBot and the Dog Aging Project: Dr. Matt Kaeberlein is a heavy hitter in the longevity field. While his name has become associated with the Dog Aging Project that he started a few years ago, his research interests span much wider.

Rejuvenation Roundup Podcast

Ryan O’Shea of Future Grind hosts this month’s podcast, showcasing the events and research discussed here.

Journal Club

Rapamycin extends life span & health span in mice & Daphnia: The Journal Club returned on our Facebook channel. Dr. Medvedik took a look at the recent paper entitled “Rapamycin treatment during development extends life span and health span of male mice and Daphnia magna”.

Advocacy and Analysis

New Initiative for a More Longevity-Friendly World: Quantum Healthy Longevity Innovation Mission is a new UK-based initiative touting a multi-pronged approach to push for longer lifespans and healthspans for everyone.

We Can Think of Worse Curses, Elon Musk: Two days ago, famous billionaire and new Twitter owner Elon Musk Tweeted that he cannot think of a worse curse than living forever, in reply to a Tweet relating to the predicted heat death of the universe.

Making Good Financial Decisions for Longevity: In a preprint published in Social Science Research Network, researchers have shown that it might be possible to protect people from making poor financial decisions earlier in life by providing them objective longevity information.

Research Roundup

Cellular Reprogramming Extends Lifespan, Healthspan in Mice: Scientists have shown that continuous low-dose induction of reprogramming factors and a single early life reprogramming treatment both significantly increase lifespan and healthspan in progeroid mice while altering their epigenetic landscape.

Klotho Reduces Arterial Calcification Through Autophagy: In a new study published in Oxidative Medicine and Cellular Longevity, the researchers have shown that klotho ameliorates vascular calcification via increased autophagy. Vascular calcification, the deposition of minerals in the cardiovascular system, is a complex pathological process that accompanies aging.

Protecting Memory Through Gut Bacteria: Researchers publishing in Nutrients have shown that adding a strain of lactic acid bacteria to the gut flora of older, memory-impaired people partially alleviates their memory problems.

Gene Therapy to Delay Reproductive Senescence: A team of Spanish researchers publishing in Aging have reported that they can delay reproductive senescence in female rats by stimulating the production of insulin growth factor 1 (IGF-1) through gene therapy.

Extracellular Vesicles from Young Stem Cells Rejuvenate Mice: Scientists have shown that injection of extracellular vesicles secreted by young adipose-derived stem cells increases fitness and promotes tissue rejuvenation in aged mice.

Astaxanthin Improves Endurance in Older Adults: In a new study published in International Journal of Environmental Research and Public Health, Japanese researchers have shown that astaxanthin supplementation improves endurance in healthy older adults.

Harnessing Senescent Cancer Cells to Fight Cancer: New research published in Cancer Discovery has outlined a potential new method of using senescent cells to encourage the immune system to attack cancer.

Correlation Between Cognitive Decline and Epigenetic Clocks: Researchers publishing in Aging have found a correlation between cognitive decline and measurements of epigenetic aging. An epigenetic clock is a biochemical test that uses DNA methylation levels and accumulation of methyl groups on DNA to determine biological age.

Protein Intake Increases Bone Density in Older Adults: Scientists have found that animal protein consumption positively correlates with bone density in older adults. Things become more complicated regarding plant protein.

The Effects of Niacin on Alzheimer’s in Mice: A study published in the Annals of Translational Medicine has shown the effects of niacin supplementation on a mouse model of Alzheimer’s and outlined the genes involved.

Arginase Inhibitor Improves “Leaky Gut” in Old Mice: According to a new study, the age-related increase in intestinal permeability that drives inflammation can be alleviated by inhibiting the enzyme arginase, a regulator of nitric oxide production.

Protein Content in an Optimal Diet: In a new study published in Nature Communications, researchers have designed guidelines for dietary amino acid consumption for optimal health.

Muscle Strength Associated with Oral Health: Researchers publishing in The Lancet have found a relationship between poor oral health and weaker muscles in people who are at least 70 years old.

Nicotinamide Riboside May Make Existing Cancer Worse: A paper published in the journal Biosensors and Bioelectronics has caused a stir in the longevity community by showing that nicotinamide riboside (NR), a precursor to NAD+, makes tumors more aggressive in a mouse model.

Exercise Might Protect from Metastatic Cancer: In a new study published in the journal Cancer Research, Israeli scientists have found that by increasing the metabolic activity of healthy cells, exercise likely pitches them against cancer cells in a battle for nutrients, which slows cancer progression.

Rapamycin Improves the Viability of Egg Cells: Researchers publishing in Aging have found that rapamycin, a molecule thoroughly researched for its effects on metabolism, improves the viability of egg cells (oocytes) grown in vitro. Decreased fertility in women occurs much more rapidly than other aspects of aging.

Air Pollution Harms Immune Function in Lungs: A new study published in Nature Medicine suggests that lifelong exposure to tiny airborne particles leads to their accumulation in lymph nodes in the lungs and to impaired immune function. With age, people become more susceptible to many diseases, with the lungs being one of the most affected organs.

How much resistance exercise is beneficial for healthy aging and longevity?: Although these analyses demonstrated an overall inverse association between resistance exercise and mortality risk from all causes and/or from cardiovascular diseases, diabetes, and cancers, this was only true up to a certain threshold.

