The government is reviewing its dietary guidelines on saturated fat following growing concerns that it’s been unfairly “demonized” in the past.
Under current recommendations, the government advises that foods high in saturated fat such as butter, cream, and cheese make up just 10% of the total calories a person eats per day.
This is largely because saturated fats were previously linked to a person having an increased risk of heart disease. But in the past few years, two studies have found there is no link between saturated fats and heart disease and several experts have said eating more saturated fats could actually be beneficial for our health.
Saturated Fats Good or Bad?
According to The Times, minutes from the saturated fats working group of the scientific advisory committee on nutrition (SACN) say the decision was made to re-examine government advice on saturated fats “in the context of recent meta-analyses that have reported no significant associations between saturated fats and cardiovascular disease”.
Food Standards Scotland also requested a review.
Speaking to the paper, lead cardiologist Aseem Malhotra said: “I don’t think there is any good evidence that eating saturated fats causes cardiovascular disease and there should not be any limit. We should instead base the official advice on the type of foods people should be eating.
“Saturated fats has been wrongly demonized because of poor science. The evidence is accumulating that sugar is the No 1 dietary culprit driving cardiovascular disease.”
The new review will look at the consumption of saturated fats in relation to overall mortality rates, heart disease, Type 2 diabetes, and cancer.
The news of the review comes after a report from the National Obesity Forum (NOF) and the Public Health Collaboration released last month questioned the advice given in the government’s official Eatwell Guide.
The report claimed that “the continued demonisation of omnipresent natural fat” was fuelling the obesity crisis, as some of the most nutritious foods available – such as meat, fish, eggs, dairy products, nuts, seeds, olive, avocados – all contain saturated fats.
It advised the public to eat more fats and cut the amount of carbohydrates they eat in order to reduce their risk of obesity and diabetes.
But the report was met with controversy, with The British Dietetic Association calling the advice “potentially dangerous” while a spokesperson from Public Health England slated it as “irresponsible”.
The new review of saturated fats is set to be published next year.
Many people are wondering about the link between salt and weight gain (or weight loss) so they are asking numerous questions: Can Salt Prevent You From Losing Weight? Can Eating Salt Prevent Weight Loss? Does salt make you fat? Fat and salt are a common and appetitive combination in food; however, the effect of either on food intake is unclear. Fat taste sensitivity has been negatively associated with dietary fat intake, but how fat taste sensitivity influences the intake of fat within a meal has, to our knowledge, not yet been investigated.
The goals of this new study were to investigate the effects of both fat and salt on ad libitum food intake and, second, to investigate the effects of fat taste sensitivity on satiation responses to fat and whether this was affected by salt.
Forty-eight healthy adults, 16 men, and 32 women, aged 18–54 years old, with a BMI between 17.8 and 34.4, were recruited to participate in this study. They attended 4 lunchtime sessions after a standardized breakfast. Meals consisted of elbow macaroni with sauce; sauces were manipulated to low-fat/low-salt, low-fat/high-salt, high-fat/low-salt and high-fat/high-salt. Also read: Obesity Could Cause 670,000 New Cancer Cases By 2035
The study found that Salt increased food and energy intakes by 11%, irrespective of if the fat content was high or low. The fat content of the meal didn’t result in people eating more food by weight, but because of its greater energy density, that meant more kilojoules were eaten.
People who were considered to be sensitive to the taste of fat ate less of the high-fat meal, but only if it was also low in salt. Ratings of hunger before, and fullness after, each meal were similar and unaffected by the meal composition.
The results of this research suggest that salt promotes passive overconsumption of energy in adults and that salt may override fat-mediated satiation in individuals who are sensitive to the taste of fat. This means that the saltiness of food is being able to influence passive over-consumption for foods high fat.
In a time when there are too many discretionary food choices available that meet the criteria for being high in fat and salt, then this research helps explain why such food could be an important driver of excess eating and subsequent weight gain. So if you still asking yourself, does salt make me fat ? does salt prevent weight loss ? in the light of this study, I would say yes definitely.
