Posts Tagged ‘obesity’

Is your child having a tough time sleeping properly? You may need to keep a check on his/her body mass index (BMI) as a new research suggests that there is a co-relation between the two and can lead to cancer in adulthood.

“Childhood obesity very often leads to adult obesity. This puts them at greater risk of developing obesity-related cancers in adulthood,” said study lead author Bernard Fuemmeler, Professor and Associate Director for Cancer Prevention and Control at the Virginia Commonwealth University.

For the study, researchers enrolled 120 children, with an average age of eight, whose mothers had participated in the Newborn Epigenetic Study both pre-birth and during early childhood.

To track the sleep-wake cycle, the children wore accelerometers continuously for 24 hours a day for a period of at least five days.

They found that shorter sleep duration, measured in hours, was associated with a higher BMI z-score (body mass index adjusted for age and sex).

Each additional hour of sleep was associated with a .13 decrease in BMI z-score and with a 1.29 cm decrease in waist circumference.

More fragmented rest-activity rhythms and increased intradaily variability — a measure of the frequency and extent of transitions between sleep and activity — were also associated with greater waist circumferences.

The study results, to be presented at Obesity and Cancer: Mechanisms Underlying Etiology and Outcomes, indicate that while sleep duration is important, examining markers of sleep quality may also be useful in designing childhood obesity prevention strategies.

“Today, many children are not getting enough sleep. There are a number of distractions, such as screens in the bedroom, that contribute to interrupted, fragmented sleep. This, perpetuated over time, can be a risk factor for obesity,” Fuemmeler said.

“Because of the strong links between obesity and many types of cancer, childhood obesity prevention is cancer prevention.”

Proper sleep in children may prevent cancer later

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Consumption of dietary fiber can prevent obesity, metabolic syndrome and adverse changes in the intestine by promoting growth of “good” bacteria in the colon, according to a study led by Georgia State University.

The researchers found enriching the diet of mice with the fermentable fiber inulin prevented metabolic syndrome that is induced by a high-fat diet, and they identified specifically how this occurs in the body. Metabolic syndrome is a cluster of conditions closely linked to obesity that includes increased blood pressure, high blood sugar, excess body fat around the waist and abnormal cholesterol or triglyceride levels. When these conditions occur together, they increase a person’s risk of heart disease, stroke and diabetes.

Obesity and metabolic syndrome are associated with alterations in gut microbiota, the microorganism population that lives in the intestine. Modern changes in dietary habits, particularly the consumption of processed foods lacking fiber, are believed to affect microbiota and contribute to the increase of chronic inflammatory disease, including metabolic syndrome. Studies have found a high-fat diet destroys gut microbiota, reduces the production of epithelial cells lining the intestine and causes gut bacteria to invade intestinal epithelial cells.

This study found the fermentable fiber inulin restored gut health and protected mice against metabolic syndrome induced by a high-fat diet by restoring gut microbiota levels, increasing the production of intestinal epithelial cells and restoring expression of the protein interleukin-22 (IL-22), which prevented gut microbiota from invading epithelial cells. The findings are published in the journal Cell Host & Microbe.

“We found that manipulating dietary fiber content, particularly by adding fermentable fiber, guards against metabolic syndrome,” said Dr. Andrew Gewirtz, professor in the Institute for Biomedical Sciences at Georgia State. “This study revealed the specific mechanism used to restore gut health and suppress obesity and metabolic syndrome is the induction of IL-22 expression. These results contribute to the understanding of the mechanisms that underlie diet-induced obesity and offer insight into how fermentable fibers might promote better health.”

For four weeks, the researchers fed mice either a grain-based rodent chow, a high-fat diet (high fat and low fiber content with 5 percent cellulose as a source of fiber) or a high-fat diet supplemented with fiber (either fermentable inulin fiber or insoluble cellulose fiber). The high-fat diet is linked to an increase in obesity and conditions associated with metabolic syndrome.

