It’s a Saturday afternoon at a kids’ birthday party. Hordes of children are swarming between the spread of birthday treats and party games. Half-eaten cupcakes, biscuits and lollies litter the floor, and the kids seem to have gained superhuman speed and bounce-off-the-wall energy. But is sugar to blame?

The belief that eating sugary foods and drinks leads to hyperactivity has steadfastly persisted for decades. And parents have curtailed their children’s intake accordingly.

Balanced nutrition is critical during childhood. As a neuroscientist who has studied the negative effects of high sugar “junk food” diets on brain function, I can confidently say excessive sugar consumption does not have benefits to the young mind. In fact, neuroimaging studies show the brains of children who eat more processed snack foods are smaller in volume, particularly in the frontal cortices, than those of children who eat a more healthful diet.

But today’s scientific evidence does not support the claim sugar makes kids hyperactive.

The hyperactivity myth

Sugar is a rapid source of fuel for the body. The myth of sugar-induced hyperactivity can be traced to a handful of studies conducted in the 1970s and early 1980s. These were focused on the Feingold Diet as a treatment for what we now call Attention Deficit Hyperactivity Disorder (ADHD), a neurodivergent profile where problems with inattention and/or hyperactivity and impulsivity can negatively affect school, work or relationships.

Devised by American paediatric allergist Benjamin Feingold, the diet is extremely restrictive. Artificial colours, sweeteners (including sugar) and flavourings, salicylates including aspirin, and three preservatives (butylated hydroxyanisole, butylated hydroxytoluene, and tert-Butrylhdryquinone) are eliminated.

Salicylates occur naturally in many healthy foods, including apples, berries, tomatoes, broccoli, cucumbers, capsicums, nuts, seeds, spices and some grains. So, as well as eliminating processed foods containing artificial colours, flavours, preservatives and sweeteners, the Feingold diet eliminates many nutritious foods helpful for healthy development.

However, Feingold believed avoiding these ingredients improved focus and behaviour. He conducted some small studies, which he claimed showed a large proportion of hyperactive children responded favourably to his diet.

Flawed by design

The methods used in the studies were flawed, particularly with respect to adequate control groups (who did not restrict foods) and failed to establish a causal link between sugar consumption and hyperactive behaviour.

Subsequent studies suggested less than 2% responded to restrictions rather than Feingold’s claimed 75%. But the idea still took hold in the public consciousness and was perpetuated by anecdotal experiences.

Fast forward to the present day. The scientific landscape looks vastly different. Rigorous research conducted by experts has consistently failed to find a connection between sugar and hyperactivity. Numerous placebo-controlled studies have demonstrated sugar does not significantly impact children’s behaviour or attention span.

One landmark meta-analysis study, published almost 20 years ago, compared the effects of sugar versus a placebo on children’s behaviour across multiple studies. The results were clear: in the vast majority of studies, sugar consumption did not lead to increased hyperactivity or disruptive behaviour.

Subsequent research has reinforced these findings, providing further evidence sugar does not cause hyperactivity in children, even in those diagnosed with ADHD.

While Feingold’s original claims were overstated, a small proportion of children do experience allergies to artificial food flavourings and dyes.

Pre-school aged children may be more sensitive to food additives than older children. This is potentially due to their smaller body size, or their still-developing brain and body.

Hooked on dopamine?

Although the link between sugar and hyperactivity is murky at best, there is a proven link between the neurotransmitter dopamine and increased activity.

The brain releases dopamine when a reward is encountered – such as an unexpected sweet treat. A surge of dopamine also invigorates movement – we see this increased activity after taking psychostimulant drugs like amphetamine. The excited behaviour of children towards sugary foods may be attributed to a burst of dopamine released in expectation of a reward, although the level of dopamine release is much less than that of a psychostimulant drug.

Dopamine function is also critically linked to ADHD, which is thought to be due to diminished dopamine receptor function in the brain. Some ADHD treatments such as methylphenidate (labelled Ritalin or Concerta) and lisdexamfetamine (sold as Vyvanse) are also psychostimulants. But in the ADHD brain the increased dopamine from these drugs recalibrates brain function to aid focus and behavioural control.

Why does the myth persist?

