Young people who sleep less may be more likely to be overweight, especially if they spend less time in rapid eye movement (REM) sleep, according to a report released on August 4, 2008 in Archives of General Psychiatry, one of the JAMA/Archives journals.
The obesity epidemic in the United States is well recognized, and has been occurring even in children. According to the background information in the article, the obesity rate in children between 6 and 11 years old has more than tripled in the last 30 years, and about 17% of the adolescents in the population are classified as obese or overweight presently. Obesity is generally caused by an uneven caloric intake and energy use balance, but there are many factors that could potentially affect obesity that are not well understood. Previously, an association has been suggested between fewer hours of sleep and a higher body mass index (BMI) in both adults and children.
To investigate this relationship in children, Xianchen Liu, M.D., Ph.D., of the University of Pittsburgh School of Medicine Department of Psychiatry and Western Psychiatric Institute and Clinic of the University of Pittsburgh Medical Center, and colleagues studied a total 335 children between the ages of 7 and 17 years. The subjects were observed using polysomnography for three nights in a row. Once sleep time, time spent in REM sleep, the time it took to fall asleep and other variables were observed, they were compared to a BMI calculation made using weight and height.
The researchers found that 14.6% of participants (49 youths) were at risk for becoming overweight, while 13.4% (45 youths) were already overweight. Comparing these children with those who had normal weights, the higher weight children slept approximately 22 fewer minutes per night. Additionally, their sleep efficiency, defined as the percentage of time that the subject remained asleep, was lower, their REM sleep time was shorter, they had less REM activity even in REM sleep, and took longer to reach their first REM sleep periods.
In all, one hour less of total sleep was associated with twice the risk of being overweight. Having one hour less of REM sleep was associated with three times the risk.
The authors note that there are many possible explanations for this association: "Although the precise mechanisms are currently under investigation, the association between short sleep duration and overweight may be attributed to the interaction of behavioral and biological changes as a result of sleep deprivation." For one, hormone levels may fluctuate differently when someone experiences loss of sleep, which could affect hunger. Additionally, the fatigue associated with sleep loss could lead to fatigue which reduces the amount of exercise experienced, thereby reducing the energy expenditure of the person.
The authors conclude that by improving sleep in this age group, some of the obesity experienced in this age group might be mitigated. "Given the fact that the prevalence of overweight among children and adolescents continues to increase and chronic sleep insufficiency becomes more prevalent in modern society, family- and school-based sleep interventions that aim to enhance sleep hygiene and increase sleep duration may have important public health implications for the prevention and intervention of obesity and type 2 diabetes in children," they say. "Furthermore, our results demonstrate an important relationship between REM sleep and high BMI and obesity, suggesting that the short sleep"obesity association may be attributed to reduced REM sleep time and decreased activity during REM sleep."
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Wednesday, August 13, 2008
Young People Who Sleep Less Have More Risk Of Being Overweight
Eating Eggs Boosts A Healthy Weight Loss Plan
A study published online in the International Journal of Obesity shows that eating two eggs for breakfast, as part of a reduced-calorie diet, helps overweight adults lose more weight and feel more energetic than those who eat a bagel breakfast of equal calories. [1] This study supports previous research, published in the Journal of the American College of Nutrition, which showed that people who ate eggs for breakfast felt more satisfied and ate fewer calories at the following meal. [2]
"People have a hard time adhering to diets and our research shows that choosing eggs for breakfast can dramatically improve the success of a weight loss plan," said Nikhil V. Dhurandhar, Ph.D., lead researcher and associate professor in the laboratory of infection and obesity at Pennington Biomedical Research Center, a campus of the Louisiana State University system. "Apparently, the increased satiety and energy due to eggs helps people better comply with a reduced-calorie diet."
Significant Weight Loss Related to Egg Breakfast
Compared to the subjects who ate a bagel breakfast, men and women who consumed two eggs for breakfast as part of a reduced-calorie diet:
- lost 65 percent more weight
- exhibited a 61 percent greater reduction in BMI
- reported higher energy levels than their dieting counterparts who consumed a bagel breakfast [1]
The egg and bagel breakfasts provided the same number of calories and had identical weights (energy density), which is an important control factor in satiety and weight loss studies.
