Category: Diet and Nutrition

Categories : Diet and Nutrition Obstetrics & Gynaecology

Fish During Pregnancy – What’s Safe, What’s Not?

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Fish consumption during pregnancy is a complex scientific topic. While fish are rich in nutrients essential to brain development, such as polyunsaturated fatty acids, selenium, iodine, and vitamin D, they also contain methyl mercury, a known neurotoxicant. This has led the US Food and Drug Administration to recommend that expectant mothers limit consumption, inadvertently causing many women to completely stop eating fish during pregnancy.

Fish consumption is an important route of methyl mercury exposure, however, efforts to understand the health risk posed by mercury are further complicated by the fact that the nutritional benefits from fish may modify or reduce the toxicity posed by mercury. A new study appearing in the American Journal of Epidemiology based on data from a cohort of residents of a coastal community in Massachusetts creates a new framework that could untangle these questions, reduce confusion, and produce clearer guidance on fish consumption for pregnant mothers.

“We propose an alternative modelling approach to address limitations of previous models and to contribute thereby to improved evidence-based advice on the risks and benefits of fish consumption,” said the authors. “In fish-eating populations, this can be addressed by separating mercury exposure into fish intake and average mercury content of the consumed fish.”

The new research comes from an analysis of data from the New Bedford Cohort, which was created to assess the health of children born to mothers residing near the New Bedford Harbor Superfund site in Massachusetts. The current study included 361 children from the cohort who were born between 1993 and 1998 and at eight years old, underwent neurodevelopment assessments, including tests for IQ, language, memory, and attention.

The researchers were able to measure mercury exposure during the third trimester of pregnancy through hair sample collected from the mothers after birth. While hair samples have been the traditional method to study maternal mercury exposure, this approach alone cannot distinguish between mothers who frequently consumed low-mercury fish compared to those who consumed a smaller quantity of high-mercury fish.

To overcome this limitation, the researchers instead created a model that includes estimates of mercury exposure per serving of fish. This was possible because mothers in the cohort also completed a food questionnaire and reported the type and frequency of fish and shellfish consumed during pregnancy. The authors estimated the average mercury levels by type of fish, and when combined with the information about the mother’s diet, they were able to create a more precise and detailed method to estimate the joint associations of pregnancy fish intake and fish mercury levels on neurodevelopment.

Using this model, the researchers found that the relation between pregnancy fish consumption and subsequent neurodevelopment varied depending on the estimated average mercury levels in the fish. Specifically, consuming low mercury-containing fish was beneficial, while consuming fish with higher levels of mercury was detrimental.

“Given methodologic limitations to previous analyses, future work expanding our alternative modelling approach to account for both the average mercury and nutritional content of fish could facilitate better estimation of the risk-benefit tradeoffs of fish consumption, a key component of many healthy diets,” said the authors.

The authors are in the process of applying this model to other large studies of maternal fish consumption, including the Seychelles Child Development Study.

Source: University of Rochester Medical Center

Categories : Diet and NutritionTags :

For Healthy Adults, Regular Multivitamins don’t Reduce Mortality Risk

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A large analysis of data from nearly 400 000 healthy US adults followed for more than 20 years has found no association between regular multivitamin use and lower risk of death. The study, led by researchers at the National Institutes of Health’s National Cancer Institute, was published in JAMA Network Open.

Many adults in the United States take multivitamins with the hope of improving their health. However, the benefits and harms of regular multivitamin use remain unclear. Previous studies of multivitamin use and mortality have yielded mixed results and been limited by short follow-up times.

To more deeply explore the relationship between long-term regular multivitamin use and overall mortality and death from cardiovascular disease and cancer, the researchers analysed data from three large, geographically diverse prospective studies involving a total of 390 124 US adults who were followed for more than 20 years. The participants included in this analysis were generally healthy, with no history of cancer or other chronic diseases.

