Oh, yeah. There are skeptics. Just watch the video clip of Dr. Bredesen visiting Dr. Oz on his show. Or talk with just about every family doctor or cardiologist my mom ever saw. And, in my mom's case, they might have been right - it was almost certainly too late and she wasn't willing to adopt big changes. Heck, I still have ups and downs and doubts about whether the program, which might help some others, will help me. And I think it is good to be skeptical....as long as we are open to new ideas and new data. Also, there is what Dr. Bredesen says about it: "It's not alternative medicine, it's NO alternative medicine".
Having said that, there certainly is good evidence that:
(1) some cases of dementia are triggered by toxins, infections, stress, diabetes, etc. And it is just logical that fixing the underlying problem would help.
(2) healthy lifestyles can help prevent dementia, or slow it down, or delay it's development. And many of these interventions fall under the category of "just being generally healthy" - they help prevent diabetes, CVD, cancer, depression, etc.
Here is one example I sometimes re-read when I have doubts. It is one of those large clinical trials looking at different types of lifestyle changes, including dietary changes. And it sure seems to have helped this population of E4s, which is very encouraging. See bolded part at the bottom.
Effect of the Apolipoprotein E Genotype on Cognitive Change During a Multidomain Lifestyle Intervention: A Subgroup Analysis of a Randomized Clinical Trial
Alina Solomon, Heidi Turunen, Tiia Ngandu, Markku Peltonen, Esko Levälahti, Seppo Helisalmi, Riitta Antikainen, Lars Bäckman, Tuomo Hänninen, Antti Jula and 10 others
IMPORTANCE: The role of the apolipoprotein E (APOE) ε4 allele as an effect modifier in lifestyle interventions to prevent cognitive impairment is still unclear. OBJECTIVE: To examine whether the APOE ε4 allele modifies the previously reported significant cognitive benefits of a multidomain lifestyle intervention (prespecified subgroup analysis). DESIGN, SETTING, AND PARTICIPANTS: The Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) was a randomized clinical trial in 6 centers across Finland (screening and randomization performed from September 7, 2009, through November 24, 2011; intervention duration, 2 years). Data analysis was performed from August 1, 2015, to March 31, 2016. The study population was at-risk older individuals from the general population. Inclusion criteria were age of 60 to 77 years; Cardiovascular Risk Factors, Aging, and Dementia risk score of at least 6 points; and cognition at a mean level or slightly lower than expected for age. Individuals with dementia or substantial cognitive impairment and conditions that prevented cooperation or safe engagement in the intervention were excluded. APOE genotype data were available for 1175 of the 1260 participants. INTERVENTIONS: Participants were randomly assigned in a 1:1 ratio to a multidomain intervention group (diet, exercise, cognitive training, and vascular risk management) or a control group (general health advice). Group allocation was not actively disclosed to participants, and outcome assessors were masked to group allocation. MAIN OUTCOMES AND MEASURES: Primary outcome was change in cognition measured through a comprehensive neuropsychological test battery. Analysis was based on modified intention to treat (participants with at least 1 postbaseline assessment). RESULTS: A total of 1109 participants (mean [SD] age, 69.3 [4.7] years; 514 [46.3%] female) were included in the analysis: 362 APOE ε4 allele carriers (173 intervention and 189 control) and 747 noncarriers (380 intervention and 367 control). The APOE ε4 carriers and noncarriers were not significantly different at baseline (except for serum cholesterol level). The difference between the intervention and control groups in annual neuropsychological test battery total score change was 0.037 (95% CI, 0.001 to 0.073) among carriers and 0.014 (95% CI, −0.011 to 0.039) among noncarriers. Intervention effect was not significantly different between carriers and noncarriers (0.023; 95% CI, −0.021 to 0.067). CONCLUSIONS AND RELEVANCE: Healthy lifestyle changes may be beneficial for cognition in older at-risk individuals even in the presence of APOE-related genetic susceptibility to dementia. Whether such benefits are more pronounced in APOE ε4 carriers compared with noncarriers should be further investigated. The findings also emphasize the importance of early prevention strategies that target multiple modifiable risk factors simultaneously. TRIAL
Four relatives with AD. Concerned, but hopeful. Introverted, but will talk about science.