>>186906, >>186907, >>186908, >>186909, >>186910, >>186911, >>186912, >>186913, >>186914, >>186915, >>186916
Craig Caplan @CraigCaplan - House returns today to consider a bipartisan agreement on children online safety legislation (KIDS Act) under suspension of the rules as well as a non-binding Lebanon war powers resolution for the 2nd time this year by Rep. Tlaib (D-MI). Her first resolution failed 92-324-2 earlier this month. @cspan
Quote:
Craig Caplan @CraigCaplan
92-324-2: House defeated a Lebanon war powers resolution by Rep. Rashida Tlaib (D-MI) to block U.S. military action against Lebanon without Congressional approval. 91 Democrats & 1 Republican Yes, 117 Democrats & 205 Republicans voted No & 2 Democrats voted Present.
https://x.com/CraigCaplan/status/2071555721120854500

Culture War Notes @culturewarnotes - Genetics and vitamins....
The MTHFR and folate conversation almost always skips the vitamin sitting one step above it.
A lot of people now know their MTHFR status, take methylfolate, maybe add B6, and watch their homocysteine. What rarely comes up is that the enzymes doing this work do not run on folate and B6 alone. They run on parts built from riboflavin, plain old vitamin B2.
Here is the chain in plain terms. Your body takes riboflavin and turns it into two working parts, called FAD and FMN. Those parts are not optional add-ons. They are built into the machines that activate the other B vitamins. The enzyme that recycles folate, MTHFR, has a piece of riboflavin locked inside it. The enzyme that converts B6 into its active form has a piece of riboflavin inside it too. And the step that lets B12 do its job in the same cycle depends on a riboflavin part as well. Riboflavin sits upstream of all three.
This matters most for the famous MTHFR variant. The common version of that gene, the one millions of people carry, does not just work a little slower. The actual problem is that the enzyme loses its grip on its riboflavin part more easily. The riboflavin falls out, and the enzyme goes quiet. Several studies have shown that giving riboflavin to people with this exact genotype lowers their homocysteine, because it helps the unstable enzyme hold its working part in place. You are not forcing the pathway. You are handing a wobbly enzyme back the piece it keeps dropping.
Now the honest limits, because this is easy to oversell. Most people are not riboflavin deficient. In well-fed populations, frank B2 deficiency is uncommon, so for the average person already getting enough, more riboflavin does not push anything higher. The strongest evidence is specific: it is in people who carry the MTHFR TT genotype, and the clearest effect has been on blood pressure and homocysteine in that group, not a general energy or mood claim. This is also not a reason to ignore folate or B6. It is a reason to recognize that fixing those while riboflavin runs low can leave the bottleneck in place. The point is not take more B2. The point is that the pathway people obsess over has a quiet first step, and if that step is short, the expensive downstream vitamins cannot do what the label promises.
Amenyah SD, et al. Biochimie. 2020
Pejchal R, et al. Biochemistry. 2006
Barile A, et al. Sci Rep. 2020
Dominguez-Salas P, et al. Am J Clin Nutr. 2013