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Infant Formula Fats Linked to Liver Disease in New Study

by Dr. Priya Deshmukh - Senior Editor, Health
written by Dr. Priya Deshmukh - Senior Editor, Health

Concerns are growing about the potential long-term health effects of infant formula, with a new study suggesting a link between certain fats commonly used in these products and the development of fatty liver disease in infants. Researchers at Virginia Tech have found that medium-chain fatty acids (MCFAs), often derived from coconut oil, may contribute to faster fat accumulation in the liver of newborn pigs compared to long-chain fatty acids (LCFAs) found in animal fats. This finding raises important questions about the composition of infant formulas and the impact of early nutrition on liver health.

Steatotic liver disease, formerly known as non-alcoholic fatty liver disease, is a condition characterized by excess fat buildup in the liver. While historically associated with obesity in adults, diagnoses are increasingly being made in children and even infants, prompting scientists to investigate the role of early-life dietary factors. The Virginia Tech study, published in the American Journal of Physiology-Endocrinology and Metabolism, sheds light on how different types of fats may affect liver metabolism during this critical developmental period.

The research team utilized a neonatal pig model, chosen since their digestive systems and fat metabolism closely resemble those of human infants. Pigs were fed either a formula rich in MCFAs or one rich in LCFAs, while maintaining equal calorie and protein intake. Within just seven days, the piglets fed the coconut oil-derived formula – rich in MCFAs – began to show signs of fat accumulation in their livers. By two weeks, this had progressed to a more severe inflammatory form of the disease, according to lead researcher Samer El-Kadi, associate professor at the School of Animal Sciences at Virginia Tech. “Even within seven days, we could observe fat starting to build up in the liver. By about two weeks, it had progressed from simple steatosis to a more severe inflammatory form of the disease,” El-Kadi stated.

What makes this finding particularly noteworthy is the difference in how the developing liver responds to fat accumulation compared to the adult liver. Traditionally, fat buildup in adults occurs when the liver slows down its fat-burning process. However, the study revealed that in developing livers, fat accumulated even as fat burning increased. “We saw the liver activate both fat-making and fat-burning pathways at the same time. Even with those adaptive responses, the developing liver became overwhelmed. That was surprising to us. Based on what we know from adult disease, increased fat burning should have been protective,” explained El-Kadi.

The Role of Medium-Chain vs. Long-Chain Fatty Acids

Infant formulas commonly utilize blends of plant-based oils to mimic the fat composition of breast milk. The study specifically compared formulas differing only in their fat source. The formula containing MCFAs was derived from coconut oil, while the other used animal fat, providing LCFAs. Researchers found that piglets fed the MCFAs accumulated liver fat at a faster rate than those fed LCFAs.

While breast milk remains the “gold standard” for infant nutrition, formula is often a critical and life-saving alternative when human milk is unavailable. El-Kadi emphasized that the goal of this research is not to discourage formula utilize, but rather to improve its composition. “The immediate benefits of feeding far outweigh any potential long-term risks. Our goal is not to discourage formula use. It’s to understand how different components of formulas affect the developing body, so they can be improved over time,” he said.

The findings underscore the importance of understanding how early nutrition shapes liver metabolism. Further research is needed to determine the long-term consequences of MCFA exposure in infant formula and to identify optimal fat compositions for infant nutrition.

Innovation in Infant Nutrition

The focus on improving infant nutrition is gaining momentum within the industry. Recently, US-based MaiaMilk launched a shelf-stable, medical-grade human donor milk powder, previously only available in neonatal intensive care units. This product, unlike traditional formulas that attempt to replicate breast milk synthetically, is made entirely from human donor milk and can now be used at home after hospital discharge.

As research continues to unravel the complexities of infant liver development and the impact of dietary fats, We see likely that we will see further innovations in infant formula designed to promote optimal health outcomes. The ongoing investigation into the role of MCFAs and LCFAs represents a crucial step towards ensuring that all infants have access to the best possible nutrition for healthy growth and development.

Disclaimer: This article provides informational content and should not be considered medical advice. Always consult with a qualified healthcare professional for any health concerns or before making any decisions related to your health or treatment.