Besides that, Salt has been proved to be linked to high blood pressure and heart disease as well.
Recently, there has beenresearch examining the connection between poultry consumption and weight gain. One study out of the Netherlands examining about 4,000 people, correlated chicken consumption with weight gain. Another study followed 89,000 people in four other countries and found that animal protein intake was associated with long-term weight gain, and poultry was the worst, with 40 percent more weight gain than red meat or processed meat.
What makes poultry so bad? Yes, chickens are fatty these days because of the way we’ve genetically manipulated them—up to ten times more fat and calories than they used to have—but one bizarre theory postulated that it might be due to an obesity-causing chicken virus. In one study, one in five obese humans tested positive to the chicken virus SMAM-1, with those exposed to the chicken virus averaging 33 pounds heavier than those testing negative.
SMAM-1 was the first chicken virus to be associated with human obesity, but not the last. The original obesity-causing chicken virus SMAM-1 was able to effectively transmit obesity from one chicken to another when caged together, similar to a human adenovirus Ad-36, a human obesity-associated virus first associated with obesity in chickens and mice. Ad-36 spreads quickly from one chicken to another via nasal, oral or fecal excretion and contamination, causing obesity in each chicken. This, of course, raises serious concerns about Ad-36-induced adiposity in humans.
The easiest way to test this hypothesis is to experimentally infect humans with the virus. However, ethical reasons preclude experimental infection of humans, and so, the evidence will have to remain indirect. In the absence of direct experimental data, we must rely on population studies, similar to how researchers nailed smoking and lung cancer. About 15 percent of Americans are already infected with Ad-36; so, we can follow them and see what happens. That’s exactly what a research team out of Taiwan did. They followed 1,400 Hispanic men and women for a decade and found that not only were those exposed to the virus fatter than those who were not, but also over the ten years, those with a history of infection had a greater percentage of body fat over time. Also read: In Fight Against Obesity, The U.S. Is Failing Women
Most studies done to date on adults have found a connection between exposure to Ad-36 and obesity, and all studies done so far on childhood obesity show an increase in the prevalence of infection in obese children compared to non-obese children. We’re now up to more than a thousand children studied with similar findings. Obese children who tested positive for the virus weighed 35 pounds more than children who tested negative.
The virus appears to both increase the number of fat cells by mobilizing precursor stem cells and increase the accumulation of fat within the cells. If we take liposuction samples of fat from people, the fat cell precursors turn into fat cells at about five times the rate in people who came to the liposuction clinic already infected. Fat taken from non-infected people that were then exposed to the virus start sucking up fat at a faster rate, potentially inducing obesity without increasing food intake.
Just as Ad-36 can be transmitted horizontally from one infected chicken to another in the same cage, subsequently causing obesity in each chicken, this same virus is also easily transmitted among humans, raising the question as to whether at least some cases of childhood obesity can be considered an infectious disease. Researchers publishing in the International Journal of Pediatric Obesity speculate that this animal adenovirus may have mutated to become a human adenovirus capable of infecting humans and causing obesity.
Video Transcript :
0:00 think twice before blaming yourself or someone else for being overweight
0:04 a new study suggests a common childhood virus could be the culprit
0:08 researchers found that children exposed to add no virus 36 an infection that
0:12 causes short-term gastrointestinal and respiratory symptoms
0:16 wait an average of 52 pounds more than children who were never infected
0:20 researchers believe this fat virus increases the body's fat cells and makes
0:24 it harder for the body to break down mature fat cells later
0:27 the result is that people affected by the virus store more fat overall
0:31 so go easy on the next overweight person you see diet and exercise may not work
New wearable technology is helping to provide novel weight loss tools. One way is by providing bite count feedback, which allows users to keep track of the number of bites during a meal.
