The QUANTIFERON®-TB Gold Plus (QFT-Plus) test is a blood test used to check for latent tuberculosis (TB) infection. It’s often recommended for people who may have been around someone with TB or who are at higher risk of exposure, such as healthcare workers or people with weakened immune systems. This test helps detect TB bacteria that may be inactive in the body but could still cause health issues if they become active later on.

Research has noted antidiabetic, anti-inflammatory, antioxidant, antimicrobial, anti-Alzheimer's, antiarthritic, cardiovascular, and wound-healing effects.

This test measures levels of phosphorylated tau217 (p-tau217) in the blood—a protein strongly linked to the development of Alzheimer’s disease and other neurodegenerative conditions. Tau proteins normally help stabilize nerve cells in the brain. However, when they become abnormally phosphorylated, as seen in Alzheimer’s, they can form toxic tangles that interfere with memory and thinking.

Why it matters:
The presence of elevated p-tau217 in plasma is a highly specific early indicator of Alzheimer's pathology, even before major symptoms appear. This biomarker is clinically validated to distinguish Alzheimer’s disease from other forms of dementia with greater accuracy than previous tau tests.

People who are new to the GFD encounter new foods and/or over-consume old favorites to compensate for the lack of wheat in the diet. Gluten-free cookies, crackers, breads and cakes often contain copious amounts of rice, amaranth, sorghum and other substitutes. Some of these new-to-the-patient foods may illicit an adverse reaction. Other foods that are often introduced to the patient on the GFD are quinoa, buckwheat and hemp. Some People may turn to the “ancient” grains (Polish wheat, spelt, barley, rye), not knowing that these contain gluten. Another problem patients often face on the GFD is the over-consumption of another starch to make up for the loss of wheat. They turn to potato, rice or corn as a substitute. This can lead to the development of a new sensitivity or the enhancement of old sensitivities.

The presence of antibodies to Quinoa is an indication of food immune reactivity. The offending food and its known cross-reactive foods should be eliminated from the diet. Quinoa is considered a beneficial food, especially for celiac patients and vegetarians. Quinoa is labeled by the scientific community as a nonallergenic food, however, severe allergic reaction to Quinoa has been reported. If a recently diagnosed gluten-reactive patient exhibits high levels of antibodies to Quinoa, it may be due to the late introduction of Quinoa into the diet.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Tryptophan and its different pathways:

The management of tryptophan converting to serotonin within the brain has some complex moving parts. Tryptophan gets converted into serotonin. High levels of stress of any type and acute/chronic infections can change this process by provoking an immune system response. Instead of serotonin being made from tryptophan in this process, two other compounds are eventually made: They are kynurenic acid which is neuroprotective and quinolinic acid which is neurodegenerative.The quinolinic acid is a NMDA-agonist, i.e. quinolinic acid, NMDA, and inflammation are best friends and like to wreak havoc when kynurenic acid is lacking. Recent research showed that patients suffering from severe depression and suicidality were found to have very high levels of inflammation and elevated NMDA activity as a result of long-term dysregulation of this pathway. The researchers’ recommended goal was to find ways to dampen the NMDA receptors and quinolinic acid in the brain.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Quinolinate is a neurotoxin derived from tryptophan. Elevated quinolinate is seen in brain and nerve tissue damage, especially in disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, motor neuron diseases, multiple sclerosis, epilepsy, amyotrophic lateral sclerosis, and major depressive disorder. We can also see elevated quinolinate due to low serotonin and need for vitamin B3 (niacin). The causes of elevated quinolinate include neuroinflammation, general inflammation, infection, phthalate exposure, and/or oral tryptophan use.

Quinolinate is a neurotoxin derived from tryptophan. Elevated quinolinate is seen in brain and nerve tissue damage, especially in disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, motor neuron diseases, multiple sclerosis, epilepsy, amyotrophic lateral sclerosis, and major depressive disorder. We can also see elevated quinolinate due to low serotonin and need for vitamin B3 (niacin). The causes of elevated quinolinate include neuroinflammation, general inflammation, infection, phthalate exposure, and/or oral tryptophan use.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

A high ratio of quinolinic acid to the tryptophan metabolite, 5-hydroxyindoleacetic acid, indicates excessive inflammation due to recurrent infections, excessive tryptophan intake, immune overstimulation, excessive adrenal production of cortisol, or excessive exposure to phthalates.

Quinolinic acid is a neurotoxic substance produced by our own bodies and a metabolite of tryptophan.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.

Kynurenic acid and Quinolinic acid are tryptophan metabolites formed through the kynurenine pathway. Tryptophan is the amino acid precursor to serotonin; its major route for catabolism is the kynurenine pathway. Important products of the kynurenine pathway include xanthurenic acid and kynurenic acid, which can further metabolize into quinolinic acid. The historical importance of this pathway has mainly been as a source of the coenzyme NAD+, which is important for all redox reactions in the mitochondria.

However, it is now understood that kynurenic and quinolinic acid have physiologic implications. This alternate pathway is upregulated in response to inflammation and stress, which can lead to deficient serotonin production. Kynurenic acid has shown some neuroprotective properties in the brain, since it can stimulate NMDA receptors. However, its importance on the periphery is still not fully elucidated. Some studies outline antiinflammatory, analgesic, antiatherogenic, antioxidative, and hepatoprotective properties to peripheral kynurenic acid.

The correlation to levels of urinary excretion needs further study. Quinolinic acid, in and of itself, can be inflammatory and neurotoxic.