Obesity and Diet 5

Anti-inflammatory diet linked to reduced risk of early death

September 13, 2018

Science Daily/Wiley

Adhering to an anti-inflammatory diet was associated with lower risks of dying from any cause, dying from cardiovascular causes, and dying from cancer in a recent Journal of Internal Medicine study.

 

In the study of 68,273 Swedish men and women aged 45 to 83 years who were followed for 16 years, participants who most closely followed an anti-inflammatory diet had an 18% lower risk of all-cause mortality, a 20% lower risk of cardiovascular mortality, and a 13% lower risk of cancer mortality, when compared with those who followed the diet to a lesser degree. Smokers who followed the diet experienced even greater benefits when compared with smokers who did not follow the diet.

 

Anti-inflammatory foods consist of fruits and vegetables, tea, coffee, whole grain bread, breakfast cereal, low-fat cheese, olive oil and canola oil, nuts, chocolate, and moderate amounts of red wine and beer. Pro-inflammatory foods include unprocessed and processed red meat, organ meats, chips, and soft-drink beverages.

 

"Our dose-response analysis showed that even partial adherence to the anti-inflammatory diet may provide a health benefit," said lead author Dr. Joanna Kaluza, an associate professor at the Warsaw University of Life Sciences, in Poland.

https://www.sciencedaily.com/releases/2018/09/180913113815.htm

High blood sugar during pregnancy ups risk of mother's type 2 diabetes, child's obesity

September 11, 2018

Science Daily/NIH/National Institute of Diabetes and Digestive and Kidney Diseases

Mothers with elevated blood glucose during pregnancy -- even if not high enough to meet the traditional definition of gestational diabetes -- were significantly more likely to have developed type 2 diabetes a decade after pregnancy than their counterparts without high blood glucose.

 

For children born to mothers with elevated or normal glucose, researchers found no statistically significant difference between the two groups of children in terms of their combined overweight and obesity, the study's primary outcome. However, when obesity was measured alone, children of mothers with elevated blood glucose were significantly more likely to be obese.

 

The results are part of a follow-up study published Sept. 11 in the Journal of the American Medical Association. Funded primarily by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institute of Health, the Hyperglycemia and Adverse Pregnancy Outcomes-Follow-up Study or HAPO-FUS, followed mothers and their children 10-14 years after birth.

 

The original HAPO study found that even modestly elevated blood glucose levels increased the risks of complications for the baby both before and shortly after birth. Based on these results many, but not all, organizations adopted a new definition of gestational diabetes, a type of diabetes that occurs during pregnancy.

 

HAPO-FUS compared the long-term effects of blood glucose levels in mothers who would have met the new definition of gestational diabetes with those who did not. Researchers aimed to learn if modest increases in blood glucose increased the mother's risk of developing type 2 diabetes or prediabetes and the risk of obesity in the mother's offspring at least a decade after giving birth.

 

The study found the harms of even modestly elevated blood glucose for both mother and child extend more than a decade. Among women with elevated blood glucose during pregnancy, nearly 11 percent had type 2 diabetes at the follow-up study visit 10-14 years after childbirth and about 42 percent had prediabetes. Of their counterparts who did not have elevated blood glucose during pregnancy, about 2 percent had type 2 diabetes and about 18 percent had prediabetes. The study examined 4,697 mothers for type 2 diabetes, prediabetes and other disorders of glucose metabolism.

 

Researchers analyzed 4,832 children for overweight and obesity, collecting data using body mass index (BMI), body fat percentage, skin fold thickness and waist circumference. They found that these measures all showed that children born to mothers with elevated glucose levels were more likely to be obese. For example, using BMI, 19 percent of children born to mothers with elevated blood glucose were obese, compared with 10 percent for children of mothers with normal glucose.

 

Adjusting for the mother's BMI reduced -- but did not eliminate -- the differences between the groups.

 

"The differences in mothers and their children due to the mother's higher blood glucose are very concerning. Even accounting for the mother's weight, glucose had an independent effect," said Dr. Barbara Linder, a study author and senior advisor for childhood diabetes research at the NIDDK. "Our findings add to the motivation to find ways to help women at high risk for gestational diabetes who are or plan to get pregnant to take steps to reduce their risk."

 

The original HAPO study looked at 23,316 mother-child pairs and found that a mother's blood sugar levels, even short of diabetes, were associated with her newborn's birth weight and body fat. HAPO results led an international panel of experts to recommend new diagnostic criteria for gestational diabetes in 2010. However, not all professional groups adopted these proposed criteria.

 

"HAPO helped redefine gestational diabetes, and now its follow up continues to raise important alarms about the long-term danger of high blood glucose levels during pregnancy," said study chair Dr. Boyd Metzger, emeritus Tom D. Spies Professor of Nutrition and Metabolism at the Northwestern University Feinberg School of Medicine, Chicago. "This study shows that both mothers with elevated blood glucose levels and their offspring are at higher risk for adverse health effects later in life. More research is needed to find interventions to help both these women and their children."

 

None of the women in HAPO-FUS were diagnosed with or treated for gestational diabetes during their pregnancy. HAPO recruited an international, racially and ethnically diverse group. Limitations of the data in HAPO include that body mass index was obtained during pregnancy, not before. As well, HAPO-FUS did not collect data on the women or children's lifestyles to evaluate other factors that could contribute to obesity or type 2 diabetes.

 

The results build on findings from other studies showing that type 2 diabetes in mothers during pregnancy is associated with obesity in that mother's offspring and that elevated blood glucose increases risk of type 2 diabetes in the woman after pregnancy.

 

"HAPO and its follow-up study have shown the detrimental long-term effects of elevated blood glucose on both mother and child and the importance of early intervention for women at risk for gestational diabetes," said NIDDK Director Dr. Griffin P. Rodgers. "We hope these results will be used to improve the health of generations to come."

https://www.sciencedaily.com/releases/2018/09/180911152429.htm

Change your diet to save both water and your health

September 10, 2018

Science Daily/European Commission Joint Research Centre

Shifting to a healthy diet is not only good for us, but it also saves a lot of fresh water, according to a new study. Compared to existing diets, the water required to produce our food could be reduced by up to 55 percent for healthy pescetarian and vegetarian diets.

 

Compared to existing diets, the water required to produce our food could be reduced by between 11% and 35% for healthy diets containing meat, 33% and 55% for healthy pescetarian diets and 35% and 55% for healthy vegetarian diets.

 

Researchers compared these three diet patterns, defined by respective national dietary guidelines, to the current actual food consumption, using available data from more than 43 thousand areas in France, the UK and Germany.

 

They found that eating more healthily could substantially reduce the water footprint of people's diets, consistent across all the geographical entities analysed in the study.

 

The study is the most detailed nationwide food consumption-related water footprint ever made, taking into account socio-economic factors of food consumption, for existing and recommended diets.

 

Influences on the food we eat

 

The scientists also show how individual food consumption behaviour -- and their related water footprints -- depend strongly on the socio-economic factors like age, gender and education level.

 

They found interesting correlations between such factors and both the water footprint of specific foods and their resulting impact on overall water footprints.

 

For example, the study shows how in France, the water footprint of milk consumption decreases with age across the municipalities analysed.

 

Across London, they show a strong correlation between the water footprint of wine consumption and the percentage of the population of each area with a high education level.

 

Background

 

The water footprint is defined as the total volume of freshwater that is used to produce goods consumed, food in this particular case.

 

The scientists used national dietary surveys to assess differences in food product group consumption between regions and socio- economic factors within regions.

 

The diet scenarios analysed in the study take into account total daily energy and protein requirements as well as maximum daily fat amounts.

 

They are based upon national dietary guidelines, in which for every food product group specific recommendations are given according to age and gender.

 

By downscaling national water footprints to the lowest possible administrative boundaries within a country, the scientists provide a useful tool for policy makers at various levels.

