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Q) What is the role of vitamin D in multiple sclerosis? Is it beneficial?
The exact etiology and pathophysiology of multiple sclerosis (MS) is still not fully understood. Research strongly suggests that there are two major causative factors: one genetic, and the other, environmental. From an environmental standpoint, multiple studies have shown that living farther from the equator, not being exposed to sunlight, and having a low vitamin D level are all correlated with increased risk for MS and MS relapse.1
Our bodies need sunlight to successfully synthesize vitamin D in the skin. Research has found that individuals with lightly pigmented skin are five times more efficient at synthesizing vitamin D in the presence of sunlight than those with darker skin.2 However, the ability to absorb sunlight is also correlated with the earth’s latitude; worse absorption occurs in areas beyond the 40th parallel (in either hemisphere), where UVB levels are too low to synthesize vitamin D four to six months out of the year.2
When exposed to UVB rays, our bodies start to synthesize vitamin D; it undergoes a transformation in the liver and then the kidneys and ultimately becomes the hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 (calcitriol).2 Calcitriol is recognized by multiple tissues throughout the body that contain vitamin D receptors. Specifically, in the central nervous system, receptors are located on microglia, activated monocytes, and B and T lymphocytes.1 In MS, myelin (the coating around the nerves) is destroyed by an immune-mediated inflammatory process involving the microglia and B and T lymphocytes. Vitamin D quiets down this inflammation, thereby reducing disability accumulation and relapse risk and resulting in fewer changes on MRI.
Vitamin D is also believed to shift the immune response to an anti-inflammatory state by focusing the response on the cytotoxic T cells often found in MS lesions, which attack neurons and oligodendrocytes.2 This theory was tested by Munger and colleagues, who used a pooled cohort of 187,000 women from the Nurses’ Health Study and Nurses’ Health Study II to assess vitamin D intake and risk for MS. Compared to women with lower vitamin D intake, those who took 700 IU/d had a 41% lower incidence of MS. Women who took ≥ 400 IU/d had a 33% lower risk for MS, compared to nonusers.3 In another evaluation of 7 million US military personnel, individuals with a serum vitamin D level of 40 ng/mL were 62% less likely to develop MS.4
In light of the anti-inflammatory effects of vitamin D and its purported reduction of MS risk, it is possible that patients with MS should begin vitamin D supplementation early to obtain maximum anti-inflammatory effects. While an optimal vitamin D goal has not been established in the literature, some studies suggest 30 to 55 ng/mL as a target range for serum vitamin D level.1
While vitamin D has been found to be well-tolerated, patients should be cautioned that very high doses can cause fatigue, abdominal cramps, nausea, vomiting, kidney damage, hypertension, hypercalcemia, and oth
Lisa Marie Fox, MSPAS, PA-C
Division of Multiple Sclerosis, Department of Neurology, Johns Hopkins Hosptial, Baltimore
1. Waubant E, Mowry E, Bowling A. The role of vitamin D in multiple sclerosis pathology and treatment: answers and opportunities. Int J MS Care. 2015;17(2):1-24.
2. Pierrot-Deseilligny C. Clinical implications of a possible role of vitamin D in multiple sclerosis. J Neurol. 2009;256(9):1468-1478.3. Munger KL, Zhang SM, O’Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62(1):60-65.
4. Munger KL, Levin LI, Hollis BW, et al. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA. 2006; 296(23):2832-2838.
5. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96(1):53-58.
Q) What is the role of vitamin D in multiple sclerosis? Is it beneficial?
The exact etiology and pathophysiology of multiple sclerosis (MS) is still not fully understood. Research strongly suggests that there are two major causative factors: one genetic, and the other, environmental. From an environmental standpoint, multiple studies have shown that living farther from the equator, not being exposed to sunlight, and having a low vitamin D level are all correlated with increased risk for MS and MS relapse.1
Our bodies need sunlight to successfully synthesize vitamin D in the skin. Research has found that individuals with lightly pigmented skin are five times more efficient at synthesizing vitamin D in the presence of sunlight than those with darker skin.2 However, the ability to absorb sunlight is also correlated with the earth’s latitude; worse absorption occurs in areas beyond the 40th parallel (in either hemisphere), where UVB levels are too low to synthesize vitamin D four to six months out of the year.2
When exposed to UVB rays, our bodies start to synthesize vitamin D; it undergoes a transformation in the liver and then the kidneys and ultimately becomes the hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 (calcitriol).2 Calcitriol is recognized by multiple tissues throughout the body that contain vitamin D receptors. Specifically, in the central nervous system, receptors are located on microglia, activated monocytes, and B and T lymphocytes.1 In MS, myelin (the coating around the nerves) is destroyed by an immune-mediated inflammatory process involving the microglia and B and T lymphocytes. Vitamin D quiets down this inflammation, thereby reducing disability accumulation and relapse risk and resulting in fewer changes on MRI.