Researchers at Clemson University wanted to analyze how providing bite count feedback might influence eaters in different situations and determine its efficacy in the presence of environmental cues linked to overeating. The study found that people who received bite count feedback ate less and reduced their overall intake during a meal. The full results are published in the Journal of the Academy of Nutrition and Dietetics. Investigators recruited young adults to consume a meal in the laboratory. In the first round, some subjects were outfitted with bite count feedback devices and given either a small or large plate. The group that received bite count feedback significantly reduced their intake regardless of plate size, although, those given larger plates still consumed more than those given smaller plates. Larger plate sizes have been positively linked to overconsumption. While providing bite count feedback helped mitigate the known influence of plate size, it was not enough to overcome it completely. Also read: Overeating May Cause More Eating By Cutting Off Fullness Signal "It was found that the presence of bite count feedback led to a reduction in overall consumption. This finding is consistent with current literature that shows feedback on consumption leads people to consume less," explained Phillip W. Jasper, PhD candidate in Human Factor Psychology, Department of Psychology, Clemson University. "It was found that this type of feedback does not eliminate the effect of environment cues such as plate size. Individuals may eat less when they receive bite count feedback, but feedback alone may not be sufficient in terms of helping them to take an 'appropriate' or 'normal' number of bites, particularly in the presence of large plates." In the second round, subjects were given either a low-bite goal (12 bites) or a high-bite goal (22 bites) for their meal. Interestingly, both groups met their goals, but the low-bite group took bigger bites, which resulted in both groups having comparable levels of consumption. This revealed a complex relationship between bite count goals and energy intake. "It is possible that this compensatory behavior is intentional, a reaction to a perceived limitation such that participants believed 12 bites to be too restricting of a goal," noted Mr. Jasper. "In other words, in an effort to reach satiety while not surpassing the given goal, participants felt as though they needed to take larger bites than they typically would." In order to effectively manage creating a realistic bite goal without making people feel like they need to overcompensate with bigger bites, investigators suggest helping patients establish a baseline level of bites across all meals plus snacks before setting any bite number goals. Following a thorough evaluation of typical behavior, practitioners can then work with patients to set personalized bite goals that are just slightly under their average, thus helping them to reduce intake through fewer bites without feeling like they have to overcompensate. "It is possible to reduce the number of bites and in an appropriate way so that individuals don't even know they're reducing their bites and their caloric intake. Over the timespan of an effective diet, that delta in energy intake really has a strong impact on overall weight gain and weight change," added Mr. Jasper. Bite count feedback is an excellent weapon against the so-called "mindless margin," or the amount people eat without really thinking about it. By providing live insight into the number of bites, people will be more likely to stop eating when appropriately full and be more aware of what they're eating. "We want people to be mindful of what they're doing. That's what's really important. We want them to be mindful of their eating, and bite count feedback is a way to keep people mindful of their eating behaviors," explained Mr. Jasper. New approaches such as providing bite count feedback can help people concerned with overweight and obesity eat less by providing them with external indicators of their energy intake. Knowing the number of bites is much less abstract than knowing the number of calories. "Self-monitoring is one of the cornerstones of successful weight loss," concluded Mr. Jasper. "By giving people bite count feedback, which is a good indicator of energy intake, they know how much they've had to eat or drink, they know their intake so they can better adjust their energy expenditure behaviors." Source: This research was funded by National Institutes of Health grant no. 2R42DK0911410-02. Article: Effects of Bite Count Feedback from a Wearable Device and Goal-Setting on Consumption in Young Adults, Phillip W. Jasper, MS, Melva T. James, PhD, Adam W. Hoover, PhD, Eric R. Muth, PhD, Journal of the Academy of Nutrition and Dietetics, doi: 10.1016/j.jand.2016.05.004, published online 23 June 2016.
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Overeating can lead to more eating, setting up a vicious cycle that promotes obesity. Now, a new study suggests one way this cycle works is that when the gut senses too many calories, it shuts off a hormone that tells the brain we are full.
