VITAMIN B-12 DEFICIENCY

WELL, HERE IS ANOTHER TOPIC THAT IS BECOMING NEAR AND DEAR TO MY HEART. AFTER WE LOST DALLIN, WE PLAYED RAPID CATCH-UP IN THE KIDS DEPT AND HAD THE LAST TWO RAPID-FIRE WITH ALL OF OUR ZERO-POP DOCS AND PEOPLE HERE IN SEATTLE WATCHING IN ABSOLUTE HORROR AS WE SINGLE-HANDEDLY BROUGHT LIFE ON THIS PLANET TO A GRINDING HALT WITH OUR MIS-GUIDED COPIOUS COPULATING.

WHILE THEY WERE OUT IN LEFT FIELD FROM A GOSPEL STANDPOINT, THEY MIGHT HAVE BEEN RIGHT ON ONE FRONT (IN HIND-SIGHT). DURING THE LAST PREGNANCY, SHAWNA'S PERSONALITY SLOWLY CHANGED FROM HER BUBBLY SELF TO A QUIET, WITHDRAWN, INTROSPECTIVE PERSON THAT I DID NOT RECOGNIZE. IT WAS A SLOW 9 MONTH NOSE-DIVE THAT CAUSED HER TO CHANGE 180 DEGREES IN HER VIEWS POLITICALLY AND RELIGIOUSLY ALONG WITH THE PERSONALITY CHANGE. SHE ALSO BECAME VERY ANXIOUS, MOODY, DEPRESSED, AND OVERWHELMED AT SEEMINGLY ORDINARY STUFF. BY THE TIME THE BABY CAME I WAS PRETTY MUCH AT MY ROPES END WITH ALL OF THESE CHANGES. I THOUGHT THEY WERE JUST PART OF THE PREGNANCY DEAL (EVEN THOUGH I HAD NOT OBSERVED THEM BEFORE IN THE PREVIOUS 4 PREGNANCIES) AND JUST KIND OF "ROLLED WITH IT".

THAT ALL CHANGED ABOUT SIX WEEKS AFTER THE BABY CAME HOME. SHAWNA STARTED HER PERIOD (WHILE BREAST FEEDING - NOT NORMAL....) WAS OVERLY AMOROUS (TO MY DELIGHT) AND BECAME WHAT WE LATER FOUND TO BE MANIC (RAPID SPEECH, THOUGHTS AND GRANDIOSE BEHAVIOR). MY WORST FEAR WAS REALIZED WHEN SHE WOULD NOT SLEEP FOR FEAR OF LOSING ANOTHER BABY IN THE NIGHT. I BEGAN TO WORRY FOR THE SAFETY OF THE KIDS - AND DID NOT WANT TO BE ANOTHER ONE OF THOSE POST-PARTUM DISASTERS YOU ALWAYS READ ABOUT. TO TOP IT ALL OFF, THE PHONE QUIT WORKING AND I WAS MORE OR LESS TRAPPED AT HOME TRYING TO DEAL WITH THIS AND COULD NOT EASILY CALL TO GET SOME ADVICE. FINALLY, I LEFT CAMYLLE AT HOME TO KEEP AN EYE ON HER MOM, AND I SPLIT FOR THE NEIGHBOR'S HOUSE TO CALL A CHURCH FRIEND WHO WAS IN THE MENTAL HEALTH FIELD. SHE WAS NOT HOME SO I CALLED THE R.S. PREZ AND SHE CAME RIGHT OVER WITH ANOTHER OF SHAWNA'S FRIENDS. THEY WERE ABLE TO COAX HER INTO THEIR SUBURBAN FOR A QUICK TRIP TO THE EMERGENCY ROOM FOR OBSERVATION. WHILE IN OBSERVATION, SHE ACTED RELATIVELY TOTALLY 'NORMAL' AND I HAD THE HARDEST TIME CONVINCING ANY NURSE OR DOCTOR THAT THERE WAS A PROBLEM. FOUR HOURS LATER AND USING ALL OF PEOPLE THAT HAD GATHERED TO HELP OUT (IT WAS QUITE THE CIRCUS), SHAWNA SPIT OUT A PILL AND BOLTED FOR THE DOOR (CONVINCED IN HER COMPROMISED STATE THAT WE WERE ALL OUT TO GET HER). SHE FINALLY ENDED UP GETTING TRANSPORTED TO A HOSPITAL THAT WAS ABLE TO SEDATE HER FOR TWO WEEKS TO GET OVER THE SLEEP DEPRIVATION AND TO PUMP HER FULL OF PSYCHOTROPICS FOR HER NOW-DIAGNOSED CONDITION OF "MANIC-DEPRESSIVE". SHE CAME HOME A ZOMBIE FROM ALL OF THE DRUGS THEY PUT HER ON, BUT THINGS WERE RELATIVELY 'NORMAL'. I WAS GRATEFUL THAT I STILL HAD MY JOB AFTER ONLY GOING INTO THE OFFICE FOR 2 DAYS OUT OF 60 AND TELECOMPUTING AND USING BANKED SICK-LEAVE AND VACATION FOR THE REMAINDER. IT PRETTY-MUCH WIPED US OUT IN THAT AREA.

I WAS ADVISED BY SEVERAL PEOPLE THAT THE STRESS OF LOSING DALLIN MAY HAVE BEEN TOO MUCH - AND THAT WE SHOULD LOOK FOR A NEW HOUSE AND A NEW START AND TO "MAKE SHAWNA AS COMFORTABLE AS POSSIBLE". I THOUGHT IT WAS ALL GOOD ADVICE - AND SO WE HAD OUR HOUSE BUILT AND BEGAN THAT PROCESS - ALL THE WHILE TRYING TO SHIELD SHAWNA FROM THE UPS AND DOWNS OF THAT STRESSFUL PROCESS. WE HAD STARTED OUR MONTANA PROJECT - BUT THAT WAS SHELVED FOR THE TIME-BEING TO FOCUS ON THE BIGGER FISH THAT WE WERE FRYING IN OUR PAN.

