Role of Vitamin D and Antioxidants in the Prevention and Treatment of Alzheimer’s Disease
Abhai Kumar, Debasis Bagchi in Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Several researchers have studied the effects of these nutrients and antioxidants on cognitive outcomes. An American cohort study among 5,115 young adults who were followed up for 25 years reported that higher intake of vitamin B (B3, B6, B9, and B12) would enhance cognitive functioning. This is supported by the fact that vitamin B complexes are involved in the metabolism of homocysteine. Elevated levels of homocysteine have been identified as a risk for dementia (Qin et al. 2017). On the contrary, some studies do not report a positive role of vitamin B on cognitive outcomes. On the other hand, the VITACOG study demonstrated that vitamin B improved cognitive outcomes in patients with normal omega fatty acid levels and reduced the rate of brain atrophy (Jerneren et al. 2015). The researchers believe that a cumulative effect from various nutrients may improve the outcome. Vitamin B is the most frequently studied nutrient compared to the others; therefore, more consistent results are available for vitamin B. In addition, a randomized controlled trial compared the effects of an over-the-counter available antioxidant with multivitamin preparation and reported that antioxidants have the potential to improve memory in the elderly (Summers et al. 2018).
Metabolic Approaches to the Treatment of Back Pain
Kohlstadt Ingrid, Cintron Kenneth in Metabolic Therapies in Orthopedics, Second Edition, 2018
Neuropathies associated with deficiencies in B1, B6, and B12 are very real and often missed, particularly if a spine provider is focused on an anatomic cause for a patients symptoms. The risk of B12 deficiency is 65% higher in patients who have been on proton pump inhibitors (PPIs) for greater than two years [70]. Supplementation with a B-complex can seem relatively straightforward; however, depending on the population, approximately 28% of individuals will have difficulty processing standard B vitamin supplements because of a mutation in MTHFR. This enzyme is the rate-limiting step in the methylation process. It catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a co-substrate for homocysteine. MTHFR variants can be identified in laboratory testing. Homocysteine levels can be measured to screen. Patients with impaired methylation can have signs of nutritional deficiencies. Eating folate-rich leafy green vegetables is recommended and if supplementation is used it should be with methyl-folate and methyl-cobalamin. A great resource is Dr. Kara Fitzgerald’s eBook Methylation Diet and Lifestyle [71].
The Multifactorial Model of Cardiovascular Pathology: Is Caffeine Pathogenic in Coronary Heart Disease?
Barry D. Smith, Uma Gupta, B.S. Gupta in Caffeine and Activation Theory, 2006
An elevation in plasma homocysteine levels (hyperhomocysteinemia) is another substantial risk factor for cardiovascular disease, accounting for an estimated 10% of CHD risk (Fowler, 2005). Homocysteine is a sulfur-containing amino acid derived from methionine during its metabolism. Hyperhomocysteinemia promotes the development of thrombosis, atherosclerosis, and oxidative damage. As many as 10 to 20% of coronary heart disease cases are causally linked to homocysteine elevation (Rogers, Sanchez–Saffon, Frol, & Diaz–Arrastia, 2003). A case-control study, for example, evaluated the relationship of homocysteine levels to 149 coronary events (74 deaths and 75 MIs) that occurred in women over a 13-year follow-up period and compared them with matched control subjects. Among women with heart disease at baseline, relative coronary risk, adjusted for other known factors, was 3.32 in the highest homocysteine quintile as compared to the lowest quintile (Knekt et al., 2001).
The role of nutrition on Parkinson’s disease: a systematic review
Published in Nutritional Neuroscience, 2023
Vittorio Emanuele Bianchi, Laura Rizzi, Fahad Somaa
A low vitamin B12 level is frequently observed in PD and predicts worsening clinical outcomes and cognitive decline [146,147]. PD patients with a low serum folate level showed mild motor impairment [148]. In early PD, Christine et al. [90] found that a standard low vitamin B12 level predicted more significant morbidity and worsening of mobility. In these patients, an elevated homocysteine level predicted more significant cognitive decline. The correlations of folate, vitamin B6/B12 dietary intake, and PD were evaluated in a hospital-based, case–control study in Japan [43], which demonstrated that low intake of vitamin B6, although not folate, vitamin B12, or riboflavin, was independently associated with an increased risk of PD. However, de Lau et al. [149], in a prospective, population-based evaluation of 5,289 subjects for a mean of 9,7 years, found that dietary intake of vitamin B6 may decrease the risk of PD.
Presence of macroproteins on the measurement of vitamin B12: studying high vitamin B12 levels using polyethylene glycol and heterophile antibody blocking tubes
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2023
In our study, simultaneous laboratory findings and clinical diagnoses of the patient group were also evaluated. Among them, patient #39 was diagnosed as having ulcerative colitis and the mean corpuscular volume (MCV) value measured at the same time was 106 fL (femtoliter) and the hemoglobin value was 119 g/L. It is known that MCV values exceed 100 fL in macrocytic anemia due to vitamin B12 deficiency [33]. Another patient with a recovery value of 4% had a diagnosis of autoimmune thyroiditis and had positive anti-thyroglobulin and anti-thyroid peroxidase antibodies. In a patient with a recovery value of 21%, it was noted that the homocysteine level measured simultaneously was 17 μmol/L (reference range: 3.7–13.9 μmol/L). High homocysteine levels are considered to be quite significant for diagnosis, especially in patients who are thought to have vitamin B12 deficiency but whose levels are found to be normal [34]. In these patients, interference in the measurement of vitamin B12 may have masked vitamin B12 deficiency.
Dietary vitamin B12 deficiency impairs motor function and changes neuronal survival and choline metabolism after ischemic stroke in middle-aged male and female mice
Published in Nutritional Neuroscience, 2023
Gyllian B. Yahn MBS, Brandi Wasek, Teodoro Bottiglieri, Olga Malysheva, Marie A. Caudill, Nafisa M. Jadavji
Having a deficiency in vitamin B12 results in a multitude of problems and can exacerbate outstanding conditions or developing conditions. A vitamin B12 deficiency is defined as low plasma and tissue levels of vitamin B12 [3]. It can affect all age ranges, however, it has a much higher prevalence within the elderly population [1,4]. A deficiency is commonly caused by malabsorption, decreased acid secretion, and reduced intrinsic factor production [4]. Vitamin B12 is an important co-factor in the conversion of homocysteine to methionine. Elevated levels of homocysteine are well associated with an increased risk for cardiovascular disease, such as ischemic stroke [5]. The recommended daily amount of vitamin B12 is 2.4 µg and the average daily diet contains a range of 3–30 µg [6]. Interestingly, only 50% of patients who are vitamin B12 deficient present with low levels of serum vitamin B12, resulting in a substantial number of undiagnosed patients [2]. Clinical manifestations can be set back due to the high amounts of hepatic storage of vitamin B12 [6].
Related Knowledge Centers
- Coronary Artery Disease
- Cysteine
- Methionine
- Methyl Group
- Amino Acid
- Ischemia
- Atherosclerosis
- Hyperhomocysteinemia
- Homologous Series
- Methylene Bridge