When pubs, bars and restaurants in England removed their largest size of wine sold by the glass, consumers drank less alcohol
Photo from Pixabay CC0
Alcohol consumption is the fifth largest contributor to premature death and disease globally. Many cues in physical and economic environments influence alcohol consumption across populations. One proposed intervention to excessive alcohol consumption is reducing the size of servings of alcoholic drinks sold by the glass, but there has been no real-world evidence for the effectiveness of this.
In the new study, researchers asked 21 licensed premises in England to remove from their menus their largest serving of wine by the glass – usually 250mL – for four weeks. The researchers then tracked the total volume of wine, beer and cider sold by each establishment.
Over the course of the four weeks, the total volume of wine sold by the licensed premises decreased by 7.6%, and there was no overall increase in beer and cider sales. There was an increase in the sales of smaller servings of wine by the glass – generally 125mL and 175mL – but no impact on sales of wine by the bottle or beer or cider sales.
“This suggests that this is a promising intervention for decreasing alcohol consumption across populations, which merits consideration as part of alcohol licensing regulations,” the authors say.
Marteau adds, “Removing the largest serving size of wine by the glass in 21 licensed premises reduced the volume of wine sold, in keeping with the wealth of research showing smaller serving sizes reduce how much we eat. This could become a novel intervention to improve population health by reducing how much we drink.”
Restricting calories is known to improve health and increase lifespan, but much of how it does so remains a mystery, especially in regard to how it protects the brain. Now, scientists from the Buck Institute for Research on Aging have uncovered a role for a gene called OXR1 that is necessary for the lifespan extension seen with dietary restriction and is essential for healthy brain aging.
“When people restrict the amount of food that they eat, they typically think it might affect their digestive tract or fat buildup, but not necessarily about how it affects the brain,” said Kenneth Wilson, PhD, Buck postdoc and first author of the study, published in Nature Communications. “As it turns out, this is a gene that is important in the brain.”
The team additionally demonstrated a detailed cellular mechanism of how dietary restriction can delay aging and slow the progression of neurodegenerative diseases. The work, done in fruit flies and human cells, also identifies potential therapeutic targets to slow aging and age-related neurodegenerative diseases.
“We found a neuron-specific response that mediates the neuroprotection of dietary restriction,” said Buck Professor Pankaj Kapahi , PhD, co-senior author of the study. “Strategies such as intermittent fasting or caloric restriction, which limit nutrients, may enhance levels of this gene to mediate its protective effects.”
“The gene is an important brain resilience factor protecting against aging and neurological diseases,” said Buck Professor Lisa Ellerby, PhD, co-senior author of the study.
Understanding variability in response to dietary restriction
Members of the team have previously shown mechanisms that improve lifespan and healthspan with dietary restriction, but it was not clear why there is so much variability in response to reduced calories across individuals and different tissues. This project was started to understand why different people respond to diets in different ways.
The team began by scanning about 200 strains of flies with different genetic backgrounds. The flies were raised with two different diets, either with a normal diet or with dietary restriction, which was only 10% of normal nutrition. Researchers identified five genes which had specific variants that significantly affected longevity under dietary restriction. Of those, two had counterparts in human genetics.
The team chose one gene to explore thoroughly, called “mustard” (mtd) in fruit flies and “Oxidation Resistance 1” (OXR1) in humans and mice. The gene protects cells from oxidative damage, but the mechanism for how this gene functions was unclear. The loss of OXR1 in humans results in severe neurological defects and premature death. In mice, extra OXR1 improves survival in a model of amyotrophic lateral sclerosis (ALS).
The link between brain aging, neurodegeneration and lifespan
To figure out how a gene that is active in neurons affects overall lifespan, the team did a series of in-depth tests. They found that OXR1 affects a complex called the retromer, which is a set of proteins necessary for recycling cellular proteins and lipids. “The retromer is an important mechanism in neurons because it determines the fate of all proteins that are brought into the cell,” said Wilson. Retromer dysfunction has been associated with age-related neurodegenerative diseases that are protected by dietary restriction, specifically Alzheimer’s and Parkinson’s diseases.
