Durk Pearson & Sandy Shaw’s®
Life Extension NewsTM
Volume 16 No. 3 • March 2013


Going Mountain Climbing? Quercetin Found To Be Protective Against High Altitude Cerebral Edema


A new paper1 starts by telling you about the dangers of traveling to high altitudes or mountain climbing without adequate acclimatization. You could end up like one of the millions of people who every year suffer from acute high altitude mountain sickness, from which 5% can develop life threatening high altitude cerebral edema. High altitude cerebral edema has been described as, “although uncommon, high altitude cerebral edema causes significant morbidity and occasionally death in otherwise perfectly healthy individuals.” The researchers1 report that their recent study “proved that oxidative stress and inflammation play an important role in high altitude cerebral edema via the redox-sensitive transcription factor, NFkappaB activation.” NFkappaB is a major regulator of inflammation-associated genes.

Another mechanism described by the researchers is hypobaric hypoxia leading to low blood oxygen saturation that triggers the production of erythropoietin (to increase the number of red blood cells). They go on to explain that increases in red blood cells induce hypoxic inflammation by producing reactive oxygen species. The researchers carried out a study to identify “a potent therapeutic agent which can reduce hypobaric hypoxia-induced oxidative stress, as well as inflammation” as a possible way to reduce high altitude cerebral edema.1 Quercetin has been found to have powerful antioxidant and antiinflammatory effects. Moreover, quercetin has been reported in several studies to reduce inflammation by attenuating the redox-sensitive transcription factor NFkappaB, as well as scavenging free radicals. The researchers compared the effects of quercetin with dexamethasone (a synthetic corticosteroid, which acts as an antiinflammatory) against high altitude cerebral edema in male Sprague Dawley rats.

In the study, rats were exposed to an altitude of 25,000 feet for 24 hours, as a result of which they showed a significant rise in various blood parameters including white blood cells, red blood cells, lymphocytes, monocytes, granulocytes, hemoglobin, platelets, MCV, and HCT (hematocrit). The authors hypothesize that increase in red blood cells, hemoglobin, and hematocrit might lead to increased blood viscosity and stasis of blood, increasing the risk of blood clots. However, administration of quercetin or dexamethasone prior to hypoxia exposure resulted in a reduction in many of these changes. Quercetin was more effective than dexamethasone as an antioxidant (decreasing reactive oxygen species and increasing superoxide dismutase) as well as an antiinflammatory by downregulating NFkappaB. Unlike dexamethasone, quercetin does not have the many side effects commonly observed in corticosteroid therapy (such as severe allergic reactions, loss of appetite, depression, diarrhea, dizziness, fever, muscle weakness, severe nausea or vomiting, swelling of feet or legs, and others).

According to the authors, the MSD (material safety data sheet) for quercetin in the rat for LD50 (dose that kills 50% of the animals) is 161 mg/kg of body weight. For a human of 70 kg, this would be equivalent to about 11,270 mg. The basic multinutrient formulation we both take daily contains in the recommended 12 capsules a day 128 mg of quercetin or nearly two orders of magnitude lower than the LD50 for rats.

Anti-inflammatory Effects of Benfotiamine Mediated By Regulation of Arachidonic Acid Pathway in Macrophages

As noted in the article (above), arachidonic acid stimulates the proliferation of prostate cancer cells through its metabolite HETE, produced by 5-lipoxygenase. Interestingly, a 2012 paper2 reports that benfotiamine, a lipid soluble form of vitamin B1 (thiamine) inhibits the formation of arachidonic acid metabolites by preventing the LPS-induced metabolizing of arachidonic acid via 5-lipoxygenase and other arachidonic acid metabolizing enzymes such as COX-2 (cyclooxygenase 2), TXB (thromboxane) synthase, and PG12 (prostacyclin) synthase. Moreover, benfotiamine has been found to be a potent blocker of AGEs (advanced glycation end products) as well as antiinflammatory against LPS (lipopolysaccharide). “Bacterial lipopolysaccharide (LPS), the structural component of the Gram-negative bacterial outer cell wall, is a potent initiator of the inflammatory response during most commonly seen bacterial infections.”2

References

1. Patir et al. Quercetin as a prophylactic measure against high altitude cerebral edema. Free Radic Biol Med. 53:659-68 (2012).
2. Shoeb and Ramana. Anti-inflammatory effects of benfotiamine are mediated through the regulation of the arachidonic acid pathway in macrophages. Free Radic Biol Med. 52:182-90 (2012).

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