Higher intakes of the B vitamins thiamine and riboflavin from the diet may reduce the incidence of premenstrual syndrome (PMS) by about 35 percent, suggest new findings. According to a new paper published in the American Journal of Clinical Nutrition, the link between B vitamins and PMS is biologically plausible since B vitamins such as thiamine and riboflavin are known to play important roles in the synthesis of various neurotransmitters involved in PMS.
While most women experience mild emotional or physical premenstrual symptoms, as many as 8-20 per cent of women experience symptoms severe enough to meet the definition of premenstrual syndrome, which can substantially interfere with daily activities and relationships. The new study, performed by researchers from the University of Massachusetts, Harvard, and the University of Iowa, indicates that increase intakes of certain B vitamins from food sources may help reduce the incidence of PMS.
Using data from 1,057 women with PMS and 1,968 women without PMS participating in the Nurses' Health Study II cohort, the researchers found that women with the highest average intakes of riboflavin two to four years prior to diagnosis were associated with a 35 percent lower incidence of PMS than women with the lowest average intakes. On the other hand, the researchers did not observe any benefits with other B vitamins, including niacin, folate, B6, and B12. In addition, supplemental intakes of these vitamins was not linked to PMS incidence, they added. “We observed a significantly lower risk of PMS in women with high intakes of thiamine and riboflavin from food sources only,” wrote the researchers. “Further research is needed to evaluate the effects of B vitamins in the development of premenstrual syndrome.”
Beyond the B vitamins, there is also some evidence for the potential of a diet rich in calcium and vitamin D to lower the risk of developing PMS, a condition that affects up to a fifth of all women. According to a study published in 2005 in the Archives of Internal Medicine (Vol. 165, pp1246-1252), researchers from the University of Massachusetts and GlaxoSmithKline reported for the first time that calcium and vitamin D may help prevent the initial development of PMS.
Source: The American Journal of Clinical Nutrition. Published online ahead of print, doi: 10.3945/ajcn.110.009530 “Dietary B vitamin intake and incident premenstrual syndrome” Authors: P.O. Chocano-Bedoya, J.E. Manson, S.E. Hankinson, W.C. Willett, S.R. Johnson, L. Chasan-Taber, A.G. Ronnenberg, C. Bigelow, E.R. Bertone-Johnson
Researchers have a new theory on why some kids get unexplained tummy aches.
In some people, the small intestine is unable to efficiently break down fructose (and sometimes other forms of sugar). This problem is sometimes referred to as fructose intolerance. The undigested fructose passes into the large intestine, where it is broken down by bacteria. A by-product of this process is the creation of carbon dioxide and hydrogen. These two gases build up in the intestine, causing bloating, gas, pain and diarrhea. In some cases, the problem can affect absorption of important nutrients, like calcium and iron.
Researchers estimate about 33 percent of Americans have some level of sensitivity to sugar, most commonly to fructose, but the symptoms are often vague. Some people with fructose intolerance can eat small amounts of the sugar and not have any problems, making diagnosis even trickier.
Daniel Lustig, M.D., Pediatric Gastroenterologist at Mary Bridge Children’s Health Center in Tacoma, WA, says patients with chronic digestive problems should have a physician’s evaluation to rule out other possible causes of the symptoms, like Celiac disease or Crohn’s disease. Once those conditions have been ruled out, he recommends a diagnostic tool called the breath hydrogen test.
A patient is given a dose of fructose. Then, periodically, he/she breathes into an air collection bag. The gases from the bag are retrieved and analyzed for the presence of hydrogen (one of the gases given off when fructose is broken down in the large intestine). Patients whose hydrogen levels exceed 20 points beyond a baseline reading are likely to be fructose intolerant.
Lustig explains the main treatment of fructose intolerance is avoidance of foods containing fructose. That includes fruits, fruit juices, sodas and processed foods and drinks with high fructose corn syrup. Since fructose is in so many foods, it can be tricky to find and hard to avoid.
Lustig recently performed a study to look at possible fructose intolerance in 245 children and adolescents (ages 2 to 18) with unexplained chronic abdominal pain, gas or bloating. The breath hydrogen test found that nearly 54 percent of the participants tested positive for fructose intolerance. Lustig says the problem appeared to be especially high among teen girls.
