What is equally visible but perhaps not as obvious is
the fact that the person has some health issues.
In 400 B.C.E. Hippocrates, who is said to be the
father of clinical medicine, said that fingernails
reveal health and inner condition. He is the first
person to identify "clubbing" as a tool for diagnosing
lung and heart disease.
Far more common than lung and heart disease are
health issues related to nerves. This fingernail
reveals that the person has nerve issues involving
balance, memory, depression, and numbness all of
which are also symptoms of low vitamin B12.
The fact is that every six months you have a new
fingernail, from cuticle to tip. The rate of growth is
about an eighth inch a month. Good vitamin B12 levels
give you white moons on all your fingers; the thumbs'
are the last to go. (Tessa Jupp, R.N., active in the
Post-Polio Network, Dec. 2001).
If your moons have disappeared, you may have been
short of vitamin B12 for a long time. If so, you may
be noticing symptoms of B12 Malabsorption Illness:
As your moons disappear, ridges may develop on your
nails. These can be faint, to very visible ridges like
wax drippings on a Chianti bottle, but finer. Lines on
top of lines may look like hogback hills. To see them
clearly use a magnifying glass or reading glasses.
If you have faint lines, hardly noticeable, then run
through the barbed issues above, looking for ones
that apply to you. If three or four do, that is a
warning that the others may be only a few years
away. If, that is, you do nothing.
Blue skin under your fingernails indicates that you
may be short of red blood cells and by extension,
the oxygen they carry. Low vitamin B12 often
affects the blood as well as nerves.
Red blood cells are supposed to divide.
For more information, click on the healthy splat...
What your fingernails may be telling you is that your
nerves are being affected by a B12 malabsorption
illness. Research follows the navigation bar below.
the fact that the person has some health issues.
In 400 B.C.E. Hippocrates, who is said to be the
father of clinical medicine, said that fingernails
reveal health and inner condition. He is the first
person to identify "clubbing" as a tool for diagnosing
lung and heart disease.
Far more common than lung and heart disease are
health issues related to nerves. This fingernail
reveals that the person has nerve issues involving
balance, memory, depression, and numbness all of
which are also symptoms of low vitamin B12.
The fact is that every six months you have a new
fingernail, from cuticle to tip. The rate of growth is
about an eighth inch a month. Good vitamin B12 levels
give you white moons on all your fingers; the thumbs'
are the last to go. (Tessa Jupp, R.N., active in the
Post-Polio Network, Dec. 2001).
If your moons have disappeared, you may have been
short of vitamin B12 for a long time. If so, you may
be noticing symptoms of B12 Malabsorption Illness:
- tingling hands and feet
numbness
memory problems
feeling exhausted
depression
sensitivity to noise
lots of brown spots
bleeding gums
burning sensation (possibly on thighs)
legs hurt and "jump" at night
pain, including bone pain in legs
balance and gait problems
heavy menstrual bleeding, or, nose bleeds
diarrhea
As your moons disappear, ridges may develop on your
nails. These can be faint, to very visible ridges like
wax drippings on a Chianti bottle, but finer. Lines on
top of lines may look like hogback hills. To see them
clearly use a magnifying glass or reading glasses.
If you have faint lines, hardly noticeable, then run
through the barbed issues above, looking for ones
that apply to you. If three or four do, that is a
warning that the others may be only a few years
away. If, that is, you do nothing.
Blue skin under your fingernails indicates that you
may be short of red blood cells and by extension,
the oxygen they carry. Low vitamin B12 often
affects the blood as well as nerves.
Red blood cells are supposed to divide.
For more information, click on the healthy splat...
What your fingernails may be telling you is that your
nerves are being affected by a B12 malabsorption
illness. Research follows the navigation bar below.
My TimeLine shows how B12 worked for me
An effective topical antibiotic
They shut off my lights. . . And I like it ! ! !
An effective topical antibiotic
They shut off my lights. . . And I like it ! ! !
Should you take Methylcobalamin?
If you are under stress, chances are you need it and already show
symptoms of low B12. Read the research below.
If you are under stress, chances are you need it and already show
symptoms of low B12. Read the research below.
