This protocol was developed for practitioners using Fullscript in the United States and the templates cannot be applied to accounts operating outside of the United States

Protocol development in integrative medicine is not typically a simple process. Individuals require individualized care, and what works for one patient may not work for another.

To establish these protocols, we first developed a Rating Scale that could be used to discern the rigor of evidence supporting a specific nutrient’s therapeutic effect.

The following protocols were developed using only A through D-quality evidence.

Class
Qualifying studies
Minimum requirements
A
Systematic review or meta-analysis of human trials
 
B
RDBPC human trials
2+ studies and/or 1 study with 50 + subjects
C
RDBPC human trials
1 study
D
Non-RDBPC human or In-vivo animal trials
 

Introduction

Cognitive Essentials for Healthy Aging provides clinicians with a structured, evidence-informed framework for supporting brain health throughout the lifespan.

This foundational clinical guide focuses on nurturing the biological processes that contribute to cognitive performance: cellular energy production, oxidative balance, inflammation regulation, and nutrient sufficiency.

What Is Cognitive Longevity?

Cognitive longevity describes the capacity to maintain attention, memory, and mental clarity by supporting the systems that influence brain function. These include mitochondrial efficiency, antioxidant capacity, inflammation balance, adequate nutrient status, and circadian rhythm alignment. 

This clinical guide emphasizes proactive, measurable approaches that help sustain optimal brain performance and overall vitality across the aging process.

Why It Matters

As patients live longer and experience increasing cognitive demands, providers are uniquely positioned to guide them in maintaining brain vitality. Everyday contributors such as oxidative stress, inflammation, and nutritional insufficiency can influence cognitive efficiency long before disease manifests.This clinical guide empowers providers to apply evidence-based and foundational measures that help sustain attention, learning, memory, and executive performance while promoting overall well-being. By focusing on these essential physiologic processes, providers can guide patients toward habits that support healthy brain function and overall well-being.

Purpose of the Clinical Guide

The Cognitive Essentials for Healthy Aging clinical guide was designed to:

  1. Simplify decision-making using standardized, evidence-rated nutrient and lifestyle interventions.
  2. Integrate laboratory and biomarker data to identify modifiable contributors to cognitive health.

Serve as the foundation for individualized care plans aimed at maintaining cognitive performance through aging.

Essential Labs

Oxidative Stress Markers 

Oxidative stress markers measure the balance between free radicals and antioxidants, which can influence neuronal health and cognitive longevity. Oxidative stress is significantly elevated in individuals with Alzheimer’s disease and mild cognitive impairment (MCI), highlighting its role in disease progression. (Schrag 2013)

Gamma-Glutamyl Transferase (GGT)

Elevated serum GGT levels are associated with increased risk of dementia, including AD and vascular dementia, likely reflecting pro-oxidant pathways contributing to neurodegeneration. (Han 2020)

Uric Acid

Lower serum uric acid (SUA) levels (< 5.0 mg/dl) are linked to increased risk and accelerated progression of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease, likely due to reduced antioxidant protection and heightened oxidative stress. (Euser 2009) In contrast, higher SUA levels (> 6.7-7.1 mg/dl) are associated with increased risk of vascular dementia and cognitive decline, potentially through pro-inflammatory and vascular injury pathways. (Tana 2018)

Homocysteine

Homocysteine is a sulfur-containing amino acid whose elevated plasma levels are associated with increased risk of cognitive decline, dementia, and vascular contributions to neurodegeneration. Elevated homocysteine promotes endothelial dysfunction, oxidative stress, and neurotoxicity, contributing to white matter lesions and brain atrophy. (Smith 2016)

High homocysteine levels promote vascular damage and neuroinflammation by increasing oxidative stress and disrupting blood-brain barrier integrity, leading to white matter lesions and neuronal injury. (Sudduth 2013) 

Test Recommended Range Evidence-Based Ranges Associated with Oxidative Stress
GGT Male: 12–68 U/L

Female: 6–40 U/L

 ≥44 IU/L in men

≥26 IU/L in women

Associated with increased risk of dementia, including Alzheimer’s and vascular dementia. 
Uric acid Male : 4–8 mg/dL   

Female : 2.5–7 mg/dL

 Lower levels (<5.0 mg/dL) are linked to increased risk and accelerated progression of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease.