They discovered a diet supplemented with inulin reduced weight gain and noticeably reduced obesity induced by a high-fat diet, which was accompanied by a reduction in the size of fat cells. Dietary enrichment with inulin also markedly lowered cholesterol levels and largely prevented dysglycemia (abnormal blood sugar levels). The researchers found insoluble cellulose fiber only modestly reduced obesity and dysglycemia

Supplementing the high-fat diet with inulin restored gut microbiota. However, inulin didn’t restore the microbiota levels to those of mice fed a chow diet. A distinct difference in microbiota levels remained between mice fed a high-fat diet versus those fed a chow diet. Enrichment of high-fat diets with cellulose had a mild effect on microbiota levels.

In addition, the researchers found switching mice from a grain-based chow diet to a high-fat diet resulted in a loss of colon mass, which they believe contributes to low-grade inflammation and metabolic syndrome. When they switched mice back to a chow diet, the colon mass was fully restored.

https://www.technologynetworks.com/tn/news/fiber-rich-diet-fights-off-obesity-by-altering-microbiota-296642?utm_campaign=Newsletter_TN_BreakingScienceNews&utm_source=hs_email&utm_medium=email&utm_content=60184554&_hsenc=p2ANqtz-9YDsGiTl44CBfQpgNtYgc43xBeVKpAbPZym9Lh_GzlHoEVts0rAwMhHHXIDam3Jit0D3aTqKGhCceUREgr6sZfLGMWpQ&_hsmi=60184554

by Laura Elizabeth Lansdowne

Researchers have gained a new understanding of the link between obesity and cancer. In the presence of excess fat, the immune surveillance system fails due to an obesity-fueled lipid accumulation in natural killer (NK) cells, preventing their cellular metabolism and trafficking. The new findings were published in Nature Immunology.1

More than 1.9 billion adults are either overweight or obese and a growing amount of evidence proposes that numerous cancer types (including liver, kidney, endometrial and pancreatic cancers)2 are more common in overweight or obese people. Cancer risk is increased in those with higher body fat, with up to 49% of certain types attributed to obesity.3

Previous findings from the GLOBOCAN project indicate that, in 2012 in the United States, approximately 28,000 new cases of cancer in men and approximately 72,000 in women were associated with being obese or overweight.4

The 2018 study1 investigated the effect of obesity on the cellular metabolism, gene expression, and function of NK cells, and its influence on cancer development.

NK cells are cells of the innate immune system that limit the spread of tumors – numerous in vitro models have shown that tumor cells are recognized as ‘targets’ by NK cells.5 These cells destroy their targets by secreting lytic granules containing perforin and apoptosis-inducing granzymes. NK cells require a greater amount of energy to support their anti-tumor activity, therefore they switch their metabolic activity from oxidative phosphorylation (OXPHOS) to glycolysis to meet the increased demand for ATP.1

The researchers discovered that NK cells in an ‘obese environment’ display increased lipid accumulation which affects their cellular bioenergetics, resulting in ‘metabolic paralysis’. This lipid-induced metabolic paralysis led to loss of anti-tumor activity both in vitro and in vivo models. They were able to mimic obesity through fatty-acid administration and by using PPARα/δ agonists, which inhibited mechanistic target of rapamycin (mTOR)-mediated glycolysis.1

However, the researchers also discovered that it was possible to reverse the metabolic paralysis by either inhibiting PPARα/δ or by blocking lipid transport, suggesting that metabolic reprogramming of NK cells could restore their anti-tumor activity in human obesity.1

Corresponding author of the study, Lydia Lynch commented on the importance of the findings in a recent press release: “Despite increased public awareness, the prevalence of obesity and related diseases continue. Therefore, there is increased urgency to understand the pathways whereby obesity causes cancer and leads to other diseases, and to develop new strategies to prevent their progression.”

