Caloric restriction and bone health -
Serum leptin, insulin, and IGF-I concentrations were determined by using rat leptin RIA and rat insulin RIA kits Linco Research, Inc.
Serum albumin and calcium and urinary calcium concentrations were determined by using an autoanalyzer Hitachi , Japan. Micro-CT scanning was performed on proximal tibiae using a μCT scanner SCANCO Medical AG, Bassersdorf, Switzerland with a resolution of 12 μm, and microstructure parameters were calculated three-dimensionally as described previously The proximal tibia was positioned to be scanned craniocaudally using slices with 12μm increments at 55 kVp and 72 μA.
On the original three-dimensional 3D image, morphometric indices, including bone volume BV , tissue volume TV , trabecular thickness Tb. Th , trabecular separation Tb. Sp , and trabecular number Tb.
N , were directly determined from the binarized volume of interest. Nonmetric parameters, such as structure model index SMI and connectivity density Conn-Dens. Sections were prepared and stained with Villanueva Goldner to discriminate between mineralized and unmineralized bone and to identify cellular components.
Histomorphometric parameters were measured at the Ito Bone Science Institute Niigata, Japan. Nomenclature and units were used according to the recommendation of the nomenclature committee of the American Society for Bone and Mineral Research.
Bone strength was assessed in femurs by the four-point bending test, according to the previously reported methods 12 , Mechanical tests were performed at the Japan Fine Ceramics Center Nagoya, Japan using a materials testing machine type ; Instron, Norwood, MA.
Specimens were loaded in the anterior-posterior plane at a constant displacement rate of 0. The distances between the upper loading and lower support points were 4 and 8 mm, respectively.
A N load cell was used to measure the load applied to the specimens, and displacement was measured with a linear variable differential transducer. Load and displacement data were collected using Merlin software Instron. Data are expressed as means ± sem. CR was started when animals reached 3 months of age.
As shown in Fig. Body weight changes in CR mice and rats. Body weight was measured every week until 28 wk and every 4—5 wk thereafter.
The time scale is provided as both time after the start of CR upper values and the age of animals lower values in weeks. at the age of 9 months. In addition, detailed microstructure analysis of trabecular bone of mice and rats revealed that after 6 months of CR, Tb. N and Tb. Th as well as Conn.
decreased significantly, whereas SMI and Tb. Sp increased Fig. Assessment of maximal load by the four-point bending test indicated that bone strength in the femurs of CR group was indeed significantly weaker than that of the control AD group Fig.
Chronic CR induces reduced bone mass, deteriorated trabecular structure, and decreased bone strength. A and B, Representative micro-CT images of trabecular bone at the proximal tibiae of AD feeding vs.
CR mice A and AD vs. CR rats B at the age of 9 months i. after 6 months of CR. C, Microstructural parameters derived from micro-CT analysis of trabecular bone at the proximal tibiae of AD vs.
CR mice. D, Bone strength after 6 months of CR was determined by maximal load at the femur by the four-point bending test. E, Reduced bone mass by CR is not due to a concomitant reduction in calcium intake.
Micro-CT scanning of proximal tibia again revealed the 3D BV decreased by this continuous CR for 6 months, as with the CR by alternate-day feeding Fig. To examine whether the decreased bone mass after chronic CR was due to suppressed bone formation, accelerated bone resorption, or a combination of both mechanisms, histomorphometric analyses were performed at the tibial metaphysis.
When CR mice aged 9 months were switched to AD feeding, the suppression of the BFR was reversed Fig. CR causes suppression of bone formation with transiently elevated bone resorption.
A, Results of histomorphometric analysis at the proximal tibiae of AD vs. CR mice after 6 months of CR. Data are normalized for the BS. B, Reversibility of the effects of CR on bone mass. C, Continuous suppression of bone formation by CR.
The time scale is provided as both the time after the start of CR upper values and the age of the animals lower values in months M. The suppressive effect of CR on bone formation was observed as early as 1 month after the initiation of CR and consistently for at least 9 months Fig.
On the other hand, a consistent change in bone resorption was not observed; osteoclast surface Oc. Collectively, these data suggest that the decreased bone mass after chronic CR is mainly due to suppressed bone formation, although a transient increase in bone resorption may have helped enhance the effect.
Biochemical markers of energy metabolism were assessed after 6 months of CR in the blood samples of rats due to the availability of a larger volume of samples.
