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The Ketogenic Diet Improves Cognitive Function

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Breaking NEWS!

The Ketogenic Diet Improves Cognitive Function

The first trial using the ketogenic diet (KD) in patients with Alzheimer’s disease was presented at the 2017 Alzheimer’s Association International Conference. It was presented in a session of the Conference that was dedicated to the potential benefits of ketones called: Brain Ketone Metabolism, Ketogenic Interventions, and Alzheimer’s disease.

As discussed in another blog post, it is known that in Alzheimer’s disease, the brain loses its ability to uptake and use glucose. This decreased glucose utilization results in decrease energy (ATP) production, causing an energy deficit in the brain. It is believed that this energy deficit then increases the risk of neuronal dysfunction and cognitive decline. Specifically, it has been shown that patients with early Alzheimer’s disease have 20-30% less glucose uptake and utilization in certain areas of the brains compared to cognitively normal older adults. Research by Dr. Cunnane has shown that the uptake and utilization of ketones are the same in brains of patients with Alzheimer’s disease compared to the brains of cognitively normal older adults. (Cunnane, 2016)

This research by Dr. Cunnane shows that the even the areas of the Alzheimer’s brains that had decreased uptake of glucose had normal uptake of ketones. The implication of this is that the neurons themselves are not dead just not able to use glucose. The hope is that ketones can help improve cognition by improving this brain energy deficit. This was the basis of the KU Alzheimer’s Disease Ketogenic Diet study. The objection of the study was to see if by changing the fuel source from glucose to ketones thru the KD, would result in improvement of cognitive symptoms in patients with Alzheimer’s disease.

The KU Alzheimer’s Disease Ketogenic Diet Feasibility and Retention Trial

The KU Alzheimer’s Disease Ketogenic Diet Feasibility and Retention Trial involved 15 patients with a diagnosis of mild Alzheimer’s disease. The 15 patients were placed on the KD and an additional triglyceride supplement for 3 months. The degree of ketosis was measured thru urine and plasma ketone levels. Cognitive function tests were assessed at baseline, at the end of the 3 months, and then a month later after back on a regular diet.

Out of the 15 patients, 5 were able to unable to achieve ketosis and dropped out of the study. The 10 that were able to get into ketosis and remain on the diet for 3 months, showed an improvement in cognitive function of 4.1 points on the Alzheimer’s Disease Assessment Scale-Cog (ADAS Cog) score. After returning back to a standard diet, the scores then dropped back down to their baselines values.

The author of the study, Dr. Swerdlow, was noted to say: “As far as Alzheimer’s studies go, a 4 point improvement in the ADAS Cog score is fairly robust.” “It suggests a meaningful improvement in cognition.” “It is greater than that seen in the cholinesterase inhibitors studies.” (Hughes, 2017)

Data from this study support the need for further studies of KD in Alzheimer’s disease. The intervention was well tolerated without serious adverse event. The main limitation of the study was adhering to the KD. (Swerdlow, 2017)   Dr. Swerdlow noted that the KD is not an easy diet to be on, and potentially an easier way to get ketones to the brain may be with supplements, which does not require such a strict low carbohydrate diet.



Cunnane, S. C. (2016). Can Ketones Help Rescue Brain Fuel Supply in Later Life? Implications for Cognitive Health During Aging and the Treatment of Alzheimer’s Disease. Frontiers in Molecular Neuroscience, 9, 1-21.

Hughes, S. (2017, August 03). Boosting Brain Ketones Metabolism: A New Approach to Alzheimer’s. Medscape Medical News.

Swerdlow, R. (2017). The KU Alzheimer’s Disease Ketogenic Diet Feasibility and Retention Trial: Results from a Pilot Study. Alzheimer’s Association International Conference.


The medical information on this site is provided as an information resource only. This information does not create any patient-physician relationship, and should not be used as a substitute for professional diagnosis and treatment.


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Can ketones be used as an alternative fuel source in the Alzheimer’s brain?

Can ketones be used as an alternative fuel source in the Alzheimer’s brain?

