N-Acetyl Cysteine

600 mg N-Acetyl cysteine boosts the chances of pregnancy continuing past 20 weeks by 190%

Pregnancy could be associated with a state of oxidative stress that could initiate and propagate a cascade of changes that may lead to miscarriage. This process of oxidative stress may be suppressed by the antioxidant effect of N-acetyl cysteine. The current study aimed to evaluate the effect of N-acetyl cysteine therapy in patients diagnosed with unexplained recurrent miscarriage. A group of patients with history of recurrent unexplained miscarriage were treated with N-acetyl cysteine 0.6 g + folic acid 500 microg/day and compared with an aged-matched group of patients treated with folic acid 500 microg/day alone. N-acetyl cysteine + folic acid compared with folic acid alone caused a significantly increased rate of continuation of a living pregnancy up to and beyond 20 weeks (odds ratio = 2.9). N-acetyl cysteine + folic acid was associated with a significant increase in the take-home baby rate as compared with folic acid alone (odds ratio = 1.98). In conclusion, N-acetyl cysteine is a well-tolerated drug that could be a potentially effective treatment in patients with unexplained recurrent miscarriage.

N-acetyl cysteine boosts pregnancy rates by 40% and lowers miscarriage odds by 60% in PCOS women

Patients with clomiphene citrate-resistant PCOS who underwent unilateral ovarian drilling were assigned randomly to receive either N-acetyl cysteine 1.2 g/d or placebo for 5 days starting at day 3 of the cycle for 12 consecutive cycles. A significant increase in both ovulation and pregnancy rates was observed in the N-acetyl cysteine group, compared with placebo [87% versus 67% (odds ratio = 1.3) and 77% versus 57% (odds ratio 1.4), respectively]. Moreover, miscarriage rates were significantly lower and live birth rates were significantly higher in the N-acetyl cysteine group [8.7% versus 23.5% (odds ratio 0.4) and 67% versus 40% (odds ratio 1.7), respectively]. In conclusion, N-acetyl cysteine is a novel adjuvant therapy after laparoscopic ovarian drilling for clomiphene citrate-resistant women with polycystic ovary syndrome (PCOS) which might help improve overall reproductive outcome.

N-acetyl cysteine boosts ovulation, progesterone and endometrial thickness in PCOS women

Patients had clomiphene citrate tablets alone or with N-acetyl cysteine 1,200 mg/day orally for 5 days starting on day 3 of the menstrual cycle. RESULTS: Ovulation rate improved significantly after the addition of N-acetyl cysteine (17.9% versus 52.1%). Although the number of mature follicles was more in the N-acetyl cysteine group (2.1 versus 3.2), the difference was not statistically significant. The mean estrogen levels at the time of human chorionic gonadotropine injection, serum progesterone levels on days 21-23 of the cycle, and the endometrial thickness were significantly improved in the N-acetyl cysteine group. CONCLUSION: N-Acetyl cysteine is proved effective in inducing or augmenting ovulation in polycystic ovary patients.

N-acetyl cysteine boosts ovulation rate from 1% to 49% in PCOS women

The patients were assigned randomly to receive either N-acetyl cysteine 1.2 g/d or placebo with clomiphene citrate for 5 days starting at day 3 of the cycle. RESULTS: Combination of clomiphene citrate and N-acetyl cysteine significantly increased both ovulation rate and pregnancy rate in women with clomiphene citrate-resistant PCOS (49.3% vs. 1.3% and 21.3% vs. 0%, respectively). No cases of ovarian hyperstimulation syndrome were reported in the N-acetyl cysteine group; two cases of miscarriage (12.5%) were reported. CONCLUSION(S): The N-acetyl cysteine as an adjuvant to clomiphene citrate was more effective than placebo for clomiphene citrate-resistant patients with PCOS. It is safe and well tolerated.

N-acetyl cysteine does not offer any additional benefit to clomid treatment

Patients in the study group were treated with clomiphene citrate (50-mg tablets) twice per day and with N-acetyl cysteine (1,200 mg/d orally) for 5 days starting on day 2 of the cycle. Patients in the control group were treated with clomiphene citrate with sugar powder. RESULT(S): There were no statistically significant differences between the two groups in the number of follicles sized >18 mm, mean estrogen levels, serum progesterone, or endometrial thickness. Pregnancy rate was comparable in both groups (22.2% vs. 27%). Miscarriage rate was comparable in both groups (6.7% in the study group vs. 7.4% in the control group). CONCLUSION(S): N-Acetyl cysteine is ineffective in inducing or augmenting ovulation in patients with unexplained infertility and cannot be recommended as an adjuvant to clomiphene citrate in such patients.