 

The methodology could also be applied to other footprints assessments -- like the carbon, land or energy footprints related to food consumption.

 

Animal products -- and especially meat -- have a high water footprint.

 

The average European diet is characterised by overconsumption in general, particularly of animal products.

 

A healthy diet would contain less sugar, crop oils, meat and animal fats, and more vegetables and fruit.

 

Due to the numerous negative impacts of an intensive livestock production system on the planet's resources and ecosystems, as well as the growing demands of non-western countries for animal products, moving to a more resource-efficient (and healthier) vegetable-rich diet in the EU is a necessity.

https://www.sciencedaily.com/releases/2018/09/180910142419.htm

Longer daily fasting times improve health and longevity in mice

Benefits seen regardless of calorie intake, diet composition in new study

September 6, 2018

Science Daily/NIH/National Institute on Aging

Increasing time between meals made male mice healthier overall and live longer compared to mice who ate more frequently, according to a new study published in the Sept. 6, 2018 issue of Cell Metabolism. Scientists from the National Institute on Aging (NIA) at the National Institutes of Health, the University of Wisconsin-Madison, and the Pennington Biomedical Research Center, Baton Rouge, Louisiana, reported that health and longevity improved with increased fasting time, regardless of what the mice ate or how many calories they consumed.

 

"This study showed that mice who ate one meal per day, and thus had the longest fasting period, seemed to have a longer lifespan and better outcomes for common age-related liver disease and metabolic disorders," said NIA Director Richard J. Hodes, M.D. "These intriguing results in an animal model show that the interplay of total caloric intake and the length of feeding and fasting periods deserves a closer look."

 

The scientists randomly divided 292 male mice into two diet groups. One group received a naturally sourced diet that was lower in purified sugars and fat, and higher in protein and fiber than the other diet. The mice in each diet group were then divided into three sub-groups based on how often they had access to food. The first group of mice had access to food around the clock. A second group of mice was fed 30 percent less calories per day than the first group. The third group was meal fed, getting a single meal that added up to the exact number of calories as the round-the-clock group. Both the meal-fed and calorie-restricted mice learned to eat quickly when food was available, resulting in longer daily fasting periods for both groups.

 

The scientists tracked the mice's metabolic health through their lifespans until their natural deaths and examined them post-mortem. Meal-fed and calorie-restricted mice showed improvements in overall health, as evidenced by delays in common age-related damage to the liver and other organs, and extended longevity. The calorie-restricted mice also showed significant improvement in fasting glucose and insulin levels compared to the other groups. Interestingly, the researchers found that diet composition had no significant impact on lifespan in the meal fed and calorie restricted groups.

 

According to the study's lead author, Rafael de Cabo, Ph.D., chief of the Translational Gerontology Branch of the NIA Intramural Research Program, scientists have studied the beneficial effects of caloric restriction for more than a century, but the impact of increased fasting times has recently come under closer scrutiny.

 

"Increasing daily fasting times, without a reduction of calories and regardless of the type of diet consumed, resulted in overall improvements in health and survival in male mice," said de Cabo. "Perhaps this extended daily fasting period enables repair and maintenance mechanisms that would be absent in a continuous exposure to food."

 

The researchers say their findings are encouraging for future studies on how these types of time-restricted eating patterns might help humans to maintain healthy weight and reduce some common age-related metabolic disorders. According to de Cabo, next steps for this research include expanding these findings to other strains of mice and other lab animal species using both sexes, and to find the potential translation of the findings in humans.

 

For more information on what the research shows about calorie restriction and fasting diets in humans visit: https://www.nia.nih.gov/health/calorie-restriction-and-fasting-diets-what-do-we-know

https://www.sciencedaily.com/releases/2018/09/180906123305.htm

Pregnant women can safely control weight gain through diet and lifestyle changes

September 6, 2018

Science Daily/Northwestern University

Many overweight/obese women gain too much weight during pregnancy. New trials showed these women can safely limit their weight gain with diet and exercise interventions. The reduced weight gain, however, did not result in fewer obstetrical complications. The finding suggests that the lifestyle changes need to start before pregnancy.

 

A new group of trials funded by the National Institutes of Health (NIH) showed that pregnant women can safely limit their weight gain with diet and exercise interventions. It is the largest set of trials in the U.S. to target pregnancy weight gain of overweight and obese women. The trials included diverse socioeconomic groups, which means the findings are generalizable to a large population.

 

"This is an important study because it affirms that women can change behaviors to control the amount of weight gained in pregnancy," said lead author Dr. Alan Peaceman, chief of maternal fetal medicine at Northwestern University Feinberg School of Medicine and a Northwestern Medicine high-risk obstetrician.

 

However, the reduced weight gain -- about four pounds per woman -- did not result in fewer obstetrical complications, including cesarean sections, diabetes, hypertension, and preeclampsia, or change the average birth weight of the baby.

 

"We think that by the time these women are already in the second trimester, it may already be late to change important outcomes," Peaceman said. "To lower the risk of obstetrical complications, they may have to start changing their lifestyle before or immediately after they conceive."

 

Investigators are hopeful that there will be longer-term benefits of the interventions in the infants, such as less childhood obesity or fewer metabolic abnormalities such as childhood diabetes.

 

The study was published Sept. 6 in the journal Obesity.

 

Seven teams of investigators recruited 1,150 participants for the LIFE-Mom trials (579 women had the lifestyle intervention, 571 had standard care), which ran from the second trimester to birth. Each trial offered a varied lifestyle intervention, but all aimed to improve diet quality and reduce calories, increase physical activity and incorporate behavior strategies such as self-monitoring.

 

Overweight and obese women are "hard nut to crack"

 

Overweight and obese women are a critical group to target, because they have higher rates of excess pregnancy weight gain and of retaining that weight postpartum. They also are more likely to have children who are obese. The majority of U.S. women of reproductive age are overweight or obese.

 

About 62 percent of the women in the intervention groups, versus 75 percent in the control groups, exceeded the National Academy of Medicine recommendations for pregnancy weight gain. The recommendation is overweight women limit their pregnancy weight gain to 15 to 25 pounds and obese women to 11 to 20 pounds, compared to 25 to 35 pounds for non-overweight women.

 

The fact that so many women in the intervention groups still exceeded the recommended weight gain shows the challenges of encouraging pregnant women to adhere to recommended diet and activity levels at a time when overeating and reluctance to exercise tend to increase, Peaceman said.

 

"It's a very hard nut to crack," he said.

 

A seesaw history of pregnancy weight gain

 

The advice doctors gave women about pregnancy weight gain has varied widely from decade to decade. In the 1950s, doctors often instructed their patients not to gain more than 15 pounds, Peaceman said.

 

By the late 1970s and early 1980s, mothers weren't gaining enough weight and were having small babies, which could lead to developmental problems in childhood. Then doctors started encouraging women to gain more weight.

 

"Doctors essentially told them that they could eat for two," Peaceman said.

 

"Then women started gaining excessively, but it wasn't thought to be a medical issue, just a cosmetic one," Peaceman said. "The attitude was, 'there's more weight for you to lose when you're done, but that is not a major medical concern'."

 

In the early 2000s, physicians started noticing that excessive pregnancy weight gain was associated with certain pregnancy complications: higher incidence of high blood pressure, gestational diabetes and cesarean sections.

 

"Then we started seeing more worrisome things," Peaceman said. "Excess maternal weight gain was not just associated with bigger babies, but those babies ended up with an increased risk of obesity and childhood diabetes."

 

A few researchers began investigating whether they could help women avoid excess weight gain during pregnancy. Trials testing different strategies for limiting pregnancy weight gain in overweight and obese women had mixed results, in part due to different populations studied and the lack of standardized clinical outcome measures.

