Some studies have reported that vitamin D may reduce the risk or symptoms of fibromyalgia by lowering inflammation.

Fibromyalgia Patient friendly summary

Fibromyalgia is a chronic syndrome of body-wide pain. Tender points are the joints, muscles, tendons, and other soft tissues. People with fibromyalgia also have persistent fatigue, memory and mood disorders, and insomnia.

Risk factors

The cause of fibromyalgia is unknown. Possible triggers include:

  • Physical or emotional trauma
  • An abnormal or over-reactive pain response
  • An infectious organism, such as a virus

Sunlight exposure and fibromyalgia risk

There is no evidence that risk or symptoms of fibromyalgia are related to sunlight exposure.

Some people with fibromyalgia have a vitamin D deficiency. If so, vitamin D from solar ultraviolet-B (UVB) would reduce the symptoms.

Vitamin D and fibromyalgia

Vitamin D levels

2Fibro vit DSeveral studies report that people with fibromyalgia have lower vitamin D levels. 

Several studies report that people with fibromyalgia have lower vitamin D levels:

  • In the United Kingdom, 43% of females with fibromyalgia had very low vitamin D levels compared to 19% without fibromyalgia.
  • In Belfast, Northern Ireland, people with fibromyalgia frequently had low vitamin D levels. The study also linked anxiety and depression to low vitamin D levels.

However, other studies have different observations:

  • In Israel and Brazil, vitamin D levels did not vary in people with or without fibromyalgia. In the same Brazilian study, there was no connection between vitamin D levels and pain intensity.
  • In Turkey, neither vitamin D levels nor bone mineral densityvaried in people with or without fibromyalgia.

In all of the above studies, vitamin D levels could be the result of disease condition rather than the cause of the disease. Thus, the evidence that vitamin D plays a role in fibromyalgia is weak at best.

3Fibbbbro vit DHow vitamin D works

Some studies have reported that vitamin D may reduce the risk or symptoms of fibromyalgia by lowering inflammation. 

Some studies have reported that vitamin D may reduce the risk or symptoms of fibromyalgia by lowering inflammation. Vitamin D reducescytokine production. Thisprotein causes inflammation. However, one study found that fibromyalgia pain was not directly affected by these compounds.


There is no evidence that vitamin D reduces the risk of fibromyalgia. However, it may reduce inflammation. Based on studies of other diseases, it might be worthwhile to keep vitamin D blood levels above 30–40 ng/mL (75–100 nmol/L).


Vitamin D has been used to treat fibromyalgia in several studies and observations:

  • In the United Arab Emirates, people diagnosed with fibromyalgia or muscle pain benefited from vitamin D. However, it was unclear whether those with muscle pain actually had fibromyalgia.
  • People in Minnesota with fibromyalgia who initially had low vitamin D levels (10–25 ng/mL [25–63 nmol/L]) participated in a clinical trial. Some people received placebos. Others took 7000 international units (IU)/day of vitamin D3 (cholecalciferol). Vitamin D3 is the type of vitamin D made in the body. After 8 weeks, those receiving placebos showed no improvement. The vitamin D3 group showed significant improvement in fibromyalgia assessment scores. However, they did not show significant improvement in most musculoskeletal symptoms or in activities of daily living. In addition, those with severe vitamin D deficiency had no symptom improvement during the trial nor one year later.
  • Diffuse back pain related to vitamin D deficiency is often diagnosed as fibromyalgia. Raising vitamin D blood levels reduces that type of pain.

Vitamin D may reduce fibromyalgia pain. Those with fibromyalgia should consider increasing their vitamin D levels above 30–40 ng/mL (75–100 nmol/L).

Find out more…

Do you want to find out more and see the research upon which this summary is based?  Read our detailed evidence summary on fibromyalgia.

Page last edited: 17 May 2011

*These statements have not been evaluated by the Food and Drug Administration. The products and information presented on this website are not intended to diagnose, treat, cure, or prevent any disease.

Additional evidence that vitamin D reduces the risk of developing autism

Additional evidence that vitamin D reduces the risk of developing autism

14 December 2012


A study just published online in the peer-reviewed journalDermato-Endocrinologyfound additional evidence that vitamin D reduces the risk of developing autism (Grant and Cannell, 2012). The study examined the variation of autism prevalence by state for those aged 6-17 years in 2010. It found that states with higher solar ultraviolet-B (UVB) doses in summer or autumn had half the rate of autism as states with the lowest doses. The study also found that in the states with the least solar UVB, black-Americans had a 40% higher rate of autism than white-Americans. Black-Americans have lower vitamin D or serum 25-hydroxyvitamin D [25(OH)D] concentrations due to their darker skin and since solar UVB is the primary source of vitamin D for most Americans.

Similar geographical variations have been noted for incidence and mortality rates for about 15 types of cancer in the United States (Grant and Garland, 2006). The UVB-vitamin D-cancer hypothesis was proposed in 1980 based on variations in colon cancer mortality rates in the United States and now has strong support from observational studies, laboratory studies of mechanisms, and limited support from randomized controlled trials. Those who have lower serum 25(OH)D concentrations have been found to have a greater risk of developing breast and colorectal cancer. In addition, those who have lower 25(OH)D concentrations at time of cancer diagnosis have a much lower survival rate for at least seven types of cancer.

Similar geographical variations in dental caries among white boys aged 12-14 years were also reported in the mid-1930s and linked to the amount of sunshine. Also, dental rank of men entering the Armed Forces for World War I and World War II also showed a similar variation with respect to solar UVB. Vitamin D reduces risk of dental caries through induction of cathelicidin, which has antibacterial effects. (Grant WB. 2011)

Thus, studies of geographical variation of disease with respect to solar UVB doses are important ways to identify a potential role of vitamin D in preventing a disease. No factor other than vitamin D production has been proposed to explain the findings for the inverse correlations between solar UVB and cancer or dental caries. Thus, the same conclusion seems very likely for autism.

This finding regarding autism leads to the question whether maternal vitamin D deficiency during pregnancy or vitamin D deficiency in early life is related to development of autism.

Regarding maternal vitamin D deficiency, other studies have found adverse effects on fetal brain development during the third trimester of pregnancy related to vitamin D deficiency, including increased risk of schizophrenia and language difficulties. Also, increased risk of autism related to springtime births has been reported in several studies.

One of the mechanisms whereby vitamin D might reduce the risk of autism is through reducing the risk of sporadic DNA mutations from influencing fetal development. Another is through reducing the risk of influenza and other infectious diseases during pregnancy, which have been linked to increased risk of schizophrenia. Also, vitamin D reduces inflammation by shiftingcytokine production towards less inflammatory cytokines.

If vitamin D deficiency during pregnancy is a risk factor for autism, then risk could be reduced by having pregnant women take 4000 IU/d vitamin D3 and raising serum 25(OH)D concentrations to above 40 ng/ml (100 nmol/l). This amount has been shown to be both safe and necessary to increase concentrations of 1,25-dihydroxyvitamin D (calcitriol), the activemetabolite of vitamin D, to optimal levels in a randomized controlled trial by Drs. Bruce Hollis, Carol Wagner and colleagues at the Medical University of South Carolina. Calcitriolcan control the expression of more than 200 genes through interacting with vitamin D receptors, which would be very important during fetal development.

Vitamin D deficiency in early life could be a risk factor for autism, although this remains to be proved. The ways that vitamin D might reduce the risk of autism in early life are by strengthening the body’s innate immune system and reducing inflammation. Vitamin D strengthens the body’s innate immune system by inducing production of cathelicidin and defensins, which can combat bacterial and viral infections. Vitamin D also shiftscytokine production away from T-helper 1 (Th1) proinflammatory ones toward Th2 cytokines. Recent studies also show vitamin D increases neurotrophins, upregulates glutathione, increases DNA repair enzymes, and protects against mitochondrial damage.

Once autism develops, symptoms may be reduced by treating vitamin D deficiency in autistic children, although this remains to be shown in randomized controlled trials. The rationale for such a statement comes from several recent studies showing vitamin D deficiency is common among autistic children and from a recent study in the Journal of Neurodevelopment that showed vitamin D levels are inversely and strongly (R=-0.86) associated with both severity on autism rating scales and serum levels of an anti-neural antibody found in autistic children.

