Atherosclerosis is still responsible for the highest number of deaths in the U.S. Approximately one million people die from the disease each year. In one article I read it said atherosclerosis is the leading killer of both men and women after the age of 46.
Atherosclerosis, a type of arteriosclerosis, is a condition in which fatty material (plaque) collects along the walls of arteries and as this fatty material thickens, and hardens it may eventually block arteries. Over time, the plaque can make the artery narrow and less flexible. In essence the artery becomes stiff.
A group of researchers now believes that vitamin D deficiency may play a role in causing the problem. In fact, they find that reduced levels of vitamin D appear to correlate with increased arterial stiffness.
I still recommend 2-3,000 IU of vitamin D 3 per day and make sure that you do some stretching. There is evidence that whole body stretching is helpful to reduce arterial stiffness.
June 16-19, 2010 in Rome, Italy — vitamin D deficiency is a common feature in patients with a range of painful rheumatic and related autoimmune disorders. What is less clear, however, is the amount of vitamin D supplementation that would benefit these patients.
Here are highlights from three recent studies:
- Researchers in the UK assessed levels of vitamin D in patients with either inflammatory joint diseases (ie, rheumatoid arthritis, RA), osteoporosis, or unexplained muscle pain (ie, myalgia) — 30 subjects in each group — compared with a control group of 90 patients with chronic back pain [Kelly et al. 2010]. Within all 180 patients (two-thirds female) the median vitamin D level was 15 ng/mL and 58% were below the normal range (defined as 20-58 ng/mL by these authors). The median vitamin D level in control patients (with back pain) was 20 ng/mL compared with statistically significant lower medians of 14 ng/mL in the RA group, 12 ng/mL in the osteoporosis group, and 12 ng/mL in the myalgia group. The authors expressed surprise that vitamin D deficiencies also were evident in persons with diffuse muscle pain but suggested that patients in all groups would benefit from vitamin D supplementation. Note: Why patients with back pain were chosen as a control group is unclear, as other research has already found such patients to be vitamin D insufficient (ie, <30 ng/mL) overall.
- A second study, conducted by Italian researchers, focused on 1,191 patients (85% female) with rheumatoid arthritis (RA) to determine a correlation between vitamin D deficiency and several clinical measures of disease activity [Idolazzi et al. 2010]. They found that levels of 25(OH)D were deficient (<20 ng/mL) in 52% of the patients not taking a vitamin D supplement and in one third of those taking supplements (?800 IU/day). In non-supplemented patients low levels of 25(OH)D significantly correlated with worse scores on 3 measures of disease activity: Health Assessment Questionnaire Disability Index, Mobility Activities of Daily Living Score, and Number of Swollen Joints Count. Significantly lower 25(OH)D levels were found in patients with active disease compared with those in disease remission and in those who were not responding to treatment compared with patients with a good response. Therefore, vitamin D sufficiency appears to be directly related to the course of rheumatoid arthritis and response to treatment; however, the authors conclude that further research is needed to assess the benefits of vitamin D supplementation in these patients.
- Another reported study from Italian researchers evaluated the impact of vitamin D supplementation in patients with either inflammatory autoimmune disease (IAD; rheumatoid arthritis, spondyloarthritis, or connective tissue diseases; n=43) and noninflammatory autoimmune disease (NIAD; osteoarthritis or osteoporosis; n=57) [Sainaghi et al. 2010]. Mean 25(OH)D levels between the two groups at outset were equivalently deficient — 12.6±7.5 ng/mL IAD group, 13.1±8.8 ng/mL NIAD group. Following daily supplementation with 800 to 1000 IU of vitamin D3 for 6 months, only 29% of all patients reached 25(OH)D levels ?30 ng/mL considered to be sufficient and there were no significant differences observed between the IAD and NIAD groups. The authors conclude that, while the amount of supplementation was not adequate to normalize 25(OH)D levels in their patients the response to vitamin D (or lack thereof) did not appear to be influenced by the presence of an inflammatory autoimmune condition.
COMMENTARY: A separate presentation at EULAR 2010, based on a large multinational survey of women with RA, reported that among the 75% who were taking analgesic medications more than 7 in 10 (72%) still experienced daily pain [Strand et al. 2010]. Two-thirds of the respondents said that they constantly look for new ideas to address pain. Therefore, the studies above are of great importance because they demonstrate that painful inflammatory and noninflammatory rheumatologic or bone conditions are generally accompanied by vitamin D deficiencies. Based on prior research, it is not surprising that daily supplementation of 800 to 1000 IU of vitamin D3 was inadequate to significantly raise 25(OH)D to more normal levels. It is disappointing that none of the 3 research teams proceeded to the next step of testing more ample vitamin D supplementation and assessing outcomes on pain relief and/or disease moderation.
Idolazzi L, Bagnato G, Bianchi G, et al. Vitamin D deficiency in rheumatoid arthritis: prevalence, determinants, and associations with disease activity. A cross-sectional study. Ann Rheum Dis. 2010;69(Suppl 3):516. Abstract SAT0093.
Kelly C, Scott K, Bell G, et al. Vitamin D levels in a spectrum of rheumatic disease. Ann Rheum Dis. 2010;69(Suppl 3:481. Abstract FRI0509.
Sainaghi PP, Bellan M, Carda S, et al. Response to vitamin D supplementation in inflammatory autoimmune diseases: a retrospective study. Ann Rheum Dis. 2010;69(Suppl 3):652. Abstract SAT0506.
Strand V, Emery P, Fleming S, Coke E. The impact of rheumatoid arthritis on women: focus on pain, productivity, and relationships. Ann Rheum Dis 2010;69(Suppl 3):748. Abstract OP0002-PARE.