 

"That's why NIH recognized the need to do this study in diverse populations and with standardized clinical outcome measures," Peaceman said. "It provides more reliable evidence."

https://www.sciencedaily.com/releases/2018/09/180906184239.htm

Obesity: We inherit the dangerous fat from Dad -- and the good fat from Mom

September 6, 2018

Science Daily/University of Southern Denmark

Brown fat cells burn off a lot of calories, whereas an excess of white fat cells make us overweight and ill. Now researchers have identified a new gene in brown fat cells; a gene that may be crucial for the future's treatment of obesity.

 

A team of researchers, led by Professor Jan-Wilhelm Kornfeld from the Department of Biochemistry and Molecular Biology, University of Southern Denmark, Elena Schmidt from the Max Planck Institute for Metabolism Research, Cologne, Germany and Martin Bilban from the Medial University, Vienna, Austria, have made a groundbreaking discovery in obesity research.

 

The team has discovered a new function of the gene H19. This gene proves to have a unique protective effect against the development of overweight and consequently could affect the onset of overweight-associated disease such as diabetes, overweight and cardiovascular diseases.

 

H19 belongs to the app. one percent of our genes, which we -- as opposed to the remaining 99 percent -- inherit exclusively from either our mother or father, the so-called monoallelic genes.

 

As a result of extensive studies, the researchers have also discovered how genes derived from our father primarily lead to the development of white fat tissue, which most often are found on the stomach, thighs and backside, and which can lead to metabolic diseases.

 

Likewise, it appears that genes from our mother primarily lead to the development of brown fat tissue, which is characterized by having a protective effect against obesity.

 

Professor Jan-Wilhelm Kornfeld and Martin Bilban are delighted with the research results.

 

In their view the results could constitute a first step towards the development of better treatments of obesity.

 

"By using mouse models, we have identified that the gene H19 performs a form of gene control in brown fat cells. We have been able to demonstrate that an overexpression of the H19 gene in mice protects against obesity and insulin resistance. In addition, we have been able to detect similar patterns of gene control in obese people. We therefore believe that our results can be the first step towards developing groundbreaking new and improved treatments for obesity-related diseases," says Professor Jan-Wilhelm Kornfeld.

https://www.sciencedaily.com/releases/2018/09/180906100438.htm

Fish oil supplement in pregnancy is linked to increase in lean and bone mass by age 6 years

September 4, 2018

Science Daily/BMJ

Taking fish oil supplements in the later stages of pregnancy is associated with a higher weight (BMI) in children in the first six years of life, but not an increased risk of overweight or obesity by age 6, a new study suggests.

 

Fish oil supplement in the later stages of pregnancy is associated with a higher body mass index (BMI) in children in the first six years of life, which is explained by an increase in total lean and bone mass at 6 years of age, but with no increase in fat mass, suggest the findings of a large randomised controlled trial published by The BMJ today.

 

Studies in animals have shown that supplementing the diet with fish oil during pregnancy affects adipogenesis (the development of fat cells). However, while trials in humans have shown that pregnant women with a higher intake of fish oil give birth to higher birth weight infants, the impact on children later in life has been unclear.

 

So a team of researchers based in Denmark and the UK set out to examine the effect of taking fish oil supplements during pregnancy on the growth and body composition of children later in life.

 

The trial involved 736 pregnant women from the Copenhagen Prospective Studies on Asthma in Childhood study who were randomised to receive n-3 long-chain polyunsaturated fatty acids (LCPUFAs) (fish oil) or olive oil (control) daily from week 24 of pregnancy week until one week after birth.

 

Height, weight, head and waist measurements were assessed 11 times from birth to age 6 years and adjusted for age and sex. These revealed a sustained higher BMI from 1 year to 6 years of age.

 

Body composition was assessed using dual-energy X-ray absorptiometry (DXA) scans at 3.5 and 6 years of age and demonstrated that the higher BMI was not the result of a higher fat percentage, but reflected a proportional increase in lean mass, bone mass, and fat mass, suggesting that the fish oil supplementation had a general growth stimulating effect.

 

At age 6, DXA scans showed children whose mothers had taken fish oil supplements while pregnant had a 395g higher total mass, 280.7g higher lean mass, 10.3g higher bone mineral content and 116.3g higher fat mass compared with children of mothers who took the control oil.

 

The researchers conclude: "The body composition at age 6 years in children given fish oil supplementation was characterised by a proportional increase in lean, bone, and fat mass suggesting a general growth stimulating effect."

https://www.sciencedaily.com/releases/2018/09/180904190616.htm

Changes in breakfast and dinner timings can reduce body fat

August 30, 2018

Science Daily/University of Surrey

Modest changes to breakfast and dinner times can reduce body fat, a new pilot study reports.

 

During a 10-week study on 'time-restricted feeding' (a form of intermittent fasting), researchers led by Dr Jonathan Johnston from the University of Surrey investigated the impact changing meal times has on dietary intake, body composition and blood risk markers for diabetes and heart disease.

 

Participants were split into two groups -- those who were required to delay their breakfast by 90 minutes and have their dinner 90 minutes earlier, and those who ate meals as they would normally (the controls). Participants were required to provide blood samples and complete diet diaries before and during the 10-week intervention and complete a feedback questionnaire immediately after the study.

 

Unlike previous studies in this area, participants were not asked to stick to a strict diet and could eat freely, provided it was within a certain eating window. This helped researchers assess whether this type of diet was easy to follow in everyday life.

 

Researchers found that those who changed their mealtimes lost on average more than twice as much body fat as those in the control group, who ate their meals as normal. If these pilot data can be repeated in larger studies, there is potential for time-restricted feeding to have broad health benefits.

 

Although there were no restrictions on what participants could eat, researchers found that those who changed their mealtimes ate less food overall than the control group. This result was supported by questionnaire responses which found that 57 percent of participants noted a reduction in food intake either due to reduced appetite, decreased eating opportunities or a cutback in snacking (particularly in the evenings). It is currently uncertain whether the longer fasting period undertaken by this group was also a contributing factor to this reduction in body fat.

 

As part of the study, researchers also examined if fasting diets are compatible with everyday life and long term commitment. When questioned, 57 percent of participants felt they could not have maintained the new meal times beyond the prescribed 10 weeks because of their incompatibility with family and social life. However, 43 per cent of participants would consider continuing if eating times were more flexible.

 

Dr Jonathan Johnston, Reader in Chronobiology and Integrative Physiology at the University of Surrey, said:

 

"Although this study is small, it has provided us with invaluable insight into how slight alterations to our meal times can have benefits to our bodies. Reduction in body fat lessens our chances of developing obesity and related diseases, so is vital in improving our overall health.

 

"However, as we have seen with these participants, fasting diets are difficult to follow and may not always be compatible with family and social life. We therefore need to make sure they are flexible and conducive to real life, as the potential benefits of such diets are clear to see.

 

"We are now going to use these preliminary findings to design larger, more comprehensive studies of time-restricted feeding."

https://www.sciencedaily.com/releases/2018/08/180830084826.htm

Switching to hunter-gatherer lifestyle may increase diversity in children's gut microbes

August 29, 2018

Science Daily/American Society for Microbiology

Immersing city dwellers in the traditional lifestyle and diet of a rainforest village for two weeks increases the diversity of the visiting children's -- but not the adults' -- gut microbiota. In a small pilot study, researchers show that the immersion visit did little to shift the adults' skin, oral, nasal and fecal microbiota.

 

An international team of researchers has shown that immersing city dwellers in the traditional lifestyle and diet of a rainforest village for two weeks increases the diversity of the visiting children's -- but not the adults' -- gut microbiota. In a small pilot study published this week in mSphere®, an open-access journal of the American Society for Microbiology, the team shows that the immersion visit did little to shift the adults' skin, oral, nasal and fecal microbiota.

