Thursday, November 30, 2017

Update on "Report on molybdenum and a currently circulating GI virus" and a little complaining about an unrelated subject

Here we are six days later, and no one else in the family has thrown up since my kindergartner awakened me in the wee hours of Thanksgiving Eve, as reported below. After she threw up, I pre-dosed everyone with 500-1000 mcg of powdered molybdenum glycinate and some zinc, including the toddler, who shares a bedroom with the kindergartner. My father-in-law (a retired engineer, so someone who likes things proven to him), my 13-year-old, my 10-year-old, and I all experienced some stomach cramping/pain at different times over the Thanksgiving holiday, so we took extra molybdenum when it happened. Everyone recovered quickly, and no one else ever threw up.

I think this is a big deal. I stumbled on a highly effective nausea preventive that doesn't appear to have any side effects. It saved my Thanksgiving get-together, too.

But how do I tell more people? I'm merely a lawyer who likes to research things more interesting than subject matter jurisdiction. (I'm putting off writing a short brief on that subject right now, in fact. Why can't people just file certified copies when the statute says to do so? Grumble, grumble.) My discovery about molybdenum helping with nausea needs to be investigated by people with the proper background. Unfortunately, there is little profit motive for anyone to research this with expensive trials, for molybdenum is found in inexpensive foods: lentils and other legumes, barley, oats, etc.

I do "cold emails" to academic researchers about molybdenum sometimes after finding out about yet another success from a friend* or relative (I give them bottles of molybdenum to have on hand for when nausea or a migraine strikes), but I rarely receive responses to those emails. Are the emails just going into researchers' spam folders along with invitations to fake conferences? Is the idea of a "cure for nausea" just too snake-oil sounding? Is it that too many people don't know anything about molybdenum's role in the human body and aren't willing to do a quick internet search before discarding my email? I don't know. It's discouraging to not know how to get the word out. Sure, some local people and family members are being helped right now, but that's a speck of sand compared to the global population. It's not enough that I'm being "passed over" by the destroying angel of nausea and vomiting; I want other people to benefit, too. My inability to "sell" an idea so easy to test is a downside of my introversion and lack of entrepreneurship. And it's a big inability--my medical-school-trained brothers basically dismiss me as a crackpot, which I do not enjoy. If it's not a published trial, they do not want to hear it, much less try it.

Yet how do I stop saying molybdenum works when I repeatedly observe its effectiveness at helping with nausea and migraine? Like Galileo, my observations render me unable to change my story. :) "And yet it works."

* A few days ago, a nurse friend of mine told me that a pregnant friend of hers had been experiencing "morning sickness" a while back. My friend loaned her a bottle of molybdenum, which she took for a week. The pregnant woman reported that her morning sickness went away. Unfortunately, I don't know what dose she took or what she weighed. But I'm happy it seems to have helped her!

(Disclaimer: I do not prescribe the use of pharmaceutical drugs in any way. I am not a physician, and I reject out of hand any attempt to hold me liable for what boils down to a discussion of food. Any use of a molybdenum supplement should be prudent and guided by the tested tolerable upper intake levels for its usage (see http://lpi.oregonstate.edu/mic/minerals/molybdenum for those limits). Any use of an isolated molybdenum supplement during pregnancy should be under the direction of a medical professional as such supplements have apparently not been tested during pregnancy.)

Friday, November 24, 2017

Report on molybdenum and a currently circulating GI virus

Wednesday morning at about 3 am, my five-year-old came to my room saying, "Mommy, my tummy really hurts." I invited her to snuggle in bed with me, hoping that she was just cold and would fall asleep with me. I was probably in groggy denial. About two minutes later, she started to vomit, so I grabbed her to me and got her to the bathroom, where she vomited in the toilet and then had a severe bout of diarrhea. Within just a few minutes she went from normal to looking as though she was on the verge of dehydration. I was momentarily frightened, but molybdenum had proven itself in the past, so I calmly cleaned up her, me, and the bathroom, after which we went down to the kitchen and I gave her some molybdenum (1000 mcg of powdered molybdenum glycinate for nausea/vomiting) and zinc (30 mg of powdered chelated zinc for the diarrhea, a use which is well-supported by research--https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3113371/). She then cuddled up on the armchair in the family room under a couple of blankets, and I gave her a container to vomit into should the need arise. Within half an hour, she reported that her tummy only hurt a little, and not much after that she fell asleep. Once she looked deeply asleep, I went back to bed. I woke at 9 am the next morning to hear her loud, chipper voice carrying through the house; she was already totally over the virus.

