Category: Diet and Nutrition

Do Sweeteners Increase Appetite? New Randomised Controlled Trial Says No

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Replacing sugar with artificial and natural sweeteners in foods has been the subject of a great deal of controversy, due to conflicting reports about their potential to increase appetite. But according to a significant new study published in eBioMedicine, it does not in fact make people hungrier as is often held – and also helps to reduce blood sugar levels.

Previous studies into whether sugar replacement with sweeteners increase appetite have been carried out but did not provide robust evidence. But the researchers say that their study, which meets the gold standard level of proof in scientific investigation, provides very strong evidence that sweeteners and sweetness enhancers do not negatively impact appetite and are beneficial for reducing sugar intake.

The double blind randomised controlled trial found that consuming food containing sweeteners produced a similar reduction in appetite sensations and appetite-related hormone responses as sugary foods. Additionally, it was found to provide some benefits such as lowering blood sugar, which may be particularly important in people at risk of developing type 2 diabetes.

The trial was led by the University of Leeds in collaboration with the The Rhône-Alpes Research Center for Human Nutrition. It is the latest study to be published by the SWEET consortium of 29 European research, consumer and industry partners which is working to develop and review evidence on long term benefits and potential risks involved in switching over to sweeteners and sweetness enhancers in the context of public health and safety, obesity, and sustainability. It was funded by Horizon Europe.

Lead author Catherine Gibbons, Associate Professor in the University of Leeds’ School of Psychology, said: “Reducing sugar consumption has become a key public health target in the fight to reduce the rising burden of obesity-related metabolic diseases such as type 2 diabetes.

“Simply restricting sugar from foods without substitution may negatively impact its taste or increase sweet cravings, resulting in difficulties sticking to a low-sugar diet. Replacing sugars with sweeteners and sweetness enhancers in food products is one of the most widely used dietary and food manufacturing strategies to reduce sugar intake and improve the nutritional profile of commercial foods and beverages.”

Principal investigator Graham Finlayson, Professor of Psychobiology in the University of Leeds’ School of Psychology, said: “The use of sweeteners and sweetness enhancers has received a lot of negative attention, including high profile publications linking their consumption with impaired glycaemic response, toxicological damage to DNA and increased risk of heart attack and stroke. These reports contribute to the current befuddlement concerning the safety of sweeteners and sweetness enhancers among the general public and especially people at risk of metabolic diseases.

“Our study provides crucial evidence supporting the day-to-day use of sweeteners and sweetness enhancers for body weight and blood sugar control.”

Until now, virtually all studies of the effects of sweeteners and sweetness enhancers on appetite and glycaemia have been conducted using beverages as the vehicle. Few studies include volunteers with overweight or obesity and few have included volunteers of both sexes.

Most studies have only compared a single sweetener, mostly aspartame, with a control, and very few studies have examined the effect of repeated daily intake of a known sweetener or sweetness enhancer in the normal diet.

The study, which is the first of its kind, looked at the effects of consuming biscuits containing either sugar or two types of food sweetener: natural sugar substitute Stevia, or artificial sweetener Neotame on 53 adult men and women with overweight or obesity. Participants were all aged 18 to 60, with overweight or obesity.

The trial consisted of three two-week consumption periods, where participants consumed biscuits with either fruit filling containing sugar; natural sugar substitute Stevia, or artificial sweetener Neotame, each separated by a break of 14–21 days. Day 1 and day 14 of the consumption periods took place in the lab.

Participants were instructed to arrive in the lab after an overnight fast, a blood sample was taken to establish baseline levels of glucose, insulin and appetite-related hormones. They were also asked to rate their appetite and food preferences.

After consuming the biscuits, they were asked to rate how full they felt over several hours. Glucose and insulin levels were measured, as were ghrelin, glucagon-like peptide 1 and pancreatic polypeptide – hormones associated with the consumption of food.

The results from the two sweetener types showed no differences in appetite or endocrine responses compared to sugar, but insulin levels measured over two hours after eating were reduced, as were blood sugar levels.

Source: University of Leeds

Inaoside A, a New Antioxidant Derived from Mushrooms

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Natural products have unique chemical structures and biological activities and can play a pivotal role in advancing pharmaceutical science. In a pioneering study, researchers from Shinshu University discovered Inaoside A, an antioxidant derived from Laetiporus cremeiporus mushrooms. This breakthrough, published in the journal Heliyon, sheds light on the potential of mushrooms as a source of therapeutic bioactive compounds.

