Wednesday, September 26, 2012

Fish Eaters Run Lower Risk of Heart Attack, Despite Some Mercury Content, Study Suggests

Eat fish, but avoid fish with the most pollutants. This is the conclusion drawn by a group of researchers at Umeå University in Sweden after having weighed the risks of mercury content against the advantages of healthful fatty acids.
The work was done as part of an international collaborative effort.

Fish is healthful food, and several studies have shown that people who eat fish have a lower risk of cardiovascular diseases than those who eat very little or no fish. At the same time, some fish contain environmental pollutants that can be hazardous to our health. One such pollutant that is suspected of increasing the risk of cardiovascular disease is methyl mercury, which is found in varying degree in different kinds of fish. If people eat fish with much pollutants, this would lead to increased risk of disease, but at the same time if people are overly cautious and eat too little fish, the risk of disease also increases.

In order to attain a better understanding of what the golden mean might be, researchers at Umeå University, in collaboration with researchers from Finland and elsewhere, examined how the risk of heart attack (acute myocardial infarction) is contingent on the amount of omega-3 fats and mercury from fish that people have in their body. The content was measured in blood and hair samples from people that had previously participated in health studies in northern Sweden and eastern Finland. The Swedish blood samples were from the Medical Biobank in Umeå. Those who experienced a heart attack after the health check-up were compared with those who did not.

The findings are now being published in American Journal of Clinical Nutrition (AJCN). It turned out that mercury was linked to increased risk, and omega-3 fatty acids to decreased risk, of having a heart attack. The increased risk from mercury was noticeable only at high levels of this environmental pollutant in the body and if the level of the protective omega-3 fatty acids was concomitantly low. In other words, what is important is the balance between healthful and hazardous substances in fish. The environmental pollutant in this study was mercury. For organic pollutants like PCB and dioxin, the problem complex is similar, but no study of this kind has yet been undertaken.

The conclusion is simple: Eat fish, but avoid fish with the most pollutants. The Swedish National Food Agency recommends that people should eat fish 2-3 times a week, but their intake of predatory fish (e.g. pike, perch, pike-perch), which contain a great deal of mercury, should be limited (see link below). This study supports that recommendation. According to a recent study from the National Food Agency, 7 of 10 Swedes eat too little fish.



http://www.sciencedaily.com/releases/2012/09/120924080303.htm


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Association Between Diets High In Total Antioxidants And Lower Risk Of Myocardial Infarction In Women

Coronary heart disease is a major cause of death in women. A new study has found that a diet rich in antioxidants, mainly from fruits and vegetables, can significantly reduce the risk of myocardial infarction. The study is published in the October issue of The American Journal of Medicine.

"Our study was the first to look at the effect of all dietary antioxidants in relation to myocardial infarction," says lead investigator Alicja Wolk, DrMedSci, Division of Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institute, Stockholm, Sweden. "Total antioxidant capacity measures in a single value all antioxidants present in diet and the synergistic effects between them."

The study followed 32,561 Swedish women aged 49-83 from September 1997 through December 2007. The women completed a food-frequency questionnaire in which they were asked how often, on average, they consumed each type of food or beverage during the last year. The investigators calculated estimates of total antioxidant capacity from a database that measures the oxygen radical absorption capacity (ORAC) of the most common foods in the United States (no equivalent database of Swedish foods exists). The women were categorized into five groups of total antioxidant capacity of diet.

During the study, 1,114 women suffered a myocardial infarction. Women in the group with the highest total antioxidant capacity had a 20% lower risk, and they consumed almost 7 servings per day of fruit and vegetables, which was nearly 3 times more than the women with the least antioxidant capacity, who on average consumed 2.4 servings.

Dr. Wolk notes that trials testing high doses of antioxidant supplements have failed to see any benefit on coronary heart disease and, in fact, in one study higher all-cause mortality was reported. "In contrast to supplements of single antioxidants, the dietary total antioxidant capacity reflects all present antioxidants, including thousands of compounds, all of them in doses present in our usual diet, and even takes into account their synergistic effects," she explains.