Because these stupid gastrointestinal viruses are so contagious, I gave everyone in the family 500-1000 mcg of molybdenum on Wednesday morning (after I woke up). Then on Thursday, close to bedtime, I noticed my teenager curled up on the family room floor. She was so out of it from a virus, probably the same one, that she didn't even fully realize she was sick. So I gave her 1000 mcg molybdenum and 30 mg zinc and sent her to get ready for bed. An hour later she complained that her stomach was still hurting, so I gave her 1000 mcg more and she went to sleep after that. The next morning (today, which is Friday), she said her stomach still hurt, so I gave her 1500 mcg more of molybdenum, after which she ate a banana. By lunchtime, she was happily serving herself turkey, stuffing, rolls, gravy, etc. from the Thanksgiving leftovers. She's recovered after just a few hours discomfort and never even vomited.

If this is the same stomach bug other local people have been telling me about in the recent past, my children should have suffered for days, not just a few hours.

I don't think molybdenum directly affected the virus because I don't know by what mechanism it could do that. But supplemental molybdenum does seem to greatly reduce the duration of a GI illness in addition to relieving the vomiting and nausea caused by it. Perhaps it does so because freeing the GI tract from a burden of excess sulfite, via support of sulfite oxidase function, somehow permits other immunity-related resources to more quickly expel the virus from the GI lining or at least protects the lining from sulfite-induced vulnerability. Some things to research next week when the holiday is over.

(Disclaimer: I do not prescribe the use of pharmaceutical drugs in any way. I am not a physician, and I reject out of hand any attempt to hold me liable for what boils down to a discussion of food. Any use of a molybdenum supplement should be prudent and guided by the tested tolerable upper intake levels for its usage (see http://lpi.oregonstate.edu/mic/minerals/molybdenum for those limits). Any use of an isolated molybdenum supplement during pregnancy should be under the direction of a medical professional as such supplements have apparently not been tested during pregnancy.)

Tuesday, November 21, 2017

More soup for you! And you, too! Soup for everyone!

I just wrote a long comment on Joanne Jacob's blog, where she posted recently about charter schools not being able to close the gender gap that is leaving more and more boys out in the cold educationally. In it, I call for a rebirth of soup popularity. It's almost winter; surely that's not too controversial a call! Below is what I wrote in the comment:

Boys are more fragile when it comes to ADHD and autism (which look similar on brain scans - https://www.sciencedaily.com/releases/2016/07/160727110911.htm). A girl may have ADHD and still get acceptable grades because spaciness alone doesn't usually create a discipline issue, while boys' higher physical energy combined with ADHD does create discipline issues and greatly disrupts their classrooms and their own educational paths. No charter is going to solve ADHD and autism just with a different school culture.

We need to find a way to ameliorate and/or prevent ADHD and autism. I might have mentioned this before, but I think a possible key is easily absorbable glycine betaine in the diet. Glycine betaine is an osmoprotectant (i.e., it protects cell walls from perturbation by dissociated aqueous NaCl) which can nevertheless be easily boiled out of plant cells. Those regions where they frequently consume the water in which glycine betaine-containing food was boiled (i.e., cuisines including barszcz, palak/spinach, and beverages/soups made with wheat and rye) are experiencing much lower burdens of autism (e.g., Poland with 1/40th the autism of the USA). 

I've been testing glycine betaine (AKA trimethylglycine) with my own Aspie child by putting it in our family milk and increasing intake of pasta cooking water and palak paneer. Glycine betaine is an inexpensive supplement because it's a byproduct of making beet sugar, and beets are one of the best vegetable sources of glycine betaine. Spinach and amaranth are two other good vegetable sources. Wheat and rye are also good grain sources of glycine betaine in the European-style diet. Glycine betaine's value lies in its role in supporting the function of the enzyme betaine-homocysteine methyltransferase, which catalyzes transformation of homocysteine to methionine, important because the next molecule, SAM-e, is used for carrying out DNA methylation. My Aspie child's emotions are stable now; the last time she had a big meltdown was when she'd been traveling and hadn't had supplemental glycine betaine for a while.

If I had a charter school, I'd add beet/rye/spinach soups to the lunch menu and see what happens. If I ran a regular public school, I'd do the same. We should learn from the Poles. The drive for convenience that has us draining away our cooking water in the West appears to be a big waste of easily-utilized, important nutrients. It's time for a soup renaissance.