Higher levels (>6.7–7.1 mg/dL) are associated with increased risk of vascular dementia and cognitive decline.
Homocysteine Male: <11.4 umol/L

Female: <10.4 umol/L

 Elevated homocysteine levels are associated with increased risk of cognitive decline, dementia, and vascular contributions to neurodegeneration. 

High levels are also associated with increased vascular damage and neuroinflammation by disrupting blood-brain barrier integrity, leading to neuronal injury.

(Han 2020)(Euser 2008)(Tana 2018)(Zhou 2019)

Inflammation

Inflammation markers reflect systemic and neuroinflammatory activity, which has been associated with cognitive decline, slower processing speed, and memory impairments. Elevated inflammatory markers have been linked to structural brain changes and reduced cognitive performance in older adults. (Xie 2022)

High-Sensitivity C-Reactive Protein (hs-CRP)

Higher midlife hs-CRP levels have been associated with greater long-term declines in overall cognition, particularly in memory performance. These findings reflect chronic, low-grade inflammation rather than acute elevations, with elevated hs-CRP indicating inflammatory activity linked to accelerated cognitive decline and increased vulnerability to late-life cognitive impairment. (Walker 2019)

Complete Blood Count 

White Blood Cell Count

Elevated white blood cell (WBC) counts (leukocytosis) (>11,000 per mm3) are independently associated with increased risk of cognitive decline and dementia in both Alzheimer’s and Parkinson’s disease. Leukocytosis has been identified as a risk factor for Parkinson’s dementia and is linked to mechanisms underlying cognitive dysfunction, suggesting that systemic inflammation may accelerate neurodegeneration. (Unda 2021) Higher WBC counts are also inversely associated with brain volume and markers of advanced brain aging, with magnetic resonance imaging (MRI) studies showing that elevated WBCs correlate with accelerated brain atrophy patterns observed in dementia. (Janowitz 2020)

Systemic Immune-Inflammation Index (SII)

The SII is calculated using the formula SII = (platelet count × neutrophil count) / lymphocyte count. This index reflects the interaction between inflammatory activity, represented by neutrophils and platelets, and immune regulation, represented by lymphocytes. Elevated SII levels indicate systemic inflammation, which has been associated with cognitive impairment and an increased risk of neurodegenerative disease. (Wang 2025)

Systemic Inflammation Response Index (SIRI)

The SIRI is calculated using the formula SIRI = (neutrophil count × monocyte count) / lymphocyte count. This index represents the balance between innate immune activation, driven by neutrophils and monocytes, and adaptive immune defense, mediated by lymphocytes. Higher SIRI values indicate a greater systemic inflammatory burden, which may contribute to cognitive decline and the progression of chronic diseases. Overall, SIRI provides a simple and accessible biomarker for assessing inflammation-related cognitive risk. (Wang 2025)

Neutrophil-Lymphocyte Ratio (NLR)

The NLR is a marker of systemic inflammation derived from standard complete blood count (CBC) results. In a meta-analysis, a high NLR was associated with a significantly greater risk of cognitive impairment (OR 2.53, 95% CI 1.67–3.82, p < 0.0001). (Hung 2022)

Comprehensive Metabolic Panel (CMP) – Aspartate Aminotransferase (AST) and Alanine Aminotransferase (ALT)

Higher AST levels and lower ALT levels have been associated with an increased risk of cognitive decline and dementia. Elevated AST and AST to ALT ratio have been correlated with poorer cognitive performance, while reduced ALT has been linked to lower cognitive scores and greater dementia risk. Liver enzyme imbalances have also been associated with structural brain changes in regions such as the hippocampus, amygdala, and thalamus, suggesting that liver dysfunction may contribute to neurodegeneration and cognitive impairment. (Gao 2024)

Test Recommended Range
hs-CRP Risk according to American Heart Association (AHA)/Centers for Disease Control and Prevention (CDC) guidelines (for ages >17 years):

  • Lower relative cardiovascular (CVD) risk: <1
  • Average relative CVD risk: 1–3
  • Higher relative CVD risk: 3.1–10
    • Consider retesting in 1–2 weeks to exclude a benign transient elevation in the baseline CRP value secondary to infection or inflammation
  • Persistent elevation upon retesting: >10 
    • May be associated with infection and inflammation
WBC 3.8–10.8 thousand/µL
SII
  • SII = (platelet count × neutrophil count) / lymphocyte count
  • SII cutoff for moderate–severe dementia: 335.15
    • Sensitivity: 90.4%
    • Specificity: 31.1%
SIRI
  • SIRI = (neutrophil count × monocyte count) / lymphocyte count
  • Range: 0.3–1.2
NLR 0.78–3.53
ALT
  • Male (≥20 years): 9–46 U/L 
  • Female (≥20 years): 6–29 U/L
AST Male:

