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Ultra-Processed Diet Leads to Extra Calories, Weight Gain

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Dietary Weight Gain and Loss
Credit: Hall et al., Cell Metabolism, 2019

If you’ve ever tried to lose a few pounds or just stay at a healthy weight, you’ve likely encountered a dizzying array of diets, each with passionate proponents: low carb, low fat, keto, paleo, vegan, Mediterranean, and so on. Yet most nutrition experts agree on one thing: it’s best to steer clear of ultra-processed foods. Now, there’s some solid scientific evidence to back up that advice.

In the first randomized, controlled study to compare the effects of ultra-processed with unprocessed foods, NIH researchers found healthy adults gained about a pound per week when they were given a daily diet high in ultra-processed foods, which often contain ingredients such as hydrogenated fats, high fructose corn syrup, flavoring agents, emulsifiers, and preservatives. In contrast, when those same people ate unprocessed whole foods, they lost weight.

Intriguingly, the weight differences on the two diets occurred even though both kinds of foods had been carefully matched from a nutritional standpoint, including calorie density, fiber, fat, sugar, and salt. For example, breakfast for the ultra-processed group might consist of a bagel with cream cheese and turkey bacon, while the unprocessed group might be offered oatmeal with bananas, walnuts, and skim milk.

The explanation for the differences appears to lie in the fact that study participants were free to eat as little or as much food as they wished at mealtimes and to snack between meals. It turns out that when folks were on the ultra-processed diet they ate significantly more—about 500 extra calories per day on average—than when they were on the unprocessed diet. And, as you probably know, more calories without more exercise usually leads to more weight!

This might not seem new to you. After all, it has been tempting for some time to suggest a connection between the rise of packaged, ultra-processed foods and America’s growing waistlines. But as plausible as it might seem that such foods may encourage overeating, perhaps because of their high salt, sugar, and fat content, correlation is not causation and controlled studies of what people actually eat are tough to do. As a result, definitive evidence directly tying ultra-processed foods to weight gain has been lacking.

To explore the possible connection in the study now reported in Cell Metabolism, researchers at NIH’s National Institute of Diabetes and Digestive and Kidney Diseases took advantage of the Metabolic Clinical Research Unit at the NIH Clinical Center, Bethesda, MD. The unit is specially equipped to study issues involving diet and metabolism.

The researchers asked 20 healthy men and women of stable weight to stay at the center for 28 days. Each volunteer was randomly assigned to eat either an ultra-processed or unprocessed diet for two consecutive weeks. At that point, they switched to the other diet for another two weeks.

Both diets consisted of three daily meals, and volunteers were given permission to eat as much food as they liked. Importantly, a team of dieticians had carefully designed the ultra-processed and unprocessed meals such that they were well matched for total calories, calorie density, macronutrients, fiber, sugars, and salt.

At lunch, for example, one of the study’s processed meals consisted of quesadillas, refried beans, and diet lemonade. An unprocessed lunch consisted of a spinach salad with chicken breast, apple slices, bulgur, and sunflower seeds with a side of grapes.

The main difference between each diet was the proportion of calories derived from ultra-processed versus unprocessed foods as defined by the NOVA diet classification system. This system categorizes food based on the nature, extent, and purpose of food processing, rather than its nutrient content.

Each week, researchers measured the energy expenditure, weight, and changes in body composition of all volunteers. After two weeks on the ultra-processed diet, volunteers gained about two pounds on average. That’s compared to a loss of about two pounds for those on the unprocessed diet.

Metabolic testing showed that people expended more energy on the ultra-processed diet. However, that wasn’t enough to offset the increased consumption of calories. As a result, participants gained pounds and body fat. The study does have some limitations, such as slight differences in the protein content of the two diets. and the researchers plan to address such issues in their future work.

During this relatively brief study, the researchers did not observe other telltale changes associated with poor metabolic health, such as a rise in blood glucose levels or fat in the liver. While a couple of pounds might not sound like much, the extra calories and weight associated with an ultra-processed diet would, over time, add up.

So, it appears that a good place to start in reaching or maintaining a healthy weight is to follow the advice shared by all those otherwise conflicting diet plans: work to eliminate or at least reduce ultra-processed foods in your diet in favor of a balanced variety of unprocessed, nutrient-packed foods.

Reference:

[1] Ultra-processed diets cause excess calorie intake and weight gain: An inpatient randomized controlled trial of ad libitum food intake. Hall KD et al. Cell Metab. 2019 May 16.

