[Editor update: Entire Sally Pachlock B12 film embedded on 21 May 2018.]They tell us that Australia has an 'aging population problem' and an associated ‘dementia epidemic’, with Alzheimers Disease the leading diagnosis. But everything that looks like Alzheimers is not Alzheimers. Vitamin B12 deficiency causes an easily treatable and reversible form of dementia which has been increasingly overlooked since the 1980s, although it was discovered in 1900 and the cure found in 1926, earning Minot and Murphy a Nobel Prize. Previously it was core medical practitioner knowledge that the ability to absorb Vitamin B12 via the gut diminishes with age and may cause dementia. [See appendix at end of article: “Useful reference documents on age, Vitamin B12 and dementia.”] This failure to absorb Vitamin B12 orally can be compensated by B12 injections and or by megadose lozenges or drops absorbed under the tongue. It used to be wide practice to give B12 injections to people over 60 monthly in Australia and many other countries, but for a variety of reasons this went out of fashion. The problem is not confined to the elderly. Children breastfeeding from mothers low in B12 have a high risk of neurological damage. Vitamin B12 cannot be supplied from vegan diets. [2a] There is also quite a large group of people of all ages, including children, who develop auto-immune pernicious anaemia (due to loss of the 'intrinsic factor') , which can and will cause brain injury, psychiatric problems, dementia, paralysis and death if untreated. However Australian, British and United States medical teaching, diagnostic and treatment guidelines are very problematic with regard to B12 deficiencies. So problematic that there is now a huge international movement where sufferers of pernicious anaemia teach each other about diagnosis and treatment, and where to access different forms of the vitamin, while they try to inform the medical profession.
As well as pernicious anaemia, many other events can affect Vitamin 12 absorption:
”Gastrointestinal disorders such as Crohn’s disease, celiac disease, enteritis and any inflammatory process will interfere with B12 absorption, even if it is correctly broken down by the body. Toxins such as mercury will interfere with the ability of B12 to cross the blood-brain barrier. Alcohol and the anesthetic nitrous oxide (often used in dental surgery) will inactivate B12; birth control pills deplete the vitamin in the body. A variety of inborn metabolic errors can also prevent normal absorption. The most well known aberration is pernicious anemia, although it is not the most common problem. Numerous medications inhibit the absorption of B12, including the many commonly prescribed drugs for heartburn, GERD and ulcers, as well as medications for diabetes, gout, some antibiotics and diuretics, the cholesterol drug Questran, and others. These drugs are commonly prescribed to the aging population, along with fistfuls of other medications that can mask the signs of B12 deficiency while worsening its effects, such as anti-depressants, drugs for insomnia, fatigue, numbness and tingling in extremities, incontinence, and tremors. Especially because of these drug interactions the aging population is at great risk for B12 deficiency. Most medical practitioners, however, will ascribe their deteriorating conditions to the ravages of age, or the complications and “natural progression” of their wrongly diagnosed diseases.” Source: http://www.westonaprice.org/book-reviews/could-it-be-b12-by-sally-pacholok-and-jeffrey-stuart/
A book by Sally M. Pacholok and Jeffrey J. Stuart called, Could It Be B12?: An Epidemic of Misdiagnoses (2007) (2011) records a nurse’s heroic efforts to get negligent hospitals to recognise and treat severe cases of B12 deficiency. For her careful and intelligent work she was shamefully persecuted. Nonetheless many doctors began to support what she was doing and continue to do so (as you can hear in the youtube clip at the top of this article.) This story is now the subject of an upcoming feature film about the cost of forgetting about B12. See the complete film below:
The forgetting of B12 is attributed in part to the streaming by US insurers of diseases into treatment categories that classified B12 deficiency as a red blood cell deformity rather than for the neurologic and other damage it does before it gets to that stage. A further complication is that compulsory addition of folic acid to many cereals  in the 1990s has had the effect of reducing the red blood cell deformity that doctors often rely on to diagnose the deficiency, without reducing the psychiatric symptoms including dementia and weaknesses and paralysis, which are then attributed to other or unknown causes, such as Alzheimers Disease and Multiple Sclerosis. The folic acid was added to reduce cases of spina bifida, which it did, but lack of B12 also causes spina bifida and unfortunately this problem has grown. “Birth defects linked to low B12.”
Sometimes B12 deficiency can be such an emergency that a blood transfusion is required to preserve life. In pernicious anaemia injections are usually preferred because the patient must take them for life and unfortunately people tend to cease taking oral supplements when they feel better, not realising or forgetting how important it is never to stop this vitamin.
