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malDigestIon - ENZYMATiC

Digestion is a dynamic process that involves mechanical and chemical actions working together to transform complex foods into absorbable nutrients. Central to this process are digestive enzymes, which are responsible for breaking down macronutrients - carbohydrates, proteins, and fats, into molecules small enough to be absorbed through the intestinal lining. 

 

These enzymes are primarily produced by pancreatic acinar cells, which are specialized cells within the pancreas responsible for synthesizing and secreting key digestive enzymes, including amylase, lipase, and proteases. These enzymes are then released into the pancreatic ducts and delivered into the small intestine for digestion.

 

When digestive enzyme production is low, or activity is impaired, it is often attributed to poor pancreatic signalling or pancreatic insufficiency. However, beyond these primary causes, intestinal inflammation and villi flattening, commonly seen in chronic infections, or inflammatory bowel disorders, can compromise the interface needed for nutrient-enzyme interaction.

 

As a result, the body's ability to chemically break down food into absorbable units becomes compromised. This condition, known as maldigestion, disrupts the proper breakdown of carbohydrates, proteins, and fats, leaving complex food particles only partially digested.

 

As a result, essential nutrients are not adequately absorbed through the intestinal lining. Over time, this can manifest as a spectrum of gastrointestinal symptoms including bloating, gas, abdominal cramping, diarrhea, fatty stools, and the presence of undigested food in stools. If left unaddressed, chronic maldigestion may also contribute to systemic issues such as nutrient deficiencies, fatigue, and impaired immune function.[1]

 

Here we focus on key digestive enzymes, and how they function:

 

Amylase
 

  • Metabolises: Complex Carbohydrates / Starch into maltose, dextrins, and simple sugars
     

  • Food sources affected: Bread, rice, pasta, potatoes, cereals, and other starch-rich foods
     

  • Deficiency Signs: Undigested starches pass into the colon, where it is fermented by gut bacteria, leading to excessive gas, bloating, watery stools, and the appearance of starchy residues in feces.

 

Protease
 

  • Metabolises: Proteins into peptides and amino acids by cleaving peptide bonds
     

  • Food sources affected: Meat, fish, eggs, dairy, legumes, soy products

 

  • Deficiency Signs: Bloating, fatigue, muscle weakness, diarrhea, and sometimes visible protein fragments or undigested meat fibers in the stool, indicating incomplete protein catabolism.
     

Lipase

 

  • Metabolises: Triglycerides / dietary fats, into monoglycerides and free fatty acids
     

  • Food sources affected: Oils, butter, cheese, fatty meats, nuts and seeds
     

  • Deficiency Signs: Clay coloured stool (not dark rich brown), greasy stool, foul-smelling stools, sometimes with visible oil slicks on the water.

 

Cellulase

 

  • Metabolises: Cellulose, a structural plant fiber made of β-1,4-linked glucose units
     

  • Food sources affected: Vegetables, fruits, grains, and fibrous plant skins
     

  • Deficiency Signs:  Bloating, gas, cramping, and the passage of visible plant fibers or vegetable skins in stools
     

Lactase / Tilactase 

 

  • Metabolises: Lactose, a disaccharide sugar composed of glucose and galactose
     

  • Food sources affected: All dairy based produces
     

  • Deficiency Signs: Symptoms occur 30 minutes to 2 hours after consuming dairy. Symptoms include bloating, cramping, excessive gas, and diarrhea, resulting from the fermentation of undigested lactose by colonic bacteria and the osmotic draw of water into the intestine.

 

Alpha-galactosidase

 

  • Metabolises: Oligosaccharides / long chain sugars

 

  • Food sources: Beans, legumes, cabbage, broccoli, whole grains

 

  • Deficiency Signs: Alpha-galactosidase is not produced by humans, which is why these foods produce gas for every individual. If your diet is naturally high in these sources for reasons such as vegan or vegetarian diet, supplementation can alleviate symptoms.
     

Xylose isomerase

 

  • Metabolises: Fructose 

 

  • Food Sources: High Fructose foods: Honey, Dates, Dried fruits, Apple, Pears, Grapes

 

  • Deficiency Signs: Xylose isomerase is not produced by humans, it is indicated for the malabsorption of fructose due to digestive issues, which appears as excessive bloating and gas after consuming fructose rich foods. 

 

[1][9]

signs & symptoms

Lientery - Undigested Food in the faeces 

 

Lientery is a condition in which recognisable, undigested food particles, such as vegetable matter, seeds, or fibrous components, are excreted in the feces and can be visibly observed.

 

Lientery often results from accelerated intestinal transit. Under normal physiological conditions, digestion and absorption require the coordinated action of digestive enzymes, followed by nutrient uptake across the small intestinal. This process is time-dependent, relying on sufficient enzyme availability and contact time for hydrolysis and absorption.

