Dr. Romi Fung, Naturopathic Doctor

03/02/2026

Do you have friends in your life that you are lucky to know? Come out on Wed. March 4 and meet new friends and acquaintances. =

02/28/2026

Come out and join us March 4th to our social gathering and meet new friends, gain connections and relax with a coffee. Register at info@seniorlink.ca

02/16/2026

Join me with Boucher Naturopathic Clinic on Monday, February 23rd, 2026 at 5:00pm PT!

Register here: https://ccnmclinics.ca/heart-health

In recognition of Heart Month in Canada, join Dr. Romi Fung, ND, Ph.D (cand.), clinic supervisor and instructor at CCNM-Boucher, in some heart-warming information about improving cardiovascular health with naturopathic approaches on Monday, Feburary 23 at 5:00pm PST. You'll learn how cardiovascular disease can develop, how blood testing helps identify certain problems, how certain lifestyle choices contribute to healthy hearts, and even how your cardiovascular health is strongly linked to your brain health!

Register now! https://ccnmclinics.ca/heart-health

02/01/2026

Welcome to the team, Jerri-Lynne!

We’re excited to welcome naturopathic intern Jerri-Lynne to the clinic!

Jerri-Lynne will be seeing patients every Tuesday from 10:00 AM – 6:00 PM, working closely under the supervision of Dr. Romi Fung, ND. She brings curiosity, compassion, and a strong commitment to patient-centred care, and we’re thrilled to have her support our community.

📍 Location:
613-6081 No. 3 Road
Richmond, BC. V6Y 2B2

🕙 Intern Clinic Hours:
Tuesdays | 10:00 AM – 6:00 PM

📞 Bookings & Inquiries:
Contact@DrRomiFungND.com
https://DrRomiFungND.Janeapp.com

If you’ve been curious about naturopathic care or are looking for supportive, supervised intern visits, this is a great opportunity. Please join us in giving Jerri-Lynne a warm welcome!

01/28/2026

Traumatic brain injury (TBI) is associated with an increased risk of dementia, with pooled estimates showing approximately 1.7 to 1.8 times higher risk compared to individuals without TBI. The relationship demonstrates a dose-response pattern, where more severe injuries and multiple TBIs confer greater risk.

The risk persists for decades after injury. A Swedish nationwide cohort study found that while the association was strongest in the first year after TBI (OR 3.52), elevated risk remained significant more than 30 years post-injury.

Proposed biological mechanisms include chronic neuroinflammation, disrupted axonal transport leading to pathological protein aggregation (amyloid-β and hyperphosphorylated tau), and polypathology on neuropathological examination.

Gardner, R. C., Bahorik, A., Kornblith, E. S., Allen, I. E., Plassman, B. L., & Yaffe, K. (2023). Systematic Review, Meta-Analysis, and Population Attributable Risk of Dementia Associated with Traumatic Brain Injury in Civilians and Veterans. Journal of neurotrauma, 40(7-8), 620–634. https://doi.org/10.1089/neu.2022.0041

Nordström, A., & Nordström, P. (2018). Traumatic brain injury and the risk of dementia diagnosis: A nationwide cohort study. PLoS medicine, 15(1), e1002496. https://doi.org/10.1371/journal.pmed.1002496

01/28/2026

Higher daily step counts are associated with a lower risk of developing dementia, with optimal risk reduction observed at approximately 9800 steps per day and meaningful benefit starting at around 3800 steps per day.

In a UK Biobank study of 78,430 adults followed for 6.9 years, the optimal dose of 9826 steps was associated with a 51% lower dementia risk (HR 0.49), while the minimal dose of 3826 steps achieved 50% of this maximum benefit (HR 0.75).

Start slow. If 10,000 steps is too much, start at 2000. Bring up your steps over time at small increments.

del Pozo Cruz, B., Ahmadi, M., Naismith, S. L., & Stamatakis, E. (2022). Association of daily step count and intensity with incident dementia in 78 430 adults living in the UK. JAMA Neurology, 79(10), 1059–1063. https://doi.org/10.1001/jamaneurol.2022.2672

01/28/2026

Lower skeletal muscle mass is associated with reduced brain-derived neurotrophic factor (BDNF) levels, and both independently correlate with increased dementia risk.

The proposed mechanism centers on myokine secretion from physically active muscle tissue. During exercise, skeletal muscle releases myokines (such as irisin and cathepsin B) that cross the blood-brain barrier and upregulate BDNF expression in the hippocampus.This exercise-induced BDNF elevation promotes neuronal survival, synaptic plasticity, and exerts anti-inflammatory neuroprotective effects.

