Friday, November 16, 2018

Probiotics: When Good Bacteria Turn Bad

As the popularity of probiotics grows, scientists are turning more of their attention to these tiny particles. With the spotlight intensifying, some researchers suspect that their impact may not be beneficial for everyone.

The concept of people improving their intestinal health by eating live organisms is not a new one but dates back almost 100 years. Today, however, the idea is mainstream. Grocery stores across the United States sell a range of products that contain probiotics and offer the promise of improved gut health.

Despite their growing popularity and impressive claims, research into the potential health benefits of probiotics is still relatively sparse and not entirely positive.

University of Texas engineers attached human cells to microchips and, depending on the cell type they chose, watched them mimic any organ in the body. The scientists were interested in understanding why inflammation arose in the digestive system. They recently published their work in the Proceedings of the National Academy of Sciences, in a study that marks the first time that an organ-on-a-chip has modeled the development of a disease.

To date, scientists have found it challenging to understand exactly why and how gut inflammation develops. The process involves communication between the epithelial cells that line the gut, the immune system, and the microbiome. These physiological components engage in a chemical dialogue that involves a dizzying array of secretions – and deciphering the interactions is difficult.

The researchers concluded that the main driver of gut inflammation is the health of the intestinal epithelium – specifically, its permeability. The intestinal epithelium is a thin layer of cells that have a protective role – namely, to prevent toxins and bacteria from the gut leaching out into the rest of the body, where they could cause harm.

As part of their study, the scientists considered the impact of probiotics. They found that so-called good bacteria might be healthful for some people but have a negative health impact for others. It seems that their influence depends on the integrity of the intestinal epithelium.



“When the gut barrier is healthy, probiotics are beneficial. When it is compromised, however, they can cause more harm than good.” – Researcher Kim

Dysfunction of the epithelial membrane – sometimes referred to as a leaky gut – appears to play a role in a wide range of health conditions, including inflammatory bowel disease, irritable bowel syndrome, obesity, food allergies, and celiac disease.

Although more work will be needed to firm up these conclusions, they call into question the current one-size-fits-all approach to probiotics. Because of their newfound popularity, understanding how they might impact individuals with compromised intestinal epithelia is vital.

My Take:
I have been posting warnings about indiscriminate use of probiotics for years. This study just uses alternate technology to reaffirm my concerns.

The lining of your gut is comprised of a single celled layer of epithelium. Every cell is replaced in the course of 36-48 hours, if and only if the gut is healthy. If not, the barrier develops gaps and “leaky gut” ensues.

This increased intestinal permeability is a major causative factor in autoimmune diseases like Crohn’s disease, Hashimoto’s thyroiditis, RA, MS and many others.

Bottom Line:
If you have taken an antibiotic recently, had chemotherapy and/or radiation therapy then take a probiotic short term – for a week or two. Take a simple one, like Lactobacillus acidophilus, as it is commonly found in most of us. Avoid complex probiotics containing many different species. The chance of a conflict with your microbiome increases as the variety of the product increases. If you feel your microbiome has been impaired take a prebiotic, like Slippery Elm Bark or apple pectin. Prebiotics feed the healthy bacteria and you never lose all of them, just the numbers are reduced. If fed properly, they will rebound.

Source: October 29, 2018 NIH

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