 

"We wanted to look at the question of whether microbiota change during a drastic, radical change of diet and lifestyle," says Maria Gloria Dominguez-Bello, a microbial ecologist at Rutgers University in New Brunswick, New Jersey who led the study with microbiologist Monica Contreras from the Venezuelan Institute of Scientific Research. "In this village, there was no market economy, no bodega, no Coca-Cola -- so this represented a radical shift in diet from a high percentage of processed foods in urban places to zero processed foods and an all-natural diet."

 

Dominguez-Bello, along with researchers from New York University and two Venezuelan institutes, took advantage of a visit planned by five, city-dwelling adult visitors -- and two of their children -- to live among an indigenous Yekwana village in the Bolivar State of Venezuela for 16 days. The village has a hunter-gatherer-gardener lifestyle and diet.

 

Typical fare includes cassava (a starchy, high-fiber tuber), corn, various wild fruits, including plantains, pineapples, and berries, fish, and small amounts of game meat and eggs gathered from wild birds. Visitors had two meals a day that consisted of soup with a bit of fish or meat. The rest of their diet consisted of "all-day snacking on cassava with fruit" says Dominguez-Bello. The visitors also bathed in the river without soap and followed the natural circadian rhythms of their hosts.

 

"The diet contains very little animal protein and it's very, very high in fiber and very low in fat," compared to Western diets, says Dominguez-Bello.

 

While it is known that people with traditional diets have higher gut microbiota diversity compared to those with urban diets, it was unknown if urban dwellers could shift the diversity of their microbiota higher simply by following a traditional lifestyle and diet. In the gut, a high diversity of microbes is considered a sign of good health.

 

Traditional people eat diets rich in unprocessed plant material, which are much more chemically complex compared to processed foods. The smorgasbord of chemicals acts as fuel for a higher variety of microbes. Traditional people use less antimicrobial medicines and compounds in daily life, which might also contribute to their increased gut microbe diversity.

 

During the 16-day visit, the researchers collected samples from the visitors' skin, mouth, nose, and from a fecal swab. Age-matched samples were also collected from villagers. The samples were sequenced and compared.

 

Surprisingly, none of the adult visitors' microbiota shifted significantly during the visit, while the two children's gut microbiota trended toward a higher number of total microbial species present. Although these results were not statistically significant and in just two subjects, the researchers saw this as interesting nonetheless, given the children's ages of 4 and 7.

 

Up to now, it was thought that children's gut microbiota become stable and more 'adult-like' by the time they reach 3 years of age. "This indicates that the window for maturing your microbiome may not be 3 years of age, but longer," says Dominguez-Bello. Her team plans to do a larger study with 12 children participating in an "immersion summer camp" to a traditional village.

 

Because the children's gut microbiota exhibited more plasticity, these results raise an interesting possibility that urban children who eat a more traditional, high-fiber, low-fat and low-processed diet early in life might cultivate a more diverse set of gut microbes. Conversely, adults may have a limited response due to their low microbiome plasticity.

 

Dominguez-Bello was not terribly surprised that the adults' gut and other microbiota changed so little: "If you take traditional people and bring them to New York, give them antibiotics and McDonald's to eat everyday, it's not surprising that they lose diversity," she says. "But if, as an urban dweller, you've already lost that gut microbe diversity and you move to a high-diversity diet, maybe you cannot 'bloom' diversity because you simply don't have those microbes present anymore."

https://www.sciencedaily.com/releases/2018/08/180829133429.htm

Father's diet could affect the long-term health of his offspring

August 29, 2018

Science Daily/University of Nottingham

New research has shown that a lack of protein in a father's diet affects sperm quality which can have a direct impact on the long-term health of their offspring.

 

The study -- 'Paternal diet programs offspring health through sperm- and seminal plasma-specific pathways in mice' -- carried out at the University of Nottingham fed male mice a poor quality diet which resulted in their offspring becoming over weight, with symptoms of type 2 diabetes and reduced expression of genes which regulate the metabolism of fat.

 

Researchers from the University of Nottingham's Schools of Medicine and Biosciences have published a report in PNAS showing that both sperm and the fluid they are carried in (seminal plasma) from male mice fed a low protein diet could affect the long-term metabolic health of their offspring.

 

There has been much research showing that sperm from men who are overweight, smoke, drink excessively or who have type 2 diabetes are often of poorer quality than sperm from healthy, fertile men. However, little is known about the impact of such lifestyle factors on the long-term health of a father's offspring. This new study bridges this gap in our understanding by using a mouse model to explore the long-term growth and metabolic health of offspring from males fed a poor quality diet.

 

Improving dietary advice given to prospective fathers

 

Dr Adam Watkins, Assistant Professor in Reproductive Biology at the University of Nottingham led the study. He said: "It is well understood that what a mother eats during pregnancy can affect the development and health of her child. As such, there is a lot of information available to women who want to become pregnant about the importance of a healthy lifestyle and good dietary choices both for their own health and that of their child. Interestingly, little, if any, advice is available for the father. Our research using mice shows that at the time of conception, the diet and well-being of the father influences the long-term growth and metabolic health of his offspring. Our study not only identifies what impact a poor paternal diet has on the health of his offspring but also starts to uncover how these effects are established''.

 

The study, carried out on mice, found that males fed a low-protein diet produced sperm with fewer chemical tags on their DNA that regulate gene expression than mice fed a normal diet. Researchers also observed that the seminal plasma suppressed maternal uterine inflammatory and immunological responses, essential for a healthy pregnancy. The researchers believe that the health of a father's offspring is affected both by the quality of a father's genetic information passed on within the sperm at conception, and by the seminal plasma-primed maternal uterine environment in which the embryo will develop.

 

Kevin Sinclair, Professor of Developmental Biology in the School of Biosciences, who collaborated on this study said: "It is important to recognise that sperm contribute more than just half of the genes that make up a child. During natural conception sperm deposited in the female reproductive tract are bathed in seminal plasma which can in itself influence pregnancy outcomes. Our study shows that the composition of seminal plasma can be altered by father's diet, and that this can also influence offspring wellbeing."

https://www.sciencedaily.com/releases/2018/08/180829115539.htm

Obesity, risk of cognitive dysfunction? Consider high-intensity interval exercise

Study first to use high-intensity interval exercise on obese individuals to test effects on cognitive dysfunction

Science Daily/December 10, 2018

Florida Atlantic University

Researchers have discovered what might be an effective strategy to prevent and combat cognitive dysfunction in obese individuals. They are the first to examine the modulatory role of an exercise-induced protein in the brain that promotes neuron survival and used high-intensity interval exercise (HIIE) in obese and normal-weight subjects. Obesity reduces the expression of this protein and lower levels are associated with Alzheimer's, Parkinson's and obesity. HIIE upregulated this protein in the obese subjects compared to normal-weight subjects.

 

It's fast-paced, takes less time to do, and burns a lot of calories. High-intensity interval exercise is widely recognized as the most time-efficient and effective way to exercise. In a first-of-its-kind study, researchers from Florida Atlantic University have discovered another important health benefit of these short bursts of intense exercise with rest intervals. It could also be an effective strategy to prevent and combat cognitive dysfunction in obese individuals.

 

Obesity reduces the expression of brain-derived neurotrophic factor (BDNF), a protein in the brain that promotes the survival of nerve cells or neurons. Lower levels of this protein are associated with Alzheimer's disease, Parkinson's disease, and obesity. Although studies have shown that obesity is a risk factor for cognitive dysfunction, the mechanisms of this relationship are not fully understood.

 

To-date, studies on exercise and BDNF response in obese populations have only used continuous moderate-intensity exercise without rest intervals. FAU researchers and collaborators from the University of Texas at Austin and Purdue University, are the first to examine the modulatory role of obesity on exercise-induced BDNF release and to use an acute high-intensity interval exercise protocol as a practical model to measure the phenomena of BDNF release in both obese and normal-weight subjects. They also examined the potential relationship of exercise-induced BDNF with blood lactate and cortisol.

