From UPI.com

Swedish researchers found women who breast feed more than 13 months were half as likely to get rheumatoid arthritis.Those who had breast fed for one to 12 months were 25 percent less likely to get the disease.The study, published online ahead of print in the Annals of the Rheumatic Diseases, also found taking oral contraceptives — suspected to protect against the disease because they contain hormones that are raised in pregnancy — did not have the same effect. Similarly, being pregnant — but not breast feeding — did not seem to have a protective effect either.

The authors said that it was difficult to say whether there was a connection between higher rates of breast feeding and a corresponding fall in the number of women affected by rheumatoid arthritis, but that the results of the study provided yet another reason why women should breast feed.

Study leader Dr. M. Pikwer of The Malmo University Hospital, in Sweden compared 136 women with rheumatoid arthritis with 544 women of a similar age without the disease.

From WebMD

The reaction of an infant’s immature immune system to a protein found in cow’s milk infant formula may explain the suspected link between early consumption of cow’s milk and an increased risk of developing type 1 diabetes later, according to a new study.

But experts who reviewed the study for WebMD say the research is mixed on the suspected link and the new report does not offer conclusive proof of cause and effect. While these experts strongly support breastfeeding, they say those mothers who can’t or choose not to breastfeed shouldn’t be alarmed by the report.

The Formula-Diabetes Theory

The protein under study, called beta-lactoglobulin, is found in cow’s milk but not human breast milk. It is similar in structure to the human protein glycodelin, writes Marcia F. Goldfarb, author of the new report.

The report is published in the letters section of the Journal of Proteome Research. Goldfarb directs Anatek-EP, a contract protein research laboratory in Portland, Maine.

An infant’s immature immune system may destroy the glycodelin in an effort to destroy the look-alike “foreign” protein beta-lactoglobulin, Goldfarb says.

Glycodelin controls the production of the body’s T-cells, which help protect against infection. If glycodelin is destroyed, there could be an overproduction of T cells, she says.

Lower body mass, high levels of good cholesterol combat cardiovascular disease, study says

From HealthDay

Breast-fed babies are less likely than bottle-fed infants to have certain cardiovascular disease (CVD) risk factors in adulthood, say U.S. researchers who analyzed two generations of participants in the Framingham Heart Study.

“Having been breast-fed in infancy is associated with a lower average body-mass index (BMI) and a higher average HDL (high-density lipoprotein, or “good” cholesterol) level in adulthood, even after accounting for personal and maternal demographic and CVD risk factors that could influence the results,” study author Dr. Nisha I. Parikh, a cardiovascular fellow at the Beth Israel Deaconess Medical Center in Boston, said in a prepared statement.

Lower BMI and high HDL both protect against CVD, noted the researchers, who found that middle-aged adults who were breast-fed as infants were 55 percent more likely to have high HDL levels than to have low HDL levels, defined as less than 50 mg/dL for women and less than 40 mg/dL for men.

Average HDL levels among adults who’d been breast-fed was 56.6 mg/dL, compared with 53.7 mg/dL for adults who’d been bottle-fed. However, the researchers said this difference was not statistically different once BMI was considered in a later analysis.

Adults who were breast-fed had a lower mean BMI than those who’d been bottle-fed — 26.1 vs. 26.9. People with a BMI higher than 25 are considered overweight and increased risk for CVD.

“This was a modest reduction in BMI [among those who'd been breast-fed], but even a modest reduction leads to a significantly reduced risk of cardiovascular disease-related death,” Parikh said.

Breast-feeding was not associated with any other adult CVD risk factors, the researchers said.

It helps high-risk infants prone to eczema, asthma and food allergies, report suggests

From HealthDay

Atopic disease — which includes eczema, asthma and food allergies — may be delayed or even prevented in high-risk infants if they are exclusively breast-fed for at least four months or fed infant formula without cow milk protein.

That’s the conclusion of a new clinical report from the American Academy of Pediatrics (AAP) that’s published in the January issue of Pediatrics. The report replaces an earlier policy statement from the AAP.