In 33% of cases, tingling and numbness are the first symptoms. Lists of symptoms Foods Containing B12 New Evidence Research Excerpts Articles Blog Discusses: intimate link between vitamin B12 and our nervous system. How I Know It's True Immunity vs the Flu Serrapeptase (for pain) "I lost memory and processing speed from undiagnosed, untreated low B12. I wish someone had warned me. That's why I did this web site." Karen Marie Kline I began my site while living in my condo where there were toxins: their affect felt like low B12. (From losing feeling I fell and hit my head on the bricks.) ... |
Research Excerpts Regarding Vitamin B12
"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.
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.
| I bet my fingernails showed signs of a deficiency at age 34!!! |
| Research linking low B12, high homocysteine, and heart disease Check this page out! |
| The bibliography for the above study contains 98 references. |
| Europe and Japan use a much higher "low" for B12 than we do in the United States. They found that mental impairment begins at levels of 550. Check it out. The U.S. low is 350 points below that, so Americans have to suffer more health loss before a blood test will alert their doctors to the problem. |
"Ask and you shall receive." So, please will
you donate, or shop?
you donate, or shop?
This is a Fingernail, Obviously
Health Boundaries Bite
| ...... |
"Symptoms in the legs, such as paresthesia, burning pains, and heaviness,
dramatically improved. The effect appeared within a few hours to one
week and lasted from several months to four years." Clinical usefulness of
intrathecal injection of methylcobalamin in patients with diabetic
neuropathy; Clinical Theraputics, 1987, research by Ide H, Fujiya S,
Asanuma Y, Tsuji M, Sakai H, Agishi Y.
dramatically improved. The effect appeared within a few hours to one
week and lasted from several months to four years." Clinical usefulness of
intrathecal injection of methylcobalamin in patients with diabetic
neuropathy; Clinical Theraputics, 1987, research by Ide H, Fujiya S,
Asanuma Y, Tsuji M, Sakai H, Agishi Y.
"An ultra-high dose of vitamin B12 has been reported to promote
peripheral nerve regeneration in experimental neuropathy. METHODS:
Nine patients received a 500 microg methylcobalamin injection 3 times a
week for 6 months. The effects were evaluated using neuropathic pain
grading and a nerve conduction study. RESULTS: Serum concentrations
of vitamin B12 were ultra-high during treatment due to the lack of
urinary excretion. After 6 months of treatment, the patients' pain or
paresthesia had lessened, and the ulnar motor and median sensory nerve
conduction velocities showed significant improvement. There were no side
effects." Intravenous methylcobalamin treatment for uremic and diabetic
neuropathy in chronic hemodialysis patients. Internal Medicine, Japan,
1999, research by Kuwabara S, Nakazawa R, Azuma N, Suzuki M,
Miyajima K, Fukutake T, Hattori T.
peripheral nerve regeneration in experimental neuropathy. METHODS:
Nine patients received a 500 microg methylcobalamin injection 3 times a
week for 6 months. The effects were evaluated using neuropathic pain
grading and a nerve conduction study. RESULTS: Serum concentrations
of vitamin B12 were ultra-high during treatment due to the lack of
urinary excretion. After 6 months of treatment, the patients' pain or
paresthesia had lessened, and the ulnar motor and median sensory nerve
conduction velocities showed significant improvement. There were no side
effects." Intravenous methylcobalamin treatment for uremic and diabetic
neuropathy in chronic hemodialysis patients. Internal Medicine, Japan,
1999, research by Kuwabara S, Nakazawa R, Azuma N, Suzuki M,
Miyajima K, Fukutake T, Hattori T.
I received an interesting email on February 10, 2008, relating to the use
of methylcobalamin to heal diabetic neuropathy in cats. I had run across
a web site about this and written to the webmaster. (I've put the site on
my Useful Websites page.)
Laurie, the site owner, responded to my email, "Goodness, cats can take as
much as 25 MG of methylcobalamin with no problem. Through Jasper's
site, I've been in touch with thousands of people over the years, and some
only needed to give their cats 3 to 6 MG per day, others needed more. An
average, I'd say, is 12 MG - and that's factoring in people whose cats'
diabetes is not regulated, so they're fighting ongoing damage and need
more of the vitamin to help them."
