The CIA doesn't want you to consume a nutritious breakfast and read the Bible out in the sun first thing in the morning. It would make you harder to control "Show me the science". Okay nerd. Reading the Bible alters brain metrics under stress and (this is a correlation, though) scripture memorization practices correlate with up to a 30% reduction in anxiety symptoms. When it comes to nutrition, the list is endless. For example: Low B12: -Reduces BH4 -Increases oxidative stress and homocysteine (which lead to all sorts of issues such as NMDA-mediated excitotoxicity, impaired hippocampal neurogenesis, blood–brain-barrier disruption, MMA-related demyelination etc) -Lowers EGF -Increases TNF-α Low B9: -Harms the production of every single neurotransmitter (folate is required to make SAMe (S-adenosylmethionine) low folate → low SAMe → increased risk of depression, anxiety, bipolar disorder, schizophrenia and cognitive decline). -Harms monoamine synthesis (via BH4 regeneration). -Harms the synthesis of melatonin, CoQ10, carnitine, creatine, phosphatidylcholine -Dietary biotin intake exhibited an approximately L-shaped nonlinear relationship with anxiety and depression risk, where risk decreased with increasing intake up to a moderate threshold. "Okay but these are for relatively healthy people, i actually have a psychiatric disease". How is not supporting your biology make sense? Let's say that you have ADHD for example. Something crucial to remember, no matter what intervention you want to try for your ADHD is that catecholamine synthesis proceeds as follows: 1. Tyrosine → L-DOPA by tyrosine hydroxylase (TH) 2. L-DOPA → dopamine by DOPA decarboxylase 3. Dopamine → norepinephrine by DBH 4. Norepinephrine → epinephrine by PNMT The key cofactors for these enzymes involved in catecholamine synthesis are: -TH requires BH4, iron and molecular oxygen. So you need methylfolate to support the salvage pathway via dihydrofolate reductase (DHFR), which converts dihydrobiopterin (BH2) back to BH4. Vitamin C that directly reduces the BH3 radical back to active BH4 during recycling. Zinc and magnesium that are required by 6-pyruvoyl-tetrahydropterin synthase (PTPS) in the de novo pathway. B2 since NADPH / NADH that are required by sepiapterin reductase (de novo) and dihydropteridine reductase L dopa needs pyridoxal 5'-phosphate as the prosthetic cofactor for the decarboxylation. DBH needs vitamin C, some copper and molecualr oxygen. PNMT's key requirement is SAMe that transfers a methyl group to form epinephrine so it needs (methylated) B6, B9, B12 and choline, magnesium and B2. And this is just the tip of the iceberg. ADHD patients might have compromised or slowed B6-dependent enzymes for example. The specific B6-dependent enzymes heavily implicated in ADHD include: 1. Dopa decarboxylase that converts L-DOPA into dopamine and 5-HTP into serotonin. 2. Glutamate decarboxylase (GAD) that converts glutamate into GABA. 3. Tryptophan metabolizing enzymes (think the kynurenine pathway) “But i don’t feel anything from B6”. A) Are you using P5P? B) Do you have enough zinc, B2 and magnesium in your system? Then zinc helps keep DAT at a healthy baseline, preventing it from vacuuming up dopamine too aggressively. DAT contains four high-affinity extracellular binding sites specifically meant for Zinc. When Zinc binds to these sites, it physically modulates the transporter’s rhythm, altering steady-state currents and optimizing reuptake. Normally, after dopamine is released into the synaptic cleft, it binds to dopamine receptors on the postsynaptic neuron to exert its effects. The DAT then clears the dopamine from the synapse and recycles it back into the presynaptic neuron. So it helps to terminate the action of dopamine by transporting it back into the presynaptic neuron. So when we inhibit it, we slow down the cleanup of dopamine and leave more of the chemical active in the synapses. Ritalin for example is a highly effective DAT inhibitor. Its structural mechanism differs completely from zinc obviously. While zinc acts as a non-competitive, allosteric clamp that locks the transporter from a side-pocket, methylphenidate operates primarily as an orthosteric blocker. It targets the S1 central binding site of the dopamine transporter. This is the exact same internal structural pocket where the dopamine molecule itself lands to be moved across the membrane. By sitting directly inside the central channel core, it acts like a physical plug and thus dopamine cannot bind to the transporter at all. Now unlike competitive inhibitors (such as cocaine or Ritalin), which bind directly to the central S1 substrate site halfway across the cell membrane, zinc acts at an entirely independent allosteric site on the outer surface of the transporter. By anchoring itself to this distinct outer pocket, zinc physically restrains the movement of the transporter. It acts as a rigid macromolecular bridge that locks the DAT machinery in an “outward-open” conformation. While the central channel remains open, the transporter is effectively paralyzed, it can no longer undergo the conformational rotation required to pull dopamine out of the synapse and back into the cell. For someone struggling with ADHD or anhedonia, this highly efficient, non-competitive blocking action provides a unique therapeutic advantage. Because zinc does not compete for the central keyhole, its ability to stop the cellular “vacuum cleaner” cannot be overridden by fluctuating concentrations of natural dopamine. It forces a baseline level of dopamine to pool within the synaptic cleft. This is why DAT inhibitors usually increase the effectiveness of stimulants. In the context of ADHD, this prolonged synaptic activity helps satisfy under-stimulated reward pathways. In the case of anhedonia this steady accumulation of active dopamine lowers the activation threshold required to feel pleasure, motivation and goal-directed drive. Other natural DAT inhibitors that you