Got ketones drdebbrain

Ketones are the preferred fuel source for our brains

What is Ketosis?

Like most people, I did not know what ketosis was or whether having ketones in the body was a good thing or not. Ketosis by definition is the just the state of having ketones in our body. Since most of us have always eaten a carbohydrate-based diet, which uses glucose as the main fuel for our brains to run on, we did not know there was anything different. However, recently I have done a lot of research and found a huge body literature supporting the multiple benefits of having ketones in our bodies and using it for fuel instead of glucose.

I recently had the honor to listen to Dr. Stephen Cunnane, one of the leading researchers on nutrition and brain development, speak on his research about ketones as fuel for the brain. I have a few take-aways from that talk and from his recent article, published in Frontiers in Molecular Neuroscience that I would like to share to, hopefully, help show that having ketones in our bodies is indeed a good thing

Ketones are the preferred fuel source for the brain

It has been known since the 1960s, that ketones are the alternative fuel source, instead of glucose, for the brain. Dr Cahill at that time showed that the liver would produces ketones when glucose levels were low, as a way of survival during times of fasting or starvation.

The amount of ketones that are taken up into the cells of the brain is directly related to the amount of ketones that are present in the blood. Such that, the more ketones that are present in the blood, the more ketones will be taken up into the brain to be used. This is different than glucose, which is pulled into the brain cells based on the brain’s energy needs. Glucose also requires the presence of insulin to open the door for glucose to get into the cells (which is an issue in some neurological disorders such as Alzheimer’s Dementia).

In adults, the liver only produces ketones when glucose supplies are low, so ketones and glucose have not been available at the same time. Now that exogenous therapeutic ketones have been developed, your body can actually have ketones present even when glucose is also around. Thus, the body potentially now can have two different fuel sources in the body at the same time. So which one does the brain prefer? Dr Cunnane researched just that question, and with the use of PET scans to show the amount uptake of glucose and ketones in the brain. He found that that amount of glucose utilization in the brain decreases as the availability of ketones to the brain increases. I.e. if the energy needs of the brain are being meet by ketones, glucose uptake decreases. Thus when ketones are around, they are actually the preferred energy substrate for the brain.

Ketones are essential to the developing infant’s brain

Ketones are essential to the developing infant. In the neonatal brain, there is insufficient glucose available to meet the very high-energy needs of the growing brain thus; it must rely heavily on ketones for fuel. Ketones are not only needed as a fuel but they are also the main substrate needed for brain lipid synthesis (brain development). Even after the infant is born the infant’s brain relies on ketones for fuel. Thus, the infant remains in a sustained state of ketosis. This ketosis is not a function of food restriction (or low glucose levels) but is due to the medium chain fatty acids (MCFAs) that are supplied from the breast milk (and some formulas). The MCFAs are then stored in the infant’s adipose tissue. After breast-feeding ends, the adipose tissues provide will enough fats for ketones to be produced for many months.

So, in summary, being in ketosis is very natural. It is the body’s way to be protective of our brain during times of starvation or fasting. It is also probably also the diet of our ancestors. It is also a very natural state, since we are born in ketosis and with breast milk stay in ketosis through out infancy. Lastly, our brain actually prefers ketones over glucose. Are you ready to see how good your brain feels with it is fueled with ketones?

Got ketones drdebbrain

Bibliography

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.
PET_Normal_brain

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?

 

Bibliography

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.
broken-brain

Treating Concussions with Ketones

broken-brain

What is a Concussion?

Head injury, whether it is from a concussion or a severe traumatic brain injury, can have long term and serious consequences. Concussions are typically described as mild traumatic brain injury. Concussions are most commonly occur from sports related injuries, such as from being tackled in football, to hitting a soccer ball off of head, or falling off a bicycle. In the US, there is estimated between 1.6 to 3.8 million sports related concussions that occur every year. The rates for concussion are highest in pediatric and adolescent age ranges. Even though concussions often do not cause structural damage to the brain, they still can causes significant symptoms. Headaches are the most common symptom seen with a concussion, but other post concussion symptoms include problems sleeping, impaired memory, dizziness, balance problems, attention problems and depression. These symptoms can last from weeks to months and in some cases even longer. (Giza, 2014)

Concussions have come to the forefront of pubic awareness with the recently discovered disease, chronic traumatic encephalopathy, which was the topic of the movie ‘Concussion’. Chronic traumatic encephalopathy (CTE) is the neurodegenerative changes that occur in the brains of individuals who have sustain multiple concussions earlier in their lives. CTE results in long-term neurological symptoms including behavioral, cognitive and motor symptoms.   The behavioral symptoms include depression, mood swings, aggression and possibly suicide. The cognitive deficits can range from memory problems to dementia. The motor symptoms vary from parkinsonian tremors to ataxia and even possibly a motor neuron disease. (Jordan, 2014)

What is the treatment of concussion?

