Vitamins in Diet – B12

Posted by admin | | Friday 4 January 2008 11:53 pm

All this vegetarian and (I’m completely averse to using “versus”) non-vegetarian discussion got me thinking. And I’ve got an article here that is almost scary, – my vegetarian friends out there must really read it and take heed!

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by Dr. R. S. Wadia
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Vitamin B12 is a member of the B complex group of vitamins. It is essential for normal metabolism and with Folic acid it combines in the production of DNA – the chemical of life responsible for all cell reproduction.

Vitamin B12 is not found in any vegetarian food. There was a belief that living vegetable sources like sprouting beans contain B12 but it is not a reliable source. Vegetables grown in fields receiving manure from human feacal material may have some Vitamin B12 but this is rather small in amount. Milk contains B12 and raw milk has a reasonable amount. However pasteurization of milk destroys B12 and if we use boiled pasteurized milk the B12 content may come down from 1.2 mg/100cc to 300-400 ug/100cc. The US health authorities say that a healthy person should have 2.4 mg a day. This would require an intake of ¾ liter boiled milk to get the daily required Vitamin B12 intake.
Non-vegetarian food – liver, eggs, meat all contains B12 so those who take non-vegetarian food regularly have a good B12 intake. Our body cannot manufacture Vitamin B12.

Causes of B12 Deficiency
Vitamin B12 deficiency is therefore noted in pure vegetarians, especially vegans (no non-vegetarian food, no eggs, no dairy intake). It is also not uncommon in those who have a non-vegetarian diet only rarely – 1 or 2 times a month, or less often. The Vitamin B12 taken in food is joined to a factor produced by the stomach called the intrinsic factor and this combination is absorbed from the lower end of the small intestine i.e. the ileum. Thus B12 deficiency will occur in those who have stomach disease (atrophic gastritis), or stomach surgery with removal of all or part of the stomach, an operation that was common for the treatment of ulcer. Other causes are chronic diarrhea, failure of absorbtion (malabsorption syndrome) and surgery with removal of the lower end of the ileum.
In India in a study done by us, hospitalized unselected persons not complaining of any symptoms of B12 deficiency had a 51% incidence of B12 deficiency. This excluded patients having stroke or myocardial infarction in which B12 deficiency may play a part.

Effects of B12 Deficiency

    a. As B12 is an adjunct for DNA synthesis, cells with rapid turn over are likely to show effects of B12 deficiency. The red blood corpuscles (RBCs) are frequently affected and the growth of the cells is abnormal. Anemia is noted. Three dietary factors are important for RBC development – Vitamin B12, folic acid, and iron. Where as iron deficiency causes the RBC’s to be small and pale, B12 and Folic acid causes the RBCs to be larger. The size of the RBC is measured as mean corpuscle volume (MCV), which is normally 75-95 ff. An MCV of more than 95 usually means B12 and Folic aid deficiency but can occur due to liver disease or low thyroid function or due to drugs. However if MCV exceeds 104 it is almost always due to B12 or Folate deficiency. Perhaps less well known is that B12 deficiency also causes reduced White Blood Cell and platelets counts also.
    b. In the nervous system B12 deficiency has multiple effects. It affects the nerves so that there is ill function of nerve with tingling and numbness in hands and feet and weakness of hands and feet. Nutritional deficiency of Vitamin B12, folate, Vitamin B1 is among the commoner cause of neuropathy seen in India and relatively easily treated. Among these nutritional neuropathies Vitamin B12 deficiency is probably the most common.
    c. B12 deficiency also affects the spinal cord. In the cord it causes malfunction of 2 important nerve tracts called the motor tracts (pyramidal tract) and the posterior column. The pyramidal tracts carry orders from the brain to the muscles to move the muscles and when they are damaged the muscles are stiff and weak. The Posterior column carries information on the position of our joints so our ability to stand steady is affected when B12 is deficient. Combined disease of these 2 tracts gives the B12 deficiency of the cord a separate name Subacute (i.e. gradually occurring) combined degeneration of the cord.
    d. Less commonly B12 deficiency causes defects in functioning of the small brain or cerebellum (causing further loss of balance). Deficiency also influences memory so that it causes forgetfulness, and failure to think clearly and understand. B12 deficiency may cause defect in the optic nerves and I have seen a person whose eyes deteriorated progressively from normal to 6/60 vision i.e. effectively 1/10th normal vision while 3 different ophthalmologists were treating him. When diagnosed as B12 deficient and corrected, his vision was restored to normal within 2 months. Just when I was wondering how I could possibly help he complained that he has tingling in hands and feet telling me he had a neuropathy (disease of the peripheral nerves) also and that made me check for B12 deficiency.