Those who were judged to be fructose intolerant were given advice on using a low-fructose diet. The investigators found that nearly 68 percent of those who followed the recommended diet had an improvement or resolution in their symptoms.
With eating disorders on the rise among boys, minorities and younger children, doctors need to keep an eye out for unexpected cases, according to the author of a new report. The stereotype that eating disorders affect only affluent, white teenage girls no longer applies, said David S. Rosen, MD, MPH, who wrote a clinical report on the topic that was published in the December issue of Pediatrics. “It’s also happening to boys, young children, people of color and middle-aged women. It’s more of an equal opportunity disorder,” said Dr. Rosen, a professor of pediatrics, internal medicine and psychiatry at the University of Michigan.
Males, for example, now represent up to 10% of all cases of eating disorders. The number of children younger than 12 who are hospitalized for eating disorders increased 119% from 1999 to 2006, according to an analysis by the Agency for Healthcare Research and Quality cited in the report (www.ncbi.nlm.nih.gov/pubmed/21115584/). Young children who develop eating disorders are more susceptible to serious medical consequences such as stunted growth and organ damage, Dr. Rosen said.
Early intervention recommended
He urges physicians, nurses, parents, school social workers and others to intervene early. Health care professionals should take note when patients, particularly young ones, make derogatory comments about their appearance or talk about going on a diet. The report said screening questions about eating patterns and body image should be asked of all preteens and adolescents.
Fewer than 1% of adolescent girls in the U.S. have anorexia, and 1% to 2% percent have bulimia. Experts estimate that between 1% and 14% of Americans exhibit some physical and psychological symptoms of an eating disorder. Male and female athletes, including gymnasts, runners and wrestlers, and performers, such as dancers and models, may be more at risk.
The report said eating disorders may have more of a genetic link, similar to alcoholism and depression, than previously thought. The discovery that some children may be genetically predisposed to the condition may “help to take away some of the blame or stigma,” Dr. Rosen said. With more children obese, physicians should choose their words carefully when counseling a child about his or her weight, Dr. Rosen said. He sees young patients with eating disorders who claim their problems with food began when their doctor told them to lose weight.
Dr. Rosen recommends that physicians discuss healthy eating practices, not dieting, with patients and focus on a healthy lifestyle, not losing weight. “There’s a perception that, like alcoholism, [an eating disorder] never goes away and that the best you can do is keep it under control,” he said. But if caught early, “most children and teens can expect to recover completely.”
Findings from a new study of 141 adults add to an ongoing medical debate over which patients with symptoms of celiac disease should go on a gluten-free diet. Published in ACS' Journal of Proteome Research, the study concludes that people currently diagnosed as “potential” celiac disease patients and not advised to follow a gluten-free diet may not be “potential” patients at all. Rather, the scientists found that these patients have the same distinctive metabolic fingerprint as patients with full-blown disease who do benefit from gluten-free diets.
In the study, Ivano Bertini and colleagues explain that celiac disease is an autoimmune digestive disorder characterized by the inability to digest a protein called gliadin, a component of gluten, which is found in wheat, rye, and barley. The condition causes diarrhea, bloating, and other symptoms in over 3 million people in the United States alone. Treatment is avoidance of foods containing gluten. But the disease is often undiagnosed or misdiagnosed. Definitive diagnosis involves biopsy of the small intestine, showing tissue damage. People with a positive blood test for the condition but no positive biopsy usually are diagnosed as “potential” celiac patients and may or may not be advised to follow a gluten-free diet.
The scientists used magnetic resonance metabolic profiling to analyze the biochemical markers in the blood and urine of 61 patients with celiac disease, 29 with potential celiac disease, and 51 healthy people. They found that those with potential disease largely shared the same profile as those with the confirmed disease and that the biochemical markers in both groups differed significantly from those of the healthy individuals. “Our results demonstrate that metabolic alterations may precede the development of small intestinal villous atrophy and provide a further rationale for early institution of gluten-free diet in patients with potential celiac disease, as recently suggested by prospective clinical studies,” the scientists conclude.
