Advanced Dried Urine Hormone Profile (NutriPATH)

16α-Hydroxyestrone (16α-OH-E1), or hydroxyestrone, also known as estra-1,3,5(10)-trien-3,16α-diol-17-one, is an endogenous steroidal estrogen and a major metabolite of estrone, as well as an intermediate in the biosynthesis of estriol. It is a potent estrogen similarly to estrone, and it has been suggested that the ratio of 16α-hydroxyestrone to 2-OH-E1, the latter being much less estrogenic in comparison and even antiestrogenic in the presence of more potent estrogens like estradiol, may be involved in the pathophysiology of breast cancer. Conversely, 16α-hydroxyestrone may help to protect against osteoporosis.

The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy-E1 is produced from 2-OH-E1 through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH-E1 and particularly 2-Methoxy-E1.

2-Methoxy-E1 has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy-E1 levels were lower in breast cancer patients than controls.

The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy estrogens are produced from 2-OH estrogens through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH estrogens and particularly 2-Methoxy estrogens.

2-Methoxy estrogens has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy estrogen levels were lower in breast cancer patients than controls.

The 2-Methoxy Estrogens are considered to be protective.

2-Methoxy-E1 is produced from 2-OH-E1 through the COMT enzyme. Anti-cancerogenic effects have been ascribed to 2-OH-E1 and particularly 2-Methoxy-E1.

2-Methoxy-E1 has shown antiproliferative effects in both hormone-dependent and hormone-independent breast cancer cells. These studies have shown that urinary 2-Methoxy-E1 levels were lower in breast cancer patients than controls.

2-hydroxyestrone and 16-hydroxyestrone are Phase I metabolites of Estrone (E1). Their ratio is of clinical significance in pre and peri-menopausal women. In post-menopausal women it does not have the same clinical significance. It is, however, hypothesized that the 2/16 ratio is important in menopausal women who are on hormone replacement therapy (HRT).

Research and clinical studies show that the 2-hydroxylated estrogens (2-OH E2 and 2-OH E1) are a safer pathway of hydroxylation than the 4-hydroxyestrogens (4-OH E2 and 4-OH E1), which bind to and damage DNA, leading to mutations that are associated with increased breast cancer risk.

Most consider 2-OH-E1 favorable

Estrogen is metabolized (primarily by the liver) down three phase I pathways. The 2-OH pathway is considered the safest because of the anti-cancer properties of 2-OH metabolites. Conversely, the 4-OH pathway is considered the most genotoxic as its metabolites can create reactive products that damage DNA. The third pathway, 16-OH creates the most estrogenic of the metabolites (although still considerably less estrogenic than estradiol) - 16-OH-E1.

20a-Dihydroprogesterone (20a-DHP), also known as 20a-hydroxyprogesterone (20a-OHP), is a naturally occurring, endogenous progestogen. It is a metabolite of progesterone, formed by the 20a-hydroxysteroid dehydrogenases (20a-HSDs). 20a-DHP can be transformed back into progesterone by 20a-HSDs. 20a-DHP has very low affinity for the progesterone receptor and is much less potent as a progestogen in comparison to progesterone.

3a- and 20a- dihydroprogesterone, have tumor-inhibitory properties in breast cancer.

3a-Dihydroprogesterone (3a-DHP), also known as 3a-hydroxyprogesterone, is an endogenous neurosteroid. It is biosynthesized by 3a-hydroxysteroid dehydrogenase from progesterone. 3a-DHP has been found to act as a positive allosteric modulator of the GABAA receptor and is described as being as active as allopregnanolone in regard to this action. In accordance, it has anxiolytic effects in animals. 3a-DHP has also been found to inhibit the secretion of follicle-stimulating hormone (FSH) from the rat pituitary gland, demonstrating possible antigonadotrophic properties.

Healthy Phase II metabolism methylates 2-hydroxy (2-OH) estrogens to the more cancer-protective 2-methoxy (2-MeO) forms, and neutralizes the potentially carcinogenic 4-OH estrogens to their 4-MeO forms.