"Vitamin B12 is not carcinogenic, teratogenic, or mutagenic. It is considered safe even at 1,000 times the RDA." Source: Baik and Russell, 1999, cited by the American Center for Disease Control, http://www.cdc.gov/ncbddd/b12/patients.html
CDB Editor 29 October 2017: The above link is no longer viable. Here is another statement on dosage level from the US CDC:
"No adverse effects have been associated with excess vitamin B12 intake from food or supplements in healthy individuals, and no UL has been set."
Source: Institute of Medicine, 1998. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline. Washington, DC: National Academy Press, cited by Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for vitamin C, vitamin E, selenium, and carotenoids. Washington, D.C.: National Academy Press; 2000, cited in 2nd National Report on Biochemical Indicators of Diet and Nutrition in the U.S. Population, p.16, https://www.cdc.gov/nutritionreport/pdf/Water.pdf.
More caution should be exercised about rapid initial dosage in relatively rare cases involving megaloblastic anaemia (big red cells) especially in the presence of heart disease.
The rate of injections depends on severity of neurological symptoms. The pharmaceutical advice accompanying Neo B12 injections suggests 1000mcg (1mg) of B12 intramuscularly every second day for one to two weeks. A lot of doctors are not aware of this.
After that the convention is weekly for 6-8 weeks. Then monthly. Some people need it more frequently and may even inject it daily with ‘pens’ like the ones that are used for insulin administration.
Unfortunately Neo B12 manufacturers and a few guides suggest that 3 monthly administration is sufficient after the initial intense treatment, however there are many warnings in the medical literature that this is usually not enough in pernicious anaemia or other mal-absorption syndromes. The patients cannot maintain levels for so long for various reasons. Patients in the UK find that the prescribing regimes there are so rigid and niggardly that many resort to buying B12 in injection form and self-injecting. The Pernicious Anaemia Society is circulating a petition to have the UK system more responsive to individual patient needs. See various forums for people with pernicious anaemia.
Lozenges and drops are not fast enough in an emergency – i.e. where there are noticeable neurological symptoms. If you take about 5mg (5000 mcg) sublingually daily for a month, by the end of a month you may reach the same dose as you would reach within 48 hrs after a single 1mg (1000mcg) injection. You can import high dose lozenges from the United States via amazon.com and also from New South Wales, Australia.
Blood level norms vary widely between countries
The levels considered 'normal range' vary greatly between different countries. In Japan 450 picograms per milliliter(pg/mL) is considered the lowest safe level, but in Australia it is 150, although guidelines advise that anyone with lower count than 350 who has symptoms, should be investigated further. The problem here is that many doctors think that the only ‘symptoms’ are deformed (macrocytic) red blood cells and attribute any neurologic symptoms to other or unknown causes or just ignore them. The patient goes away but the disease progresses and they may finish up in psychiatric facilities, nursing homes or dead.
I have experienced this lackadaisical treatment for two members of my family, leaving both disabled by brain injury. In both cases blood tests had been done which were well below the danger level, but they were ignored, again in both cases, by neurologist and a range of GPs in a particular clinic. When, as a carer with power of medical attorney I finally twigged to the cause and requested records of tests and new tests, the responses by the practitioners were awfully predictable: “But they don’t have macrocytosis.” “Oh, does she have symptoms?” (In a patient who had developed profound dementia over three years). “Oh, but his symptoms were caused by an accident.” (But they preceded the accident.) It seems that with B12 deficiencies people cannot even trust neurologists, let alone GPs to do the right thing. We therefore need to arm ourselves with knowledge and re-educate GPS. What we can do with our anger and despair at the needless suffering, I am not too sure. I find it hard to write about, but I write about it because I want to warn people.
This is a disease of frequently subtle onset:
"...because the liver is a very efficient storage organ for vitamin B12, even completely deficient diets in healthy adults might not result in low serum vitamin B12 levels for several years. Conversely, apparently healthy adults, especially the elderly, consuming diets rich in naturally occurring vitamin B12 can still develop a significant deficiency because of undetected malabsorption. It is possible for vitamin B12 deficiency to develop in a much shorter period of time (months) in some people." (Source: American Center for Disease Control, "Detection and Diagnosis.")
The disease runs in families as well as occurring with no family history.
Getting the norms changed, sensitizing clinics to neuro and psyche symptoms, diagnosing and treating the vitamin deficiency is very difficult because formal recognition of so far ignored cases could open up retrospective opportunities for legal suits. If the phenomena is as widespread as it seems to be, then we would be looking at huge class actions. Maybe we still are, since the evidence is so abundant, you wonder how long the medical and pathology definitions can resist this.
