When Does Hungry Become Hangry?

Jennifer MacCormack wrote . . . . . .

Have you ever been grumpy, only to realize that you’re hungry?

Many people feel more irritable, annoyed, or negative when hungry – an experience colloquially called being “hangry.” The idea that hunger affects our feelings and behaviors is widespread – from advertisements to memes and merchandise. But surprisingly little research investigates how feeling hungry transforms into feeling hangry.

Psychologists have traditionally thought of hunger and emotions as separate, with hunger and other physical states as basic drives with different physiological and neural underpinnings from emotions. But growing scientific evidence suggests that your physical states can shape your emotions and cognition in surprising ways.

Prior studies show that hunger itself can influence mood, likely because it activates many of the same bodily systems, like the autonomic nervous system and hormones, that are involved in emotion. For example, when you’re hungry, your body releases a host of hormones including cortisol and adrenaline, often associated with stress. The result is that hunger, especially at greater intensity, can make you feel more tense, unpleasant and primed for action – due to how these hormones make you feel.

But is feeling hangry just these hunger-induced feelings or is there more to it? This question inspired the studies that psychologist Kristen Lindquist and I conducted at UNC-Chapel Hill. We wanted to know whether hunger-induced feelings can transform how people experience their emotions and the world around them.

Negative situations set the scene for hanger

An idea in psychology known as affect-as-information theory holds that your mood can temporarily shape how you see the world. In this way, when you’re hungry, you may view things in a more negative light than when you’re not hungry. But here’s the twist.

People are most likely to be guided by their feelings when they’re not paying attention to them. This suggests that people may become hangry when they aren’t actively focused on their internal feelings, but instead wrapped up in the world around them, such as that terrible driver or that customer’s rude comment.

To test whether hungry people are more likely to become hangry in negative situations when they aren’t focused on their feelings, we designed three different studies. In the first two, run online with U.S. adults, we asked people – some hungry, some full – to look at negative, positive and neutral emotional images. Then they saw an ambiguous figure: a Chinese character or pictograph they’d never seen before. We asked participants whether they thought the pictograph meant something pleasant or unpleasant.

Hungry people who saw negative images thought the pictographs meant something more unpleasant. However, hungry people’s ratings after positive or neutral emotional pictures were no different than the not-hungry people.

This suggests that the hangry bias doesn’t occur when people experience positive or even neutral situations. Instead, hunger only becomes relevant when people confront negative stimuli or situations. But why would hunger only matter in negative situations?

Affect-as-information theory also suggests that people are more likely to use their feelings as information about the world around them when those feelings match the situation they’re in. Hunger likely only becomes relevant in negative situations because hunger itself produces unpleasant feelings – making it easier to mistake the cause of those feelings to be the negative things around you, rather than your hunger.

Tuning in to your feelings

In the final study, we recreated in the laboratory a frustrating situation to test how hunger and awareness – or lack thereof – might cause hanger.

We assigned two random groups of undergraduate students to fast for at least five hours or eat a full meal before coming to our lab. There we assigned them to write a story that was meant either to direct their attention to emotional information, or to not focus on emotions at all. Then everyone did a long, tedious computer task. At the end of the task, we secretly programmed the computer to “crash.” The researcher blamed the participant for the computer malfunction and told them they’d have to redo the task once it was fixed.

It turned out that hungry people who hadn’t focused on feelings beforehand exhibited more signs of being hangry. They reported feeling more stressed, hateful and other negative emotions and rated the researcher as being more “judgmental,” compared to full individuals and the hungry people who did write about emotions earlier.

These findings suggest that feeling hangry occurs when your hunger-induced negativity gets blamed on the external world around you. You think that person who cut you off on the road is the one who made you angry – not the fact that you’re ravenous. This seems to be a fairly unconscious process: People don’t even realize they’re making these attributions.

Our data suggest that paying attention to feelings may short circuit the hangry bias – and even help reduce hanger once you notice it.