  •  20–49 years: 10–40 U/L
  •  ≥50 years: 10–35 U/L 

Female: 

  • 20–44 years: 10–30 U/L
  • ≥45 years: 10–35 U/L

(Algul 2025)(Choi 2024)(Myers 2004)(Quest Diagnostics)

Nutrients

Nutrient markers assess levels of essential vitamins, minerals, and cofactors that support brain structure and function, with evidence showing optimal nutrient levels are linked to preservation of brain networks and reduced risk of neurodegeneration. (Zwilling 2024)

Iron, Ferritin

Excess iron in the brain contributes to oxidative stress and neurodegeneration by promoting the generation of reactive oxygen species (ROS) and lipid peroxidation. With age, iron accumulates in specific brain regions. Dysregulation of iron homeostasis amplifies oxidative stress and cellular damage, playing a key role in the pathogenesis of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease. (Ward 2014)

Elevated serum ferritin is associated with an increased risk of stroke, a condition that shares vascular pathology with dementia and contributes to cognitive decline. Iron overload can damage vascular and neuronal tissues by generating reactive oxygen species, triggering inflammation and causing endothelial injury. (Zheng 2025)

Both iron deficiency (ID) and iron deficiency anemia (IDA) are associated with deficits in cognitive performance, behavioral regulation, and motor development. These effects are thought to arise from disruptions in hippocampal architecture, impaired mitochondrial function, altered dopamine metabolism, and delayed or dysregulated myelination during critical neurodevelopmental windows. (Jáuregui-Lobera 2014)

Vitamin D (25-OH)

Vitamin D supports long-term cognitive health by modulating neuroinflammation, maintaining calcium homeostasis, and promoting neuronal growth and repair. (Muir 2011) Low serum vitamin D levels are linked to increased risk of dementia and poorer cognitive function in older adults. (Balion 2012)(Etgen 2012)

Magnesium – Red Blood Cell (RBC)

RBC magnesium reflects intracellular magnesium status, which is critical for neuronal function. Both low and high serum magnesium levels are associated with increased dementia risk. (Kieboom 2017)

Omega-3 Fatty Acids

Omega-3 fatty acids support cognitive health, with benefits most pronounced in individuals with MCI. Improvements are observed in attention, processing speed, and working memory. (Mazereeuw 2012)

Zinc

Zinc is an essential trace element critical for central nervous system function, regulating synaptic activity and neuronal signaling. Low serum zinc levels are associated with cognitive decline and dementia conversion in Parkinson’s disease patients. (Lee 2023)

B Vitamins: B12, Folate, B6

Vitamin B12 and folate are essential for one-carbon metabolism and DNA synthesis. Supplementation lowers homocysteine, a neurotoxic amino acid associated with cognitive decline and dementia. Benefits are most evident in patients with MCI or early Alzheimer’s disease who are not receiving folate-fortified foods. (Chen 2021)

Maintaining optimal B-vitamin status helps support healthy homocysteine metabolism, which has been associated with favorable cognitive outcomes in adults with elevated homocysteine levels. (Smith 2010)

Test Recommended Range
Vitamin D (25-OH) 30–100 ng/mL
B vitamins The following reference ranges apply to individuals ≥18 years 

  • Folate: >5.4 ng/mL
  • B1 (thiamine): 78–185 nmol/L
  • B2: 6.2–39.0 nmol/L
  • B3: ≤110 ng/mL
  • B5: <275 ng/mL
  • B6: 2.1–21.7 ng/mL
  • B12: 200–1,100 ng/mL
OmegaCheck®
  • Low CVD risk level: ≥5.5
  • Moderate CVD risk level: 3.8–5.4
  • High CVD risk level: ≤3.7 
RBC magnesium ≥18 years: 4.0–6.4 mg/dL
Zinc (serum/plasma) ≥18 years: 60–130 µg/dL
Iron Male (mcg/dL):

 •  4–19 years: 27–164

 •  20–29 years: 50–195         

 •  ≥30 years: 50–180         

 •  20–49 years: 40–190

 •  ≥50 years: 45–160

 Female (mcg/dL):        

