NutriNews

In animal nutrition, fibers are defined as the portion of dietary polysaccharides that cannot be digested by the enzymes of the small intestine. Instead, these complex carbohydrates either pass to the colon where they are fermented by the microbiota, or they remain unfermented and are excreted in the feces. This distinction gives rise to two important fractions: fermentable fibers, which produce beneficial short-chain fatty acids during fermentation, and non-fermentable fibers, which provide bulk and mechanical stimulation along the digestive tract. The challenge in Asia is that diets are heavily based on rice, corn and soybean meal, which provide too little insoluble fibre. As a result, diets are fibre-deficient and unbalanced. In Thailand and Vietnam, where corn–soy-based diets dominate, the total dietary fiber level is typically 2–3% crude fiber (CF) and 6–10% neutral detergent fiber (NDF). By the time digestible nutrients are absorbed in the small intestine, fiber becomes the dominant fraction in the distal gut, often more than 60% of the remaining dry matter. This means that, even if fiber represents a modest proportion of the diet at intake, it is the dominant fraction by the time digesta reaches the hindgut. Despite this central role, the use of fiber in monogastric nutrition remains poorly understood, and misconceptions continue to circulate. How fibers act in the gut The action of dietary fibers in pigs and poultry is first and foremost mechanical. Unlike starches and proteins that dissolve and disappear during digestion, fibers remain as solid particles in the intestinal contents. This solid phase exerts physical pressure against the intestinal wall, stimulating peristalsis, the rhythmic contractions that move digesta forward. Without fibers, the intestinal contents would be mostly liquid, and peristalsis would be severely impaired. Fibers also act as a scraping agent. They help to remove excess mucus and reduce bacterial adhesion

You might not expect chickens or shrimp to be deep thinkers, but inside every cell they’re running a complex decision-making system based on methylation—deciding what genes to express, what fats to burn, and how to stay cool under pressure. It’s biochemistry’s version of high-speed multitasking, and it all depends on one key ingredient: methyl groups. Supporting this cycle with the right nutrients isn’t just smart nutrition—it’s giving your animals the tools to outthink their stress.The methylation cycle refers to a series of biochemical reactions where methyl groups, small carbon-based molecules (–CH₃), are transferred from one molecule to another. These reactions are fundamental to the functioning of animal cells. Liver Health and Lipid Metabolism Methylation is involved in synthesizing phosphatidylcholine, essential for fat transport. A deficiency in methyl donors can lead to fatty liver syndrome, especially in poultry and fish fed high-energy diets. Homocysteine Detoxification Homocysteine is a toxic by-product of methionine metabolism. If not remethylated back to methionine or converted to cysteine, it can accumulate and impair cardiovascular and neurological function. Efficient methylation keeps homocysteine levels in check. Synthesis of creatine and carnitine These two molecules are essential for muscle energy and fat metabolism. When methyl donors are insufficient, animals may struggle to maintain optimal muscle growth or efficiently mobilize energy from fat, leading to slower gains or poorer feed conversion. Embryonic development In breeding animals, methylation is central to reproductive success and embryonic development, with studies showing improved hatchability and litter performance when methyl donors are supplemented in maternal diets. Gut tight junctions Even the structure of the gut itself, villus height, crypt architecture, and epithelial integrity benefits from robust methylation. This is particularly important during early life stages or under stress conditions, where gut function is most vulnerable. Gene Regulation Methylation modifies DNA, turning genes “on” or “off.”

