Last updated on 30th November 2008
Here are a couple of studies on smoking, a couple on B vitamins, a couple on vitamin D, and an intriguing study on iron. The smoking papers underline the varieties of damage this habit produces. So the Pasco et al study shows that, for women, being a smoker is associated with double the risk of developing subsequent major depression. The Strandberg research challenges any notion of "Eat, drink and be merry for tomorrow we die". This study of 1658 men reports that "During the 26-year follow-up of this socioeconomically homogeneous male cohort, HRQoL (quality of life) deteriorated with an increase in daily cigarettes smoked in a dose-dependent manner. Never-smokers lived longer than heavy smokers, and their extra years were of better quality." Basically smoking not only shortens life by about 7 to 10 years, but it also screws up the quality of the reduced number of years one is left with. With the vitamin B research, two studies on supplementation (Aisen et al & Zhang et al) showed no benefits in reducing subsequent dementia in those with early signs of Alzheimer disease, and no benefits in reducing cancer risk in women already at increased risk of cardiovascular disease (this latter study was in the States where folate supplementation is already included universally in flour). Two studies on vitamin D include one (Wagner et al) increasing the official recommendation on vitamin D supplementation for kids in the States: "It is now recommended that all infants and children, including adolescents, have a minimum daily intake of 400 IU of vitamin D beginning soon after birth. The current recommendation replaces the previous recommendation of a minimum daily intake of 200 IU/day of vitamin D supplementation beginning in the first 2 months after birth and continuing through adolescence." The Zold et al study suggests vitamin D deficiency increases the risk of developing a variety of autoimmune diseases "systemic lupus erythematosus, rheumatoid arthritis, insulin-dependent diabetes mellitus, and inflammatory bowel disease." Finally the Insel et al study found that maternal anaemia in pregnancy increased the subsequent risk of schizophrenia in offspring "For every 1-g/dL increase in mean maternal hemoglobin concentration, a 27% decrease in the rate of SSDs (schizophrenia spectrum disorders) was observed." If replicated and confirmed this is going to be a very important finding.
Aisen, P. S., L. S. Schneider, et al. (2008). "High-Dose B Vitamin Supplementation and Cognitive Decline in Alzheimer Disease: A Randomized Controlled Trial." JAMA 300(15): 1774-1783. [Abstract/Full Text]
Context Blood levels of homocysteine may be increased in Alzheimer disease (AD) and hyperhomocysteinemia may contribute to disease pathophysiology by vascular and direct neurotoxic mechanisms. Even in the absence of vitamin deficiency, homocysteine levels can be reduced by administration of high-dose supplements of folic acid and vitamins B6 and B12. Prior studies of B vitamins to reduce homocysteine in AD have not had sufficient size or duration to assess their effect on cognitive decline. Objective To determine the efficacy and safety of B vitamin supplementation in the treatment of AD. Design, Setting, and Patients A multicenter, randomized, double-blind controlled clinical trial of high-dose folate, vitamin B6, and vitamin B12 supplementation in 409 (of 601 screened) individuals with mild to moderate AD (Mini-Mental State Examination scores between 14 and 26, inclusive) and normal folic acid, vitamin B12, and homocysteine levels. The study was conducted between February 20, 2003, and December 15, 2006, at clinical research sites of the Alzheimer Disease Cooperative Study located throughout the United States. Intervention Participants were randomly assigned to 2 groups of unequal size to increase enrollment (60% treated with high-dose supplements [5 mg/d of folate, 25 mg/d of vitamin B6, 1 mg/d of vitamin B12] and 40% treated with identical placebo); duration of treatment was 18 months. Main Outcome Measure Change in the cognitive subscale of the Alzheimer Disease Assessment Scale (ADAS-cog). Results A total of 340 participants (202 in active treatment group and 138 in placebo group) completed the trial while taking study medication. Although the vitamin supplement regimen was effective in reducing homocysteine levels (mean [SD], -2.42 [3.35] in active treatment group vs -0.86 [2.59] in placebo group; P < .001), it had no beneficial effect on the primary cognitive measure, rate of change in ADAS-cog score during 18 months (0.372 points per month for placebo group vs 0.401 points per month for active treatment group, P = .52; 95% confidence interval of rate difference, -0.06 to 0.12; based on the intention-to-treat generalized estimating equations model), or on any secondary measures. A higher quantity of adverse events involving depression was observed in the group treated with vitamin supplements. Conclusion This regimen of high-dose B vitamin supplements does not slow cognitive decline in individuals with mild to moderate AD.
