- Ohio State Battles Back from Slow Start to Defeat No. 14 Seed James Madison, 80-66, in First Round of NCAA Tou Eleven Warriors
- Ohio State vs. James Madison – First Round NCAA tournament extended highlights March Madness
- James Madison vs. Ohio State – Women’s College Basketball Game Recap – March 18, 2023 ESPN
- OSU women’s basketball rallies from down 16 to defeat James Madison in NCAA opener 247Sports
- Ohio State Women’s Basketball Confident About Ability to Make Deep NCAA Tournament Run | Eleven Warriors Eleven Warriors
- View Full Coverage on Google News
Tag Archives: slow
Investigational Anti-amyloid Treatment Started Before Alzheimer’s Symptoms Did Not Slow Memory Loss – Neuroscience News
- Investigational Anti-amyloid Treatment Started Before Alzheimer’s Symptoms Did Not Slow Memory Loss Neuroscience News
- Eli Lilly Alzheimer’s treatment solanezumab failed to slow disease progression CNBC
- Pharmalittle: Pharmacies are battlegrounds in the abortion debate; Lilly Alzheimer’s drug failed to prevent memory loss in study STAT
- Lilly’s 10-year bet on treating Alzheimer’s before symptoms start ends in failure FierceBiotech
- Eli Lilly Stock: Decade-Long Effort In Alzheimer’s Treatment Fails | Investor’s Business Daily Investor’s Business Daily
- View Full Coverage on Google News
Slow TCA flux and ATP production in primary solid tumours but not metastases
Frayn, K. N. & Evans, R. Human Metabolism: A Regulatory Perspective (John Wiley & Sons, 2019).
Warburg, O. The metabolism of carcinoma cells. J. Cancer Res. 9, 148–163 (1925).
Google Scholar
Warburg, O. The metabolism of tumors in the body. J. Gen. Physiol. 8, 519–530 (1927).
Google Scholar
Vander Heiden, M. G., Cantley, L. C. & Thompson, C. B. Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science 324, 1029–1033 (2009).
Liberti, M. V. & Locasale, J. W. The Warburg effect: how does it benefit cancer cells? Trends Biochem. Sci. 41, 211–218 (2016).
Google Scholar
Cori, C. F. & Cori, G. T. The carbohydrate metabolism of tumors: III. The rate of glycolysis of tumor tissue in the living animal. J. Cancer Res. 12, 301–313 (1928).
Crabtree, H. G. Observations on the carbohydrate metabolism of tumours. Biochem. J. 23, 536–545 (1929).
Google Scholar
Fletcher, J. W. et al. Recommendations on the use of 18F-FDG PET in oncology. J. Nucl. Med. 49, 480–508 (2008).
Birsoy, K. et al. An essential role of the mitochondrial electron transport chain in cell proliferation is to enable aspartate synthesis. Cell 162, 540–551 (2015).
Google Scholar
Ju, Y. S. et al. Origins and functional consequences of somatic mitochondrial DNA mutations in human cancer. eLife 3, e02935 (2014).
Weinberg, F. et al. Mitochondrial metabolism and ROS generation are essential for Kras-mediated tumorigenicity. Proc. Natl Acad. Sci. USA 107, 8788–8793 (2010).
Google Scholar
Sullivan, L. B. et al. Supporting aspartate biosynthesis is an essential function of respiration in proliferating. Cell 162, 552–563 (2015).
Google Scholar
Viale, A. et al. Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function. Nature 514, 628–632 (2014).
Google Scholar
Gorelick, A. N. et al. Respiratory complex and tissue lineage drive recurrent mutations in tumour mtDNA. Nat Metab. 3, 558–570 (2021).
Google Scholar
Hui, S. et al. Glucose feeds the TCA cycle via circulating lactate. Nature 551, 115–118 (2017).
Hensley, C. T. et al. Metabolic heterogeneity in human lung tumors. Cell 164, 681–694 (2016).
Google Scholar
Mason, G. F. et al. Simultaneous determination of the rates of the TCA cycle, glucose utilization, α-ketoglutarate/glutamate exchange, and glutamine synthesis in human brain by NMR. J. Cereb. Blood Flow Metab. 15, 12–25 (1995).
Google Scholar
Jucker, B. M., Lee, J. Y. & Shulman, R. G. In vivo 13C NMR measurements of hepatocellular tricarboxylic acid cycle flux. J. Biol. Chem. 273, 12187–12194 (1998).
Google Scholar
Petersen, K. F. et al. Mitochondrial dysfunction in the elderly: possible role in insulin resistance. Science 300, 1140–1142 (2003).
Google Scholar
Wijnen, J. P. et al. In vivo 13C magnetic resonance spectroscopy of a human brain tumor after application of 13C-1-enriched glucose. Magn. Reson. Imaging 28, 690–697 (2010).
Google Scholar
Yuan, J., Bennett, B. D. & Rabinowitz, J. D. Kinetic flux profiling for quantitation of cellular metabolic fluxes. Nat. Protoc. 3, 1328–1340 (2008).
Google Scholar
Befroy, D. E. et al. Direct assessment of hepatic mitochondrial oxidative and anaplerotic fluxes in humans using dynamic 13 C magnetic resonance spectroscopy. Nat. Med. 20, 98–102 (2014).