 

Results of study, published in the journal Experimental Biology and Medicine, show that the BDNF response to acute high-intensity interval exercise was greater than continuous moderate-intensity exercise in obese subjects when compared to normal-weight subjects. Similarly, although acute high-intensity interval exercise induced greater blood lactate and plasma cortisol levels than continuous moderate-intensity exercise, obese subjects produced less blood lactate, but showed no difference in cortisol than normal-weight subjects.

 

These findings suggest that acute high-intensity interval exercise may be a more effective protocol to upregulate BDNF expression in an obese population, independent of increased lactate and cortisol levels.

 

"High-intensity interval exercise is a time-efficient strategy with similar or superior physiological benefits that promotes the expression of a growth factor typically associated with brain health, yet that appears to be down regulated in obesity," said Chun-Jung (Phil) Huang, Ph.D., lead author and an associate professor in the Exercise Biochemistry Laboratory, Department of Exercise Science and Health Promotion, in FAU's College of Education. "The relative simplicity and efficacy of high-intensity interval exercise supports its use as a preventive measure and as an intervention to combat obesity and other chronic disease conditions."

 

For the study, male subjects participated in a counterbalanced and caloric equated experiment of high-intensity interval exercise. The high-intensity interval exercise protocol consisted of a five minute walking or jogging warm-up, followed by four high-intensity intervals lasting four minutes each, followed by three minutes of active recovery followed by each high-intensity interval. Blood samples were collected prior to, immediately following exercise, and an hour into recovery for measurements of serum BDNF, blood lactate, and plasma cortisol.

 

Other findings from the study show statistically significant differences between the obese and normal-weight groups for body weight, BMI, systolic and diastolic blood pressures, and waist/hip circumferences and ratio. In addition, both the obese and normal-weight groups had comparable heart rate responses during both exercise protocols, demonstrating a similar relative exercise intensity and effort between groups. Therefore, the BDNF response was likely not influenced by disparities between aerobic fitness, with a greater level in obese subjects than normal-weight subjects following acute high-intensity interval exercise vs. continuous moderate-intensity exercise.

 

"Increased levels of cortisol have been shown to down regulate BDNF expression, however, this relationship in response to exercise still remains equivocal," Huang. "Specifically, our study and others, did not observe any correlation between cortisol and BDNF following either acute high-intensity exercise or continuous moderate-intensity exercise protocol, yet, the report of such is opposite."

 

Aerobic training has been shown to not only provide beneficial anti-inflammatory and cardiovascular benefits, but also reductions in age-related cognitive decline. It also has been shown to preserve brain volume and potentially improve blood flow.

 

The Centers for Disease Control and Prevention estimates that about 93.3 million Americans were classified as obese in 2016. The annual medical costs of obesity were estimated at around $147 billion in 2008.

https://www.sciencedaily.com/releases/2018/12/181210091027.htm

When fathers exercise, children are healthier, even as adults

October 22, 2018

Science Daily/Ohio State University Wexner Medical Center

Most parents know that the diet and exercise habits of a pregnant woman impacts the health of her baby, but little is known about how a father's health choices are passed to his children. A new study finds that lifestyle practices of fathers prior to conception may have a major impact on the lifelong health of their children.

 

In a new study led by Kristin Stanford, a physiology and cell biology researcher with The Ohio State University College of Medicine at the Wexner Medical Center, paternal exercise had a significant impact on the metabolic health of offspring well into their adulthood.

 

Laurie Goodyear of the Joslin Diabetes Center and Harvard Medical School co-led the study, published today in the journal Diabetes.

 

"This work is an important step in learning about metabolic disease and prevention at the cellular level," said Dr. K. Craig Kent, dean of the Ohio State College of Medicine.

 

Recent studies have linked development of type 2 diabetes and impaired metabolic health to the parents' poor diet, and there is increasing evidence that fathers play an important role in obesity and metabolic programming of their offspring.

 

Stanford is a member of Ohio State's Diabetes and Metabolism Research Center. Her team investigated how a father's exercise regimen would affect his offspring's metabolic health. Using a mouse model, they fed male mice either a normal diet or a high-fat diet for three weeks. Some mice from each diet group were sedentary and some exercised freely. After three weeks, the mice bred and their offspring ate a normal diet under sedentary conditions for a year.

 

The researchers report that adult offspring from sires who exercised had improved glucose metabolism, decreased body weight and a decreased fat mass.

 

"Here's what's really interesting; offspring from the dads fed a high-fat diet fared worse, so they were more glucose intolerant. But exercise negated that effect," Stanford said. "When the dad exercised, even on a high-fat diet, we saw improved metabolic health in their adult offspring."

 

Stanford's team also found that exercise caused changes in the genetic expression of the father's sperm that suppress poor dietary effects and transfer to the offspring.

 

"We saw a strong change in their small-RNA profile. Now we want to see exactly which small-RNAs are responsible for these metabolic improvements, where it's happening in the offspring and why," Stanford said.

 

Previous studies from this group have shown that when mouse mothers exercise, their offspring also have beneficial effects of metabolism.

 

"Based on both studies, we're now determining if both parents exercising has even greater effects to improve metabolism and overall health of offspring. If translated to humans, this would be hugely important for the health of the next generation," Goodyear said.

 

The researchers believe the results support the hypothesis that small RNAs could help transmit parental environmental information to the next generation.

 

"There's potential for this to translate to humans. We know that in adult men obesity impairs testosterone levels, sperm number and motility, and it decreases the number of live births," Stanford said. "If we ask someone who's getting ready to have a child to exercise moderately, even for a month before conception, that could have a strong effect on the health of their sperm and the long-term metabolic health of their children."

 

Other Ohio State researchers involved in the study were Lisa Baer, Adam Lehnig and Joseph White.

 

Funding from the National Institutes of Health supported this research.

https://www.sciencedaily.com/releases/2018/10/181022085844.htm

Inflammation can lead to circadian sleep disorders

Novel technology turns inflammation on and off, affecting body clock in mice

October 31, 2018

Science Daily/Northwestern University

Inflammation, which is the root cause of autoimmune disorders including arthritis, type 1 diabetes, irritable bowel syndrome and Crohn's disease, has unexpected effects on body clock function and can lead to sleep and shiftwork-type disorders, a new study in mice found.

 

The study was published in the journal Genes & Development.

 

The study used a new technology -- a genetic switch -- to turn inflammation on and off in genetically modified mouse models. When researchers deactivated inflammation, the mouse was unable to tell what time it was and was unable to keep an intact rest-activity cycle.

 

In addition to this new technology, the study was novel because, for the first time, scientists saw a link between what causes inflammation and what controls the body's clock.

 

In inflammatory diseases, the body experiences an excess of a genetic factor known as NF-kappa beta (NFKB), the study found. NFKB is a catalyst for a set of chain reactions, or pathway, that leads to the pain and tissue destruction patients feel in inflammatory diseases. That same chain-reaction catalyst also controls the body's clock.

 

"NFKB alters the core processor through which we tell time, and now we know that it is also critical in linking inflammation to rest-activity patterns," said senior author Dr. Joseph Bass, the Charles F. Kettering Professor of Medicine and director of the Center for Diabetes and Metabolism at Northwestern University Feinberg School of Medicine.

 

When people have sore muscles and take an ibuprofen to reduce the inflammation, they are essentially trying to turn down the activation of inflammation, which is similar to what the authors did in this study, Bass said.

 

The findings also have implications for diet and provide a detailed roadmap to understanding the fundamental mechanisms by which inflammation -- including the inflammation that occurs when someone chronically consumes a high-fat diet -- and likely other instigators lead to circadian disorders.

 

The scientists sought to understand how a high-fat diet might affect the perception of time at the tissue level, which is what led to their study of inflammation, said first author Hee-Kyung Hong, research assistant professor of endocrinology at Feinberg.