might be aware of are ginkgo and saffron. “What about copper?” At basic doses such as 10-15mg/day, eating just 100 grams of beef liver/week does the trick. "Cool but i'll just take my meds". Nutrition is a prerequisite for your meds to work as much as they can. Even low ferritin can cook your response to stimulants such as modafinil and Adderall. Your stimulants do not actually create new dopamine out of thin air. Instead, they act like a pump that forces your brain to release and utilize the dopamine you already have. Amphetamines for example, reverse the dopamine transporter and promote release from vesicles while also inhibiting reuptake. Modafinil is more of a reuptake inhibitor (plus other effects when it comes to histame, orexin etc). So they are not factories that create dopamine out of nothing. However, to build dopamine in the first place, your brain relies on a specific enzyme called tyrosine hydroxylase. This enzyme cannot function without iron acting as its structural cofactor. Here's why. Tyrosine hydroxylase requires ferrous iron (Fe²⁺) as a cofactor, along with tetrahydrobiopterin (BH4) and oxygen. The iron is structural to the catalytic mechanism (non-heme iron enzyme that generates a high-valent Fe(IV)=O intermediate). So low iron availability impairs this step. On top, iron deficiency also alters the structure of the brain's dopamine D2 receptors and these receptors become less sensitive. Because the receptors are sluggish, it takes a much higher concentration of a stimulant to force a response. And this is just ONE marker/nutrient. Several other nutrients matter for dopamine synthesis and signaling, and a few have at least correlational or adjunctive evidence related to stimulant response. Iron is one of the better-supported ones, but it is not the only cofactor. Dopamine synthesis has two main enzymatic steps with specific requirements: -Tyrosine → L-DOPA via tyrosine hydroxylase (TH) This needs iron (Fe²⁺) + tetrahydrobiopterin (BH4) + oxygen. -L-DOPA → dopamine via aromatic L-amino acid decarboxylase (AADC) This needs vitamin B6 as pyridoxal-5-phosphate (PLP). So in the first step, BH4 is the other obligatory cofactor for TH (and for tryptophan hydroxylase in serotonin synthesis). It is made from GTP and regenerated with help from the folate cycle. So low BH4 or poor recycling can bottleneck the pathway even if tyrosine and iron are sufficient (so it can be related to low B9 or vitamin C). Then PLP is required for the final conversion of L-DOPA to dopamine so a deficiency can impair that step. Etc Also never forget that no amount of caffeine or meds can fix a neuron that physically lacks the energy to fire. Working to optimize or balance your neurotransmitters is largely ineffective if your cells are not producing enough ATP. The creation of neurotransmitters from amino acid precursors requires enzymatic steps that are ATP-dependent processes. So without enough cellular energy, your brain cannot efficiently build these chemical messengers. Once neurotransmitters are made, they must be actively pumped into storage sacs called vesicles. This relies on V-ATPase, an enzyme that also requires direct ATP consumption to move neurotransmitters against their concentration gradient. To send a signal, neurons must fire and then reset their electrical balance. The sodium-potassium pump resets the neuron's membrane potential after an action potential. This single process consumes roughly HALF of the total energy used by the entire brain. Then after a neurotransmitter is released into the synaptic cleft, it needs to be cleared or recycled via reuptake transporters. These transporters also rely on the ion gradients maintained by ATP-driven pumps. So without sufficient ATP, your brain cells lack the basic power needed to manufacture, store, release, and clean up neurotransmitters. To build what feels like "unlimited willpower," you must shift from viewing willpower as a moral choice or a mental muscle and start viewing it as a metabolic resource. "I'll just take a multivitamin and call it a day". Not how this works. Kiwis for example (yes, the fruit) can help with depression in 4 days. This was a 28-day dietary intervention with 155 adults who had low baseline levels of Vitamin C and, besides the placebo group, they either: -Took 250 mg of vitamin C -Ate two SunGold kiwifruits The group eating the actual kiwifruit reported significant improvements in vitality and mood within just 4 days. Am i saying that vitamin C does not matter? Of course not. Getting less than 93.61 mg of vitamin C per day is heavily linked to depression. Also vitamin C made fluoxetine way more effective in pediatric patients being treated for major depressive disorder. Of course, this link (between low vitamin C and depression) is deeply rooted in fact such as that: -The brain is highly susceptible to oxidative stress -Vitamin C serves as a required cofactor to synthesize serotonin, dopamine, and norepinephrine -The highest concentrations of vitamin C in the entire body are found in the amygdala, hippocampus, and hypothalamus The point is to take your nutrition seriously. For more about the brain: fitandball.gumroad.com/l/bra…

Crazy how “being mean is bad” has some necessary carveouts for people you personally don’t like

It’s not hateful to say that Mormonism isn’t Christianity. It’s the truth. If you do not repent and believe in the true gospel, you will be eternally offended by what Jesus will say to you when you meet him.

You’re gonna find it hard for me to care about your orthodox beliefs when I don’t believe in your truth claims to begin with bubbers

this is the shit I be talking about with her. She's entirely too old and far into her career to play the "I didn't know" card when it comes to the company she keeps

Mormons call Christians brothers and sisters because they so desperately want us to do the same for them. They want us to call them Christian brothers and sisters, which they are not.