The search for novel bioactive compounds from natural sources has gained considerable momentum in recent years due to the need for new therapeutic agents to combat various health challenges. Among a diverse array of natural products, mushrooms have emerged as a rich reservoir of bioactive molecules with potential pharmaceutical and nutraceutical applications. The genus Laetiporus has attracted attention for its extracts exhibiting antimicrobial, antioxidant, and antithrombin bioactivities. The species Laetiporus cremeiporus, spread across East Asia, has also been reported to show antioxidant properties. However, the identification and characterisation of specific antioxidant compounds from this species have not been conducted.

In a groundbreaking study, researchers led by Assistant Professor Atsushi Kawamura from the Department of Biomolecular Innovation, Institute for Biomedical Sciences, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, along with Hidefumi Makabe from the Department of Agriculture, Graduate School of Science and Technology, Shinshu University, and Akiyoshi Yamada from the Department of Mountain Ecosystem, Institute for Mountain Science, Interdisciplinary Cluster for Cutting Edge Research, Shinshu University, recently discovered the antioxidant compound derived from L. cremeiporus.

The researchers collected fresh fruiting bodies of L. cremeiporus from the Ina campus of Shinshu University. The obtained extracts were concentrated and partitioned between water and ethyl acetate. After this, the extracts were subjected to advanced chromatographic techniques, which led to the successful isolation of Inaoside A, a new antioxidant phenolic compound, along with three other well-characterised bioactive compounds, i.e., 5′-S-methyl-5′-thioadenosine (MTA), nicotinamide, and adenosine.

“Our study marks the pioneering discovery of Inaoside A from an extract of the edible mushroom Laetiporus cremeiporus. To date, there has been only one prior report on the biological function of an extract of L. cremeiporus. We are the first to uncover the isolation of an antioxidant compound from L. cremeiporus,” states Professor Kawamura, highlighting the breakthrough research.

Next, the researchers wanted to determine the structure of the newly found antioxidant compound. For this, they utilised one and two- dimensional NMR and other spectroscopic analyses. The structure of Inaoside A revealed a planar configuration. With a molecular formula of C17H24O7, the compound was found to feature a distinctive ribose moiety, identified as α-ribofuranoside through stereochemical analysis. Subsequent investigation into the absolute stereochemistry confirmed the D-ribose configuration, thereby reinforcing the planar structure of this compound.

The mushroom extracts were then isolated into fractions to determine the antioxidant activities of the four isolated bioactive compounds. These fractions were then examined by DPPH radical scavenging and superoxide dismutase assays. The findings were noteworthy as the DPPH radical scavenging activity exhibited by Inaoside A was significant, showing 80% inhibition at 100μg/mL, indicative of its significant antioxidant properties. The IC50 value of Inaoside A was determined to be 79.9μM, further highlighting its efficacy as an antioxidant agent.

What are the objectives of the researchers following the discovery of Inaoside? Professor Kawamura reveals, “We are now focusing on investigating the chemical compositions and biological properties of natural compounds obtained from mushrooms. Our goal is to uncover the potential of edible mushrooms as functional foods through this discovery.”

The identification of Inaoside A as an antioxidant from Laetiporus cremeiporus marks a significant breakthrough in natural product research, highlighting the potential of mushrooms as a source of therapeutic bioactive compounds. These findings may lead to the development of novel antioxidant-based therapies for various health conditions. Further studies should focus on synthetic research and detailed investigations into the biological activity of Inaoside A, aiming to harness its potential as a pharmaceutical lead compound.

Source: Shinshu University

Molecule Present in both the Body and Coffee Improves Muscle Function in Ageing

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A research consortium led by Nestlé Research in Switzerland and the Yong Loo Lin School of Medicine, National University of Singapore (NUS Medicine) made a recent discovery that the natural molecule trigonelline – present in coffee, fenugreek, and also in the human body – can help to improve muscle health and function. The researchers published their findings in Nature Metabolism.

In an international collaboration among the University of Southampton, University of Melbourne, University of Tehran, University of South Alabama, University of Toyama and University of Copenhagen, the work builds on a previous collaborative study that described novel mechanisms of human sarcopenia.

Sarcopenia is a condition where cellular changes that happen during ageing gradually weaken the muscles in the body and lead to accelerated loss of muscle mass, strength and reduced physical independence.