If vitamin D is a risk factor for autism, then autistic children should have their serum 25(OH)D concentration raised to above 30-40 ng/ml, which could take 1000-2000 IU/d vitamin D3, or more depending on such factors as genetics, weight and amount of time spent in the sun.


Grant WB. A review of the role of solar ultraviolet-B irradiance and vitamin D in reducing risk of dental caries. Dermatoendocrinol. 2011;3(3):193-198. Open access

Grant WB, Cannell JJ. Autism prevalence in the United States with respect to solar ultraviolet-B doses: An ecological study. Dermatoendocrinol. 2012;4(4): epub December 2012 (open access)

Grant WB, Garland CF. The association of solar ultraviolet B (UVB) with reducing risk of cancer: multifactorial ecologic analysis of geographic variation in age-adjusted cancer mortality rates. Anticancer Res. 2006 Jul-Aug;26(4A):2687-99.


William B. Grant, Ph.D.
Sunlight, Nutrition, and Health Research Center
P.O. Box 641603
San Francisco, CA 94164-1603, USA

Page last edited: 14 December 2012

Vitamin D Status and the Risk of Cardiovascular Disease Death

Vitamin D Status and the Risk of Cardiovascular Disease Death


  1. 1.    Annamari Kilkkinen,
  2. 2.    Paul Knekt,
  3. 3.    Antti Aro,
  4. 4.    Harri Rissanen,
  5. 5.    Jukka Marniemi,
  6. 6.    Markku Heliövaara,
  7. 7.    Olli Impivaara and
  8. 8.    Antti Reunanen
  9. Correspondence to Dr. Annamari Kilkkinen, National Institute for Health and Welfare, P.O. Box 30, FI-00271 Helsinki, Finland (e-mail:



Oxford Journals

Vitamin D Status and the Risk of Cardiovascular Disease Death

Annamari Kilkkinen,

Paul Knekt,

Antti Aro,

Harri Rissanen,

Jukka Marniemi,

Markku Heliövaara,

Olli Impivaara and

Antti Reunanen

Correspondence to Dr. Annamari Kilkkinen, National Institute for Health and Welfare, P.O. Box 30, FI-00271 Helsinki, Finland (e-mail:

Received April 24, 2009.

Accepted July 1, 2009.

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Accumulating evidence suggests that inadequate vitamin D levels may predispose people to chronic diseases. The authors aimed to investigate whether serum 25-hydroxyvitamin D (25(OH)D) level predicts mortality from cardiovascular disease (CVD). The study was based on the Mini-Finland Health Survey and included 6,219 men and women aged ≥30 years who were free from CVD at baseline (1978–1980). During follow-up through 2006, 640 coronary disease deaths and 293 cerebrovascular disease deaths were identified. Levels of 25(OH)D were determined from serum collected at baseline. Cox’s proportional hazards model was used to assess the association between 25(OH)D and risk of CVD death. After adjustment for potential confounders, the hazard ratio for total CVD death was 0.76 (95% confidence interval (95% CI): 0.60, 0.95) for the highest quintile of 25(OH)D level versus the lowest. The association was evident for cerebrovascular death (hazard ratio = 0.48, 95% CI: 0.31, 0.75) but not coronary death (hazard ratio = 0.91, 95% CI: 0.70, 1.18). A low vitamin D level may be associated with higher risk of a fatal CVD event, particularly cerebrovascular death. These findings need to be replicated in other populations. To demonstrate a causal link between vitamin D and CVD, randomized controlled trials are required.

Key words

cardiovascular diseases

cohort studies


vitamin D


Interest in vitamin D has intensified lately, with a growing body of evidence suggesting that adequate vitamin D status is required for optimal health (1, 2). The importance of vitamin D for bone health has long been acknowledged. Recent evidence suggests that vitamin D can also play a role in reducing the risk of several other diseases, including cardiovascular disease (CVD).

Vitamin D, whether ingested or synthesized in the skin, is metabolized in the human body into 25-hydroxyvitamin D (25(OH)D) and further into the biologically active form, 1,25-dihydroxyvitamin D (1, 2). Receptors for vitamin D have been found in many different cells, including cardiomyocytes and vascular endothelial cells, giving it the potential to have wide-ranging vascular effects (36). Evidence from ecologic, animal, and clinical studies also supports a potential beneficial role for vitamin D in the development of CVD (3, 4, 710). Furthermore, vitamin D status has been demonstrated to be associated with several established risk factors for CVD (11) and prevalent CVD (12). Epidemiologic evidence, however, is limited and inconclusive; both inverse associations (1315) and no associations (16) between vitamin D status and CVD risk have been reported. In addition, vitamin D supplementation had no influence on CVD incidence and mortality in the Women’s Health Initiative trial (17, 18). In the present study, we extended previous research on vitamin D and CVD by evaluating whether serum 25(OH)D level predicts mortality from coronary and cerebrovascular diseases in a cohort of more than 6,000 Finnish men and women.

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The Mini-Finland Health Survey was carried out in 1978–1980 in 40 areas of Finland (19). A 2-stage random sample (n = 8,000) was drawn from the population register to represent Finnish men and women aged 30 years or more. A total of 7,217 subjects (90% of the sample) participated in the survey, which included a health examination. Of these, 890 subjects who had a history of (or findings suggestive of) CVD at baseline and 108 subjects who did not have a serum sample available for 25(OH)D analysis were excluded. This resulted in a cohort of 6,219 subjects.


Fasting blood samples were taken during a health examination and kept frozen at −20°C until 2003, when 25(OH)D levels were determined by radioimmunoassay (DiaSorin, Inc., Stillwater, Minnesota). The interassay coefficient of variation for 25(OH)D determination was 7.80% at the mean level of 47.3 nmol/L (n = 167) and 9.12% at the level of 131.3 nmol/L (n = 135). The proportion of quality-control samples was 13.5%.

Serum total and high density lipoprotein cholesterol levels were determined with a direct modification of the Liebermann–Burchard method (20) in 1978–1980. The level of high density lipoprotein cholesterol was analyzed from the supernatant of the serum after precipitation of low density lipoprotein cholesterol and very low density lipoprotein cholesterol with magnesium/dextran sulfate. Serum triglyceride levels were analyzed enzymatically (Boehringer Mannheim GmbH, Mannheim, Germany). Low density lipoprotein cholesterol level was calculated according to the Friedewald formula: total cholesterol − high density lipoprotein cholesterol − 0.45 × total triglyceride level. Plasma glucose level was measured using the glucose oxidase method (Boehringer Mannheim) in 1978–1980, and cotinine level was measured by radioimmunoassay (Diagnostic Products Corporation, Los Angeles, California) in 1999.

The health examination included electrocardiographic recordings and blood pressure measurements. Height and weight were measured, and body mass index (weight (kg)/height (m)2) was calculated. Subjects with chronic disease histories, symptoms, or findings suggestive of cardiovascular, respiratory, or musculoskeletal diseases were asked to participate in a standardized physical examination conducted by specially trained physicians. At the end of the examination, the physicians made diagnostic assessments on the basis of all available documents, self-reported disease histories, symptoms, and clinical signs and findings. Angina pectoris was defined as typical chest pain brought on by exertion and relieved by nitroglycerine or rest. Myocardial infarction was defined as a positive history in the medical records, old myocardial infarction found upon electrocardiography, or a typical self-reported history of myocardial infarction treated in a hospital. Stroke was defined as a positive history in the medical records or a typical self-reported history of stroke treated in a hospital.

Information on socioeconomic background, symptoms, diseases, medications, and lifestyle was collected via questionnaires and interviews. Educational level was categorized into 2 groups (low, 0–9 years; high, ≥10 years) and marital status into 4 groups (unmarried, married (including common-law marriage) or in a committed relationship, widowed, divorced). Leisure-time physical activity was assessed with a question about the duration, intensity, and frequency of physical activity, and subjects were classified as inactive, occasionally active, or regularly active. Categories of alcohol consumption (ethanol intake; 0, 1–14.9, or ≥15 g/week) were derived from responses to questionnaire items concerning average weekly consumption of beer, wine, and liquor during the preceding month. Both self-reported information on smoking habits and serum cotinine level were used to generate the smoking variable. Subjects who reported that they had never smoked or had quit smoking and had a serum cotinine level of 100 ng/mL or less were categorized as nonsmokers. The rest of the subjects were divided into tertiles (cutoff points, 405 ng/mL and 767 ng/mL) based on their serum cotinine level.

