Tag Archives: keto diet

Man with alzheimers[This article discusses health improvements based, at least in part, on a ketogenic diet. Dr. Loren Cordain and many others, including The Paleo Diet editorial review board, don’t recommend or endorse long-term ketogenic dieting for the general public. They do acknowledge that it can be effective if used short-term and as a therapeutic measure for Alzheimer’s and other diseases.]

Peter Dredge’s book Beating Alzheimer’s, the enemy at the gate: turning despair into hope and action [1], recounts his wife Ann’s early-onset Alzheimer’s diagnosis and their intense struggle with both the disease and “conventional” medical treatment. They refused to accept what most of us believe; that Alzheimer’s is unstoppable, incurable, and irreversible (at one-point Ann was offered euthanasia.) Instead, they researched every nontraditional alternative.

They discovered the work of Dr. Mary Newport [2] and Dr. Dale Bredesen [3] and using that work as a guide, they achieved both short term relief from the worst symptoms, and measurable reversal of the condition. Ann, initially given only three months to live, is sometimes referred to as “probably the first New Zealander to come back from end-stage Alzheimer’s” [4].

Diet and supplementation contributed heavily to Ann’s progress. Drs. Newport and Bredesen, among many others, have exhaustively researched how the conventional Western diet, heavy in carbs, sugar, inflammatory oils and additives, can create a “perfect storm” in the brain. While food choices are not the only Alzheimer’s culprits, dietary changes can be pivotal in slowing—and even reversing—cognitive decline.

 

Dr. Newport and coconut oil

Dr. Newport’s husband Steve also suffered early-onset Alzheimer’s. Frustrated by conventional medicine’s lack of options, she began her own internet research. As passionately and painstakingly described in her book Alzheimer’s Disease – What If There Was A Cure? The Story of Ketones, [3] she discovered research on a prototype “medical food” (Ketasyn, a forerunner of Axona [5]) for dementia patients. The food was based on medium-chain triglycerides derived from coconut and palm kernel oil. Since the food itself was not yet available, Dr. Newport calculated the available MCT’s in coconut oil and added this to Steve’s diet.

Steve responded dramatically and immediately to coconut oil, and later MCT oil, consuming both regularly. His caregivers, including Dr. Newport, all noticed that he “was back,” with improved life and coping skills (dexterity, gait, personality,) better short-term memory, and measurably improved cognitive exam scores. Two years later, “stable” MRI results showed that there had been little, if any, additional brain atrophy during this oil-supplementation phase.

Steve did not experience a miracle cure, but rather measurable, intermittent relief from the worst symptoms of Alzheimer’s over fifteen years. Average life expectancy after diagnosis is 3-11 years [6]. During this time, the family diet was gradually modified along more classic ketogenic, or at least lower-carb lines. Steve also later used prototype “ketone esters,” then being developed by Dr. Richard Veech et al. [7]

Like Steve, Ann Dredge also responded quickly to a 60/40 MCT to coconut oil mixture. Four ounces each day, caused her daily, hour-long full-body twitching episodes to disappear. The same mixture could alleviate any rare recurrence. Dressing herself became much easier, and the oil mixture would also help calm Ann during what Peter calls “more-delusional episodes” of anxiety and confusion.

Ann also follows a ketogenic diet, exercises when possible, minimizes stress, and continues to use the oil mixture to this day. Symptoms often resume or intensify if she misses a dose. [1]

 

Ketones and the brain

Dr. Newport’s original 2008 case study [8], available on her website, succinctly introduces ketones, and ketosis, in the context of Alzheimer’s and other chronic diseases. Ketosis, the body’s use of fat-derived “ketone bodies” for energy (instead of glucose) has been widely popularized in the last few years due to the ketogenic diet craze.

As most keto dieters know, our bodies (and brains) come “factory equipped” to function in the absence of exogenous glucose. While we manufacture some glucose internally, due to our ability to survive on ketones, we don’t need to consume additional glucose in order to maintain bodily function. Keto texts, including Dr. Newport’s, often refer to starvation or fasting as a normal context for ketosis, but low-enough carbohydrate dieting produces the same result.

