Vitamin B12 deficiency takes on many forms, including depression and limited mobility. Learn what you can do to ensure your body gets enough of this vital nutrient.
In "Could It Be B12," Sally Pacholok and Jeffrey J. Stuart explore the symptoms of B12 vitamin deficiency, often misdiagnosed as depression, mobility disorders, or other diseases.
B12 deficiency is a public health crisis that even most doctors don’t know exists. In Could It Be B12? (Quill Driver Books, 2011), authors Sally Pacholok and Jeffrey J. Stuart give a complete and authoritative guide to B12 deficiency and its treatment. This section comes from the chapter, “An Invisible Epidemic.”
A silent crippler stalks millions of Americans—and you may be one of them.
This crippler is a master of masquerade, striking different people in different ways. It afflicts one person with tremors, makes another depressed or psychotic, and causes agonizing leg and arm pains or paralysis in still another. It can mimic Alzheimer’s disease, multiple sclerosis, early Parkinson’s disease, diabetic neuropathy, or chronic fatigue syndrome. It can make both men and women infertile, or cause developmental disabilities in their children. Other times, it lurks silently, stealthily increasing its victims’ risk of deadly diseases, ranging from strokes and heart attacks to cancer.
This medical disorder stems from a vitamin deficiency, but your standard multivitamin pill won’t prevent it in many cases, and even some higher-dose oral formulas of this vitamin may not help. It’s considered an “old people’s disease” by doctors, but it can strike any person at any age, and it sometimes hits children the hardest.
The disorder I’ve described is vitamin B12 deficiency. If you develop this deficiency, it’s easy to spot, easy to treat, and easy to cure—but only if your doctor diagnoses you before it’s too late. Unfortunately, that frequently doesn’t happen.
The cases we’ll describe in the pages of this book involve people of every age and from every walk of life: babies, children, young men and women, middle-aged people, and senior citizens.
Among them are the following:
• A thirty-five-year-old man who starts wetting himself, and who can no longer walk steadily or grip with his hands.
• An eight-month-old baby who loses her speech, stops responding to her parents, and eventually can’t even sit up by herself.
• A twenty-year-old woman who becomes severely depressed and who attempts to kill herself.
• A grandfather transformed, in three months, from a healthy jogger into a depressed, confused man, diagnosed with senile dementia.
• A two-year-old child who exhibits severe developmental delay and is diagnosed with autism.
• A young woman unable to conceive a baby.
• A fifty-four-year-old woman experiencing paranoid delusions and violent outbursts, coupled with symptoms that her doctor diagnoses as multiple sclerosis.
• An eighty-year-old man who develops balance problems, falls, and fractures his hip.
• A ballet dancer who undergoes cosmetic surgery and ends up nearly unable to walk.
• A middle-aged woman accused by her doctors of being an alcoholic and a “drug seeker” when she complains of intense, chronic back and leg pain.
• A seventy-eight-year-old with foot and leg numbness diagnosed as incurable diabetic neuropathy.
• A senior citizen whose doctors attribute his repeated falls to “mini-strokes.”
All of these very different patients have one thing in common: Their doctors have failed to properly diagnose them. They’ve been labeled with a dozen different disorders, ranging from incurable diseases to hypochondria, but in reality, they all suffer from the same medical condition: vitamin B12 deficiency.
This isn’t a new or fad disease. In fact, you’ll find it listed in the textbooks of any first-year medical student. It’s not a rare disease, either: If you’re over forty, you’re at an elevated risk for dangerous B12 deficiency, and if you’re over sixty, you have up to a 40 percent chance of having potentially dangerous low B12 levels. The lower your serum B12 gets, and the longer you have signs and symptoms, the greater your potential for injury and poor outcomes.
To understand why B12 deficiency can hurt or even kill you, and why this deficiency is so common even in seemingly healthy people, it’s important to know a little about what vitamins are—and why B12 is unique.