In the journal Nutrition & Diabetes, researchers at Thomas Jefferson University, Philadelphia, PA, describe how they came to this conclusion after observing mice on high-calorie diets. In previous research on colon cancer using non-obese mice, the team had come across a hormone called uroguanylin that is produced in the small intestine and then travels to the brain where it signals fullness. Building on their earlier work, senior author and professor Scott A. Waldman, chair of pharmacology and experimental therapeutics, and colleagues decided to explore how uroguanylin might be involved in promoting obesity. They put mice on high-calorie, obesity-inducing diets for 14 weeks and monitored what happened to uroguanylin in their guts and brains. The researchers found that the small intestines of the overfed mice stopped producing uroguanylin. Prof. Waldman notes:
"What's interesting is that it didn't matter whether the mice were lean and overfed, or obese and overfed - uroguanylin production stopped in both groups of animals when they got too many calories."
When they examined the animals' brains, the team found the receptors for the hormone were intact - and had even increased in number - showing it was the lack of production rather than poor reception that had stopped the fullness signal reaching the brain. Stressed endoplasmic reticulum might play a role When the overfed mice were then put on a low-calorie diet, their small intestines began producing the hormone again. These effects are the opposite of what we know about other obesity-related hormones like insulin and leptin, Prof. Waldman explains. Production of these hormones goes up as weight increases, but here, "it's not the obese state that's causing the masalah but rather it's the calories," he adds. Also read: Have You Ever Heard About Fat Virus ? Virus In Chicken Linked To ObesityDo Drugs Compared by FDA To discover what the underlying mechanism might be, the team examined the cells in the small intestine responsible for uroguanylin production. They had a hunch that it might have something to do with the endoplasmic reticulum (ER) - a cell compartment that acts like a mini factory for proteins and hormones. The ER can stop working if it gets stressed. When the researchers gave the mice tunicamycin, a chemical that causes ER stress, the animals stopped producing uroguanylin. The team also found that giving overfed, obese mice a chemical known to relieve ER stress caused their gut to resume production of the hormone. The researchers suggest in combination with other approaches, hormone replacement of uroguanylin may become an important component of therapy to reverse obesity. However, a lot more research needs to be done first. As with cancer, there are many steps to becoming obese that are not easily reversed. Future studies need to find out, for example, whether the uroguanylin pathway is important early or late in the process, and how big an influence it has compared with other pathways.
In an analysis that included nearly 30,000 overweight or obese adults, compared with placebo, orlistat, lorcaserin, naltrexone-bupropion, phentermine-topiramate, and liraglutide were each associated with achieving at least 5 percent weight loss at 52 weeks, and phentermine-topiramate and liraglutide were associated with the highest odds of achieving at least 5 percent weight loss, according to a study appearing in the June 14 issue of JAMA. Approximately 1.9 billion adults are overweight and 600 million are obese worldwide. Identifying effective long-term treatment strategies for overweight and obesity is of paramount importance. The U.S. Food and Drug Administration (FDA) has approved 5 weight loss drugs (orlistat, lorcaserin, naltrexone-bupropion, phentermine-topiramate, and liraglutide) for long-term use in obese (body mass index [BMI] ? 30) or overweight (BMI ? 27) individuals with at least 1 weight-associated condition (type 2 diabetes, hypertension, hyperlipidemia). Data on the comparative effectiveness of these drugs are limited. Siddharth Singh, M.D., M.S., of the University of California, San Diego, La Jolla, and colleagues conducted a systematic review and meta-analysis of randomized clinical trials that included overweight and obese adults treated with FDA-approved long-term weight loss agents for at least 1 year compared with another active agent or placebo. Twenty-eight randomized clinical trials with 29,018 patients (median age, 46 years; 74 percent women; median baseline body weight, 222 lbs.; median baseline BMI, 36.1) were included.