A lack of testing for food allergies is putting children's health at risk and could lead to life threatening reactions, a study has found. The study, Adverse reactions to food in New Zealand children age 0-5 years, was published in the New Zealand Medical Journal. It looked at a cross-section of 110 children who had attended Plunket clinics. It found 44 had experienced an adverse reaction to food, but only four had been clinically evaluated. Those children were found to have adverse reactions to food allergens, including a life threatening peanut allergy. Two others had been hospitalised with systemic symptoms, but neither had undergone testing for food allergy. “If these children have food allergies, they remain at risk for continued and possibly severe reactions,” the study said.
Parents modifying children's diets or breastfeeding mothers cutting out food without advice from a physician or dietician could also have adverse affects, it said. “Failure to thrive is commonly seen in children experiencing FA (food allergy) as a result of multiple foods being removed from their diet.” The data indicated adverse reactions to food were a public health concern and may be under investigated — even when symptoms were severe, the study said.
“There is an urgent need to investigate the epidemiology, diagnosis, and prevention of FA (food allergy) in New Zealand to reduce morbidity, improve child health, and reduce the burden to health costs.” Thirty-three of the children were reported to have eczema. Ten had worsening symptoms two hours after eating, the study said. Symptoms improved in six of them with dietary changes. Doctors had prescribed topical therapy for 18 of those children with eczema, but symptoms had persisted.
“One possible explanation for this observation is undiagnosed FA (food allergy). Without testing, allergic triggers for eczema could not be identified in these participants.” Further investigation of food allergy as the cause of eczema was warranted, the study said.
Adverse reactions to food worldwide in children was an increasing concern and food allergy was as common in New Zealand as in other countries, the study said. The study was conducted by the Auckland District Health Board and led by Associate Professor Rohan Ameratunga and lead researcher Dr Christine Crooks. Allergy New Zealand chief executive Penny Jorgensen said the study was “really disturbing” because it highlighted that many children were not being assessed for food allergy. The risk was the potential for life-threatening reactions, she said.
A new study shows that adolescents who take acetaminophen, better known as Tylenol, have a higher risk of asthma, allergic nasal conditions and the skin disorder eczema.
Acetaminophen is widely viewed as a very safe drug—one reason why hospitals use it routinely as a painkiller instead of aspirin or ibuprofen. The major problem associated with it is liver damage caused by overdoses. Recently, however, there has been a growing drumbeat about possible dangers from the drug. One study, for example, found that acetaminophen increased the risk of hearing loss in men. And some others have hinted that the drug is linked to asthma in newborns whose mothers used the drug during pregnancy and in young children exposed to it.
The new findings were reported in the American Journal of Respiratory and Critical Care Medicine by researchers in the International Study of Asthma and Allergies in Childhood. The team, headed by epidemiologist Richard Beasley of the Medical Research Institute in Wellington, New Zealand, gave written questionnaires to 322,959 13- and 14-year-olds in 50 countries exploring their use of acetaminophen, other drugs, and asthma symptoms. They were also shown a video containing five scenes of clinical asthma and asked whether they had experienced any symptoms similar to those shown. About 73% of the teens said they had used acetaminophen at least once in the previous year and 30% said they had used it monthly.
Taking into account maternal education, smoking, diet and siblings, the team found that those subjects who had used the drug at least once per year were 43% more likely to have asthma, while those who used it at least monthly were 2.5 times as likely to suffer from the condition. The risk of rhinoconjunctivitis (a severe nasal congestion) was 38% higher for those who used it once per year and 2.39 times as high for those who used it at least monthly. The comparable increases in risk for eczema were 31% and 99%, respectively.
Overall, the increased risk of asthma associated with acetaminophen was 41%, the authors found. That could, at least in part, explain why there has been an increase in the prevalence of asthma in the 50 years since the drug was introduced. Given the widespread use of the drug, it could also represent a large public health problem.
But—and it is a very big but—the study shows only an association, not causality. That could only be determined by a randomized clinical trial, which the authors recommend. Furthermore, the study relies on the recall of teenagers. Recall is notoriously inaccurate in adults, and it is probably worse in adolescents, clouding the results. For the time being then, you can probably continue to feel comfortable giving the drug to your children.
