Weight Loss Promoted By Drug Combination In Polycystic Ovary Syndrome

Women with polycystic ovary syndrome, or PCOS, lost significantly more weight when they took two drugs that are traditionally used to treat diabetes, rather than either drug alone, a study from Slovenia demonstrates. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

PCOS is the leading cause of infertility among women. In the United States, the disorder affects approximately 5 million women, according to the U.S. Department of Health and Human Services Office of Women's Health. This translates to 1 in 10 to 20 women, overall, who are affected. The disease probably is genetic, although the exact causes are still unknown.

In PCOS, the ovaries produce excessive amounts of male sex hormones, or androgens. The name of the disease derives from small cysts that form on the ovaries, which do not produce enough of the hormone that triggers ovulation. When this occurs, the ovarian follicles, which have filled with fluid in preparation for ovulation, remain as cysts when ovulation fails to take place. In addition to infertility, symptoms include excessive hair growth in areas that usually are relatively hairless; obesity; menstrual irregularity; thinning or balding hair on the scalp; prediabetes or diabetes; and anxiety or depression. Weight loss in these women leads to higher chances of conception, improved pregnancy outcomes and improved metabolic profile.

Treatment varies depending upon the severity of the disease, and includes lifestyle modifications and drug therapy. Some of the same medications that are used to treat diabetes also improve PCOS symptoms. One of these medications, metformin, works by regulating the hormone insulin and by suppressing androgen activity, which, in turn, helps control blood-sugar levels and has beneficial effects on ovarian function. The problem with metformin, however, is that it does not always aid with weight loss.

Because of this, investigators examined different drug combinations to see which ones caused the most weight loss. In addition to metformin, they administered another diabetes medication called liraglutide, both alone and in combination with metformin, to determine which approach led to the greatest amount of weight loss.

They found that patients who took the combined drugs lost 6.5 kilograms (kg), or about 14 pounds, on average, compared to about 4 kg, or almost 9 pounds, on liraglutide alone, and 1 kg, or about 2 pounds, on metformin alone. Furthermore, 22 percent of participants on the combined treatment lost a significant amount of weight, defined as 5 percent or more of their body weight, compared to 16 percent of those on liraglutide. No one in the metformin group achieved this amount of weight loss. In terms of body-mass index and waist circumference, the combined-treatment group saw greater improvements than either of the single-medication groups. For both of these measurements, liraglutide alone outperformed metformin alone.

"The effect of metformin on weight reduction in polycystic ovary syndrome is often unsatisfactory," said study author Mojca Jensterle Sever, MD, PhD, who served as lead author with Andrej Janez, MD, PhD, a fellow consultant at the University Medical Center in Ljubljana, Slovenia. "Short-term combined treatment with liraglutide and metformin appears better than either metformin or liraglutide alone on weight loss and decrease in waist circumference in obese women with PCOS who had been previously poor responders regarding weight reduction on metformin alone."

The main side effect was nausea, which occurred more often with liraglutide than with metformin. The nausea did improve with time, however, and was not associated with weight loss.

Study participants comprised 36 women with PCOS who had lost less than 5 percent of their body weight on a six-month course of metformin preceding the study. Their average age was 31 years. Investigators randomly assigned them to one of three treatment groups for the 12-week study, including metformin alone, liraglutide alone, and both medications.

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Research Links Two Genes To Obesity And Health Disorders

Family DNA may influence development of Metabolic Syndrome.

Two genes may be linked to obesity and health disorders according to new research by the TOPS Obesity and Metabolic Research Center at the Medical College of Wisconsin. The study of obese individuals from four generations of families shows that hereditary DNA may influence development of Metabolic Syndrome, a cluster of conditions effecting one in five Americans, which dramatically increases the risk for heart disease and diabetes. So far, the TOPS families' DNA samples have made it possible for researchers to query almost one million variations in genes that are associated with whether or not someone develops the Metabolic Syndrome and how the disease surfaces in different people.

Soon to be published in Obesity, the official journal of The Obesity Society, the report reveals evidence of two new genes that significantly impact weight gain. One gene affects the growth and development of newborn infants, as well as regulation of glucose/insulin response, lipid profiles, and body weight in adults. The other gene affects pro-inflammatory pathways, which are precursors of traits of Metabolic Syndrome.

"Our genome-wide survey could lead to the creation of early diagnostic tools for detecting risks for developing obesity, as well as the discovery of drugs targeted specifically to these genes," said Yi (Sherry) Zhang, Ph.D., instructor, Department of Medicine, Human & Molecular Genetics Center at the Medical College of Wisconsin. "This is the first published work of our genome-wide survey, and we expect a series of reports will soon follow to address other aspects of this complex disease," she added.

Zhang and her colleagues from the TOPS Obesity Center have been working to determine the full picture of the genetic makeup that encourages development of Metabolic Syndrome, including body composition, insulin resistance, and circulating blood levels of the hormone leptin, which is exclusively produced by fatty tissue.

"We've all heard such common expressions as, 'You have your mom's eyes,' or 'I developed high blood pressure in my '40s, just like my grandfather," notes Barbara Cady, TOPS President. "When we discuss 'inheritance' like this, we're relating to a question that scientists have been striving to answer for decades: how does our genetic makeup determine our traits? Knowing which genes are detrimental to our health may help researchers develop a strategic plan to treat or even prevent the symptoms that are caused by these genes."

This research is the latest in a series of papers based on the TOPS Obesity and Metabolic Research samples housed at the Medical College of Wisconsin as part of an ongoing partnership.

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Adolescent Obesity Associated With Hearing Loss

Obese adolescents are more likely than their normal-weight counterparts to have hearing loss, according to results of a new study. Findings showed that obese adolescents had increased hearing loss across all frequencies and were almost twice as likely to have unilateral (one-sided) low-frequency hearing loss. The study was recently e-published by The Laryngoscope, a journal published by the American Laryngological, Rhinological and Otological Society.

"This is the first paper to show that obesity is associated with hearing loss in adolescents," said study first author Anil K. Lalwani, MD, professor and vice chair for research, Department of Otolaryngology/Head & Neck Surgery, Columbia University Medical Center.

The study found that obesity in adolescents is associated with sensorineural hearing loss across all frequencies (the frequency range that can be heard by humans); sensorineural hearing loss is caused by damage to the inner-ear hair cells. The highest rates were for low-frequency hearing loss - 15.16 percent of obese adolescents compared with 7.89 percent of non-obese adolescents. People with low-frequency hearing loss cannot hear sounds in frequencies 2,000 Hz and below; they may still hear sounds in the higher frequencies (normal hearing range is from 20 Hz to 20,000 Hz). Often they can still understand human speech well, but may have difficulty hearing in groups or in noisy places.

