TAI CHI, VITAMIN B & THE HUMAN BRAIN JULY/AUGUST 2024

Ever walk into a room and forget what you were intending to get?  This started happening more often (up to 3 times daily) until Dr. Le, my neurologist, recommended B-12, B-6 Folic Acid for its role in nourishing neurons in the brain and nervous system and improving memory. Now this might happen once a week.  So this would be a perfect add-in if you have a loved one dealing with memory issues.  But don't take my word for it, check out the research.

From WebMD

"Vitamin B12 is an essential nutrient that helps the body create DNA, nourishes the brain and nervous system. It occurs naturally in meat, fish, and dairy products.  A lack of B12 can put you at higher risk for a specific type of anemia that makes you feel weak and tired."

Brain Health

"Vitamin B12 is an essential nutrient for the neurons in the brain. Brain atrophy, which refers to the loss of neurons in the brain, is associated with memory loss and dementia.

In one randomized trial, older adults with early-stage dementia who were given vitamin B12 supplements to lower their blood homocysteine levels demonstrated a slower rate of cognitive and clinical decline.

Another study found that low B12 levels, even within the normal range, contribute to poor memory performance.  More studies are needed before researchers can be certain of the impact of B12 supplementation on memory loss and dementia." 

Reduced Risk of Macular Degeneration

Supplementing with vitamin B12 is believed to lower homocysteine in the bloodstream, which may help prevent age-related macular degeneration, an eye disease that can cause blindness in older adults. In one study of 5,000 women age 40 and up, those who took supplements of vitamins B12, B6, and folic acid had 34% fewer cases of macular degeneration after seven years than a placebo group. Their risk of severe degeneration was 41% lower.

Vitamin B complex and cognition Memory 

FROM THE NATIONAL CENTER FOR BIOTECHNOLOGY INFORMATION   https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1123448/#B11

• Conclusions:  There is evidence that folate deficiency may contribute to the cognitive impairment of the ageing brain, sometimes leading to reversible dementia but also increasing the risk of Alzheimer's disease and vascular dementia, perhaps by methylation related processes or by homocysteine mediated vascular or neurotoxic mechanisms.

• One reason for the apparently high incidence of folate deficiency in elderly people is that folate concentrations in serum and cerebrospinal fluid fall and plasma homocysteine rises with age, perhaps contributing to the ageing process.
• In a case-control study of 164 patients with Alzheimer's disease, cognitive decline was significantly associated with raised plasma homocysteine and lowered serum folate (and vitamin B-12) concentrations.
• In a prospective community based study of 370 healthy elderly Swedish subjects, folate or vitamin B-12 deficiency doubled the risk of subsequently developing Alzheimer's disease.  Recently the much larger and longer Farmlingham community based study confirmed that a raised plasma homocysteine concentration doubled the risk of developing Alzheimer's and non-Alzheimer's dementia.
• The selective effects of folate deficiency on episodic memory were suspected to be related to encoding and retrieval mechanisms. Wahlin et al extended their studies of the same populations to include a wider range of cognitive functions—spatial orientation, visuospatial functioning, perceptual motor speed, attention, short term memory, and verbal fluency. They found an overall effect of folate status on cognitive function, whereas the overall effect of vitamin B-12 status did not approach statistical significance, although it added to the effects of reduced folate status. In particular, there were specific effects on visuospatial functioning, cognitive shift and flexibility, attention, working memory, and phonemic search, but only marginal effects on spatial orientation, primary memory, and category fluency. The pattern of cognitive dysfunction is claimed to resemble that in normal aging—that is, impairment in tasks that involve little structure, are unfamiliar, speeded, and attention demanding and involve complex processing of information.
• Snowden et al studied prospectively 30 elderly nuns from the same environmental and nutritional background. They died at the mean age of 91 (range 78 to 101) years, and half had neuropathological lesions of Alzheimer's disease. Of 18 nutritional factors examined, only serum folate was significantly negatively correlated with atrophy of the neocortex, especially in the 15 nuns with Alzheimer's disease but also in those with minimal atherosclerosis and no infarcts.
• Unusually, folic acid in the form of methylfolate is present in cerebrospinal fluid in humans in concentrations three times greater than in serum.  The active transport mechanism for methylfolate across the blood-brain barrier strictly limits the entry of the vitamin, perhaps for reasons concerned with the excitatory (convulsant) properties of folic acid.

** Some studies suggest that folate deficiency affects the nervous system only at certain not very well defined critically low concentrations of folic acid or high concentrations of homocysteine.

• Other data, especially in relation to some cognitive impairments in otherwise healthy elderly people in the community, suggest more of a continuum, with folate levels related to performance even within the “normal range.” This raises questions about the optimum nutritional environment for the healthy brain, which may not be closely related to arbitrary blood levels.
• further clinical trials in precisely defined clinical categories are needed, but they should be long term (at least six months to one year) as the impact of folate is slow and cumulative over many months, perhaps because blood-brain barrier mechanisms limit entry to the brain. Small doses over the long term may be preferable to larger doses in the short or long term, not least because of risks to the nervous system, especially in vitamin B-12 deficiency and epilepsy.  It is not clear which folate formulation is preferable: folic acid, folinic acid, or perhaps methylfolate (the transport form across the blood-brain barrier).

*****The best way forward may be to undertake large scale community based studies of folate supplementation or food fortification to explore the preventive potential of the vitamin for mood and cognitive disorders. Such studies are being designed or undertaken for the possible prophylaxis of vascular disease and could be adapted to address the question of preventing or reducing depression and dementia, including vascular dementia, while taking into account the special requirements of the nervous system.

From the National Institutes of Health on B-12 

"Vitamin B12 is required for the development, myelination, and function of the central nervous system; healthy red blood cell formation; and DNA synthesis."

Similarly, supplementation with vitamin B12 alone or with other B vitamins does not appear to decrease the risk or slow the progression of dementia or Alzheimer’s disease in older adults. A Cochrane Review evaluated the effects of vitamin and mineral supplements on cognitive function and dementia in people with mild cognitive impairment. Taking these B vitamins for 6 to 24 months had no apparent effect on episodic memory, executive function, speed of processing, or quality of life, although one study found a slower rate of brain atrophy over 2 years."

Here's Mayo Clinic on B-12

"Left untreated, a vitamin B-12 deficiency can lead to anemia, fatigue, muscle weakness, intestinal problems, nerve damage and mood disturbances.  Research on the use of vitamin B-12 for specific activities and conditions shows:

• Heart and blood vessel disease. Studies show that the combination of these vitamins doesn't seem to reduce the risk or severity of cardiovascular disease and stroke.
• Dementia. Vitamin B-12 deficiency is associated with dementia and low cognitive function, but it's not clear whether vitamin B-12 supplements might help prevent or treat dementia."