Currently, there is no medical treatment for concussion except supportive measures. Other than the prevention of concussion in the first place, there is no medical ways to prevent it from progressing into CTE.

What is the pathobiology of concussion?

The underlying pathobiology of concussion has been well described. The shaken brain causes a disruption of the cellular membranes. This then causes a release of chemicals; potassium to flow out of the cells and calcium to flow into the cells. This triggers a cortical spreading depression of the neurons, which then results in the release of glutamate from the cells. The brain needs energy, or ATP to reestablish a balance or homeostasis of these chemicals. ATP is produced in the mitochondria of the cell after the uptake of glucose thru the process of glycolysis.(Giza, 2014)

Immediately after the brain injury there is then a transient increase in glucose uptake, followed by a prolonged decreased in glucose uptake and decrease glycolysis. This impairment in glucose uptake and glycolysis results in an over decreased in ATP production. This time of energy crisis or metabolic dysfunction of the brain is variable, ranging from days to months, depending on severity of injury and age of the brain.(Prins, 2104) Other changes that are occurring in the brain during this time include; increased glutamate excitotoxic damage and increased free radical production. During this time of metabolic dysfunction the brain is felt to be more vulnerable to a second injury. (Giza, 2014)

Is there an alternate fuel source that can be used?

Ketones are the only known natural alternative of glucose that can be used for cerebral energy metabolism. The advantage of using ketones is that they produce ATP thru beta- oxidation not thru glycolysis. Thus ketones are able to bypass the glucose metabolic derangements that are seen associated with brain injuries. ATP supply is also increased from mitochondria biogenesis that is seen with ketones. (Streijger, 2016) In the injured brain, ATP stores have been to be restored after administration of a ketone, beta-hydroxybutyate. (Prins, 2004) Ketones may also benefit the injured brain by their antioxidant effect, ability to increase the antioxidant glutathione and reduce free radical production. (Gano, 2014) Ketones also have been shown to protect cells against glutamate-induced neurotoxicity. (Ziegler, 2003) Hence, using Ketones as an as alternate fuel source instead of glucose, as therapeutic treatment of head injury is appealing.

How does this translate clinically?

There have not been any trials, as of yet, in humans. In studies using adolescent rats, the ketogenic diet has been shown to improve outcomes both with cognitive and motor function, following traumatic brain injury.   When the rats are pretreated with ketogenic diet they were found to have 58% less cortical injury volumes and better neuronal preservation. (Streijger, 2016)

For maximum neuroprotective effects, it is best to be in a state of ketosis (a state where the body is producing ketones) prior to any brain injury. The next best is to start it as soon as possible after the injury. Typically, if you start a ketogenic diet, it may take a while, up to several days, before you will be in ketosis. Another option, which can be used either in place of, or in addition to a ketogenic diet, is to use a ketone supplement. This supplement will get your body in the state of ketosis in less than 60 minutes. This supplement is not currently FDA approved for the treatment of concussion or other diseases. However, the researchers, who are currently using this supplement in research studies for concussion and head injury, are very excited about its potential. They currently recommended it for anyone who plays contact sports and are discussing potential uses in college and profession sports.

protect-brain-football

Bibliography

Gano, L. (2014). Ketogenic Diet, mitochondria, and neurological diesases. Journal Lipid Research, 55, 2211-2228.
Giza, C. C. (2014). An Introduction to Sports Concussions. Continuum Lifelong learning in Neurology, 20 (6), 1545-1551.
Jordan, B. (2014). Chronic Traumatic Encephalopathy and other long-term sequelae. Continuum, lifelong learning in Neurology, 20 (6)1588-1604.
Prins, M. (2004). Increased cerebral uptake and oxidation of exogenous BHB improves ATP following traumatice brain injury in adult rats. Journal of Neurochemistry, 90, 666-672.
Prins, M. M. (2014). The collective therapeutic potential of cerebralketone metabolism in traumatic brain injury. Journal of Lipid Research, 55, 2450-2457.
Streijger, F. (2016). Ketogenic Diet and Ketones for the Treatment of Traumatic Brain and Spinal Cord Injury. In S. Masino (Ed.), Ketogenic Diet and Metabolic Therapies (pp. 133-146). Oxford.
Ziegler, D. (2003). Ketogenic diet increases glutathion peroxidase activity in rat hippocampus. Neurochem Res, 28, 1793-1797.
parkinsons-word-brain-get-fit