Dementia is a progressive neurological disorder resulting in a decline in cognitive function that interferes with daily activities. The most common cause of dementia is Alzheimer’s Dementia (AD). There is currently no treatment for AD and the cause of AD is still unknown. One thing that is well established, is that there is deteriorating brain glucose utilization, both uptake and metabolism, in the Alzheimer’s brain. This is based on decades of research looking at glucose uptake in brains using PET scans. These studies have shown a 20-25% global decreased brain glucose utilization compared to normal age related controls. (See picture below) This decreased glucose utilization is localized regionally in the parietal, posterior cingulate and temporal cortex of the brain. This pattern of decreased utilization is relatively specific to AD compared to other forms of dementia and normal aging itself and is used to help diagnose people who have AD. In the past this pattern of decreased glucose utilization seen in patients with AD, generally, was believed to be a consequence of neuronal cell death.

alzheimers-PET ok

Recent evidence now reveals that this brain energy deficit is present long before the clinical diagnosis or even before the symptoms of AD start. Specifically, glucose utilization has been shown to be 9% lower in cognitively normal individuals older than 65 years of age compared to younger cognitively normal individuals. The glucose deficit is also present in adults who are less than 40 years of age who have genetic or lifestyle risk factors for AD, even before having cognitive symptoms. For example young women who have polycystic ovarian syndrome (PCOS) have been shown to have decreased brain glucose utilization deficit similar to what would be seen in people in their 70s and 80s. PCOS patients have mild insulin resistance, which is associated with an increased risk of AD. Is it plausible then that this deficit of brain glucose utilization may exacerbate or may even be the cause of, instead of the consequence of neuronal loss in AD. One theory proposed is that it is a vicious cycle in decreased glucose utilization that then causes deteriorating neuronal function, which then results in a higher demand for glucose, with the eventual emergence of cognitive decline.

So what if there is another fuel that the brain can use other than glucose?

Dr. Cahill showed in the 1960s that ketones are the main alternative fuel source/energy supply for the brain as a way to protect the brain in times of starvation. It is also known that  infant rely on ketones as the main fuel source due to the metabolic stresses that occur with the rapidly growing infant brain. (see prior blog post) So if the human species relies on ketones to confront these energy challenges why couldn’t it work for the aging or Alzheimer’s brain?

It is has been shown that the brain uptake of ketones is proportional to the plasma ketone levels, but does this change in the aging brain or AD brain? Dr Cunnane looked at just this question. He used PET studies to show that the brain uptake of ketones is the same in patients with AD as compared to age matched cognitively healthy controls. The brain ketone utilization in AD was proportional to the plasma concentration and was the same as age matched controls. I repeat, the areas of the brain that showed decreased glucose utilization in the Alzheimer’s brain had normal uptake and utilization of ketones. This, to me is very exciting! As a neurologist I have always believed that decreased glucose utilizations in patients with AD, was a sign that those brain cells were dead. This data by Dr. Cunnane, however, shows that those cells are just not able to use glucose but can use ketones, thus are NOT dead.

So then would fueling the body with ketones be a potential treatment option of AD?

Babies are born into ketosis and stay in ketosis because the breast milk contains medium chain fatty acids which are rapidly absorbed and transformed quickly into ketones.  Coconut oil is another medium chain fatty acids. When medium chain fatty acids such as coconut oil are added to the diet in patients with AD, cognitive benefits have been shown. Clinical trials using ketogenic interventions in AD have also shown improvement with cognitive function. (see prior blog post) This suggests that interventions that increase ketone levels may have beneficial therapeutics in patients with AD and deserve further study.

The take home message, to me is: there is an impairment of glucose uptake and metabolism in the brain in patients with Alzheimer disease (AD). However, the brain uptake of ketones remains the same in AD as compared to healthy controls. There for interventions that increase ketones availability, either with a ketogenic diet or ketone supplements may help improve the energy deficits seen in the AD and aging brain. Though we do not know if there will be clinical benefits without further study.  Isn’t worth a try?



Cunnane, S. (2011). Brain fuel metabolism, aging, and Alzheimer’s disease. Nutrition, 27, 3-20.
Cunnane, S. C. (2016). Can Ketones compensate for deteriorating brain glucose uptake during aging? Implications for the risk and treatment of Alzheimer’s disease. Annuals of the New York Academy of Science, 1367, 12-20.
Cunnane, S. C. (2016). Can Ketones Help Rescue Brain Fuel Supply in Later life? Implications for Cognitive Health during Aging and the Treatment of Alzheimer’s Disease. Frontiers in Molecular Neuroscience, 9, 1-21.
The medical information on this site is provided as an information resource only. This information does not create any patient-physician relationship, and should not be used as a substitute for professional diagnosis and treatment.

