Between vitamin C and scurvy: how to prevent the "sailor's disease"

IN BRIEF

• Scurvy is the severe clinical manifestation of prolonged vitamin C deficiency, with signs related to connective tissue fragility and impaired immune function.
• Vitamin C is an essential cofactor for enzymes that stabilize collagen and influences numerous biological processes; body reserves are depleted within weeks–months.
• Most modern cases are observed in people with diets extremely poor in fruits and vegetables, in contexts of social vulnerability, or in the presence of conditions that increase demand or reduce absorption.
• Prevention is based on a diet rich in vitamin C or targeted supplementation; doses and routes of administration determine different plasma concentrations and physiological effects.

Abstract: what does science say?

Vitamin C (ascorbic acid) is an essential water-soluble micronutrient for humans. Evidence indicates that its prolonged deficiency causes scurvy, characterized by gum bleeding, bruising, slow wound healing, and, in advanced cases, systemic complications. Pharmacokinetic studies show that bioavailability and plasma concentrations depend on dose, frequency, and route of administration: moderate oral doses (100–200 mg/day) saturate tissues under normal conditions, while pharmacological concentrations require intravenous administration. Epidemiological research documents the persistence of hypovitaminosis even in high-income countries, especially in vulnerable groups. However, many observed associations between vitamin C levels and disease outcomes remain observational and require cautious interpretation.

Causes and Physiology of Vitamin C

Vitamin C is essential as an electron donor and as a cofactor for a family of enzymes that catalyze hydroxylation reactions in various tissues. Among the most well-known reactions are the hydroxylations of proline and lysine, which are necessary to stabilize the triple-helix structure of collagen: without this activity, the collagen formed is unstable, and connective tissues become fragile. This mechanism explains why prolonged deficiency results in peripheral hemorrhagic phenomena, difficulty in wound healing, and loss of mucosal integrity [1].

From a pharmacokinetic perspective, vitamin C has dose-dependent dynamics: plasma levels increase with oral intake, but beyond certain dosages, the absorption percentage decreases, and the excess is excreted in the urine. To achieve very high plasma concentrations, such as those studied in experimental or therapeutic contexts, intravenous administration is necessary; the differences between administration routes have practical implications for clinical and experimental use [1][6].

Clinical Symptoms and Presentation of Scurvy

Scurvy initially manifests with non-specific symptoms such as fatigue, irritability, loss of appetite, and musculoskeletal pain. As the deficiency worsens, more specific signs appear: swollen and bleeding gums, widespread ecchymoses and petechiae, delayed wound healing, and capillary fragility. In children, bone pain and difficulty walking may be observed. In advanced cases, secondary infections, anemia, and, rarely, fatal outcomes can occur if left untreated [3].

Today, scurvy is relatively rare in the general population but continues to be reported in patients with severely restricted diets, individuals with alcohol dependence, isolated elderly people, and, sometimes, in disadvantaged socioeconomic contexts. Modern case series and clinical reports confirm that, despite the availability of vitamin C-rich foods, the disease can still manifest when intake is insufficient for months [3][4].

Risk Factors and Vulnerable Populations

Surveys of large populations show that vitamin C deficiency is more frequent in low-income groups, smokers, and individuals with diets poor in fruits and vegetables [4]. Medical conditions that reduce intestinal absorption or increase requirements (e.g., some gastrointestinal disorders, recent surgeries, acute infections, inflammatory states) also increase the risk of hypovitaminosis. Eating disorders and extremely restrictive diets are known causes of modern scurvy; a recent review describes the co-occurrence of scurvy in people with anorexia nervosa [5].

Other frequent causes include chronic alcohol use, social isolation, and certain therapies or conditions that accelerate vitamin C turnover. For these reasons, it is important to assess individual risk and not limit oneself to considering scurvy as a disease of the past [4][5].

Absorption, Doses, and Pharmacokinetics

The bioavailability of vitamin C after oral administration is high at modest doses but progressively decreases as the dose increases: for example, the absorbed fraction decreases when exceeding a few hundred milligrams per dose, with greater urinary excretion of the excess [1]. This pattern explains why regular intakes in the order of 100–200 mg/day are sufficient to maintain saturated tissue levels under normal conditions, while intravenous administrations have been used to achieve pharmacological levels in certain clinical research studies [6].

Pharmacokinetic studies have also shown that very high single oral doses produce transient plasma peaks that return to baseline levels within 24 hours, while repeated or fractionated administrations maintain more stable levels. The choice of dose and frequency must therefore consider the objective: deficiency prevention, tissue support, or experimental uses [1][6].

