Fueling My Brain

Nutrition, Gut Health, and Daily Routine

"Let food be thy medicine."
— Hippocrates (But let’s pair that wisdom with what peer-reviewed science actually tells us.)

The Evidence-Based Foundation for Brain Nutrition

Let’s be clear. Food is not a miracle cure for bipolar disorder. But pretending it doesn’t affect your brain is equally irresponsible. The idea that “it’s all in your head” ignores decades of research showing that what you eat directly impacts your central nervous system, neurotransmitter synthesis, inflammation, energy metabolism, and mood regulation.

If you live with a serious psychiatric condition like bipolar disorder, nutrition is not optional. It’s a variable in the system. A modifiable input. And it deserves the same attention as medication or therapy—not as a replacement, but as a critical part of a multidisciplinary strategy.

I’ve lived this. And I’ve also studied it. I hold a Master of Science in Exercise Physiology and Sports Nutrition, and I’ve spent years applying what I know from the lab to real life with a bipolar brain.

This post isn’t fluff. It’s what the research says, what I’ve tested personally, and what I believe every person with a mood disorder deserves to know.

The Brain Is a Metabolically Demanding Organ

Your brain is a high-output system. Despite being roughly two percent of your body mass, it consumes twenty to twenty-five percent of your resting metabolic rate (Clarke & Sokoloff, 1999). That demand increases during acute stress or emotional dysregulation.

Bipolar disorder is associated with changes in how the brain creates and uses energy—especially in the mitochondria, which are like tiny batteries inside brain cells. It also affects how your brain uses sugar (glucose) for fuel, and how well it manages oxidative stress—a chemical tug-of-war between damage and repair inside your cells (known as redox balance). This is not a philosophical idea. It's measurable.

Brain scans using a technology called magnetic resonance spectroscopy have shown that people with bipolar disorder often have trouble producing clean, efficient energy inside brain cells, especially during episodes. Dysfunctional mitochondria may impair energy production in neural tissue, which contributes to mood instability and cognitive dysfunction (Stork & Renshaw, 2005; Andreazza et al., 2010).

Put simply: if your brain can’t generate or regulate energy efficiently, you’re going to feel it. That’s why nutrition isn’t just about "eating clean." It’s about supporting the bioenergetic demands of a vulnerable system.

What Makes the Bipolar Brain Nutritionally Unique?

Here’s what we know so far from emerging research:

• Mitochondrial Dysfunction: Impaired energy production can increase susceptibility to depressive and manic episodes. Supporting mitochondrial health through nutrients like CoQ10, creatine, and B-vitamins may help stabilize energy regulation.

• Oxidative Stress: People with bipolar disorder often show elevated markers of oxidative stress. This makes antioxidant support (like omega-3s, magnesium, and polyphenols) critical.

• Excitotoxicity: Bipolar brains can have heightened glutamate activity, which leads to overstimulation and damage to neurons. Nutrients like magnesium and N-acetylcysteine (NAC) may help calm the brain when it’s firing too fast or too often, protecting it from the kind of overstimulation that can cause mood swings or burnout.

• Genetic Polymorphisms: Some people have a genetic variant called MTHFR that makes it harder to convert folic acid into its active form (L-methylfolate). That’s important, because this active form is critical for brain chemicals like serotonin and dopamine to function properly. Supplementing with L-methylfolate instead of folic acid can be beneficial in these cases.

Your brain isn’t just sensitive. It’s high performance. It needs fuel and support like an elite machine.

Blood Glucose Regulation and Mood: What the Data Shows

If there’s one factor that consistently affects my bipolar symptoms on a day-to-day basis, it’s blood sugar. And no, that’s not just anecdotal.

Glucose is the brain’s primary fuel source. Large fluctuations in blood glucose are associated with increased cortisol, disrupted cognition, and mood dysregulation. When your blood sugar drops too low (hypoglycemia), your body hits the panic button—epinephrine, norepinephrine, and cortisol rise to bring sugar levels back up (Cryer, 2008).

In healthy individuals, mild hypoglycemia may result in fatigue or irritability. In a brain already prone to emotional lability, that same drop can precipitate panic, rage, or intrusive thoughts. I’ve personally experienced this. And numerous studies show that individuals with mood disorders often have altered glucose-insulin dynamics and greater susceptibility to glycemic shifts (Liu et al., 2022; Holt et al., 2010).

That’s why I structure my meals around protein, fiber, and fat. I rarely eat simple carbohydrates alone. And when I do indulge—say, with a treat like gluten-free cookies—I pair it with a protein source to blunt the glycemic impact.