There was no significant difference in serum calcium concentrations between the AD and CR groups Fig. Accordingly, serum leptin concentrations as well as insulin, IGF-I, and blood sugar levels were significantly reduced after long-term CR Fig.
It is conceivable, therefore, that an altered signaling of these hormones may have affected bone metabolism under CR. Blood biochemical characteristics under long-term CR. The results of serum, whole blood, and plasma biochemistry in AD white bars vs.
CR black bars rats is shown. Blood was collected at the age of 9 months i. CR reduces bone mass through leptin signaling and sympathetic nervous tone. CR black bar regimen for 4 months. Representative micro-CT images are shown to the right.
D, Expression of NMU in the hypothalamus of CR vs. AD mice. RNA was extracted from the hypothalamus after CR for the indicated periods in months, M and subjected to quantitative RT-PCR.
E, Involvement of the sympathetic nervous system. The decrease in bone mass by CR was prevented by propranolol Pro , a β-blocker, whereas isoproterenol Iso , a β-stimulant, reduced BV in AD mice. Consistent with this notion are the results that the expression of neuromedin U NMU , a mediator of the antiosteogenic action of leptin in the hypothalamus 15 , was increased in the hypothalamus of CR mice in the face of reduced circulating leptin concentrations, compared with the AD group Fig.
It has been demonstrated that the suppression of bone formation induced by leptin is mediated through an increased sympathetic nervous tone and signaling through the β2-adrenergic receptor expressed on osteoblasts To examine the involvement of the sympathetic nervous system in the suppressive effect of CR on bone, the effect of blocking adrenergic tone on bone mass under the CR regimen was examined.
Conversely, when mice were treated with isoproterenol, a β-stimulant, BV decreased, even in the AD group, down to the CR level Fig. Treatment with isoproterenol did not cause a further reduction in BV in CR mice Fig. These results are consistent with our concept that the reduced BV by CR is mediated through increased activity of the sympathetic nervous system.
We examined the time course of the effects of CR on 3D BV. After CR was initiated at the age of 3 months, there was a significant decrease in bone mass at 3 months of CR i. at the age of 6 months , and a clear-cut reduction in BV was also observed after 6—9 months of CR i.
at the age of 9—12 months Fig. However, the effect of CR on BV became more and more obscure thereafter, and after 13—17 months of CR i. at the age of 16—20 months , BV was indistinguishable between CR and AD mice Fig.
In fact, after 24 months of CR i. at the age of 27 months , CR mice exhibited a modestly but significantly higher bone mass than the AD control group Fig. CR protects against age-related bone loss by reducing bone turnover. A, Changes in the 3D BV fraction at the proximal tibiae of AD white bars vs.
CR black bars mice, as determined by micro-CT, were followed at the indicated times. The time scale is provided as both the time after the start of CR upper values and the age of mice in months lower values.
B, Representative micro-CT images of trabecular bone in the proximal tibiae of AD vs. CR mice at natural death at the indicated age in months M. C, Microstructural parameters derived from micro-CT analysis of trabecular bone at the proximal tibiae of life-long CR mice black bars.
The age at death is provided below in months M as the mean ± sem. D, Results of histomorphometric analysis of the proximal tibiae of AD white bars vs.
CR black bars mice after 24 months of CR. Oc, Number of osteoclasts. Because CR extends the maximal lifespan, the average age of CR mice at death was higher than that of the control AD group Detailed microstructure analysis indicates that the higher bone mass in CR mice was associated with increased Tb.
Th and connectivity and decreased SMI Fig. The protective effects of lifelong CR on age-related bone loss and microstructural deterioration were also confirmed in F rats Fig.
CR protects against age-related bone loss and microstructural deterioration in F rats. A, Representative micro-CT images of trabecular bone at the proximal tibiae of AD vs.
CR F rats at natural death at the indicated age in months M. B, Microstructural parameters derived from micro-CT analysis of trabecular bone at the proximal tibiae of AD white bars vs.
CR black bars F rats. The age at death is provided below in months M as mean ± sem for each group. Finally, to gain some insight into the mechanism by which CR countered age-related bone loss, histomorphometric analysis was performed at the tibiae at the age of 27 months i.
after 2 yr of CR. The results indicate that the number of osteoclasts N. With respect to indices of bone formation, the osteoblast surface Ob. These data suggest that the higher bone turnover rate in aged AD animals is mitigated by CR and that CR counters the aging-related bone loss by reducing bone turnover.
Thus, regulation of bone turnover appears to be a protective strategy deployed by CR against skeletal aging. Nutrition, especially the intake of calcium and vitamin D, is an important remedy for maintaining bone health.