Because the study population was so large and included lengthy follow-up and extensive information on demographics and lifestyle factors, the researchers were able to mitigate the effects of possible biases that may have influenced the findings of other studies. For example, people who use multivitamins may have healthier lifestyles in general, and sicker patients may be more likely to increase their use of multivitamins.

The analysis showed that people who took daily multivitamins did not have a lower risk of death from any cause than people who took no multivitamins. There were also no differences in mortality from cancer, heart disease, or cerebrovascular diseases. The results were adjusted for factors such as race and ethnicity, education, and diet quality. 

The researchers noted that it is important to evaluate multivitamin use and risk of death among different kinds of populations, such as those with documented nutritional deficiencies, as well as the potential impact of regular multivitamin use on other health conditions associated with aging.

Source: NIH/National Cancer Institute

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Surprisingly, Benefits of Dietary Fibre Vary Significantly between Individuals

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Nutritionists generally advise everyone to eat more dietary fibre, but a new study suggests that its effects on health can vary, suggesting that recommendations should be tailored to each individual’s gut microbiome. The study, published in Gut Microbes, focused on resistant starch, a category of dietary fibre found in such foods as bread, cereals, green bananas, whole-grain pasta, brown rice and potatoes.

The researchers identified the gut microbe species that change in response to two different types of resistant starch. They found evidence that each individual may have a unique response to eating a resistant starch, with some people benefiting and others experiencing little or no effect. The reason for the variation appears tied to the level of diversity and composition of a person’s gut microbiome.

“Precision nutrition definitely has a use in determining what dietary fibre we should tell people to eat,” said Angela Poole, assistant professor of molecular nutrition and senior author of the study.

“This is critical because we’ve had public messaging advising people to eat more dietary fibre for decades,” Poole said. “At the same time, less than 10% of people eat the recommended intake. Since there are many different types of dietary fibre and carbohydrates, a better strategy would be to collect data on each person and tell them which dietary fibre they can eat to get the most bang for their buck.”

Resistant starch comes in five types, and resists degradation by human digestive enzymes until it reaches the gut. There, it acts as a substrate for certain gut microbes to produce short chain fatty acids, which are important in signaling pathways that regulate glucose and lipid metabolism. Multiple microbe species may work together to create the fatty acids.

In the study, Poole and colleagues tested three dietary treatments on 59 participants over seven weeks.

The team had three different types of crackers manufactured. Two crackers had the same ingredients, except one contained resistant starch type 2, which occurs naturally, and the other contained resistant starch type 4, which is human-made. A third control cracker was digestible by human enzymes, similar to white bread, and the researchers expected none of the bacteria to act on the control.

Subjects were then divided into two groups. The first group ate the resistant starch type 2 cracker first, followed by the control, and then resistant starch type 4. Each cracker type was eaten for 10 days, with five days of no cracker consumption between treatments. The second group reversed the order, also with the control in the middle.

They then sequenced the microbiomes of each participant before and after each treatment. For resistant starch type 2, more than 30 bacteria changed in abundance, including Ruminococcus bromii, which is considered a keystone resistant starch degrader in the human gut. For type 4, more than 20 bacteria changed. And for the control, nothing changed.

“For the resistant starch crackers, we could detect that 20 or 30 of them were changing, but how much they changed and whether they changed at all, for each of those bacteria, depended on the person,” Poole said.

Similarly, each resistant starch type changed different short chain fatty acids, with variable levels of fatty acid increases and decreases based on the individual. For resistant starch type 2, the researchers identified a subset of 13 bacteria that predicted change in amounts of propionate, a type of short chain fatty acid. Also for resistant starch 2, by knowing the diversity of an individual’s gut microbiome, the researchers could roughly predict if two types of short chain fatty acids (acetate and butyrate) were going to increase.