What are your thoughts on this new research? Share your comments below, and let’s continue the conversation.

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Health

Liver-on-a-Chip Models Human Rejection & Regeneration for Transplants

by Dr. Priya Deshmukh - Senior Editor, Health
written by Dr. Priya Deshmukh - Senior Editor, Health

Researchers have developed a novel “liver-on-a-chip” model that closely mimics the human liver, offering a promising new tool for studying liver regeneration and the complex process of transplant rejection. This innovative platform, described as a vascularized liver tissueoid-on-a-chip (LToC), could significantly advance our understanding of these critical areas and potentially lead to more personalized strategies for liver transplantation.

Liver transplantation remains the gold standard for patients with finish-stage liver disease, but challenges persist in optimizing outcomes and minimizing the risk of rejection. Current research is hampered by a lack of experimental models that accurately replicate the intricate architecture and immune interactions within the human liver. This new technology aims to bridge that gap, providing a more physiologically relevant system for investigation.

The LToC, engineered by researchers at the Terasaki Institute for Biomedical Innovation, is composed of human hepatic progenitor cells and intrahepatic portal vein endothelial cells. Within a week of being established in a dynamic perfusion culture, the tissueoid self-assembled into a functioning microvascular network, maturing over 49 days into a tissue resembling a human liver. The team demonstrated sustained viability, preserved vascular integrity, and active liver function, including the secretion of key proteins like albumin and urea, according to a study published in Advanced Materials.

The mature tissueoid contains a diverse range of liver cell types – hepatocytes, cholangiocytes, Kupffer cells, stellate cells, and endothelial cells – mirroring the complexity of a native human liver. This cellular diversity is crucial for accurately modeling liver function and response to injury or immune attack.

Modeling Immune-Mediated Rejection

To test the platform’s ability to simulate real-world scenarios, the researchers exposed the LToC to allogeneic T cells – immune cells from a genetically different donor. This exposure triggered responses characteristic of cellular rejection, including reduced tissue viability, disruption of the endothelial lining of blood vessels, loss of liver-specific markers, increased expression of HLA-I (a marker of immune activation), and a surge in pro-inflammatory cytokines. Specifically, levels of IL-6, TNF-α, IL-1β, IFN-γ, granzyme A and B, and perforin increased, mirroring patterns observed during clinical transplant rejection.

“This liver tissueoid-on-a-chip enables us to recreate key aspects of liver regeneration and immune-mediated rejection within a human-relevant, vascularized tissue architecture,” explained Dr. Abdul Rahim Chethikkattuveli Salih, the first author of the publication.

Dr. Vadim Jucaud, Principal Investigator and Assistant Professor at the Terasaki Institute, added, “By integrating functional vasculature, multiple liver cell types, and immune responsiveness into a single platform, this system allows us to study transplant biology in a more physiologically meaningful way. This approach has the potential to support immunosuppressive drug evaluation and advance more personalized strategies for liver transplantation.”

A Legacy of Innovation in Transplantation

This research builds upon the pioneering work of Dr. Paul I. Terasaki, a renowned figure in organ transplantation research. Dr. Terasaki’s work focused on improving the lives of transplant patients through innovation, and the Terasaki Institute continues to uphold that mission. The institute’s commitment to patient-centered, translational technologies aims to translate laboratory discoveries into tangible benefits for those awaiting or undergoing transplantation.

Dr. Jucaud, a doctoral scholar trained by Dr. Terasaki, emphasized the personal significance of carrying forward his mentor’s vision. “Dr. Terasaki believed that meaningful innovation in transplantation must always be driven by its potential to improve patients’ lives,” he said. “As one of the last doctoral scholars trained by Dr. Paul I. Terasaki, carrying forward his vision, through innovative, translational science that bridges engineering, immunology, and transplantation, holds deep personal significance to me.”

The development of this vascularized tissueoid-on-a-chip represents a significant step forward in the field of liver transplantation research. The ability to model complex biological processes in a human-relevant system opens new avenues for understanding disease mechanisms and developing more effective therapies.

