Functional Medicine Approach to Dementia and Alzheimer’s Disease
Is Dementia or Alzheimers disease a result of toxic overload ? nutritional deficiencies ? what about mitochondrial dysfunction ? genomic predispositions ? disruption of our Microbiome ? or perhaps all of the above ? Functional Medicine takes a personalized approach in assessing and treating the root cause(s) of memory decline. The following are some abstracts supporting these findings.
Risk of Alzheimer‘s disease with metal concentrations in whole blood and urine: A case-control study using propensity score matching.
Environmental exposure to heavy metals is suspected to result in neuropathology damage and cognitive impairment. We aimed to explore the association of Alzheimer‘s disease (AD) risk with the internal dose of heavy metals by constructing a hospital-based case-control study and using propensity-score-matching methods. We investigated 170 patients with AD and 264 controls from the Department of Neurology and Family Medicine, China Medical University Hospital in Taiwan. All patients with AD received clinical neuropsychological examination and cognitive-function assessments, including the mini-mental status examination and clinical dementia rating scale. We also constructed a propensity-score-matched population of 82 patients with AD and 82 controls by matching age, gender, education, and AD-related comorbidity. Blood levels with cadmium, lead, mercury, selenium, and urinary arsenic profile were measured. Logistic regression models and 95% confidence intervals (CIs) were applied to estimate AD risk. After stratification by respective quartile cutoffs of heavy metals, the AD risk of study participants with high urinary inorganic arsenic (InAs%) or low dimethylarsinic acid (DMA%) significantly increased (p?<?0.05), as similarly found in the propensity-score-matched population. In addition, people with a low median level of selenium and high median level of InAs%, or/and a low median level of DMA% had approximately two- to threefold significant AD risk. Urinary arsenic profiles may be associated with increased AD risk. Repeat measurements of heavy metals with large sample size and the surveying of potential exposure sources are recommended in future studies.
Yang YW, Liou SH, Hsueh YM, Lyu WS, Liu CS, Liu HJ, Chung MC, Hung PH, Chung
CJ. Risk of Alzheimer’s disease with metal concentrations in whole blood and
urine: A case-control study using propensity score matching. Toxicol Appl
Pharmacol. 2018 Jul 17;356:8-14. doi: 10.1016/j.taap.2018.07.015. [Epub ahead of
print] PubMed PMID: 30025849.
Alzheimer‘s disease and other neurodegenerative diseases may be due to nutritional deficiencies secondary to unrecognized exocrine pancreatic insufficiency.
Alzheimer‘s disease (AD) may be related to nutritional deficiencies from exocrine pancreatic insufficiency (EPI) with mal-absorption of essential nutrients, vitamins and minerals. EPI occurs in about twenty percent of the elderly population, sometimes without obvious symptoms, a number similar to the incidence of AD. Other Neurological degenerative diseases with potential nutritional components such as Parkinson’s disease, frailty of age and Multiple Sclerosis, a disease with increased activity from vitamin D deficiency, may also be related to untreated exocrine pancreatic insufficiency causing impaired absorption of essential dietary elements. Testing of patients with Neurological degenerative diseases for EPI may enable correction of underlying nutritional deficiencies with enzyme replacement as necessary, possibly resulting in improvement of the underlying Neurological condition.
Brenner SR. Alzheimer’s disease and other neurodegenerative diseases may be due to nutritional deficiencies secondary to unrecognized exocrine pancreatic insufficiency. Med Hypotheses. 2017 May;102:89-90. doi: 10.1016/j.mehy.2017.03.020. Epub 2017 Mar 15. PubMed PMID: 28478840.
Mitochondrial abnormalities in Parkinson’s disease and Alzheimer‘s disease: can mitochondria be targeted therapeutically?
Mitochondrial abnormalities have been identified as a central mechanism in multiple neurodegenerative diseases and, therefore, the mitochondria have been explored as a therapeutic target. This review will focus on the evidence for mitochondrial abnormalities in the two most common neurodegenerative diseases, Parkinson’s disease and Alzheimer‘s disease. In addition, we discuss the main strategies which have been explored in these diseases to target the mitochondria for therapeutic purposes, focusing on mitochondrially targeted antioxidants, peptides, modulators of mitochondrial dynamics and phenotypic screening outcomes.
Macdonald R, Barnes K, Hastings C, Mortiboys H. Mitochondrial abnormalities in Parkinson’s disease and Alzheimer’s disease: can mitochondria be targeted therapeutically? Biochem Soc Trans. 2018 Jul 19. pii: BST20170501. doi: 10.1042/BST20170501. [Epub ahead of print] Review. PubMed PMID: 30026371.
Alzheimer‘s disease in the omics era.
Recent progresses in high-throughput technologies have led to a new scenario in investigating pathologies, named the “Omics era”, which integrate the opportunity to collect large amounts of data and information at the molecular and protein levels together with the development of novel computational and statistical tools that are able to analyze and filter such data. Subsequently, advances in genotyping arrays, next generation sequencing, mass spectrometry technology, and bioinformatics allowed for the simultaneous large-scale study of thousands of genes (genomics), epigenetics factors (epigenomics), RNA (transcriptomics), metabolites (metabolomics) and proteins(proteomics), with the possibility of integrating multiple types of omics data (“multi -omics”). All of these technological innovations have modified the approach to the study of complex diseases, such as Alzheimer‘s Disease (AD), thus representing a promising tool to investigate the relationship between several molecular pathways in AD as well as other pathologies. This review focuses on the current knowledge on the pathology of AD, the recent findings from Omics sciences, and the challenge of the use of Big Data. We then focus on future perspectives for Omics sciences, such as the discovery of novel diagnostic biomarkers or drugs.
Sancesario GM, Bernardini S. Alzheimer’s disease in the omics era. Clin Biochem. 2018 Jun 18. pii: S0009-9120(17)31078-0. doi: 10.1016/j.clinbiochem.2018.06.011. [Epub ahead of print] Review. PubMed PMID: 29920246.
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