Tetrahydrofolate is the basic, reduced form of folate from which other forms of reduced folate are made.

Active and Inactive Forms of Folate:

Dihydrofolate (DHF) is the dietary form of folate, whilst folic acid is the synthetic form of folate used in supplements and to fortify the food supply. These forms of folate are not biologically active; they must undergo enzymatic transformation to L-methylfolate in order to be used by cells. L-methylfolate, unlike the other folates, is able to cross the blood-brain barrier for use in the CNS. The conversion of dihydrofolate (DHF) and folic acid to L-methylfolate occurs through a three or four step process:

1. Folic acid is converted to DHF by the dihydrofolate reductase enzyme (DHFR)

2. DHF is then converted to tetrahydrofolate (THF)

3. THF is converted to 5,10-methyleneTHF

4. 5,10-methyleneTHF is converted to L-methylfolate by the methyltetrahydrofolate reductase enzyme (MTHFR).

Transforming Growth Factor (TGF) plays a crucial role in tissue regeneration, cell differentiation, embryonic development, and regulation of the immune system. Transforming growth factor beta is found in hematopoietic (blood-forming) tissue and initiates a signaling pathway that suppresses the early development of cancer cells. It enhances the deposition of extracellular matrix and may play potential role in wound healing and cirrhosis formation. Many cells synthesize TGF-b and almost all of them have specific receptors for this peptide.

TGF Beta-1 is a protein that has important regulatory effects throughout innate immune pathways.  This protein helps control the growth and division (proliferation) of cells, the process by which cells mature to carry out specific functions (differentiation), cell movement (motility), and the self-destruction of cells (apoptosis).  The TGF Beta-1 protein is found throughout the body and plays a role in development before birth, the formation of blood vessels, the regulation of muscle tissue and body fat development, wound healing, and immune system function (especially regulatory T-cells).

TGF Beta-1 can impair T-regulatory cell function, which in turn contributes to the activation of autoimmunity, yet TGF Beta-1 also plays a role in suppressing autoimmunity. Neurologic, autoimmune and many other systemmic problems also are found with high TGF Beta-1.

Th/To antibodies target RNase P and mitochondrial RNase ribonucleoprotein complexes. These antibodies are found in 2% to 5% of SSc patients and are primarily associated with lcSSc. Th/To antibodies are rarely found in other autoimmune diseases but can occur in patients with localized scleroderma.

Patients with Th/To antibodies often develop both ILD and PAH and thus have a poorer prognosis than other patients with lcSSc.

The TH1/TH2 ratio measures the balance between T-helper type 1 (TH1) and T-helper type 2 (TH2) cells. These are subsets of CD4+ T-helper cells that regulate the immune system by driving different types of immune responses:

• TH1 Cells: Promote cellular immunity, targeting intracellular pathogens (e.g., viruses, some bacteria) and cancer cells.
• TH2 Cells: Promote humoral immunity, stimulating antibody production to combat extracellular pathogens (e.g., parasites) and allergens.

The TH1/TH2 ratio reflects the overall immune system balance:

• A balanced ratio supports effective immunity against infections while avoiding excessive inflammation or hypersensitivity.
• An imbalanced ratio may indicate susceptibility to certain diseases, chronic inflammation, or immune dysregulation.

The Th17/Treg ratio is a critical marker offering significant insights into the immune system's regulatory mechanisms. Th17 cells (T-helper 17) and Treg cells (regulatory T cells) represent two distinct subsets of CD4+ T cells with opposing functions in the immune response.

Th17 cells are pro-inflammatory and play a crucial role in the body's defense against pathogens and in the pathogenesis of various autoimmune and inflammatory diseases. They are characterized by the production of interleukin-17 (IL-17) and other inflammatory cytokines.

On the other hand, Treg cells are responsible for maintaining immune tolerance and preventing autoimmune responses by suppressing the activity of effector T cells, including Th17 cells.

SOURCES:

Fish, shellfish, plants, cigarettes, soil, air, water, electronic devices, switches and closures for the semi-conductor industry, glass for medical procedures.

NUTRIENT INTERACTIONS:

Some of its toxic effects results from interference with biological functions of potassium.

SOURCES:

Fish, shellfish, plants, cigarettes, soil, air, water, electronic devices, switches and closures for the semi-conductor industry, glass for medical procedures.

NUTRIENT INTERACTIONS:

Some of its toxic effects results from interference with biological functions of potassium.

Fecal thallium (Tl) provides an indication of Tl that has been excreted from the body in bile, and to a lesser extent recent oral exposure to the element. The biliary fecal route is the primary route of Tl excretion from the body, although about 35% is excreted in urine. Tl is rapidly and near completely absorbed when ingested, inhaled or brought into contact with skin.

Thallium is a highly toxic heavy metal which is generally tasteless and odorless, and doesn’t have physiological functions in the body.

Thallium (Tl) is a highly toxic element which, like lead and mercury, accumulates in many body tissues. Hair levels reflect chronic accumulation of Tl, but alopecia occurs about two weeks after ACUTE Tl poisoning. Thallium occurs naturally in some minerals, and magmatic and sedimentary rock, consequently in soil, water, and air. Industrially, Tl is used in lenses and prisms, as an alloy with mercury in low temperature thermometers, and in the preparation of high density liquids.

Sources:

Fish, shellfish, plants, cigarettes, soil, air, water, electronic devices, switches and closures for the semiconductor industry, glass for medical procedures.

Nutrient interactions:

Some of its toxic effects results from interference with biological functions of potassium.

Severe, painful neurological and gastrointestinal symptoms occur from thallium poisoning; alopecia is the most characteristic sign, as it is coupled with a black pigment at the hair root. Nausea, vomiting, and diarrhea have been reported. Thallium exposure may occur due to soil contamination with thallium-containing pesticides although they have been banned since 1972. Specimens used for thallium detection include urine, which is the main route of excretion, and hair. Blood levels have been measured, but thallium is rapidly cleared, so exposure must be acute to achieve accurate results. Treatment for high thallium levels include Prussian blue, DMSA, or activated charcoal for ingested thallium. BAL, D-penicillamine and EDTA are contraindicated.

SOURCES:

Fish, shellfish, plants, cigarettes, soil, air, water, electronic devices, switches and closures for the semi-conductor industry, glass for medical procedures.

NUTRIENT INTERACTIONS:

Some of its toxic effects results from interference with biological functions of potassium.

This calculation includes the daily metabolites of cortisol (5-alpha THF, THF) and cortisone (THE) which maybe a better representation of daily cortisol output than measuring cortisol and cortisone alone due to metabolism differences in the liver (with thyroid hormone) and fatty tissues.

This calculation includes the daily metabolites of cortisol (5-alpha THF, THF) and cortisone (THE) which maybe a better representation of daily cortisol output than measuring cortisol and cortisone alone due to metabolism differences in the liver (with thyroid hormone) and fatty tissues.

High levels can indicate increased cortisol secretion or hyperthyroidism.

Low levels may indicate decreased cortisol secretion or hypothyroidism.