According to the World Health Organization (WHO), the global number of people living with dementia is set to triple to 150 million by 2050. The condition which involves cognitive decline and eventual death can affect people in ways they cannot perceive and others fail to understand. In the early stages performers like the late Terry Jones forget their lines, CEOs make impulsive decisions to the detriment of their company, laws may be broken, and loved ones may suddenly seem distant and uncaring. The ability to predict and understand such events, should they occur, would be of benefit to society. Biomarkers may provide such an opportunity.
Nutrition and metabolism go awry in many conditions, often at very early stages, and the authors of a recent paper headed by Maartje I. Kester of the Alzheimer Center Amsterdam, published in the Journal of the American Medical Directors Association (JAMDA), reasoned that this may be the case in dementia. Conditions related to dietary intake such as hypertension, diabetes, and obesity have already been identified as risk factors for dementia. Dietary intervention might even slow or halt cognitive decline.
Metabolic changes are known to occur in patients with Alzheimer’s, however knowledge of the predemetia stages such as mild cognitive impairment (MCI) are less well characterized. The authors tested the association of nutritional biomarkers measured in biobanked blood and cerebral spinal fluid (CSF) with clinical with progression of subjective cognitive decline (SCD) or MCI. The Amsterdam Dementia Cohort was retrospectively screened for patients with a baseline diagnosis of SCD or MCI who also had sufficient blood/CSF volumes and at least 1 year of clinical follow-up.
The study found that overall raised high-density lipoprotein (HDL) levels were associated with clinical progression. In the SCD subgroup, high folate and low bilirubin levels were associated with cognitive decline. In the MCI subgroup, low CSF S-adenosylmethionine (SAM) and high theobromine were associated with progression and high HDL, cholesterol, iron, and 1,25(OH)2 vitamin D were associated with cognitive decline.
The association of high iron and vitamin D with progression in MCI was not replicated in the SCD cohort. The authors noted that iron and vitamin D levels show day and night variation with short half-lives, which may have biased their results.
A limitation of the study is that no attempt was made to determine the causation of the biomarker changes. It is an open question as to whether dementia drove the changes, or whether diet led to the development of dementia. No analysis of the potential impact of genetics on nutritional status was made. Non-fasting blood samples were used and there was no data on dietary intake or supplement use among the participants. The study size was relatively small with only 299 participants and the authors noted that the study results will require verification through replication.
The authors concluded that “we observed stage- and subtype-dependent nutritional biomarker profiles associated with clinical progression in memory-clinic patients with SCD and MCI. These results show that nutritional biomarker changes in predementia stages are subtle, but studied as nutritional biomarkers profiles, combinations of nutritional biomarkers are highlighted that can potentially be of value to select patients for dietary intervention trials.”
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