Overall, their results told the story of how dietary restriction slows brain aging by the action of mtd/OXR1 in maintaining the retromer. “This work shows that the retromer pathway, which is involved in reusing cellular proteins, has a key role in protecting neurons when nutrients are limited,” said Kapahi. The team found that mtd/OXR1 preserves retromer function and is necessary for neuronal function, healthy brain aging, and lifespan extension seen with dietary restriction.
“Diet is influencing this gene. By eating less, you are actually enhancing this mechanism of proteins being sorted properly in your cells, because your cells are enhancing the expression of OXR1,” said Wilson.
The team also found that boosting mtd in flies caused them to live longer, leading researchers to speculate that in humans excess expression of OXR1 might help extend lifespan. “Our next step is to identify specific compounds that increase the levels of OXR1 during aging to delay brain aging,” said Ellerby.
“Hopefully from this we can get more of an idea of why our brains degenerate in the first place,” said Wilson.
“Diet impacts all the processes in your body,” he said. “I think this work supports efforts to follow a healthy diet, because what you eat is going to affect more than you know.”
Low-carbohydrate diets of mostly plant-based proteins and fats with healthy carbohydrates such as whole grains were associated with slower long-term weight gain than low-carbohydrate diets of mostly of animal proteins and fats with unhealthy carbohydrates like refined starches, according to a new study led by Harvard T.H. Chan School of Public Health. The study was published in JAMA Network Open.
“Our study goes beyond the simple question of, ‘To carb or not to carb?'” said lead author Binkai Liu, research assistant in the Department of Nutrition. “It dissects the low-carbohydrate diet and provides a nuanced look at how the composition of these diets can affect health over years, not just weeks or months.”
While many studies have shown the benefits of cutting carbohydrates for short-term weight loss, little research has been conducted on low-carbohydrate diets’ effect on long-term weight maintenance and the role of food group quality.
Using data from the Nurses’ Health Study, Nurses’ Health Study II, and Health Professionals Follow-up Study, the researchers analysed the diets and weights of 123 332 healthy adults from 1986 to 2018.
Each participant provided self-reports of their diets and weights every four years.
The researchers scored participants’ diets based on how well they adhered to five categories of low-carbohydrate diet: total low-carbohydrate diet (TLCD), emphasising overall lower carbohydrate intake; animal-based low-carbohydrate diet (ALCD), emphasising animal-based proteins and fats; vegetable-based low-carbohydrate diet (VLCD), emphasising plant-based proteins and fats; healthy low-carbohydrate diet (HLCD), emphasising plant-based proteins, healthy fats, and fewer refined carbohydrates; and unhealthy low-carbohydrate diet (ULCD), emphasising animal-based proteins, unhealthy fats, and carbohydrates coming from unhealthy sources such as processed breads and cereals.
The study found that diets comprised of plant-based proteins and fats and healthy carbohydrates were significantly associated with slower long-term weight gain. None of these diets strictly excluded animal or dairy products.
Participants who increased their adherence to TLCD, ALCD, and ULCD on average gained more weight compared to those who increased their adherence to HLCD over time.
These associations were most pronounced among participants who were younger (< 55 years old), overweight or obese, and/or less physically active.
The results for the vegetable-based low carbohydrate diet were more ambiguous: Data from the Nurses’ Health Study II showed an association between higher VLCD scores and less weight gain over time, while data around VLCD scores from the Nurses’ Health Study and Health Professionals Follow-up Study were more mixed.
“The key takeaway here is that not all low-carbohydrate diets are created equal when it comes to managing weight in the long-term,” said senior author Qi Sun, associate professor in the Department of Nutrition.
“Our findings could shake up the way we think about popular low-carbohydrate diets and suggest that public health initiatives should continue to promote dietary patterns that emphasise healthful foods like whole grains, fruits, vegetables, and low-fat dairy products.”