Definite hypertension was defined as systolic blood pressure ≥170 mm Hg and diastolic blood pressure ≥100 mm Hg or the use of antihypertensive medication. Of the remaining members of the study population, those with systolic blood pressure ≥160 mm Hg and diastolic blood pressure ≥95 mm Hg were considered to have mild hypertension and those with systolic blood pressure <140 mm Hg and diastolic blood pressure <90 mm Hg were considered to be normotensive. All other subjects were considered to have borderline hypertension. Diabetes mellitus was defined as a self-reported history of diabetes that had been diagnosed and treated by a physician or a fasting plasma glucose level ≥6.7 mmol/L. In Finland, which is situated geographically between 60°N latitude and 70°N latitude, biologically effective ultraviolet B irradiation for production of vitamin D by the skin is provided by sunshine during the summer months only; therefore, serum 25(OH)D levels are higher between June and September than during the rest of the year. Because the baseline examinations were conducted in different seasons, the subjects were divided into 2 seasonal groups, winter (October–May) and summer (June–September).


Incident cases of fatal CVD were identified through linkage with Statistics Finland, using the Finnish nationwide individual identification number as the identity link. The Eighth, Ninth, and Tenth revisions of the International Classification of Diseases (ICD-8, ICD-9, and ICD-10, respectively) were used for coding the causes of death. Deaths with ICD codes 410–414 (ICD-8 and ICD-9) and I20–I25 (ICD-10) were classified as coronary heart disease deaths. Cerebrovascular deaths included those due to subarachnoid hemorrhage (ICD-8 and ICD-9 code 430, ICD-10 code I60), hemorrhagic stroke (ICD-8 and ICD-9 code 431, ICD-10 code I61), ischemic stroke (ICD-8 and ICD-9 codes 433–434, ICD-10 code I63), or other unspecified cerebrovascular causes (ICD-8 codes 435–438, ICD-9 codes 432 and 435–438, ICD-10 codes I6 and I64–I69).


The Cox proportional hazards model was used to estimate hazard ratios and 95% confidence intervals for total CVD, coronary heart disease, and cerebrovascular deaths according to quintile of serum 25(OH)D level. The follow-up period was defined as the time from the baseline examination to the date of CVD death, death from other causes, or the end of follow-up (December 31, 2006)—whichever came first. All analyses were adjusted for age (in years, as a continuous variable) and sex (model 1). Multivariable analyses (model 2) also included adjustment for the following a priori potential confounders: marital status, educational level, body mass index, alcohol consumption, smoking, leisure-time physical activity, and season of baseline examination. We defined 2 additional models, one of which further included serum levels of high and low density lipoprotein cholesterol (model 3) and another that also included blood pressure and diabetes (model 4).

In secondary analyses, the subjects who died of CVD within the first 4 years of follow-up or were aged 70 years or older at baseline were excluded. In addition, interactions between vitamin D and the potential effect-modifying factors (blood pressure, smoking, age, sex, body mass index, season of baseline examination, serum total, high and low density lipoprotein cholesterol levels, leisure-time physical activity, alcohol consumption and diabetes) were assessed in the main multivariable model (model 2). Because the results of these secondary analyses were essentially similar for total CVD, coronary heart disease, and cerebrovascular mortality, only the results for total CVD are presented. The vitamin D–stroke association was also analyzed according to subtypes of stroke (hemorrhagic and ischemic); these analyses were conducted using tertiles of serum 25(OH)D because of the small number of cases. In addition, subjects were divided into 2 categories using commonly applied cutoff points for low (<50 nmol/L) and high (≥50 nmol/L) levels of vitamin D (1).

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The study population consisted of 2,817 men and 3,402 women with a mean age of 49.4 years (standard deviation (SD), 13.6) at baseline. The mean serum 25(OH)D level was 43.4 nmol/L (SD, 19.7) (45.7 nmol/L (SD, 20.3) in men and 41.5 nmol/L (SD, 18.9) in women), with 67.6% of the population having a level less than 50 nmol/L. Older and highly educated subjects were more likely to have a higher vitamin D status than younger and less-educated subjects, respectively (Table 1). Heavy smoking, high alcohol consumption, low leisure-time physical activity, high body mass index, diabetes, hypertension, and a poor serum lipid profile were also associated with low serum 25(OH)D level.

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Table 1.

Baseline Characteristics of Participants According to Quintile of Serum 25-Hydroxyvitamin D Level, Mini-Finland Health Survey, Finland, 1978–1980a

During a median follow-up period of 27.1 years (range, 9 days–28.9 years), 640 coronary heart disease deaths (358 in men and 282 in women) and 293 cerebrovascular disease deaths (122 in men and 171 in women) were identified. Cerebrovascular events included 175 ischemic strokes, 43 hemorrhagic strokes, 22 subarachnoid hemorrhages, and 53 other unspecified cerebrovascular events.

There was an inverse association between serum 25(OH)D level and total CVD mortality when results were adjusted for age and sex only (for the highest quintile in model 1 vs. the lowest, hazard ratio (HR) = 0.71, 95% confidence interval (CI): 0.58, 0.87; P for trend < 0.001 (Table 2)). Adjustment for potential confounders, including also marital status, educational level, body mass index, alcohol consumption, smoking, leisure-time physical activity, and season of baseline examination, only slightly attenuated the association (in model 2, HR = 0.76, 95% CI: 0.61, 0.95; P for trend = 0.005). Further adjustment for serum high and low density lipoprotein cholesterol levels (in model 3, HR = 0.75, 95% CI: 0.59, 0.94; P for trend = 0.004) and diabetes and blood pressure (in model 4, HR = 0.80, 95% CI: 0.64, 1.01; P for trend 0.012) did not notably change the results. Moreover, the results remained essentially similar after the exclusion of subjects who died of CVD during the first 4 years of follow-up (in model 2, HR = 0.76, 95% CI: 0.60, 0.96; P for trend = 0.008) or were 70 years of age or older at baseline (in model 2, HR = 0.79, 95% CI: 0.61, 1.03; P for trend = 0.029). No statistically significant interaction was observed between 25(OH)D level and age (P for interaction = 0.95), alcohol consumption (P = 0.53), body mass index (P = 0.49), diabetes (P = 0.32), blood pressure (P = 0.81), leisure-time physical activity (P = 0.30), season of baseline examination (P = 0.75), sex (P = 0.74), smoking (P = 0.24), or serum total (P = 0.12), high density lipoprotein (P = 0.23), or low density lipoprotein (P = 0.13) cholesterol level.

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Table 2.

Hazard Ratios for Cerebrovascular and Coronary Disease Mortality According to Quintile of Baseline Serum 25-Hydroxyvitamin D Level, Mini-Finland Health Survey, Finland, 1978–1980

An inverse association was found between serum 25(OH)D level and mortality from cerebrovascular disease (for the highest quintile in model 1 vs. the lowest, HR = 0.47, 95% CI: 0.31, 0.70; P for trend < 0.001 (Table 2)). Results from multivariable analyses were rather similar (in model 2, HR = 0.48, 95% CI: 0.31, 0.75; P for trend = 0.002), indicating that there was little confounding by the covariates. Further adjustment for serum high and low density lipoprotein cholesterol concentrations (in model 3, HR = 0.50, 95% CI: 0.32, 0.77; P for trend = 0.003) and diabetes and blood pressure (in model 4, HR = 0.52, 95% CI: 0.33, 0.80; P for trend = 0.004) did not change the results. In the analyses conducted according to subtype of stroke, the multivariable adjusted hazard ratios (for the highest tertile in model 2 vs. the lowest) for hemorrhagic and ischemic stroke were 0.61 (95% CI: 0.26, 1.46; P for trend = 0.29) and 0.60 (95% CI: 0.38, 0.93; P for trend = 0.050), respectively (Table 3).

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Table 3.

