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Supplementing with B vitamins can reduce risk of Alzheimer’s


Taking large amounts of B vitamins might benefit patients with Alzheimer’s disease. An Oxford study showed that supplementation slowed down the progression of the neurodegenerative disease and improved cognitive function.

The clinical trial involved 156 older people with mild cognitive impairment. The participants were at considerable risk of developing Alzheimer’s and dementia.

Oxford University researchers randomly divided the participants into two groups. The control group got a placebo, while the treatment group received 800 micrograms of folic acid (vitamin B9), 20 milligrams of vitamin B6, and 500 micrograms of vitamin B12 every day. The experiment lasted for two years.

Before starting the experiment, the researchers checked the atrophy levels of the patients’ grey matter. They continued doing so throughout the trial period.

One of the markers of Alzheimer’s disease and dementia is the atrophy of grey matter. On magnetic resonance imaging (MRI) scans, this shows up as shrinkage in the amount of grey matter in the brain.

The Oxford researchers noted that members of both groups displayed reduced amounts of grey matter. However, the participants who took B vitamin supplements enjoyed much less grey matter atrophy than the placebo group. (Related: Green tea and carrots could reverse dementia, restore memory.)

Taking B-vitamins helps minimize the symptoms of Alzheimer’s disease

Further analysis showed that the participants who experienced the fastest atrophy of grey matter also displayed increased levels of homocysteine. Interestingly, the same people received the greatest benefit from taking B vitamin supplements.

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The Oxford researchers concluded that B vitamins can slow down cognitive decline by reducing homocysteine levels. Decreasing homocysteine levels reduces the atrophy rate of grey matter.

They followed up on their MRI scans and homocysteine level analysis by conducting neuropsychological tests on the participants. The researchers looked for connections between grey matter atrophy and neuropsychological function.

Based on the results of their tests, they found that B vitamins helped reduce the decline in neuropsychological scores that came with grey matter atrophy.

“Our results show that B-vitamin supplementation can slow the atrophy of specific brain regions that are a key component of the Alzheimer’s disease process and that are associated with cognitive decline,” the researchers said.

Take natural folate instead of synthetic folic acid

Other studies link homocysteine levels with cardiovascular disease. People with high levels of homocysteine experience faster progression of atherosclerosis.

Depending on the age and health of a person, blood homocysteine levels are considered to be high when they reach 10 to 15 micromoles per liter (umol/L). For their experiment, the Oxford researchers considered 11 umol/L as high.

Homocysteine plays an important role in methylation, a process that transfers methyl groups from one molecule to another. Adding a methyl group to an oxidative toxin causes the body to get rid of the harmful molecule as fast as possible.

When a person has high levels of homocysteine, he often has increased concentrations of oxidative radicals and toxins in his bloodstream and liver. These harmful molecules can cause oxidative stress that damages blood vessels and cells, such as the neurons that comprise much of the brain.

Many nutrients act as methyl donors. By adding methyl groups to toxins, they help the body detoxify and heal itself. The nutrients also prevent mutation of cellular DNA.

B-vitamins are good methyl donors. Take folate, the natural form of vitamin B9, instead of synthetic folic acid.

Folate is found in many plant-based foods. Asparagus, beets, broccoli, cauliflower, collard greens, lentils, mustard greens, parsley, romaine lettuce, spinach, and turnips are good sources of natural vitamin B9. For supplements, take 5-methyltetrahydrofolate (5-MTHF) instead of folic acid.

Sources include:

GreenMedInfo.com

PNAS.org



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