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Thursday, April 25, 2024
Weight Loss

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Obesity can have severe effects on a person’s quality of life and lifespan. Research shows that it substantially increases the risk of a wide range of diseases, including type 2 diabetes, cardiovascular disease, and some cancers.

Despite the long-established health risks, however, recent decades have seen an inexorable rise in rates of obesity throughout the world.

One study found that between 1980 and 2015, the prevalence of obesity doubled in more than 70 countries and steadily increased in most others.

According to the World Health Organization (WHO), in 2016, more than 650 million adults had obesity. Overweight and obesity now claim the lives of more than 2.8 million people each year.

A major challenge for researchers is to distinguish the effects of genetics from those of lifestyle on the progression of obesity and its effects on health.

A team of researchers, led by two from the Obesity Research Unit at the University of Helsinki, in Finland, used an ingenious way to do this.

By studying 49 pairs of identical twins who did not share the same body mass index, or BMI, readings, they removed the effect of genes from the equation.

Identical, or monozygotic, twins have the same genetic makeup. They experience almost identical conditions in the womb and usually have very similar upbringings.

This means that the differences between the twins in the study arose from the influence of their environment or lifestyle as adults, rather than their genes or conditions during childhood.

The researchers have published their findings in the journal Cell Reports Medicine.

Biopsies of fat and muscle

First, the researchers took blood samples and biopsies of fat, or adipose, tissue and skeletal muscle tissue from the volunteers.

They then used a variety of molecular techniques to analyze the transcription of genes, production of proteins, and processing of metabolites in the two types of tissue.

A key finding was that the activity of mitochondria, the power plants of cells, was reduced in the muscle and adipose tissue of people with obesity.

The change was more marked in adipose than in muscle tissue.

Meanwhile, there was also increased inflammation in the tissues from twins with obesity, compared with their leaner siblings.

The changes in adipose tissue, but not muscle tissue, were associated with adverse health effects, including fatty liver disease and insulin resistance, conditions that have been linked to the development of diabetes.

Reduced power output

“If mitochondria […] are compared to the engine of a car, you could say that the power output decreases as weight increases,” explains senior author Prof. Kirsi Pietiläinen, also of the university’s Obesity Research Unit.

The researchers believe that these underperforming mitochondria produce more of the harmful reactive oxygen species, or free radicals, that stoke inflammation.

“A low-powered mitochondrial engine may also generate toxic exhaust fumes, which can cause a pro-inflammatory state in adipose tissue and, consequently, the onset of diseases associated with obesity,” explains Prof. Pietiläinen.

“What was surprising was that the mitochondrial pathways in muscle had no association with these adverse health effects,” she adds.

Another notable finding was that mitochondria in the adipose and muscle tissue of individuals with obesity were less efficient at breaking down a type of amino acid. These acids are the building blocks of proteins.

“This finding was of particular significance because the reduced breakdown of these amino acids and the resulting heightened concentration in blood have also been directly linked with prediabetic changes and the accumulation of liver fat in prior twin studies,” says Prof. Pietiläinen.

The researchers observe that in people with obesity, excessive nutrients may upset the control of catabolic and anabolic processes, reactions that break down and assemble organic molecules, respectively.

They write:

“We argue that, because of a high nutrition load, adipose tissue and skeletal muscle tissue no longer sufficiently shift between catabolic and anabolic reactions in acquired obesity. Consequently, the cells in these tissues increase their [internal] communication and activate emergency responses, such as inflammation.”

They acknowledge that the major limitation of their study was its cross-sectional design, meaning that it focused on a single point in time.

While the study identified associations between obesity and the various metabolic and health measures, it could not prove the existence of any causal relationships, as a result of this design

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According to the Centers for Disease Control and Prevention (CDC), the prevalence of obesity among adults in the United States increased from 30.5% in 1999–2000 to 42.4% in 2017–2018.

The prevalence of severe obesity almost doubled over the same period, from 4.7% to 9.2%.

One of the factors behind the steep rise in obesity rates may be the intensive marketing of high calorie, nutrient-poor food in restaurants, on screens, and on billboards.

Past research suggested that children with excess weight or obesity are more susceptible to food advertising, which may cause a cycle of weight gain and overeating.

Whether adults with obesity are also more prone to food marketing was unclear, however.

Researchers in Canada and France have found that women with obesity also appear to be more vulnerable to marketing — but that weight loss due to bariatric surgery can free them from the cycle.

If the scientists had found that marketing still holds sway over people after weight loss, this would imply an inbuilt vulnerability to overeating.

“That would mean people are endowed with unchangeable psychological characteristics that would always make them more responsive to marketing — which would make it very difficult to sustain a medically recommended weight,” says the study’s lead researcher Yann Cornil, Ph.D., from the University of British Columbia (UBC) in Vancouver, Canada.

“But one of the positive things is that after significant weight loss, people become less responsive to marketing, such that it is more sustainable to remain at a lower body mass index,” he adds.

The research, which was a collaboration between UBC and the Pitié-Salpêtrière University Hospital in Paris, France, appears in the Journal of Consumer Psychology.