"These results have several important public health implications," said Dr. Lalwani, who is also an otolaryngologist at NewYork-Presbyterian Hospital/Columbia University Medical Center. "Because previous research found that 80 percent of adolescents with hearing loss were unaware of having hearing difficulty, adolescents with obesity should receive regular hearing screening so they can be treated appropriately to avoid cognitive and behavioral issues."

Although the overall hearing loss among obese adolescents was relatively mild, the almost 2-fold increase in the odds of unilateral low-frequency hearing loss is particularly worrisome. It suggests early, and possibly ongoing, injury to the inner ear that could progress as the obese adolescent becomes an obese adult. Future research is needed on the adverse consequences of this early hearing loss on social development, academic performance, and behavioral and cognitive function.

"Furthermore, hearing loss should be added to the growing list of the negative health consequences of obesity that affect both children and adults - adding to the impetus to reduce obesity among people of all ages," said Dr. Lalwani.

In the United States, nearly 17 percent of children are obese, defined as having a body mass index (BMI) of =95 percentile. (BMI in children is expressed as a percentile; adult BMI is expressed as a number based on weight and height.) Obesity and its associated morbidities have been identified as a risk factor for hearing loss in adults.

The study analyzed data from nearly 1,500 adolescents from the National Health and Nutrition Examination Survey - a large, nationally representative sample of adolescents between the ages of 12 and 19, conducted from 2005 to 2006 by the National Center for Health Statistics of the Centers for Disease Control and Prevention. Participants were interviewed at home, taking into account family medical history, current medical conditions, medication use, household smokers, socioeconomic and demographic factors, and noise-exposure history.

Dr. Lalwani and his colleagues speculate that obesity may directly or indirectly lead to hearing loss. Although additional research is needed to determine the mechanisms involved, they theorize that obesity-induced inflammation may contribute to hearing loss. Low plasma levels of the anti-inflammatory protein adiponectin, which is secreted from adipose tissue, have been found in obese children, and low levels in obese adults have been associated with high-frequency hearing loss (which affects a person's ability to understand speech). Obesity also may contribute indirectly to hearing loss as a result of its comorbidities, including type 2 diabetes, cardiovascular disease, and high cholesterol - all of which have been reported to be associated with loss of peripheral hearing (relating to the outer, middle, and inner ear).

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Identifying Genetic Markers In Overweight Newborns Could Prevent Obesity In Later Life

Similar genetic variations occur in both overweight newborns and obese adults, a large study finds. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Our data suggest that adult obesity and newborn adiposity share, in part, a common genetic background," said study lead author Reeti Chawla, MD, fellow in pediatric endocrinology at Ann & Robert H. Lurie Children's Hospital of Chicago and the Northwestern University Feinberg School of Medicine, in Chicago, IL. "Allowing earlier identification of high-risk newborns may allow for earlier interventions to take place to possibly prevent obesity later in life. "

Obesity has become an epidemic worldwide. In the United States alone, more than one-third of adults are obese, according to the Centers for Disease Control and Prevention. Excess weight and obesity are related to numerous health problems, including heart disease, type 2 diabetes, stroke and some cancers. Since being obese in childhood increases the risk of adult obesity, medical researchers are interested in identifying early risk factors, or genetic markers, to help predict who is at greater risk for weight gain.

One of these genetic markers is called a single nucleotide polymorphism, or SNP, which is a naturally occurring genetic variant within the general population. In this case, investigators used SNPs related to adult obesity to identify genetic markers associated with higher newborn weight and skinfold thickness.

Investigators were able to identify 144 SNPs associated with birth weight or skinfold thickness. Since some of these 144 SNPs are closely linked and inherited together, they then narrowed the group down to 45 SNPs that are related to higher fat among newborns.

Investigators obtained the genetic data of 4,465 newborns from a large, multi-ethnic study examining the association between maternal blood-sugar levels and risk of poor pregnancy outcome. The study, called the Hyperglycemia and Adverse Pregnancy Outcomes, or HAPO, comprised mothers and infants from diverse ethnic backgrounds, including 1,095 Afro-Caribbean, 1,363 European, 616 Mexican-American and 1,207 of Thai descent.

Chawla said that she and her team now are using the 45 SNPs identified in this study to develop a genetic risk score "to determine whether bearing a large number of these SNPs predicts which newborns are at risk for increased fat at birth and, potentially, obesity later in life."

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Fat Tissues In Sheep Affected By Prenatal Exposure To BPA

New research suggests that fetal exposure to the common environmental chemical bisphenol A, or BPA, causes increased inflammation in fat tissues after birth, which can lead to obesity and metabolic syndrome. Results of the animal study were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

Found in plastic water bottles, older baby bottles and many other consumer products, BPA is a known hormone disrupter with estrogen-like properties. Prior research has linked BPA in both animals and humans to obesity and the metabolic syndrome, which is a cluster of metabolic risk factors that increase the chance of later developing diabetes, heart disease and stroke.

"This research is the first study to show that prenatal exposure to BPA increases postnatal fat tissue inflammation, a condition that underlies the onset of metabolic diseases such as obesity, diabetes and cardiovascular disease," said the study's lead author, Almudena Veiga-Lopez, DVM, PhD, a research investigator at the University of Michigan, Ann Arbor.

She said the study, which examines the effects of BPA on sheep, improves the understanding of how prenatal BPA exposure regulates the inflammatory response in offspring in the tissues that are relevant to development of metabolic disease. The study was conducted in the laboratory of Vasantha Padmanabhan, MS, PhD, Professor at the University of Michigan, Ann Arbor, with funding from the National Institutes of Health's National Institutes of Environmental Health Sciences. Veiga-Lopez said sheep have similar body fat to that in humans, including visceral (deep belly) fat and subcutaneous fat, which is directly below the skin.

The researchers fed two groups of pregnant sheep corn oil, either with nothing added to it or with added BPA at a dose needed to achieve BPA levels similar to those seen in human cord blood in the umbilical cord blood of the sheep offspring. Of the female offspring from the sheep, half from each group were overfed at approximately 6 weeks of age. All female offspring then were divided into four groups of nine to 12 animals each: (1) non-BPA-exposed controls that received a normal diet, (2) BPA-exposed offspring that received a normal diet, (3) overfed, obese controls and (4) overfed, obese BPA-exposed offspring.

