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What to Eat to Reverse Osteoporosis Naturally! Bone health and weight management weight is often Muscle soreness prevention heallth healthy living. Managsment weight loss could be detrimental Injury prevention nutrition your bone densityespecially in postmenopausal women. Losing too much bone mangaement can bring on Muscle soreness prevention and lead to a managejent risk of fractures. According to the National Institutes of Healththe reduction in bone mineral density following weight loss is caused by decreased mechanical stress of the bones during movement and increased calcium loss. Rapid weight loss methods with low-energy diet programs of less than calories per day have been linked to the cause of lasting bone density loss in postmenopausal women. Read on for tips on losing weight and reducing your risk of bone density loss that could lead to osteoporosis.Bone health and weight management -
Weight changes have been commonly assessed as the difference between baseline and a single follow-up. However, during this period, individuals may experience repeated episodes of weight loss and subsequent weight gain or weight cycling.
These weight variations have been associated with negative effects on skeletal health in younger individuals [ 32, 33 ]. The few available studies in the elderly suggest that weight cycling increases their risk of fracture [ 34, 35 ].
These findings were closely related to the extent of variability in weight [ 34 ] and the number of weight cycling episodes between the ages of 25 and 50 years [ 35 ]. This section addresses the findings of interventional studies focused on lifestyle changes resulting in weight loss. Interventional studies that explored the effects of weight loss through lifestyle modification on skeletal health outcomes in obese older adults.
A month randomized controlled trial RCT comprised obese and frail older adults [ 36, 37 ]. They also experienced synchronous increases in osteocalcin bone formation and C-telopeptide of type I collagen or CTX bone resorption levels and decreases in hip BMD at 6 and 12 months compared to baseline [ 36, 37 ].
Hip structure analysis based on DXA-acquired BMD images revealed decreases in cross-sectional area and cortical thickness and increases in buckling ratio at the hip in the weight loss group at 12 months [ 31 ].
Collectively, these changes suggest bone degradation secondary to weight loss achieved by diet rather than a normalization of BMD relative to weight loss. Importantly, the prescribed diet in this arm was characterized by a moderate energy deficit, while providing sufficient quantities of protein, calcium, and vitamin D [ 36 ].
These data suggest that even well-planned weight loss diets may not suffice to maintain skeletal health in the elderly. In contrast to hip BMD, lumbar spine and total body BMD appear to be unaffected by weight loss in this age group [ 36, 38, 39 ].
It is uncertain whether these findings were actual treatment effects or were flawed by measurement error. In the presence of obesity or during aging, calcifications originating from atherosclerotic lesions within the aorta or osteophytes may artificially mask bone reduction [ 9 ].
Nevertheless, these findings in obese elderly individuals are consistent with those of a meta-analysis of diet-induced weight loss studies [ 9 ].
The majority of the studies was conducted in younger adults and indicated similar skeletal responses to this weight loss approach with age [ 9 ].
Several studies have addressed the combined effects of exercise and caloric restriction on bone health [ 31, 36, 37, ]. In an earlier investigation, older women were offered counseling on diet and physical activity to induce weight loss [ 40 ].
Weight loss was a significant predictor of total body BMD, but not spine or hip BMD [ 40 ]. Interestingly, total body and hip BMD declined not only in the weight loss group but also in controls [ 40 ]. The study was not informative about the individual contributions of diet and exercise to weight loss and bone loss, and the participants did not follow a specific exercise program under supervision.
However, the data revealed the importance of including a control group with no weight loss, given that aging itself is associated with bone deterioration.
Haywood et al. Total body BMD was assessed by DXA as the sole skeletal health outcome at baseline and at 12 weeks follow-up. The exercise plus very low-calorie diet group experienced greatest weight loss, accompanied by a small, but significant, reduction in total body BMD; no significant changes were observed in the other study arms [ 41 ].
Additional evidence on the effects of exercise added to weight loss were obtained from 2 further RCTs [ 36, 42 ]. In a first small cohort, the effects of a lifestyle intervention consisting of caloric restriction, calcium and vitamin D supplementation, and a combined aerobic and resistance training program were compared to no treatment.