The most surprising result was that the control digestible cracker led to the greatest gains of short chain fatty acids. More work is needed to understand why, but Poole suspects that the order of cracker consumption was key to the result. Since many microbes are involved in making short chain fatty acids, she hypothesises that eating a resistant starch first primed the gut to produce the fatty acids when that person ate the digestible starch.

“That’s one of the major takeaways, maybe I can get away with eating a French baguette some of the time, and it may be better than just eating whole grain all the time,” Poole said. “But I have to test that, and it probably varies between people.”

Source: Cornell University

Categories : Diet and NutritionTags :

Time to Debunk Four Persistent Myths about Intermittent Fasting

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In a new article published in Nature Reviews Endocrinology, researchers at the University of Illinois Chicago debunk four common myths about the safety of intermittent fasting. 

Intermittent fasting as a weight loss method has grown increasingly popular, with a large body of research demonstrating its safety. Despite this, several myths about fasting have spread among clinicians, journalists and the general public: that fasting can lead to a poor diet or loss of lean muscle mass, cause eating disorders, or decrease sex hormones. 

In a new commentary, UIC researchers debunk each of these. They base their conclusions on clinical studies, some of which they conducted and some done by others. 

“I’ve been studying intermittent fasting for 20 years, and I’m constantly asked if the diets are safe,” said lead author Krista Varady, professor of kinesiology and nutrition at UIC. “There is a lot of misinformation out there. However, those ideas are not based on science; they’re just based on personal opinion.”  

There are two main types of intermittent fasting. With alternate-day eating, people alternate between days of eating a very small number of calories and days of eating what they want. With time-restricted eating, people eat what they want during a four- to 10-hour window each day, then don’t eat during the rest of the day. The researchers conclude both types are safe despite the popular myths.

Their conclusions: 

Intermittent fasting does not lead to a poor diet: The researchers point to studies showing the intake of sugar, saturated fat, cholesterol, fibre, sodium and caffeine do not change during fasting compared with before a fast. And the percentage of energy consumed in carbohydrates, protein and fat doesn’t change, either.  

Intermittent fasting does not cause eating disorders: None of the studies show that fasting caused participants to develop an eating disorder. However, all the studies screened out participants who had a history of eating disorders, and the researchers say that those with a history of eating disorders should not try intermittent fasting. They also urge paediatricians to be cautious when monitoring obese adolescents if they start fasting, because this group has a high risk of developing eating disorders. 

Intermittent fasting does not cause excessive loss of lean muscle mass: The studies show that people lose the same amount of lean muscle mass whether they’re losing weight by fasting or with a different diet. In both cases, resistance training and increased protein intake can counteract the loss of lean muscle. 

Intermittent fasting does not affect sex hormones: Despite concerns about fertility and libido, neither oestrogen, testosterone nor other related hormones are affected by fasting, the researchers said. 

Source: University of Illinois Chicago

Categories : Diet and Nutrition Mental HealthTags :

High-fat Diets can Interfere with Serotonin Pathways, Fuelling Anxiety

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Photo by Jonathan Borba

New research from CU Boulder shows that turning to junk food when we’re stressed out may backfire. The study found that in animals, a high-fat diet disrupts resident gut bacteria, alters behaviour and, through a complex pathway connecting the gut to the brain, influences brain chemicals in ways that fuel anxiety.

“Everyone knows that these are not healthy foods, but we tend to think about them strictly in terms of a little weight gain,” said lead author Christopher Lowry, a professor of integrative physiology at CU Boulder. “If you understand that they also impact your brain in a way that can promote anxiety, that makes the stakes even higher.”

For the study, published in the journal Biological Research in May, Lowry worked with first author Sylvana Rendeiro de Noronha, a doctoral student at the Federal University of Ouro Preto in Brazil.

In a previous study, the team found that rats fed a high-fat diet consisting primarily of saturated fat showed increases in neuroinflammation and anxiety-like behaviour.

While evidence is mixed, some human studies have also shown that replacing a high-fat, high-sugar, ultra-processed diet with a healthier one can reduce depression and anxiety.