Wednesday, November 15, 2017

Thin people

As a weight-conscious American woman, I often wonder, "Why are southeast Asians so thin? Why are eastern Europeans so often thinner young adults than western Europeans (except for the French)? Why is my third child downright skinny?"

I think that Dr. Jason Fung's theories on obesity resulting from insulin resistance--which can be acquired in the womb--help explain why some people seem programmed to be thinner.

In order to avoid developing insulin resistance, one needs to avoid subjecting one's body to chronic high levels of insulin, which insulin is stimulated by high glucose levels in the blood. With my third child, and only with her, I exercised a lot during pregnancy, often taking long walks that lasted into early evening and apparently resulted in me using up all my circulating glucose; I have a strong memory of getting weak and hungry on those walks but pushing through anyway. 

Southeast Asians regularly eat a plant we call water spinach (AKA kangkong, ong choy, Ipomoea aquatica) that is proven in rats to inhibit glucose absorption and decrease blood glucose levels. (https://www.ncbi.nlm.nih.gov/pubmed/17651914, https://www.ncbi.nlm.nih.gov/pubmed/11746851, https://www.ncbi.nlm.nih.gov/pubmed/10967485) Certainly, genetics also plays a role, but if you've seen southeast-Asian-Americans whose gestational development and childhood occurred in the USA, you've probably noticed that they tend not to be as skinny as their peers raised in Asia.

Eastern Europeans eat rye bread much more than western Europeans, and rye bread also slows down glucose absorption. (https://www.ncbi.nlm.nih.gov/pubmed/25370913) However, some people in the rye-consuming countries, such as in Finland, also drink caffeinated coffee throughout the day, and caffeinated coffee appears to decrease insulin sensitivity and increase glucose (http://care.diabetesjournals.org/content/27/12/2990/, http://ajcn.nutrition.org/content/87/5/1254.full, https://www.ncbi.nlm.nih.gov/pubmed/28031026), so a rye bread effect in them might be counteracted by their constant coffee consumption.

If I could go back in time to my pregnant self, I'd have a lot to tell me.

Wednesday, November 8, 2017

Schizophrenia, tyrosinase, ginseng, capers, and tyrosinase inhibitors (tea, mate, kojic acid, etc.)

The Texas church shooting two days ago has been weighing heavily on me, for I have a relative with schizophrenia. She refuses mental health treatment. She showed signs of early schizophrenia as early as her adolescence in that she had no close friends despite being able to engage in work, social events, and family events relatively well. Cold, distant, and detached describes her pretty well back then. (http://schizophrenia.com/earlysigns.htm) Then over the next two decades came hypersensitivity, ruminating thoughts, suicidal thoughts and hostility, hygiene neglect, lack of insight, nonsensical logic, delusions, affective flattening, and abusive behavior. It's a horrible thing to watch happen to a loved one, especially because the person, due to brain dysfunction, is convinced that nothing is wrong with her and that her problems are all due to mistreatment by others.

I think that tyrosinase activity is a key to schizophrenia. Tyrosinase is a copper-containing enzyme that is connected to both melanin and dopamine production. Tyrosinase is expressed in the brain. (http://onlinelibrary.wiley.com/doi/10.1111/j.1471-4159.2005.03019.x/full) One way researchers bring about schizophrenia in lab rats is by giving them the copper chelator cuprizone. (https://www.pubfacts.com/detail/28989170/Olig2-Silence-Ameliorates-Cuprizone-Induced-Schizophrenia-Like-Symptoms-in-Mice, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058516/)  A look at an epidemiology map of schizophrenia quickly gives rise to a supposition that melanin and schizophrenia might be inversely related (https://en.wikipedia.org/wiki/Epidemiology_of_schizophrenia), and higher melanin appears associated with altered dopamine signalling-connected sensitivity (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5569050/). Dopamine dysfunction is  involved in schizophrenia. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4032934/) As rats grow up, their cutaneous tyrosinase goes from making dopamine to making melanin in a way that temporally mirrors the common adolescent/young adult onset of early signs of schizophrenia in humans. (https://www.ncbi.nlm.nih.gov/pubmed/12832289)

I did some searching to see what could upregulate tyrosinase expression or increase its activity. Lymphoid enhancer-binding factor-1 (LEF-1) regulates tyrosinase gene transcription; overexpression of LEF-1 increases tyrosinase gene promoter activity, while LEF-1 knockdown decreases tyrosinase expression. (http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0143142) This is a promising finding, for LEF-1 is underexpressed in schizophrenia patients. (http://europepmc.org/articles/PMC1888575) Components of ginseng root can upregulate tyrosinase expression, too (https://www.hindawi.com/journals/ecam/2014/892073/), and ginseng root extract does not have a net effect of suppressing tyrosinase activity (https://www.ncbi.nlm.nih.gov/pubmed/12808298).