References

1. Michelet, X., et al. Metabolic reprogramming of natural killer cells in obesity limits antitumor responses. Nature Immunology. (2018) https://www.nature.com/articles/s41590-018-0251-7
2. Mason, L. E., The Link Between Cancer and Obesity. Technology Networks. Available at: https://www.technologynetworks.com/cancer-research/articles/the-link-between-cancer-and-obesity-298207. Accessed: November 12, 2018
3. Renehan, A. G., et al. Body-mass index and incidence of cancer: a systematic review and meta-analysis of prospective observational studies. Lancet. (2008) 371, 569–578
4. Arnold, M., et al. Global burden of cancer attributable to high body-mass index in 2012: a population-based study. Lancet Oncol. (2015) 16(1): 36–46
5. Vivier, E., et al. Functions of natural killer cells. Nature Immunology. (2008) 9, 503–510

https://www.technologynetworks.com/cancer-research/news/obesity-and-cancer-fat-clogged-immune-cells-fail-to-fight-tumors-311744?utm_campaign=NEWSLETTER_TN_Breaking%20Science%20News&utm_source=hs_email&utm_medium=email&utm_content=68543465&_hsenc=p2ANqtz–8ZbNt7sDLF6bujB3qX9CeJA-hpSQwPHeSLoR5Ju1WYXA6SnOEepdO0o-J7qw_1aGB3nfwldpf30hV3pAvVi7SzJa8fw&_hsmi=68543465


A fluorescent probe creates a heat map of copper in white fat cells. Higher levels of copper are shown in yellow and red. The left panel shows normal levels of copper from fat cells of control mice, and the right panel shows cells deficient in copper.
Credit: Lakshmi Krishnamoorthy and Joseph Cotruvo Jr./UC Berkeley

A new study is further burnishing copper’s reputation as an essential nutrient for human physiology. A research team led by a scientist at the Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) and at the University of California, Berkeley, has found that copper plays a key role in metabolizing fat.

Long prized as a malleable, conductive metal used in cookware, electronics, jewelry and plumbing, copper has been gaining increasing attention over the past decade for its role in certain biological functions. It has been known that copper is needed to form red blood cells, absorb iron, develop connective tissue and support the immune system.

The new findings, to appear in the July print issue of Nature Chemical Biology but published online today, establishes for the first time copper’s role in fat metabolism.

The team of researchers was led by Chris Chang, a faculty scientist at Berkeley Lab’s Chemical Sciences Division, a UC Berkeley professor of chemistry and a Howard Hughes Medical Institute investigator. Co-lead authors of the study are Lakshmi Krishnamoorthy and Joseph Cotruvo Jr, both UC Berkeley postdoctoral researchers in chemistry with affiliations at Berkeley Lab.

“We find that copper is essential for breaking down fat cells so that they can be used for energy,” said Chang. “It acts as a regulator. The more copper there is, the more the fat is broken down. We think it would be worthwhile to study whether a deficiency in this nutrient could be linked to obesity and obesity-related diseases.”

Dietary copper

Chang said that copper could potentially play a role in restoring a natural way to burn fat. The nutrient is plentiful in foods such as oysters and other shellfish, leafy greens, mushrooms, seeds, nuts and beans.

According to the Food and Nutrition Board of the Institute of Medicine, an adult’s estimated average dietary requirement for copper is about 700 micrograms per day. The Food and Nutrition Board also found that only 25 percent of the U.S. population gets enough copper daily.

“Copper is not something the body can make, so we need to get it through our diet,” said Chang. “The typical American diet, however, doesn’t include many green leafy vegetables. Asian diets, for example, have more foods rich in copper.”

But Chang cautions against ingesting copper supplements as a result of these study results. Too much copper can lead to imbalances with other essential minerals, including zinc.

Copper as a ‘brake on a brake’

The researchers made the copper-fat link using mice with a genetic mutation that causes the accumulation of copper in the liver. Notably, these mice have larger than average deposits of fat compared with normal mice.

The inherited condition, known as Wilson’s disease, also occurs in humans and is potentially fatal if left untreated.

