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Retraining the brain to beat stress is the key to losing weight and keeping it off, a leading Australian neuroscientist says.
There’s overwhelming evidence that many people who lose weight through dieting quickly regain it.
This is because people have learned to ignore their brain – an organ which has been dictating behaviour since prehistoric times – and have accepted emotional eating that comes with living an over-stressed lifestyle, according to Professor Selena Bartlett from QUT’s Institute of Health and Biomedical Innovation.
Diets can in fact make us fatter and more stressed, says Prof Bartlett
“When we are stressed our brain seeks pleasure and that’s the problem,” says Prof Bartlett.
And the more stress you experience, the more your brain seeks pleasure to counter it.
Choosing to beat stress in order to loose weight has long been advocated by US neuroscientist, Dr Caroline Leaf.
Stress, like real food, is not inherently bad – it makes people alert and ready for action.
But it depends on how a person reacts to stress that determines the outcome of a situation and in this case weight loss, according to Dr Leaf.
“Thoughts are real things that occupy mental real estate,” she said during her 2015 TEDx talk on the power of our thoughts.
If a person chooses to react wrongly to a challenging situation, they enter stage two of the stress reaction.
“During this stage, high levels of cortisol circulate in the blood for extended periods of time, in turn contributing to prolonged high blood sugar that can also lead to insulin resistance, pre- diabetes, and weight gain, since prolonged high levels of cortisol lead to the accumulation of fat instead of fat breakdown.
“In this toxic situation, fat tends to accumulate around the middle of the body and is a risk factor for heart disease,” writes Dr Leaf.
In fact, prolonged, high levels of cortisol can lead to Cushing’s Syndrome – characterised by fat accumulation around the middle and back of the human body.
The good news is that it’s possible to override the way the amygdala – the emotional part of our brain – responds to stress, says Prof Bartlett.
“When the rational brain is in charge; sustainable weight loss is possible,” she said.
PROFESSOR BARTLETT’S FIVE STEPS TO HELP MAKE THIS HAPPEN:
1. Be compassionate to your brain – it is an amazing organ that can be severely damaged by stress, especially in childhood while it’s developing.
2. Get to know the brain – an awareness of how the amygdala – an almond-shape set of neurons located deep in the brain’s medial temporal lobes – drives your behaviour is critical to overriding unhealthy impulses.
3. Identify when your amygdala is taking over in stressful situations and acknowledge when you’re tempted by the urge to eat comforting food, like sugar.
4. Replace food and alcohol with deep breathing, stretching, walking, running or any movement that feels good.
5. Reduce sugar and alcohol intake and increase cardiovascular and high intensity exercise – these will help to heal your brain of its stress-induced damage and build a strong, healthy body.
Does it seem like kicking a sugar habit is as hard as dropping the cigarettes and cold ones?
It turns out there’s a good reason behind that — a group of researchers have found that sugar, alcohol, and nicotine are all addicting in the same way.
“What we’ve shown is that the brain changes after long-term sugar consumption. It’s actually the same as what happens with alcohol and nicotine,” lead author of the study, Queensland University of Technology’s Professor Selena Bartlett, told The Huffington Post Australia.
The study found that changes to the brain’s neurons, caused by long-term consumption of sugar, drove test subjects to seek ever-higher levels of dopamine by consuming even more sugar — the same way an addiction to nicotine or alcohol works.
The researchers also found that in animals, sugar addiction can be treated with a drug used to help people quit smoking. They used an FDA-approved drug, varenicline, to stop sugar addiction in rats.
But while the study showed such a treatment is possible, Professor Bartlett said it’s not necessarily desirable.
“I’m not advocating a direct drug treatment for sugar addiction,” she told HuffPost Australia.
“But it is game-changing, in the sense you can demonstrate that alcohol and nicotine and sugar are changing the brain in exactly the same way.”
The findings could also help us better understand ways to treat sugar addiction and reduce the contribution it makes to Australia’s obesity problem.
In 2014-2015, 63.4 percent of Australian adults were overweight or obese — well over half of our nation’s population. That was an increase from 1995, where 56.3 percent of the population were overweight or obese.
Experts have called for a sugar tax to help arrest rising obesity rates. While Professor Bartlett said a sugar tax could help to create change, it wasn’t the only culprit in rising obesity levels.
“It’s not all sugar. Everything in moderation is fine. It’s things like supersizing, sugar in all sorts of foods, it’s difficult for the brain to reduce consumption because it feels so good. Combined with sedentary behaviour, that’s what’s driving the obesity rate higher,” Professor Bartlett told HuffPost Australia.
