I’ve had elevated LH for at least a decade (LH always above top of normal range). I asked my urologist what the long term health impact would be if I continued to have high LH. He said “nothing”. Wow.
I’m making a list of potential negative health effects due to chronically elevated LH. Please post if you know of any that I miss, or if you have references in addition to the ones I list below.
Leydig cell desensitization
“Hormones and their actions”, Volume 18, Part 2 By Brian A. Cooke, Roger John Benjamin King, H. J. van der Molen
Several reports indicate that LH induced desensitization can be reversed. Reversal of LH-induced desensitization of adenylate cyclase in testis Leydig cells has been found to be dependent on the time and concentration of LH used [78]; at low phys- iological concentrations of LH the desensitization was completely reversed during incubation of cells for 2 h in the absence of further hormone. With higher concen- trations of LH however, the cells remained unresponsive to further challenges with the hormone over the same time period.
Early onset Alzheimer disease
“Dysregulation of the Hypothalamic-Pituitary-Gonadal Axis with Menopause and Andropause Promotes Neurodegenerative Senescence”, Atwood et al., J Neuropathol Exp Neurol, 2005 (http://p973.ccmu.edu.cn/4-zuixinjinzhan/1/7.pdf )
LH is known to cross the blood-brain barrier and LH receptors are expressed in the brain with the highest expression in brain regions susceptible to AD neuropathology (71). In addition, pyramidal neurons contain intracytoplasmic LH and pyramidal neurons in AD brains contain significantly greater amounts than age-matched controls (71). Further evidence that gonadotropins may play a role in AD is found with studies from individuals with DS who have elevated serum concen- trations of gonadotropins throughout life and develop AD-like neuropathology if they live into the fourth decade (72). In sharp contrast to the general population, males with DS de- velop these neuropathologic changes earlier and more often than their female counterparts. The reversal in gender predilec- tion cannot be explained on the basis of sex steroid concen- trations since there is no difference between DS individuals and the general population. However, the increase in gonado- tropin concentrations is more pronounced and occurs at an earlier age in DS males than in DS females (64).
Of interest: “Can regulating LH halt Alzheimers?” http://alzheimersweekly.com/content/can-regulating-lh-halt-alzheimers
Also: http://www.curaxispharma.com/index.php?option=com_content&view=article&id=22&Itemid=29
Testicular and Adrenal cancer
“High levels of luteinizing hormone analog stimulate gonadal and adrenal tumorigenesis in mice transgenic for the mouse inhibin-alpha-subunit promoter/Simian virus 40 T-antigen fusion gene”, Mikola et al., Oncogene (2003) 22, 3269â??3278. High levels of luteinizing hormone analog stimulate gonadal and adrenal tumorigenesis in mice transgenic for the mouse inhibin-α-subunit promoter/Simian virus 40 T-antigen fusion gene | Oncogene
The gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), are the main regulators of gonadal differentiation, growth and steroidogenesis. It is therefore to be expected that they are involved in the appearance and/or maintenance of gonadal tumors. Among human gonadal malignancies, ovarian tumors are the commonest, with the poorest prognosis. In attempts to improve the diagnostics and treatment of ovarian cancers, it is essential to learn more about their pathogenesis, including the regulation of their aggressive growth and invasion, and to develop better predictive markers. It has often been suggested that LH could promote the development of certain types of ovarian and testicular cancer. This is supported by epidemiological findings showing an increased incidence of ovarian cancer after menopause, when circulating gonadotropin levels are elevated (Wise et al., 1996). There are also data showing that ovarian stimulation with gonadotropins is associated with an increased incidence of granulosa cell tumors (Willemsen et al., 1993). In addition, certain activating mutations of the LH receptor (LHR) gene have been shown to cause Leydig cell tumors in humans (Liu et al., 1999), while the results of in vitro studies have demonstrated that LH and FSH can stimulate the growth of human ovarian carcinoma cells (Simon et al., 1983; Wimalasena et al., 1992).
Elevated estradiol (and follow-on health effects of elevated estradiol)
“Acute stimulation of aromatization in Leydig cells by human chorionic gonadotropin in vitro”, Valladares and Payne, Proc. Nat. Acad. Sci., 1979. http://www.pnas.org/content/76/9/4460.full.pdf
The data presented in this report unequivocally demonstrate that Leydig cells from mature rats have the capacity to aromatize testosterone to estradiol. Furthermore, hCG acutely stimulates aromatization in purified Leydig cells. HCG stimulation of estradiol production from testosterone was demonstrated with saturating concentrations of testosterone. This observation indicates that the effect of hCG is on stimulation of the aromatase enzyme(s) and is not due to increased production of testosterone, the substrate for aromatase.
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This is a good idea for a thread. I think if we have knowledgeable people help build it, we can get it stickeyed eventually.
I would like to eventually add a discussion on WHY your LH can be chronically elevated, and things to do to both diagnose and correct that issue.
Work in progress.