If you’ve ever made a fruit salad, perhaps you know the chef’s trick of sprinkling a little lemon or lime juice over the fruit to keep it from turning brown. Well, in many ways, your body is just like that fruit.
Every time you eat, breathe or move, your body uses fuel created from the food you eat to produce energy. But just as a car using gasoline as fuel releases harmful by-products in the process in the form of exhaust, so, too, does your body’s energy-producing efforts produce a dangerous by-product — free radicals.
What are Free Radicals?
Free radicals are highly reactive forms of oxygen that are missing an electron. The terms “free radicals” and “oxidation” are used interchangeably due to the role oxygen plays when it comes to free radicals. You see, when a free radical comes into contact with normal molecules, it tries to steal an electron, damaging the healthy cell and its DNA. In fact, some estimates show that every cell in your body takes 10,000 oxidative hits to its DNA daily!
Oxidation and free radical damage have long been believed to be a risk factor of many chronic diseases that accompany aging, including heart disease, eye degeneration, memory loss, damage from UV light and cancer. Fortunately, there is one thing that can offset oxidation caused by free radical damage: antioxidants.
The Power of Antioxidants
Antioxidants gobble up as many free radicals as they can and deactivate them, preventing them from doing damage. If damage has already occurred, they may give the free radical an electron to stabilize it, or combine with it to form a different, more stable compound.
There are many recognized antioxidants, but the one of the most well-known is vitamin E. Study after study has shown that vitamin E is a potent antioxidant that can help prevent and even treat free radical damage.
However, there has been quite a bit of disagreement as to one particular oxidation-related disease and the effectiveness of vitamin E.
The Cholesterol Conundrum
It has been widely accepted that high LDL (bad) cholesterol levels are linked to heart disease. But, over the past 20 years, a new school of thought has emerged.
Turns out, LDL cholesterol isn’t “bad.” In fact, it’s quite good. Virtually every cell and hormone in your body is formed from cholesterol. What makes LDL cholesterol “bad” is oxidation. Let me explain.
Since rust occurs due to oxidation, I will use a car as an example. Picture a shiny, new metal fender on your car. It’s strong, sturdy and reliable. Now leave your car out in the rain or snow for months on end. After an extended period of time, that same fender will change color, weaken and become less reliable. That’s because it has oxidized.
The same thing happens to cholesterol. In its natural state, it is healthy and normal. But when it oxidizes, it becomes dangerous. And it is this oxidized LDL cholesterol that is linked to atherosclerosis and other cardiovascular conditions. Enter vitamin E.
The Vitamin E Debate
Vitamin E has long been studied as a potent antioxidant against LDL cholesterol oxidation and heart disease that can follow suit. However, the actual effectiveness of vitamin E is hotly debated.
In petri dishes and in animal studies, vitamin E routinely proves itself to be quite effective in preventing atherosclerosis. However, human studies are a bit more controversial.
On one hand, eight different studies spanning 12 years have found that vitamin E is effective at preventing atherosclerosis in humans. And then there are the 11 studies performed over 11 years that come to the complete opposite conclusion.
What is going on? According to a recent study, quite a bit.
A Question of What and When
According to a January 2011 study, “Do free radicals play causal role in atherosclerosis?”, from the Journal of Clinical Biochemistry and Nutrition, there are two critical factors that affect vitamin E’s ability to offset LDL oxidation — the type of oxidation and the duration and timing of use. 1
LDL cholesterol can become oxidized in a few ways — four in fact. Of these four, free radical damage is one, and the other three are lipoxygenase, cytochrome P450, and singlet oxygen, in case you were wondering.
Turns out, vitamin E is only effective in fighting the free radical form of oxidation. It is not effective against the other three. OK, first problem solved.
As for the timing issue, according to the study, LDL oxidation in humans often occurs over several years, if not decades. However, in animal and cell studies, the oxidation is contrived and usually forced.
This is a critical point. It means that the introduction of vitamin E is taking place nearly simultaneously with the beginning onset of oxidation. However, in people, the oxidation has been brewing slowly and steadily before person starts taking the vitamin E.
When you look at it this way, it becomes clear that it is rather unrealistic to think that a year or two of vitamin E supplementation could undo the damage done by decades of oxidative stress. Problem two solved.
Based on these two realizations, researchers concluded that vitamin E could be an effective preventative and therapeutic treatment for atherosclerosis caused by LDL oxidation if the oxidation is caused by free radical damage and if the supplement is taken early on.
What This Means for You
While a lot of this study is quite technical and does help explain the disparity in the vitamin E studies, there is one key takeaway: Start taking vitamin E early and often.
Look for a natural vitamin E supplement that contains d-alpha-tocopherol. Avoid the dl-form — that extra “l” means it is not natural. And aim for 200–400 IU a day.
Note: If you are on a blood thinner, check with your doctor before taking vitamin E, as it may cause your blood to become too thin.
1Niki, E. Do free radicals play causal role in atherosclerosis? Low density lipoprotein oxidation and vitamin E revisited. Journal of Clinical Biochemistry and Nutrition. 2011 Jan;48(1):3-7.