One important problem during sarcopenia is that the cellular cofactor NAD+ declines during ageing, while mitochondria, the energy powerhouses in our cells, produce less energy.

The study team discovered that levels of trigonelline were lower in older people with sarcopenia.

Providing this molecule in pre-clinical models resulted in increased levels of NAD+, increased mitochondrial activity and contributed to the maintenance of muscle function during ageing.

NAD+ levels can be enhanced with different dietary precursors like the essential amino acid L-tryptophan (L-Trp), and vitamin B3 forms such as nicotinic acid (NA), nicotinamide (NAM), nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN).

Assistant Professor Vincenzo Sorrentino from the Healthy Longevity Translational Research Programme at NUS Medicine added, “Our findings expand the current understanding of NAD+ metabolism with the discovery of trigonelline as a novel NAD+ precursor and increase the potential of establishing interventions with NAD+-producing vitamins for both healthy longevity and age-associated diseases applications.”

Nutrition and physical activity are important lifestyle recommendations to maintain healthy muscles during ageing. “We were excited to discover through collaborative research that a natural molecule from food cross-talks with cellular hallmarks of ageing. The benefits of trigonelline on cellular metabolism and muscle health during ageing opens promising translational applications,” said Jerome Feige, Head of the Physical Health department at Nestlé Research.

Source: National University of Singapore, Yong Loo Lin School of Medicine

Avid Appetite in Childhood Linked to Symptoms of Eating Disorder Later on

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An enthusiastic response to food in early childhood may be linked to a higher likelihood of experiencing eating disorder symptoms in adolescence, according to a new study led by researchers at UCL and Erasmus University Rotterdam.

The study, published in The Lancet Child & Adolescent Health, looked at survey data from 3670 young people in the UK and the Netherlands to investigate how appetite traits in early childhood might relate to the likelihood of developing eating disorder symptoms up to 10 years later.

The team also found that a slower pace of eating and feeling full more quickly (high sensitivity to satiety) in early childhood may be protective against developing some eating disorder symptoms later.

Co-lead author Dr Ivonne Derks (UCL Institute of Epidemiology & Health Care) said: “Although our study cannot prove causality, our findings suggest food cue responsiveness may be one predisposing risk factor for the onset of eating disorder symptoms in adolescence.

“However, high responsiveness to food is also a normal and very common behaviour and should be seen as just one potential risk factor among many rather than something to cause parents worry.”

Higher food responsiveness was linked to a 16% to 47% increase in the odds of reporting eating disorder symptoms, including binge eating symptoms, uncontrolled eating, emotional eating, restrained eating and compensatory behaviours.

The 47% increase was found for binge eating symptoms (eating a very large amount of food and/or experiencing the feeling of loss of control over eating), meaning that adolescents whose parents rated them highest on food responsiveness were almost three times more likely to report binge eating symptoms compared to adolescents whose parents scored them lowest.

A 16% increase in odds was found for restrained eating, whereby a person restricts their intake of food to lose weight or avoid weight gain.

Just like food responsiveness, emotional overeating in early childhood was also linked with higher odds of engaging in compensatory behaviours, which are intended to avoid weight gain, such as skipping meals, fasting and excessive exercise.

In turn, some appetite traits seemed to be protective against developing eating disorder symptoms later. Higher satiety responsiveness – that is, feeling full more quickly after eating, and feeling full for longer – was linked to lower odds of uncontrolled eating (defined as the extent to which someone feels out of control and eats more than usual) and compensatory behaviours.

A slower pace of eating, meanwhile, was linked to lower odds of compensatory behaviours and restrained eating.

The researchers also found that appetite traits such as food fussiness, emotional undereating (eating less due to low mood), and enjoyment of food in early childhood were not linked to later eating disorder symptoms in adolescence.

For the study, the researchers looked at data from two separate longitudinal studies: Generation R, following children born in Rotterdam, the Netherlands, between 2002 and 2006, and Gemini, which follows twins born in England and Wales in 2007.

Appetite traits were assessed based on parents’ questionnaire responses when the children were aged four or five. Eating disorder symptoms were self-reported by the then adolescents themselves at ages 12 to 14, when eating disorder symptoms typically start to emerge.

About 10% of the adolescents reported binge eating symptoms, where people eat an unusual amount of food and/or experience the feeling of loss of control over eating. Next to that, 50% reported at least one behaviour to compensate their food intake or to avoid gaining weight, such as skipping a meal.

