Why Expensive Wine Appears to Taste Better

When a bottle costs more, the reward center in the brain plays a trick on us

Price labels influence our liking of wine: The same wine tastes better to participants when it is labeled with a higher price tag. Scientists from the INSEAD Business School and the University of Bonn have discovered that the decision-making and motivation center in the brain plays a pivotal role in such price biases to occur. The medial pre-frontal cortex and the ventral striatum are particularly involved in this. The results have now been published in the journal “Scientific Reports”.

Previous work from INSEAD Associate Professor of Marketing Hilke Plassmann’s research group did show that a higher price, for instance for chocolate or wine, increased the expectation that the product will also taste better and in turn affects taste processing regions in the brain. “However, it has so far been unclear how the price information ultimately causes more expensive wine to also be perceived as having a better taste in the brain,” says Prof. Bernd Weber, Acting Director of the Center for Economics and Neuroscience (CENs) at the University of Bonn. The phenomenon that identical products are perceived differently due to differences in price is called the “marketing placebo effect”. As with placebo medications, it has an effect solely due to ascribed properties: “Quality has its price!”

The researchers assessed how different prices are translated into corresponding taste experiences in the brain, even if the wine tasted does not differ. 30 participants took part in the study, of which 15 were women and 15 were men, with an average age of around 30 years.

Wine tasting while lying down

The wine tasting took place lying down in an MRI scanner, allowing brain activity to be recorded “online” while participants were tasting the wines. Each time, the price of the wine was shown first. Only then around a milliliter of the respective wine was administrated to the test person via a tube in their mouths. The participants were then asked to rate via a button on a nine-point scale how good the wine tasted to them. Their mouths were then rinsed with a neutral liquid and the next identical wine sample was given for tasting. All of the experiments were performed in the brain scanner at the Life & Brain Center at the University of Bonn.

“The marketing placebo effect has its limits: If, for example, a very low-quality wine is offered for 100 euros, the effect would predictably be absent,” says Prof. Weber. This is why the researchers conducted the tests using an average to good quality red wine with a retail bottle prize of 12 €. In the MRI scanner, the price of this wine was shown randomly as 3, 6 and 18 €. In order to make the study as realistic as possible, the participants were given 45 euros of initial credit. For some of the tastings, the displayed sum was deducted from this account in some of the trials.

“As expected, the subjects stated that the wine with the higher price tasted better than an apparently cheaper one,” reports Professor Hilke Plassmann from the INSEAD Business School, with campuses in Fontainebleau (France), Singapore and Abu Dhabi. “However, it was not important whether the participants also had to pay for the wine or whether they were given it for free.” Identical wine leads to a better taste experience when a greater quality expectation is associated with the wine due to its price.

The measurements of brain activity in the MRI scanner confirmed this. The research team discovered that above all parts of the medial pre-frontal cortex and also the ventral striatum were activated more when prices were higher. While the medial pre-frontal cortex particularly appears to be involved in integrating the price comparison and thus the expectation into the evaluation of the wine, the ventral striatum forms part of the brain’s reward and motivation system. “The reward and motivation system is activated more significantly with higher prices and apparently increases the taste experience in this way,” says Prof. Weber.

How can placebo effects be inhibited?

“Ultimately, the reward and motivation system plays a trick on us,” explains INSEAD post-doctoral fellow Liane Schmidt. When prices are higher, it leads us to believe that a taste is present that is not only driven by the wine itself, because the products were objectively identical in all of the tastings. “The exciting question is now whether it is possible to train the reward system to make it less receptive to such placebo marketing effects,” says Prof. Weber. This may be possible by training one’s own physical perception – such as taste – to a greater extent.

Source : University of Bonn


Japanese-style Pork Belly and Cabbage Pot


300g pork belly slices
1 kg Chinese cabbage (suey choi)
1 stalk leek, finely shredded
3 onion, shredded
1 tsp minced ginger


2 tbsp dashi granules
6 cups water
2 tbsp soy sauce
1/2 tsp sea salt


  1. Peel off the leaves of the cabbage and layer between them the pork slices. Cut the stack of cabbage and pork into smaller stacks of about 5 cm wide. Arrange the stacks in the pot as shown in the picture below.

  2. Add the broth ingredients to the pot. Bring to a boil. Turn down heat and simmer with the lid on until the pork is done and the cabbage is tender.
  3. Mix in the leek, onion and ginger and cook for a few more minutes. Serve the dish in the pot.

Source: Japanese magazine

In Pictures: Limited-time offer of Character Food and Drink at Cafe Costa Mesa in Osaka, Japan

Sanrio’s Popular Character Gutama

Mapping The Brain’s Microbiome: Can Studying Germs In The Brain Lead To A Cure For Alzheimer’s?