At 15 months of age, sheep underwent a glucose tolerance test, to measure their insulin and blood sugar levels. Seven months later, the researchers collected samples of the animals' visceral and subcutaneous fat tissues to evaluate levels of two biological markers of inflammation. These biomarkers were CD68, a marker for inflammatory cells, and adiponectin, a molecule with a known role in the development of metabolic syndrome. When the adiponectin level decreases or CD68 expression increases, inflammation is worse, according to Veiga-Lopez.

Adiponectin was decreased and CD68 expression was raised in the visceral fat of both obese groups, and CD68 expression also was raised in the subcutaneous fat in normal weight, BPA-exposed female offspring, Veiga-Lopez reported. She said these results suggest that "prenatal BPA exposure and postnatal diet may interact to modulate inflammatory mechanisms in fat deposits."

Both obese groups had hyperinsulinemia, or high insulin levels, a precursor to insulin resistance, which is a prediabetic state, Veiga-Lopez reported. However, she said prenatal exposure to BPA did not lead to insulin resistance in sheep, as was true in a previous mouse study. She speculated that the hyperinsulinemia in obese offspring stems from changes that occurred in the two inflammatory markers in the visceral fat deposit.

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Research Breakthrough Of Essential Molecule Reveals Important Targets In Diabetes And Obesity

Insulin is the most potent physiological anabolic agent for tissue-building and energy storage, promoting the storage and synthesis of lipids, protein and carbohydrates, and inhibiting their breakdown and release into the circulatory system. It also plays a major role in stimulating glucose entry into muscle tissue, where the glucose is metabolized and removed from the blood following meals. But gaps exist in understanding the precise molecular mechanisms by which insulin regulates glucose uptake in fat and muscle cells.

A research team led by Assia Shisheva, Ph.D., professor of physiology in Wayne State University's School of Medicine, has made breakthrough advancements on a molecule that may provide more answers to this mystery.

The conserved phospholipid enzyme, PIKfyve, was discovered in Shisheva's lab in 1999. Based on studies in cultured cells, the lab has implicated PIKfyve in the insulin-regulated glucose transport activation, which led to the development of a unique mouse model with PIKfyve ablation, or removal, in muscle (MPlfKO), the tissue responsible for the majority of postprandial glucose disposal.

In Shisheva's recent paper, "Muscle-specific PIKfyve gene distribution causes glucose intolerance, insulin resistance, adiposity and hyperinsulinemia but not muscle fiber-type switching," published online in the American Journal of Physiology - Endocrinology and Metabolism, Shisheva and her research team characterize whether this new model exhibits metabolic defects.

"Our team found a striking metabolic phenotype in the MPIfKO mice consisting of glucose intolerance and insulin resistance at an early age and on a normal diet," said Shisheva, a resident of Royal Oak. "We also revealed that PIKfyve is essential for normal insulin signaling to GLUT4/glucose transport in muscle and provided the first in vivo evidence for the central role of PIKfyve in the mechanisms regulating healthy blood glucose levels, or glucose homeostasis."

In addition, the research team found that these metabolic disturbances were followed by increased animal fat (adiposity) and elevated levels of insulin (hyperinsulinemia), but not abnormal amounts of lipids or cholesterol in the blood (dyslipidemia).

"The combined phenotype manifested by the MPlfKO mouse closely recapitulates the cluster of typical features in human prediabetes including systemic glucose intolerance and insulin resistance, hyperinsulinemia and increased visceral obesity without dyslipidemia," said Shisheva.

"Therefore, our mouse model, in addition to providing novel mechanisms of insulin resistance, represents a valuable tool for exploring new preclinical strategies to improve treatments in individuals with prediabetes."

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CNIO Researchers Discover A New Gene Involved In Obesity

RAP1 is a gene that also protects telomeres. This is the first time that a link has been found between these structures that shorten with ageing and obesity

The discovery of an unexpected function for a gene that was associated to another process in the organism might be a solution in search of a problem, a clue to unsuspected connections. That is what has happened with RAP1, a gene that protects telomeres - the ends of chromosomes - after researchers from the Spanish National Cancer Research Centre (CNIO) surprisingly discovered its key role in obesity.

"We still don't know what evolutionary significance to attach to it, but it is at the very least interesting that a telomere gene is related to obesity", says Maria Blasco, CNIO director and co-author of the study published in the journal Cell Reports.

RAP1 forms part of the shelterin complex, a group of proteins that make up the protective hood of telomeres - the DNA sequence at the ends of chromosomes that shortens with each cellular division and thus measures the ageing of the organism. There are six shelterins, and CNIO's Telomeres & Telomerase Group, which studies them in-depth, has discovered that RAP1, contrary to the rest, is not essential for the survival of the organism; but that does not mean RAP1 is not important. The reverse is rather the case: when comparing the genomes of different species, it can be observed that RAP1 is the most conserved shelterin of all. Despite the long history of evolutionary changes, RAP1 has not changed; it is present even in yeast. This normally implies an important role in the organism, but which one?

CNIO researchers had discovered that RAP1, in addition to being located in telomeres, is also present in the rest of the chromosome; they supposed it acts regulating the action of other genes. In order to analyse this other potential function, and its importance in the organism, CNIO researchers created a lineage of mice without RAP1 and, to their surprise, discovered a model for obesity.

MICE LACKING RAP1 GAIN MORE WEIGHT

"Mice - especially female mice - without RAP1 do not eat more, but do gain weight. They suffer from metabolic syndrome, accumulate abdominal fat and present high glucose and cholesterol levels, amongst other symptoms", says Paula Martínez, first-author of the study.

The reason is that RAP1 plays an important role in the regulation of genes involved in metabolism. In particular, researchers have discovered that it acts on the same signalling pathway mediated by another protein: PPAR- gamma (PPAR-?). In fact, PPAR-? deficient mice suffer from a type of obesity "surprisingly similar" to that seen in mice without RAP1.

The next step in the research will be to study if RAP1 also plays a role in human obesity. "This discovery adds an element to the obesity equation, and opens up a possible new link between metabolic dysfunction and ageing, via a protein present in telomeres", says Blasco.

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Your Weight, Eating Behavior, Likely Impacted By What You Believe Causes Obesity

Whether a person believes obesity is caused by overeating or by a lack of exercise predicts his or her actual body mass, according to new research published in Psychological Science, a journal of the Association for Psychological Science.

Obesity has become a pressing public health issue in recent years, with two-thirds of U.S. adults classified as overweight or obese and similar trends unfolding in many developed nations. Researchers Brent McFerran of the Ross School of Business at the University of Michigan and Anirban Mukhopadhyay of Hong Kong University of Science and Technology wondered whether individual beliefs might play a role in these trends.

