04 Mar Exercise to reverse dementia
Published just a few days ago in the Journal Current Alzheimer Research is an excellent study out of the Division of Behavioral Neurology, Department of Neurology, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Taiwan. Living a sedentary lifestyle with trivial or no exercise at all is a significant preventable risk factor for cognitive decline and Alzheimer’s dementia.
Previous studies examined the role of aerobic exercise such as brisk walking, cycling, swimming and other activities that increase heart rate for at least 30-50 minutes in reducing the risk of cognitive decline as adults age, but resistance or strength training has not been studied as much. In this study, CL Tsai et al recruited 55 patients with mild cognitive impairment and randomized them to Aerobic Exercise (AE) or Resistance Exercise (RE) and measured cognitive performance, trophic factors that increase growth of neurons and their connections (good), and inflammatory cytokines that cause loss of neurons and connections (bad).
Importantly, BOTH groups showed improved cognitive performance (memory) but the mechanism of biological action were different between the two groups. The principle mechanism of action in the AE group was a significant increase in brain derived neurotrophic factor (BDNF, helpful biomarkers) and a decrease in levels of insulin, TNF-α, and IL- 15 (harmful biomarkers). In the RE group, improvement was also documented but the mechanism was entirely different, with this group showing an increase in IGF-1 and decreased IL-15 levels.
By comparing two different exercise types in the same study, measuring the most important beneficial and harmful biomarkers, this study advances in a significant way our understanding of how exercise is neuroprotective, and what the specific biological mechanisms are that explain these results.
At DeerFields we are currently treating 40 patients with dementia using the Bredesen Protocol and about 50% of our patients are showing early signs of cognitive improvement, which is remarkable in that conventional medicine has not been able to identify a single drug treatment protocol that modifies the devastating natural history of this disease. The Bredesen protocol includes a significant component of exercise and what this research is suggesting is that both aerobic AND resistance exercise improve cognition through different biological mechanisms and probably should be combined.
Our in house exercise physiologist and human performance coach, Anthony Barsby, recommends combining both aerobic and resistance exercise in the course of a typical week and it is now clear that we need both to slow down, stop, and in many cases reverse cognitive decline.
What to do?
Exercise, ideally first thing in the morning when fasting. Walking, swimming, treadmill, elliptical, stationary bicycle etc. for 30-60 minutes every other day combined with body-weight or light weight strength training, pushups, squats and planks on the other days all supplemented with High Intensity Interval Training (HIIT).
Key to success?
Knowing is not doing. Even after you learn about important advances in reversing the risk of disease, only about 5% of people actual initiate change, leaving 95% of people doing the same thing day in and week out. From behavioural medicine research, the key to adopting the advice provided above is to start with the minimum effective dose of exercise every day which is 10 minutes. Start low and go slow. Invite a family member or friend to join you. And reach out to your DeerFields team for a personalized exercise plan to help you progress once you start a daily ritual.
Dr. Randy Knipping BSc MD CCFP FAARFM ABAARM
Curr Alzheimer Res. 2019 Feb 28. doi: 10.2174/1567205016666190228125429. [Epub ahead of print]
Distinctive effects of aerobic and resistance exercise modes on neurocognitive and biochemical changes in individuals with mild cognitive impairment.
Decreased levels of the neuroprotective growth factors, low-grade inflammation, and reduced neurocognitive functions during aging are associated with neurodegenerative diseases, such as Alzheimer’s disease. Physical exercise modifies these disadvantageous phenomena while a sedentary lifestyle promotes them.
The purposes of the present study included investigating whether both aerobic and resistance exercise produce divergent effects on the neuroprotective growth factors, inflammatory cytokines, and neurocognitive performance, and further exploring whether changes in the levels of these molecular biomarkers are associated with alterations in neurocognitive performance.
Fifty-five older adults with amnestic MCI (aMCI) were recruited and randomly assigned to an aerobic exercise (AE) group, a resistance exercise (RE) group, or a control group. The assessment included neurocognitive measures [e.g., behavior and event-related potential (ERP)] during a task-switching paradigm, as well as circulating neuroprotective growth factors (e.g., BDNF, IGF-1, VEGF, and FGF-2) and inflammatory cytokine (e.g., TNF-α, IL-1β, IL-6, IL-8, and IL-15) levels at baseline and after either a 16-week aerobic or resistance exercise intervention program or a control period.
Aerobic and resistance exercise could effectively partially facilitate neurocognitive performance [e.g., accuracy rates (ARs), reaction times during the heterogeneous condition, global switching cost, and ERP P3 amplitude] when the participants performed the task switching paradigm although the ERP P2 components and P3 latency could not be changed. In terms of the circulating molecular biomarkers, the 16-week exercise interventions did not change some parameters (e.g., leptin, VEGF, FGF-2, IL-1β, IL-6, and IL-8). However, the peripheral serum BDNF level was significantly increased, and the levels of insulin, TNF-α, and IL- 15 levels were significantly decreased in the AE group, whereas the RE group showed significantly increased IGF-1 levels and decreased IL-15 levels. The relationships between the changes in neurocognitive performance (AR and P3 amplitudes) and the changes in the levels of neurotrophins (BDNF and IGF-1)/inflammatory cytokines (TNF-α) only approached significance.
These findings suggested that in older adults with aMCI, not only aerobic but also resistance exercise is effective with regard to increasing neurotrophins, reducing some inflammatory cytokines, and facilitating neurocognitive performance. However, the aerobic and resistance exercise modes likely employed divergent molecular mechanisms on neurocognitive facilitation.
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