The dark side of serotonin

To better understand what may be driving the fat-anxiety connection, Lowry’s team divided male adolescent rats into two groups: Half got a standard diet of about 11% fat for nine weeks; the others got a high-fat diet of 45% fat, consisting mostly of saturated fat from animal products.

The typical American diet is about 36% fat, according to the Centers for Disease Control and Prevention.

Throughout the study, the researchers collected faecal samples and assessed the animals’ gut microbiome. After nine weeks, the animals underwent behavioural tests.

When compared to the control group, the group eating a high-fat diet, not surprisingly, gained weight. But the animals also showed significantly less diversity of gut bacteria. Generally speaking, more bacterial diversity is associated with better health, Lowry explained. They also hosted far more of a category of bacteria called Firmicutes and less of a category called Bacteroidetes. A higher Firmicutes to Bacteroidetes ratio has been associated with the typical industrialised diet and with obesity.

The high-fat diet group also showed higher expression of three genes (tph2, htr1a, and slc6a4) involved in production and signalling of the neurotransmitter serotonin – particularly in a region of the brainstem known as the dorsal raphe nucleus cDRD, which is associated with stress and anxiety.

While serotonin is often billed as a “feel-good brain chemical,” Lowry notes that certain subsets of serotonin neurons can, when activated, prompt anxiety-like responses in animals. Notably, heightened expression of tph2, or tryptophan hydroxylase, in the cDRD has been associated with mood disorders and suicide risk in humans.

“To think that just a high-fat diet could alter expression of these genes in the brain is extraordinary,” said Lowry. “The high-fat group essentially had the molecular signature of a high anxiety state in their brain.”

A primal gut-brain connection

Just how a disrupted gut can change chemicals in the brain remains unclear. But Lowry suspects that an unhealthy microbiome compromises the gut lining, enabling bacteria to slip into the body’s circulation and communicate with the brain via the vagus nerve, a pathway from the gastrointestinal tract to the brain.

“If you think about human evolution, it makes sense,” Lowry said.  “We are hard-wired to really notice things that make us sick so we can avoid those things in the future.”

Lowry stresses that not all fats are bad, and that healthy fats like those found in fish, olive oil, nuts and seeds can be anti-inflammatory and good for the brain.

But his research in animals suggests that exposure to an ultra-high-fat diet consisting of predominantly saturated fats, particularly at a young age, could both boost anxiety in the short-term and prime the brain to be more prone to it in the future.

His advice: Eat as many different kinds of fruits and vegetables as possible, add fermented foods to your diet to support a healthy microbiome and lay off the pizza and fries. Also, if you do have a hamburger, add a slice of avocado. Research shows that good fat can counteract some of the bad.

Rodrigo Cunha de Menezes, professor of physiology at Federal University of Ouro Preto in Brazil, is co- senior author on this paper.

Source: University of Colorado Boulder

Categories : Cardiovascular Disease Diet and NutritionTags :

Study Links Xylitol to Increased Cardiovascular Risk

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Cleveland Clinic researchers found higher amounts of the sugar alcohol xylitol are associated with increased risk of cardiovascular events like heart attack and stroke. They confirmed the association in a large-scale patient analysis, preclinical research models and a clinical intervention study, published in the European Heart Journal.

Xylitol is a common sugar substitute used in sugar-free candy, gums, baked goods and oral products like toothpaste. Over the past decade, the use of sugar substitutes, including sugar alcohols and artificial sweeteners, has increased significantly in processed foods that are promoted as healthy alternatives.

The team, led by Stanley Hazen, MD, PhD, had also previously revealed a similar link between erythritol and cardiovascular risk last year. Xylitol is not as prevalent as erythritol in keto or sugar-free food products in the US but is common in other countries.

