Health
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.
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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.
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