Tests of susceptibility

The scientists compared the susceptibility to food marketing of three groups of women:

  • Group one: Comprising 73 women with severe obesity who were due to receive bariatric surgery (gastric bypass or band), which involves surgically altering the digestive system to promote weight loss.
  • Group two: Consisting of 41 women with moderate weight, who the scientists referred to as “lean controls.” The team matched these individuals to the first group in terms of their age, gender, income, employment, and marital status.
  • Group three: Comprising 29 women with obesity who were not in line to receive bariatric surgery or any other weight loss procedure.

The researchers tested the patients with obesity who were due for surgery before the procedure, then 3 and 12 months afterward.

They tested the second group twice, 6 months apart, and the third group only once.

The tests measured participants’ susceptibility to three common marketing strategies that portray food and portion sizes as more healthy than they actually are.

The first strategy, called the “health halo” effect, involves framing a product as natural or healthy.

The researchers asked participants to estimate the calorie content of 4 “healthy” snacks, including apple juice and granola bars, and 4 “indulgent” snacks, including a can of cola and chocolate bars.

In reality, the “healthy” snacks all contained more calories than the “indulgent snacks.”

The second marketing strategy involves downplaying portion sizes by renaming them, which tends to make people overeat.

The researchers asked participants to imagine choosing a portion of fries or a drink from a range of three options.

There were labels providing the actual size of each portion in grams or centiliters (cl), but these names either understated the sizes (as “mini,” “small,” and “medium”) or overstated them (as “medium,” “large,” and “extra-large.”)

The third marketing strategy involves omitting the smallest option in a size range, which can also lead to people choosing larger portions.

In this test, participants chose from a menu with 47, 65, and 95 cl size options, or from a menu with 24, 47, and 65 cl size variants.

The tests revealed that women with obesity were significantly more responsive than those with a moderate weight to the health halo and size labeling effects.

Crucially, however, women with obesity who underwent bariatric surgery were no more susceptible to these marketing ploys 12 months after the procedure than the control group with moderate weight.

Reward and motivation

In their paper, the scientists note neuroscientific research suggesting that brain regions involved in reward and motivation are more active in those with obesity.

They add that bariatric surgery may “rewire” the brain’s reward system in favor of more healthy food choices.

Alternatively, they write, the psychological impact of undergoing radical surgery to reduce their weight may motivate patients to eat more healthily.

At any rate, it remains unclear whether people who lose weight through other means, for example, through exercise or dieting, also become less responsive to food marketing.

The authors acknowledge that their study had some other limitations.

For example, they tested women with obesity only up to 12 months after surgery, so the durability of the effects beyond this point is unknown.

In addition, all the participants were adult French women. “Future research should therefore examine a larger and more diverse sample of people with obesity, including men and adolescents,” they write.

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For people who may wish to lose weight, plant-based diets could be the best solution thanks to the way in which they influence metabolism.

That is the takeaway from a recent study published in the JAMA Network Open.

According to the research results, switching to a low fat, plant-based diet could boost the body’s metabolism enough to burn excess weight and fat — even without vigorous exercise.

Researchers with the Physicians Committee for Responsible Medicine (PCRM) partnered with Dr. Kitt Petersen and Dr. Gerald Shulman of Yale University. Together, they conducted a 16-week trial where participants in the intervention group adopted a low fat, vegan diet.

The study team hoped to find the full impact of a low fat, vegan diet. Could it improve metabolism, reduce visceral fat, and aid in significant weight loss?

Initially, 3,115 people responded to the flyers distributed by the research team. Of these, 244 met the criteria for participation in the study.

Eligible study participants had overweight, with body mass indexes ranging between 28 and 40, and were aged 25–75.

Researchers randomly split the study participants into two groups. The first group followed a 4-month-long low fat, vegan diet, eating fruits, vegetables, pulses, and grains in serving sizes comparable to what they ordinarily consumed at mealtimes. The second group, functioning as the control group, did not change their dietary habits.

Members of both groups curbed their daily alcohol consumption for the duration of the study. Women could drink a single alcoholic beverage daily, while men could have up to two drinks per day. Neither group began an exercise routine or deviated from any existing physical habits during the 16-week trial.

Study outcome and implications

Researchers took measurements at the beginning and end of the trial. By the end of the study, the plant-based diet group averaged an 18.7% increase in their after-meal calorie burn. They also saw an average weight loss of about 14 pounds (lb).

Additionally, the vegan diet group experienced a decrease in insulin resistance and a reduction in body fat. Crucially, this group saw a significant loss of visceral fat, the more detrimental type of fat that gets stored around the internal organs.

By contrast, the control group experienced no significant loss of weight or reduction in body fat. After comparing the two groups, it was clear to researchers that the low fat, vegan diet had a measurable impact on the weight and health of the intervention group.

Lead study author Dr. Hana Kahleova, director of clinical research at the PCRM, considers the results “groundbreaking for the 160 million Americans struggling with overweight and obesity.”

She adds, “Over the course of years and decades, burning more calories after every meal can make a significant difference in weight management.”

Findings back up existing research

These findings are consistent with a number of previous studies that have shown plant-based diets to be associated with reduced excess body fat. As reviewed recently by Rami S. Najjar and Rafaela G. Feresin in Nutrient:

“Plant-based diets can reduce body fat […] [and] cumulatively lead to reduced calorie intake and increased energy expenditure.”

