|
I would like to share some of my research regarding the results of a study release last May. On May 20, 2010, researchers from the Harvard School of Public Health presented their findings from a study exploring the possible relationship between the use of fertility drugs and autism spectrum disorder (ASD). The scientists reported to attendees at the International Meeting for Autism Research in Philadelphia that women who used fertility drugs to get pregnant had almost double the risk of having a child with ASD verses nonusers. The drugs studied included Clomid (clomiphene citrate) and Pergonal (gonadotropin).
This recent study is part of a growing body of research that strengthens the argument that Clomid and other fertility drugs are a cause of ASD via their ability to deny cholesterol to a developing embryo shortly after conception. About 58% of ASD children have low total cholesterol ([160 mg/dL) and about 19% have extremely low total cholesterol ([100 mg/dL). The average level for children is 165 mg/dL. It has also been observed that a high percentage of children (71-86%) born with Smith-Lemli-Opitz syndrome (SLOS), in addition to a wide array of birth defects are also born with ASD. Infants with SLOS are born with a defective enzyme that impairs the body’s ability to convert a precursor (7-dehydrocholesterol) to cholesterol. Cholesterol is essential for growth of the myelin membranes that cover the brain and abnormalities in the myelin sheath are believed to be a contributing cause of ASD. Many experts thus believe that low cholesterol during early embryonic development is one of the causes of ASD.
Clomid has a long half-life and is present during the embryonic period (first 8 weeks) even when taken before conception. Studies have shown it to be biologically active for up to 54 days after ingestion and that it can accumulate over successive cycles of treatment. In the Harvard study they found that the longer the use of fertility drugs, the higher the risk of developing ASD. A critically important fact – and one not known by most physicians prescribing the drug – is that Clomid is a cholesterol inhibitor and impairs its production by acting upon enzymes in the body similar to Lipitor and other statin drugs. Its chemical structure is also similar to the cholesterol-reducing drug, Triparanol, which was briefly available during the 1960s. Animal studies have shown that Clomid and Triparanol both act on the same enzyme and affect developing organs in a similar way, with Triparanol being slightly more potent.
Pergonal (also known as human menopausal gonadotropin or hMG) likewise reduces cholesterol, but by way of a different mechanism. Namely, it suppresses cholesterol levels in early pregnancy via its ability to elevate estrogen production. Studies have established that following hyperstimulation of the ovaries by Pergonal, the resulting elevated estrogen during the luteal (post-ovulation) phase of the cycle suppresses the level of total cholesterol. In fact, there is an inverse correlation between concentrations of estrogen and the level of total cholesterol – the higher the level of estrogen, the lower the concentration of total cholesterol.
The GOOD NEWS is that with the knowledge of HOW fertility drugs can negatively impact the human embryo, we can develop a means of eliminating or offsetting that risk. Animal studies have shown that cholesterol supplementation can offset the presence of birth defects in pregnant animals receiving a cholesterol-inhibiting drug, that would otherwise produce offspring with birth defects absent the supplementation. Thus, the key is maintaining the proper level of cholesterol throughout pregnancy when taking Clomid and other fertility drugs.
Everyone using fertility drugs is looking not only to have a baby, but also one who is healthy and normal. The path to seeing more and more healthy and normal babies can only occur only if we examine and analyze studies, such as the one out of Harvard, and explore ways to offset the risk factors.
Reply
|
