Nutritional deficiency in 111 Russian patients with Alzheimer's and Parkinson's disease, and what travelled with it
- A prospective study from Nizhny Novgorod followed 111 patients aged 50 to 89 with neurodegenerative disease, 66 with Alzheimer's disease (59.5%) and 45 with Parkinson's disease (40.5%), at a first visit and again two months later. There was no control group.
- Nutritional deficiency or risk of it was found in 31 patients (28%). In the Alzheimer's group 15 had deficiency (62.5%) and 9 had risk (37.5%); in the Parkinson's group 3 had deficiency (42.9%) and 4 had risk (57.1%).
- Deficiency or risk was associated with dysphagia, oral apraxia, tooth loss and impaired chewing (r = 0.3, p < 0.001), and with depression and affective disturbances (p < 0.05).
- Flagged patients received dietary advice, a conversation with relatives and, where needed, enteral supplements. At two months body mass index had risen in all of them.
This is a two-visit study in Russian neurology patients with no comparison group. The authors screened 111 people with Alzheimer's or Parkinson's disease for nutritional deficiency and corrected it where they found it. The sample has a neurodegenerative diagnosis, not a primary psychiatric one, so depression here is a measured accompanying feature.
Who was flagged, and the findings alongside
Screening used the Mini Nutritional Assessment (MNA) and body mass index, with haemoglobin, albumin, lipids, urea and creatinine as laboratory markers. Anxiety, depression, chewing, swallowing and teeth were also assessed. Thirty-one patients had deficiency or risk. In Alzheimer's disease this was more frequent at moderate to severe dementia, and in Parkinson's disease at a more advanced stage and with more marked motor symptoms (both p < 0.05). Low albumin and haemoglobin and raised creatinine went with deficiency or risk (p < 0.05), as did depression and affective disturbances.
What was done, and what a non-physician can do
Flagged patients got dietary recommendations and a talk with relatives. Supplements were calculated at 30–35 kcal/kg per day, not less than 400 kcal per day, with 1 g of protein/kg per day; patients with dysphagia received a modified-texture diet. After two months body mass index had risen in every treated patient. Without a comparison group the study cannot say what produced that change.
The rest is the author's view, not the authors' position. A psychologist or psychiatrist who sees a person with dementia or Parkinson's disease already sits across from them for an hour. The MNA is a questionnaire that fits into that visit. A look at the teeth, a question about coughing at meals and a note of recent weight loss cost little more. The task stops at noticing and passing on: a short note to the neurologist, the family doctor or a dietitian. Treating the deficiency belongs to them, but without someone noticing it, it may not be raised at all.
In 111 patients with Alzheimer's or Parkinson's disease, nutritional deficiency or risk was found in 31 and went with chewing and swallowing problems and with depression.
One centre, 111 patients, two visits two months apart and no control group. Deficiency or risk was measured alongside depression, so the direction of the link is not known.