Endo 2013

SAN FRANCISCO – Vitamin D deficiency may help explain why obese children are more at risk than others for allergies and asthma, according to an observational cross-sectional study.

"In our population, we found that the allergic profile was increased in obese adolescents," said lead investigator Dr. Candace Percival, a pediatric endocrinology fellow at the Uniformed Services University of the Health Sciences in Bethesda, Md.

Fifty-four boys and girls 10-18 years old who were at or above the 85th percentile for age- and sex-adjusted body mass index and 32 normal-weight controls participated in the project. The investigators tested for blood levels of vitamin D, immunoglobulin E (IgE), leptin, adiponectin, and cytokines that contribute to allergy and asthma.

As expected, based on previous obesity studies, higher BMIs correlated significantly with higher leptin and lower adiponectin levels, both of which have been linked to enhanced allergic response. Obesity correlated significantly with increased levels of IgE, IL (interleukin)-6 and IL-13 as well; the obese subjects were all also vitamin D deficient.

However, "when we ran a multivariate analysis controlling for vitamin D deficiency, we found that the statistical significance of correlations between cytokines and IgE with BMI disappeared. The relationship between BMI and ... markers of allergic disease seemed to depend on vitamin D deficiency; it was a dependent cofactor for adolescents having this allergy profile. It’s hard to say if there’s any sort of causal relationship, [but] this makes us wonder if vitamin D may be a mediator of the increased risk for allergy in the setting of obesity," Dr. Percival said at the Endocrine Society’s annual meeting.

It’s not an unreasonable thought. "Past research has shown that vitamin D is important for normal immune system function. It has both anti-inflammatory and antiallergic effects. Vitamin D deficiency is very common in obese individuals [and] is associated with an increased risk for allergy and asthma; it may skew the immune system towards an allergic response," she said.

The next step is to see if vitamin D supplements make a difference in biochemical markers and symptoms of allergic response in obese adolescents. Dr. Percival said she hopes to initiate that trial.

The authors said they had no relevant financial disclosures. The study was funded by Walter Reed National Military Medical Center and the Diabetes Action Research and Education Foundation in Washington, D.C.

aotto@frontlinemedcom.com

SAN FRANCISCO – Vitamin D deficiency may help explain why obese children are more at risk than others for allergies and asthma, according to an observational cross-sectional study.

"In our population, we found that the allergic profile was increased in obese adolescents," said lead investigator Dr. Candace Percival, a pediatric endocrinology fellow at the Uniformed Services University of the Health Sciences in Bethesda, Md.

Fifty-four boys and girls 10-18 years old who were at or above the 85th percentile for age- and sex-adjusted body mass index and 32 normal-weight controls participated in the project. The investigators tested for blood levels of vitamin D, immunoglobulin E (IgE), leptin, adiponectin, and cytokines that contribute to allergy and asthma.

As expected, based on previous obesity studies, higher BMIs correlated significantly with higher leptin and lower adiponectin levels, both of which have been linked to enhanced allergic response. Obesity correlated significantly with increased levels of IgE, IL (interleukin)-6 and IL-13 as well; the obese subjects were all also vitamin D deficient.

However, "when we ran a multivariate analysis controlling for vitamin D deficiency, we found that the statistical significance of correlations between cytokines and IgE with BMI disappeared. The relationship between BMI and ... markers of allergic disease seemed to depend on vitamin D deficiency; it was a dependent cofactor for adolescents having this allergy profile. It’s hard to say if there’s any sort of causal relationship, [but] this makes us wonder if vitamin D may be a mediator of the increased risk for allergy in the setting of obesity," Dr. Percival said at the Endocrine Society’s annual meeting.

It’s not an unreasonable thought. "Past research has shown that vitamin D is important for normal immune system function. It has both anti-inflammatory and antiallergic effects. Vitamin D deficiency is very common in obese individuals [and] is associated with an increased risk for allergy and asthma; it may skew the immune system towards an allergic response," she said.

The next step is to see if vitamin D supplements make a difference in biochemical markers and symptoms of allergic response in obese adolescents. Dr. Percival said she hopes to initiate that trial.

The authors said they had no relevant financial disclosures. The study was funded by Walter Reed National Military Medical Center and the Diabetes Action Research and Education Foundation in Washington, D.C.

aotto@frontlinemedcom.com

SAN FRANCISCO – Vitamin D deficiency may help explain why obese children are more at risk than others for allergies and asthma, according to an observational cross-sectional study.

"In our population, we found that the allergic profile was increased in obese adolescents," said lead investigator Dr. Candace Percival, a pediatric endocrinology fellow at the Uniformed Services University of the Health Sciences in Bethesda, Md.

