Countering demand for ineffective health remedies: Do consumers respond to risks, lack of benefits, or both?

OBJECTIVE: We tested whether targeting the illusion of causality and/or misperceptions about health risks had the potential to reduce consumer demand for an ineffective health remedy (multivitamin supplements). DESIGN: We adopted a 2 (contingency information: no/yes) × 2 (fear appeal: no/yes) factorial design, with willingness-to-pay as the dependent variable. The contingency information specified, in table format, the number of people reporting a benefit vs. no benefit from both multivitamins and placebo, plus a causal explanation for lack of efficacy over placebo. The fear appeal involved a summary of clinical-trial results that indicated multivitamins can cause health harms. The control condition received only irrelevant information. MAIN OUTCOME MEASURE: Experimental auctions measured people's willingness-to-pay for multivitamins. Experiment 1 (N = 260) elicited hypothetical willingness-to-pay online. Experiment 2 (N = 207) elicited incentivised willingness-to-pay in the laboratory. RESULTS: Compared to a control group, we found independent effects of contingency information (-22%) and the fear appeal (-32%) on willingness-to-pay. The combination of both interventions had the greatest impact (-50%) on willingness-to-pay. CONCLUSION: We found evidence that consumer choices are influenced by both perceptions of efficacy and risk. The combination of both elements can provide additive effects that appear superior to either approach alone.

Reducing demand for ineffective health remedies: overcoming the illusion of causality.

OBJECTIVE: We tested a novel intervention for reducing demand for ineffective health remedies. The intervention aimed to empower participants to overcome the illusion of causality, which otherwise drives erroneous perceptions regarding remedy efficacy. DESIGN: A laboratory experiment adopted a between-participants design with six conditions that varied the amount of information available to participants (N = 245). The control condition received a basic refutation of multivitamin efficacy, whereas the principal intervention condition received a full contingency table specifying the number of people reporting a benefit vs. no benefit from both the product and placebo, plus an alternate causal explanation for inefficacy over placebo. MAIN OUTCOME MEASURES: We measured participants' willingness to pay (WTP) for multivitamin products using two incentivized experimental auctions. General attitudes towards health supplements were assessed as a moderator of WTP. We tested generalisation using ratings of the importance of clinical-trial results for making future health purchases. RESULTS: Our principal intervention significantly reduced participants' WTP for multivitamins (by 23%) and increased their recognition of the importance of clinical-trial results. CONCLUSION: We found evidence that communicating a simplified full-contingency table and an alternate causal explanation may help reduce demand for ineffective health remedies by countering the illusion of causality.

Efficiency of long-term tetrahydrobiopterin monotherapy in phenylketonuria.

Phenylketonuria, an inborn error of phenylalanine metabolism, occurs with a frequency of about 1 in 10,000 births and is treated with a strict dietary regimen. Recently, some patients with PKU have been found to show increased tolerance towards phenylalanine intake while receiving tetrahydrobiopterin (BH(4)) supplementation. We have treated two infants with BH(4)-responsive PKU with BH(4) for more than 2 years. No additional dietary control was required to maintain blood phenylalanine concentrations in the desired range. Both children have shown normal development. Generally, our results suggest that BH(4) treatment might be an option for some patients with mild PKU, as it frees them from dietary restrictions and thus improves their quality of life.

A hypothesis on the biochemical mechanism of BH(4)-responsiveness in phenylalanine hydroxylase deficiency.

We describe six children with tetrahydrobiopterin (BH(4)) responsive phenylalanine hydroxylase (PAH) deficiency. All patients carry two mutant alleles in the PAH gene. Cofactor deficiency was excluded. The effect of BH(4) administration was studied by correlating different oral BH(4) doses with plasma phenylalanine levels under defined protein intake. Our results indicate that oral BH(4) supplementation may be used as long-term treatment for individuals with BH(4)-responsive PAH deficiency, either without or in combination with a less restrictive diet. Previous in vitro studies have demonstrated that BH(4) inhibits PAH tetramers but activates PAH dimers. This may indicate, that BH(4)-responsiveness results from BH(4) induced stabilization of mutant PAH dimers. In addition, interindividual differences in the cellular folding apparatus may determine the tertiary structure and the amount of mutant PAH dimers and hence may account for divergent BH(4)-responsiveness reported for the same PAH genotype.

Deficits in selective and sustained attention processes in early treated children with phenylketonuria--result of impaired frontal lobe functions?

UNLABELLED: Twenty normally intelligent children with early treated phenylketonuria (PKU) (IQ: mean = 101.4, SD = 10.0; age: mean = 10 years 11 months, SD = 1.3 years) and 20 healthy controls, matched for age, sex and IQ, were assessed for their selective (Stroop Task) and sustained attention (Test-d-2). Using positron emission tomography an activation of the frontal lobe during the Stroop task had previously been demonstrated. In addition to the Stroop Task and the Test-d-2, a short-term memory test as a "non-frontal-lobe-function-task" was administered to all subjects. Group comparisons demonstrated that PKU children had specific deficits in selective and sustained attention, which were significantly correlated with the concurrent serum phenylalanine concentration. CONCLUSION: The results give evidence that even dietary treated children with PKU were suffering from impaired attentional control mechanisms in spite of a normal IQ. The deficits might be the result of impaired frontal lobe functions.

Glycogen storage disease type I and III and pyruvate carboxylase deficiency: results of long-term treatment with uncooked cornstarch.

Three patients with glycogen storage disease type I (GSD-I), three with glycogen storage disease type III (GSD-III) and one with pyruvate carboxylase deficiency (PCD) could be successfully switched over from continuous nocturnal gastric drip feeding (GDF) to nocturnal feeding with uncooked cornstarch in yoghurt or "quark" (CSF) at the age of 4-20 years. The new kind of therapy is much more convenient for the patients. When followed up to 30 months, patients on CSF showed the same clinical and laboratory findings as during the last two years with GDF. CSF was not introduced to three patients with GSD-I. Two of them refused the permanent starch-yoghurt meals. In the third patient the morning blood glucose concentrations were too variable.

Glycogen storage disease type I. Results of treatment with frequent daytime feeding, combined with nocturnal intragastric feeding and with administration of an alpha-glucosidase inhibitor.

Seven patients with glycogen disease type I have been treated with nocturnal intragastric feeding combined with frequent daytime feeding. Follow-up shows a striking improvement in their clinical condition including growth rate. Determination of biochemical parameters reveals a significant increase in mean blood glucose levels and a significant decrease of lactate, pyruvate, alanine, uric acid, triglycerides, and SGOT in blood. Additional administration of an alpha-glucosidase inhibitor in four patients caused a significant increase in blood lactate despite unchanged blood glucose levels.