Thursday, June 30, 2016

Egg for breakfast

We're going to be learning about Austria for the first two weeks of July. A typical Austrian breakfast is a roll with butter/cheese/jam/etc., a cup of coffee or hot cocoa, and an egg. I look forward to breakfasts that include egg for a while. Typically, we just have cold cereal (the kind without cyanocobalamin and folic acid these days) and milk because it's convenient. But it really doesn't seem to be the best way to start every single day, especially if one is trying to avoid weight gain and Type II diabetes. A recent study shows some clear advantages from including an egg as part of one's breakfast.
This study evaluated appetite and glycemic effects of egg-based breakfasts, containing high and moderate protein (30 g protein and 20 g protein +7 g fiber, respectively) compared to a low-protein cereal breakfast (10 g protein) examined in healthy adults (N = 48; age 24 ± 1 yr; BMI 23 ± 1 kg/m2; mean ± SE). Meals provided 390 kcal/serving and equal fat content. Food intake was measured at an ad libitum lunch meal and blood glucose response was measured. Visual analog scales (VAS) were used to assess hunger, satisfaction, fullness, and prospective food intake. The egg-based breakfast meal with high protein produced greater overall satiety (p < 0.0001), and both high protein and moderate protein with fiber egg-based breakfasts reduced postprandial glycemic response (p < 0.005) and food intake (p < 0.05) at subsequent meal (by 135 kcal and 69 kcal; effect sizes 0.44 and 0.23, respectively) compared to a cereal-based breakfast with low protein and fiber.
"The effects of the combination of egg and fiber on appetite, glycemic response and food intake in normal weight adults – a randomized, controlled, crossover trial," [Abstract], http://www.tandfonline.com/doi/full/10.1080/09637486.2016.1196654

Eggs are a bit messy to prepare, especially in comparison with a bowl of cereal and milk, but it's time my older children learn to fry them!

Monday, June 27, 2016

Published!

Here's a link to the letter to the editor that my friend and I submitted to the International Journal of Food Sciences and Nutrition. The gist of it is that research, especially over the past 10 years or so, points to mechanisms explaining how a rise in folic acid intake could have caused increases in autism spectrum disorders and inattentive-type ADHD and that we would be prudent to consider using folate supplements that don't inhibit the enzyme dihydrofolate reductase the way folic acid does.

http://www.tandfonline.com/eprint/E4IhDdijbZIMRfYh4T28/full

Update: All 50 of the free downloads from the publisher are already gone, so here's a 30-second slide show video I made from part of the letter and its supporting references.


Saturday, June 25, 2016

Cyanocobalamin - a very poor choice, part 2

When the body has to detoxify cyanide, the most well-known pathway is facilitated by the enzyme rhodanese, which converts cyanide to thiocyanate, which is then excreted via the kidneys. But what does thiocyanate do to us before it's excreted? I'm sure there are other things I haven't come across yet, but my early research has turned up studies showing that thiocyanate induces hypothyroidism in weaned mice and is associated with neurological diseases. Then there's a website for anesthesiologists saying
Thiocyanate toxicity causes anorexia, fatigue, and mental status changes, including psychosis, weakness, seizures, tinnitus, and hyperreflexia. Thiocyanate is usually excreted in the urine. Toxicity can be minimized by avoiding prolonged administration of nitroprusside and by limiting drug use in patients with renal insufficiency. If necessary, thiocyanate can be removed by dialysis.
I fear I'm going to sound like a broken record before I'm done with researching cyanocobalamin, but we should really be using other forms of cobalamin (B12) in our breakfast cereal and vitamin supplements. Instead of adding to the body's cyanide load, we could be decreasing our suffering from cyanide and its metabolites if we used hydroxocobalamin. Hydroxocobalamin and cyanocobalamin are both synthetic, but at least hydroxocobalamin dissociates more easily and helps reduce the body's cyanide and thiocyanate loads. I'll have to do more research later on methylcobalamin and adenosylcobalamin, the forms of B12 that naturally occur in food (mostly animal products).

