Getting serious about citrus 

It’s not news that vitamin C is critical to human health; however, our interest in addressing it has waxed and waned with medical trends since the days of lime-sucking sailors. For at least the last 20 years, the mainstream healthcare community in the U.S. has been in a relative dark age regarding the importance of vitamin C deficiency. We’ve failed to recognize its prevalence, to understand the clinical implications to our patients, and to identify and implement effective remediation strategies—a failure compounded by a continued lack of emphasis on social determinants of health in clinical practice. 

Recently, I tested a patient for vitamin C levels in a last-ditch effort to figure out what was causing her symptoms. This woman, who had been eating a relatively healthy diet that should have been meeting her FDA recommended daily allowance, had near-zero plasma levels of vitamin C. Once we realized this, she and I identified several risk factors in her history: uncontrolled type 2 diabetes, long-term methadone maintenance therapy, low-level chronic inflammation, metabolic syndrome, intermittent cocaine use, and high levels of socioeconomic stress. Supplementation with 1,000 mg of ascorbic acid daily improved her wound healing, joint pain, mood, and constipation. After realizing that many other patients shared those risk factors, I tested a few others. Out of the six individuals I tested, four had “deficient” or scurvy-levels of vitamin C, one was low end of normal, and one was normal.  

We were taught in school that people should “eat their vitamins,” that vitamin supplementation caused “cachexia of the wallet,” and that “vitamin C deficiency is rare in the U.S. and other industrialized countries.” While perhaps that holds true for middle class white men, it’s not true for everyone. The most recent NHANES dataset that includes data on plasma ascorbic acid levels shows that 6.9-7.1% of Americans surveyed are deficient to levels that would result in clinically significant morbidity. A “rare” disease according to the FDA is one that affects fewer than 200,000 people in the US; the NHANES data suggest that vitamin C deficiency affects more than 23 million Americans. That is clearly far from “rare.” 

Vitamin C plays a critical role in reversing the effects of chronic inflammation as an antioxidant. This means that those who have metabolic syndrome, autoimmune or autoinflammatory disease, heart disease, diabetes, cancer, etc. run through vitamin C more quickly than those who do not have chronic inflammation. Without sufficient vitamin C to meet their needs for the vitamin’s various purposes, these patients will have subclinical signs of scurvy such as impaired wound healing, frequent infections (especially respiratory infections), low mood, joint pain, and brain fog; all these symptoms are easily blamed on their chronic illness or other things and would rarely cause us to consider a vitamin deficiency. Long term, they’re at higher risk for the development and progression of cardiovascular disease. However, since they’re taking in some vitamin C, the levels are usually not low enough for long enough to tip over into clinical scurvy symptoms. 

Once a documented deficiency exists, the next step is repletion, but that may not be as simple as “take # mg of vitamin C daily.” This is because there’s no agreement on what the ideal plasma level for repletion is or even if plasma levels should be the target; there’s no agreement on a therapeutic dose; there are risks associated with repletion in patients with undiagnosed hypercalciuria; and there are interactions between high-dose vitamin C supplementation and the Freestyle Libre glucose monitor. To date, I’ve had patients take anywhere from 250 mg to 1000 mg daily of additional vitamin C depending on the extent of their symptoms and documented deficiency. Of those with deficiencies, two of the four initially identified did follow up testing and both had normal levels after six weeks without obvious adverse effects.  

This isn’t just about vitamin C, however. I believe that this demonstrates how easy it is to forget about the diverse implications of poverty when it interacts—as it so often does—with chronic disease. My patients don’t have scurvy because they’re poor or because they have chronic disease. They have scurvy because they are poor AND have chronic disease. We watch people like them suffer more from the consequences of these chronic diseases than wealthier people who are otherwise similar but throw up our hands in frustration rather than investigate further. This is the proverbial shot across the bow warning us all to be more attentive to the often subtle, but rarely insignificant, effects poverty can have on our patients’ health. 

This piece expresses the views solely of the author. It does not necessarily represent the views of any organization, including Johns Hopkins Medicine.