Vitamin D is also believed to shift the immune response to an anti-inflammatory state by focusing the response on the cytotoxic T cells often found in MS lesions, which attack neurons and oligodendrocytes.2 This theory was tested by Munger and colleagues, who used a pooled cohort of 187,000 women from the Nurses’ Health Study and Nurses’ Health Study II to assess vitamin D intake and risk for MS. Compared to women with lower vitamin D intake, those who took 700 IU/d had a 41% lower incidence of MS. Women who took ≥ 400 IU/d had a 33% lower risk for MS, compared to nonusers.3 In another evaluation of 7 million US military personnel, individuals with a serum vitamin D level of 40 ng/mL were 62% less likely to develop MS.4
In light of the anti-inflammatory effects of vitamin D and its purported reduction of MS risk, it is possible that patients with MS should begin vitamin D supplementation early to obtain maximum anti-inflammatory effects. While an optimal vitamin D goal has not been established in the literature, some studies suggest 30 to 55 ng/mL as a target range for serum vitamin D level.1
While vitamin D has been found to be well-tolerated, patients should be cautioned that very high doses can cause fatigue, abdominal cramps, nausea, vomiting, kidney damage, hypertension, hypercalcemia, and oth
Lisa Marie Fox, MSPAS, PA-C
Division of Multiple Sclerosis, Department of Neurology, Johns Hopkins Hosptial, Baltimore
Q) What is the role of vitamin D in multiple sclerosis? Is it beneficial?
The exact etiology and pathophysiology of multiple sclerosis (MS) is still not fully understood. Research strongly suggests that there are two major causative factors: one genetic, and the other, environmental. From an environmental standpoint, multiple studies have shown that living farther from the equator, not being exposed to sunlight, and having a low vitamin D level are all correlated with increased risk for MS and MS relapse.1
Our bodies need sunlight to successfully synthesize vitamin D in the skin. Research has found that individuals with lightly pigmented skin are five times more efficient at synthesizing vitamin D in the presence of sunlight than those with darker skin.2 However, the ability to absorb sunlight is also correlated with the earth’s latitude; worse absorption occurs in areas beyond the 40th parallel (in either hemisphere), where UVB levels are too low to synthesize vitamin D four to six months out of the year.2
When exposed to UVB rays, our bodies start to synthesize vitamin D; it undergoes a transformation in the liver and then the kidneys and ultimately becomes the hormonally active form of vitamin D, 1,25-dihydroxyvitamin D3 (calcitriol).2 Calcitriol is recognized by multiple tissues throughout the body that contain vitamin D receptors. Specifically, in the central nervous system, receptors are located on microglia, activated monocytes, and B and T lymphocytes.1 In MS, myelin (the coating around the nerves) is destroyed by an immune-mediated inflammatory process involving the microglia and B and T lymphocytes. Vitamin D quiets down this inflammation, thereby reducing disability accumulation and relapse risk and resulting in fewer changes on MRI.
Vitamin D is also believed to shift the immune response to an anti-inflammatory state by focusing the response on the cytotoxic T cells often found in MS lesions, which attack neurons and oligodendrocytes.2 This theory was tested by Munger and colleagues, who used a pooled cohort of 187,000 women from the Nurses’ Health Study and Nurses’ Health Study II to assess vitamin D intake and risk for MS. Compared to women with lower vitamin D intake, those who took 700 IU/d had a 41% lower incidence of MS. Women who took ≥ 400 IU/d had a 33% lower risk for MS, compared to nonusers.3 In another evaluation of 7 million US military personnel, individuals with a serum vitamin D level of 40 ng/mL were 62% less likely to develop MS.4
In light of the anti-inflammatory effects of vitamin D and its purported reduction of MS risk, it is possible that patients with MS should begin vitamin D supplementation early to obtain maximum anti-inflammatory effects. While an optimal vitamin D goal has not been established in the literature, some studies suggest 30 to 55 ng/mL as a target range for serum vitamin D level.1
While vitamin D has been found to be well-tolerated, patients should be cautioned that very high doses can cause fatigue, abdominal cramps, nausea, vomiting, kidney damage, hypertension, hypercalcemia, and oth
Lisa Marie Fox, MSPAS, PA-C
Division of Multiple Sclerosis, Department of Neurology, Johns Hopkins Hosptial, Baltimore
1. Waubant E, Mowry E, Bowling A. The role of vitamin D in multiple sclerosis pathology and treatment: answers and opportunities. Int J MS Care. 2015;17(2):1-24.
2. Pierrot-Deseilligny C. Clinical implications of a possible role of vitamin D in multiple sclerosis. J Neurol. 2009;256(9):1468-1478.3. Munger KL, Zhang SM, O’Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62(1):60-65.
4. Munger KL, Levin LI, Hollis BW, et al. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA. 2006; 296(23):2832-2838.
5. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96(1):53-58.
1. Waubant E, Mowry E, Bowling A. The role of vitamin D in multiple sclerosis pathology and treatment: answers and opportunities. Int J MS Care. 2015;17(2):1-24.
2. Pierrot-Deseilligny C. Clinical implications of a possible role of vitamin D in multiple sclerosis. J Neurol. 2009;256(9):1468-1478.3. Munger KL, Zhang SM, O’Reilly E, et al. Vitamin D intake and incidence of multiple sclerosis. Neurology. 2004;62(1):60-65.
4. Munger KL, Levin LI, Hollis BW, et al. Serum 25-hydroxyvitamin D levels and risk of multiple sclerosis. JAMA. 2006; 296(23):2832-2838.
5. Ross AC, Manson JE, Abrams SA, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96(1):53-58.