Healthy Phase II metabolism methylates 2-hydroxy (2-OH) estrogens to the more cancer-protective 2-methoxy (2-MeO) forms, and neutralizes the potentially carcinogenic 4-OH estrogens to their 4-MeO forms.

4-Methoxyestradiol (4-ME2) is an endogenous, naturally occurring methoxylated catechol estrogen and metabolite of estradiol that is formed by catechol O-methyltransferase via the intermediate 4-hydroxyestradiol.

Neutralized version of carcinogenic 4-OH-E1

4-OHE1and 4-OH-E2 are referred to as the “bad” estrogens, along with 16a-OHE1. They are primarily produced by CYP1B1 and CYP34A, respectively, enzymes localized in tissues, including breast and prostate as well as liver. Some have suggested that increased expression of CYP1B1 and 4-hydroxylation of estradiol are biomarkers of tumorigenesis.

Human breast cancer tissue produces much higher levels of 4-OH than 2-OH, while normal breast tissue produces approximately equal amounts of the two metabolites. Women taking hormone therapy with a polymorphism in CYP1B1 had twice the risk of developing breast cancer compared to other HRT users.

- The 4-OH pathway is considered the most genotoxic as its metabolites can create reactive products that damage DNA.

- Estrone is hydroxylated through Phase 1 detox to form 4-OH-E1. In Phase 2 it is methylation to form 4-MeE1. When 4-OH-E1 is properly methylated to 4-MeE1 it is relatively benign as the 4-MeE1 is easily eliminated and risks are low.

- When it is not methylated 4-OH-E1 builds up. Then it converts to 3,4-Quinones which are carcinogenic similarly to the 16 pathway. Women with uterine fibroids may have increased levels of 4-OH-E1. High levels of estrogen across the board are associated with heavy cycles.

5a,3a–androstanediol is a neuroactive steroid that enhances dopamine activity, important for mood elevation.

5a-DHT is a testosterone metabolite. 

5a-DHT is essential for the development of the male sex characteristics before birth, particularly the formation of the external genitalia. In the adult, 5a-DHT is needed to develop and maintain male gender characteristics, such as facial hair, deep voice, and muscle growth. In women, 5a-DHT may induce the onset of puberty and causes the body and pubic hair growth.

Increased 5a-DHT levels are found in about 40% of patients with idiopathic hirsutism and 35% of patients with polycystic ovarian syndrome (=PCOS).

Allopregnanediol, or 5a-pregnane-3a,20a-diol, is an endogenous metabolite of progesterone and allopregnanolone and an isomer of pregnanediol.

Allopregnanolone, also known as brexanolone, is a medication and a naturally produced steroid that acts on the brain. Allopregnanolone possesses a wide variety of effects, including, in no particular order, antidepressant, anxiolytic, stress-reducing, rewarding, prosocial, antiaggressive, prosexual, sedative, pro-sleep, cognitive, memory-impairment, analgesic, anesthetic, anticonvulsant, neuroprotective, and neurogenic effects.

DHEA and androstenedione are made almost exclusively by the adrenal gland (although a smaller amount is made in the ovaries). These hormones appear in urine as DHEA-S (DHEA-Sulfate), androsterone and etiocholanolone.

Androsterone is a DHEA metabolite via the 5-alpha-reductase pathway. The 5-alpha pathway is more androgenic. 

Bisphenol A (BPA) is a xenoestrogen, exhibiting estrogen-mimicking, hormone-like properties that raise concern about its suitability in some consumer products and food containers. Bisphenol A (BPA) is an organic synthetic compound and it is a starting material for the synthesis of plastics, primarily certain polycarbonates and epoxy resins, as well as some polysulfones and certain niche materials. BPA is an endocrine-disrupting chemical that has been found to bind to both of the nuclear estrogen receptors. A recent exposure to plastic that released excessive amounts of BPA into a food or a beverage could be identified by high levels of urinary BPA.

Corticosterone, also known as 17-deoxycortisol, is a steroid hormone of the corticosteroid type produced in the cortex of the adrenal glands. Corticosterone has multiple effects on memory. The main effects are seen through the impact of stress on emotional memories as well as long term memory. With emotional memories, corticosterone is largely associated with fear memory recognition. Not only does corticosterone have effects on emotional memories but memory recognition and consolidation as well.

