How To Get Rid Of Brain Fog

How To Get Rid Of Brain Fog: Understanding Causes and Targeted Treatment

Brain fog is one of those frustrating symptoms that can make you feel like you’re thinking through a thick haze. You might struggle to find the right words, forget why you walked into a room, or feel like your mental processing speed has dropped to a crawl. While “brain fog” is a colloquial term rather than a medical diagnosis, it refers to very real cognitive difficulties including reduced mental clarity, inability to concentrate, forgetfulness, and slowed thinking.

Here’s the important truth: brain fog is a symptom, not a diagnosis. It’s your body’s way of signalling that something deeper needs attention. Understanding what’s causing your brain fog is essential to understanding how to get rid of brain fog effectively.

Check out our other blogs on brain fog here.

What Does the Research Tell Us About Brain Fog?

Research characterises brain fog as a constellation of symptoms involving reduced cognition, difficulty concentrating and multitasking, as well as loss of short and long-term memory. Studies show that people experiencing brain fog often describe it as slow thinking, confusion, lack of concentration, forgetfulness, or haziness in thought processes.

Brain fog appears across numerous conditions including chronic fatigue syndrome, long COVID, hypothyroidism, menopause, autoimmune diseases, mast cell activation disorders, and following chemotherapy. The common thread? These conditions all involve underlying biological mechanisms that disrupt normal brain function.

The Multifactorial Nature of Brain Fog

There is no singular treatment for brain fog because there is no singular cause. The key to addressing brain fog effectively is investigating and understanding the mechanisms contributing to your specific symptoms. Research has identified several common underlying causes:

1. Gut Imbalances and the Gut-Brain Axis

The connection between gut health and cognitive function is increasingly well-established. Your gut microbiome communicates bidirectionally with your brain through what scientists call the gut-brain axis. This communication occurs through multiple pathways including the vagus nerve, immune system signalling, and microbial metabolites that can cross the blood-brain barrier.

Research demonstrates that gut microbiome produce metabolites like short-chain fatty acids (SCFAs) that affect mucosal immunity, immune responses, and ultimately cognitive function. Studies have shown correlations between gut microbiota diversity and enhanced cognitive flexibility and executive function.

Gut dysbiosis—an imbalance in the gut microbiome—is strongly associated with cognitive decline. When the intestinal barrier becomes compromised (often called “leaky gut”), there’s an elevation in inflammatory mediators and metabolites that can activate immune responses and promote inflammatory processes. These alterations may ultimately contribute to cognitive impairments through their impact on brain neurons.

Key considerations for gut health and brain fog:

• SIBO (Small Intestinal Bacterial Overgrowth): Overgrowth of bacteria in the small intestine can impair nutrient absorption and increase inflammatory compounds that affect brain function
• Intestinal permeability (leaky gut): When tight junctions in the gut lining become compromised, inflammatory molecules can enter the bloodstream and potentially cross the blood-brain barrier
• Microbiome diversity: Reduced diversity of beneficial gut bacteria is linked to increased inflammation and cognitive symptoms
• Digestive function: Poor digestion can lead to nutrient deficiencies that directly impact brain health

Testing and treatment approach: If gut dysfunction is suspected, comprehensive stool testing can evaluate microbiome diversity, beneficial and pathogenic bacteria, markers of intestinal permeability, and digestive function. Treatment typically involves addressing infections or overgrowths, healing the intestinal lining with nutrients like L-glutamine and zinc, replenishing beneficial bacteria with targeted prebiotics, and supporting digestive function.

Discover the reasons for your gut symptoms.

View our gut health tests

2. Vitamin B12 Deficiency

Vitamin B12 is essential for neurological and cognitive health, playing critical roles in myelin integrity (the protective coating around nerves), neurotransmitter synthesis, and homocysteine metabolism. Research clearly demonstrates that low serum vitamin B12 levels are associated with neurodegenerative disease and cognitive impairment.

B12 deficiency disrupts these processes, leading to neurotoxic effects including oxidative stress, vascular damage, and neurodegeneration. Studies show that vitamin B12 deficiency can cause cognitive symptoms ranging from mild impairment to reversible dementia. One study found that among patients with cognitive impairment and B12 deficiency, vitamin B12 supplementation resulted in improved cognitive function, with mean MMSE scores improving significantly after treatment.