Fifty-four boys and girls 10-18 years old who were at or above the 85th percentile for age- and sex-adjusted body mass index and 32 normal-weight controls participated in the project. The investigators tested for blood levels of vitamin D, immunoglobulin E (IgE), leptin, adiponectin, and cytokines that contribute to allergy and asthma.

As expected, based on previous obesity studies, higher BMIs correlated significantly with higher leptin and lower adiponectin levels, both of which have been linked to enhanced allergic response. Obesity correlated significantly with increased levels of IgE, IL (interleukin)-6 and IL-13 as well; the obese subjects were all also vitamin D deficient.

However, "when we ran a multivariate analysis controlling for vitamin D deficiency, we found that the statistical significance of correlations between cytokines and IgE with BMI disappeared. The relationship between BMI and ... markers of allergic disease seemed to depend on vitamin D deficiency; it was a dependent cofactor for adolescents having this allergy profile. It’s hard to say if there’s any sort of causal relationship, [but] this makes us wonder if vitamin D may be a mediator of the increased risk for allergy in the setting of obesity," Dr. Percival said at the Endocrine Society’s annual meeting.

It’s not an unreasonable thought. "Past research has shown that vitamin D is important for normal immune system function. It has both anti-inflammatory and antiallergic effects. Vitamin D deficiency is very common in obese individuals [and] is associated with an increased risk for allergy and asthma; it may skew the immune system towards an allergic response," she said.

The next step is to see if vitamin D supplements make a difference in biochemical markers and symptoms of allergic response in obese adolescents. Dr. Percival said she hopes to initiate that trial.

The authors said they had no relevant financial disclosures. The study was funded by Walter Reed National Military Medical Center and the Diabetes Action Research and Education Foundation in Washington, D.C.

aotto@frontlinemedcom.com

There are no randomized controlled trials in which pregnant women in one group are exposed to endocrine-disrupting chemicals while a similar control group is protected from the same chemicals. It’s ethically impossible.

Still, evidence is mounting of the potential harm to fetuses from environmental exposure to bisphenol A (BPA) and other endocrine disruptors in human case-control and epidemiological studies, as well as in studies of animals or human cells. BPA is a synthetic estrogen used in carbonless receipts, plastic bottles, food-can liners, and more.

At the Endocrine Society’s Annual Meeting, a French study linked BPA exposure to higher risk for male babies to be born with undescended testicles. Investigators in Chicago grafted human prostate stem cells into mice and showed that exposure to BPA while tissues are developing produced greater risk for prostate cancer later in life. Building on prior human epidemiological studies suggesting that BPA exposure is associated with risk for metabolic syndrome, a study of pregnant sheep found that fetal exposure to BPA increased inflammation in fat tissue after birth, which can lead to obesity and metabolic syndrome.

The findings are "striking" in that they each connect fetal exposure to BPA with later development of disease, said Dr. Joanna Spencer-Segal of the University of Michigan, Ann Arbor, who moderated a press briefing on endocrine disruptors.

Dr. Patrick Fénichel and his associates screened all 6,246 boys born at one hospital after 34 weeks’ gestation and matched two normal male newborns with each of the 52 born with isolated cryptochordism. Umbilical cord blood assays showed that infants with cryptochordism had significantly lower levels of insulin-like peptide 3 (INSL-3), one of two hormones that regulate testicular descent. Blood levels of BPA were inversely correlated with INSL-3 levels – the more BPA on board, the lower the level of the hormone, said Dr. Fénichel, professor and head of the endocrinology department at the University Hospital, Nice, France.

Gail S. Prins, Ph.D. and her associates took the mice with human prostate stem cells and gave them BPA in levels found in humans for 2 weeks. When the prostate tissue had matured a month after grafting, they gave the mice estrogen and testosterone to mimic hormonal changes in aging men. Over the next 4 months, 33%-45% of the 27 mice exposed to varying amounts of BPA developed high-grade prostate intraepithelial neoplasia or prostate adenocarcinoma, compared with 12% of the 34 control mice, said Dr. Prins, professor of urology at the University of Illinois, Chicago.

Almudena Veiga-Lopez, D.V.M., Ph.D., and her associates randomized 12 pregnant sheep to be fed corn oil with or without BPA, and studied their 33 offspring. In each group, they overfed half of the offspring to make them obese. At 15 months of age, fat tissue in the obese sheep had abnormal levels of two markers of inflammation – CD68 and adiponectin – and the CD68 levels also were abnormal in normal-weight female offspring of mother sheep who had been fed BPA, reported Dr. Veiga-Lopez, also of the University of Michigan. Tissue inflammation can be a precursor to metabolic diseases such as obesity, diabetes, or cardiovascular disease, she pointed out.

