Walnuts protect against cardiovascular disease, and thanks to a small human study published by Ella Haddad in Nutrition Journal we better understand why. Walnuts prevent ‘bad cholesterol’ LDL from oxidising and thus reduce the chance of LDL causing damage to blood vessels.
People who eat lots of nuts live longer than people who don’t. This is mainly because nuts reduce the chance of developing fatal cardiovascular disease. Nutritionists agree on this, but how and why nuts have this effect remains an unknown quantity.
Researchers at Loma Linda University in the US tried to find out more about how walnuts work by doing an experiment on 16 adults. On one occasion the subjects were given breakfast that consisted of 90 g walnuts [Walnut] and on another occasion a breakfast based on oil, white bread and egg protein [Control].
After consuming the control meal, the amount of oxidised LDL in the blood rose. LDL is a bit like a molecular oil tanker, which transports cholesterol through your blood vessels. Oxidised LDL is like a leaking oil tanker. A small oil leak means that the blood vessel walls have to absorb lots of cholesterol and bad fats, and as a result the vessels become narrower.
After consuming walnuts the amount of oxidised LDL did not increase. The researchers believe that this was partly due to the vitamin E analogue gamma tocopherol. Walnuts contain large amounts of gamma tocopherol, and after eating walnuts the concentration of this protective vitamin rose in the subjects’ blood.
Nuts also contain catechins. Together with the gamma tocopherol these reduce the effect of aggressive molecules, free radicals, the researchers believe. And as a result gamma tocopherol and catechins also protect LDL against oxidation.
The researchers base this theory on other observations: they found a higher antioxidant effect [ORAC] in the blood after the walnut meal and also less malondialdehyde. Malondialdehyde is a marker for free radical activity.
Effect of a walnut meal on postprandial oxidative stress and antioxidants in healthy individuals.
In vitro studies rank walnuts (Juglans regia) among the plant foods high in antioxidant capacity, but whether the active constituents of walnuts are bioavailable to humans remains to be determined. The intention of this study was to examine the acute effects of consuming walnuts compared to refined fat on meal induced oxidative stress. At issue is whether the ellagitannins and tocopherols in walnuts are bioavailable and provide postprandial antioxidant protection.
A randomized, crossover, and controlled-feeding study was conducted to evaluate a walnut test meal compared to one composed of refined ingredients on postprandial serum antioxidants and biomarkers of oxidative status in healthy adults (n?=?16) with at least 1 week between testing sessions. Following consumption of a low phenolic diet for one day and an overnight fast, blood was sampled prior to the test meals and at intervals up to 24 hours post ingestion and analyzed for total phenols, malondiadehyde (MDA), oxidized LDL, ferric reducing antioxidant power (FRAP), hydrophilic and lipophilic oxygen radical absorbance capacity (ORAC), uric acid, catechins and urinary excretion of phenylacetate metabolites and of urolithin A.
Mixed linear models demonstrated a diet effect (P?< ?0.001) for plasma ?-tocopherol but not for ?-tocopherol with the walnut meal. Following the walnut test meal, the incremental 5 hour area under the curve (AUC(0-5h)) was reduced 7.4% for MDA, increased 7.5% for hydrophilic and 8.5% for lipophilic ORAC and comparable for total phenols, FRAP and uric acid. Oxidized LDL was reduced at 2 hours after the walnut meal. Plasma concentrations of gallocatechin gallate (GCG), epicatechin gallate (ECG) and epicallocatechin gallate (EGCG) increased significantly at 1 hour after the walnut test meal. Quantities of urolithin-A excreted in the urine were significantly higher following the walnut meal.
Compared to the refined control meal, the walnut meal acutely increased postprandial ?-tocopherol and catechins and attenuated some measures of oxidative stress.
PMID: 24410903 [PubMed – in process] PMCID: PMC3893411