Links:

Obesity (National Institute of Diabetes and Digestive and Kidney Diseases/NIH)

Healthy Eating Plan (National Heart, Lung, and Blood Institute/NIH)

Body Weight Planner (NIDDK/NIH)

Kevin D. Hall (NIDDK/NIH)

Metabolic Clinical Research Unit (NIDDK/NIH)

NIH Support: National Institute of Diabetes and Digestive and Kidney Diseases


Study Finds No Benefit for Dietary Supplements

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Eating healthy
Credit: iStock/Artfully79

More than half of U.S. adults take dietary supplements [1]. I don’t, but some of my family members do. But does popping all of these vitamins, minerals, and other substances really lead to a longer, healthier life? A new nationwide study suggests it doesn’t.

Based on an analysis of survey data gathered from more than 27,000 people over a six-year period, the NIH-funded study found that individuals who reported taking dietary supplements had about the same risk of dying as those who got their nutrients through food. What’s more, the mortality benefits associated with adequate intake of vitamin A, vitamin K, magnesium, zinc, and copper were limited to food consumption.

The study, published in the Annals of Internal Medicine, also uncovered some evidence suggesting that certain supplements might even be harmful to health when taken in excess [2]. For instance, people who took more than 1,000 milligrams of supplemental calcium per day were more likely to die of cancer than those who didn’t.

The researchers, led by Fang Fang Zhang, Tufts University, Boston, were intrigued that so many people take dietary supplements, despite questions about their health benefits. While the overall evidence had suggested no benefits or harms, results of a limited number of studies had suggested that high doses of certain supplements could be harmful in some cases.

To take a broader look, Zhang’s team took advantage of survey data from tens of thousands of U.S. adults, age 20 or older, who had participated in six annual cycles of the National Health and Nutrition Examination Survey (NHANES) between 1999-2000 and 2009-2010. NHANES participants were asked whether they’d used any dietary supplements in the previous 30 days. Those who answered yes were then asked to provide further details on the specific product(s) and how long and often they’d taken them.

Just over half of participants reported use of dietary supplements in the previous 30 days. Nearly 40 percent reported use of multivitamins containing three or more vitamins.

Nutrient intake from foods was also assessed. Each year, the study’s participants were asked to recall what they’d eaten over the last 24 hours. The researchers then used that information to calculate participants’ nutrient intake from food. Those calculations indicated that more than half of the study’s participants had inadequate intake of vitamins D, E, and K, as well as choline and potassium.

Over the course of the study, more than 3,600 of the study’s participants died. Those deaths included 945 attributed to cardiovascular disease and 805 attributed to cancer. The next step was to look for any association between the nutrient intake and the mortality data.

The researchers found the use of dietary supplements had no influence on mortality. People with adequate intake of vitamin A, vitamin K, magnesium, zinc, and copper were less likely to die. However, that relationship only held for nutrient intake from food consumption.

People who reported taking more than 1,000 milligrams of calcium per day were more likely to die of cancer. There was also evidence that people who took supplemental vitamin D at a dose exceeding 10 micrograms (400 IU) per day without a vitamin D deficiency were more likely to die from cancer.

It’s worth noting that the researchers did initially see an association between the use of dietary supplements and a lower risk of death due to all causes. However, those associations vanished when they accounted for other potentially confounding factors.

For example, study participants who reported taking dietary supplements generally had a higher level of education and income. They also tended to enjoy a healthier lifestyle. They ate more nutritious food, were less likely to smoke or drink alcohol, and exercised more. So, it appears that people who take dietary supplements are likely to live a longer and healthier life for reasons that are unrelated to their supplement use.

While the study has some limitations, including the difficulty in distinguishing association from causation, and a reliance on self-reported data, its findings suggest that the regular use of dietary supplements should not be recommended for the general U.S. population. Of course, this doesn’t rule out the possibility that certain subgroups of people, including perhaps those following certain special diets or with known nutritional deficiencies, may benefit.

These findings serve up a reminder that dietary supplements are no substitute for other evidence-based approaches to health maintenance and eating nutritious food. Right now, the best way to live a long and healthy life is to follow the good advice offered by the rigorous and highly objective reviews provided by the U.S. Preventive Services Task Force [3]. Those tend to align with what I hope your parents offered: eat a balanced diet, including plenty of fruits, veggies, and healthy sources of calcium and protein. Don’t smoke. Use alcohol in moderation. Avoid recreational drugs. Get plenty of exercise.

References:

[1] Trends in Dietary Supplement Use Among US Adults From 1999-2012. Kantor ED, Rehm CD, Du M, White E, Giovannucci EL. JAMA. 2016 Oct 11;316(14):1464-1474.