Causes of B12 deficiency:

• Dietary insufficiency: Particularly in vegetarians and vegans, as B12 is primarily found in animal products
• Malabsorption: Conditions affecting the stomach or small intestine, including atrophic gastritis, celiac disease, Crohn’s disease, or previous gastric surgery
• Pernicious anaemia: An autoimmune condition where the body cannot produce intrinsic factor, which is necessary for B12 absorption
• Medications: Proton pump inhibitors (PPIs), metformin, and some antibiotics can interfere with B12 absorption
• Age: Absorption naturally decreases with age

Testing and treatment: Testing should include serum B12 levels, and in some cases, methylmalonic acid (MMA) and homocysteine levels, which are more sensitive markers of functional B12 deficiency. The good news is that research shows oral vitamin B12 supplements are as effective as injections for most people with confirmed B12 deficiency. Those with severe deficiency or malabsorption issues may require higher doses or parenteral (injectable) forms initially.

3. Hypothyroidism

Hypothyroid-associated brain fog is a well-documented phenomenon. Symptoms commonly include fatigue, depressed mood, and cognitive difficulties in memory and executive function. Research shows these symptoms often predate the diagnosis of hypothyroidism, and the magnitude of cognitive impairment can range from mild to severe.

Studies demonstrate that hypothyroidism impacts cognitive function through multiple mechanisms. Thyroid hormones exert potent effects on the brain, influencing neurotransmitter systems (particularly acetylcholine, which is crucial for memory), synaptic plasticity, neurite growth, and neurogenesis. Thyroid hormones also enhance mitochondrial function and ATP production—critical in an energy-demanding organ like the brain.

One study of over 5,000 patients with hypothyroidism found that brain fog was associated most frequently with fatigue and cognitive symptoms, affecting up to 79% of participants.

Key considerations:

• Even when TSH levels are “adequately” controlled on levothyroxine, some patients continue to experience cognitive symptoms
• Subclinical hypothyroidism (slightly elevated TSH with normal free T4) may still cause cognitive impairment, particularly in people under 75 years old
• Some individuals may need combination T4/T3 therapy or optimisation of cofactors needed for thyroid hormone conversion (selenium, zinc, iron)
• It’s essential to rule out Hashimoto’s thyroiditis, an autoimmune condition that may require additional immune modulation

Testing and treatment: Comprehensive thyroid testing should include TSH, free T4, free T3, reverse T3, and thyroid antibodies (TPO and thyroglobulin antibodies). Treatment involves optimising thyroid hormone levels, addressing any autoimmune components, and ensuring adequate cofactor nutrients. Some patients benefit from addressing concurrent issues like adrenal dysfunction or sex hormone imbalances.

4. Mast Cell Activation and Histamine Intolerance

Mast cells are immune cells located throughout the body, particularly at boundaries between internal and external environments (like the gut lining, respiratory tract, and skin). When activated, mast cells release numerous inflammatory mediators, with histamine being one of the most significant.

Research shows that brain fog characterises patients with mast cell disorders, and that histamine and other mast cell mediators can activate microglia in the brain, causing focal brain inflammation. Mast cells are located perivascularly in the brain, particularly in the leptomeninges and hypothalamus, where they contain most of the brain’s histamine. Studies demonstrate that abnormally high or low histamine concentrations in the brain are found in various neurological and psychiatric conditions.

Brain fog is a common complaint in those with mast cell activation syndrome (MCAS) and histamine intolerance. When inflammatory agents including histamine are released from mast cells, they may activate microglia and increase the risk of brain inflammation, leading to symptoms of cognitive dysfunction.