In animal nutrition, nothing is arbitrary, especially when it comes to trace minerals. Copper, for instance, is required at just 10 to 20 ppm in most swine and poultry diets, a remarkably small quantity compared to other essential nutrients. This raises a simple but important question: If nature sets the copper requirement so low, is there a reason for it, and could we increase the dosage without consequences? Over the past decades, nutritionists have demonstrated that increasing copper to pharmacological levels (150–250 ppm), particularly in growing piglets or broilers, has consistent benefits on performance. Short-term use improves average daily gain (ADG), feed conversion ratio (FCR), and gut health. However, when used over longer periods, during grower or finisher stages, this high copper inclusion can backfire. Performance gains may plateau or reverse, and the risk of toxicity increases, with evidence of liver accumulation, and tissue stress. This paradox leads to a broader reflection: What if the redox potential of ingredient plays a role in their toxicity implications? What Is Redox Potential ? Redox potential (or reduction potential) is a measure of how easily a substance can gain or lose electrons during a chemical reaction. It’s expressed in volts (V) and reflects the electron-transfer activity of an element. In biological systems, this property is crucial: many enzymes require trace minerals to accept or donate electrons as part of metabolic and detoxification processes. Each mineral has a characteristic redox potential, especially those that cycle between ionic states. Minerals with high redox potential will strongly attract electrons. Inside the cell, if unbound, these minerals can interact directly with DNA, proteins, lipids, and cell membranes, stealing electrons and denaturing their structure. This silent oxidative attack weakens the integrity of muscle cells, denatures proteins, and initiates lipid peroxidation. The consequences, though invisible during feeding, become apparent

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In animal nutrition, particularly for monogastric species like swine and poultry, feed formulation goes far beyond meeting basic nutritional needs. One critical yet often underestimated factor influencing performance, gut health, and nutrient absorption is feed viscosity. This is especially relevant in Southeast Asia, where the widespread use of fibrous by-products such as rice bran, cassava and copra meal presents new challenges in formulation. As local feed ingredients and strategies evolve, understanding and managing viscosity becomes essential for every nutritionist seeking to improve efficiency and profitability. What is Feed Viscosity? Feed viscosity refers to the thickness or resistance to flow of the digesta in the gastrointestinal tract. When feed is mixed with digestive secretions, certain components, particularly soluble fibers, can form viscous gels. This gel-like environment slows down nutrient absorption, impairs enzyme activity, and creates favorable conditions for harmful microbial growth. But not all fibers behave the same way. Only soluble fibers increase viscosity because they dissolve in water and form molecular networks that bind water and thicken the intestinal contents. Common examples in the Southeast Asian context include pectins in cassava, arabinoxylans in rice bran, and mannans in copra meals. Both pigs and poultry are affected by viscous diets, but poultry are more sensitive due to their shorter gastrointestinal tract and faster transit time. In broilers, increased viscosity is directly linked to reduced nutrient absorption and wet litter problems. In piglets, the impact is milder but still significant, particularly in the post-weaning phase when the digestive system is immature. With growing use of non-traditional fiber sources in Asian piglet diets, attention to viscosity is more important than ever. What Causes Feed Viscosity? Viscosity mainly arises from soluble non-starch polysaccharides (NSPs) complex carbohydrates found in many plant-based feed ingredients. In Southeast Asia, key sources include: Arabinoxylans in rice bran and corn

In piglet nutrition, zinc oxide has long been a trusted ally. For decades, nutritionists have relied on it to fight post-weaning diarrhea, boost gut health, and help young pigs thrive through their most fragile weeks. Yet behind this familiar white, black or yellow powder lies a deeper truth: not all zinc oxide is created equal. While many feed formulators focus on the dosage, how many kilograms per ton, how many weeks in the program, the real story, and often the real problem, comes down to something less obvious: the physical and chemical nature of the zinc oxide itself. The analysis of multiple zinc oxide sources used across Asia and beyond has enabled to identify three distinct families of products, illustrated by different color and each behaving differently in the piglet’s digestive tract and each with its own consequences for antibacterial efficacy. Family One: White, Fast, and Short-Lived The first family of zinc oxide products is typically white in color and comes mostly from Asian sources. These products have small particle size, low density, but relatively high surface area. At first, they look like strong performers. The high surface area suggests plenty of material ready to interact with bacteria, giving a sharp antibacterial punch, on paper at least. But once these small, light particles hit the piglet’s stomach acid, they dissolve rapidly, sometimes too rapidly. The zinc ions release so quickly that by the time they meet bacteria, the antibacterial effect has already faded away. To compensate, nutritionists often increase the dosage, usually pushing up to 3 kilograms per ton of feed. But this raises serious concerns: Toxicity risks, especially if used for more than two weeks Reduction of feed intake as zinc taste is rejected by piglets Blocking actions of phytases Environmental burdens due to zinc excretion Regulatory red flags

