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There is now substantial evidence that cardiovascular disease (atherosclerosis, hypertension, high cholesterol) are diseases of chronic inflammation & oxidative stress (1).

A review of human clinical trials for Sulforaphane showed significant reductions in LDL cholesterol levels (2).

Interestingly, high LDL cholesterol may increase the production of oxygen free radicals (ROS), leading to oxidation of LDL-C, which sets the stage for the development of atherosclerosis (3). Notably dietary (direct) antioxidants (e.g. Vit C) have disappointed in clinical trials to prevent CVD. Using the bodies endogenous antioxidant (i.e. indirect) shows considerably more promise.

Nitric Oxide (NO) production reduces with age, and with the presence of Oxidative stress (4, 5). The reduction of NO (and increase superoxide) promotes endothelial dysfunction (6) and hypertension, and cause inflammatory processes such as atherosclerosis.

Numerous animal models show reductions in oxidative stress and inflammation when given Sulforaphane, leading to reduction in BP (20mmHg) 3, and the downregulation of inflammatory markers (TNFα and others).

Atherosclerosis is associated with long term inflammation of the arterial walls. Again numerous animal studies have shown that Sulforaphane reduces inflammation in vascular adhesions (7).


Recent Pat Inflamm Allergy Drug Discov. 2009 Jan;3(1):73-80, Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer.

Mol Nutr Food Res. 2015 May; 59(5): 918–926

Role of oxidized low density lipoprotein in atherogenesis.Witztum JL, Steinberg D J Clin Invest. 1991 Dec; 88(6):1785-92

Ghosh et al., Br J Pharmacol 141(4):562-573, 2004

PNAS May 4, 2004 101 (18) 7094-7099;

Endothelial dysfunction and hypertension in aging.Higashi Y, Kihara Y, Noma K Hypertens Res. 2012 Nov; 35(11):1039-47.

Oxid Med Cell Longev. 2015; 2015: 407580