Causes of mast cell activation and histamine intolerance:

• Genetic predisposition: Some people have genetic variants affecting mast cell stability or histamine metabolism
• Environmental triggers: Toxins, mould exposure, infections, stress
• Impaired histamine breakdown: Deficiency or dysfunction of DAO (diamine oxidase) and HNMT (histamine-N-methyltransferase), the enzymes that break down histamine
• Gut dysfunction: Since DAO is primarily produced in the small intestine, gut inflammation or damage can impair histamine breakdown
• Nutrient deficiencies: DAO requires copper, vitamin B6, and vitamin C to function optimally

Testing and treatment approach: Diagnosis can be challenging as mast cell mediators fluctuate. Testing may include serum tryptase, serum histamine, 24-hour urine histamine and N-methylhistamine, and prostaglandin D2. DAO levels can also be measured. Treatment focuses on stabilising mast cells with natural compounds (like quercetin, vitamin C, and omega-3 fatty acids) or medications (such as cromolyn sodium or ketotifen), blocking histamine receptors with H1 and H2 antihistamines, supporting DAO function with cofactor nutrients, following a lower-histamine diet during active phases, and identifying and removing triggers.

5. Hormonal Changes (Menopause)

Brain fog during the menopausal transition, sometimes called “meno-fog,” is common and well-documented. Longitudinal studies find small but reliable declines in objective memory performance as women transition into perimenopause, and these declines are not explained by advancing age alone.

Changes in sex steroid hormones, particularly 17β-estradiol, play a key role. Estrogen has potent effects on the brain, influencing cholinergic neurotransmitter systems relevant to memory, enhancing synaptic plasticity, promoting neurogenesis, and improving mitochondrial function. During menopause, declining estrogen levels can therefore directly impact cognitive processes.

Research shows that women’s experience of brain fog during menopause extends beyond memory complaints, affecting a broad range of cognitive abilities including attention, processing speed, and executive function. Studies indicate brain fog is tied to the severity of certain menopause symptoms, especially depression, sleep disturbances, and vasomotor symptoms (hot flashes).

Key considerations:

• Brain fog often appears during perimenopause when hormone levels are fluctuating, not just after menopause
• Sleep disruption from night sweats and hot flashes contributes significantly to cognitive symptoms
• Mood changes (anxiety, depression) can exacerbate cognitive difficulties
• For most women, cognitive symptoms improve after the transition to postmenopause

Treatment approach: Management involves addressing menopausal symptoms comprehensively. This may include hormone replacement therapy (HRT) for appropriate candidates during the early menopausal transition, improving sleep quality through sleep hygiene and potentially cognitive behavioural therapy for insomnia, stress management techniques, regular exercise which supports cognitive function and mood, and nutritional support including omega-3 fatty acids, B vitamins, and antioxidants.

6. Inflammation and Neuroinflammation

Chronic inflammation, particularly neuroinflammation, is increasingly recognised as a central mechanism in brain fog across multiple conditions. Research demonstrates that brain fog may be due to inflammatory molecules, including cytokines that can activate microglia (the brain’s immune cells) and cause focal brain inflammation.

Studies on long COVID patients with brain fog show evidence of sustained neuroinflammation, blood-brain barrier disruption, and elevated inflammatory markers including glial fibrillary acidic protein (GFAP) and transforming growth factor-β (TGFβ). Inflammatory cytokines play a significant role in reducing long-term potentiation and long-term depression—processes critical for learning and memory—as well as reducing neurogenesis and dendritic sprouting.

The relationship between systemic inflammation and cognitive function is bidirectional. Chronic inflammatory conditions can lead to brain fog, while addressing inflammation often improves cognitive symptoms.

Sources of chronic inflammation:

• Chronic infections (viral, bacterial, parasitic)
• Autoimmune conditions
• Food sensitivities and allergies
• Environmental toxin exposure
• Chronic stress
• Poor sleep quality
• Sedentary lifestyle
• Diet high in processed foods and refined sugars

Testing and treatment: Testing may include inflammatory markers like high-sensitivity CRP, ESR, cytokine panels, and autoimmune antibodies. Treatment involves identifying and addressing sources of inflammation, adopting an anti-inflammatory diet rich in colourful vegetables, omega-3 fatty acids, and polyphenols, using targeted anti-inflammatory supplements like curcumin, omega-3s, and specialised pro-resolving mediators, optimising sleep and stress management, and regular moderate exercise which has anti-inflammatory effects.