Google Scholar
Nöh, K., Wahl, A. & Wiechert, W. Computational tools for isotopically instationary 13C labeling experiments under metabolic steady state conditions. Metab. Eng. 8, 554–577 (2006).
Martin, A. W. & Fuhrman, F. A. The relationship between summated tissue respiration and metabolic rate in the mouse and dog. Physiol. Zool. 28, 18–34 (1955).
Sokoloff, L. et al. The [14c]deoxyglucose method for the measurement of local cerebral glucose utilization: theory, procedure, and normal values in the conscious and anesthetized albino Rat. J. Neurochem. 28, 897–916 (1977).
Google Scholar
Hostetler, K. Y. & Landau, B. R. Estimation of the pentose cycle contribution to glucose metabolism in tissue in vivo. Biochemistry 6, 2961–2964 (1967).
Google Scholar
Munger, J. et al. Systems-level metabolic flux profiling identifies fatty acid synthesis as a target for antiviral therapy. Nat. Biotechnol. 26, 1179–1186 (2008).
Google Scholar
Fueger, B. J. et al. Impact of animal handling on the results of 18F-FDG PET studies in mice. J. Nucl. Med. 47, 999–1006 (2006).
Google Scholar
Wolfe, R. R. Tracers in Metabolic Research: Radioisotope and Stable Isotope/Mass Spectometry Methods (A.R. Liss, 1984).
Donovan, C. M. & Brooks, G. A. Endurance training affects lactate clearance, not lactate production. Am. J. Physiol. Endocrinol. Metab. 244, E83–E92 (1983).
Google Scholar
Levy, M. N. Uptake of lactate and pyruvate by intact kidney of the dog. Am. J. Physiol. 202, 302–308 (1962).
Google Scholar
Murashige, D. et al. Comprehensive quantification of fuel use by the failing and nonfailing human heart. Science 370, 364–368 (2020).
Google Scholar
Jang, C. et al. Metabolite exchange between mammalian organs quantified in pigs. Cell Metab. 30, 594–606 (2019).
Google Scholar
Piskounova, E. et al. Oxidative stress inhibits distant metastasis by human melanoma cells. Nature 527, 186–191 (2015).
Google Scholar
Ubellacker, J. M. et al. Lymph protects metastasizing melanoma cells from ferroptosis. Nature 585, 113–118 (2020).
Google Scholar
Fischer, G. M. et al. Molecular profiling reveals unique immune and metabolic features of melanoma brain metastases. Cancer Discov. 9, 628–645 (2019).
Google Scholar
Rodrigues, M. F. et al. Enhanced OXPHOS, glutaminolysis and β-oxidation constitute the metastatic phenotype of melanoma cells. Biochem. J. 473, 703–715 (2016).
Google Scholar
Momcilovic, M. et al. In vivo imaging of mitochondrial membrane potential in non-small-cell lung cancer. Nature 575, 380–384 (2019).
Google Scholar
Nicholls, D. G. & Locke, R. M. Thermogenic mechanisms in brown fat. Physiol. Rev. 64, 1–64 (1984).
Google Scholar
Divakaruni, A. S. & Brand, M. D. The regulation and physiology of mitochondrial proton leak. Physiology 26, 192–205 (2011).
Google Scholar
Brown, G. C. Control of respiration and ATP synthesis in mammalian mitochondria and cells. Biochem. J. 284, 1–13 (1992).
Google Scholar
Pavlova, N. N. & Thompson, C. B. The emerging hallmarks of cancer metabolism. Cell Metab. 23, 27–47 (2016).
Google Scholar
Bauduin, H., Colin, M. & Dumont, J. E. Energy sources for protein synthesis and enzymatic secretion in rat pancreas in vitro. Biochim. Biophy. Acta 174, 722–733 (1969).
Google Scholar
Campagne, R. N. & Gruber, M. Amino acid and energy requirements of protein synthesis in rat pancreatic tissue in vitro. Biochim. Biophys. Acta 55, 353–360 (1962).
Google Scholar
Neinast, M. D. et al. Quantitative analysis of the whole-body metabolic fate of branched-chain amino acids. Cell Metab. 29, 417–429 (2019).
Google Scholar
Lassen, N. A., Munck, O. & Thaysen, J. H. Oxygen consumption and sodium reabsorption in the kidney. Acta Physiol. Scand. 51, 371–384 (1961).
Google Scholar
Müller, M. J. Hepatic fuel selection. Proc. Nutr. Soc. 54, 139–150 (1995).
Frauwirth, K. A. et al. The CD28 signaling pathway regulates glucose metabolism. Immunity 16, 769–777 (2002).
Google Scholar
Lapidot, T. et al. A cell initiating human acute myeloid leukaemia after transplantation into SCID mice. Nature 367, 645–648 (1994).
Google Scholar
Storz, P. Acinar cell plasticity and development of pancreatic ductal adenocarcinoma. Nat. Rev. Gastroenterol. Hepatol. 14, 296–304 (2017).
Google Scholar
Rajasekaran, S. A. et al. Reduced expression of beta-subunit of na,k-atpase in human clear-cell renal cell carcinoma. J. Urol. 162, 574–580 (1999).
