Oxidative stress is a critical factor in cardiometabolic conditions. As previously demonstrated by the PREDIMED study, high-risk CVD patients have low antioxidant enzymatic activity and a high pro-oxidative state. Therefore, reactive oxygen species (ROS) scavengers have been highlighted for their protection against CVD. Sulforaphane, a sulfur-containing isothiocyanate (ITC), is distributed in cruciferous vegetables. In fact, Foods rich in sulforaphane possess anticancer functions as well as anti-inflammatory and antioxidant properties, reducing the risk of developing CVD.
The onset pathology of CVD relies on the heart and vessels’ dysfunction, affecting the circulatory system until it fails. Nevertheless, let us not forget that the ecosystem in which this condition is possible has insulin resistance (IR) as the primary trigger. On that same note, IR is associated with increased visceral fat contributing to a low-grade inflammatory state. Besides this, CVD has been and will continue to be a medical and economic burden in developed countries.
Some of the mediators contributing to these conditions’ onset continue to be low physical activity, abundant calorie-dense foods, high-stress settings, and availability of tobacco products. On the other hand, the traditional nutritional patterns based on whole-grain cereals, fruits, and vegetables, less availability to highly processed foods, and physical activity are proven to have a protective effect against CVD.
ROS and CVD
With increased heart rate, elevated production of ROS will appear. Indeed, this is thought to contribute to contractile and endothelial dysfunction, extracellular remodeling of the heart, and myocyte apoptosis. Furthermore, two molecular antioxidant processes are involved; the first one is redox-active and short-lived; it can also contribute to ROS production. On the other hand, the second one involves indirect antioxidants’ action; it’s long-lived and does not have a pro-oxidant effect. Therefore, the introduction of health-promoting antioxidant foods is needed to decrease the risk of CVD.
Sulforaphane is a metabolite of glucoraphanin (Grn), which in turn is the main glucosinolate (GLS) in broccoli. The production of sulforaphane is only possible when this is released due to plat injury. For example, chewing will chemically change the structure of glucoraphanin in conjunction with the enzyme myrosinase. Furthermore, this action will release glucose and sulfate, leaving the sulforaphane (SFN) molecule free to function.
However, ITC and sulforaphane cytoprotective effect as an indirect antioxidant is associated with the fact that they can conjugate with glutathione (GSH), contributing to phase activation II enzymes and scavenging of ROS. Besides this, SFN can regulate the nuclear factor erythroid-derived 2- (NF-E2) related factor 2- (Nrf2-) antioxidant response element (ARE) pathway. Consequently, this action upregulates the expression of a range of antioxidant enzymes, including HO-1, NQO1, GST, γ-glutamyl cysteine ligase (GCL), and glutathione reductase (GR).
SFN induces Nrf2 accumulation by inhibiting proteasomal degradation of the bZIP protein. In turn, bZIP protein can be sequestered by Keap1. This would result in a down-regulation of ARE-driven genes, eventually reflecting in low phase II enzymes activity. When SFN interacts with the Nrf2-Keap1 complex, it modifies keap1’s cysteine residues allowing Nrf2 to translocate to the nucleus.
SFN mediated effects
The introduction of SFN to our diet has been shown to have beneficial effects on wellbeing. However, the surprising factor is that even when SFN is cleared from the body in a few hours, it has been shown to exert prolonged protection against radical induce damage.
- SFN induced Nrf2 activity in astrocytes; a cell type highly involved in defense against oxidative stress in the brain. This resulted in increased antioxidant enzymes like NQO1 and HO-1 over a period that extended up to 48h after the broccoli ingestion.
- Besides this, glutathione levels were elevated for more than 20 h, resulting in peroxide-clearing and resistance towards superoxide and diminished cell damage.
- A reduced ROS- concentration was seen in cardiomyocytes as well as decreased DNA fragmentation. Also, an increased level of antioxidants and phase II enzymes were seen as part of the intervention with SFN.
Hypertension and SFN
Oxidative stress is associated with reduced production of nitric oxide (NO), resulting in platelet aggregation and endothelial dysfunction. Besides this, the overproduction of ROS represents a possible driver of hypertension.
- When Grn (found in broccoli) was included in males’ diet, it showed decreased oxidative stress associated problems, resulting in an improvement in blood pressure. This same result was found when females introduced broccoli to their diets.
- The SFN-mediated protection against platelet aggregation has been well- documented. It is believed that SFN can decrease collagen-induced glycoprotein IIb/IIIa activation and thromboxane A2 formation.
- In a study performed with Wistar rats, the ingestion of SFN resulted in a lower concentration of oxidized GSH, increased GR and GPx activity. Consequently, these improvements reflected in better endothelial relaxation and lower blood pressure.
Body composition and SFN
Obesity is a triggering component associated with hypertension. When SFN was included in the high-fat diet of C57BL/6N mice, it attenuated visceral adiposity, adipocyte hypertrophy, and fat accumulation in the liver. Furthermore, body composition plays a vital role in every assessment. A BIA can procure in-depth information about your nutritional status and risk factors.
The protective effects of SFN against oxidative stress is a great discovery. To link the ingestion of a simple cruciferous vegetable and bioactive compound SFN to its products to mitigate ROS deleterious results is empowering. ROS production is unavoidable, but now it is clear that the inclusion of a simple compound can protect against CVD. The official dose of SFN for humans is 0.5mg/kg, which means that a man of 70 kilograms can eat 12g of broccoli per day to prevent CVD. Oh wow! – Ana Paola Rodríguez Arciniega, MS
From your kitchen to your genes
Yesterday I was running late and out salad, but I had a broccoli head in mi fridge, onion, and orange bell pepper. I decided to make a quick fix with these three ingredients, and after a few minutes, I had to prepare a side dish.
1 broccoli head, cleaned and chopped
¼ red onion, chopped
1 bell pepper, chopped (orange, yellow, or red)
5 tbsp olive oil
1 tsp mustard
1-2 tbsp turmeric
On a big saucepan, introduce 2 tbsp of olive oil.
Add the vegetables and cook for 5 minutes, with a closed lid.
Mix 5 tbsp of olive oil with the mustard and turmeric and add it to the vegetables.
Mix well and close the lid for 2 minutes more.
Bai, Yang et al. “Sulforaphane Protects against Cardiovascular Disease via Nrf2 Activation.” Oxidative medicine and cellular longevity vol. 2015 (2015): 407580. doi:10.1155/2015/407580
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Dr. Alex Jimenez DC, MSACP, CCST, IFMCP*, CIFM*, CTG*
Licensed in Texas & New Mexico