Co-senior author Dr Clare Llewellyn (UCL Institute of Epidemiology & Health Care) said: “While the role of appetite in the development of obesity has been studied for many decades, this is the first study to comprehensively examine the role of appetite traits in the development of eating disorder symptoms.

“Eating disorders can be harder to treat effectively once they develop and so it would be better to prevent them from occurring in the first place. Our work in identifying risk factors in early life aims to support the development of possible prevention strategies. These could, for instance, involve providing extra support to children at higher risk.”

Appetite traits are divided into food approach appetitive traits (eg, food responsiveness, enjoyment of food, emotional overeating) and food avoidance traits (eg, satiety responsiveness, food fussiness, slowness in eating, emotional undereating).

The researchers found that non-responsive feeding practices, such as putting pressure on children to eat or using food as a reward or to soothe emotions, were linked to a higher likelihood of specific eating disorder symptoms later. However, the associations were small and varied between the two cohorts, and the researchers said further replication studies were needed.

Source: University College London

How the Body’s Organs Respond to Seven Days without Food

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New findings reveal that the body undergoes significant, systematic changes across multiple organs during prolonged periods of fasting. The results published in Nature Metabolism, demonstrate evidence of health benefits beyond weight loss, but also show that any potentially health-altering changes appear to occur only after three days without food.

By identifying the potential health benefits from fasting and their underlying molecular basis, researchers from Queen Mary University of London’s Precision Healthcare University Research Institute (PHURI) and the Norwegian School of Sports Sciences provide a road map for future research that could lead to therapeutic interventions – including for people that may benefit from fasting but cannot undergo prolonged fasting or fasting-mimicking, such as ketogenic, diets.

Over millennia, humans have developed the ability to survive without food for prolonged periods of time. Fasting is practiced by millions of people throughout the world for different medical and cultural purposes, including health benefits and weight loss. Since ancient times, it has been used to treat diseases such as epilepsy and rheumatoid arthritis.

During fasting, the body changes its source and type of energy, switching from consumed calories to using its own fat stores. However, beyond this change in fuel sources, little is known about how the body responds to prolonged periods without food and any health impacts – beneficial or adverse – this may have. New techniques allowing researchers to measure thousands of proteins circulating in our blood provide the opportunity to systematically study molecular adaptions to fasting in humans in great detail.

Researchers followed 12 healthy volunteers taking part in a seven-day water-only fast. The volunteers were monitored closely on a daily basis to record changes in the levels of around 3000 proteins in their blood before, during, and after the fast. By identifying which proteins are involved in the body’s response, the researchers could then predict potential health outcomes of prolonged fasting by integrating genetic information from large-scale studies.

As expected, the researchers observed the body switching energy sources – from glucose to fat stored in the body – within the first two or three days of fasting. The volunteers lost an average of 5.7kg of both fat mass and lean mass. After three days of eating after fasting, the weight stayed off – the loss of lean was almost completely reversed, but the fat mass stayed off.

For the first time, the researchers observed the body undergoing distinct changes in protein levels after about three days of fasting – indicating a whole-body response to complete calorie restriction. Overall, one in three of the proteins measured changed significantly during fasting across all major organs. These changes were consistent across the volunteers, but there were signatures distinctive to fasting that went beyond weight loss, such as changes in proteins that make up the supportive structure for neurons in the brain.

Claudia Langenberg, Director of Queen Mary’s Precision Health University Research Institute (PHURI), said:

“For the first time, we’re able to see what’s happening on a molecular level across the body when we fast. Fasting, when done safely, is an effective weight loss intervention. Popular diets that incorporate fasting — such as intermittent fasting — claim to have health benefits beyond weight loss. Our results provide evidence for the health benefits of fasting beyond weight loss, but these were only visible after three days of total caloric restriction — later than we previously thought.”

Maik Pietzner, Health Data Chair of PHURI and co-lead of the Computational Medicine Group at Berlin Institute of Health at Charité, said:

“Our findings have provided a basis for some age-old knowledge as to why fasting is used for certain conditions. While fasting may be beneficial for treating some conditions, often times, fasting won’t be an option to patients suffering from ill health. We hope that these findings can provide information about why fasting is beneficial in certain cases, which can then be used to develop treatments that patients are able to do.”

Source: Queen Mary University of London

Are Ultra-processed Foods the New ‘Silent Killer’?