Although these studies provide a valuable glimpse into the ways that physical states, like hunger, can temporarily shape our feelings and behaviors, they are only a first step. For example, our studies only address hunger effects in healthy populations where individuals eat regularly. It would be interesting to look at how feeling hangry could change with long-term dieting or conditions like diabetes or eating disorders.

These studies alongside other emerging science suggest that our bodies can deeply shape how we think, feel and act – whether we realize it or not. We’re generally aware that emotions like feeling stressed can influence our health, but the reverse direction is also true. Our bodies and physical health have the power to shape our mental lives, coloring who we are and the way we experience the world around us.

Warding off hanger

Here are three pro tips to help keep your hunger from going full-blown hangry.

First, it may seem obvious, but pay more attention to your hunger. People vary a lot in how sensitive they are to hunger and other bodily cues. Maybe you don’t notice you’re hungry until you’re already ravenous. Plan ahead – carry healthy snacks, eat a protein-filled breakfast or lunch to give you lasting energy – and set yourself reminders to eat regularly. These basic precautions help prevent you from becoming overly hungry in the first place.

But what if you’re already super hungry and can’t eat right away? Our findings suggest people are more likely to be biased by hunger in negative situations. Maybe you’re stuck in bad traffic or you have a stressful deadline. In these cases, try to make your environment more pleasant. Listen to an amusing podcast while you drive. Put on pleasant music while you work. Do something to inject positivity into your experience.

Most importantly, your awareness can make all the difference. Yes, maybe you’re hungry and starting to feel road rage, overwhelmed with your task deadline, or wounded by your partner’s words. But amid the heat of those feelings, if you can, step back for a moment and notice your growling stomach. This could help you recognize that hunger is part of why you feel particularly upset. This awareness then gives you the power to still be you, even when you’re hungry.

Source : The Conversation

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Baked Chicken Marinated with Tequila and Lime Served with Chili Ginger Garlic Sauce and Baked Potato

Ingredients

1 whole chicken de-jointed or 4 chicken thighs bone in, skin on and 4 chicken drumsticks with skin on
75 ml tequila blanco
zest and juice of 2 limes
1/4 tsp chilli flakes, plus more for garnish
2 tbsp olive oil
2 tsp salt flakes

Chili Ginger Garlic sauce

100 g red chillies, roughly chopped
2 cloves garlic, crushed
10 cm piece (50 g) ginger, peeled and roughly chopped
1 tsp fine sea salt, or to taste
4 tsp sunflower oil
2 tsp sugar
juice of 1 lime

Baked Potato

4 brush potatoes, washed
200 g coconut yoghurt, to serve
1/2 cup chopped coriander leaves
salt, to taste

Garnish

1 avocado, mashed
leaves of 1 Romaine lettuce, torn
finely chopped coriander leaves
lime wedges

Method

  1. Preheat oven to 220ºC.
  2. Place potatoes onto a baking tray lined with baking paper. Pierce several holes into each potato using a skewer. Season with salt and pepper and bake in the oven until soft, about 45 minutes.
  3. Meanwhile, mix coconut yoghurt and chopped coriander together in a bowl until combined. Season with salt, to taste, cover with plastic wrap and set aside in the fridge.
  4. Place chicken pieces into a large zip lock bag. Add marinade ingredients and seal bag, pushing out air first. Place onto a tray and into the fridge for at least 45 minutes or overnight.
  5. To make the sauce, place all ingredients into a bowl and puree with a hand blender. Set aside to rest for at least 15 minutes before use.
  6. Once chicken has marinated, remove chicken pieces from the bag, reserving marinating liquid in the bag. Pour about half of the marinade over the chicken pieces. Place chicken onto a shallow baking tray and bake in the oven for 25 minutes.
  7. Remove chicken from oven and pour the remaining marinade over the chicken pieces. Continue to bake until golden brown, about 25-30 minutes. Check that chicken is cooked through and remove from oven. Remove chicken pieces from the baking tray and set aside, keeping warm.
  8. Add some boiling water to the baking dish to loosen the pan juices and stir to create a slightly thick sauce. Set aside until required.
  9. To serve, place some torn lettuce leaves and a dollop of mashed avocado on the plate. Place two pieces of chicken onto a plate and sprinkle with chili flakes. Place a Baked Potato onto the plate, slice potato open and fill with some of the coriander coconut yoghurt dressing. Dollop some of the Chili Ginger and Garlic sauce to the side. Drizzle some of the reserved pan juices over the chicken and sprinkle with chopped coriander. Serve with a wedge of lime.

