Danish experiment reveals: You can satisfy your appetite just by looking at pictures of food on your phone.

The results may lead to a new form of treatment for overeating.
The results may lead to a new form of treatment for overeating.

The internet is overflowing with pictures of food: On news sites, social media and the banner ads that pop up everywhere.

Many of the food images are uploaded to sell specific foods. The idea is that the images on Facebook or Instagram will make us yearn for a McDonalds burger, for example. In other words, the image awakens our hunger.

New research from Aarhus University now shows that the images can actually have the opposite effect. At least if we see pictures of the same product repeatedly. 

A number of experiments reveal that we can get a sense of satiety if we see the same image more 30 times. Tjark Andersen, who recently defended his PhD at Department of Food Science at Aarhus University, explains more.

“In our experiments, we showed that when the participants saw the same food picture 30 times, they felt more satiated than before they had seen the picture. The participants who were shown the picture many times also chose a smaller portion than those who had only seen the picture three times, when we subsequently asked about the size of portion they wanted,” he says.

Tricking your brain into feeling full
It may sound strange that the participants felt full without actually eating anything. But this is really quite natural, explains Tjark Andersen. How we think about food has a large influence on our appetite. 

“Your appetite is more closely linked with your cognitive perception than most of us think. How we think about our food is very important,” he says, and continues:

“Studies have shown that if you make people aware of different colours of Jelly Beans, even if they have eaten all they can in red Jelly Beans, will still want the yellow ones. Even if both colours taste completely the same.”

Within brain research, these findings are explained with so-called grounded cognition theory.  For example, if you imagine putting your teeth in a juicy apple, the same areas of the brain are stimulated as if you actually take a bite of an apple.

“You will receive a physiological response to something you have only thought about. That’s why we can feel fully satisfied without eating anything,” he says.

A large online experiment
Tjark Andersen and his colleagues are not the first to discover that we can get feel full by looking at pictures of food. Other research groups have previously shown this. 

The new research from Aarhus University is that they examined the number of repetitions needed – and whether variation in the images removes the sense of satiety.

“We know from previous studies that images of different types of food don’t have the same effect on satiety. That’s why you can really feel full after the main course but still have room for dessert. Sweet things are a completely different type of food,” he says.

To investigate whether variation in food completely removes the sense of satiety, Tjark Andersen and his colleagues designed a number of online experiments. They ended up getting more than 1,000 people through their digital experiments.

First they showed a picture of just orange M&Ms. Some participants were shown the picture three times, others 30 times. The group that saw most pictures the M&M felt most satiated afterwards, explains Tjark Andersen.

“They had to answer how many M&Ms between 1 and 10 they wanted. The group which had seen 30 images of orange chocolate buttons, chose a smaller amount than the other two groups.”

Afterwards, they repeated the experiment. This time with M&Ms in different colours. The colours did not change the result.

Finally, they replaced the M&Ms with Skittles. Unlike M&Ss, Skittles taste different depending on the colour.

“If colour didn’t play a role, it must be the imagined taste. But we found no major effect here either. This suggests that more parameters than just colour and flavour have to change before we can make a effect on satiety,” he explains.

Could be used as a weight loss strategy
Since 1975, the number of overweight people worldwide has tripled. According to the WHO, obesity is one of the biggest health challenges facing humans. And the reason why we become too fat is that we eat too much food and too much unhealthy food and we do not take enough exercise.

This is where Tjark Andersen’s results come into the play. Perhaps they can be applied as a method to control appetite, he says. 

“Think if you developed an app based on a Google search. Let’s say you wanted pizza. You open the app. Choose pizza – and it shows a lot of photos of pizza while you imagine eating it. In this way, you could get a sense of satiety and maybe just stop wanting pizza.”

Perhaps his results can best be used to ensure that you don’t start a meal. The participants in the study only chose slightly fewer Skittles or M&Ms, corresponding to less than 50 calories.

“You won’t save many calories unless you completely refrain from starting a meal. But perhaps the method can be used for this as well. It’d be interesting to investigate,” he says.

Social media are overflowing with food
Tjark Andersen and a number of other researchers are studying how food advertisements on social media affect us, because we are constantly being confronted with delicious food. 

A few years ago, an American research group tried to find out how many advertisements with food we encounter on average when we are on social media. The researchers monitored a number of young people and mapped out the content they met.

On average, the young people saw 6.1 of food-related posts in 12 hours. The vast majority of the posts were pictures of food – and more than a third were about desserts or other sweet food.

