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.
Curcumin, a natural phytochemical from turmeric that is used as a spice in curry, holds promise in treating or preventing liver damage from an advanced form of a condition known as fatty liver disease, new Saint Louis University research suggests. Curcumin is contained in turmeric, a plant used by the Chinese to make traditional medicines for thousands of years. SLU's recent study highlights its potential in countering an increasingly common kind of fatty liver disease called non-alcoholic steatohepatitis (NASH). Linked to obesity and weight gain, NASH affects 3 to 4 percent of U.S. adults and can lead to a type of liver damage called liver fibrosis and possibly cirrhosis, liver cancer and death.
“My laboratory studies the molecular mechanism of liver fibrosis and is searching for natural ways to prevent and treat this liver damage,” said Anping Chen, Ph.D., corresponding author and director of research in the pathology department of Saint Louis University. The findings were published in the September 2010 issue of Endocrinology. “While research in an animal model and human clinical trials are needed, our study suggests that curcumin may be an effective therapy to treat and prevent liver fibrosis, which is associated with non-alcoholic steatohepatitis (NASH).”
High levels of blood leptin, glucose and insulin are commonly found in human patients with obesity and type 2 diabetes, which might contribute to NASH-associated liver fibrosis. Chen's most recent work tested the effect of curcumin on the role of high levels of leptin in causing liver fibrosis in vitro, or in a controlled lab setting. “Leptin plays a critical role in the development of liver fibrosis,” he said.
High levels of leptin activate hepatic stellate cells, which are the cells that cause overproduction of the collagen protein, a major feature of liver fibrosis. The researchers found that among other activities, curcumin eliminated the effects of leptin on activating hepatic stellate cells, which short-circuited the development of liver damage (Courtesy of EurekAlert!, a service of AAAS).
Reference: Youcai Tang, Anping Chen. Curcumin Protects Hepatic Stellate Cells against Leptin-Induced Activation in Vitro by Accumulating Intracellular Lipids. Endocrinology Vol. 151, No. 9 4168-4177 begin_of_the_skype_highlighting 9 4168-4177 end_of_the_skype_highlighting. doi:10.1210/en.2010-0191
Metabolic syndrome is a cluster of risk factors which can result in heart disease and diabetes. Researchers have now found that poor diet and lack of exercise that lead to an imbalance in metabolism may also increase a child's risk of developing asthma.
Dr. Giovanni Piedimonte and researchers from West Virginia University School of Medicine analyzed data from nearly 18,000 children aged 4 to 12 years who were taking part in the Coronary Artery Risk Detection in Appalachian Communities (CARDIAC) project. Factors considered included triglyceride levels and evidence of acanthosis nigricans, which are raised patches of brown skin that are often biomarkers for insulin resistance.
The team also considered body mass index or BMI, and almost 21% of the children were considered obese. Fourteen percent of the children had asthma.
The researchers found that asthma prevalence among the children was strongly associated with certain symptoms of metabolic syndrome including dyslipidemia and abnormal glucose metabolism, but not weight status. Although those who were obese were more likely to have asthma, even children of a healthy weight who had imbalanced metabolism were at increased risk.
Certain metabolic factors participate in the asthma disease process by contributing to inflammation of the airways in the lungs and hyperreactivity (contraction of smooth muscle in the bronchial walls), says Dr. Piedimonte. He says that strict monitoring and control of triglyceride and glucose levels early in life may play a role in the management of chronic asthma in children.
Dr. Piedimonte would like to see the findings used as further support for universal lipid screening in children. “The rationale is that by using selective screening, we would have missed over a third of children with significant genetic dyslipidemia,” he said.
Both poor diet – one lacking in antioxidants but high in fat – and inadequate exercise play a role in the metabolic syndrome, a group of risk factors that increase the risk for coronary artery disease, stroke, and type 2 diabetes. The goal of treatment is often weight loss (if overweight), a minimum of 30 minutes of daily moderate intensity exercise, and a lowering of cholesterol, blood pressure and blood sugar through diet or medication.
Cottrell L, et al “Metabolic abnormalities in children with asthma” Am J Respir Crit Care Med 2010; DOI: 10.1164/rccm.201004-0603OC.
Working in the laboratory, the scientists isolated fragments of DNA in cells to study the effects of exposure to calcitriol, the “active” form of vitamin D. Their findings are published in the journal Genome Research.
Vitamin D influences DNA through a “go-between” protein called the vitamin D receptor (VDR). The protein is activated by the vitamin and attaches itself to DNA at the binding sites the researchers identified. VDR binding was enriched in disease-associated regions of the genetic code and also areas linked to traits such as tanning, height and hair colour.