This is not “diet culture.” It’s physiology.

Micronutrients and Mood: What the Literature Actually Says

Forget macros for a second. Micronutrient sufficiency matters—especially for the brain. Micronutrients are vitamins and minerals your brain needs in tiny but essential amounts to function well. Think of them as spark plugs for your brain chemistry.

Let’s walk through the big hitters with evidence:

Magnesium: Essential cofactor for more than 300 enzymatic reactions, many related to neurotransmitter activity, NMDA receptor modulation, and HPA axis function. Meta-analyses suggest that magnesium supplementation may improve symptoms of depression and anxiety, particularly in deficient populations (Boyle et al., 2017).

Zinc: Involved in neuroplasticity, antioxidant defense, and synaptic signaling. Low zinc status is associated with increased depressive symptoms, and some research supports zinc supplementation as an adjunct to antidepressants (Swardfager et al., 2013).

B-Vitamins (B6, B12, Folate): Critical for methylation, homocysteine regulation, and monoamine synthesis. Deficiencies can impair serotonin and dopamine metabolism and are commonly observed in individuals with mood disorders (Young, 2007).

Vitamin D: More than just a bone-health vitamin. Vitamin D doesn’t just help your bones—it acts more like a hormone for your brain, influencing which genes get turned on or off and helping regulate inflammation and mood.

Low vitamin D levels are associated with greater severity of depressive symptoms, though causality is still debated (Anglin et al., 2013).

Omega-3 Fatty Acids: EPA and DHA are integral components of neuronal membranes. Meta-analyses indicate that EPA-predominant omega-3 supplementation may reduce depressive symptoms, especially in bipolar depression (Sublette et al., 2011).

So no, taking these isn’t “woo.” It’s evidence-based nutritional psychiatry.

In my case, I use a high-quality greens powder that contains a broad spectrum of micronutrients, probiotics, and enzymes. I also supplement with fish oil, magnesium glycinate, vitamin D3 with K2, and creatine monohydrate. These are not exotic. They are clinically relevant and dosed according to current literature.

Inflammation and Bipolar Disorder: The Emerging Consensus

Bipolar disorder is not just about dopamine and serotonin. It’s about immune signaling and chronic low-grade inflammation.

During mood episodes, the brain often shows signs of inflammation, like when you get sick. Chemical messengers called cytokines—including IL-6, TNF-alpha, and CRP—are often too high, which can make symptoms worse and affect clear thinking. (Munkholm et al., 2013). Elevated CRP correlates with worse executive function and greater episode severity.

What causes neuroinflammation? Multiple factors: oxidative stress, sleep disruption, trauma, and yes—poor diet.

A diet high in ultra-processed foods, added sugars, and industrial trans fats promotes inflammation through multiple pathways. A poor diet can cause “leaky gut,” where bacterial fragments (like LPS) sneak into the bloodstream and trigger inflammation. It also throws off the balance of your gut microbes (gut dysbiosis), which affects immune signaling and mood. (Calder et al., 2011). That doesn’t mean one cookie will ruin your brain, but patterns matter.

For me, minimizing inflammation means eating mostly whole foods, avoiding alcohol, sleeping 8 hours a night, and using proven anti-inflammatory agents like omega-3s and curcumin phytosome. I also incorporate exercise, cold exposure, and sauna, all of which reduce inflammatory markers over time.

This is not restrictive. It’s rational.

Gut-Brain Axis: More Than a Buzzword

Let’s talk gut health without the pseudoscience.

The gut-brain axis is the two-way highway between your gut and your brain. It communicates through nerves, hormones, and your immune system—and plays a major role in how you feel emotionally and mentally.

Approximately 90 percent of serotonin is produced in the gut. Healthy gut bacteria produce helpful byproducts (short-chain fatty acids) that can strengthen the blood-brain barrier (your brain’s security system), calm the HPA axis (your internal stress response), and reduce inflammation.

There is preliminary evidence linking gut dysbiosis to increased anxiety, depression, and even bipolar spectrum disorders (Dinan and Cryan, 2017). That said, the evidence on probiotic supplementation is still evolving. Not all strains are beneficial, and results are highly individualized.

My approach is pragmatic. I don’t eat sauerkraut every day or down kombucha like a religion. I avoid gluten due to celiac disease, limit highly processed foods, and take a greens supplement with clinically supported probiotic strains. I also consume Greek yogurt occasionally for natural probiotics and aim for at least 25–35 grams of fiber daily from oats, potatoes, vegetables, and berries.