The reductions in hip BMD were correlated with elevations in CTX ~fold and osteocalcin ~fold , indicating that the bone loss was mediated by an uncoupling of bone formation from resorption, favoring the latter.
BMD was maintained at the lumbar spine, which was suggested to be a bone-protective effect of exercise [ 42 ]. In a subsequent study by the same group, obese and frail older adults were randomized to no treatment, caloric restriction, exercise without weight loss, or caloric restriction combined with exercise [ 36 ].
The group that was randomized to caloric restriction combined with exercise experienced less hip bone loss than those who followed caloric restriction alone.
Unlike the group subjected to caloric restriction, the combined exercise and caloric restriction group did not experience changes in bone turnover markers or bone structure cross-sectional area, cortical thickness, and volumetric BMD at the 1-year follow-up, although trabecular microarchitecture was not assessed [ 31, 37 ].
These results suggest that a combination of resistance and aerobic training added to a weight loss program can lessen the bone loss induced by weight reduction. More recent studies have focused on the exercise type that would be most beneficial for weight loss in obese older individuals [ 39, 44, 45 ].
In a 6-month RCT, Villareal et al. Beaver et al. Volumetric BMD and cortical thickness estimates at the hip and femoral neck assessed by CT scans were significantly declined in all groups, with the most pronounced changes seen in the diet-induced weight loss group [ 39 ].
In a pooled analysis of the 3 treatment groups, bone strength estimated with subject-specific finite-element models based on CT-derived parameters was reduced by 6.
Although this sub-analysis was not powered to detect between-group differences, finite-element models can be used to provide better predictions of bone strength and fracture risk in future weight loss interventions.
Taken together, these findings suggest that resistance training exerts bone-sparing effects in weight loss interventions which, however, may not always be captured by BMD assessed by DXA. The discrepant results between the studies may be explained by differences in exercise regimens and the baseline characteristics of the study populations.
Frail and obese individuals are possibly more responsive to the effects of exercise training. In a month follow-up of a 1-year weight loss intervention [ 36 ], Waters et al. Similarly, Beavers et al. Both studies support unfavorable changes in skeletal health due to long-term weight loss.
These studies were subject to reporting bias because they were based on subsets of the initial groups and did not include individuals with no weight loss. Nevertheless, they underpin the need for follow-up studies to evaluate weight management approaches in the elderly and characterize skeletal health outcomes associated with sustained weight loss or multiple weight loss attempts.
We investigated the available evidence on the mechanistic links between weight loss and bone loss in obese older individuals or relevant aged animal models. We also discuss speculative contributors to bone loss during weight loss which, however, have been poorly investigated in obese elderly under weight loss and require further elucidation.
The effects of weight loss on skeletal outcomes during aging are likely multifactorial and may be mediated by i mechanical unloading, ii changes in body composition, iii restriction of important nutrients for bone metabolism and health, iv alterations in gonadal hormones and endocrine factors that co-regulate energy and bone metabolism, and v changes in inflammatory factors.
These factors appear to affect the balance between bone formation and resorption. This, in turn, mediates changes in the macro- and microstructure of bone as well as bone material, which determine bone strength and, ultimately, the risk of fractures Fig.
They also influence other geriatric outcomes such as physical function or falls, which are known to modify the risk of fracture [ 37, 44, 48 ] Fig. Bone adapts its mass, structure, and strength to the loads applied by muscle contractions as a result of physical activity or gravitational forces i.
Several lines of evidence support mechanical unloading as a mediator of the effects of weight loss on bone. First, diet-induced weight loss consistently results in bone loss at the weight-bearing hip rather than total body [ 36, 37, 39 ].
Second, changes in muscle mass and strength are correlated with bone changes in the hip in older individuals; these effects are largely explained by the gravitational forces exerted by muscles on bone [ 37 ]. Third, exercise and especially resistance training incorporated in weight loss programs can preserve fat-free mass and reduce the negative skeletal effects of weight loss [ 31, 37 ].