Makes 4 servings.

Source: Nigella Lawson

Video: Master Sushi Chef Yumi Chiba

Chef Yumi Chiba has spent her career trying to figure out one of sushi’s most illusive specialities at her restaurant Anago no Uotake, Japan.

Watch video at You Tube (9:36 minutes) . . . . .

Scientist Says Salt Won’t Give You a Heart Attack If You are Healthy

Dr. James Dinicolantono wrote . . . . . . . . .

For more than 40 years, we’ve been told eating too much salt is killing us. Doctors say it’s as bad for our health as smoking or not exercising, and government guidelines limit us to just under a teaspoon a day.

We’re told not to cook with it and not to sprinkle it on our meals. The white stuff is not just addictive, goes the message — it’s deadly. Too much of it causes high blood pressure, which in turn damages our hearts. We must learn to live — joylessly, flavourlessly but healthily — without it.

Well, I’m here to tell you that all of that is wrong. As a leading cardiovascular research scientist — based at Saint Luke’s Mid-America Heart Institute, Missouri — I’ve contributed extensively to health policy and medical literature.

I am associate editor of the British Medical Journal’s Open Heart, published in partnership with the British Cardiovascular Society, and I sit on the editorial advisory board of several other medical journals.

In my work, I’ve examined data from more than 500 medical papers and studies about salt. And this is what I’ve learned: there was never any sound scientific evidence to support this low salt idea. What’s more, as I explain in my new book, eating too little of it can cause insulin resistance, increased fat storage and may even increase the risk of diabetes — not to mention decreasing our sex drive.

Current daily guidelines limit you to 2.4 g of sodium, which translates to 6 g of salt (or sodium chloride) or slightly less than a teaspoonful.

If you have high blood pressure, or belong to a group considered to be at greater risk of developing it — such as being over 60 or Afro-Caribbean — doctors even advise you to cut your intake to two-thirds of a teaspoon of salt per day.

Yet salt is an essential nutrient that our bodies depend on to live. And those limits go against all our natural instincts. When people are allowed as much salt as they fancy, they tend to settle at about a teaspoon-and-a-half a day. This is true all over the world, across all cultures, climates and social backgrounds.

If you’ve been struggling to cut your intake, it may come as a relief to learn your salt cravings are normal, a biological need akin to our thirst for water.

We are essentially salty people. We cry salt, we sweat salt and the cells in our bodies are bathed in salty fluids. Without salt we’d not be able to live. And it’s not only our bodies that work this way.

A yen for salt drives the elephants of Kenya to walk into the pitch-black caves of Mount Elgon to lick sodium sulphate salt crystals off the walls. Gorillas have been known to follow elephants to eat the salt-rich droppings, while monkeys that groom one another don’t do so to eat fleas, but to enjoy their salty skin secretions.

Salt is so fundamental to life that a deficiency of it acts as a natural contraceptive in all sorts of animals, including us.

A diet low in salt reduces the sex-drive, inhibits the chances of getting pregnant and affects the birth weight of infants. Clinical studies show that low-salt diets can increase the risk of erectile dysfunction, fatigue and the age at which females become fertile.

Salt helps the body withstand accidents and other traumas. Besides excessive bleeding, we experience a loss of other fluids in states of shock — for example, from burns. As the injured areas soak up fluids to speed healing, the body needs its salt reserves to keep the blood circulating and fend off vascular collapse.

So why do almost all doctors tell us that salt is bad for us?