No gimmicks. Just patterns that support gut integrity and reduce inflammation.

My Daily Routine: Structure That Supports Stability

Routine is a keystone habit in my recovery. It’s not rigid, but it’s rhythmic. Here’s how I build my day to support stability:

Wake: Between 6:30 and 7:30 a.m., depending on recovery data from my Garmin.

Morning: Light exposure within 15 minutes, mindfulness breath meditation, then supplements and breakfast. My morning stack includes vitamin D, magnesium, creatine, fish oil, and my greens powder. I time this with food to maximize absorption and reduce nausea.

Mid-Morning: Green tea and work. I save caffeine until cortisol naturally dips post-wake.

Workout: Between 1:00 and 2:00 p.m., after a pre-workout meal containing protein and carbs. Post-lift, I have a shake or whole food meal.

Evening: I taper stimulation. I do NSDR (non-sleep deep rest), a second meditation or body scan, dinner, light reading or TV, and avoid screens within an hour of bed.

Bedtime: Between 9:30 and 10:30. I take a sleep support stack of glycine, magnesium, and herbal support like passionflower or valerian if needed.

This rhythm reinforces circadian alignment, blood sugar balance, and nervous system regulation—key factors in mood stability.

A Moderate Approach to Macros

I used to track every gram of food obsessively. It worked until it didn’t. Today, I still hit macro targets most days, but I use a flexible structure instead of rigid tracking. I am a muscular 215 lbs and aim for roughly 200 grams of protein, 400 grams of carbs, 90 grams of fat, and 30 plus grams of fiber.

Instead of logging every bite, I build my days around consistent meals:

Breakfast: High-protein smoothie with oats, fruit, nut butter, and whey.

Lunch: Lean protein, potatoes or rice, vegetables.

Pre-workout: Fruit, rice cakes, or honey with whey or a protein bar.

Post-workout: Shake or meal with protein and carbs.

Dinner: Protein, starch, vegetables, and healthy fats.

Evening snack: Greek yogurt or cottage cheese with fruit and granola.

Yes, I eat gluten-free Oreos sometimes. No, I don’t feel guilty. Because health isn’t about restriction—it’s about patterns, context, and consistency.

Sample Day Plans for Different Needs

Instead of a rigid meal plan, think of these as blueprints for different mental states:

Stabilizing Day (after poor sleep or stress spike):

• Breakfast: Smoothie with whey, oats, berries, nut butter

• Snack: Hard-boiled eggs and a banana

• Lunch: Chicken, sweet potato, spinach, olive oil

• Snack: Greek yogurt with almonds

• Dinner: Salmon, rice, roasted carrots

• Evening: Herbal tea, glycine, magnesium

High-Functioning Day (focus + productivity):

• Breakfast: Eggs, avocado toast (GF), berries

• Snack: Protein bar or turkey slices + apple

• Lunch: Lean beef, jasmine rice, broccoli

• Pre-workout: Rice cakes and whey

• Post-workout: Chicken and potatoes

• Dinner: Turkey stir-fry with veggies + rice

Reset Day (after indulgence):

• Breakfast: Green smoothie with protein, flax, frozen berries

• Snack: Cottage cheese and cucumber

• Lunch: Grilled chicken salad with olive oil and avocado

• Snack: Celery and peanut butter

• Dinner: White fish, quinoa, steamed veggies

This is flexibility with purpose.

Red Flags: Signs Your Diet Might Be Working Against You

Pay attention to these early warning signals:

• You feel jittery, panicky, or irritable after meals

• You crash in the afternoon even with good sleep

• Your thoughts speed up or spiral after sugar/caffeine

• You skip meals and notice mood swings escalate

• You feel obsessive or ashamed about food choices

These signs aren’t moral failings—they’re data. Your brain is asking for better support.

Disordered Eating, Orthorexia, and the Mental Health Trap

Mental health circles can unintentionally foster perfectionism around food. I’ve seen it and lived it. The irony is that obsession over food quality can become a new form of instability. When your identity depends on eating perfectly, even a minor deviation can feel catastrophic.

That’s not health. That’s anxiety in disguise.

What I preach now is moderation, evidence, and self-compassion. Eat in a way that supports your brain, not punishes it. Be consistent, not obsessive. Allow flexibility, not chaos.

My Grocery Staples

Protein: Chicken, turkey, eggs, egg whites, protein powder, Greek yogurt, cottage cheese, deli turkey.

Carbs: Potatoes, rice, oats, rice cakes, bananas, blueberries, strawberries, gluten-free bread, gluten-free treats in moderation.

