Fingernails and Vitamin B12 deficiency

"Depression seems characteristic of most vitamin B deficiencies." British Journal of Psychiatry
. June 1990.

"Pernicious anemia results from a deficiency of cobalamin, or vitamin B12. The neurological
symptoms associated with cobalamin deficiency were identified more than 100 years ago.
Today, cobalamin deficiency is more likely to be recognized in its earlier stages, and the
associated neurological symptoms are more easily reversed by vitamin B12 treatment."
Neurologic aspects of cobalamin deficiency, Medicine, July 1991, research by: Heaton,
Savage, Brust, Garrett, Lindenbaum.

"Of 369 patients with documented cobalamin deficiency seen over a 17-year period, 189
developed neurological symptoms. In 114 cases, the neurological symptoms were the first
indications of the vitamin deficiency. The most common initial complaint was paresthesia, or
abnormal sensation, which affected more than 70 percent of the patients with neurological
symptoms. These abnormal sensations took the form of a 'pins and needles' feeling, numbness,
or tingling. In 10 cases, these feelings were strong enough to be considered disabling by the
patient. In 122 episodes of deficiency, neurological abnormalities were found at the time of
initial diagnosis. The most common was reduced sensitivity to vibration, which was observed in
107 episodes. Proprioception, the awareness of position and movements of the body, was
impaired or absent in the toes or ankles in 72 episodes." Ibid.

"The majority of cases improved with treatment; moderate or severe neurologic disability was
known to persist in only 6.3 percent of the patients who received adequate follow-up. Eleven
of the 18 patients with mental impairment had a complete response to vitamin B12 therapy."
Ibid.

"The extent of nervous system dysfunction was clearly related to the duration of neurologic
symptoms before treatment." Ibid.

"In the 10 episodes in which the pretreatment severity score was 20 or greater a complete
response was seen in only 2 and residual neurologic dysfunction was observed in all of the 8
episodes in which the severity score was more than 23 before therapy." Ibid.

"Duration of symptoms correlated quantitatively with post-treatment severity." Ibid.

"When mental impairment occurred, however, it was frequently the most disabling and
dominant neurologic abnormality." Ibid.

"A striking feature of our patients was the high degree of responsiveness to Cbl [cobalamin]
therapy." Ibid.

"The severity score was reduced by 50% or greater after treatment in 91% of the episodes.
Residual long-term moderate or severe neurologic disability was noted following only 7 (6.3%)
episodes." Ibid.

"Vitamin B12 deficiency causes abnormalities in both the blood and in neurological function. In
many patients, the neurological abnormalities resulting from vitamin B12 deficiency become
apparent before any blood abnormalities develop. These neurological abnormalities may cover
a wide spectrum, ranging from abnormal sensations and impairment of vibration sensitivity to
conditions as severe as abnormal gait and even dementia." Cerebrospinal fluid methylmalonic
acid levels in normal subjects and patients with cobalamin deficiency, by Stabler, Allen,
Barrett, Savage, Lindenbaum. Neurology. Oct. 1991.

"Among patients with cobalamin deficiency, the blood level of methylmalonic acid was about
eight times greater than among controls. However, in the cerebrospinal fluid, the level of
methylmalonic acid was, on the average, 600 times greater than among control patients." Ibid.

"Cobalamin deficiency worsens with increasing age and has been implicated in declining
cognitive functions in elderly persons. Early diagnosis and treatment of cobalamin deficiency
are thus important in preventing or slowing down neuropsychiatric disorders in the elderly."
Review: cobalamin deficiency and mental impairment in elderly people, Age and Ageing, Nov.
1995.

"Cobalamin deficiency increases with advancing age and is found in 3% to 42% of persons aged
65 and over." Ibid.

"It has been shown that nearly 50% of patients with low serum cobalamin and a normal
Schilling test are unable to absorb protein-bound cobalamin as opposed to the free cobalamin
used in the Schilling test." Ibid.

