Lipids derived from red wine, beers, and their dealcoholized variants

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Lipids in wine and beer

Our group has been studying the bioactivities of lipids present in beer and wine against platelet aggregation for more than 20 years. This stream of research was spearheaded by Emeritus Professor Constantinos A Demopoulos. Under his inspirational mentoring, our group grew over the years and now we are Academics in 3 Universities studying how the polar lipids (PL) present in beer and wine can inhibit platelet aggregation and hence the related atheromatosis.

 

Why did we choose wine and beer?

It has been known for many years, that during fermentation, bioactive lipids are bioformed. Hence, fermented foods and drinks (yoghurt, cheese, beer and wine) have much higher nutritional value than their unfermented foods (e.g. milk) and distillates (e.g. vodka and whiskey) whose nutritional value is practically zero! Using our approach, as published here, we can measure the anti-thrombotic activities of PL present in any food and feed. In our latest publication, here, we have studied the PL in wines and beers and their dealcoholized variants in relation to their capacity to inhibit (in vitro) the aggregation of platelets and hence exhibit a cardioprotective and anti-inflammatory potential.

The highlights of our paper are:

  1. Polar lipids and Total lipids of beer, red wine, and their dealcoholized variants inhibit PAF-induced platelet aggregation.
  2. LC-MS showed that the polar lipid fatty acid composition was characterized by high levels of saturated fatty acids.
  3. Lipid extracts from dealcoholized beverages have comparable antiplatelet activity to their alcoholic counterparts.

We studied: commercially produced stout (Guinness), lager (Heineken), red wine (120 Santa Rita Cabernet Sauvignon) and the alcohol-free equivalents of all beverages (Guinness 0%, Heineken 0% and Dealcoholized 120 Santa Rita Cabernet Sauvignon).

 

What next?

Our paper (titled “Bioactive lipids derived from red wine, beers, and their dealcoholized variants inhibit platelet-activating factor (PAF) induced platelet activation in vitro”) shows that during the dealcoholization the cardioprotective activities of PL in wine and beer are not removed and hence the zero% alcohol beer and wine, they still have strong cardioprotective activities. As a matter of fact the zero% alcohol drinks have lower IC50 values than the original drinks (see table 2 of our paper); this suggests that the dealcoholized drinks have stronger anti-platelet activities.

This study, the first of its kind, could show the way on how we can further develop zero% alcohol drinks. These drinks are becoming more popular and this trend is expected to grow even further in the future.

The wine and beer industry have lots to gain with data like ours as they could promote even further the nutritional profile of the zero% alcohol drinks.