In a commentary accompanying the article, Pamela Powers Hannley, MPH, Managing Editor of The American Journal of Medicine, observes that with the industrialization of our food supply, Americans began to consume more total calories and more calories from processed food high in fat and sugar. As a result, obesity rates began to climb steadily. "Although weight-loss diets abound in the US, the few which emphasize increasing intake of fruits and vegetables actually may be on the right track," she says. "Yet only 14% of American adults and 9.5% of adolescents eat five or more servings of fruits or vegetables a day."

http://www.medicalnewstoday.com/releases/250604.php


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Risk Of Heart Disease Increased By Vitamin D Deficiency

New research from the University of Copenhagen and Copenhagen University Hospital shows that low levels of vitamin D are associated with a markedly higher risk of heart attack and early death. The study involved more than 10,000 Danes and has been published in the well-reputed American journal Arteriosclerosis, Thrombosis and Vascular Biology.

Vitamin D deficiency has traditionally been linked with poor bone health. However, the results from several population studies indicate that a low level of this important vitamin may also be linked to a higher risk of ischemic heart disease, a designation that covers heart attack, coronary arteriosclerosis and angina. Other studies show that vitamin D deficiency may increase blood pressure, and it is well known that high blood pressure increases the risk of heart attack.Low levels of vitamin D are associated with a markedly higher risk of heart attack.

"We have now examined the association between a low level of vitamin D and ischemic heart disease and death in the largest study to date. We observed that low levels of vitamin D compared to optimal levels are linked to 40% higher risk of ischemic heart disease, 64% higher risk of heart attack, 57% higher risk of early death, and to no less than 81% higher risk of death from heart disease," says Dr. Peter Brøndum-Jacobsen, Clinical Biochemical Department, Copenhagen University Hospital.

The scientists have compared the 5% lowest levels of vitamin D (less than 15 nanomol vitamin per litre serum) with the 50% highest levels (more than 50 nanomol vitamin per litre serum). In Denmark, it is currently recommended to have a vitamin D status of at least 50 nanomol vitamin per litre serum.

The higher risks are visible, even after adjustment for several factors that can influence the level of vitamin D and the risk of disease and death. This is one of the methods scientists use to avoid bias.

Blood samples from more than 10,000 Danes

The population study that forms the basis for this scientific investigation is the Copenhagen City Heart Study, where levels of vitamin D were measured in blood samples from 1981-1983. Participants were then followed in the nationwide Danish registries up to the present.

"With this type of population study, we are unable to say anything definitive about a possible causal relationship. But we can ascertain that there is a strong statistical correlation between a low level of vitamin D and high risk of heart disease and early death. The explanation may be that a low level of vitamin D directly leads to heart disease and death. However, it is also possible that vitamin deficiency is a marker for poor health generally," says Børge Nordestgaard, clinical professor at the Faculty of Health and Medical Sciences, University of Copenhagen and senior physician at Copenhagen University Hospital

. Long-term goal is prevention

The scientists are now working to determine whether the connection between a low level of vitamin D and the risk of heart disease is a genuine causal relationship.

If this is the case, it will potentially have a massive influence on the health of the world population. Heart disease is the most common cause of adult death in the world according to the World Health Organization (WHO), which estimates that at least 17 million people die every year from heart disease.

"The cheapest and easiest way to get enough vitamin D is to let the sun shine on your skin at regular intervals. There is plenty of evidence that sunshine is good, but it is also important to avoid getting sunburned, which increases the risk of skin cancer. Diet with a good supply of vitamin D is also good, but it has not been proven that vitamin D as a dietary supplement prevents heart disease and death," says Børge Nordestgaard.
http://www.medicalnewstoday.com/releases/250651.php


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Saturday, September 22, 2012

Manipulating hormone receptors may help in the fight against obesity

In the body's ongoing effort to maintain a healthy weight, an arsenal of cellular proteins called androgen receptors is critical for blocking fat accumulation. Now researchers reporting in the September issue of the Cell Press Journal Chemistry & Biology have discovered that naturally occurring steroids called glucocorticoids can thwart the receptors' activity, ultimately encouraging fat buildup.

"This has implications in this era of an obesity epidemic," says senior author Dr. Michael Mancini, from Baylor College of Medicine. "If you can reduce glucocorticoids, you might be able to upregulate, or increase, androgen receptor activity and regulate fat storage."