BEING THE PROBLEM-SOLVING ENGINEER THAT I AM, I DUG RIGHT INTO THIS PROBLEM TRYING TO FIND SOMEONE WHO HAD LICKED IT. I STAYED AWAY FROM CONVENTIONAL MEDICINE KNOWING THAT THEIR SOLUTION WAS JUST MORE EXPENSIVE PSYCHOTROPICS THAT JUST TREATED THE SYMPTOMS AND NOT THE UNDERLYING ROOT CAUSE. WHILE SHAWNA WAS STABILIZED ON THE PSYCHOTROPICS, SHE WAS NOT THE WOMAN I HAD MARRIED. THE DRUGS TOOK ALL THE HIGHS AND LOWS AWAY FROM HER PERSONALITY - I MIGHT AS WELL HAVE BEEN MARRIED TO ONE OF THOSE LIFE-LIKE ROBOTS FROM HONDA. I FELT LIKE MY MARITAL AND FAMILIAL QUALITY OF LIFE WAS AROUND 20% - NOTHING TO WRITE HOME ABOUT.... THE OLDER KIDS WERE GETTING FRUSTRATED ABOUT IT, AS WELL. THEY COULD SENSE THE MARKED CHANGE IN THEIR MOTHER. ON TOP OF THAT, CAMYLLE ENDED UP PLAYING MOTHER WHILE I WAS AWAY AT WORK BECAUSE JUST THE THOUGHT OF MAKING A SIMPLE DINNER OR CLEANING UP A MESS AROUND THE HOUSE HORRIBLY OVERWHELMED SHAWNA AND SOME DAYS, DEPENDING ON THE CLOCKING OF HER MENSTRUAL CYCLE ESTROGEN/PROGESTERONE AND TESTOSTERONE. OUR FAMILY WAS REACHING THE BREAKING POINT. AROUND THAT TIME, I HAD A SINGULAR DREAM UNLIKE ANY OTHER I HAD EVER HAD AND I SEEMED TO GET THE IDEA THAT WE WOULD FIND A CURE FOR THIS - OUTSIDE OF PRIESTHOOD POWER AND THE BLESSINGS SHAWNA HAD RECEIVED. WITH OUR GREAT RESOURCES OF KNOWLEDGE, SOMETIMES IT IS JUST FINDING THE RIGHT KEY TO UNLOCK THAT KNOWLEDGE IN A WORLD WHERE TRUTH IS OFTEN NOT SOUGHT OUT - AND OFTEN SUPPRESSED DUE TO THE "DESIGNS OF CONSPIRING MEN". SORRY FOR YOU GOOD DOCTORS OUT THERE, BUT I HAVE LEARNED TO DESPISE OUR EXISTING CORRUPTED MEDICAL SYSTEM THAT, BY DESIGN, ONLY FOCUSES ON THE SYMPTOMS. I SUGGEST IF YOU ARE KNOWINGLY PART OF THAT SYSTEM, INSTEAD OF THE SOLUTION YOU WILL EXIT THE SCENE SHORTLY WITH THE REST THAT OPERATE ON BAD PRINCIPLE. THE EXISTING SYSTEM WILL LARGELY NOT BE INTACT WHEN THE SAVIOR MAKES HIS APPEARANCE AND WILL BE REPLACED BY A SYSTEM THAT ONLY HAS THE PATIENT'S BEST INTERESTS IN MIND - NOT THE DRUG COMPANIES'.

SO, FOLLOWING THE SPIRIT AND DIGGING AROUND ON THE INTERNET, I FOUND A STORY OF AN ENGINEER FROM THE CARDSTON AREA (LDS) WHO HAD 8 KIDS AND WHOSE WIFE LOST THE BATTLE TO POST-PARTUM BI-POLAR DEPRESSION AND WHO TOOK HER OWN LIFE. TO MAKE THINGS WORSE, TWO OF HIS KIDS BEGAN SHOWING SIMILAR SYMPTOMS (THIS SHOWED A HEREDITARY FACTOR) AND HE WAS SCARED THAT HE WOULD POSSIBLY LOSE THEM. HE MENTIONED HIS PROBLEM TO A FRIEND WHO WAS A PIG FARMER WHO SAID THAT WHEN HE HAD PIGS THAT WOULD DEVELOP A "SYNDROME" THAT WOULD CAUSE THEM TO EAT AT THE EARS AND TAILS OF THE OTHER PIGS IN THE HERD. THE COMMON CURE WAS TO ISOLATE THEM, FEED THEM A FEED RICH IN VITAMINS AND MINERALS FOR SEVERAL WEEKS AND THEN PLACE THEM BACK IN THE GENERAL POPULATION WITH NO FURTHER SIGNS OF TROUBLE. PIGS ARE CLOSE TO HUMANS PHYSIOLOGICALLY, SO THIS GOOD BROTHER ASKED HIS FRIEND FOR THE FORMULATION AND DUPLICATED IT IN USP GRADE VITAMINS ETC. HE GAVE THE CONCOCTION TO HIS KIDS AND WITHIN A FEW MONTHS THEY WERE SHOWING NO RESIDUAL SIGNS OF THE PROBLEMS THEY HAD STARTED WITH.