 

One of the reasons Western diet contributes to diabetes, cardiovascular disease and even certain cancers is thought to be the inappropriate trigger of inflammation, so a unifying idea is that impaired time-keeping may be one of the links between diet and disease.

 

"We don't know the reasons, but this interaction between the inflammation and clocks is not only relevant to understanding how inflammation affects the brain and sleep-wake cycle but also how immune or fat cells work," Hong said.

https://www.sciencedaily.com/releases/2018/10/181031124858.htm

Link between hunger and mood explained

The sudden drop in glucose we experience when we are hungry can impact our mood

September 25, 2018

Science Daily/University of Guelph

The study used rats to examine the impact on emotional behavior of a sudden drop in blood sugar. When the rats were given a glucose blocker, researchers found they had higher levels of cortisol. They also showed signs of stress and sluggish behavior similar to a poor mood. To prove the behavior wasn't just a lack of glucose to the muscles, researchers then gave them a common antidepressant and the behavior disappeared.

 

It seems "hangry" isn't just a made-up term.

 

University of Guelph researchers have revealed that the sudden drop in glucose we experience when we are hungry can impact our mood.

 

"We found evidence that a change in glucose level can have a lasting effect on mood," said Prof. Francesco Leri, Department of Psychology. "I was skeptical when people would tell me that they get grouchy if they don't eat, but now I believe it. Hypoglycemia is a strong physiological and psychological stressor."

 

Published in the journal Psychopharmacology, the study examined the impact of a sudden glucose drop on emotional behaviour by inducing hypoglycemia in rats.

 

"When people think about negative mood states and stress, they think about the psychological factors, not necessarily the metabolic factors," said PhD student Thomas Horman, who led the study. "But we found poor eating behaviour can have an impact."

 

The rats were injected with a glucose metabolism blocker causing them to experience hypoglycemia, and were then placed in a specific chamber. On a separate occasion, they were given an injection of water and placed in a different chamber. When given the choice of which chamber to enter, they actively avoided the chamber where they experienced hypoglycemia.

 

"This type of avoidance behaviour is an expression of stress and anxiety," said Leri. "The animals are avoiding that chamber because they had a stressful experience there. They don't want to experience it again."

 

The researchers tested blood levels of the rats after experiencing hypoglycemia and found more corticosterone, an indicator of physiological stress.

 

The rats also appeared more sluggish when given the glucose metabolism blocker.

 

"You might argue that this is because they need glucose to make their muscles work," said Leri. "But when we gave them a commonly used antidepressant medication, the sluggish behaviour was not observed. The animals moved around normally. This is interesting because their muscles still weren't getting the glucose, yet their behaviour changed."

 

This finding supports the idea that the animals experienced stress and depressed mood when they were hypoglycemic, he said.

 

For people who experience anxiety or depression, the study results have implications for treatment, said Horman.

 

"The factors that lead someone to develop depression and anxiety can be different from one person to the next. Knowing that nutrition is a factor, we can include eating habits into possible treatment."

 

These findings also provide insight into the connection between depression and diseases such as obesity, diabetes, bulimia and anorexia, Horman said.

 

Having established that hypoglycemia contributes to negative mood states, the researchers plan to determine whether chronic, long-term hypoglycemia is a risk factor for developing depression-like behaviours.

 

While missing one meal may make you "hangry," Horman said, these findings suggest your mood could be impacted if meal-skipping becomes a habit.

 

"Poor mood and poor eating can become a vicious cycle in that if a person isn't eating properly, they can experience a drop in mood, and this drop in mood can make them not want to eat. If someone is constantly missing meals and constantly experiencing this stressor, the response could affect their emotional state on a more constant level."

https://www.sciencedaily.com/releases/2018/09/180925115218.htm

Say Hello to a Healthy Gut and Goodbye to Digestive Problems

By Scott Sanders

www.cancerwell.org

<info@cancerwell.org>

Some people can eat whatever they want without any issues. Others have negative reactions to certain foods and diets. If you’re one of many people who experience occasional digestive problems, it’s time to learn about how you can use the food you consume to heal you from the inside out. 

Digestive ailments hit everyone at some point in their lives, and they can be temporary inconveniences or chronic conditions. Who hasn’t had diarrhea, constipation, bloating, vomiting, or an upset stomach at some point? But there are many who suffer from serious conditions like gallstones, celiac disease, Crohn’s disease, ulcerative colitis, irritable bowel syndrome, and more. According to Everyday Health, 20 percent of Americans are affected by GERD, over 25 million have gallstones, and approximately 10 to 15 percent are affected by irritable bowel syndrome. Disruptive stomach conditions can be caused by what you eat, but they can also be treated by what you eat. 

Nutrition

Eating whole, unprocessed foods is the best way to heal the gut. Learn to read nutrition labelsto see what ingredients make up your food. Preservatives and additives make your digestive system work harder and cause other health issues. Some foreign ingredients simply shouldn’t be eaten. Buy your food fresh rather than from packages. The more ingredients in the food, the more you should avoid it.

Food Elimination

Digestive conditions and autoimmune diseases generally call for special diets. To see which foods affect you in negative ways, try an elimination diet that removes specific foods for one month. You can start by cutting out the foods that typically cause issues (such as gluten, dairy, corn, soy, sugar, and alcohol) and reintroduce them slowly to see how they affect you. Another option is to cut out one thing at a time to monitor any differences. If you’re willing to stick with a strict diet, the autoimmune protocoldiet helps reduce intestinal inflammation. 

Gut Health

Since your gut processes all of your body’s nutrients, the health of your digestive tract is important to your overall wellbeing. When things are off in your gut, the rest of your body feels off, too. Gut healthcould affect everything from your brain to your skin to your weight-loss efforts. 

Your gut contains both good bacteria and bad bacteria. Known as microbiomes, these microorganisms live inside your digestive tract. The friendly bacteriain your gut include Bifidobacterium, Lactobacillus, Saccharomyces Boulardii, Bacillus Coagulans, and Akkermansia microbes. They protect against harmful microbes, promote digestive health, aid in digestion, improve the immune system, produce vitamins, impact the metabolism, and have other positive effects on intestinal health. 

Disease

The good bacteria may prevent and treat diseases, such as inflammatory conditions, heart disease, and even cancer. Gut health is linked to cancer in many ways. Digestive issues are often due to cancer and side effects of treatments. Constipation, nausea, stomach cramps, weight loss, and digestion problems can occur as a result of pain medication, chemotherapy, or the cancer itself. 

Sometimes, it’s the gut health that helps treat cancer. An immunotherapy called Checkpoint Inhibition can shrink tumors, but studieshave shown that gut health could have something to do with the patient’s response to it. By altering the gut microbiome, patients develop a better response to the immunotherapy. More good bacteria means better immune cells to kill the cancer cells. 

Probiotics

Healthy people who don’t have underlying medical problems may want to consider adding probioticsto their daily routine. Probiotics contain the same helpful microorganisms that are present in our bodies. You can ingest probiotics through supplements or in foods such as yogurt, kefir, kimchi, sauerkraut, tempeh, and kombucha (which also has antioxidants).

Exercise

Let’s not discount the importance of exercise for overall health. A healthy diet can heal your body, but never underestimate the role of physical fitness in a holistic approach to healing digestive ailments. Any form of cardiovascular exercise can help move digestive waste through your system. Yogais a great activity to practice, especially when it comes to reducing bloat.

There is no one-size-fits-all approach to intestinal health and treating digestive disorders. Each body is different. It takes trial and error, listening to your body, and seeing a doctor when natural methods don’t provide results. When the solutions finally do come, you’ll get to relish in the joy of eating again.

How sleep loss may contribute to adverse weight gain

August 23, 2018

Science Daily/Uppsala University

One night of sleep loss has a tissue-specific impact on the regulation of gene expression and metabolism in humans, according to researchers. This may explain how shift work and chronic sleep loss impairs our metabolism and adversely affects our body composition.