Analysis of the mice with Wilson’s disease revealed that the abnormal buildup of copper was accompanied by lower than normal lipid levels in the liver compared with control groups of mice. The researchers also found that the white adipose tissue, or white fat, of the mice with Wilson’s disease had lower levels of copper compared with the control mice and correspondingly higher levels of fat deposits.

They then treated the Wilson’s disease mice with isoproterenol, a beta agonist known to induce lipolysis, the breakdown of fat into fatty acids, through the cyclic adenosine monophosphate (cAMP) signaling pathway. They noted that the mice with Wilson’s disease exhibited less fat-breakdown activity compared with control mice.

The results prompted the researchers to conduct cell culture analyses to clarify the mechanism by which copper influences lipolysis. The researchers used inductively coupled plasma mass spectroscopy (ICP-MS) equipment at Berkeley Lab to measure levels of copper in fat tissue.

“It had been noted in cattle that levels of copper in the feed would affect how fatty the meat was,” said Chang. “This effect on fat deposits in animals was in the agricultural literature, but it hadn’t been clear what the biochemical mechanisms were linking copper and fat.”

The new work builds upon prior research from Chang’s lab on the roles of copper and other metals in neuroscience. In support of President Barack Obama’s BRAIN Initiative, Berkeley Lab provided Chang seed funding in 2013 through the Laboratory Directed Research and Development program. Chang’s work continued through the BRAIN Tri-Institutional Partnership, an alliance with Berkeley Lab, UC Berkeley and UC San Francisco.

Of the copper in human bodies, there are particularly high concentrations found in the brain. Recent studies, including those led by Chang, have found that copper helps brain cells communicate with each other by acting as a brake when it is time for neural signals to stop.

While Chang’s initial focus was on the role of copper in neural communications, he branched out to investigations of metals in fat metabolism and other biological pathways. This latest work was primarily funded by the National Institutes of Health.

https://www.sciencedaily.com/releases/2016/06/160606200439.htm

They found that copper binds to phosphodiesterase 3, or PDE3, an enzyme that binds to cAMP, halting cAMP’s ability to facilitate the breakdown of fat.

“When copper binds phosphodiesterase, it’s like a brake on a brake,” said Chang. “That’s why copper has a positive correlation with lipolysis.”

Hints from cows

The connection between copper and fat metabolism is not altogether surprising. The researchers actually found hints of the link in the field of animal husbandry.

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While researching the brain’s learning and memory system, scientists at Johns Hopkins say they stumbled upon a new type of nerve cell that seems to control feeding behaviors in mice. The finding, they report, adds significant detail to the way brains tell animals when to stop eating and, if confirmed in humans, could lead to new tools for fighting obesity. Details of the study were published by the journal Science today.

“When the type of brain cell we discovered fires and sends off signals, our laboratory mice stop eating soon after,” says Richard Huganir, Ph.D., director of the Department of Neuroscience at the Johns Hopkins University School of Medicine. “The signals seem to tell the mice they’ve had enough.”

Huganir says his team’s discovery grew out of studies of the proteins that strengthen and weaken the intersections, or synapses, between brain cells. These are an important target of research because synapse strength, particularly among cells in the hippocampus and cortex of the brain, is important in learning and memory.

In a search for details about synapse strength, Huganir and graduate student Olof Lagerlöf, M.D., focused on the enzyme OGT — a biological catalyst involved in many bodily functions, including insulin use and sugar chemistry. The enzyme’s job is to add a molecule called N-acetylglucosamine (GlcNAc), a derivative of glucose, to proteins, a phenomenon first discovered in 1984 by Gerald Hart, Ph.D., director of the Johns Hopkins University School of Medicine’s Department of Biological Chemistry and co-leader of the current study. By adding GlcNAc molecules, OGT alters the proteins’ behavior.

To learn about OGT’s role in the brain, Lagerlöf deleted the gene that codes for it from the primary nerve cells of the hippocampus and cortex in adult mice. Even before he looked directly at the impact of the deletion in the rodents’ brains, Lagerlöf reports, he noticed that the mice doubled in weight in just three weeks. It turned out that fat buildup, not muscle mass, was responsible.

