Quercetin & Vitamin E
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Laurance Johnston, Ph.D.

The Occam’s Razor principle dictates that the simplest of competing theories should be chosen. I prefer a more colloquial variation called KISS or “Keep it Simple, Stupid.” Although I’m a former National-Institutes-of-Health (NIH) division director, I believe our scientific policies for generating new SCI solutions often ignore KISS wisdom. In allegiance to the God of science and its dogma, we have adopted complex and burdensome strategies for developing new treatments, which - albeit ensuring the sanctity of the anointed scientific process - create few real-world SCI treatments.

A case in point is methylprednisolone (MP), a drug commonly administered after injury. Although NIH subjected MP to more complex, time-consuming, and costly clinical trials than any other SCI drug in history, many are now challenging its true effectiveness. If the most scientifically scrutinized SCI drug can’t cut the mustard over time, perhaps we should consider more simple options that wouldn’t take decades to evaluate and reevaluate.

Such options include nutritional and herbal approaches, which, given already extensive human use and presumed safety, would be relatively easy to incorporate into treatment regimens. For example as discussed previously, animal studies suggest that 1) Ginkgo biloba, a widely consumed herbal medicine, 2) melatonin, an extensively used sleep aid, and 3) every-other-day fasting may be neuroprotective after injury.

This update discusses the neuroprotective potential of two other nutritional approaches: quercetin and vitamin E.


Belonging to the flavonoid family of molecules, quercetin imbues coloring to many foods, including apples, red onions, red grapes, tomatoes, raspberries, and other berries. Evidence suggests that it is beneficial for cancer, prostatitis, heart disease, cataracts, allergies/inflammation, and respiratory disorders.

An antioxidant, quercetin scavenges free radicals and inhibits damage-perpetuating, post-injury lipid peroxidation. Basically, after the initial mechanical injury, a complicated physiological chain reaction generates free-radicals, which steal electrons from the lipids in neighboring neuronal membranes, resulting in further cell death.

Post-injury hemorrhaging causes the hemoglobin within red blood cells to disintegrate, releasing oxidized iron, which triggers lipid peroxidation. Quercetin binds to this iron, preventing it from reacting with the lipids on neighboring cells. In addition to its antioxidant characteristics, quercetin has other properties that augment its neuroprotective potential. For example, it is 1) lipophilic (i.e., affinity for fat or lipid), allowing it to diffuse through cell membranes and scavenge free radicals within the cells, 2) anti-inflammatory, and 3) anti-edematous, i.e., inhibits damage-causing swelling.

Dr. E. Schultke and colleagues (2003, Canada) assessed the impact of treating experimentally injured rats with quercetin. Different doses of quercetin or saline (i.e., controls) were injected into the body cavity one hour after injury and every 12 hours thereafter for either 4 or 10 days. Recovery of hind-limb function was evaluated by a scale which assesses functional recovery on a gradation from 0 (no hind-limb movement) to 21 (normal walking).

Although no controls walked, two-thirds of the quercetin-treated animals recovered some ability to do so. Supporting the idea that iron mediates damage, the tissue of the injured cords of control animals tested positive for iron, but no iron was detected in the cords of quercetin-treated animals.

The investigators reported the results of a somewhat similar investigation in 2009. Although no control animals regained sufficient hind-limb function to walk, approximately 50% of the rats treated with twice-daily doses of quercetin over three or ten days were able to walk.  In general, the rats that were treated with quercetin for a longer duration recovered more function. Compared to controls, more spinal-cord tissue was preserved in the quercetin-treated rats.

Vitamin E

Vitamin E is a generic term for a class of molecules called tocopherols, the most physiologically ubiquitous being alpha-tocopherol (illustration). Vitamin E is found in vegetable oils, whole grains, dark green leafy vegetables, nuts and seeds, and legumes. Supplementation may promote cardiovascular and eye health, and prevent cancer and age-related cognitive decline.

Like quercetin, vitamin E is an antioxidant that protects neuronal membranes from lipid-peroxidation.

Dr. Royal Saunders and co-investigators (1987, Ohio) investigated the effects on lipid peroxidation of treating experimentally injured cats with a combination of vitamin E and another antioxidant, selenium. Cats were orally pretreated with the combination for five days before injury. Compared to untreated controls, the spinal-cord tissue at the injury site of the antioxidant-treated cats had fewer molecules associated with lipid-peroxidation.

Former PVA scientific advisor, Dr. Douglas Anderson et al (1988, Ohio) evaluated vitamin-E’s effect in cats with experimental SCI. The cats were treated orally with the vitamin for five days before and after injury. Functional recovery was assessed by improvements in walking, running, and stair climbing.

Four weeks post-injury, vitamin-E treated cats recovered 72% of their pre-injury function compared to only 20% for similarly injured but untreated controls. The investigators concluded that vitamin-E pretreatment “was extraordinarily effective in promoting functional recovery…” However, they noted that because vitamin E enters the central nervous system slowly, it’s probably not a viable candidate for treating SCI. (see below)

Dr. Kenichi Iwasa and associates (1989, Japan) compared the recovery of rats fed a diet containing vitamin E at a level 25 times that fed to controls. The high vitamin-E diet was consumed for eight to ten weeks before experimental injury. Hind-limb function was assessed using a scale ranging from 0 (no movement) to 4 (complete recovery). One day after injury, the vitamin-E-treated rats had a hind-limb score of 3.5 compared to 2.4 for controls. In addition, vitamin-E supplementation enhanced the recovery of nerve conductivity and spinal-cord blood flow, and reduced the level of lipid-peroxidation-associated molecules. Finally, microscopic examination of the injured cord tissue showed less damage, such as bleeding and edema, in vitamin-E-treated animals.

This investigative team later (1990) compared recovery in rats fed the aforementioned control diet with rats fed a vitamin-E-deficient diet (specifically, 20-times less). In other words, this study compared controls to vitamin-E-deficient and not -supplemented animals. The results indicated that vitamin-E-deficient rats had 1) less recovery of hind-limb function, 2) less restoration of spinal-cord blood flow, 3) more compromised nerve conduction, 4) more bleeding and edema, and 5) a greater production of lipid-peroxidation-related chemicals.

Recently, Dr. Al Jadid and colleagues (2009, Saudi Arabia) reconfirmed vitamin E’s neuroprotective effects. Injured rats were divided into three groups: saline-treated controls and two groups that received different levels of vitamin E. Supplementation was started at the time of injury and continued for 14 days.

Post-injury functional recovery was measured using an activity cage, which uses horizontal and vertical sensors to measure movements. Rats who recovered greater function would trigger the sensors more. Both vitamin-E supplemented groups had statistically significant functional improvements by the end of the study compared to controls. The results suggest that vitamin E, even when administered after injury, may be a useful SCI treatment option.


Clearly, many therapeutic agents look promising in animal research, but fall short when used in humans. Although I have no idea whether quercetin, vitamin E or other nutritional approaches are truly neuroprotective after human injury, common sense suggests that there is little to lose and perhaps much to gain by including them in our SCI-treatment regimen.

Adapted from article appearing in February 2010 Paraplegia News (For subscriptions, call 602-224-0500) or go to www.pn-magazine.com.