Metabolic rate and aging -
These findings are the first evidence based on longitudinal data showing that a blunted capacity to reduce BMR with age is a significant risk factor for mortality in the general population. We confirmed that BMR declines with age 25 , 26 , 36 , 37 and showed that the rate of decline accelerates at older ages Interestingly, the age-related decline of BMR was blunted in participants who died compared to those who were still alive at the end of the follow-up period.
These results are compatible with the notion that long-lived individuals are able to preserve a low energy metabolism, perhaps reflecting good health status.
The discrepancy in BMR between individuals who died and those who survived may indicate pathological conditions causing a homeostatic dysregulation that substantially increase minimum energy requirements. A potential clinical application of this concept stems from the hypothesis that an excessively high BMR, such as one caused by uncontrolled inflammation, is an early index of the perturbation of health status.
As a consequence, BMR may help clinicians to monitor the effectiveness of their interventions. We acknowledge that the present study has limitations. The BLSA sample is not representative of the general population because it mostly includes highly educated individuals of high socioeconomic status who are considered healthy at study entry.
Data were collected from through Women were enrolled in the study only from The longitudinal BMR evaluation based on the same methodology and performed in the same clinical setting at the Gerontology Research Center in Baltimore over a period of decades is a unique feature of the BLSA.
However, we caution the readers about the difficulty of detecting early thyroid dysfunction based only on physical examination. During —, thyroid-stimulating hormone TSH radioimmunoassay or triiodothyronine T 3 determinations were not available for the BLSA participants, and later they were measured only in a subgroup.
However, to our knowledge this study is unique because of the open panel design and the length of follow-up of the participants. Additionally, the BLSA is particularly suited to address the scientific question of this manuscript, and our findings have important potential scientific implications.
By showing that BMR is independently related to mortality in humans, and that persons who died had a blunted age-related BMR decline compared to those who survived, our study may open new research perspectives to investigate the role of energy expenditure in influencing both health status and duration of life.
Decision Editor: Darryl Wieland, PhD, MPH. Changes in basal metabolic rate BMR with aging. A, Data collected on BMR in all participants and at all time-points using nonparametric smoothing functions dashed line for men; solid line for women.
B, Longitudinal trend of BMR by age decade solid lines and limited to men. Longitudinal predicted values are from a fully adjusted mixed-effects regression model.
Dashed lines , participants who were still alive at the end of the follow-up period; solid lines, participants who died during the follow-up period. Functional form of the relationship between basal metabolic rate BMR and mortality in the Baltimore Longitudinal Study of Aging BLSA male participants.
Excess mortality reported on the y axis is defined as the absolute difference between the observed and the estimated mortality hazard. Estimate solid line and confidence intervals dashed lines were adjusted for age, race, calendar date of visit, weight, body mass index BMI , total physical activity, smoking status, creatinine excretion, muscle strength, and white blood cell count.
Note that BMR between Table shows the mortality risk ratio from longitudinal data according to participant groups. Notes : Survivors are participants who were still alive at the end of the follow-up; decedents are those who died during the follow-up.
Differences among censored and participants who died have been estimated using the Student t or chi-square test, as adequate. Characteristics of Follow-Ups on BLSA Participants According to Final Vital Status.
BMR and Mortality Risk Estimated From Longitudinal Data in Male BLSA Participants. Notes : In Model 3, missing data for total physical activity, creatinine, and muscle strength, and in Model 4, missing data for systolic and diastolic blood pressure, cancer, and diabetes were imputed using multiple imputation inference 34, Mortality Rates and Relative Risks for Mortality According to BMR Groups at Baseline and Using Longitudinal Data in Male BLSA Participants.
Characteristics of BLSA Participants Across the BMR Groups Based on Time-Dependent Approach. Statistical comparisons for continuous variables were performed by Bonferroni multiple comparison test when one-way analysis of variance was significant. Statistical comparisons for proportion were performed by Mantel-Haenszel chi-square test.
This research was supported by the Intramural Research Program of the National Institutes of Health, National Institute on Aging.
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Mortality and morbidity in laboratory-maintained Rhesus monkeys and effects of long-term dietary restriction. J Gerontol A Biol Sci Med Sci. Lane MA, Mattison JA, Roth GS, Brant LJ, Ingram DK. Effects of long-term diet restriction on aging and longevity in primates remain uncertain.
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J Nutr Biochem. Heilbronn LK, de Jonge L, Frisard MI, et al. Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial.
