Kinder and his colleagues assessed the prevalence of vitamin D deficiency in a cohort of patients with interstitial lung disease, who are often treated with corticosteroids. The detrimental effect of chronic use of corticosteroids on bone health has been well established, according to the researchers. Of the patients included in the study, 51 had interstitial lung disease and 67 had other forms of interstitial lung disease related to autoimmune connective tissue diseases.
A vitamin D insufficiency was defined as a serum level of less than 30 ng/mL. A level of less than 20 ng/mL was considered deficient. Both insufficient and deficient levels were prevalent in the study. In the overall sample, lower vitamin D levels were associated with reduced forced vital capacity (P=0.01). When the analysis was restricted to patients with connective tissue disease, both forced vital capacity and diffusing capacity of lung for carbon monoxide — a measure of the lung’s ability to transfer gases from the air to the blood — were significantly reduced (P<0.05 for both). After adjustment for several potential confounders — including age, corticosteroid use, race, and season, the presence of connective lung disease was a strong predictor of vitamin D insufficiency (OR 11.8, 95% CI 3.5 to 40.6).
According to the researchers, a pathogenic role of low vitamin D in the development of autoimmune diseases such as interstitial lung disease is plausible because of the immunoregulatory role of the biologically active form of vitamin D, 1,25-(OH)2D. “All cells of the adaptive immune system express vitamin D receptors and are sensitive to the action of 1,25-(OH)2D,” they wrote. “High levels of 1,25-(OH)2D are potent inhibitors of dendritic cell maturation with lower expression of major histocompatibility complex class II molecules, down-regulation of costimulatory molecules, and lower production of proinflammatory cytokines.” “A common theme in the immunomodulatory functions of vitamin D is that higher levels are immunosuppressive,” they continued, “which is consistent with a potential role for hypovitaminosis D in the pathogenesis of autoimmune disorders.”
In a statement, Len Horovitz, MD, a pulmonary specialist at Lenox Hill Hospital in New York City, commented that “vitamin D is known to promote wound healing, and to benefit the immune system. So it is not surprising to find that patients with immune lung disorders are vitamin D deficient.” He said that all of his patients are screened and treated for vitamin D deficiency with supplements. The study authors noted that further research is needed to determine whether supplementation is associated with improved outcomes. The study was limited, Kinder and his colleagues wrote, by its use of patients from a single center in Cincinnati.
In addition, the cross-sectional design of the study did not evaluate whether vitamin D supplementation is associated with any improved clinical outcomes. To examine that issue, the team called for prospective controlled interventional studies to determine whether vitamin D7 supplements can ameliorate symptoms and improve outcomes in connective tissue disease-related interstitial lung disease.
Source reference: Hagaman J, et al “Vitamin D deficiency and reduced lung function in connective tissue-associated interstitial lung diseases” Chest 2011; DOI: 10.1378/chest.10-0968.
People who weigh more have lower circulating levels of Vitamin D according to recent research conducted at the Rikshospitalet-Radiumhospitalet Medical Center in Oslo, Norway and published in the Journal of Nutrition. Lead researcher, Zoya Lagunova, MD and her colleagues measured the serum levels of Vitamin D and 1,25(OH)2D in 1,779 patients at a Medical and Metabolic Lifestyle Management Clinic in Oslo, Norway. The associations among 1,25(OH)(2)D, serum 25-hydroxyvitamin D [25(OH)D], and body composition were analyzed. Lagunova noted that generally people with higher BMI had lower levels of Vitamin D. Age, season, and gender were also found to influence serum 1,25(OH)(2)D.
Vitamin D is not a true vitamin, but rather a vitamin-steroid thought to play a key role in the prevention of cancer, cardiovascular disease, diabetes, multiple sclerosis and other diseases. It is likely not coincidental that obesity is also a risk factor for many of these diseases. Vitamin D is vital to the regulation of calcium. Studies have shown that calcium deficiency increases the production of synthase, an enzyme that converts calories into fat. It has been shown that calcium deficiency can increase synthase production by up to 500 percent. Vitamin D has also been shown to play a role in the regulation of blood sugar levels; proper blood sugar regulation is vital to the maintenance of a healthy weight. Vitamin D is produced from sunlight and converted into various metabolites. It is stored in fat tissue. According to Lagunova, obese people may take in as much Vitamin D as other people; however, because it is stored in fat it may be less available. This may result in lower circulating levels of Vitamin D.
A previous study conducted by Shalamar Sibley, MD, MPH, an assistant professor of medicine at the University of Minnesota, showed that subjects who have higher levels of Vitamin D at the start of a weight loss diet lose more weight than those with lower levels. The study measured Vitamin D levels of 38 overweight men and women both before and after following an 11-week calorie-restricted diet. Vitamin D levels at the start of diet was an accurate predictor of weight loss…those with higher levels of Vitamin D lost more weight. It was found that for every nanogram increase in Vitamin D precursor, there was an 1/2 pound increase in weight loss.