These are hardly the first studies to trigger alarm about BPA and similar chemicals. Our report from the Endocrine Society’s 2012 meeting highlighted studies showing that children’s weight correlated with their blood levels of another endocrine disruptor, di(2-ethylhexyl)phthalate, and that prenatal exposure to a mixture of endocrine disruptors caused long-term adverse changes in the developing brains of rats.

There’s no easy way to avoid all of these chemicals at the moment, though pregnant women should try, the speakers said. What are really needed are tougher international regulations requiring industry to test new chemicals for safety before introducing them to the market, Dr. Prins said.

All speakers reported having no financial disclosures.

–By Sherry Boschert

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

There are no randomized controlled trials in which pregnant women in one group are exposed to endocrine-disrupting chemicals while a similar control group is protected from the same chemicals. It’s ethically impossible.

Still, evidence is mounting of the potential harm to fetuses from environmental exposure to bisphenol A (BPA) and other endocrine disruptors in human case-control and epidemiological studies, as well as in studies of animals or human cells. BPA is a synthetic estrogen used in carbonless receipts, plastic bottles, food-can liners, and more.

At the Endocrine Society’s Annual Meeting, a French study linked BPA exposure to higher risk for male babies to be born with undescended testicles. Investigators in Chicago grafted human prostate stem cells into mice and showed that exposure to BPA while tissues are developing produced greater risk for prostate cancer later in life. Building on prior human epidemiological studies suggesting that BPA exposure is associated with risk for metabolic syndrome, a study of pregnant sheep found that fetal exposure to BPA increased inflammation in fat tissue after birth, which can lead to obesity and metabolic syndrome.

The findings are "striking" in that they each connect fetal exposure to BPA with later development of disease, said Dr. Joanna Spencer-Segal of the University of Michigan, Ann Arbor, who moderated a press briefing on endocrine disruptors.

Dr. Patrick Fénichel and his associates screened all 6,246 boys born at one hospital after 34 weeks’ gestation and matched two normal male newborns with each of the 52 born with isolated cryptochordism. Umbilical cord blood assays showed that infants with cryptochordism had significantly lower levels of insulin-like peptide 3 (INSL-3), one of two hormones that regulate testicular descent. Blood levels of BPA were inversely correlated with INSL-3 levels – the more BPA on board, the lower the level of the hormone, said Dr. Fénichel, professor and head of the endocrinology department at the University Hospital, Nice, France.

Gail S. Prins, Ph.D. and her associates took the mice with human prostate stem cells and gave them BPA in levels found in humans for 2 weeks. When the prostate tissue had matured a month after grafting, they gave the mice estrogen and testosterone to mimic hormonal changes in aging men. Over the next 4 months, 33%-45% of the 27 mice exposed to varying amounts of BPA developed high-grade prostate intraepithelial neoplasia or prostate adenocarcinoma, compared with 12% of the 34 control mice, said Dr. Prins, professor of urology at the University of Illinois, Chicago.

Almudena Veiga-Lopez, D.V.M., Ph.D., and her associates randomized 12 pregnant sheep to be fed corn oil with or without BPA, and studied their 33 offspring. In each group, they overfed half of the offspring to make them obese. At 15 months of age, fat tissue in the obese sheep had abnormal levels of two markers of inflammation – CD68 and adiponectin – and the CD68 levels also were abnormal in normal-weight female offspring of mother sheep who had been fed BPA, reported Dr. Veiga-Lopez, also of the University of Michigan. Tissue inflammation can be a precursor to metabolic diseases such as obesity, diabetes, or cardiovascular disease, she pointed out.

These are hardly the first studies to trigger alarm about BPA and similar chemicals. Our report from the Endocrine Society’s 2012 meeting highlighted studies showing that children’s weight correlated with their blood levels of another endocrine disruptor, di(2-ethylhexyl)phthalate, and that prenatal exposure to a mixture of endocrine disruptors caused long-term adverse changes in the developing brains of rats.

There’s no easy way to avoid all of these chemicals at the moment, though pregnant women should try, the speakers said. What are really needed are tougher international regulations requiring industry to test new chemicals for safety before introducing them to the market, Dr. Prins said.

All speakers reported having no financial disclosures.

–By Sherry Boschert

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

There are no randomized controlled trials in which pregnant women in one group are exposed to endocrine-disrupting chemicals while a similar control group is protected from the same chemicals. It’s ethically impossible.

Still, evidence is mounting of the potential harm to fetuses from environmental exposure to bisphenol A (BPA) and other endocrine disruptors in human case-control and epidemiological studies, as well as in studies of animals or human cells. BPA is a synthetic estrogen used in carbonless receipts, plastic bottles, food-can liners, and more.

