What is the causal relationship between food additives sugar consumption and adhd

Most of the evidence for a genetic inheritance model of causality comes from role in ADHD include food additives, sugar ingestion, and maternal use of alcohol Similarly, results assessing the relationship between sugar consumption and. Preliminary research suggests that the link between maternal smoking and ADHD health benefit of reducing maternal nicotine and alcohol use during pregnancy. There are persistent assertions that dietary sugar, food additives, and/ or If there is any causal relationship between diet and ADHD, the contribution of. Unfortunately, the causal pathways of ADHD are largely unknown; ADHD is a for the effect of food additives elimination (concurrently providing a food or elimination of one specific food or food component (e.g. sugar or AFC), .. 74] of five studies, and noted an important difference in a third study [71].

All relevant data are within the paper and its Supporting Information files. The underlying causes include both genetic and environmental factors and may differ between individuals. The efficacy of diet treatments in ADHD was recently evaluated in three reviews, reporting divergent and confusing conclusions based on heterogeneous studies and subjects. To address this inconsistency we conducted a systematic review of meta-analyses of double-blind placebo-controlled trials evaluating the effect of diet interventions elimination and supplementation on ADHD.

Methods Our literature search resulted in 14 meta-analyses, six of which confined to double-blind placebo-controlled trials applying homogeneous diet interventions, i. I2 was calculated to assess heterogeneity if necessary and additional random effects subgroup meta-regression was conducted if substantial heterogeneity was present.

Further FFD research should focus on establishing the underlying mechanisms of food e. Children with ADHD are at risk for impaired academic performance [ 2 ], social isolation and peer problems [ 3 ], substance abuse [ 4 ], aggressive behavior and delinquency [ 56 ]. Recent research has shown that suffering from ADHD may result in decreased life expectancy with more than double the risk of premature death from unnatural causes, like accidents, compared to people without ADHD [ 11 ].

In sum, ADHD seriously affects the quality of life of child, parents and siblings [ 38 ], incurs high economic costs [ 1213 ] and is a long-term burden on families and society [ 14 ]. Psychostimulants are first-choice pharmacological treatment [ 15 ] and have shown beneficial short-term efficacy, i.

However, children taking psychostimulants may still meet the ADHD-criteria [ 22 ] and complete normalization of behavior is rare [ 23 — 25 ]. Furthermore, medication non-adherence occurs frequently [ 2627 ]: Apart from common side effects like sleep and appetite problems [ 1417 ], medication may also affect growth and long-term bone health [ 31 ].

Finally, drug treatment does not attenuate the increased risk for school dropout and unemployment [ 6 ]. In sum, better treatments preferentially aimed at prevention of ADHD in young children [ 22 ] and at targeting the underlying causes are welcome [ 14 ].

Attention-Deficit/Hyperactivity Disorder: Is it Time to Reappraise the Role of Sugar Consumption?

Apart from the involvement of many genes with a small effect [ 33 ], multiple pre- peri- and postnatal environmental factors may be risk factors for ADHD [ 3435 ]. One of these conditions, though controversial [ 35 ], is diet [ 39 — 42 ]. The Feingold studies were followed by other elimination diet studies [ 45 ], investigating the effects of either artificial food color AFC elimination or of a diet eliminating many foods and additives, i.

The main aim of reviews is to summarize the evidence on a specific topic, of which both researchers and clinicians may benefit [ 47 ].

However, the three reviews show divergent conclusions, i. This divergence in conclusions might be explained by the fact that in previous reviews the results of uncontrolled and un-blinded studies [ 40 ], of studies amalgamating different types of diet interventions [ 40 — 42 ] and of meta-analyses not specifically aimed at children with ADHD or hyperactive behavior [ 4142 ] were included. The importance of identifying agents that contribute to obesity There is an abundance of research related to obesity etiology and prevention in regard to decreasing caloric intake and increasing energy expenditure.

Agents in our food supply have immense potential to affect metabolism due to continuous exposure and potential interactions among multiple compounds. It is critical that we identify these obesogens in our food supply in order to facilitate obesity prevention and treatment [ 34 ]. Unfortunately, many of the obesogenic compounds in our food supply were added deliberately to enhance production instead of being added to enhance nutrition.

Attention-Deficit/Hyperactivity Disorder: Is it Time to Reappraise the Role of Sugar Consumption?

For example, pesticides are added to ward off insects during farming; BPA is a strong, clear plastic that has ideal properties for making bottles and coating cans; and mono- and diglycerides are added to emulsify the fat and water in foods to achieve a favorable texture. Simple exclusion of these compounds may not be possible until alternatives are developed, but then these novel compounds must be tested. Like pharmaceuticals, thorough testing is time-consuming and expensive.

Obesogen identification and characterization is in its infancy, and much of the scientific evidence supporting the relationship between synthetic compounds and the obesity epidemic is currently weak.

Strong, evidence-based scientific support is derived from randomized, controlled trials, ideally cross-over design, that comprise four steps: However, the bulk of evidence relating environmental contaminants and obesity is derived from epidemiological studies which are correlational by nature. While correlations are important, they are limited in that conclusions about causal relationships are impossible.

Well-designed animal studies provide strong evidence within the animal model, but must be confirmed in humans. Cell studies are important for deriving mechanisms that may link certain compounds to obesity, yet provide only weak evidence for the global phenomenon the obesity epidemic. It is important to note that in evaluating foods for their contribution to obesity, we may identify ingredients that prevent obesity.

Also, anthocyanins potent color compounds from grapes, purple corn, blueberries, and other plants may reduce oxidative stress, prevent obesity, and help control diabetes in cell culture, animal models, and humans [ 57 ]. Again, not all compounds in a class are equal; for example, although the hydrocolloid guar gum may prevent obesity mentioned aboveanother hydrocolloid called carrageenan, found commonly in chocolate milk and ice cream, may contribute to insulin resistance in mice [ 58 ].

What in our food is making us fat? There are many aspects of the average Western diet that may promote obesity.