| Vitamin B12 Research (Excerpts) |
| NOTE: When I talk about how our fingernails reflect our B12 health, I do not mean that they are the sole symptom anyone should consider. From my observations, our fingernails provide an excellent way to see that we might have a vitamin B12 problem. And, if we do, there will most certainly be other symptoms. To understand the other symptoms, it is a good idea to read the research, or at least excerpts from it. |
Health Boundaries Bite
Research Excerpts Re: 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.
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.
| The bibliography for the above study contains 98 references. |
| Europe and Japan use a higher "low" for B12 than we do here 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 suffer more health loss before a blood test will alert their doctors to the problem. |
"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.
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.
"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 methyl-
cobalamin 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
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 methyl-
cobalamin 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
Incidentally, 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.
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.
| ...... |
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.
| ...... |
http://www.health-boundaries-bite.com
Your fingernails reflect your health --
Learn some warning signs --
Karen Kline
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)
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