Conversely, physical inactivity and low muscle mass result in dysfunctional myokine secretion, contributing to reduced BDNF levels and cognitive impairment.

Higher serum BDNF levels are associated with reduced dementia risk.

Oudbier, S. J., Goh, J., Looijaard, S. M. L. M., Reijnierse, E. M., Meskers, C. G. M., & Maier, A. B. (2022). Pathophysiological Mechanisms Explaining the Association Between Low Skeletal Muscle Mass and Cognitive Function. The journals of gerontology. Series A, Biological sciences and medical sciences, 77(10), 1959–1968. https://doi.org/10.1093/gerona/glac121

Qian, F., Liu, J., Yang, H., Zhu, H., Wang, Z., Wu, Y., & Cheng, Z. (2022). Association of plasma brain-derived neurotrophic factor with Alzheimer's disease and its influencing factors in Chinese elderly population. Frontiers in aging neuroscience, 14, 987244. https://doi.org/10.3389/fnagi.2022.987244

01/27/2026

Higher cognitive reserve is associated with a 40-60% reduced risk of dementia, even among individuals with significant brain pathology. This protective relationship operates through both reduced accumulation of neuropathology and enhanced compensatory mechanisms that allow individuals to maintain cognitive function despite existing brain damage.

Cognitive reserve operates largely independent of brain pathology. While higher reserve is associated with somewhat lower pathological burden, the majority of its protective effect (approximately 80%) operates through mechanisms other than preventing pathology accumulation.

Key evidence-based strategies in increasing cognitive reserve include:

🧠 Physical activity: Both aerobic exercise (walking, swimming) and resistance training improve cardiovascular health and cognitive function
🧠 Cognitively stimulating activities: Reading, playing cognitively engaging games, education classes such as learning a new language
🧠 Cardiovascular risk factor management: Treatment of hypertension, diabetes, and other vascular risk factors, particularly in midlife
🧠 Mediterranean diet: Emphasizing green leafy vegetables, fish, and healthy fats
🧠 Social engagement: Regular meaningful social interactions, though cognitive complexity appears more protective than social contact alone
🧠 Adequate sleep and stress management
🧠 Smoking cessation and limiting alcohol use

Nelson, M. E., Jester, D. J., Petkus, A. J., & Andel, R. (2021). Cognitive Reserve, Alzheimer's Neuropathology, and Risk of Dementia: A Systematic Review and Meta-Analysis. Neuropsychology review, 31(2), 233–250. https://doi.org/10.1007/s11065-021-09478-4

Oveisgharan S, Wilson RS, Yu L, Schneider JA, Bennett DA. Association of Early-Life Cognitive Enrichment With Alzheimer Disease Pathological Changes and Cognitive Decline. JAMA Neurol. 2020;77(10):1217–1224. doi:10.1001/jamaneurol.2020.1941 #

01/27/2026

Neurofilament light chain (NfL) is a strong predictor of dementia risk and cognitive decline as a result of a brain injury, with elevated levels in both CSF and blood associated with increased risk of progression from normal cognition to mild cognitive impairment (MCI) or dementia.

NfL levels can remain elevated for over a decade in individuals at risk for dementia, beginning in the presymptomatic phase and continuing through clinical progression. In sporadic Alzheimer's disease, plasma NfL levels begin diverging from controls approximately 9.6 years before clinical diagnosis and continue rising throughout the disease course.

Testing for NfL can shed light on your recovery from your head trauma, even when asymptomatic.

The duration of elevation correlates with disease severity and progression rate—individuals with faster cognitive decline show steeper NfL increases over time. In population-based cohorts, peripheral GFAP and NfL elevations can be detected up to 15 years before dementia diagnosis.

Singh, R. K., Bekena, S., Damera, N., Zhu, Y., Trani, J. F., & Babulal, G. M. (2025). The relationships between cerebrospinal fluid neurofilament light chain and hippocampal atrophy with cognitive decline. Journal of Alzheimer's disease : JAD, 107(3), 1143–1153. https://doi.org/10.1177/13872877251365219

de Wolf, F., Ghanbari, M., Licher, S., McRae-McKee, K., Gras, L., Weverling, G. J., Wermeling, P., Sedaghat, S., Ikram, M. K., Waziry, R., Koudstaal, W., Klap, J., Kostense, S., Hofman, A., Anderson, R., Goudsmit, J., & Ikram, M. A. (2020). Plasma tau, neurofilament light chain and amyloid-β levels and risk of dementia; a population-based cohort study. Brain : a journal of neurology, 143(4), 1220–1232. https://doi.org/10.1093/brain/awaa054

Lehmann, S., Schraen-Maschke, S., Vidal, J. S., Blanc, F., Paquet, C., Allinquant, B., Bombois, S., Gabelle, A., Delaby, C., Hanon, O., & BALTAZAR Study Group (2023). Blood Neurofilament Levels Predict Cognitive Decline across the Alzheimer's Disease Continuum. International journal of molecular sciences, 24(24), 17361. https://doi.org/10.3390/ijms242417361

01/27/2026

Strength training is associated with a reduced risk of developing dementia, with evidence suggesting both protective effects from higher muscle strength and cognitive benefits from resistance exercise interventions, particularly when performed at least twice weekly for six months or longer.