Looking ahead, researchers plan to utilize the LToC platform to evaluate the efficacy of different immunosuppressive drugs and explore personalized treatment strategies for liver transplant recipients. Further refinement of the model and validation with clinical data will be crucial for translating these findings into improved patient care.

Disclaimer: This article provides informational content and should not be considered medical advice. Please consult with a qualified healthcare professional for any health concerns or before making any decisions related to your health or treatment.

What are your thoughts on the potential of organ-on-a-chip technology to revolutionize transplant medicine? Share your comments below.

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Health

The Link Between Sorbitol and Increased Risk of Steatotic Liver Disease

by Dr. Priya Deshmukh - Senior Editor, Health
written by Dr. Priya Deshmukh - Senior Editor, Health

Sorbitol: The ‘Healthy’ Sugar Substitute Linked to Liver Issues, New research Reveals

Table of Contents

St. Louis, MO – For years, sugar alcohols like sorbitol have been marketed as healthier alternatives to refined sugar, often found in “sugar-free” candies, gums, and naturally occurring in fruits like apples and peaches. However, groundbreaking new research from Washington University in St. Louis challenges this assumption, suggesting sorbitol may not be as harmless as previously believed.

The study, published in Science Signaling, builds upon previous work by Professor Gary Patti and his team detailing the detrimental effects of fructose on the liver and othre bodily systems. Patti’s earlier research demonstrated how fructose can fuel cancer cell growth and contribute to steatotic liver disease, a condition affecting approximately 30% of adults globally.

The latest findings reveal a surprising connection: because sorbitol is chemically “one transformation away from fructose,” it can trigger similar harmful effects. experiments conducted on zebrafish showed that sorbitol, whether consumed directly or produced naturally in the gut from glucose, is ultimately converted into fructose in the liver.

“There are many roads to fructose in the liver, and potential detours,” Patti explained, highlighting the complex interplay between sorbitol and glucose consumption, and the crucial role of gut bacteria.

While sorbitol metabolism has historically been linked to high glucose levels in pathological conditions like diabetes, the research demonstrates that even in healthy individuals, glucose levels in the gut can rise sufficiently after eating to initiate sorbitol production.

However, the impact of sorbitol isn’t uniform. The presence of specific Aeromonas bacterial strains in the gut can effectively degrade sorbitol into a harmless byproduct. “It can be produced in the body at significant levels. But if you have the right bacteria, turns out, it doesn’t matter,” Patti stated.

The problem arises when individuals lack these beneficial bacteria, allowing sorbitol to bypass degradation and travel to the liver, where it’s converted into a fructose derivative.

The research indicates that gut bacteria generally handle modest levels of sorbitol, such as those found in fruit. Though, excessive glucose intake – leading to increased glucose-derived sorbitol – or high dietary sorbitol consumption can overwhelm the gut’s capacity, triggering the problematic conversion in the liver.

This discovery raises critical questions about the true health benefits of option sweeteners, particularly for individuals with diabetes and other metabolic disorders who rely on “sugar-free” products.Further examination is needed to determine whether these sweeteners truly offer a healthy alternative to traditional table sugar.

Could reducing sorbitol intake be a preventative measure for individuals with risk factors for NAFLD,such as obesity or diabetes?

The Link Between Sorbitol and Increased Risk of Steatotic Liver Disease

Understanding Steatotic Liver Disease (NAFLD/NASH)

Steatotic liver disease,encompassing Non-Alcoholic Fatty Liver Disease (NAFLD) and its more severe form,Non-Alcoholic Steatohepatitis (NASH),is a growing global health concern. Characterized by an accumulation of fat in the liver, it can progress to cirrhosis, liver failure, and even liver cancer. While often linked to obesity, diabetes, and metabolic syndrome, emerging research highlights a potential, often overlooked, contributor: excessive sorbitol consumption. This article explores the connection between sorbitol, fatty liver, and the increasing risk of NAFLD, offering insights into prevention and management.

How Sorbitol Impacts Liver Health

Sorbitol, a sugar alcohol commonly found in fruits like apples, pears, and peaches, and widely used as a sweetener in sugar-free products (gum, candies, medications), isn’t fully absorbed by the small intestine.This incomplete absorption leads to several metabolic consequences that can strain the liver.