N-acetyl cysteine does not significantly improve pregnancy rate in women with male factor infertility

Women undergoing intracytoplasmic sperm injection cycles due to male factor infertility were randomly assigned to receive either long protocol or long protocol plus N-acetyl cysteine. Clinical pregnancy was the primary outcome. Clinical pregnancy rate was insignificantly higher in N-acetyl cysteine group (52.6%) than control (47.4%).

N-acetyl cysteine protects pregnancy from maternal inflammation

Maternal infection or inflammation may induce fetal inflammatory responses and potentially fetal brain injury. We sought to determine whether prophylactic n-acetylcysteine, a known antiinflammatory, may modulate the fetal cytokine response to maternal lipopolysaccharide (an endotoxin injected to create a strong immune response). N-acetyl cysteine before lipopolysaccharide injection significantly reduced the fetal IL-6 and IL-1 beta response. Fetal IL-10 was not attenuated by any treatment. N-acetyl cysteine attenuated both maternal pro- and antiinflammatory responses to lipopolysaccharide injection. CONCLUSION: Maternal N-acetyl cysteine suppressed fetal and maternal inflammatory responses to maternal lipopolysaccharide injection. These results suggest that prophylactic N-acetyl cysteine may protect the fetus from maternal inflammation.

Glutathione peroxidase is lower in women who miscarry

Red cell and plasma glutathione peroxidase activities of women who had had a miscarriage were significantly lower than in both normal pregnancies and the control group (n-acetyl cysteine is a precursor to glutathione peroxidase). The decreased activities of the antioxidant enzymes, red cell and plasma glutathione peroxidase, may play an important role in the aetrology of miscarriage.

N-acetyl cysteine reduces mercury levels in woman and fetus

Many people, by means of consumption of seafood or other anthropogenic sources, are exposed to levels of methylmercury that are generally considered to be quite low, but that may nevertheless produce irreversible brain damage, particularly in unborn babies. Because N-acetyl cysteine is effective at enhancing methylmercury excretion when given either orally or intravenously, can decrease brain and fetal levels of methylmercury, has minimal side effects, and is widely available in clinical settings, N-acetyl cysteine should be evaluated as a potential antidote in humans.

N-acetyl cysteine prevents heart disease in offspring induced by maternal low protein diet

A maternal low protein diet throughout gestation significantly impairs recovery of the 6-month-old adult rat heart to myocardial ischaemia-reperfusion-induced injury. Undernutrition during development may increase susceptibility to coronary hard disease by impairing recovery from coronary events. Pre-treatment with N-acetyl cysteine prevented this impairment of recovery in maternal low protein male offspring and improved recovery in all females. Myocardial infarct size was not different between dietary groups after ischaemia-reperfusion, but N-acetyl cysteine pre-treatment significantly reduced the degree of infarction.

N-acetyl cysteine helps prevent diabetes induced birth defects and miscarriage

We found decreased Bcl-2, increased Bax and cleaved Caspase 3 proteins in embryos from diabetic rats. Moreover, we found increased activation of Caspase 3 in cells from embryos previously exposed to a diabetes-like environment (in vivo, in vitro) compared to cells from control embryos, which was normalized by supplementation of N-acetylcysteine or apoptosis inhibitor. Additionally, we found increased dysmorphogenesis in embryos exposed to a diabetic environment in vivo and in vitro. Exposure to a diabetic milieu during organogenesis increases apoptosis in embryonic cells and dysmorphogenesis in embryos. Enhanced apoptotic rate may have a role in diabetic embryopathy by inducing disturbed embryonic maturation, increased rates of resorptions and congenital malformations.