In a statement, McNeil Consumer Healthcare, which manufactures Tylenol, said that the drug “has over 50 years of clinical history to support its safety and effectiveness” and that no clinical trial has demonstrated that the drug causes asthma.
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.
Organophosphate pesticides act by disrupting neurotransmitters, particularly acetylcholine, which plays an important role in sustaining attention and short-term memory.
“Given that these compounds are designed to attack the nervous system of organisms, there is reason to be cautious, especially in situations where exposure may coincide with critical periods of fetal and child development,” said he study's lead author Amy Marks.
Earlier this year, a different study by researchers at Harvard University associated greater exposure to organophosphate pesticides in school aged children with higher rates of attention deficit hyperactivity disorder (ADHD) symptoms.
“These studies provide a growing body of evidence that organophosphate pesticide exposure can impact human neurodevelopment, particularly among children. We were especially interested in prenatal exposure because that is the period when a baby's nervous system is developing the most,” said Eskenazi.
More than 300 children were tested and the researchers were continuing to follow the children as they get older and expect to present more results in the years to come. The current findings were published in the journal Environmental Health Perspectives.
Source: New York Post
The study involved participants in the Chicago Health and Aging Project, a longitudinal study of risk factors for Alzheimer's disease involving a population of older adults on Chicago's south side. At three year intervals, the entire population completed a brief self-report measure of depressive symptoms and clinical evaluations for Alzheimer's disease.
Initial analyses focused on a group of 357 individuals who developed Alzheimer's disease during the course of the study. The study found a barely perceptible increase in depressive symptoms, a rate of 0.04 symptoms per year, during six to seven years of observation before the diagnosis of Alzheimer's disease and no change during two to three years of observation after the diagnosis.
Because dementia may reduce the accuracy of self-report, in a subgroup of 340 participants, researchers conducted additional analyses of change in depressive symptoms by interviewing family, friends and other who were close to the study participants. Neither Alzheimer's disease nor its precursor, mild cognitive impairment, was associated with change in depressive symptoms during a mean of three years of observation.
The results were consistent across all demographics. There was no evidence that sex, age, education or race modified the trajectory of depressive symptoms before or after Alzheimer's disease was diagnosed.
“Here is this terrible disease that robs people of who they are and their ability to function and yet it doesn't make them depressed,” said Wilson. “Alzheimer's may disrupt the ability to have prolonged bouts of negative emotions, in much the same way it disrupts many other activities.”
The study authors suggest additional studies of patients with Alzheimer's disease for longer periods to determine if depressive symptoms may eventually decrease as the disease becomes more severe.
In addition, researchers at Rush continue to look at why depression increases the risk of Alzheimer's disease.
The study was supported by funding from the National Institutes of Health (NIH)/ National Institute on Aging (NIA). Co-authors include G.M. Hoganson, BS; K.B. Rajan, PhD; L.L. Barnes, PhD; C.F. Mendes de Leon, PhD; and D.A. Evans, MD.
People with mild cognitive impairment can be affected by a reduction in their ability to think, such as reduced memory and a short attention span.
“We wanted to find out whether highly educated patients with mild cognitive impairment differed in terms of tolerance of the disease from patients with intermediate and low levels of education,” says Rolstad.
By analysing the patients' spinal fluid, the researchers were able to examine whether there were signs of dementia in the brain.
“Highly educated patients with mild cognitive impairment who went on to develop dementia over the next two years had more signs of disease in their spinal fluid than those with intermediate and low levels of education,” says Rolstad.
Despite having more disease in the brain, the highly educated patients showed the same symptoms of the disease as their less well educated counterparts. This means that patients with higher levels of education tolerate more disease in the brain.
The researchers also studied patients with mild cognitive impairment who did not go on to develop dementia over the next two years.
“We found that the highly educated patients who did not develop dementia during the course of the study showed signs of better nerve function than those with lower levels of education,” says Rolstad. “This finding means that the highly educated not only tolerate more disease in the brain but also sustain less nerve damage during the early stages of the disease.”
The results indicate that a higher reserve capacity delays the symptoms of dementia and the progress of the disease. This can help the care sector to be more aware of dementia in highly educated patients, and thus increase the chances of the correct treatment being given.