Study leader Dr Sreeram Ramagopalan, from the Wellcome Trust Centre for Human Genetics, at Oxford University, said: “There is now evidence supporting a role for vitamin D in susceptibility to a host of diseases. Vitamin D supplements during pregnancy and the early years could have a beneficial effect on a child's health in later life. “Some countries, such as France, have instituted this as a routine public health measure.”
Vitamin D is chiefly made in the body as a result of the skin's exposure to sunlight. A small number of foods also contain the vitamin, including oily fish and eggs, but 90% comes from being in the sun. In many northern countries, a lack of sun can lead to vitamin D deficiency. Over-zealous use of sunscreen can also prevent vitamin D production. It is estimated that more than half the UK population do not get enough vitamin D, and worldwide a billion people may be deficient in the vitamin. Lack of vitamin D affects bone growth and development, leading to rickets in children and bone fractures in adults.
The study supports the theory that lighter, more sun-sensitive skins evolved as people migrated north out of Africa to maximise vitamin D production in the body. A significant number of the VDR binding sites were in DNA regions where genetic changes are commonly found in people of European and Asian descent.
“Vitamin D status is potentially one of the most powerful selective pressures on the genome in relatively recent times,” said co-author Professor George Ebers, also from the Wellcome Trust Centre for Human Genetics. “Our study appears to support this interpretation and it may be we have not had enough time to make all the adaptations we have needed to cope with our northern circumstances.”
Researchers employed imaging techniques to examine and analyze brain anatomical differences between 55 female IBS patients and 48 female control subjects. Patients had moderate IBS severity, with disease duration from one to 34 years (average 11 years). The average age of the participants was 31.
Investigators found both increases and decreases of brain grey matter in specific cortical brain regions.
Even after accounting for additional factors such as anxiety and depression, researchers still discovered differences between IBS patients and control subjects in areas of the brain involved in cognitive and evaluative functions, including the prefrontal and posterior parietal cortices, and in the posterior insula, which represents the primary viscerosensory cortex receiving sensory information from the gastrointestinal tract.
“The grey-matter changes in the posterior insula are particularly interesting since they may play a role in central pain amplification for IBS patients,” said study author David A. Seminowicz, Ph.D., of the Alan Edwards Centre for Research on Pain at McGill University. “This particular finding may point to a specific brain difference or abnormality that plays a role in heightening pain signals that reach the brain from the gut.”
Decreases in grey matter in IBS patients occurred in several regions involved in attentional brain processes, which decide what the body should pay attention to. The thalamus and midbrain also showed reductions, including a region – the periaqueductal grey – that plays a major role in suppressing pain.
“Reductions of grey matter in these key areas may demonstrate an inability of the brain to effectively inhibit pain responses,” Seminowicz said.
The observed decreases in brain grey matter were consistent across IBS patient sub-groups, such as those experiencing more diarrhea-like symptoms than constipation.
“We noticed that the structural brain changes varied between patients who characterized their symptoms primarily as pain, rather than non-painful discomfort,” said Mayer, director of the UCLA Center for Neurobiology of Stress. “In contrast, the length of time a patient has had IBS was not related to these structural brain changes.”
Mayer added that the next steps in the research will include exploring whether genes can be identified that are related to these structural brain changes. In addition, there is a need to increase the study sample size to address male-female differences and to determine if these brain changes are a cause or consequence of having IBS.
The study was funded by the National Institutes of Health.
Additional authors include M. Catherine Bushnell, Ph.D., of McGill University, and Jennifer B. Labus, Joshua A. Bueller, Kirsten Tillisch and Bruce D. Naliboff, Ph.D., all of UCLA.
People with celiac disease may develop osteoporosis due to immune-system attacks on bone tissue (N Engl J Med. 2009; 361:1459-1465). Although osteoporosis is a known complication of celiac disease, scientists have always believed that it occurred because celiac patients cannot properly absorb calcium and vitamin D from their diet and were therefore unable to maintain healthy bone tissue.
At the heart of this development is the protein osteoprotegerin, which plays a crucial role in maintaining bone health by controlling the rate at which bone tissue is removed. Researchers from the United Kingdom's University of Edinburgh and University of Liverpool detected autoantibodies against osteoprotegerin in several patients with celiac disease.
“Such autoantibodies may be associated with the development of high-turnover osteoporosis, but whether autoantibodies against osteoprotegerin commonly contribute to the pathogenesis of osteoporosis in patients with celiac disease remains to be determined,” the investigators conclude.
The team looked at how NK cells (natural killer cells – a type of immune cell) reacted to Helicobacter pylori. These cells are an important part of the immune system as they can both recognise and kill cells that are infected by viruses and bacteria as well as tumour cells.
