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68/100

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Treatments

Topic: Risk, prevention and care in population studies

Objective To compare the effects of a 4-week high-saturated fat/high-glycemic index (HIGH) diet with a low-saturated fat/low-glycemic index (LOW) diet on insulin and lipid metabolism, cerebrospinal fluid (CSF) markers of Alzheimer disease, and cognition for healthy adults and adults with amnestic mild cognitive impairment (aMCI). Design Randomized controlled trial. Setting Veterans Affairs Medical Center clinical research unit. Participants Forty-nine older adults (20 healthy adults with a mean [SD] age of 69.3 [7.4] years and 29 adults with aMCI with a mean [SD] age of 67.6 [6.8] years). Intervention Participants received the HIGH diet (fat, 45% [saturated fat, > 25%]; carbohydrates, 35%-40% [glycemic index, > 70]; and protein, 15%-20%) or the LOW diet (fat, 25%; [saturated fat, Main outcome measures The CSF concentrations of β-amyloid (Aβ42 and Aβ40), tau protein, insulin, F2-isoprostanes, and apolipoprotein E, plasma lipids and insulin, and measures of cognition. Results For the aMCI group, the LOW diet increased CSF Aβ42 concentrations, contrary to the pathologic pattern of lowered CSF Aβ42 typically observed in Alzheimer disease. The LOW diet had the opposite effect for healthy adults, ie, decreasing CSF Aβ42, whereas the HIGH diet increased CSF Aβ42. The CSF apolipoprotein E concentration was increased by the LOW diet and decreased by the HIGH diet for both groups. For the aMCI group, the CSF insulin concentration increased with the LOW diet, but the HIGH diet lowered the CSF insulin concentration for healthy adults. The HIGH diet increased and the LOW diet decreased plasma lipids, insulin, and CSF F2-isoprostane concentrations. Delayed visual memory improved for both groups after completion of 4 weeks of the LOW diet. Conclusion Our results suggest that diet may be a powerful environmental factor that modulates Alzheimer disease risk through its effects on central nervous system concentrations of Aβ42, lipoproteins, oxidative stress, and insulin.

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APA 7th

Bayer-Carter, J. L., Green, P. S., Montine, T. J., VanFossen, B., Baker, L. D., Watson, G. S., et al. (2011). Diet intervention and cerebrospinal fluid biomarkers in amnestic mild cognitive impairment. Archives of neurology. https://doi.org/10.1001/archneurol.2011.125

Vancouver

Bayer-Carter JL, Green PS, Montine TJ, VanFossen B, Baker LD, Watson GS, et al. Diet intervention and cerebrospinal fluid biomarkers in amnestic mild cognitive impairment. Archives of neurology. 2011. doi:10.1001/archneurol.2011.125. PMID: 21670398.

BibTeX

@article{bayercarter2011-21670398,
  author  = {Bayer-Carter, J. L. and Green, P. S. and Montine, T. J. and VanFossen, B. and Baker, L. D. and Watson, G. S. and Bonner, L. M. and Callaghan, M. and others},
  title   = {{Diet intervention and cerebrospinal fluid biomarkers in amnestic mild cognitive impairment}},
  journal = {Archives of neurology},
  year    = {2011},
  doi     = {10.1001/archneurol.2011.125},
  pmid    = {21670398},
  url     = {https://doi.org/10.1001/archneurol.2011.125}
}

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Key findings

Results For the aMCI group, the LOW diet increased CSF Aβ42 concentrations, contrary to the pathologic pattern of lowered CSF Aβ42 typically observed in Alzheimer disease.
Conclusion Our results suggest that diet may be a powerful environmental factor that modulates Alzheimer disease risk through its effects on central nervous system concentrations of Aβ42, lipoproteins, oxidative stress, and insulin.

Why it matters

In people with amnestic mild cognitive impairment, a 4-week low-saturated-fat/low-glycemic-index diet raised levels of a cerebrospinal fluid Alzheimer marker in the direction opposite to the pattern usually seen in the disease. The authors suggest diet may influence Alzheimer risk through effects on these central nervous system markers, but this was a short 4-week study of 49 people and does not show whether diet changes dementia outcomes.

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Study details

Study designrandomized controlled trial
Participants29
Evidence strengthHigh

How this study scored 68/100

Published in a peer-reviewed journal, and it is a randomized controlled trial. Scored zero for effect reported because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Archives of neurology)
Journal's citation record	3 / 4	Archives of Neurology: journal h-index 353 (OpenAlex, 2026-10-29)
Study design	11 / 12	A randomized controlled trial
Strength of evidence	5 / 5	Rated “high” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2011 — within 20 year(s) of the newest study here
Sample size	1 / 4	29 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomized / blinded	1 / 2	Randomized (as stated in the record)
Times cited	5 / 7	Cited 154 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	9.1 citations a year over 17 year(s) since 2011
Impact for its field and year	4 / 6	Cited 9.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 13 other studies in this library
Still being cited	1 / 4	Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Suzanne Craft: h-index 103 (OpenAlex, whole career)
Institution's track record	3 / 3	University of Washington: institution h-index 3,540 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 3 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 21670398)
Free to read	0 / 2	Behind a paywall — scores zero
Total	68 / 100	—

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