“Our studies show only long term, excessive consumption is bad, changes the brain. If you have a teaspoon of sugar in your coffee, you’re not going to get addicted.”
With obesity rates on the rise worldwide and excess sugar consumption considered a direct contributor, the search has been on for treatments to reverse the trend. Now a world-first study led by QUT may have the answer.
Neuroscientist Professor Selena Bartlett from QUT’s Institute of Health and Biomedical Innovation said the study, which has just been published by international research journal PLOS ONE, shows drugs used to treat nicotine addiction could be used to treat sugar addiction in animals.
The publication coincides with another paper by the team — Prolonged Consumption of Sucrose in a Binge-Like Manner, Alters the Morphology of Medium Spiny Neurons in the Nucleus Accumbens Shell — being published in Frontiers in Behavioral Neuroscience. It shows that long chronic sugar intake can cause eating disorders and impact on behaviour.
“The latest World Health Organisation figures tell us 1.9 billion people worldwide are overweight, with 600 million considered obese,” said Professor Bartlett who is based at the Translational Research Institute.
“Excess sugar consumption has been proven to contribute directly to weight gain. It has also been shown to repeatedly elevate dopamine levels which control the brain’s reward and pleasure centres in a way that is similar to many drugs of abuse including tobacco, cocaine and morphine.
“After long-term consumption, this leads to the opposite, a reduction in dopamine levels. This leads to higher consumption of sugar to get the same level of reward.
“We have also found that as well as an increased risk of weight gain, animals that maintain high sugar consumption and binge eating into adulthood may also face neurological and psychiatric consequences affecting mood and motivation.
“Our study found that Food and Drug Administration (FDA) approved drugs like varenicline, a prescription medication trading as Champix which treats nicotine addiction, can work the same way when it comes to sugar cravings.”
PhD researcher Masroor Shariff said the study also put artificial sweeteners under the spotlight.
“Interestingly, our study also found that artificial sweeteners such as saccharin could produce effects similar to those we obtained with table sugar, highlighting the importance of reevaluating our relationship with sweetened food per se,” said Mr Shariff.
Professor Bartlett said varenicline acted as a neuronal nicotinic receptor modulator (nAChR) and similar results were observed with other such drugs including mecamylamine and cytisine.
“Like other drugs of abuse, withdrawal from chronic sucrose exposure can result in an imbalance in dopamine levels and be as difficult as going ‘cold turkey’ from them,” she said.
“Further studies are required but our results do suggest that current FDA-approved nAChR drugs may represent a novel new treatment strategy to tackle the obesity epidemic.”
The full Neuronal Nicotinic Acetylcholine Receptor Modulators Reduce Sugar Intake paper can be read on PLOS ONE.
Could you image a world without sugar? A life without that spectacular sweet taste in your mouth?
Sugar is something that we consume constantly as it is everywhere. Several reports estimate that up to 75% of all foods and beverages contain high amounts of added sugars (Ford and Dietz, 2013; Bray and Popkin, 2014). In fact, excess sugar consumption is implicated as one of the essential and underlying components of the current obesity epidemic, which has now become a worldwide problem.
It is nowadays well established that sugar can exert an extremely powerful impact on the brain reward system, the same system that tells us what we like and what we dislike. Interestingly, sugar may trigger the same dopamine-mediated biological mechanisms that recreational drugs such as cocaine, amphetamines, morphine and nicotine do. Upon an increase in the levels of dopamine, the reward’s mediator, we are confronted with cravings. Moreover, animal studies have clearly shown that long-term consumption of palatable foods can cause changes in the brain reward pathways, which suggests an imbalance in the normal reward processing homeostasis. But how exactly does sugar affect the brain? Here, Dr. Nicole Avena tries giving her answer, suggesting that an overload of sugar spikes dopamine levels and leaves you craving more and more. From this point of view, shared by many neuroscientists, one could legitimately start wondering whether sugar addiction may be treated as any other drug addiction.
A recent study published in PLOS ONE by Shariff and colleagues demonstrates that sugar addiction and nicotine dependency may share some common biochemical substrates. In particular, a common mechanism may take place at the level of the neuronal nicotinic acetylcholine receptors (nAChRs). In fact, the authors of the study observed that Varenicline, a partial agonist of nAChRs able to reduce nicotine cravings and withdrawal symptoms, was also able to efficiently reduce sugar consumption in rats.
Using an intermittent-access two-bottle choice test, Shariff and colleagues report that Varenicline strongly reduced sugar intake, thus breaking down the need for sugar consumption. Indeed, such “therapeutic” effects on sugar craving were also observed when another nAChRs ligand was used, thus suggesting that nicotine and sugar share common pathways. In addition to these pharmacological experiments, the authors of the current study also found that long-term sucrose exposure results in an increase in the expression of nAChR receptor subunits in the nucleus accumbens (NAc), a brain region known to be highly involved in the rewarding properties of addictive substances.
