Nonsense. DHEA is a byproduct downstream from progesterone. Just try googling first.

Are you supplementing with DHEA-S? It is known to elevate progesterone levels. If not, perhaps another supplement?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380904/

•Inhibits 5 alpha-reductase activity. 5 alpha-reductase participate in 3 metabolic pathways: bile acid biosynthesis, androgen and estrogen metabolism, and prostate cancer. There are three isoenzymes of 5-alpha reductase, which vary in different tissues with age.

•Helps balance blood glucose. Improves insulin resistance. Plays an important role in the signaling of insulin release and pancreatic function, and may affect the susceptibility to diabetes or gestational diabetes.
•Is calming, due to it’s action on the GABA receptor sites. GABA is a calming neurotransmitter, this prevents an excessive response to stress and reduces cortisol which is catabolic breaking down tissue.
•Brain neurotransmitter and myelinator. Progesterones are neuromodulators and are neuro-protective, neurogenic, and regulate neurotransmission and myelination. Myelin sheaths are made of progesterone. There is also evidence that the addition of progesterone can also help remyelinate damaged axons due to trauma, restoring some lost neural signal conduction
*Produces the neurotransmitters- dopamine and serotonin. Enhances serotonin. Increases gene expression for DNA repair mechanisms in serotonin neurons, thereby rendering them less vulnerable to stress-induced DNA fragmentation.
•Has well-described protective effects against numerous insults in a variety of cell models, animal models and in humans, including strokes, concussions, and spinal injuries.
•The key mediator of progesterone’s beneficial effects is on the family of growth factors called neurotrophins in the central nervous system.
•Acts as an antiinflammatory agent and regulates the immune response.
•Increases T cells synergistically with Vitamin D. Progesterone with vitamin D promotes generation of induced regulatory T cells with increased stability.
• Is responsible for immune function in cooperation with vitamin D which fail with lowered progesterone and lowered vitamin D causing autoimmune disorders and other diseases.
•Improves blood pressure. Is a vasodilator, thus enhancing blood flow which allows nutrients to reach the hair follicle (a reason for baldness. Estrogen on the other hand constricts the smooth muscle found in blood vessels.)
•Acts as an antioxidant by increasing levels of superoxide dismutase, glutathione and catalase (which catalase is deficient in gray hair).
•Inhibits lipid peroxidation (a high level of pro-inflammatory LDLs leads to increased lipid peroxidation). Progesterone protects against lipid peroxidation.

•Inhibits mast cells responsible for the increase in histamine.
•Maintains and lengthens telomeres and stabilizes DNA.

•Inhibits Tumor Necrosis Factor-alpha.
•Appears to prevent endometrial cancer (involving the uterine lining) by regulating the effects of estrogen.
•Causes cancer apoptosis at progesterone levels comparable to the third trimester.
•Suppresses the stress hormones. Cortisol uses up progesterone. Higher progesterone suppresses cortisol.
•Suppresses the mTOR pathway. http://www.sciencedirect.com/science/article/pii/S0960076014000934 “Anti-tumor effects of progesterone in human glioblastoma multiforme: Role of PI3K/Akt/mTOR signaling” (Rapamycin does the job of decreased progesterone)
• Increases the tumor suppressor p53 to suppress cancer http://www.ncbi.nlm.nih.gov/pubmed/9846203 “Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53.”
•Raises epidermal growth factor-1 (EGF-1) levels, a factor often used to induce proliferation, and used to sustain cultures, of stem cells.
•Stimulates progenitor cells and promotes stem cell growth with estrogen/testosterone. http://www.ncbi.nlm.nih.gov/pubmed/24395108 “Progesterone stimulates progenitor cells in normal human breast and breast cancer cells.” http://www.the-scientist.com/?articles.view/articleNo/28895/title/Hormones-promote-stem-cell-growth/ “Hormones promote stem cell growth” Using our own stem cells with progesterone being a signal molecule is how our body renews itself.
*Adequate progesterone keeps women’s
*Progesterone is one of the anabolic hormones which stimulate connective tissue growth- including bone, cartilage, tendon ligaments, guts, cornea, liver, lymphatic organs, heart, vessels, lungs, adipose tissue, nervous systems, meninges, spinal cord, skin.
*Every cell in our body has progesterone receptors.
. *Men maintain higher progesterone levels slightly longer than women, so they are sometimes able to produce sperm for reproduction to impregnate women when they are advanced in age, whereas progesterone levels drop when women are in peri-menopause beginning in the mid 30’s. When women finally become menopausal, their progesterone production virtually stops. Women are not born with a finite supply of eggs causing menopause. Plus, even after menopause you still have many eggs left. http://news.sciencemag.org/2012/02/stem-cells-may-make-eggs-found-women Healthy ovaries nourished with progesterone which nourish egg producing stem cells will allow stem cells to keep replacing old eggs with new eggs over time unless progesterone levels drop. Once progesterone drops, then menopause means further hormone unbalancing and de-stabilization. Once progesterone drops in both men and women, this means the quality of the house/factory to build eggs and babies- testes/ovaries/endometrium in the uterus have weakened connective tissue. Ovaries/testes which produce eggs/sperm, become weakened with reduced progesterone, then egg/sperm production slows/ceases. Research shows progesterone keeps the endometrium healthy to implant an embryo and maintain a pregnancy. Also, eating the placenta stops apoptosis of ovarian germ-line stem cells (because the placenta is rich in progesterone).