Google Scholar
Chang, C.-H. et al. Metabolic competition in the tumor microenvironment is a driver of cancer progression. Cell 162, 1229–1241 (2015).
Google Scholar
Kamphorst, J. J. et al. Human pancreatic cancer tumors are nutrient poor and tumor cells actively scavenge extracellular protein. Cancer Res. 75, 544–553 (2015).
Google Scholar
Tasdogan, A. et al. Metabolic heterogeneity confers differences in melanoma metastatic potential. Nature 577, 115–120 (2020).
Google Scholar
Reinfeld, B. I. et al. Cell-programmed nutrient partitioning in the tumour microenvironment. Nature 593, 282–288 (2021).
Google Scholar
Brindle, K. M. Imaging metabolism with hyperpolarized 13C-labeled cell substrates. J. Am. Chem. Soc. 137, 6418–6427 (2015).
Google Scholar
Davidson, S. M. et al. Environment impacts the metabolic dependencies of Ras-driven non-small cell lung cancer. Cell Metab. 23, 517–528 (2016).
Google Scholar
Herranz, D. et al. Metabolic reprogramming induces resistance to anti-NOTCH1 therapies in T cell acute lymphoblastic leukemia. Nat. Med. 21, 1182–1189 (2015).
Google Scholar
Kang, Y. et al. A multigenic program mediating breast cancer metastasis to bone. Cancer Cell 3, 537–549 (2003).
Google Scholar
Minn, A. J. et al. Genes that mediate breast cancer metastasis to lung. Nature 436, 518–524 (2005).
Google Scholar
Esposito, M. et al. TGF-β-induced DACT1 biomolecular condensates repress Wnt signalling to promote bone metastasis. Nat. Cell Biol. 23, 257–267 (2021).
Google Scholar
Chiles, E. et al. Fast LC-MS quantitation of glucose and glycerol via enzymatic derivatization. Anal. Biochem. 575, 40–43 (2019).
Google Scholar
Wang, L. et al. Spatially resolved isotope tracing reveals tissue metabolic activity. Nat. Methods 19, 223–230 (2022).
Gupta, M., Sonnett, M., Ryazanova, L., Presler, M. & Wühr, M. Quantitative proteomics of Xenopus embryos I, sample preparation. Methods Mol. Biol. 1865, 175–194 (2018).
Google Scholar
Hughes, C. S. et al. Single-pot, solid-phase-enhanced sample preparation for proteomics experiments. Nat. Protoc. 14, 68–85 (2019).
Google Scholar
Rappsilber, J., Mann, M. & Ishihama, Y. Protocol for micro-purification, enrichment, pre-fractionation and storage of peptides for proteomics using StageTips. Nat. Protoc. 2, 1896–1906 (2007).
Google Scholar
Li, J. et al. TMTpro-18plex: The expanded and complete set of TMTpro reagents for sample multiplexing. J. Proteome Res. 20, 2964–2972 (2021).
Google Scholar
Su, X., Lu, W. & Rabinowitz, J. D. Metabolite spectral accuracy on orbitraps. Anal. Chem. 89, 5940–5948 (2017).
Google Scholar
Levenberg, K. A method for the solution of certain non-linear problems in least squares. Quart. Appl. Math. 2, 164–168 (1944).
Google Scholar
Marquardt, D. W. An algorithm for least-squares estimation of nonlinear parameters. J. Soc. Ind. Appl. Math. 11, 431–441 (1963).
Google Scholar
Hui, S. et al. Quantitative fluxomics of circulating metabolites. Cell Metab. 32, 676–688 (2020).
Google Scholar
Ghergurovich, J. M. et al. Local production of lactate, ribose phosphate, and amino acids by human triple-negative breast cancer. Med 2, 736–754 (2021).
Google Scholar
Petersen, M. C., Vatner, D. F. & Shulman, G. I. Regulation of hepatic glucose metabolism in health and disease. Nat. Rev. Endocrinol. 13, 572–587 (2017).
Google Scholar
Brown, R. P., Delp, M. D., Lindstedt, S. L., Rhomberg, L. R. & Beliles, R. P. Physiological parameter values for physiologically based pharmacokinetic models. Toxicol. Ind. Health 13, 407–484 (1997).
Google Scholar
West, D. B., Boozer, C. N., Moody, D. L. & Atkinson, R. L. Dietary obesity in nine inbred mouse strains. Am. J. Physiol. 262, R1025–R1032 (1992).
Google Scholar
Burkholder, T. J., Fingado, B., Baron, S. & Lieber, R. L. Relationship between muscle fiber types and sizes and muscle architectural properties in the mouse hindlimb. J. Morphol. 221, 177–190 (1994).
Google Scholar
Mathewson, M. A., Chapman, M. A., Hentzen, E. R., Fridén, J. & Lieber, R. L. Anatomical, architectural, and biochemical diversity of the murine forelimb muscles. J. Anat. 221, 443–451 (2012).
Kim, Y. S. Human tissues: chemical composition and photon dosimetry data. Radiat. Res. 57, 38–45 (1974).
Google Scholar
Goldman, M. J. et al. Visualizing and interpreting cancer genomics data via the Xena platform. Nat. Biotechnol. 38, 675–678 (2020).