“This study again shows the immediate need for investigating sugar alcohols and artificial sweeteners, especially as they continue to be recommended in combatting conditions like obesity or diabetes,” said Dr Hazen. “It does not mean throw out your toothpaste if it has xylitol in it, but we should be aware that consumption of a product containing high levels could increase the risk of blood clot related events.”

In this new study, researchers identified that high levels of circulating xylitol were associated with an elevated three-year risk of cardiovascular events in an analysis of more than 3000 patients in the US and Europe. A third of patients with the highest amount of xylitol in their plasma were more likely to experience a cardiovascular event. To confirm the findings, the research team conducted pre-clinical testing and found that xylitol caused platelets to clot and heightened the risk of thrombosis. Researchers also tracked platelet activity from people who ingested a xylitol-sweetened drink versus a glucose-sweetened drink and found that every measure of clotting ability significantly increased immediately following ingestion of xylitol but not glucose.

The authors note that further studies assessing the long-term cardiovascular safety of xylitol are warranted. The research had several limitations, including that clinical observation studies demonstrate association and not causation.

Source: Cleveland Clinic

Categories : Ageing Diet and NutritionTags :

Less of a Specific Amino Acid Extends Lifespan and Health in Mice

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New research in mice has demonstrated that not having too much of a certain amino acid – present in many foods commonly eaten by overweight or obese individuals – extends their lifespan and reduces the incidence of diseases such as cancers.

“We like to say a calorie is not just a calorie,” says Dudley Lamming, a professor and metabolism researcher at the University of Wisconsin School of Medicine and Public Health. “Different components of your diet have value and impact beyond their function as a calorie, and we’ve been digging in on one component that many people may be eating too much of.”

Lamming is the lead author of a new study in mice, published recently in the journal Cell Metabolism showing that cutting down the amount of a single amino acid called isoleucine can, among other benefits, extend their lifespan, make them leaner and less frail as they age and reduce cancer and prostate problems, all while the mice ate more calories.

Amino acids are the molecular building blocks of proteins, and Lamming and his colleagues are interested in their connection to healthy aging.

In earlier research, data from UW–Madison’s Survey of the Health of Wisconsin showed the scientists that Wisconsinites with higher body mass index measurements tend to consume more isoleucine, an essential amino acid. Isoleucine is plentiful in foods including eggs, dairy, soy protein and many kinds of meat.

To better understand its health effects, Lamming and collaborators from across disciplines at UW–Madison fed genetically diverse mice either a balanced control diet, a version of the balanced diet that was low in a group of about 20 amino acids, or a diet formulated to cut out two-thirds of the diet’s isoleucine. The mice, which began the study at about six months of age (equivalent to a 30-year-old person) got to eat as much as they wanted.

“Very quickly, we saw the mice on the reduced isoleucine diet lose adiposity – their bodies got leaner, they lost fat,” says Lamming, while the bodies of the mice on the low-amino-acid diet also got leaner to start, but eventually regained weight and fat.

Mice on the low-isoleucine diet lived longer – on average 33% longer for males and 7% longer for females. And, based on 26 measures of health, including assessments ranging from muscle strength and endurance to tail use and even hair loss, the low-isoleucine mice were in much better shape during their extended lives.

“Previous research has shown lifespan increase with low-calorie and low-protein or low-amino-acid diets starting in very young mice,” says Lamming, whose work is supported by the National Institutes of Health. “We started with mice that were already getting older. It’s interesting and encouraging to think a dietary change could still make such a big difference in lifespan and what we call ‘healthspan,’ even when it started closer to mid-life.”

The mice on the low-isoleucine diets chowed down, eating significantly more calories than their study counterparts – probably to try to make up for getting less isoleucine, according to Lamming. But they also burned far more calories, losing and then maintaining leaner body weights simply through adjustments in metabolism, not by getting more exercise.

At the same time, Lamming says, they maintained steadier blood sugar levels and male mice experienced less age-related prostate enlargement. And while cancer is the leading cause of death for the diverse strain of mice in the study, the low-isoleucine males were less likely to develop a tumour.