The internet and, in particular, social media can be a contributory factor in our becoming increasingly overweight. But it may also be the solution.

Only the future will tell.

Obesity is more prevalent in people with type 1 diabetes than previously thought


People with type 1 diabetes should be screened regularly for obesity and chronic kidney disease, according to a study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.

Almost half of the adults in the United States have obesity, a chronic progressive disease characterized by an individual having an excess of body fat. Obesity is one of the leading causes of death in the United States, and people with obesity are at an increased risk for many serious diseases and health conditions such as diabetes, heart and liver disease. Obesity is a main risk factor for developing type 2 diabetes, but it has not been previously seen as a major complication in type 1 diabetes.

In type 1 diabetes, the body completely stops making insulin. In type 2 diabetes, the body produces insulin, but the cells do not respond to insulin as well as they should and later in the disease often do not make enough insulin. Type 2 diabetes is more likely to occur in people who are over the age of 40, overweight, and have a family history of diabetes, although more and more younger people, are developing type 2 diabetes.

“Our study shows that obesity rates in adults with type 1 diabetes are increasing and mirror the rates in the general adult population,” said Elizabeth Selvin, Ph.D., M.P.H., of Johns Hopkins Bloomberg School of Public Health and John Hopkins University in Baltimore, Md. “Our research also highlights the high risk of kidney disease in people with type 1 diabetes. Kidney disease is often considered more common in people with type 2 diabetes, but our data shows adults with type 1 diabetes actually had a higher risk of kidney disease than those with type 2.”

The researchers studied data from 4,060 people with type 1 diabetes and 135,458 people with type 2 diabetes from the Pennsylvania based Geisinger Health System between 2004-2018. They found 37% of people with type 1 diabetes had obesity, and the prevalence of kidney disease was higher in people with type 1 diabetes than those with type 2 after adjusting for age differences (16% vs. 9% in 2018).

“Our results highlight the need for interventions to prevent weight gain and end-stage kidney disease in people with type 1 diabetes,” Selvin said.

Obesity is a critical risk factor for type 2 diabetes, regardless of genetics


Obesity increases the risk of developing type 2 diabetes by at least 6 times, regardless of genetic predisposition to the disease, concludes research published in Diabetologia (the journal of the European Association for the Study of Diabetes [EASD]). The study is by Dr Theresia Schnurr and Hermina Jakupovi?, Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark, and colleagues.

Using data from a case-cohort study nested within the Diet, Cancer and Health cohort in Denmark, the authors examined the joint association of obesity, genetic predisposition, and unfavourable lifestyle with incident type 2 diabetes (T2D). The study sample included 4,729 individuals who developed type 2 diabetes during a median 14.7 years of follow-up, and a randomly selected cohort sample of 5,402 individuals (the control group).

The mean age of all participants was 56.1 years (range 50-65) and 49.6% were women. Overall, 21.8% of all participants were classified as obese, 43.0% as overweight and 35.2% as having normal weight; and 40.0% of the participants had a favourable lifestyle, 34.6% had an intermediate lifestyle and 25.4% had an unfavourable lifestyle.

Genetic predisposition was quantified using a genetic risk score (GRS) comprising 193 known type 2 diabetes-associated genetic variants and divided into 5 risk groups of 20% each (quintiles), from lowest (quintile 1) to highest (quintile 5) genetic risk. Lifestyle was assessed by a lifestyle score composed of smoking, alcohol consumption, physical activity and diet. Statistical modelling was used to calculate the individual and combined associations of the GRS, obesity and lifestyle score with developing T2D.

Compared with people of normal weight, those with obesity were almost six times more likely to develop T2D, while people who were overweight had a 2.4 times increased risk. For genetic risk, those with the highest GRS were twice as likely to develop T2D as those with the lowest, while those with the unhealthiest lifestyle were 18% more likely to develop T2D than those with the healthiest.

Individuals who ranked high for all three risk factors, with obesity, high GRS and unfavourable lifestyle, had a 14.5 times increased risk of developing T2D, compared with individuals who had a normal body weight, low GRS and favourable lifestyle. Notably, even among individuals with a low GRS and favourable lifestyle, obesity was associated with 8.4 times increased risk of T2D compared with normal weight individuals in the same genetic and lifestyle risk group.

The authors conclude: “The results suggest that type 2 diabetes prevention by weight management and healthy lifestyle is critical across all genetic risk groups. Furthermore, we found that the effect of obesity on type 2 diabetes risk is dominant over other risk factors, highlighting the importance of weight management in type 2 diabetes prevention.”