From an initial online survey, they discovered that people seem to subscribe to one of two major beliefs about the primary cause of obesity:

"There was a clear demarcation," says McFerran. "Some people overwhelmingly implicated poor diet, and a roughly equal number implicated lack of exercise. Genetics, to our surprise, was a far distant third."

McFerran and Mukhopadhyay wanted to dig deeper to see if the pattern could be replicated and, if so, what implications it might have for behavior. They conducted a series of studies across five countries on three continents.

Data from participants in Korea, the United States, and France showed the same overall pattern: Not only did people tend to implicate diet or exercise as the leading cause of obesity, people who implicated diet as the primary cause of obesity actually had lower BMIs than those who implicated lack of exercise.

"What surprised me the most was the fact that we found lay theories to have an effect on BMI over and above other known factors, such as socio-economic status, age, education, various medical conditions, and sleep habits," says McFerran.

The researchers hypothesized that the link between people's beliefs and their BMI might have to do with how much they eat.

A study with Canadian participants revealed that participants who linked obesity to lack of exercise ate significantly more chocolates than those who linked obesity to diet. And a study with participants in Hong Kong showed that participants who were primed to think about the importance of exercise ate more chocolate than those primed to contemplate diet.

These findings provide evidence that our everyday beliefs about obesity may actually influence our eating habits - and our body mass.

According to Mukhopadhyay, this is "the first research that has drawn a link between people's beliefs and the obesity crisis, which is growing as fast as people's waistlines are."

The new findings suggest that, in order to be effective, public health campaigns may need to target people's beliefs just as much as they target their behaviors.

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Relationship Between Short-Term Antidepressant Use, Stress, High-Fat Diet And Long-Term Weight Gain

Short-term use of antidepressants, combined with stress and a high-fat diet, is associated with long-term increases in body weight, a new animal study finds. The results were presented Sunday at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Our study suggests that short-term exposure to stress and antidepressants, rather than a high-calorie, high-fat diet alone, leads to long-term body weight gain, accompanied with increased bone and spleen weights," said study lead author Suhyun Lee, a PhD candidate in the medical sciences at the John Curtin School of Medical Research at the Australian National University in Canberra, Australia.

Antidepressants are among the most prevalent medications today, accounting for millions of prescriptions each year. In the United States, physicians wrote more than 1.5 million prescriptions for antidepressants in 2009, while physicians in Australia wrote more than 12 million of these prescriptions in 2008.

At the same time, obesity rates are climbing in developed countries worldwide. Among adults in both the United States and Australia, two-thirds are overweight or obese. Being overweight or obese is a risk factor for many serious diseases, including heart disease, which is the leading cause of death among adults in the United States and Australia.

Unfortunately, weight gain is one of the main side effects associated with antidepressants. The amount of excess weight varies between patients, but some have reported increases as high as 7 percent of the amount they weighed at the start of their antidepressant treatment.

In this study, male rats treated with the antidepressant fluoxetine after induced stress had significantly increased body weight compared to control animals. In addition to greater overall body weight, animals in the antidepressant group also developed greater bone and spleen weights, compared to animals in the control group.

"These findings may implicate different pathophysiological mechanisms in stress and antidepressant related obesity when compared to obesity that is solely diet-induced," Lee said.

During the follow-up, investigators also compared behavior between the drug and control groups. This comparison showed that the antidepressants reduced anxiety among the animals in response to induced stress. After the stressful periods, which involved physical restraint, the fluoxetine-treated animals exhibited significantly fewer symptoms of anxiety, compared to the control animals.

The study involved a two-week period of repeated restraint stress, combined with antidepressant treatment among one group of animals, and saline administration among the control group. After the two-week period, both groups of animals received a high-fat diet for 295 days.

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New Tool To Measure Sugar Consumption

Scientists at the University of Alaska Fairbanks identified a new tool that can dramatically improve the notoriously inaccurate surveys of what and how much an individual eats and drinks. Their research is published in the June 2013 issue of the Journal of Nutrition.

Conventional wisdom says that consumption of sugar-sweetened beverages such as soda and fruit juice is a significant contributor to obesity and chronic disease risk, but the science surrounding this issue is inconclusive. Part of the problem is that in a typical diet survey few people accurately and consistently recall what they consumed. The problem becomes exaggerated when people underreport foods they know are less healthy for them, like sugars.

"We were looking for an objective biomarker that could accurately measure long-term sugar intake from a single blood or hair sample" said Diane O'Brien, project leader and biologist with the UAF Center for Alaska Native Health Research at the Institute of Arctic Biology.

The biomarker O'Brien and her CANHR research group pilot-tested was the ratio of two different carbon atoms (heavy carbon 13 and light carbon 12) which are incorporated into plants during photosynthesis. The ratio, called an isotopic signature, is distinct in corn and sugar cane, which are the sources of nearly all of the sugars found in sugar-sweetened beverages.

"We used the isotopic signature of alanine an amino acid and building block of protein that essentially traps the carbon from dietary sugar so that it can be measured in the protein component of hair or blood," O'Brien said.

Even after foods and beverages are consumed, metabolized, transported in blood and stored in body tissues, these isotopic signatures remain largely intact. The more sugar-sweetened beverages an individual consumes, the greater alanine's carbon isotope ratio will be. Importantly, O'Brien's group found that alanine was uncorrelated with other foods that can contribute to elevated carbon ratios.

Although the use of isotope signatures to study food webs and diet is not new, previous efforts to accurately measure sweetener intake have not been particularly successful. The use of alanine and the technique employed by O'Brien's group makes their findings particularly exciting.

"Even for validated and well-accepted biomarkers of diet, associations with self-reported intake are generally very weak. Our biomarker was able to explain almost half of the variation in self-reported sugar-sweetened beverage intake, which in this field is a very high level of explanatory power," said O'Brien.

The scientists' findings are also being used in other health and diet-related research.

"Diane's research program has provided CANHR with incredibly valuable objectively measured biomarkers of food intake," said CANHR Director Bert Boyer. "These biomarkers are currently being used to help us understand the role polyunsaturated fatty acids play in disease prevention, including the modification of genetic risk."

The tool is not without its drawbacks, caution the authors.

"The gas chromatography-combustion-isotope ratio mass spectrometry process we used isn't inexpensive and or widely available," O'Brien said. "We expect that our findings will be most useful as a calibration tool, either for self-reported dietary data or more high-throughput biomarkers of sweetener intake."