“Basically, it probably does not matter what pregnant or lactating women eat,” said Dr. Frank Greer, an author of the report, professor of pediatrics at the University of Wisconsin and chairman of the AAP Committee on Nutrition.

“The best prevention for atopic [allergic] disease is exclusive breast-feeding for four months,” he added. “And if your infant comes from a family with significant atopic disease, then weaning from breast milk to a partially or extensively hydrolyzed [hypoallergenic] formula [without cow milk protein] may delay or prevent the onset of atopic disease, especially atopic dermatitis [eczema].”

Greer added that this recommendation would also apply to formula-fed infants who are at risk for atopic disease.

The timing and introduction of solid foods has no protective effect on the prevention of atopic disease, according to the new report.

“With the increase in asthma and food allergies that we’ve seen recently, we had hoped that maternal diet, breast-feeding and early childhood diet might all have some factor in decreasing incidence,” said Dr. Jennifer Wu, an obstetrician/gynecologist at Lenox Hill Hospital in New York City. “Unfortunately, it doesn’t seem to significantly impact, according to studies already done. The only one that seems to be impacted is the atopic dermatitis, which is decreased by about one third by breast-feeding. But the studies that have been done so far have not proven that breast-feeding will significantly impact childhood asthma or food allergies.”

The incidence of allergic diseases such as asthma, food allergies and various skin conditions has exploded during the past few decades. In children 4 years of age and younger, the incidence of asthma has risen 160 percent, while the incidence of atopic dermatitis has almost tripled. And the incidence of peanut allergy has doubled just during the past decade, according to the report.

While genetics certainly plays a role in the development of these diseases, environmental factors such as diet are also strongly related.

The new report reviewed different evidence on nutrition during pregnancy, breast-feeding and the first year of life that might affect the development of allergic disease. Its major findings are as follows:

Currently, there is no evidence that what a mother eats during pregnancy or breast-feeding plays a major role in preventing atopic disease in infants. There is some evidence, however, that avoiding certain foods during breast-feeding may help prevent atopic eczema.

Exclusive breast-feeding for at least four months for infants at high-risk of developing atopic disease decreases the risk of developing eczema and cow milk allergy during the first two years of life.

In high-risk infants who aren’t breast-fed exclusively for four to six months, the use of hydrolyzed infant formula (as opposed to formula containing cow milk) may delay or prevent the onset of atopic dermatitis.

Exclusive breast-feeding for at least three months protects an infant against wheezing in early life.

There is no good evidence to support the use of soy-based infant formula to prevent allergies.

There is no evidence to suggest that delaying the introduction of solid foods before the recommended 4 to 6 months of age will have an effect on the development of atopic disease.

There is no convincing evidence to suggest that any dietary intervention will prevent atopic disease after 4 to 6 months of age.

“It’s a mixed picture,” Wu said. “We don’t have proven efficacy for breast-feeding. It may mean that we need more robust studies and a longer-term follow-up for kids.”

The new report is titled “Effects of Early Nutritional Interventions on the Development of Atopic Disease in Infants and Children: The Role of Maternal Dietary Restriction, Breastfeeding, Timing of Introduction of Complementary Foods, and Hydrolyzed Formulas.”

From HealthScout

Researchers have identified the chemical pathway by which a mother’s smoking before and after pregnancy might reduce her daughter’s fertility by as much as two-thirds.

Cigarette smoking during pregnancy has been shown in retrospective studies to affect the fertility of a woman’s offspring, but this is the first study to offer an explanation of the biology behind the effect, the Canadian scientists claim.

A team at the Samuel Lunenfeld Research Institute at Mount Sinai Hospital in Toronto investigated the impact of polycyclic aromatic hydrocarbons (PAH), a byproduct of smoking, on mouse fertility.

Researchers injected three groups of female mice with a low-dose mixture of PAH: One group received PAH before conception and again when they were providing milk for their pups; one group received PAH only before conception; and the third group received PAH only during lactation. A fourth control group did not receive PAH but were mated at the same time as the others. The total amount of PAH given to each mouse over the three-week injection cycle was equivalent to 25 packs of cigarettes, according to the researchers. The exposed mice did not have fewer pups in their own litters, but when researchers investigated the number of eggs in their female offspring, they found about 70 percent fewer follicles available to produce eggs.