Cortisol is a steroid hormone synthesized from cholesterol by a multienzyme cascade in the adrenal glands. It is the main glucocorticoid in humans and acts as a gene transcription factor influencing a multitude of cellular responses in virtually all tissues. Cortisol plays a critical role in glucose metabolism, maintenance of vascular tone, immune response regulation, and in the body's response to stress. Its production is under hypothalamic-pituitary feedback control.

Cortisone, a downstream metabolite of cortisol, provides an additional variable to assist in the diagnosis of various adrenal disorders, including abnormalities of 11-beta-hydroxy steroid dehydrogenase (11-beta HSD), the enzyme that converts cortisol to cortisone. Deficiency of 11-beta HSD results in a state of mineralocorticoid excess because cortisol (but not cortisone) acts as a mineralocorticoid receptor agonist. Licorice (active component glycyrrhetinic acid) inhibits 11-beta HSD and excess consumption can result in similar changes.

The evaluation of the creatinine concentration in the urine does only serve as an admeasurement of the individual efficiency of the kidney. High values point to an urine concentration, low values to a strong dilution. Only the consideration of these circumstances allowes to evaluate the requested analyte correctly.

The evaluation of the creatinine concentration in the urine does only serve as an admeasurement of the individual efficiency of the kidney. High values point to an urine concentration, low values to a strong dilution. Only the consideration of these circumstances allowes to evaluate the requested analyte correctly.

The evaluation of the creatinine concentration in the urine does only serve as an admeasurement of the individual efficiency of the kidney. High values point to an urine concentration, low values to a strong dilution. Only the consideration of these circumstances allowes to evaluate the requested analyte correctly.

The evaluation of the creatinine concentration in the urine does only serve as an admeasurement of the individual efficiency of the kidney. High values point to an urine concentration, low values to a strong dilution. Only the consideration of these circumstances allowes to evaluate the requested analyte correctly.

Creatinine values are measured to correct results for urine dilution.

Creatinine is a waste product produced by muscles from the breakdown of a compound called creatine. Creatinine is filtered from the blood by the kidneys and released into the urine.

The amount of creatinine produced in the body is dependent on muscle mass and is relatively constant for an individual. The amount of creatinine removed from the blood depends on both the filtering ability of the kidneys and the rate at which blood is carried to the kidneys.

Deoxycorticosterone (DOC) is a steroid hormone synthesized in the adrenal gland and is a precursor for the synthesis of cortisol and aldosterone. The levels of DOC of pregnant women are extraordinarily high compared with those in men and nonpregnant women. The major diagnostic utility of measurement of steroid synthesis intermediates such as Deoxycorticosterone is in diagnosing disorders of steroid synthesis.

DHEA-S is the sulfate ester of DHEA and only a part of DHEA testing. If this marker was low it would mean that there is potential inflammation blocking DHEA being converted to DHEA-S. 

The ratio of potentially toxic urinary estrogens (i.e. 2- and 4-catechols of estradiol and estrone) to inert estriol has been used for many years as an index of breast cancer risk.

Epitestosterone, or isotestosterone is an endogenous steroid and an epimer of the androgen sex hormone testosterone. It is a weak competitive antagonist of the androgen receptor (AR). Structurally, epitestosterone differs from testosterone only in the configuration at the hydroxy-bearing carbon, C17. Epitestosterone is believed to form in a similar way to testosterone; studies found that around 50% of epitestosterone production in human males can be ascribed to the testis, although the exact pathway of its formation is still the subject of research. It has been shown to accumulate in mammary cyst fluid and in the prostate. Epitestosterone levels are typically highest in young males; however, by adulthood, most healthy males exhibit a testosterone to epitestosterone ratio (T/E ratio) of about 1:1

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.

Has weak estrogen activity. Considered to be a protective estrogen. Most prevalent estrogen in pregnancy.

Produced by the ovaries, the estrone hormone is one of three types of estrogen, and it is one of the major hormones found in the bodies of postmenopausal women. While research into estrone function is still ongoing, since it is the least powerful of the three estrogen types, women should still understand this hormone and its known effects on the body.