Hazard Ratios for Various Subtypes of Stroke According to Tertile of Baseline Serum 25-Hydroxyvitamin D Level, Mini-Finland Health Survey, Finland, 1978–1980

In model 1, with adjustment for age and sex only, an inverse association was found between serum 25(OH)D level and the risk of coronary heart disease death (for the highest quintile vs. the lowest, HR = 0.83, 95% CI: 0.65, 1.06; P for trend = 0.037 (Table 2)). After adjustment for potential confounders, the hazard ratios were no longer statistically significant (in model 2, HR = 0.91, 95% CI: 0.70, 1.18; P for trend = 0.20). No single risk factor was responsible for the attenuation. Further inclusion of serum high and low density lipoprotein cholesterol concentrations in the model did not change the results (in model 3, HR = 0.87, 95% CI: 0.67, 1.14; P for trend = 0.12). In the model 4 that also included diabetes and blood pressure, the hazard ratio for the highest quintile versus the lowest was 0.96 (95% CI: 0.73, 1.25; P for trend = 0.28).

In further analysis based on the cutoff value of 50 nmol/L for serum 25(OH)D level, the multivariable adjusted hazard ratio (for high vitamin D category in model 2 vs. low vitamin D category) for total CVD death was 0.88 (95% CI: 0.75, 1.03). For mortality from cerebrovascular disease and coronary heart disease, the corresponding hazard ratios were 0.58 (95% CI: 0.42, 0.79) and 1.04 (95% CI: 0.86, 1.25), respectively.

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This cohort study provided evidence that a low circulating level of vitamin D may predict a higher risk of CVD death. The observed association was particularly striking for mortality from cerebrovascular disease; subjects in the highest quintile of serum 25(OH)D level had less than half the risk of cerebrovascular death as those in the lowest quintile.

Epidemiologic evidence on the association between vitamin D and the risk of CVD is limited. In the Health Professionals Follow-up Study, men with a high circulating level of vitamin D had half the risk of myocardial infarction as men with vitamin D insufficiency (14). Similarly, a study of German adults who were undergoing elective cardiac catheterization showed a 2-fold risk of CVD death among persons in the lowest quartile of baseline vitamin D level compared with those in the highest quartile (13). In addition, among participants in the Framingham Offspring Study cohort, vitamin D deficiency was associated with an increased risk of CVD (relative risk = 1.62, 95% CI: 1.11, 2.36) (15). However, in contrast to our findings, the association was observed only in hypertensive subjects, not in those without hypertension (15). Moreover, in a recent cohort study based on data from the Third National Health and Nutrition Examination Survey, Melamed et al. (16) could not find a statistically significant association between vitamin D status and CVD mortality in the general population. Note, however, that data on coronary heart disease and cerebrovascular events were pooled in the Third National Health and Nutrition Examination Survey (16) and in most earlier studies (13, 15), whereas we analyzed deaths from coronary heart disease and cerebrovascular disease separately. Indeed, our findings suggest that vitamin D might have a more important role in the prevention of cerebrovascular disease, especially ischemic stroke, than in the etiology of coronary heart disease. There is no obvious explanation for this finding, and confirmation in other studies is required. However, although coronary heart disease and cerebrovascular disease share important risk factors, the impact of some risk factors (e.g., blood lipids and blood pressure) varies (21). This may imply different underlying mechanisms for these diseases and offers a possible explanation for the differences in our results for cerebrovascular disease and coronary heart disease.

Although the exact mechanisms by which an adequate vitamin D status may protect against CVD are not fully understood, experimental studies indicate that vitamin D is one of the most potent hormones for suppressing the renin-angiotensin system and thus for regulating blood pressure (4). The vascular effects of vitamin D also include inhibition of thrombosis (3) and arterial calcification (22). Furthermore, several types of cells, including vascular smooth muscle cells and lymphocytes, express receptors for vitamin D and have the ability to convert circulating 25(OH)D to 1,25-dihydroxyvitamin D, which in turn can reduce the proliferation of lymphocytes and the production of cytokines (5, 6). Because there is increasing evidence that systemic inflammation plays an important role in the development of atherosclerosis (23), the antiinflammatory properties of vitamin D warrant further exploration. Vitamin D deficiency, on the other hand, increases the secretion of parathyroid hormone, which has been shown to contribute to pathologic changes in the cardiovascular system (24). Further studies are required to clarify the vitamin D–CVD association and the mechanisms behind the association. Data from supplementation trials of the effects of vitamin D on bone health could provide useful information.

The mean serum 25(OH)D values in our study were approximately of the same order of magnitude as those previously found in Finland (25) but somewhat lower than those generally observed in other European (13, 26) and American (12) populations. There is no absolute consensus as to what the optimal range for serum 25(OH)D levels should be. However, relatively high concentrations of 25(OH)D (>75 nmol/L) are required to maintain normal parathyroid hormone levels, and even higher concentrations (≥83–121 nmol/L) are suggested to be desirable for cancer prevention (27). Although optimal levels for cardiovascular protection may differ from those, it is noteworthy that the values in our cohort were substantially lower than those previously thought to be sufficient (27).

The main strengths of the present study lay in the prospective design and the fairly large nationally representative population sample. In addition, information on CVD mortality was obtained from the nationwide mortality register, which is based on death certificates and has been shown to have reasonably good validity (28, 29). A further strength of the study was the information on CVD and its risk factors at baseline from the physician’s examination. However, while the detailed data on multiple CVD risk factors allowed adjustment for potential confounders, we cannot rule out the possibility of residual confounding. It can be speculated that persons with chronic illness may have reduced serum vitamin D levels because of their limited exposure to sunlight and inadequate dietary intake of vitamin D. This raises the possibility that low vitamin D status is only a nonspecific indicator of chronic illness rather than a direct contributor to disease pathogenesis. It is important to acknowledge potential confounding by dietary factors, as we did not have information on vitamin D intake from diet and supplements. The major dietary source of vitamin D is fatty fish, consumption of which is suggested to be protective against CVD because of its n-3 polyunsaturated fatty acid content (30). A recent meta-analysis, however, did not show a definite effect of omega-3 fatty acids on CVD events (31).

A further limitation of this study was the use of a single measurement of vitamin D. It can be questioned whether serum 25(OH)D level measured at a single point in time reflects only recent exposure rather than long-term exposure. Nevertheless, in 1 study, the correlation coefficient for correlation between 2 measurements of vitamin D taken 3 years apart appeared to be moderately high, 0.70 (32), suggesting that a single serum measurement of this compound could be a useful tool in epidemiologic studies. Such measurement, however, fails to take into account the intraindividual seasonal variation in serum 25(OH)D levels. Inclusion of the season of baseline examination as a potential confounder in the model or the use of it as an effect-modifying factor did not substantially change our results. Because serum samples were stored at −20°C up to 25 years before the determination of vitamin D level, a change in vitamin D concentrations during storage is a potential concern. However, vitamin D metabolites in blood stored at 24°C for up to 72 hours have been shown to remain intact (33), and only a minimal decline is observed for plasma 25(OH)D level for up to 4 years of storage at −20°C (34). Although the evidence suggests that 25(OH)D is a stable compound (3335), we cannot rule out the possibility that levels might have changed during storage at −20°C. Finally, the use of mortality rather than incidence data was a potential limitation of the study.

In conclusion, our results suggest that a low circulating level of vitamin D may be associated with a higher risk of fatal CVD events. Although a possible causal link between vitamin D and CVD is biologically plausible, further investigations from different populations with repeated measurements of vitamin D are warranted. To demonstrate a causal link between vitamin D status and the risk of CVD, randomized controlled clinical trials are required. Because CVD remains the leading cause of death in most developed countries, identification of new CVD risk factors (such as vitamin D) is an area of much interest, both scientifically and among the lay public. Our findings may have profound public health implications; while the prevalence of suboptimal vitamin D levels has been observed to be high worldwide, vitamin D status can be rather inexpensively and easily improved through supplementation or lifestyle measures.

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Author affiliation: National Institute for Health and Welfare, Helsinki, Finland.

This work was supported in part by the Social Insurance Institution of Finland.

Conflict of interest: none declared.

