SACRAMENTO – Dr. Ron Chapman, director of the California Department of Public Health (CDPH) and state health officer, on Wednesday warned consumers not to eat Pappy’s Chipotle Sauce Marinade with “Best Before” dates between Feb. 2013 and Feb. 2014 because the product contains undeclared allergens.
Pappy’s Fine Foods of Fresno, Calif., is voluntarily recalling the Pappy’s Chipotle Sauce Marinade because the product label failed to declare food allergens (wheat and fish) in the ingredient statements.
The recall was initiated after a routine inspection by CDPH identified the labeling deficiency. No illnesses have been reported at this time.
Pappy’s Chipotle Marinade Sauce is packaged in a 14-fluid-ounce glass bottle with a white label. It has a UPC (Universal Product Code) of 009502001119.
Only products with a Best Before date between Feb. 2013 and Feb. 2014 are subject to this recall. The Best Before date is printed on the cap.
People who have an allergy or severe sensitivity to wheat or fish run the risk of a life-threatening allergic reaction that requires immediate medical attention should they consume these products.
Consumers who have experienced allergic reaction after consuming this product should contact their health care provider
Consumers that observe the products being offered for sale are encouraged to report their findings to the CDPH toll free complaint line at 800-495-3232.
Soldiers preoccupied with threat at the time of enlistment or with avoiding it just before deployment were more likely to develop post-traumatic stress disorder (PTSD), in a study of Israeli infantrymen.
Such pre-deployment threat vigilance and avoidance, interacting with combat experience and an emotion-related gene, accounted for more than a third of PTSD symptoms that emerged later, say National Institutes of Health scientists, who conducted the study in collaboration with American and Israeli colleagues.
“Since biased attention predicted future risk for PTSD, computerized training that helps modify such attention biases might help protect soldiers from the disorder,” said Daniel Pine, M.D., of the NIH’s National Institute of Mental Health (NIMH).
Pine, Yair Bar-Haim, Ph.D. External Web Site Policy, of Tel Aviv University, and colleagues, report their findings, Feb. 13, 2013, in the journal JAMA Psychiatry.
Bar-Haim’s team tracked 1085 male Israeli soldiers from recruitment through combat deployment during 2008-2010, to pinpoint how shifting attitudes toward threat interact with other factors to predict symptoms that develop after exposure to dangers.
They expected that the more soldiers paid attention to avoiding threats just before and during deployment, the more they would suffer PTSD symptoms.
Researchers measured threat attention biases over the course of soldiers’ first year of service: at the time of recruitment, about six months later — just before deployment to combat — and six months after deployment. Data from all three time points was collected for 487 of the soldiers.
Soldiers performed a computerized task that required paying attention to locations of neutral words, such as “data” or threatening words, such as “dead.” A faster reaction time for identifying the location of threat words indicated increased threat vigilance. Slower reaction times to such word locations indicated attention away from threat, or threat avoidance.
The study also examined how threat attention bias vulnerability might be moderated by other factors, including the gene that codes for the protein on neurons that recycles the brain chemical messenger serotonin from the synapse.
Versions of this serotonin transporter gene had been previously linked to PTSD risk. Evidence suggests that people with gene versions that result in less efficient recycling may be overly vigilant toward threats under normal circumstances.
Yet there is also evidence that having these low-efficiency versions may help people cope with dangerous conditions, when such heightened vigilance may be adaptive.
As expected, soldiers who experienced higher combat exposure – e.g., served in units operating outside Israel’s security fence – tended to show more threat vigilance than those with less stressful assignments.
Compared to soldiers who were neither vigilant nor avoidant, soldiers with greater vigilance at recruitment or avoidance at six months – on the eve of deployment – had more PTSD symptoms at the end of their first year of service.
Although serotonin gene type had no direct effect on symptoms, the low efficiency gene version, combined with high threat vigilance, appeared to confer some protection to soldiers who experienced high combat exposure.
“Their natural tendency to attend to threats may lead to less adaptive emotional responses and elevated anxiety when environmental conditions are safe and stable, but to perfectly normal and adaptive responses in combat, where vigilance toward minor threats is crucial for survival,” explained Pine.
Bias toward threats showed no such association with PTSD symptoms in those with the high efficiency version of the gene. Nor did gene type interact with threat bias to predict PTSD in solders with low combat exposure.
Similarly, among the low combat exposure group, a history of traumatic experiences, self-reported combat experience, threat bias or gene type had no bearing on PTSD symptoms.
Higher pre-deployment PTSD symptoms and failure to complete high school also predicted higher post-deployment PTSD risk.
“Extreme adaptation challenges, such as those arising from soldiers’ shifting exposures to relatively safe and acutely hostile environments, may produce shifting psychological and behavioral symptoms of hyper-vigilance and avoidance,” explained the researchers.