Google Scholar
Kanehisa, M. & Goto, S. KEGG: Kyoto Encyclopedia of Genes and Genomes. Nucleic Acids Res. 28, 27–30 (2000).
Google Scholar
Chen, E. Y. et al. Enrichr: interactive and collaborative HTML5 gene list enrichment analysis tool. BMC Bioinform. 14, 128 (2013).
Sonnett, M., Gupta, M., Nguyen, T. & Wühr, M. Quantitative proteomics for Xenopus embryos II, data analysis. Methods Mol. Biol. 1865, 195–215 (2018).
Google Scholar
Sonnett, M., Yeung, E. & Wühr, M. Accurate, sensitive, and precise multiplexed proteomics using the complement reporter ion cluster. Anal. Chem. 90, 5032–5039 (2018).
Google Scholar
High Blood Pressure Medication Shown To Slow Aging and Extend Lifespan
A study recently published in the journal Aging Cell found that administering rilmenidine, a medication used to treat hypertension, to animals at both young and older ages increases lifespan and enhances overall health markers, similar to the effects of caloric restriction.
Researchers have discovered that the hypertension drug rilmenidine can extend lifespan and slow aging.
New research findings, published on January 20 in the journal Aging Cell, show that animals treated with rilmenidine, currently used to treat hypertension (high blood pressure), at young and older ages increase lifespan and improve health markers, mimicking the effects of caloric restriction. Rilmenidine, which is a prescription medication, is marketed under the brand names Albarel, Hyperium, Iterium, and Tenaxum.
They also demonstrate that the healthspan and lifespan benefits of rilmenidine treatment in the roundworm C. elegans are mediated by the I1-imidazoline receptor nish-1, identifying this receptor as a potential longevity target.
Unlike other drugs previously studied for this purpose by the researchers, the widely-prescribed, oral antihypertensive rilmenidine has the potential for future translatability to humans as side effects are rare and non-severe.
To date, a caloric restriction diet has been considered the most robust anti-aging intervention, promoting longevity across
Reference: “Rilmenidine extends lifespan and healthspan in Caenorhabditis elegans via a nischarin I1-imidazoline receptor” by Dominic F. Bennett, Anita Goyala, Cyril Statzer, Charles W. Beckett, Alexander Tyshkovskiy, Vadim N. Gladyshev, Collin Y. Ewald and João Pedro de Magalhães, 20 January 2023, Aging Cell.
DOI: 10.1111/acel.13774
This study was undertaken by researchers from the University of Liverpool, ETH Zürich, and Harvard Medical School, and funded by the Swiss National Science Foundation, LongeCity, and the Biotechnology and Biological Sciences Research Council.
Hypertension Drug Shown to Extend Lifespan And Slow Aging in Animals : ScienceAlert
The hypertension drug rilmenidine has been shown to slow down aging in worms, an effect that in humans could hypothetically help us live longer and keep us healthier in our latter years.
Rilmenidine was picked for this latest study because past research has shown it mimics the effects of caloric restriction on a cellular level. Reducing available energy while maintaining nutrition within the body has been shown to extend lifespans in several animal models.
Whether this translates to human biology, or is a potential risk to our health, is a topic of ongoing debate. Finding ways to achieve the same benefits without the costs of extreme calorie cutting could lead to new ways to improve health in old age.
In a series of tests conducted by an international team of researchers, young and old Caenorhabditis elegans worms treated with the drug – which is normally used to treat high blood pressure – lived longer and presented higher measures in a variety of health markers in the same way as restricting calories, as the scientists had hoped.
“For the first time, we have been able to show in animals that rilmenidine can increase lifespan,” says molecular biogerontologist João Pedro Magalhães, from the University of Birmingham in the UK. “We are now keen to explore if rilmenidine may have other clinical applications.”
The C. elegans worm is a favorite for studies, because many of its genes have similarities to counterparts in our genome. Yet in spite of these similarities, it is still a rather distant relation to humans.
Further tests showed that gene activity associated with caloric restriction could be seen in the kidney and liver tissues of mice treated with rilmenidine. In other words, some of the changes that caloric restriction gives in animals and thought to confer certain health benefits also appear with a hypertension drug that many people already take.
Another discovery was that a biological signaling receptor called nish-1 was crucial in the effectiveness of rilmenidine. This particular chemical structure could be targeted in future attempts to improve lifespan and slow down aging.
“We found that the lifespan-extending effects of rilmenidine were abolished when nish-1 was deleted,” write the researchers in their published paper. “Critically, rescuing the nish-1 receptor reinstated the increase in lifespan upon treatment with rilmenidine.”
Low-calorie diets are hard to follow and come with a variety of side effects, such as hair thinning, dizziness, and brittle bones. It’s early days still, but the thinking is that this hypertension drug could confer the same benefits as a low-calorie diet while being easier on the body.
What makes rilmenidine a promising candidate as an anti-aging drug is that it can be taken orally, it’s already widely prescribed, and its side effects are rare and relatively mild (they include palpitations, insomnia and drowsiness in a few cases).
There’s a long way to go yet in figuring out if rilmenidine would work as an anti-aging drug for actual humans, but the early signs in these worm and mice tests are promising. We now know much more about what rilmenidine can do, and how it operates.