 

Epidemiological studies have shown that the risk for obesity and type 2 diabetes is elevated in those who suffer from chronic sleep loss or who carry out shift work. Other studies have shown an association between disrupted sleep and adverse weight gain, in which fat accumulation is increased at the same time as the muscle mass is reduced -- a combination that in and of itself has been associated with numerous adverse health consequences. Researchers from Uppsala and other groups have in earlier studies shown that metabolic functions that are regulated by e.g. skeletal muscle and adipose tissue are adversely affected by disrupted sleep and circadian rhythms. However, until now it has remained unknown whether sleep loss per se can cause molecular changes at the tissue level that can confer an increased risk of adverse weight gain.

 

In the new study, the researchers studied 15 healthy normal-weight individuals who participated in two in-lab sessions in which activity and meal patterns were highly standardised. In randomised order, the participants slept a normal night of sleep (over eight hours) during one session, and were instead kept awake the entire night during the other session. The morning after each night-time intervention, small tissue samples (biopsies) were taken from the participants' subcutaneous fat and skeletal muscle. These two tissues often exhibit disrupted metabolism in conditions such as obesity and diabetes. At the same time in the morning, blood samples were also taken to enable a comparison across tissue compartments of a number of metabolites. These metabolites comprise sugar molecules, as well as different fatty and amino acids.

 

The tissue samples were used for multiple molecular analyses, which first of all revealed that the sleep loss condition resulted in a tissue-specific change in DNA methylation, one form of mechanism that regulates gene expression. DNA methylation is a so-called epigenetic modification that is involved in regulating how the genes of each cell in the body are turned on or off, and is impacted by both hereditary as well as environmental factors, such as physical exercise.

 

"Our research group were the first to demonstrate that acute sleep loss in and of itself results in epigenetic changes in the so-called clock genes that within each tissue regulate its circadian rhythm. Our new findings indicate that sleep loss causes tissue-specific changes to the degree of DNA methylation in genes spread throughout the human genome. Our parallel analysis of both muscle and adipose tissue further enabled us to reveal that DNA methylation is not regulated similarly in these tissues in response to acute sleep loss," says Jonathan Cedernaes who led the study.

 

"It is interesting that we saw changes in DNA methylation only in adipose tissue, and specifically for genes that have also been shown to be altered at the DNA methylation level in metabolic conditions such as obesity and type 2 diabetes. Epigenetic modifications are thought to be able to confer a sort of metabolic "memory" that can regulate how metabolic programmes operate over longer time periods. We therefore think that the changes we have observed in our new study can constitute another piece of the puzzle of how chronic disruption of sleep and circadian rhythms may impact the risk of developing for example obesity," notes Jonathan Cedernaes.

 

Further analyses of e.g. gene and protein expression demonstrated that the response as a result of wakefulness differed between skeletal muscle and adipose tissue. The researchers say that the period of wakefulness simulates the overnight wakefulness period of many shift workers assigned to nightwork. A possible explanation for why the two tissues respond in the observed manner could be that overnight wakefulness periods exert a tissue-specific effect on tissues' circadian rhythm, resulting in misalignment between these rhythms. This is something that the researchers found preliminary support for also in this study, as well as in an earlier similar but smaller study.

 

"In the present study we observed molecular signatures of increased inflammation across tissues in response to sleep loss. However, we also saw specific molecular signatures that indicate that the adipose tissue is attempting to increase its capacity to store fat following sleep loss, whereas we instead observed signs indicating concomitant breakdown of skeletal muscle proteins in the skeletal muscle, in what's also known as catabolism. We also noted changes in skeletal muscle levels of proteins involved handling blood glucose, and this could help explain why the participants' glucose sensitivity was impaired following sleep loss. Taken together, these observations may provide at least partial mechanistic insight as to why chronic sleep loss and shift work can increase the risk of adverse weight gain as well as the risk of type 2 diabetes," says Jonathan Cedernaes.

 

The researchers have only studied the effect of one night of sleep loss, and therefore do not know how other forms of sleep or disruption of circadian misalignment would have affected the participants' tissue metabolism.

 

"It will be interesting to investigate to what extent one or more nights of recovery sleep can normalise the metabolic changes that we observe at the tissue level as a result of sleep loss. Diet and exercise are factors that can also alter DNA methylation, and these factors can thus possibly be used to counteract adverse metabolic effects of sleep loss," says Jonathan Cedernaes.

https://www.sciencedaily.com/releases/2018/08/180823095946.htm

Food for thought: How the brain reacts to food may be linked to overeating

July 19, 2018

Science Daily/Penn State

The reason why some people find it so hard to resist finishing an entire bag of chips or bowl of candy may lie with how their brain responds to food rewards, according to researchers who found that when certain regions of the brain reacted more strongly to being rewarded with food than being rewarded with money, those people were more likely to overeat.

 

In a study with children, researchers found that when certain regions of the brain reacted more strongly to being rewarded with food than being rewarded with money, those children were more likely to overeat, even when the child wasn't hungry and regardless of if they were overweight or not.

 

Shana Adise, a postdoctoral fellow at the University of Vermont who led the study while earning her doctorate at Penn State, said the results give insight into why some people may be more prone to overeating than others. The findings may also give clues on how to help prevent obesity at a younger age.

 

"If we can learn more about how the brain responds to food and how that relates to what you eat, maybe we can learn how to change those responses and behavior," Adise said. "This also makes children an interesting population to work with, because if we can stop overeating and obesity at an earlier age, that could be really beneficial."

 

Previous research on how the brain's response to food can contribute to overeating has been mixed. Some studies have linked overeating with brains that are more sensitive to food rewards, while others have found that being less sensitive to receiving food rewards makes you more likely to overeat.

 

Additionally, other studies have shown that people who are willing to work harder for food than other types of rewards, like money, are more likely to overeat and gain weight over time. But the current study is the first to show that children who have greater brain responses to food compared to money rewards are more likely to overeat when appealing foods are available.

 

"We know very little about the mechanisms that contribute to overeating," Adise said. "The scientific community has developed theories that may explain overeating, but whether or not they actually relate to food intake hadn't yet been evaluated. So we wanted to go into the lab and test whether a greater brain response to anticipating and winning food, compared to money, was related to overeating."

 

For the study, 59 children between the ages of 7 and 11 years old made four visits to the Penn State's Children's Eating Behavior Laboratory.

 

During the first three visits, the children were given meals designed to measure how they eat in a variety of different situations, such as a typical meal when they're hungry versus snacks when they're not hungry. How much the children ate at each meal was determined by weighing the plates before and after the meals.

 

On their fourth visit, the children had fMRI scans as they played several rounds of a game in which they guessed if a computer-generated number would be higher or lower than five. They were then told that if they were right, they would win either money, candy or a book, before it was revealed if they were correct or not.

 

The researchers found that when various regions of the brain reacted more to anticipating or winning food compared to money, those children were more likely to overeat.

 

"We also found that the brain's response to food compared to money was related to overeating regardless of how much the child weighed," Adise said. "Specifically, we saw that increased brain responses in areas of the brain related to cognitive control and self control when the children received food compared to money were associated with overeating."

 

Adise added that this is important because it suggests there may be a way to identify brain responses that can predict the development of obesity in the future.

 

Kathleen Keller, associate professor of nutritional sciences, Penn State, said the study -- recently published in the journal Appetite -- backs up the theory that an increased brain response in regions of the brain related to rewards is associated with eating more food in a variety of situations.

 

"We predicted that kids who had an increased response to food relative to money would be the ones to overeat, and that's what we ended up seeing," Keller said. "We specifically wanted to look at kids whose brains responded to one type of a reward over another. So it wasn't that they're overly sensitive to all rewards, but that they're highly sensitive to food rewards."

 

Keller said the findings give insight into how the brain influences eating, which is important because it could help identify children who are at risk for obesity or other poor eating habits before those habits actually develop.