- Weaker compared to Estradiol (Research says the estrogenic activity is about 4% of estradiol’s activity)

- Most abundant in menopause

- Made via aromatization in several tissues like fat and muscle

- Converts into estradiol (E2)

Estrone (E1) is also made by the ovary but in fat tissue in lesser quantities. While not as abundant in circulation as estradiol, estrone excess can still increase the risk for estrogen dominant cancers and estrogen dominant symptoms such as breast tenderness, heavy menstrual cycles, headaches, and erectile dysfunction and breast development in men just like estradiol. Estrone is commonly thought to be more abundant during menopause. 

Estradiol and estrone can interconvert into each other. 

Etiocholanolone is a DHEA metabolite that is excreted in the urine. It is produced from androstenedione and the 5-beta-reductase metabolic pathway. It is helpful in evaluating adrenal and androgen function.

Cortisol is a hormone produced by the adrenal glands, which are located on top of the kidneys. It is normally released in response to events and circumstances such as waking up in the morning, exercising, and acute stress.

In the Advanced Dried Urine Hormone Profile (NutriPATH) test there are 4 individual free cortisol readings that were measured at different times throughout one day:

- Free Cortisol (1st Morning)
- Free Cortisol (2nd Morning)
- Free Cortisol (Evening)
- Free Cortisol (Night)

When you are looking at Free Cortisol (1st Morning) it is essential to also look at Free Cortisol (2nd Morning). The difference between those 2 cortisol samples is called the cortisol awakening response (or CAR). 

An elevated CAR would mean that the difference between those 2 markers is really big.

Different possible reasons for an elevated CAR:

- an overactive HPA axis (=plays an important role in the stress response), ongoing job-related stress (anticipatory stress for the day)

- blood sugar dysregulation

- pain (i.e. waking with painful joints or a migraine), 

- and general depression (not Seasonal affective disorder/”winter depression”)

Neither the waking nor post-waking cortisol results correlated to Major Depressive Disorder, but the CAR calculation (the change between the first two samples) does. So this means that if your morning free cortisol reading spikes up high first thing in the morning, there is something to look at. Is there an overactivity to stress? Are you anticipating a stressful day at work? If your morning free cortisol levels are high, this can be due to stress or anticipating stress. 

This is the 2nd cortisol sample of the day. Usually measured 30 to 60 minutes after waking. 

Cortisol is a hormone produced by the adrenal glands, which are located on top of the kidneys. It is normally released in response to events and circumstances such as waking up in the morning, exercising, and acute stress.

In the Advanced Dried Urine Hormone Profile (NutriPATH) test there are 4 individual free cortisol readings that were measured at different times throughout one day:

- Free Cortisol (1st Morning)
- Free Cortisol (2nd Morning)
- Free Cortisol (Evening)
- Free Cortisol (Night)

When you are looking at Free Cortisol (2nd Morning) it is essential to also look at Free Cortisol (1st Morning). The difference between those 2 cortisol samples is called the cortisol awakening response (or CAR). 

An elevated CAR would mean that the difference between those 2 markers is really big.

Different possible reasons for an elevated CAR:

- an overactive HPA axis (=plays an important role in the stress response), ongoing job-related stress (anticipatory stress for the day)

- blood sugar dysregulation

- pain (i.e. waking with painful joints or a migraine), 

- and general depression (not Seasonal affective disorder/”winter depression”)

Neither the waking nor post-waking cortisol results correlated to Major Depressive Disorder, but the CAR calculation (the change between the first two samples) does. So this means that if your morning free cortisol reading spikes up high first thing in the morning, there is something to look at. Is there an overactivity to stress? Are you anticipating a stressful day at work? If your morning free cortisol levels are high, this can be due to stress or anticipating stress. 

This is the 3rd cortisol sample of the day. Usually measured in the afternoon/evening. 

Cortisol is a hormone produced by the adrenal glands, which are located on top of the kidneys. It is normally released in response to events and circumstances such as waking up in the morning, exercising, and acute stress.