Seventy-five percent or more of Americans, teenage and older, are Vitamin D deficient according to a recent study published in the Archives of Internal Medicine. According to the Gallup-Healthways Well-Being Index, 26.5% of American are obese. More research needs to be conducted into the exact role Vitamin D plays in obesity and weight loss and the possibility of increased Vitamin D consumption (through the form of supplementation and/or increased sun exposure) being a key factor to achieving a healthy weight.
The most common type of breast cancer in older women — estrogen and progesterone receptor (ER/PR) positive breast cancer — has been linked to a protein that fends off aging-related cellular damage. A new study led by Vanderbilt-Ingram Cancer Center researcher David Gius, M.D., Ph.D., now shows how a deficiency in this aging-associated protein may set the stage for these tumors to develop.
The findings, published in Molecular Cell, provide information that could assist in the screening, prevention and treatment of these common age-related cancers. While the young are certainly not spared cancer’s wrath, cancer is primarily a disease of aging, with the majority of cases occurring in people over 50. However, the biological processes that underlie this association are not clear.
“The connection between aging and cancer is one of the most established phenomena in cancer research,” said Gius, associate professor of Cancer Biology, Pediatrics and Radiation Oncology. “The problem to address this clinically significant question is that this field lacks in vivo models to study this.”
In the late-1990s, proteins called “sirtuins” were linked to extended lifespan observed in several species maintained on a calorically restricted diet. These nutrient-sensing sirtuin proteins seemed to defend against aging-related cellular damage. Sirtuins are present in all living organisms, with humans having seven different sirtuin proteins. “When (the sirtuins) were discovered, it seemed obvious to conclude that there might be a mechanistic connection between the genes that determine length of survival and cancer,” Gius said. Previously, while at the National Cancer Institute, Gius and colleagues created mice lacking some of these sirtuins.
They reported last January in Cancer Cell that when they knocked out Sirt3 — a sirtuin localized in the mitochondria, the cellular “power plants” — the mice developed ER/PR positive breast tumors, the most common type of breast cancer in postmenopausal women. These tumors also exhibited increased levels of damaging free radicals and “reactive oxygen species” (ROS) — including superoxide, the primary metabolite of oxygen in the mitochondria — which provided an important clue as to how Sirt3 deficiency might permit these tumors to develop. “The mechanism, at least in part, for why these mice develop receptor positive breast cancer is altered mitochondrial ROS, including superoxide,” Gius said. But how deficiency in a longevity gene led to increased ROS was not clear. Since superoxide is generally removed from the cell with the help of a detoxifying enzyme called manganese superoxide dismutase (MnSOD), Gius hypothesized that the Sirt3 deficiency may abnormally regulate MnSOD.
In the current study, the researchers show that Sirt3 knockout mice have decreased MnSOD activity despite having normal levels of the protein. Gius and colleagues determined that the MnSOD in Sirt3 knockout mice was abnormally modified (with a chemical “acetyl” group) at a specific amino acid (lysine 122). This aberrant modification of MnSOD reduced the enzyme’s ability to detoxify superoxide and appeared to explain the increase in ROS in Sirt3 knockout mouse tumors. “These results suggest that aberrant regulation of MnSOD plays a role in receptor positive breast cancer,” said Gius.
Gius and colleagues also developed an antibody that can assess the acetylation status of MnSOD, which he says can potentially be used “to screen breast tissue samples to determine what women are at risk for (receptor positive) cancer or for recurrence because of this dysregulation of MnSOD.” Additionally, agents that target the acetylation of this amino acid on MnSOD may be useful as chemopreventive therapies in women at risk of these cancers and of recurrence, he noted. The research was supported by grants from the National Cancer Institute and the Department of Defense.
There are many situations where referral may be indicated including:
a new diagnosis requiring specific dietary modification (eg. diabetes, food allergy, abnormal blood lipids)
poor understanding of dietary management (eg. a patient who has had diabetes for years but has poor blood glucose control)
significant unintentional weight change (either weight loss or gain)
evidence of recent poor food intake, poor appetite or difficulty preparing or eating food (eg. poor dentition or social isolation)
deterioration of symptoms or change in care needs (especially for cancer or HIV patients or the elderly)
any nutritional deficiencies (eg. anaemia or iodine deficiency)
changes in medication prescribed that may affect dietary intake
alternative methods of feeding (eg. enteral)
texture modified food (dysphagic patients)
periodic review for chronic conditions.
When referring, it is useful to include relevant medical history, recent biochemical and metabolic test results, and details of any medications currently prescribed.