In the fall 2016 MPDN article on dietary supplements, I noted that there are studies indicating Parkinson disease (PD) patients may be deficient in vitamins B6, B12, and D. I find that when people learn this they often assume it would be a good idea to pick up some vitamins at the grocery store as a preventive measure. That is not the right move, and is probably a result of years of advertising by industry, to create the false image that vitamins are always safe, and more is better. Vitamins are not benign, and one should not blindly take them.
Instead, just as I advised in the supplement article, if a qualified doctor has found a low level, that doctor can advise you on whether or not you should take a vitamin. If that is the case, stick to the dose directed by your doctor. Don’t improvise, don’t listen to unqualified, however well-meaning people, and don’t believe the majority of what you read on the internet about the topic of vitamins. With vitamins, too little or too much may lead to serious health problems.
Having said that, let’s discuss B12 (cyanocobalamin). Several studies have shown an association with low B12, the total amount of levodopa someone has taken, and peripheral neuropathy (nerve damage in the hands and feet). In other words, the more levodopa someone has taken, the greater the risk might be of that person running low on B12. Low B12 is a common cause of nerve damage. People with PD treated with oral levodopa have a higher prevalence of a mild, chronic sensory neuropathy, though rare cases of severe, subacute neuropathy similar to Guillain-Barré syndrome have been reported (1). The great majority of both types of cases were associated with low B12 levels. The association became more obvious after the dopamine pump was introduced in Europe (2, 3). Continuous infusion of carbidopa/levodopa intestinal gel (LCIG) was associated with a peripheral neuropathy and vitamin B12 and/or B6 deficiency. Cases of LCIG-associated neuropathy often responded to vitamin supplementation without the need for stopping the pump. Investigators advocated for monitoring of vitamin B12 and B6 status before and after patients start LCIG, and vigilance for signs of neuropathy, such as numbness in the feet, tingling, or even burning sensations.
In addition, neuropathy is not the only problem low B12 can cause. Every nerve in the body uses B12, and without it, disease occurs. It might make sense then, to know that B12 deficiency can also cause blindness, memory loss, dementia, and spinal cord damage, which may become permanent. Some patients have told me they know about these issues, and have learned that B12 deficiency can also cause anemia. The logic goes that since they are not anemic, they have nothing to worry about. They are unfortunately wrong. The neurologic damage associated with B12 deficiency is usually established before a person develops anemia. You can’t rely on the presence or absence of anemia to screen for low B12.
Though it is stored in the liver, doctors check B12 with a blood test (with an at least four hour fast prior to drawing blood). It is advisable not to take vitamins before the test, as these will falsely elevate the level, rendering the test useless. Most of the time a level over 300 pg/mL is considered normal. The tricky part is that “normal” levels of this vitamin vary from person to person, and for some a level somewhat under 300 pg/mL may be fine. Fortunately, there is a way to sort this out. Because B12 is necessary for certain enzymes to work, low B12 can cause a buildup in the blood of substances that would have otherwise been broken down, such as methylmalonic acid (MMA) and homocysteine (HC). Think about it like a scale is tipped. When a borderline low B12 level is present and MMA and HC are high, one has a deficiency. In fact, because the B12 blood test may be falsely elevated, MMA is actually a more sensitive test for the state of a person’s B12 storage. In the above-referenced LCIG patients, all of these lab tests verified deficiency.
If B12 is low, it can be replaced by high-dose shots, or sometimes by high-dose tablets, which should again be directed by a doctor. The orally absorbed B12 goes directly into the bloodstream and may be better absorbed than swallowed pills, though some of these are also very effective.
Under normal circumstances, we get B12 from dietary sources, and the minimum daily requirement is about 2.5 mcg, with a recommended daily intake of 6 mcg (six millionths of a gram). A person’s liver will store about 3 mg of B12. A typical American diet contains about 20 mcg of B12 daily, almost all coming from meat or dairy products. Vegan diets can lead to deficiency, and no vegetable product is known to contain a reliable source of biologically active B12. There is some data that the mori, or purple laver of edible seaweed used to wrap sushi might contain sufficient biologically active B12 (4). If a healthy person were to stop ingesting B12 suddenly, deficiency might take up to five years to develop because of those high liver stores.
There are a multitude of other ways one might develop B12 deficiency. These include, but are not limited to: bariatric surgery, taking certain other medications such as proton pump inhibitors or metformin, inhalation of laughing gas (nitrous oxide) and some other inhaled anesthetics, allergic gastritis, and Helicobactor pylori infection. In my neurology group practice B12 deficiency is diagnosed daily.
In the U.S., there is no guideline to check B12 among PD patients. It sounds like a good idea to me, though.
REFERENCES
- Uncini et al. J Neurol Neurosurg Psychiatry. 2014 Aug 28. Polyneuropathy associated with duodenal infusion of levodopa in Parkinson’s disease: features, pathogenesis and management.
- Müller et al. Parkinsonism Relat Disord. 2013;19(5):501-7. Peripheral neuropathy in Parkinson’s disease: levodopa exposure and implications for duodenal delivery.
- Santos-García et al. J Neurol. 2012;259(8):1668-72. Polyneuropathy while on duodenal levodopa infusion in Parkinson’s disease patients: we must be alert.
- Watanabe, et al. Biosci Biotechnol Biochem 2000;64(12):2712-05. Characterization of a vitamin B12 compound in the edible purple laver, Porphyra yezoensis.