Ketones and Parkinson’s Disease

Parkinson’s disease (PD) is the second most common neurodegenerative disease. Parkinson’s disease is a progressive neurodegenerative disorder, characterized by tremors, slowness of movement, rigidity and problems with balance. These symptoms are believed to be due to the degeneration of the dopaminergic neurons in the substantia nigra. The mechanism of this neurodegeneration in PD remains unclear. (Masino, 2016) Currently, there is only symptomatic treatment.  There are no treatments available currently for delaying or preventing this neuronal damage that causes PD.

parkinsons-word-brain-get-fit

One of the potential theories of what causes this degeneration of the substantia nigra, is from mitochondrial dysfunction, specifically, impaired complex I activity of the electron transport chain.(VanItallie, 2005) Impairment of the mitochondrial results in decreased energy (ATP) production. As with most neuro-degenerative disorders there is probably also a component of  increased inflammation. (Masino, 2016) Another theory is that there is increased oxidative stress. (Shaafi, 2015) This increased oxidative stress is from increased levels of reactive oxygen species.  The antioxidant Glutathione is also decreased levels in patients with PD.(Cheng, 2009)

The ketogenic diet (KD) has been used for treatment for drug resistant epilepsy since the 1920s. There is  mounting research that ketones are neuroprotective thus ketones and the KD are increasingly being studied in a number of other neurological disorders; including Alzheimer’s dementia, ALS, autism, cancer, stroke, traumatic brain injury and even Parkinson’s disease. (Gano, 2014)   Ketones are produced naturally from the liver under conditions of sustained low glucose levels, such as times of starvation or when on a ketogenic diet. The ketogenic diet is a high fat, low carbohydrate diet that metabolically shifts the body from using glucose to ketones as it main source of fuel. When present, ketones are the preferred fuel source for the brain. (Cunnane, 2011)

Ketones have several benefits that are potentially neuroprotective.  One of the potential neuroprotective benefit of ketones in PD is from the improved energy (ATP) production. There are three different ways that using ketones instead of glucose as a fuel result in more ATP. First of all ketones have been shown to bypass the blocked pathway in the mitochondria that is damaged in PD, thus the previously damaged mitochondria are now able to produce ATP. (Gano, 2014) Secondly, ketones have also been shown to actually stimulate new mitochondrial to form.  (Gasior, 2006)  Lastly, ketones are a more efficient source of energy (produce more ATP) per unit of oxygen compared to glucose.

Another potential neuroprotective benefit of ketones is from the anti-inflammation and anti-oxidant effects of ketones. This has been shown in several different animal model of PD. One study looked at mice, which were treated with the neurotoxin MPTP. MTPT causes a neurodegeneration of the dopamine neurons similar to what is seen in PD. The mice which were treated with KD prior to injection with MPTP, were shown to have had decreased pro-inflammatory cytokines (interleukin-1 beta, interleukin-6, and tumor necrosis factor-alpha) levels in the substantia nigra. Importantly, this resulted in preserved levels of dopamine and protection against the motor dysfunction typically caused my MPTP. (Yang, 2010)

In another study using the rat model of PD induced by 6-OHDA also showed neuroprotective effects of ketones. The KD pretreated rats were found to have the dopaminergic neurons of the substantia nigra protected from the neurotoxicity of the 6-OHDA. The researchers felt that this was possibly due to decrease oxidative stress. They found less ROS and increased level of the antioxidant glutathione in the rats on the KD compared to those on normal diet. (Cheng, 2009)

So does this improved ATP production, decrease inflammation and decreased oxidative stress correlate with clinical improvement? A recent study looked just at that. In the PD model of rats, the rats feed a KD had improved motor function compared to rats feed a normal diet. (Shaafi, 2016)