Infants born extremely prematurely need enrichment in addition to breast milk, but it wasn’t clear as to whether enrichments were made from breast milk or cow’s milk had an effect on the risk of severe complications. This has been investigated by a large clinical study led by Linköping University, Sweden, published in eClinicalMedicine.
Infants born extremely prematurely, between weeks 22 and 27 of pregnancy, are among the most vulnerable patients in healthcare, at high risk of serious complications and mortality.
There is strong research support for giving breast milk to these children rather than formula made from cow’s milk. Formula based on cow’s milk is known to increase severe the risks for intestinal inflammation and sepsis.
“In Sweden, all extremely preterm infants receive breast milk from their mother or donated breast milk. Despite this, almost one in ten children get a severe inflammation of the intestine called necrotising enterocolitis. It’s one of the worst diseases you can have. At least three out of ten children die and those who survive often have neurological problems afterwards,” says Thomas Abrahamsson, professor at Linköping University and senior physician at the neonatal department at the University Hospital in Linköping, who led the current study.
Historically, there have been very few studies on extremely preterm infants where treatments have been compared against each other.
Therefore, there is a great need for clinical studies that can provide scientific support for how these children should be treated to have better chances of survival and a good life.
In some countries, such as Sweden, infants are fed exclusively with either their mother’s breast milk or donated breast milk.
However, in order for extremely preterm infants to grow as well as possible, they need more nutrition than breast milk contains. This is why breast milk is supplemented with extra protein, so-called enrichment.
The enrichment has previously been made from cow’s milk. But there have been suspicions that cow’s milk-based enrichment increases the risk of severe complications. Today, there is enrichment that is based on donated breast milk, and which has begun to be used in healthcare in some places.
The big question is whether it can reduce the risk of diseases in extremely preterm infants.
The current study, called N-Forte (the Nordic study on human milk fortification in extremely preterm infants), is the largest that has been carried out to seek answers to this question.
The results have been eagerly awaited by paediatricians and others caring for these fragile infants.
“We concluded that it doesn’t matter whether extremely preterm infants get enrichment made from cow’s milk or made from donated breast milk,” says Thomas Abrahamsson.
Although the study indicates that there was no difference between the two options, its results can be useful – the breast milk enrichment is fairly expensive.
“On the one hand, we’re disappointed that we didn’t find a positive effect of enrichment based on breast milk. On the other hand, it’s a large and well-done study and we can now say with great certainty that it doesn’t have an effect in this patient group. This is also important knowledge, so that we don’t invest in expensive products that don’t have the desired effect,” says Thomas Abrahamsson.
The N-Forte study included 228 extremely preterm infants, randomised 1:1 to receive enrichment made from breast milk and cow’s milk respectively.
The researchers examined whether the two groups differed in the incidence of necrotising enterocolitis, sepsis and death.
Of the children treated with breast milk-based enrichment, 35.7% had these complications, while the corresponding proportion was 34.5% in the group receiving cow’s milk-based enrichment, which means that there was no difference between the groups.
The results of the study are in line with a smaller study from Canada published in 2018, where researchers also saw no difference between the two types of enrichment on necrotising enterocolitis and severe sepsis.
A new study from UC Riverside has added more reasons to stick to New Year’s diet resolutions: it showed that that high-fat diets affect genes linked not only to obesity, colon cancer and irritable bowels, but also to the immune system, brain function, and potentially COVID risk.
While other studies have examined the effects of a high-fat diet, this one is unusual in its scope. UCR researchers fed mice three different diets over the course of 24 weeks where at least 40% of the calories came from fat. Then, they looked not only at the microbiome, but also at genetic changes in all four parts of the intestines.
One group of mice ate a diet based on saturated fat from coconut oil, another got a monounsaturated, modified soybean oil, a third got an unmodified soybean oil high in polyunsaturated fat. Compared to a low-fat control diet, all three groups experienced concerning changes in gene expression, the process that turns genetic information into a functional product, such as a protein.
