Background Brain energy metabolism is impaired in Alzheimer’s disease (AD), which may be mitigated by a ketogenic diet. We conducted a randomized crossover trial to determine whether a 12-week modified ketogenic diet improved cognition, daily function, or quality of life in a hospital clinic of AD patients. Methods We randomly assigned patients with clinically confirmed diagnoses of AD to a modified ketogenic diet or usual diet supplemented with low-fat healthy-eating guidelines and enrolled them in a single-phase, assessor-blinded, two-period crossover trial (two 12-week treatment periods, separated by a 10-week washout period). Primary outcomes were mean within-individual changes in the Addenbrookes Cognitive Examination - III (ACE-III) scale, AD Cooperative Study - Activities of Daily Living (ADCS-ADL) inventory, and Quality of Life in AD (QOL-AD) questionnaire over 12 weeks. Secondary outcomes considered changes in cardiovascular risk factors and adverse effects. Results We randomized 26 patients, of whom 21 (81%) completed the ketogenic diet; only one withdrawal was attributed to the ketogenic diet. While on the ketogenic diet, patients achieved sustained physiological ketosis (12-week mean beta-hydroxybutyrate level: 0.95 ± 0.34 mmol/L). Compared with usual diet, patients on the ketogenic diet increased their mean within-individual ADCS-ADL (+ 3.13 ± 5.01 points, P = 0.0067) and QOL-AD (+ 3.37 ± 6.86 points, P = 0.023) scores; the ACE-III also increased, but not significantly (+ 2.12 ± 8.70 points, P = 0.24). Changes in cardiovascular risk factors were mostly favourable, and adverse effects were mild. Conclusions This is the first randomized trial to investigate the impact of a ketogenic diet in patients with uniform diagnoses of AD. High rates of retention, adherence, and safety appear to be achievable in applying a 12-week modified ketogenic diet to AD patients. Compared with a usual diet supplemented with low-fat healthy-eating guidelines, patients on the ketogenic diet improved in daily function and quality of life, two factors of great importance to people living with dementia. Trial registration This trial is registered on the Australia New Zealand Clinical Trials Registry, number ACTRN12618001450202. The trial was registered on August 28, 2018.
There is considerable evidence that pro-cholinergic agents can cause depressed mood. However, there are also published case reports of a rare association between cholinesterase inhibitors and mood elevation in patients with pre-existing major functional psychiatric disorders, or organic disorders other than dementia. This report adds to the literature by describing a case of mood elevation in a patient without pre-existing psychiatric disorder.
A wider POA and non-POA services mapping is required to determine the level of services for clinical populations that have high and complex clinical needs. DHB funders should review the expected population growth in people aged 65+ and consider increasing the funding for these under-served clinical populations.
Objective: To investigate the changes in publicly funded memory clinics in New Zealand’s since the last survey in 2008. Method: We conducted an online survey of the 20 District Health Boards (DHBs) and gathered information on the recently discontinued or established memory clinics. Results: We found dedicated memory clinics in the seven DHBs that have the largest older persons populations in New Zealand. Those DHBs that had discontinued their memory clinics did so because they opted for a more integrated approach using their primary care based dementia care pathway. Increased waiting times, low staffing ratios, variance in cognitive screening tests and patient demographics were reported. Conclusions: There is significant variability in the structure of memory clinics in New Zealand. These clinics could benefit from collaboration and bench-marking of their services.
Objective The primary objective was to survey the Psychiatry of Old Age (POA) service resources in New Zealand: number of psychiatrists, inpatient beds, and community psychogeriatric beds. A secondary objective was to compare the POA service resources reported by frontline clinicians with official government data. Methods The New Zealand Branch of Faculty of POA collected information from a POA representative in each of the 20 districts, along with official government data. Results Information from 17 services were obtained. POA service resources varied greatly between districts. There were discrepancies between the New Zealand Branch of Faculty of POA and official government data. The number of old age psychiatrist FTEs per 10,000 older adults ranged from 0.3 to 1.1 (mean = 0.7). The number of inpatient beds per 10,000 older adults ranged from 0.0 to 4.1 (mean = 1.6); and the number of psychogeriatric beds per 10,000 older adults ranged from 0.0 to 22.7 (mean = 12.6). Conclusions There is an urgent need to address the official government data discrepancies and POA service resource inequalities. This can ensure the “postcode” system that determines psychiatric care for older adults can be effectively eliminated. We also found the number of POA inpatient beds is below the internationally recommended level.
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