It is worth noting that the PCRM and Yale University researchers focused on people without a history of diabetes. The pool of participants also skewed heavily toward one gender, with females constituting 86% of all participants.

Additional research might be needed for those already experiencing related health issues, or with a more balanced group of participants.

Still, there is enough existing research to suggest that no matter a person’s current diabetes status, their health outcomes could improve through following a diet mainly consisting of fruits and vegetables.

At least one participant in the clinical study decided to make a permanent change to his lifestyle. Sam T., who lost 34 lb during the 4-month study, continued with the plant-based diet. He reached his goal weight and began partaking in half-marathons and marathons.

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Although obesity is common, there are many misconceptions associated with it — and these myths often fuel social stigma. In this edition of Medical Myths, we tackle five of the most common misunderstandings about obesity.

According to the Centers for Disease Control and Prevention (CDC), in the United States, 42.4% of adults have obesity. Globally, the World Health Organization (WHO) estimate that around 650 million adults have obesity.

People are growing increasingly aware of the health issues associated with obesity. However, despite public health campaigns, myths continue unabated. Many of the most common myths drive stigma that can impact the mental health of people with obesity.

For instance, the results of one 2020 meta-analysis on the subject indicate “a stronger association between weight stigma and diminished mental health with increasing body mass index [BMI].”

Addressing the myths that surround obesity is important. With this in mind, this article will tackle five of the most prevalent misunderstandings around this condition.

1. To reduce obesity, just eat less and move more

In many cases, consuming more calories than the body needs for a prolonged amount of time is the direct cause of obesity. Indeed, the vast majority of measures for reducing obesity aim to lower caloric intake, increase physical activity, or both.

Although diet and exercise are important factors, several unrelated factors can also play a significant part in obesity.

These factors, which people often forget about, include insufficient sleep, psychological stress, chronic pain, endocrine (hormone) disruptors, and the use of certain medications.

In these cases, overeating, for instance, may be a symptom rather than a cause.

Also, some of these factors work together to increase the chance of obesity. As an example, stress can increase the chance of obesity. Due to the prevalence of weight stigma, obesity can be stressful for some people, thereby increasing stress levels and sparking a negative feedback loop.

Added to this, stress can impact sleep quality, and this, in turn, might cause sleep deprivation, which is another factor in the development of obesity. Sleep deprivation also appears to increase stress levels. As one paper explains, “stress hormone levels correlate positively with decreased sleep duration.”

Sleep apnea, wherein a person stops breathing for short periods during sleep, is more prevalent in people with overweight or obesity. Again, a cycle can form: As they gain weight, their sleep apnea may worsen, which can lead to sleep deprivation, which can lead to further weight gain.

As another example, there appears to be an association between chronic pain and obesity. The reasons for this relationship are sure to be complex and differ from person to person, but they likely include chemical factors, sleep, depression, and lifestyle.

It is not difficult to see how chronic pain would both increase stress levels and impact sleep, adding to the negative loops outlined above.

Stress, sleep, and pain are just three interlinking factors that can drive obesity. Each person’s case will be different, but simply receiving an instruction to “move more and eat less” might not be an adequate intervention.

As this article will continue to reiterate, calorie intake and exercise are vital factors in reducing obesity, but they do not tell the whole tale.

2. Obesity causes diabetes

Obesity does not directly cause diabetes. It is a risk factor for type 2 diabetes, but not everyone with obesity will develop type 2 diabetes, and not everyone with type 2 diabetes has obesity.

Obesity is also a risk factor for gestational diabetes, which occurs during pregnancy, but it is not a risk factor for type 1 diabetes.powered by Rubicon Project

3. People with obesity are lazy

An inactive lifestyle is a factor in obesity, and becoming more active can aid weight loss, but there is more to obesity than inactivity.

One 2011 study used accelerometers to measure the activity levels of 2,832 adults, aged 20–79 years, for 4 days. Their step counts reduced as their weight increased, but the differences were not as significant as one might predict, particularly for women.

The list below shows the women’s weights and how many steps they took per day during this study:

  • those with a “healthy” weight: 8,819 steps
  • those with overweight: 8,506 steps
  • those with obesity: 7,546 steps

When one considers that someone with overweight or obesity expends more energy with each step, the difference between the groups’ overall energy expenditures may be even more slight.

This does not mean that physical activity is not essential for good health, but the story is more complex.

Another factor to consider is that not all people are able to perform physical activity. For instance, some physical disabilities can make moving challenging or impossible.

Also, certain mental health issues can severely impact motivation — and there appears to be a relationship between depression and obesity, which further deepens the complexity.

Aside from physical and mental health issues, some people with obesity may also have a negative body image, which might make leaving their home a more daunting prospect.

4. If your close relatives have obesity, so will you

The relationship between obesity and genetics is complex, but someone whose relatives have obesity will not necessarily develop the condition themselves. However, their chance of doing so is higher.

Understanding the role of genes and the environment in isolation is difficult; people who share similar genes often live together and, therefore, may have similar dietary and lifestyle habits.

In 1990, a group of researchers published a study that helped split genes from the environment. The results appeared in The New England Journal of Medicine.

The scientists investigated twins who had been brought up apart and compared them with twins who had been brought up together. In this way, they hoped to tease apart the impact of genetics and the environment. Overall, they conclude:

“[G]enetic influences on [BMI] are substantial, whereas the childhood environment has little or no influence.”

