LH and Miscarriage

Elevated LH, FSH, estrogen, prolactin, DHEAS linked to recurrent miscarriage

FSH, estradiol, LH, prolactin and DHEAS concentrations were significantly higher in the unexplained recurrent miscarriage group than in the explained recurrent miscarriage group, although serum concentrations of all hormones were within the normal range.


Abnormal LH secretion found in 81% of women with recurrent miscarriage

Twenty-one women with recurrent early miscarriage and 10 multiparous (having had multiple children) controls were investigated; 81% of recurrent miscarriage and 10% control subjects had polycystic ovaries. Mean mid-follicular and mid-luteal serum LH and follicle stimulating hormone (FSH) levels were similar in both groups. 81% of women with recurrent miscarriage had either raised urinary LH excretion or a premature LH surge; 10% of control subjects had a premature LH surge. Total LH excretion during the cycle and mean follicular phase serum testosterone was significantly greater with early pregnancy loss than in the control group, the difference in LH being greatest in the early luteal phase. Urinary estrogen was raised in the early luteal phase of the cycle in the group with early miscarriage; there was no difference between the groups in progesterone excretion. These data demonstrate abnormalities in LH secretion in 81% of women with recurrent miscarriage. Inappropriately raised LH levels may have adverse effects on the developing oocyte or endometrium either directly, or indirectly by causing an elevation in testosterone and estrogen levels.


High LH found in 8% of women with unexplained recurrent miscarriage

Hypersecretion of luteinising hormone or ultrasonographic features of polycystic ovarian disease was present in 8% and 7.8% of women with unexplained recurrent miscarriage, respectively. The free androgen index was elevated in 14.6% of subjects. In the mid-luteal phase, low progesterone level was found in 17.4% and delayed endometrial development was noted in 27.1% of women. Although women with recurrent miscarriage women and delayed endometrium had significantly lower progesterone levels than those with normal endometrial development, only 8/24 had mid-luteal progesterone levels below 30 nmol/L. Recurrent miscarriage was not associated with hyperprolactinaemia or abnormal thyroid function test. CONCLUSIONS: Endocrinological and endometrial abnormalities are present in about a quarter of women with unexplained recurrent miscarriage.


LH is higher in unexplained miscarriage

Serum levels of superoxide dismutase, catalase, LH, FSH as well as TNF-alpha in serum and the expression of TNF-alpha positive cells in placental tissues, were assayed in women suffering from unexplained first trimester miscarriage. Two groups were included, the first was represented by 16 women with unexplained first trimester miscarriage (number of miscarriages: 3-5) and the second one included 24 women with unexplained first trimester miscarriage (number of miscarriages > 5). The control groups included 20 women within their first trimester of pregnancy and 20 non pregnant healthy females within their follicular phase. The obtained results showed a highly significant decrease in serum levels of superoxide dismutase and catalase, in the unexplained first trimester miscarriage groups compared to control groups. Higher serum levels of TNF-alpha were detected in unexplained first trimester miscarriage groups compared to control groups. A significant increase in serum levels of LH was encountered between unexplained first trimester miscarriage groups compared to control groups; on the other hand the mean levels of FSH expressed no significant changes among unexplained first trimester miscarriage groups as compared to first trimester pregnancies control group. A positive correlation was noticed between serum levels of TNF-alpha and the levels of LH. We conclude that antioxidant enzymes (catalase, superoxide dismutase), TNF-alpha, LH and FSH may play a major role in the pathogenesis of unexplained first trimester miscarriage.


High LH disturbs fertility, increases risk of miscarriage, due to premature egg maturation

High tonic serum concentrations of luteinizing hormone (LH) in the follicular phase, frequently witnessed in PCOS, have been associated with decreased reproductive function. Impaired rates of fertilization, conception and miscarriage are obtained when LH levels are high before oocytes are collected, during ovulation induction or in women with regular cycles. Conversely, treatment that decreases LH concentrations, such as GnRH analogue or laparoscopic ovarian puncture, eases induction of ovulation and pregnancy and improves miscarriage rates. Tonic hypersecretion of LH appears to induce premature oocyte maturation, causing the problems with fertilization and miscarriage.

http://www.ncbi.nlm.nih.gov/pMenstrual Cycle and Miscarriageubmed/10627767

LH is increased in women with recurrent miscarriage

A total of 31 women suffering from habitual miscarriage have been examined when not pregnant. Both increased and normal prolactin levels were recorded. In hyperprolactinemia the level of the luteinizing hormone (LH) secretion was high and no ovulatory peaks were detected, whereas in normal prolactin secretion the level of LH was moderately increased during all phases of the menstrual cycle. Secretion of follicle-stimulating hormone was normal in both groups. Sex steroid secretion was disturbed.


Medical intervention to lower LH does not improve miscarriage rate

106 women with a history of three or more consecutive first trimester miscarriages, polycystic ovaries, and hypersecretion of luteinising hormone were studied. Women were randomised before conception to receive pituitary suppression with a luteinising hormone releasing hormone analogue followed by low dose ovulation induction and luteal phase progesterone (group 1) or were allowed to ovulate spontaneously and then given luteal phase progesterone alone or luteal phase placebo alone (group 2). No drugs were prescribed in pregnancy. Conception rates in the pituitary suppression and luteal phase support groups over six cycles were 80% and 82%respectively. Live birth rates were 65% and 76% respectively. In the luteal phase support group there was no difference in the outcome of pregnancy between women given progesterone and those given placebo pessaries. Live birth rates from an intention to treat analysis were 52% in the group given pituitary suppression and 63% in the controls. CONCLUSIONS: Prepregnancy suppression of high luteinising hormone concentrations in ovulatory women with recurrent miscarriage and hypersecretion of luteinising hormone does not improve the outcome of pregnancy. The outcome of pregnancy without pituitary suppression is excellent.