Plant-based or not, high-fat is bad
“Word on the street is that plant-based diets are better for you, and in many cases that’s true. However, a diet high in fat, even from a plant, is one case where it’s just not true,” said Frances Sladek, a UCR cell biology professor and senior author of the new study.
The study, published in Scientific Reports, documents the many impacts of high-fat diets. Some of the intestinal changes did not surprise the researchers, such as major changes in genes related to fat metabolism and the composition of gut bacteria. For example, they observed an increase in pathogenic E. coli and a suppression of Bacteroides, which helps protect the body against pathogens.
Other observations were more surprising, such as changes in genes regulating susceptibility to infectious diseases. “We saw pattern recognition genes, ones that recognise infectious bacteria, take a hit. We saw cytokine signalling genes take a hit, which help the body control inflammation,” Sladek said. ‘So, it’s a double whammy. These diets impair immune system genes in the host, and they also create an environment in which harmful gut bacteria can thrive.”
The team’s previous work with soybean oil documents its link to obesity and diabetes, both major risk factors for COVID. This paper now shows that all three high-fat diets increase the expression of ACE2 and other host proteins that are used by COVID spike proteins to enter the body.
Additionally, the team observed that high-fat food increased signs of stem cells in the colon. “You’d think that would be a good thing, but actually they can be precursors to cancer,” Sladek said.
In terms of effects on gene expression, coconut oil showed the greatest number of changes, followed by the unmodified soybean oil. Differences between the two soybean oils suggest that polyunsaturated fatty acids in unmodified soybean oil, primarily linoleic acid, play a role in altering gene expression.
Negative changes to the microbiome in this study were more pronounced in mice fed the soybean oil diet. This was unsurprising, as the same research team previously documented other negative health effects of high soybean oil consumption.
Soybeans are fine, but watch the oil
In 2015, the team found that soybean oil induces obesity, diabetes, insulin resistance, and fatty liver in mice. In 2020, the researchers team demonstrated the oil could also affect genes in the brain related to conditions like autism, Alzheimer’s disease, anxiety, and depression.
Interestingly, in their current work they also found the expression of several neurotransmitter genes were changed by the high fat diets, reinforcing the notion of a gut-brain axis that can be impacted by diet.
The researchers have noted that these findings only apply to soybean oil, and not to other soy products, tofu, or soybeans themselves. “There are some really good things about soybeans. But too much of that oil is just not good for you,” said UCR microbiologist Poonamjot Deol, who was co-first author of the current study along with UCR postdoctoral researcher Jose Martinez-Lomeli.
Also, the studies were conducted using mice, and mouse studies do not always translate to the same results in humans. However, humans and mice share 97.5% of their working DNA. Therefore, the findings are concerning, as soybean oil is the most commonly consumed oil in the United States, and is increasingly being used in other countries, including Brazil, China, and India.
By some estimates, Americans tend to get nearly 40% of their calories from fat, which mirrors what the mice were fed in this study. “Some fat is necessary in the diet, perhaps 10 to 15%. Most people though, at least in this country, are getting at least three times the amount that they need,” Deol said.
Readers should not panic about a single meal. It is the long-term high-fat habit that caused the observed changes. Recall that the mice were fed these diets for 24 weeks. “In human terms, that is like starting from childhood and continuing until middle age. One night of indulgence is not what these mice ate. It’s more like a lifetime of the food,” Deol said.
That said, the researchers hope the study will cause people to closely examine their eating habits.
The holiday season is a time for joy and celebration but many Americans admit the endless flurry of activities make it difficult to eat healthy, exercise and get adequate rest, according to a new survey from The Ohio State University Wexner Medical Center.
Two-thirds of those surveyed said they overindulge in food, nearly 45% said they take a break from exercise and more than half report feeling tired and have less time for themselves. Plus, a third admit they drink more alcohol during the holidays.