At the Endocrine Society’s Annual Meeting, a French study linked BPA exposure to higher risk for male babies to be born with undescended testicles. Investigators in Chicago grafted human prostate stem cells into mice and showed that exposure to BPA while tissues are developing produced greater risk for prostate cancer later in life. Building on prior human epidemiological studies suggesting that BPA exposure is associated with risk for metabolic syndrome, a study of pregnant sheep found that fetal exposure to BPA increased inflammation in fat tissue after birth, which can lead to obesity and metabolic syndrome.

The findings are "striking" in that they each connect fetal exposure to BPA with later development of disease, said Dr. Joanna Spencer-Segal of the University of Michigan, Ann Arbor, who moderated a press briefing on endocrine disruptors.

Dr. Patrick Fénichel and his associates screened all 6,246 boys born at one hospital after 34 weeks’ gestation and matched two normal male newborns with each of the 52 born with isolated cryptochordism. Umbilical cord blood assays showed that infants with cryptochordism had significantly lower levels of insulin-like peptide 3 (INSL-3), one of two hormones that regulate testicular descent. Blood levels of BPA were inversely correlated with INSL-3 levels – the more BPA on board, the lower the level of the hormone, said Dr. Fénichel, professor and head of the endocrinology department at the University Hospital, Nice, France.

Gail S. Prins, Ph.D. and her associates took the mice with human prostate stem cells and gave them BPA in levels found in humans for 2 weeks. When the prostate tissue had matured a month after grafting, they gave the mice estrogen and testosterone to mimic hormonal changes in aging men. Over the next 4 months, 33%-45% of the 27 mice exposed to varying amounts of BPA developed high-grade prostate intraepithelial neoplasia or prostate adenocarcinoma, compared with 12% of the 34 control mice, said Dr. Prins, professor of urology at the University of Illinois, Chicago.

Almudena Veiga-Lopez, D.V.M., Ph.D., and her associates randomized 12 pregnant sheep to be fed corn oil with or without BPA, and studied their 33 offspring. In each group, they overfed half of the offspring to make them obese. At 15 months of age, fat tissue in the obese sheep had abnormal levels of two markers of inflammation – CD68 and adiponectin – and the CD68 levels also were abnormal in normal-weight female offspring of mother sheep who had been fed BPA, reported Dr. Veiga-Lopez, also of the University of Michigan. Tissue inflammation can be a precursor to metabolic diseases such as obesity, diabetes, or cardiovascular disease, she pointed out.

These are hardly the first studies to trigger alarm about BPA and similar chemicals. Our report from the Endocrine Society’s 2012 meeting highlighted studies showing that children’s weight correlated with their blood levels of another endocrine disruptor, di(2-ethylhexyl)phthalate, and that prenatal exposure to a mixture of endocrine disruptors caused long-term adverse changes in the developing brains of rats.

There’s no easy way to avoid all of these chemicals at the moment, though pregnant women should try, the speakers said. What are really needed are tougher international regulations requiring industry to test new chemicals for safety before introducing them to the market, Dr. Prins said.

All speakers reported having no financial disclosures.

–By Sherry Boschert

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SAN FRANCISCO – Teenage girls with anorexia have less anxiety about gaining weight if their estrogen levels have been returned to normal, according to a small, randomized study, researchers from Massachusetts General Hospital and Harvard Medical School in Boston reported.

If confirmed in additional studies, it is an important finding, because anxiety about weight gain can sabotage anorexia nervosa treatment. "Physiological estrogen replacement is a potential strategy to reduce ... anxiety and improve chances of successful treatment," said lead investigator Dr. Madhusmita Misra, a pediatric endocrinologist and associate professor of pediatrics at Harvard Medical School in Boston.

Her team randomized female patients aged 13-18 years to 100-mcg transdermal estradiol twice weekly with cyclic progesterone 10 days/month, or to placebo patches and pills.

After 18 months, 20 girls on active treatment, when compared with 17 on placebo, had a significant decrease in trait anxiety, the tendency to experience anxiety as assessed by the State-Trait Anxiety Inventory for Children (–3.05 vs. 2.07, P = .01). Patients with the greatest estrogen level increases had the greatest reductions in trait anxiety scores (P = .001).

The girls were amenorrheic, with baseline estrogen levels far below normal; the intervention restored them to physiologic levels. They all met DSM-IV anorexia criteria, had bone ages of at least 15 years old, and were under treatment.

There were no significant between-group baseline differences in body mass index, psychotropic medication use, age, estrogen levels, questionnaire scores, and other factors, including weight gain over the 18 months. "We did various multiple adjustments to be sure there were not any confounders driving this association," Dr. Misra said.

Estrogen replacement did not directly affect eating attitudes assessed by the Eating Disorders Inventory II questionnaire, or body-shape perceptions assessed by the Body Shape Questionnaire (BSQ-34). However, it did seem to prevent an increase in body dissatisfaction and state anxiety – current anxiety – with weight gain, something noted in the placebo group and common in anorexia nervosa treatment.