The present study demonstrates that under physiological conditions, the amount of total caloric intake per se has a profound impact on bone remodeling. Under these conditions, bone resorption and subsequently bone formation are stimulated, with a net balance such that the former exceeds the latter, resulting in bone loss and structural deterioration.
CR with relatively increased calcium content failed to reverse the reduction in bone mass, which lends further support to our conclusion that a reduction in caloric, not calcium intake, is responsible for the decreased bone formation and bone mass induced by CR.
Bone remodeling, performed by bone-resorbing osteoclasts and bone-building osteoblasts, functions under hormonal 19 , 20 , neuronal 21 , immunological 22 , and mechanical 23 , 24 control. Recently, much attention has been focused on the central control of bone remodeling Mice harboring genetic mutations in leptin signaling and the sympathetic nervous system have provided powerful tools in dissecting molecular pathways that link energy homeostasis to bone remodeling 16 , However, the physiological conditions under which the pathway operates have been elusive.
Our data suggest that changes in leptin signaling may be involved in the suppression of bone formation and osteopenia after chronic CR. The effects of leptin on bone metabolism appear to be complex and to depend on the site and type of bone analyzed.
In addition, leptin treatment partially prevents the bone loss induced by ovariectomy in the trabecular bone of the proximal tibia in rats 27 and counters the inhibition of the longitudinal effects of calorie deprivation in young mice Leptin can affect bone metabolism not only through the central nervous system 16 but also through a peripheral pathway by acting directly on the cells in bone 29 , A recent study demonstrates that NMU-deficient mice exhibit high bone mass with increased bone formation and are resistant to the antiosteogenic effects of leptin and isoproterenol, suggesting that NMU is a mediator of the antiosteogenic action of the leptin-sympathetic nervous system The data show that treatment with propranolol blocked the suppressive effect of CR on bone.
Taken together with the link between central leptin signaling and the peripheral sympathetic nervous system 17 , one plausible hypothesis is that leptin signaling regulates bone metabolism in response to CR through increased activity of the sympathetic nervous system.
However, the data cannot rule out the possibility that the adrenergic receptor responds to CR independently of leptin signaling. Importantly, this study discloses another and unexpected aspect of CR, namely a protective effect against age-related bone loss during the latter half of life.
Histomorphometric analysis of 1- vs. Although CR animals had gained less bone during young adulthood, they maintained a higher bone mass after 27 months of age.
This protection from skeletal aging is likely to be attained by reducing bone turnover, because reduced osteoclast number and activity with a reduced bone formation rate was observed in aged CR mice compared with the AD group.
At present, there is no evidence for the involvement of leptin signaling in the slower age-related bone loss in the CR group, and more studies are required to identify which factor s specifically elicited by the CR regimen provides protection against skeletal aging by reducing bone turnover.
In conclusion, if the present results were to extrapolate to humans, it would follow that excessive dieting during young adulthood would be discouraged, whereas a mild reduction in calorie intake after middle age would be encouraged to help slow the aging of the skeleton.
It remains to be determined whether CR during the latter half of life alone has a protective effect or a whether combination of AD and CR, i. AD feeding until 1 yr of age followed by CR thereafter, would be even more effective in maintaining skeletal health in rodents, both by increasing peak bone mass and by slowing the rate of age-related bone loss.
We thank Drs. Akio Inui Kagoshima University and Mineko Fujimiya Shiga Medical University for instructions on hypothalamus isolation and valuable suggestions, Dr.
Shu Takeda Tokyo Medical and Dental University for discussion and PCR primers for NMU, Ms. Akemi Ito Ito Bone Science Institute for technical assistance with the bone histomorphometry, Japan Fine Ceramics Center Nagoya, Japan for mechanical tests of bone samples, Dr.
Sunao Takeshita NCGG for comments on the manuscript, and members of NCGG for stimulating discussion. Pacific Edit reviewed the manuscript before submission. This study was supported in part by grants from Daiko Foudation to K.
and from the Program for Promotion of Fundamental Studies in Health Sciences of the National Institute of Biomedical Innovation of Japan MF and to K. Sambrook P , Cooper C Osteoporosis. Lancet : — Google Scholar.
Ralston SH , de Crombrugghe B Genetic regulation of bone mass and susceptibility to osteoporosis. Genes Dev 20 : — Kanis JA Diagnosis of osteoporosis and assessment of fracture risk. Weindruch R , Sohal RS Seminars in medicine of the Beth Israel Deaconess Medical Center. Caloric intake and aging.