Insel, B. J., C. A. Schaefer, et al. (2008). "Maternal Iron Deficiency and the Risk of Schizophrenia in Offspring." Arch Gen Psychiatry 65(10): 1136-1144. [Abstract/Full Text]
Context Iron is essential for brain development and functioning. Emerging evidence suggests that iron deficiency in early life leads to long-lasting neural and behavioral deficits in infants and children. Adopting a life course perspective, we examined the effects of early iron deficiency on the risk of schizophrenia in adulthood. Objective To determine whether maternal iron deficiency, assessed by maternal hemoglobin concentration during pregnancy, increases the susceptibility to schizophrenia spectrum disorders (SSDs) among offspring. Design Data were drawn from a population-based cohort born from 1959 through 1967 and followed up for development of SSD from 1981 through 1997. Participants Of 6872 offspring for whom maternal hemoglobin concentration was available, 57 had SSDs (0.8%) and 6815 did not (99.2%). Main Outcome Measure Prospectively assayed, the mean value of maternal hemoglobin concentration was the primary exposure. Hemoglobin concentration was analyzed as a continuous and a categorical variable. Results A mean maternal hemoglobin concentration of 10.0 g/dL or less was associated with a nearly 4-fold statistically significant increased rate of SSDs (adjusted rate ratio, 3.73; 95% confidence interval, 1.41-9.81; P = .008) compared with a mean maternal hemoglobin concentration of 12.0 g/dL or higher, adjusting for maternal education and ethnicity. For every 1-g/dL increase in mean maternal hemoglobin concentration, a 27% decrease in the rate of SSDs was observed (95% confidence interval, 0.55-0.96; P = .02). Conclusions The findings suggest that maternal iron deficiency may be a risk factor for SSDs among offspring. Given that this hypothesis offers the potential for reducing the risk for SSDs, further investigation in independent samples is warranted.
Pasco, J. A., L. J. Williams, et al. (2008). "Tobacco smoking as a risk factor for major depressive disorder: population-based study." The British Journal of Psychiatry 193(4): 322-326. [Abstract/Full Text]
Background Smoking is disproportionately prevalent among people with psychiatric illness. Aims To investigate smoking as a risk factor for major depressive disorder. Method A population-based sample of women was studied using case-control and retrospective cohort study designs. Exposure to smoking was self-reported, and major depressive disorder diagnosed using the Structured Clinical Interview for DSM-IV-TR (SCID-I/NP). Results Among 165 people with major depressive disorder and 806 controls, smoking was associated with increased odds for major depressive disorder (age-adjusted odds ratio (OR)=1.46, 95% CI 1.03-2.07). Compared with non-smokers, odds for major depressive disorder more than doubled for heavy smokers (>20 cigarettes/day). Among 671 women with no history of major depressive disorder at baseline, 13 of 87 smokers and 38 of 584 non-smokers developed de novo major depressive disorder during a decade of follow-up. Smoking increased major depressive disorder risk by 93% (hazard ratio (HR)=1.93, 95% CI 1.02-3.69); this was not explained by physical activity or alcohol consumption. Conclusions Evidence from cross-sectional and longitudinal data suggests that smoking increases the risk of major depressive disorder in women.
Strandberg, A. Y., T. E. Strandberg, et al. (2008). "The Effect of Smoking in Midlife on Health-Related Quality of Life in Old Age: A 26-Year Prospective Study." Arch Intern Med 168(18): 1968-1974. [Abstract/Full Text]
Background Smoking shortens life expectancy by 7 to 10 years. However, it is unclear whether the enhanced longevity of nonsmokers produces increased disability and decreased quality of life during these extra final years. This study evaluates the long-term effect of smoking in midlife on health-related quality of life (HRQoL) in old age. Methods Prospective cohort study with a 26-year follow-up of 1658 white men (born 1919-1934) of similar socioeconomic status who were participating in the Helsinki Businessmen Study. All men were healthy at baseline in 1974, when cardiovascular risk factors and smoking habits were assessed. The participants were reevaluated with the use of mailed questionnaires in 2000; HRQoL was measured with the use of the RAND 36-Item Health Survey (similar to the Medical Outcomes Study Short-Form Health Survey) and related to the baseline smoking status. Total mortality through 2000 was determined from Finnish national registers. Results Participants who had never smoked (n = 614) lived a mean of 10 years longer than heavy smokers (>20 cigarettes daily; n = 188). Among survivors in 2000 (n = 1131), the never-smokers had the highest (ie, best) scores on all RAND 36-Item Health Survey scales. The differences were greatest between never-smokers and heavy smokers, ranging from 4 points on the scale of social functioning to 14 points on the physical functioning scale. The physical component summary score showed a graded deterioration of HRQoL with an increasing number of cigarettes smoked daily (P = .01). Conclusions During the 26-year follow-up of this socioeconomically homogeneous male cohort, HRQoL deteriorated with an increase in daily cigarettes smoked in a dose-dependent manner. Never-smokers lived longer than heavy smokers, and their extra years were of better quality.
