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How vitamin E prevents cell aging

How Vitamin E Can Help Prevent Cellular Senescence

Vitamin E is at the top of the list when it comes to antioxidants because of its ability to fend off free radicals and protect against oxidative stress that causes the break down of our cells or cellular senescence. Free radicals are things that we are exposed to daily such as pollution, UV rays, radiation, smoking, and even a poor diet. Oxidative stress is caused by an imbalance between free radicals and antioxidants and while oxidative stress is a normal process, a severe enough imbalance can cause serious health issues. So how does vitamin E play a factor in this process?

What is Cellular Senescence?

Cellular senescence is when the cells in our body stop the process of division. In the 1960s, two scientists, Leonard Hayflick and Paul Moorhead were performing experiments on human cells and discovered that they had set lifespan and that the cells ceased creating and dividing after a set amount of divisions. Hayflick and Moorhead were the first to associate cellular senescence with the process of aging, later it was also associated as a process in helping to protect against cancers. Further, cellular senescence has also recently been associated with other biological processes such as tissue repair, development, and aging and age-related disorders.

Premature cellular senescence caused by free radicals increases the aging process in our bodies which can result in a weakened immune system, diseases, infections, and early aging. The process of cellular senescence can be initiated, triggered, or sped up through a variety of stress-related factors that can occur from internal or environmentally damaging factors such as oxidative stress.

What is Vitamin E?

Vitamin E is a group of fat-soluble vitamins that protect our immune system by fighting off free radicals and has been studied extensively for its abilities in how it can benefit our health, healing, the slowing of the aging process, as well assisting in preventing certain diseases such as cancers and heart disease. Ensuring that you get enough vitamin E is a great way of looking out for and maintaining your health as well as the early prevention of cellular senescence. Talk to your doctor first before taking any vitamin E supplements.

Good Food Sources of Vitamin E:

  • Dark green leafy vegetables
  • Wheat Germ Oil
  • Sunflower Seeds
  • Olive oil
  • Abalone
  • Avocado
  • Peanuts
  • Hazelnuts
  • Almonds
  • Oatmeal
  • Soybeans
  • Wheat and wheat germ
  • Brown rice
  • Sweet potatoes
  • Watercress

Vitamin E and Cellular Senescence

There have been a variety of studies on vitamin E that demonstrate vitamin E’s potential in reducing cellular senescence.

  • In one study, a low intake of vitamin E was shown to accelerate cellular senescence in those who have cardiovascular disease.
  • Further, in another study that tested two different types of human cells, vitamin E supplementation was shown to also help delay cellular senescence in a laboratory setting.
  • Vitamin E was also shown to help reduce age-related declines in the immune system in rats.
  • In other tests involving topical vitamin E for wounds on rats, the rats that had the topical vitamin E applied showed an increase in wound closure as well as a decrease in scarring.
  • When vitamin E is used in or with sunscreen, it is more effective in blocking out UV rays, which help prevent cellular senescence in our skin.

In Conclusion

Vitamin E appears to be a key nutrient and essential antioxidant when it comes to the aging of our cells and in staying as healthy as possible. As research continue with vitamin E and its impact with cellular senescence, science may one day find a way to work with vitamin E to delay the aging process of our cells. Such discoveries could mean that people could live longer lives with extended vitality or with a more youthful appearance, as well as reducing the impact of diseases like cancers and cardiovascular disease.

Sources:

https://en.wikipedia.org/wiki/Cellular_senescence

https://pubmed.ncbi.nlm.nih.gov/9054499/


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