A Personalised Approach to Treating Brain Fog

Given the multifactorial nature of brain fog, effective treatment requires:

1. Comprehensive evaluation: Work with a healthcare practitioner who will investigate potential underlying causes rather than simply treating symptoms
2. Appropriate testing: Based on your symptoms and history, this might include thyroid function tests, vitamin B12 and other nutritional markers, comprehensive stool testing, inflammatory markers, hormone panels, and specialised tests for mast cell disorders
3. Targeted treatment: Address the specific mechanisms contributing to your brain fog
4. Lifestyle optimisation: Regardless of the underlying cause, supporting overall brain health through quality sleep, stress management, regular movement, and an anti-inflammatory diet will support recovery
5. Patience: Brain fog often doesn’t resolve overnight. Improvement is typically gradual as underlying issues are addressed

Conclusion

Brain fog is frustrating and can significantly impact your quality of life, but it’s important to remember that it’s a symptom pointing to underlying imbalances. The good news is that brain fog is often reversible once the root causes are identified and addressed.

Whether your brain fog stems from gut dysfunction, nutritional deficiencies, thyroid imbalances, mast cell activation, hormonal changes, or chronic inflammation—or a combination of these factors—there are evidence-based approaches to investigation and treatment. By taking a comprehensive, individualised approach and working with knowledgeable healthcare practitioners, you can clear the fog and regain your mental clarity.