N Engl J Med : — Kalu DN , Hardin RR , Cockerham R , Yu BP , Norling BK , Egan JW Lifelong food restriction prevents senile osteopenia and hyperparathyroidism in F rats.
Mech Ageing Dev 26 : — Sanderson JP , Binkley N , Roecker EB , Champ JE , Pugh TD , Aspnes L , Weindruch R Influence of fat intake and caloric restriction on bone in aging male rats. J Gerontol A Biol Sci Med Sci 52 : B20 — B In contrast, Bahijri et al.
examined the effects of intermittent fasting on bone markers during the Muslim holiday of Ramadan in which observers fast from sunrise until sunset and found decreased evening PTH levels after two weeks of IF.
This study did not include an assessment of bone mineral density and it is unclear if this effect is due to caloric restriction, sleep disturbance, or other factors such as alteration in mineral intake with evening serum calcium significantly higher during Ramadan Significant discrepancies exist within this literature, especially with regard to the length of intervention, degree of restriction, etc.
A relatively small sample size is an additional limitation, particularly for the human subject trials. This underscores the need for future work to replicate previous study designs and provide independent corroboration of findings in diverse patient populations. That said, it is generally consistent across species and multiple studies that caloric restriction negatively influences bone mass; at present, it appears that intermittent fasting may not.
It is important to note, however, that bone mass is only one aspect of fracture risk and measurements of fracture rate, bone strength, and bone quality are generally lacking in the studies detailed here.
Future study is required to address this important limitation of the current literature. These articles were screened by CH and AE for relevance to the topic, eliminating publications.
Intramural funds for the publication of this work were provided to JWL by Marian University. Copyright: © Lowery JW. This article is distributed under the terms of the Creative Commons Attribution 4. Home Articles Article Details. Introduction Osteoporosis is a chronic condition characterized by low bone mass and places individuals at increased risk for fracture.
Bone Remodeling and Bone Health Bone matrix is produced by cells called osteoblasts and resorbed by cells called osteoclasts. Caloric Restriction and Bone Health In this section, we discuss the existing studies examining the impact of caloric restriction on bone health with an emphasis on molecular markers of bone remodeling.
Intermittent Fasting and Bone Health In this section, we discuss the relatively limited data examining the impact of intermittent fasting on bone health.
Conflict of Interest The authors declare no conflicts of interest. References Scaturro D, Vitagliani F, Terrana P, Tomasello S, Camarda L, Letizia Mauro G: Does the association of therapeutic exercise and supplementation with sucrosomial magnesium improve posture and balance and prevent the risk of new falls?
Aging Clin Exp Res Capozzi A, Scambia G, Lello S: Calcium, vitamin D, vitamin K2, and magnesium supplementation and skeletal health. Maturitas , Bielemann RM, Martinez-Mesa J, Gigante DP: Physical activity during life course and bone mass: a systematic review of methods and findings from cohort studies with young adults.
BMC Musculoskelet Disord , Tenforde AS, Sayres LC, Sainani KL, Fredericson M: Evaluating the relationship of calcium and vitamin D in the prevention of stress fracture injuries in the young athlete: a review of the literature.
PM R , 2 10 : Weaver AA, Houston DK, Shapses SA, Lyles MF, Henderson RM, Beavers DP, Baker AC, Beavers KM: Effect of a hypocaloric, nutritionally complete, higher-protein meal plan on bone density and quality in older adults with obesity: a randomized trial. Am J Clin Nutr , 2 Ciobanu O, Elena Sandu R, Tudor Balseanu A, Zavaleanu A, Gresita A, Petcu EB, Uzoni A, Popa-Wagner A: Caloric restriction stabilizes body weight and accelerates behavioral recovery in aged rats after focal ischemia.
Aging Cell , 16 6 Sandesara PB, Sperling LS: Caloric Restriction as a Therapeutic Approach to Heart Failure: Can Less Be More in Mice and Men?
Circ Heart Fail , 11 3 :e de Lucia C, Gambino G, Petraglia L, Elia A, Komici K, Femminella GD, D'Amico ML, Formisano R, Borghetti G, Liccardo D et al: Long-Term Caloric Restriction Improves Cardiac Function, Remodeling, Adrenergic Responsiveness, and Sympathetic Innervation in a Model of Postischemic Heart Failure.