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confidence interval


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Vitamin D Status and the Risk of Cardiovascular Disease Death


Dra. Cristina Sales – «Saber comer é pura informação»

Dra . Cristina Sales –  «Saber comer é pura informação»

Por Célia Rosa. Fotografia de Pedro Granadeiro/GI


E se o seu organismo não reconhecer aquilo que você come como um alimento? Defende-se, inflama-se, fica doente. É o que fazem muitos dos produtos que levamos à boca. Cristina Sales, médica e especialista em alimentação, garante que na origem da maioria das doenças que afetam o homem do século XXI está o que comemos e o modo como o fazemos. É que os alimentos são veículos de comunicação: dizem às células como devem comportar-se.

Precisamos de mudar a forma como nos alimentamos?

_É obrigatório que o façamos porque a alimentação que a população dos países ocidentais, incluindo Portugal, passou a fazer nos últimos cinquenta anos é o que está na origem da maior parte das doenças endócrinas, metabólicas, autoimunes, degenerativas e alérgicas. As novas epidemias devem-se sobretudo aos estilos de vida e à alimentação que fazemos desde o pós-guerra.

A alimentação é decisiva para a saúde e o bem-estar mas está a provocar doenças e a aumentar a mortalidade precoce?

_A geração dos nossos filhos terá uma esperança de vida mais reduzida do que a nossa por causa dos estilos de vida e da alimentação. Primeiro, os produtos altamente processados pela indústria alimentar conduzem a uma desnutrição em nutrientes fundamentais e ingerimos uma grande quantidade de calorias vazias. Segundo, são muito diferentes dos alimentos originais e o organismo não sabe lidar com eles, não os reconhece como alimentos. Depois, há uma sobrecarga tóxica inerente à alimentação que provém dos agroquímicos (da produção), dos conservantes, corantes e adoçantes que são adicionados para preservar os produtos durante mais tempo e para os manter bonitinhos.

São alimentos para ver…

_Os produtos que nos chegam ao prato foram feitos para vender e não para comer. Não têm nada que ver com os alimentos que ingerimos e que nos fizeram viver e sobreviver ao longo de milhões de anos. Esta mudança ocorreu tão depressa que o organismo não está adaptado para gerir, digerir e assimilar estes produtos, pelo contrário, vê-os como substâncias estranhas e reage, inflamando-se.

Como é que podemos livrar-nos dessa teia?

_As escolhas alimentares são condicionadas pela publicidade, as pessoas não são ensinadas a escolher. Quem é que é ensinado a consumir maçãs ou laranjas? Ninguém. A informação que passa de forma subliminar através dos anúncios da TV e dos jornais é que se deve beber sumo de maçã e de laranja. Mas se alguém ler os rótulos das embalagens verifica que contém imenso açúcar, frutose, acidificantes, etc., e o que falta é a maçã e a laranja. É preciso informar, ensinar e consciencializar a população.

A atitude da indústria alimentar tem de mudar?

_No global sim, mas também depende do que a indústria faz. A conservação de alimentos através da congelação, por exemplo, é perfeita. Os legumes congelados são uma ótima opção, por vezes mais económica, e chegam ao consumidor mais frescos e com mais nutrientes do que os que são mantidos durante cinco ou seis dias nas cadeias de distribuição. Já quando falamos de alimentos que têm de levar uma quantidade enorme de aditivos para serem consumidos – é o caso das carnes de muito má qualidade e dos aproveitamentos que se fazem dos restos dos mariscos – é diferente. Sempre que tivermos de dobrar a língua muitas vezes para conseguir ler o que está escrito nos rótulos é porque não é comida. Não compre. Será qualquer coisa que do ponto de vista nutricional, químico e metabólico está muito longe do alimento original.

Está a falar de alimentos que duram ad eternum?

_Por exemplo. Como é que duram? Fizeram-se estudos com hambúrgueres e batatas fritas – uns feitos em casa, com carne picada, e batatas que foram descascadas, outros com produtos processados e embalados – e verificou-se que ao fim de trinta ou quarenta dias alguns hambúrgueres se mantinham iguaizinhos. Não se degradaram, ao contrário dos que foram feitos em casa, que estavam estragados três dias depois. Ora alguém acha que uma coisa daquelas pode ser comida?

Quando ingerimos produtos desse tipo como é que o organismo reage?

_Defende-se e inflama-se ou agarra naquelas coisas que não considera importantes e arruma-as nos depósitos de lixo, que são as células gordas. Estas, além de serem o nosso reservatório de energia, são também o depósito de substâncias tóxicas que o organismo não metaboliza ou não utiliza para impedir que entrem nos circuitos mais nobres. Esta acumulação de lixo cria bloqueios bioquímicos e alterações metabólicas que impedem as células de trabalhar em condições. Hoje ninguém sabe que consequências é que isto tem para o cérebro e o sistema imunitário e para o bom trabalho hepático e digestivo. Os circuitos da toxicidade são cruzados – se uma pessoa come de vez em quando um gelado, um iogurte, umas bolachas ou um sumo que tem um determinado corante é uma coisa, mas se o faz com regularidade, ao fim de seis meses já ultrapassou as doses suportáveis e entra em sobrecarga tóxica.

E o que é que acontece?

_Veja-se o ácido fosfórico, um aditivo que está presente em alimentos de consumo diário, como os cereais de pequeno-almoço e os refrigerantes. Quem ingere estes produtos todos os dias, além de ficar com o sistema acidificado e perder cálcio (uma compensação do organismo que depois predispõe à osteoporose), também fica numa excitação – o ácido fosfórico é um estimulante cerebral e é óbvio que uma criança que de manhã come um prato de cereais chega à escola e não para quieta. O ácido fosfórico altera o comportamento e em determinadas concentrações é neurotóxico.

Como é que os alimentos atuam no organismo?

_Os alimentos servem para construir tecido, osso, órgãos, etc., e para nos darem energia, mas o que as ciências da nutrição têm vindo a mostrar é que os alimentos são essencialmente moduladores do comportamento celular – são informadores das células, dizem-lhes como devem funcionar. Imagine que tem um prato com uma determinada quantidade de proteínas (peixe ou carne) e outra de hidratos de carbono. Só a proporção entre a quantidade de carne e batatas ingeridas vai informar o organismo da necessidade de produzir uma hormona ou outra, neste caso insulina (que é a hormona do armazenamento) ou glucagon (a hormona do desarmazenamento).

Explique lá melhor…

_Se comer mais proteínas do que hidratos de carbono vai produzir mais glucagon e induzir o metabolismo a ir buscar gordura acumulada para disponibilizar às células, ou seja, vai desarmazenar. Mas se comer mais arroz, massa ou batatas vai dar uma ordem em sentido contrário, vai dizer que é precisa mais insulina e vai acumular gordura.

Mas se as pessoas forem ativas podem queimar essa energia…

_Isso é outra coisa, o que importa reter é que na proporção hidratos de carbono/proteínas a quantidade de açúcar que chega aos sensores do tubo digestivo aciona imediatamente uma ordem de libertação de glucagon ou de insulina. Se a indicação é libertar glucagon, o organismo vai usar a gordura acumulada, se a ordem for para libertar insulina, o organismo vai armazenar gordura. Isto é pura informação.

Quem quer perder peso tem de saber isso, certo?

_Se a pessoa tiver consciência da informação que dá ao corpo tem muito mais capacidade para o modular. Outro exemplo. A leptina, a hormona que sinaliza o apetite, que depende sobretudo do ritmo solar. Ora, uma pessoa equilibrada, que durma de noite e trabalhe de dia, produz mais leptina de manhã (e tem apetite) e ao fim do dia produz menor quantidade (o apetite diminui). Se uma pessoa comer muito à noite estraga este equilíbrio e a certa altura está sempre com fome porque inutilizou os sensores da leptina. Nós somos mamíferos e de noite, quando dormimos, não precisamos de comer. O nosso corpo tem a sabedoria para sinalizar o apetite em função da hora do dia – comer muito à noite estraga essa sinalização, faz ter apetite a toda a hora.

A alimentação é bioquímica?

_Os alimentos são veículos de comunicação. Se fizer uma refeição de gordura saturada – uma sopa com um chouriço e depois um cozido à portuguesa – dá um sinal à cárdia (esfíncter entre o estômago e o esófago) para alargar e é assim que ocorrer o refluxo gastroesofágico e aparece a azia. A gordura saturada é um sinal que se dá à cárdia para se manter aberta. Se no dia seguinte a mesma pessoa só comer azeite ou gorduras de peixe não terá azia. Sabe porquê? É que o azeite ajuda a fechar a cárdia. Este é outro exemplo que ilustra a importância do conhecimento. Pessoas mais esclarecidas fazem escolhas mais acertadas.