What is astonishing to me about that, and WONDERFUL, is that it is
exactly what I found when I got rid of my peripheral neuropathy when I
was having a B12 shot a day, which is about the same as 25 to 30 mg of
methylcobalamin a day in lozenges.
Not "exactly" really, because a cat is tiny and I am 6 feet tall and heavy.
of methylcobalamin to heal diabetic neuropathy in cats. I had run across
a web site about this and written to the webmaster. (I've put the site on
my Useful Websites page.)
Laurie, the site owner, responded to my email, "Goodness, cats can take as
much as 25 MG of methylcobalamin with no problem. Through Jasper's
site, I've been in touch with thousands of people over the years, and some
only needed to give their cats 3 to 6 MG per day, others needed more. An
average, I'd say, is 12 MG - and that's factoring in people whose cats'
diabetes is not regulated, so they're fighting ongoing damage and need
more of the vitamin to help them."
What is astonishing to me about that, and WONDERFUL, is that it is
exactly what I found when I got rid of my peripheral neuropathy when I
was having a B12 shot a day, which is about the same as 25 to 30 mg of
methylcobalamin a day in lozenges.
Not "exactly" really, because a cat is tiny and I am 6 feet tall and heavy.
Thank you everyone who's left a message. I had no
idea I would get so many lovely messages when I put
a response box here. However, I'm now getting
dozens of viagra ads a day which apparently the
spammer does not realize are never published...
If you'd like to ask me a question, email me. I'll
respond just as well as I did using the comments box.
idea I would get so many lovely messages when I put
a response box here. However, I'm now getting
dozens of viagra ads a day which apparently the
spammer does not realize are never published...
If you'd like to ask me a question, email me. I'll
respond just as well as I did using the comments box.
| ...... |
"Vitamin B12 has the largest and most complex chemical structure of all
the vitamins. It is unique among vitamins in that it contains a metal ion,
cobalt. For this reason cobalamin is the term used to refer to compounds
having vitamin B12 activity. Methylcobalamin and 5-deoxyadenosyl
cobalamin are the forms of vitamin B12 used in the human body." Brody T.
Nutritional Biochemistry. 2nd ed. San Diego: Academic Press; 1999.
the vitamins. It is unique among vitamins in that it contains a metal ion,
cobalt. For this reason cobalamin is the term used to refer to compounds
having vitamin B12 activity. Methylcobalamin and 5-deoxyadenosyl
cobalamin are the forms of vitamin B12 used in the human body." Brody T.
Nutritional Biochemistry. 2nd ed. San Diego: Academic Press; 1999.
"Before becoming pregnant, women need to get enough vitamin B12 in
addition to folic acid to cut their risk of having a baby with a serious
birth defect of the brain and spinal cord... Irish women with the lowest
vitamin B12 levels were five times more likely to have a baby with a neural
tube defect than those with the highest levels... Neural tube defects can
lead to lifelong disability or death." The two most common ones are spina
bifida, in which the spinal cord and back bones do not form properly, and
anencephaly, a fatal condition in which the brain and skull bones do not
develop normally. Dr. James Mills, U.S. National Institutes of Health.
Pediatrics, March 2009
"An absolutely critical point is that women have to consider this before
they become pregnant because once they realize they are pregnant it's
likely to be too late," Mills,said in a telephone interview.
The study involved almost 1,200 women in Ireland who gave blood samples
during early pregnancy, which were analyzed to determine vitamin B12
levels. The women in the lowest 25 percent of vitamin B12 levels were five
times more likely than those in the highest 25 percent to have had a baby
with a neural tube defect.
The researchers suggested that women have vitamin B12 levels above 300
nanograms per liter before getting pregnant. Dr. James Mills, U.S.
National Institutes of Health. Pediatrics, March 2009
addition to folic acid to cut their risk of having a baby with a serious
birth defect of the brain and spinal cord... Irish women with the lowest
vitamin B12 levels were five times more likely to have a baby with a neural
tube defect than those with the highest levels... Neural tube defects can
lead to lifelong disability or death." The two most common ones are spina
bifida, in which the spinal cord and back bones do not form properly, and
anencephaly, a fatal condition in which the brain and skull bones do not
develop normally. Dr. James Mills, U.S. National Institutes of Health.