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 its 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-hydroxybutyrate 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 this same patient is 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 why 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 by 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 a 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 phosphorylated tau protein formation, the neuropathology associated with AD. Ketones have also been shown to have a neuroprotective effect on the hippocampal neurons from both glutamate and amyloid beta toxicity. The hippocampi in rats that are fed a ketogenic diet have also had an increasing amount of mitochondria. The neuroprotective 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, the 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. Behavioral Pharmacology (17), 431-439.

Hashim, S. W. (2014). Ketone body therapy: from the ketogenic diet to the oral administration 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.


The medical information on this site is provided as an information resource only. This information does not create any patient-physician relationship, and should not be used as a substitute for professional diagnosis and treatment.
tip for healthy brain

Tips to keeping your brain healthy

8 ways to keep your brain healthy

As  Neurologist I am frequently asked, “what can I take to keep my brain healthy to help prevent Alzheimer’s dementia”.  My answer is that there is no simple pill to keep your brain healthy, but these 8 tips are a great place to start.

  1. Exercise your body: More and more studies are coming out which reinforces what I have long believed, that exercise is the best prescription I can give to prevent Alzheimer’s dementia.
  1. Exercise your brain: Your brain is the most powerful ‘muscle’ of all. If you don’t use it you will lose it!
  1. Keep blood sugars under control: Diabetes increases your risk for Alzheimer’s dementia, as does having high blood sugar levels, in general, even without diabetes.
  1. Consider changing your diet to low carbohydrate high fat diet: A ketogenic diet has been shown to improve brain function, (and it will decrease your risk for diabetes). If you are not ready for that significant of a change, at least start adding more healthier fats into your diet such as: olive oil, DHE, Omega 3 fatty acids and coconut oil.
  1. Keep hydrated, drink more water: You should be drinking half your body weight in ounces of water each day. Example: if you weigh 150 pounds, you should drink 75 ounces of water each day.
  1. Increase your daily intake of antioxidants: Antioxidants help protect your brain from damaging free radicals.  Some common antioxidants include Vitamin C and E along with selenium and flavonoids. The best sources of natural antioxidants are fruits and vegetables.
  1. Decrease stress: If you are unable to limit the amount of stress you have in your life, at least find a healthy way to deal with it. My personal favorite is exercise!
  1. Get more sleep:  Preferably between 7-8 hours per night.


alz brain

Exercise prevents Alzheimer’s pathology

Exercise can prevent Alzheimer’s pathology in the brain

Age is considered the #1 risk factor for the development of Alzheimer’s Dementia (AD). The pathological changes in the brain of a patient with AD include abnormal beta–amyloid deposition in plaques and neurofibrillary tangles  resulting in neuronal loss and shrinkage of the brain. These changes, however, can be seen as early as 30 years before clinical symptoms occur but increase as we age.

As of yet there are not any drug or medical treatments that have been shown to prevent or reverse these changes in the brain of patients with AD. However, a recent study just published in the November 2014 issue of Neurology showed that exercise lessens these preclinical pathological biomarkers of AD.

Prior to this recent study, we had multiple studies that showed the following: (1) exercise can help to preserve memory as we age; (2) exercise has been shown to improve cognition in patients who already have Alzheimer’s and (3) exercise can improve brain volumes, most specifically, in the memory processing areas of the brain, the hippocampus. This is the first study that specifically looks at the pathological changes of AD resulting from exercise.

This study looked at late middle-aged adults (ages 40-65 at entry) who were cognitively normal but at high risk for AD. They investigated whether engagement in physical activity lessons age association alterations in beta-amyloid accumulation, cerebral glucose metabolism, hippocampal volume and cognitive function. Being physically active was based on the American Heart Association recommendation of 30 minute of moderate exercise 5 days a week.

The study found was that the physically active individuals had less beta-amyloid burden, improved glucose metabolism, hippocampal volume, immediate memory, and visuospatial ability compared to physically inactive persons.  This study provides more confirmatory support to the many other studies that show the beneficial effect of physical activity on the aging brain.

Since physical exercise has been shown to improve cognition, improve brain volumes and now decrease the age related disease markers of AD what are you waiting for? There is so much we do not have control over in our lives, but this is not one of them. You have the power to get and keep your brain fit and, potentially, prevent AD.  If you do not know where to start I would be happy to help find a program just for you.


Dr Deb

Works Cited:

Okonwo, O. e. (2014). Physical activity attenuates age-related biomarker alterations in preclinical AD. Neurology , 83, 1753-1760.

