Homocystene is an amino acid that circulates in the blood. It is produced when the body breaks down protein. Low homocysteine levels are considered healthy. Elevated levels are problematic for a number of reasons. High levels …
- Are a marker of inflammation
- Cause dementia
- Can cause strokes
- Damage artery walls
- Increase blood clot risks
- Compromise the cardiovascular system.

A reason homocysteine levels can be too high in the case of Parkinsons is that certain medicines delete vitamins B6, B12 and folic acid (vitamin B9). How do you reduce unusually high levels of homocysteine? Increase the intake of vitamins B6, B12 and folic acid – the ones that just happen already to be chronically deficient.
Supplements of course can be taken to supplement low levels of B vitamins. Alternatively, certain foods boost the level of B vitamins. The following foods are rich in vitamins B6, B12 and folic acid:
- Spinach
- Beef liver
- Chicken liver
- Chickpeas
- Sunflower seeds
- Wild salmon
- Eggs
- Clams
- Oysters
- Sardines
- Lentils
Research on Homocysteine Levels and Parkinsons
Heliyon. 2024 Nov 6;10(21):e40191. Association analyses of nutritional markers with Parkinson’s disease and Alzheimer’s disease
Abstract
Introduction: Parkinson’s disease (PD) and Alzheimer’s disease (AD) are common neurodegenerative diseases with multifaceted etiology. Nutritional and metabolic abnormalities are frequently implicated in PD and AD. In this observational study, we analyzed a series of nutritional markers, and aimed to understand their association with AD and PD risk.
Methods: A total of 424 PD patients, 314 AD patients, and 388 healthy controls were included. Nutritional markers including Hemoglobin A1c, vitamin B12, folate, apolipoprotein B (ApoB), apolipoprotein A1 (ApoA1), low-density lipoprotein (LDL), high-density lipoprotein, triglyceride, total cholesterol (TC), uric acid and homocysteine (HCY) were measured. Significance for odds ratios examining was P < 0.0045 after bonferroni correction.
Results: Multifactor risk analysis showed that ApoB, LDL, and TC reduce PD risk, while homocysteine HCY increase PD risk. ApoA1 and HCY are protective and risk factors for AD, respectively.
Conclusion: The cross-sectional study demonstrates that HCY and lipid metabolism markers are associated with PD and AD risks. Our findings support the involvement of one-carbon metabolism and lipid metabolism disturbance in PD and AD.
Nutrients. 2025 Apr 11;17(8):1325. Homocysteine, Nutrition, and Gut Microbiota: A Comprehensive Review of Current Evidence and Insight
Abstract
Homocysteine, a sulfur-containing amino acid, is an intermediate product during the metabolism of methionine, a vital amino acid. An elevated concentration of homocysteine in the plasma, named hyperhomocysteinemia, has been significantly related to the onset of several diseases, including diabetes, multiple sclerosis, osteoporosis, cancer, and neurodegenerative disorders such as dementia, Alzheimer’s and Parkinson’s diseases.
An interaction between metabolic pathways of homocysteine and gut microbiota has been reported, and specific microbial signatures have been found in individuals experiencing hyperhomocysteinemia.
Furthermore, some evidence suggests that gut microbial modulation may exert an influence on homocysteine levels and related disease progression. Conventional approaches for managing hyperhomocysteinemia typically involve dietary interventions alongside the administration of supplements such as B vitamins and betaine.
The present review aims to synthesize recent advancements in understanding interventions targeted at mitigating hyperhomocysteinemia, with a particular emphasis on the role of gut microbiota in these strategies. The emerging therapeutic potential of gut microbiota has been reported for several diseases.
.Acta Neurol Belg. 2025 Apr;125(2):435-444. Diagnostic values of serum levels of ?-synuclein, homocysteine and leucine-rich ?2 glycoprotein for predicting cognitive impairment in Parkinson’s diseas
Abstract
Background: ?-synuclein, homocysteine (Hcy) and leucine-rich ?2-glycoprotein (LRG) have been shown to correlate to Parkinson’s disease (PD). However, it remains unclear whether these factors are associated with the occurrence of cognitive impairment (CI) in PD patients.
Methods: This study initially enrolled eligible PD patients without cognitive impairment. Blood samples were collected to measure serum levels of ?-synuclein, Hcy, and LRG using enzyme-linked immunosorbent assay. After one year of treatment, patients were divided into CI group and non-CI groups based on their Montreal Cognitive Assessment (MoCA) scores. Baseline clinical characteristics and the levels of these three factors were compared between the two groups. Additionally, Receiver Operating Characteristic (ROC) analysis was used to assess the predictive value of these factors for the occurrence of CI in PD patients.
Results: The study included 102 eligible PD patients without baseline CI, divided into 65 patients in the non-CI group and 37 patients in the CI group after one year, based on the MoCA scores. Serum levels of ?-synuclein, Hcy, and LRG in the CI group were 0.42 ± 0.33 ng/mL, 19.85 ± 6.31 µmol/L, and 14.53 ± 5.11 ng/mL respectively, compared to 0.04 ± 0.03 ng/mL, 14.32 ± 5.25 µmol/L, and 11.67 ± 3.10 ng/mL in the non-CI group. Patients in the CI group had MoCA scores below 26, indicating cognitive impairment. ROC analysis revealed that ?-synuclein, Hcy, and LRG levels effectively predicted the occurrence of CI in PD patients.
Conclusions: Serum levels of ?-synuclein, homocysteine and glycoprotein were elevated in the CI group compared to the non-CI group, suggesting that these factors may serve as predictors of cognitive impairment in PD patients.
Robert Rodgers PhD
Founder 2004
Parkinsons Recovery ®
Road to Recovery from Parkinsons Disease





