Your body needs thirteen different vitamins in order to stay alive and remain healthy. These tiny molecules participate in thousands of chemical reactions that build your tissues and organs, provide you with energy from the food you eat, clean the toxins from your body, protect you against infections, repair damage, and allow your cells to communicate with each other.
Your body can’t make vitamins by itself, so it depends on you to provide them by eating the right foods. Some (the fat-soluble vitamins) can be stored; others, including the B vitamins, are water-soluble and need to be “restocked” every day. If you don’t take in enough of a particular vitamin, your supplies dwindle, causing a marginal deficiency and, eventually, a deficiency disease such as scurvy (vitamin C deficiency) or beriberi (vitamin B1 deficiency). The bigger the drain on your stores, the more serious the consequences will be—up to and including death.
Of the thirteen vitamins your body needs, one is vitamin B12. It acts, in many ways, much like the other dozen vitamins. But in other important ways, vitamin B12 is an oddity, and some of the quirks that make it different also make it harder for millions of people to get enough of it.
Among its distinctions, B12 is the only vitamin that contains a trace element—cobalt—which explains its scientific name, cobalamin. Because B12 is produced in the gut of animals, it’s also the only vitamin that you can’t obtain from plants or sunlight. Plants don’t need B12, so they don’t produce or store it.
To obtain B12 from your diet, you need to eat meat, poultry, fish, eggs, dairy products, or foods fortified with B12—or, if you don’t eat these foods, you need to take supplements. However, even a diet high in B12, augmented with a supplement, isn’t sufficient for many people.
In fact, while the Institute of Medicine (IOM) reports that you need only a tiny amount of B12 each day (two to four micrograms or about a millionth of an ounce), it’s remarkably easy to become deficient in this nutrient. While deficiency often occurs in vegans or vegetarians who fail to take the right supplements, the majority of B12-deficient people eat plentiful amounts of the vitamin—it’s just that their bodies can’t absorb or use it.
Why? Because to get from your mouth into your bloodstream, vitamin B12 must follow a complex pathway, and a roadblock in any part of that pathway can cause your B12 levels to plummet. Here’s a highly simplified explanation of this pathway:
1. The vitamin B12 in your food is bound to animal proteins, and first must be freed. To split the B12 and the protein apart, your body uses an enzyme called pepsin, which can be produced in sufficient amounts only if there is enough hydrochloric acid available in your stomach.
2. Your stomach also produces intrinsic factor (IF), a protein that makes its way into your intestine to be available for a later step in the B12 pathway.
3. Next, other proteins called R-binders ferry the B12 into your small intestine.
4. In the intestine, intrinsic factor latches onto the B12 (with the help of enzymes called pancreatic proteases) and carries it to the last section of the small intestine, the ileum. The cells that line the ileum contain receptors that grab onto the B12-IF complex, pulling it into the bloodstream.
5. In the bloodstream, another protein, transcobalamin II, carries vitamin B12 to the various cells of the body, and then transports the excess to the liver for storage.
This complicated B12 metabolism process, far more complex than that for any other vitamin, can break down at any point. The most famous (but not the most common) breakdown in this process is pernicious anemia (an autoimmune disease), a hereditary disorder that once subjected its sufferers to physical and mental deterioration and eventually a terrible death. The disease occurs when the body fails to produce intrinsic factor, making the B12 consumed in the diet useless. In 1926, two doctors, George Richards Minot and William Parry Murphy, discovered that feeding half a pound of liver per day to their patients with pernicious anemia dramatically reversed their symptoms. The physicians, along with Dr. George Hoyt Whipple (who had earlier found that liver reversed pernicious anemia symptoms in dogs), won the 1934 Nobel Prize in medicine for their life-saving discovery.
It is unknown whether people in the early twentieth century died from “pernicious anemia,” which is an autoimmune phenomenon, or whether other causes of B12 deficiency played a role. The bottom line is that even today, untreated B12 deficiency, whatever its cause, can be “pernicious” or deadly.