Symptoms of B12 Deficiency
With mild deficiency of B12 there might be only non-specific symptoms of tiredness, fatigue, general unwell-ness and perhaps a mild tingling in the limbs.
When B12 deficiency produces a neuropathy, the main symptoms would be tingling, pins and needles sensation in the legs first and hands later. This may progress to a mild weakness in the hands and a feeling as if walking on cotton wool. In India persons complain that their slippers fall off from their feet and they may not even realize it for some time. This is due to a combination of weakness of the toes and general loss of sensation. Similarly objects fall out of their hands.

When the deficiency gets more severe the spinal cord is affected and there is stiffness of the limbs, increasing weakness, and loss of balance. The eyes can compensate the loss of balance in B12 deficiency, so it is more noticeable in the dark and while washing their face, etc.

Finally B12 deficiency may cause loss of higher function of the brain and there is increasing forgetfulness and irritability. B12 deficiency and more often folate deficiency can cause depression. In a study of 213 continuously depressed patients, Dr. Fava found a folic acid deficiency in 19% and B12 deficiency in 12%. He noted that the low folate group were more likely to fail to respond to treatment. 35% of this group failed standard treatments for depression, whereas in the normal folate group, there was a 20% failure rate.

Besides neurological manifestations B12 deficiency can produce anemia which causes tiredness, fatigue and rarely breathlessness on exertion. In a patient with B12 deficiency, folic acid can prevent or treat the anemia but will allow the neurological symptoms to progress. So in our collection of cases of neurological complications due to B12 deficiency, 35% did not have anemia, that is, their hemoglobin was greater than 11g/ml.

The irony of all these conditions is that once diagnosed, correction in the levels of Vitamin B12 can correct a seemingly serious illness within a couple of months!

How common it is to see neurologic disease due to B12 deficiency? In the 70’s a study in Bombay found only 5 cases of B12 deficiency in 3 years. This was a gross underestimate. In 2001 we reported over 150 cases seen at the Ruby Hall Clinic, Pune in 3 years. The increased diagnostic rate was markedly due to the availability of a relatively simple test for B12 in blood. With the test available, more and more cases were tested and more and more abnormalities were found.
Thus B12 deficiency clearly produces blood disorders chiefly anemia, and a variety of neurologic disease.

But the next interesting, and frightening finding was the importance of B12 deficiency in the cause of stroke and myocardial infarction (heart attacks) and strokes, which we reported in the Indian Academy of Neurology meeting in 2001.

Part 2
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by Dr. R. S. Wadia

Bear with me, I’ve tried to keep this simple and get to the (vegetarian) point quickly…

For some years now it has been known that raised levels of an aminoacid Homocysteine in blood increases the chances of vascular disease.

Boushey et al did 17 different research studies of Homocysteine and vascular disease. In these studies normal levels of serum Homocysteine were set at 5-15 µmol/L. It was found that those with Homocysteine levels in the upper-most 10% of normal have a vascular disease risk 2.5 times greater than those at a lower level. This risk rate is as high or higher than the risk associated with smoking and high cholesterol. It was calculated that for every 5 µmol/L rise in Homocysteine the risk increased 1.5 times.

What cause the raised Homocysteine? Homocysteine is raised with renal failure, low thyroid state and some drugs and rare genetic disorders. But the most important cause of high serum Homocysteine is reduced folic acid or Vitamin B12 or Pyridoxine, in that order of importance (in Western studies). In the US it was found that the addition of 400 ug (i.e. less than ½ mg) of folic acid to a daily diet caused a 25% drop in the Homocysteine level in about a month’s time. Therefore, in 1998 as a public health policy the US started putting folic acid in all breakfast cereals. The plan automatically lowered homocysteine levels in the population, reducing myocardial infarction, stroke and peripheral vascular disease in the population as a whole.

