Surprising Research ! Link Between Saturated Fats And Heart Disease Questioned

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.

Source: huffingtonpost.co.uk

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Obesity And Cancer Risk: Obesity Could Cause 670,000 New Cancer Cases By 2035

Over the next 20 years there will be 670,000 new cases of obesity-related cancer if nothing is done to tackle the growing epidemic, new research suggests.

The Obesity Health Alliance estimates that around 40 million adults in the UK will be overweight or obese by 2035, which could result in more than 7.6 million new cases of diseases.


Experts predict this will cause an additional 4.62 million cases of Type 2 diabetes, 1.63 million cases of coronary heart disease and 670,000 new cases of cancer.

 OBESITY LINKED CANCERS

They have now called on the government to introduce a strong childhood obesity strategy to combat the growing crisis.

According to experts, even the smallest of changes could make a massive difference to public health.

A 1% shift in the number of people putting on extra weight each year until 2035 could avoid around 77,000 cases of disease including 45,000 cases of Type 2 diabetes in the year 2035 alone.

How Obesity Lead to Cancer:

how obesity leads to cancer

Alison Cox, Cancer Research UK’s director of prevention and member of the Obesity Health Alliance, said: “These numbers are shocking and it’s difficult to think of the impact this will have on public health and an already strained NHS.”

“Without bold action, the next generation will face more disease and live shorter lives.”

“Kids are bombarded with advertisements for unhealthy food and if we are to give our children the chance for better and healthier lives, it’s vital the government’s childhood obesity strategy restricts this kind of marketing.”

To tackle the obesity epidemic, the Obesity Health Alliance is calling on the government to introduce a strong childhood obesity strategy without delay.

Also, read Does Salt Make You Fat?

They said it must include restricting junk food advertising on TV before the 9 pm watershed, tightening online marketing to align with broadcast regulations, as well as setting targets for industry to reduce the amount of sugar and fat in food.

Modi Mwatsama, director of policy and global health at the UK Health Forum and member of the Obesity Health Alliance, said: “This study is a wake-up call for the government and shows a daunting future if no strong action is taken against the obesity epidemic.”

“We can’t expect industry to make changes on their own and people need help making healthier choices.”

“The government must lead the way by creating a level playing field with independent, regulated targets for reducing the amount of sugar, fat and salt in food.”

“Without government action, our children face a life of disease and early death.”

obesity and cancer risk infographic

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In Fight Against Obesity, The U.S. Is Failing Women | Latest News

About 41 percent of women and 35 percent of men are obese, according to survey data collected as recently as 2014 and reported in one of the studies.

A decade earlier, about 38 percent of women and 34 percent of men were obese, the study found. Only the increase for women was large enough to be sure it wasn’t due to chance.


Over this same period, obesity rates for teens rose from about 17 percent to 21 percent, CDC researchers report in the second study.

“The most recent data before this point showed no increases overall in youth, men or women over the previous decade,” said Cynthia Ogden, a CDC researcher who worked on both studies.

“These trends are not explained by changes in age or educational levels in the population or by changes in the distribution of race-ethnic groups in the population or changes in smoking status,” Ogden added by email.

Globally, 1.9 billion adults are overweight or obese, according to the World Health Organization. Obesity increases the risk of heart disease, diabetes, kidney complications, joint disorders and certain cancers.

Also, read Surprising Research ! Link Between Saturated Fats And Heart Disease Questioned

Both studies analyzed data from a nationally representative survey of the U.S. population that includes questions about weight and height. Researchers looked at participants’ body mass index (BMI), a measure of weight relative to height, to assess trends in obesity over time.

For adults, a BMI between 18.5 and 24.9 is considered healthy, 25 to 29.9 is overweight, 30 or above is obese and 40 or higher is morbidly obese.

An adult who is 5’9” tall and weighs from 125 to 168 pounds would have a healthy weight and a BMI of 18.5 to 24.9, according to the U.S. Centers for Disease Control and Prevention. An obese adult at that height would weigh at least 203 pounds and have a BMI of 30 or more.

Almost 6 percent of men and 10 percent of women have what’s known as “class 3” obesity, with a BMI of at least 40 and the most severe risk of health complications tied to their weight, the CDC study of adults found.

If there’s a sliver of good news in all this data, it’s for the youngest children, ages 2 to 5, the CDC youth study found.

For these kids, obesity rates declined from about 14 percent a decade ago to 9 percent in the most recent survey.

Over that period, obesity rates for children ages 6 to 11 dipped slightly, but not enough to rule out the possibility that this was due to chance.

One limitation of both studies is that people in surveys tend to say they are taller and lighter than they really are, which can downplay obesity rates calculated from BMI, the authors note. BMI also doesn’t distinguish between fat and muscle.

Even so, the two studies suggest that huge investments to reverse the U.S. obesity epidemic over the past three decades haven’t done much to diminish the problem, Dr. Jody Zylke and Dr. Howard Bauchner, deputy editor and editor-in-chief of JAMA, respectively, wrote in an editorial.

“The rates among children and adults are driven by the same factors,” said Dr. Lili Lustig, a family medicine researcher at Cleveland Clinic in Ohio who wasn’t involved in the study.

Lack of exercise is part of the problem, and so is what people eat, Lustig added by email.

“We have done a deplorable job of helping parents understand food as a prescription for health,” Lustig said by email. “If a parent does not understand the value of food choices, how can you expect their children and the next generation to have any better understanding?”

SOURCE: Journal of the American Medical Association, online June 7, 2016.

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Does Salt Make You Fat ? New Research About Salt And Weight Gain

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. 

Salt, Sodium, Health - Infographic

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Have You Ever Heard About Fat Virus ? Virus In Chicken Linked To Obesity

Recently, there has been research 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

0:36 as well for them as they do for you

From: nutritionfacts.org

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Count Bites Not Calories ! Wearable Technology To Lose Weight

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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Bite Counter.

Overeating May Cause More Eating By Cutting Off Fullness Signal: Uroguanylin

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.

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