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The Importance Of A Father's Diet Before Conception

When fathers eat a high-fat diet before conception of offspring, the male offspring have increased body weight after weaning and high body fat in midlife despite eating a low-fat diet, a new study in mice finds. The results were presented at The Endocrine Society's 95th Annual Meeting in San Francisco.

"Many researchers have studied the effects of maternal diet on the risk of obesity in their children. We found that the father's diet also affects the offspring in ways that are inherited," said the study's principal investigator, Felicia V. Nowak, MD, PhD, associate professor of molecular endocrinology at Ohio University in Athens.

The inherited differences in metabolism in the offspring of obese fathers appear to be epigenetic - changes in how genes are expressed that are "not hardwired" into the genes, meaning that they are modifiable by internal and external environmental factors, Nowak said. The cause of these changes was not behavioral because the offspring did not observe what their fathers ate nor did they have access to a high-fat diet, she noted.

In their study, the researchers fed male mice a 13-week diet that was either high fat (45 percent of calories derived from fat) or low fat (10 percent of calories from fat; control mice) but contained the same number of calories. The mice that ate the high-fat food became obese. All mice were mated with females that had received the matched low-fat diet. All their offspring received standard laboratory mouse chow.

The mouse pups underwent testing of their body weight and fat at various ages: 20 days, which was right after weaning and is similar in age to human infants or toddlers, according to Nowak; 6 weeks, which is roughly equivalent to adolescence; 6 months, or young adulthood; and finally 12 months, or older adulthood.

Compared with offspring from control mice, the male offspring of paternal mice with diet-induced obesity had higher body weight starting at 6 weeks of age, and the increased weight was still present at 6 and 12 months, the authors reported. In addition, at 6 months, the male offspring of the obese paternal mice had a higher percentage of total body fat than control offspring did. There were, however, no observed differences in the amount of brown fat, the calorie-burning fat that both rodents and humans have.

Surprisingly, male offspring of the high-fat-fed paternal mice also showed increases in voluntary running at 6 weeks. Female offspring ran more than male offspring at 6 months and 12 months, Nowak said. She said they are studying possible causes for this behavior, which might offset the increased body fat and reduce the offspring's risk of metabolic disease such as diabetes and heart disease.

"Increasing numbers of children and adolescents are affected by obesity," Nowak said. "It is essential that we identify markers for early detection and prediction of obesity and diabetes. This will enable individuals to make healthy lifestyle choices and receive targeted health care interventions to delay or prevent the related disabilities and increase life expectancy."

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Postnatal Obesity Triggered During Pregnancy

During pregnancy, the health of the mother and the intrauterine environment can have dramatic and lasting effects on the child.

Intrahepatic cholestasis of pregnancy (ICP) is a liver disease that affects 0.5-2% of pregnant women and is characterized by increased bile acid levels in the maternal serum.

In this issue of the Journal of Clinical Investigation, Catherine Williamson and colleagues at Imperial College London studied the long term impact of ICP in a cohort of Finnish families. They found that as teenagers, individuals born to women with ICP had altered metabolic profiles and increased BMI.

To further understand this effect, Williams and colleagues developed a mouse model of ICP and found that offspring of ICP mothers were more susceptible to metabolic disease and diet-induced obesity.

In the companion commentary, Susan Murphy of Duke University points out that the mouse model of ICP may also be useful in identifying other factors that predispose individuals to metabolic syndrome.

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Healthy Living Learned By Example

Kids whose moms encourage them to exercise and eat well, and model those healthy behaviors themselves, are more likely to be active and healthy eaters, according to researchers at Duke Medicine.

Their findings, published online in the International Journal of Obesity,remind parents that they are role models for their children, and underscore the importance of parental policies promoting physical activity and healthy eating.

Exercise and healthy diets are critical in fighting childhood obesity, a considerable problem in the United States, where over a quarter of kids ages two to five are already overweight or obese.

"Obesity is a complex phenomenon, which is influenced by individual biological factors and behaviors," said study author Truls Østbye, M.D., PhD, professor of community and family medicine at Duke. "But there are variations in obesity from one society to another and from one environment to another, so there is clearly something in the environment that strongly influences the obesity epidemic."

The home environment and parenting can influence a child's health by shaping dietary and physical behaviors, such as providing access to fruits and vegetables or encouraging kids to play outside.

"The 'obesiogenic' environment is broad and multi-faceted, including the physical neighborhood environment, media and advertising, and food tax policies, but we feel that the home environment is critical, particularly among children. However, we didn't have a lot of evidence as to how important this was," Østbye said.

In this study, Østbye and his colleagues examined the relationship between the home environment and behaviors related to obesity - dietary and exercise habits - among preschoolers.

The researchers studied data from 190 kids, ages two to five, whose mothers were overweight or obese. They collected information on the children's food intake over the past week, with foods rated as junk food or healthy food. To gauge their levels of physical activity, the children wore accelerometers for a week, which measured moderate to vigorous physical activity as well as sedentary time.

The mothers reported information about their children's environments, including family policies around food and physical activity, accessibility of healthy versus junk foods, availability of physical activity equipment, and whether they model healthy eating or exercise for their kids.

When they analyzed the data, the researchers found significant associations between these environmental measures and the preschoolers' physical activity and healthy versus junk food intake. They concluded that to promote healthy behaviors in children, a healthy home environment and parental role modeling are important.

For example, limiting access to junk foods at home and parental policies supporting family meals increased the amount of healthy foods kids ate. Overall, the home environment had more influence on the children's dietary habits than on their physical activity levels.

This study reminds parents that their children are watching and learning from observing their behaviors, both good and bad.

"It's hard for parents to change their behaviors, but not only is this important for you and your own health; it is also important for your children because you are a role model for them," said Marissa Stroo, a co-investigator on the study. "This might be common sense, but now we have some evidence to support this."

The researchers also looked at socioeconomic factors of the mothers, including their education levels and whether they worked, to see if this had an effect on the children's behaviors. The mother's socioeconomic factors did not affect their kids' physical activity, but had mixed results when it came to their dietary habits.

Further research is needed to better understand how a mother's socioeconomic factors influence her child's health, but it is possible that different strategies may be needed to prevent obesity in children depending on a mother's education and work status. More research is also necessary to see if the influence of the home environment changes as children get older, and if parenting strategies should adapt accordingly.

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Causal Relationship Between Adiposity And Heart Failure, And Elevated Liver Enzymes

New evidence supports a causal relationship between adiposity and heart failure, and between adiposity and increased liver enzymes, according to a study published this week in PLOS Medicine. The study, conducted by Inga Prokopenko, Erik Ingelsson, and colleagues from the ENGAGE (European Network for Genetic and Genomic Epidemiology) Consortium, also provides additional support for several previously shown causal associations such as those between adiposity and type 2 diabetes, metabolic syndrome, dyslipidemia, and hypertension.

