| Physical changes in the brain. Elevated
homocysteine in Alz-heimer’s
disease is associated with atrophy of the temporal medial lobe of the brain,
the site of the hippocampus. Other studies show a relation between increased
plasma homocysteine and a significant decrease in the width of the cerebral
cortex and the width and volume of the hippocampus.4
Folate, B Vitamins Key to Prevention
A basic regimen of folate and B- vitamin
supplementation has been shown effective in preventing hyperhomocysteinemia.
Folate and folic acid. Folate is found in foods such as green leafy vegetables,
legumes, citrus fruits, grain, berries, and liver; folic acid is the form in
which folate appears in supplements and fortified foods. Dietary folate from
a mixed diet, however, has a 50% lower bioavailability than synthetic folic
acid.12
Vitamin B6. Requirements for vitamin B6 rise with increased intake of protein.
The richest dietary sources of vitamin B6 include chicken, fish, liver, and
eggs; other sources are soybean, oats, whole wheat products, peanuts, and walnuts.
Dairy products and red meat are relatively poor sources of vitamin B6.12
Vitamin B12. Vitamin B12 or cobalamin, a cofactor with folate in the recycling
of homocysteine to methionine, is essential in many aspects of human metabolism.
Bacteria, fungi, and algae synthesize vitamin B12 but yeasts, higher plant
forms, and animals cannot. Animal products are the source of vitamin B12 in
the human diet.12
The therapeutic effects of folic acid and B-vitamin supplementation were reported
in a recent Austrian study, in which 9 of 31 patients with dementia and hyperhomocysteinemia
were treated with 50 mg of vitamin B1, 50 mg of vitamin B6, 5000 mcg of folic
acid, and 5 mcg of vitamin B12. After four weeks of treatment, serum homocysteine
concentrations returned to normal in all nine patients, dropping from 17.3
to 10.7 micromoles/liter.13
 |
Vegetarians, especially vegans, are at a high risk for vitamin B12 deficiency,
which can lead to anemia, elevated homocysteine levels, and irreversible neurological
damage. A one-year study of healthy vegetarians found that while all subjects
exhibited low levels of vitamin B12, these levels were inversely related to
the amount of animal (e.g., dairy) products they consumed. While vegans had
the lowest vitamin B12 levels and the highest concentrations of plasma homocysteine,
those who took vitamin supplements had plasma vitamin B12 concentrations similar
to those of non-vegetarians. The study also found that vitamin B12 levels declined
and homocysteine levels increased with advancing age.14
Antioxidants Counter Risk of Dementia
Oxidative stress and neuronal
apoptosis are pathological features in dementia; the presence of
amyloid beta peptide, a feature of Alzheimer’s dementia,
increases neurotoxicity. Antioxidants thus have an important role in blocking
these oxidative reactions and preventing apoptotic death of neurons. In a
recent study, Alzheimer’s disease patients taking vitamin E showed
a slowing down of cognitive decline15; in experimental studies, a wide variety
of antioxidants, including phytochemicals, have shown the ability to prevent
oxidative damage.16
Vitamins E and C. Combined treatment with antioxidants has been found to be
effective in improving memory in animal studies and in reducing the risk of
Alzheimer’s disease dementia. In a study from Brazil, investigators tested
homocysteine’s effects in inducing memory impairment in rats and antioxidants’ ability
to prevent the deleterious homocysteine effects. Rats pretreated for a week
with vitamins C and E were injected with homocysteine before and after being
trained to master a task. Memory was severely impaired in the homocysteine-treated
group while “treatment with vitamins E and C prevented amnesia.”17
A study of 633 persons aged 65 years and older, with a follow-up period
of 4.3 years, found that none of the participants taking vitamin C and E
supplements had Alzheimer’s disease at the end of the follow-up period,
compared with the predicted incidence of 3.9 observed in non-users of supplements.18
Antioxidant levels decrease with age and are low in people with cognitive impairment.
In a study from the University of Perugia in Italy, investigators
measured antioxidant levels in the plasma and cells of 25 elderly
patients with mild cognitive impairment, 63 patients with Alzheimer’s disease, and 53 controls.
The antioxidants measured were uric acid; vitamins A, E, and C; and carotenoids,
including lutein, zeaxanthin, beta-cryptoxanthin, lycopene, and alpha and beta
carotene. Also measured were the activities of plasma and red blood cell superoxide
dismutase (SOD) and plasma glutathione peroxidase. The findings showed that
patients with cognitive impairment and Alzheimer’s disease had low antioxidant
levels, compared to control subjects. The study’s authors suggested that
as mild cognitive impairment represents an early stage in Alzheimer’s
disease and oxidative damage is an early pathological event in dementia, “an
increased intake of antioxidants in patients with mild cognitive impairment
”19 Phytochemicals Also Offer Protection
Ginkgo biloba, curcumin, and
aged garlic extract are phytochemicals that have been shown to
reduce oxidative damage, thus counteracting vascular damage and
neurodegeneration.
Ginkgo. Ginkgo biloba supplementation has been shown to improve cognition in
people with certain forms of dementia.20 Studies now suggest that some of its
protective effects in vascular dementia may be due to reducing oxidative stress
and preventing platelet aggregation that give rise to blood clots.
Curcumin. Present in curry, curcumin is a potent antioxidant with anti-inflammatory
effects. Studies on an Alzheimer’s disease mouse model show that dietary
curcumin reduced oxidative damage and decreased amyloid beta peptides in the
brain by 43-50%. In studies on the PC12 neuron cell model, curcumin was more
effective than alpha tocopherol in preventing amyloid beta peptide toxicity.21
Aged garlic extract. Garlic contains
a wide range of active constituents, which are enhanced by a special process
that yields aged garlic extract (Kyolic™).22 Aged garlic extract protects the vascular system by inhibiting platelet aggregation,
reducing inflammation, and preventing coronary plaque in humans; aged garlic
extract also has neuroprotective effects, reducing homocysteine levels23, preventing
amyloid beta peptide toxicity in PC12 neurons,24 and apoptotic death, and improving
memory in senility-prone mice.25
In a four-week study at Penn State University, researchers fed rats a folate-deficient
diet and Kyolic aged garlic extract, and compared their homocysteine levels
to those in rats fed a folate-fortified diet and aged garlic extract. Aged
garlic extract reduced plasma homocysteine by 30% in folate-deficient animals,
but not at all in animals with adequate folate. The results suggest that aged
garlic extract may serve as a surrogate for folate treatment in hyperhomocysteinemia.25
Summary: Lowering Homocysteine Lowers Dementia Risk
Elevated plasma
homocysteine (hyperhomocysteinemia) is a major risk factor for
dementia, including Alzheimer’s disease. Hyperhomo-cysteinemia
commonly results from a deficiency in folate and vitamins B6 and B12, and
supplementation with these nutrients is the mainstay preventive and therapeutic
treatment for hyperhomocysteinemia. Vegetarians, especially vegans, often
have low levels of vitamin B12 and elevated homocysteine, but supplementation
with vitamin B12 can return their plasma concentrations to levels of nonvegetarians.
Antioxidant levels decline as a result of normal aging and dementia. Increasing
your intake of vitamins C and E—along with phytochemicals such as aged
garlic extract, ginkgo biloba, and curcumin that have been shown in experiments
to prevent oxidant damage and brain cell death by apoptosis—also may
help stave off dementia. |