One twin study from 1986 reached similar conclusions. The researchers found that the weights of adopted children correlated with the weights of their biological parents, but not with those of their adoptive parents.

Although more recent studies have identified a more significant role for the environment, genetics do appear to play an important part in obesity.

In recent years, scientists have searched for the genes that influence the chance of obesity. As the CDC explain, in most people with obesity, “no single genetic cause can be identified. Since 2006, genome-wide association studies have found more than 50 genes associated with obesity, most with very small effects.”

One gene that is linked to obesity is a variant of a gene called FTO. This variant, according to one 2011 study, is associated with a 20–30% increased chance of obesity.

Although genetics are important, this does not mean that obesity is inevitable for someone whose relatives have the condition. The above study, which involved individuals with the FTO gene variant, looked at the role of exercise. As the paper explains:

“Using data from over 218,000 adults, the authors found that carrying a copy of the susceptibility gene increased the odds of obesity by 1.23-fold. But the size of this influence was 27% less in the genetically susceptible adults who were physically active.”

A review and meta-analysis that investigated the same gene variant came to a similar conclusion. The authors explain that people with the FTO variant “respond equally well to […] weight loss interventions and thus genetic predisposition to obesity associated with the FTO minor allele can be at least partly counteracted through such interventions.”

However, it is important to reiterate the point that these interventions alone may not be helpful for some people.

5. Obesity does not impact health

This is a myth. There are several conditions associated with obesity. For instance, obesity increases the risk of diabetes, high blood pressure, cardiovascular disease, osteoarthritis, sleep apnea, and some mental health conditions.

That said, even modest weight loss can provide health benefits. According to the CDC, “weight loss of 5–10% of your total body weight is likely to produce health benefits, such as improvements in blood pressure, blood cholesterol, and blood sugars.”

Also, a review of existing literature in the BMJ concludes that weight loss interventions “may reduce premature all-cause mortality in adults with obesity.”

Obesity is highly prevalent. Currently, the stigma surrounding the condition is unhelpful and can be damaging. We need to address it whenever we encounter it.

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Two studies involving postmenopausal females found that sedentary behavior increased their risk of developing heart failure and that walking lowered their risk of high blood pressure.

For people spending more time at home as a result of the COVID-19 pandemic, the new research provides an impetus to go for more walks and avoid sitting too long in front of computer or television screens.

In the two studies, which the University at Buffalo (UB), NY, led, researchers found that postmenopausal females who went for brisk walks and spent less time sitting or lying down during their waking hours had a lower risk of hypertension and heart failure, respectively.

“Walking and moving are simple activities that can be easily integrated into our daily lives,” says Jean Wactawksi-Wende, Ph.D., dean of UB’s School of Public Health and Health Professions (SPHHP) and a co-author of both studies.

The research drew upon data collected over several years from females who took part in the Women’s Health Initiative. The participants were 50–79 years of age at the start of the studies.

The results suggest that regardless of overall levels of physical activity, walking more and being less sedentary can benefit cardiovascular health.

“Sit less, walk more for heart health,” advises Michael LaMonte, Ph.D., research associate professor of epidemiology at the SPHHP.

LaMonte was the senior author on the paper that linked walking to a reduced risk of hypertension and first author on the paper that found an association between sedentary behavior and an increased risk of heart failure.

Walking and hypertension

The walking research followed 83,435 females who did not have a diagnosis of hypertension, heart failure, coronary heart disease, or stroke at the start of the study.

All of the participants reported that they could walk at least one block without assistance.

During the average follow-up period of 11 years, 38,230 participants received a diagnosis of hypertension.

After adjusting for other possible contributing factors, including other types of physical exercise, the participants who walked the most were 11% less likely to develop hypertension than those who walked the least.

Participants who were among the fastest walkers had a 21% lower risk of hypertension compared with those who walked the slowest.

Even after adjusting the figures to account for the overall amount of time that each participant spent walking and the distance they covered, a walking speed of at least 2 miles per hour was associated with a significant reduction in the risk of hypertension.

The study suggests that walking briskly has a more significant effect on hypertension risk than either the total distance or the duration of walks.

“To put it simply, get your steps in, and try to make them quick,” says Connor Miller, who was the lead researcher on the study, which he worked on while obtaining his master’s in epidemiology at UB. He is now an epidemiologist at Roswell Park Comprehensive Cancer Center in Buffalo.

“Our work adds to growing evidence that you don’t necessarily have to be an avid jogger or cyclist to gain health benefits from physical activity,” he adds.

The findings of this study appear in the journal Hypertension.

Sedentary behavior and heart failure

The study of sedentary behavior followed 80,982 females who had not received a diagnosis of heart failure at the start of the study and were able to walk at least one block unassisted.

The participants regularly filled out questionnaires that included questions about the amount of time they spent sitting or lying down in their waking hours.

During the average follow-up period of 9 years, there were 1,402 cases of hospitalization for heart failure.

In their analysis, the researchers adjusted the figures to account for a wide range of other possible confounding factors, including the participants’ age, race/ethnicity, smoking status, alcohol consumption, and use of hormone replacement therapy.

Compared with the participants who reported sitting for no more than 4.5 hours a day, sitting for 4.6–8.5 hours a day was associated with a 14% increased risk of heart failure.