Wagner, C. L., F. R. Greer, et al. (2008). "Prevention of Rickets and Vitamin D Deficiency in Infants, Children, and Adolescents." Pediatrics 122(5): 1142-1152. [Abstract/Full Text]
Rickets in infants attributable to inadequate vitamin D intake and decreased exposure to sunlight continues to be reported in the United States. There are also concerns for vitamin D deficiency in older children and adolescents. Because there are limited natural dietary sources of vitamin D and adequate sunshine exposure for the cutaneous synthesis of vitamin D is not easily determined for a given individual and may increase the risk of skin cancer, the recommendations to ensure adequate vitamin D status have been revised to include all infants, including those who are exclusively breastfed and older children and adolescents. It is now recommended that all infants and children, including adolescents, have a minimum daily intake of 400 IU of vitamin D beginning soon after birth. The current recommendation replaces the previous recommendation of a minimum daily intake of 200 IU/day of vitamin D supplementation beginning in the first 2 months after birth and continuing through adolescence. These revised guidelines for vitamin D intake for healthy infants, children, and adolescents are based on evidence from new clinical trials and the historical precedence of safely giving 400 IU of vitamin D per day in the pediatric and adolescent population. New evidence supports a potential role for vitamin D in maintaining innate immunity and preventing diseases such as diabetes and cancer. The new data may eventually refine what constitutes vitamin D sufficiency or deficiency.
Zhang, S. M., N. R. Cook, et al. (2008). "Effect of Combined Folic Acid, Vitamin B6, and Vitamin B12 on Cancer Risk in Women: A Randomized Trial." JAMA 300(17): 2012-2021. [Abstract/Full Text]
Context Folate, vitamin B6, and vitamin B12 are thought to play an important role in cancer prevention. Objective To evaluate the effect of combined folic acid, vitamin B6, and vitamin B12 treatment on cancer risk in women at high risk for cardiovascular disease. Design, Setting, and Participants In the Women's Antioxidant and Folic Acid Cardiovascular Study, 5442 US female health professionals aged 42 years or older, with preexisting cardiovascular disease or 3 or more coronary risk factors, were randomly assigned to receive either a daily combination of folic acid, vitamin B6, and vitamin B12 or a matching placebo. They were treated for 7.3 years from April 1998 through July 31, 2005. Intervention Daily supplementation of a combination of 2.5 mg of folic acid, 50 mg of vitamin B6, and 1 mg of vitamin B12 (n = 2721) or placebo (n = 2721). Main Outcome Measures Confirmed newly diagnosed total invasive cancer or breast cancer. Results A total of 379 women developed invasive cancer (187 in the active treatment group and 192 in the placebo group). Compared with placebo, women receiving the active treatment had similar risk of developing total invasive cancer (101.1/10 000 person-years for the active treatment group vs 104.3/10 000 person-years for placebo group; hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.79-1.18; P = .75), breast cancer (37.8/10 000 person-years vs 45.6/10 000 person-years, respectively; HR, 0.83; 95% CI, 0.60-1.14; P = .24), or any cancer death (24.6/10 000 person-years vs 30.1/10 000 person-years, respectively; HR, 0.82; 95% CI, 0.56-1.21; P = .32). Conclusion Combined folic acid, vitamin B6, and vitamin B12 treatment had no significant effect on overall risk of total invasive cancer or breast cancer among women during the folic acid fortification era (in the USA).
Zold, E., P. Szodoray, et al. (2008). "Vitamin D deficiency in Undifferentiated Connective Tissue Disease." Arthritis Res Ther 10(5): R123. [PubMed]
ABSTRACT: INTRODUCTION: Both experimental and clinical data provide evidence that vitamin D is one of those important environmental factors that can increase the prevalence of certain autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, insulin-dependent diabetes mellitus, and inflammatory bowel disease. The aim of the present study was to investigate the prevalence of vitamin D insufficiency in patients with undifferentiated connective tissue disease (UCTD). METHODS: Plasma 25(OH)D3 levels in 161 UCTD patients were measured both in summer and winter periods. Autoantibody profiles (ANA, anti-U1 RNP, anti-SSA, anti-SSB, anti-Jo1, anti-Scl70, anti-dsDNA, anti-centromere, anti-cardiolipin, RF, anti-CCP) and the patients' clinical symptoms were assessed. RESULTS: Plasma levels of 25(OH)D3 in UCTD patients were significantly lower compared to controls both in summer and winter periods (UCTD-summer: 33+/-13.4 ng/ml vs. control: 39.9+/-11.7 ng/ml; p=0.01; UCTD-winter: 27.8+/-12.48 vs. control 37.8+/-12.3 ng/ml; p=0.0001). The presence of dermatological symptoms (photosensitivity, erythema, chronic discoid rash) and pleuritis was associated with low levels of vitamin D. During the average 2.3 years follow-up period 35/161 patients (21.7 %) with UCTD further developed into well established connective tissue disease (CTD). Patients who progressed into CTDs had the lower vitamin D levels than those who remained in UCTD stage (Vitamin D levels: CTD: 14.7+/- 6.45 ng/ml vs. UCTD: 33.0+/- 13.4 ng/ml, p=0.0001). CONCLUSIONS: In patients with UCTD a seasonal variance in levels of 25(OH)D3 was identified and showed that these levels were significantly lower than in controls during the corresponding seasons. Our results suggest that vitamin D deficiency in UCTD patients may play a role in the subsequent progress into well-defined CTDs.