For a concise list of qualities found to affect one's risk of miscarriage, see: Causes of Miscarriage

How to lower LH levels

LH levels are dependent on insulin sensitivity

The decrease in LH concentrations is inversely related to the severity of insulin resistance. It is possible that the decrease in LH secretion with weight reduction is more dependent on the absolute levels of insulin sensitivity than on the degree of general adiposity.


Insulin increases LH

Hyperinsulinemia increases GNRH pulse activity leading to disorderly LH and FSH activity, as seen in Polycystic ovary syndrome (PCOS).


Weight loss in infertile, overweight women lowers LH, insulin, testosterone, boosts SHBG

We studied follicular phase LH and FSH secretion and glucose metabolism before and after weight reduction in 10 severely overweight infertility patients. A 6-week very low calorie diet was followed by a 4-week normocaloric period. We observed a decrease of 8% in percent body fat mass and a 5% reduction in waist to hip ratio. Mean LH decreased by 45%, whereas mean FSH remained unchanged. Insulin-stimulated glucose uptake increased by 41%, which was accounted for by a significant increase in nonoxidative glucose disposal. Serum sex hormone-binding globulin concentrations increased by 39%, and insulin-like growth factor (IGF)-binding protein-1 (IGFBP-1) levels increased by 46%. Fasting serum insulin concentrations decreased by 38%, those of leptin by 37%, those of androstenedione by 32%, those of testosterone by 20%, and those of dehydroepiandrosterone sulfate by 13%. The percent change in LH correlated negatively with glucose uptake and the increase in serum sex hormone-binding globulin and positively with the percent change in waist to hip ratio . The absolute LH levels after weight reduction correlated significantly with fasting insulin concentrations and negatively with glucose uptake. Our findings suggest that weight reduction with a very low calorie diet results in a decrease in LH concentrations, a reduction in the LH/FSH ratio, and FSH predominance favoring folliculogenesis.


Soy decreases LH, FSH, estrogen, free T3 and DHEAS

Isoflavones were consumed in soy protein powders and provided relative to body weight (control diet, 10 +/- 1.1; low isoflavone diet, 64 +/- 9.2; high isoflavone diet, 128 +/- 16 mg/day) for three menstrual cycles plus 9 days in a randomized cross-over design. During the last 6 weeks of each diet period, plasma was collected every other day for analysis of estrogens, progesterone, LH, and FSH. Diet effects were assessed during each of four distinctly defined menstrual cycle phases. Plasma from the early follicular phase was analyzed for androgens, cortisol, thyroid hormones, insulin, prolactin, and sex hormone-binding globulin. The low isoflavone diet decreased LH and FSH levels during the periovulatory phase. The high isoflavone diet decreased free T3 and dehydroepiandrosterone sulfate levels during the early follicular phase and estrone levels during the midfollicular phase. No other significant changes were observed in hormone concentrations or in the length of the menstrual cycle, follicular phase, or luteal phase.


Vitex increases progesterone and estrogen, lowers LH and prolactin

Vitex induced significant increase in the uterine weight of ovariectomized rats at two dose levels comparable to that of control group. Significant increases in plasma progesterone and total estrogens levels were shown at the two dose levels when compared to that of control group. On the other side, the extract induced significant reduction in luteinizing and plasma prolactin hormones.


Myo-inositol lowers LH, testosterone, and insulin resisitance

After 3 months of myo-inositol administration, plasma LH, testosterone, free testosterone, insulin and insulin resistance index resulted significantly reduced; no significant changes were observed in plasma FSH and androstenedione levels.


Low Vitamin D impairs egg production, elevates LH and FSH

Vitamin D deficiency caused uterine hypoplasia and impaired folliculogenesis in mice. Elevated serum levels of LH and FSH revealed hypergonadotropic hypogonadism in these mice.


6 weeks of exercise lowered LH

Free testosterone showed a decreasing trend of 19-25% with 6 weeks of training on 6 days a week in recreational athletes. Cortisol release was reduced, follicle-stimulating hormone (FSH)-synthesis-secretion capacity was increased after training, and the luteinizing hormone (LH)-synthesis-secretion capacity reduced.


LH Information

High LH found in fibrocystic breast sufferers

LH levels in fibrocystic disease and fibroadenoma groups were significantly increased.


LH rises with increasing age

Among U.S. women aged 35-60 years, median FSH and LH levels began to increase for women in their late 40s and reached a plateau for women in their early 50s.


High testosterone is caused by high LH

PCOS develops when the ovaries overproduce androgens (eg, testosterone). Androgen overproduction often results from overproduction of LH (luteinizing hormone), which is produced by the pituitary gland.


LH triggers the production of androgens which can then be used to create estrogen

Luteinizing hormone (LH) is essential to provide the androgen substrate for estrogen synthesis, which in turn contributes to oocyte maturation and may play a relevant role in optimizing fertilization and embryo quality.


LH raises testosterone, FSH raises estrogen

In the ovaries, LH acts on theca and interstitial cells to produce progestins and androgens, and FSH acts on granulosa cells to stimulate aromatization of these precursor steroids to estrogen.


GnRH and estrogen stimulate LH release

As progesterone decreases, GnRH rises and causes stimulation of LH and FSH. FSH causes maturation of follicles past the antral stage. The dominant follicle establishes itself and is the main follicle that grows. The growing follicle produces estrogen in the granulosa cells. Estrogen actually peaks before ovulation and it is the estrogen that causes the final LH release.

Other topics covered under Hormones:

Adiponectin, Estrogen, FSH, GnRH, LH, PCOS, Progesterone, Prolactin, SHBG, Testosterone