“We found that a special type of NK cells was active against the stomach ulcer bacterium,” says Åsa Lindgren. “These NK cells produced cytokines, which are the immune system's signal substances and act as a defence against the intruder.”
The researchers' results suggest that NK cells can play an important role in the immune defence against Helicobacter pylori. Previous research has also shown that a high proportion of NK cells in tumour tissue has contributed to a better prognosis and longer survival for patients with stomach cancer, as these cells help to eliminate the tumour cells.
The researchers therefore believe that activation of the NK cells can play a key role in stopping tumours from developing, and that reduced NK-cell activity can increase the risk of cancer developing. Åsa Lindgren hopes that these findings can be used to develop new ways of diagnosing and treating stomach cancer.
“This would make it possible to diagnose stomach cancer at an early stage, which, in turn, could mean a better prognosis for the patients.”
Thirty years ago Maria de Sousa, then at the beginning of her career, noticed that lymphocytes were attracted to places with surplus of iron. This, together with
1- the fact that the vertebrate immune system (IS) was incredibly more complex that those of its ancestors (and evolution rarely increases complexity, which is energetically costly, unless something is gained)
2- the IS unique capacity to reach everywhere in the body
led her to a revolutionary new idea – could this new complexity be evolutionary sound, because it allowed the IS to perform some important new function, maybe protecting the body against iron toxicity?
In fact iron, although an essential element for most life forms, can also be toxic to these same organisms when free (not attached to proteins). This means that in this form it needs to be “watched” and regulated around the clock. In vertebrates, this is done through hepcidin, a liver protein that “moves” iron between cells and plasma according to the body needs (or potential dangers). The problem is that the hepcidin liver cells have limited mobility so a complementary far reaching iron control system was needed. Lymphocytes, with their unique capacity to move throughout the body were the perfect candidates and since 1978, de Sousa and her group have been chasing this idea.
Much of their work has been done on hemochromatosis – a disease where there are problems in the absorption of iron through the digestive track leading to too much iron in the organism and to its toxic accumulation in the organs.
From this work we know now that hemochromatosis patients also have a defective IS, and more, that their iron overload levels correlate with their lymphocyte deficiency – the less lymphocytes they have the more severe the disease. Work in animal models with iron overload problems or instead, with lymphocyte deficiencies have again found links between excess of iron in the body and deficient IS further supporting de Sousa's “immuno-iron idea”.
And meanwhile, human lymphocytes were shown to produce several proteins crucial for the regulation of iron levels – ferritin, which acts as the body storage of iron (so holding to it when there is too much in the body or releasing it when there is deficiency) and ferroportin, which is the cells' iron “exit door” (again releasing or retaining iron as necessary) . The fact that lymphocytes had both proteins gave them the potential to be a “mobile” and easily “mobilizable” iron-storage compartment, characteristics perfect for an important role in iron homeostasis.
Nevertheless, the exact mechanism how this could happen remained elusive
But hepcidin, the central piece of iron regulation, is known to be also an important player in the immune response what has raised the possibility that it could be in it the clue to this problem. In fact, during infection hepcidin shuts down the “door” through which iron leaves the cell (ferroportin) reducing iron availability in the plasma and thus helping to control infection – as bacteria need iron to divide. And now several studies have shown that hepcidin is produced by a variety of cells involved in the immune response. Finally, last year, a study suggested, for the first time, that lymphocytes were also capable of producing the protein putting the possibility that hepcidin could actually be “the missing link” of de Sousa's theory.
To clarify this hypothesis Jorge Pinto, Maria de Sousa and colleagues at the Institute for Molecular and Cell Biology (IBMC) of Porto University looked at hepcidin production in human lymphocytes in situations of toxic iron concentrations or immune activation, as de Sousa's theory proposed that lymphocytes could play a role in both situations. They found that hepcidin not only was produced by all classes of lymphocytes, but also that its production increased both in the presence of high quantities of iron, and when lymphocytes were activated, backing de Sousa's proposals.
Pinto explains: “We show, for the first time, that lymphocytes can “feel” the toxic levels of iron in circulation and respond by increasing their own capacity to retain it within, restoring “normality”. The same mechanism is seen being used in situations of (iron) demand, such as when the cells are activated by the occurrence of an infection and need to divide.”
They also found something else totally unexpected – that hepcidin was involved in this second mechanism, suggesting an even closer dependence between the two systems than de Sousa had thought.
To Hal Drakesmith, a researcher at the University of Oxford working on the possibility of manipulating iron transport as a way to combat infections such as HIV, malaria and Hepatitis C these results raise particularly interesting questions as he explains “This seems to suggest that control of iron metabolism may be an integral component of lymphocyte immunity. Withholding iron from pathogens is an accepted part of our defence against infection, but a role for lymphocytes in controlling iron transport has not been proposed before.
