Here is an excerpt from my book which is available on Amazon Here is a link Prevent Alzheimer's Autism and Stroke with 7 Supplements, 7 Lifestyle Choices and a Dissolved Mineral
We all know the difference between walking and running when we exercise. When walking both our heart and breathing rates are slightly increased and when running our heart and breathing rates are significantly increased. This increase in heart and breathing rates keeps the oxygen level of our blood, brain, and muscles constant. When performed regularly both of these aerobic exercises, walking and running, increase our aerobic fitness and endurance. When a several minute sprint is added to this aerobic exercise routine we push our heart and breathing rate to the limit where we can no longer get sufficient oxygen into our blood. This is called anaerobic exercise. It results in lower than normal oxygen levels in our brain and muscles and painful lactic acid build-up in our muscles.
Aerobic exercise when performed correctly is not painful and will prevent or postpone the onset of Alzheimer’s. I recommend non-impact exercise performed by walking, rowing, stepping, and bicycling. In order to be effective aerobic exercise should be performed at least three times a week for 40 minutes with a heart rate of 60% to75% of your peak heart rate reserve. Your peak heart rate reserve is the difference between your resting heart rate and your maximum heart rate. Your maximum heart rate is 220 beats per minute (bpm) minus your age in years. For example if you are 70 years of age with a resting heart rate of 50 bpm, your maximum heart rate is 220 – 70 = 150 bpm and your peak heart rate reserve is the 100 bpm difference between 50 and 150 bpm . In this example 60% to 75% of your peak heart rate reserve is therefore 110 to 125 bpm. Before beginning an aerobic exercise program I recommend a doctor supervised stress test.
The results of a multi-year study of 18,670 men and women were recently published in the Archives of Internal Medicine. The study, beginning in 1970, involved a mid-life fitness evaluation. Then 30 years later, when the participants were in their 70’s and 80’s, their medical records were checked. The results revealed that those who were most aerobically fit in their 40’s and 50’s suffered from AD only in the final five years of their lives. Those who were less fit in their 40’s and 50’s suffered from AD in the final 10 to 20 years of their lives. Even though both groups had the same frequency of getting AD, those who were most aerobically fit at mid-life lived longer and suffered with AD for a shorter period time than those who were less fit492.
In our brains during aerobic exercise there is a choreographed production of biochemicals that are both neuron growth promoters and neuroprotective cleansing agents counteracting the effects of accumulated aluminum and associated Aβ plaques:
Neuropeptide YY (a.k.a. PYY) – Aerobic exercise stimulates the production of a small neuropeptide called PYY493. Injections of PYY in mice has been found to lower both aluminum absorption from the gut into the blood by 54% and aluminum accumulation in the brain by 86%494. This dramatic decrease in aluminum accumulation in the brain suggests that PYY not only decreases absorption but also cleanses the brain of aluminum.
In humans aerobic exercise increases PYY production by 23-24% both during and after acute and long-term exercise training495,496. In addition PYY levels remain high for an hour after exercise495. Rising PYY levels are observed during and after exercise in adolescents and adults with a normal body mass index (BMI) and in adolescents with a BMI in the 85th percentile or higher, but surprisingly not significantly in obese adults493,496,497. This is possibly due to obese adults having less PYY in their blood than those with normal BMI498. Lower PYY in the blood of obese adults may account for why each unit of BMI at midlife predicts earlier onset of AD by 6.7 months209. Lower PYY in the blood of obese adults results in more aluminum accumulation in their brains and a higher risk of AD.
In addition to lowering aluminum accumulation, PYY is a regulator of energy metabolism496. Protein consumption, but not carbohydrate consumption, also increases PYY production498. PYY is produced by cells in the stomach and released into the blood. When PYY reaches the hypothalamus in the brain, the feeling of hunger is decreased493,496. High PYY levels cause appetite suppression in those people with both normal and high BMIs494-496,498. Therefore for optimum appetite suppression eat some protein and eat slowly to allow the PYY to reach your hypothalamus.
Somatotropin and Somatostatin – In AD patients Aβ plaque accumulation is observed almost a decade before cognitive impairment. Removal of the Aβ plaque may postpone the onset of cognitive impairment. Somatotropin and somatostatin facilitate the removal of Aβ plaques from the brain. Physical exercise has been shown to stimulate the anterior pituitary gland of the brain to produce the peptide hormone somatotropin (a.k.a. human growth hormone)500. In response to high levels of somatotropin for periods longer than 15 minutes501, the peptide hormone somatostatin is produced by the hypothalamus to inhibit somatotropin production. Therefore thirty minutes of aerobic exercise causes somatotropin levels to peak and decline and somatostatin levels to increase in the brain500,502.
Neprilysin is a membrane bound zinc-dependent enzyme that degrades Aβ peptides and Aβ plaques. The activity of neprilysin is increased by aerobic exercise because somatostatin enhances neprilysin’s activity503. Somatostatin levels decline with age and are reduced by 47% in the temporal cortex of the brains of AD patients as compared with normal brains504. These changes may contribute to the increase in Aβ plaques in the brains of AD patients. Aerobic exercise for 30 minutes increases the level of somatostatin that in turn increases neprilysin’s rate of Aβ plaque degradation thereby postponing the onset of AD and possibly preventing AD.