 

"Until we know the root cause of overeating and other food-related behaviors, it's hard to give good advice on fixing those behaviors," Keller said. "Once patterns take over and you overeat for a long time, it becomes more difficult to break those habits. Ideally, we'd like to prevent them from becoming habits in the first place."

https://www.sciencedaily.com/releases/2018/07/180719085413.htm

Obesity + aging linked to Alzheimer's markers in the brain

Study finds most neurodegeneration in hippocampus of overweight, middle-age mice

June 28, 2018

Science Daily/American Physiological Society

A new study suggests that when a high-fat, high-sugar diet that leads to obesity is paired with normal aging, it may contribute to the development of Alzheimer's disease. In addition, researchers discovered that certain areas of the brain respond differently to risk factors associated with Alzheimer's.

 

Alzheimer's disease, the most common form of dementia, is a progressive brain disorder that leads to loss of cognitive skills and memory and causes significant changes in behavior. Aging is a significant risk factor for Alzheimer's. Previous studies suggest that diet-related obesity is also associated with development of the disease.

 

Researchers from Brock University in Ontario, Canada, looked at the effects of an obesity-inducing diet on insulin signaling (the process that tells the body how to use sugar), and markers of inflammation and cellular stress. These factors have been found to be involved in the progression of Alzheimer's disease during the aging process in mice. One group of mice received a high-fat, high-sugar diet ("HFS"), while the control group ate a normal diet. The researchers measured the animals' inflammation and stress levels in the hippocampus and the prefrontal cortex in the brain after 13 weeks on the assigned diets. They compared the brains of aged mice to those of a younger set of baseline mice. The hippocampus is near the center of the brain and is responsible for long-term memory. The prefrontal cortex, at the front of the brain, oversees complex cognitive, emotional and behavioral function.

 

Compared to the control group, the HFS group had significantly higher markers of inflammation, insulin resistance (altered insulin signaling) and cellular stress in areas of the hippocampus thought to be involved in the progression of Alzheimer's disease. The prefrontal cortex region of the HFS group showed more signs of insulin resistance, but inflammation and cellular stress markers did not change. The "region specific differences between the prefrontal cortex and hippocampus in response to aging with a HFS diet [indicates] that the disease pathology is not uniform throughout the brain," the researchers wrote.

 

The control group's inflammation levels were also increased after the trial when compared to the baseline readings. These results supports the theory that aging alone plays a role in the progression of Alzheimer's disease, and obesity exacerbates the effects of aging on brain function.

 

"This study provides novel information in relation to the mechanistic link between obesity and the transition from adulthood to middle age and signaling cascades that may be related to [Alzheimer's] pathology later in life," the research team wrote. "These results add to our basic understanding of the pathways involved in the early progression of [Alzheimer's] pathogenesis and demonstrate the negative effects of a HFS diet on both the prefrontal cortex and hippocampal regions."

https://www.sciencedaily.com/releases/2018/06/180628151649.htm

Adolescents who consume diet high in saturated fats may develop poor stress skills

Rat study provides insights into impact of diet on brain functioning during critical developmental period

June 13, 2018

Science Daily/Loma Linda University Adventist Health Sciences Center

Adolescents who consume a diet high in saturated fats may develop poor stress coping skills, signs of post-traumatic stress disorder as adults.

 

"The teen years are a very critical time for brain maturation, including how well (or not) we'll cope with stress as adults," said Dr. Johnny Figueroa, Assistant Professor, Division of Physiology, Department of Basic Sciences and Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine. "The findings of our research support that the lifestyle decisions made during adolescence -- even those as simple as your diet -- can make a big difference in our ability to overcome every day challenges."

 

The study, "Exposure to an obesogenic diet during adolescence leads to abnormal maturation of neural and behavioral substrates underpinning fear and anxiety," investigated the impact of an obesogenic Western-like high-saturated fat diet on the development of brain areas involved in responding to fear and stress. Study findings demonstrate that the consumption of an obesogenic diet during adolescence has a profound effect on phasic and sustained components of fear in the adult rat. Notably, the rats that consumed the high-saturated fat diet exhibited more anxiety, problems with associative and non-associative learning processes and an impaired fear-startle response.

 

Startle reflexes, which are studied in humans and lab animals, have a prominent role in anxiety and PTSD research. In this study, consumption of an obesogenic diet during adolescence reduced the extinction of fear memories -- a major impairment observed in people suffering from PTSD. In addition to not properly learning fear associations, the rats on the high-saturated fat diet incorrectly assessed the level of threat. This suggests that obesity and associated metabolic alterations may predispose individuals to PTSD-related psychopathology.

 

Researchers reported that the animals in the high-saturated fat diet group exhibited alterations in the structure of brain regions associated with PTSD, including the amygdala and the prefrontal cortex. Notably, the group found that the left-brain hemisphere seems to be more vulnerable to the effects of high-saturated fat diet consumption and obesity-related metabolic alterations. Understanding the neural networks that predispose obese adolescents to developing anxiety and stress-related disorders may help target metabolic measures to alleviate the burden of mental illness in this growing population.

 

Figueroa said the study leaves other questions open for further investigation, such as replicability in human subjects and if the alterations seen in the brain structures are permanent or whether the effects can be reversed. Study limitations include lack of clarity on how the high-saturated fat diet impacts the adult brain, and whether the effects of the obesogenic diet on the fear response are related to deficits in fear memory consolidation, retrieval and expression.

https://www.sciencedaily.com/releases/2018/06/180613113738.htm

Sleep loss linked to nighttime snacking, junk food cravings, obesity, diabetes

June 1, 2018

Science Daily/University of Arizona Health Sciences

Nighttime snacking and junk food cravings may contribute to unhealthy eating behaviors and represent a potential link between poor sleep and obesity.

 

The study was conducted via a nationwide, phone-based survey of 3,105 adults from 23 U.S. metropolitan areas. Participants were asked if they regularly consumed a nighttime snack and whether lack of sleep led them to crave junk food. They also were asked about their sleep quality and existing health problems.

 

About 60 percent of participants reported regular nighttime snacking and two-thirds reported that lack of sleep led them to crave more junk food.

 

The researchers found that junk food cravings were associated with double the increase in the likelihood of nighttime snacking, which was associated with an increased risk for diabetes. They also found that poor sleep quality seemed to be a major predictor of junk food cravings, and that junk food cravings were associated with a greater likelihood of participants reporting obesity, diabetes and other health problems.

 

"Laboratory studies suggest that sleep deprivation can lead to junk food cravings at night, which leads to increased unhealthy snacking at night, which then leads to weight gain. This study provides important information about the process, that these laboratory findings may actually translate to the real world," noted Michael A. Grandner, PhD, MTR, UA assistant professor of psychiatry and director of the UA Sleep and Health Research Program and the UA Behavioral Sleep Medicine Clinic. "This connection between poor sleep, junk food cravings and unhealthy nighttime snacking may represent an important way that sleep helps regulate metabolism."

 

"Sleep is increasingly recognized as an important factor in health, alongside nutrition," said Christopher Sanchez, UA undergraduate nutrition and dietetics major, who is the lead author of the study and a student research assistant in the Sleep and Health Research Program directed by Dr. Grandner. "This study shows how sleep and eating patterns are linked and work together to promote health."

 

William D. "Scott" Killgore, PhD, UA professor of psychiatry, medical imaging and psychology, and director of the UA Social, Cognitive and Affective Neuroscience (SCAN) Lab, also contributed to the study.

 

UA Health Sciences sleep researchers work as interdisciplinary teams, conducting research and leading clinical trials to assess how sleep affects memory, mental health, stress, alertness and decision-making, and how environmental factors affect sleep. Sleep and wakefulness disorders affect an estimated 15 to 20 percent of U.S. adults, according to the U.S. Department of Health and Human Services.

https://www.sciencedaily.com/releases/2018/06/180601171900.htm

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