The researchers also found that blood lipids were not impacted during the two month study. They found that blood levels of HDL and LDL cholesterol, as well as triglycerides, did not vary compared to baseline cholesterol blood levels in subjects who ate either the bagel or egg breakfasts. These findings add to more than 30 years of research that conclude that healthy adults can enjoy eggs without significantly impacting their risk of heart disease.
New Emphasis on the Importance of High-Quality Protein
This study adds to the growing body of research which supports the importance of high-quality protein in the diet. The American Journal of Clinical Nutrition (AJCN) published a special issue in May 2008, which contains nine articles that focus on the value of high-quality protein in the American diet. A major finding was that not getting enough high-quality protein may contribute to obesity, muscle wasting (loss) and increased risk of chronic disease. [3,4]
Jump Start the Morning with Eggs
Jackie Newgent, registered dietitian and chef, stresses the importance of obtaining adequate high-quality protein when advising consumers about weight loss. "Eggs are a good source of all-natural, high-quality protein, so they can help keep you satisfied longer, making it easier to resist tempting snacks," said Newgent. "Nearly half of an egg's protein, and many of the other nutrients, are found in the yolk, so make sure to eat the whole egg for maximum benefits."
Newgent suggests these nutrition tips for a successful weight loss plan:
- Manic Monday: Make a batch of hard-cooked eggs on Sunday, so you'll have all-natural, high-quality protein meals for your on-the-go schedule during the week. Plus, eggs are incredibly affordable. At an average of $1.93 per dozen (or $0.16 per egg), [5] eggs are one of the most affordable high-quality protein foods in the marketplace.
- In-a-Minute Morning Meal: In less than 60 seconds, you can prepare an egg breakfast to help jump start your day. Simply beat one whole egg in a microwave-safe mug then cook in the microwave oven on high for 60 seconds. Slide the egg onto a whole grain English muffin. Add flavor with a sprinkling of fresh herbs, salsa, or cheese. Serve fresh seasonal fruit slices, like peaches in the summer, on the side for a balanced meal.
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Scientists Identify Another Piece Of The Weight-Control Puzzle - Research Finds Role For GABA Neurotransmitter In Maintaining Energy Balance
Controlling body weight is a complicated process, as any frustrated dieter might attest. But as scientists continue to investigate the brain's intricate neurocircuitry and its role in maintaining energy balance, they are forming a clearer picture of the myriad events that lead to weight gain and weight loss.
In the August 10 on-line issue of Nature Neuroscience, a study led by scientists at Beth Israel Deaconess Medical Center (BIDMC) identifies another piece of this complex puzzle, demonstrating that the neurotransmitter GABA --one of the master communicators among neurons - plays a role in controlling energy balance.
"Body weight maintenance is made up of three basic stages," explains the paper's senior author Bradford Lowell, MD, PhD, an investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC whose laboratory is working to identify the specific neurocircuits responsible for controlling food intake and/or energy through functional neuroanatomical mapping studies.
"In the first stage, the brain receives sensory input from the body [including information provided by circulating hormones such as leptin and ghrelin and from fuels such as glucose and fatty acids]," says Lowell, who is also a Professor of Medicine at Harvard Medical School.
In the second stage, he adds, the brain integrates this sensory information with cues it has received from the environment (such as aromas and other enticements) along with information gathered from the organism's emotional state. Then, in the final stage, the brain's neurocircuitry takes over, enabling the brain to make appropriate alterations in food intake and energy expenditure in order to maintain energy balance - and prevent weight gain and obesity.
Previous work had primarily focused on identifying the neuropeptides involved in this process. And indeed, this group of neurotransmitters often proves essential to maintaining energy balance - but not always.
"It is well known that AgRP [Agouti-related protein] neurons play a critical role in feeding and energy balance regulation," explains Qingchun Tong, PhD, a postdoctoral fellow in the Lowell laboratory and the study's first author. "However, the deletion of AgRP and NPY [two neuropeptides released from the AgRP neurons] produces little metabolic effect."
An alternate theory proposed that release of the GABA neurotransmitter was mediating the function of AgRP neurons, an idea that had long been postulated but never examined.
To test this hypothesis, Tong and his colleagues generated a group of mice with disrupted release of GABA specifically from the AgRP neurons. As predicted, the genetically altered mice exhibited profound metabolic changes.
"The mice with AgRP neuron-specific disruption of GABA release were lean, had higher energy expenditure and showed resistance to diet-induced obesity," says Tong. "We also found that these animals showed reduced food intake response to the hormone ghrelin. This suggests to us that the neurocircuit engaging GABA release from the AgRP neurons mediates at least part of ghrelin's appetite-stimulating action."