Effects of nicotinamide mononucleotide on older patients with diabetes and impaired physical performance: A prospective, placebo-controlled, double-blind study: In older male patients with diabetes and impaired physical performance, NMN supplementation for 24 weeks was safe, but did not improve grip strength and walking speed.

Genistein effect on cognition in prodromal Alzheimer’s disease patients. The GENIAL clinical trial: This study shows that genistein may have a role in therapeutics to delay the onset of Alzheimer’s dementia in patients with prodromal Alzheimer’s disease.

Bioactive Yoghurt Containing Curcumin and Chlorogenic Acid Reduces Inflammation in Postmenopausal Women: Bioactive yoghurt fortified with curcumin and chlorogenic acid has the potential to reduce inflammatory mediators; however, a larger and longer-term study is required to confirm these findings.

Impact of probiotics on muscle mass, muscle strength and lean mass: a systematic review and meta-analysis of randomized controlled trials: Probiotic supplementation enhances both muscle mass and global muscle strength; however, no beneficial effects were observed in total lean mass.

Rapamycin not dietary restriction improves resilience against pathogens: a meta-analysis: Rapamycin treatment significantly increased post-infection survival rate, while dietary restriction reduced post-infection survival. These results show that immunomodulation caused by rapamycin treatment is beneficial to survival from acute infection.

Comparative Effects of Low-Dose Rosuvastatin, Placebo and Dietary Supplements on Lipids and Inflammatory Biomarkers: Among individuals with increased 10-year risk for atherosclerotic cardiovascular disease, rosuvastatin 5 mg daily lowered harmful cholesterol significantly more than placebo, fish oil, cinnamon, garlic, turmeric, plant sterols, and red yeast rice.

Positive social factors prospectively predict younger epigenetic age: Findings from the Health and Retirement Study: Perceived support from and contact with close others, particularly friends, may have implications for healthy biological aging. Notably, the effect sizes for friends were comparable to the effect of body mass index on epigenetic age.

In vivo partial reprogramming by bacteria promotes adult liver organ growth without fibrosis and tumorigenesis: Mycobacterium leprae infection of adult nine-banded armadillos promotes in vivo liver growth. Enlarged infected livers are functionally and architecturally normal without tumors, partial reprogramming to progenitor/regeneration state drives liver growth, and bypassing of normal liver growth restriction offers safer repair interventions.

Autologous NK cells propagated and activated ex vivo decrease senescence markers in human PBMCs: Activated NK cells decrease senescent cells in vitro and immunosenescence in humans based on the biomarkers p16 and β-galactosidase.

Glutaminase inhibitors rejuvenate human skin via clearance of senescent cells: a study using a mouse/human chimeric model: Selective removal of senescent dermal fibroblasts can improve the skin aging phenotype, indicating that the glutaminase inhibitor BPTES may be an effective novel therapeutic agent for skin aging.

Unsupervised learning of aging principles from longitudinal data: The AI-developed dynamic frailty indicator changed along with hallmarks of aging, including frailty index, molecular markers of inflammation, senescent cell accumulation, and responded to life-shortening (high-fat diet) and life-extending (rapamycin) treatments.

Deep phenotyping and lifetime trajectories reveal limited effects of longevity regulators on the aging process in C57BL/6J mice: Many putative anti-aging interventions influence phenotypes long before the onset of detectable age-dependent change but, importantly, do not alter the rate of phenotypic change. Hence, they have limited effects on aging.

Is life expectancy higher in countries and territories with publicly funded health care? Global analysis of health care access and the social determinants of health: These findings demonstrate how, if made widely available, publicly funded health care could extend longevity of life. If combined with programs to reduce the burden of social determinants, a substantial impact can be made to promote more equitable distribution of life expectancies across the world.

Aging, Equality and the Human Healthspan: The author responds to a previous paper, stating that an intervention that slows down the rate of molecular and cellular decline from the inborn aging process will likely be one of the most important public health advancements of the twenty-first century.

Cellular enlargement – A new hallmark of aging?: Taken together, the researchers found mounting evidence linking cellular enlargement to aging and age-related diseases. Therefore, they encourage researchers from seemingly unrelated areas to take a fresh look at their data from the perspective of cell size.

News Nuggets

The Quantum Healthy Longevity Innovation Mission Launches: The National Innovation Centre for Ageing and Collider Health launch the Quantum Healthy Longevity Innovation Mission with a keynote by Lord Bethell, former Parliamentary Under Secretary of State for Technology, Innovation and Life Sciences, to shift ‘sickcare’ to a new model based on proactive prevention.

Longevity Biotech Fellowship Announces Launch: On Deck Longevity Biotech and the founders of LessDeath.org have collaborated to start the Longevity Biotech Fellowship, a new initiative focusing on bringing upcoming professionals into the longevity industry.

FDA Purges NMN From the List of Supplements: Reversing its own earlier decision, the FDA has informed an NMN manufacturer that the molecule can no longer be marketed as part of dietary supplements. Another company that is testing NMN as a drug probably contributed to the decision, which is not being enforced as of now.