I MENTIONED THIS TO SHAWNA. SHE WENT TO A NATUROPATHIC DOCTOR SHE WOULD SEE OCCASIONALLY, WHO THEN ORDERED BLOOD TESTS FOR VITAMIN LEVELS. THE DOC CONFIRMED WHAT SHOULD HAVE BEEN SEEN BY A COMPETENT PHYSICIAN UP FRONT - B12 LEVELS WERE ROCK BOTTOM. SHAWNA WAS AT A BLOOD SERUM LEVEL OF 200 PICO-GRAMS PER DECILITER OF BLOOD AND A NORMAL LEVEL IS 3-5 TIMES THAT AND A BABY'S LEVELS ARE 10 TIMES THAT (WHICH IS HOW SHAWNA GOT IN HER CONDITION - SHE WAS BEING DEPLETED BY OUR ANNELISE WHO WAS TRYING TO GET ENOUGH FOR HER DEVELOPING BODY). ODDLY, I WAS SKEPTICAL AND WOULD JOKE TO SHAWNA ABOUT HER "WITCH DOCTOR" AND VOO-DOO MEDICINE. SHAWNA PERSISTED FOR ABOUT 5-6 WEEKS WITH VERY HIGH DOSAGE INTRA-MUSCULAR INJECTIONS OF B12 WHICH LITERALLY CAUSED THE "EMOTIONAL CLOUDS TO PART AND THE SUN COME OUT". I COULDN'T BELIEVE IT. JUST AS SHAWNA FADED OVER 9 MONTHS INTO A "ZOMBIE" I DIDN'T RECOGNIZE - INTO SOMEONE WHO EASILY COULD HAVE TAKEN HER OWN LIFE DUE TO OVERWHELMING DEPRESSION/ANXIETY - SHE WAS COMING BACK RIGHT BEFORE MY EYES (A YEAR LATER WE I KNOW WE ARE TOTALLY OUT OF THE WOODS). I WENT FROM CAUTIOUS SKEPTIC TO COMPLETE BELIEVER IN B12 AS AN ABSOLUTE ESSENTIAL ELEMENT FOR MIND (NERVOUS SYSTEM) AND BODY HEALTH. DUE TO ITS COMPLEXITY AS THE ONLY METAL-BASED (COBALT) AMINO ACID VITAMIN, JUST ONE OF THE STEPS OF ITS ASSIMILATION PROCESS THAT IS COMPROMISED CAN LEAD TO ITS DEFICIENCY AND CATASTROPHIC RESULTS THAT WE SAW. SINCE SOME STEPS IN THIS PROCESS CAN BE INFLUENCED BY EXTERNAL FACTORS SUCH AS HEREDITY, THE FACT THAT SHAWNA HAD ONE PERSON ON EACH SIDE OF HER FAMILY THAT SUFFERED FROM IT INCREASED HER RISK. THE OTHER THING THAT BROUGHT IT ABOUT WAS THE INDUCTION OF EXTREME STRESS DUE TO A MAJOR LIFE EVENT (LOSING A CHILD QUALIFIES IN THE EXTREME - AND THERE WAS MORE THAT LED TO THIS THAT I WILL PROBABLY BLOG LATER THAT IS WAY MORE FASCINATING THAN THIS LITTLE JOURNEY WE WERE SENT ON).

ANYWAY, THIS WHOLE EPISODE QUITE NEARLY LED TO THE END OF OUR MARRIAGE (I HAVE NOT EVEN SCRATCHED THE SURFACE AS TO HOW BIZARRE THINGS GOT, OUT OF RESPECT FOR SHAWNA AND THE FACT THAT THOSE DAYS DO NOT REPRESENT WHO SHE IS WHO IS A PERSON WHO IS ROCK SOLID SPIRITUALLY AND EMOTIONALLY) AS I LOST THE WILL TO COPE WITH MY WIFE'S BIZARRE SYMPTOMS. AS A SIDE NOTE, 90% OF MARRIAGES THAT HAVE AT LEAST ONE PARTNER WHO SUFFERS BI-POLAR SYMPTOMS LEADS TO DIVORCE. I DON'T THINK A TEMPLE MARRIAGE NECESSARILY INNOCULATES ONE AGAINST THIS TREND EITHER. TO MAKE THINGS WORSE, 70% OF COUPLES WHO LOSE A CHILD END UP DIVORCED DUE TO THE STRESS THAT COMES FROM THAT EVENT. THE COMPOSITE ODDS OF OUR MARRIAGE SURVIVING FOR THE THREE YEARS WE WERE IN THIS CONDITION WAS EFFECTIVELY 3%. THE ONLY THING THAT KEPT ME GOING AT PARTICULARLY DIFFICULT PERIODS WERE FREQUENT VISITS TO THE TEMPLE THAT SERVED TO RE-CHARGE ME SPIRITUALLY, A HIGH DOSE OF IRISH STUBBORNNESS..., AND A GOOD BROTHER WHO OPENED UP ABOUT HIS WIFE'S PROBLEM AND HOW HE DEALT WITH IT AND CONVINCED ME THAT I WAS A FOOL FOR NOT REALIZING SHAWNA'S THEORETICAL LONG-SUFFERING HAD THE SITUATION BEEN FLIPPED. THERE IS AN EXTREMELY HIGH INCIDENCE OF USE OF MOOD ALTERING DRUGS IN THE CHURCH - I BELIEVE UTAH LEADS THE CHARGE IN THIS AREA FOR ALL 50 STATES - AND THIS COULD ACCOUNT FOR HIGHER THAN EXPECTED DIVORCE RATES, TEEN-PREGNANCY RATES THAT MIRROR 'THE WORLD' AND OTHER BAFFLING PROBLEMS THAT DEFY THE TEACHINGS WE ARE GIVEN. THAT OUTSIDE OF THE PROBLEMS OF JUST GOOD OLD-FASHIONED LEVELS OF SIN THAT MIGHT BE EXPECTED AMONG PROPERLY-TRAINED LDS FOLK.