A series of studies to examine the function of glutamate and GABA release from other groups of neurons are currently underway as investigators continue to dissect the brain's neurocircuitry.
"As these new findings demonstrate, GABA release is an important component that mediates the function of AgRP neurons," says Tong. "Discoveries such as this will ultimately help us to design an efficient strategy to tackle the current epidemic of obesity and metabolic disease."
This work was funded, in part, by grants from the National Institutes of Health and support from the North American Association for the Study of Obesity.
In addition to Lowell and Tong, coauthors include BIDMC investigators Chian-Ping Ye and Juli Jones and University of Texas Southwestern Medical Center investigator Joel Elmquist.
Beth Israel Deaconess Medical Center is a patient care, teaching and research facility of Harvard Medical School and consistently ranks among the top four in National Institutes of Health funding among independent hospitals nationwide. BIDMC is clinically affiliated with the Joslin Diabetes Center and is a research partner of Dana-Farber/Harvard Cancer Center. BIDMC is the official hospital of the Boston Red Sox. For more information, visit http://www.bidmc.harvard.edu.
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5 Tips to Get a Flat Stomach
- Did you you know that crunches and situps actually do NOT flatten your abs effectively?
- Did you know that there is a specific type of exercise that burns belly fat faster than cardio?
- Did you know that certain foods such as soy proteins, "diet" drinks, and others can actually increase your stomach fat?
More details in the article below.
5 Facts You MUST Understand if You Are Ever Going to Lose Your Belly Fat & Get Six Pack Abs
1. Many so-called "health foods" are actually cleverly disguised junk foods that actually stimulate you to gain more belly fat... yet the diet food marketing industry continues to lie to you so they can maximize their profits.
2. Ab exercises like crunches, sit-ups, and ab machines are the LEAST effective method of getting flat six pack abs. We'll explore what types of exercises REALLY work in a minute.
3. Boring repetitive cardio exercise routines are NOT the best way to lose body fat and uncover those six pack abs. I'll show you the exact types of unique workouts that produce 10x better results below.
4. You DON'T need to waste your money on expensive "extreme fat burner" pills (that don't work) or other bogus supplements. A special class of natural foods is much more effective. I'll tell you about these natural foods and their powers below.
5. Ab belts, ab-rockers, ab-loungers, and other infomercial ab-gimmicks... they're all a complete waste of your time and money. Despite the misleading infomercials, the perfectly chiseled fitness models in the commercials did NOT get their perfect body by using that "ab contraption"... they got their perfect body through REAL workouts and REAL nutrition strategies.
Decisions Under Pressure: It's All In The Heart Beat
A person's heart rate can reveal a lot about how they make decisions when feeling stressed, a Queensland University of Technology academic says.
Economics Associate Professor Uwe Dulleck, from the QUT Business Faculty, said stress in the workplace wasn't necessarily a bad thing, because it was, in fact, a natural reaction that had been given a negative connotation.
Professor Dulleck is leading the Australian arm of a study that was awarded an Australian Research Council grant to study the effects of both positive and negative stress on workers' decision-making.
"The study will use heart rate monitors to measure the stress of people 'on the job' and in the controlled environment of an experimental economics computer laboratory as they interact and communicate," Professor Dulleck said.
"We will measure how much they are stressed in certain situations and whether that is positive or negative stress, this will be measured against how they behaved and what decisions they made - whether they made rational or emotional decisions."
Professor Dulleck said negative stress could be detected by measuring a person's heart beat and its variations over short intervals of time.
"If the heart rate varies, it shows that the body is relaxed with an activity and is feeling positive stress," he said. "In this case the body is more flexible to react to the demands of the situation".
"But if the variations are very limited it shows that the body is not at ease with this activity. This kind of stress hardens the body and makes it operate in a more regular way. In such situations, the body works more like a motor engine - highly efficient in some respects but also more likely to break if unexpected challenges arise.
"We are trying to find what effect this has on decision-making."
Professor Dulleck said study participants would be monitored as they played two games: a game of chance to see what kind of decisions they made when uncertain; and a negotiation game, both before and after socialising with their "opponent", to see what affect communication had on cooperation.
"We will also look at whether they took high or low risks in the game of chance, to learn about attitudes towards risk and whether an individual's worry is over losing money, or the risk of chance itself," he said.
