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Vitamin E and quercitin.

The Occam's Razor principle dictates that the simplest of competing theories should be chosen. I prefer a more colloquial variation called KISS-- "Keep it Simple, Stupid."

Although I'm a former National Institutes of Health (NIH) division director, I believe our scientific policies for generating new spinal-cord injury (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 methyll nisolone (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 individuals are now challenging its true effectiveness. If the most scientifically scrutinized SCI drug can't cut the mustard over time, perhaps we should consider simpler 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 article discusses the neuroprotective potential of two other nutritional approaches: quercetin and vitamin E.

Quercetin

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 it is beneficial for preventing cancer, prostatitis, heart disease, cataracts, allergies/inflammation, and respiratory disorders.

An antioxidant, quercetin scavenges free radicals and inhibits damage-perpetuating, postinjury 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.

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Postinjury 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:

* Lipophilic (i.e., the affinity for fat or lipid), allowing it to diffuse through cell membranes and scavenge free radicals within the cells

* Anti-inflammatory

* 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 4 or 10 days. Recovery of hind-limb function was evaluated by a scale that assesses functional recovery on a gradation from 0 (no hind-limb movement) to 21 (normal walking).

Although no control animals walked, two thirds of the quercetin-treated rats 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 those treated with quercetin.

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 having twice-daily doses of quercetin over three or ten days were able to walk. In general, those 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 (see illustration on p. xx). 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) studied the effects on lipid peroxidation of treating experimentally injured cats with a combination of vitamin E and another antioxidant, selenium. Cats were orally pre-treated 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.

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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 postinjury, vitamin-E treated cats recovered 72% of their pre-injury function compared to only 20% for similarly injured but untreated con-trots. The investigators concluded that vitamin-E pretrearment "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 SCT (see following information).

Dr. Kenichi Iwasa and associates (1989, Japan) compared the recovery of rats fed a diet containing vitamin Eat a level 25 times that given to control animals. 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 vita-min-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. 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 those on 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 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.

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

Conclusion

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 there is little to lose and perhaps much to gain by including them in our SCI-treatment regimen.

Contact: laurancejohnston@msn.com.

S. LAURANCE JOHNSTON, PhD

KISS Candidates

Animal studies suggest the following commonly consumed, presumably relatively innocuous substances or practices have neuroprotective potential after acute spinal-cord injury (SCI):

Nutritional:

Melatonin--A pineal gland hormone consumed as a sleep aid (PN, October 2009)

Vitamin E -- A key vitamin found in and added to many foods

Quercetin -- A substance imbuing color to many foods Fasting (PN, October 2007)

Herbal:

Ginkgo biloba -- One of the world's most consumed and ancient plant-based medicines (PN, February 2008)

Buyang Huanwu decoction -- A traditional Chinese herbal mixture used to treat paralysis (PN, April 2009)

Pharmaceutical:

Ibuprofen -- An anti-inflammatory pain killer

Lipitor -- A cholesterol-lowering agent (PN, February 2008)
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Title Annotation:healing options
Author:Johnston, S. Laurance
Publication:PN - Paraplegia News
Date:Feb 1, 2010
Words:1294
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