Yes I will donate❤️

Date Posted: November 30, 2022

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Making Good Financial Decisions for Longevity

In a preprint published in Social Science Research Network, researchers have shown that it might be possible to protect people from making poor financial decisions earlier in life by providing them objective longevity information [1].

Do you save up?

It is now well-accepted that income positively correlates with life expectancy. Indeed, poverty is a strong risk factor for all-cause mortality. Moreover, the rich enjoy up to a decade of more disability-free life compared to the poor [2].

In many cases, however, it is not simply about earnings but in how well these earnings are allocated. Saving up a percentage of monthly income can make a big difference later in life.

According to a study published in 2018, approximately 60% of older adults regret not having saved more during their working years [3]. There could be many reasons why people choose not to save money, including poor judgement about their expected longevity.

In this study, the researchers explored if accurate information about individual survival probabilities increases regret for undersaving earlier in life and, therefore, potentially prevents poor financial decision making.

If not, you’ll regret it

The researchers conducted a survey among 1,764 American adults over the age of 50 (average age of 72.5), asking them if they experience regret regarding the financial decisions they had made when they were younger. Around 60% of the participants were female, and three-quarters considered themselves to be in good health.

The participants were divided into three groups. The T1 group was asked about subjective survival probabilities prior to the regret questions. The T2 group was also asked to estimate how much longer they expect to live, but they were provided additional objective information about longevity for their age group prior to the regret-related questions. The control group answered the regret-related questions only.

Apart from asking the participants “Do you think that what you saved was too little, about right, or too much?”, the researchers also included questions about long-term care insurance and about longevity insurance. This is a form of ‘reverse’ life insurance that is steadily paid out during older ages instead of to beneficiaries at death.

Participants who had not purchased any such insurance were asked if they would have done it given another chance. In addition, the participants were asked if they regret being financially dependent on someone else and if they regret quitting work too soon.

The results showed that about 60% of respondents regretted not having saved more, 40% regretted not having bought long-term care insurance, about 40% regretted not working longer, and 10% regretted being financially dependent on others.

Interestingly, better educated and healthier participants regretted less about undersaving and having stopped working too early. Somewhat unsurprisingly, wealthier people were less likely to regret not having saved enough and not having purchased long-term care insurance.

Know your longevity probabilities

Finally, the researchers show that providing objective longevity information increases the participants’ financial regret. In other words, when people are given probabilities about how much longer they are likely to live, they consider saving more money, buying insurance that makes sense for such a long lifespan, and making decisions to protect themselves against financial problems throughout their lives.

On the other hand, no difference in terms of financial regret was shown between the control group and the T1 group. Therefore, it is not enough to ask people about their subjective survival probabilities. Instead, it is important to inform members of the public what their chances are to survive at older ages.

Abstract

Older people often express regret about financial decisions made earlier in life that left them susceptible to old-age insecurity. Prior work has explored one outcome, saving regret, or peoples’ expressed wish that they had saved more earlier in life. The present paper extends attention to five additional areas regarding financial decisions, examining whether older Americans also regret not having insured better, claimed benefits and quit working too early, and becoming financially dependent on others. Using a controlled randomized experiment conducted on 1,764 respondents age 50+ in the Health and Retirement Study, we show that providing people objective longevity information does alter their self-reported financial regret. Specifically, giving people information about objective survival probabilities more than doubled regret expressed about not having purchased long term care, and it also boosted their regret by 2.4 times for not having purchased lifetime income. We conclude that information provision can be a potent, as well as cost-effective, method of alerting people to retirement risk.

Conclusion

This study demonstrates that inaccurate perception of individual longevity prospects seems to be a major reason why older people end up with financial regrets. It is thus of paramount importance that members of the general public consider their own longevity to help them avoid making financial mistakes earlier in life and secure lifelong financial stability. This only becomes more true in a world with considerably longer lifespans.

Yes I will donate❤️

Literature

[1] Hurwitz, A. & Mitchell, O. S. Financial Regret at Older Ages and Longevity Awareness. (2022) doi:10.2139/ssrn.4283158

[2] Zaninotto, P. et al. Socioeconomic Inequalities in Disability-free Life Expectancy in Older People from England and the United States: A Cross-national Population-Based Study. J. Gerontol. A Biol. Sci. Med. Sci. 75, 906–913 (2020)

[3] Börsch-Supan, A. H., Bucher-Koenen, T., Hurd, M. D. & Rohwedder, S. Saving Regret. (2018) doi:10.3386/w25238

Date Posted: November 29, 2022

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Air Pollution Harms Immune Function in Lungs

A new study published in Nature Medicine suggests that lifelong exposure to tiny airborne particles leads to their accumulation in lymph nodes in the lungs and to impaired immune function [1].

Age-related lung diseases and pollution

With age, people become more susceptible to many diseases, with the lungs being one of the most affected organs. Lung cancer is highly age-related, and prognoses are worse in older people [2]. As we know from the COVID-19 and the annual flu epidemics, infectious diseases that attack lungs also become much deadlier with age [3]. Could it be that lifelong exposure to air pollution contributes to pulmonary decline?

In this new study, the researchers were able to put this hypothesis to the test using actual human lymph nodes obtained from 84 organ donors aged 11 to 93 with no history of smoking. Lymph nodes house immune cells and are at the center of the immune response that is supposed to protect against both cancer and infections.