Professor Dulleck said knowing what caused positive and negative stress in individuals and what effect this had on decision making would help businesses improve work for their staff and managers.
"Knowing how stress affects people's behaviour will help in designing training programs for employees as well as achieving a better work-life balance and avoiding burn-out syndromes," he said.
The study is being undertaken in conjunction with Associate Professor Benno Torgler and Dr Cameron Newton from the QUT Centre of Philanthropy and Nonprofit Studies, and three Austrian business partners; a human resources company, a construction company and a nonprofit organization.
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Yoga And Meditation Change Gene Response To Stress
Research from the US suggests that mind body techniques like yoga and meditation that put the body in a state of deep rest known as the relaxation response, are capable of changing how genes behave in response to stress.
The study is the work of researchers at Benson-Henry Institute for Mind/Body Medicine at Massachusetts General Hospital (MGH) and the Genomics Center at Beth Israel Deaconess Medical Center (BIDMC) and is published online in the open-access journal PLoS One.
Mind-body practices that produce a relaxation response have been used by people across cultures for thousands of years to prevent and treat disease, wrote the authors in their background to the study.
The relaxation response is characterized by reduction in oxygen intake, increase in exhalation of nitric oxide, and lower psychological distress. Many experts see it as the counterpart to the "flight or fight" stress response that has already been shown by a number of studies to have a distinct pattern of physiological and gene expression changes (called "transcriptional profile").
The researchers for this study wanted to test the idea that the relaxation response also produces changes in gene expression.
The researchers recruited three groups of people. In the first group (called the M group) there were 19 long term practitioners who had been practising various ways of producing the relaxation response every day for a long time (for instance with daily yoga, repeated prayer or meditation practice).
In the second group were another 19 people who they called the "healthy controls" (group N1), who were not daily practitioners, and the third group was like the healthy controls group, except these 20 people completed 8 weeks of relaxation response training (this group was N2).
The researchers assessed transcriptional profiles of the people in all three groups from blood samples.
They found the expressions of a total of 2,209 genes were significantly different between groups M and N1, and a total of 1,561 genes were similarly significantly different between groups N2 and N1.
More importantly, however, was the fact 433 of the genes were common to both sets of comparisons: the same ones were different between M and N1 and between M and N2, so even short term practise of the relaxation response appeared to produce changes in these 433 gene expressions.
Further analysis using techniques called gene ontology and gene set enrichment, showed that groups M and N1 (the long term and the short term practitioners of the relaxation response) exhibited similar physiological changes such as in "cell metabolism, oxidative phosphorylation, generation of reactive oxygen species and response to oxidative stress".
A second phase of the study involving 5 N1 healthy controls, 5 N2 short term practitioners, and 6 M long term practitioners, was done to validate a significant number of genes and pathways.
The authors concluded that:
"This study provides the first compelling evidence that the RR [relaxation response] elicits specific gene expression changes in short-term and long- term practitioners."
They wrote that their findings suggest:
"Consistent and constitutive changes in gene expression resulting from RR may relate to long term physiological effects," and that "Our study may stimulate new investigations into applying transcriptional profiling for accurately measuring RR and stress related responses in multiple disease settings."
Dr Herbert Benson, director emeritus of the Benson-Henry Institute and co-senior author of the study said:
"Now we've found how changing the activity of the mind can alter the way basic genetic instructions are implemented," said Benson.
Dr Towia Libermann, director of the BIDMC Genomics Center and also co-senior author of the study added that:
"This is the first comprehensive study of how the mind can affect gene expression, linking what has been looked on as a 'soft' science with the 'hard' science of genomics."
"It is also important because of its focus on gene expression in healthy individuals, rather than in disease states," explained Libermann.
The authors said their study showed that the relaxation response changed the expression of genes involved with inflammation, programmed cell death and the handling of free radicals. Free radicals are normal byproducts of metabolism that the body neutralizes in order to stop damage to cells and tissues.
Co-lead author of the study Dr Jeffery Dusek formerly of the Benson-Henry Institute and now with the Abbott Northwestern Hospital in Minneapolis said:
"Changes in the activation of these same genes have previously been seen in conditions such as post-traumatic stress disorder; but the relaxation-response-associated changes were the opposite of stress-associated changes and were much more pronounced in the long-term practitioners."