“With a global aging population, the benefits of delaying aging, even if slightly, are immense,” says Magalhães.
The research has been published in Aging Cell.
New study finds 6 ways to slow memory decline and lower dementia risk
While researchers have long known that there is a link between dementia and factors such as social isolation and obesity, the size and scope of the new study adds substantial evidence to a global body of research that suggests a healthy lifestyle may help brains age better.
It also suggests that the effects of a healthy lifestyle are beneficial even for people who are genetically more susceptible to memory decline — a “very hope-giving” finding for the millions of individuals around the world who carry the APOEε4 gene, a major risk factor for Alzheimer’s disease, said Eef Hogervorst, chair of biological psychology at Loughborough University, who was not involved in the study.
Memory naturally declines gradually as people age. Some older people may develop dementia, an umbrella term that can include Alzheimer’s, and generally describes a deterioration in cognitive function that goes beyond the normal effects of aging. But for many, “memory loss can merely be senescent forgetfulness,” write the authors of the BMJ study — like forgetting the name of that TV program you used to love, or that pesky fact you wanted to look up.
Memory loss is no less damaging for being gradual, and age-related memory decline can in some cases be an early symptom of dementia. But the good news, the researchers say, is that it “can be reversed or become stable rather than progress to a pathological state.”
The BMJ study was conducted in China between 2009 and 2019. Researchers conducted tests on over 29,000 people ages 60 and older and then tracked their progress or decline over time — what’s known as a population-based cohort study. Although more than 10,500 participants dropped out of the study over the next decade — some participants died or stopped participating — the researchers still used the data collected from those individuals in their analysis.
At the start of the study, researchers conducted baseline memory tests as well as testing for the APOE gene. They also surveyed participants about their daily habits. Participants were sorted into one of three groups — favorable, average and unfavorable — based on their lifestyle.
The six modifiable lifestyle factors the researchers focused on included:
- Physical exercise: Doing at least 150 minutes of moderate or 75 minutes of vigorous activity per week.
- Diet: Eating appropriate daily amounts of at least seven of 12 food items (fruits, vegetables, fish, meat, dairy products, salt, oil, eggs, cereals, legumes, nuts and tea).
- Alcohol: Never drank or drank occasionally.
- Smoking: Never having smoked or being a former smoker.
- Cognitive activity: Exercising the brain at least twice a week (by reading and playing cards or mah-jongg, for example).
- Social contact: Engaging with others at least twice a week (by attending community meetings or visiting friends or relatives, for example).
Over the course of the study, the researchers found that people in the favorable group (four to six healthy factors) and average group (two to three) had a slower rate of memory decline over time than people with unfavorable lifestyles (zero to one healthy factor).
People living favorable lifestyles that included at least four healthy habits were also less likely to progress to mild cognitive impairment and dementia.
The results show that “more is better of these behaviors,” says Hogervorst — in other words, the more healthy lifestyle factors you can combine, the better your chances of preserving your memory and staving off dementia.
Notably, this held true even for people who carried the APOE gene associated with a higher risk of Alzheimer’s disease.
“These results provide an optimistic outlook, as they suggest that although genetic risk is not modifiable, a combination of more healthy lifestyle factors are associated with a slower rate of memory decline, regardless of the genetic risk,” wrote the study authors.
The study stands out because of its size and follow-up over time, and because it was conducted in China, whereas “most publications are based on western high income countries,” Carol Brayne, a professor of public health medicine at the University of Cambridge who researches older people and dementia, said in an email.
However, the study authors acknowledge several limitations, including that people’s own reports of health behaviors may not be fully accurate, and that the people who took part in the study were more likely to be leading healthy lives to begin with.
Some of the study’s findings differ from the results of other large studies conducted in the United States and in Europe, says Hogervorst. For instance, the BMJ study found that the lifestyle factor with the greatest effect on reducing memory decline was a balanced diet. Other studies have suggested that diet matters less in old age than physical and mental exercise, says Hogervorst.
Still, its results align with the broad scientific consensus that there is a link between how we live and our cognitive function as we age — and perhaps more important, suggest that it may never be too late to improve your brain health.
“The overall message from the study is a positive one,” Snorri B. Rafnsson, associate professor of aging and dementia at the University of West London, said in an email. “Namely, that cognitive function, and especially memory function, in later life maybe positively influenced by regularly and frequently engaging in different health related activities.”
Six lifestyle choices to slow memory decline named in 10-year study | Memory
A combination of healthy lifestyle choices such as eating well, regularly exercising, playing cards and socialising at least twice a week may help slow the rate of memory decline and reduce the risk of dementia, a decade-long study suggests.
Memory is a fundamental function of daily life that continuously declines as people age, impairing quality of life and productivity, and increasing the risk of dementia.
Evidence from previous research has been insufficient to evaluate the effect of healthy lifestyle on memory trajectory, but now a study suggests that combining multiple healthy lifestyle choices – the more the better – is linked with softening the speed of memory decline.
“A combination of positive healthy behaviours is associated with a slower rate of memory decline in cognitively normal older adults,” researchers from the National Center for Neurological Disorders in Beijing, China, wrote in the BMJ.
Practising multiple healthy lifestyle choices together “was associated with a lower probability of progression to mild cognitive impairment and dementia”, they added.
