So, Let's imagine this is a Fingernail
.
Vitamin B12 History
More Symptoms & Illustrations

Learn about Methylcobalamin, the active form of B12

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.

.


Like a healthy plant, your fingernails grow. And, just
as leaves show the health of a plant, your fingernails
reveal your health and inner condition. (Hippocrates,
400 B.C.E.)

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
a lot 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; nose bleeds
diarrhea
Before your moons disappear, ridges 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 look like hogback hills. To see them
clearly, use a magnifying glass or reading glasses.

If you have faint lines, no more noticeable than the
tassels on the wheat in the image to the left, then run
through the barbed issues above, looking for ones
that apply to you. If three or four do, then be
warned 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.

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.
.

In 33% of cases, tingling
and numbness are the
first symptoms.

New Evidence

Research Excerpts
More symptoms
Foods Containing B12
Articles
How I Know It's True

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've just lost my condo.
The courts have let me
down. But curiously, if
they had not, I would not
have made these pages.



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.

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.
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.





Order Methylcobalamin Now and begin taking it

Excellent natural health reference books
Love quotes, roses to grow and diamonds
Stressed? Need to Relax?
This is How I've been Losing Weight
Neat things
Is there someone you want to send flowers to?
Nuts and Bolts of the office
Good quotes and shopping
Want to see my garden?

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.

Attached Thumbnails

 

I seem to have many of the symptoms. They never made sense before and I never actually was able to connect them to each other before.

I'll be mentioning this to my NP at my next appt, May 1st.

Hi! I'm a newbie to this forum and read your article with a great deal of interest! Wouldn't it be wonderful if they found all these MS symptoms could be reversed with 2 simple vitamins!

However, I digress! My neuro has me on Metanex which is a combo prescription of B6 and B12. My insurance covers it but I don't know what the criteria is for approval. Mine went through without a wimper but be forewarned, there is no generic as yet. I do not know what the actual cost of the medication is as I am a military dependent and have a very low copay.

Prayers and Hugs,

Tina

I've had my B12 checked multiple time and it's always at a very high level (I supplement quite regularly with the B's). But I don't have the white crescents on any of my nails except for my thumbs. But I know it's not because of low B12 levels though since I've never tested low for B12 levels and I supplement.

Same here Wannabe, always have!

I have b-12 deficiency and take supplementals shots for over a year now; I was diagnosed a year earlier with a movement disorder, Essential Tremor. I now have a vitamin D deficiency; I'm 47 years old. Neuro/MDS will not rule out MS as the tremors progress and I have issues with balance, weakness in knees...severely low b-12 (117 when caught) caused peripheral neuropathy...on lots of meds for the tremor....now with the vitamin D deficiency diagnosis yesterday (17) - I'm further concerned I've got early MS...any thoughts?

Moi Aussi: High levels of B12 *800*, and normal urine and serum mma, but crescents only on thumbs, and ridges on all nails.

Great book: Could it Be B12? written by a nurse and doctor. Get it at Amazon. What an eye opener the book was. It agrees that the cutoff of B12 is too low and should be at least 350 or more. It also shows how you can have normal serum MMA levels, normal serum B12 and abnormal urine MMA. Urine MMA is the definitive test for B12 problems (Pernicious Anemia) , which is an MS mimicker. And so treatable. Cheaply.

I've ordered the book after reading a review/info on the web. Thanks for the information. On other news for movement disorder, I take Propranolol (40mg) 1x a day and Primidone (50mg) 4x per day. Doctor has never suggested taking drugs for MS or Parkinson's but wondering if I should push it? What I'm taking has helped some but I still have internal tremors that are maddening at times...Jon

Thank you so much for the information. I am taking B12 shots due to the deficiency. Also have the MTRF gene checked. If you are B12 deficient, usually you are also low on folic acid and should take L5MTF.