“Holiday travel, activities with friends and family, and trying to get a bunch of things done can cause people to lose track of their healthy habits,” said Barbara Bawer, MD, family medicine physician at Ohio State Wexner Medical Center and clinical assistant professor of family and community medicine at The Ohio State University College of Medicine.
“If one healthy habit drops off, it can affect other areas very quickly.”
To make it through the holiday season with healthy habits intact, Bawer suggests trying to stick to a normal routine as much as possible while giving yourself some grace.
“Once you’re out of a routine, which typically happens around the holidays, it’s really hard to get back on track partly because the motivation is no longer there,” said Bawer.
When the invitations start to pile up and decadent menus feels tempting, Bawer offers this advice, “Remember that it’s OK to say no.”
To keep healthy habits in check, try the following:
Diet: When it comes to sustaining healthy eating habits, it’s important to plan ahead. If you have an evening event, don’t starve yourself all day. Eat a high protein, low carb meal earlier in the day so you don’t overeat.
You can indulge with a favorite dish or dessert but it’s OK to say no to sampling every entrée or treat so you’re not eating excess calories at each event.
Exercise: Try to keep the same exercise schedule. If an obligation prevents you from going to a fitness centre or going for a run, be flexible. It’s OK to say no to the gym and consider doing an activity with family and friends that keeps you moving like going for a walk or playing a game of basketball.
Sleep: Go to sleep and wake up at your normal times, even when travelling. Limit the use of supplements like melatonin, as long-term use can disrupt healthy sleep-wake cycles. It’s OK to say no to some invitations if you feel like you’re going to overextend yourself.
Alcohol: People may drink more during the holidays but binge drinking is never a healthy choice. Binge drinking is when a man consumes five drinks or a woman consume four drinks in one setting. It’s OK to say no to excessive drinking. If you do drink, try to stick to the recommended two drinks for men or one drink for women. Avoid drinking on an empty stomach and drink plenty of water.
“Small, consistent changes and slowly adding to them can help you reach your health goals,” Bawer said.
Survey results and methodology This survey was conducted on behalf of The Ohio State University Wexner Medical Center by SSRS on its Opinion Panel Omnibus platform. The SSRS Opinion Panel Omnibus is a national, twice-per-month, probability-based survey. Data collection was conducted from Oct. 20-23 among a sample of 1 007 respondents. The survey was conducted via web (n = 977) and telephone (n = 30) and administered in English. The margin of error for total respondents is +/-3.6 percentage points at the 95% confidence level. All SSRS Opinion Panel Omnibus data are weighted to represent the target population of U.S. adults ages 18 or older.
A study published in Nature Communications has revealed that the time at which we eat could influence our risk of developing cardiovascular disease. This study, suggests that eating a late first or last meal is associated with a higher risk of cardiovascular disease. It also appears that a longer night-time fasting duration is associated with a reduced risk of cerebrovascular disease such as stroke. The findings, suggest the importance of daily meal timing and rhythm in reducing cardiovascular disease risk.
The study was led by scientists from INRAE, the Barcelona Institute for Global Health, Inserm, and the Université Sorbonne Paris Nord.
Diet plays a major role in the development and progression of cardiovascular diseases. The modern lifestyle of Western societies has led to specific eating habits such as eating dinner late or skipping breakfast. In addition to light, the daily cycle of food intake (meals, snacks, etc) alternating with periods of fasting synchronizes the peripheral clocks, or circadian rhythms, of the body’s various organs, thus influencing cardiometabolic functions such as blood pressure regulation. Chrononutrition is emerging as an important new field for understanding the relationship between the timing of food intake, circadian rhythms and health.
Scientists used data from 103,389 participants in the NutriNet-Santé cohort (79% of whom were women, with an average age of 42) to study the associations between food intake patterns and cardiovascular disease. To reduce the risk of possible bias, the researchers accounted for a large number of confounding factors, especially sociodemographic factors (age, sex, family situation, etc.), diet nutritional quality, lifestyle and sleep cycle.