---

References

1. Ocon AJ. Caught in the thickness of brain fog: exploring the cognitive symptoms of Chronic Fatigue Syndrome. Front Physiol. 2013;4:63. https://pubmed.ncbi.nlm.nih.gov/23576989/
2. Ross AJ, Medow MS, Rowe PC, Stewart JM. What is brain fog? An evaluation of the symptom in postural tachycardia syndrome. Clin Auton Res. 2013;23(6):305-311. https://pubmed.ncbi.nlm.nih.gov/23999934/
3. Hugon J, Msika EF, Queneau M, Farid K, Paquet C. Long COVID: cognitive complaints (brain fog) and dysfunction of the cingulate cortex. J Neurol. 2022;269(1):44-46. https://pubmed.ncbi.nlm.nih.gov/34143277/
4. Delgado-Alonso C, Díez-Cirarda M, Pagán J, et al. Comprehensive clinical characterisation of brain fog in adults reporting long COVID symptoms. J Neurol Neurosurg Psychiatry. 2022;93(10):1040-1046. https://pubmed.ncbi.nlm.nih.gov/35743516/
5. Vogt NM, Kerby RL, Dill-McFarland KA, et al. Gut microbiome alterations in Alzheimer’s disease. Sci Rep. 2017;7:13537. https://pubmed.ncbi.nlm.nih.gov/29045397/
6. Ghaisas S, Maher J, Kanthasamy A. Gut microbiome in health and disease: Linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. Pharmacol Ther. 2016;158:52-62. https://pubmed.ncbi.nlm.nih.gov/26627987/
7. Chen Y, Xu J, Chen Y. Regulation of neurotransmitters by the gut microbiota and effects on cognition in neurological disorders. Nutrients. 2021;13(6):2099. https://pubmed.ncbi.nlm.nih.gov/34205349/
8. Foster JA, Rinaman L, Cryan JF. Stress & the gut-brain axis: Regulation by the microbiome. Neurobiol Stress. 2017;7:124-136. https://pubmed.ncbi.nlm.nih.gov/29276734/
9. Mayer EA, Knight R, Mazmanian SK, Cryan JF, Tillisch K. Gut microbes and the brain: paradigm shift in neuroscience. J Neurosci. 2014;34(46):15490-15496. https://pubmed.ncbi.nlm.nih.gov/25392516/
10. Cryan JF, O’Riordan KJ, Cowan CSM, et al. The microbiota-gut-brain axis. Physiol Rev. 2019;99(4):1877-2013. https://pubmed.ncbi.nlm.nih.gov/31460832/
11. Shi H, Wang Q, Zheng M, et al. Supplement of microbiota-accessible carbohydrates prevents neuroinflammation and cognitive decline by improving the gut microbiota-brain axis in diet-induced obese mice. J Neuroinflammation. 2020;17(1):77. https://pubmed.ncbi.nlm.nih.gov/32127019/
12. Li B, He Y, Ma J, et al. Mild cognitive impairment has similar alterations as Alzheimer’s disease in gut microbiota. Alzheimers Dement. 2019;15(10):1357-1366. https://pubmed.ncbi.nlm.nih.gov/31434623/
13. Riaz Rajoka MS, Zhao H, Lu Y, et al. Anticancer potential against cervix cancer (HeLa) cell line of probiotic Lactobacillus casei and Lactobacillus paracasei strains isolated from human breast milk. Food Funct. 2018;9(5):2705-2715. https://pubmed.ncbi.nlm.nih.gov/29682653/
14. Smith KJ, Butler T, Baune BT. Differential effects of depressive symptom dimensions on cardio-metabolic risk factors: a mendelian randomization study. Front Genet. 2021;12:634995. https://pubmed.ncbi.nlm.nih.gov/33815479/
15. Shirvani-Rad S, Tabatabaei-Malazy O, Mohseni S, et al. Is there any link between cognitive impairment and gut microbiota? A systematic review. Dement Geriatr Cogn Disord. 2022;51(1):1-15. https://pubmed.ncbi.nlm.nih.gov/35263739/
16. Moore E, Mander A, Ames D, et al. Cognitive impairment and vitamin B12: a review. Int Psychogeriatr. 2012;24(4):541-556. https://pubmed.ncbi.nlm.nih.gov/22221769/
17. McCaddon A, Regland B, Hudson P, Davies G. Functional vitamin B12 deficiency and Alzheimer disease. Neurology. 2002;58(9):1395-1399. https://pubmed.ncbi.nlm.nih.gov/12011290/
18. Smith AD, Refsum H. Homocysteine, B vitamins, and cognitive impairment. Annu Rev Nutr. 2016;36:211-239. https://pubmed.ncbi.nlm.nih.gov/27431367/
19. Health Quality Ontario. Vitamin B12 and cognitive function: an evidence-based analysis. Ont Health Technol Assess Ser. 2013;13(23):1-45. https://pubmed.ncbi.nlm.nih.gov/24379897/
20. O’Leary F, Samman S. Vitamin B12 in health and disease. Nutrients. 2010;2(3):299-316. https://pubmed.ncbi.nlm.nih.gov/22254022/