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Nowadays, ultra-processed foods are packed with a bewildering range of additives: there are common ones like oil, fat, and sugar. There are also emulsifiers such as carrageenan, mono- and diglycerides, carboxymethylcellulose, polysorbate and soy lecithin. These continue to strip food of healthy nutrients while introducing other ingredients that could also be detrimental to human health.

Hundreds of novel ingredients never encountered by human physiology are now found in nearly 60% of the average adult’s diet and nearly 70% of children’s diets in the United States.

While obesity and lack of physical activity are well recognised contributors to avoidable morbidity and mortality, another emerging hazard is the unprecedented consumption of these ultra-processed foods in the standard American diet. This may be the new “silent” killer, as was unrecognised hypertension in previous decades.

Physicians from Florida Atlantic University’s Schmidt College of Medicine explored this hypothesis and provide important insights to health care providers in a battle where the entertainment industry, the food industry and public policy do not align with their patients’ needs. Their findings are published in a commentary in The American Journal of Medicine.

First generation of doctors to see a reduction in life expectancy

“Those of us practicing medicine in the US today find ourselves in an ignominious and unique position – we are the first cohort of health care professionals to have presided over a decline in life expectancy in 100 years,” said Dawn H. Sherling, MD, corresponding author, associate program director for the internal medicine residency and an associate professor of medicine, FAU Schmidt College of Medicine. “Our life expectancy is lower than other economically comparable countries. When we look at increasing rates of non-communicable diseases in less developed nations, we can see a tracking of this increase along with increasing consumption of ultra-processed foods in their diets.”

Although professional organizations such as the American College of Cardiology cautions patients to “choose minimally processed foods instead of ultra-processed foods” in their 2021 dietary guidelines, there is a caveat that “there is no commonly accepted definition for ultra-processed foods, and some healthy foods may exist within the ultra-processed food category.”

“When the components of a food are contained within a natural, whole food matrix, they are digested more slowly and more inefficiently, resulting in less calorie extraction, lower glycaemic loads in general, and lower rise in triglyceride-rich lipoproteins after eating, which could result in atherosclerotic plaque,” said Allison H. Ferris, MD, senior author, an associate professor and chair, Department of Medicine, and director of the internal medicine residency program, FAU Schmidt College of Medicine. “Therefore, even if the troublesome additives were removed from the ultra-processed food, there would still be concern for an over-consumption of these products possibly leading to obesity, diabetes and heart disease.”

The authors add that public health organisations are increasingly making use of the NOVA classification system, which divides foods into four categories – whole foods, culinary ingredients (items like butter, oil and salt), traditionally processed foods (such as bread and yogurt made with few ingredients), and ultra-processed foods – or those foods that are industrially made and use ingredients not normally found in a domestic kitchen.

According to the authors, one plausible mechanism to explain the hazards is that ultra-processed foods contain emulsifiers and other additives that the mammalian gastrointestinal tract mostly does not digest. They may act as a food source for our microbiota, and as such may be creating a dysbiotic microbiome that can, in the right host, promote disease.

“Additives, such as maltodextrin, may promote a mucous layer that is friendly to certain species of bacteria that are found in greater abundance in patients with inflammatory bowel disease,” said Sherling. “When the mucous layer is not properly maintained, the epithelial cell layer may become vulnerable to injury, as has been shown in feeding studies using carrageenan in humans and other studies in mice models, using polysorbate-80 and cellulose gum, triggering immunologic responses in the host.”

Food companies as powerful as the 20th century’s tobacco companies

The authors add that there have been marked increases in colorectal cancer in the US, especially among younger adults. They opine that increased ultra-processed food consumption may be a contributor as well as to several other gastrointestinal diseases.

“Whether ultra-processed foods contribute to our currently rising rates of non-communicable disease requires direct testing in analytic studies designed a priori to do so,” said Charles H. Hennekens, MD, FACPM, co-author, the First Sir Richard Doll Professor of Medicine and senior academic advisor, FAU Schmidt College of Medicine. “In the meantime, we believe it is incumbent upon all health care professionals to discuss the benefits of increasing consumption of whole foods and reducing consumption of ultra-processed foods with their patients.”

The authors also opine that just as the dangers of tobacco began to emerge during the middle of the prior century, decades passed before the preponderance of the evidence and the efforts of forward-thinking health officials prompted policy change to discourage the use of cigarettes. They say there is likely to be a similar path for ultra-processed foods.