Norepinephrine - Norepinephrine both counteracts the negative effect of aluminum on the working memory and improves the working memory in the frontal cortex of the brain505-507. Aerobic exercise increases norepinephrine plasma levels by as much as 14 fold in both men and women508,509. People who exercise regularly (i.e. trained people) produce more norepinephrine than people who do not exercise regularly (i.e. untrained people). More than twice the amount of norepinephrine is produced during equivalent aerobic exercise performed by trained versus untrained men and women of 22-45 years of age509,510. Trained 65 year old men produce 50% more norepinephrine than untrained men of the same age while aerobically exercising510.
The locus coeruleus (a.k.a. LC, locus ceruleus), located in the brain stem, is the principle norepinephrine producing site of the brain511. In the brains of AD patients there is up to an 80% loss of the norepinephrine producing LC neurons511. For details on how norepinephrine counteracts aluminum’s negative impact on working memory see “Neurochemistry of Memory Improvement by Exercise” at the end of this chapter.
Brain Derived Neurotrophic Factor (a.k.a. BDNF) - Aerobic exercise stimulates the production of BDNF in the brain that has been found to stimulate the process of neurogenesis. Neurogenesis is involved in creating a network of neuronal connections required for memory storage. Neurogenesis also adds volume to the hippocampus. Hippocampal volumes are larger in more-fit older adults and these larger hippocampal volumes are associated with improved spatial memory. BDNF levels are lower in the the brains of those 90+ year olds with dementia versus those without dementia512.
The hippocampal region of the brain is where short-term memories are converted to long-term memories and where long-term episodic and spatial relationship memories are pre-sorted, processed, and stored. The dentate gyrus in the hippocampus is one of several regions in the brain where neural stem cells are converted to new neurons in a process called neurogenesis that continues to occur throughout one’s lifetime. Neurogenesis in the adult human hippocampus was first observed in 1998 using a chemical label that permanently integrates into the DNA of dividing brain cells513. This finding was confirmed in 2013 by analyzing radioactive carbon in the DNA of brain cells. The amount of radioactive carbon in human DNA declined after 1963, due to the above ground nuclear test ban treaty, providing a marker to distinguish old from new DNA. From the amount of radioactive carbon in DNA of 55 deceased patients it was found that one third of the hippocampal neurons are renewed throughout one’s life amounting to the addition of 1400 new neurons a day159. In spite of this increase in neurons, hippocampal volume declines 1-2% per year as a part of ageing. In individuals with mild cognitive impairment there is a larger decline than normal and with AD this decline in volume is much more pronounced.
In 2011 a study of 120 older adults was published514. In this study, the older adults were paid to excercise for one year. At 6 and 12 months their hippocampal volume, BDNF serum levels, and spatial memories were tested. Half of the study group (mean age of 67.6) walked aerobically for 40 minutes 3 days a week while maintaining 60-75% of their peak heart rate reserve. The other half of the study group (mean age of 65.5) did not aerobically excercise but instead non-aerobically exercised for 40 minutes 3 days a week with:
· four muscle toning exercises using dumbells or resistance bands
· two exercises designed to improve balance
· one yoga sequence
· one exercise of their choice
Hippocampal volume increased 2% over the year in the group that aerobically exercised by walking and declined by 1.4% in the other group. Also in the group that exercised aerobically by walking both spatial memory improvement and increased serum BDNF levels correlated with increased hippocampal volume. These results indicate that starting an aerobic exercise program in later life can lead to improvements in hippocampal volume, spatial memory, and cognitive function. An aerobic exercise program will prevent or postpone the onset of AD.
Aluminum Excretion by Sweating During Exercise – Perspiration is another way that aluminum is excreted by the body. Sweating while exercising lowers aluminum levels in the body515. It has been shown that a diet that includes a mineral water high in dissolved silicic acid facilitates this pathway for aluminum excretion516.
A neurochemical mechanism has been proposed to explain how norepinephrine, produced during aerobic exercise, improves one’s working memory and counteracts the negative effect of accumulated aluminum on the working memory. Working memory is defined as the brain’s capacity to retain, manipulate and utilize information. The prefrontal cortex is the location of working memory. In the prefrontal cortex co-located on the neuronal dendrites there are both:
· Hyperpolarized cyclic nucleotide – gated ion channels (HCN)
· Alpha 2A adrenergic receptors (AAR)
Cyclic adenosine monophosphate (cAMP) in the brain holds HCN channels open lowering synaptic efficiency and preventing information required for the working memory to be passed across synapses. Norepinephrine produced during aerobic exercise stimulates the AARs that inhibit cAMP biosynthesis from ATP. This lowers the cAMP concentration that in turn keeps HCN channels closed, thereby improving working memory in the prefrontal cortex505.
Aging human brains have higher levels of cAMP and this holds HCN channels open in ageing brains. The accumulated aluminum in older brains inhibits the calcium/calmodulin complex from activating the enzyme PDE4A that normally degrades cAMP. Therefore aluminum increases the cAMP concentration in aging brains506. Agents like norepinephrine that inhibit cAMP production or close HCN channels can restore normal working memory in the prefrontal cortex and reverse the effects of accumulated aluminum507. Therefore aerobic exercise reverses the negative effect of accumulated aluminum on the working memory.
Another stimulant for AARs is guanfacine that also improves working memory and mental attention in the prefrontal cortex. Guanfacine is sold under the brand name Intuniv as a time-release pill. Resveratrol, sold for improved mitochondrial and cardiac function, increases cAMP and therefore can’t be recommended506.