A far more common cause of B12 deficiency, especially in people over fifty, is a condition called atrophic gastritis, an inflammation and deterioration of the stomach lining. Atrophic gastritis reduces the secretion of the stomach acid that is needed to separate vitamin B12 from protein—a problem often made worse by proton-pump inhibitors and antacids or other medications. In addition, older people have smaller numbers of the cells that produce intrinsic factor.
It’s not just the elderly, however, who are at risk. People of any age who undergo gastric surgery for weight loss (gastric bypass), or have partial or complete stomach resections for other reasons, are also candidates for B12 deficiency. This is because they lose the cells that produce hydrochloric acid and intrinsic factor. Intestinal surgery involving partial or complete removal of the ileum will also cause B12 deficiency, because receptors needed for the absorption of B12 are located in this area.
In addition, gastrointestinal disorders such as Crohn’s disease (an inflammatory intestinal disease), enteritis, “blind loop” syndrome, or celiac disease can interfere with the absorption of B12, even if it’s broken down correctly by the body. So can alcohol and many medications, ranging from gastroesophageal reflux (GERD) drugs to ulcer drugs to diabetes medications. Exposure to nitrous oxide, either during surgery (including dental surgery) or through recreational drug abuse, can inactivate B12. Toxins such as mercury interfere with B12’s ability to cross the blood–brain barrier and reach the neurons where it’s needed. And, a variety of inborn errors of B12 metabolism, which we’ll discuss in later chapters, can interfere with B12 metabolism at any step from beginning to end. This is why people who say, “I can’t be deficient—I take a vitamin pill every day” are wrong.
People who can’t metabolize B12 from food often can’t make use of it efficiently in pill form either, so many of the supplements on the market won’t guarantee that you’re safe. The National Institute of Health acknowledges that only about 10 mcg of a 500 mcg oral supplement (which is listed as 8,333% of daily value [DV]) is actually absorbed by healthy people. And, if you’re already B12-deficient, the few micrograms of B12 you’ll get from a standard supplement (6 mcg) will do as little good as trying to fill an empty swimming pool with a teaspoon of water each day. A person with B12 deficiency needs thousands, not just tens or hundreds, of micrograms of B12 every day—and in some cases, even people taking thousands of micrograms of oral B12 may benefit more by being treated with injections.
Some high-dose over-the-counter lozenges (containing more than 1,000 mcg of B12) can be effective over time, but people who are severely deficient and have neurologic symptoms initially need to be treated aggressively with B12 injections. Since B12 symptoms eventually become irreversible, it’s important to treat the problem quickly and aggressively. Patients can be switched to high-dose B12 lozenges afterward, but must be monitored by their physicians to assure that this route is effective.
It’s important to note that most of the studies mentioned below underestimate the prevalence of deficiency, because, as we’ll explain later, many deficient people have “normal” serum B12 levels.
Tufts University researchers, analyzing data from the large-scale Framingham Offspring Study, found that nearly 40 percent of participants between the ages of twenty-six and eighty-three had plasma B12 levels in the “low normal” range—a level at which many people begin experiencing neurological symptoms. Nearly 9 percent had outright deficiency, and 16 percent exhibited near-deficiency. Remarkably, low serum B12 was as common in younger participants as in the elderly.
• Smaller studies report that 15 to 20 percent of seniors have a vitamin B12 deficiency.
• A recent study found that 40 percent of hospitalized elderly patients had low or borderline serum B12 levels.
• Over 80 percent of long-term vegans who do not adequately supplement their diets with B12, and over 50 percent of long-term vegetarians, show evidence suggestive of B12 deficiency.
In June 2009, the CDC reported that B12 deficiency is present in one out of every 31 people over the age 50.5 What’s more, this alarming statistic underreports the true incidence of B12 deficiency. That’s because the researchers defined B12 deficiency as a serum B12 level under 200 pg/ml. It’s well documented that many people whose serum B12 is between 200pg/ml and 350pg/ml have a vitamin B12 deficiency.
This excerpt has been reprinted with permission from Could It Be B12? By Sally Pacholok, R.N., B.S.N. and Jeffrey J. Stuart, D.O., published by Quill Driver Books, 2011.
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