 

When bowel transit is abnormally fast, as occurs during carbohydrate maldigestion and malabsorption, the osmotic forces draw water into the lumen, increasing motility and reducing absorption time. 

 

As a result, food particles may pass through the gastrointestinal tract without complete enzymatic digestion in the small intestine. Additionally, limited time within the colon due to osmotic pressure also impairs microbial fermentation of unabsorbed substrates, ultimately leading to the excretion of visibly undigested vegetable matter, seeds, or fibrous components.[10][11]

 

Bloating + Flatulence

 

Under normal conditions, digestive enzymes break down carbohydrates, fats, and proteins into absorbable components in the small intestine. When these enzymes are lacking, macronutrients remain only partially digested. These undigested food particles then pass into the colon, where they become substrates for fermentation by resident gut microbiota. 

 

This microbial fermentation process generates gases such as hydrogen, methane, and carbon dioxide. The buildup of these gases in the intestinal lumen leads to increased intra-abdominal pressure, resulting in the sensation of bloating, visible abdominal distension, and flatulence.[4]

 

Steatorrhea

 

Undigested or unabsorbed fats passing through the gastrointestinal tract typically cause symptoms of Steatorrhea, which causes the faeces to present as such, in varying degrees:

 

  • Shiny, greasy, or oily appearance

  • Mid brown / clay colour

  • Floats in the bowel

  • Malodourous - foul in smell [ Stool or Gas ]

 

Enzyme deficiency, particularly from lipase, which is essential for fat digestion results in dietary not being effectively broken down and absorbed in the small intestine. These unabsorbed fats pass through the gastrointestinal tract and are excreted in the stool, leading to the hallmark signs of steatorrhea [6][7]

 

Strong urges to defecate

 

In extreme carbohydrate maldigestion, when the sugar load exceeds the colonic bacteria’s ability to ferment it, unabsorbed carbohydrates create a strong osmotic influx of fluid into the intestinal lumen, increasing small-bowel distension and accelerating transit, which extends into a pronounced, sometimes sudden urge to defecate, and the stool can often pass as soft or loose. [10]

 

Chronic Digestive Complaints [ Biofilms ] 

 

Biofilms protect microbial communities by encasing them in a matrix that functions as a shield from, making pathogens highly resistant to antimicrobial support and immune defenses. They are implicated in up to 80% of chronic GI and systemic infections.

 

Enzymes, particularly cellulase and amylase are crucial for breaking down the biofilm matrix. This degradation disrupts biofilm structure, enhancing antimicrobial access and clearance of microbes. Therefore, when digestive enzyme levels are low biofilm breakdown is impaired, fostering persistent infections.[5]

 

Low Fecal Elastase [ Stool Testing ]

 

Beyond signs and symptoms, functional stool assessment can test for Elastase, which is an enzyme that creates a marker for pancreatic enzyme output. Normal fecal elastase levels are over 200 µg/gl, while test results indicating near 200 µg/g or below are suggestive of pancreatic insufficiency and poor enzyme output.[8]
 

This testing can be authorised at an additional cost, please email info@remedylane-co.com.au

Causes

Exocrine Pancreatic Insufficiency (EPI) 

 

EPI is a condition in which the pancreas fails to produce or deliver sufficient quantities of digestive enzymes, specifically lipase, amylase, and protease to the small intestine. The mechanism behind this deficiency stems from damage to the pancreatic acinar cells, which are responsible for producing these digestive enzymes. This damage can occur due to a variety of reasons, resulting in a progressive loss of functional pancreatic tissue and function, leading to enzyme deficiencys.[2]

 

Chronic Stress

 

Chronic stress causes a series of harmful effects in the pancreas. It increases the production of TNF-α, a key inflammatory molecule, and attracts immune cells into the pancreatic tissue. At the same time, it disrupts blood flow in the pancreas, causing cycles of reduced oxygen supply and reoxygenation, which leads to oxidative stress. These changes damage the internal structure of pancreatic acinar cells, particularly the actin cytoskeleton, which helps maintain proper cell shape and function. 

 

As a result, the pancreas struggles to release digestive enzymes properly, especially amylase in response to the hormone CCK, and begins activating trypsinogen inside the pancreas rather than in the intestine. This premature enzyme activation causes the pancreas to start digesting itself, leading to inflammation and tissue injury, further worsening enzyme output.[14]

 

Hypochlorydria - Under Acid Stomach

 

Under normal physiological conditions, gastrin, which is a hormone released by the stomach in response to protein, stimulates the secretion of hydrochloric acid. This surge of gastric acid lowers the stomach pH, which is crucial for triggering the downstream pancreatic stimulation cascade. 

 

One of the most critical components of this cascade is the release of a substance called secretin in the first part of the small intestine below the stomach, which is strongly dependent on the presence of acidic chyme entering.