Does primary ovarian insufficiency affect your risks for obesity and diabetes?

Obesity
Obesity

Are overweight women less fertile? Does primary ovarian insufficiency increase risks for obesity and diabetes? For years the controversy regarding the connection between reproductive health and body mass index has continued. A new study assessed the effect of ovarian reserve on obesity and glucose metabolism and found no correlation. Study results are published online today in Menopause, the journal of The North American Menopause Society (NAMS).

Ovarian reserve has been defined as the number and quality of a woman’s eggs. A low ovarian reserve means that the number and/or quality of eggs a woman has is low for her age, making it more difficult for her to become pregnant. But low ovarian reserve can have other health ramifications beyond fertility. A number of previous studies have suggested that a lower reserve is linked to an increase in the storage of fat and impaired ability to process insulin, putting a woman at greater risk for diabetes.

However, in this latest study involving more than 1,000 participants and follow-up of 16 years, researchers concluded that a woman’s level of ovarian reserve was not associated with her risk of becoming obese or diabetic. The study specifically evaluated changes in a woman’s level of antimüllerian hormone (AMH), which is found in the blood and helps to estimate the duration of a woman’s reproductive lifespan, ultimately determining that this biomarker does not predict cardiometabolic risk.

Study results appear in the article, “Do trends of adiposity and metabolic parameters vary in women with different ovarian reserve status? A population-based cohort study.”

“Although previous research has clearly established a link between early menopause and cardiovascular disease risk, the present study showed that lower ovarian reserve, as measured by a single AMH level, was not associated with greater over time trends in adiposity and markers of glucose metabolism. Additional study is needed to determine how best to predict cardiometabolic risk in women with and without primary ovarian insufficiency in order to initiate appropriate risk reduction strategies,” says Dr. Stephanie Faubion, NAMS medical director.

Genetic links between depression and obesity explored




Obesity - an overview

Obesity – an overview

“Genetic variants linked to high BMI can lead to mental health issues,” reports The Guardian.

Depression is more common among people who are obese. But previous studies have not been able to determine whether there is a direct cause and effect relationship. So it could be the case that depression causes weight gain rather than the other way around, or indeed both could be true.




Also, it could be the complications associated with obesity, such as type 2 diabetes, are contributing to depression rather than the obesity itself.

This latest study attempted to use a genetic technique to focus on the direct effect of obesity on depression, removing the effect of other lifestyle and health factors. The researchers looked at the DNA of around half a million adults with white European ancestry in the UK.

The researchers looked at 73 genetic variations which had previously been linked to higher BMI. Some of these had also been linked to a reduction in risk of metabolic complications such as high cholesterol or blood sugar levels, rather than the increase that might be expected.

The researchers found that having a combination of the genetic variants which were associated with higher BMI was also associated with depression. This was some evidence that it was even the case when a person had the variants which reduced their risk of metabolic complications. This may suggest that obesity influences depression risk through psychological rather than metabolic changes; at least in some cases.

While we cannot change our DNA, taking regular exercise and eating healthily can help people achieve or maintain a healthy weight, and also help people with depression. Read more about how exercise can boost your mood and improve your health.




Where did the story come from?
The study was carried out by researchers from The University of Exeter Medical School, the University of South Australia Cancer Research Institute and King’s College London.

The researchers were funded by the Diabetes Research and Wellness Foundation, the Australian Research Training Program, the UK Medical Research Council, the Wellcome Trust, the European Research Council, the Royal Society, the Gillings Family Foundation, Diabetes UK, the National Institute for Health Research (NIHR) Biomedical Research Centre, Maudsley NHS Foundation Trust and King’s College London. The study was published in the peer-reviewed International Journal of Epidemiology on an open access basis so it is free to read online.

The Guardian reported the study accurately, including a mention of the limitations. The Mail Online provided sketchy details of the study, skirting over any of the genetic analysis and concluding that the psychological impact of being overweight increases the risk of depression, when this was only suggested by the results and not proven.

What kind of research was this?
This was a case-control study, comparing the genetic makeup of people with and without depression.

Depression is more common among people who are obese. However, it is not known whether obesity can directly increase a person’s risk of depression, whether the reverse is true, or both are true.

So researchers carried out a particular type of case-control study known as a Mendelian randomisation study, where researchers focused on genes known to be associated with disease risk and health outcomes rather than lifestyle factors.

The idea behind this type of study is the exact combination of DNA that people inherit from their parents is random. So the analysis reduces the possibility that other factors (confounders) are causing the links seen between obesity and depression.

