Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis
Vitamin C easily crosses the blood brain barrier and its transport into the brain is mediated by glucose transporters. Vitamin C concentrations in the brain exceed those in blood by 10-fold. In humans, hypovitaminosis C correlated with brain damage in patients with head trauma (Stroke. 2001;32:898-902). The vitamin C has important functions in the brain, for example, protecting neuronal membranes from oxidative damage acting as a scavenger of free radicals.
Another free radical scavenger Vitamin E (-tocopherol) inhibits the amyloid peptide characteristic for Alzheimer’s disease known to induced cell death (Biochemical and Biophysical Research Communications Volume 186, Issue 2, 31 July 1992, Pages 944-950).
The results of a study of Guinea Pigs’s fed either on normal or vitamin-deficient diets showed that while moderate deficiencies of vitamins E or C didn’t result in serious brain changes, their combined moderate deficienciescaused degenerative changes in the guinea pig brains in only 5 days after vitamins were removed from the feed.
Interestingly, the deficiencies in either E or C vitamins had only moderate consequences, but their combination caused severe brain lesions – inflammation, cell death with necrosis and apoptosis and animals’ death (Nutr. 136:1576-1581, June 2006).
Combined deficiency in vitamins C and E is a risk factor for neuronal death and brain necrosis.
Vitamin C easily crosses the blood brain barrier and its transport into the brain is mediated by glucose transporters. Vitamin C concentrations in the brain exceed those in blood by 10-fold. In humans, hypovitaminosis C correlated with brain damage in patients with head trauma (Stroke. 2001;32:898-902). The vitamin C has important functions in the brain, for example, protecting neuronal membranes from oxidative damage acting as a scavenger of free radicals.
Another free radical scavenger Vitamin E (-tocopherol) inhibits the amyloid peptide characteristic for Alzheimer’s disease known to induced cell death (Biochemical and Biophysical Research Communications Volume 186, Issue 2, 31 July 1992, Pages 944-950).
The results of a study of Guinea Pigs’s fed either on normal or vitamin-deficient diets showed that while moderate deficiencies of vitamins E or C didn’t result in serious brain changes, their combined moderate deficienciescaused degenerative changes in the guinea pig brains in only 5 days after vitamins were removed from the feed.
Interestingly, the deficiencies in either E or C vitamins had only moderate consequences, but their combination caused severe brain lesions – inflammation, cell death with necrosis and apoptosis and animals’ death (Nutr. 136:1576-1581, June 2006).
What is the problem?
Vitamin D deficiency has been linked not only to bone health, but also some types of cancer, lowered immune function, and kidney disease. Recent studies showed that vitamin D may preserve cognitive function exerting its neuroprotective effects via the vitamin D receptors abundantly expressed in regions frequently affected in cases of neurodegenerative diseases such as the hypothalamus, substantia nigra, cortex and hippocampus. An increased incidence of Alzheimer’s disease, schizophrenia and depression (including depression as a symptom of fibromyalgia and chronic fatigue syndrome, Clinical Rheumatology 1434-9949, 26, 4, April 2007) associated with vitamin D deficiency were reported (J Chem Neuroanat 2005;29:21-30.)
What are the causes?
Decreased bioavailability of vitamin D can be caused by malabsorption often present in cystic fibrosis, celiac disease, Whipple’s disease, Crohn’s disease, bypass surgery, and medications that reduce cholesterol absorption. 86,87
Obesity also educes availability of vitamin D locking it in the body fat depots.
Anticonvulsants, glucocorticoids
Inadequate sun exposure including that due to excessive sunscreen use
(N Engl J Med 2007;357:266-81)
Prevention by supplementation
Most experts agree that current recommendations for daily intake of vitamin D are in fact inadequate: without adequate sun exposure, children and adults require approximately 800 to 1000 IU per day (J Clin Invest 2006;
116:2062-72; Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American
Society for Bone and Mineral Research, 2006:129-37; Endocrinology. Philadelphia: W.B.Saunders, 2001:1009-28)
Related post: Both hypervitaminosis D3 and hypovitaminosis D3 cause premature aging of CNS
What is the problem?
Vitamin D deficiency has been linked not only to bone health, but also some types of cancer, lowered immune function, and kidney disease. Recent studies showed that vitamin D may preserve cognitive function exerting its neuroprotective effects via the vitamin D receptors abundantly expressed in regions frequently affected in cases of neurodegenerative diseases such as the hypothalamus, substantia nigra, cortex and hippocampus. An increased incidence of Alzheimer’s disease, schizophrenia and depression (including depression as a symptom of fibromyalgia and chronic fatigue syndrome, Clinical Rheumatology 1434-9949, 26, 4, April 2007) was proved to be associated with vitamin D deficiency (J Chem Neuroanat 2005;29:21-30.)
What are the causes?
- Decreased bioavailability of vitamin D can be caused by malabsorption often present in cystic fibrosis, celiac disease, Whipple’s disease, Crohn’s disease, bypass surgery, and medications that reduce cholesterol absorption.
- Obesity also educes availability of vitamin D locking it in the body fat depots.
- Anticonvulsants, glucocorticoids
- Inadequate sun exposure including that due to excessive sunscreen use
(N Engl J Med 2007;357:266-81)
Prevention by supplementation
Most experts agree that current recommendations for daily intake of vitamin D are in fact inadequate: without adequate sun exposure, children and adults require approximately 800 to 1000 IU per day (J Clin Invest 2006; 116:2062-72; Primer on the metabolic bone diseases and disorders of mineral metabolism. 6th ed. Washington, DC: American Society for Bone and Mineral Research, 2006:129-37; Endocrinology. Philadelphia: W.B.Saunders, 2001:1009-28)