The discovery came after Dr. Mancini and his team searched for genes or signals expressed specifically by human fat cells with the hope of gaining a better understanding of fat deposition and the development of obesity. They used a novel approach that combined gene expression studies with automated microscopy and specialized image analyses.

The approach showed that the androgen receptor is both expressed and functional during the early stages of fat cell differentiation. "Activation of the androgen receptor can inhibit the early stages of human fat maturation," says first author Dr. Sean Hartig, also from Baylor College of Medicine. The finding makes sense because androgens such as testosterone, which bind to androgen receptors, are known to favorably direct muscle differentiation, regulate muscle mass, and increase lean body mass as humans age.

The researchers also found that glucocorticoids decrease androgen receptor activity and alter the effects of androgens on fat storage. The result is deposition of fat throughout the body, particularly in the abdominal region. "Using a custom-developed image analysis software platform usually found only in large pharmaceutical screening centers, we applied specific algorithms to sensitively detect the glucocorticoid inhibition of androgen receptor activity," says Dr. Mancini.

The research suggests that treatment strategies that modulate the activity of glucocorticoids and the androgen receptor—perhaps in combination—may help combat obesity.
###

Hartig et al.: "Feed-forward Inhibition of Androgen Receptor Activity by Glucocorticoid Action in Human Adipocytes."

In the body's ongoing effort to maintain a healthy weight, an arsenal of cellular proteins called androgen receptors is critical for blocking fat accumulation. Now researchers reporting in the September issue of the Cell Press Journal Chemistry & Biology have discovered that naturally occurring steroids called glucocorticoids can thwart the receptors' activity, ultimately encouraging fat buildup.
"This has implications in this era of an obesity epidemic," says senior author Dr. Michael Mancini, from Baylor College of Medicine. "If you can reduce glucocorticoids, you might be able to upregulate, or increase, androgen receptor activity and regulate fat storage."
The discovery came after Dr. Mancini and his team searched for genes or signals expressed specifically by human fat cells with the hope of gaining a better understanding of fat deposition and the development of obesity. They used a novel approach that combined gene expression studies with automated microscopy and specialized image analyses.
The approach showed that the androgen receptor is both expressed and functional during the early stages of fat cell differentiation. "Activation of the androgen receptor can inhibit the early stages of human fat maturation," says first author Dr. Sean Hartig, also from Baylor College of Medicine. The finding makes sense because androgens such as testosterone, which bind to androgen receptors, are known to favorably direct muscle differentiation, regulate muscle mass, and increase lean body mass as humans age.
The researchers also found that glucocorticoids decrease androgen receptor activity and alter the effects of androgens on fat storage. The result is deposition of fat throughout the body, particularly in the abdominal region. "Using a custom-developed image analysis software platform usually found only in large pharmaceutical screening centers, we applied specific algorithms to sensitively detect the glucocorticoid inhibition of androgen receptor activity," says Dr. Mancini.
The research suggests that treatment strategies that modulate the activity of glucocorticoids and the androgen receptor—perhaps in combination—may help combat obesity.
###

Hartig et al.: "Feed-forward Inhibition of Androgen Receptor Activity by Glucocorticoid Action in Human Adipocytes."


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Thursday, August 16, 2012

Risk Of Bladder Cancer Increased For Over 15 Million Americans Taking Diabetes Drugs

A popular class of diabetes drugs increases patients' risk of bladder cancer, according to a new study published online this month in the Journal of the National Cancer Institute. Researchers from the Perelman School of Medicine at the University of Pennsylvania found that patients taking thiazolidinedione (TZDs) drugs - which account for up to 20 percent of the drugs prescribed to diabetics in the United States - are two to three times more likely to develop bladder cancer than those who took a sulfonylurea drug, another common class of medications for diabetes.

The authors say the findings are especially important since diabetic patients are known to already be at a slightly increased risk of this type of cancer as compared to the generation population, in which about 30 in 100,000 people develop bladder cancer. Among diabetes patients overall, the incidence of this cancer is typically about 40 out of 100,000.

The authors of the new study analyzed 60,000 Type 2 diabetes patients from the Health Improvement Network (THIN) database in the United Kingdom. They found that patients treated with the TZD drugs pioglitazone (Actos) or rosiglitzaone (Avandia) for five or more years had a two-to-three-fold increase in risk of developing bladder cancer when compared to those who took sulfonylurea drugs. Among patients taking TZDs for that length of time, the team's analysis indicates that 170 patients per 100,000 would be expected to develop the disease. About 60 in 100,000 of those who take sulfonylurea drugs - such as glipizide (Glucotrol) - would be expected to develop bladder cancer.