Particles accumulate in macrophages

The first thing the researchers noticed was that lung lymph nodes were often black in color, contrary to intestinal lymph nodes. The prevalence of black lung lymph nodes was much higher in older donors, matching the color of the most ubiquitous air pollutants from burning fuels. Microscopy images confirmed the accumulation of particulate matter with age, especially past the age of 40, in lung lymph nodes but not in intestinal lymph nodes.

Lymph nodes are complex structures that contain immune cells of various types. The researchers hypothesized that particulates are mainly found within innate immune cells that can engulf foreign pathogens in a process called phagocytosis. In lymph nodes, those are mostly macrophages and dendritic cells. As expected, particulate matter was found almost exclusively in a subset of cells called CD68+CD169- macrophages. Those cells are the most active scavengers of dying and dead cells and other debris.

Decreased phagocytosis

The researchers then went on to determine if particle accumulation actually affects macrophage function. Controlling for other variables, such as age, they found that key activation and phagocytosis markers decrease with age specifically in CD68+CD169− macrophages in lung lymph nodes but not in intestinal lymph nodes.

To further investigate this loss of function, the researchers assessed the actual effects of carbon particulates that they had isolated from urban environmental sources on human macrophages in vitro. The cells readily devoured the black particles, but this hampered their phagocytic abilities compared to particle-free controls.

Interestingly, particle accumulation did not affect the proliferation of the macrophages, but aging did. The researchers suggest that with age, the proliferation, and hence the turnover, of macrophages slows down. Cells spend more time in the lymph nodes before being replaced with new cells, which leads to more particle accumulation.

Altered cytokine production

In addition to engulfing pathogens, macrophages also secrete cytokines that modulate the immune response. By staining lymph nodes with antibodies, the researchers found that black particulates significantly decrease the production of the antiviral cytokine IFN-α and of the pro-inflammatory cytokines TNF-α and IL-6, indicating loss of function.

Accumulation of particles also affected the complex architecture of lymph nodes. Follicles that contain B cells became more dispersed, and the number of lymphatic vessels declined with age in the areas affected by particle accumulation. In contrast, no such structural changes were observed in intestinal lymph nodes, which apparently do not suffer from accumulation of airborne particles.

In conclusion, our results provide direct evidence that the environment can have cumulative and adverse effects on our immune system with age. We show how environmental pollutants specifically target immune cells within lymphoid organs, which carry out essential immune surveillance functions. These findings can inform how we monitor and study our immune system—in health and disease and with age.

Conclusion

Air pollution has been linked to various health problems [4], but the underlying mechanisms are still being investigated. In this study, the researchers were able to use actual human organs to lend some support to the idea that air pollution contributes to age-related decline in immune response that disproportionately affects lungs.

Yes I will donate❤️

Literature

[1] Ural, B. B., Caron, D. P., Dogra, P., Wells, S. B., Szabo, P. A., Granot, T., … & Farber, D. L. (2022). Inhaled particulate accumulation with age impairs immune function and architecture in human lung lymph nodes. Nature Medicine, 1-11.

[2] Tas, F., Ciftci, R., Kilic, L., & Karabulut, S. (2013). Age is a prognostic factor affecting survival in lung cancer patients. Oncology letters, 6(5), 1507-1513.

[3] Meiners, S., Eickelberg, O., & Königshoff, M. (2015). Hallmarks of the ageing lung. European Respiratory Journal, 45(3), 807-827.

[4] Brunekreef, B., & Holgate, S. T. (2002). Air pollution and health. The lancet, 360(9341), 1233-1242.

Date Posted: November 29, 2022

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Raising Awareness that Aging is a Problem Worth Solving

There has been plenty going on here at Lifespan.io, so we thought it was time to give you a little update on what’s been happening.

Meet us at the Longevity Summit 2022

The Longevity Summit 2022 is happening on December 6-7 at the Buck Institute for Research on Aging, and Lifespan.io is an official media partner! As a special bonus to our readers, you can purchase tickets here with a 15% discount using the code LifespanIO.

Our Executive Director Stephanie Dainow will be hosting a discussion panel during the event. If you are at the conference, please do come and say hello, as we are always interested in meeting people in the industry and exploring ways to collaborate.

New SENS Research and Life Noggin videos about aging

We have joined forces with the SENS Research Foundation recently to produce a video series about the causes of aging on our popular Youtube channel, Life Noggin.

Our Life Noggin channel uses a pop-sci style to explain science and technology, in a fun and engaging way. With an audience of 3.26 million subscribers, it allows us to engage the wider science community about all the amazing research on aging happening in the lab right now. This is just one example of how we are helping to build a strong community that supports research towards longer, healthier lives.

According to the SENS model of aging, there are seven sources of damage that make us age. We are making a video for each of these and, more importantly, how we might fix that damage. Right now, the mitochondrial dysfunction (MitoSENS), senescent cells (ApoptoSENS), and cellular waste (LysoSENS) episodes are ready for you to enjoy.

We would like to thank the SENS Research Foundation for sponsoring this video series. If you are interested in sponsoring your own video on Life Noggin, please feel free to get in touch with us.

Learn about how we are working to solve aging

One of the things people don’t always realize is just how much we do. We are best known for our news coverage of the aging research and rejuvenation field, but there is a lot more to our organization than that!