How does raised Homocysteine cause increased strokes and heart attacks?
Homocysteine increases atherogenesis i.e. it makes the blood vessels narrow and hard and therefore more likely to be blocked. Homocysteine also increases the chances of blood clotting, and that together with the narrowing vessels are a lethal combination. Moreover Homocysteine causes clotting of veins also beside arteries. Most diseases, which cause arteries to clog – high BP, cholesterol, smoking do not cause clotting in veins or vice versa, but raised homocysteine levels affect both arteries and veins.

Several years ago when we first heard of the importance of Homocysteine, I heard a foreign lecturer talk about Homocysteine in India. She pointed out that that though folic acid was common in Indian foods, there still seemed to be a population with higher than usual Homocysteine levels. It was she who first brought to our notice that given the large vegetarian population, it was possibly Vitamin B12 that played the bigger part in raising Homocysteine levels here.

We mounted a study of Homocysteine and B12 levels in stroke and found that if we considered all ischaemic (reduced blood supply) strokes, as many as 80% of all cases showed high levels of Homocysteine! There were many patients with levels greater than 50 µmol/L! If it is true that for each 5 µmol/L rise the risk of stroke goes up 1.5 times then the chances of stroke in those of 50ng/dl would be 12 times that of a person with normal levels. Frightening! In all 150 cases studied by us only 7 had low folic acid levels.

In India strokes in younger person below age 45 are more common than in the West and in our study of this category, 92% had homocysteine greater than 16 µmol/L. And in patients with Venous thrombosis (blood clot in a vein) 75% had high levels of Homocysteine. In this study raised Homocysteine was the commonest risk factor for ischaemic strokes in India, more than hypertension, diabetes, cholesterol, smoking, family medical history, etc.

This is only part of the story. The important part is the role of diet.
Our studies showed that if the person was a pure vegetarian and had a stroke, the chances of his having a high homocysteine was higher than if he was a non-vegetarian. And of the 35 pure vegetarians with stroke, 31 had Vitamin B12 levels below the lowest limit of normal i.e. less than 200 pg/ml, and 4 others were borderline normal. In those who were vegetarian and ate meats or poultry just once a week or less, the findings were similar. It is only in people who ate non vegetarian food more often than 5 times a week, that homocysteine levels were usually normal.

Simultaneously, we studied healthy people, – those without stroke, heart attacks, peripheral vascular disease, renal failure, etc. We found 51% of this population also has B12 deficiency with raised Homocysteine levels. The findings were so alarming that we wondered if there was an error. But at the KEM Hospital, Pune, a completely independent study was being carried out by Dr. Yagnik, who was sending his samples to Norway for testing. He found roughly 77% of ‘normal’ Puneites have below normal Vitamin B12 levels, with raised homocysteine. Since I read this paper at the Indian Academy of Neurology Meet in 2001, several neurologists in Pune, Bombay, Western and Southern India have found the same findings. Interestingly, in south India the trend is not so striking and the incidence is not so high.

This brings me to the next point. Contrary to the usually held notion, the incidence of stroke in India is higher than in the US, UK, or the Western world. There are studies in individual towns and at the district level but unfortunately there are no official figures. The mortality from stroke in India is 2.4 times higher than the US & UK. Recognised studies in UK on the incidence of myocardial infarction (heart attack) and stroke in Asian Indians living in the UK is significantly higher than the white population, though it is the whites who smoke more, and eat more animal fat, etc. Why is this? One explanation is Indians have more central obesity i.e. bigger tummies, probably as a genetic trait and this makes us prone to strokes and heart attacks. A second may be our tendency to vegetarianism.

What next?
To summarize, vegetarian diet is deficient in Vitamin B12. Low B12 causes raised Homocysteine. Raised Homocysteine is a potent cause for strokes, myocardial infarction, and venous thrombosis. In the Indian population of stroke patients, 80% have been found to have homocysteine above the highest level of normal. Seven years ago US health authorities decided to add folic acid to breakfast cereals to try and lower Homocysteine in the general population. We have proven B12 deficiency; we have high levels of homocysteine. It is about time the Government used routine B12 supplementation as a major public health programme to prevent two of the largest killers in the Adult Indian population.

    If you are vegetarian, or have a low intake of meats, this is what you can do for yourself. Just take 1.5 mg of Vitamin B12 daily. It could save you thousands on future coronary treatments, and keep you walking and moving freely for years longer. It may even prevent dementia, the disease all older people are most worried about.