"Another manifestation of cobalamin deficiency is altered mental status, which consists of
impairment of attention span, memory abstraction, or other intellectual functions with or
without abnormalities of behaviour, mood, affect, or logical thought. Neuropsychiatric
symptoms may be the initial, or the only, manifestations of cobalamin deficiency." Ibid.

"Cobalamin deficiency may result in a variety of mental symptoms, such as organic psychosis,
dementia paranoia, memory impairment, mania, slow mentation, hallucinations, and depression."
Ibid.

"A finding of low serum cobalamin levels in Alzheimer's disease and multi-infarct dementia,
but not in other forms of dementia or cognitive impairment, would suggest that cobalamin
deficiency may cause specific types of dementia and is not the result of dementia with
consequently insufficient dietary intake of cobalamin." Ibid.

"In a recent study 18 subjects with low serum cobalamin and evidence of cognitive dysfunction
were investigated. Only patients who had symptoms for less than 1 year showed improvement
after therapy. The best clinical responders had been symptomatic for less than 6 months." Ibid
.

"These investigations indicate that the duration of the cobalamin deficiency plays an essential
role in the degree of improvement of neuropsychiatric symptoms after treatment." Ibid.

"This is important, because cobalamin deficiency may have to be acknowledged as a significant
cause of neuropsychiatric disorders in elderly people. Early treatment may prevent
irreversibility of the neuropsychological features and organic lesions of the brain related to
the deficiency." Ibid.

"Classical disorders such as pernicious anemia are the cause of this deficiency in only a small
proportion of the elderly. A more frequent problem is food-cobalamin malabsorption which
usually arises from atrophic gastritis and hypochlorhydria but other mechanisms seem to be
involved in some patients." Cobalamin, the stomach, and ageing. American Journal of Clinial
Nutrition. Oct. 1997.

"The partial nature of this form of malabsorption produces a more slowly progressive
depletion of cobalamin than does the more complete malabsorption engendered by disruption
of intrinsic factor-mediated absorption. The slower progression of depletion probably
explains why mild, preclinical deficiency is associated with food-cobalamin malabsorption more
often than with pernicious anemia." Ibid.

"Attention has shifted recently to the challenge of milder cobalamin deficiency states in which
signs such as megaloblastic anemia are not apparent. This is a much more common problem than
classical deficiency. This entity has emerged largely because of the application of sensitive
metabolic tests to patients." Mild cobalamin deficiency. The Western Journal of Medicine.
June 1998.

"An examination of the relationship of plasma cobalamin (vitmin B(12)) level to overall
psychological distress, specific mood states, and major depressive disorder was conducted in
159 bereaved men... findings suggest that cobalamin level may be physiologically related to
depressed and anxious mood level, as well as to syndromal depression." Cobalamin level is
related to self-reported and clinically rated mood and to syndromal..." Health Source -
Consumer Edition, 2000.

"In community-dwelling older women, metabolically significant vitamin B(sub 12) deficiency is
associated with a twofold risk of severe depression." Vitamin B12 deficiency and depression in
physically disabled older women: epidemiologic evidence from the Women's Health and Aging
Study. American Journal of Psychiatry. May 2000. (Authors include Stabler)

"Evidence for vitamin [B.sub. 12] deficiency usually involves combinations of low serum vitamin
[B.sub.12] levels, clinical and metabolic abnormalities, and therapeutic response. Identification
of the underlying cause is important in the diagnosis of vitamin [B.sub. 12] deficiency that is
usually attributed to malabsorption. Helicobacter pylori is one of the most common causes of
peptic ulcer disease worldwide and a major cause of chronic superficial gastritis leading to
atrophy of gastric glands. It is suggested that there maybe a causal relationship between H
pylori and food cobalamin malabsorption." Helicobacter pylori--Is It a Novel Causative Agent
in Vitamin [B.sub.12] Deficiency? Archives of Internal Medicine. May 2000.