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A network-based analysis of systemic inflammation in humans. Ferrannini E. The theoretical bases of indirect calorimetry: a review.
Ravussin E, Lillioja S, Anderson TE, Christin L, Bogardus C. Determinants of hour energy expenditure in man. Methods and results using a respiratory chamber. J Clin Invest. Shock NW, Yiengst MJ.
Age changes in basal respiratory measurements and metabolism in males. Tzankoff SP, Norris AH. Effect of muscle mass decrease on age-related BMR changes. J Appl Physiol.
Peters J, van Slyke DD. Respiratory Metabolism. Quantitative Clinical Chemistry. Volume II. Baltimore: Williams and Wilkins Company; Hare RS. Endogenous creatinine in serum and urine. Proc Soc Exp Biol Med.
Talbot LA, Metter EJ, Fleg JL. Leisure-time physical activities and their relationship to cardiorespiratory fitness in healthy men and women years old. Med Sci Sports Exerc. Ainsworth BE, Haskell WL, Leon AS, et al.
Compendium of physical activities: classification of energy costs of human physical activities. Although a number of studies have been conducted in animals, studies in humans are too scarce to conclude whether an accumulation of oxidative damage also occurs with aging.
In addition, the accumulation of oxidative stress seems to be dependent on the choice of markers of oxidative stress as well as the type of tissue studied. Both factors make it difficult to come to a conclusion on the effect of age on oxidative stress.
For example, oxidative damage to DNA and proteins was increased in skeletal muscle of older patients and was decreased in blood cells after calorie restriction 21 , 25 , In contrast, data regarding lipid peroxidation are more confusing. Studies using malondialdehyde MDA as a marker of lipid peroxidation have indicated an increase in lipid peroxidation as a result of increasing age 41 , However, data from the Framingham Study actually observed a decrease in isoprostanes, a more reliable marker of lipid peroxidation, in individuals ranging from 33 to 88 years old In the current study, there were no differences in any markers of oxidative stress among the three groups.
Such results directly contradict the well accepted theory that oxidative stress increases with age. There was a trend for the aged individuals to have more DNA damage than either of the other groups; this trend supports the idea that nonagenarians may be protected from oxidative damage to DNA.
In healthy individuals, the accumulation of oxidative stress may be small and may require larger studies to observe age-related differences. In addition, one of the requirements of the study was that individuals had to be able to come to the testing facility to be tested. Participants with diabetes were also excluded.
Therefore, it is possible that the study design selected healthier older participants and that this may mask or dilute any differences between groups or relationships that otherwise would have been detected. Furthermore, it is recognized that the accumulation of oxidative stress is greater in postmitotic tissues such as skeletal muscle and brain than in other cell types with faster turnover rates such as blood , which may partially account for the fact that there were no differences detected between groups with regard to protein carbonyls in serum However, a recent study in rats reported that 8-OhdG significantly increased with age in peripheral lymphocytes as well as in heart, skeletal muscle, brain, liver, and intestine The current study used the Comet assay in whole blood, a generally accepted method to assess DNA fragmentation in humans, but did not reveal any differences between groups.
Our validation studies of the assay provide a strong reliability of the test and also show that using only lymphocytes or all nucleated cells in blood did not change the outcome. There is still disagreement as to whether RMR declines with age independent of changes in body weight and body composition and whether such a decrease contributes to the aging process and determination of life span.
However, the measurement of RMR in animals, especially rodents, is notoriously difficult when compared to measurement in humans in whom strict cooperation can be obtained during the procedure. Therefore, it may not be possible to apply conclusions from rodent studies to humans when it comes to aging and energy metabolism.
In humans, earlier observations of a decline in RMR with age were later supported by reports of lower RMR in older individuals when compared to younger individuals even after adjusting for FFM 45— Others have reported that the decline in RMR may be due to the decline in cell mass only.
The decline in physical activity with age has also been implicated as a potential cause for the reduction in RMR with age, even if there is no clear relationship between RMR and maximal oxygen consumption, an index of the level of physical activity 49 , In the current study, RMR was lower in each of the older groups compared to the young group, and this situation persisted after adjustment for body weight and composition.
The relationship between RMR and total T3 serum concentrations suggests that one of the determinants of the variability in RMR may be the activity of the thyroid axis. Possible other reasons for this decline in RMR with aging include lower sympathetic nervous system SNS activity, lower sensitivity to the activity of the SNS, smaller organ size, or lower overall energy intake.