 •  20–49 years: 40–190

 •  ≥50 years: 45–160
Ferritin Male (ng/mL):

•  19–59 years: 38–380 

•  >59 years: 24–380 L

 Female (ng/mL):

•  41–60 years: 16–232 

•  >60 years: 16–288 

(Chen 2018)(Quest Diagnostics)

Ingredients

Multivitamin, Multimineral 

Dosing: Dosing may vary depending on the specific product and should be tailored to the patient’s nutritional needs and goals, such as nutrient repletion or metabolic support. Healthcare providers should consult product-specific guidelines and adjust the dosage based on the patient’s unique requirements and response. 

Supporting evidence:

  • Multivitamin supplementation has been studied as a safe, accessible strategy to support cognitive function in older adults. (Baker 2023)(Yeung 2023)
  • In the large COSMOS-Mind randomized clinical trial (RCT) (n=2,262; mean age 73 years), daily multivitamin–mineral supplementation for three years helped significantly improve global cognition, episodic memory, and executive function compared with placebo, with the strongest benefits observed in participants with cardiovascular disease. (Baker 2023)
  • In the COSMOS-Web trial (n=3,562), daily multivitamin use helped improve episodic memory performance after one year and maintain this benefit over three years of follow-up, corresponding to a 3-year reduction in age-related memory decline. (Yeung 2023)

Magnesium L-Threonate

Dosing: 2 grams per day for 12 weeks 

Supporting evidence:

  • Magnesium L-threonate may more effectively raise brain magnesium levels compared to other forms, potentially enhancing synapse density and plasticity in regions important for memory and executive function. (Liu 2016)
  • A 12-week randomized, double-blind, placebo-controlled (RDBPC) trial in adults aged 50–70 with cognitive impairment found that magnesium L-threonate significantly improved overall cognitive ability (p=0.003), reduced cognitive fluctuation, and nearly restored impaired executive function. (Liu 2016)
  • In a placebo-controlled study of 109 healthy adults, daily supplementation with a Magtein®PS formula (2 g/day for 30 days) helped lead to significant improvements in all memory test categories and overall memory quotient, with the largest gains observed in older participants. (Zhang 2022)

Omega-3 Fatty Acids

Dosing: 2,000–4,000 mg/day of combined docosahexaenoic acid (DHA) + eicosapentaenoic acid (EPA) for 6–12 months

Supporting evidence:

  • Omega-3 fatty acids (DHA and EPA) support neuronal membrane integrity, modulate inflammation, and may improve synaptic function, mechanisms linked to cognitive health. (Stavrinou 2020)(Shahinfar 2025)(Yang 2024)
  • A meta-analysis of 12 trials in elderly adults with MCI (n=1,124) found that DHA/EPA supplementation helped improve global cognition (standardized mean difference [SMD] 0.51), though no benefits were seen for language fluency, executive function, or depression. (Yang 2024)
  • In a 6-month RDBPC trial of older adults with MCI, a high-dose formula containing EPA (810 mg), DHA (4,140 mg), gamma-linolenic acid (GLA) (1,800 mg), linoleic acid (LA) (3,150 mg), and antioxidant vitamins improved cognitive scores (Addenbrooke’s Cognitive Examination-Revised [ACE-R], Mini-Mental State Examination [MMSE]), Stroop Color and Word Test (STROOP) performance, functional capacity, fatigue, and sleepiness compared with placebo. (Stavrinou 2020)
  • A dose-response meta-analysis of 58 RCTs found that each 2,000 mg/day increment of omega-3 supplementation was associated with improvements in attention, perceptual speed, primary memory, visuospatial function, and global cognition, though effects varied by domain and followed non-linear dose relationships. However, doses above 3,000 mg/day offered no extra benefit and sometimes showed diminishing effects. (Shahinfar 2025)

Creatine Monohydrate

Dosing: 5 grams per day for 6–24 weeks 

  • Note the brain may require higher doses and/or longer loading phases (e.g., 20 g/day × 4 weeks) than those used to raise muscle creatine.