ON THAT NOTE, IN SHAWNA'S TWISTED MENTAL STATE, IMHO SHE WAS QUITE CAPABLE OF DOING ANYTHING FROM A "MARY K. LETOURNEAU" TO THE "TEXAS TOAST" (BOTH WOMEN WERE RECENT POST-PARTUMS WHEN THEY PLUNGED OFF THE DEEPT END) AND ALOT OF STUFF IN BETWEEN THAT I HAVE SEEN IN HUNDREDS OF CASES THAT I HAVE BUMPED INTO AND WITNESSED ANECDOTALLY. I WOULD NOT HAVE BELIEVED IF I HAD NOT SEEN IT AND EXPERIENCED IT IN A REAL WAY. WITH THINGS BACK IN BALANCE, I NEVER EXPECT TO WITNESS THIS KIND OF TROUBLE FOR THE REST OF OUR LIVES TOGETHER - AS SHAWNA IS PROBABLY MORE SANE THAN I AM RIGHT NOW.....:) IT IS A TRUE MIRACLE AND A FULFILLMENT OF THAT DREAM (TO BE RECORDED LATER) AND PART THREE OF THE "DALLIN DREAM" THAT I WILL POST THE TRANSCRIPT OF AND LINK AT A LATER TIME.

THE ONE THING THAT I WALKED AWAY FROM THIS WHOLE CONVOLUTED THING WITH WAS A COMPLETE AND TOTAL WITNESS THAT GOD LOVES US AND IS INTIMATELY INVOLVED WITH EACH OF HIS CHILDREN IN HELPING THEM REACH THEIR FULL POTENTIAL IN THIS LIFE. I ALSO LEARNED THAT, IF LIFE IS A CAKE WALK, THEN WE ARE NOT GETTING ANY GOOD FROM THIS MORTAL PROBATION. SO BUCKLE UP, DO WHAT IS RIGHT AND ENJOY THE RIDE THAT IS LIFE!!

GOD TRULY WILL NEVER GIVE YOU MORE THAN YOU CAN HANDLE.

HERE IS MORE INFO ON B12 FOR THOSE OF YOU THAT HAVE FAMILY THAT MAY BE STRUGGLING ALONG THESE LINES. THIS IS ONE OF THE MORE CONCISE EXPLANATIONS OF THE ROLE OF B12 THAT I HAVE COME ACROSS:



Micronutrient Information Center
Vitamin B12

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 (1). The form of cobalamin used in most supplements, cyanocobalamin, is readily converted to 5-deoxyadenosyl and methylcobalamin in the body. In mammals, cobalamin is a cofactor for only two enzymes, methionine synthase and L-methylmalonyl-CoA mutase (2).

Function

Cofactor for methionine synthase

Methylcobalamin is required for the function of the folate-dependent enzyme, methionine synthase. This enzyme is required for the synthesis of the amino acid, methionine, from homocysteine. Methionine in turn is required for the synthesis of S-adenosylmethionine, a methyl group donor used in many biological methylation reactions, including the methylation of a number of sites within DNA and RNA (3). Methylation of DNA may be important in cancer prevention. Inadequate function of methionine synthase can lead to an accumulation of homocysteine, which has been associated with increased risk of cardiovascular diseases (diagram).

Cofactor for L-methylmalonyl-CoA mutase

5-Deoxyadenosylcobalamin is required by the enzyme that catalyzes the conversion of L-methylmalonyl-CoA to succinyl-CoA. This biochemical reaction plays an important role in the production of energy from fats and proteins. Succinyl CoA is also required for the synthesis of hemoglobin, the oxygen carrying pigment in red blood cells (3).

Deficiency

Vitamin B12 deficiency is estimated to affect 10%-15% of individuals over the age of 60 (4). Absorption of vitamin B12 from food requires normal function of the stomach, pancreas, and small intestine. Stomach acid and enzymes free vitamin B12 from food, allowing it to bind to other proteins called R proteins (3). In the alkaline environment of the small intestine, R proteins are degraded by pancreatic enzymes, freeing vitamin B12 to bind to intrinsic factor (IF), a protein secreted by specialized cells in the stomach. Receptors on the surface of the small intestine take up the IF-B12 complex only in the presence of calcium, which is supplied by the pancreas (5). Vitamin B12 can also be absorbed by passive diffusion, but this process is very inefficient—only about 1% absorption of the vitamin B12 dose is absorbed passively (2).

Causes of vitamin B12 deficiency

The most common causes of vitamin B12 deficiency are: 1) an autoimmune condition known as pernicious anemia and 2) food-bound vitamin B12 malabsorption. Although both causes become more common with increasing age, they are separate conditions (4).

Pernicious anemia

Pernicious anemia has been estimated to be present in approximately 2% of individuals over 60 (6). Although anemia is often a symptom, the condition is actually the end stage of an autoimmune inflammation of the stomach, resulting in destruction of stomach cells by one's own antibodies. Progressive destruction of the cells that line the stomach causes decreased secretion of acid and enzymes required to release food-bound vitamin B12. Antibodies to intrinsic factor (IF) bind to IF preventing formation of the IF-B12 complex, further inhibiting vitamin B12 absorption. If the body's vitamin B12 stores are adequate prior to the onset of pernicious anemia, it may take years for symptoms of deficiency to develop. About 20% of the relatives of pernicious anemia patients also have pernicious anemia, suggesting a genetic predisposition. Treatment of pernicious anemia generally requires injections of vitamin B12 to bypass intestinal absorption. High-dose oral supplementation is another treatment option, because consuming 1,000 mcg (1 mg)/day of vitamin B12 orally should result in the absorption of about 10 mcg/day (1% of dose) by passive diffusion (4). In fact, high-dose oral therapy is considered to be as effective as intramuscular injection (7-10).

Food-bound vitamin B12 malabsorption

Food-bound vitamin B12 malabsorption is defined as an impaired ability to absorb food or protein-bound vitamin B12, although the free form is fully absorbable (11). In the elderly, food-bound vitamin B12 malabsorption is thought to result mainly from atrophic gastritis, a chronic inflammation of the lining of the stomach that ultimately results in the loss of glands in the stomach (atrophy) and decreased stomach acid production. Because stomach acid is required for the release of vitamin B12 from the proteins in food, vitamin B12 absorption is diminished. Decreased stomach acid production also provides an environment conducive to the overgrowth of anaerobic bacteria in the stomach, which further interferes with vitamin B12 absorption (3). Because vitamin B12 in supplements is not bound to protein, and because intrinsic factor (IF) is still available, the absorption of supplemental vitamin B12 is not reduced as it is in pernicious anemia. Thus, individuals with food-bound vitamin B12 malabsorption do not have an increased requirement for vitamin B12; they simply need it in the crystalline form found in fortified foods and dietary supplements.