Benson said that people across different cultures have been using mind body techniques for thousands of years. They found that it didn't particularly matter which techniques was used, whether it was meditation, yoga, breathing, or repetitive praying, they acted via the same underlying mechanism.
"Now we need to see if similar changes occur in patients who use the relaxation response to help treat stress-related disorders, and those studies are underway now".
Libermann said they used "cutting edge" genomic analysis and the "latest bioinformatics tools to identify potential gene functions, generating hypotheses that can then be tested in laboratory or clinical studies."
"There are a lot of differences in gene expression between one healthy person and another, so it is challenging to analyze the kinds of subtle changes we are seeing and identify what changes are significant and what are just background noise," explained Libermann.
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Gene/Stress Interaction Increases Cognitive Decline In Elderly
The negative effects of stress on cognitive functioning appear to be amplified by a genetic variation associated with Alzheimer's disease, a new federally funded study has found. The genetic variation may, in effect, accelerate the development of age-related cognitive decline by as much as eight years.
Researchers from the Baltimore Memory Study report in The American Journal of Psychiatry (AJP), the official journal of the American Psychiatric Association, that a high level of the stress hormone cortisol in study participants aged 50 to 70 years was associated with worsened cognitive abilities. The researchers also found that the effect was greater among those with a common form of the gene for apolipoprotein E (APOE), which has been shown to increase the risk for Alzheimer's disease.
This gene-environment interaction is reported by Brian Lee, M.H.S., Brian Schwartz, M.D., and colleagues at Johns Hopkins University. The group's findings will be presented online on July 1 under AJP in Advance . The effect appears to increase as the number of copies of a specific APOE gene in the individual increases. Everyone inherits two versions of the APOE gene, known as alleles - one from each parent. The most common APOE alleles are epsilon-2, -3, and -4. Having at least one epsilon-4 allele increases an individual's risk of late-onset Alzheimer's disease. Individuals with two copies of the esiplon-4 version of the gene are particularly susceptible to the damaging effects of cortisol in the brain.
"Our findings indicate that the APOE epsilon-4 allele may increase vulnerability of the aging brain to elevated cortisol levels," said lead author Lee, a doctoral student in epidemiology at the Johns Hopkins Bloomberg School of Public Health. "While our results remain to be replicated, the observed cortisol-APOE interaction is intriguing since both cortisol and APOE have been implicated in cognitive decline associated with aging as well as in Alzheimer's disease."
The effects on cognitive functioning extended to six of the seven areas that were studied: language, eye-hand coordination, executive functioning, verbal memory/learning, visual memory, and ability to copy a complex visual design.
The deficits are similar in magnitude to those seen with advancing age. The authors estimated the equivalent years of increased age, represented by the poorer cognition of the study participants with high cortisol and the epsilon-4 form of the APOE gene. For language ability, the lower scores of people with high cortisol levels and one epsilon-4 copy were comparable to an age increase of eight years. For those with two epsilon-4 copies, the comparable age increase was even larger.
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Late Onset Hypogonadism, ADAM, Andropause: What Is It And What Is The Treatment?
Late-onset hypogonadism (LOH), or androgen decline in the aging male, is a syndrome caused by the well-known decline in gonadal production of androgens in males that occurs with aging. It is characterized by clinical symptoms that accompany low serum androgen levels. LOH affects a wide range of organ systems and has a broad severity of clinical presentations. Sexual dysfunction, including erectile dysfunction (ED), decreased libido, difficulty achieving orgasm, and decreased penile sensation, is usually the presenting complaint, although fatigue, depressed mood, impaired cognition, and decreased muscle mass are other common symptoms. If these symptoms are found in conjunction with low serum testosterone (T), a diagnosis of LOH may be made. Universally accepted guidelines for a level of T to define or treat LOH have not been established. In general, when the T level is found to be at or below the lower limit of normal, in conjunction with symptoms, treatment is appropriate.
The incidence of LOH is rising. Serum T levels decrease with age and according to U.S. Census data from 2000, the U.S. population of men 65 years of age and older is projected to double by the year 2030. An extrapolation from the Massachusetts Male Aging Study found a prevalence of LOH of almost half a million new cases per year in men in their fifth, sixth, and seventh decades of life. The principal treatment for LOH is androgen replacement, also known as testosterone replacement therapy (TRT). With the rising incidence of LOH and better understanding of treatment benefits, the use of TRT has been steadily increasing in recent years. This rise is evidenced by a 500% increase in prescription sales of T since 1993.