Alz-dementia word

Alzheimer’s Dementia

 What is Alzheimer’s Dementia and how can I prevent it?

As a neurologist I often get asked:  How can I prevent myself from getting Alzheimer’s?   My normal answer is to increase your physical and mental activity and keep yourself healthy and you will keep your brain healthy.  I will explain the reasoning below along with some basic information regarding Alzheimer’s dementia (AD)

What is Alzheimer’s Dementia?

Alzheimer’s dementia is the most common cause of dementia. Dementia by definition is a progressive decline in cognitive functioning.  It is a decline in thinking, remembering and reasoning to an extent that it interferes with a person’s daily life and activities.  Per estimates from the Alzheimer’s Association, 5.3 million Americans have AD. This number is estimated to triple in the next 40 years as the population continues to age and live longer.

How do you diagnosis AD?

Currently doctors can only diagnosis AD clinically, based on symptoms and excluding other causes of dementia that can be treated (vitamin deficiencies, hydrocephalus, tumors, depression etc). Unfortunately, the only way to confirm the diagnosis AD is by autopsy of your brain. The pathological changes that are seen in the brains of patients of AD include amyloid plaques (abnormal clumps of amyloid proteins) and neurofibrillary tangles (abnormal bundles of fibers).  It is unclear how or why these plaques and tangles form.  Once they are there, neurons in the brain lose their ability to function and communicate with each other.  Over time the neurons eventually die causing brain atrophy (shrinking of the brain). This process is thought to start up to 30 years before clinical symptoms develop.

What causes AD?

Scientists are not sure what causes AD.  It is most likely due to a combination of genetic, environmental and lifestyle factors. We do know some of the risk factors that can increase your risk of develop AD.  The more risk factors you have the more likely you are to develop AD.

What are the Risk Factors for Dementia?

  • The biggest risk factor for developing AD is age.  Currently the risk of AD doubles every 5 years after age of 65.
  • Genetics:  Genetics plays a big part in what is called “familial AD” which is a young onset AD (typically onset in the 40-50s). This type is autosomal dominant and has strong connection to genetics. This type of AD, however, only accounts for 5% of all AD.  The most common type of AD, “late onset AD” may be linked to an abnormal gene: the apolipoprotein E.  The linkage is not however 100%.  Thus not everyone who has this abnormal gene gets AD, and you may still get AD even if you don’t have the abnormal ApO E gene.
  • Diabetes (DM):   Studies have shown that people with DM are twice as likely to develop AD.  The good news is that people who are at risk for diabetes who changed their lifestyles could reduce their risk of DM by 58% over a 3 year period, thus possibly decreasing their risk for developing AD.   There may be several different reasons why people with diabetes are at an increased risk of dementia.
      • First of all they have an increased risk of having a stroke which itself increases the risk of dementia.
      • DM itself also causes micro-vascular disease which decreases blood flow into the brain thus increasing risk for dementia.
      • AD could be from a problem with the way the brain uses insulin. Nerve cells require a lot of energy; they get this energy from glucose and oxygen.  With diabetes cells lose their ability to respond to insulin, and brain is not able to use glucose properly.  (Think of it as DM of the brain).
      • Insulin also is known to regulate the metabolism of beta-amyloid and tau (the building blocks of the AD pathology) in the brain.
  • Depression:  A meta-analysis of 13 studies showed that people with a history of depression had almost a two times increased risk of dementia compared to controls without depression.
  • Cardiovascular disease:
    • Hypertension: Studies have shown people who have uncontrolled high blood pressure in midlife, are more likely to develop AD.  Hypertension also increases the risk for stroke.
    • High cholesterol: Cholesterol is felt to drive the production of beta amyloid.
    • Increased risk of stroke, patients with DM, hypertension, and high cholesterol are all associated with an increase of having strokes.  Having a stroke is felt to double your risk for dementia.
    • Belly fat:  Obesity has been associated with an increase risk of dementia.  The association between dementia and body weight appears to be most associated with a larger “waist to height” ratios than “body-mass index”.  The association is also greater for obesity during midlife instead of late life obesity.  A 2008 study in the journal “Neurology” found that people in their 40’s who have the highest amount of abdominal fat were more likely to have dementia when they reached their 70s. They found that those with the highest amount of belly fat were nearly 3 times more likely to develop dementia than those with the lowest amount of belly fat.
  • Head injury:  The best data to date show that people who have had moderate to severe traumatic brain injury have a 2-4 fold increase risk of dementia.  There is unclear association with mild head injuries or concussions.  More and more evidence is emerging regarding the risk of dementia after multiple head injuries as seen in boxers and professional football players (what is described in the literature as “chronic traumatic encephalopathy”)
  • Physical inactivity: A meta-analysis of 16 prospective studies and a systemic review of 24 longitudinal studies show that the lowest physical activity groups are associated with higher risks of developing AD.  The good news is that the risks of AD can be decreased with higher levels of physical activity as shown in a study reported in 2012.  Exercise has been shown to improve memory and to increase the size of the hippocampus (the area in the brain that works with memory), by 2% thus reversing age related volume loss by 1-2 years.
  • Cognitive inactivity and low education levels: Multiple studies have showed that the risk for dementia is lower in people who have higher education levels, intelligence, occupational attainment, and mentally stimulating leisure activities.  These studies are supported by randomized control studies, which reported cognitive interventions in healthy older adults are associated with improvement in cognitive function.