Pernicious Anaemia and Macrocytosis
"The accepted normal range, created many decades ago, is based on hematologic (blood) changes and not neurologic changes, and thus contributes significantly to late diagnosis." Source: Pacholok, Sally M.; Stuart, Jeffrey J. (2011-01-01). Could It Be B12?: An Epidemic of Misdiagnoses (p. 14). Linden Publishing. Kindle Edition. "
As I have already alluded, many doctors have been taught that pernicious anaemia is largely a blood disorder where the red cells that carry oxygen become visibly deformed (under the microscope). They have been taught that until this happens, the disease is not very serious. In reality, brain injury can occur well before the blood cell deformity occurs, and the blood cell deformity may never occur, especially now that most people are exposed to compulsory Folic Acid supplements in cereals. As well as classic brain injury, spinal lesions occur, crippling people with low B12 and mimicking Multiple Sclerosis.
"We believe that the “normal” serum B12 threshold needs to be raised from 200 pg/ml to at least 450 pg/ml because deficiencies begin to appear in the cerebral spinal fluid (CSF) below 550 pg/ml.10, 11, 12 At this time, we believe normal serum B12 levels should be greater than 550pg/ml. For brain and nervous system health and prevention of disease in older adults, serum B12 levels should be maintained near or above 1,000 pg/ml." Source: Pacholok, Sally M.; Stuart, Jeffrey J. (2011-01-01). Could It Be B12?: An Epidemic of Misdiagnoses (p. 11). Linden Publishing. Kindle Edition.
It is over a century since medical scientists discovered the link between B12 and mental illness, but in the early 21st century, “very few mentally ill patients are being evaluated for underlying B12 deficiency, and only a minute percentage receive the adjunctive urinary MMA test that can also assist in diagnosis.” Source: Pacholok, Sally M.; Stuart, Jeffrey J. (2011-01-01). Could It Be B12?: An Epidemic of Misdiagnoses (pp. 87-88). Linden Publishing. Kindle Edition. "
 I visited my mother’s 90 year old friend, who is a retired pharmacist a few days ago and raised the subject of B12 with her. She immediately said, “The minute someone turned 60 the doctors used to give them monthly Vitamin B12 injections. It was a very good earner for our pharmacy! And then it kind of went out of fashion.” She would have begun dispensing from her father’s pharmacy around 1942 or so.
 The intrinsic factor is a substance secreted by the stomach which enables the body to absorb vitamin B12. It is a glycoprotein. It can be destroyed by alcohol, various drugs, including antacids, beta blockers, some antibiotics and some illnesses. Discussed above as factors affecting Vitamin B12 absorption.
 Regulations for mandatory fortification of wheat flour with folic acid are currently in place in 53 countries although in many cases these regulations have not been implemented . In 2006, the World Health Organization and the Food and Agricultural Organization of the United Nations published guidelines to help countries to set the Target Fortification Level, the Minimum Fortification Level, the Maximum Fortification Level and the Legal Minimum Level of folic acid to be used to fortify flour with folic acid]. In the United States, mandatory fortification of enriched cereal grain products with folic acid was authorized in 1996 and fully implemented in 1998. Source: #B23-nutrients-03-00370">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3257747/#B23-nutrients-03-00370
APPENDIX: Useful reference documents on age, Vitamin B12 and dementia
Vitamin B12 deficiency common among elderly people
MOLNLYCKE, SWEDEN. Swedish researchers have discovered that many older people are deficient in
vitamin B-12. Their study involved 368 men and women aged 75 years or older. Analysis of blood serum
showed that 11 per cent of the participants were deficient in cobalamin (vitamin B-12). The researchers
point out that a vitamin B-12 deficiency has been linked to neuropsychiatric disorders such as memory
loss and dementia. The researchers discovered several cases of gastritis (inflammation of the lining of
the stomach) and two cases of celiac disease among patients with low serum values of cobalamin. They
conclude that routine screening for a vitamin B-12 deficiency is justified in the case of older people.
In a separate letter to the Journal of the American Geriatrics Society doctors from the Union
Memorial Hospital in Baltimore report on a case of vitamin B-12 deficiency. The patient, an 85-year-old
man, had developed progressive memory loss and lethargy over a two-year period. Although his serum
level of vitamin B-12 was within the currently accepted range, the doctors decided to proceed with vitamin
B-12 therapy. The patient received an intramuscular injection of 1000 micrograms of vitamin B-12 for
three consecutive days, then 1000 micrograms weekly for a month, and then one injection every month.