Sitting for more than 8.5 hours per day was associated with a 54% increased risk of heart failure.

Even among females with the highest levels of recreational physical activity, the risk of heart failure was significantly raised if they spent more than 9.5 hours per day sitting or lying down.

“This latter finding points to the need to not only promote more physical activity for heart failure prevention but to also promote interruption of sedentary time throughout the day,” says LaMonte.

In their paper, the researchers say that the risks of heart failure associated with prolonged sedentary behavior are on a par with those for obesity and diabetes.

Other studies suggest that sedentary behavior promotes the development of atherosclerosis (narrowing of the arteries supplying the heart muscle), the authors write, which, in turn, increases a person’s risk of heart failure.

They report their findings in the journal Circulation: Heart Failure.

Medical News Today have reported a range of other possible negative health effects of sedentary behavior, including obesity, type 2 diabetes, and cancer.

Limitations of the research

Both studies had some limitations in common.

The researchers could not rule out the possibility that some participants had undiagnosed underlying health conditions at the start of the study. These could have affected their walking and sedentary behavior.

Also, both studies relied upon the participants’ estimates of how far and fast they walked or the amount of time they spent sitting or lying down.

Finally, the study of sedentary behavior only gauged the total time that people spent sitting or lying down. Other research, using accelerometers to record participants’ movements, suggests that the length of each uninterrupted bout of sedentary behavior is also an important factor.

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Encouraging people to eat more dried fruit — without added sugar — could be an effective way to boost their intake of vital nutrients, researchers have concluded.

Low consumption of fruit in the United States and other countries is a major contributor to diet-related disease and disability, according to a recent analysis.

Fruit is a good source of nutrients, such as fiber and potassium, that many people lack in their diet. It also contains bioactive nutrients that provide extra health benefits, including polyphenols and carotenoids.

Research suggests that eating fruit is associated with a lower risk of cardiovascular disease, cancer, and type 2 diabetes.

However, only about 24% of females and 14% of males in the U.S. eat the recommended daily amount of fruit, according to the National Cancer Institute.

Several factors might contribute to people’s low intake of fresh fruit, including limited availability, high cost, and perishability.

Recommending that people eat more dried fruit could be one solution.

Healthful snack?

Dried fruit offers several advantages over fresh fruit in terms of cost, availability, and ease of storage and transport. It could also replace more unhealthful snack food that is high in sugar, salt, and saturated fat.

At the same time, however, there are concerns about overconsumption leading to excess calorie intake because dried fruit is such an “energy dense” form of fruit.

Previous observational studies have found that eating dried fruit is associated with health benefits. However, the evidence is inconclusive because people who eat more dried fruit may tend to have a more healthful diet and lifestyle overall.

The new study by researchers at Pennsylvania (Penn) State University in University Park aimed to get around this difficulty by comparing days when particular participants reported eating dried fruit with days when they ate none.

They found that people tended to consume more key nutrients on the days they ate dried fruit, including dietary fiber and potassium. However, they also consumed more calories.

“Dried fruit can be a great choice for a nutritious snack, but consumers might want to be sure they’re choosing unsweetened versions without added sugar,” says Valerie Sullivan of Johns Hopkins Bloomberg School of Public Health in Baltimore, MD, who was a grad student at Penn State when she led the study.

“Portion sizes can also be tricky because a serving of dried fruit is smaller than a serving of fresh since the water has been taken out. But the positive is that dried fruit can help people potentially consume more fruit because it’s portable, it’s shelf-stable, and can even be cheaper.”

The research appears in the Journal of the Academy of Nutrition and Dietetics.

Health and nutrition survey

For their analysis, the scientists drew on survey responses from 25,590 individuals who took part in the National Health and Nutrition Examination Survey (NHANES) 2007–2016.

The respondents provided information about the food they had consumed in the past 24 hours (called “dietary recalls”).

Dried fruit accounted for only 3.7% of all the fruit consumed. However, a total of 1,233 participants reported consuming dried fruit on one out of two dietary recalls, allowing the scientists to compare their intake on these days.

Data were also available on the participants’ health, including their body mass index (BMI), waist circumference, and seated resting blood pressure.

Even after adjusting for demographic and lifestyle factors, the participants who ate significant amounts of dried fruit tended to have better diets, a lower BMI, a smaller waist circumference, and lower systolic blood pressure compared with those who did not.

When the researchers compared the days when a participant ate dried fruit with those when they did not, they found that the average intake of total carbohydrate, dietary fiber, potassium, and polyunsaturated fat was greater on the days they ate dried fruit.

Active lifestyle

Taken together, the findings suggest that people who ate dried fruit expended more energy, compensating for the extra calories.

“In our study, people who consumed dried fruits had a higher calorie intake but a lower BMI and waist circumference, which suggests they were more physically active,” says co-author Penny Kris-Etherton, Evan Pugh University Professor of Nutritional Sciences at Penn State.

“So, when incorporating dried fruits, pay attention to calories and be sure to substitute out calories from low nutrient foods for dried fruits to get the greatest benefit of eating dried fruits,” she adds.

The researchers write that eating dried fruit tended to increase total fruit consumption, rather than replacing other forms of fruit. “Thus, increasing dried fruit consumption might help Americans achieve greater fruit intakes.”