Atrophic gastritis

Atrophic gastritis is thought to affect 10%-30% of people over 60 years of age, and the condition is frequently associated with infection by the bacteria, Heliobacter pylori. H. pylori infection induces chronic inflammation of the stomach, which may progress to peptic ulcer disease, atrophic gastritis, and/or gastric cancer in some individuals. The relationship of H. pylori infection to atrophic gastritis, gastric cancer, and vitamin B12 deficiency is presently an area of active research (4).

Other causes of vitamin B12 deficiency

Other causes of vitamin B12 deficiency include surgical resection of the stomach or portions of the small intestine where receptors for the IF-B12 complex are located. Conditions affecting the small intestine, such as malabsorption syndromes (celiac disease and tropical sprue), may also result in vitamin B12 deficiency. Because the pancreas provides critical enzymes as well as calcium required for vitamin B12 absorption, pancreatic insufficiency may contribute to B12 deficiency. Since vitamin B12 is found only in foods of animal origin, a strict vegetarian (vegan) diet has resulted in cases of vitamin B12 deficiency. Alcoholics may experience reduced intestinal absorption of vitamin B12 (2). Individuals with acquired immunodeficiency syndrome (AIDS) appear to be at increased risk of deficiency, possibly related to a failure of the IF-B12 receptor to take up the IF-B12 complex (3). Long-term use of acid-reducing drugs has also been implicated in vitamin B12 deficiency (see Drug interactions).

Symptoms of vitamin B12 deficiency

Vitamin B12 deficiency results in impairment of the activities of B12-requiring enzymes. Impaired activity of methionine synthase may result in elevated homocysteine levels, while impaired activity of L-methylmalonyl-CoA mutase results in increased levels of a metabolite of methylmalonyl-CoA called methylmalonic acid (MMA). Individuals with mild vitamin B12 deficiency may not experience symptoms, although blood levels of homocysteine and/or MMA may be elevated (12).

Megaloblastic anemia

Diminished activity of methionine synthase in vitamin B12 deficiency inhibits the regeneration of tetrahydrofolate (THF) and traps folate in a form that is not usable by the body (diagram), resulting in symptoms of folate deficiency even in the presence of adequate folate levels. Thus, in both folate and vitamin B12 deficiencies, folate is unavailable to participate in DNA synthesis. This impairment of DNA synthesis affects the rapidly dividing cells of the bone marrow earlier than other cells, resulting in the production of large, immature, hemoglobin-poor red blood cells. The resulting anemia is known as megaloblastic anemia and is the symptom for which the disease, pernicious anemia, was named (3). Supplementation with folic acid will provide enough usable folate to restore normal red blood cell formation. However, if vitamin B12 deficiency is the cause, it will persist despite the resolution of the anemia. Thus, megaloblastic anemia should not be treated with folic acid until the underlying cause has been determined (5).

Neurologic symptoms

The neurologic symptoms of vitamin B12 deficiency include numbness and tingling of the arms and, more commonly, the legs, difficulty walking, memory loss, disorientation, and dementia with or without mood changes. Although the progression of neurologic complications is generally gradual, such symptoms are not always reversible with treatment of vitamin B12 deficiency, especially if they have been present for a long time. Neurologic complications are not always associated with megaloblastic anemia and are the only clinical symptom of vitamin B12 deficiency in about 25% of cases (6). Although vitamin B12 deficiency is known to damage the myelin sheath covering cranial, spinal, and peripheral nerves, the biochemical processes leading to neurological damage in B12 deficiency are not well understood (3).

Gastrointestinal symptoms

Tongue soreness, appetite loss, and constipation have also been associated with vitamin B12 deficiency. The origins of these symptoms are unclear, but they may be related to the stomach inflammation underlying some cases of B12 deficiency, or to the increased vulnerability of rapidly dividing gastrointestinal cells to impaired DNA synthesis (6).

The Recommended Dietary Allowance (RDA)

The current RDA was revised by the Food and Nutrition Board (FNB) of the Institute of Medicine in 1998. Because of the increased risk of food-bound vitamin B12 malabsorption in older adults, the FNB recommended that adults over 50 years of age get most of the RDA from fortified food or vitamin B12-containing supplements (6).
Recommended Dietary Allowance (RDA) for Vitamin B12
Life Stage Age Males (mcg/day) Females (mcg/day)
Infants 0-6 months 0.4 (AI) 0.4 (AI)
Infants 7-12 months 0.5 (AI) 0.5 (AI)
Children 1-3 years 0.9 0.9
Children 4-8 years 1.2 1.2
Children 9-13 years 1.8 1.8
Adolescents 14-18 years 2.4 2.4
Adults 19-50 years 2.4 2.4
Adults 51 years and older 2.4* 2.4*
Pregnancy all ages - 2.6
Breast-feeding all ages - 2.8

*Vitamin B12 intake should be from supplements or fortified foods due to the age-related increase in food bound malabsorption.