Sulfur is an essential element in animal nutrition, present in many feed ingredients and additives. It is a key component of amino acids like methionine and cysteine and is necessary for protein synthesis and metabolic functions. However, excessive sulfur intake, whether from organic or inorganic sources, can cause significant toxicity issues in both swine and poultry. In animal feeding practices, several key contributors to sulfur intake consistently stand out: DDGS, lysine sulfate, copper sulfate and high-sulfur protein meals such as canola and soybean meals can increase the total sulfur load. Canola meal, soybean meal, and other protein-rich by-products contain significant amounts of organic sulfur, primarily in the form of sulfur-containing amino acids like methionine and cysteine. Canola meal, for instance, contains around 0.6-0.8% total sulfur. Although this sulfur is organic rather than inorganic sulfate, excessive inclusion of these meals can still increase the overall sulfur load in the diet. DDGS, a by-product of ethanol production, contains around 0.5-1% total sulfur, which includes both organic sulfur from protein content and inorganic sulfate. The sulfur content in DDGS primarily originates from the use of sulfuric acid during the ethanol production process to control pH and clean equipment. Due to its high protein and energy content, DDGS is commonly included at rates of 5-10% in animal diets contributing approximately 50 to 100 grams of sulfur per ton of feed. Lysine Sulfate Lysine sulfate, used as a cost-effective lysine source, contains 20-25% sulfate. In typical diets, lysine sulfate is included at 0.5-1%. Since sulfate itself contains about 33% sulfur, we can expect approximately 330-825 grams of sulfur per ton of feed, making lysine sulfate one of the main sources of sulfur, particularly in swine and poultry rations. Copper Sulfate Copper sulfate (CuSO₄·5H₂O) contains about 40% sulfate. When copper sulfate is used as a growth

The acidification of the stomach serves as the first natural line of defense against bacterial contamination in the gut. This function is particularly crucial for piglets and chicks, as their ability to produce gastric acids is limited in early life. A well-acidified stomach not only helps with digestion through activaction of pepsinogen enzyme and solubilisation of minerals but also prevents pathogenic bacteria from reaching the intestines, reducing the risk of infections and improving overall gut health. To support this process, various organic and inorganic acids are commonly incorporated into animal feed. Formic acid, propionic acid, citric acid, fumaric acid, and lactic acid are among the most widely used acidifiers. These acids effectively lower the pH in the stomach, creating an environment that inhibits harmful bacteria while enhancing nutrient absorption. However, their application is not without challenges. When used at inclusion rates of 10 to 15 kg per ton of feed, these acids often exhibit strong odors and corrosive properties, making handling and storage difficult for feed manufacturers. In certain situations, such as when formulating premixes, manufacturers seek non-corrosive alternatives to achieve stomach acidification. This need has led to the adoption of an indirect acidification strategy, which focuses on lowering the Acid Binding Capacity (ABC) of the diet rather than directly introducing acids. By reducing the ABC of feed, it becomes easier for the piglet or chick’s natural gastric acid secretion to maintain an optimal pH, without the drawbacks associated with traditional acidifiers. The Role of Acid Binding Capacity in Feed Acidification Acid Binding Capacity (ABC) measures the buffering effect of a diet—essentially, the amount of acid required to lower its pH to a target level. Ingredients with high ABC values require more acid to achieve the same pH reduction, placing a greater burden on the animal’s digestive system and necessitating