“The multinational companies that produce ultra-processed foods are just as, if not more, powerful than tobacco companies were in the last century, and it is unlikely that governments will be able to move quickly on policies that will promote whole foods and discourage the consumption of ultra-processed foods,” said Sherling. “Importantly, health care providers also should remain cognizant of the difficulties that many of our patients have in being able to afford and find healthier options, which calls for a broader public health response.”

Source: Florida Atlantic University

Excessive Protein Consumption Increases Atherosclerosis Risk

Cardiovascular pitfalls to increasing protein intake discovered

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University of Pittsburgh School of Medicine researchers discovered a molecular mechanism by which excessive dietary protein could increase atherosclerosis risk. The study, published in Nature Metabolism, combined small human trials with in vitro human and mouse cell experiments.

It showed that consuming over 22% of dietary calories from protein can lead to increased activation of immune cells that play a role in atherosclerotic plaque formation, driving the disease risk.

Furthermore, the scientists showed that one amino acid, leucine, seems to have a disproportionate role in driving the pathological pathways linked to atherosclerosis, or stiff, hardened arteries.

“Our study shows that dialling up your protein intake in pursuit of better metabolic health is not a panacea. You could be doing real damage to your arteries,” said senior and co-corresponding author Babak Razani, MD, PhD, professor of cardiology at Pitt.

“Our hope is that this research starts a conversation about ways of modifying diets in a precise manner that can influence body function at a molecular level and dampen disease risks.”

According to a survey of an average American diet over the last decade, Americans generally consume a lot of protein, mostly from animal sources.

Further, nearly a quarter of the population receives over 22% of all daily calories from protein alone.

That trend is likely driven by the popular idea that dietary protein is essential to healthy living, says Razani.

But his and other groups have shown that overreliance on protein may not be such a good thing for long-term health.

Following their 2020 research, in which Razani’s laboratory first showed that excess dietary protein increases atherosclerosis risk in mice, his next study in collaboration with Bettina Mittendorfer, PhD, a metabolism expert at the University of Missouri, Columbia, delved deeper into the potential mechanism and its relevance to the human body.

To arrive at the answer, Razani’s laboratory, led by first-authors Xiangyu Zhang, Ph.D., and Divya Kapoor, M.D., teamed up with Mittendorfer’s group to combine their expertise in cellular biology and metabolism and perform a series of experiments across various models, from cells to mice to humans.

“We have shown in our mechanistic studies that amino acids, which are really the building blocks of the protein, can trigger disease through specific signaling mechanisms and then also alter the metabolism of these cells,” Mittendorfer said.

“For instance, small immune cells in the vasculature called macrophages can trigger the development of atherosclerosis.”

Based on initial experiments in healthy human subjects to determine the timeline of immune cell activation following ingestion of protein-enriched meals, the researchers simulated similar conditions in mice and in human macrophages, immune cells that are shown to be particularly sensitive to amino acids derived from protein.

Their work showed that consuming more than 22% of daily dietary calories through protein can negatively affect macrophages that are responsible for clearing out cellular debris, leading to the accumulation of a “graveyard” of those cells inside the vessel walls and worsening of atherosclerotic plaques overtime.

Interestingly, the analysis of circulating amino acids showed that leucine, an amino acid enriched in animal-derived foods like beef, eggs and milk, is primarily responsible for abnormal macrophage activation and atherosclerosis risk, suggesting a potential avenue for further research on personalized diet modification, or “precision nutrition.”

Razani is careful to note that many questions remain to be answered, mainly: What happens when a person consumes between 15% of daily calories from protein as recommended by the USDA and 22% of daily calories from protein, and if there is a ‘sweet spot’ for maximising the benefits of protein (such as muscle gain) while avoiding kick-starting a molecular cascade of damaging events leading to cardiovascular disease.

The findings are particularly relevant in hospital settings, where nutritionists often recommend protein-rich foods for the sickest patients to preserve muscle mass and strength.

“Perhaps blindly increasing protein load is wrong,” Razani said.

“Instead, it’s important to look at the diet as a whole and suggest balanced meals that won’t inadvertently exacerbate cardiovascular conditions, especially in people at risk of heart disease and vessel disorders.”

Razani also notes that these findings suggest differences in leucine levels between diets enriched in plant and animal protein might explain the differences in their effect on cardiovascular and metabolic health.