The authors investigated whether adiposity is causally related to various cardiometabolic traits using a Mendelian randomization analysis, in which the variation in genes associated with conditions is used to assess the causal relationship between conditions. It is known that a genetic variant (rs9939609) within the genome region that encodes the fat-mass- and obesity-associated gene (FTO) is associated with increased BMI. Using genetic and health data collected in 36 population-based studies of nearly 200,000 individuals of European descent, the authors measured the strength of the causal association between BMI and cardiometabolic traits and found that higher BMI had a causal relationship with heart failure, type 2 diabetes, metabolic syndrome, dyslipidemia, hypertension, increased blood levels of liver enzymes, and several other cardiometabolic traits.

As with all Mendelian randomization studies, the reliability of the causal associations reported here depends on several assumptions made by the researchers. The authors report, "The present study addressing the role of BMI in 24 traits in up to 198,502 individuals provides novel insights in the causal effect of obesity on heart failure and increased liver enzymes levels."

They also say that this study "provides robust support to the causal relationship between obesity and a number of cardiometabolic traits reported previously. These results support global public prevention efforts for obesity in order to decrease cost and suffering from [type 2 diabetes] and heart failure."

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Longest-Ever Intervention Study Investigating Whether Weight Loss Reduces The Risk Of Heart Disease For Patients With Type 2 Diabetes

A landmark study investigating the long-term effects of weight loss on the risks of cardiovascular disease among patients with Type 2 diabetes has now concluded, with significant results published in the New England Journal of Medicine.

Conducted at the University of Pittsburgh and at clinical facilities throughout the United States, the multicenter clinical trial investigated the effects of an intensive lifestyle intervention program, intended to achieve and maintain weight loss in overweight or obese people with Type 2 diabetes, on rates of cardiovascular disease. Begun in 2001, the trial enrolled more than 5,000 people at 16 clinical centers across the United States and is the longest intervention study of its type ever undertaken for patients with diabetes.

John Jakicic, chair and professor in the Department of Health and Physical Activity in Pitt's School of Education and Director of the Physical Activity and Weight Management Research Center, served as principal investigator for the University of Pittsburgh's role in the study. He, along with colleagues throughout the University, is among the researchers comprising the national Look AHEAD (Action for Health in Diabetes) Research Group, which carried out the study and authored the New England Journal of Medicine paper.

Among the study's main findings is that weight loss among members of the study's Intensive Lifestyle Intervention group, provided with a program of weight management and increased physical activity, resulted in no difference in heart attacks and strokes when compared with the study's control group, the Diabetes Support and Education group, which was provided with only general health information and social support.

The effect of the intervention program on weight loss, however, was significant: Participants in the intervention group lost 8.7 percent of their initial body weight after one year of the study versus 0.7 percent among the control group's members; the intervention group also maintained a greater weight loss, 6 percent of their initial weight, versus 3.5 percent for the control group, at the study's conclusion.

The Look AHEAD study is the first to achieve such sustained weight loss. A weight loss of 5 percent or more in short-term studies is considered to be clinically significant and has been shown to improve control of blood pressure, blood sugar, cholesterol, and other risk factors. Comparable weight loss can also help prevent the development of Type 2 diabetes in overweight and obese adults.

"While the findings from the Look AHEAD study did not support that engagement in a weight- loss intervention was effective for reducing the onset of cardiovascular disease incidence or mortality, this does not mean that overweight adults with diabetes should not lose weight and become more physically active," said Jakicic. "Rather, there is an overwhelming amount of evidence from this study to date that has shown that weight loss and physical activity were associated with numerous other health benefits.

"These include improving physical function and quality of life, reduction in risk factors such as lipids and blood pressure with less reliance on medication, better diabetes control with less reliance on medication, improved sleep, psychological and emotional health benefits, and many others," Jakicic said. "Thus, adults with diabetes can begin to realize many of these health benefits with even modest reductions in body weight and modest increases in physical activity."

The study sought to determine whether weight loss achieved with a lifestyle program would help individuals with diabetes live longer and develop less cardiovascular disease. While short-term studies had shown that weight loss improved control of blood sugar and mitigated risk factors for heart disease and stroke in overweight and obese individuals with Type 2 diabetes, the longer-term effects of weight loss were not well studied. In particular, it was unknown whether weight loss achieved with a lifestyle intervention alone could reduce the risk of heart disease in people with Type 2 diabetes.

Type 2 is the most common form of diabetes, affecting approximately 25 million Americans over the age of 20. Complications of Type 2 diabetes include heart disease and stroke, high blood pressure, blindness, kidney disease, the nervous system disease known as neuropathy, and amputations. The total cost of Type 2 diabetes in 2012 was estimated to be $245 billion. This disease, for which there is no cure but which involves ongoing treatment, can be managed with diet, physical activity including regular exercise equal to at least 30 minutes of brisk walking each day, modest weight loss, and a variety of medications. The Look AHEAD study has shown that these lifestyle factors are effective for improving the management of Type 2 diabetes.

Study participants were individuals between 45 and 75 years of age with Type 2 diabetes and a body-mass index of 25 or greater. Sixty percent of the study participants were women, while 37 percent were from ethnic and racial minority groups.

The University of Pittsburgh's General Clinical Research Center and Clinical Translational Research Center served as participating clinical sites, with researchers here recruiting more than 330 participants over a three-year span. Jakicic credited the Division of Endocrinology within the Department of Medicine and the Department of Psychiatry in Pitt's School of Medicine, and the Department of Epidemiology in Pitt's Graduate School of Public Health, with the success of the local clinical trials.

Participants were assigned randomly to the Intensive Lifestyle Intervention group or the Diabetes Support and Education group. Members of the Intensive Lifestyle Intervention group were enrolled in a weight management program that provided individual and group support for making changes in eating behaviors and engaging in physical activity. The intervention program focused on home-based, functional activities including helping participants balance, climb stairs, and get out of a chair, among other examples. Diabetes Support and Education group members received what Jakicic called "usual care, with some very infrequent support on general health topics that were not related to diet, physical activity, or weight loss."

Participants were required to have their own health care providers manage their diabetes and other conditions. Look AHEAD did not provide medical care, but it did assist participants in finding a health care provider if they did not have one.