The authors acknowledge that their study did not prove that eating dried fruit improves health, only that there seems to be an association. People who are likely to eat dried fruit may have better health for other reasons, such as taking more exercise or leading less stressful lives.

In addition, they note that the survey relied on the participants’ recollection of what they had eaten over the past 24 hours and their ability to estimate quantities accurately.

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A clinical trial has found that a monoclonal antibody reduces low-density lipoprotein (LDL) cholesterol levels by 50% in people with an inherited condition called familial hypercholesterolemia.

Individuals with high levels of low-density lipoprotein (LDL) or “bad” cholesterol in their blood are at increased risk of developing atherosclerosis (narrowed arteries) and cardiovascular disease.

Doctors define severe hypercholesterolemia as untreated LDL cholesterol levels of at least 190 milligrams per deciliter (mg/dl) of blood.

Cardiologists in the U.S. recommend that individuals who are at very high risk of cardiovascular disease due atherosclerosis aim for an LDL cholesterol level of around 70 mg/dl of blood.

Lifestyle changes can help reduce LDL, but people usually need to take cholesterol-lowering drugs to reach this goal. In addition, certain genetic differences can make achieving this objective more difficult for some people.

Worldwide, approximately 1 in 250 adults have an inherited condition called heterozygous familial hypercholesterolemia. This usually results from mutations in a gene for a receptor that removes LDL from the bloodstream.

Doctors usually prescribe a standard “triple therapy” of three types of cholesterol-lowering drugs for hypercholesterolemia:

  • A high dose of a statin, which reduces the amount of cholesterol the body produces.
  • A PCSK9 inhibitor, which boosts the number of LDL receptors in the liver.
  • Ezetimibe, which limits the absorption of cholesterol from the intestine.

For individuals whose LDL cholesterol level remains too high despite taking the maximum tolerable dose of this drug combination, a new drug called evinacumab that acts on a different target may soon be available.

A clinical trial published in The New England Journal of Medicine suggests that evinacumab could further reduce LDL levels in these individuals by around 50%.

This would be good news for people with mutations in the gene for the LDL receptor who don’t respond particularly well to PCSK9 inhibitors.

“There’s an unmet need for agents that address refractory hypercholesterolemia through a pathway that’s independent of the LDL receptor,” explains principal investigator Robert Rosenson, MD, Director of Cardiometabolic Disorders at the Icahn School of Medicine at Mount Sinai in New York, N.Y.

“If approved by the U.S. Food and Drug Administration, evinacumab may potentially fill that clinical gap for patients by reducing severely elevated LDL cholesterol,” he adds.

Breaking down lipids

Evinacumab is a monoclonal antibody that targets a protein called angiopoietin-like 3 (ANGPTL3). Normally, ANGPTL3 inhibits enzymes that break down lipids, including LDL, high-density lipoprotein (HDL), and triglycerides.

People with a faulty version of the gene that makes ANGPTL3 have abnormally low levels of these lipids in their blood. As a result, their chance of developing coronary artery disease is 41% lower than the general population.

By disabling ANGPTL3 with an antibody, drug developers hoped to recreate these beneficial effects in people with very high cholesterol levels.

In this phase II clinical trial, the researchers randomly assigned 272 people to receive either evinacumab — through intravenous or subcutaneous administration at various doses — or placebo treatments.

Most of the participants had heterozygous familial hypercholesterolemia.

After 16 weeks, LDL cholesterol had fallen by an average of 56% compared with placebo in those who received a subcutaneous dose of 450 mg of evinacumab weekly.

Among those who received a monthly intravenous injection of 15 mg evinacumab per kilogram of body weight, LDL cholesterol fell by 50.5% compared with the placebo group.

The authors note that some people prefer subcutaneous administration because they can do it themselves at home, avoiding the need to take time off work to visit a clinic.

Commenting on the findings, Dr. Rosenson concludes:

“Our study demonstrates that a regimen of either subcutaneous or intravenous evinacumab can have a significant impact on LDL cholesterol […] If approved for use in this setting, evinacumab could potentially arm cardiologists with a major new add-on therapy to bring patients with [heterozygous familial hypercholesterolemia] to or closer to their cholesterol-lowering goal.”

Racial diversity

The authors concede that their study had some limitations. For example, the numbers in each arm of the study were relatively small, and treatment lasted only 16 weeks.

In addition, the racial diversity of participants was not as broad as the researchers had hoped, so the results may not apply to all people in the wider population.

One of the people treated with subcutaneous evinacumab had difficulty breathing, and another had a mild anaphylactic reaction.

The pharmaceutical company Regeneron, which makes evinacumab, sponsored the study.

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More than four billion people could be overweight by 2050, with 1.5 billion of them obese, if the current global dietary trend towards processed foods continues, a first-of-its-kind study predicted Wednesday.

Warning of a health and environmental crisis of “mind-blowing magnitude”, experts from the Potsdam Institute for Climate Impact Research (PIK) said that global food demand would leap 50 percent by mid-century, pushing past Earth’s capacity to sustain nature.

Food production already hoovers up three-quarters of the world’s freshwater and one-third of its land — and accounts for up to a third of greenhouse gas emissions.