The results show that having a first meal later in the day (such as when skipping breakfast), is associated with a higher risk of cardiovascular disease, with a 6% increase in risk per hour delay. For example, a person who eats for the first time at 9 am is 6% more likely to develop cardiovascular disease than someone who eats at 8 am When it comes to the last meal of the day, eating late (after 9 pm) is associated with a 28% increase in the risk of cerebrovascular disease such as stroke compared with eating before 8 pm, particularly in women. Finally, a longer duration of night-time fasting – the time between the last meal of the day and the first meal of the following day – is associated with a reduced risk of cerebrovascular disease, supporting the idea of eating one’s first and last meals earlier in the day.
These findings, which need to be replicated in other cohorts and through additional scientific studies with different designs, highlight a potential role for meal timing in preventing cardiovascular disease. They suggest that adopting the habit of eating earlier first and last meals with a longer period of night-time fasting could help to prevent the risk of cardiovascular disease.
This is a pseudo-colored image of high-resolution gradient-echo MRI scan of a fixed cerebral hemisphere from a person with multiple sclerosis.
Credit: Govind Bhagavatheeshwaran, Daniel Reich, National Institute of Neurological Disorders and Stroke, National Institutes of Health
For decades, scientists have noted an intriguing similarity between a deficiency in vitamin B12 – an essential nutrient that supports healthy development and functioning of the central nervous system (CNS) – and multiple sclerosis (MS), a chronic disease in which the body’s immune system attacks the CNS and which can produce neurodegeneration.
Both vitamin B12 deficiency and MS produce similar neurological symptoms, including numbness or tingling in hands and feet, vision loss, difficulty walking or speaking normally and cognitive dysfunction, such as problems with memory.
In a new study, published in Cell Reports, researchers at Sanford Burnham Prebys, with collaborators elsewhere, describe a novel molecular link between vitamin B12 and MS that takes place in astrocytes – important non-neuronal glial cells in the brain.
The findings by senior study author Jerold Chun, MD, PhD, professor and senior vice president of neuroscience drug discovery, and Yasuyuki Kihara, PhD, research associate professor and co-corresponding author, and colleagues suggest new ways to improve the treatment of MS through CNS-B12 supplementation.
“The shared molecular binding of the brain’s vitamin B12 carrier protein, known as transcobalamin 2 or TCN2, with the FDA-approved MS drug fingolimod provides a mechanistic link between B12 signaling and MS, towards reducing neuroinflammation and possibly neurodegeneration,” said Chun.
“Augmenting brain B12 with fingolimod or potentially related molecules could enhance both current and future MS therapies.”
In their paper, the team at Sanford Burnham Prebys, with collaborators at University of Southern California, Juntendo University in Japan, Tokyo University of Pharmacy and Life Sciences and State University of New York, focused on the molecular functioning of FTY720 or fingolimod (Gilenya®), a sphingosine 1-phosphate (S1P) receptor modulator that suppresses distribution of T and B immune cells errantly attacking the brains of MS patients.
Working with an animal model of MS as well as human post-mortem brains, the researchers found that fingolimod suppresses neuroinflammation by functionally and physically regulating B12 communication pathways, specifically elevating a B12 receptor called CD320 needed to take up and use needed B12 when it is bound to TCN2, which distributes B12 throughout the body, including the CNS. This known process was newly identified for its interactions with fingolimod within astrocytes. Importantly, the relationship was also observed in human MS brains.
Of particular note, the researchers reported that lower levels of CD320 or dietary B12 restriction worsened the disease course in an animal model of MS and reduced the therapeutic efficacy of fingolimod, which occurred through a mechanism in which fingolimod hitchhikes by binding to the TCN2-B12 complex, allowing delivery of all to the astrocytes via interactions with CD320, with component losses disrupting the process and worsening disease.
These new findings further support to the use of B12 supplementation – especially in terms of delivering the vitamin to astrocytes within the brain – while revealing that fingolimod can correct the impaired astrocyte-B12 pathway in people with MS.