Dietary amino acids are linked to a gene called mTOR that appears to be a lever on the aging process in mice and other animals as well as to a hormone that manages the body’s response to cold and has been considered a potential diabetes drug candidate for human patients. But the mechanism behind the stark benefits of low-isoleucine intake is not well understood. Lamming thinks the new study’s results may help future research pick apart causes.

“That we see less benefit for female mice than male mice is something we may be able to use to get to that mechanism,” he says.

While the results are promising, humans do need isoleucine to live, and reducing isoleucine from a diet that hasn’t been preformulated by a mouse chow company is not an easy task.

“We can’t just switch everyone to a low-isoleucine diet,” Lamming says. “But narrowing these benefits down to a single amino acid gets us closer to understanding the biological processes and maybe potential interventions for humans, like an isoleucine-blocking drug.”

The Survey of the Health of Wisconsin showed that people vary in isoleucine intake, with leaner participants tending to eat a diet lower in isoleucine. Other data from Lamming’s lab suggest that overweight and obese Americans may be eating significantly more isoleucine than they need.

“It could be that by choosing healthier foods and healthier eating in general, we might be able to lower isoleucine enough to make a difference,” Lamming says.

Source: University of Wisconsin-Madison

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For Healthy Adults, New Guideline Recommends only Daily Allowance of Vitamin D

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Guideline recommends vitamin D higher than the recommended daily allowance for children, pregnant people, adults over 75 and adults with prediabetes

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Healthy adults under the age of 75 are unlikely to benefit from taking more than the daily intake of vitamin D recommended by the Institutes of Medicine (IOM) and do not require testing for vitamin D levels, according to a new Clinical Practice Guideline issued today by the Endocrine Society. For children, pregnant people, adults older than 75 years and adults with high-risk prediabetes, the guideline recommends vitamin D higher than the IOM recommended daily allowance.

Vitamin D use and blood vitamin D levels have been associated with many common diseases. However, whether vitamin D supplementation lowers the risk of these diseases and what vitamin D blood levels are needed for better health have been debated for years.

In this new guideline, the panel of experts established guidelines for vitamin D use and testing for vitamin D levels in healthy persons without established indications for vitamin D treatment or testing. The guideline relied on clinical trials to develop the recommendations.

The guideline, titled “Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline,” was published online and will appear in the August 2024 print issue of The Journal of Clinical Endocrinology & Metabolism (JCEM), a publication of the Endocrine Society.

“The goal of this guideline was to address the vitamin D requirements for disease prevention in a generally healthy population with no underlying conditions that would put them at risk of impaired vitamin D absorption or action,” said Marie Demay, M.D., of Harvard Medical School and Massachusetts General Hospital in Boston, Mass. Demay is the chair of the panel that developed the guideline. “Healthy populations who may benefit from higher dose vitamin D supplements are those 75 and older, pregnant people, adults with prediabetes, and children and adolescents 18 and younger, but we do not recommend routine testing for vitamin D levels in any of these groups.”

Key recommendations from the guideline include:

  • We suggest against vitamin D supplements at doses beyond the reference dietary intakes recommended by the IOM in healthy adults under 75 years old.
  • We identified the following populations that may benefit from supplementation above the intakes recommended by the IOM because of the potential to reduce specific health risks:
    • Children and adolescents 18 and younger—potential to prevent nutritional rickets and to reduce the chance of respiratory infections.
    • Individuals 75 and older—potential to lower mortality risk.
    • Pregnant people—potential to reduce risk of pre-eclampsia, intra-uterine mortality, preterm birth, small-for-gestational age birth and neonatal mortality.
    • People with prediabetes—potential to reduce progression to diabetes.
  • In adults ages 50 years and older who have indications for vitamin D supplementation or treatment, we suggest daily, lower-dose vitamin D instead of non-daily, higher-dose vitamin D.
  •  We suggest against routine testing for 25-hydroxyvitamin D levels in any of the populations studied, since outcome-specific benefits based on these levels have not been identified. This includes 25-hydroxyvitamin D screening in people with dark complexion or obesity.