Providing a long-term overview of changing global eating habits between 1965 and 2100, the researchers used an open-source model to forecast how food demand would respond to a variety of factors such as population growth, ageing, growing body masses, declining physical activity and increased food waste.

They found that “business as usual” — a continuation of current trends — will likely see more than four billion people, or 45 percent of the world’s population, overweight by 2050.

The model predicted that 16 percent would be obese, compared with nine percent currently among the 29 percent of the population who are overweight.

“The increasing waste of food and the rising consumption of animal protein mean that the environmental impact of our agricultural system will spiral out of control,” said Benjamin Bodirsky, lead author of the study published in Nature Scientific Reports.

“Whether greenhouse gasses, nitrogen pollution or deforestation: we are pushing the limits of our planet — and exceeding them.”

While trends vary between regions, the authors said that global eating habits were moving away from plant- and starch-based diets to more “affluent diets high in sugar, fat, and animal-source foods, featuring highly-processed food products”.

At the same time, the study found that as a result of increasing inequality along with food waste and loss — food that is produced but not consumed due to lack of storage or overbuying — around half a billion people will still be undernourished by mid-century.

“There is enough food in the world — the problem is that the poorest people on our planet have simply not the income to purchase it,” said co-author Prajal Pradhan.

“And in rich countries, people don’t feel the economic and environmental consequences of wasting food.”

The UN’s Intergovernmental Panel on Climate Change warned in a special report last year that humanity will face increasingly painful trade-offs between food security and rising temperatures within decades unless emissions are curbed and unsustainable farming and deforestation are halted.

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Image credit: LeoPatrizi/Getty Images

A recent study reveals that losing fat without reducing muscle mass results in a significantly lower risk of heart failure in people with type 2 diabetes.

In the United States, around 1 in 10 people have diabetes, and 90–95% of them have type 2 diabetes. Type 2 diabetes usually develops after age 45. Estimates suggest that by 2045, 700 million adults worldwide will have this condition.

Type 2 diabetes usually begins as insulin resistance. This is a condition wherein the body’s cells no longer react to the insulin the pancreas produces to control blood sugar.

Genetics, ethnicity, and advancing age all play a role in the development of insulin resistance and diabetes. However, excess weight, a lack of exercise, an unhealthful diet, and smoking may be driving factors in its occurrence.

Once doctors diagnose this condition, the primary treatments they advise generally include taking medications and making certain lifestyle changes, such as losing weight and improving the diet.

As diabetes nearly doubles the risk of death due to heart disease or stroke and increases the risk of having heart failure by a factor of two in males and five in females, many researchers are focusing on preventing these and similar health complications for those with diabetes.

Heart failure, or congestive heart failure, occurs when the heart muscle does not pump the blood adequately. This leads to a buildup of fluid in the lungs or legs, or sometimes both.

Heart failure has a number of potential causes. For example, after a heart attack (when the heart muscle sustains damage due to a lack of oxygen), the muscle is weak and cannot pump well.

Heart failure can also occur due to type 2 diabetes. This is as a result of direct harm to the heart muscle from raised blood sugar and systemic inflammation associated with the condition.

One prevention strategy includes weight loss for people with overweight or obesity. However, not much is known regarding what type of weight loss has the most impact on reducing the risk of diabetes-related heart issues.

The study

To investigate this further, researchers at the University of Texas Southwestern Medical Center (UTSW) in Dallas analyzed data from the Look AHEAD study.

This is a randomized trial investigating weight loss due to intensive lifestyle intervention, consisting of healthful eating and increased physical activity versus support and education alone in people with type 2 diabetes.

The UTSW research, which appears in the journal Circulation, received funding from the National Heart, Lung, and Blood Institute, the Texas Health Resources Clinical Scholars Program, and the National Institutes of Health (NIH).

The researchers selected 5,103 people from the Look AHEAD study who did not have heart failure at the beginning of the study. The participants also had sufficient baseline measurements needed for prediction equations to estimate how much fat mass and lean (muscle) mass they had.

Data on the participants’ weight and waist circumference were available at the beginning of the study and over a 4-year period. The team also noted hospitalizations for heart failure over a 12-year time frame.

During the trial’s 12-year follow-up, 257 study participants were hospitalized for heart failure treatment.

In the Look AHEAD study, scientists used a scanning technique called dual-energy X-ray absorptiometry (DXA) to determine body composition in a subset of about 1 in 5 of the participants. These participants also had information recorded on factors such as height, weight, waist circumference, and ethnicity.

This meant that the researchers could validate existing equations that predict the proportion of fat mass and lean mass from these factors, which are simple to collect compared with the much more complicated process of conducting a DXA scan.

The researchers’ analysis of the subset of participants with DXA scans provided a new equation specific to this study group. They applied this new equation to the remaining participants without a DXA scan to accurately predict their fat mass and lean mass.

This revealed that adults in the study who had lost weight were less likely to develop heart failure if they lowered their fat mass and waist circumference. However, losing lean mass did not change their risk.

The investigators note that although the risk of heart failure decreased in those who lost body fat and reduced their waist circumference, the study data showed no significant reductions in heart attack risk.

The team also considered the participants’ ejection fraction (EF) ratio. This is a measurement of the amount of blood leaving the heart with each contraction.

