I am stating this at the beginning of this post because the studies linked below are about dementia and Alzheimer’s Disease (AD).
I don’t believe I have early dementia. I have, however, been struggling with a side effect of aggressive cancer treatment called
Over the past dozen or so years I have read about chemobrain, dementia, cognitive decline, long covid, and they all seem to share symptoms. While my chemobrain is relatively mild when compared to, say, Alzheimer’s, I share symptoms such as deficiencies in;
My interpretation is that the four symptoms listed above are well-know to many/most people over the age of, what 65-70?
So when I talk about brain health, I am talking about improving or healing the typical symptoms common to many of us older folks. It is not about AD, for example, it is about brain health.
To be clear, I do not consider nutritional supplementation (Vitamin D3, C, B12, etc.) to be a silver bullet cure for brain, heart, muscle, etc. health. I consider nutritional supplementation to be one piece of our brain health puzzle.
On that note, please see the studies linked and excepted below. Deficiencies in
according to the studies linked below, contribute to “all- cause” dementia. My interpretation of “all-cause” dementia is that deficiencies in D3. Magnesium, Folate and Vitamin C worsen brain health. You are more likely to be diagnosed with AD if you are deficient in these four vitamins. Based on my research and personal experience anyway.
While this post focuses on nutritional supplementation and our brain health, I have researched the brain health benefits of other evidence-based but non-conventional therapies such as exercise, nutrition and brain games. If you have questions or comments about your own brain health, chemobrain, cognitive decline, AD, please scroll down the page and post a question or a comment.
I will reply to you ASAP.
“Results: During a mean follow-up of 5.6 years, 171 participants developed all-cause dementia, including 102 cases of Alzheimer disease. Using Cox proportional hazards models, the multivariate adjusted hazard ratios (95% confidence interval [CI]) for incident all-cause dementia in participants who were severely 25(OH)D deficient (<25 nmol/L) and deficient (≥25 to <50 nmol/L) were 2.25 (95% CI: 1.23–4.13) and 1.53 (95% CI: 1.06–2.21) compared to participants with sufficient concentrations (≥50 nmol/L). The multivariate adjusted hazard ratios for incident Alzheimer disease in participants who were severely 25(OH)D deficient and deficient compared to participants with sufficient concentrations were 2.22 (95% CI: 1.02–4.83) and 1.69 (95% CI: 1.06–2.69). In multivariate adjusted penalized smoothing spline plots, the risk of all-cause dementia and Alzheimer disease markedly increased below a threshold of 50 nmol/L.
Conclusion: Our results confirm that vitamin D deficiency is associated with a substantially increased risk of all-cause dementia and Alzheimer disease. This adds to the ongoing debate about the role of vitamin D in nonskeletal conditions.
Objective: To determine if serum magnesium levels are associated with the risk of all-cause dementia and Alzheimer disease.
Methods: Within the prospective population-based Rotterdam Study, we measured serum magnesium levels in 9,569 participants, free from dementia at baseline (1997-2008). Participants were subsequently followed up for incident dementia, determined according to the DSM-III-R criteria, until January 1, 2015. We used Cox proportional hazard regression models to associate quintiles of serum magnesium with incident all-cause dementia. We used the third quintile as a reference group and adjusted for age, sex, Rotterdam Study cohort, educational level, cardiovascular risk factors, kidney function, comorbidities, other electrolytes, and diuretic use.
Results: Our study population had a mean age of 64.9 years and 56.6% were women. During a median follow-up of 7.8 years, 823 participants were diagnosed with all-cause dementia. Both low serum magnesium levels (≤0.79 mmol/L) and high serum magnesium levels (≥0.90 mmol/L) were associated with an increased risk of dementia (hazard ratio [HR] 1.32, 95% confidence interval [CI] 1.02-1.69, and HR 1.30, 95% CI 1.02-1.67, respectively).
Conclusions: Both low and high serum magnesium levels are associated with an increased risk of all-cause dementia. Our results warrant replication in other population-based studies.
“To investigate the role of folate deficiency/possible deficiency in the risk of AD and the benefical effect of sufficient folate intake on the prevention of AD, a systematic review and meta-analysis were performed. The Web of Science, PubMed, CENTRAL, EBSCO, CNKI, CQVIP, and Wanfang databases were searched.
The analysis of cross-sectional studies showed that the standardized mean difference (SMD) was −0.60 (95% confidence interval (CI): −0.65, −0.55), indicating that plasma/serum folate level is lower in AD patients than that in controls.
Moreover, the combined odds ratio (OR) of case-control studies was 0.96 (95% CI: 0.93, 0.99), while the combined ORs were 0.86 (95% CI: 0.46, 1.26) and 1.94 (95% CI: 1.02, 2.86) in populations with normal levels of folate (≥13.5 nmol/L) and folate deficiency/possible deficiency (<13.5 nmol/L), respectively.
In addition, the risk ratio (RR) of the cohort studies was 1.88 (95% CI: 1.20, 2.57) in populations with folate deficiency/possible deficiency.
Furthermore, when the intake of folate was equal to or higher than the recommended daily allowance, the combined RR and hazard ratio (HR) were 0.44 (95% CI: 0.18, 0.71) and 0.76 (95% CI: 0.52, 0.99), respectively.
These results indicate that folate deficiency/possible deficiency increases the risk for AD, while sufficient intake of folate is a protective factor against AD…”
“Vitamin B12 deficiency is a cause of reversible dementia that must be ruled out in the evaluation of neurocognitive decline. We present a case of neurocognitive decline secondary to B12 deficiency where the workup was obscured by multiple competing diagnoses and treatment with empiric B12 supplementation reversed symptoms.
Although the pretest probability was low, the morbidity from undiagnosed B12 deficiency is high, warranting a trial of B12 supplementation that resolved the patient’s symptoms.”
“Blood folate levels diminish with age.
According to the authors of the latest study, “Evidence suggests that serum folate deficiency increases the likelihood of deficits in cognitive performance and neurological functioning….”
The findings appear in the journal Evidence-Based Mental Health.
“…Additionally, several risk factors associated with cognitive decline depend on chronological age. It is well recognized that the process of aging is associated with a decline in cognitive ability and brain function….
Recent investigations have highlighted the importance of vitamin C in maintaining brain health and its association with cognitive function in both cognitively intact and impaired cohorts. The present review explores previous literature that has evaluated differences in plasma/brain vitamin C between genders and during aging.
It then assesses whether these age and gender-related differences may affect the relationship between plasma/brain vitamin C and cognition.
The purpose of this review was to examine the evidence for a link between plasma/brain vitamin C and cognition and the impact of gender and age on this relationship.
Epidemiological studies have frequently shown higher vitamin C plasma concentrations in women. Similarly, aging has been systematically associated with reductions in plasma vitamin C levels. A range of animal studies has demonstrated potential gender and age-related differences in vitamin C brain distribution and utilization.
The reviewed literature suggests that gender differences in plasma and brain vitamin C may potentially contribute to differences in gender-associated cognitive ability, particularly while females are pre-menopausal.
Additionally, we can propose that age-associated differences in plasma and brain vitamin C may be potentially linked to age-associated cognitive differences, with older cohorts appearing more vulnerable to experience declines in plasma vitamin C concentrations alongside compromised vitamin C brain regulation…”