At the molecular level, the skeletal effects of mechanical unloading during diet-induced weight loss are supported by elevations in sclerostin levels [ 31 ]. Sclerostin is produced by osteocytes, the bone mechanosensors, and acts on bone formation through inhibition of the canonical Wnt signaling pathway.
The latter regulates osteoblastic differentiation, proliferation, and activity. Despite the significant role of mechanical unloading on bone responses to weight loss, it cannot explain the skeletal changes that occur at non-weight-bearing sites [ ], or continued bone loss after a weight loss plateau [ 47 ].
Obese older individuals have been shown to lose fat-free mass not only during single weight loss interventions but also during weight cycling [ 36, 41, 42 ].
In the latter, weight regain is predominantly accompanied by the acquisition of fat mass rather than fat-free mass [ 50 ]. In addition to the aforementioned mechanical link between muscle and bone, these tissues are connected through bidirectional signaling.
Muscle mass also affects skeletal health through its role in physical performance and fall prevention; this emphasizes the need for strategies aimed at the maintenance of muscle mass during weight loss.
A recent systematic review of weight loss RCTs in obese elderly person provided a summary of current evidence on the subject. The review showed that caloric restrictions combined with exercise attenuated the reductions in muscle and bone mass seen in diet-only study arms and resulted in greatest improvements in physical performance [ 48 ].
The relationship between bone and adipose tissue during weight loss appears to be particularly strong during aging. For example, in a population-based prospective study in older men, fat loss — and not loss of lean body mass — was strongly associated with hip bone loss in older men who lost weight over 2 years [ 16 ].
These results likely reflect the actions of fat mass in modulating bone health above and beyond its effects on skeletal loading. Several endocrine factors that link bone and adipose tissue have been identified [ 52 ]; these appear to mediate skeletal responses to weight loss during aging see below.
The current published literature supports the role of bone marrow adipose tissue in bone and energy metabolism and osteogenesis [ 53 ]. Marrow adipocytes have a common origin with osteoblasts, both arising from mesenchymal stem cells. Alterations in the mesenchymal stem cells lineage allocation may contribute to the associations between increased marrow adipose tissue and the elevated risk of fracture in osteoporosis, anorexia nervosa, and diabetes [ 53 ].
Limited animal and human data suggest that marrow fat is reduced during weight loss [ 54, 55 ]; these reductions may also attenuate bone loss. Given the age-related increase in marrow adipose tissue [ 56 ], it would be interesting to explore changes in bone marrow and their contribution to skeletal outcomes during weight loss in obese elderly.
Macro- and micronutrient deficiencies are common among elderly individuals, due to altered lifestyle or metabolism. These may be exacerbated by energy-deficient diets, which frequently lack key nutrients for skeletal health including protein, vitamin D, and calcium.
This suggests that higher doses of these nutrients or other combined strategies might be needed to mitigate the undesirable weight-loss-induced effects on the skeletal system. The contribution of endocrine factors such as estrogens, insulin-like-growth-factor-1 IGF-1 , leptin, and adiponectin to bone loss observed after weight loss has been detailed elsewhere [ 8 ].
Hereby, we summarize the key findings in older obese individuals. Although reductions in estradiol levels have been reported in obese older women and men during weight loss, possibly due to the reduction of fat mass, these were not correlated with bone loss.
Thus, estradiol probably exerts indirect rather than direct effects on bone responses to weight loss [ 37, 42, 56 ]. IGF-1 reductions have been inconsistently reported in older adults under energy or protein restriction [ 37, 42 ]. However, it is unclear whether the absence of changes reflects true effects of the intervention or whether IGF-1 reductions are masked by increases in its binding proteins [ 60 ].
A reduction in leptin, an adipokine significantly involved in the regulation of energy metabolism and with established central and peripheral effects on bone [ 56 ], is a consistent finding among obese elderly weight losers [ 37, 42 ]. In contrast, the role of adiponectin, another adipokine with potential action on bone [ 61 ], in skeletal changes in obese elderly under weight loss remains poorly understood.
