Exercise to prevent Alzehimer’s dementia

Dementia is a defined as a cognitive decline resulting in a decline in daily function. The most common cause of dementia is Alzheimer’s Dementia (AD). In the United States there are over 5.3 million people in the United States who have AD. This number is estimated to triple by 2050. The main risk factor for developing AD is aging. The majority of other major risk factors including diabetes, obesity, and physical inactivity, are potentially modifiable thus we have control over. (Barnes, 2011)

Out of all the risk factors physical inactivity may have the largest impact on prevention of AD. It has been estimated that over 1.1 million cases of AD are potentially attributable to physical inactivity.(Barnes, 2011) Such that those who engage in the highest physical activity have been estimated to have a decreased risk of AD by 45% compared to lowest physical activity category. (Hamer, 2009)

Exercise has indirect effects of improving your brain by improving health conditions that are also risk factors for AD. Specifically exercise results in weight loss that then decreases risk of obesity. Diabetes and hypertension are also improved with exercise. Improvement in these health conditions, then, potentially may result in a decrease risk of strokes.

Epidemiological studies have shown that increased lifetime engagement in physical activity can reduce the risk of developing dementia in cognitively normal elderly persons. (Taafee, 2007) Specially, moderate activity during mid-life is associated with 39% decreased risk of developing mild cognitive impairment (which is one of first stage of AD). The good new is that even starting an exercise program later in life is also associated with a 32% lower risk for mild cognitive impairment. (Bherer, 2013).

Evidence is also growing that exercise may not only reduce the risk of dementia but also have some benefit in improving memory as we age and if you already have dementia. Exercise has been shown to preserves memory, processing speed, and executive function that typically decline with age. (Bherer, 2013) Exercise in patients with dementia overall has a positive effect on cognitive function based on a meta- analysis of 18 randomized studies. (Groot, 2016) Exercise also improves balance, mobility and thus reduced the risk of falls.

The beneficial effects of exercise are supportive by the brain imaging research that has been done. These studies have noted a decrease rate of the shrinking of brain in those who have higher aerobic fitness levels. Also shown is that the area involved in memory, the hippocampus, has a larger volume with exercise. (Kelly, 2014)

How exercise is believed to result in these changes are of course not completely know. Things that are believed is that exercise has neuro-protective effects on the brain. One of the main factors believed to be contributive to age related diseases and AD is oxidative stress mediated by reactive oxygen species. Exercise has been shown to decreases reactive oxygen species and increases the activity of antioxidant systems.   Exercise also increases a neuropeptide, brain derived neurotropic factor (BDNF) that helps to promote neurogenesis in the hippocampus. (Radak, 2010) (Bherer, 2013)

How much exercise is needed? To reduce risk of cognitive decline in cognitively normal persons over the age of 65 the World Health Organization recommends: A weekly minimum of 150 minutes of moderate intensity aerobic activity or 75 minutes of vigorous intensity aerobic activity. (Groot, 2016) I would also recommend adding some muscle strengthening exercises to help improve strength. To help prevent falls consider adding in some yoga or Tai Chi to help with balance.




Barnes, D. Y. (2011). The projected effect of risk factor reduction on Alzheimer’s disease prevalence. Lancet Neurology, 10, 819-828.

Bherer, L. E. (2013). A Review of the Effects of Physical Activity and Exercise on Cognitive and Brain Functions in Older Adults. Journal of Aging Research, 1-8.

Erickson, E. E. (2011). Exercise training increases size of hippocampus and improves memory. Proceeding of the National Academy of Sciences of the United States of America , 108 (7), 3017-3022.

Groot, C. E. (2016). The effect of physical activity of cognitive function in patients with dementia: A meta-analysis of randomized control trials. Ageing Research Reviews , 25, 13-23.

Hamer, M. C. (2009). Physical activity and risk of neurodegenerative disease: a systemic review of prospective evidence. Psychol. Med , 39, 3-11.

Kelly, M. E. (2014). The impact of exercise on the cognitive functioning of healthy older adults: A systemic review and meta-analysis. Aging Research Reviews , 16, 12-31.

Radak, Z. E. (2010). Exercise Plays a Preventive Role Against Alzhemier’s Diease. Journal of Alzheimer’s Diease , 20, 777-783.

Soli, F. (2011). Physical activity and risk of cognitive decline: a meta- analysis of prospective studies. Journal of Internal Medicine, 269, 107-117.

Taafee, D. e. (2007). Physical activity, physical function, and incident dementia in elderly men: the Honolulu-Asia Aging Study. Journal Gerontology , 63 (5), 529-535.



Brain aging and memory loss due to Dementia and Alzheimer's disease with the medical icon of a group of color changing autumn fall trees in the shape of a human head losing leaves as a loss of thoughts and intelligence function.

Can Alzheimer’s disease be treated with ketones?

Brain aging and memory loss due to Dementia and Alzheimer's disease with the medical icon of a group of color changing autumn fall trees in the shape of a human head losing leaves as a loss of thoughts and intelligence function.

The brain’s main fuel source is glucose. However, it has been shown that the brains of people who have Alzheimer dementia (AD) are not able to utilize glucose as well as normal people. When there is not enough glucose to meet it’s metabolic needs, the neurons that work the hardest, i.e. those involved with memory and cognition are the first ones to be compromised and thus show impairment. So the question is: is there another fuel that the brain can use?