The scientists said it is possible that other S1P receptor modulators on the market, such as Mayzent®, Zeposia® and Ponvory®, may access at least parts of this CNS mechanism. The study supports B12 supplementation with S1P receptor modulators with the goal of improving drug efficacy for this class of medicines.
The study also opens new avenues on how the B12-TCN2-CD320 pathway is regulated by sphingolipids, specifically sphingosine, a naturally occurring and endogenous structural analogue of fingolimod, toward improving future MS therapies, Chun said.
“It supports creating brain-targeted B12 formulations. In the future, this mechanism might also extend to novel treatments of other neuroinflammatory and neurodegenerative conditions.”
New research that had participants compare the taste perception of less processed foods with ultra-processed foods (UPFs), found that UPFs were no more pleasant tasting than less processed foods. The University of Bristol-led findings, published in the journal Appetite, support the theory that humans are programmed to learn to like foods with more equal amounts of carbohydrate and fat. Carbohydrate (including sugars) and fat provide most of the calories in human diets.
The study wanted to test the common but largely untested assumptions that food energy density (calories per gram), level of processing, and carbohydrate-to-fat ratio are key factors influencing food liking and desirability.
In the experiment, involving 224 adult volunteers, participants were presented with colour images of between 24 and 32 familiar foods, varying in energy density, level of processing (including UPFs), and carbohydrate-to-fat ratio. There were 52 different foods in total, including avocado, grapes, cashew nuts, king prawns, olives, blueberry muffin, crispbread, pepperoni sausage, and ice cream.
Participants were then asked to rate the foods for taste pleasantness (liking), desire to eat, sweetness, and saltiness while imagining tasting them. The validity of this method was confirmed by, for example, finding a strong relationship between sweetness ratings and food sugar content.
Results from the study showed that, on average, UPFs were no more liked or desired than processed or unprocessed foods. But foods that combined more equal amounts (in calories) of carbohydrate and fat were more liked and desired than foods equivalent in calories but mostly from either carbohydrate or fat. This is known, from previous research, as the ‘combo’ effect.
Further results revealed that foods with higher amounts of dietary fibre were less liked and desired, and foods tasting more intense (mainly related to the level of sweetness and saltiness), were more liked and desired.
Lead author Professor Peter Rogers found the results for UPFs surprising. He said: “Our results challenge the assumption that ultra-processed foods are ‘hyperpalatable’, and it seems odd that this has not been directly tested before.
“However, whilst ultra-processing didn’t reliably predict liking (palatability) in our study, food carbohydrate-to-fat ratio, food fibre content, and taste intensity did – actually, together, these three characteristics accounted for more than half of the variability in liking across the foods we tested.
“The results for sweetness and saltiness, are consistent with our innate liking for sweetness and saltiness. And the results for carbohydrate-to-fat ratio and fibre might be related to another important characteristic that determines food liking.
“Our suggestion is that humans are programmed to learn to like foods with more equal amounts of carbohydrate and fat, and lower amounts of fibre, because those foods are less filling per calorie. In other words, we value calories over fullness.
“In turn, this trait helps us to maximise calorie intake and build up fat reserves when food is abundant – which is adaptive in circumstances when food supplies are uncertain or fluctuate seasonally, but not when food is continuously available in excess of our immediate needs.”
The researchers at the Nutrition and Behaviour Group are currently testing the calories versus fullness idea in further studies of food liking and meal preferences, including across different countries and cuisines.
Trans-vaccenic acid (TVA), a long-chain fatty acid found in meat and dairy products from grazing animals such as cows and sheep, improves the ability of CD8+ T cells to infiltrate tumours and kill cancer cells, according to a new study by researchers from the University of Chicago.
The research, published in Nature, also shows that cancer patients with higher levels of TVA circulating in the blood responded better to immunotherapy, suggesting potential as a nutritional complement to conventional cancer therapy. Although trans fatty acids that are industrially produced are known to be harmful to health, natural ones such as TVA are linked to health benefits. But the researchers don’t envision prescribing diets packed with red meat and cheese – rather, TVA would be a supplement.
