The role of nutrition and body composition in peripheral arterial disease

Abstract

Peripheral arterial disease (PAD) has not been as extensively investigated as other cardiovascular diseases. However, the available data suggest that nutrition-based treatment strategies have the potential to reduce the cost-economic burden of PAD substantially. Abdominal obesity is associated with PAD and prospective and cross-sectional studies have shown that a low dietary intake of folate and reduced synthesis of vitamin D are associated with an increased risk of PAD and severe walking impairment in patients who have the disease. However, dietary patterns that are associated with decreased cardiovascular risk might protect against PAD. A small number of clinical trials have provided evidence that increased intakes of niacin and insoluble fiber might be associated with decreased levels of LDL cholesterol and thrombogenic biomarkers, as well as increased serum levels of HDL cholesterol in patients with PAD. However, little evidence that antioxidants, vitamins B(6) and B(12), or essential fatty acid supplements improve clinical outcomes in these patients exists. Overall, data on the effects of nutrition, body composition, and nutritional supplementation on the risk, progression, and prognosis of PAD are scarce. Further research into these areas is required to allow the development of evidence-based nutritional guidelines for the prevention and treatment of the disease.

Figure 1

Potential effects of vitamin B₁₂ and folate deficiencies, and the Cys66Thr variant of the MTHFR gene on homocysteine regulation and PAD etiology. Vitamin B₁₂ and the folate substrate 5-methyltetrahydrofolate are cofactors for methionine synthase, which catalyzes the conversion of homocysteine to methionine. Deficiencies in vitamin B₁₂ or folate could, therefore, disrupt homocysteine homeostasis, leading to accumulation of homocysteine, hyperhomocysteinemia, and an increased risk of PAD. Methylenetetrahydrofolate reductase is required for the conversion of folate substrates. The Cys667Thr variant of the enzyme has reduced catalytic efficiency, so the presence of the variant might also lead to disruption of homocysteine homeostasis and possibly increase the risk of PAD. Abbreviations: B₆, vitamin B₆; B₁₂, vitamin B₁₂; PAD, peripheral arterial disease.

Figure 2

Potential effects of vitamin D deficiency on the risk and progression of atherosclerosis and PAD. a | PAD-induced leg pain and discomfort can lead to decreased walking ability and an increase in sedentary, home-centered habits. This lifestyle, in turn, decreases the frequency and duration of sun exposure, which might lead to a self-reinforcing cycle in which vitamin D deficiency leads to abnormal calcium absorption, hyperparathyroidism, and even greater leg pain and discomfort. b | Vitamin D deficiency caused by inadequate sun exposure, dietary intake, or both might result in aberrant calcium metabolism and bone mineralization pathways. These irregularities might lead to alterations in the function of arterial smooth muscle cells and promote calcium deposition on arterial walls, arterial stiffness, and increased risk of atherosclerosis.