Supporting evidence:

  • Creatine plays a key role in brain energy homeostasis, buffering ATP supply during high energy demand. Supplementation increases brain creatine stores in some studies, which may support short-term memory and reasoning under cognitively demanding conditions. (Prokopidis 2023)
  • A systematic review and meta-analysis of RCTs (10 RCTs, 8 in meta-analysis) found creatine supplementation helped significantly improve memory compared with placebo (SMD = 0.29, p=0.02), with the greatest effects in older adults (ages 66–76, SMD = 0.88). (Prokopidis 2023)
  • Individual RCTs show variable outcomes: Rae (2003) reported that 5 g/day of creatine for 6 weeks significantly improved working memory (backward digit span) and reasoning (Raven’s matrices) in young vegetarian adults (p < 0.0001), while a larger trial (n=123, mixed vegetarians/omnivores) found only small, borderline benefits on working memory with no clear effects on reasoning. (Rae 2003)(Sandkühler 2023)

Ginkgo (Ginkgo biloba)

Dosing: 120 mg twice daily (total 240 mg/day) for at least 24 weeks

Supporting evidence: 

  • Ginkgo biloba extract (EGb 761) has been investigated for its antioxidant, anti-inflammatory, and neuroprotective effects, which may help stabilize or slow cognitive decline in Alzheimer’s disease and MCI. (Solfrizzi 2015)(Yuan 2017)
  • A meta-analysis including 2,561 patients found that EGb 761 at 240 mg/day for 22–26 weeks significantly improved cognition, activities of daily living, and global clinical ratings compared with placebo, particularly in those with neuropsychiatric symptoms. (Tan 2015)
  • An overview of 12 systematic reviews reported that Ginkgo biloba extract may have beneficial effects on cognitive performance, functional ability, and overall clinical impression at doses greater than 200 mg/day administered for at least 22 weeks. However, effects were not observed with lower doses or shorter treatment durations. (Yuan 2017)

Bacopa (Bacopa monnieri)

Dosing: 300–450 mg per day for 6–12 weeks

Supporting evidence:

  • Bacopa monnieri contains bacosides that may enhance synaptic communication, support neuronal repair, and provide antioxidant protection, mechanisms linked to improved learning and memory. (Pase 2012)(Kongkeaw 2014)(Kumar 2016)
  • In a 6-week RDBPC trial of 60 medical students, 300 mg/day of standardized Bacopa monnieri extract (Bacognize®) significantly improved multiple measures of memory and cognitive function compared with placebo. (Kumar 2016)
  • A systematic review of six RCTs (all 12 weeks, 300–450 mg/day standardized extracts) found consistent improvements in memory free recall, though effects in other cognitive domains were less studied. (Pase 2012)
  • A meta-analysis of nine RCTs (n=518, ≥12 weeks) demonstrated significant improvements in attention speed (reduced choice reaction time) and executive function (Trail Making Test B performance), supporting benefits beyond memory. (Kongkeaw 2014)

Lifestyle Recommendations

Nutrition

Risk Factors

Diets high in saturated fats, added sugars, and ultra-processed foods are associated with an increased risk of neurodegenerative diseases, including Alzheimer’s and Parkinson’s disease. These dietary patterns promote systemic inflammation, oxidative stress, insulin resistance, and gut dysbiosis, collectively accelerating neuronal aging and cognitive decline. (Solfrizzi 2017) Conversely, adequate intake of key nutrients—such as omega-3 fatty acids, B vitamins (B6, B12, folate), vitamin D, and antioxidants—supports neuroprotection by reducing amyloid deposition, Tau pathology, and neuroinflammation. (Bianchi 2019)

Interventions

Adherence to diets rich in vegetables, fruits, whole grains, legumes, nuts, fish, and olive oil (e.g., Mediterranean or Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND)-style diets), has been shown to reduce the risk of cognitive decline and dementia, likely through mechanisms including reduced oxidative stress, improved vascular health, and enhanced neurotrophic signaling. (Scarmeas 2006) A 2022 meta-analysis (31 cohort studies, 5 RCTs) further found that high adherence to the Mediterranean diet was associated with a 25% lower risk of MCI and a 29% lower risk of Alzheimer’s disease, along with better memory performance. (Fu 2022) Supporting long-term brain health can also involve:

  • Ensuring adequate intake of omega-3 fatty acids from fatty fish or supplements to support synaptic plasticity and reduce neuroinflammation
  • Optimizing B-vitamin status to maintain homocysteine levels and prevent vascular and neuronal damage
  • Increasing consumption of polyphenol-rich foods (berries, dark chocolate, green tea) to provide antioxidant and anti-inflammatory neuroprotection
  • Encouraging dietary patterns that support a healthy gut microbiome, which influences neuroimmune signaling and cognitive resilience