The benefits of TRT are easily recognized, primarily because as levels of serum T normalize, desired improvements in sexual function, libido, and mood, as well as in overall quality of life are reached. TRT also has a positive effect on cardiovascular health; one well-documented effect of TRT is a decrease in total cholesterol and low-density lipoprotein (LDL)1. Recent studies have shown a link between hypogonadism and a high-risk and increasingly prevalent syndrome called metabolic syndrome, also known as insulin resistance syndrome, or syndrome X. Metabolic syndrome is characterized by at least 3 of the following: abdominal obesity, hypertriglyceridemia, low high-density lipoprotein (HDL), hyperglycemia, and hypertension2. Laaksonen and colleagues have suggested that hypogonadism is an element of metabolic syndrome based on their large population-based study. Treatment of LOH with TRT may improve the symptoms of metabolic syndrome, and vice versa, treatment of metabolic syndrome may improve the symptoms of LOH.
Despite its benefits, TRT has a number of contraindications, and questions remain regarding its effects on prostate health. Benign prostatic hyperplasia (BPH) is an androgen-sensitive disease which is accelerated by endogenous and exogenous T. The incidence of BPH increases with age, and prostate volume is decreased in hypogonadal men compared to men with normal serum T. Prostate volumes of men with LOH undergoing TRT increase up to the levels of age-matched controls, but TRT has not been shown to drastically increase prostate volume beyond that of eugonadal men of the same age. Similar to BPH, prostate cancer (CaP) is exquisitely androgen sensitive. First-line treatment for metastatic CaP is androgen deprivation, either through bilateral orchiectomy or medical castration with gonadotropin-releasing hormone agonists. While numerous studies have failed to show that exogenous T is a direct cause of CaP, the fact that CaP is androgen sensitive raises the question of whether T can awaken a clinically insignificant CaP or augment a CaP into a higher Gleason grade.
Short-term changes in prostate-specific antigen (PSA) levels during TRT have been reported. Much of this data is derived from relatively small, often retrospective studies. A definitive double-blind, randomized, placebo-controlled study on the effect TRT has on PSA has yet to be published. A systematic review of 18 studies of short-term TRT for men with LOH performed in 2003 found an average PSA increase of 0.3 ng/mL, and a systematic review of 6 other published studies of TRT in slightly older men with LOH found a slightly higher average PSA increase of 0.43 ng/mL. The long-term effects TRT has on PSA, however, have yet to be reported.
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Worry And Sleepless Nights Increase Risk Of Diabetes In Men
New research claims that psychological distress including anxiety, insomnia, depression, apathy and fatigue can more than double the risk of developing Type 2 diabetes in older men.
Scientists looked at 2,127 men, born between 1938 and 1957, who had normal blood glucose levels. They determined their level of psychological distress both at the beginning and end of the study. The men were tested for diabetes eight to ten years later and it was found that the men with the highest levels of psychological distress were 2.2 times more likely to develop Type 2 diabetes than those with the lowest levels. Altogether 103 men developed Type 2 diabetes. The study also looked at 3,100 middle-aged women but found that there was not an increased risk of diabetes in those with high levels of psychological distress.
More research is needed
"It is intriguing that the increased risk of diabetes occurs in men only and it would be interesting to find out why. The results suggest that it could be due to a hormonal or behavioural influence. We already know from previous studies that stress is considered to be a risk factor for Type 2 diabetes and others have looked at the link between sleep disorders, such as insomnia, and the condition. This research appears to confirm that there might be something in this," said Dr Iain Frame, Director of Research at Diabetes UK.
"We know that risk factors which increase the risk of Type 2 diabetes are being white and over 40 years old, or of black or South Asian origin and over 25 years old, having a family member with the condition, being overweight and having high blood pressure. If you have two or more of these risk factors, you should see your GP for a simple test."
Other factors
Professor Anders Ekbom from the Unit of Clinical Epidemiology at the Karolinska Institute, Sweden, conducted the study. "Genetic and environmental factors are involved in the development of Type 2 diabetes. We already knew that psychological distress and depression are risk factors for heart disease and suspected they may play a part in developing Type 2 diabetes, which is corroborated by this research," he said."
The link could be a result of the way psychological distress affects the brain's role in regulating hormones or perhaps because depression influences a person's diet and level of physical activity in a negative way."
The study was published in the journal 'Diabetic Medicine'.
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