Even though the evidence on the role of vitamin D in health and disease has increased over the last decade, the panel noted many limitations in the available evidence. For example, many of the large clinical trials were not designed for several of the outcomes that they reported, and the studied populations had vitamin D blood levels that most would consider adequate to begin with. Based on insufficient evidence, the panel could not determine specific blood-level thresholds for 25-hydroxyvitamin D for adequacy or for target levels for disease prevention.

Source: The Endocrine Society

Categories : Dermatology Diet and NutritionTags :

UV Exposure Increases Appetite but Suppresses Weight Gain

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In a novel study, a team of dermatologists evaluated the effect of ultraviolet (UV) exposure on appetite and weight regulation. They found that UV exposure raises norepinephrine levels, decreases leptin levels, and induces the browning of subcutaneous fat, thereby increasing energy expenditure. These results potentially pave the way for new approaches to prevent and treat obesity and metabolic disorders. Their findings appear in the Journal of Investigative Dermatology, published by Elsevier.

Co-first authors Qing-Ling Quan, MD, PhD, and Eun Ju Kim, PhD, Department of Dermatology, Seoul National University Hospital, explained, “Recent evidence has suggested that UV exposure limits body weight gain in mouse models of obesity. Subcutaneous fat is a critical organ in regulating energy homeostasis. Alongside previous studies on the effects of UV exposure on obesity and metabolic disorders, our team was inspired by our prior discovery that, although UV rays do not directly reach subcutaneous fat when exposed to the skin, they can regulate the metabolism of subcutaneous fat. This led us to hypothesise that skin exposure to UV rays could play a significant role in systemic energy homeostasis, prompting this research.”

Investigators discovered that when exposed to UV radiation consistently, mice fed a normal diet and those on a high-fat diet exhibited increased appetite due to a decrease in leptin, a key hormone in appetite regulation. But there was no weight increase – they found that UV radiation inhibits weight gain by enhancing secretion of the neurotransmitter norepinephrine, which not only decreases leptin but also increases energy expenditure through the “browning” of subcutaneous fat.

The increased energy intake, driven by heightened appetite, is converted to heat and burned before it can accumulate in subcutaneous fat, thus preventing weight gain.

This research provides new insights into the impact of UV exposure on appetite and weight regulation, opening possibilities for novel approaches in the prevention and treatment of obesity and metabolic disorders. Specifically, uncovering the mechanism by which UV radiation prevents weight gain could offer new approaches to dietary regulation and weight loss, providing innovative insights into health and obesity management that could positively impact human health.

Lead investigator Jin Ho Chung, MD, PhD, Department of Dermatology, Seoul National University Hospital, Seoul National University College of Medicine, explained, “This study elucidates the mechanism by which UV exposure can increase appetite while inhibiting weight gain. These findings contribute significantly to understanding the effects of UV radiation on energy metabolism and homeostasis and open new avenues for exploring prevention and treatment strategies for obesity and metabolic disorders. Notably, the fact that UV radiation lowers leptin levels and increases norepinephrine, thereby promoting the browning of subcutaneous fat and increasing energy expenditure, provides a groundbreaking clue for the development of obesity treatment strategies. This research demonstrates that UV exposure not only affects the skin but also plays a deep role in our body’s energy metabolism and homeostasis processes. However, further research is needed on the long-term effects and safety of UV exposure, and there should be significant interest in developing new therapeutic approaches that utilise the efficacy of UV radiation.”

