- Gram-negative genus in the Proteobacteria phylum.

- Normal gut flora.

- Escherichia coli (E. coli) is the primary species in this genus.

- Most E. coli are nonpathogenic (pathogenic E. coli strains are measured separately).

The Esterified/Free Ratio measures the balance between esterified (acylcarnitine) and free carnitine in your bloodstream. This ratio helps assess how efficiently your mitochondria transport and break down fatty acids for energy. An elevated ratio may suggest impaired fatty acid oxidation or increased metabolic stress, while a low ratio may point to reduced acylcarnitine formation or low metabolic demand. This marker is commonly used in evaluating metabolic function, mitochondrial efficiency, and nutritional carnitine status.

The esterified/free carnitine ratio, often measured in clinical settings, is a valuable indicator of carnitine metabolism balance within the body. This ratio compares the amount of carnitine bound to fatty acids (esterified carnitine) to the amount of carnitine in its free, unbound form. A balanced ratio is crucial for efficient energy production, as carnitine plays a key role in transporting fatty acids into mitochondria for oxidation.

Your estimated Average Glucose (eAG) number is calculated from the result of your A1c test. Like the A1c, the eAG shows what your average blood sugars have been over the previous 2 to 3 months, but instead of a percentage, the eAG is in the same units (mg/dl) as your blood glucose meter.

The CHD Risk is based on the T. Chol/HDL ratio. Other factors affect CHD Risk such as hypertension, smoking, diabetes, severe obesity, and family history of premature CHD.

Estradiol (Estrogen) is a female hormone, produced primarily in the ovary. The amount of estrogen produced depends on the phase of the menstrual cycle.

Men also produce estradiol, but only very small amounts.

Shortly before ovulation, estradiol levels surge and then fall immediately after ovulation. They then rise again and remain elevated until 2-3 days before menstruation.

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

Estradiol (E2) is critical for assessing the estrogenic activity and hormonal balance in women. Estradiol, the most potent of the three major estrogens (which also include estrone and estriol), plays a pivotal role in female reproductive health, influencing the menstrual cycle, fertility, and secondary sexual characteristics.

Estradiol is primarily produced by the ovaries in premenopausal women and, to a lesser extent, by adipose tissue and the adrenal glands. Its production is stimulated by follicle-stimulating hormone (FSH) and luteinizing hormone (LH). In postmenopausal women, estradiol levels significantly decrease due to diminished ovarian function, with a relative increase in the importance of peripheral sources like adipose tissue for its production.

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

Estrogens play a critical role in female sexual development, menstrual function, protein synthesis, cardiovascular function, bone formation and remodeling, cognitive function, emotional balance and other important health factors. The estrogenic potency of estradiol is 12 times that of estrone and 80 times that of estriol. Estradiol is the primary estrogen in premenopausal women. Estrone is the second most potent estrogen compared to estradiol.

Estradiol (E2) is produced in women mainly in the ovary. The testes and adrenal glands are the principal source of estradiol in men. In women, normal levels of estradiol provide for proper ovulation, conception, and pregnancy, while also promoting healthy bone structure and regulating cholesterol levels.

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

Estradiol is the main "female" hormone. The full name is 17-beta-Estradiol.

Current research indicates that, in some people, this hormone may play a role in the loss of bone density, prevents male bodies from clearing DHT out of the prostate gland, and can stimulate estrogen-sensitive tumor growth (if estrogen-sensitive cancer cells are already present).

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

The most physiologically active estrogen. Binds to both to ER and Estrogen Receptor Beta (ERβ). Estradiol, made in the ovary, rapidly converts to estrone. Poor symptom control with estrogen replacement may suggest the need for improving absorption or increasing estradiol.

Estradiol is the main "female" hormone. The full name is 17-beta-Estradiol.

Current research indicates that, in some people, this hormone may play a role in the loss of bone density, prevents male bodies from clearing DHT out of the prostate gland, and can stimulate estrogen-sensitive tumor growth (if estrogen-sensitive cancer cells are already present).

Men need to produce estrogen through a process involving an enzyme called aromatase that transforms testosterone into estradiol.

Aging men sometimes have too much aromatase activity, which causes their testosterone to convert to excess estradiol. This results in depletion of vital testosterone while spiking estradiol to unsafe ranges.