Waldman M, Cohen K, Yadin D, Nudelman V, Gorfil D, Laniado-Schwartzman M, Kornwoski R, Aravot D, Abraham NG, Arad M et al: Regulation of diabetic cardiomyopathy by caloric restriction is mediated by intracellular signaling pathways involving 'SIRT1 and PGC-1alpha'. Cardiovasc Diabetol , 17 1 Halpern B, Mendes TB: Intermittent fasting for obesity and related disorders: unveiling myths, facts, and presumptions.
Arch Endocrinol Metab Dorling JL, Martin CK, Redman LM: Calorie restriction for enhanced longevity: The role of novel dietary strategies in the present obesogenic environment.
Ageing Res Rev , Pifferi F, Aujard F: Caloric restriction, longevity and aging: Recent contributions from human and non-human primate studies. Prog Neuropsychopharmacol Biol Psychiatry , Redman LM, Ravussin E: Caloric restriction in humans: impact on physiological, psychological, and behavioral outcomes.
Antioxid Redox Signal , 14 2 Rynders CA, Thomas EA, Zaman A, Pan Z, Catenacci VA, Melanson EL: Effectiveness of Intermittent Fasting and Time-Restricted Feeding Compared to Continuous Energy Restriction for Weight Loss. Nutrients , 11 Ayub N, Faraj M, Ghatan S, Reijers JAA, Napoli N, Oei L: The Treatment Gap in Osteoporosis.
J Clin Med , 10 Greenblatt MB, Tsai JN, Wein MN: Bone Turnover Markers in the Diagnosis and Monitoring of Metabolic Bone Disease. Clin Chem , 63 2 Hadjidakis DJ, Androulakis, II: Bone remodeling.
Ann N Y Acad Sci , Gao Y, Patil S, Jia J: The Development of Molecular Biology of Osteoporosis. Int J Mol Sci , 22 Hamrick MW, Ding KH, Ponnala S, Ferrari SL, Isales CM: Caloric restriction decreases cortical bone mass but spares trabecular bone in the mouse skeleton: implications for the regulation of bone mass by body weight.
J Bone Miner Res , 23 6 Devlin MJ, Cloutier AM, Thomas NA, Panus DA, Lotinun S, Pinz I, Baron R, Rosen CJ, Bouxsein ML: Caloric restriction leads to high marrow adiposity and low bone mass in growing mice. J Bone Miner Res , 25 9 Shen CL, Zhu W, Gao W, Wang S, Chen L, Chyu MC: Energy-restricted diet benefits body composition but degrades bone integrity in middle-aged obese female rats.
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Connor Natural beetroot juice. Hernon 1,2 anc, Abduallah Elsayed 3Raphael M. Vicente 4Ariane Zamarioli caloric restriction and bone healthNone A. Kacena 3,5,6Jonathan W. Lowery 1,2,3,5,6. CR and IF are dietary interventions used in rehabilitative healthcare for augmenting weight loss and also proposed for recovery of conditions such as stroke and heart failure.Restrictioj restriction, especially in combination with exercise, can make bones smaller and weaker, according to new resyriction in mice. Abd contrast, exercising while on restridtion full ajd diet jealth benefit restrictioj health, say the researchers.
Healtth describe their investigation and restricttion results in annd recent Journal of Bone and Mineral Research paper. Maya Styner, rsstriction associate professor of medicine at the Resttiction of North Hfalth at Immune system defense Hill.
Bbone is not an inert material but very much caloriv it is hdalth renewing itself. During childhood, caloric restriction and bone health bone formation happens faster boone removal of old bone, resulting Delectable Refreshment Selection bigger, heavier, and denser bones.
Bone calpric continues outpacing bone removal until around calooric age of 20—30 years, during which time it peaks caloric restriction and bone health most people. They can do this by getting regular exercise, restrkction smoking, caloric restriction and bone health drinking too much alcohol, and ensuring that they have a sufficient amount of vitamin D caloric restriction and bone health calcium in abd diet.
Osteoporosis occurs when restridtion formation is too slow, when anr is too quick, or both. The condition, which tends caoric affect females healht often than OMAD and weight maintenance, weakens bones restgiction makes them more likely to fracture.
Scientists suggest gealth one reason osteoporosis is more caloric restriction and bone health in females is because their bones heapth to be healtg and thinner. Another reason could be destriction menopause csloric on a sudden drop in estrogena hormone that restrriction protect amd. Styner suggests that the new findings could be particularly caloric restriction and bone health for women hone as they age, their bone nad starts restrictkon deteriorate rwstriction.