Taking N-acetyl cysteine before infection protects fetus; N-acetyl cysteine after onset hurts

The present study investigated the effects of N-acetyl cysteine on lipopolysaccharide injection-induced (injection creates the same inflammatory effect of infection) intrauterine fetal death and intrauterine growth restriction. Results showed that pretreatment with N-acetyl cysteine significantly alleviated LPS-induced fetal mortality and reversed lipopolysaccharide injection-induced growth and skeletal development retardation. By contrast to pretreatment, when administered after lipopolysaccharide injection, N-acetyl cysteine did not protect against lipopolysaccharide injection-induced intrauterine fetal death and intrauterine growth restriction and in fact aggravated lipopolysaccharide injection-induced preterm labor. Pretreatment with N-acetyl cysteine improves fetal survival and reverses lipopolysaccharide injection-induced fetal growth and skeletal development retardation, whereas posttreatment with N-acetyl cysteine aggravates lipopolysaccharide injection-induced preterm labor.

N-acetyl cysteine helps protect placenta from high homocysteine levels

Hyperhomocystinemia is a thrombophilic condition associated with placental dysfunction. Homocysteine-thiolactone induced a concentration dependent increase in total cell death and death by apoptosis, compared with control. Vitamin C ameliorated apoptosis in cytotrophoblasts, whereas N-acetylcysteine ameliorated cell death in syncytiotrophoblasts. CONCLUSION: Homocysteine-thiolactone enhances apoptosis in cultured human trophoblast, and the effect can be limited by antioxidants.

N-acetyl cysteine reduces incidence of birth defects caused by maternal consumption of alcohol

In the present study, the hypothesis that coadministration of N-acetyl cysteine and ethanol by means of liquid diet on days 7 and 8 of pregnancy in mice would reduce ethanol's teratogenicity was tested. Although the lower dosage of N-acetyl cysteine (300 mg/kg) resulted in a decrease in the incidence of ocular defects in both the left and right eyes, this reduction was not statistically significant. However, doubling the N-acetyl cysteine concentration did yield a significant change; as compared with the group treated with ethanol alone, the incidence of ocular abnormalities was diminished by 22%. These results show the potential of an orally administered compound with proven clinical efficacy to reduce ethanol's teratogenic effects and support the premise that oxidative damage plays an important mechanistic role in fetal alcohol spectrum disorders.

1000 mg N-acetyl cysteine per kilogram of body weight per day causes infertility

The toxic effects of i.v. administration of N-acetyl-cysteine, a component of parenteral nutrition solutions, on fertility and embryonic development were investigated in male and female rats at doses of 100, 300, and 1000 mg kg-1 day-1. Infertility was observed in females in the 1000-mg/kg group (equivalent to 54,000 mg /day for a 120 lb woman) throughout the period from before mating to embryogenesis. No effect of N-acetyl-cysteine on the reproductive ability of the male rats was seen.

N-acetyl cysteine does not cause birth defects in rats or rabbits

With regard to the reproductive and developmental toxicity of orally administered N-acetyl-cysteine, Bonanomi and Gazzaniga
reported that no effects were observed in a male rat fertility study at daily doses of 250–1000 mg/kg, in a rat teratogenicity study at daily doses of 500–2000 mg/kg, in a rabbit teratogenicity study at daily doses of 250–1000 mg/kg, and in a rat peri- and postnatal study at daily doses of 250–1000 mg/kg. Johnston et al. also reported that oral administration at a dose of 500 mg/kg/day from
Gestational Day (GD) 6 to GD16 showed no teratogenic effects in the rabbit. Thus, a number of studies have examined the reproductive and developmental toxicity of orally administered N-acetyl-cysteine.

1.8g N-Acetyl cysteine improves insulin resistance and lowers testosterone in PCOS subjects

Patients were treated for 5-6 weeks with N-acetyl cysteine at a dose of 1.8 g/day orally. A dose of 3 g/day was arbitrarily chosen for massively obese subjects. Six of 31 obese patients with PCOS were treated with placebo and served as controls. Fasting glucose, fasting insulin, and glucose area under curve were unchanged after treatment. Insulin area under curve after oral glucose tolerance test was significantly reduced, and the peripheral insulin sensitivity increased after N-acetyl cysteine administration, whereas the hepatic insulin extraction was unaffected. The N-acetyl cysteine treatment induced a significant fall in testosterone levels and in free androgen index values. In analyzing patients according to their insulinemic response to oral glucose tolerance test, normoinsulinemic subjects and placebo-treated patients did not show any modification of the above parameters, whereas a significant improvement was observed in hyperinsulinemic subjects. CONCLUSION(S): N-acetyl cysteine may be a new treatment for the improvement of insulin circulating levels and insulin sensitivity in hyperinsulinemic patients with polycystic ovary syndrome.

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