* Fructose Metabolism: Sorbitol is metabolized primarily in the liver via the sorbitol pathway, ultimately converting to fructose. Excessive fructose intake is strongly linked to de novo lipogenesis – the creation of new fat in the liver. This process directly contributes to liver fat accumulation.

* Osmotic Effect: Because sorbitol isn’t fully absorbed, it draws water into the intestines, potentially causing bloating, gas, and diarrhea. This osmotic effect can also disrupt gut microbiota balance.

* Gut Microbiome Disruption: An imbalanced gut microbiome (dysbiosis) is increasingly recognized as a key player in NAFLD growth. Sorbitol can feed certain bacteria, leading to an overgrowth of species that promote inflammation and increase intestinal permeability – frequently enough referred to as “leaky gut.”

* Increased Oxidative Stress: The metabolic processes involved in sorbitol breakdown can generate reactive oxygen species (ROS), contributing to oxidative stress in the liver. Oxidative stress damages liver cells and exacerbates inflammation.

Sorbitol Sources & Daily Intake considerations

Many are unaware of the hidden sorbitol in their diet. Beyond naturally occurring sources, it’s prevalent in:

* Sugar-Free Foods: Look for sorbitol on ingredient lists of sugar-free candies, chewing gum, baked goods, and desserts.

* Medications: Sorbitol is used as an excipient (inactive ingredient) in liquid medications, syrups, and some tablets.

* Diet Sodas & “Healthy” Drinks: Some beverages marketed as low-sugar or healthy utilize sorbitol as a sweetener.

* Fruit Juices & Concentrates: While fruits contain sorbitol naturally, concentrated forms like juice can deliver a notable dose.

Recommended Daily Intake: While there isn’t a universally agreed-upon limit, consuming over 50 grams of sorbitol daily can cause gastrointestinal distress. For individuals predisposed to liver disease, even lower amounts might potentially be problematic.

Identifying Individuals at Higher Risk

Certain populations are more vulnerable to the negative effects of sorbitol on liver health:

* Individuals with Pre-existing NAFLD: Sorbitol can accelerate disease progression.

* People with Fructose Malabsorption: Those who struggle to metabolize fructose will experience amplified effects from sorbitol’s conversion.

* Individuals with Insulin Resistance: Insulin resistance impairs the liver’s ability to regulate fat metabolism, making it more susceptible to sorbitol-induced fat accumulation.

* Those with Gut Dysbiosis: An already imbalanced gut microbiome is more easily disrupted by sorbitol.

* Individuals on High-Fructose Diets: Combining sorbitol with other fructose sources (high-fructose corn syrup) creates a synergistic effect, increasing liver stress.

Diagnostic Tools & Monitoring

Detecting early signs of steatosis is crucial. Common diagnostic tools include:

  1. Liver Function Tests (LFTs): Blood tests that assess liver enzyme levels (ALT, AST). Elevated levels can indicate liver damage.
  2. Ultrasound: A non-invasive imaging technique to visualize the liver and detect fat accumulation.
  3. fibroscan: A specialized ultrasound that measures liver stiffness, indicating the degree of fibrosis (scarring).
  4. Liver Biopsy: The gold standard for diagnosing NASH, involving a tissue sample analysis.

Regular monitoring of LFTs and imaging studies is recommended for individuals with risk factors or suspected sorbitol-related liver issues.

Dietary Strategies & Management

Managing sorbitol intake is a key component of a liver-healthy lifestyle:

* Read Food Labels Carefully: Become a label detective and avoid products with sorbitol, particularly if you have risk factors.

* Limit Sugar-Free Products: Reduce consumption of sugar-free candies, gum, and baked goods.

* Choose Whole Fruits Over Juices: Whole fruits provide fiber and nutrients,mitigating some of sorbitol’s negative effects.

* Reduce Fructose Intake: Limit high-fructose corn syrup and other fructose-rich foods.

