Currently there are around 700,000 people in the UK with dementia and it is believed that these figures are set to rise to one million in the next 10 years because of the ageing population. The National Institute of Health and Clinical Excellence (NICE) guidance is that people with dementia should only be offered antipsychotic drugs if they are severely distressed or there is an immediate risk of harm to the person or others. However the use of sedatives in dementia has repeatedly been condemned due to the increasing evidence that the use of such drugs in dementia patients significantly increases their risk of death. One such study published earlier this year followed 165 patients with Alzheimer’s disease living in care homes in Oxfordshire, Tyneside, London and Edinburgh. Patients who were already taking anti-psychotics either continued on their treatment, or given a dummy pill for a year and then followed up over a period of three years. After two years, 46% of patients who had been treated with anti-psychotics were alive compared with 71% on the placebo. Three years after the start of the study, fewer than a third of people on anti-psychotics were alive compared to nearly two-thirds taking the placebo (Ballard et al, 2009). A recent review ordered by the Department of Health outlines the over prescription of antipsychotic drugs to treat aggression and agitation in people with dementia and contrary to NICE guidance. The review authored by Professor S. Banerjee goes as far as suggesting that up to two thirds of those individuals with dementia receiving anti-psychotic drugs are prescribed them unnecessarily.
So why is it that pharmaceutical drugs, with such well documented findings in terms of their negative health effects, continue to be prescribed? It certainly appears that they are offered as a ‘quick fix’ regardless of the long term consequences. Originally discovered in the 1950s, anti-psychotics were found to block receptors in the dopamine pathway and used quite successfully in the treatment of schizophrenia and bi-polar disorder before being introduced as treatment for dementia where their actions serve as nothing other than “chemical restraints”. It seems shameful that pharmaceutical companies can benefit in such situations whilst nutraceutical companies struggle to get clearance for health claims from the Medicines and Healthcare products Regulatory Agency (MHRA). This government agency is responsible for ensuring that medicines and medical devices work and are acceptably safe, and consistently rejects claims for many well-known safe and commonly used nutritional products.
The benefits of fish oil and the role of long-chain fatty acids in brain chemistry and in dementia are generally accepted but not endorsed. Ironically the side effects of consuming fish oils include only relatively minor complications (gastrointestinal upset, nausea, headaches) when compared with the potentially very serious sides effects of some pharmaceutical products. Given that long-chain fatty acids are involved in the dopamine pathway influencing dopamine concentration, number of vesicles and D2 receptors, and have been beneficial in studies where the dopamine pathway is known to be involved such as schizophrenia and attention deficit hyperactivity disorder (ADHD), would it not be prudent to suggest a role of fatty acids as a regular or add-on treatment in individuals with dementia? The recent positive findings of the role of eicosapentaenoic acid EPA in reducing cerebral atrophy in Huntington’s disease is certainly indicative that non-pharmaceutical products need to be investigated and that their role in dementia, not only in the treatment but in the prevention of the condition, is sadly underrated at the expense of the patient.
Ballard C, Hanney ML, Theodoulou M, Douglas S, McShane R, Kossakowski K, Gill R, Juszczak E, Yu LM, Jacoby R; DART-AD investigators. (2009) The dementia antipsychotic withdrawal trial (DART-AD): long-term follow-up of a randomised placebo-controlled trial. Lancet Neurol. 2009 8:151-7.
Puri BK, Bydder GM, Manku MS, Clarke A, Waldman AD, Beckmann CF. (2008) Reduction in cerebral atrophy associated with ethyl-eicosapentaenoic acid treatment in patients with Huntington’s disease. J Int Med Res. 36:896-905