Disease Prevention

Homocysteine and cardiovascular disease

The results of more than 80 studies indicate that even moderately elevated levels of homocysteine in the blood increase the risk of cardiovascular diseases (13), though the mechanism by which homocysteine increases the disease risk remains the subject of a great deal of research. The amount of homocysteine in the blood is regulated by at least three vitamins: folate, vitamin B12, and vitamin B6 (diagram). Analysis of the results of 12 homocysteine-lowering trials showed folic acid supplementation (0.5-5 mg/day) had the greatest lowering effect on blood homocysteine levels (25% decrease); co-supplementation with folic acid and vitamin B12 (mean 0.5 mg/day or 500 mcg/day) provided an additional 7% reduction (32% decrease) in blood homocysteine concentrations (14). The results of a sequential supplementation trial in 53 men and women indicated that after folic acid supplementation, vitamin B12 became the major determinant of plasma homocysteine levels (15). Some evidence indicates that vitamin B12 deficiency is a major cause of elevated homocysteine levels in people over the age of 60. Two studies found blood methylmalonic acid (MMA) levels to be elevated in more than 60% of elderly individuals with elevated homocysteine levels. An elevated MMA level in conjunction with elevated homocysteine, in the absence of impaired kidney function, suggests either a vitamin B12 deficiency or a combined B12 and folate deficiency (16). Thus, it is important to evaluate vitamin B12 status as well as kidney function in older individuals with elevated homocysteine levels prior to initiating homocysteine-lowering therapy. For more information regarding homocysteine and cardiovascular diseases, see the article on folic acid.

Although increased intake of folic acid and vitamin B12 has been found to decrease homocysteine levels, it is not presently known whether increasing intake of these vitamins will translate to reductions in risk for cardiovascular diseases. However, several randomized placebo-controlled trials are presently being conducted to determine whether homocysteine lowering through folic acid and other B vitamin supplementation reduces the incidence of cardiovascular diseases. A meta-analysis of data from four of the ongoing trials shows that B vitamin supplementation had no significant effect on risk of coronary heart disease or stroke, but only about 14,000 participants were included in analysis and thus any conclusions are limited (17). Nevertheless, the completion of ongoing clinical trials should help to answer whether or not supplemental B vitamins lower risk for cardiovascular diseases.

Cancer

Folate is required for synthesis of DNA, and there is evidence that decreased availability of folate results in strands of DNA that are more susceptible to damage. Deficiency of vitamin B12 traps folate in a form that is unusable by the body for DNA synthesis. Both vitamin B12 and folate deficiencies result in a diminished capacity for methylation reactions (diagram). Thus, vitamin B12 deficiency may lead to an elevated rate of DNA damage and altered methylation of DNA, both of which are important risk factors for cancer. A recent series of studies in young adults and older men indicated that increased levels of homocysteine and decreased levels of vitamin B12 in the blood were associated with a biomarker of chromosome breakage in white blood cells. In a double-blind, placebo-controlled study, the same biomarker of chromosome breakage was minimized in young adults who were supplemented with 700 mcg of folic acid and 7 mcg of vitamin B12 daily in cereal for two months (18).

Breast cancer

A case-control study compared prediagnostic levels of serum folate, vitamin B6, and vitamin B12 in 195 women later diagnosed with breast cancer and 195 age-matched women who were not diagnosed with breast cancer (19). Among women who were postmenopausal at the time of blood donation, the association between blood levels of vitamin B12 and breast cancer suggested a threshold effect. The risk of breast cancer was more than doubled in women with serum vitamin B12 levels in the lowest quintile (1/5) compared to women in the four highest quintiles. The investigators found no relationship between breast cancer and serum levels of vitamin B6, folate, or homocysteine. A case-control study in Mexican women (475 cases and 1,391 controls) reported that breast cancer risk for women in the highest quartile (1/4) of vitamin B12 intake was 68% lower than those in the lowest quartile (20). Stratification of the data revealed that the inverse association between dietary vitamin B12 intake and breast cancer risk was stronger in postmenopausal women compared to premenopausal women, though both associations were statistically significant. Because these studies were observational, it cannot be determined whether decreased serum levels of vitamin B12 or low dietary vitamin B12 intakes were a cause or a result of breast cancer. Previously, there has been little evidence to suggest a relationship between vitamin B12 status and breast cancer risk. However, high dietary folate intakes have been associated with reduced risk for breast cancer in several studies, and some studies have reported that vitamin B12 intake may modify this association (21, 22).

Neural tube defects

Neural tube defects (NTD) may result in anencephaly or spina bifida, devastating and sometimes fatal birth defects. The defects occur between the 21st and 27th days after conception, a time when many women do not realize they are pregnant (23). Randomized controlled trials have demonstrated 60% to 100% reductions in NTD cases when women consumed folic acid supplements in addition to a varied diet during the month before and the month after conception. Increasing evidence indicates that the homocysteine-lowering effect of folic acid plays a critical role in lowering the risk of NTD (24). Homocysteine may accumulate in the blood when there is inadequate folate and/or vitamin B12 for effective functioning of the methionine synthase enzyme. Decreased vitamin B12 levels in the blood and amniotic fluid of pregnant women have been associated with an increased risk of NTD, suggesting that adequate vitamin B12 intake in addition to folic acid may be beneficial in the prevention of NTD.

Alzheimer's disease and dementia

Individuals with Alzheimer's disease often have low blood levels of vitamin B12. One study found lower vitamin B12 levels in the cerebrospinal fluid of patients with Alzheimer's disease than in patients with other types of dementia, though blood levels of vitamin B12 did not differ (25). The reason for the association of low vitamin B12 status with Alzheimer's disease is not clear. Vitamin B12 deficiency, like folate deficiency, may lead to decreased synthesis of methionine and S-adenosylmethionine, thereby adversely affecting methylation reactions. Methylation reactions are essential for the metabolism of components of the myelin sheath of nerve cells as well as neurotransmitters. Also, moderately increased homocysteine levels as well as decreased folate and vitamin B12 levels have been associated with Alzheimer's disease and vascular dementia.