Although neither were measured in the present study, previous studies have indicated that SNS activity is related to energy expenditure and that the decline in RMR in older men may be directly due to a decline in energy intake 49— Contrary to our hypothesis, RMR was not a significant determinant of urinary isoprostane concentrations, serum protein carbonyl concentrations, or DNA fragmentation.
Loft and colleagues 29 found a positive relationship between hour oxygen consumption and urinary excretion of 8-oxodG in women. However, free radical production does not necessarily increase in direct proportion to total oxygen consumption because electron leak is not constant across tissues.
In addition, free radical production is highest in the resting state when adenosine triphosphate ATP demand is low Therefore, one would expect a direct relationship between markers of oxidative stress and RMR rather than total energy expenditure, which is the sum of RMR, the thermic effect of food, and the energy needed to sustain physical activity as observed by Loft and colleagues These discrepancies indicate that a number of factors, not just energy expenditure, contribute to the production of free radicals.
Although there was no relationship between RMR and markers of oxidative stress, nonagenarians had significantly lower RMR with no significant differences in oxidative stress.
Could the lower RMR in nonagenarians be an adaptive response in an effort to attenuate the age-related accumulation of oxidative stress? This question could not be answered by the present study design.
Furthermore, our cross-sectional study design lends itself to limitations because it is impossible to know who from the younger individuals will live beyond 90 years. Because we did not directly measure free radical production, antioxidant concentrations, or antioxidant intake, it is impossible to determine if older individuals produce more free radicals but also have an enhanced capacity to defend against them.
In addition, we did not control for the presence of some diseases of aging or medication usage hypertension and dyslipidemia. Recent data indicate that many disease states are associated with oxidative stress and that the medications used to treat these conditions can also influence oxidative stress; these factors may have affected the current results 54 , Such studies would indicate whether individuals with a lower metabolic rate throughout life have less oxidative damage and therefore live longer.
The current study supports previous findings of an age-related decline in RMR that cannot be fully explained by changes in FFM or FM.
Interestingly, nonagenarians may be protected from the age-related increase in oxidative damage to DNA, but the reduced RMR could not be directly implicated in the mechanism of oxidative stress because no relationship was found between metabolic rate and oxidative damage.
Decision Editor: Luigi Ferrucci, MD, PhD. Relationship between resting metabolic rate RMR and fat-free mass FFM. Markers of oxidative stress in the three different age groups. There were no significant differences in isoprostanes, protein carbonyls, or DNA fragmentation by the Comet or Fragment Length Analysis using Repair Enzymes FLARE assay between the three age groups.
Notes : Values are means ± standard error of the mean with ranges in brackets. This research was supported by the Louisiana Board of Regents through the Millennium Trust Health Excellence Fund [HEF —06 ], by the National Institute on Aging P01AG , and by the National Institute of General Medical Sciences GM and GM Members of the Louisiana Healthy Aging Study: Meghan Allen, Arturo M.
Arce, Mark A. Batzer, Lauri O. Byerley, Pauline Callinan, Cathy M. Champagne, Katie E. Cherry, Yu-wen Chiu, James P. DeLany, Melissa J. deVeer, Devon A. Dobrosielski, Andrea Ermolao, Elizabeth T. Fontham, Paula J. Geiselman, Valentina Greco, Sibte Hadi, Tiffany Hall, Karri Hawley, Scott W.
Herke, Hui-Chen Hsu, Sangkyu Kim, Beth Kimball, Christina King-Rowley, Kim Landry, Li Li, Hui-Yi Lin, Kay Lopez, John D. Mountz, Emily Olinde, Kim Pedersen, Jennifer C. Rood, Henry Rothschild, Ryan A. Russell, Donald Scott, Jennie Silva, Nicole Standberry, L.
Joseph Su, Jessica Thomson, Crystal Traylor, Cruz Velasco-Gonzalez, Jerilyn A. Walker, Xui Yun Wang, Michael A. Welsch, David A. Welsh, Robert H. Wood, and Pili Zhang. We acknowledge and thank everyone working on the Louisiana Healthy Aging Study from four sites, i.
Most of all, we thank all the participants who enrolled in the Louisiana Healthy Aging Study. Austad SN. Theories of aging: an overview. Aging Milano.
Greenberg JA. Organ metabolic rates and aging: two hypotheses. Med Hypotheses. Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. Ku HH, Brunk UT, Sohal RS. Relationship between mitochondrial superoxide and hydrogen peroxide production and longevity of mammalian species.