* Support Gut Health: Consume probiotic-rich foods (yogurt, kefir

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Health

Sweetener & Liver Health: Risks & Concerns

by Dr. Priya Deshmukh - Senior Editor, Health
written by Dr. Priya Deshmukh - Senior Editor, Health

The Hidden Cost of “Healthy” Sweeteners: How Sorbitol Could Be Harming Your Liver

Nearly one-third of adults worldwide grapple with non-alcoholic fatty liver disease, and the culprit isn’t always what you think. While excessive sugar consumption is a known risk factor, a growing body of research suggests that even sugar alternatives – particularly the sugar alcohol sorbitol – may be quietly contributing to the problem. New findings reveal that sorbitol isn’t simply inertly passed through the body, but can be converted into fructose in the liver, triggering a cascade of metabolic issues.

Sorbitol: From “Harmless” to Hazardous?

For decades, sweeteners like aspartame, sucralose, and sugar alcohols like sorbitol have been marketed as healthier options for those looking to reduce their refined sugar intake. But a team led by Gary Patti at Washington University in St. Louis is challenging that assumption. Their research, published in Science Signaling, builds on previous work demonstrating the detrimental effects of fructose on liver health and even its potential to fuel cancer cell growth. The surprising discovery? Sorbitol, often found in “low-calorie” candies, gums, and even naturally occurring in stone fruits, is just “one transformation away” from fructose.

The Gut-Liver Connection: It’s Complicated

The process isn’t straightforward. Patti’s team utilized zebrafish to demonstrate that sorbitol, produced naturally in the gut from glucose, can ultimately be converted into fructose within the liver. The pathway depends heavily on individual factors: glucose and sorbitol consumption levels, and – crucially – the composition of your gut microbiome. While sorbitol production was initially linked to high glucose levels in conditions like diabetes, the research shows even healthy individuals can produce significant amounts of sorbitol in the gut after eating.

“It can be produced in the body at significant levels,” Patti explains. “But if you have the right bacteria, it doesn’t matter.” Certain bacterial strains, like Aeromonas, effectively break down sorbitol into harmless byproducts. However, if these beneficial bacteria are absent or overwhelmed, sorbitol bypasses degradation and heads straight to the liver, where it’s converted into a fructose derivative. This highlights the critical role of gut health in metabolizing these sugar alcohols.

Beyond Diabetes: A Wider Metabolic Risk

This is particularly concerning for individuals with diabetes or other metabolic disorders who may rely on “sugar-free” products. But even those without pre-existing conditions aren’t immune. While gut bacteria can handle modest amounts of sorbitol – like that found in a piece of fruit – excessive consumption, either through dietary sorbitol or glucose-derived sorbitol, can overwhelm the system. The more glucose and sorbitol consumed, the greater the strain on the gut microbiome’s ability to process it effectively.

The Protein Bar Paradox

The ubiquity of sorbitol in processed foods adds another layer of complexity. Patti himself was surprised to discover his favorite protein bar was loaded with the sugar alcohol. This underscores the challenge of avoiding both sugar and alternative sweeteners, as many products contain a cocktail of both. This hidden presence of sorbitol is a key reason why simply switching to “diet” or “sugar-free” options isn’t necessarily a healthy solution.

Future Research & Personalized Nutrition

While this research provides a crucial piece of the puzzle, further investigation is needed. Patti’s lab is now focused on understanding the specific mechanisms by which bacteria clear sorbitol, and how to optimize gut health to mitigate its potential harmful effects. This could pave the way for personalized nutrition strategies tailored to an individual’s gut microbiome composition and metabolic profile. The emerging field of metabolomics – the large-scale study of small molecules, like sorbitol and fructose, within the body – will be instrumental in this effort. Read the original research in Science Signaling.

The Bottom Line: No Free Lunch

The message is clear: there’s no easy escape from the metabolic consequences of sugar consumption. Whether it’s refined sugar, artificial sweeteners, or seemingly harmless sugar alcohols like sorbitol, the body responds in complex ways. Prioritizing a whole-food diet, minimizing processed foods, and nurturing a healthy gut microbiome are essential steps towards protecting your liver and overall metabolic health. What are your predictions for the future of sugar alternatives? Share your thoughts in the comments below!

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