"We have shown" before "that physiologic estrogen replacement is very important for normalizing the rate of bone accrual" in teenage girls with the condition (J. Bone. Miner. Res. 2011;26:2430-8). "This seems to be an additional benefit. These findings have the potential to [affect] therapy in anorexia nervosa with early implementation of estrogen replacement in girls who are estrogen deficient. [But,] more studies are necessary to confirm these findings; it would be premature to advise estrogen replacement just for anxiety issues," Dr. Misra said.

Estradiol levels during the study increased a mean of 117.0 pg/mL in treated girls, and 22.4 pg/mL in the placebo group.

The investigators said they have nothing to disclose. The National Institutes of Health funded the work.

aotto@frontlinemedcom.com

SAN FRANCISCO – Teenage girls with anorexia have less anxiety about gaining weight if their estrogen levels have been returned to normal, according to a small, randomized study, researchers from Massachusetts General Hospital and Harvard Medical School in Boston reported.

If confirmed in additional studies, it is an important finding, because anxiety about weight gain can sabotage anorexia nervosa treatment. "Physiological estrogen replacement is a potential strategy to reduce ... anxiety and improve chances of successful treatment," said lead investigator Dr. Madhusmita Misra, a pediatric endocrinologist and associate professor of pediatrics at Harvard Medical School in Boston.

Her team randomized female patients aged 13-18 years to 100-mcg transdermal estradiol twice weekly with cyclic progesterone 10 days/month, or to placebo patches and pills.

After 18 months, 20 girls on active treatment, when compared with 17 on placebo, had a significant decrease in trait anxiety, the tendency to experience anxiety as assessed by the State-Trait Anxiety Inventory for Children (–3.05 vs. 2.07, P = .01). Patients with the greatest estrogen level increases had the greatest reductions in trait anxiety scores (P = .001).

The girls were amenorrheic, with baseline estrogen levels far below normal; the intervention restored them to physiologic levels. They all met DSM-IV anorexia criteria, had bone ages of at least 15 years old, and were under treatment.

There were no significant between-group baseline differences in body mass index, psychotropic medication use, age, estrogen levels, questionnaire scores, and other factors, including weight gain over the 18 months. "We did various multiple adjustments to be sure there were not any confounders driving this association," Dr. Misra said.

Estrogen replacement did not directly affect eating attitudes assessed by the Eating Disorders Inventory II questionnaire, or body-shape perceptions assessed by the Body Shape Questionnaire (BSQ-34). However, it did seem to prevent an increase in body dissatisfaction and state anxiety – current anxiety – with weight gain, something noted in the placebo group and common in anorexia nervosa treatment.

"We have shown" before "that physiologic estrogen replacement is very important for normalizing the rate of bone accrual" in teenage girls with the condition (J. Bone. Miner. Res. 2011;26:2430-8). "This seems to be an additional benefit. These findings have the potential to [affect] therapy in anorexia nervosa with early implementation of estrogen replacement in girls who are estrogen deficient. [But,] more studies are necessary to confirm these findings; it would be premature to advise estrogen replacement just for anxiety issues," Dr. Misra said.

Estradiol levels during the study increased a mean of 117.0 pg/mL in treated girls, and 22.4 pg/mL in the placebo group.

The investigators said they have nothing to disclose. The National Institutes of Health funded the work.

aotto@frontlinemedcom.com

SAN FRANCISCO – Teenage girls with anorexia have less anxiety about gaining weight if their estrogen levels have been returned to normal, according to a small, randomized study, researchers from Massachusetts General Hospital and Harvard Medical School in Boston reported.

If confirmed in additional studies, it is an important finding, because anxiety about weight gain can sabotage anorexia nervosa treatment. "Physiological estrogen replacement is a potential strategy to reduce ... anxiety and improve chances of successful treatment," said lead investigator Dr. Madhusmita Misra, a pediatric endocrinologist and associate professor of pediatrics at Harvard Medical School in Boston.

Her team randomized female patients aged 13-18 years to 100-mcg transdermal estradiol twice weekly with cyclic progesterone 10 days/month, or to placebo patches and pills.

After 18 months, 20 girls on active treatment, when compared with 17 on placebo, had a significant decrease in trait anxiety, the tendency to experience anxiety as assessed by the State-Trait Anxiety Inventory for Children (–3.05 vs. 2.07, P = .01). Patients with the greatest estrogen level increases had the greatest reductions in trait anxiety scores (P = .001).

The girls were amenorrheic, with baseline estrogen levels far below normal; the intervention restored them to physiologic levels. They all met DSM-IV anorexia criteria, had bone ages of at least 15 years old, and were under treatment.

