Dopamine Synthesis: Genes, lifestyle, diet, and dopamine optimization
Hi there,
One of my goals this year for Genetic Lifehacks is to fill in the gaps of topics that I haven't completely covered. In updating my article on dopamine receptors, I realized that I had never written about dopamine synthesis in detail.
So this week's new article explains dopamine synthesis, genes, and supplements/diet to optimize dopamine. I've also created a pathway diagram explaining dopamine synthesis (in the new Pathway Diagrams section for members).
In the Mood and Brain section, you'll now find Dopamine Receptors, Dopamine Synthesis, GABA, Serotonin, Tryptophan, BDNF, COMT, MAO -- as well as all the other articles on cognitive function, mood, ADHD, etc.
I have NMDA receptors, glutamate, and ketamine on my list to write about soon. My question to all of you -- what am I missing in the brain function section that you would like to know about? If you see something missing there, shoot me a quick email reply and let me know.
Gratefully yours,
Debbie
Dopamine Synthesis Genes
Key takeaways:
~ Dopamine synthesis begins with the conversion of tyrosine to l-DOPA, which is then converted to dopamine.
~ The key enzymes in this synthesis are TH (tyrosine hydroxylase) and DDC.
~ Genetic variants in these genes, along with lifestyle, diet, and other environmental factors, affect dopamine levels.
~ Testing can show you where you’re at, and supplements or dietary changes can help optimize dopamine levels.
What I've been reading:
1) Luteolin Is More Potent than Cromolyn in Their Ability to Inhibit Mediator Release from Cultured Human Mast Cells
Cromolyn is a commonly prescribed drug for inhibiting mast cell degranulation. This study compared luteolin, a natural supplement, to cromolyn and found that luteolin was superior for mast cell inhibition.
One problem, though, is that luteolin is not as easily absorbed or bioavailable as prescription drugs. Read all about luteolin.
This is a concerning pre-print from researchers at Brown University that I hope will be followed up with more research on the topic. For context, p53 is a tumor suppressor gene that regulates cell division. The preprint shows that the spike 2 subunit suppresses the transcription of p53, which isn't good when it comes to preventing cancer.
3) The microbiota drives diurnal rhythms in tryptophan
metabolism in the stressed gut
This new study in Cell Reports explains: "Chronic stress disrupts diurnal rhythmicity and the microbiota-gut-brain
axis. Here, Gheorghe et al. show that acute stress alters microbial tryptophan metabolism and gut barrier integrity and
that diurnal rhythmicity is a feature of tryptophan-metabolizing bacteria. Normal diurnal rhythms in gut barrier function and host tryptophan metabolism are dependent on the microbiota."
Essentially, stress causes changes to the gut microbiome with alterations in tryptophan metabolism. There's a circadian rhythm controlling our tryptophan metabolism and circadian rhythm also controls bacterial tryptophan metabolism. Thus, the time of day when you're stressed matters to your gut barrier function. The study is interesting in that it only took 15 minutes of stress to alter the gut microbiome (in mice).