Free Radic Biol Med. Sohal RS, Allen RG. Relationship between metabolic rate, free radicals, differentiation and aging: a unified theory. Basic Life Sci. Adelman R, Saul RL, Ames BN. Oxidative damage to DNA: relation to species metabolic rate and life span.
Proc Natl Acad Sci U S A. Speakman JR, Talbot DA, Selman C, et al. Uncoupled and surviving: individual mice with high metabolism have greater mitochondrial uncoupling and live longer. Aging Cell. Droge W. Free radicals in the physiological control of cell function.
Physiol Rev. Arnaiz SL, Travacio M, Llesuy S, Boveris A. Hydrogen peroxide metabolism during peroxisome proliferation by fenofibrate.
Biochim Biophys Acta. Beckman KB, Ames BN. The free radical theory of aging matures. Strobel HW, Coon MJ. Effect of superoxide generation and dismutation on hydroxylation reactions catalyzed by liver microsomal cytochrome P J Biol Chem.
Turrens JF, Boveris A. Generation of superoxide anion by the NADH dehydrogenase of bovine heart mitochondria. Biochem J. Hamilton ML, Guo Z, Fuller CD, et al. A reliable assessment of 8-oxodeoxyguanosine levels in nuclear and mitochondrial DNA using the sodium iodide method to isolate DNA.
Nucleic Acids Res. Morrow J, Hill K, Burk R, et al. A series of prostaglandin F2-like compounds are produced in vivo in humans by a non-cyclooxygenase, free radical-catalyzed mechanism. Stadtman ER. Protein oxidation and aging. Halliwell B, Gutteridge JMC.
Free Radicals in Biology and Medicine. New York: Oxford University Press; Murphy MP, Echtay KS, Blaikie FH, et al. Superoxide activates uncoupling proteins by generating carbon-centered radicals and initiating lipid peroxidation: studies using a mitochondria-targeted spin trap derived from alpha-phenyl- N-tert -butylnitrone.
Brand MD. Uncoupling to survive? The role of mitochondria inefficiency in human ageing. Exp Gerontol. Fano G, Mecocci P, Veccheet J, et al. Age and sex influence on oxidative damage and functional status in human skeletal muscle.
J Muscle Res Cell Motil. Hamilton ML, Van Remmen H, Drake JA, et al. Does oxidative damage to DNA increase with age? Mecocci P, Fano G, Fulle S, et al.
Age-dependent increases in oxidative damage to DNA, lipids, and proteins in human skeletal muscle. Barja G, Herrero A. Oxidative damage to mitochondrial DNA is inversely related to maximum life span in the heart and brain of mammals.
FASEB J. Sohal RS, Weindruch R. Oxidative stress, caloric restriction, and aging. The researchers analyzed average total daily energy expenditures, which include the calories we burn doing everything from breathing and digesting food to thinking and moving our bodies.
And this was the first time that we had the ability to do this with a really big data set that would allow us to pull apart the effects of body size and age and gender and all these things on our energy expenditures over the day. Take, for instance, the finding that metabolic rate declines in seniors, which might have been expected.
We can say, 'No, no, no, it's more than that. Results did not show that metabolic rates spiked upward during the teen years or pregnancy, as commonly thought, or that there were specific differences between men and women after accounting for body size and composition.
Registered dietitian Colleen Tewksbury, a senior research investigator at the University of Pennsylvania and a spokesperson for the Academy of Nutrition and Dietetics, said the new study is surprising. But if changing metabolism is not playing a role in weight gain at certain points in adult life, there could be other contributing factors, she said.
It's more likely a much more complex web of lots of different changes happening at once. So that could be changes to food intake.
It could be changes in activity levels. It can be where they're living, what they have access to, what are their sleep changes. Malin said the findings, for instance, contradict the belief that adults experience a decline in metabolism as they move from their 20s into their 30s and that this may be contributing to the obesity epidemic.
Pontzer said the findings in early life highlight the critical importance of infant nutrition meeting the increasing energy demands of growing babies. In addition, he said, the study results could have implications for how much medicine people need at various ages, when they could be metabolizing drugs differently.
In a commentary published with the new study, Timothy Rhoads and Rozalyn Anderson, who work in geriatrics at the University of Wisconsin, said the findings also may have implications for the study of age-related diseases.