There were no significant between-group baseline differences in body mass index, psychotropic medication use, age, estrogen levels, questionnaire scores, and other factors, including weight gain over the 18 months. "We did various multiple adjustments to be sure there were not any confounders driving this association," Dr. Misra said.

Estrogen replacement did not directly affect eating attitudes assessed by the Eating Disorders Inventory II questionnaire, or body-shape perceptions assessed by the Body Shape Questionnaire (BSQ-34). However, it did seem to prevent an increase in body dissatisfaction and state anxiety – current anxiety – with weight gain, something noted in the placebo group and common in anorexia nervosa treatment.

"We have shown" before "that physiologic estrogen replacement is very important for normalizing the rate of bone accrual" in teenage girls with the condition (J. Bone. Miner. Res. 2011;26:2430-8). "This seems to be an additional benefit. These findings have the potential to [affect] therapy in anorexia nervosa with early implementation of estrogen replacement in girls who are estrogen deficient. [But,] more studies are necessary to confirm these findings; it would be premature to advise estrogen replacement just for anxiety issues," Dr. Misra said.

Estradiol levels during the study increased a mean of 117.0 pg/mL in treated girls, and 22.4 pg/mL in the placebo group.

The investigators said they have nothing to disclose. The National Institutes of Health funded the work.

aotto@frontlinemedcom.com

SAN FRANCISCO – Skipping breakfast triggered acute insulin resistance and elevated levels of free fatty acids in nine obese, nondiabetic women, compared with a day on which they ate breakfast in a randomized crossover trial.

If just 1 day of missing breakfast could do this, then skipping breakfast regularly over time may lead to further metabolic derangements, such as chronic insulin resistance and possible progression to type 2 diabetes mellitus, Dr. Elizabeth A. Thomas suggested.

The findings give clinicians one more tool to try to convince patients to eat a healthy breakfast, she said at the annual meeting of the Endocrine Society.

She and her associates studied the women on two separate days, approximately 1 month apart, and randomized them to receive breakfast or no breakfast at the first visit and the opposite at the second visit. They asked the women not to exercise prior to each visit and gave them a standardized dinner the night before the study day. Fasting laboratory measures were taken the morning of the study day, and 4 hours later, the participants were given a standardized lunch. The investigators took blood samples every 30 minutes after lunch for 3 hours and later gave them a standardized dinner.

Levels of insulin and glucose did not differ significantly between groups before lunch. Insulin and glucose levels were significantly higher after lunch on the days that the women skipped breakfast, representing acute insulin resistance, reported Dr. Thomas, an endocrinology fellow at the University of Colorado, Aurora.

Insulin levels rose significantly higher on the no-breakfast days, compared with after breakfast within 1 hour of the meal, and remained significantly higher at 2 hours. Similarly, the increase in glucose levels was significantly higher on the no-breakfast days within 1 hour of eating and remained significantly elevated, compared with levels on the breakfast days.

Free fatty acid levels were suppressed following breakfast, as would be expected, and thus were higher before lunch on days without breakfast. Both the total and incremental area under the curve (AUC) for free fatty acids after lunch were higher on the no-breakfast days, compared with breakfast days, suggesting that prelunch free fatty acid levels were not the cause of the increased AUC, she said.

Prelunch triglyceride levels were lower on no-breakfast days than on breakfast days. The total AUC for triglyceride levels after lunch was lower on no-breakfast days, compared with breakfast days, but the incremental AUC did not differ significantly between groups, suggesting that the prelunch triglyceride levels were driving the difference in total AUC, Dr. Thomas said.

Indirect calorimetry measures showed decreased energy expenditure on no-breakfast days and a significantly reduced respiratory quotient, which indicates greater fat oxidation, she said.

Previous epidemiologic and longitudinal studies have found associations between breakfast skipping and greater weight gain and risk for type 2 diabetes, but most of these were small studies focused on lean subjects, and none have shown a causal relationship, Dr. Thomas said. Few other short-term studies have assessed the effects of breakfast skipping on metabolic parameters and appetite.

In the study, the insulin total AUC was 12,322 microIU/mL x 180 minutes on no-breakfast days, compared with 8,882 microIU/mL x 180 minutes on breakfast days. The glucose total AUC was 20,775 vs. 18,126 mg/dL x 180 minutes on no-breakfast and breakfast days, respectively.

Prelunch free fatty acid levels on no-breakfast and breakfast days, respectively, were 705 vs. 287 microEq/L, and the total AUC for free fatty acids was 33,980 vs. 25,692 microEq/L x 180 minutes. The incremental AUC for free fatty acids was –92,980 vs. –26,008 microEq/L x 180 minutes. Prelunch triglyceride levels were 86 vs. 121 mg/dL on no-breakfast and breakfast days, respectively. The triglyceride total AUC was 17,352 vs. 24,060 mg/dL x 180 minutes on days without and with breakfast, respectively.