Inflammation also contributes to sarcopenia by accelerating protein degradation and slowing down protein synthesis in the muscle [ 56 ]. It is widely accepted that aging, obesity, and exercise are characterized by chronic low-grade inflammation, and weight loss reduces inflammatory markers [ ].
However, the effects of weight loss and exercise on inflammatory molecules and processes in relation to skeletal health outcomes in older obese individuals require further elucidation. Besides, a complex interplay exists between bone and inflammatory factors derived from muscle, adipose tissue, brain, the immune system, and host — gut microbiota interactions, which might be further modified by weight loss and exercise during aging [ 66 ].
Animal studies complement and extend research in humans by allowing a detailed examination of caloric restriction, exercise, or nutrient manipulation under standardized conditions and by addressing mechanistic aspects.
One of the strengths of animal studies is the existence of similarities in age-related bone loss and obesity among animals and humans. Further advantages of animal studies include the accurate control of diet and exercise, the employment of many study arms, and the ability to analyze changes at different levels [ ].
These advantages are contrasted by a significant diversity among different animal models. The use of animal models requires knowledge of the respective bone anatomy, physiology, energy homeostasis, and the differences between these parameters in animals and humans [ ].
Despite the differences, meticulously designed experimental studies in animals, accompanied by critical data interpretation, have great potential to enhance our knowledge in this area. Surprisingly, we found no previous study on the effects of caloric restriction on skeletal health in obese aged animals, underpinning a significant literature gap in this age group.
Current evidence is derived from research in lean aged animals [ 57, ] or obese mature animals [ ], which cannot be extrapolated to obese aged animals. As such, we hereby present available animal models that capture age-related bone loss and obesity.
We also propose potentially relevant models, which, however, require validation prior to their use in future weight loss interventions Fig. Advantages and disadvantages of small e. Excellent reviews have described animal models of senile osteoporosis [ 67, 79 ] and obesity [ 68, 80 ]; however, models including both phenotypes are scarce [ 81 ].
A simple and useful model may be the application of a diet-induced obesity DIO paradigm in young, mature, or aged animals.
In the DIO paradigm, animals are provided ad libitum access to energy-dense diets, and the progression of obesity and its metabolic consequences are monitored [ 76, 81 ]. Despite its validity and relevance to human obesity, the DIO paradigm is influenced by animal characteristics e.
Similarly, aged Sprague-Dawley rats have severe abnormalities in trabecular bone and imbalanced bone turnover favoring bone resorption [ 87 ]. Furthermore, progressive increases in body fat percentage and body fat to lean mass ratio have been reported in Sprague-Dawley rats monitored from the age of 8 to 24 months [ 88 ].
Dietary manipulations and characterization of the body composition of animals with senile osteoporosis may provide new alleys of investigation. The same is true for the determination of skeletal features in established animal models of obesity.
For instance, senescence-accelerated mouse-P lines are featured by an accelerated aging phenotype and a short lifespan [ 89 ]. The senescence-accelerated mouse-P6 mice have been established as a model of senile osteoporosis: they exhibit low peak bone mass due to low bone formation and are prone to spontaneous fractures [ 90 ].
Nevertheless, these mice have not been used in diet-induced weight loss interventions. Finally, the use of larger animal models such as dogs, sheep, and pigs might be promising for future research because they offer significant advantages compared to smaller animals [ 79 ].
These include their greater phenotypical similarities to humans and the possibility to collect larger blood volumes over time for biochemical analyses Fig.
Nevertheless, their use in age-related research is hampered by their long life span, high costs, handling, housing requirements, and ethical implications. The effects of intentional weight loss in obese older individuals are of clinical significance because this population is susceptible to poor musculoskeletal health even prior to weight reduction.