A few Metzbolic for this include Glucose monitoring devices loss, being Metabolic rate and aging active Mehabolic the natural aging of your metabolic processes. It also determines Metabolic rate and aging many calories you burn per day. The faster your metabolism, the more calories you burn. The speed of your metabolism is influenced by four key factors 1 :. Other things that can affect your metabolism include age, height, muscle mass and hormonal factors 1.Metabolic rate and aging -
Guidelines from the department of Health and Human Services recommend performing muscle-strengthening activities, such as lifting weights, resistance band exercises or body weight exercise like push-ups, sit-ups, etc.
at least two days per week. To fuel a healthy metabolism you should eat a variety of nutrient dense foods from each food group. Nutrient dense foods are foods that have a high nutrient to calorie ratio such as lean meats, vegetables and whole grains. Consuming fiber-rich foods and drinking plenty of water may particularly benefit metabolic health by aiding digestion and lowering blood sugar and cholesterol.
The reasons for this are not entirely understood, but experts believe a combination of physiological, environmental and behavioral changes are to blame. Research indicates that the following tips can help promote longer, more restful sleep:. However, research indicates that if we start early, we are much more likely to maintain a consistent, healthy body weight, which can be vital for preserving metabolic function, reducing our risk for many chronic conditions and maintaining functional independence well into our golden years.
Kate Lyden, Ph. In this role she designs, implements and supports clinical studies related to physical activity and sleep. She works in close collaboration with academic partners to bring together industry know-how with academic innovation.
Prior to joining Misfit, Inc. Her research examined the effects of interrupting sedentary time with short and continuous bouts of moderate intensity walking on metabolic outcomes in overweight adults. She developed methodologies to quantify physical activity, sedentary behavior and sleep using wearable sensors, and used these techniques to understand the dose-response relationship between physical activity and sedentary behavior and chronic disease.
After completing his Ph. in Exercise Science from the University of Massachusetts, Amherst, Dr. Edward Melanson started his research career as a post-doctoral fellow at the University of Colorado Anschutz Medical Campus.
His research has focused on the effects of lifestyle factors exercise, diet, sleep on energy balance and substrate metabolism. Melanson is currently an Associate Professor in the Division of Endocrinology, with a secondary appointment in the Division of Geriatric Medicine.
He is a long time member of the IMAGE research group Investigations in Metabolism, Aging, Gender and Exercise. Melanson has published more than 55 peer-reviewed journal articles, as well as 11 review articles and several book chapters.
With his collaborators, Dr. Melanson is actively conducting research aimed at understanding the mechanisms via which sleep restriction and alterations in circadian physiology impact metabolism and body weight regulation, as well as mechanisms by which the menopause contributes to weight gain.
Located in the CSU Health and Medical Center W. Lake Street Campus Delivery Fort Collins, CO Email: [email protected].
Apply to CSU Contact CSU Disclaimer Equal Opportunity Privacy Statement. Search Search. Metabolism The term metabolism describes all biochemical reactions that occur inside of our bodies to maintain life. Aging and Metabolism As we age, metabolic processes do not operate as well as when we were younger.
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According to recent findings arte in Scienceahd reaches Self-care for anxiety peak much earlier in Metabolic rate and aging Anti-cellulite cream Metabolic rate and aging down much later than Metagolic previously thought. Before Digestive system support into the details Metabooic the new research, ratf define a few Metaholic. Metabolism is the combination of all the chemical processes that Metabollc an rte to sustain life. For humans, this includes conversion of energy from food into energy for life-sustaining tasks such as breathing, circulating blood, building and repairing cells, digesting food, and eliminating waste. The minimum amount of energy needed to carry out these basic processes while an organism is fasting and at rest is known as the basal metabolic rateor BMR, which can be calculated using a variety of online calculators that take into account an individual's height, weight, age, and sex. BMR is often referred to as resting metabolic rate, or RMR. Total energy expenditure TEE is a combination of BMR, plus energy used for physical activities and energy used to digest food known as dietary thermogenesis. Carmelinda Metabolic rate and aging, E. Jeffrey Metter, Vojtech Melenovsky, Antonio Cherubini, Samer S. Najjar, Alessandro Metabklic, Umberto Meatbolic, Dan L. Despite Metabolic rate and aging controversies from animal studies on Mtabolic relationship between basal metabolic rate BMR and longevity, Visceral fat and cholesterol levels BMR is a risk factor for mortality has never been tested in humans. We evaluate the longitudinal changes in BMR and the relationship between BMR and mortality in the Baltimore Longitudinal Study of Aging BLSA participants. BMR and medical information were collected at the study entry and approximately every 2 years in participants men over a year follow-up. Data on all-cause and specific-cause mortality were also obtained.
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