Robin Seaton Jefferson wrote . . . . . . .

Could it really all come down to infection? Two scientists and a team of researchers are trying to find out.

Harvard researchers, Dr. Rudolph Tanzi and Robert D. Moir, PhD, are heading up a team, funded by the Cure Alzheimer’s Fund and the Good Ventures Foundation, that has taken on mapping the microbiome, the population of microorganisms, some helpful and some pathological, that exists inside the brain. The monumental task, dubbed The Brain Microbiome Project, will, they hope, tell them if amyloid beta plaques–known to initiate the pathological cascade of Alzheimer’s disease—are being made to protect the brain and if so, from what? In earlier studies, Tanzi and Moir showed that the main component of amyloid plaques in the brains of Alzheimer’s patients—the amyloid beta protein—is an “antimicrobial peptide” used by the brain’s immune system to protect itself against infection.

“If we can find out what microbes are the most common triggers of amyloid plaques, we may be able to later target those microbes with a vaccine,” Tanzi said.

A neurogeneticist, Tanzi, is vice-chair of neurology, director of the Genetics and Aging Research Unit at Massachusetts General Hospital and serves as the Joseph P. and Rose F. Kennedy Professor of Neurology at Harvard Medical School. Tanzi co-discovered all three early-onset familial Alzheimer’s disease genes and identified several others as leader of the Cure Alzheimer’s Fund Alzheimer’s Genome Project.

Robert D. Moir, PhD is an assistant professor in neurology at Harvard Medical School and Massachusetts General Hospital. His research focuses on the biochemical and cellular mechanisms involved in neurodegeneration in Alzheimer’s disease (AD) and aging.

The team’s theory is that amyloid-beta proteins are acting as saviors rather than slayers of brain cells, by surrounding viruses, bacteria and fungi, and clumping the offending pathogens into a ball so they can not harm the brain. Their actions would seem to be protective rather than destructive, but the problem lies in that these clumps then cause inflammation and the formation of neurotoxic tangles that lead to the death of nerve cells and Alzheimer’s disease.

By studying dozens of autopsied normal and Alzheimer’s brains, Tanzi and Moir hope to determine what kinds of microbial pathogens get into the brain or are already living in the brain and whether certain ones are more abundant in the brains of Alzheimer’s disease patients and trigger plaques, later leading to dementia.

To begin the process, they took autopsied brain tissue from a region of the brain that was ravaged by Alzheimer’s and ground it up into a broth of sorts. In doing so, they found that the ground, “homogenized” tissue was absolutely deadly to microbes—as much as 100 times more potent than penicillin, Tanzi said.

He said the tissue owed its lethality to those same amyloid-beta proteins—the ones that form plaques, which clog the brains of people with Alzheimer’s. He said the tissue’s ability to destroy microbes was greater than any other homogenized tissue or broth that was created from the brains of people without dementia or even from regions of diseased brains that didn’t have the plaques.

The results of that study, published in 2010, forced Tanzi and Moir to consider a new theory about the cause of Alzheimer’s disease—one that hypothesized that plaques might actually form to help the brain fight infection. Until then, amyloid-beta was thought to be purposeless, another unwanted overgrowth from old age, similar to nose hair. Only this one cannot simply be plucked. This one is ultimately responsible for the process that leads to Alzheimer’s disease in some people.

Now they are contending that amyloid-beta may perhaps play a crucial role in protecting the brain from attacks by bacteria, yeast, fungi and viruses. And if amyloid-beta are accumulating simply to fight a persistent infection, this new theory could lead to groundbreaking new therapies for treating or even preventing Alzheimer’s.

Tanzi said the team is hypothesizing that specific types of microbes will be more abundant and are the culprits behind triggering the plaque formation that initiate the pathological spiral of events in Alzheimer’s. While the study is unbiased, looking for any and all microbes present in the brain, they are also specifically looking at Lyme disease bacteria Borrelia and Bartonella, Chlamydia bacteria and various species of bacteria that grow in inflamed gums in periodontal disease. They are also concentrating on various types of the Herpes virus. Once the team has mapped the microbiome—or what specific pathogens live in the brain—they can begin to determine whether specific microbes are more abundant in Alzheimer’s disease, Tanzi said.

At one time scientists considered the brain to be immune-privileged. In other words, they once thought that the brain was completely sterile, owing its protection from pathogens to the blood-brain barrier (BBB), or the highly selective semi-permeable membrane that separates the circulating blood from brain fluid in the central nervous system (CNS). Scientists have known for some time that microbes can pass through the BBB after entering through the sinus cavities or bloodstream, for example. What’s new is that scientists are learning how the brain deals with infection.