Researchers analysed 29,000 adults aged over 60 with normal cognitive function who were part of the China Cognition and Aging Study.
At the start of the study in 2009, memory function was measured using tests and people were checked for the APOE gene, which is the strongest risk-factor gene for Alzheimer’s disease. The subjects were then monitored for 10 years with periodic assessments.
A healthy lifestyle score combining six factors was calculated: a healthy diet; regular exercise; active social contact; cognitive activity; non-smoking; and not drinking alcohol.
Based on their score, ranging from zero to six, participants were put into lifestyle groups – favourable (four to six healthy factors), average (two to three healthy factors), or unfavourable (0 to 1 healthy factors) – and into APOE-carrier and non-carrier groups.
A healthy diet was deemed as eating at least seven out of 12 food groups: fruits, vegetables, fish, meat, dairy, salt, oil, eggs, cereals, legumes, nuts and tea.
Writing, reading, playing cards or other games at least twice a week was the second area of healthy behaviour.
Other areas included drinking no alcohol, exercising for more than 150 minutes a week at moderate intensity or more than 75 at vigorous intensity, and never having smoked or being an ex-smoker.
Social contact at least twice a week was the sixth healthy behaviour, including activities such as visiting family and friends, attending meetings or going to parties.
After accounting for factors likely to affect the results, the researchers found that each individual healthy behaviour was associated with a slower-than-average decline in memory over 10 years.
A healthy diet had the strongest effect on slowing memory decline, followed by cognitive activity and then physical exercise.
People with the APOE gene who had healthy lives on the whole also experienced a slower rate of memory decline than those with APOE who were the least healthy.
Overall, people with four to six healthy behaviours or two to three were almost 90% and almost 30% respectively less likely to develop dementia or mild cognitive impairment relative to those who were the least healthy, the BMJ reported.
Dr Susan Mitchell, head of policy at Alzheimer’s Research UK, said: “This is a well-conducted study, which followed people over a long period of time, and adds to the substantial evidence that a healthy lifestyle can help to support memory and thinking skills as we age.
“Too few of us know that there are steps we can all take to reduce our chances of dementia in later life.”
Personal trainer: These are the signs you have a slow metabolism and quick ways you can boost it
A personal trainer has shared the 13 signs you have a slow metabolism, and how you can boost yours to achieve your goal weight fast.
Rachael Attard, from Sydney, said while you might not think about it, metabolism has a ‘huge impact on our health’, particularly when it comes to weight loss and gain.
‘Simply put, metabolism is the internal process by which your body expends energy and burns calories,’ Rachael wrote on Instagram.
‘It works 24/7 by converting the food and nutrients you consume into energy.’
Rachael said some of the factors that can impact your metabolism include your genes, hormones, lack of sleep, diet, dehydration, age, stress and the medications you’re taking.
A personal trainer has shared the 13 signs you have a slow metabolism, and how you can boost yours to achieve your goal weight fast (Rachael Attard pictured)
Rachael (pictured) said some of the factors that can impact your metabolism include your genes, hormones, lack of sleep, diet, dehydration, age, stress and medications you’re taking
Some of the most common signs your metabolism is low include chronic fatigue and low energy, not feeling hungry in the morning and weight gain for no apparent reason.
Those with a slow metabolism might also experience constipation, depression, thinning hair, dry skin and brittle nails, as well as brain fog, hair loss and feeling cold all the time.
‘Other common signs frequent headaches, a low pulse rate and constant cravings for sugar and carbohydrates,’ Rachael said.
But you can address your metabolism – and the PT uses a few simple ‘tried and tested tricks’ to give hers a boost, like eating a protein-rich breakfast (pictured)
But you can address your metabolism – and the PT uses a few simple ‘tried and tested tricks’ to give hers a boost, particularly after the holiday season, when you might be feeling sluggish from over-eating and drinking.
The first thing Rachael said she does is she will have a hot cup of water and lemon.
‘Lemons are a great way to boost your metabolism, because they are high in vitamin C and antioxidants, which help your immune system,’ Rachael wrote on her website.
She said if you want to up the metabolism kick even more, you can add some cayenne pepper and ginger, which will help to promote a healthy digestive system, ‘making it easier for your metabolism to power through calories’.
Rachael (pictured) also recommends drinking a cup of warm water with lemon and making your regular water is icy cold
Next, the fitness pro always recommends that you drink icy cold water, as studies have shown this can help your metabolism.
‘By drinking cold water, your body has to work harder and burn more calories to process it. The study mentioned above found that you can burn 25 per cent more calories just by drinking cold water,’ Rachael said.
You can also still enjoy your cup of coffee, as studies have also shown that coffee and green tea also help with your metabolism – leading to more calories burned through the day.
Finally, Rachael (pictured) said increasing your muscle mass will work wonders at boosting your metabolism, and this comes from lifting weights
‘There are some foods that naturally increase your metabolism and protein is one of them,’ Rachael said.
‘Your body burns lots more calories digesting protein than it does compared to fat and protein.’
For this reason, she recommends a protein-rich breakfast like healthy protein smoothies, yoghurt or eggs, taking care to limit sweeteners.
Finally, Rachael said increasing your muscle mass will work wonders at boosting your metabolism.