The complex interplay between diet, behaviour and societal beliefs endures. Expecting sugar to change your child’s behaviour can influence how you interpret what you see. In a study where parents were told their child had either received a sugary drink, or a placebo drink (with a non-sugar sweetener), those parents who expected their child to be hyperactive after having sugar perceived this effect, even when they’d only had the sugar-free placebo.

The allure of a simple explanation – blaming sugar for hyperactivity – can also be appealing in a world filled with many choices and conflicting voices.

Healthy foods, healthy brains

Sugar itself may not make your child hyperactive, but it can affect your child’s mental and physical health. Rather than demonising sugar, we should encourage moderation and balanced nutrition, teaching children healthy eating habits and fostering a positive relationship with food.

In both children and adults, the World Health Organization (WHO) recommends limiting free sugar consumption to less than 10% of energy intake, and a reduction to 5% for further health benefits. Free sugars include sugars added to foods during manufacturing, and naturally present sugars in honey, syrups, fruit juices and fruit juice concentrates.

Treating sugary foods as rewards can result in them becoming highly valued by children. Non-sugar rewards also have this effect, so it’s a good idea to use stickers, toys or a fun activity as incentives for positive behaviour instead.

While sugar may provide a temporary energy boost, it does not turn children into hyperactive whirlwinds.

Amy Reichelt, Senior Lecturer (Adjunct), Nutritional neuroscientist, University of Adelaide

This article is republished from The Conversation under a Creative Commons license. Read the original article.

As many of us hit the gym or go for a run to recover from the silly season, you might notice a bit of extra muscle soreness.

This is especially true if it has been a while between workouts.

A common misunderstanding is that such soreness is due to lactic acid build-up in the muscles.

Research, however, shows lactic acid has nothing to do with it. The truth is far more interesting, but also a bit more complex.

It’s not lactic acid

We’ve known for decades that lactic acid has nothing to do with muscle soreness after exercise.

In fact, as one of us (Robert Andrew Robergs) has long argued, cells produce lactate, not lactic acid. This process actually opposes not causes the build-up of acid in the muscles and bloodstream.

Unfortunately, historical inertia means people still use the term “lactic acid” in relation to exercise.

Lactate doesn’t cause major problems for the muscles you use when you exercise. You’d probably be worse off without it due to other benefits to your working muscles.

Lactate isn’t the reason you’re sore a few days after upping your weights or exercising after a long break.

So, if it’s not lactic acid and it’s not lactate, what is causing all that muscle soreness?

Muscle pain during and after exercise

When you exercise, a lot of chemical reactions occur in your muscle cells. All these chemical reactions accumulate products and by-products which cause water to enter into the cells.

That causes the pressure inside and between muscle cells to increase.

This pressure, combined with the movement of molecules from the muscle cells can stimulate nerve endings and cause discomfort during exercise.

The pain and discomfort you sometimes feel hours to days after an unfamiliar type or amount of exercise has a different list of causes.

If you exercise beyond your usual level or routine, you can cause microscopic damage to your muscles and their connections to tendons.

Such damage causes the release of ions and other molecules from the muscles, causing localised swelling and stimulation of nerve endings.

This is sometimes known as “delayed onset muscle soreness” or DOMS.

While the damage occurs during the exercise, the resulting response to the injury builds over the next one to two days (longer if the damage is severe). This can sometimes cause pain and difficulty with normal movement.

The upshot

Research is clear; the discomfort from delayed onset muscle soreness has nothing to do with lactate or lactic acid.

The good news, though, is that your muscles adapt rapidly to the activity that would initially cause delayed onset muscle soreness.

So, assuming you don’t wait too long (more than roughly two weeks) before being active again, the next time you do the same activity there will be much less damage and discomfort.

If you have an exercise goal (such as doing a particular hike or completing a half-marathon), ensure it is realistic and that you can work up to it by training over several months.

Such training will gradually build the muscle adaptations necessary to prevent delayed onset muscle soreness. And being less wrecked by exercise makes it more enjoyable and more easy to stick to a routine or habit.

Finally, remove “lactic acid” from your exercise vocabulary. Its supposed role in muscle soreness is a myth that’s hung around far too long already.

Robert Andrew Robergs, Associate Professor – Exercise Physiology, Queensland University of Technology and Samuel L. Torrens, PhD Candidate, Queensland University of Technology

This article is republished from The Conversation under a Creative Commons license. Read the original article.