"Diabetes is one the most common chronic diseases worldwide, affecting 285 million people. There are many factors clinicians must weigh in deciding which drug to use to control a patient's diabetes, and these new data provide important information to include in that decision-making process," said the study's lead author, Ronac Mamtani, MD, an instructor in the division of Hematology-Oncology in Penn's Abramson Cancer Center. "Our study shows that doctors who care for patients with diabetes should be very aware of any bladder-related symptoms patients might be having, like blood in the urine, and take steps to further evaluate those issues."

Though most patients in the United States no longer take Avandia since it was linked to severe cardiovascular problems, Actos is the ninth most commonly prescribed drug in the nation, accounting for some 15 million prescriptions each year. The drug is a common choice when Type 2 diabetes patients' illnesses can no longer be controlled with the first-line diabetes drug Metformin.

Based on previous data examining safety risks among patients taking Actos, the FDA has already warned that it may be associated with a risk of bladder cancer, and France and Germany have removed the drug from their markets. The new findings add to mounting evidence against the entire class of TZDs, as one of the first studies examining this type of risk among people taking both types of TZDs and among those taking sulfonylurea drugs.

"The risk does seem to be common among both drugs in the TZD class, and the fact that we have compared bladder cancer risk among patients taking each of those drugs provides essential information, because a safety warning on a drug is only useful to a doctor when they have knowledge of the same risks for an alternative drug," Mamtani says. "We believe our study will help doctors and their patients weigh the potential benefits and risks when selecting between different diabetes medication."
http://www.medicalnewstoday.com/releases/248984.php


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Wednesday, August 15, 2012

Weight Training May Lower Your Diabetes Risk

Men who do weight training or resistance training on a regular basis may be able to lower their risk of developing type 2 diabetes, according to a new study published online this week.

Weight training is a form of resistance training, where the aim is to develop strength in the skeletal muscles by resisting force through the use of free weights, for example dumbbells and barbells.

Writing in the 6 August online-first issue of the Archives of Internal Medicine, researchers from the Harvard School of Public Health (HSPH) and the University of Southern Denmark, describe how they found men who practise weight training about 30 minutes a day on 5 days a week may be able to lower their risk for type 2 diabetes by up to 34%.

And they show how men may be able to lower their risk further, by 59%, if they combine weight training with aerobic exercise like brisk walking or running.

The researchers wanted to do the study because while we already know there is a strong link between aerobic exercise and reduced risk for type 2 diabetes, the link with weight training on its own was not so clear.

Evidence from recent trials has shown that resistance training can improve glycemic control in patients with type 2 diabetes, even without aerobic training, and in fact this has led to the recommendation that people with type 2 diabetes incorporate resistance training into their exercise schedule three times a week.


Man exercising with dumbbells at gym
A combination of weight training and aerobic exercise together appears to show the greatest reduction in type 2 diabetes risk.
But this is the first study to show that weight training on its own may prevent type 2 diabetes.

This could be an important finding, as lead author Anders Grøntved, a visiting researcher in the Department of Nutrition at HSPH and a doctoral student in exercise epidemiology at the University of Southern Denmark, told the press, because "many people have difficulty engaging in or adhering to aerobic exercise".

Senior author Frank Hu, professor of nutrition and epidemiology at HSPH, said:

"This study provides clear evidence that weight training has beneficial effects on diabetes risk over and above aerobic exercise."

He said the effects are probably due to increased muscle mass and improved insulin sensitivity.

"To achieve the best results for diabetes prevention, resistance training can be incorporated with aerobic exercise," he added.

For the study, Grøntved and colleagues used data on 32,002 men who took part in the Health Professionals Follow-up Study from 1990 to 2008.

The data included questionnaires that the men had filled in every two years and answered questions about how much time they spent every week doing weight training and aerobic exercise.

Over the study period, 2,278 of the men were newly diagnosed with type 2 diabetes.