We publish news stories, run research crowdfunding campaigns, host an annual conference, produce free educational articles, and create edutainment videos to engage policymakers and the general public.

If you are curious about what exactly Lifespan.io does, we have been busy updating our website to explain that. Check out our new “What we do” page to find out about all the things we are doing to help solve aging.

The Rejuvenation Roadmap gets a new lease of life

As part of our commitment to education we operate a curated database called the Rejuvenation Roadmap. This visual resource tracks some of the most important aging interventions and technologies being developed in the field.

We are aware that the Roadmap is not as comprehensive as we would like, and so we are delighted to announce that staff member and researcher Stephen Christopher Rose is stepping up to take on the role of curator.

He started his masters work in Bioengineering at Harvard University in 2013 and he is currently completing his PhD at SUNY Polytechnic University in Albany, NY. His dissertation is focused on the role of the senescent cell burden in the development of fibrotic disease.

The Roadmap will be seeing more regular updates and new companies will be added, so keep an eye out for them.

Lifespan.io speaks to students at Virginia Commonwealth University

On November 2, Lifespan.io’s Ryan O’Shea spoke with Virginia Commonwealth University PhD and pre-med students about the work of Lifespan.io and the importance of messaging, public outreach, and novel approaches to funding and innovation in our quest to overcome human biological aging. The students were primarily from the laboratory of Dr. Alaattin Kaya, who has previous experience at the laboratory of Dr. Vadim Gladyshev at Harvard Medical School.

Dr. Kaya’s course syllabus features content from Lifespan.io, and the students are working with the Lifespan.io team to help collectively determine how advocacy organizations can best serve the needs of students, scientists, and the general public.

This is one of numerous examples of the types of direct outreach that Lifespan.io engages in. If you have a group that would benefit from hearing from a Lifespan.io representative, please reach out and let us know!

We won the 2022 Greatnonprofits badge

For the fourth year in a row we have been awarded a Greatnonprofits badge for 2022. This marks us as a non-profit organization of merit and it’s thanks to the community who support us.

Life Extension Advocacy Foundation Inc Nonprofit Overview and Reviews on GreatNonprofits

Volunteer. Donate. Review.

From all of us here at Lifespan.io, thank you to everyone who has left us a review and for telling the world why our work is so important.

All of our content is 100% free for everyone to enjoy, but it does mean that we rely on the help of people like you. Every contribution really helps, no matter if it’s big or small. You can also support us by making a monthly or one-off donation or in other ways at no cost to you.

Date Posted: November 28, 2022

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Rapamycin Improves the Viability of Egg Cells

Researchers publishing in Aging have found that rapamycin, a molecule thoroughly researched for its effects on metabolism, improves the viability of egg cells (oocytes) grown in vitro.

Another approach towards a known problem

Decreased fertility in women occurs much more rapidly than other aspects of aging, and advanced maternal age has a substantial impact on pregnancy outcomes [1]. Researchers have previously approached this problem over multiple promising angles, including NAD+ and fibrosis, finding that oxidative stress and mitochondrial dysfunction are significant contributors.

These researchers have previously examined the effects of rapamycin on egg cells taken from mice, finding that it reduces reactive oxygen species (ROS) and protects against DNA damage [2]. This study builds on that work, using oocytes from aged mice and from women over the age of 35.

Effects on maturation, activity, and DNA protection

Taking oocytes from 40- to 48-week-old mice and cultivating them in vitro, the researchers found that 86% of the rapamycin-treated group matured, while only 75% of the control group matured. After a parthenogenic activation treatment, a form of simulated fertilization, more eggs in the rapamycin group showed signs of activation (54% to 41%) and cellular division (48% to 33%).

Similar positive effects were shown on chromosomal abnormalities. Roughly 39% of the control group had misaligned chromosomes, while only 20% of the rapamycin group did. Effects on chromosomal spindles and mitochondrial membranes seemed positive but were not statistically significant.

However, the effects on ROS and DNA damage were substantial and visible. Fluorescence from ROS was 14 in the rapamycin group and 49 in the control group In the control group, the relative fluorescence of the DNA damage marker γ-H2AX was roughly 2.5 times that of the rapamycin group.

Fertilized human oocytes benefit as well

Finally, the researchers examined a total of 131 oocytes taken from human women who had volunteered for in vitro fertilization. 64 of these oocytes were in the control group, and 67 were in the rapamycin group. While the rapamycin group showed greater maturation and germinal vesicle formation, due to the relatively low sample size, these positive results did not reach the level of statistical significance.

However, fertilized oocytes did benefit in a specific and important way. Comparing 39 fertilized eggs from the control group and 34 from the rapamycin group, they found that the rates of normal fertilization were no different, but the number of high-quality embryos was substantially different: the rapamycin group had 12, while the control group had only 5. These are the embryos that are most likely to survive through development and childbirth.

Conclusion

The researchers note that these results are positive, but not as positive as they might have liked. Rapamycin was shown to ameliorate many problems with chromosomes and genetic damage. However, it appears to be unable to help cells repair double-stranded DNA breaks, which are more common in oocytes derived from women over 35, and the researchers believe that this may have affected the results.

