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Aside from medical treatment, there are lifestyle changes women can make to help lower their testosterone levels. However, research reveals that some pre-menopausal women with high testosterone levels may be asymptomatic, meaning they never experience symptoms. Many women with high testosterone levels will have irregular menses or no period at all. "There are no established optimal testosterone levels for women, so most clinicians use a lab reference range to diagnose a woman with high testosterone," Dr. Dorr says. It’s important to note that for people assigned female at birth (AFAB), there’s no exact number for determining high testosterone levels, also known as hyperandrogenism. In comparison, normal testosterone levels for men ages 19 years and older are typically between 240–950 ng/dL. High levels of testosterone in females may indicate polycystic ovary syndrome (PCOS), adrenal tumors, ovarian tumors, or hermaphroditism (having both female and male sex organs).
The imbalance of the hypothalamic–pituitary–ovarian axis furthermore negatively affected the development and function of the reproductive system of female progeny . Data showed that DEHP induced the altered development of the primordial germ cells, germ cell survival, meiotic progression and increased follicle atresia . The US case-control study included 527 mothers of sons with testicular cancer and 562 mothers of controls aged 20–29.
On the other side, Brehm et al. noticed increased levels of estradiol in female CD mice after the prenatal exposure to DEHP at 20, 500, 750 mg/kg/day. For instance, Martinez-Arguelles et al. and Meltzer et al. observed that in female Sprague-Dawley rats, prenatal DEHP exposure at 300 mg/kg/day induced a decrease in estradiol levels. In contrast, some studies are showing that phthalates induced linear toxicity 176,181. Phthalates, like hormones, exert their physiological effects instead in low as in high doses. For instance, reproductive toxicity is related to the side chain length of phthalates.
Other male reproductive disorders related to phthalate exposure include dysfunctions of puberty. In vitro studies demonstrated that DEHP exposure at 40, 80 and 160 μM and dibutyl phthalate (DBP) exposure at 10 and 100 mg/L caused the apoptosis of TM3 Leydig cells and Sertoli cells of Male Sprague-Dawley rats, respectively 72,73. Estradiol and progesterone are essential hormones for postnatal female reproductive system development and to enable ovarian and menstrual cycle, pregnancy, and labor. In this review, we attempted to present an overview of the current knowledge concerning the phthalates’ effect on reproductive health at multiple levels. The aim of this review was to compile the evidence concerning the association between phthalates and reproductive diseases, phthalates-induced reproductive disorders, and their possible endocrine and intracellular mechanisms. Di-n-butyl phthalate (DnBP) is classified as an endocrine disruptor, negatively impacting testosterone levels in human males.
Phthalates alter cell proliferation and apoptosis via crosstalk between MAPK, NF-kB, PI3K/Akt, and NR. Phthalates modulate the activity of signaling pathways, such as MAPK, NF- κB, and PI3K/Akt, to delay apoptosis and stimulate cell proliferation. These activities could lead to prostate and ovarian cancer onset 110,201. DnBP induced cancer onset via the interaction with ER and the modulation of the MAPK signaling pathway . In the study by Giammona et al. , MEHP was administered orally to several rodent species and strains (1 g/kg to gld and B6 mice and Sprague-Dawley rats; 2 g/kg to Fisher rats). Maternal exposure to DEHP at 40 μg/kg inhibited the DNA methylation of Igf2r and Peg3 genes in F1 and F2 mouse oocytes . Depending on the number of generations affected by epigenetic influence, there are transgenerational or multigenerational effects .
Specifically, studies have argued that BAT provides a more accurate reflection of androgen status than total testosterone (55, 57). In other words, those with high exposure levels may not show the strongest associations or even associations in the same direction as those with lower concentrations of exposure. Another potential reason for the different associations by age are differences in the distribution of phthalate metabolite concentrations.
In vitro studies showed that DEHP exposure decreased as well as the increased expression of estrogen receptor 200,201. Similarly, in men with benign prostatic hyperplasia, estradiol levels, testosterone and steroidogenic enzymes aromatase, and 5α-reductase were increased . For example, Ha et al. observed that with the increasing dose of DEHP in Sprague-Dawley rats, levels of testosterone, FSH and LH decreased. For instance, Hannon et al. , showed that the exposure to DEHP at 10 µg/mL increased the levels of Cyp19a1, Hsd17b1 and exposure to DEHP at 100 µg/mL decreased levels of those enzymes in cultured mouse antral follicles. The dose of phthalates can also be the source of conflict in results. Phthalate diesters with a side chain length of C4-6, such as DEHP, DBP or BBzP, are able to interfere with reproductive health .
Postnatal exposure to BBzP in male Sprague-Dawley rats at 10 and 100 mg/kg/day increased the expression of Lhr . Postnatal exposure to DEHP in female Wistar rats at 10 mg/kg/day increased the expression of Fshr . Postnatal exposure to DEHP in female Wistar rats at and 1000 mg/kg/day increased the expression of Gnrhr 132,176. Phthalates can affect the HPG axis and steroidogenesis through interaction with genes for GPCRs—receptors for GnRH on pituitary cells, receptors for FSH and LH on Leydig cells, ovarian cells—granulosa and thecal cells.
In some instances, insurance may fully or partially cover the costs of in-person or at-home testosterone testing. There are at-home testing kits available online, but the results are best discussed with a healthcare provider. A healthcare provider can provide additional support on medical and natural treatments based on a person’s unique health problems. According to Dr. Gaither, certain nutrients, such as vitamin B, zinc, omega-3 fatty acids, magnesium, and protein, can naturally boost testosterone. It’s important to mention that some methods are similar to those mentioned for high testosterone treatment. Menopause is often the reason why women experience a change in their sex drive. A healthcare provider can develop a treatment plan that aims to lower ovarian or adrenal androgen production.

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