Some but not all studies have associated elevated homocysteine concentrations or decreased serum levels of vitamin B12 with an increased risk of Alzheimer's disease. A case-control study of 164 patients with dementia of Alzheimer's type included 76 cases in which the diagnosis of Alzheimer's disease was confirmed by examination of brain cells after death (26). Compared to 108 control subjects without evidence of dementia, subjects with dementia of Alzheimer's type and confirmed Alzheimer's disease had higher blood homocysteine levels and lower blood levels of folate and vitamin B12. Measures of general nutritional status indicated that the association of increased homocysteine levels and diminished vitamin B12 status with Alzheimer's disease was not due to dementia-related malnutrition (26). In another study, low serum vitamin B12 (< 150 pmol/L) or folate (< 10 nmol/L) levels were associated with a doubling of the risk of developing Alzheimer's disease in 370 elderly men and women followed over three years (27). In a sample of 1,092 men and women without dementia followed for an average of ten years, those with higher plasma homocysteine levels at baseline had a significantly higher risk of developing Alzheimer's disease and other types of dementia (28). Specifically, those with plasma homocysteine levels greater than 14 micromol/L had nearly double the risk of developing Alzheimer's disease. A study in 650 elderly men and women reported that the risk of elevated plasma homocysteine levels was significantly higher in those with lower cognitive function scores (29). A prospective study in 816 elderly men and women reported that those with elevated homocysteine levels
(> 15 micromol/L) had a significantly higher risk of developing Alzheimer's disease or dementia, but vitamin B12 status was not related to risk of Alzheimer's disease or dementia in this study (30). Similarly, another prospective study in 965 older adults found that vitamin B12 status was not related to the risk of Alzheimer's disease (31). Further, a prospective study in 1,041 older adults, followed for a median of 3.9 years, found that vitamin B12 dietary intake was not associated with risk of developing Alzheimer's disease (32).

B vitamin supplementation is commonly used to treat hyperhomocysteinemia. A recent randomized, double-blind, placebo-controlled clinical trial in 253 older individuals with plasma homocysteine concentrations equal to or greater than 13 micromol/L found that daily B vitamin supplementation (1 mg folic acid, 0.5 mg vitamin B12, and 10 mg vitamin B6) for two years did not affect measures of cognitive performance despite an average 4.36 micromol/L reduction in plasma homocysteine concentrations (33). Another randomized, double-blind, placebo-controlled study in 195 elderly adults reported that oral vitamin B12 supplementation (1 mg daily) for six months had no effect on measures of cognitive function (34). Several of the homocysteine-lowering trials primarily focused on assessing cardiovascular disease risk will also assess measures of cognitive function (35). Thus, the findings of these ongoing trials may provide insight into whether long-term B vitamin supplementation is protective against dementia.

Depression

Observational studies have found as many as 30% of patients hospitalized for depression are deficient in vitamin B12 (36). A cross-sectional study of 700 community-living, physically disabled women over the age of 65 found that vitamin B12 deficient women were twice as likely to be severely depressed as non-deficient women (37). A population-based study in 3,884 elderly men and women with depressive disorders found that those with vitamin B12 deficiency were almost 70% more likely to experience depression than those with normal vitamin B12 status (38). The reasons for the relationship between vitamin B12 deficiency and depression are not clear but may involve S-adenosylmethionine (SAMe). Vitamin B12 and folate are required for the synthesis of SAMe, a methyl group donor essential for the metabolism of neurotransmitters whose bioavailability has been related to depression. This hypothesis is supported by several studies that have shown supplementation with SAMe improves depressive symptoms (39-42). Because few studies have examined the relationship of vitamin B12 status and the development of depression over time, it cannot yet be determined if vitamin B12 deficiency plays a causal role in depression. However, due to the high prevalence of vitamin B12 deficiency in older individuals, it may be beneficial to screen for vitamin B12 deficiency as part of a medical evaluation for depression.

Sources

Food sources

Only bacteria can synthesize vitamin B12. Vitamin B12 is present in animal products such as meat, poultry, fish (including shellfish), and to a lesser extent milk, but it is not generally present in plant products or yeast (1). Fresh pasteurized milk contains 0.9 mcg per cup and is an important source of vitamin B12 for some vegetarians (6). Those vegetarians who eat no animal products need supplemental vitamin B12 to meet their requirements. Also, individuals over the age of 50 should obtain their vitamin B12 in supplements or fortified foods like fortified cereal because of the increased likelihood of food-bound vitamin B12 malabsorption.

Most people do not have a problem obtaining the RDA of 2.4 mcg/day of vitamin B12 in food. In the United States, the average intake of vitamin B12 is about 4.5 mcg/day for young adult men, and 3 mcg/day for young adult women. In a sample of adults over the age of 60, men were found to have an average dietary intake of 3.4 mcg/day and women had an average dietary intake of 2.6 mcg/day (6). Some foods with substantial amounts of vitamin B12 are listed in the table below along with their vitamin B12 content in micrograms (mcg). For more information on the nutrient content of specific foods, search the USDA food composition database.
Food Serving Vitamin B12 (mcg)
Clams (steamed) 3 ounces 84.0
Mussels (steamed) 3 ounces 20.4
Crab (steamed) 3 ounces 8.8
Salmon (baked) 3 ounces* 2.4
Rockfish (baked) 3 ounces 1.0
Beef (cooked) 3 ounces 2.1
Chicken (roasted) 3 ounces 0.3
Turkey (roasted) 3 ounces 0.3
Egg (poached) 1 large 0.6
Milk (skim) 8 ounces 0.9
Brie (cheese) 1 ounce 0.5

*A three-ounce serving of meat or fish is about the size of a deck of cards.

Supplements

Cyanocobalamin is the principal form of vitamin B12 used in supplements but methylcobalamin is also available as a supplement. Cyanocobalamin is available by prescription in an injectable form and as a nasal gel for the treatment of pernicious anemia. Over-the-counter preparations containing cyanocobalamin include multivitamin, vitamin B-complex, and vitamin B12 supplements (43).