[2] Association among dietary supplement use, nutrient intake, and mortality among U.S. adults. Chen F, Du M, Blumberg JB, Ho Chui KK, Ruan M, Rogers G, Shan Z, Zeng L, Zhang. Ann Intern Med. 2019 Apr 9. [Epub ahead of print].

[3] Vitamin Supplementation to Prevent Cancer and CVD: Preventive Medication. U.S. Preventive Services Task Force, February 2014.

Links:

Office of Dietary Supplements (NIH)

Healthy Eating Plan (National Heart, Lung, and Blood Institute/NIH)

National Health and Nutrition Examination Survey (Centers for Disease Control and Prevention, Atlanta)

U.S. Preventive Services Task Force (Rockville, MD)

Fang Fang Zhang (Tufts University, Boston)

NIH Support: National Institute on Minority Health and Health Disparities


Connecting Senescent Cells to Obesity and Anxiety

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Graphical Abstract
Adapted from Ogrodnik et al., 2019, Cell Metabolism.

Obesity—which affects about 4 in 10 U.S. adults—increases the risk for lots of human health problems: diabetes, heart disease, certain cancers, and even anxiety and depression [1]. It’s also been associated with increased accumulation of senescent cells, which are older cells that resist death even as they lose the ability to grow and divide.

Now, NIH-funded researchers have found that when lean mice are fed a high-fat diet that makes them obese, they also have more senescent cells in their brain and show more anxious behaviors [2]. The researchers could reduce this obesity-driven anxiety using so-called senolytic drugs that cleared away the senescent cells. These findings are among the first to provide proof-of-concept that senolytics may offer a new avenue for treating an array of neuropsychiatric disorders, in addition to many other chronic conditions.

As we age, senescent cells accumulate in many parts of the body [3]. But cells can also enter a senescent state at any point in life in response to major stresses, such as DNA damage or chronic infection. Studies suggest that having lots of senescent cells around, especially later in life, is associated with a wide variety of chronic conditions, including osteoporosis, osteoarthritis, vascular disease, and general frailty.

Senescent cells display a “zombie”-like behavior known as a senescence-associated secretory phenotype (SASP). In this death-defying, zombie-like state, the cells ramp up their release of proteins, bioactive lipids, DNA, and other factors that, like a zombie virus, induce nearby healthy cells to join in the dysfunction.

In fact, the team behind this latest study, led by James Kirkland, Mayo Clinic, Rochester, MN, recently showed that transplanting small numbers of senescent cells into young mice is enough to cause them weakness, frailty, and persistent health problems. Those ill effects were alleviated with a senolytic cocktail, including dasatinib (a leukemia drug) and quercetin (a plant compound). This drug cocktail overrode the zombie-like SASP phenotype and forced the senescent cells to undergo programmed cell death and finally die.

Previous research indicates that senescent cells also accumulate in obesity, and not just in adipose tissues. Moreover, recent studies have linked senescent cells in the brain to neurodegenerative conditions, including Alzheimer’s disease, and showed in mice that dasatinib and quercetin helps to alleviate neurodegenerative disease [4,5]. In the latest paper, published in the journal Cell Metabolism, Kirkland and colleagues asked whether senescent cells in the brain also could explain anxiety-like behavior in obesity.

The answer appears to be “yes.” The researchers showed that lean mice, if allowed to feast on a high-fat diet, grew obese and became more anxious about exploring open spaces and elevated mazes.

The researchers also found that the obese mice had an increase in senescent cells in the white matter near the lateral ventricle, a part of the brain that offers a pathway for cerebrospinal fluid. Those senescent cells also contained an excessive amount of fat. Could senolytic drugs clear those cells and make the obesity-related anxiety go away?

To find out, the researchers treated lean and obese mice with a senolytic drug for 10 weeks. The treatment didn’t lead to any changes in body weight. But, as senescent cells were cleared from their brains, the obese mice showed a significant reduction in their anxiety-related behavior. They lost their anxiety without losing the weight!

More preclinical study is needed to understand more precisely how the treatment works. But, it’s worth noting that clinical trials testing a variety of senolytic drugs are already underway for many conditions associated with senescent cells, including chronic kidney disease [6,7], frailty [8], and premature aging associated with bone marrow transplant [9].

As a matter of fact, just after the Cell Metabolism paper came out, Kirkland’s team published encouraging though preliminary, first-in-human results of the previously mentioned senolytic drug dasatinib in 14 people with age-related idiopathic pulmonary fibrosis, a condition in which lung tissue becomes damaged and scarred [10]. Caution is warranted as we learn more about the associated risks and benefits, but it’s safe to say we’ll be hearing a lot more about senolytics in the years ahead.