A forma como nos alimentamos dita o comportamento das células?

_Quando ingeridas, as gorduras saturadas e as gorduras ómega 6 (provenientes essencialmente dos animais e dos cereais, sobretudo da soja) são a estrutura a partir da qual as células fazem substâncias pró-inflamatórias. As gorduras ómega 3 – provenientes das algas e dos peixes – são as que permitem que as células produzam substâncias anti-inflamatórias. Se uma pessoa tem uma doença inflamatória (por exemplo, uma alergia, artrite ou doença autoimune) e come muita gordura saturada, esta vai funcionar como substrato para a fogueira e agravar o processo inflamatório da doença que já tem. Ao contrário, se a pessoa ingerir gorduras ómega 3, vai ser capaz de construir extintores de incêndio para que as suas células produzam anti-inflamatórios.

Há outros exemplos?

_Se uma pessoa tem tendência depressiva porque não consegue produzir serotonina em quantidade suficiente, deve comer os alimentos que têm os aminoácidos precursores da serotonina – a carne de peru, por exemplo, é extremamente rica em triptofano, que é um precursor da serotonina. Se a pessoa souber isto, no outono, quando o tempo fica mais escuro, porque é que não há de comer mais carne de peru em vez de carne de vaca?

A alimentação e o processo digestivo podem agravar ou controlar certas doenças?

_Sim, se uma pessoa tem uma predisposição genética para a diabetes, Alzheimer, etc., a doença só vai manifestar-se se o gene for ativado. Mas o que as pessoas precisam de saber é que os genes também podem ser desativados – é a modulação genética através da nutrigenética. Como? O que ativa ou suprime a expressão dos genes é a presença de determinados fitoquímicos, substâncias que também se encontram nos alimentos.

Podemos dizer que há alimentos anti-inflamatórios?

_Claramente. Os que têm ómega 3 – sardinha, cavala e os peixes das águas frias do Norte. Algumas substâncias vegetais dos legumes (tomate), frutos (quivi) e especiarias (a curcuma, que confere a cor amarela ao caril) também têm efeito modulador de alguns genes pró-inflamatórios. Mas alimentos anti-inflamatórios devem ser consumidos, independentemente de se ter doença ou não. Hoje sabe-se que um cérebro com Alzheimer já está inflamado vinte anos antes da manifestação da doença. Todas as doenças degenerativas começam com processos inflamatórias, as autoimunes também. Não conhecemos é as causas.

Há substâncias que devem mesmo ser eliminadas da alimentação?

_Os aditivos químicos. Falo das substâncias químicas que não são alimentos, que são usadas pela indústria alimentar e podem ser geradoras de inflamação em contacto com o organismo. A vida corrente não nos permite evitar todos os aditivos, mas se estivermos despertos para esta realidade teremos mais atenção, faremos escolhas mais saudáveis e ingerimos menores quantidades.

E as gorduras?

_As gorduras ómega 6, que se encontram nas margarinas e nos óleos e que são provenientes da soja, do milho e do amendoim, são claramente pró-inflamatórias. Precisamos de ómega 6 no organismo, mas em quantidades muito reduzidas. O problema é que a cadeia alimentar atual é geradora de uma alimentação extraordinariamente rica em ómega 6 e pobre em ómega 3. Basta pensar que, dantes, as galinhas e as vacas comiam erva, agora comem rações provenientes da soja; os peixes comiam algas, agora comem rações também com soja. Os produtos alimentares que usamos são essencialmente da linha produtora de ómega 6.

Nos supermercados temos centenas de alimentos à escolha. Precisamos de tanta coisa?

_Não precisamos de tantos produtos alimentares, necessitamos é de maior diversidade alimentar. Essas centenas ou milhares de produtos que vemos nas prateleiras são provenientes de quatro ou cinco alimentos – cereais, lácteos, açúcares e gorduras – e da indústria de processamento. Se olharmos para a quantidade de legumes, frutos, oleaginosas e peixe que as pessoas comem no dia a dia verificamos que não há variedade alimentar, as pessoas comem quase sempre o mesmo. Já pensou na variedade de saladas que é possível fazer? Mas se perguntar a alguém qual é a que come diz-lhe alface e tomate.

No supermercado fazemos escolhas condicionadas pela publicidade e o marketing. Como podemos fugir a isso?

_Só vai mudar com a informação dos cidadãos. Nos países do Norte da Europa, onde a população é muito mais esclarecida, não encontramos nos supermercados esta quantidade enorme de alimentos-lixo – basta verificar que o espaço ocupado por refrigerantes, cereais de pequeno-almoço e óleos alimentares é muito reduzido. Exatamente o oposto do que se passa em Portugal.

A crise económica e as dificuldades das famílias podem piorar ainda mais a alimentação dos portugueses?

_Também pode acontecer o contrário. Numa altura em que todos sentimos uma necessidade absoluta de gerir muito bem os orçamentos familiares, devemos fazer listas de compras de forma racional. E antes de comprar certos produtos alimentares, é obrigatório perguntar: «Preciso mesmo disto? Vale a pena? Faz-me ficar mais forte, vital, inteligente? Tem mais nutrientes?» Ocasionalmente, podemos comprar os tais alimentos que não comportam nenhum valor acrescentado mas que agradam ao paladar, mas isso é num dia de festa.

De que produtos podemos e devemos mesmo prescindir quando vamos às compras?

_Devemos tirar os refrigerantes, cereais com açúcar, pastelaria, óleos e margarinas – para cozinhar devemos usar o azeite, só azeite. Todos os refrigerantes são um estrago de dinheiro – as pessoas devem beber água. Os cereais com açúcar (os de pequeno-almoço e as bolachas) também são prescindíveis – devemos escolher cereais completos, integrais, que até são mais baratos. Compare-se o preço de uma caixa de cereais de pequeno-almoço com o de um pacote de flocos de aveia, que são altamente nutritivos. A aveia é muito mais barata e muito nutritiva.

Mas comprar carne magra e peixe gordo, frutos e hortaliças é muito mais dispendioso…

_Mas há estratégias que podem ser implementadas. Uma é comprar carne de melhor qualidade e comer menos quantidade e menos vezes. É preferível comer carne três vezes por semana em vez de comer carne gorda todos os dias. Além disso, toda a gente ganha se fizer uma alimentação vegetariana dois dias da semana e em vez da carne comer, por exemplo, arroz de feijão ou grão-de-bico com massa. Se se acrescentar hortaliças, ervas aromáticas e azeite, podemos dizer que são refeições perfeitas. Menos carne, mas de melhor qualidade; mais peixe (incluindo cavala e sardinhas, frescas ou em conserva de azeite) e ovos (podem ser consumidos três ou quatro por semana) são opções a privilegiar.

Não retira massa, arroz ou batatas ao seu carrinho de compras?

_Não, mas reduzo as quantidades ingeridas. No prato devemos ter pequenas porções de massa, arroz ou batatas e maior quantidade de hortaliças, legumes e leguminosas.

Fala-se muito na responsabilidade social da indústria farmacêutica, que ganha dinheiro à custa do tratamento dos doentes. E quanto à responsabilidade social da indústria alimentar, que ganha dinheiro atirando-nos para a doença?

_A indústria alimentar está a fazer maus alimentos, mas a verdade é que as pessoas só compram o que querem. Sei que quanto menor é a informação maior é a permeabilidade ao marketing, mas o caminho também se faz através da informação dos cidadãos e da sua responsabilização. Custa-me imenso ver nas caixas de supermercado que as pessoas aparentemente mais pobres também são as que levam os carrinhos repletos de produtos inúteis e nefastos para a sua saúde. É preciso repensar a política alimentar e inovar.