Movement

Risk Factors

A sedentary lifestyle significantly undermines brain health and resilience with aging. Lack of regular exercise contributes to impaired cerebral perfusion, reduced neurotrophic signaling (e.g., brain-derived neurotrophic factor [BDNF]), chronic inflammation, insulin resistance, and vascular dysfunction, all of which promote neuronal aging and cognitive impairment.  (Ahlskog 2011)(Lautenschlager 2008)) Older adults who do not engage in regular aerobic or resistance exercise demonstrate faster brain atrophy and reduced hippocampal volume, correlating with poorer memory and executive function outcomes.

Interventions

Engaging in regular physical activity—including aerobic exercise, resistance training, and balance or mobility exercises—slows cognitive decline and reduces dementia risk. (Northey 2018) Moderate-intensity aerobic exercise for at least 150 minutes per week (or 75 min of vigorous activity) improves cerebral blood flow and supports neurogenesis, while resistance training 2–3 times per week enhances executive function and helps maintain brain volume. Combined exercise programs integrating aerobic, resistance, and balance training have been shown to improve global cognition in older adults. (Lautenschlager 2008) Incorporating incidental movement throughout the day, such as standing breaks, walking, or using stairs, further supports vascular and neurocognitive health.

Stress

Risk Factors

Chronic psychological stress represents another important driver of neurodegeneration. Persistent activation of the hypothalamic-pituitary-adrenal (HPA) axis elevates cortisol and promotes chronic inflammation, mitochondrial dysfunction, and impaired synaptic plasticity—mechanisms that accelerate neuronal aging and cognitive decline. (Lupien 1998)(Johansson 2010) High stress levels in older adults are associated with hippocampal atrophy and reduced performance in memory and executive domains.

Interventions

Stress reduction strategies may help preserve cognitive function and slow neurodegenerative processes. Evidence-based interventions such as mindfulness practices, including meditation and deep breathing, have been shown to reduce psychological stress and improve well-being by modulating HPA axis activity and lowering systemic inflammation. (Goyal 2014) Social support and structured relaxation techniques, including yoga or tai chi, have also been shown to improve stress resilience and protect brain health over time.

Sleep

Risk Factors

Sleep is a critical period for neuroprotection and memory consolidation, and its disruption has far-reaching consequences for brain health. Insufficient or poor-quality sleep fosters amyloid-β accumulation, Tau pathology, oxidative stress, and systemic inflammation, impairing neuroprotection and hastening cognitive decline. (Ju 2014)(Lim 2013)) Both short sleep duration (<6 hours) and excessive sleep (>9 hours) are linked to higher dementia risk and poorer cognitive performance in aging populations.

Interventions

Improving sleep quality and duration supports cognitive longevity. Evidence-based strategies include maintaining a consistent sleep schedule, optimizing sleep hygiene (e.g., limiting screen time before bed, reducing caffeine intake), treating sleep apnea with continuous positive airway pressure (CPAP) therapy, and promoting exposure to natural light during the day to support circadian rhythm entrainment. (Ju 2014)

Environment 

Risk Factors

Environmental exposures also shape long-term brain health, with toxicants serving as silent but powerful contributors to neurodegenerative disease risk. Heavy metals (lead, mercury, cadmium, arsenic, aluminum), pesticides, solvents, and air pollution introduce oxidative stress, chronic neuroinflammation, protein aggregation, mitochondrial dysfunction, and disrupted neurotransmission, thereby accelerating neuronal loss and cognitive decline. (Nabi 2022)(Power 2010) Chronic exposure to air pollution, particularly fine particulate matter (PM2.5), has been linked to reduced brain volume and impaired cognitive function in older adults.

Interventions

Minimizing exposure to environmental toxins may support long-term cognitive health. Strategies include using water and air filtration systems, avoiding areas with high air pollution, reducing use of pesticides and industrial solvents, and ensuring adequate dietary intake of antioxidants and neuroprotective nutrients to counteract oxidative stress. (Nabi 2022)

Disclaimer

The Fullscript Integrative Medical Advisory team has developed or collected these protocols from practitioners and supplier partners to help health care practitioners make decisions when building treatment plans. By adding this protocol to your Fullscript template library, you understand and accept that the recommendations in the protocol are for initial guidance and may not be appropriate for every patient.

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