There are a handful of studies to indicate that ginseng root might actually be able to help ameliorate schizophrenia. A small study nearly a decade ago found that schizophrenia patients who took panax ginseng (AKA Korean ginseng) were less likely to have "flat affect" and other negative symptoms (negative in the sense of there being an absence of normal motivation, pleasure, etc.); the dosage was 200 mg/day, and it was taken for eight weeks. (https://www.cbsnews.com/news/ginseng-may-help-treat-schizophrenia/) A 2015 study subjected pregnant mice to stress and then found that ginseng could reverse the prenatal stress-caused behavioral changes in the offspring. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4249748/)

If ginseng can really help with schizophrenia, wouldn't it have been noticed sooner? Ginseng is very important in traditional Chinese medicine. However, something else is very important in Chinese culture: tea, which just so happens to inhibit tyrosinase. (https://www.medscape.com/medline/abstract/10576599) Moreover, throughout eastern Asia, people regularly eat foods containing kojic acid, an important tyrosinase inhibitor in the field of skin-lightening research. (https://www.ncbi.nlm.nih.gov/pubmed/27725765, https://www.researchgate.net/publication/289283346_Inhibition_of_tyrosinase_activity_on_dopamine_hydrochloride_by_kojic_acid)

There are many tyrosinase inhibitors that are in the human diet. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705500/) There's mate in South America. (http://www.koreascience.or.kr/article/ArticleFullRecord.jsp?cn=HJPHBN_2015_v41n4_391) Perhaps mate is why Uruguay has more of a schizophrenia burden than Argentina despite being full of European-ancestry people and otherwise having a similar diet, for Uruguayans are mate-obsessed. There's rosmarinic acid, named after the culinary herb rosemary, which contains it. (http://agris.fao.org/agris-search/search.do?request_locale=es&recordID=KR2005011915) There's arbutin, found in bearberries, pear skins, and wheat. (https://www.ncbi.nlm.nih.gov/pubmed/8632348) It would take a supercomputer (good thing we live in the 21st century) to calculate the tyrosinase inhibition caused by an individual's diet, and the frequency of intake of the inhibitors would also need to be taken into account, for rare is the person who eats rosemary all day, while green tea at every meal is the rule in Japan and mate lovers in Uruguay seem to spend every waking hour cuddling their mate gourds.

The human diet doesn't appear to contain much in the way of tyrosinase boosters (http://www.mdpi.com/1420-3049/22/8/1303/htm). There are capers (https://link.springer.com/content/pdf/10.1007%2F978-90-481-3419-9_127.pdf) and watery grapefruit and pomelo extracts (https://www.ncbi.nlm.nih.gov/pubmed/20857432).  And then there is the possibility of ginseng root candy being a tyrosinase booster, so I will probably be giving some to my relative for Christmas this year.* This paucity of dietary tyrosinase boosters compared with the plethora of tyrosinase inhibitors is exactly what one would expect to find with an intractable issue like schizophrenia, for if tyrosinase activity is a key to schizophrenia, any tyrosinase boosters in the diet should have started to make themselves manifest by now by decreasing the prevalence of schizophrenia where they are consumed. But who consumes pomelo extract and capers regularly? (Actually, the countries where capers are most often eaten do in fact mostly show up at the bottom of the list for schizophrenia burden...I'm starting to get cautiously optimistic about my little hypothesis....my relative is getting capers for Thanksgiving.) And any tyrosinase boost from ginseng root might have been noted earlier were it not for the simultaneous consumption of tyrosinase-inhibiting tea in China.

* As with everything, ginseng shouldn't be overused. There are published case reports of two men who ended up with manic psychosis from using huge doses of ginseng (15-20 grams/day). (https://www.researchgate.net/publication/261289619_Manic_Psychosis_Associated_With_Ginseng_A_Report_of_Two_Cases_and_Discussion_of_the_Literature) One can always get too much of a good thing.