“Crucially – says Pinto – we still believe that the main regulator of systemic iron levels is the liver but not only are lymphocytes (and not liver cells) able to sense toxic forms of iron, but they are also able to travel and be activated in specific places where the pathogens accumulate helping to control infection. “
These results are a major step to understand the link between the IS and iron and, if confirmed in live organisms –all this work was done on human cells in the laboratory – can be the beginning of a totally different view of what the immune system is and how to approach immunologic problems.
As Hal Drakesmith says “the paper describes several new findings which are highly likely to be of interest and importance to the iron and immunity fields of research” A simple example is the anaemia that usually accompanies chronic inflammatory diseases and that so far can not be clearly explained. Pinto and Sousa's results suggest that lymphocyte chronic activation, so characteristic of these diseases, by leading to hepcidin production could be part of the phenomenon as iron is an integral part of red blood cells.
Pinto, de Sousa and colleagues now plan to go back to those diseases of iron overload associated to immune abnormalities and see if hepcidin proves to be, in fact, the connection between them. Other possibility is the construction of mice without the hepcidin gene in the bone marrow – where lymphocytes develop – to analyse the changes that this could bring to both iron homeostasis and the immune response.
Whatever happens this is a strikingly interesting story with decades of persistence and believe behind it and which, I am sure, still has much to tell us.
By Catarina Amorim
To this end, the following emotional variables have been specified: those relative to emotional experience —the frequency of positive and negative emotions, anxiety, low self-esteem and the influence of diet, weight and the body shape on the emotional state—; negative perception of emotions, negative attitude to emotional expression, alexithymia —the inability to identify own emotions and to express them verbally— and the manner of controlling negative emotions.
Moreover, another variable has also been taken into account: the need for control. This variable is not strictly emotional, but has a clear emotional component, given that people with a high need for control, experience anxiety and unwellness when perceiving lack of control.
Study of women
In order to undertake the study, 433 women took part; 143 of these suffered from some kind of eating disorder and 145 in risk of contracting one. The results of the study show that, in general, the majority of the variables put forward can be used as predictive of suffering an eating disorder. The variables which, above all, alert to greater risk of developing an eating disorder are when the emotional state of the person is excessively influenced by diet, weight and body shape, when self-esteem is low, and when, in anxiety situations, emotions are not expressed and the person tends to act in an impulsive manner.
These results have important implications, above all when drawing up prevention programmes for eating disorders. With the data obtained, it can be said that many of the emotional variables dealt with in Ms Pascual's work should be taken into account when drawing up these prevention programmes.
Eating disorders are very serious illnesses that have dire consequences for the sufferer, both physically as well as psychologically and socially, and there are disorders that are evermore widespread. Much research has been undertaken in order to find out the factors involved in their development, but the role played by the various emotional variables at the onset of these disorders has hardly been investigated. This thesis presented at the UPV/EHU focused on this matter more deeply.
Lonely fruit and vegetables seems to be a national phenomenon. According to the USDA, fewer than 15 percent of elementary students eat the recommended 5 or more servings of fruits and vegetables every day. Furthermore, average fruit and vegetable intake among 6-11 year olds is only 3.5 servings a day.
Does low fruit and vegetable intake really matter when children are young? Chronic illness such as heart disease, stroke, and cancer are usually concerns for adults. However, life-long positive eating habits (such as eating low fat foods, consuming foods with high fiber, eating less processed foods) are habit-forming when started young. Furthermore, certain diseases such as diabetes and high cholesterol are starting to appear in children who are overweight. Finally, fruits and vegetables have so many naturally occurring vitamins, minerals, phytochemicals, and fiber that are good for your health.
Are our busy lifestyles to blame? Certainly, if you have kids you are getting in the car to go somewhere (to a restaurant, to soccer practice, etc.). Packaged food such as chips or power bars are very convenient and there is something about opening up a package that seems so easy compared to slicing up that lonely piece of fruit. It really is just a mindset though. Once you start packing up the fruits and veggies in Tupperware containers you will get in the habit. Plus, fruits and veggies are low in calories and fill you up.
We are constantly bombarded with food advertisements and not necessarily for healthy food such as fruits and vegetables. In fact, children 2 to 11 years old are exposed to an average of 150 to 200 hours of commercial messages, or 20,000 commercials a year and the majority of these advertisement are for cereals, candies, or other sweets.
So, what is a parent to do? Role modeling is my motto. If you are eating your fruits and vegetables, your children will too. In 2002, researchers at Pennsylvania State University examined parental pressure (“finish your vegetables” or “do as I say”) vs. role modeling (“do as I do”) among 191 five year old girls. The results showed that a daughter's fruit and vegetable intake was positively related to their parent's reported fruit and vegetable intake.
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