Prospective studies suggest that weight loss is associated with bone loss, impaired bone microstructure, and a higher risk of fractures in elderly. However, these associations often reflect the negative impact of unintentional weight loss in underweight older individuals rather than the effects of intentional weight loss in their obese counterparts.
Interventional studies support the worsening of musculoskeletal health outcomes. Nevertheless, these effects appear to be relatively small following a single weight loss attempt and their contribution to the risk of fractures is unknown. The limited body of data from weight maintenance studies is a cause of concern.
These show that bone loss persists during this phase. Given the long-term implications of intentional weight loss or repeated weight reduction efforts, strategies to attenuate the harmful effects of weight loss on bone are clinically relevant but remain understudied in this group.
The most compelling evidence for such strategies is derived from studies that combined caloric restriction with resistance training.
Some older individuals cannot or do not wish to perform exercise training. Thus, future work should be focused on alternative approaches that may counteract, if not prevent, bone loss during active weight loss and weight maintenance. Simultaneously, the assessment of other geriatric outcomes and biochemical markers could provide mechanistic links between weight loss and bone loss.
To this end, the use of relevant animal models serves as a unique opportunity to understand the pathophysiology of weight-loss-associated bone alterations, as well as develop and test potential counteracting strategies for obese elderly.
All other authors have no conflicts of interest to declare. All authors reviewed and approved the final manuscript. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest.
filter your search All Content All Journals Gerontology. Advanced Search. Skip Nav Destination Close navigation menu Article navigation. Volume 66, Issue 1. Epidemiological Studies. Interventional Studies. Animal Studies. Statement of Ethics.
Disclosure Statement. Funding Sources. Author Contributions. Article Navigation. Review Articles June 28 Is Weight Loss Harmful for Skeletal Health in Obese Older Adults? Subject Area: Geriatrics and Gerontology. Maria Papageorgiou ; Maria Papageorgiou. a Department of Pathophysiology and Allergy Research, Center of Pathophysiology, Infectiology, and Immunology, Medical University of Vienna, Vienna, Austria.
b Department of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, United Kingdom. This Site. Google Scholar. Katharina Kerschan-Schindl ; Katharina Kerschan-Schindl.
c Department of Physical Medicine, Rehabilitation and Occupational Therapy, Medical University of Vienna, Vienna, Austria. Thozhukat Sathyapalan ; Thozhukat Sathyapalan. Peter Pietschmann Peter Pietschmann. pietschmann meduniwien. Gerontology 66 1 : 2— Article history Received:. Cite Icon Cite.
toolbar search Search Dropdown Menu. Good sources of calcium include dairy products, almonds, broccoli, kale, canned salmon with bones, sardines and soy products, such as tofu. If you find it difficult to get enough calcium from your diet, ask your doctor about supplements.
Pay attention to vitamin D. Your body needs vitamin D to absorb calcium. For adults ages 19 to 70, the RDA of vitamin D is international units IUs a day. The recommendation increases to IUs a day for adults age 71 and older. Good sources of vitamin D include oily fish, such as salmon, trout, whitefish and tuna.
Additionally, mushrooms, eggs and fortified foods, such as milk and cereals, are good sources of vitamin D. Sunlight also contributes to the body's production of vitamin D. If you're worried about getting enough vitamin D, ask your doctor about supplements. If you're concerned about your bone health or your risk factors for osteoporosis, including a recent bone fracture, consult your doctor.
He or she might recommend a bone density test. The results will help your doctor gauge your bone density and determine your rate of bone loss. By evaluating this information and your risk factors, your doctor can assess whether you might be a candidate for medication to help slow bone loss. There is a problem with information submitted for this request.
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Antioxidant-rich Berries is a managrment disease characterized managemeny decreases in bone strength and Muscle soreness prevention density. It affects weihht than million people worldwide and is more common in people assigned female at birth. Traditionally, low body mass index BMI has been associated with a higher risk of osteoporosisbut research suggests this may be true at the opposite end of the spectrum may as well. Carrying excess weight may have both protective and harmful effects on bone health. Once upon a time, obesity was thought to be mainly protective against osteoporosis.
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