In their investigation, Dr. Styner and colleagues focused on bone heaoth fat. Scientists Natural muscle soreness remedies not fully understand restrition this type healh fat restridtion. They suspect that it is harmful to bones in humans resttiction other mammals.
Previous studies have suggested that lower levels of bone marrow fat are usually caolric indication of good bone reshriction. In earlier festriction, Dr.
Styner had examined restrition calorie consumption relates Personalized weight loss bone marrow fat and how exercise might influence this link. Those none showed, for example, that levels of bone marrow fat go up when excess calorie consumption leads to obesity.
They also found that when mice of a normal weight and mice with obesity exercised, it caused a drop in their bone marrow fat and improved their bone density. The purpose of the new study was to find out what happens to bone marrow fat and bone health during calorie restriction.
The researchers split mice into two groups. The calorie restricted mice received supplements of minerals and vitamins so that these nutrient intakes matched those of the mice on the normal diet. The team then gone the mice again, into sedentary and exercise subgroups, and monitored them for 6 weeks.
The results showed that although the calorie restricted mice lost weight, their bone marrow fat levels went up significantly. These mice also experienced a decrease in bone quantity. The researchers conclude that the bone loss in the calorie restricted mice was due to calorie reduction alone and not lack of nutrients, since the mice had the calodic vitamin and mineral intake as their regular diet counterparts.
The team found that, as expected from previous studies, adding exercise to calorie restriction led to a reduction in bone marrow fat. However, it unexpectedly also led to a cqloric in overall quantity and quality of bone. The researchers were surprised to find that under conditions of calorie restriction, exercise appears to make bones more fragile — not more robust.
They are already planning further investigations to better understand the function of bone marrow fat. In particular, they wish to learn about the underlying mechanisms that cause diet and exercise to produce the effects that they found.
Bone density decreases with time. Some people have a risk of developing weak or brittle bones. Learn how to increase or maintain bone density here. Paget's disease is the second most common bone disorder after osteoporosis, and involves a distortion of the normal skeletal architecture.
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Medical News Today. Health Conditions Health Products Discover Tools Connect. Calorie restriction plus exercise can make bones more fragile. By Catharine Paddock, Ph. on September 13, — Fact checked by Jasmin Collier. Share on Pinterest Can restricting calories and exercising make bones smaller and weaker?
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: Caloric restriction and bone health| The effects of calorie restriction, intermittent fasting and vegetarian diets on bone health | Related articles in PubMed Linking bone marrow fat with decreased bone mineral density among Indian patients with osteoporotic fracture. Annu Rev Nutr — Our study, therefore, provides novel information on the skeletal effects of CR- and EX-induced weight loss. Hyldstrup LAndersen TMcNair PBreum LTransbol I Bone metabolism in obesity: changes related to severe overweight and dietary weight reduction. Published : 22 March Calcif Tissue Int ;36 suppl 1 S S61 PubMed Google Scholar Crossref. The data reported in this article were obtained as part of an investigation of the feasibility of CR in healthy volunteers Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy [CALERIE]. |
| Calorie Restriction Does Not Appear To Induce Bone Loss In Overweight Adults | ScienceDaily | All subjects who provided follow-up data at any time point are included in the analysis. Between-group comparisons of categorical baseline variables were performed using χ 2 tests or Fisher exact tests. Between-group comparisons of continuous baseline variables were performed using analysis of variance. Longitudinal analyses were carried out using mixed-model repeated-measures analysis of variance. The primary focus of these analyses was on the significance of the interaction between group and time point. Analyses testing for within-group changes also were performed using mixed-model repeated-measures analysis of variance. Select mixed models were adjusted for sex, age, and current hormone therapy use depending on the outcomes examined. Data are presented in tables as least squares mean ± SE. Data are presented in text as mean ± SD. The data analysis was generated using SAS statistical software version 9. Of the 48 subjects who started the intervention, 46 completed the study; 1 woman dropped out of the CR group at 6 months because of the inability to comply with the diet prescription, and 1 man dropped out of the EX group at 9 months because of medical reasons unrelated to the study. The 3 groups did not differ on baseline demographic and clinical characteristics except for age, with the EX group being slightly older than the CR group Table 1. Most participants were overweight BMI, The proportion of women receiving hormone therapy did not differ among the groups. One woman in the HL group and 1 woman in the EX group discontinued hormone therapy after the 3-month time point. Therefore, for