So the next question then is, how does this translate clinically in humans with PD? To date there is only one small human study, that I am aware of. This study placed 7 PD patients on a KD, 5 of which remained on the KD for 28 days. Those 5 patients had on average a 43% reduction of their Unified Parkinson’s Diseases Rating scale. The clinically improved symptoms included: resting tremor, freezing, balance, gait, mood and energy level.(VanItallie, 2005)

In summary, animal studies, when exposed to neurotoxins that would typically cause PD, showed that ketones resulted in decrease inflammation, decrease ROS, and increase ATP production compared to animals on standard diets.  These findings correlated with improved dopamine levels and improved motor function.   There, however is limited data on how this translates to clinical benefits in PD patients.  The one study using the KD in PD patients has encouraging results, but more studies are needed.

Currently one of the limitation is that the KD is very hard to stick with.  Luckily there is another way to get into ketosis;  the use of *ketone supplement.   This supplement, which is a blend of ketone salts, that 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 PD or any other disease. However, based on what the research suggests for PD and other neurological conditions, if something as simple as drinking this supplement could help, why not give it a try?

a-new-fuel

Bibliography

Cheng, B. (2009). Ketogenic diet protects dopaminergic neurons against 6-OHDA neurotoxicity via up-regulating glutathione in a rat model of Parkinson’s disease. Brain Research , 1286, 25-31.
Cunnane, S. E. (2011). Brain fuel metabolism, aging and Alzheimer’s disease. Nutrition (27), 3-20.
Gano, L. (2014). Ketogenic diets, mitochondria, and neurological diseases. Journal of Lipid Research , 55, 2211-2228.
Gasior, M. (2006). Neuroprotective and disease-modifying effects of the ketogenic diet. Behavioral Pharmacology , 17, 431-439.
Masino, S. A. (2016). Ketogenic Diet and Metabolic Therapies. (S. A. Masino, Ed.) Oxford.
Shaafi, S. (2015). Modulatory role of ketogenic diet on neuroinflammation; a possible drug naive strategy to treatment of Parkinson’s disease. Advances in Bioscience and Clinical Medicine , 3 (4), 43-47.
Shaafi, S. (2016). The efficacy of the ketogenic diet on motor functions in Parkinson’s disease: A rat model. Iranian Journal of Neurology , 15 (2), 63-69.
VanItallie, T. (2005). Treatment of Parkinson disease with diet-induced hyperketonemia: A feasibility study. Neurology , 65, 728-730.
Yang, X. (2010). Neuroprotective and Anti-inflammatory Activities of Ketogenic Diet on MPTP-induced Neurotoxicity. Journal of Molecular Neuroscience , 42, 145–153.
*These products are not intended to are not intended to diagnose prevent treat or cure any disease. If you are under medical supervision for any allergy, disease, taking prescription medications or you are breastfeeding contact your medical provider before adding any new supplements to your daily regimen.
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.

 

Bibliography

 

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.

 

 

Fuel your body with the power of ketones

Ketones are an alternative fuel source for our brain and body.

Our bodies need energy to preform our daily activities. This energy is at the molecular level is called ATP. ATP is produced in the mitochondria of all cells. It however also takes energy to produce ATP. This energy comes from the break down of one of two different fuel sources, glucose or ketones.

  1. Glucose is the broken down to produce ATP by the process called glycolysis
    1. Glucose comes from
      1. Carbohydrates that we eat
      2. The break down of the stored glucose in the form of glycogen
      3. Protein from our diet that break down into amino acids into glycogen then into glucose
  2. Ketones are broken down to produce ATP thru the process called Beta- oxidation
    1. Ketones are formed by the break down of fats.
      1. There are 3 different ketones (ketone bodies):
        1. Acetoacetate
        2. Beta-hydroxybutyrate
        3. Acetone

How can I get into ketosis?

  1. Starvation
  2. Intense exercise
  3. Eating ketogenic diet (70% fats, 20% proteins and 5% carbohydrates)
  4. Adding endogenous ketone supplement

The majority of the US population is currently only fueled by glucose, since the body is not able to tap into the second fuel source of ketones until it has run out of glucose. Our bodies however are designed to use either ketones or glucose as a mechanism to protect our species in times of starvation. Just think about how we lived in the caveman days when there was not any grocery stores or McDonalds on every block.  In the summer and spring when food was plentiful, cavemen would eat more food and pack on and store the extra as fat.  Then in the fall and winter when food was scarce, the cavemen would live off that extra stored fat by switch over from using glucose to ketones as primary fuel source.