“Effect of medroxyprogesterone acetate (synthetic progesterone) on the response of the rat mammary gland to carcinogenesis.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2246992 /
http://www.pnas.org/content/102/7/2490.full

Another experiment shows results that demonstrate that (real) progesterone at a concentration similar to that seen during the third trimester of pregnancy exhibited a strong antiproliferative effect on at least two breast cancer cell lines. Apoptosis was induced in the progesterone receptor expressing T47-D breast cancer cells. “Progesterone inhibits growth and induces apoptosis in breast cancer cells: inverse effects on Bcl-2 and p53.” https://www.ncbi.nlm.nih.gov/pubmed/11559549

It is suggested that androgens and progesterone might play an etiologic role in ovarian carcinogenesis [37]. Pregnancy results in increases in maternal circulating progesterone due to production from the placenta. Among cell lines of normal human ovarian surface epithelium and ovarian cancer epithelium, low doses of progesterone were shown to stimulate cell growth in both cell lines whereas high doses resulted in cell growth inhibition [38]. In contrast, among the same cell lines exposed to estrone and 17-β estradiol, there was continued cell growth stimulation with increasing levels of hormone [38]. While it has been suggested that estrone exerts limited effect on ovarian surface epithelium cells, the link between Hormone Therapy and ovarian cancer risk suggested in these and other data suggest that estrone, and perhaps synthetic components of Hormone Therapy, might enhance neoplastic changes in ovarian epithelium. “Estrogen, Progesterone and Epithelial Ovarian Cancer.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2729759/

Our data have identified folicle stimulating hormone, luteinizing hormone, estrone, estradiol, testosterone, DHT, and low-dose progesterone as positive growth regulators for ovarian cancer cells. Conversely, progesterone at high concentrations has been shown to be a potent antiproliferative factor for ovarian cancer cells. (Doesn’t say if they used synthetic progesterone.) “Expression of Gonadotropin Receptor and Growth Responses to Key Reproductive Hormones in Normal and Malignant Human Ovarian Surface Epithelial Cells.”
http://www.annclinlabsci.org/content/28/6/360.abstract

Progesterone lowers follicle stimulating hormone and luteinizing hormone (that climb with age) back down to normal levels.

Estrone the carcinogenic form of estradiol common in older women and men,(reference: “Age Trends in Estradiol and Estrone Levels Measured Using Liquid Chromatography Tandem Mass Spectrometry in Community-Dwelling Men of the Framingham Heart Study.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3660115/) may be converted in the liver back into estradiol by a NAD conversion, In my mind, an important reason to keep NAD levels up to normalize estradiol/estrone levels with age. .

In enzymology, an estradiol 17beta-dehydrogenase (EC 1.1.1.62) is an enzyme that catalyzes the chemical reaction.

estradiol-17beta + NAD(P)+ (rightleftharpoons) estrone + NAD(P)H + H+

The 3 substrates of this enzyme are estradiol-17beta, NAD+, and NADP+, whereas its 4 products are estrone, NADH, NADPH, and H+.

This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is estradiol-17beta:NAD(P)+ 17-oxidoreductase. Other names in common use include 20alpha-hydroxysteroid dehydrogenase, 17beta,20alpha-hydroxysteroid dehydrogenase, 17beta-estradiol dehydrogenase, estradiol dehydrogenase, estrogen 17-oxidoreductase, and 17beta-HSD. This enzyme participates in androgen and estrogen metabolism.

Estrone is known to be a carcinogen for human females as well as a cause of breast tenderness or pain, nausea, headache, hypertension, and leg cramps in the context of non-endogenous exposure. https://en.wikipedia.org/wiki/Estrone

True