The women had a mean age of 29 years and a mean body mass index of 31 kg/m². Eight women said that they habitually eat breakfast. Dr. Thomas hopes to expand the study to 20 women and to include more women who habitually skip breakfast. She also plans to control for exercise in a future study.

The medical literature reports that roughly 10%-20% of Americans routinely skip breakfast, she said. Dr. Lisa Fish of the University of Minnesota, Minneapolis, who moderated a press briefing on Dr. Thomas’s study, said that many American breakfasts are high in carbohydrates and low in protein, and that eating a more balanced meal at the start of the day would be healthier.

Dr. Thomas reported having no financial disclosures. The study was funded by the Endocrine Fellows Foundation, the National Institutes of Health, and the Colorado Nutrition Obesity Research Center.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SAN FRANCISCO – Skipping breakfast triggered acute insulin resistance and elevated levels of free fatty acids in nine obese, nondiabetic women, compared with a day on which they ate breakfast in a randomized crossover trial.

If just 1 day of missing breakfast could do this, then skipping breakfast regularly over time may lead to further metabolic derangements, such as chronic insulin resistance and possible progression to type 2 diabetes mellitus, Dr. Elizabeth A. Thomas suggested.

The findings give clinicians one more tool to try to convince patients to eat a healthy breakfast, she said at the annual meeting of the Endocrine Society.

She and her associates studied the women on two separate days, approximately 1 month apart, and randomized them to receive breakfast or no breakfast at the first visit and the opposite at the second visit. They asked the women not to exercise prior to each visit and gave them a standardized dinner the night before the study day. Fasting laboratory measures were taken the morning of the study day, and 4 hours later, the participants were given a standardized lunch. The investigators took blood samples every 30 minutes after lunch for 3 hours and later gave them a standardized dinner.

Levels of insulin and glucose did not differ significantly between groups before lunch. Insulin and glucose levels were significantly higher after lunch on the days that the women skipped breakfast, representing acute insulin resistance, reported Dr. Thomas, an endocrinology fellow at the University of Colorado, Aurora.

Insulin levels rose significantly higher on the no-breakfast days, compared with after breakfast within 1 hour of the meal, and remained significantly higher at 2 hours. Similarly, the increase in glucose levels was significantly higher on the no-breakfast days within 1 hour of eating and remained significantly elevated, compared with levels on the breakfast days.

Free fatty acid levels were suppressed following breakfast, as would be expected, and thus were higher before lunch on days without breakfast. Both the total and incremental area under the curve (AUC) for free fatty acids after lunch were higher on the no-breakfast days, compared with breakfast days, suggesting that prelunch free fatty acid levels were not the cause of the increased AUC, she said.

Prelunch triglyceride levels were lower on no-breakfast days than on breakfast days. The total AUC for triglyceride levels after lunch was lower on no-breakfast days, compared with breakfast days, but the incremental AUC did not differ significantly between groups, suggesting that the prelunch triglyceride levels were driving the difference in total AUC, Dr. Thomas said.

Indirect calorimetry measures showed decreased energy expenditure on no-breakfast days and a significantly reduced respiratory quotient, which indicates greater fat oxidation, she said.

Previous epidemiologic and longitudinal studies have found associations between breakfast skipping and greater weight gain and risk for type 2 diabetes, but most of these were small studies focused on lean subjects, and none have shown a causal relationship, Dr. Thomas said. Few other short-term studies have assessed the effects of breakfast skipping on metabolic parameters and appetite.

In the study, the insulin total AUC was 12,322 microIU/mL x 180 minutes on no-breakfast days, compared with 8,882 microIU/mL x 180 minutes on breakfast days. The glucose total AUC was 20,775 vs. 18,126 mg/dL x 180 minutes on no-breakfast and breakfast days, respectively.

Prelunch free fatty acid levels on no-breakfast and breakfast days, respectively, were 705 vs. 287 microEq/L, and the total AUC for free fatty acids was 33,980 vs. 25,692 microEq/L x 180 minutes. The incremental AUC for free fatty acids was –92,980 vs. –26,008 microEq/L x 180 minutes. Prelunch triglyceride levels were 86 vs. 121 mg/dL on no-breakfast and breakfast days, respectively. The triglyceride total AUC was 17,352 vs. 24,060 mg/dL x 180 minutes on days without and with breakfast, respectively.

The women had a mean age of 29 years and a mean body mass index of 31 kg/m². Eight women said that they habitually eat breakfast. Dr. Thomas hopes to expand the study to 20 women and to include more women who habitually skip breakfast. She also plans to control for exercise in a future study.