“The potential for this type of mechanistic research to inform future dietary guidelines is quite exciting,” he said.

Source: University of Pittsburgh

Switching to Vegan or Keto Diets Impacts Immune System

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Researchers at the National Institutes of Health observed rapid and distinct immune system changes in a small study of people who switched to a vegan or a ketogenic (“keto”) diet. They found that the vegan diet prompted responses linked to innate immunity while the keto diet prompted responses associated with adaptive immunity. Metabolic changes and shifts in the participants’ microbiomes were also observed. More research is needed to determine if these changes are beneficial or detrimental and what effect they could have on nutritional interventions for diseases such as cancer or inflammatory conditions.

Scientific understanding of how different diets impact the human immune system and microbiome is limited. Therapeutic nutritional interventions, which involve changing the diet to improve health, are not well understood, and few studies have directly compared the effects of more than one diet. The keto diet is a low-carbohydrate diet that is generally high in fat. The vegan diet eliminates animal products and tends to be high in fibre and low in fat.

The study was conducted by researchers from the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the Metabolic Clinical Research Unit in the NIH Clinical Center.

The 20 participants were diverse with respect to ethnicity, race, gender, body mass index (BMI), and age. Participants sequentially ate vegan and keto diets for two weeks, in random order. Each person ate as much as desired of one diet (vegan or keto) for two weeks, followed by as much as desired of the other diet for two weeks. People on the vegan diet, which contained about 10% fat and 75% carbohydrates, chose to consume fewer calories than those on the keto diet, which contained about 76% fat and 10% carbohydrates. Throughout the study period, blood, urine, and stool were collected for analysis.

The effects of the diets were examined using a “multi-omics” approach that analysed multiple data sets to assess the body’s biochemical, cellular, metabolic, and immune responses, as well as changes to the microbiome.

Participants remained on site for the entire month-long study, allowing for careful control of the dietary interventions. Switching exclusively to the study diets caused notable changes in all participants.

The vegan diet significantly impacted pathways linked to the innate immune system, including antiviral responses. On the other hand, the keto diet led to significant increases in biochemical and cellular processes linked to adaptive immunity, such as pathways associated with T and B cells.

The keto diet affected levels of more proteins in the blood plasma than the vegan diet, as well as proteins from a wider range of tissues, such as the blood, brain and bone marrow. The vegan diet promoted more red blood cell-linked pathways, including those involved in heme metabolism, which could be due to the higher iron content of this diet.

Additionally, both diets produced changes in the microbiomes of the participants, causing shifts in the abundance of gut bacterial species that previously had been linked to the diets.

The keto diet was associated with changes in amino acid metabolism – an increase in human metabolic pathways for the production and degradation of amino acids and a reduction in microbial pathways for these processes – which might reflect the higher amounts of protein consumed by people on this diet.

The distinct metabolic and immune system changes caused by the two diets were observed despite the diversity of the participants, which shows that dietary changes consistently affect widespread and interconnected pathways in the body. More study is needed to examine how these nutritional interventions affect specific components of the immune system. According to the authors, the results of this study demonstrate that the immune system responds surprisingly rapidly to nutritional interventions. The authors suggest that it may be possible to tailor diets to prevent disease or complement disease treatments, such as by slowing processes associated with cancer or neurodegenerative disorders.

Source: NIH/National Institute of Allergy and Infectious Diseases

People with Gluten Sensitivity have Negative Effects – Even When Eating a Placebo

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Symptoms of gluten sensitivity are partly to do with people’s expectations, if celiac disease and wheat allergy have been excluded as causes. Recent research at the universities of Maastricht and Leeds shows that the expectation that gluten causes gastrointestinal complaints plays a crucial role in whether or not people experience these symptoms. These results, published in The Lancet Gastroenterology and Hepatology, indicate a direct involvement of the interaction between the brain and the intestines – the ‘gut-brain axis’ – in the experience of complaints after ingesting gluten.

Fear of gluten

A growing number of people are reducing their gluten intake due to self-reported digestive complaints, despite the fact that celiac disease and wheat allergy have been ruled out. The cause of their symptoms is often unclear. The researchers therefore wanted to investigate the effects of expectations on symptoms experienced after gluten intake. More than 80 subjects with self-reported gluten sensitivity took part in a psychological study and were divided into four groups. The results were unequivocal: people who thought they were eating food containing gluten reported more symptoms, while those who thought their food was gluten-free reported fewer symptoms.