“Mothers, mice in this case, exposed to PAHs — environmental pollutants found in cigarette smoke, car exhaust, smoke produced by fossil fuel combustion, as well as in smoked food –before pregnancy and/or during breast-feeding, but not during pregnancy, can cause a reduction in the number of eggs in the ovaries of their female offspring by two-thirds. This limits the window in which the daughter will be able to reproduce,” explained lead researcher Dr. Andrea Jurisicova.

Further analysis indicated that the effects of PAHs on the number of follicles in female offspring were mediated through a receptor that affects the expression of a gene that makes a protein that causes cells to die. The researchers then demonstrated similar effects in human ovarian tissue transplanted into immunocompromised mice.

Jurisicova described the process: “Toxic compounds were injected under the skin of mice and were picked up by the bloodstream and carried throughout the body until they reached the ovaries. Once at the ovaries, they passed through the cell membrane and bound to the receptor. When this happens, it activates the receptor, which then enters the cell nucleus. The receptor then finds a specific DNA sequence that turns on the gene, which accumulates and eventually kills the eggs.”

“This study now is providing a chemical pathway, which is very nice,” said Dr. Norman Edelman, consultant for scientific affairs with the American Lung Association. The new data provides biological support for epidemiological results, such as the previously observed reduction in fertility among daughters of smoking women, he added.

Whether the news will have an impact on a woman’s decision to smoke is another question, said Edelman.

“If we do our job right and these results get good press, this data could remind women of what they are doing to their unborn fetuses,” Edelman said.

Another expert noted this latest finding adds to a growing body of evidence that shows a strong connection between smoking and fertility.

“I think it is an interesting study, but it doesn’t add much new. Other studies have shown similar outcomes. The theory is that smoking could affect the follicles or the fallopian tubes,” said Dr. Amos Grunebaum, director of obstetrics at New York Weill Cornell Medical Center, in New York City. “We have known for many years that smoking affects fertility on many levels.”

“The key is women should quit smoking before they are thinking of getting pregnant,” Grunebaum said.

The Canadian researchers did offer some good news in their report, published in the Dec. 3 edition of the Journal of Clinical Investigation. Injecting resveratrol in the mice who were exposed to PAH prevented the reduction in egg follicles in their offspring. Resveratrol is a naturally occurring antioxidant found in wine and grape skins. However, that reversal of damage does not mean that women who smoke can counter the effects with a nutritional supplement or a glass of red wine, the researchers stressed.

“We have found that oral consumption of resveratrol as a food supplement, at least in mice, is not effective, as levels of resveratrol do not reach sufficient amount in the bloodstream to provide protection,” Jurisicova said.

Although the findings do not define the length of time between quitting smoking and healthier fertility in offspring, Jurisicova noted that previous studies have shown that women who smoke have better results with in vitro fertilization one year after they quit smoking. The mice in the current study conceived up to two weeks after their final PAH injection, which is approximately equivalent to three menstrual cycles in women.

The effect of a mother’s cigarette smoking is not limited to her female children. A study published in the Jan. 1 issue of the American Journal of Epidemiology suggested that the male offspring of mothers who smoke have lower sperm counts.

There is still more research to be done, Jurisicova noted.

“We hope to continue studying the female offspring to see if they enter the mouse version of menopause earlier than mice whose mothers were not exposed to PAHs,” Jurisicova said. “We also hope to study if their reduced fertility passes on to subsequent generations, and if the granddaughters are predisposed to similar problems.”

More information

Need to quit smoking? Visit the U.S. Surgeon General or the National Institutes of Health.

SOURCES: Norman H. Edelman, M.D., consultant, scientific affairs, American Lung Association; Andrea Jurisicova, M.D., assistant professor, University of Toronto, and Canada Research Chair, Molecular and Reproductive Medicine, Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto; Amos Grunebaum, M.D., director, obstetrics, New York Weill Cornell Medical Center, New York City; Dec. 3, 2007, Journal of Clinical Investigation