 

In states of hypochlorhydria, where stomach acid production is reduced, insufficient acidity means secretin is inadequate and without adequate secretin, the pancreas receives a weak signal to secrete digestive enzymes, especially lipase, amylase, and proteases. The pancreas also secretes insufficient  bicarbonate, which results in a suboptimal pH environment in the duodenum, also reducing enzyme solubility and activity.[3]

 

Nutritional deficiencies

 

Nutritional deficiencies such as Copper and Zinc play a primary role in pancreatic enzyme output insufficiency. 

 

Copper is essential to the structure and function of pancreatic acinar cells, which produce key digestive enzymes. Deficiency has been linked to acinar cell degeneration and impairs vagal signaling required for enzyme secretion.

 

Zinc plays a vital role in pancreatic enzyme synthesis and cellular signaling. Deficiency has been linked to enzyme secretion impairments.[14][15]

 

Intestinal Villi Damage [ Dysbiosis ]

 

The intestinal villi plays a critical role in both the production of brush-border enzymes and in creating the appropriate environment for pancreatic enzyme activity. When the intestinal lining is damaged due to infections, dysbiosis and inflammatory conditions, enzyme production is often impaired, and there is reduced surface area for enzyme action and nutrient absorption, leading to compromised digestion and malabsorption of essential macronutrients.[1]

 

Inflammation 


IL-1β, IL-18, and TNF-α are specific proinflammatory cytokines that directly contribute to damage of cells within the pancreas, known as acinar cells, which are responsible for producing digestive enzymes.[12]


These cytokines are notably upregulated under conditions such as chronic alcohol consumption, smoking, oxidative stress, and infections, particularly bacterial endotoxins like LPS driven by conditions such as SIBO and dysbiosis. 


Aging

 

As individuals age, there is a gradual decline in digestive efficiency, particularly in the secretion of endogenous digestive enzymes. This reduction is most notable after the fourth decade of life, and becomes more pronounced in elderly populations. 

 

Older adults are also more likely to experience atrophy of gastrointestinal tissues, slower gastric emptying, and reduced bile flow, which may further compromise enzyme activation and activity in the digestive tract. [1]

References 
 

[1].https://www.metagenicsinstitute.com.au/tech-data/high-potency-vegetarian-digestive

[2] https://www.ncbi.nlm.nih.gov/books/NBK555926/

[3] https://pubmed.ncbi.nlm.nih.gov/340322/

[4].https://pmc.ncbi.nlm.nih.gov/articles/PMC2890937/pdf/WJG-16-2978.pdf

[5].https://www.sciencedirect.com/science/article/pii/S0021925822007955

[6] https://pubmed.ncbi.nlm.nih.gov/21377551/

[7] https://www.ncbi.nlm.nih.gov/books/NBK541055/

[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC6910206/

[9].https://www.bioceuticals.com.au/product-training/flyers/multigest-enzymes

[10] https://pmc.ncbi.nlm.nih.gov/articles/PMC9099680/

[11] https://www.ncbi.nlm.nih.gov/books/NBK553106/

[12] https://pmc.ncbi.nlm.nih.gov/articles/PMC5292603/

[13] https://pmc.ncbi.nlm.nih.gov/articles/PMC6842873/

[14] https://pmc.ncbi.nlm.nih.gov/articles/PMC4024789/

[15] https://pmc.ncbi.nlm.nih.gov/articles/PMC7572834/

[16] https://pubmed.ncbi.nlm.nih.gov/30000941/

[17].https://www.researchgate.net/publication/285028880_Traditional_and_medicinal_uses_of_Carica_papaya

[18] https://www.scielo.br/j/cta/a/KgGvx6c5BDTFBmybSXnrPvs/

[19] https://pubmed.ncbi.nlm.nih.gov/23394986/

[20] https://pmc.ncbi.nlm.nih.gov/articles/PMC8534447/

[21] https://www.ncbi.nlm.nih.gov/books/NBK54127/

[22] https://aab.copernicus.org/articles/67/571/2024/

[23] https://botanyjournals.com/assets/archives/2022/vol7issue7/7-7-21-894.pdf

[24] https://pmc.ncbi.nlm.nih.gov/articles/PMC4446506/

[25] https://pmc.ncbi.nlm.nih.gov/articles/PMC8072924/

[26].https://www.sciencedirect.com/science/article/abs/pii/S0023643813003368

[27] https://pmc.ncbi.nlm.nih.gov/articles/PMC8719756/

[28] https://pmc.ncbi.nlm.nih.gov/articles/PMC9914867/

[29] https://pmc.ncbi.nlm.nih.gov/articles/PMC11171741/

[30] https://pmc.ncbi.nlm.nih.gov/articles/PMC5828430/

[31].https://www.sciencedirect.com/science/article/pii/S092422442200070X

[32].https://www.sciencedirect.com/science/article/pii/S0753332223016566

[33] https://www.nature.com/articles/s41598-021-86648-7

[34].https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2024.1357803/full

[35] https://pmc.ncbi.nlm.nih.gov/articles/PMC9623659/

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