The orthodox medical view on salt is based on a straightforward hypothesis, which says eating higher levels of salt leads to higher levels of blood pressure — end of story.

But as with so many simplistic health theories, this is based on a fundamental misunderstanding, compounded by faulty science.

The faulty hypothesis goes like this: when we eat salt, we get thirsty, so we drink more water.

The dangerous myth that salt raises blood pressure began more than 100 years ago

The excess salt causes the body to hold on to that water to dilute the saltiness of the blood.

That water retention increases blood volume, which leads to higher blood pressure, and thus to heart disease, strokes and other serious conditions.

Although this makes sense in theory, there’s a problem: the facts don’t back it up.

Evidence in medical literature suggests approximately 80 per cent of people with normal blood pressure (that is, a reading of below 120 over 80) do not suffer any signs of raised blood pressure — none at all — when they increase their salt intake.

Among those with prehypertension, or higher blood pressure, three quarters are not sensitive to salt. And even among those with full-blown high blood pressure, more than half — about 55 per cent — are totally immune to salt’s effects.

The dangerous myth that salt raises blood pressure began more than 100 years ago, with French scientists Ambard and Beauchard. They based their findings on studies of just six patients.

Successive researchers misinterpreted and misused their data, building on a theory that earned media attention without any solid foundation in fact.

In the early Fifties, at Brookhaven National Laboratory in New York, Dr Lewis Dahl was determined to make science fit his own preconceptions.

A man of ‘strong convictions’, he was a proponent of racial theories that claimed Japanese people had high levels of hypertension while Inuit tribes did not — and that this was due to the amount of salt in their diets.

He proposed to prove this with experiments on rodents. However, as even Dr Dahl was obliged to concede, normal rats are not sensitive to salt. It does nothing to their blood pressure.

So he decided to selectively modify them through in-breeding over several generations to create what are now known as ‘Dahl salt-sensitive rats’.

That’s right: Dahl created salt-sensitive rats in a lab and then used them to prove his hypothesis that salt affected blood pressure.

Dahl popularised the notion that salt is nothing but a flavouring we add to food. He cited medical studies that, he claimed, were proof humans could survive on a quarter of the recommended levels.

But a closer look at the papers he promoted is alarming: one 1945 experiment into a low-salt diet may have killed people.

One patient placed on a restricted salt regime died soon afterwards, and another sustained circulatory collapse, due to inadequate supplies of oxygen and nutrients to the tissues — a classic symptom of salt deprivation.

One of Dahl’s most dramatic experiments involved giving human baby food with high salt content to his special salt-sensitive rats. It killed them, which Dahl proclaimed as proof that baby food could be lethal for human infants, too.

Of course, human babies are much larger than rats, and the salt-sensitive rats had been genetically engineered to suffer from hypertension.

But based partly on this research, the Committee on Nutrition at the American Academy of Paediatrics concluded that infants were consuming too much sodium, and manufacturers began to lower the salt content in all kinds of food.

The link between high blood pressure and salt was established in the public mind, on the most spurious of pretexts.

But this misinformation did not take hold worldwide. The average Korean, for instance, eats over 4g of sodium a day. They feast on tteokguk, a broth-based soup full of salt, and bulgogi, grilled meat marinated in a sea of sodium-packed soy sauce. They eat kimchi — cabbage preserved in salt — with every meal.

Yet Koreans have some of the world’s lowest rates for hypertension, coronary heart disease and death due to cardiovascular disease. This is known as the ‘Korean Paradox’. South Korea also has one of the lowest death rates from coronaries in the world, along with Japan and France.

What do people from these three countries have in common? They all eat a very high-salt diet.

The Mediterranean diet, too, widely recommended as heart-healthy, is not exactly low in salt — think of all those anchovies and sardines. Even where blood pressure does increase, the benefits of a higher salt intake — a lower heart rate, reduced insulin levels, more balanced adrenal hormones and better kidney function — are likely to outweigh any risks.