"Food cobalamin is released as a stable complex with gastric R binder and its absorption
depends on the initial release from the binders in food. Food-cobalamin malabsorption is
marked by the inability to release cobalamin from food. Therefore, cobalamin cannot be taken
up by intrinsic factor for absorption. Release of cobalamin from food requires acid and
pepsin, and most food-cobalamin malabsorptive states can be traced to gastric defects.
However, other mechanisms may also play a role." Ibid.

"It has been proposed that pernicious anemia may represent the final phase of a process that
begins with H pylori--associated gastritis and evolves through progressive levels of atrophy
until parietal cell mass is entirely lost." Ibid.

"In a retrospective study that was conducted in 1994 and 1995, we demonstrated that a
majority (55%) of cases of cyanocobalamin (vitamin [B.sub.12]) deficiency were related to the
inability to release cobalamin from food and that pernicious anemia was a rare condition
(17%). In a second retrospective study that was conducted between 1995 and 1998, we
confirmed that food cobalamin malabsorption was emerging as a major cause of vitamin
[B.sub.12] deficiency. We found that 68 patients (60%) had a vitamin [B.sub.12] deficiency
caused by food cobalamin malabsorption and 7 subjects (6%) had pernicious anemia." Food
Cobalamin Malabsorption: A Usual Cause of Vitamin [B.sub.12] Deficiency. Archives of
Internal Medicine. July 2000.

"There is little reason to treat food cobalamin malabsorption differently than pernicious
anemia." Ibid.

"The objective of this study was to investigate whether cognitive functioning is affected in
adolescents (aged 10-16 y) with marginal cobalamin status as a result of being fed a
macrobiotic diet up to an average age of 6 y... Conclusion: Our data suggest that cobalamin
deficiency, in the absence of hematologic signs, may lead to impaired cognitive performance in
adolescents." American Journal of Clinical Nutrition. Sept. 2000.

"Patients with mild-moderate dementia and elevated plasma homocysteine levels improved
clinically with increased test scores after vitamin substitution." Improvement of cognitive
functions after cobalamin/folate supplementation in elderly patients with dementia and
elevated plasma homocysteine. Alternative Medicine Review. Oct. 2001.

"Mild cobalamin (Cbl) deficiency is frequently found in older persons and is associated with
cognitive and cerebral abnormalities... Conclusion. Electrographic signs of improved cerebral
function and improved cognitive function were found after Cbl supplementation in older
subjects with low plasma Cbl concentrations who were free of significant cognitive impairment.
These improvements were related to a reduction of plasma tHcy concentration." Cobalamin
supplementation improves cognitive and cerebral function in older, cobalamin-deficient
persons. The Journals of Gerontology, Series A. Dec. 2001.

"Megalin has previously been shown to bind and mediate endocytosis of transcobalamin
(TC)-[B.sub.12]. However, the physiological significance of this has not been established, and
other TC-[B.sub.12] binding proteins have been suggested to mediate renal uptake of this
vitamin complex. The present study demonstrates by the use of megalin-deficient mice that
megalin is, in fact, essential for the normal renal reabsorption of TC-vitamin [B.sub.12] and
for renal accumulation of this highly conserved vitamin." Megalin is essential for renal
proximal tubule reabsoption and accumulation of transcobalamin-[B.sub.12]. The American
Journal of Physiology. March 2002.

"Elevated metabolites of the enzyme cofactor cobalamin in elderly patients may predict the
future development of cognitive dysfunction, especially in men, according to a study presented
at the annual meeting of the American Geriatrics Society. High levels of methylcitric acid and,
to a lesser degree, other cobalamin (vitamin [B.sub.12] metabolites correlated significantly
with lower scores on many sections of the California Verbal Learning Test (CVLT), reported
Dr. Angela Garcia of Queen's University, Kingston, Ont." Cobalamin markers could signal
cognitive decline. (Nondemented Elderly Patients). Family Practice News. Oct. 2002.