When the team monitored the feeding patterns of the mice, they found that those missing OGT ate the same number of meals — on average, 18 a day — as their normal littermates but tarried over the food longer and ate more calories at each meal. When their food intake was restricted to that of a normal lab diet, they no longer gained extra weight, suggesting that the absence of OGT interfered with the animals’ ability to sense when they were full.

“These mice don’t understand that they’ve had enough food, so they keep eating,” says Lagerlöf.

Because the hippocampus and cortex are not known to directly regulate feeding behaviors in rodents or other mammals, the researchers looked for changes elsewhere in the brain, particularly in the hypothalamus, which is known to control body temperature, feeding, sleep and metabolism. There, they found OGT missing from a small subset of nerve cells within a cluster of neurons called the paraventricular nucleus.

Lagerlöf says these cells already were known to send and receive multiple signals related to appetite and food intake. When he looked for changes in the levels of those factors that might be traced to the absence of OGT, he found that most of them were not affected, and the activity of the appetite signals that many other research groups have focused on didn’t seem to be causing the weight gain, he adds.

Next, the team examined the chemical and biological activity of the OGT-negative cells. By measuring the background electrical activity in nonfiring brain cells, the researchers estimated the number of incoming synapses on the cells and found that they were three times as few, compared to normal cells.

“That result suggests that, in these cells, OGT helps maintain synapses,” says Huganir. “The number of synapses on these cells was so low that they probably aren’t receiving enough input to fire. In turn, that suggests that these cells are responsible for sending the message to stop eating.”

To verify this idea, the researchers genetically manipulated the cells in the paraventricular nucleus so that they would add blue light-sensitive proteins to their membranes. When they stimulated the cells with a beam of blue light, the cells fired and sent signals to other parts of the brain, and the mice decreased the amount they ate in a day by about 25 percent.

Finally, because glucose is needed to produce GlcNAc, they thought that glucose levels, which increase after meals, might affect the activity of OGT. Indeed, they found that if they added glucose to nerve cells in petri dishes, the level of proteins with the GlcNAc addition increased in proportion to the amount of glucose in the dishes. And when they looked at cells in the paraventricular nucleus of mice that hadn’t eaten in a while, they saw low levels of GlcNAc-decorated proteins.

“There are still many things about this system that we don’t know,” says Lagerlöf, “but we think that glucose works with OGT in these cells to control ‘portion size’ for the mice. We believe we have found a new receiver of information that directly affects brain activity and feeding behavior, and if our findings bear out in other animals, including people, they may advance the search for drugs or other means of controlling appetites.”

http://www.eurekalert.org/pub_releases/2016-03/jhm-pcc031416.php

houston

Diabetes is so common in Patricia Graham’s neighbourhood that it has its own slang term. “At churches you run into people you ain’t seen in years, and they say, ‘I’ve got sugar,’” she says.

Graham does not quite have “sugar”, but when foot surgery in 2014 reduced her activity level, her blood sugar level soared. And there is a history of diabetes in her family: three of four brothers and her mother, who lost a leg to it.

So three times a week she comes to the smart, modern Diabetes Awareness and Wellness Network (Dawn) centre in Houston’s third ward, a historically African American district near downtown. Used by about 520 people a month, Dawn is in effect a free, city-run gym and support group for diabetics and pre-diabetics: a one-stop shop for inspiration, information and perspiration. Last Friday Graham, 68, was there for a walking session.

Not that she or the half-dozen other participants went anywhere. This was walking on the spot to pulsating music. Had the class stepped outside they would have enjoyed perfect conditions for a stroll: a blue sky and a temperature of 21C. If they had worked up an appetite, a soul food restaurant was only a 15-minute walk away, serving celebrated (if not exactly sugar-free) food that belies its unpromising location in a standard shopping mall on a busy road next to a dialysis centre.