After adjusting for possible influencing factors, such as other types of physical activity, watching TV, coffee, alcohol, smoking, family history of diabetes and ethnicity, plus a number of dietary factors, the researchers found a "dose-response" relationship between weight training and reduced risk of type 2 diabetes, in that even a modest amount of weight training appeared to help lower the risk of type 2 diabetes a bit.

Compared with men who did no weight training, the ones who did up to 59 minutes a week had a 12% reduced risk for type 2 diabetes.

And doing between 60 and 149 minutes of weight training a week reduced the risk of type 2 diabetes by 25%, and doing at least 150 minutes a week reduced it by 34%.

When they looked at aerobic exercise, the researchers found, as expected, a similar dose-response relationship.

Up to 59 minutes a week of aerobic exercise reduced the risk for type 2 diabetes by 7%, compared to not doing it at all.

And doing 60 to 149 minutes of aerobic exercise reduced the risk of type 2 diabetes by 31%, while doing at least 150 minutes a week reduced it by 52%.

Grøntved and colleagues also found that weight training and aerobic exercise together had the greatest effect: men who did more than 150 minutes of aerobic exercise, and also at least 150 minutes of weight training every week had a 59% reduced risk of type 2 diabetes.

Grøntved said there now need to be more studies to confirm these findings, and also to find out if the same is true for women.

Type 2 diabetes is a major health problem throughout the world and it is rising.

The World Health Organization estimates that 346 million people have the disease, and deaths related to it are expected to double between 2005 and 2030, with more than 80% of them occuring in low and middle income countries.

Some of the researchers on the study were supported by grants from the National Institutes of Health in the US.

Written by Catharine Paddock PhD
Copyright: Medical News Today
http://www.medicalnewstoday.com/articles/248853.php


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Butter Flavoring Ingredient in Microwave Popcorn, Thought Safe for Food Industry Workers, Is a Respiratory Hazard

ScienceDaily (Aug. 13, 2012) — The ingredient 2,3-pentanedione (PD), used to impart the flavor and aroma of butter in microwave popcorn, is a respiratory hazard that can also alter gene expression in the brain of rats. Manufacturers started using PD when another butter flavoring, diacetyl, was found to cause bronchiolitis obliterans, a life-threatening and nonreversible lung disease in workers who inhaled the substance. New research on PD with implications for "popcorn workers' lung" is published in The American Journal of Pathology and indicates that acute PD exposure has respiratory toxicity which is comparable to diacetyl in laboratory animals.
"Our study demonstrates that PD, like diacetyl, damages airway epithelium in laboratory studies. This finding is important because the damage is believed to be the underlying cause of bronchiolitis obliterans," says lead investigator Ann F. Hubbs, DVM, PhD, DACVP, Health Effects Laboratory Division of the National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, WV. "Our study also supports established recommendations that flavorings should be substituted only when there is evidence that the substitute is less toxic than the agent it replaces."

The study included groups of rats exposed for six hours to different concentrations of PD, a comparable concentration of diacetyl, or filtered air. Since the investigators observed signs of delayed toxicity, they exposed additional rats to PD, and further microscopically examined the brains, lungs, and nasal tissues from these rats 0-2 hours, 12-14 hours, and 18-20 hours after exposure. investigators then evaluated changes in gene expression in discrete brain regions.

The investigators found respiratory epithelial injury in the upper nose, comparable to that caused by diacetyl that progressed through 12 to 14 hours post-exposure. They also found that PD exposure caused necrosis and apoptosis in the olfactory neuroepithelium and activation of caspase 3, a protein that plays a role in cell death, in axons of olfactory nerve bundles. Signs consistent with neurotoxicity included increased expression of the inflammatory mediators, interleukin-6 and nitric oxide synthase-2, as well as decreased expression of vascular endothelial growth factor A in the olfactory bulb, striatum, hippocampus, and cerebellum.

"Our study is a reminder that a chemical with a long history of being eaten without any evidence of toxicity can still be an agent with respiratory toxicity when appropriate studies are conducted," says Dr. Hubbs. "It suggests several intriguing potential mechanisms for the toxicity of inhaled volatile α-diketones, reveals mRNA changes in the brain, documents olfactory neurotoxicity, and clearly demonstrates that the remarkable airway toxicity of diacetyl is shared with its close structural relative, PD."

http://www.sciencedaily.com/releases/2012/08/120813115450.htm


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