What can I do to prevent AD?

Dr. Deborah Barnes from University of California, San Francisco looked at seven potentially modifiable risk factors for AD: diabetes, midlife hypertension, midlife obesity, smoking, depression, cognitive inactivity, and physical inactivity.  She estimates that up to a half of all the AD cases worldwide might be attributable to these risk factors.  She states that if risk factors prevalence were decreased by 25% then prevalence of AD could potentially be lowered by over 3 million cases worldwide.

Out all of the risk factors, the one that has the largest impact on AD prevention in the US is physical inactivity.  It is estimated that if 25% of sedentary people start exercising, potentially 230,000 cases of AD in the US could be avoided.  Low education potentially contributed to the largest proportion of AD cases worldwide; thus with a 25% reduction in low education and cognitive inactivity could potentially lower AD prevalence by 1.375 million worldwide and 91,000 cases in US.

Are there any medical treatments to prevent AD?

Currently there are NO medications that have been shown to decrease your risk for AD.  There are 4 medications that have been approved by the FDA to treat AD: Aricept, Exelon, Razadyne, and Namenda.  These medications provide modest benefit in slowing the rate of cognitive decline, but they do not change the underlying disease process.

“So how can I prevent AD from occurring?”

The corner stone of dementia prevention, until disease-modifying agents are available, is risk factor modification.  Thus you should try to decrease the bad things that may increase your risk for dementia: midlife obesity, midlife high blood pressure, diabetes, strokes, and tobacco use. Then you need to work on improving the things that have been shown to decrease your risk for dementia: increasing mental activity, regular exercise, remaining socially active, and have a healthy diet.

This site is purely informative and should not be considered medical advice. It is not intended to be used to diagnosis or treat any disease.  Please consult your physician before starting any fitness program or new supplement.



Amen, D. Use Your Brain to Change your Age.

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

Buchman, A. B. (2012). Total daily physical activity and the risk of AD and cognitive decline in older adults. Neurology , 13231329.

Desai, A. K. (2010). Healthy Brain Aging: A Road Map. Clinical Geriatric Medicine , 1-16.

Erickson, K. I. (2011). Exercise training increases size of hippocampus and improves memory. Proceeding of the National Academy of Sciences , 3017-3022.

Paturel, A. (2009, July/August). Your Heart, Your Belly and Alzheimer’s: People with so-called metabolic syndrome may be at a higher risk of developing Alzheimer’s dementia. Neurology Now , pp. 18-25.


The best foods to eat to prevent dementia

The best foods to eat to prevent Dementia

Unfortunately, there is no pill to prevent Alzheimer’s dementia (AD).  Even the medication that is available for AD does not prevent it or help improve your memory.  The medications just slow down the natural progression of decline in your memory.  So what can you do to help keep your brain healthy?  Well as discussed in an prior post Alzheimer’s Dementia, the best way is a combination of increase physical and mental activity along with healthy eating.  This blog is going to focus on the foods that have been shown to help keep your brain healthy.

It is now known that as your belly grows; your brain tends to shrink.  There is a direct correlation between obesity and the shrinking of the area of the brain that is responsible for memory and recall; the hippocampus.  It has also been found that being overweight doubles your risk of developing Alzheimer’s dementia and being obese will quadruple that risk. So an important goal of eating healthy is for weight loss.  However, being on a brain healthy diet is more than just going on a weight lose diet. It is also about choosing foods that can help keep our brains healthy.

