She did experience one side effect: diarrhea, which is also something she experiences when she takes magnesium. The diarrhea is annoying enough that she is only going to take molybdenum when a migraine is coming on, but the molybdenum definitely helped her. If magnesium and molybdenum are supporting her body in turning sulfite into sulfate by facilitating suddenly higher levels of sulfite oxidase activity, diarrhea is exactly what one would expect to see, for there is anecdotal evidence that a sudden increase in sulfates in drinking water can trigger diarrhea and a 2012 study connected copper sulfate with diarrhea (https://www.ncbi.nlm.nih.gov/pubmed/22687538).
I've written to researchers in the field of migraines about sulfite possibly being a cause of migraine headaches, but the ones I contacted either ignored my emails or did not take seriously the possibility that sulfite could be involved. That is unfortunate, for there are many recently published research articles about how hydrogen sulfide, a precursor of sulfite, is made in the brain. I'll list a few here:
- https://www.ncbi.nlm.nih.gov/pubmed/20149843: "In conclusion, H(2)S exerts a protective effect against cerebral hypoxia induced neuronal cell death via K(ATP)/PKC/ERK1/2/Hsp90 pathway. Our findings emphasize the important neuroprotective role of H(2)S in the brain during cerebral hypoxia."
- https://www.ncbi.nlm.nih.gov/pubmed/12392053: Hydrogen sulfide as a neuromodulator.
- https://www.ncbi.nlm.nih.gov/pubmed/25747482: "We as well as others have also shown that H2S has antioxidant, antiapoptotic, and anti-inflammatory properties against various neurodegenerative disorders such as stroke, Alzheimer's disease, and vascular dementia."
- https://www.ncbi.nlm.nih.gov/pubmed/26019015: "During transsulfuration pathways, Hcy is metabolized into hydrogen sulfide (H2S), which is a synaptic modulator, as well as a neuro-protective agent."
- https://www.ncbi.nlm.nih.gov/pubmed/18754702: "Hydrogen sulfide (H2S) is recognized as a neuromodulator as well as neuroprotectant in the brain. H2S can be produced from cysteine by enzymes such as cystathionine beta-synthase. However, a mechanism for releasing H2S under physiologic conditions has not been identified. Here we show that H2S is released from bound sulfur, an intracellular store of sulfur, in neurons and astrocytes of mice and rats in the presence of physiologic concentrations of endogenous reducing substances glutathione and cysteine. The highest pH to release H2S from another sulfur store, acid-labile sulfur, which is localized mainly in mitochondria, is 5.4. Because mitochondria are not in the acidic condition, acid-labile sulfur may not be a physiologic source of H2S. Free H2S is immediately absorbed and stored as bound sulfur. Our novel method, using silver particles to measure free H2S, shows that free H2S is maintained at a low level in basal conditions. Alkalinization of the cytoplasm is required for effective release of H2S from bound sulfur, and this condition is achieved in astrocytes by the high concentrations of extracellular K+ that are normally present when nearby neurons are excited."
- https://www.ncbi.nlm.nih.gov/pubmed/24800864: "Hydrogen sulfide (H2S) has been recognized as a signaling molecule as well as a cytoprotectant. It modulates neurotransmission, regulates vascular tone, and protects various tissues and organs, including neurons, the heart, and kidneys, from oxidative stress and ischemia-reperfusion injury."
- https://www.ncbi.nlm.nih.gov/pubmed/24466346: "Hydrogen sulfide (H2S), a novel gaseous mediator, has been recognized as an important neuromodulator and neuroprotective agent in the central nervous system. The present study was undertaken to study the effects of exogenous H2S on traumatic brain injury (TBI) and the underlying mechanisms. The effects of exogenous H2S on TBI were examined by using measurement of brain edema, behavior assessment, propidium iodide (PI) staining, and Western blotting, respectively. Compared to TBI groups, H2S pretreatment had reduced brain edema, improved motor performance and ameliorated performance in Morris water maze test after TBI. Immunoblotting results showed that H2S pretreatment reversed TBI-induced cleavage of caspase-3 and decline of Bcl-2, suppressed LC3-II, Beclin-1 and Vps34 activation and maintained p62 level in injured cortex and hippocampus post TBI. The results suggest a protective effect and therapeutic potential of H2S in the treatment of brain injury and the protective effect against TBI may be associated with regulating apoptosis and autophagy."
- https://www.ncbi.nlm.nih.gov/pubmed/26111628: "Endogenous production of H2S in the brain was significantly inhibited by SAH. The protein levels of the predominant H2S-generating enzymes in the brain, including cystathionineb-synthase (CBS) and 3-mercaptopyruvate sulfur transferase (3MST), were also correspondingly reduced by SAH, while treatment with NaHS restored H2S production and the expressions of CBS and 3MST. More importantly, NaHS treatment could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, braincell apoptosis, inflammatory response, and cerebral vasospasm) after SAH. In vitro, H2S protects neurons and endothelial function by functioning as an antioxidant and antiapoptotic mediator. "
- https://www.ncbi.nlm.nih.gov/pubmed/25388401: "The current study indicates that H2S may function as an effective neuromodulator to regulate striatal neurotransmission and provides insight into the potential of H2S for PD therapy."
- https://www.ncbi.nlm.nih.gov/pubmed/24643521: "Hydrogen sulfide (H(2)S), a well-known toxic gas, is regarded as endogenous neuromodulator and plays multiple roles in the central nervous system under physiological and pathological states, especially in secondary neuronal injury. Recent studies have shown relatively high concentrations of hydrogen sulfide (H(2)S) in the brain and also cytoprotective effects of endogenous and exogenous H(2)S in models of in vitro and in vivo ischemic injury. H(2)S protects neurons by functioning as an anti-oxidant, anti-inflammatory, and anti-apoptotic mediator and by improving neurological function. Moreover, it protects neurons from glutamate toxicity."
Moreover, we know that when someone becomes deficient in molybdenum, headaches are one of the symptoms of that deficiency (http://ncp.sagepub.com/content/8/6/277.abstract). Also, we now know that sulfite oxidase deficiency affects the brain starting in the cerebral cortex and striatum (https://www.ncbi.nlm.nih.gov/pubmed/27523630). The cerebral cortex appears associated with migraine onset (https://www.ncbi.nlm.nih.gov/pubmed/24042483) and exhibits abnormalities in migraine patients (https://www.ncbi.nlm.nih.gov/pubmed/23533286).
If any readers of this blog know a physician, medical researcher, naturopath, nutritionist, or chiropractor who would be interested in looking into a sulfite connection to migraines, please tell them about this possibility. Testing molybdenum supplements for migraine alleviation is much less controversial than testing it (or any supplement) on patients with nausea and vomiting of pregnancy, for no one wants to take the tiniest chance of harming a developing fetus (which is as it should be).