these 2 participants, follow-up data collected after 3 months were not used. The changes in BMD at the total hip and intertrochanter were significantly different from the corresponding changes total hip: 1. In contrast, despite the decrease in body weight in the EX group, there were no significant changes in BMD in this group, and there were no significant differences in BMD changes between the EX and HL groups. Bone markers and hormones over the study period are given in Table 3 and Figure 2. C-telopeptide of type I collagen levels significantly increased in the CR group and EX group at 6 months, while C-telopeptide of type I collagen levels did not change in the HL group. Although there were no significant changes in bone-specific alkaline phosphatase levels from baseline within each group, the change in bone-specific alkaline phosphatase at 6 months in the EX group was greater than the corresponding changes in the CR and HL groups. There were no significant changes in osteocalcin concentrations. Leptin concentrations decreased in the CR and EX groups compared with no changes in the HL group. There were no significant changes in serum estradiol levels. Accordingly, intake of macronutrients such as protein and fat also decreased in the CR compared with the EX and HL group. The intake of many micronutrients increased in the EX and CR groups, although not in the HL group. Seven-day Physical Activity Recall Questionnaire findings indicated that MET hours per day increased in the EX group from Heart rate monitors revealed that the EX group exercised 5. Maintaining adequate bone mass helps reduce fracture risk in old age. Although bone loss often accompanies CR-induced weight loss in obese persons, 10 - 18 the clinical implications of this adverse effect are unclear because obesity is associated with increased bone mass. In addition, it is unknown whether EX-induced weight loss causes the same decrease in bone mass as CR-induced weight loss. Therefore, we conducted a 1-year randomized controlled trial to evaluate the effect of similar weight loss induced by either CR or EX on BMD in nonobese, middle-aged adults. The results of the present study show that EX-induced weight loss does not change BMD, whereas CR-induced weight loss decreases BMD in the lumbar spine, total hip, femoral neck, and intertrochanter. Changes in body weight correlated directly with changes in BMD in the CR group but not in the EX group. These findings have important implications in designing an appropriate weight-loss therapy program in middle-aged adults, particularly in the subset of patients who may already be at increased risk for bone fracture. Thus, there is little information on the effects of EX-induced weight loss on BMD. To our knowledge, only 1 previous study compared the effects of CR- and EX-induced weight loss on BMD. In the present study, we carefully monitored energy balance eg, using food diaries and heart rate monitors to 1 reduce caloric intake without changing energy expenditure in the CR group and 2 increase energy expenditure without changing caloric intake in the EX group. Our study, therefore, provides novel information on the skeletal effects of CR- and EX-induced weight loss. Despite both weight loss and increased bone turnover in the CR and EX groups, only the CR group had a significant decrease in BMD. A common explanation given for the bone loss induced by weight loss is reduction in mechanical stress on the weight-bearing skeleton ie, hip and spine. As expected with weight loss, we found that leptin levels decreased similarly in the EX and CR groups. Accordingly, fat mass decreased to a similar extent approximately 6 kg in the EX and CR groups, as previously reported. Therefore, our results do not support an important role for leptin. There were also no significant changes in estradiol levels, despite use of an ultrasensitive estradiol assay. However, these findings must be interpreted cautiously because approximately one third of female subjects were receiving hormone therapy although we enrolled only women using a stable dose prior to the study. These findings are consistent with previous reports demonstrating that 1 the association with BMD is stronger for weight than for estrogen concentrations 9 and 2 estrogen production may not be the most significant predictor of BMD. There is little information regarding markers of bone turnover during weight loss, 10 , 20 , 37 and to our knowledge the present study is the first to measure C-telopeptide of type I collagen, a sensitive marker of bone resorption. However, the increase in bone turnover was detrimental only in the CR group, while the EX group did not have a significant decrease in BMD even after 1 year. The changes in bone-specific alkaline phosphatase levels marker of bone formation in the EX group were greater than in the CR group, suggesting less imbalance in the bone remodeling cycle. The strengths of the present study include the randomized controlled trial design, the comprehensive assessments of energy intake and expenditure, and the high rate of compliance of participants. A limitation is that the dual-energy x-ray absorptiometry provided information on bone quantity but not bone quality eg, microarchitecture , which is an additional determinant of fracture risk. Because the present study was part of a parent study of the feasibility of CR in humans and effects on body composition, 23 an additional limitation is the relatively small