Pediatrics, March 2009
"An absolutely critical point is that women have to consider this before
they become pregnant because once they realize they are pregnant it's
likely to be too late," Mills,said in a telephone interview.
The study involved almost 1,200 women in Ireland who gave blood samples
during early pregnancy, which were analyzed to determine vitamin B12
levels. The women in the lowest 25 percent of vitamin B12 levels were five
times more likely than those in the highest 25 percent to have had a baby
with a neural tube defect.
The researchers suggested that women have vitamin B12 levels above 300
nanograms per liter before getting pregnant. Dr. James Mills, U.S.
National Institutes of Health. Pediatrics, March 2009
 |
| |
 |
| |
 |
| |
 |
| |
 |
| |
 |
| |
 |
| |
 |
| |
 |
Methylcobalamin is the form of B12 that our bodies make and need and use. Learn
about Methylcobalamin.
B12/Methylcobalamin is safe because what our bodies don't use, they excrete: You
don't have to worry that Methylcobalamin will hurt you. If you need B12 and take
Methylcobalamin, your health will significantly improve within two months.
Significantly. No doubt. I know from experience. (This is like Stravinsky who said,
"Inspiration is never wrong. If it turns out to be wrong, it wasn't an inspiration.)
(And, though true, I put that quote here to amuse you.)
Methylcobalamin lozenges work even if you have B12 malabsorption illness, which is
increasingly common, especially in people who have lots of stress, take antacids or
some other medications... see the list of conditions contributing to malabsorption.
 |  |  |  |  |  |  |  |
| http://www.health-boundaries-bite.com Your fingernails reflect your health -- Learn some warning signs -- Karen Kline |
"Seven men and four women with symptomatic diabetic neuropathy were
treated with Methylcobalamin (2,500 micrograms in 10 ml of saline)
injected intrathecally... Symptoms in the legs, such as paresthesia,
burning pains, and heaviness, dramatically improved... Methylcobalamin
in spinal fluid was 114 +/- 32 pg/ml before intrathecal injection (n=5)
and 4,752 +/- 2,504 pg/ml one month after... Methylcobalamin caused
no side effects. Clinical usefulness of intrathecal injection of
Methylcobalamin in patients with neuropathy - Ide H Fujiya S Asanuma
Y Tsuji M Sakai H Agishi Y, Clin Ther (1987)
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder
affecting both upper and lower motor neurons... We have shown the
ultra-high-dose methylcobalamin (25 mg/day i.m.) slows down the
progressive reduction of the CMAP (compound muscle action potential)
amplitudes in ALS in the short term (4 weeks). The latencies of SSR
(sympathetic skin response) were shorter after treatment (50 mg/day
i.v., 2 weeks). In the long-term effect of methylcobalamin (50 mg/day
i.m., twice a week), the survival time (or the period to become
respirator-bound) was significantly longer in the treated group than
in the untreated. Clinical trials of ultra-high-dose methylcobalamin in
ALS Izumi Y, Kaji R. Brain Nerve (2007)
treated with Methylcobalamin (2,500 micrograms in 10 ml of saline)
injected intrathecally... Symptoms in the legs, such as paresthesia,
burning pains, and heaviness, dramatically improved... Methylcobalamin
in spinal fluid was 114 +/- 32 pg/ml before intrathecal injection (n=5)
and 4,752 +/- 2,504 pg/ml one month after... Methylcobalamin caused
no side effects. Clinical usefulness of intrathecal injection of
Methylcobalamin in patients with neuropathy - Ide H Fujiya S Asanuma
Y Tsuji M Sakai H Agishi Y, Clin Ther (1987)
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder
affecting both upper and lower motor neurons... We have shown the
ultra-high-dose methylcobalamin (25 mg/day i.m.) slows down the
progressive reduction of the CMAP (compound muscle action potential)
amplitudes in ALS in the short term (4 weeks). The latencies of SSR
(sympathetic skin response) were shorter after treatment (50 mg/day
i.v., 2 weeks). In the long-term effect of methylcobalamin (50 mg/day
i.m., twice a week), the survival time (or the period to become
respirator-bound) was significantly longer in the treated group than
in the untreated. Clinical trials of ultra-high-dose methylcobalamin in
ALS Izumi Y, Kaji R. Brain Nerve (2007)