The brain actually prefers to use ketones as a fuel when it is available.

There are 3 main reasons why ketones are a better source of energy for your brain.

  1. Ketones produce more ATP than glucose.
  2. Ketones are a cleaner less toxic source of energy since they produce less carbon dioxide and free radicals than when the body uses glucose as a fuel source
  3. Unlike glucose, ketones do not depend on insulin to get into the cells for use.

Are you often fatigued in the middle of the day? Do you have a hard time and need more energy to get thru a busy day at work, a long workout or just for a day of play? If so, instead of reaching for a high calorie candy bar, soda or energy drink, which will cause you to crash in a couple of hours, consider changing your fuel source to ketone based instead of glucose.

 

Hello from Dr. Deb

 

An alternative approach to Neurology

Hello Dr. Deb here. I just wanted to say thanks for liking my Facebook page @ https://www.facebook.com/BrainBodyFitness/. I also wanted to introduce myself to those who do not know me. I am currently 48 years old. I am a wife and a mom of wonderful 2 young girls. I have been practicing neurology for over 18 years. I specialize in headache medicine but still manage all types of neurological diseases including Alzheimer’s dementia, seizures, strokes, multiple sclerosis and Parkinson’s disease. However pain and migraines are the conditions I see the most.

I started this website and my Facebook page because over the years my approach to the practice of medicine and specifically neurology has changed. I previously believed that my job was just to find the right pill for your symptoms. I since have come to the conclusion that sometimes the best medicine is not a pill that I can give, but a healthy life style that you choose for yourself. I have discovered this both thru my patients but also with my personal experience. I too suffer from migraines and depression but since making some changes with exercise and changes my diet to include ketosis I have had significant improvement in my symptoms.

Over the last couple of years I have been doing more and more research on the powers of exercise, nutrition and most recently the benefits of ketones. I will be making a series of videos over the next several of weeks so that I can share with some of what I have learned.  I hope that you will find some value in these videos.

Sincerely,

Dr. Deb

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?

Bibliography

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.

 

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.

 

fuel pump

Benefits of fueling your body with ketones

Why Ketones are a better fuel source than glucose

Where do our bodies get the energy to fuel our activities of daily living? 

Glucose is the main fuel source of our bodies, but there is another type of fuel that is available to our bodies, ketones.  Ketones are a natural by-product of fat metabolism.  When the body has run out of glucose to use as fuel it will switch fuel sources and start converting fat into fatty acids and then into ketones.  Our bodies were designed to use this duel source of energy based on how we lived in the caveman days.  In the summer and spring when food was plentiful, cavemen would eat more food and pack on the extra and store it as fat.  Then in the fall and winter when food was scarce, the cavemen would live off that extra stored fat.   Nowadays, since food supply is plentiful all year around and there is no physiological need or demand to live off the stored fat, thus we may just keep packing it on, all year around.

What are the differences between ketones and glucose as a source of energy?

Research suggests that ketones are a better, cleaner source of energy for the body and actually provide more energy than glucose.  Unlike glucose, ketones do not depend on insulin to get into the cells for use. Ketones produce less carbon dioxide and free radicals than when the body uses glucose as a fuel source thus are less toxic for our body, making it a cleaner fuel source. Unfortunately, ketones are harder energy source for our bodies to tap into since they require your body to be in either a starvation mode or at least be in a state of very low in carbohydrates.  Nowadays, the most common way of getting the body to produce ketones, or be in a state of ketosis, is by being on a very low carb diet i.e. a ketogenic diet.  Typically, a ketogenic diet consists of 5-10% carbohydrates, 20-25% protein and 65-75% fats.  As you can imagine this is not easy to achieve.

For those who do achieve ketosis, the benefits to the body and the brain are impressive.  Here are just a few of the benefits that are suggested by the research:

1) Better Brain Function

As a Neurologist this is the benefit of ketosis I have to list first.  If ketones are available, then they are the preferred fuel for the brain over glucose.  Subjectively, this means improved focus and mental cognition.  Objectively, it has been shown to improve memory in patients with Alzheimer’s dementia.  A ketogenic diet has been used for over 80 years in the treatment of difficult to control seizures.  It is also being studied in: Parkinson’s disease, ALS, traumatic brain injury, and hypoxic brain injury.  Ketosis has also been shown to be beneficial in patients with migraine headaches, ADD, PTSD and depression.