The medical literature reports that roughly 10%-20% of Americans routinely skip breakfast, she said. Dr. Lisa Fish of the University of Minnesota, Minneapolis, who moderated a press briefing on Dr. Thomas’s study, said that many American breakfasts are high in carbohydrates and low in protein, and that eating a more balanced meal at the start of the day would be healthier.

Dr. Thomas reported having no financial disclosures. The study was funded by the Endocrine Fellows Foundation, the National Institutes of Health, and the Colorado Nutrition Obesity Research Center.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert

SAN FRANCISCO – Skipping breakfast triggered acute insulin resistance and elevated levels of free fatty acids in nine obese, nondiabetic women, compared with a day on which they ate breakfast in a randomized crossover trial.

If just 1 day of missing breakfast could do this, then skipping breakfast regularly over time may lead to further metabolic derangements, such as chronic insulin resistance and possible progression to type 2 diabetes mellitus, Dr. Elizabeth A. Thomas suggested.

The findings give clinicians one more tool to try to convince patients to eat a healthy breakfast, she said at the annual meeting of the Endocrine Society.

She and her associates studied the women on two separate days, approximately 1 month apart, and randomized them to receive breakfast or no breakfast at the first visit and the opposite at the second visit. They asked the women not to exercise prior to each visit and gave them a standardized dinner the night before the study day. Fasting laboratory measures were taken the morning of the study day, and 4 hours later, the participants were given a standardized lunch. The investigators took blood samples every 30 minutes after lunch for 3 hours and later gave them a standardized dinner.

Levels of insulin and glucose did not differ significantly between groups before lunch. Insulin and glucose levels were significantly higher after lunch on the days that the women skipped breakfast, representing acute insulin resistance, reported Dr. Thomas, an endocrinology fellow at the University of Colorado, Aurora.

Insulin levels rose significantly higher on the no-breakfast days, compared with after breakfast within 1 hour of the meal, and remained significantly higher at 2 hours. Similarly, the increase in glucose levels was significantly higher on the no-breakfast days within 1 hour of eating and remained significantly elevated, compared with levels on the breakfast days.

Free fatty acid levels were suppressed following breakfast, as would be expected, and thus were higher before lunch on days without breakfast. Both the total and incremental area under the curve (AUC) for free fatty acids after lunch were higher on the no-breakfast days, compared with breakfast days, suggesting that prelunch free fatty acid levels were not the cause of the increased AUC, she said.

Prelunch triglyceride levels were lower on no-breakfast days than on breakfast days. The total AUC for triglyceride levels after lunch was lower on no-breakfast days, compared with breakfast days, but the incremental AUC did not differ significantly between groups, suggesting that the prelunch triglyceride levels were driving the difference in total AUC, Dr. Thomas said.

Indirect calorimetry measures showed decreased energy expenditure on no-breakfast days and a significantly reduced respiratory quotient, which indicates greater fat oxidation, she said.

Previous epidemiologic and longitudinal studies have found associations between breakfast skipping and greater weight gain and risk for type 2 diabetes, but most of these were small studies focused on lean subjects, and none have shown a causal relationship, Dr. Thomas said. Few other short-term studies have assessed the effects of breakfast skipping on metabolic parameters and appetite.

In the study, the insulin total AUC was 12,322 microIU/mL x 180 minutes on no-breakfast days, compared with 8,882 microIU/mL x 180 minutes on breakfast days. The glucose total AUC was 20,775 vs. 18,126 mg/dL x 180 minutes on no-breakfast and breakfast days, respectively.

Prelunch free fatty acid levels on no-breakfast and breakfast days, respectively, were 705 vs. 287 microEq/L, and the total AUC for free fatty acids was 33,980 vs. 25,692 microEq/L x 180 minutes. The incremental AUC for free fatty acids was –92,980 vs. –26,008 microEq/L x 180 minutes. Prelunch triglyceride levels were 86 vs. 121 mg/dL on no-breakfast and breakfast days, respectively. The triglyceride total AUC was 17,352 vs. 24,060 mg/dL x 180 minutes on days without and with breakfast, respectively.

The women had a mean age of 29 years and a mean body mass index of 31 kg/m². Eight women said that they habitually eat breakfast. Dr. Thomas hopes to expand the study to 20 women and to include more women who habitually skip breakfast. She also plans to control for exercise in a future study.

The medical literature reports that roughly 10%-20% of Americans routinely skip breakfast, she said. Dr. Lisa Fish of the University of Minnesota, Minneapolis, who moderated a press briefing on Dr. Thomas’s study, said that many American breakfasts are high in carbohydrates and low in protein, and that eating a more balanced meal at the start of the day would be healthier.

Dr. Thomas reported having no financial disclosures. The study was funded by the Endocrine Fellows Foundation, the National Institutes of Health, and the Colorado Nutrition Obesity Research Center.

sboschert@frontlinemedcom.com

On Twitter @sherryboschert