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Current Landscape of Pharmacotherapies for Sarcopenia
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<blockquote data-quote="madman" data-source="post: 275536" data-attributes="member: 13851"><p><em><strong> *In summary, the exact role of vitamin D supplementation in the prevention and treatment of sarcopenia <u>remains uncertain due to the high heterogeneity of studies and the conflicting results of RCTs</u>.</strong></em></p><p></p><p></p><p></p><p></p><p><strong>2 Nutritional intervention for sarcopenia</strong></p><p></p><h3>2.2. Vitamins</h3><h4><strong>2.2.1. Vitamin D</strong></h4><h4><strong>2.2.1.1. Mechanisms</strong></h4><p><em><strong>The vitamin D/VDR axis plays a key role in regulating biological processes central to sarcopenic muscle atrophy, such as proteolysis, mitochondrial function, cellular senescence, and adiposity (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B72" target="_blank">72</a>).</strong> First, vitamin D deficiency appears to lead to increased muscle protein breakdown via the ubiquitin-proteasomal pathway (UPP) and autophagy and upregulation of AMPK and members of the renin-angiotensin system (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B73" target="_blank">73</a>, <a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B74" target="_blank">74</a>). Second, permanent exit from the cell cycle (senescence) is a critical aging phenomenon, and the vitamin D/VDR axis has been shown to have regulatory control (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B75" target="_blank">75</a>). Third, low vitamin D states may lead to impaired mitochondrial function (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B76" target="_blank">76</a>), and active 1,25(OH)2D3 can increase oxygen consumption rates and fission/fusion dynamics (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B77" target="_blank">77</a>, <a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B78" target="_blank">78</a>). Fourth, low vitamin D states may lead to increased adiposity in muscle (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B79" target="_blank">79</a>), and those who are overweight have an increased risk of deficits in muscle mass and function (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B80" target="_blank">80</a>).</em></p><p></p><p></p><p></p><h4><strong>2.2.1.2. Clinical studies</strong></h4><p><em>Vitamin D is a fat-soluble vitamin synthesized in the skin, 90% of which comes from UV exposure and 10% from the diet. Vitamin D deficiency is now considered a global public health problem, and elderly individuals are at greater risk of vitamin D deficiency due to poor intestinal absorption, reduced sun exposure, and chronic renal insufficiency. Lower 25-(OH)-VD levels are thought to be associated with adverse changes in muscle mass and physical function (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B81" target="_blank">81</a>). Yang et al. (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B82" target="_blank">82</a>) fed mice a vitamin D-deficient diet for 24 weeks and immobilized them to determine the extent of skeletal muscle atrophy. As a result, vitamin D deficiency accelerated the decrease in gastrocnemius muscle mass, muscle fiber cross-sectional area, and grip strength; moreover, vitamin D supplementation inhibited the decrease in grip strength. The team also performed a cross-sectional analysis of 4,139 older adults, and linear regression analysis showed that serum 25 hydroxyvitamin D and physical activity were linearly associated and interacted with timed running time and grip strength. However, in another study in which the control group took a placebo daily and the intervention group took 800 IU of vitamin D orally daily, no differences were found between the two groups in leg push-up strength, function, or lean body mass after 1 year (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B83" target="_blank">83</a>). <strong>According to the systematic reviews and meta-analyses, vitamin D supplementation alone did not improve muscle strength or SPPB scores, on the contrary, significantly decreased SPPB scores (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B84" target="_blank">84</a>).</strong> When vitamin D was taken together with whey protein and leucine, the muscle mass of the limbs of patients with sarcopenia could be effectively increased even without physical exercise, and when combined with physical exercise, not only muscle mass increases but muscle strength and performance could also be significantly improved (<a href="https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B85" target="_blank">85</a>). <strong>However, we cannot be sure of the effectiveness of vitamin D supplementation alone, due to the presence of protein and amino acids. In summary, the exact role of vitamin D supplementation in the prevention and treatment of sarcopenia <u>remains uncertain due to the high heterogeneity of studies and the conflicting results of RCTs</u>.</strong></em></p></blockquote><p></p>