A combination treatment of NAD+ boosters, rapamycin or rapalogs, and additional compounds that enhance DNA repair may be the near-future path forward for improving the success rates of in vitro fertilization. More research in this area is clearly needed.

Yes I will donate❤️

Literature

[1] Attali, E., & Yogev, Y. (2021). The impact of advanced maternal age on pregnancy outcome. Best Practice & Research Clinical Obstetrics & Gynaecology, 70, 2-9.

[2] Yang, Q., Xi, Q., Wang, M., Long, R., Hu, J., Li, Z., … & Jin, L. (2022). Rapamycin improves the quality and developmental competence of mice oocytes by promoting DNA damage repair during in vitro maturation. Reproductive Biology and Endocrinology, 20(1), 1-11.

Date Posted: November 25, 2022

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Exercise Might Protect from Metastatic Cancer

In a new study published in the journal Cancer Research, Israeli scientists have found that by increasing the metabolic activity of healthy cells, exercise likely pitches them against cancer cells in a battle for nutrients, which slows cancer progression [1].

Higher metabolic activity

Physical activity provides many health benefits, and it can even lower the risk of developing cancer [2]. However, the mechanisms responsible for this are largely unknown. These scientists proposed an intriguing hypothesis: that in physically active people, tissues and organs compete with cancer cells for nutrients, leading to slower cancer progression.

First, the researchers studied exercise-associated changes in mice. In physically active mice, significant upregulation of energy metabolism (carbohydrate metabolism, glycolysis, oxidative phosphorylation, and mitochondrial biogenesis) was observed in all tissues examined. However, blood glucose levels did not differ before and after exercise, suggesting that the metabolic alterations were caused by changes in the organs themselves. Measurements on individual cells showed highly elevated glycolysis and more active mitochondria in cells taken from active mice. These results are in line with what we already know about the effects of exercise [3].

Less metastatic cancer in humans and mice

The researchers then examined a cohort of 2,734 people from the Israeli National Cancer Registry. Physical activity was assessed at baseline via a questionnaire, and the follow-up period was an impressive 20 years. A statistical analysis showed no significant difference in the incidence of non-metastatic cancer, but there was a major difference in cancers that reached the highly metastatic stage (SEER 7). High-intensity exercise seemed to lead to an especially hefty risk reduction: 73% less metastatic cancer.

Next, the researchers created a mouse cancer model based on melanoma, which is prone to metastasizing to distant organs and lymph nodes. The active group was subjected to 8 weeks of intensive treadmill activity prior to subcutaneous inoculation with melanoma cells. After some time, the primary tumors were excised, and, following a period of recovery, physical activity in the study group resumed. In the end of the experiment, metastasis was assessed.

The number of melanoma cells was significantly reduced in the lungs and liver of the active group compared to controls, and there was the same downward trend, though not statistically significant, in lymph nodes; the sample sizes in this experiment were small, which affected statistical power. Moreover, exercise also seemed to decrease the size of the primary tumors.

Because this reduction in primary tumor size could have affected the intensity of metastasis, the researchers ran another experiment, forgoing primary tumor formation and instead directly injecting cancer cells into circulation. In yet another experiment, the study group exercised only prior to, but not after, the inoculation. In all the experiments, the spread of cancer in the study group was significantly reduced compared to controls. According to the researchers, these results show that exercise dampens future metastasis by priming organs and tissues even prior to the emergence of cancer.

Wrestling nutrients from cancer

Switching to in vitro, the researchers co-cultured cells taken from active and inactive mice with melanoma cells. In the presence of exercise-primed cells, melanoma cells seemed to fare far worse, with either decreased proliferation (when co-cultured with lung cells) or increased apoptosis (when co-cultured with liver and lymph node cells).

Because previous results suggested that increased metabolic activity causes more stiff competition and ultimately affects cancer progression, the researchers ran another interesting experiment: they treated cells taken from active mice with rapamycin, which reduces metabolic activity by blocking mTOR. Indeed, treating healthy cells with rapamycin increased the proliferation and survival of the neighboring melanoma cells.

While this last result is intriguing, rapamycin is currently the most effective drug for lifespan extension in mice [4]. Considering that mice die mostly of cancer, it seems that rapamycin’s effects on cancer risk are positive overall. However, the specific connection uncovered by the researchers deserves a closer look.

By analyzing gene expression in melanoma cells on various cancer stages, the researchers found that in metastatic melanoma, metabolic pathways were greatly enriched compared to primary tumors. This might explain why exercise seems to work better in preventing metastasis than the first appearance of cancer: the higher the metabolic demands of cancer cells, the more they are vulnerable to competition from nutrient-hungry exercise-primed cells.

Finally, the researchers showed that cells taken from melanoma metastases in exercising mice were less metabolically active than those from sedentary controls. This also seems to support the “competition hypothesis”: higher metabolic demands of healthy cells leave fewer nutrients for cancer to chow on.

Conclusion

This study lends initial support to a hypothesis that exercise-related changes in healthy cells make life harder for cancer (especially metastatic cancer) by increasing competition for nutrients. Considering that metastatic cancer is mostly incurable with current treatments, any advancements in this field are most welcome and warrant more extensive studies.

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Literature

[1] Sheinboim, D., Parikh, S., Manich, P., Markus, I., Dahan, S., Parikh, R., … & Levy, C. (2022). An exercise-induced metabolic shield in distant organs blocks cancer progression and metastatic dissemination. Cancer Research, 82(22), 4164-4178.

[2] Minihan, A. K., Patel, A. V., Flanders, W. D., Sauer, A. G., Jemal, A., & Islami, F. (2021). Proportion of Cancer Cases Attributable to Physical Inactivity by US State, 2013-2016. Medicine and Science in Sports and Exercise.

[3] Moghetti, P., Bacchi, E., Brangani, C., Donà, S., & Negri, C. (2016). Metabolic effects of exercise. Sports Endocrinology, 47, 44-57.

[4] Miller, R. A., Harrison, D. E., Astle, C. M., Baur, J. A., Boyd, A. R., De Cabo, R., … & Strong, R. (2011). Rapamycin, but not resveratrol or simvastatin, extends life span of genetically heterogeneous mice. The Journals of Gerontology: Series A, 66(2), 191-201.

Date Posted: November 24, 2022

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Lifespan.io Presents at MIRAI 2.0 R&I Week 2022

At MIRAI 2.0 Research and Innovation Week 2022, I joined Swedish and Japanese researchers in discussing future-focused innovations related to aging.

What does the future hold?

If you want to talk about the future in Japanese, there are two words to choose from: shorai (将来) and mirai (未来). The former describes a more tangible future that’s just about to come. The latter, on the other hand, denotes a mysterious future that’s far ahead and can be as fantastic as your imagination allows.

Therefore, it’s easy to guess that MIRAI 2.0, a collaboration between Japanese and Swedish universities, is an endeavor to facilitate innovation and entrepreneurship towards a bright and shiny future. Innovators from the two countries gather together every year to form research partnerships.

This year, the conference brought together researchers, entrepreneurs, and government officials to discuss “sustainable transformation towards a better world”. One of the sessions was exclusively dedicated to aging, with scientists and policymakers sharing their insights about challenges brought on by an aging society.

As I was sitting in the audience waiting for my turn to present Lifespan.io’s activities in crowdfunding and popularizing aging research, I couldn’t stop thinking about one of the presenter’s questions: “Do you believe immortality is achievable in the future?” Not many people raised their hands to signal “yes”.

I was not among them, because I do not believe we can eradicate all causes of human mortality. Nevertheless, when the time came for me to present, I proudly announced that we at Lifespan.io do believe that the major killer of humanity will one day be eradicated. An aging-free future is what we are striving for.

Robots, AI, devices

The Aging Session started with an informative talk by Tomohiro Shibata about robots and assistive devices used in care facilities in Japan. There are several assistive technologies the members of Prof. Shibata’s lab are working on, including a robot to assist the elderly in putting on clothes.

Both caregivers and frail people could benefit from assistive devices, such as transfer aids that help a caregiver lift an immobile person. Despite such devices being introduced in care facilities country-wide, Prof. Shibata noted that human contact is of paramount importance and is unlikely to be replaced by robots.

The Japanese government also realizes that with almost 30% of its population over 65 years of age, Japan is facing major challenges. Therefore, the government supports the development of various robotic care devices.

Göran Eriksson and Lame M. Kenalemang presented their research on cosmetic apps developed by such companies as Olay, L’Oréal, and Neutrogena, which give skincare recommendations based on the user’s skin analysis using AI. Although this sounds promising, there is no way to know what data is used as input or how skin scores are calculated in these apps. Therefore, it wouldn’t hurt to be somewhat skeptical when you get the results of your selfie assessment.

Aging and exercise

Jennifer Frankel talked about the effect of physical exercise on the aging brain. Her group designed a HIIT program for older adults that showed effectiveness in increasing aerobic capacity, lowering blood pressure, and improving working memory. The results of the study are not published yet, but once it is, we intend to publish the details of a safe HIIT program that you could follow in your 60s and beyond.

Jimmy Falk presented his research on postural control in older adults. The ability to resist falling when confronted with a slippery or shaky surface varies and generally declines with age. A common strategy when walking on an icy road is stiffening the leg muscles.

However, the more older adults stiffen their ankles in response to a surface perturbation (e.g. a sudden movement on a train), the higher the risk of a fall. This is explained by poorer leg muscle strength and is more common among older females than males. Therefore, one strategy to prevent falls is to combine leg strength and balance exercises.

Miki Tachiyama talked about her research on the psychological effects of various physical exercise programs for active older adults. Her group introduced a “GrandCheer” exercise routine for senior Japanese females that entails a cheerleader-like dance, including pom-pom routines. Compared to strength training, yoga, and ballet, GrandCheer, along with hula dancing and Zumba, improved the psychological well-being of the participants. The social nature and costumed performance of these activities could be the key to their success in improving the mental health of the participants.

A member of Takayuki Akimoto‘s lab presented research on a mouse model of progeria and metabolic changes caused by a gene knockout. Although Akimoto’s lab is focusing on how mechanical stress during exercise controls muscular plasticity, there are other research projects aimed at uncovering the molecular mechanisms of aging and developing therapeutic interventions.