Low salt intake has several side-effects that magnify our risk of heart disease, such as increased heart rate, compromised kidney function, underactive thyroid glands, heightened insulin levels — a risk factor for diabetes — as well as heightened cholesterol.

All through lack of salt. This white crystal that has been unfairly demonised for many decades is diverting blame from the real culprit of these illnesses.

High blood pressure, cardiovascular disease and chronic kidney disease can all be caused by the real health hazard, excessive consumption of sugar.

We all need salt to live. But you could go the rest of your life, and probably extend its span, if you never ingested another gram of added sugar.

It is extraordinary that no food advertisement or leaflet in your GP’s surgery ever tells you that a low-salt diet doesn’t just increase your risk of an elevated heart rate, it practically guarantees it. This harmful effect occurs in nearly everyone who restricts salt intake.

The damage done by an average increase of four heartbeats a minute is compounded by other salt-related stresses inflicted on our bodies by modern life.

We lose salt by following fashionable diets such as low-carb regimes. Some medications cause salt loss. Intestinal problems including Crohn’s disease, ulcerative colitis, irritable bowel syndrome and leaky gut also decrease salt absorption.

And kidney damage from refined carbs and sugar will reduce those organs’ capacity to retain salt.

We may discover that low-salt guidelines have created more heart disease than they ever prevented.

They may even have been a contributing factor in the greatest public health challenge of our time: the rising epidemic of diabetes, caused in part by an increasingly common, yet little-known, phenomenon called ‘internal starvation’.

To understand this, we need to begin by looking at the obesity epidemic. The conventional explanation for this is an imbalance between the consumption of calories and our expenditure of energy — in other words, we eat more than we burn off. We’re told to eat less and move more, though it’s obvious this strategy isn’t working for everyone.

Consuming too little salt can set into motion an unfortunate cascade of changes that result in insulin resistance, an increase in sugar cravings, an out-of-control appetite and ultimately internal starvation, sometimes known as hidden cellular semi-starvation, which promotes weight gain.

Someone who appears massively overweight on the outside may be literally starving on the inside.

When you start restricting your salt intake, your body will do anything to try to hold on to it.

Unfortunately, one of its main defence mechanisms is to increase insulin levels, which it does by becoming more resistant to insulin itself. The body is then less able to shuttle glucose into cells.

That means more and more insulin is secreted to control blood glucose. This keeps the body’s stored fat and protein reserves locked away. The fat cannot be converted into energy. To make matters worse, salt restriction also stimulates hormones such as renin, angiotensin and aldosterone. They help retain the ebbing salt levels, but they also increase the absorption of fat.

So a low-salt diet doesn’t just force the body to pile on fat, but prevents it from being burned off. No wonder ‘Eat Less Move More’ can make no difference for some.

It gets worse. If you slash salt intake dramatically, you could also develop an iodine deficiency, since salt is our best source of iodine. We need iodine for proper thyroid function, without which the metabolic rate may slow down.

A slower metabolic rate results in the body storing more fat, particularly in the organs, which in turn promotes insulin resistance. Once again, weight gain results.

Plus, low-salt diets increase the risk of overall dehydration. That’s a problem because well-hydrated cells consume less energy.

Dehydrated cells leave you feeling exhausted, which encourages you to consume more calories — which are immediately translated into weight gain.

Exercise now seems unappealing. Your body cannot access its stored energy and so the brain switches into conservation mode, trying to hang on to every calorie.

Even though weight is piling on, every function in the body is behaving as though it’s fighting to survive a full-scale famine.

So how much salt should you be eating? Many healthy people needn’t worry about overloading. The body takes care of any excess. Research suggests the optimal range for healthy adults is between 3g and 6g of sodium a day — about one-and-a-third to two-and-two-thirds of a teaspoon of salt.

Listen to your body. It has a built-in ‘salt thermostat’, an interconnected set of brain sensors that monitor sodium supplies in an effort to avoid activating those starvation hormones.