By the fifth injection his mental status had vastly improved and his lethargy had completely vanished. The
doctors conclude that the levels of serum vitamin B-12 concentrations currently considered normal in the
United States may be too low and should be reassessed. The lower limit of 200 pg/mL is based on the
level that causes abnormalities in the blood (pernicious anaemia). In contrast the lower limit in Japan and
some European countries is 500-550 pg/mL and is based on the level that causes mental manifestations
such as dementia and memory loss. The doctors suggest that a trial of vitamin B-12 therapy is warranted
in patients with borderline cobalamin serum levels as it is effective and inexpensive.
Eggersten, Robert, et al. Prevalence and diagnosis of cobalamin deficiency in older people. Journal of
the American Geriatrics Society , Vol. 44, No. 10, October 1996, pp. 1273-74
Goodman, Mark, et al. Are U.S. lower normal B-12 limits too low? Journal of the American Geriatrics
Society, Vol. 44, No. 10, October 1996, pp. 1274-75
NEW YORK, NY. Researchers at Columbia University have confirmed that elderly people often suffer
from a lack of vitamin B12 (cobalamin). The deficiency is usually only discovered when patients develop
megaloblastic anaemia. However, before this stage is reached, cobalamin-deficient individuals may
develop neuropsychiatric damage and show signs of disorientation and confusion. The researchers
evaluated 548 men and women aged 67 to 96 years and compared their cobalamin and folate status to
that of 117 healthy, younger control subjects. They found that 40.5 per cent of the elderly people suffered
from a vitamin B12 deficiency versus only 17.9 per cent in the younger group. There was no significant
difference in folate status between the two groups. The researchers also found that people who took oral
supplements containing vitamin B12 and folate (6 micrograms and 400 micrograms per day respectively)
were much less likely to suffer from a deficiency than were people who did not supplement. They point
out that as people age they become less and less able to absorb vitamin B12 from food and therefore are
likely to develop a deficiency. As gastric atrophy progresses vitamin B12 status can only be maintained
by taking high oral doses of cobalamin (500-1000 micrograms daily) or by routine intramuscular injections
providing 1 mg per month. The researchers also point out that a vitamin B12 deficiency leads to an
accumulation of homocysteine in the blood. An increased serum concentration of homocysteine and its
derivatives is now recognized as a major risk factor in heart disease and stroke.
Lindenbaum, John, et al. Prevalence of cobalamin deficiency in the Framingham elderly population.
American Journal of Clinical Nutrition, Vol. 60, July 1994, pp. 2-11
Allen, Lindsay H. and Casterline, Jennifer. Vitamin B-12 deficiency in elderly individuals: diagnosis and
requirements. American Journal of Clinical Nutrition, Vol. 60, July 1994, pp. 12-14
LEUVEN, BELGIUM. An international team of researchers have confirmed that elderly people often
suffer from a deficiency of vitamins B-6, B-12 and folic acid. Their investigation involved 99 healthy young
people (aged 19-55), 64 healthy elderly subjects (aged 65-88), and 286 elderly hospitalized patients
(aged 61-97). The researchers measured the blood concentrations of the vitamins in all subjects as well
as the concentration of certain metabolic products that tend to build up if a vitamin deficiency is present.
They found that 9% of the healthy elderly subjects had a low vitamin B-6 level as compared to more than
51% for the hospitalized patients. Corresponding numbers for vitamin B-12 and folic acid were 6% and
5%, and 5% and 19% respectively. Of perhaps greater significance was the finding that in 63% of the
healthy elderly subjects and in 83% of the elderly patients the researchers observed an increased serum
concentration of one or more of the metabolic products that indicate a deficiency in vitamin B-6, B-12 or
folate. Thus an elevated level of the metabolite (methylmalonic acid), which indicates a B-12 deficiency,
was found in 23% of the healthy elderly people and in 39% of the elderly hospitalized patients. Recent
experiments have shown that weekly injections of vitamin B-12, B-6, and folate are highly effective in
normalizing the elevated metabolite concentrations in elderly people.