A productive session

There were plenty of important topics raised during the Aging Session, including policies that let people work for longer into older ages with the possibility of retirement, the verbal strategies that healthcare practitioners should follow when talking to people with serious diseases, ways to optimize the location of medical facilities, and the ways that people of different ages perceive technologies to support active aging. Although some of the topics discussed and the solutions available on the market, including assistive technologies, seem like band-aids and don’t address the root causes of aging, they remain necessary in the absence of anti-aging therapeutics.

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Date Posted: November 23, 2022

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We Can Think of Worse Curses, Elon Musk

Two days ago, famous billionaire and new Twitter owner Elon Musk Tweeted that he cannot think of a worse curse than living forever, in reply to a Tweet relating to the predicted heat death of the universe.

A consistent argument

This is not Elon Musk’s first mention of opposition to longer lifespans. In a March 26 interview with Business Insider, he noted that most modern political leaders are considerably older than in past eras and opposed the idea of life extension on the grounds that it would facilitate a gerontocracy, expressing the opinions that old people with old ideas would be out of touch with the average person and cause a halt in social advancement. While he did not express a fear of immortal dictators, that argument shares many of the same characteristics.

The inability of many older people to properly adapt to new situations is not a magical property of chronological age. Instead, the inability to form new memories and learn new things can be traced to biological impairments in neurogenesis, the creation of new neurons, which becomes impaired by, among other things, exposure to old serum. With this biological origin in mind, it is somewhat disconcerting to see a noted transhumanist such as Musk, who has co-founded a company developing brain-computer interfaces, concerned about an ossified gerontocracy for this reason.

In that same interview, he also stated that he would like political leaders to be within 10 to 20 years of the average age. In a world with widespread and effective life extension, this would be a gradually narrowing characteristic.

Living forever, immortality, and life extension

We at Lifespan.io, along with every other responsible life extensionist, do not discuss “living forever” or “immortality” as part of the goals of life extension. Forever is a very long time, and making someone actually immortal would entail removing all possible causes of death for that person. Some people use the term “biological immortality” or negligible senescence, which is the removal of all age-related causes of death; if you were biologically immortal, your body’s processes would indefinitely sustain your life instead of gradually failing due to age-related diseases. This is not the same as actually living forever or being truly invincible.

Some transhumanists see life extension as a stepping stone to a greater goal: removing more and more causes of death, biological and otherwise. As a life extension advocacy organization, this sort of far-future thinking is simply beyond our scope. Instead, we focus on the age-related diseases that are actively causing harm, misery, and death to billions of ordinary human beings right now.

Worse curse #1: Alzheimer’s disease

We have written extensively on potential treatments for Alzheimer’s disease, but these articles do not usually discuss the human tragedies involved. People who suffer from Alzheimer’s forget who they are. They lose the ability to remember their own spouses and children and can no longer perform the basic functions of everyday life. Their loved ones are left helplessly watching as their minds gradually deterioriate. Whether or not Alzheimer’s is a fate worse than death is a thorny and delicate ethical question, but to suggest that it is a fate worse than living healthy and not dying is, on every ethical level, nonsensical.

Worse curse #2: Sarcopenia

The age-related loss of muscle known as sarcopenia, and the concept of frailty more generally, destroy the ability of older individuals to take care of themselves. It often turns children into caregivers, as the aging parents can simply no longer physically do the things they need to live safe and comfortable lives. People with sarcopenia and related mobility impairments, such as arthritis, become more and more disabled, gradually losing autonomy and the ability to do the things they loved. This is also certainly a worse curse than staying in good health indefinitely.

Worse curse #3: Stroke

Like Alzheimer’s, stroke is much more frequent in older people and causes brain damage; unlike Alzheimer’s, the damage occurs all at once. Not all strokes are fatal. The American Stroke Association has an extensive site detailing what might happen to someone after a stroke. This includes drastic behavior changes, vision problems, language problems, partial paralysis, or even complete, ‘locked-in’, whole-body paralysis. Having an indefinite healthy lifespan cannot be a worse curse than that.

Worse curse #4: Cancer

The incidence of cancer, of course, increases with age. Like aging, cancer is not a single disease; cancers vary wildly in their prognoses and treatment. With modern methods, some cancers, such as melanoma, are relatively easy to deal with if they are detected and treated early; other cancers, such as pancreatic, have much worse prognoses. Cancer is often an exceptionally agonizing condition, with the pain getting worse and worse as the condition proceeds to its fatal conclusion. It is difficult to believe that staying alive and healthy can be a worse curse than this.

Worse curse #5: Inevitable aging

Nearly everyone in the world has, since a very young age, known that they are going to grow old and die. Nearly everyone has also come to accept this. This is, and has been throughout all of human history, entirely correct: without interventions, everyone in the world, including you and all of your friends and family members, will one day die of age-related diseases if nothing else. Unlike Elon Musk, we believe that we can, and should, use all available technologies to change whatever is possible to change about this situation for the good of all humanity. Having the sword of slow death by aging hanging over your head is a worse curse than not having it there.

In summary

Elon Musk’s Tweet can be understood in the context of far-future transhumanism or near-future life extension. It is wrong in both cases. Obviously, we can’t survive an actual heat death of the universe, and the idea that we will simply run out of things to do and become bored in the far future is highly unlikely. Even if it is the case, that’s a problem for our future selves to deal with – if age-related diseases don’t kill us first.

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