2) Better Athletic Performance

Forget carb loading, for better athletic performance.  Ketones are a better energy source for your workouts.  Ketones provides  more ATP (adenosine triphosphate) than glucose.  Subjectively, many people who achieve ketosis report feeling of increased energy levels.  Having more ATP means more energy to workout longer and harder. Objectively, several studies on endurance athletes have shown that athletes who are in ketosis are able to perform at a higher level for a longer period of time.

3) Fat Loss

When your body is in ketosis it is now literally a ‘fat burning machine’.  Without having carbohydrates/glucose around for energy, your body starts releasing stored fat, which then will be turned into ketones for energy. Thus, inches drop off faster than with a low-fat high carb diet because you are actively burning up your stored fat.  Additionally, high fat diet have a protein (muscle) sparing effect so if you are calorie restricted, your body will be protected against breakdown of skeletal muscle as a source of fuel.

4) Improved Diabetes

Diabetes is either due to a decreased insulin production (type 1 diabetes) or insulin resistance (type 2 diabetes). Insulin is required to transport glucose into the cells for use.   In type 1 diabetes, there is not enough insulin around for the amount of glucose in the body. In type 2 diabetes, the cells are ‘resistant’ to the insulin that is around, and the cells are not able to process the glucose. Since all carbohydrates we eat break down into glucose, treatment of diabetes is often focused around lowering the glucose level, thus eating a low carb diet is recommended. Studies in individuals with type 2 diabetes using either, a very low carbohydrate or a ketogenic diet have had impressive results. These studies have showed that the participants were able to decrease or completely withdrawal off of the use of insulin, along with having major weight loss in a matter of just a few weeks. Also, it has been reported that eating a high fat, ketogenic diet can also improve insulin sensitivity, meaning the insulin that is around works better.

5) Less Inflammation

One of the ketones produced by the body is beta-hydroxybutyrate, has been shown to have an anti-inflammatory effect. Reports show individuals eating a ketogenic diet have some symptomatic improvement from rheumatoid arthritis, polycystic ovary disease, migraine headaches, eczema, and other conditions caused by inflammatory processes.

If ketosis is so good for you then why isn’t everyone doing it?

Well, first of all, most mainstream nutritionists and the USDA still recommend carbohydrates as a main staple of our diet.  Second, we live in a world that is addicted to carbohydrates.  Thus, most people simply cannot adhere to the strict diet that is required to get into and stay in ketosis through nutritional adjustments of eating so few carbohydrates.

So what if there was a supplement of exogenous ketones that could put you in therapeutic ketosis within an hour, despite your diet, and allow you to potentially to tap into the above-mentioned benefits without having to be on a strict ketogenic diet?  Sounds too good to be true, doesn’t it?   Luckily, such a supplement was developed under US Department of Defense commissioned research for use in Navy Seal divers to prevent seizures that could occur in association with using high-oxygen re-breathers (oxygen toxicity).   A ketone supplement that was inspired based on that research and has been released for sale to the public.  If you would like more information about this new ketone supplement check it out.

If you would like some help starting a ketogenic diet I would be happy to help.

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Bibliography

Di Lorenzo, C. e. (2015). Migraine improvement during short lasting ketogenesis: a proof-of concept study. European Journal of Neurology (22), 170–177.
D’Agostino, D. P. (2013). Therapeutic ketosis with ketone ester delays central nervous system oxygen toxicity seizures in rats. American Journal of Physiology. Regulatory, Integrative and Comparative Physiology, 304, R829–R836.
Paoli, A. E. (2013). Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. European Journal of Clinical Nutrition (67), 789-796.
Stafstrom, C. R. (2012). The Ketogenic diet as a treatment paradigm for diverse neurological disorders. Frontiers in Pharmacology, 3, 1-8.
Youm, Y. (2015). Ketone body β-hydroxybutyrate blocks the NLRP3 inflammasome-mediated inflammatory disease. Nature Medicine, 21 (3), 263–269.
These statements have not been evaluated by the Food and Drug Administration. These products are not intended to are not intended to diagnose prevent treat or cure any disease.
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.