21. Hama Y, Hamano T, Shirafuji N, et al. Influences of vitamin B12 supplementation on cognition and homocysteine in patients with vitamin B12 deficiency and cognitive impairment. Nutrients. 2022;14(7):1494. https://pubmed.ncbi.nlm.nih.gov/35406106/
22. Reynolds EH. The neurology of folic acid deficiency. Handb Clin Neurol. 2014;120:927-943. https://pubmed.ncbi.nlm.nih.gov/24365359/
23. Andrès E, Affenberger S, Zimmer J, et al. Current hematological findings in cobalamin deficiency. A study of 201 consecutive patients with documented cobalamin deficiency. Clin Lab Haematol. 2006;28(1):50-56. https://pubmed.ncbi.nlm.nih.gov/16451399/
24. McCaddon A. Vitamin B12 in neurology and ageing; clinical and genetic aspects. Biochimie. 2013;95(5):1066-1076. https://pubmed.ncbi.nlm.nih.gov/23174551/
25. Stabler SP. Clinical practice. Vitamin B12 deficiency. N Engl J Med. 2013;368(2):149-160. https://pubmed.ncbi.nlm.nih.gov/23301732/
26. Quadros EV. Advances in the understanding of cobalamin assimilation and metabolism. Br J Haematol. 2010;148(2):195-204. https://pubmed.ncbi.nlm.nih.gov/19832808/
27. Dali-Youcef N, Andrès E. An update on cobalamin deficiency in adults. QJM. 2009;102(1):17-28. https://pubmed.ncbi.nlm.nih.gov/18990719/
28. Spence JD. Metabolic vitamin B12 deficiency: a missed opportunity to prevent dementia and stroke. Nutr Res. 2016;36(2):109-116. https://pubmed.ncbi.nlm.nih.gov/26826426/
29. Green R, Allen LH, Bjørke-Monsen AL, et al. Vitamin B12 deficiency. Nat Rev Dis Primers. 2017;3:17040. https://pubmed.ncbi.nlm.nih.gov/28660890/
30. Rizzo G, Laganà AS, Rapisarda AM, et al. Vitamin B12 among vegetarians: status, assessment and supplementation. Nutrients. 2016;8(12):767. https://pubmed.ncbi.nlm.nih.gov/27916823/
31. Samuels MH, Bernstein LJ. Brain fog in hypothyroidism: what is it, how is it measured, and what can be done about it. Thyroid. 2022;32(7):752-763. https://pubmed.ncbi.nlm.nih.gov/35414261/
32. Ettleson MD, Raine A, Batistuzzo A, et al. Brain fog in hypothyroidism: understanding the patient’s perspective. Endocr Pract. 2022;28(3):257-264. https://pubmed.ncbi.nlm.nih.gov/34890786/
33. Haskard-Zolnierek K, Wilson C, Pruin J, et al. The relationship between brain fog and medication adherence for individuals with hypothyroidism. Clin Nurs Res. 2022;31(3):445-452. https://pubmed.ncbi.nlm.nih.gov/34348493/
34. Gulseren S, Gulseren L, Hekimsoy Z, et al. Depression, anxiety, health-related quality of life, and disability in patients with overt and subclinical thyroid dysfunction. Arch Med Res. 2006;37(1):133-139. https://pubmed.ncbi.nlm.nih.gov/16314199/
35. Berent D, Zboralski K, Orzechowska A, Gałecki P. Thyroid hormones association with depression severity and clinical outcome in patients with major depressive disorder. Mol Biol Rep. 2014;41(4):2419-2425. https://pubmed.ncbi.nlm.nih.gov/24443213/
36. Bauer M, Goetz T, Glenn T, Whybrow PC. The thyroid-brain interaction in thyroid disorders and mood disorders. J Neuroendocrinol. 2008;20(10):1101-1114. https://pubmed.ncbi.nlm.nih.gov/18673409/
37. Jabbar A, Pingitore A, Pearce SH, et al. Thyroid hormones and cardiovascular disease. Nat Rev Cardiol. 2017;14(1):39-55. https://pubmed.ncbi.nlm.nih.gov/27708278/
38. Biondi B, Cooper DS. The clinical significance of subclinical thyroid dysfunction. Endocr Rev. 2008;29(1):76-131. https://pubmed.ncbi.nlm.nih.gov/17991805/
39. Chaker L, Bianco AC, Jonklaas J, Peeters RP. Hypothyroidism. Lancet. 2017;390(10101):1550-1562. https://pubmed.ncbi.nlm.nih.gov/28336049/
40. Ittermann T, Völzke H, Baumeister SE, et al. Diagnosed thyroid disorders are associated with depression and anxiety. Soc Psychiatry Psychiatr Epidemiol. 2015;50(9):1417-1425. https://pubmed.ncbi.nlm.nih.gov/25735418/
41. Theoharides TC, Tsilioni I, Ren H. Recent advances in our understanding of mast cell activation – or should it be mast cell mediator disorders? Expert Rev Clin Immunol. 2019;15(6):639-656. https://pubmed.ncbi.nlm.nih.gov/30884251/