What it means in practice

For the general population, deficiency prevention is based on a diet that daily includes food sources rich in vitamin C: citrus fruits, kiwis, strawberries, bell peppers, leafy green vegetables, and potatoes. In good health, regular dietary intake is generally sufficient to maintain adequate plasma levels. National nutritional guidelines define recommended dosages; however, some experts consider intakes of around 100–200 mg/day useful to achieve "saturated" tissue concentrations under normal demand conditions [2].

In at-risk individuals (smokers, people with malnutrition, malabsorption, or severely restricted diets), a more careful assessment of nutritional status may be indicated, and, if necessary, supplementation. In specific clinical contexts (e.g., severe infections, surgery, or sequestration of vitamin C in inflammatory processes), requirements may increase and necessitate different strategies; however, therapeutic decisions must be made by the treating physician based on clinical evaluation and laboratory data [2][6].

Diagnosis and interventions

How scurvy is diagnosed

Diagnosis is based on dietary history, clinical picture, and confirmation by measuring plasma ascorbate levels. Low plasma levels (<11 μmol/L) are indicative of clinically relevant deficiency. Since early signs can be non-specific, it is important to consider the possibility in patients with known risk factors and compatible signs [4].

Treatment and clinical response

Scurvy treatment is simple and generally rapid: oral administration of vitamin C at doses recommended by a doctor tends to lead to symptom improvement within days to weeks; more severe signs require appropriate medical monitoring. In documented cases, the clinical response to supplementation is often marked and rapid [3].

Limitations of Evidence

Many claims regarding the benefits of vitamin C stem from observational studies, pharmacokinetic studies, case series, and heterogeneous clinical trials. This heterogeneity makes it difficult to establish clear causal relationships for many conditions other than overt scurvy. For example, the association between plasma vitamin C levels and the risk of certain chronic diseases has been documented in epidemiological studies, but not always confirmed by randomized intervention trials [4][8].

Regarding respiratory infections, systematic reviews and meta-analyses show modest effects on symptom duration and usefulness in conditions of extreme physical stress, but consistent therapeutic results in patients with established infections are limited and variable: the methodological quality of studies, differences in dosage, and route of administration complicate conclusions [7].

Finally, many studies do not evaluate differentiated effects based on baseline nutritional status, so the impact of supplementation may be greater in deficient individuals compared to the general population. Interpreting observational correlations as evidence of efficacy therefore requires caution and critical contextualization [7][8].

Key points to remember

• Vitamin C is essential for collagen synthesis and many enzymatic reactions; its prolonged deficiency causes scurvy.
• Scurvy remains possible today, especially in people with extremely limited diets or conditions that increase demand or reduce absorption. Modern clinical cases confirm this [3][4].
• To prevent hypovitaminosis, the daily diet should include fruits and vegetables rich in vitamin C; supplementation is reserved for selected cases under medical supervision [2].
• Pharmacokinetics differ by route and dose: very high plasma levels require the intravenous route, while regular oral intake achieves tissue saturation under normal conditions [1][6].

Editorial conclusion

Scurvy is a rare but still relevant disease today in people with diets severely lacking in vitamin C or with conditions that increase its consumption or reduce its absorption. The biology underlying the disease is well understood: vitamin C is necessary for collagen stability and numerous cellular functions. Effective prevention is achieved by prioritizing a varied diet rich in fruits and vegetables; where necessary, supplementation interventions and targeted clinical evaluations are valid tools. When reading the evidence, it is important to distinguish between observational associations and causal demonstrations, and always evaluate the individual clinical context. This general information does not replace medical advice for specific cases.

Editorial note

This update was prepared according to criteria of transparency and reliability: the scientific claims contained herein are supported by selected and verified peer-reviewed literature by DOI. The content is for informational and educational purposes and does not constitute individual therapeutic recommendations.

SCIENTIFIC RESEARCH

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2. [2] Carr AC, Maggini S. Vitamin C and Immune Function. Nutrients. 2017;9(11):1211. https://doi.org/10.3390/nu9111211
3. [3] Bhatia A, Gupta N, et al. Scurvy presenting with limp and weakness: a case report. BMC Pediatr. 2019;19:228. https://doi.org/10.1186/s12887-019-1605-5
4. [4] Schleicher RL, Carroll MD, Ford ES, Lacher DA. Serum vitamin C and the prevalence of vitamin C deficiency in the United States: NHANES 2003–2004. Am J Clin Nutr. 2009;90(5):1252–1263. https://doi.org/10.3945/ajcn.2008.27016
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7. [7] Hemilä H, Chalker E. Vitamin C for preventing and treating the common cold. Cochrane Database Syst Rev. 2013;1:CD000980. https://doi.org/10.1002/14651858.CD000980.pub4
8. [8] (Review) Vitamin C: A Comprehensive Review of Its Role in Health, Disease Prevention, and Therapeutic Potential. Molecules. 2025;30(3):748. https://doi.org/10.3390/molecules30030748