Thursday, June 23, 2016

Cyanocobalamin - a very poor choice, part 1

We humans have cyanide in our bodies. It's a fairly simple, small molecule, so that's not surprising. Not only are we exposed to it from some foods (especially cassava), smoking, combustion of some materials, and some poisons and medications, but it turns out that our bodies make it! Who knew? The research on endogenous (i.e., made in the body) hydrogen cyanide (a poisonous cyanide compound) focuses on mammalian brain tissue:
Cyanide is generated in neurons and this report examines the two different receptors which mediate cyanide formation in neuronal tissue. An opiate receptor blocked by naloxone increases cyanide production both in rat brain and in rat pheochromocytoma (PC12) cells. A muscarinic receptor in PC12 cells releases cyanide and the effect is blocked by atropine. In rat brain, in vivo, a muscarinic agonist inhibits cyanide generation, possibly by acting on receptor subtypes different from those in PC12 cells. Cyanide generation by a muscarinic agonist in PC12 cells is blocked by pertussis toxin but that caused by an opiate is not. Thus, two different receptors and two different second messenger systems can mediate cyanide generation in PC12 cells. In parallel with the in vivo data, cultured primary rat cortical cells also show decreased cyanide release following muscarinic stimulation. Both blockade of cyanide generation by muscarinic receptor activation and cyanide release by opiate agonists from cortical cells are pertussis toxin insensitive. Similarly, little cyanide generation was seen following cholera toxin treatment. These data indicate that opiate receptors increase and muscarinic receptors decrease cyanide production in rat brain tissue by G-protein independent mechanisms. This work supports the suggestion that the powerful actions of cyanide may be important for neuromodulation in the CNS.
Abstract from https://www.ncbi.nlm.nih.gov/pubmed/15099699.

In very small amounts, it looks like our body finds cyanide useful. Too much cyanide is to be avoided, though, for it can cause seizures, coma, and death. Among other detoxification pathways, our body has an enzyme called rhodanese that helps us convert cyanide to thiocyanate (which apparently causes hypothyroidism, which is a problem, but not as big a problem as cyanide). Too high a cyanide load overwhelms the body's ability to detoxify cyanide before it can cause harm. However, even low-level exposure to cyanide over a long period of time apparently can harm us, so it's important to minimize our intake of cyanide-containing substances.
Chronic exposure to cyanide has been associated with development of pancreatic diabetes, hypothyroidism, and several neurological diseases in both humans and animals. However, there is a limited number of experimental models for these pathologies. Thus, in the present study 0, 0.15, 0.3, or 0.6 mg KCN/kg body weight/day was administered for 3 months to 26 rats. On the last day, plasma samples were obtained for glucose, cholesterol, and thyroidal hormone measurement, and the pancreas, thyroids, and whole central nervous system were collected for histopathologic study. There were no significant difference in plasma concentrations of the substances measured between groups, and no lesions were found in the pancrease or thyroid. The CNS of experimental animals revealed the presence of spheroids on the ventral horn of the spinal cord, neuron loss in the hippocampus, damaged Purkinje cells, and loss of cerebellar white matter. In conclusion, cyanide administration could promote neuropathological lesions in rats without affecting pancreas or thyroid gland metabolism.
Abstract from "Effects of low-dose long-term cyanide administration to rats," https://www.ncbi.nlm.nih.gov/pubmed/12481854.

Because it's stable (and so cheaper), the form of vitamin B12 that is typically put into fortified foods and vitamins is cyanocobalamin. "Cyano" stands for "cyanide." It seems to be generally assumed that 1) the cyanocobalamin will dissociate into cyanide and cobalamin (useable B12) during digestion, and 2) the cyanide dose from cyanocobalamin is too low to harm us. However, a recent study of brain tissue found that cyanocobalamin is present in the brain. If it dissociates in the brain--which is kind of the point of supplementing with cyanocobalamin in the first place as we want the benefit of the cobalamin--the cyanide will be added to that from endogenous hydrogen cyanide in the central nervous system. And if it doesn't dissociate in the brain, then it isn't helping us meet our brain's cobalamin needs.

I believe cyanocobalamin is a very poor choice of B12 supplement. The evidence clearly indicates that cyanide and its less toxic metabolite, thiocyanate, could exacerbate or even cause hypothyroidism and cyanide-related neurological problems. Cyanocobalamin is far from the only form of B12 available. There is even one form of B12, hydroxocobalamin, that is used to treat cyanide poisoning because the cobalamin binds more tightly to the "cyano" than to the "hydroxo" (hydroxyl), and our bodies can excrete the resulting cyanocobalamin.

Saturday, June 4, 2016

All that research wasn't in vain

For several months a high school friend, who happens to be an RN and have MTHFR mutations, and I have been researching medical science and nutrition, with an emphasis on MTHFR-related processes. We drafted a letter to the editor on some important connections we made and submitted it to three different journals. It has been under review for some time, but we found out today that the third journal will accept it for publication after we make a few changes.

Truly, science is for everyone. My friend and I are both currently housewives taking care of several children. Well-educated housewives, to be sure, with a definite STEM bent. We were the two girls our high school sent to an area conference on "Women in Math and Science" one year. But I could never have been the person in the lab coat, slicing and dicing mouse brains. Emotionally, I would have a very hard time doing that. But I can see patterns, use logic, and follow where the data lead. As can anyone now, thanks to the people in the lab coats who create research data and the PubMed database. I am very grateful to live in a time and place where scientific knowledge is so readily accessible to all.