The Look AHEAD study was intended to run for 13.5 years, the maximum length of time researchers had determined might be required to see a difference in heart disease between two groups. After 11 years, however, the Look AHEAD Data and Safety Monitoring Board, an independent monitoring board that provides recommendations to the National Institutes of Health, reviewed the data the study had collected and determined that Look AHEAD could reach the definite conclusion that there were no differences in cardiovascular disease rates between the study's two groups.

Speculating on the failure of weight loss to reduce the risk of cardiovascular disease, researchers suggested that even greater weight loss may be necessary to reduce cardiovascular risk in diabetes patients who are overweight or obese. They also suggested that by providing participants in both groups, and their health care providers, with annual feedback on the participants' blood pressure, lipids, and blood sugar control, the cardiovascular disease risks for all experiment participants may have been reduced at a comparable rate.

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In Animal Model, Dietary Fructose Found To Cause Liver Damage

The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories.

However, a new study conducted in an animal model at Wake Forest Baptist Medical Center showed that fructose rapidly caused liver damage even without weight gain. The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.

The study is published in the American Journal of Clinical Nutrition.

"Is a calorie a calorie? Are they all created equal? Based on this study, we would say not," said Kylie Kavanagh, D.V.M., assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.

In a previous trial which is referenced in the current journal article, Kavanagh's team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period. Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group. They developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.

The big question for the researchers was what caused the liver damage. Was it because the animals got fat from eating too much, or was it something else?

To answer that question, this study was designed to prevent weight gain. Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference. Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.

Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.

Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain. At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through fecal samples and intestinal biopsies.

"What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor," Kavanagh said. "Six weeks in monkeys is roughly equivalent to three months in humans."

In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there. It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.

One of the limitations of the study was that it only tested for fructose and not dextrose. Fructose and dextrose are simple sugars found naturally in plants.

"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said. "What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.

"The liver damage began even in the absence of weight gain. This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems."

The Wake Forest Baptist team plans to begin a new study using the same controls but testing for both fructose and dextrose over a longer time frame.

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Helping Prevent Obesity Among Children Via Community-Based Programs

When it comes to confronting childhood obesity, researchers at the Johns Hopkins Bloomberg School of Public Health conclude that community-based approaches are important. A systematic review of childhood obesity prevention programs found that community-based intervention programs that incorporate schools and focus on both diet and physical activity are more effective at preventing obesity in children. The results of the study appear online in Pediatrics.

"In measuring the effectiveness of community-based programs that impact childhood obesity - more comprehensive interventions are definitely better," said Sara Bleich, PhD, associate professor inof Health Policy and Management and lead author on the paper. "The research shows that in order to help prevent obesity among children, we must focus on both diet and exercise in the communities where children live and go to school since the environment is a key contributor to obesity risk. Focusing on the community is especially important for children since they generally have little or no control over their environment."

This shift toward a stronger community focus is echoed in a recent Institute of Medicine (IOM) report, Accelerating Progress in Obesity Prevention, which recommends a comprehensive approach to childhood obesity prevention that includes the community.

Researchers examined nine studies that featured community-based interventions and found that, among those, the two interventions that included a school component effectively prevented obesity or overweight in children. Common characteristics found across most of the nine studies included the use of multiple intervention components (e.g., health education and family outreach), the inclusion of settings other than just the community (e.g., school, home, primary care, child care), and a focus on children at middle school age or younger.

"While additional research is needed to assess the full impact of community-based interventions on the prevention of childhood obesity, our conclusions indicate that more comprehensive approaches, which attempt to modify diet and exercise in the community with engagement from the schools, weigh in everyone's favor," said Bleich.

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Study Sheds Light On Molecular Basis For Metabolic Health And Disease

Inside each of us is our own internal timing device. It drives everything from sleep cycles to metabolism, but the inner-workings of this so-called "circadian clock" are complex, and the molecular processes behind it have long eluded scientists. But now, researchers at the Gladstone Institutes have discovered how one important protein falls under direct instructions from the body's circadian clock. Furthermore, they uncover how this protein regulates fundamental circadian processes - and how disrupting its normal function can throw this critical system out of sync.

In the latest issue of the Journal of Neuroscience, Gladstone Investigator Katerina Akassoglou, PhD, and her team reveal in animal models how the production of the p75 neurotrophin receptor (p75NTR) protein oscillates in time with the body's natural circadian clock - and how these rhythmic oscillations help regulate vital metabolic functions. This discovery underscores the widespread importance of p75NTR by offering insight into how the circadian clock helps maintain the body's overall metabolic health.

Virtually every organism on the planet - from bacteria to humans - has a circadian clock, a biological timing mechanism that oscillates with a period of about 24 hours and is coordinated with the cycle of day and night. And while it runs independent of external cues, it is influenced by the rhythms of light, temperature and food availability. Intriguingly, recent studies have also found a link between circadian clocks and metabolism.

"Important metabolic functions are also heavily influenced by circadian clocks, which is why activities such as chronic night-shift work - which can cause a misalignment of this clock - increase one's risk for metabolic and autoimmune diseases such as obesity, Type 2 diabetes, cancer and multiple sclerosis," said Dr. Akassoglou. Dr. Akassoglou is also a professor of neurology at the University of California, San Francisco, (UCSF) with which Gladstone is affiliated. "In this study, we pinpointed p75NTR as an important molecular 'link' between circadian clocks and metabolic health."

Originally, p75NTR was only thought to be active in the nervous system. Later studies found it to be active in many cell types throughout the body, suggesting that it impacts a variety of biological functions. Last year, Gladstone researchers discovered that p75NTR was present in the liver and in fat cells, and that it regulates glucose levels in the blood - an important metabolic process. Since these findings uncovered a link between p75NTR and metabolism, the research team tested - first in a petri dish and then in animal models - whether there was also a link between p75NTR and the circadian clock.

The team focused on two genes called Clock and Bmal1. These so-called "circadian regulator genes," and others like them, are found throughout the body. Their activity controls the body's circadian clock. The researchers wanted to see if there was a connection between these circadian genes and p75NTR.

"Our initial experiments revealed such a connection," recalls Gladstone Postdoctoral Fellow Bernat Baeza-Raja, PhD, the paper's lead author. "In individual cells, we saw that p75NTR production was controlled by Clock and Bmal1, which bind directly to the gene that codes for the p75NTR and start production of the protein."

But perhaps even more important than how p75NTR was produced was when. The team found that p75NTR production, like the circadian clock genes themselves, oscillated in a 24-hour cycle - in sync with the cells' natural circadian rhythm. Experiments in mouse models further supported these findings.