They propose that computer-based attention bias modification techniques (see below) be tested in both soldiers prior to deployment as well as in PTSD patients, in combination with evidence-based cognitive therapies.
Long a source of sibling rivalry, birth order may raise the risk of first-born children developing diabetes or high blood pressure, according to a recent study accepted for publication in The Endocrine Society's Journal of Clinical Endocrinology & Metabolism (JCEM).
First-born children have greater difficulty absorbing sugars into the body and have higher daytime blood pressure than children who have older siblings, according to the study conducted at the University of Auckland's Liggins Institute in New Zealand.
The study was the first to document a 21 percent drop in insulin sensitivity among first-born children.
“Although birth order alone is not a predictor of metabolic or cardiovascular disease, being the first-born child in a family can contribute to a person's overall risk,” said Wayne Cutfield, MBChB, DCH, FRACP, of the University of Auckland.
With family size shrinking in many countries, a larger proportion of the population is made up of first-born children who could develop conditions like type 2 diabetes, coronary artery disease, stroke and hypertension.
The research findings may have significant public health implications for nations like China, where the one-child policy has led to a greater segment of the population being composed of first-born children.
The study measured fasting lipid and hormonal profiles, height, weight and body composition in 85 healthy children between the ages of 4 and 11.
The 32 first-born children who participated in the study had a 21 percent reduction in insulin sensitivity and a 4 mmHg increase in blood pressure.
The good news for oldest and only children? The study found they tended to be taller and slimmer than their later-born counterparts, even after the height and body mass index of their parents was taken into account.
The metabolic differences in younger siblings might be caused by physical changes in the mother's uterus during her first pregnancy.
As a result of the changes, nutrient flow to the fetus tends to increase during subsequent pregnancies.
For this study, researchers focused on children because puberty and adult lifestyle can affect insulin sensitivity.
“Our results indicate first-born children have these risk factors, but more research is needed to determine how that translates into adult cases of diabetes, hypertension and other conditions,” Cutfield said.
Other researchers working on the study include: A. Ayyavoo, T. Savage, J. Derraik and P. Hofman of the University of Auckland.
The article, “First-born Children Have Reduced Insulin Sensitivity And Higher Daytime Blood Pressure Compared To Later-born Children,” appears in the March 2013 issue of JCEM.
Having diabetes doubles a person's risk of dying after a heart attack, but the reason for the increased risk is not clear.
A new University of Iowa study suggests the link may lie in the over-activation of an important heart enzyme, which leads to death of pacemaker cells in the heart, abnormal heart rhythm, and increased risk of sudden death in diabetic mice following a heart attack.
“Many studies have shown that patients with diabetes are at especially high risk for dying from a myocardial infarction (heart attack). Our study provides new evidence that this excess mortality could involve a pathway where oxidized CaMKII enzyme plays a central role,” said Mark Anderson, M.D., Ph.D., UI professor and chair and executive office of internal medicine, and senior author of the study published Feb. 15 in the Journal of Clinical Investigation.
Diabetes affects more than 8 percent of the U.S. population, and heart attack is the most common cause of death in people with diabetes.
Diabetes also causes increased oxidative stress – a rise in the level of so-called reactive oxygen species (ROS) that can be damaging to cells.
In 2008, Anderson's lab showed that CaMKII (calcium/calmodulin-dependent protein kinase II) is activated by oxidation.
The new study links oxidative stress caused by diabetes to increased death risk after a heart attack through the oxidation-based activation of the CaMKII enzyme.
“Our findings suggest that oxidized CaMKII may be a 'diabetic factor' that is responsible for the increased risk of death among patients with diabetes following a heart attack,” said lead study author Min Luo, D.O., Ph.D., a cardiology fellow in the UI Department of Internal Medicine.
Luo and her colleagues used a mouse model of diabetes to probe the link between the disease and an increased risk of death from heart attack.
The study showed that heart rates in the diabetic mice slowed dramatically and, like humans with diabetes, the mice had double the death rate after a heart attack compared to non-diabetic mice.
Evidence from the diabetic mice suggested that the excess deaths following heart attack was due to heart rhythm abnormalities, prompting the team to investigate the heart's pacemaker cells, which control heart rate.
Looking at the diabetic mice, the team found that pacemaker cells had elevated levels of oxidized CaMKII enzyme and more cell death than pacemaker cells in non-diabetic mice. The levels of oxidation and cell death were further increased in the diabetic mice following a heart attack.
When the team blocked oxidation-based activation of the enzyme, fewer pacemaker cells died, and the diabetic mice maintained normal heart rates and were protected from the increased death risk following a heart attack.
The findings suggest that preventing or reducing activation of the CaMKII enzyme in specific heart cells may represent a new approach for reducing the risk of death due to heart attack in patients with diabetes.