In the Advanced Dried Urine Hormone Profile (NutriPATH) test there are 4 individual free cortisol readings that were measured at different times throughout one day:

- Free Cortisol (1st Morning)
- Free Cortisol (2nd Morning)
- Free Cortisol (Evening)
- Free Cortisol (Night)

This is the 4th cortisol sample of the day (=evening/night).

Cortisol is a hormone produced by the adrenal glands, which are located on top of the kidneys. It is normally released in response to events and circumstances such as waking up in the morning, exercising, and acute stress.

In the Advanced Dried Urine Hormone Profile (NutriPATH) test there are 4 individual free cortisol readings that were measured at different times throughout one day:

- Free Cortisol (1st Morning)
- Free Cortisol (2nd Morning)
- Free Cortisol (Evening)
- Free Cortisol (Night)

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Free Cortisone (1st Morning) can help to confirm the marker Free Cortisol (1st Morning).

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Free Cortisone (2nd Morning) can help to confirm the marker Free Cortisol (2nd Morning).

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Free Cortisone (Evening) can help to confirm the marker Free Cortisol (Evening).

Cortisone is the inactive form of cortisol. Cortisone shows minimal biological activity per se, reflecting negligible affinity for the glucocorticoid and aldosterone receptors. The kidney, colon and saliva gland have lots of activity for changing cortisol to cortisone (active to inactive) to keep cortisol off the aldosterone receptor. Cortisone is converted back in the liver, fat, etc. (inactive to active).

Free Cortisone (Night) can help to confirm the marker Free Cortisol (Night).

Melatonin is not technically an adrenal or sex hormone however it is highly involved in the entire endocrine system. It is made in small amounts in the pineal gland in response to darkness and stimulated by Melanocyte Stimulating Hormone (MSH). 

Melatonin is not technically an adrenal or sex hormone however it is highly involved in the entire endocrine system. It is made in small amounts in the pineal gland in response to darkness and stimulated by Melanocyte Stimulating Hormone (MSH). 

Melatonin is not technically an adrenal or sex hormone however it is highly involved in the entire endocrine system. It is made in small amounts in the pineal gland in response to darkness and stimulated by Melanocyte Stimulating Hormone (MSH). 

Melatonin is not technically an adrenal or sex hormone however it is highly involved in the entire endocrine system. It is made in small amounts in the pineal gland in response to darkness and stimulated by Melanocyte Stimulating Hormone (MSH). 

Based on the optimal luteal levels of urinary Pgdiol (about 1300-2000 µg/g creatinine) an optimal working range for the ratio of this progesterone metabolite to estradiol was established based on the median level of urinary estradiol (1.37 µg/g creatinine). Thus the optimal working ratio of urinary Pgdiol to estradiol in the premenopausal woman during the peak luteal phase should be in the neighborhood of about 1000 to 1500.

Progesterone itself is not readily found in the urine. Instead, this test measures pregnanediol (a progesterone metabolite). Pregnanediol is well-established in research literature as a reliable marker for progesterone levels.

Testosterone is the major androgen in the body. It is converted to dihydrotestosterone by 5-alphareductase, and to estradiol by aromatase.

This is one of the three cortisol metabolites. The total some of the three cortisol metabolites gives us a good indication of the overall cortisol production in your body. 

Two of the 3 metabolites are the active form of cortisol (THF). The other metabolite is in the inactive form cortisone.

This particular marker (a-THF) hence is an active cortisol metabolite.

This is one of the three cortisol metabolites. The total some of the three cortisol metabolites gives us a good indication of the overall cortisol production in your body. 

Two of the 3 metabolites are the active form of cortisol (THF). The other metabolite is in the inactive form cortisone.

This particular marker (b-THE) hence is an inactive cortisone metabolite.

Cortisol is a stress hormone produced by the adrenal glands and is the primary agent used in our body’s flight or fight response to threatening stimuli.

The inactive or “storage form” of adrenal glucocorticoid. Can be reversibly transformed to cortisol. Clinically, cortisone may reflect a measure of adrenal reserve when compared to cortisol. Ideally, cortisone will be about 30% higher than cortisol when both are at optimal levels. Values at the high end or low end of the reference range are generally not optimal.