Inflammation Markers (LPS)

This marker assesses the genetic potential of your microbiome to produce Lipopolysaccharides (LPS), also known as endotoxins. These bacterial molecules are among the most potent inflammatory triggers recognized by the human immune system. Low production capacity indicates a peaceful ecosystem, while a high LPS load is the main driver of low-grade systemic inflammation.

LPS is not a toxin that bacteria release to deliberately attack us; in reality, it is a normal structural component of the outer wall of a specific group of bacteria called Gram-negative (highlighting the Proteobacteria and Bacteroidetes phyla).

As long as these bacteria and their LPS walls remain safely confined within the digestive tract and are expelled with feces, there is no problem. The biological crisis, clinically known as Metabolic Endotoxemia, occurs when two things happen simultaneously:

• There is an overgrowth of LPS-rich bacteria (dysbiosis).
• The intestinal barrier weakens or becomes permeable (Leaky Gut).

When this happens, LPS fragments filter through the intestinal wall and enter your bloodstream. Your immune system, upon detecting LPS in the blood, mistakenly assumes there is a generalized infection and sounds all emergency alarms, unleashing an inflammatory cytokine response throughout your body.

The continuous leakage of LPS into the bloodstream keeps the immune system in a state of chronic hypervigilance, which has long-term negative systemic effects:

• Insulin Resistance and Obesity: Metabolic endotoxemia is one of the fundamental causes of the modern obesity epidemic. LPS directly interferes with insulin receptors in muscle and liver cells, forcing the body to store more fat and dramatically increasing the risk of Type 2 Diabetes.
• Neuroinflammation ("Brain Fog"): Inflammatory molecules triggered by LPS can travel to the brain and alter the blood-brain barrier. This is closely associated with chronic fatigue, lack of concentration (brain fog), mood swings, and even the development of neurodegenerative disorders.
• Atherosclerosis: LPS promotes the formation of cholesterol plaques in the arteries by activating inflammatory responses in the blood vessel walls, increasing cardiovascular risk independently of diet.

Unlike blood tests that measure circulating LPS, this metagenomic marker predicts the potential for endogenous LPS synthesis directly from the gut ecosystem through Shotgun sequencing.

Our bioinformatic algorithm quantifies the abundance of genetic pathways responsible for Lipid A biosynthesis (the toxic portion of LPS), specifically mapping key genes such as lpxC, lpxD, kdtA, and lpxK.

At low levels, the ecosystem has reduced pro-inflammatory potential, typically dominated by Gram-positive butyrate-producing bacteria (which do not have LPS). Higher levels reflect an excess of Gram-negative bacterial biomass. If accompanied by markers of compromised gut barrier (Item 47) or excess Proteobacteria (Item 12), clinical intervention is a priority. Dietary strategy includes drastically reducing saturated fats (which act as "vehicles" transporting LPS across the intestinal wall) and increasing polyphenol and Omega-3 (EPA/DHA) intake to silence TLR4 inflammatory receptors.