But most of Houston is not built for walking, even on a sunny January day. There’s the constant traffic belching fumes that linger in the humid air; the uneven sidewalks that have a pesky habit of vanishing halfway along the street; the sheer distances to cover in this elongated, ever-expanding metropolis. Walking can feel like a transgressive act against Houston’s car-centric culture of convenience – and its status as the capital of the north American oil and gas industry.

It’s one reason why Houston regularly finishes top, or close, in surveys that crown “America’s fattest city”. Unsurprisingly, it has a diabetes problem as outsized as its residents’ waistlines. By 2040, one in five Houstonians is predicted to have the disease.

According to data from pharmaceutical company Novo Nordisk, the prevalence of type 2 diabetes in the city is 9.1% – with an estimated one in four of these being undiagnosed. Almost a third of adult Houstonians self-describe as obese, according to a 2010-11 survey. Without action, the number of people with diabetes is projected to nearly treble by 2040 to 1.1 million people, with diabetes-related costs soaring from $4.1bn in 2015 to $11.4bn by 2040.

Graham is alarmed by the damage diabetes is wreaking on her community. “I was talking to my friends and saying, so many of the people we grew up with got diabetes and lost limbs,” she says. “It’s not even so much the seniors any more, it’s the young people. But it doesn’t scare them. They act like they’re not afraid.”

Another Dawn member, Verne Jenkins, was diagnosed three years ago. “I had picked up a bit of weight that I shouldn’t have,” says the 63-year-old. “I knew what to eat, I knew what I was doing, I just got out of control.”

Jenkins loves to bake but has cut back on carbs, red meat, salt and sugar, abstaining from one of her guilty pleasures, German chocolate cake. Not that it’s easy in a city with so much choice: “All these wonderful restaurants, all these different kinds of cuisines, of course you’re going to try some. I imagine it leads to our delinquency,” she says.

Graham has watched her diet since she was in her 20s. “I eat pretty good,” she said. “‘She eats like white folks’ – that’s what they tell me!”

Time poverty

Diabetes is a major cause of death, blindness, kidney disease and amputations in the US. While federal researchers announced last year that the rate of new diabetes cases dropped from 1.7 million in 2009 to 1.4 million in 2014, in Texas the percentage of diagnosed adults rose from 9.8% in 2009 to 11% in 2014.

Houston, America’s fourth-largest city, is one of five participating in the Cities Changing Diabetes programme, along with Mexico City, Copenhagen, Tianjin and Shanghai. Vancouver and Johannesburg are soon to join the project, which attempts to understand, publicise and combat the threat through cultural analysis.

“The majority of people with diabetes live in cities,” says Jakob Riis, an executive vice-president at Novo Nordisk, one of the lead partners in the programme alongside the Steno Diabetes Center and University College London. “We need to rethink cities so that they are healthier to live in … otherwise we’re not really addressing the root cause of the problem.”

One of the programme’s key – and perhaps surprising – findings, however, is that assessing the risk of developing diabetes is not as simple as dividing the population according to income and race. The problem is broad – much like Houston itself.

The view stretches for miles from Faith Foreman’s eighth-floor office next to the Astrodome, the famous old indoor baseball stadium. It’s an impressive sight, but for someone tasked with tackling the city’s diabetes epidemic, also a worrying one: the sheer scale of the urban sprawl is part of the problem. The threat of the disease has expanded along with the city.

A low cost of living and a strong jobs market helped Houston become one of the fastest growing urban areas in the US. In response, the city loosened its beltways. Its third major ring road is under construction, with a northwestern segment set to open soon that is some 35 miles from downtown.

Once completed, the Grand Parkway – whose northwestern segment has just opened – will boast a circumference of about 180 miles. That is far in excess of the 117 miles of the M25, although about 14 million people live inside the boundary of London’s orbital motorway, more than twice as many as reside in the Houston area.