What did the research involve?
The researchers used genetic information from about 450,000 UK adults with white European ancestry who had volunteered to be part of the UK Biobank, and have their DNA studied for research purposes.

The researchers identified 48,791 people with depression and 291,995 people without depression (controls) whose BMI had been measured, and compared their DNA.

People were identified as having had depression based on having reported either:

that they had seen a GP or psychiatrist for nerves, anxiety, or depression and experienced at least 2 weeks where they felt depressed or unenthusiastic
UK national hospital records indicated that they had a diagnosis of recurrent major depressive disorder (MDD) or single-episode MDD
The researchers also looked at whether analysing only those people with a hospital recorded diagnosis or who reported being diagnosed with depression by a professional affected their results.

The researchers looked specifically at whether genetic variations which have been found to be associated with obesity were also more common in people with depression.

As “markers” for obesity, if these genetic variations were more common in people with depression, this would suggest that obesity could be contributing to people’s risk of developing depression.

The researchers looked at 73 genetic variations which had been linked to having a higher BMI. The researchers excluded variants which had been linked to having a higher BMI but had stronger links to other conditions or traits such as smoking or lipid levels. Of the 73 variants, 43 were in or near to genes which could have an impact on brain and nervous system function and development (so they could theoretically be affecting depression risk directly) and 30 were not. Also, 14 of the variants were associated with increased BMI but reduced risk of metabolic disease (so these would not be influencing depression through these metabolic factors).

If the variants associated with a higher BMI, but not any of the metabolic consequences of obesity, were found to be more common in people with depression, this might suggest that the link between obesity and depression relates to psychological effects.

The researchers also looked at men and women separately, as it could be that the psychological impact of obesity might be greater in women because of issues around body image. They also repeated their analyses on a second sample of 45,591 people with depression and 97,647 controls from another study group (the Psychiatric Genetics Consortium).

What were the basic results?
The researchers found that individuals who were obese had a 45% higher chance of having depression than those in the healthy BMI range (odds ratio (OR) 1.45, 95% confidence interval (CI) 1.41 to 1.49). This link was stronger in women than in men.

Having a combination of genetic variants associated with a higher BMI (about 5kg/m2 higher) was associated with an 18% increase in the odds of having depression (OR 1.18, 95% CI 1.09 to 1.28). The link was slightly stronger in women than men, but the difference was not large enough to rule out that this occurred by chance.

The researchers found similar results when they carried out further analyses to make sure their findings were robust, for example, by excluding people without a hospital recorded diagnosis of depression.

The links to depression were stronger when looking at the BMI-linked variants which were also linked to brain or nervous system related genes. But again the difference was not large enough to rule out that it occurred by chance.

The link with depression was also found for BMI-linked variants which were associated with favourable metabolic profile, but only once data from the Biobank and Psychiatric Genetics Consortium samples were pooled.

How did the researchers interpret the results?
The researchers concluded that having a higher BMI is likely to contribute to directly increasing an individual’s chances of developing depression.

Some medications used to treat depression can cause weight gain. People who are depressed may be less likely to take good care of themselves, including eating healthily and taking regular exercise, and this may also impact their weight.

Conclusion

This study provides evidence that the link seen between obesity and depression may, at least in part, be due to a direct impact of weight on a person’s risk of depression.

This study was very large, and used many complex analyses to look at the relationship between weight, genetics, and depression. The researchers used a study design which aimed to remove the chance of factors other than weight impacting the results. They also carried out several additional analyses to test their results and make sure they were reliable.

For example, the way that people were classified as having or not having depression may not have been entirely accurate, as it was based partly on people’s reports of having seen a medical professional for “nerves, anxiety or depression”. Some people might have had depression but not sought help, or might not have had a diagnosis of depression had they been fully assessed. However, when the researchers excluded people who did not have a hospital recorded diagnosis of depression, they got similar results.

While this study contributes to what is known about the links between obesity and depression, there is still much to be learned. For example, the findings suggest the link may be psychological but researchers will now have to look more closely at how obesity might contribute to depression risk.

It is also worth bearing in mind that the causes of depression are likely to be complex, with many factors potentially playing a role. Also, the results may not apply to people of different ethnicities.

If you are overweight or obese and you are also troubled by low mood or depression then it may be a good idea to seek help for both issues at the same time.

What we do know is that mental and physical health are interrelated, and regular physical activity and eating healthily are likely to be beneficial for both.

Analysis by Bazian
Edited by NHS Website