42. Theoharides TC, Stewart JM, Hatziagelaki E, Kolaitis G. Brain “fog,” inflammation and obesity: key aspects of neuropsychiatric disorders improved by luteolin. Front Neurosci. 2015;9:225. https://pubmed.ncbi.nlm.nih.gov/26190965/
43. Molderings GJ, Haenisch B, Bogdanow M, et al. Pharmacological treatment options for mast cell activation disease. Naunyn Schmiedebergs Arch Pharmacol. 2016;389(7):671-694. https://pubmed.ncbi.nlm.nih.gov/27132234/
44. Afrin LB, Ackerley MB, Bluestein LS, et al. Diagnosis of mast cell activation syndrome: a global “consensus-2”. Diagnosis (Berl). 2021;8(2):137-152. https://pubmed.ncbi.nlm.nih.gov/32324159/
45. Weinstock LB, Pace LA, Rezaie A, et al. Mast cell activation syndrome: a primer for the gastroenterologist. Dig Dis Sci. 2021;66(4):965-982. https://pubmed.ncbi.nlm.nih.gov/32857277/
46. Afrin LB, Pohlau D, Raithel M, et al. Mast cell activation disease: an underappreciated cause of neurologic and psychiatric symptoms and diseases. Brain Behav Immun. 2015;50:314-321. https://pubmed.ncbi.nlm.nih.gov/26162709/
47. Frieri M, Patel R, Celestin J. Mast cell activation syndrome: a review. Curr Allergy Asthma Rep. 2013;13(1):27-32. https://pubmed.ncbi.nlm.nih.gov/23065327/
48. Valent P, Akin C, Metcalfe DD. Mastocytosis: 2016 updated WHO classification and novel emerging treatment concepts. Blood. 2017;129(11):1420-1427. https://pubmed.ncbi.nlm.nih.gov/28031180/
49. Maintz L, Novak N. Histamine and histamine intolerance. Am J Clin Nutr. 2007;85(5):1185-1196. https://pubmed.ncbi.nlm.nih.gov/17490952/
50. Comas-Basté O, Sánchez-Pérez S, Veciana-Nogués MT, et al. Histamine intolerance: the current state of the art. Biomolecules. 2020;10(8):1181. https://pubmed.ncbi.nlm.nih.gov/32824107/
51. Maki PM, Jaff NG. Brain fog in menopause: a health-care professional’s guide for decision-making and counseling on cognition. Climacteric. 2022;25(6):570-578. https://pubmed.ncbi.nlm.nih.gov/36178170/
52. Weber MT, Rubin LH, Maki PM. Cognition in perimenopause: the effect of transition stage. Menopause. 2013;20(5):511-517. https://pubmed.ncbi.nlm.nih.gov/23615643/
53. Henderson VW, Popat RA. Effects of endogenous and exogenous estrogen exposures in midlife and late-life women on episodic memory and executive functions. Neuroscience. 2011;191:129-138. https://pubmed.ncbi.nlm.nih.gov/21664950/
54. Epperson CN, Sammel MD, Freeman EW. Menopause effects on verbal memory: findings from a longitudinal community cohort. J Clin Endocrinol Metab. 2013;98(9):3829-3838. https://pubmed.ncbi.nlm.nih.gov/23836935/
55. Weber MT, Maki PM, McDermott MP. Cognition and mood in perimenopause: a systematic review and meta-analysis. J Steroid Biochem Mol Biol. 2014;142:90-98. https://pubmed.ncbi.nlm.nih.gov/23583279/
56. Greendale GA, Huang MH, Wight RG, et al. Effects of the menopause transition and hormone use on cognitive performance in midlife women. Neurology. 2009;72(21):1850-1857. https://pubmed.ncbi.nlm.nih.gov/19470968/
57. Maki PM, Sundermann E. Hormone therapy and cognitive function. Hum Reprod Update. 2009;15(6):667-681. https://pubmed.ncbi.nlm.nih.gov/19468048/
58. Rocca WA, Bower JH, Maraganore DM, et al. Increased risk of cognitive impairment or dementia in women who underwent oophorectomy before menopause. Neurology. 2007;69(11):1074-1083. https://pubmed.ncbi.nlm.nih.gov/17761551/
59. Sherwin BB. Estrogen and cognitive functioning in women: lessons we have learned. Behav Neurosci. 2012;126(1):123-127. https://pubmed.ncbi.nlm.nih.gov/22004261/
60. Maki PM. Critical window hypothesis of hormone therapy and cognition: a scientific update on clinical studies. Menopause. 2013;20(6):695-709. https://pubmed.ncbi.nlm.nih.gov/23715379/
61. Kavanagh E. Long Covid brain fog: a neuroinflammation phenomenon? Oxford Open Immunol. 2022;3(1):iqac007. https://pubmed.ncbi.nlm.nih.gov/36846556/