sample size. Our findings must be considered preliminary, particularly as it was not powered to examine sex differences in BMD responses. We controlled for the effect of sex by including it as a covariate in the mixed-model analysis of variance. Most participants were overweight, so the results should be cautiously extended to nonoverweight populations. In summary, 1 year of CR and 1 year of EX induced similar weight loss, but only CR-induced weight loss was accompanied by significant decreases in BMD. Our results provide evidence that EX-induced weight loss is associated with preservation of BMD at important clinical sites of fracture. Therefore, EX has the important advantage over CR by protecting against bone loss. However, because the amount of EX required to achieve clinically meaningful weight loss is large, a more practical approach for weight reduction is a combination of CR and EX. Our results suggest that regular EX should be included as part of a comprehensive weight loss program to offset the adverse effects of CR on bone. Correspondence: Dennis T. Villareal, MD, Forest Park Blvd, Washington University School of Medicine, St Louis, MO dvillare wustl. Author Contributions: Dr Villareal had full access to all the data in the study and takes responsibility for the integrity and the accuracy of the data analysis. Study concept and design : Holloszy and Schechtman. Acquisition of data : Villareal and Weiss. Analysis and interpretation of data : Villareal, Fontana, Weiss, Racette, Steger-May, Schechtman, Klein, and Holloszy. Drafting of the manuscript : Villareal, Fontana, Racette, Steger-May, Schechtman, and Klein. Critical revision of the manuscript for important intellectual content : Villareal, Fontana, Weiss, Racette, Schechtman, Klein, and Holloszy. Statistical analysis : Steger-May and Schechtman. Obtained funding : Holloszy. Administrative, technical, and material support : Holloszy, Villareal, Fontana, Racette, and Klein. Study supervision : Villareal, Weiss, and Racette. Dr Weiss was supported by grant AG from the National Institutes of Health. full text icon Full Text. 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Racette SBWeiss EVillareal DT et al. One year of caloric restriction in humans: feasibility and effects on body composition and abdominal adipose tissue. J Gerontol A Biol Sci Med Sci ; PubMed Google Scholar Crossref. Weiss EPRacette SBVillareal DT et al. Improvements in glucose tolerance and insulin action induced by increasing energy expenditure or decreasing energy intake: a randomized controlled trial. Accessed September 1, Although fat in the bone is poorly understood, to date it is thought to be harmful to bones of mammals, including humans, because it makes bone weaker. Less fat is usually an indication of better bone health. Exercise in both obese and normal weight mice decreased bone marrow fat and improved the density of bones. The latest study looked at what happens to bone marrow fat and overall bone health when restricting calories. There were four groups of mice in all — a group on a regular diet RD , a group on a calorie-restricted CR diet, a RD group that exercised RD-E , and a CR group that exercised CR-E. Mice in the CR group ate 30 percent less than what RD mice ate. A 30 percent reduction would equal a diet of 1, calories per day, which is around the amount suggested to most women trying to lose weight at a rate of one pound a week. Both CR groups of mice were given supplements of vitamins and minerals to match the amount the RD group received from the extra food they ate. This, Styner says, is an indication that the effect on bone health was from calorie restriction, and not a lack of nutrients. When exercise was introduced to the CR group, bone marrow fat decreased as it had in previous studies, but the overall quantity and quality of bone decreased as well. Instead of making bones more robust, exercise made bones more fragile when paired with calorie restriction. Your calorie intake and exercise routine can have a great impact on the strength of your bones and your risk for break or fracture. Styner says her team is now planning to conduct more research to understand the purpose of bone marrow fat and why it is affected by diet and exercise. This study was funded by grants from the National Institutes of Health NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases NIAMS. |
| Caloric restriction in young, overweight adults does not adversely affect bone health | J Bone Miner Res — Article CAS PubMed Google Scholar Ding C, Parameswaran V, Udayan R et al Circulating levels of inflammatory markers predict change in bone mineral density and resorption in older adults: a longitudinal study. They were offered information about a healthy diet 25 but only received it if requested. J Clin Endocrinol Metab ; PubMed Google Scholar. Am J Clin Nutr S—S Article CAS PubMed Google Scholar Veronese N, Solmi M, Caruso MG et al Dietary fiber and health outcomes: an umbrella review of systematic reviews and meta-analyses. Leptin inhibits osteoclast generation. Results Body weight decreased similarly in the CR and EX groups |
| Access this article | As shown in Fig. Veronese N, Shivappa N, Hebert J et al Pro-inflammatory dietary pattern is associated with fractures in women: an eight year longitudinal cohort study. Online ISSN Print ISSN Copyright © Endocrine Society. Download references. Journal Article. |
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