And when the team genetically modified a group of mice so that it lacked the circadian Clock gene, everything else fell out of sync. The circadian oscillation of p75NTR production was disrupted, and p75NTR levels dropped.

However, what was most fascinating, say the researchers, was how a drop in p75NTR levels then affected a variety of circadian clock systems. Specifically, the regular oscillations of other circadian genes in the brain and the liver became disrupted, as well as genes known to regulate glucose and lipid metabolism.

"The finding that a loss of p75NTR affected circadian and metabolic systems is strong evidence that this protein is intricately tied to both," said Life Sciences Institute Director Alan Saltiel, PhD, who is also a professor at the University of Michigan and was not involved in the study. "It will be fascinating to see what additional insight Dr. Akassoglou and her team will uncover as they continue to examine the role of p75NTR in circadian clocks and metabolic function."

"While these findings reveal p75NTR to be an important link between circadian clocks and metabolism, the system is complex, and there are likely other factors at play," said Dr. Akassoglou. "We are currently working to identify the relationship between the circadian clock, metabolism and the immune system, so that one day we could develop therapies to treat diseases influenced by circadian clock disruption - including not only obesity and diabetes, but also potentially multiple sclerosis and even Alzheimer's disease."

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Obese Women Who Skip Breakfast At Greater Risk For Insulin Resistance

Overweight women who skip breakfast experience acute, or rapid-onset, insulin resistance, a condition that, when chronic, is a risk factor for diabetes, a new study finds. The results, which were presented at The Endocrine Society's 95th Annual Meeting in San Francisco, suggest that regularly skipping breakfast over time may lead to chronic insulin resistance and thus could increase an individual's risk for type 2 diabetes.

"Our study found that acute insulin resistance developed after only one day of skipping breakfast," said the study's lead author, Elizabeth Thomas, MD, an endocrinology fellow at the University of Colorado School of Medicine in Aurora.

In insulin resistance, a person requires more insulin to bring their glucose, or blood sugar, into a normal range, she explained.

Thomas and co-workers studied nine nondiabetic women, with an average age of 29, who were overweight or obese. The study took place on two days about a month apart. Subjects were randomly assigned to receive either breakfast or no breakfast at the first visit and the opposite at the second visit. Four hours later, all subjects ate the same standardized lunch at each visit. They had blood samples taken every 30 minutes after lunch for three hours to test their insulin and glucose levels.

It is normal for glucose levels to rise after eating a meal, which then triggers insulin production. The researchers found, however, that the women's insulin and glucose levels after lunch were significantly higher on the day they skipped breakfast than on the day when participants ate breakfast. The higher levels demonstrated acute insulin resistance because of skipping breakfast, according to Thomas.

It was not clear if this "heightened metabolic response" was temporary or lasting, but it may contribute to the development of chronic insulin resistance, she said. When the body becomes permanently resistant to the effects of the hormone insulin, sugar builds up in the blood, which can lead to prediabetes and diabetes over time.

"This information should help health care providers in counseling patients as to why it is better to eat a healthy, balanced breakfast than to skip breakfast," Thomas said.

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Trying To Lose Weight? Go Herbal

These days, there is a great need for overweight Americans to lose those excess pounds. Being healthy would not only lead them to have a healthier lifestyle but it will also literally lighten their load, and improve their overall well-being.

There is a long list of dieting options available. There are exercise programs, exercise machines, dietary supplements, dietary food and drinks, diet pills - there are even soaps which claim to help you lose pounds while you bathe.

One other available option to shed off those unwanted pounds is to go herbal.

Herbal weight loss products have been in great demand for people who want to lose weight the natural way. However, when you take herbal supplements to lose weight, you would have to wait for a longer time for the results because of the more subtle effects of medicines which came from plants and natural herbs.

Here are some herbal weight loss options that you might want to consider:

1. Herbal weight loss products

There are a lot of herbal weight loss products available in the market now. You can check out the Internet and you will find a lot of herbal weight loss pills and products.

Be careful, however, as there are some products which claim to be safe and natural because they are herbal, but some actually have side effects because of non-extensive research on the effects of these products.

Here are some ingredients and chemicals which make up some herbal weight loss products that you should watch out for, as they might have harmful effects to your health:

> Senna. This is an herbal laxative. Senna is a main ingredient in weight loss teas, and it works by stimulation the colon. The downside effect of this herb is dehydration. It can also lead to colon problems and can become addictive. Some people, when addicted, are unable to perform bowel movements without it, so watch out.

> Chromium picolinate. This is a synthetic compound found in herbal weight loss products. Chromium is a nutrient which helps regulate blood-sugar level. However, this ingredient, when taken in high doses, may cause damage in the chromosomes. It can also lead to dehydration.

> St. John's wort. This supplement increases the production of a chemical in the brain. If not used properly, it may cause eye and skin sensitivity, mild gastrointestinal distress, fatigue and itching.

Although a lot of herbal products claim to be safe and natural, it is better to scrutinize the ingredients and research about the effects of the product itself before going for these herbal dietary pills.

2. Organic food

In Wichita, Kansas, organic food has found its way to more homes and restaurants. Organic food devotees believe that consuming organic goodies help their bodies as well as the environment.

A person who buys organically raised eggs and vegetables claim to be healthier, and they are not spending money on doctors and prescriptions as these keep them healthier and away from the hospital. This could also be an option for weight watchers, as organic food is known to be kinder to your weight than chemically-processed food products.

3. Green Tea

Studies show that intake of green tea, or green tea extracts burns extra calories. Also, green tea with caffeine can increase fat burning by up to 40% thereby reducing fat.

This is one good option for those who want to lose weight. In a study done, people who took green tea were found to lose 2 to 3 times more weight than those who did not drink green tea.

These results show that green tea is a natural product for the treatment of obesity. Thus, it also makes for a healthier dietary option, not to mention the good effects that it has on the body as compared to caffeine. A cup of tea gives an emmediate energy lift without the side effects of caffeine.

3. Caffeine

Coffee provides an energy boost to increase fat burning. Caffeine also provides a likelihood to be active, which in turn increases your rate of calorie burn.

4. Immortality Herb

This herb, whose scientific name is Gymnostemna Pentaphyllum, is known to have the following benefits:

> increases healthy blood flow

> reduces artery blocks

> aids healthy blood pressure

> increases the rate of fat burning

5. Apple Cider Vinegar

There are pills and food supplements whose main ingredient is apple cider vinegar. Here are the benefits of taking this herbal option:

> weight loss

> improved cholesterol level

> improved high blood pressure

> helps prevent rheumatoid arthritis