The answer luckily is yes! Ketone bodies (KB) or ketones are another fuel source for the brain and the body. Acetoacetate and Beta-hydroxybutrate are collectively known as ketone bodies (KB). KB are normal metabolites that are manufactured by the liver as an alternative fuel for the body and the brain when dietary sources of carbohydrates are in short supply, a process called ketosis. Ketone bodies can be produced in healthy individuals either during times of fasting or by eating a ketogenic diet. The ketogenic diet was first introduced, over 80 years ago, as a dietary treatment of uncontrolled epilepsy in children. The ketogenic diet is diet consisting of high amounts of fat and low amounts of carbohydrates. Other ways of producing ketones nutritionally are by eating high amounts of medium chain triglycerides (MCTG) such as coconut oil repetitively throughout the day.

When ketones are available they are a better fuel source for the brain in patients with AD for several reasons. First of all ketones do not need insulin for uptake into the cell, so it is easier for the brain to get this fuel source compared to glucose. This decrease usage of glucose is visible on brain PET scans, which look at the uptake of glucose. In patients with early AD, there is a 14% overall decrease in the uptake of glucose compared to normal controls. In contrast, when these same patient are placed in brain PET scans looking at the uptake of ketones, the uptake is the same both in the patients with early AD and normal controls.

Other possible theories on way ketones are a better source of fuel for patients with AD is that they are a more efficient source of energy. First of all ketones produce more energy (ATP) compared to glucose. Secondly, the mitochondria, the cells that produce the body’s energy, are believed to be impaired in patients with AD. Ketones, however, are able to bypass the blocked site of the energy pathway, the Krebs cycle, in the mitochondria. This allows the mitochondria to produce energy more efficiently when it is fueled with ketones.

There have been several published clinical studies looking at the effects of ketosis in patients with mild cognitive impairment and AD. The results have shown improved cognitive performance in patients who are in ketosis either from eating a ketogenic diet or from a diet consisting of very high dose of MCTG oils (20- 70 g/day). This improvement in memory was positively correlated the urinary ketone levels, i.e. the higher the level of ketones in the body, the better the cognitive effect.

Even more exciting than the fact that the ketogenic diet has been shown to help memory in people with AD, is that there is also evidence that being in ketosis might also have some disease modifying benefits in AD. In mouse models of AD, a ketogenic diet has been shown to actually improve the pathology associated with AD. Specifically, the mouse brains were found to have less beta- amyloid formation and less phospholated tau protein formation, the neuropathology associated with AD. Ketones have also been shown to have a neuro-protective effect on the hippocampal neurons from both glutamate and amyloid beta toxicity. The hippocampi in rats that are fed a ketogenic diet have also have an increase amount of mitochondria. The neuro-protective effect thus may result from enhanced energy reserves, which improves the ability of the neurons to resist metabolic challenges. Another possibility is that ketone metabolism as compared to glucose metabolism generates less free radicals and lower oxidative stress, thus resulting in improved antioxidant capacity, decrease CNS inflammation, and thus less cell death.

There are potentially 2 problems associated with the ketogenic diet. 1) It is very difficult to adhere to, especially in people who have dementia, who are not self motivated to stick with the diet. 2) Eating a high carbohydrate meal while on the ketogenic diet would potentially throw the person out of therapeutic ketosis and it   may take a day or two to get back in, thus taking several days before seeing any benefits again. Up until now the only other alternative to the ketogenic diet to produce therapeutic ketosis is the repetitive ingestion of high does of MCTG. The problem with it is: the doses high enough to produce therapeutic ketosis are often associated with significant GI side effects. Additionally, taste of MCTG is often difficult to swallow.

Luckily now there is a better way. There is a now a ketone supplement available to the public. This supplement, which is a proprietary blend of ketone mineral salts, puts your body into a state of therapeutic ketosis within 60 minutes of drinking it without having to be on a strict ketogenic diet.

Now, this ketone supplement is not an approved treatment by the FDA for treatment of AD or any other disease for that matter. However, I am so convinced, based on what the research suggests on what the Alzheimer’s brain needs to function at its optimal level. Along with what the potential benefits of being in the state of ketosis offers, including how it could work for the Alzheimer’s brain that I personally drink it myself and have also recommended it to my parents. Since there is no known cure for AD or proven treatment yet available, if something as simple as drinking this supplement twice a day would help with your memory would you give it a try?


Cunnane, S. C. (2016). Can ketones compensate for deteriorating brain glucose uptake during aging? Implications for the risk and treatment of Alzheimer’s disease. Annals of the New York Academy of Sciences, 1367, 12-20.

Cunnane, S. e. (2011). Brain fuel metabolism, aging and Alzheimer’s disease. Nutrition (27), 3-20.

Gano, L. B. (2014). Ketogenic diets, mitochondria, and neurological diseases. Journal of Lipid Research, 55, 2211-2228.

Gasior, M. e. (2006). Neuroprotective and disease modifying effects of the ketogenic diet. Behavoral Pharmacology (17), 431-439.

Hashim, S. W. (2014). Ketone body therapy: from the ketogenic diet to the oral administartion of ketone ester. Journal of Lipid Research, 55, 1818-1826.

Krikorian, R. E. (2012). Dietary ketosis enhances memory in mild cognitive impairment. Neurobiology of Aging, 425 (e19).

Newport, M. T. (2015). A new way to produce hyperketonemia: Use of ketone ester in a case of Alzheimer’s disease. Alzheimer’s & Dementia, 11, 99-103.


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