In reality, the food given to half of each group contained gluten, while for the other half it was gluten-free. In all of the groups people’s expectations played a prominent role in whether or not they reported symptoms after eating. “In our research, we see a so-called nocebo effect when people eat gluten,” says researcher Marlijne de Graaf. “If people expect gluten to produce negative effects, they experience symptoms, even if it turns out afterwards that they weren’t actually eating gluten. Although the cause is partly ‘in the mind’, this doesn’t mean that the symptoms are not real.”

Gut-brain axis

The results of this study indicate a clear involvement of the interaction between the brain and the intestines in gluten sensitivity, a subject on which knowledge is as yet limited. The researchers therefore now want to concentrate on unravelling the mechanisms that determine the importance of expectation and exposure along the gut-brain axis. ‘Due to the influence of interactions between the brain and the intestines, people can genuinely experience symptoms such as stomach ache, bloating or diarrhoea after eating gluten,’ says Daisy Jonkers, professor of Intestinal Health at Maastricht University. ‘But the cause of these complaints is not only eating gluten, so a gluten-free diet isn’t the only solution.’

To treat this problem, the researchers want to conduct further studies on the influence of the brain on the development of bowel complaints. ‘For example, we’d like to know exactly which areas in the brain are involved,” says Jonkers, “and we also want to find out what substances play a role in the communication between the brain and the gut, and whether people might respond differently to them. It’s also quite possible that some people can’t tolerate wheat products because of substances in wheat other than gluten, and that there is indeed something in wheat that can lead to overstimulation of the immune system, for example, or excessive production of gas by the gut flora. This is also something we’d like to investigate.”

Source: Maastricht University

Meat Builds Muscle Proteins Better than Equivalent Vegan Dishes

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Older adults require more protein but eat less than younger people, making it a challenge for them to maintain muscle mass. Eating a meal with meat ensures that muscle proteins are built faster than a vegan meal with the same amount of protein. This study, published in The Journal of Nutrition, was the first to compare the speed at which muscle proteins are being made after eating a complete meal with animal or plant proteins.

Every two to three months the proteins in human muscle are completely renewed. In order to make muscle proteins, we need protein from food, for example from animal sources such as meat, cheese and yoghurt, or from plant products such as beans, nuts and soymilk. Previous research on protein powders showed that animal proteins have better muscle-building properties than plant proteins. “But in reality, we do not get our proteins in powder form, but through complete meals,” says study author and PhD student Philippe Pinckaers. “Those meals contain different types of protein and other nutrients such as fibres, fats and carbohydrates. These nutrients affect how proteins are released from the diet and influences the making of muscle proteins.”

To investigate how muscles respond after eating a complete meal, Pinckaers asked 16 participants aged over 65 to come to the lab twice for a dinner meal.

Dining out in the lab

On one day, the participants sat down to a meal with quinoa with chickpeas, broad beans, soy beans and soy sauce was on the menu, while on the other day the menu consisted of a beef tartlet, potatoes, green beans, apple sauce and herb butter. Both meals had similar amounts of protein, fat, carbohydrates and calories. Prior to the meals, participants were administered an infusion of special amino acids.

“The amino acids administered via the infusion were marked, as it were with a flag,” Pinckaers explains. “We took small pieces of muscle tissue from the participants and were able to measure the amount of ‘flags’ in them. If more flags are measured, it means that muscle proteins are built up faster, which is beneficial for muscles. In this way, we found that after eating a meal with animal protein, muscle protein was built up faster than after eating a vegan meal. This means that a vegan meal does not have the same capacity to make muscle proteins as a meal that includes animal proteins.” This difference arises partly because plant-based foods are harder to digest, and because they naturally contain fewer essential amino acids.

Context is key  

The results do not mean that everyone should eat meat or other animal products, clarifies professor of exercise science and lead researcher Luc van Loon. “Healthy people can very well compensate for the lower quality of plant proteins by eating more of them.” For elderly or frail patients it is a bit more complicated. “Elderly people actually need more protein in order to reach the same level of muscle protein synthesis, when compared to young individuals. However, they actually eat less. Also, patients with reduced appetite or who do not exercise much, for example during hospitalisation, may have trouble consuming a sufficient amount of protein. For them, it is therefore important to choose protein sources that stimulate the making of muscle proteins as much as possible. The best sources in this situation would be proteins from animal products.”

Source: Maastricht University