Safety

Toxicity

No toxic or adverse effects have been associated with large intakes of vitamin B12 from food or supplements in healthy people. Doses as high as 1 mg (1000 mcg) daily by mouth or 1 mg monthly by intramuscular (IM) injection have been used to treat pernicious anemia without significant side effects. When high doses of vitamin B12 are given orally, only a small percentage can be absorbed, which may explain the low toxicity. Because of the low toxicity of vitamin B12, no tolerable upper intake level (UL) was set by the Food and Nutrition Board in 1998 when the RDA was revised (6).

Drug interactions

A number of drugs reduce the absorption of vitamin B12. Proton pump inhibitors (e.g., omeprazole and lansoprazole), used for therapy of Zollinger-Ellison syndrome and gastroesophageal reflux disease (GERD), markedly decrease stomach acid secretion required for the release of vitamin B12 from food but not from supplements. Long-term use of proton pump inhibitors has been found to decrease blood vitamin B12 levels. However, vitamin B12 deficiency does not generally develop until after at least three years of continuous therapy (44). Another class of gastric acid inhibitors known as H2-receptor antagonists (e.g., Tagamet, Pepsid, Zantac), often used to treat peptic ulcer disease, has also been found to decrease the absorption of vitamin B12 from food. Because inhibition of gastric acid secretion is not as prolonged as with proton pump inhibitors H2-receptor antagonists have not been found to cause overt vitamin B12 deficiency even after long-term use (45). Individuals taking drugs that inhibit gastric acid secretion should consider taking vitamin B12 in the form of a supplement because gastric acid is not required for its absorption. Other drugs found to inhibit vitamin B12 absorption from food include cholestyramine (a bile acid-binding resin used in the treatment of high cholesterol), chloramphenicol and neomycin (antibiotics), and colchicine (anti-gout medicine). Metformin, a medication for individuals with type 2 (non-insulin dependent) diabetes, decreases vitamin B12 absorption by tying up free calcium required for absorption of the IF-B12 complex. This effect is correctable by drinking milk or taking calcium carbonate tablets along with food or supplements (5). Previous reports that megadoses of vitamin C destroy vitamin B12 have not been supported (46) and may have been an artifact of the assay used to measure vitamin B12 levels (6).

Nitrous oxide, a commonly used anesthetic, inhibits both of the vitamin B12- dependent enzymes and can produce many of the clinical features of vitamin B12 deficiency, such as megaloblastic anemia or neuropathy. Because nitrous oxide is commonly used for surgery in the elderly, some experts feel vitamin B12 deficiency should be ruled out prior to its use (4, 12).

Large doses of folic acid given to an individual with an undiagnosed vitamin B12 deficiency could correct megaloblastic anemia without correcting the underlying vitamin B12 deficiency, leaving the individual at risk of developing irreversible neurologic damage (6). For this reason the Food and Nutrition Board of the Institute of Medicine advises that all adults limit their intake of folic acid (supplements and fortification) to 1000 mcg (1 mg) daily.

Linus Pauling Institute Recommendation

A varied diet should provide enough vitamin B12 to prevent deficiency in most individuals 50 years of age and younger. Individuals over the age of 50, strict vegetarians, and women planning to become pregnant should take a multivitamin supplement daily or eat a fortified breakfast cereal, which would ensure a daily intake of 6 to 30 mcg of vitamin B12 in a form that is easily absorbed. Higher doses of vitamin B12 supplements are recommended for patients taking medications that interfere with its absorption (see Drug interactions).

Older adults (> 50 years)

Because vitamin B12 malabsorption and vitamin B12 deficiency are more common in older adults, some respected nutritionists recommend that adults older than 50 years take 100 to 400 mcg/day of supplemental vitamin B12, an amount provided by a number of vitamin B-complex supplements.

References

Written in March 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University

IF THIS IS NOT ENOUGH OF A WITNESS JUST FOR BI-POLAR CURES, ALOT OF OTHER PEOPLE OUT THERE ARE SUFFERING FROM CANCERS AND OTHER CONDITIONS THAT ARE CURABLE WITH THE CORRECT BALANCING OF VITAMINS AND MINERALS IN THE BODY. THE FATHER OF AN OLD FLAME (QUITE NEARLY MY FIANCE HAD CIRCUMSTANCES BEEN SLIGHTLY DIFFERENT) OF MINE IS SUFFERING FROM ESOPHAGAEL CANCER THAT MIGHT WELL HAVE BEEN CAUSED BY A MINERAL DEFICIENCY (MOLYBDENUM). I HOPE THEY HAVE THE COURAGE AND ARE AWAKE ENOUGH TO AT LEAST INVESTIGATE THIS AS A POSSIBILITY. AS BRIGHAM YOUNG USED TO SAY, THERE ARE ALOT OF PEOPLE WHO ARE RESTING (SIX FEET UNDER) BECAUSE THEY WERE TOO DULL OF SENSES TO GET TO THE TRUTH.

PEOPLE WHO AVOID THE 'FRINGES' FOR THE SAFETY OF THE MAIN STREAM IN THE RIVER OF LIFE, SOMETIMES NEVER RESIDE IN THE REAL TRUTH. THIS IS WHY JESUS WAS CONSIDERED SUCH A RADICAL AT THE TIME - HE HAD TO LEAVE THE SAFETY OF A CORRUPTED MAINSTREAM TO RE-ESTABLISH WHERE THE TRUTH LAY. I AM JUST GRATEFUL (EVEN THANKFUL ON THIS THANKSGIVING WEEKEND) THAT I HAVE LEARNED TO SWIM AWAY A LITTLE FROM THE 'SAFETY' OF THE CROWD AND HAVE HAD THE QUIET STRENGTH TO BE RIDICULED AND STILL KNOW THAT I HAVE BEEN DOING THE RIGHT THING ALL ALONG. ALL THE WHILE, HAVING THE SPIRIT AND A LIVING PROPHET AS MY GUIDE TO KEEP PERSPECTIVE TO AVOID THE WHIRLPOOLS OF LIFE THAT DO LURK OUT THERE.