Large homes sprout in the shadow of recently opened sections, promising cheap middle-class living with a heavy cost: a commute to central Houston of up to 90 minutes each way during rush hour, with minimal public transport options.
“A lot of time in Houston is spent in a car,” says Foreman, assistant director of Houston’s Department of Health and Human Services. This informs one of the Cities Changing Diabetes study’s most notable findings: that “time poverty” is among the risk factors in Houston for developing type 2 diabetes.

This means that young, relatively well-off people can also be considered a vulnerable population segment, even though they might not fit the traditional profile of people who may develop type 2 diabetes – that is, aged over 45, with high blood pressure and a high BMI, and perhaps disadvantaged through poverty or a lack of health insurance.

“You generally think of marginalised, lower income communities in poverty as your keys to health disparities but I think what we learned from our data in Houston is that we now have to expand the definition of what vulnerable is and what at-risk means. Just because we live in an urban environment, we may all indeed be vulnerable,” says Foreman.

In other words, not only its residents’ dietary choices but the way Houston is constructed as a city appears to be contributing to its diabetes problem, so tackling the issue requires architects as well as doctors; more sidewalks as well as fewer steaks.

Urban isolation is a key challenge, says David Napier of UCL, the lead academic for Cities Changing Diabetes. “Houston is growing so quickly and also expanding geographically at such a rapid rate. When you look at how difficult it is for people just to get out and walk, or walk to work; the fact that so many people commute long distances, spend a lot of time eating out – they have a number of obstacles to overcome,” he says.

A city with notoriously lax planning regulations is now making a conscious effort to put more care into its built environment, with more public transport, expanded bike trails, better parks and denser, more walkable neighbourhoods all evident in recent years, even as the suburbs continue to swell.

Foreman’s agency has more input when officials gather to map out the future city. “That is something that has been a big change over the last two or three years in Houston,” she says. “We are at the table and we are working with city planning to make those decisions.”

But prevention is a vital focus as well as treatment. Along with his team, Stephen Linder of the University of Texas’ school of public health – the local academic lead for Houston’s Cities Changing Diabetes research – gathered data on 5,000 households in Harris County, which includes much of the Houston area.

“One way to approach this project wasn’t to focus on diabetes itself but rather to look at some of the preconditioned social factors that seemed to generate the patterns of living that then led to the clinical signs that would designate people as being prediabetic,” he says from his office at the Texas Medical Center near downtown Houston – the world’s largest medical complex.

“These were people who had neither disadvantage nor biological risk factors. They tended to be the youngest group and would normally escape any kind of assessment – we called them the ‘time-pressured-young’. They’re the ones who did the long commutes; they’re the ones whose perception was they could not manage their day’s worth of stuff, that they have no time for anything.”

For this group, obesity is so prevalent in Houston that it distorts an understanding of what a healthy weight is, Linder found. “Their perception of their health was affected by their peers as opposed to other sorts of references. If all of their peers were overweight then in a relative sense they were fine. The judgments were about one’s peers and not relative to any sort of expert standard,” he says.

Three neighbourhoods were identified as having the highest concentration of people vulnerable to developing diabetes, and a Dallas-area research company, 2M, conducted detailed interviews with 125 residents. One place was particularly surprising: Atascocita, a desirable middle-class area near a large lake and golf courses, about 30 miles north of downtown.

Houston has become, according to a 2012 Rice University study, the most ethnically diverse large metropolitan area in the US. But this cosmopolitan air – one of the qualities sought by any place seeking to become a globally renowned city – may also unwittingly be contributing to the diabetes crisis, the study found.

Some in Atascocita, Linder said, “emphasised this sense of change and transition in their neighbourhoods, that that was a source of stress for them and that they were resistant to making changes in their own lives given the flux that was around them. Because that group happened to be older, even though they were economically secure they did have some other chronic diseases and they satisfied our biorisk characteristics.

“We call them concerned seniors. They weren’t making changes because there was too much else going on for them. And so if we were to say to them ‘you’ve got to change your diet’, they’d say ‘no, I can’t handle any more changes’.”