“There are many studies trying to decipher the link between diet and human health, and it’s very difficult to understand the underlying mechanisms because of the wide variety of foods people eat. But if we focus on just the nutrients and metabolites derived from food, we begin to see how they influence physiology and pathology,” said Jing Chen, PhD, professor of medicine at UChicago and one of the senior authors. “By focusing on nutrients that can activate T cell responses, we found one that actually enhances anti-tumour immunity by activating an important immune pathway.”
Searching for nutrients that activate immune cells
Chen’s lab focuses on understanding how metabolites, nutrients and other molecules circulating in the blood influence the development of cancer and response to cancer treatments. For the new study, they started with a database of around 700 known metabolites that come from food and assembled a ‘blood nutrient’ compound library consisting of 235 bioactive molecules derived from nutrients. They screened the compounds in this new library for their ability to influence anti-tumour immunity by activating CD8+ T cells, which are critical for killing cancerous or virally infected cells.
After the scientists evaluated the top six candidates in both human and mouse cells, they saw that TVA performed the best. TVA is the most abundant trans fatty acid present in human milk, but the body cannot produce it on its own. Only about 20% of TVA is broken down into other byproducts, leaving 80% circulating in the blood. “That means there must be something else it does, so we started working on it more,” Chen said.
Feeding mice a diet enriched with TVA significantly reduced the tumour growth potential of melanoma and colon cancer cells compared to mice fed a control diet. The TVA diet also enhanced the ability of CD8+ T cells to infiltrate tumours.
The team also performed a series of molecular and genetic analyses to understand how TVA was affecting the T cells. These included a new technique for monitoring transcription of single-stranded DNA called kethoxal-assisted single-stranded DNA sequencing, or KAS-seq, developed by Chuan He, PhD, professor of chemistry at UChicago and another senior author of the study. These additional assays, done by both the Chen and He labs, showed that TVA inactivates a receptor on the cell surface called GPR43 which is usually activated by short-chain fatty acids often produced by gut microbiota. TVA overpowers these short-chain fatty acids and activates a cellular signaling process known as the CREB pathway, which is involved in a variety of functions including cellular growth, survival, and differentiation. The team also showed that mouse models where the GPR43 receptor was exclusively removed from CD8+ T cells also lacked their improved tumour fighting ability.
Finally, working with other researchers, the team analysed blood samples taken from patients undergoing CAR-T cell immunotherapy treatment for lymphoma. They saw that patients with higher levels of TVA tended to respond to treatment better than those with lower levels. They also tested leukaemia cell lines and saw that TVA enhanced the ability of an immunotherapy drug to kill leukaemia cells.
TVA as a supplement
The study suggests that TVA could be used as a dietary supplement to help various T cell-based cancer treatments, although Chen points out that it is important to determine the optimised amount of the nutrient itself, not the food source. There is a growing body of evidence about the detrimental health effects of consuming too much red meat and dairy, so this study shouldn’t be taken as an excuse to eat more cheeseburgers and pizza; rather, it indicates that nutrient supplements such as TVA could be used to promote T cell activity. Chen thinks there may be other nutrients that can do the same.
“There is early data showing that other fatty acids from plants signal through a similar receptor, so we believe there is a high possibility that nutrients from plants can do the same thing by activating the CREB pathway as well,” he said.
‘The new research also highlights the promise of this ‘metabolomic’ approach to understanding how the building blocks of diet affect our health. Chen said his team hopes to build a comprehensive library of nutrients circulating in the blood to understand their impact on immunity and other biological processes like aging.
“After millions of years of evolution, there are only a couple hundred metabolites derived from food that end up circulating in the blood, so that means they could have some importance in our biology,” Chen said. “To see that a single nutrient like TVA has a very targeted mechanism on a targeted immune cell type, with a very profound physiological response at the whole organism level — I find that really amazing and intriguing.”