The researchers found that a median 23 percent of placebo participants had at least 5 percent weight loss vs 75 percent of participants taking phentermine-topiramate, 63 percent of participants taking liraglutide, 55 percent taking naltrexone-bupropion, 49 percent taking lorcaserin, and 44 percent taking orlistat. All active agents were associated with significant excess weight loss compared with placebo at 1 year: phentermine-topiramate, 19.4 lbs.; liraglutide, 11.7 lbs.; naltrexone-bupropion, 11 lbs.; lorcaserin, 7.1 lbs.; and orlistat, 5.7 lbs. Compared with placebo, liraglutide and naltrexone-bupropion were associated with the highest odds of adverse event-related treatment discontinuation. "Ultimately, given the differences in safety, efficacy, and response to therapy, the ideal approach to weight loss should be highly individualized, identifying appropriate candidates for pharmacotherapy, behavioral interventions, and surgical interventions. Historically, concerns regarding the long-term safety profile of pharmacotherapy for weight loss have limited their clinical use, particularly among medications with significant adrenergic actions or central appetite-suppressing actions. Short-term clinical trials may not provide comprehensive information on the long-term safety of these agents, and prospective postmarketing surveillance studies are warranted," the authors write. Ressource: Association of Pharmacological Treatments for Obesity With Weight Loss and Adverse Events: A Systematic Review and Meta-analysis, Rohan Khera, MD; Mohammad Hassan Murad, MD, MPH; Apoorva K. Chandar, MBBS, MPH; Parambir S. Dulai, MD; Zhen Wang, PhD; Larry J. Prokop, MLS; Rohit Loomba, MD, MHSc; Michael Camilleri, MD; Siddharth Singh, MD, MS, JAMA, doi:10.1001/jama.2016.7602, published 14 June 2016.
Kyoto University researchers have found that fish oil transforms fat-storage cells into fat-burning cells, which may reduce weight gain in middle age. Fish oil activates receptors in the digestive tract, fires the sympathetic nervous system, and induces storage cells to metabolize fat.
The team explains in Scientific Reports that fish oil activates receptors in the digestive tract, fires the sympathetic nervous system, and induces storage cells to metabolize fat.
Fat tissues don't all store fat. So-called "white" cells store fat in order to maintain energy supply, while "brown" cells metabolize fat to maintain a stable body temperature. Brown cells are abundant in babies but decrease in number with maturity into adulthood.
A third type of fat cell -- "beige" cells -- have recently been found in humans and mice, and have shown to function much like brown cells. Beige cells also reduce in number as people approach middle age; without these metabolizing cells, fat continues accumulating for decades without ever being used.
The scientists investigated whether the number of these beige cells could be increased by taking in certain types of foods.
"We knew from previous research that fish oil has tremendous health benefits, including the prevention of fat accumulation," says senior author Teruo Kawada. "We tested whether fish oil and an increase in beige cells could be related."
The team fed a group of mice fatty food, and other groups fatty food with fish oil additives. The mice that ate food with fish oil, they found, gained 5-10% less weight and 15-25% less fat compared to those that did not consume the oil.
They also found that beige cells formed from white fat cells when the sympathetic nervous system was activated, meaning that certain fat-storage cells acquired the ability to metabolize.
"People have long said that food from Japan and the Mediterranean contribute to longevity, but why these cuisines are beneficial was up for debate," adds Kawada. "Now we have better insight into why that may be."
Source: Eiri Ono/Kyoto University
Journal Reference:Minji Kim, Tsuyoshi Goto, Rina Yu, Kunitoshi Uchida, Makoto Tominaga, Yuriko Kano, Nobuyuki Takahashi, Teruo Kawada. Fish oil intake induces UCP1 upregulation in brown and white adipose tissue via the sympathetic nervous system. Scientific Reports, 2015; 5: 18013 DOI: 10.1038/srep18013
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