This matters since food portions are no exception to the “everything’s bigger in Texas” cliche, while Houston’s location near Mexico and the deep south, its embrace of the Lone Star state’s love of barbecued red meat and its enormous variety of restaurants serving international cuisine combine to unhealthy effect.

“The food that had a traditional aspect to it tended not to be the healthiest food – southern food that’s fried and lots of butter and lots of starch, then there’s African American soul food and then there’s Hispanic heavy fat, prepared tamales and the like, and so we found people kind of gravitated to what the UCL people called nourishing traditions,” Linder said.

“People used food as not only a reinforcement of tradition and ritual but also as a way of connecting socially. You’ve moved here from somewhere else, it’s a way to reinforce your identity, it’s a real cultural asset to have, but in a biological sense it’s not the best thing.”

For Linder, one lesson is that generalised advice about healthy eating that has long been part of diabetes awareness efforts may not be effective locally, given the complexity and variety of Houston’s neighbourhoods and the social factors that make populations vulnerable to diabetes.

“It does make the task of dietary change a much more complex one than the simple messages about changing your diet, eat more fruit and vegetables, get more colour on your plate would suggest. Those things bounce off, it’s not a useful set of interventions then for that particular group who rely on these nourishing traditions and find some solace in the change around them,” he said.

Foreman agrees that a targeted approach is vital. “How do you change diabetes in Houston? One neighbourhood at a time, in a sense, but at the same time you have bigger things that you can change systemwide in policies and how you work together collaboratively,” she said. “But then as you narrow it and get more granular it is neighbourhood, and what works in one neighbourhood may or may not work in another.”

Patricia Graham is hoping that the Dawn programme expands to other parts of the city to combat the dangerous union of unhealthy traditional food with a modern convenience culture. “Everything is food, and I mean lots of it and all the time,” she said. “Some people don’t know how to cook without grease or butter. That’s just the way we learn.”

http://www.theguardian.com/cities/2016/feb/11/houston-health-crisis-diabetes-sugar-cars-diabetic?CMP=oth_b-aplnews_d-1

Thanks to Kebmodee for bringing this to the It’s Interesting community.

A recent study has shown that fibroblast growth factor 21 (FGF21), a liver-generated hormone, suppresses the FGF21 is produced in response to high carbohydrate levels, in which it enters the bloodstream and signals the brain to suppress the preference for sweets. Matthew Potthoff, assistant professor of pharmacology in the University of Iowa Carver College of Medicine, noted that this is the “first liver-derived hormone that regulates sugar intake specifically.”consumption of simple sugars.

Earlier studies have shown how some hormones affect appetite. However, these do not regulate any specific macronutrient (eg, carbohydrate, protein, fat) and are produced in organs other than the liver. FGF21 has been known to boost insulin sensitivity but the new findings “can help people who might not be able to sense when they’ve had enough sugar, which may contribute to diabetes,” said Lucas BonDurant, a doctoral student and co-first author in the study.

Researchers used genetically-engineered mouse models and pharmacological approaches to study FGF21 in regulating sugar cravings. Normal mice were injected with FGF21 and were given a choice between a normal diet and a sugar-enriched diet. These mice did not completely stop eating sugar but consumed 7 times less than normal. The team also looked at mice that either did not produce FGF21 at all or overproduced FGF21 (>500 times more than normal mice). When presented with the same two diets as the normal mice, researchers saw that the mice that didn’t produce FGF21 all consumed more sugar whereas the mice that overproduced FGF21 consumed less sugar.

Study findings support the conclusion that FGF21 decreased appetite and sugar intake. It did not, however, decrease intake of all sugars (eg, sucrose, fructose, glucose) nor did it affect the intake of complex carboydrates. The new data may help patients who are obese or have diabetes, researchers noted. More studies are needed to see if other hormones exist to regulate appetite for specific macronutrients comparable to the effects of FGF21 on carbohydrate intake.

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