However, as co-corresponding author Dong Hun Lee, MD, PhD, Institute of Human-Environment Interface Biology, Seoul National University, noted, “Because UV exposure can accelerate skin aging and promote skin cancer, it is advisable to minimise UV exposure and protect the skin with sunscreen. Thus, our research team plans to conduct follow-up studies to develop new strategies that could mimic the effects of UV radiation for obesity and metabolic regulation.”

Source: Elsevier

Categories : Allergies Diet and NutritionTags :

Celiac Disease: New Findings on the Effects of Gluten

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May 16 is International Celiac Day. Celiac disease is a chronic autoimmune condition that occurs in around 1% of the world’s population. It is triggered by the consumption of gluten proteins from wheat, barley, rye and some oats. A gluten-free diet protects celiac patients from severe intestinal damage. Together with colleagues, chemist Dr Veronica Dodero from Bielefeld University was able to determine new details on how certain gluten-derived molecules trigger leaky gut syndrome in celiac disease.

The key finding of the study: a particular protein fragment formed in active celiac disease forms nanosized structures, the so-called oligomers, and accumulates in a gut epithelial cell model. The technical name of the molecule is 33-mer deamidated gliadin peptide (DGP). The study team has now discovered that the presence of DGP oligomers may open the tightly closed gut lining, leading to the leaky gut syndrome. The study has now been published in the journal Angewandte Chemie.

Wheat peptides causing leaky gut

Gluten proteins cannot be completely broken down by the gut. This can lead to the formation of large gluten fragments (peptides) in our gut. In cases of active coeliac disease, researchers discovered that the enzyme tissue transglutaminase 2 (tTG2) present in humans modifies a specific gluten peptide, resulting in the formation of the 33-mer DGP. This usually happens in a part of our gut called the lamina propria. However, recent research has shown that this process can also occur in the gut lining.

‘Our interdisciplinary team characterized the formation of 33-mer DGP oligomers through high-resolution microscopy and biophysical techniques. We discovered the increased permeability in a gut cell model when DGP accumulates, reports Dr. Maria Georgina Herrera, the first author of the study. She is researcher at the University of Buenos Aires in Argentina and was a postdoctoral fellow at Bielefeld.

When the intestinal barrier is weakened

Leaky gut syndrome occurs when the lining of the intestine becomes permeable, allowing harmful substances to enter the bloodstream, leading to inflammatory responses and different diseases. In celiac disease, there’s debate about the early stages of increased permeability. The mainstream theory suggests that chronic inflammation in coeliac disease leads to a leaky gut. However, there is a second theory that proposes that gluten’s effects on gut lining cells are the primary cause. In this view, gluten directly damages the cells of the intestinal lining, making them permeable, which triggers chronic inflammation and potentially leads to celiac disease in predisposed people.

However, since gluten is consumed daily, what molecular triggers lead to the leaky gut in celiac disease patients? If 33-merDGP oligomers are formed, they may damage the epithelial cell network, allowing gluten peptides, bacteria, and other toxins to pass massively into the bloodstream, leading to inflammation and, in celiac disease, autoimmunity.

‘Our findings reinforce the medical hypothesis that impairment of the epithelial barrier promoted by gluten peptides is a cause and not a result of the immune response in celiac patients,’ says the lead author of the study, Dr Veronica Dodero from the Bielefeld Faculty of Chemistry.

The relationship between 33-mer DGP and Celiac Disease

Human leukocyte antigens (HLAs) are proteins found on the surface of cells in the body. They play a crucial role in the immune system by helping it distinguish between self (the body’s own cells) and non-self (foreign substances like bacteria or viruses). In celiac disease, two specific HLA proteins, namely HLA-DQ2 and HLA-DQ8, are strongly associated with the condition. The 33-mer DGP fits perfectly with HLA-DQ2 or HLA-DQ8 and triggers an immune response, leading to inflammation and small intestine villous atrophy. This strong interaction turns the DGP into what scientists call a superantigen. For those affected, a gluten-free diet is the only lifelong therapy.

Source: Bielefeld University