Joosten, Etienne, et al. Metabolic evidence that deficiencies of vitamin B-12 (cobalamin), folate, and
vitamin B-6 occur commonly in elderly people. American Journal of Clinical Nutrition, Vol. 58, No. 3,
September 1993, pp. 468-76
See also the following peer reviewed statement in the Journal of the American Geriatric Society, in response to a letter from Dr Soloman, who speaks in the film at the top of this article, ""Diagnosing and Treating Vitamin B12 Deficiency .:
Response Letter to Lawrence Solomon
To the Editor: We appreciate Dr. Solomon's interest in our recent study of vitamin B12 and peripheral nerve function. We agree that B12 deficiency is only one risk factor for poor peripheral nerve function, and many older adults with “normal” B12 levels may have subclinical B12 deficiency, as shown according to methylmalonic acid (MMA) levels, and have poor peripheral nerve function. Because diabetes mellitus accounts for only approximately 40% of prevalent cases of peripheral neuropathy and half of incident cases,#R1" rid="R1" class="bibr popnode tag_hotlink tag_tooltip jig-ncbipopper" id="__tag_381065392">1 additional risk factors need to be identified in individuals without diabetes mellitus. Clinicians are often unable to determine a reasonable cause of neuropathy in older adults. We recognize that older adults with “normal” serum B12 levels (>260 pmol/L) can still have high MMA levels. A recent review showed that homocysteine and MMA levels may be high for serum B12 levels up to 400 pmol/L.#R2" rid="R2" class="bibr popnode tag_hotlink tag_tooltip jig-ncbipopper" id="__tag_381065393">2 Therefore, the cut point of 260 pmol/L may be inadequate for determining associations with poor peripheral nerve function. More importantly, the clinical deficient cutpoint of 148 pmol/L may need to be reexamined because many older adults with “clinically normal” B12 levels may have nerve deficits caused by low B12 availability. Thus, clinicians may believe that, because their patients' serum B12 level is “clinically normal,” poor B12 is not causing the symptoms of peripheral neuropathy and B12 replacement is not needed.
Unfortunately, MMA or homocysteine levels are not available for those with B12 levels greater than 260 pmol/L to determine those with “functional B12 deficiency.” In our study, in those with low serum B12 (<260 pmol/L), no significant difference existed in MMA levels between older adults with (358.9 ± 252.1 nmol/L) and without diabetes mellitus (323.5 ± 213 nmol/L) (P = .20). The analysis that Dr. Solomon has performed is important to determine that “functional B12 deficiency” is probably present in a substantial proportion of older adults, particularly in older adults with diabetes mellitus. The use of metformin, which impairs absorption of B12 found naturally in food (animal products), accentuates this relationship in older adults with diabetes mellitus.#R3" rid="R3" class="bibr popnode jig-ncbipopper">3,#R4" rid="R4" class="bibr popnode jig-ncbipopper">4 The role of “functional B12 deficiency” and the threshold of vitamin B12 levels affecting peripheral nerve function in older adults is a critical future direction of our work.
This work was funded by National Institute on Aging (NIA) Contracts N01-AG-6–2101, N01-AG-6–2103, and N01-AG-6–2106 and supported in part by the NIA Intramural Research Program of the National Institutes of Health (NIA Grant R01-AG 028050, Strotmeyer ES; and National Institute of Nursing Research Grant R01-NR012459), University of Pittsburgh Claude D. Pepper Older Americans Independence Center (P30-AG024827) Pilot Grant (Strotmeyer ES), and NIA training Grant T32-AG-000181 KL.
Conflict of Interest: The authors have no financial or personal conflicts of interests to disclose.
Author Contributions: Leishear and Strotmeyer: analysis and interpretation of data; preparation of manuscript. Studenski, Ferrucci, de Rekeneire, Kritchevsky, Vinik, Hogervorst, Harris, and Newman: preparation of manuscript.
Sponsor's Role: Not applicable.
Kira Leishear, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania, Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland.
Stephanie A. Studenski, Division of Geriatric Medicine, Department of Medicine School of Medicine, University of Pittsburgh, Pittsburgh Pennsylvania.
Luigi Ferrucci, Longitudinal Studies Section, Clinical Research Branch National Institute on Aging, Baltimore, Maryland.
Nathalie de Rekeneire, Section of Geriatrics, School of Medicine, Yale University New Haven, Connecticut.
Stephen B. Kritchevsky, Sticht Center on Aging, School of Medicine, Wake Forest University, Winston-Salem, North Carolina.
Aaron I. Vinik, Division of Endocrinology and Metabolism, Department of Medicine, Eastern Virginia Medical School, Strelitz Diabetes Center, Norfolk, Virginia.
Eva Hogervorst, Department of Human Sciences, Loughborough University, Loughborough, UK.
Tamara B. Harris, Laboratory of Epidemiology, Demography and Biometry Intramural Research Program, National Institute on Aging, Bethesda, Maryland.
Anne B. Newman, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania Division of Geriatric Medicine, Department of Medicine School of Medicine, University of Pittsburgh, Pittsburgh Pennsylvania.
Elsa S. Strotmeyer, Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania.