32 replies to this topic

[timar]

This recent study brings some interesting, biomarker-related insights into the protective role of nuts:

Effect of a walnut meal on postprandial oxidative stress and antioxidants in healthy individuals.

Haddad EH, Gaban-Chong N, Oda K, Sabaté J.


BACKGROUND: 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.

METHODS: 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.

RESULTS: Mixed linear models demonstrated a diet effect (P < 0.001) for plasma γ-tocopherol but not for α-tocopherol with the walnut meal. Following the walnut test meal, the incremental 5 hour area under the curve (AUC0-5h) 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.

CONCLUSIONS: Compared to the refined control meal, the walnut meal acutely increased postprandial γ-tocopherol and catechins and attenuated some measures of oxidative stress.

[APBT]

Consider the sacha inchi (Inca peanut) with its favorable n-3 to n-6 ratio.

 

http://en.wikipedia....netia_volubilis

The seeds of Inchi have high protein (27%) and oil (35 - 60%) content, and the oil is rich in the essential fatty acids omega-3 linolenic acid ( 45-53% of total fat content) andomega-6 linoleic acid ( 34-39% of fat content), as well as non-essential omega-9 ( 6-10% of fat content).^[1] They are also rich in iodine,^{[citation needed]}vitamin A,^{[citation needed]} and vitamin E. 

 

http://pubs.rsc.org/...fo/c3fo60688k#!divAbstract

Alpha-linolenic acid (ALA) is an essential n-3 PUFA; its n-3 LCPUFA derivatives EPA and DHA, which have diverse beneficial effects, are scarce in the human diet. In recent years nontraditional vegetable oils rich in ALA (up to 45%) have been developed as new alternatives to increase ALA consumption. This work evaluated the accretion of ALA, EPA and DHA into the phospholipids extracted from erythrocytes, liver, kidney, small intestine, heart, quadriceps and the brain in rats fed sunflower (SFO), canola (CO), Rosa canina (RCO), sacha inchi (Plukenetia volubilis, SIO) and chia (Salvia hisp�nica, ChO) oils. Five experimental groups (n = 12 per group) were fed for 21 days with SFO (1% ALA), CO (10% ALA), RCO (33% ALA), SIO (49% ALA), and ChO (64% ALA). SIO and ChO allowed higher ALA accretion in all tissues, except the brain, and a reduction in the content of arachidonic acid in all tissues except the brain. EPA was increased in erythrocytes, liver, kidney, small intestine, heart and quadriceps, but not in the brain. DHA was increased in the liver, small intestine and brain tissues. Our results demonstrate that ALA, when provided in significant amounts, can be converted into n-3 LCPUFA, mostly DHA in the liver and brain. It is suggested that oils rich in ALA, such as SIO and ChO, are good sources for obtaining higher tissue levels of ALA, also allowing its selective conversion into n-3 LCPUFA in some tissues of the rat. 

 

[Mind]

Just reading through this thread again because of the very polarized advice regarding omega-6 oils vs omega-3 oils.

 

I have taken to eating a lot of nuts in the last couple of years. I like them. They are filling. It helps me to avoid worse food like hi-carb snacks.

 

However, they are high in omega-6. Depending upon who you talk to, you are either going to improve your mortality risks by a small degree by eating more nuts (and omega-6), or you are going to die near instantly by eating too much.

 

Dr. Mercola avoid omega-6 as much as possible and it is hard to argue with his success. 70 years old and dead-lifting 400 pounds.

 

Large epidemiological studies show higher omega-6 is not bad and might lower bad cholesterol levels a tiny bit.

 

I do think that people consume too much omega-6 in the SAD diet. All processed and boxed food, almost all mass-produced soups and salad dressings, and many other common products are stuffed to the gills with soybean oil and other high omega-6 refined seed oils. Too much is probably bad for you.

 

I suspect moderation in nut consumption along with an overall healthy diet, is a net benefit for health.

 

Anyone have recent data to share about how good or bad omega-6 and nut consumption might be?