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.

An article published this week in the prestigious journal Nature Medicine documents what is believed to be the first evidence that Alzheimer’s disease can be transmitted from person to person.

The finding arose from long-term follow up of patients who received human growth hormone (hGH) that was taken from brain tissue of deceased donors.

Preparations of donated hGH were used in medicine to treat a variety of conditions from 1959 onwards – including in Australia from the mid 60s.

The practice stopped in 1985 when it was discovered around 200 patients worldwide who had received these donations went on to develop Creuztfeldt-Jakob disease (CJD), which causes a rapidly progressive dementia. This is an otherwise extremely rare condition, affecting roughly one person in a million.

What’s CJD got to do with Alzehimer’s?

CJD is caused by prions: infective particles that are neither bacterial or viral, but consist of abnormally folded proteins that can be transmitted from cell to cell.

Other prion diseases include kuru, a dementia seen in New Guinea tribespeople caused by eating human tissue, scrapie (a disease of sheep) and variant CJD or bovine spongiform encephalopathy, otherwise known as mad cow disease. This raised public health concerns over the eating of beef products in the United Kingdom in the 1980s.

Human growth hormone used to come from donated organs

Human growth hormone (hGH) is produced in the brain by the pituitary gland. Treatments were originally prepared from purified human pituitary tissue.

But because the amount of hGH contained in a single gland is extremely small, any single dose given to any one patient could contain material from around 16,000 donated glands.

An average course of hGH treatment lasts around four years, so the chances of receiving contaminated material – even for a very rare condition such as CJD – became quite high for such people.

hGH is now manufactured synthetically in a laboratory, rather than from human tissue. So this particular mode of CJD transmission is no longer a risk.

What are the latest findings about Alzheimer’s disease?

The Nature Medicine paper provides the first evidence that transmission of Alzheimer’s disease can occur via human-to-human transmission.

The authors examined the outcomes of people who received donated hGH until 1985. They found five such recipients had developed early-onset Alzheimer’s disease.

They considered other explanations for the findings but concluded donated hGH was the likely cause.

Given Alzheimer’s disease is a much more common illness than CJD, the authors presume those who received donated hGH before 1985 may be at higher risk of developing Alzheimer’s disease.

Alzheimer’s disease is caused by presence of two abnormally folded proteins: amyloid and tau. There is increasing evidence these proteins spread in the brain in a similar way to prion diseases. So the mode of transmission the authors propose is certainly plausible.

However, given the amyloid protein deposits in the brain at least 20 years before clinical Alzheimer’s disease develops, there is likely to be a considerable time lag before cases that might arise from the receipt of donated hGH become evident.

When was this process used in Australia?

In Australia, donated pituitary material was used from 1967 to 1985 to treat people with short stature and infertility.

More than 2,000 people received such treatment. Four developed CJD, the last case identified in 1991. All four cases were likely linked to a single contaminated batch.

The risks of any other cases of CJD developing now in pituitary material recipients, so long after the occurrence of the last identified case in Australia, are considered to be incredibly small.

Early-onset Alzheimer’s disease (defined as occurring before the age of 65) is uncommon, accounting for around 5% of all cases. Below the age of 50 it’s rare and likely to have a genetic contribution.

The risk is very low – and you can’t ‘catch’ it like a virus

The Nature Medicine paper identified five cases which were diagnosed in people aged 38 to 55. This is more than could be expected by chance, but still very low in comparison to the total number of patients treated worldwide.

Although the long “incubation period” of Alzheimer’s disease may mean more similar cases may be identified in the future, the absolute risk remains very low. The main scientific interest of the article lies in the fact it’s first to demonstrate that Alzheimer’s disease can be transmitted from person to person in a similar way to prion diseases, rather than in any public health risk.

The authors were keen to emphasise, as I will, that Alzheimer’s cannot be contracted via contact with or providing care to people with Alzheimer’s disease.

Steve Macfarlane, Head of Clinical Services, Dementia Support Australia, & Associate Professor of Psychiatry, Monash University

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