Can you imagine sharing some genes with worms?! Yes, worms. The tiny, slimy guys we are all used to seeing in soil, among flowers or on trees. In a recent study, researchers found a new gene called SKN-1B in the C. elegans worm. This gene helps brain cells detect when the animal has eaten, and helps them send a signal to tell the worm it’s had enough food.
These researchers pointed out that if this incredible molecular control is present in worms, it may exist in humans too. Nrf2 is the name of a human protein thought to mediate food-related mechanisms and to regulate satiety in a way that resembles what happens in worms. Nrf2 exerts its core activities during inflammation and oxidative stress, an imbalance between production of free radicals and the body’s antioxidant defenses.
Activated Nrf2 pushes the production of antioxidant and anti-inflammatory molecules, which reduces oxidative stress and avoids cellular damage. In addition, Nrf2 carries out its anti-inflammatory activity by directly inhibiting production of pro-inflammatory molecules. Woah, that’s great, but how do Nrf2’s abilities correlate with food-related mechanisms and weight control?
The center of appetite is located in the hypothalamus , which registers satiety and sends you messages to stop eating. After a meal, the stomach releases a protein called GLP-1 which stimulates insulin secretion to keep blood glucose levels balanced. Your fat tissue then sends messages to the hypothalamus through a protein called leptin. This protein both warns the hypothalamus that enough food has been eaten and that there is sufficient energy to run the day’s activities. It also stimulates a protein called AMPK which makes cells internalize glucose, lowering sugar levels in the blood.
Oxidative stress in the hypothalamus interferes with ALL the above-mentioned finely tuned messages, altering the activity of leptin and leading to cells being unable to internalize glucose. This leads to high blood glucose levels and weight gain, since fat tissue fails to release leptin and to communicate satiation. Nrf2 acts as a hypothalamic oxidative stress reducer, restoring leptin and satiation signals.
Nrf2’s role in lowering oxidative stress and detoxifying the body from free radicals is potentially useful in treating obesity. Excess in fat tissue underlies a systemic low-grade chronic inflammation due to fat cells increasing in number and dimensions and becoming unable to receive the right amount of oxygen from blood. This shortage in oxygen and the release of pro-inflammatory cytokines not only reinforces the body’s inflammatory state but also augments systemic oxidative stress. Free radicals further aggravate obesity by pushing fat cells to grow and increase in number, reinforcing inflammation.
Now, the real point is: do we have the power to stimulate Nrf2 in some way? Of course we have! Crucifers and foods high in vitamin D have the potential to stimulate Nrf2. Cruciferous vegetables include broccoli, cabbage, cauliflower, Brussels sprouts, kale, and radish. The molecule produced by crucifers that is able to induce Nrf2 is called sulforaphane and is considered an indirect antioxidant since it needs Nrf2 to actually detoxify the body. Vitamin D can preserve DNA stability by activating Nrf2. Sources of vitamin D include salmon, rainbow trout, mushrooms, tuna, whole milk and high-fat cheese.
So what are you waiting for? Stuff your fridge with broccoli, cauliflowers, kale and various types of fish high in vitamin D. These will boost your Nrf2 activity, preserve your body from oxidative damage and inflammation, and help you avoid weight gain.