A medicina que Cristina Sales exerce dá pelo nome de medicina funcional integrativa – reúne diferentes disciplinas, profissionais e recursos terapêuticos, é centrada na pessoa e procura entender onde estão os desequilíbrios que desencadeiam a doença. Para uns, trata-se de uma abordagem vanguardista, mais adaptada aos pacientes, ao tratamento e controlo das chamadas doenças da civilização. Para outros, a prática médica de Cristina Sales ainda gera alguma desconfiança. Quem não receia são os doentes que a procuram – sobretudo pessoas que vivem com doenças crónicas (alergias, enxaquecas, fadiga crónica, doenças inflamatórias, endócrinas, metabólicas e autoimunes) e que não encontraram resposta satisfatória para os problemas que as afetam até chegarem ao seu consultório no Porto. Uma consulta com a médica dura hora e meia e não se marca de um dia para o outro. Porque os pacientes já são muitos e porque as palestras e conferências em que Cristina Sales é oradora convidada são frequentes.

– – –

A correcção terapêutica da deficiência em vitamina D3 nas doenças auto-imunes é uma opção terapêutica baseada em evidência científica

Segundo a experiência pioneira do Dr Cicero Coimbra, MD, PhD, Professor Associado de Neurologia e Neurociência da Universidade Federal de São Paulo, Brasil, a correcção terapêutica dos níveis sanguíneos de vitamina D3, pela toma continuada de doses elevadas, ou muito elevadas, de vitamina D3 sob controlo médico, pode reverter em parte ou na totalidade os sintomas da doença e mesmo fazer a doença entrar em remissão. (14)


A correcção terapêutica da deficiência em vitamina D3 nas doenças auto-imunes é uma opção terapêutica baseada em evidência científica


Por Dra Cristina Sales


Dra Cristina Sales na revista Notícias Magazine

Foto e entrevista em Quarta-Feira, 20 Junho, 2012

Autoimunes e Vitamina D3

Doenças autoimunes e vitamina D3

Criamos uma consulta multidisciplinar para aplicação do protocolo de correcção terapêutica da deficiência em vitamina D3 nas doenças auto-imunes que segue a metodologia e tem o apoio do Dr Cícero Coimbra, seu autor.

A 1ª etapa do protocolo de correcção terapêutica da deficiência em vitamina D3 nas doenças auto-imunes, que é constituida por uma consulta médica e uma consulta de nutrição.

Ambas as consultas são agendadas para o mesmo dia.

As consultas médicas serão realizadas pela Dra Cristina Sales ou pela Dra Filomena Vieira.

As consultas de nutrição serão realizadas pela Dra Daniela Seabra ou pela Dra Helena Santos.

Para marcação de consulta queira informa-se clicando aqui .

Informação científica:

A correcção terapêutica da deficiência em vitamina D3 nas doenças autoimunes é uma opção terapêutica baseada em evidência científica


A investigação científica recente mostrou que a vitamina D3, para além do conhecido papel no metabolismo do cálcio e processo de ossificação, tem múltiplas acções no organismo, com relevância para uma importante intervenção no sistema imunitário.

A amplitude da sua acção e o facto de todas as células do organismo humano terem receptores para esta substância sugerem tratar-se não de uma vitamina mas de uma pró-hormona (1).


A síntese da vitamina D3, no organismo humano, é feita pela pele e depende totalmente da sua exposição solar. Para produzir a quantidade necessária de vitamina D3 é preciso expor ao sol as pernas, braços, pescoço e face durante, pelo menos, 15minutos, ao inicio da manhã ou ao fim da tarde quando a inclinação do sol provoca uma sombra do tamanho da pessoa.
A vida urbana moderna e o uso de protectores solares impossibilitam a produção de vitamina D3 na quantidade suficiente. O afastamento da zona geográfica onde se habita do equador representa mais um factor de risco.
Verifica-se, por outro lado, que a grande maioria da população dos países industrializados é deficitária em vitamina D3. O deficit de vitamina D3 promove a osteoporose e as patologias dentárias, aumenta a incidência dos cancros de mama, de próstata e de cólon e de doenças cardiovasculares.


Há pessoas cujo perfil genético interfere, de forma dramática, no metabolismo da vitamina D3, condicionando níveis sanguíneos muito baixos de vitamina D3 (2).
A grande maioria das pessoas com doenças auto-imunes pertence a este grupo populacional e apresenta uma grave deficiência em vitamina D3.


De entre as doenças auto-imunes, a esclerose múltipla é aquela em que a evidência científica é mais contundente. Existem mais de 3.600 (3) estudos científicos publicados que mostram a relação entre esclerose múltipla e deficiência em vitamina D3.


A alta frequência de surtos e elevada severidade das sequelas neurológicas (paraplegia, cegueira) correlaciona-se com níveis circulantes mais baixos de vitamina D tanto em adultos (4, 5) como em crianças (6).


Em 1986 um estudo mostrou que a vitamina D3, em doses modestas (5.000 UI por dia) foi capaz de reduzir em mais de 50% a frequência de surtos em portadores de esclerose múltipla (7).


Em 2007 um estudo envolvendo 12 doentes por um período de 28 semanas mostrou que a administração de doses progressivamente elevadas ao longo de 7 meses  (a partir da dose semanal de 28.000 UI = 4.000 UI por dia, até ser atingida a dose semanal de 280.000 UI = 40.000 UI por dia), levaram à redução das lesões activas em comparação com o número de lesões activas encontradas nos mesmos pacientes antes desses 7 meses, não sendo verificada a ocorrência de efeitos colaterais (8).


Um estudo “duplo-cego, randomizado” publicado em 2012, mostra a redução do número de lesões activas no grupo tratado com doses relativamente baixas de vitamina D (20.000 UI por semana) durante apenas 1 ano, além de diversas outras melhoras, sem efeitos colaterais verificados (9), em comparação com o grupo que recebeu apenas interferon + placebo.


Em Junho 2012, a publicação científica “Currente Opinion in Neurology” num artigo intitulado “Vitamin D and multiple sclerosis: epidemiology, immunology, and genetics” conclui “continuarem a acumular-se evidências em relação ao papel protector da vitamina D contra o risco da esclerose múltipla se desenvolver e contra a progressão da doença (10).
Um dado da maior relevância na abordagem terapêutica das doenças auto-imunes é que a acção imunitária da vitamina D3 diminui a resposta auto-imune ao mesmo tempo que mantém, ou mesmo aumenta, a capacidade de defesa face a doenças infecto-contagiosas.
De facto, na qualidade de potente pró-hormona imuno-reguladora, a vitamina D inibe a resposta imunológica direccionada contra o próprio organismo  (denominada pelos imunologistas como “TH17”), tanto em indivíduos saudáveis (11) como nos portadores de esclerose múltipla (12)  sem inibir a resposta direccionada contra infecções e pelo contrário, potencializando a resposta antimicrobiana, tal como se verifica, por exemplo, no tratamento da tuberculose pulmonar (13).


Se a evidência científica é especialmente bem suportada no caso da esclerose múltipla, a correcção terapêutica da deficiência em vitamina D3 assume-se como um dever ético e pode beneficiar igualmente os doentes com outras doenças auto-imunes – artrite reumatóide, lupus, diabetes tipo1, tiroidite de Hashimoto – que apresentem deficit de vitamina D3.
Segundo a experiência pioneira do Dr Cicero Coimbra, MD, PhD, Professor Associado de Neurologia e Neurociência da Universidade Federal de São Paulo, Brasil, a correcção terapêutica dos níveis sanguíneos de vitamina D3, pela toma continuada de doses elevadas, ou muito elevadas, de vitamina D3 sob controlo médico, pode reverter em parte ou na totalidade os sintomas da doença e mesmo fazer a doença entrar em remissão. (14)


As DDR – doses diárias recomendadas – de vitamina D3 que ao longo de décadas têm sido 200, 400 ou 600 UI, mostram-se totalmente desadequadas para repor o nível sérico nos doentes cujos perfis genéticos condicionam o normal metabolismo da vitamina D3, desde a sua absorção até ao seu efeito biológico.


As pessoas portadoras de EM são parcialmente resistentes à vitamina D em decorrência de polimorfismos genéticos (2)necessitando,  portanto, de doses muito maiores para obterem o mesmo efeito biológico dessa potente pró-hormona imuno-reguladora.

A administração diária de 1.000 UI eleva a concentração plasmática de vitamina D em cerca de 5 ng/mL(12.5 nmol/L); já a administração diária de 5.000 UI eleva a concentração plasmática de vitamina D em cerca de 36 ng/mL(90 nmol/L); a administração diária de 10.000 UI eleva a concentração plasmática de vitamina D em cerca de 64 ng/mL (160 nmol/L) (15).


