Let’s talk about two common types of anemia I see in my patients. They are self explanatory like iron-deficiency anemia. Megaloblastc anemia refers to a deficiency of folic acid and/or vitamin B12, and pernicious anemia refers to B12-deficiency specifically.
Every single cell in your body requires folic acid and vitamin B12 in order to “mature” and therefore function properly. All cells start off immature (and large in size) and become smaller when they mature. Thus, the term “megaloblastic” refers to the fact the cells stay large in size (mega) without these vitamins. “Macrocytic anemia” is also a term for this condition.
In regards to folic acid deficiency, we run in to some of the same situations as in iron-deficiency – when asking the question: Why is their a deficiency?
The answers are either: a) insufficient consumption of foods containing folic acid; b) lack of absorption; c) an inability to convert folic acid to its active form, and d) complications of its utilization from certain drugs.
In regards to answer “a”, you must obviously consume folic acid through the foods you eat. Some of the best foods that contain high amounts of folic acid (or folate as it is referred to when in food) are: lentils, beans peas, broccoli, spinach, collards, okra, asparagus, and citrus fruits.
As far as answer “b”, regarding absorption – this could result from:
1) Your intestinal villi are literally clogged up due to poor food choices, thus not allowing for absorption of folic acid (and most definitely other nutrients as well). To “fix” this, you would need to change your diet, and probably have to take supplements that would help detoxify the small intestine. Examples would be a whole food diet and/or fiber (to “scrub” them clean), bentonite clay (to absorb the toxins), and/or mucilaginous herbs that could help “dissolve” out the toxins.
2) Digestive conditions that can compromise the absorption of folic acid (and any nutrients) are: Crohn’s disease, ulcerative colitis, irritable bowel syndrome, leaky gut syndrome, colon cancer, and perhaps others.
Now for answer “c”. Folic acid (or folate) needs to be converted to 5-methyltetrahydrofolate (5-MTHF) in order to actually perform its necessary functions at the cellular level. This inability to convert usually results from a genetic defect. If there is a genetic defect, you may have to take a dietary supplement that contains the converted form.
The medications that interfere with folic acid utilization are: anticonvulsants (dilantin, phenytoin, and primidone), metformin (for diabetes), sulfasalizine (for Crohn’s disease and ulcerative colitis), triamterine (a diuretic), and barbituates.
Wait! A few more things regarding less common causes (that I see) of folic acid deficiency are: alcohol abuse, kidney dialysis, and liver disease. And as you’ll see below, more is required during pregnancy and lactation to prevent neural tube defects in the fetus; and for the growing baby.
Let’s now discuss vitamin B12 deficiency. Why would someone be deficient? The answers here are either: a) insufficient consumption of foods containing vitamin B12; b) failure to properly absorb B12; c) lack of a substance called intrinsic factor in the stomach (related to absorption); and d) inactive or oxidized B12.
Let’s start with answer “a”. Please be aware that B12 is only contained naturally in animal foods! You can get certainly get it in vegetarian food sources, but that means it has been “fortified”. Also, even though the algae product known as spirulina lists B12 on the label; apparently it is simply an analogue of B12 and may actually cause you to become even more B12 deficient. Read this is you are concerned. Foods high in B12 are basically every animal product known.
Answers “b” and “c” relate to an inability to absorb B12. One possibility is for the same reasons as folic acid. See above. Additionally, vitamin B12 requires a substance called intrinsic factor which is produced by (parietal) cells in the stomach, in order for proper absorption. Stomach tumors, atrophic gastritis, pancreatic enzyme insufficiency, resection of the part of the small intestine that absorbs B12, autoimmunity towards the stomach cells or intrinsic factor itself, and an excess consumption of alcohol may be prevent B12 absorption through intrinsic factor complications. See a reference here on the above. “Pernicious anemia” refers to B12-deficiency anemia when the cause is specifically related to atrophic gastritis/destruction of parietal cells or destruction of intrinsic factor (usually from an autoimmune reaction).
Lastly, I’ll talk about “d”. Vitamin B12 is known as cobalamin. This is because the mineral cobalt a necessary part of the B12 complex. B12 needs to be converted to methylcobalamin or hydroxycobalamin to actually get used properly, which depends on genetic factors. If this conversion does not occur, B12 will be inactive. Also, a person under oxidative stress (too many free radicals) may cause cobalt to become oxidized and again not allow B12 to work properly. In this case, it’s possible to have normal B12 levels on blood analysis, but it will be inactive at the cellular level and thus not work. These people will need to decrease their exposure to free radicals; and mostly likely have to supplement with antioxidants and B12 also.
RDA’s for folic acid and B12 are in the following charts provided by the National Institutes of Health:
|Males and Females
|Males and Females
|19 and older||2.4||2.6||2.8|
In conclusion, symptoms of folic acid deficiency are as follows: fatigue, diarrhea, loss of appetite, weight loss, weakness, sore tongue, headaches, heart palpitations, irritability, forgetfulness, and high blood levels of homocysteine (to be discussed in another article).
Symptoms of vitamin B12 deficiency are: fatigue, weakness, constipation, loss of appetite, weight loss, numbness and tingling in the hands and feet, difficulty maintaining balance, depression, confusion, dementia, poor memory, and soreness of the mouth or tongue.
Blood tests can be run to determine folic acid and B12 status. Especially a complete blood count (with “random distribution of weight” or RDW; and “mean corpuscular volume” or MCV) to check for the red blood cells’ size and associated anemias. A blood test can also confirm a problem with the gene associated with failure to convert folic acid to its active form.
Vitamin B12 can be measured in blood, but remember if your cobalt has been oxidized, it can show normal levels when in fact the B12 isn’t working. Methylmalonic acid is a good test (and rarely or never run) for B12 status.
And finally, homocysteine levels can spot a folic acid and/or B12 deficiency. Homocysteine is related to cardiovascular and neurological problems. Again, I’ll discuss that in another article.
I also use in-office, applied kinesiology muscle tests when I suspect deficiencies in these vitamins. HOWEVER, I still consider it prudent to use blood tests to see exactly what my patient’s levels are.
ANOTHER VITALLY IMPORTANT POINT! The blood lab’s ranges are often too wide to pick up sub-clinical deficiencies in these vitamins, that may still be causing your symptoms. I use narrower functional ranges for myself and my patients.
Proper food choices and quantities and/or supplements can correct deficiencies. HOWEVER, do not take more than 1,000 micrograms of folic acid without B12. This is because folic acid supplementation this high can trigger B12 deficiency symptoms. In particular, it can cause IRREVERSIBLE nerve damage because of B12 deficiency. Most supplements contain both vitamins together to prevent this. And the only supplements I’ve seen with 1,000 micrograms (and NO B12) in one tablet or capsule are prescription only. Go figure.
Well, that’s a lot to consider for just two vitamins. But then again, they are obviously extremely important!
Some information in this article was derived from the National Institutes of Health website.
Dr. Robert D’Aquila – NYC Chiropractor – Applied Kinesiology
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