There is scientific evidence that points to certain foods that may promote brain health while others may cause damage and thus should be avoided.

Foods to eat:

  1. Eat foods that are a good source of B and D vitamins.  It has long been recognized that some nutritional deficiencies can cause dementia, specifically, Vitamin B12, thiamine, folate, and most recently Vitamin D
  2. Consume omega 3 fatty acids. Low levels of omega 3 fatty acids have been associated with depression, anxiety, obesity, attention deficit disorder, suicide, and increase risk of Alzheimer’s dementia.  There are three omega 3 fatty acids.  Docosahexaenoic acid (DHA) and eicospentaenoic acid (EPA) which come from fish oils and alpha linolenic acid (ALA) which comes from plant sources.  DHA is the main component of brain synapse and makes up a large portion of the gray matter in the brain. Lower DHA levels are associated with a smaller brain size.  Omega 3 fatty acids reduces inflammation, combats the plaque buildup associated with Alzheimer’s and increases the blood flow to your brain.  Boosting omega 3 fatty acids in your diet is one of the best things that you can do for your weight, mood, brainpower and longevity.
  3. Consume dietary antioxidants.  Antioxidants such as vitamin E, vitamin C, and beta-carotene protect the body and the brain against the destructive effects of free radicals.  Excessive free radical formation causes cell death and tissue damage.  A study done in rats showed that rats who ate a diet rich in blueberries showed better ability to learn new motor skills and gain protection against strokes. There is evidence that that these natural antioxidants activate the brains natural house cleaning mechanisms to clean up the toxic proteins that are linked to age related memory loss and mental decline.
  4. Eat balance portions of protein, carbohydrates, and good fats at each meal.  Having protein at each meal helps to balance blood sugar levels, which can cause “brain fog” from eating simple carbohydrates. Or recently more evidence points to eating a low carb high fat diet.  See more in recent blog post.

One simple way that I am able to get in my all that I need to fuel my body and my brain is by drinking Shakeology.  Besides the benefits of helping you lose weight and reduce craving, Shakeology is also packed with more than 70 of the most nutritious whole food ingredients that your body needs.

  1. There are a total of 13 vitamins that are considered essential for proper body function and Shakeology has them all including Vitamin B1, B12, folic acid, and Vitamin D.
  2. Shakeology also includes short chain omega fatty acids ALA from natural plant based sources of the sachi inchi, chia seed, and flax seed.  However, it is unclear if the ALA gets converted to EPA or DHA so supplementing it with DHA and EPA is still recommended.
  3. It contains some of the most potent antioxidants to help protect the body from free radicals from oxidizing and destroying cells. It also helps support your body’s immune function and promote healthy aging.  The antioxidants in Shakeology include, acai berry, acerola cherry, bilberry, blueberries, cacao, camu-camu, coconut flower nectar, goji berries, pomegranate, rose hips, luo han guo, grape seed, and green tea. Did you know that the American Heart Association and the American Cancer Society recommend eating between 5 and 9 serving of antioxidant rich fruits and vegetables a day; Shakeology meets this recommendation with just one serving.
  4. Shakeology contains about 16 grams of protein and 20 grams of total carbohydrates of which 5 grams is fiber to give you a balanced meal.  Even though it seems to have a high ratio of carbohydrate, it has a low glycemic index averaging 24 (13-46 depending on formulation), which is lower than most fruits and vegetables.  This help to stabilize your sugar and insulin levels and give you the energy your body and your brain needs throughout the day.

“So why can’t I just take a multivitamin that gives some of those nutrients that I need?”  You may ask, well you can. However, unlike some multivitamin pills, Shakeology uses whole food sources of nutrients.  The benefits of using whole food is that the nutrients are preserved as close to their natural state as possible.  This allows your body to better absorb and more efficiently use these nutrients, as intended in nature.

Now I am not saying that drinking Shakeology is going to prevent you from having Alzhemier’s dementia.  Just like the label says: “these statements have not been evaluated by the FDA.”  “This product (Shakeology) is not intended to diagnosis, treat, cure, or prevent and disease”.  However, as a Neurologist I personally drink Shakeology on a daily basis for many reasons, just one of which is to help keep my brain healthy.



This information is not intended to replace the advice of a doctor. Shakeology is not intended to diagnose, treat, cure, or prevent any disease or been evaluated by theFood and Drug Administration.