“Excess sugar consumption has been proven to contribute directly to weight gain. It has also been shown to repeatedly elevate dopamine levels which control the brain’s reward and pleasure centers in a way that is similar to many drugs of abuse including tobacco, cocaine and morphine” says Pr. Selena Bartlett, neuroscientist at the Queensland University of Technology (QUT) and senior author of the study. “We have also found” continues Bartlett, “that as well as an increased risk of weight gain, animals that maintain high sugar consumption and binge eating into adulthood may also face neurological and psychiatric consequences affecting mood and motivation.”
Interestingly, the same team has also recently published another report showing the effect of long-term sugar consumption on the morphology of accumbal neurons, also known as medium-sized spiny neurons (MSNs) (Klenowski et al., 2016). Klenowski and colleagues showed that prolonged binge-like sucrose consumption significantly decreased the total dendritic length of MSNs compared to age-matched control rats. In addition, they found that the restructuring of these neurons resulted primarily from reduced distal dendritic complexity.
Conversely, “increased spine densities at the distal branch orders of Nac shell MSNs from long-term sucrose consuming rats” were observed. Altogether, these data strongly suggest that sugar addiction may be able to alter behavioral responses (cravings) as well as to induce specific morphological adaptations.
These observations, combined with studies demonstrating the contribution of excessive sugar intake to changes in reward circuitry and the development of addictive-like behaviors and emotional states in animal models (Avena et al., 2008; Benton, 2010; Ventura et al., 2014), warrant the need for further investigation. Astonishingly, the team of Serge Ahmed has shown that intense sweetness can surpass cocaine reward, even in drug-sensitized and -addicted individuals (Lenoir et al., 2007). Could sugar be the worst legal drug? Could sugar be the most abused drug? These and other studies all strongly point to one simple conclusion: sugar, especially when abused, can be extremely dangerous. Therefore, action in the form of social change, such as taxation of junk food and sugar sweetened beverages (Cornelsen and Carriedo, 2015), as well as educational interventions on nutrition and food consumption, is urgent for the wellbeing of our society.
- Ford, ES., and Dietz, WH (2013). Trends in energy intake among adults in the United States: findings from NHANES. Am. J. Clin. Nutr. 97, 848–853. doi: 10.3945/ajcn.112.052662
- Bray, GA, and Popkin, BM (2014). Dietary sugar and body weight: have we reached a crisis in the epidemic of obesity and diabetes?: health be damned! Pour on the sugar. Diabetes Care 37, 950–956. doi: 10.2337/dc13-2085
- Shariff M, Quik M, Holgate J, Morgan M, Patkar OL, Tam V, Belmer A, Bartlett SE (2016). Neuronal nicotinic acetylcholine receptor modulators reduce sugar intake. PLoS One. 2016 Mar 30;11(3):e0150270. doi: 10.1371/journal.pone.0150270. eCollection 2016.
- Klenowski PM, Shariff MR, Belmer A, Fogarty MJ, Mu EW, Bellingham MC, Bartlett SE (2016). Prolonged Consumption of Sucrose in a Binge-Like Manner, Alters the Morphology of Medium Spiny Neurons in the Nucleus Accumbens Shell. Front Behav Neurosci. 2016 Mar 23;10:54. doi: 10.3389/fnbeh.2016.00054. eCollection 2016.
- Avena, N. M., Rada, P., and Hoebel, B. G. (2008). Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci. Biobehav. Rev. 32, 20–39. doi: 10.1016/j.neubiorev.2007.04.019
- Benton, D. (2010). The plausibility of sugar addiction and its role in obesity and eating disorders. Clin. Nutr. 29, 288–303. doi: 10.1016/j.clnu.2009.12.001
- Ventura, T., Santander, J., Torres, R., and Contreras, A. M. (2014). Neurobiologic basis of craving for carbohydrates. Nutrition 30, 252–256. doi: 10.1016/j.nut.2013.06.010
- Lenoir, M., Serre, F., Cantin, L., and Ahmed, S. H. (2007). Intense sweetness surpasses cocaine reward. PLoS ONE 2:e698. doi: 10.1371/journal.pone.0000698
- Cornelsen, L and Carriedo, A (2015). Health-related taxes on foods and beverages. http://foodresearch.org.uk/wp-content/uploads/2015/06/Food-and-beverages-taxes-final-amended.pdf