The data showed that reducing body fat mass by 10% resulted in a 22% lower risk of heart failure with preserved EF ratio and a 24% lower risk of heart failure with reduced EF ratio.

“Our study suggests that simply losing weight is not enough. We may need to prioritize fat loss to truly reduce the risk of heart failure.” – Study co-author Dr. Kershaw Patel, a cardiologist at Houston Methodist Hospital in Texas

Supporting evidence

A study from May this year, which appears in the journal Circulation Research, compared obesity phenotypes, diabetes, and cardiovascular diseases.

The comparison suggests that some people who have a healthy weight or overweight but an excess amount of fat deposits around the internal organs and under the skin have a higher risk of diabetes and heart disease.

The researchers say that it is not possible to determine the risk of cardiovascular disease and type 2 diabetes based on body mass index (BMI) alone — mostly because body composition is so diverse.

They suggest that since excessive amounts of fat tissue largely define cardiovascular risks, reducing body fat is critical for prevention.

Implications and limitations

The results of the UTSW study suggest that for people with diabetes who also have overweight, losing weight, in general, may not be adequate to reduce heart health risks.

If further studies replicate these findings, it could confirm that losing weight by shedding visceral fat from around the organs — rather than losing muscle mass — is a key factor when it comes to reducing the risk of heart failure in type 2 diabetes.

The study authors also say that further investigation is necessary to determine if building or maintaining muscle in addition to losing fat mass would be even more effective in reducing the risk of diabetes-related heart failure.

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A high fat, low carb diet reversed heart failure in a mouse model of the condition. A 24-hour fast also led to improvements, mimicking the physiological effects of the diet.

In people with heart failure, the muscle on the right or left side of the heart — or on both sides — weakens. This impairment limits the organ’s ability to pump blood around the body, causing fatigue and shortness of breath, among other symptoms.

The leading causes are high blood pressure, diabetes, and ischemic heart disease, in which the heart muscle becomes starved of oxygen.

The National Heart, Lung, and Blood Institute estimate that about 5.7 million people in the United States have heart failure.

There is currently no cure, but medications and lifestyle changes can improve people’s quality of life and increase their lifespan.

Healthy heart muscle can draw upon a variety of chemical energy sources, depending on the circumstances. One of these is a molecule called pyruvate, which the body generates during the breakdown of the sugar glucose.

However, conditions such as heart failure and diabetes reduce this flexibility, starving the muscle of the fuel it needs to function effectively.

Fuel shuttle

Researchers have now traced this loss of flexibility to a transporter protein that shuttles pyruvate into mitochondria — the so-called power stations of cells.

Known as the mitochondrial pyruvate carrier (MPC) complex, it comprises two subunits: MPC1 and MPC2.

Researchers at the Saint Louis University School of Medicine in St. Louis, MO, led a team who discovered that the production of both subunits is reduced in failing human hearts.

The researchers compared heart tissue samples from people undergoing heart surgery with tissue samples from donor hearts that were healthy but unsuitable for transplant.

They then showed that mice that lack the gene for producing MPC2 steadily develop heart failure over time. Their hearts became outsized, or hypertrophied, and the organs’ ability to pump blood diminished.

Crucially, the scientists found that they could reverse the damage to the animals’ heart muscle by simply feeding them a special diet for 3 weeks.

“Interestingly, this heart failure can be prevented or even reversed by providing a high fat, low carbohydrate ‘ketogenic’ diet,” explains Kyle S. McCommis, Ph.D., assistant professor of biochemistry and molecular biology at the university, who led the research.

“A 24-hour fast in mice, which is also ‘ketogenic,’ also provided significant improvement in heart remodeling,” he adds.

Ketogenic diet

The ketogenic diet has been growing in popularity in recent years, with research suggesting that it has a range of possible health benefits. These include supporting weight loss, improving heart health, and preventing seizures in some types of epilepsy.

By severely restricting the intake of carbohydrates, such as glucose and other sugars and starches, the diet forces the body to break down fat, producing molecules called ketones that it can use as fuel. Intermittent fasting may achieve similar effects, though adhering to the regimen can be challenging.

The new research indicates that a ketogenic diet promotes the breakdown of fatty acids in heart muscle cells. This process produces an alternative fuel called acetyl-CoA, which the mitochondria can use as an energy source instead of pyruvate.

“Thus, these studies suggest that consumption of higher fat and lower carbohydrate diets may be a nutritional therapeutic intervention to treat heart failure,” says McCommis.

The scientists showed that the diet reversed heart failure by promoting the breakdown of fatty acids in mitochondria rather than ketones. Supplying the mitochondria with extra ketones only slightly improved heart failure.

Converging evidence

The findings from this study appear in the journal Nature Metabolism.

Two studies by other research groups, which feature in the same issue, independently show that the MPC transporter protein plays a central role in heart failure.

P. Christian Schulze and Jasmine M. F. Wu, who are both cardiologists from the University Hospital Jena in Germany, have written a comment article for the journal about the three papers.

While several questions remain unanswered about the regulation of MPC levels in healthy and failing hearts, they conclude:

“The current findings suggest a role for specific ketogenic diets as a supportive, nonpharmacologic treatment in people with heart failure.”

The cardiologists speculate that the findings could also inspire the development of new drugs for heart failure that work by boosting the breakdown of fatty acids in heart muscle cells.

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