Part 3
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B12 Deficiency and Dementia
The story from Rotterdam and Framingham
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Dementia is a chronic progressive loss of a persons ‘higher’ function. The loss is ‘global’, that is, complete. The most important loss may be of memory but there are other higher functions, which may be lost in dementia, including speech, orientation to time and place, abstract thinking, personality and self-care. When this higher function loss reaches a level where it interferes with activities of daily living it is called dementia.

Dementia is common, and with a larger percentage of the population living longer, it is getting commoner. There are many different causes of dementia and the commonest is Alzheimer’s disease. The second is vascular dementia due to poor blood supply, and both being common, mixed cases of Alzheimer’s and vascular dementia is also common. A recent classification puts pure Alzheimer’s as 35%, pure vascular as 10% and mixed as 15%. Recently Hackinshi et al pointed out that we have come to realize that the risk factors for dementia are advancing age, hypertension, raised cholesterol, smoking, diabetes and raised Homocysteine, and all are also risk factors for vascular disease, so most dementias must be due to mixed pathology. Heredity also plays a part as some Alzheimer’s cases, some vascular disorders and one group of dementia called fronto temporal dementia are hereditary.

As all the factors that influence vascular disease cause dementia, diet has to play a part in its effect on cholesterol, on hypertension, diabetes and on Homocysteine.

The effect of Homocysteine in dementia was brought out in the Framingham Study and from a study from Rotterdam. (Rotterdam Scan study). Framingham is a small town near Boston. Virtually the entire population of Framingham was studied in 1960-70. Blood samples were taken and stored. All data was collected and recorded and the population is being studied regularly to see the occurrence of complications. The Framingham study told us the relation of hypertension and stroke and heart attacks. They also followed cholesterol, and tri-glycerides levels, and established their importance in long-term complications.

Regarding dementia, the Framingham Study reported on 1092 older persons without dementia, and followed it up for 8 years. In 8 years, 111 developed dementia. The researchers had blood samples and histories of these people taken at the ‘base line’ at start of the study, and then 8 years after and in 2002 they reported that if they divided the population by Homocysteine levels they found those with Homocysteine level 14 mmol/L and above had in 8 years, 1.9 times the risk of developing dementia compared to the rest of the group. The persons were divided into 4 groups by Homocysteine levels and the risk for dementia of the lowest 1/4th was 1. The risk for the 2nd quartile was 1.3 that for the 3rd was 1.3 and for the top 1/4th was 2.2 times the lowest. And of course as already mentioned, the factor which influenced Homocysteine level most, is the folic acid, and B12 level. In general, in all populations studied in Thailand, Chile, Australia and India the B12 level of vegetarians is lower than that of meat eaters and their Homocysteine levels are significantly higher.

A new Rotterdam study has confirmed these findings. Here again 1015 participants who were elderly and not having dementia or any prior history of stroke were studied at the beginning, and then followed up after 3-4 years for the occurance of dementia. In this period 30 developed dementia. They had done brain scans at the beginning and found that if the patient had, in the initial scan small areas of silent brain infarction (damage to tissues) these patients had 2.26 times greater chance of developing dementia than those who did not have the original patch. Others tested has white matter hypo-densities in the base line scan, and their chance of developing dementia was 3 times those where these were not noted.
Silent Brain Infarction (SBI) and white matter hypo-densities were both related to serum Homocysteine. If patients were divided into 4 quartiles of Homocysteine level, the top quartile was 3 times as likely to show SBI or white matter hypo-densities (WMH) on scan as the ones in the lowest quarter. So high Homocysteine level causes increase SBI and WMH, and these are associated with a 3-fold risk of dementia. Even if a patient of SBI did not develop dementia there was a greater decline of global function than in those without SBI.

    There is no question that strokes raised Homocysteine levels are caused by B12 and Folic acid deficiency. So as we pointed out in stroke you could check your serum Homocysteine and serum B12 Folate level and if the Homocysteine is high you should take Folate and B12. Vitamin B12 has a very low potential for toxicity. No adverse effects have been associated with excess vitamin B12 intake from food and supplements in healthy individuals. If you are a pure vegetarian or only take a meat/poultry/egg/fish diet rarely, you should take a supplement of 1-2 mg Vitamin B12 daily with folic acid and thereby hope to reduce the chance of getting dementia (or stroke or heart attack) and thus live healthier for longer.



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    Is it true that consuming RO water causes vitamin B12 deficiency

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    Is it true that consuming RO water causes vitamin B12 deficiency

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