She said the amount of calories you burn per day is made up of three things:
‘First, it’s your resting (or basal) metabolic rate – so how many calories you burn at rest,’ she said.
‘Then, it’s Thermogenesis – how many calories you burn through digestion (this sort of falls under the resting metabolic rate category).
‘Finally, it’s your physical activity – so how many calories you burn during exercise.’
But it’s the resting or basal metabolic rate (RMR or BMR) that makes up 60 to 85 per cent of your daily calories burned, and the only way to increase that is to boost your muscle mass.
The PT recommends you do this by lifting some weights at the gym or adding some resistance training into your workouts.
For more information about Rachael Attard, you can visit her website here.
China’s Shrinking Population Is Deeper Problem Than Slow Growth for Its Economy
Economists said China’s shrinking population poses a major future challenge for the world’s second-largest economy, while President Xi Jinping’s top economic adviser sought Tuesday to restore investor confidence after one of the most disappointing growth rates in decades.
China has already rolled back the zero-Covid policies that restrained growth for much of 2022, setting the stage for a recovery this year. The U-turn, in the wake of public protests, was part of a broad policy reset aimed at boosting the economy, including an easing of regulations on the property sector and signals that the clampdown on the tech sector has ended.
Beijing is now betting on a robust rebound in economic activities as officials increasingly signal that the recent wave of infections is reaching its peak. Some government advisers say the central leadership likely will announce a growth target of between 5% and 5.5% for 2023 at the coming legislative sessions in March. China on Tuesday posted 3% growth for 2022, its second-worst growth rate since 1976.
Speaking to the World Economic Forum in Davos, Mr. Xi’s top economic adviser, Vice Premier Liu He, sought to send a message to investors and executives that China’s growth would return to prepandemic levels this year as the country reopens.
On a Davos panel titled “China’s Next Chapter,” speakers also projected optimism. China’s reopening and exit from its zero-Covid policy is the “most positive catalyst” for global markets this year, said
Hong Kong Exchanges and Clearing Ltd.
’s Chief Executive
Nicolas Aguzin.
Vice Premier Liu He sought to restore investor confidence in China at the World Economic Forum in Davos, Switzerland.
Photo:
Markus Schreiber/Associated Press
“If China produces a solid growth number for 2023, 5% or 5% plus, that will actually underpin much global growth for the year to come,” said
Kevin Rudd,
president and CEO of Asia Society.
China’s recent measures, however, won’t address a host of challenges, some of which were exacerbated by the pandemic. A rapidly aging population, slowing growth in productivity, high debt levels and rising social inequality will weigh on the country’s economic ascent for decades to come, economists said.
On Tuesday, the same day that China posted 3% growth, the second-worst growth rate since 1976, it also said that for the first time since 1961, its population shrank.
China’s population dropped by 850,000 to 1.412 billion. The shift toward a shrinking population, which came faster than Beijing had projected, marks a watershed moment in China’s history with profound implications for its economy and its status as the world’s factory floor.
The demographic milestone comes when, despite its enormous size, China’s economy is still that of a middle-income, developing country, as measured by average worker incomes when compared with the U.S. and other rich-country peers. China’s leaders have long held the ambition of leapfrogging the U.S. to become the world’s biggest economy, a task made harder by this strengthening demographic headwind, economists say.
The global economy has grown to rely on China’s vast pool of workers for manufactured goods.
Photo:
Kyodonews/Zuma Press
“The likelihood of China someday overtaking the U.S. as No. 1 economy has just gone down a notch,” said Roland Rajah, lead economist at the Lowy Institute, a Sydney think tank.
The global economy has grown to rely on China’s vast pool of factory workers for manufactured goods, and its consumers represent a growing market for Western-made cars and luxury goods. A dwindling population means fewer consumers when China is under pressure to power growth through greater consumption instead of investment and exports.
Any rebound in consumption will also likely be constrained by a weak labor market and a housing downturn that has eroded the wealth of Chinese families. The jobless rate among people age 16 to 24 remained elevated at 16.7% in December, versus the peak of near 20% last summer. Growth in disposable income per capita could slow to around 4% each year in the next five years, downshifting from around 8% before the pandemic, according to David Wang, chief China economist at
Credit Suisse.
A smaller workforce will likely restrain economic growth. An economy can only grow by adding workers or producing more with the workers it has. China’s working-age population, which peaked around 2014, is expected to fall by 0.2% a year until 2030, according to S&P Global Ratings.
Productivity growth has been slowing. It slid to 1.3% on average in the 10 years through 2019, from 2.7% in the preceding decade, according to estimates from the Conference Board, a nonprofit research organization.
“It seems like it’s going to get old before it gets rich,” said Andrew Harris, deputy chief economist at Fathom Consulting in London.
There are some grounds for optimism, economists say. China could make better, more productive use of underemployed urban workers in state-owned enterprises as well as those still laboring in the countryside.
It is also adding automation and related technology to its factories rapidly, replacing or augmenting its shrinking pool of workers. Advances in robotics, artificial intelligence and other high-tech sectors that could turbocharge worker productivity “is the potential out for China,” Mr. Harris said, though he added whether it will succeed or not is unclear.