And your brain would much prefer that you simply eat salt rather than having to scavenge it from vulnerable parts of the body.

So next time you feel a craving for salt, do yourself a favour and give in to it. Your body says these things for a reason.

Drop the guilt — not the salt.

Source: The Daily Mail


Read also:

Nutrient Reference Values for Australia and New Zealand – Sodium . . . . .

World Health Organization – Salt Reduction . . . . .

Diabetes Linked to Risk for Parkinson’s Disease

Alan Mozes wrote . . . . . . . . .

Men and women with type 2 diabetes may face a significantly higher risk of developing Parkinson’s disease later in life, new British research suggests.

The finding of a link followed the tracking of Parkinson’s diagnoses among millions of diabetic and non-diabetic patients who use the National Health Service in England.

Study author Dr. Thomas Warner said that, after accounting for conditions that might mimic Parkinson’s, the research showed that those with type 2 diabetes had a 32 percent greater risk of later developing the progressively debilitating neurological disorder.

Escalated risk was even more dramatic among younger diabetes patients, aged 25 to 44, who were found to face a fourfold greater likelihood of eventually developing Parkinson’s, according to the report.

And adults with diabetes who had already developed diabetes-related health complications — including damage to the retina, kidneys or nerves — faced a 49 percent hike in their Parkinson’s risk.

Nevertheless, Warner stressed, “it is vital to realize that, overall, the majority of diabetic patients do not develop Parkinson’s disease.”

Although the study could not prove a cause-and-effect relationship, Warner cited two possible reasons for a link between the two diseases.

First, he said, there could be “shared genetic predisposition to develop [both] type 2 diabetes and Parkinson’s.”

And then “there may be shared pathways in leading to development of diabetes and Parkinson’s,” he added. While the exact nature of such a connection remains unclear, Warner suggested it might involve the insulin production and glucose control problems that characterize diabetes.

“Unlike most tissues in the body, brain cells are almost totally reliant on glucose as a source of energy,” Warner noted. “So if there is a problem in how insulin controls the use of glucose by cells, this may affect certain groups of brain cells selectively.”

Warner is a professor of clinical neurology with the University College London Institute of Neurology, as well as the Queen Square Brain Bank for Neurological Disorder, both in London.

He and his colleagues published their findings online in the journal Neurology.

For their study, the investigators used data from the English “Hospital Episode Statistics” database to identify 2 million British patients newly diagnosed with diabetes from 1999 through 2011.

This group was then stacked up against 6 million British patients who had initially sought care during the same time frame for non-diabetes related issues, such as sprains, varicose veins, appendectomies or hip replacements.

The researchers found that just over 14,000 of the 2 million in the diabetes group were later diagnosed with Parkinson’s, compared with about 21,000 of the 6 million others. That translated into a more than 30 percent greater risk for Parkinson’s among those with diabetes, the researchers said.

Among diabetic patients 25 to 44 years old, 58 of over 130,700 people developed Parkinson’s, compared with 280 out of nearly 2.6 million similarly aged non-diabetics. That translated into a fourfold greater Parkinson’s risk among those with diabetes, the researchers said.

Drug regimens and smoking histories were not considered in the current analysis; nor were patients seeking diabetes care outside a hospital setting.

Dr. Michael Okun, medical director of the National Parkinson’s Foundation, called the findings “not surprising, as the collective evidence from multiple studies has been converging on the idea of some link or association between Parkinson’s and diabetes.”

According to Okun, “There are many potential explanations for a link between the two diseases, but in younger patients, genetics likely plays a key role. In older patients, the degenerative process itself may disrupt brain-driven endocrine pathways, including those related to insulin and to sugar management.”

Okun, who also serves as the chair of neurology at the University of Florida in Gainesville, said, “At this point the mechanisms are unknown, and will require careful research.”

He said it’s “important to stress that although diabetes drugs are currently candidates to treat or prevent Parkinson’s disease, we are not recommending this approach until more compelling data is available.”

Source: HealthDay


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