Fats: Olive oil, avocado, peanut butter, almonds.

Veggies: Spinach, zucchini, carrots, broccoli, low sodium v8.

Supplements: Creatine monohydrate, magnesium glycinate, vitamin D with K2, fish oil, greens powder, glycine, passionflower.

Bottom Line: Feed the Brain You Have

This chapter is not about following my diet. It’s about learning to nourish the brain you have—a brain that is metabolically demanding, inflammation-prone, and uniquely responsive to nutritional inputs.

Use food as a lever. Not as a cure, but as a stabilizer.

You don’t need a perfect diet. You need a sustainable one.

You don’t need to follow my plan. You need to build yours—with intelligence, intention, and compassion.

Your brain is not broken. It’s a high-performance system.

Feed it like it matters. Because it does.

Scientific Citations

Anglin, R. E. S., Samaan, Z., Walter, S. D., & McDonald, S. D. (2013). Vitamin D deficiency and depression in adults: systematic review and meta-analysis. The British Journal of Psychiatry, 202(2), 100–107. https://doi.org/10.1192/bjp.bp.111.106666

Andreazza, A. C., Kauer-Sant’Anna, M., Frey, B. N., Bond, D. J., Kapczinski, F., Young, L. T., & Yatham, L. N. (2010). Oxidative stress markers in bipolar disorder: a meta-analysis. Journal of Affective Disorders, 111(2-3), 135–144. https://doi.org/10.1016/j.jad.2008.04.013

Boyle, N. B., Lawton, C., & Dye, L. (2017). The effects of magnesium supplementation on subjective anxiety and stress—A systematic review. Nutrients, 9(5), 429. https://doi.org/10.3390/nu9050429

Calder, P. C., Ahluwalia, N., Brouns, F., Buetler, T., Clement, K., Cunningham, K., … & Verschuren, P. M. (2011). Dietary factors and low-grade inflammation in relation to overweight and obesity. British Journal of Nutrition, 106(S3), S5–S78. https://doi.org/10.1017/S0007114511005460

Clarke, D. D., & Sokoloff, L. (1999). Circulation and energy metabolism of the brain. In G. J. Siegel et al. (Eds.), Basic Neurochemistry: Molecular, Cellular and Medical Aspects (6th ed.). Lippincott-Raven.

Cryer, P. E. (2008). Hypoglycemia in diabetes: Pathophysiology, prevalence, and prevention. American Journal of Managed Care, 14(7 Suppl), S69–S76.

Dinan, T. G., & Cryan, J. F. (2017). Gut instincts: microbiota as a key regulator of brain development, ageing and neurodegeneration. The Journal of Physiology, 595(2), 489–503. https://doi.org/10.1113/JP273106

Holt, R. I. G., de Groot, M., & Golden, S. H. (2014). Diabetes and depression. Current Diabetes Reports, 14(6), 491. https://doi.org/10.1007/s11892-014-0491-3

Liu, Y., Dai, M., Bi, Y., Xu, M., Xu, Y., Li, M., … & Ning, G. (2022). Association between blood glucose levels and depression symptoms in Chinese adults: A prospective cohort study. Psychoneuroendocrinology, 135, 105597. https://doi.org/10.1016/j.psyneuen.2021.105597

Munkholm, K., Vinberg, M., & Kessing, L. V. (2013). Cytokines in bipolar disorder: a systematic review and meta-analysis. Journal of Affective Disorders, 144(1-2), 16–27. https://doi.org/10.1016/j.jad.2012.06.009

Stork, C., & Renshaw, P. F. (2005). Mitochondrial dysfunction in bipolar disorder: Evidence from magnetic resonance spectroscopy research. Molecular Psychiatry, 10(10), 900–919. https://doi.org/10.1038/sj.mp.4001706

Sublette, M. E., Ellis, S. P., Geant, A. L., & Mann, J. J. (2011). Meta-analysis of the effects of eicosapentaenoic acid (EPA) in clinical trials in depression. Journal of Clinical Psychiatry, 72(12), 1577–1584. https://doi.org/10.4088/JCP.10m06634

Swardfager, W., Herrmann, N., Mazereeuw, G., Goldberger, K., Harimoto, T., & Lanctôt, K. L. (2013). Zinc in depression: A meta-analysis. Biological Psychiatry, 74(12), 872–878. https://doi.org/10.1016/j.biopsych.2013.05.008

Young, S. N. (2007). Folate and depression—a neglected problem. Journal of Psychiatry & Neuroscience, 32(2), 80–82.