Meanwhile, China remains tied to its old playbook of fueling growth by encouraging governments and companies to borrow more to fund investments, a model that economists warn will be unsustainable in the long run.
The country’s overall debt as a share of its economy reached a high during the pandemic, as local governments borrowed to finance infrastructure projects and boost the economy. As of June 2022, credit to the nonfinancial sector reached $51.8 trillion, or 295% of gross domestic product, according to data from the Bank for International Settlements.
China’s policies throughout the pandemic have focused heavily on the supply-side rather than the demand-side of the economy. Unlike many countries in the West, the Chinese government refrained from handing out cash to households, directing most of its efforts toward supporting manufacturers.
“The systemic problems that China had in its economy before Covid are still there,” said
George Magnus,
an economist and research associate at Oxford University, “In some aspects, the pandemic made them worse.”
A dwindling population means fewer consumers as China is under pressure to power growth through consumption.
Photo:
Qilai Shen/Bloomberg News
Despite the optimism expressed by some speakers in Davos, investors and corporate executives both inside and outside China remain wary of Beijing’s willingness to sufficiently roll back its restrictions on businesses of the past few years to re-embrace private capital.
Mr. Liu sought to allay those concerns during his Tuesday speech. He told the Davos crowd that a return to a planned economy, where the party-state dictates economic activities, is impossible.
But economists say Mr. Xi’s drive for self-sufficiency across a range of industries and his penchant for dictating how private business should be run will continue to sap vitality from the economy.
To achieve self-reliance in key sectors, Beijing has focused on channeling low-cost loans to favored sectors, such as semiconductors, renewable energy and pharmaceuticals. But the spending, which often involves less-productive state-owned enterprises, has also been plagued by waste and corruption, economists say, with limited evidence of real innovation.
“Xi’s desire to make sure that the Party’s control extends across society runs far deeper than his commitment to growing a market economy,” said Mark Williams, chief Asia economist at Capital Economics.
—Rebecca Feng contributed to this article.
Write to Stella Yifan Xie at stella.xie@wsj.com and Jason Douglas at jason.douglas@wsj.com
Copyright ©2022 Dow Jones & Company, Inc. All Rights Reserved. 87990cbe856818d5eddac44c7b1cdeb8
After a slow start, SpaceX’s Falcon Heavy rocket is about to hit its stride
Enlarge / A Falcon Heavy rocket rolls to the launch pad on Saturday January 14 2023.
Trevor Mahlmann
Nearly five years have passed since the massive Falcon Heavy rocket made its successful debut launch in February 2018. Since then, however, SpaceX’s heavy lift rocket has flown just three additional times.
Why? It’s partly because there is simply not all that much demand for a heavy lift rocket. Another factor is that SpaceX has increased the performance of its Falcon 9 rocket so much that it can complete a lot of the missions originally manifested on the Falcon Heavy. However the main reason for the low cadence has been due to a lack of readiness of payloads for the new rocket, particularly from the US Department of Defense.
But now this trickle of Falcon Heavy launches may turn into a flood. As early as Saturday, from Florida, the first of potentially five launches of the heavy lift rocket this year could take place.
First up is the USSF-67 mission. This will be the second Falcon Heavy mission for the US Space Force, and the rocket will be carrying two payloads into geostationary orbit. The first of the two vehicles on board is named CBAS-2, for Continuous Broadcast Augmenting SATCOM. This is essentially a communications relay satellite, which the Space Force says will support operations by augmenting “existing military satellite communication capabilities and continuously broadcast military data through space-based satellite relay links.”
The second payload, called Long Duration Propulsive ESPA-3A, is actually a spacecraft “bus.” It will host five different, smaller payloads and provide power and propulsion before dropping these vehicles into various orbits. Among these five payloads is a prototype “crypto/interface encryption” satellite that will deliver secure space-to-ground communications capability.
“This is a complex mission and truly represents what Assured Access to Space is about and is why we’re so enthusiastic about this upcoming launch,” Maj. Gen. Stephen Purdy, program executive officer for Assured Access to Space, said in a news release.
SpaceX completed a hot fire test of the rocket on Tuesday, and declared that the vehicle was ready for liftoff. The rocket will use a brand new core stage, and side-mounted boosters that have flown into space one time, as side-mounted boosters on the USSF-44 Falcon Heavy mission that launched on Nov. 1 2022. SpaceX will again attempt to recover these side boosters, at its land-based landing zones, for a future mission. The center core will be expended.
The launch is scheduled for 5:55pm ET (22:55 UTC) from Launch Complex 39A at Kennedy Space Center. Weather conditions are favorable for the launch attempt. (Update: SpaceX delayed the launch until Sunday evening after preparations for an attempt Saturday fell behind schedule).
The timing for this launch is noteworthy, as the launch window opens just 10 minutes after sunset. This will be the first time that the Falcon Heavy rocket has launched in twilight, and it should be visible for hundreds of kilometers up and down the Florida coast. Trevor Mahlmann will be on hand for Ars to provide unique views of this large launch vehicle.
Future Falcon Heavy missions this year include a commercial mission for the satellite communications company ViaSat in March, the Space Force’s USSF-52 mission in April, a commercial mission for EchoStar in May, and the Psyche asteroid mission for NASA in October. All of those dates, as ever in the launch business, are subject to change.