References:

[1] Adult obesity facts (Centers for Disease Control and Prevention)

[2] Obesity-induced cellular senescence drives anxiety and impairs neurogenesis. Ogrodnik M et al. Cell Metabolism. 2019 Jan 3.

[3] Aging, Cell Senescence, and Chronic Disease: Emerging Therapeutic Strategies. Tchkonia T, Kirkland JL. JAMA. 2018 Oct 2;320(13):1319-1320.

[4] Tau protein aggregation is associated with cellular senescence in the brain. Musi N, Valentine JM, Sickora KR, Baeuerle E, Thompson CS, Shen Q, Orr ME. Aging Cell. 2018 Dec;17(6):e12840.

[5] Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline. Bussian TJ, Aziz A, Meyer CF, Swenson BL, van Deursen JM, Baker DJ. Nature. 2018 Oct;562(7728):578-582.

[6] Inflammation and Stem Cells in Diabetic and Chronic Kidney Disease. ClinicalTrials.gov, Sep 2018.

[7] Senescence in Chronic Kidney Disease. Clinicaltrials.gov, Sep 2018.

[8] Alleviation by Fisetin of Frailty, Inflammation, and Related Measures in Older Adults (AFFIRM-LITE). Clinicaltrials.gov, Dec 2018.

[9] Hematopoietic Stem Cell Transplant Survivors Study (HTSS Study). Clinicaltrials.gov, Sep 2018.

[10] Senolytics in idiopathic pulmonary fibrosis: Results from a first-in-human, open-label, pilot study. Justice JN, Nambiar AN, Tchkonia T, LeBrasseur K, Pascual R, Hashmi SK, Prata L, Masternak MM, Kritchevsky SB, Musi N, Kirkland JL. EBioMed. 5 Jan. 2019. [Epub ahead of print]

Links:

Healthy Aging (National Institute on Aging/NIH)

Video: Vail Scientific Summit James Kirkland Interview (Youtube)

James Kirkland (Mayo Clinic, Rochester, MN)

NIH Support: National Institute on Aging; National Institute of Neurological Disorders and Stroke


Has an Alternative to Table Sugar Contributed to the C. Diff. Epidemic?

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Ice cream sundae

Thinkstock/piyaphat50

Most of us know how hard it is to resist the creamy sweetness of ice cream. But it might surprise you to learn that, over the past 15 years or so, some makers of ice cream and many other processed foods—from pasta to ground beef products—have changed their recipes to swap out some of the table sugar (sucrose) with a sweetening/texturizing ingredient called trehalose that depresses the freezing point of food. Both sucrose and trehalose are “disaccharides.” Though they have different chemical linkages, both get broken down into glucose in the body. Now, comes word that this switch may be an important piece of a major medical puzzle: why Clostridium difficile (C. diff) has emerged as a leading cause of hospital-acquired infections.

A new study in the journal Nature indicates that trehalose-laden food may have helped fuel the recent epidemic spread of C. diff., which is a microbe that can cause life-threatening gastrointestinal distress, especially in older patients getting antibiotics and antacid medicines [1, 2]. In laboratory experiments, an NIH-funded team found that the two strains of C. diff. most likely to make people sick possess an unusual ability to thrive on trehalose, even at very low levels. And that’s not all: a diet containing trehalose significantly increased the severity of symptoms in a mouse model of C. diff. infection.


Creative Minds: Potential Diabetes Lessons from Binge-Eating Snakes

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Secor with a snake

Stephen Secor/Credit: Secor Lab

Many people would do just about anything to avoid an encounter with a snake. Not Stephen Secor. Growing up in central New York State, Secor was drawn to them. He’d spend hours frolicking through forest and field, flipping rocks and hoping to find one. His animal-loving mother encouraged him to keep looking, and she even let him keep a terrarium full of garter snakes in his bedroom. Their agreement: He must take good care of them—and please make sure they don’t get loose.

As a teen, Secor considered a career as a large-animal veterinarian. But a college zoology course led him right back to his fascination with snakes. Now a professor at the University of Alabama, Tuscaloosa, he’s spent 25 years trying to understand how some snakes, such as the Burmese python shown above, can fast for weeks or even months, and then go on a sudden food binge. Secor’s interest in the feast-or-famine digestive abilities of these snakes has now taken an unexpected turn that he never saw coming: a potential treatment to help people with diabetes.


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