[QUOTE="madman, post: 275536, member: 13851"] [I][B] *In summary, the exact role of vitamin D supplementation in the prevention and treatment of sarcopenia [U]remains uncertain due to the high heterogeneity of studies and the conflicting results of RCTs[/U].[/B][/I] [B]2 Nutritional intervention for sarcopenia[/B] [HEADING=2]2.2. Vitamins[/HEADING] [HEADING=3][B]2.2.1. Vitamin D[/B][/HEADING] [HEADING=3][B]2.2.1.1. Mechanisms[/B][/HEADING] [I][B]The vitamin D/VDR axis plays a key role in regulating biological processes central to sarcopenic muscle atrophy, such as proteolysis, mitochondrial function, cellular senescence, and adiposity ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B72']72[/URL]).[/B] First, vitamin D deficiency appears to lead to increased muscle protein breakdown via the ubiquitin-proteasomal pathway (UPP) and autophagy and upregulation of AMPK and members of the renin-angiotensin system ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B73']73[/URL], [URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B74']74[/URL]). Second, permanent exit from the cell cycle (senescence) is a critical aging phenomenon, and the vitamin D/VDR axis has been shown to have regulatory control ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B75']75[/URL]). Third, low vitamin D states may lead to impaired mitochondrial function ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B76']76[/URL]), and active 1,25(OH)2D3 can increase oxygen consumption rates and fission/fusion dynamics ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B77']77[/URL], [URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B78']78[/URL]). Fourth, low vitamin D states may lead to increased adiposity in muscle ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B79']79[/URL]), and those who are overweight have an increased risk of deficits in muscle mass and function ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B80']80[/URL]).[/I] [HEADING=3][B]2.2.1.2. Clinical studies[/B][/HEADING] [I]Vitamin D is a fat-soluble vitamin synthesized in the skin, 90% of which comes from UV exposure and 10% from the diet. Vitamin D deficiency is now considered a global public health problem, and elderly individuals are at greater risk of vitamin D deficiency due to poor intestinal absorption, reduced sun exposure, and chronic renal insufficiency. Lower 25-(OH)-VD levels are thought to be associated with adverse changes in muscle mass and physical function ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B81']81[/URL]). Yang et al. ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B82']82[/URL]) fed mice a vitamin D-deficient diet for 24 weeks and immobilized them to determine the extent of skeletal muscle atrophy. As a result, vitamin D deficiency accelerated the decrease in gastrocnemius muscle mass, muscle fiber cross-sectional area, and grip strength; moreover, vitamin D supplementation inhibited the decrease in grip strength. The team also performed a cross-sectional analysis of 4,139 older adults, and linear regression analysis showed that serum 25 hydroxyvitamin D and physical activity were linearly associated and interacted with timed running time and grip strength. However, in another study in which the control group took a placebo daily and the intervention group took 800 IU of vitamin D orally daily, no differences were found between the two groups in leg push-up strength, function, or lean body mass after 1 year ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B83']83[/URL]). [B]According to the systematic reviews and meta-analyses, vitamin D supplementation alone did not improve muscle strength or SPPB scores, on the contrary, significantly decreased SPPB scores ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B84']84[/URL]).[/B] When vitamin D was taken together with whey protein and leucine, the muscle mass of the limbs of patients with sarcopenia could be effectively increased even without physical exercise, and when combined with physical exercise, not only muscle mass increases but muscle strength and performance could also be significantly improved ([URL='https://www.frontiersin.org/articles/10.3389/fnut.2023.1189522/full#B85']85[/URL]). [B]However, we cannot be sure of the effectiveness of vitamin D supplementation alone, due to the presence of protein and amino acids. In summary, the exact role of vitamin D supplementation in the prevention and treatment of sarcopenia [U]remains uncertain due to the high heterogeneity of studies and the conflicting results of RCTs[/U].[/B][/I] [/QUOTE]
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