“The news is that the amyloid plaques which trigger disease are being made for a reason, and maybe they are made to protect the brain from viruses, bacteria and fungus,” Tanzi said.

“We’re now seeing that the brain is not sterile. It has bacteria, viruses and fungus such as yeast and even larger parasites such as amoebas. Even nematodes have been found in the brain,” he said. “So as we get older, our blood-brain barrier begins to break down and microbes start to leak in. Or maybe you can have a stroke or get hit on the head and the blood-brain barrier is damaged. Again, microbes can leak in. You can also have viruses in the human genome that can be activated, like members of the Herpes virus family.”

“When a virus, fungus or bacteria get into the brain they activate the amyloid beta proteins which stick to them and fight them to keep them away from the brain cells,” Tanzi said. “This forms plaques by gluing these infectious microbes together into a ball. They then form fibers that form a web. That network of fibers entombs the microbes so they can’t infect the cell. It then forms a plaque.”

So, if Tanzi and Moir are right, the plaques are trying to protect the brain as they accumulate, but instead go haywire and trigger neuro-inflammation, tangles and nerve cell death, leading to dementia.

If they are right, mapping these microbes could bring an end to generations of suffering from a disease that until recently scientists knew next to nothing about, a progressive, degenerative brain disease that the Alzheimer’s Association predicts will destroy the memories of some 14 million Americans by 2050.

Only recently did Tanzi make the bold statement that he believes scientists could have a solid plan for eradicating Alzheimer’s disease by 2025.

Tanzi said his new drug, called a “Gamma Secretase Modulator (GSM), will be at least a part of the prescription for stopping Alzheimer’s disease plaque pathology from leading to symptoms. The GSM, developed with colleague Steve Wagner of the University of California San Diego (UCSD) and the National Institutes of Health (NIH) Blueprint Neurotherapeutics Network, is expected to enter clinical safety trials with the National Institutes of Health (NIH) by the end of the year. He also warns that in using GSM’s or any therapies aimed at lowering brain amyloid levels, we should not wipe out amyloid in the brain, but rather “dial it down,” given the purpose amyloid appears to serve as an antimicrobial substance.

Tanzi said he and Moir and their team will continue to pursue this new avenue even as his GSM goes into trials. He still believes the disease can be eradicated in his lifetime. The possibility that it could come down to something as simple as infection is not surprising, he said. “No matter what disease you look at, in the end things usually come down to infection and inflammation.”

Source: Forbes

Cholesterol Crystals are Sure Sign a Heart Attack May Loom

A new Michigan State University study on 240 emergency room patients shows just how much of a role a person’s cholesterol plays, when in a crystallized state, during a heart attack.

George Abela, lead author and chief cardiologist at MSU, analyzed the material that was obstructing the coronary arteries of patients who had suffered a heart attack and found that 89 percent of them had an excessive amount of these crystallized structures, referred to as cholesterol crystals.

The research is now published online in the American Journal of Cardiology.

These crystals are released from plaque that can build up in the heart and is often made up of fat, calcium and other substances as well. When this material hardens over time in the arteries, it’s known as atherosclerosis.

“In previous studies, we showed that when cholesterol goes from a liquid to a solid, or crystal state, it expands in volume like ice and water,” Abela said. “This expansion inside the wall of the artery can tear it and block blood flow causing a heart attack or stroke.”

After heart attack patients entered the emergency room, Abela and his team suctioned out this plaque. They were able to see that clusters of large crystals had formed and were able to break through the plaque and walls of the arteries and then released into the heart. This caused damage by blocking blood flow.

“We now know to what great extent these crystals are contributing to a heart attack,” Abela said.

This latest research also reconfirms what Abela discovered in an earlier study that cholesterol crystals activated the production of inflammation molecules, known as Interleukin-1 beta, which aggravate, or inflame, coronary arteries.

“Now that we’ve shown how extensive cholesterol crystals are irritating and blocking off these arteries, treatments that dissolve these crystals may be used to reduce heart damage,” Abela said.

Some of these treatments can include the use of statin drugs – often used to lower one’s cholesterol – aspirin and solvents such as alcohol that can be injected in low doses into a vein during a heart attack. Using these options could allow doctors to improve patient outcomes and save more lives.

A recent clinical trial using an already FDA-approved antibody, known as canakinumab, has also shown to block the Interleukin-1 beta inflammation molecule and reduce the chances of a cardiac event.

“Saving heart muscle is the most important aspect of treating a heart attack,” Abela said. “So, if we are able to provide patients with better, more targeted treatments, then this could help open up and calm down the aggravated artery and protect the heart muscle from injury.”

Abela also added that by simply controlling one’s cholesterol by eating a healthy diet, exercising and taking statin medications as needed, could be the best way to prevent these crystals from forming.

Source: Michigan State University

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