Observational data demonstrate a strong inverse relationship between muscle strength and dementia risk. In community-dwelling older adults, those with high handgrip strength had approximately 61% lower risk of developing Alzheimer's disease compared to those with low strength.

Intervention studies show that resistance training produces measurable cognitive improvements and structural brain changes. Randomized controlled trials demonstrate that resistance exercise enhances global cognition and memory in older adults.

Train your muscles. Protect your brain.

What are you waiting for? Get lifting! Start light and build up. Consider engaging a personal trainer to ensure safety.

Marston, K. J., Brown, B. M., Rainey-Smith, S. R., & Peiffer, J. J. (2019). Resistance Exercise-Induced Responses in Physiological Factors Linked with Cognitive Health. Journal of Alzheimer's disease : JAD, 68(1), 39–64. https://doi.org/10.3233/JAD-181079

Nicola, L., Loo, S. J. Q., Lyon, G., Turknett, J., & Wood, T. R. (2024). Does resistance training in older adults lead to structural brain changes associated with a lower risk of Alzheimer's dementia? A narrative review. Ageing research reviews, 98, 102356. https://doi.org/10.1016/j.arr.2024.102356

01/27/2026

The APOE gene is the strongest genetic risk factor for late-onset Alzheimer's disease, with the ε4 allele substantially increasing risk and the ε2 allele conferring protection relative to the common ε3 allele.

Carrying one APOE ε4 allele increases AD risk approximately 3.7-fold, while two copies increase risk up to 12-fold.

APOE4 drives AD pathogenesis through multiple mechanisms, most prominently by promoting earlier and more abundant amyloid-β deposition. The protein also modulates tau pathology, neuroinflammation, synaptic integrity, lipid transport, glucose metabolism, and cerebrovascular function through both Aβ-dependent and Aβ-independent pathways.

I help people who’ve tested for APOE understand what their results actually mean by translating genetic risk into clear, actionable steps. Together, we focus on the modifiable factors that matter most for brain health, so genes inform prevention rather than define destiny.

Raulin, A. C., Doss, S. V., Trottier, Z. A., Ikezu, T. C., Bu, G., & Liu, C. C. (2022). ApoE in Alzheimer's disease: pathophysiology and therapeutic strategies. Molecular neurodegeneration, 17(1), 72. https://doi.org/10.1186/s13024-022-00574-4

Serrano-Pozo, A., Das, S., & Hyman, B. T. (2021). APOE and Alzheimer's disease: advances in genetics, pathophysiology, and therapeutic approaches. The Lancet. Neurology, 20(1), 68–80. https://doi.org/10.1016/S1474-4422(20)30412-9

01/26/2026

The relationship between homocysteine and dementia risk shows a clear dose-response pattern in the moderate-to-high range. In the Framingham Study, plasma homocysteine >14 μmol/L nearly doubled the risk of Alzheimer's disease.

The dose-response relationship is non-linear, with risk steadily increasing between approximately 8-15 μmol/L and plateauing thereafter. An international consensus statement identifies moderately raised homocysteine (>11 μmol/L) as a modifiable risk factor, with relative risks ranging from 1.15 to 2.5 in elderly populations.

Testing homocysteine and seeing your levels can be a powerful step in assessing your cognitive health.

Seshadri, S., Beiser, A., Selhub, J., Jacques, P. F., Rosenberg, I. H., D’Agostino, R. B., Wilson, P. W. F., & Wolf, P. A. (2002). Plasma homocysteine as a risk factor for dementia and Alzheimer’s disease. New England Journal of Medicine, 346(7), 476–483. https://doi.org/10.1056/NEJMoa011613

Chen, S., Honda, T., Ohara, T., Hata, J., Hirakawa, Y., Yoshida, D., Shibata, M., Sakata, S., Oishi, E., Furuta, Y., Kitazono, T., & Ninomiya, T. (2020). Serum homocysteine and risk of dementia in Japan. Journal of neurology, neurosurgery, and psychiatry, 91(5), 540–546. https://doi.org/10.1136/jnnp-2019-322366