A terapêutica com doses elevadas, ou muito elevadas, de vitamina D3 comporta alguns riscos. Por isso, este tratamento deve ser acompanhado por um regime alimentar específico e ser sujeito a uma monitorização médica e laboratorial regular para um ajuste adequado e personalizado das doses terapêuticas da vitamina D3.



(1) Norman AW. From vitamin D to hormone D: fundamentals of the vitamin D endocrine system essential for good health. American Journal of Clinical Nutrition. August 2008. vol. 88 no. 2 491S-499S

(2) Sundqvist E, Bäärnhielm M, Alfredsson L,  Hillert J, Olsson T,  Kockum I. Confirmation of association between multiple sclerosis and CYP27B1. European Journal of Human Genetics. 2010 December; 18(12): 1349–1352.

(3) Scirus [homepage]. Acedido em Junho 2012. Disponível em: feita por “vitamin D” (“multiple sclerosis”))

(4) Smolders J. Association of vitamin D metabolite levels with relapse rate and disability in multiple sclerosis. Multiple Sclerosis Journal. November 2008 vol. 14 no. 9 1220-1224.

(5) Weinstock-Guttman B, Zivadinov R, Qu J, Cookfair D, Duan X, Bang E, Bergsland N, Hussein S, Cherneva M, Willis L, Heininen-Brown M, Ramanathan M. Vitamin D metabolites are associated with clinical and MRI outcomes in multiple sclerosis patients. Journal of Neurology, Neurosurgery & Psychiatry. 2011 Feb;82(2):189-95.

(6) Mowry EM, Krupp LB, Milazzo M, Chabas D, Strober JB, Belman AL, McDonald JC, Oksenberg JR, Bacchetti P, Waubant E. Vitamin D status is associated with relapse rate in pediatric-onset multiple sclerosis. Annals of Neurology. 2010 May; 67(5):618-24.

(7) Goldberg P, Fleming MC, Picard EH. Multiple sclerosis: Decreased relapse rate through dietary supplementation with calcium, magnesium and vitamin D. Medical Hypotheses. Volume 21, Issue 2, October 1986, Pages 193–200.

(8) Kimball SM, Ursell MR, O’Connor P, Vieth R. Safety of vitamin D3 in adults with multiple sclerosis. American Journal of Clinical Nutrition. September 2007. vol. 86 no. 3 645-651.

(9) Soilu-Hänninen M,  Åivo J,  Lindström BM, et al. A randomised, double blind, placebo controlled trial with vitamin D3 as an add on treatment to interferon ß-1b in patients with multiple sclerosis. Journal of Neurology Neurosurgery and Psychiatry. 2012; 83:565-571.

(10) Simon, Kelly C.; Munger, Kassandra L.; Ascherio, Alberto. Vitamin D and multiple sclerosis: epidemiology, immunology, and genetics. Current Opinion in Neurology. June 2012 – Volume 25 – Issue 3 – p 246–251
(11) Aideen C Allen, Siobhan Kelly, Sharee A Basdeo, et al. A pilot study of the immunological effects of high-dose vitamin D in healthy volunteers. Multiple Sclerosis Journal. March 28, 2012.

(12) J.M. Burton, S. Kimball, R. Vieth, et al. A phase I/II dose-escalation trial of vitamin D3 and calcium in multiple sclerosis. Neurology. 2010 June 8; 74(23): 1852–1859.

(13) Martineau AR, Timms PM, Bothamley GH, et al. High-dose vitamin D3 during intensive-phase antimicrobial treatment of pulmonary tuberculosis: a double-blind randomised controlled trial. The Lancet, Volume 377, Issue 9761, Pages 242 – 250, 15 January 2011.

(14) Vitamina D – Por uma outra terapia (Vitamin D – For an alternative therapy). Documentário online em:

(15) Heaney RP, Davies KM, Chen TC, Holick MF, Barger-Lux MJ. Human serum 25-hydroxycholecalciferol response to extended oral dosing with cholecalciferol. American Journal of  Clinical Nutrition. 2003 Jan;77(1):204-10.


Australian and New Zealand Bone and Mineral Society and Osteoporosis Australia release new guidelines

1946_sunglasses_hat_in_sunVitamin D news

Australian and New Zealand Bone and Mineral Society and Osteoporosis Australia release new guidelines

18 February 2013

Sunshine is good, according to new guidelines set by the Australian and New Zealand Bone and Mineral Society and Osteoporosis Australia (ANZBMS).

ANZBMS put together a working group to reevaluate and redraft a position statement on vitamin D, specifically for adolescents and children. They previously released a statement in 2006. Their new guidelines were based on a systematic review of literature stored in the MEDLINE database between 1946 and July 2011.

In their position statement, ANZBMS recognized sunlight as “the most important source of vitamin D,” noting that it can provide up to 90% of vitamin D requirements if sought after adequately. They recommended that adults and pregnant women seek moderate sun exposure and be careful not to burn. They also encouraged general physical outdoor activity.

However, ANZBMS did not recommend moderate sun exposure for children and adolescents, carefully noting that those under 18 should avoid burning and use protective measures to do so, like use of clothing and shade.

For vitamin D levels, they recommended a level of over 20 ng/ml (50 nmol/l). Since levels drop in the wintertime, the working group recommended that levels may need to be at least as high as 24-28 ng/ml (60-70 nmol/l) in the summer to ensure levels over 20 ng/ml in the winter.

Have a child or adolescent with vitamin D deficiency? The ANZBMS also released treatment guidelines. For those aged 1-18 years old, the working group recommended deficiency be treated with 1,000-2,000 IU/day for 3-6 months. For those under 12 months old, they recommended the use of 1,000 IU/day for severe deficiency and 400 IU/day for mild deficiency for three months. They also recommended a “maintenance” dose of 400 IU for all ages under 18, for those that are not deficient.

The new position statement is intended for primary care providers and specialists involved in the care of children and pregnant women.


Paxton GA et al. Vitamin D and health in pregnancy, infants, children and adolescents in Australia and New Zealand; a position statement. Medical Journal of Australia, 2013

Page last edited: 18 February 2013

Vitamin D levels of professional ballet dancers: Winter vs. Summer

“Further studies on the impact of vitamin D3 supplementation on markers of bone metabolism, muscle function and injury profile would help to enhance our understanding of this important area of metabolism in athletes/dancers.”


Vitamin D Council

Vitamin D news

Vitamin D levels of professional ballet dancers: Winter vs. Summer

19 February 2013

Professional ballerinas have a high incidence of vitamin D deficiency, improving slightly during summer months. Dancers also are more likely to get injured during the winter, according to research published in theJournal of Science and Medicine in Sport.

Roger Wolman, MD, of the Royal National Orthopaedic Hospital in Stanmore, UK, and colleagues recruited 18 ballet dancers from a single international touring dance company. The participants were professional Caucasian dancers who dance an average of 6-8 hours per day, 38 hours per week. A lifestyle questionnaire and blood samples were completed in February and August 2010. Company doctors kept track of any injuries that occurred during the study period.

Dr Wolman and colleagues found that during winter season, all dancers were either insufficient, characterized as 10-30 ng/ml, or deficient,< 10 ng/ml. During summer months the authors noted significant improvement, with 3 dancers with vitamin D levels >30 ng/ml, while 14 were insufficient and 2 deficient. The authors also found that serum parathyroid hormone (PTH) significantly decreased during this time. Chronically high PTH is associated with vitamin D deficiency and can lead to problems with the thyroid.

There was a significant decrease in incidence of injury between winter and summer months (p<0.05). Interestingly, the authors noticed that among female dancers, taking an oral contraceptive had a significant beneficial effect on vitamin D status, PTH, and markers of healthy bone. They conclude,

“Further studies on the impact of vitamin D3 supplementation on markers of bone metabolism, muscle function and injury profile would help to enhance our understanding of this important area of metabolism in athletes/dancers.”


Wolman R, Wyon MA, Koutedakis Y, Nevill AM, Eastell R, Allen N. Vitamin D status in professional ballet dancers: Winter vs. summer. Journal of Science and Medicine in Sport. 2013.

Page last edited: 19 February 2013

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