Interestingly, full ketosis is not the only way to increase available ketones—especially for use by the brain.

High fat foods and supplements like coconut or MCT oil can provide medium-chain triglycerides, which are readily converted to ketones. These become available immediately in the bloodstream. MCT oil supplementation, in particular, has been shown to increase bioavailable ketones even without reducing dietary carbohydrates [13]. The brain will preferentially use available ketones even if glucose is also present. That is, full ketosis is not required for the brain to take advantage of ketones [9]. One reason, or perhaps the main reason, for this is that ketones freely cross the blood-brain barrier.

Glucose, on the other hand, requires a more complex chemical process (involving insulin) to be made available to the brain.

Alzheimer’s is often characterized by insulin insensitivity in the brain and has been called “Type 3 Diabetes” by some researchers [10]. They theorize that the brain atrophies over time as glucose provides less and less available energy—even if ingested in prodigious amounts. They also note that the brain can develop this insensitivity even if the patient is not clinically “diabetic” [11].

 

Strong anecdotal evidence

Steve and Ann’s quick reactions to ingesting medium- and long-change triglycerides, metabolized into ketone bodies, appears to show that energy deprivation in the brain could be a major contributor to Alzheimer’s.

Dr. Newport carefully gathered numerous testimonials in her books, which she received during heroic efforts to raise awareness of Steve’s progress, both within and outside of the medical community. Not everyone responds as quickly or easily as Steve, or Ann Dredge, but even the slightest improvement can be welcome to the afflicted, as well as desperate family members or caregivers.

It should be noted that this “oil therapy” is not a cure but appears to slow, arrest and mitigate—sometime even reverse—multiple gross Alzheimer’s symptoms.

According to Dr. Dale Bredesen (a neurologist specializing in Alzheimer’s research,) insulin resistance is only one of several possible contributing co-factors to Alzheimer’s and other dementias. Nevertheless, his own protocol is also based on a ketogenic diet, including supplemental MCT or coconut oil. [3] His book also contains many corroborative case studies and testimonials.

Dr. Bredesen’s protocol will be examined in a subsequent article.

 

Lack of mainstream acceptance

The Dredges, Newports, and Dr. Bredesen have all experienced resistance on many levels as they explored or tried to promote awareness of these ideas.

Peter Dredge recounts repeated instances of vigorous opposition to the idea that Alzheimer’s could be treated. He has often been treated very negatively and was even threatened with legal proceedings to remove Ann from his care. His courageous refusal to accept conventional medicine’s death sentence on his beloved wife is a strong theme throughout his book. Ann is still with us.

Dr. Newport similarly describes being repeatedly stymied as she tried to follow conventional pathways to raise awareness of Steve’s modest recovery. Attempts to exhibit or speak at Alzheimer’s Association-sponsored events were denied or shut down, once with a public announcement that the Association “did not support” coconut oil research. She was also privately told that “extensive clinical trials” would be needed before her ideas could be publicly discussed.

As Dr. Bredesen’s book [3] shows, money for “extensive clinical trials” is controlled by various institutional review boards and hard to come by. His own protocol was denied funding as “too complicated,” despite many successful case studies [12].

Conventional medicine’s intransigence, especially when faced with effective but non-traditional methodologies, is well known to Paleo readers—many of whom have resolved serious health conditions by abandoning conventional dietary advice.

The stories of Peter and Ann Dredge, and the work of Drs. Newport and Bredesen, deserve much wider awareness.

 

REFERENCES:

  1. Beating Alzheimer’s, The Enemy at the Gate: Turning Despair into Hope and Action EBook: Peter Dredge: Gateway. https://www.amazon.com/Beating-Alzheimers-Enemy-Gate-Turning-ebook/dp/B07HH67GV3/ref=sr_1_4 crid=1OL2PXR69Y6EO&keywords=beating+alzheimers&qid=1560174789&s=gateway&sprefix=beating+al%2Caps%2C187&sr=8-4.
  2. Newport, Mary T. Alzheimer’s Disease: What If There Was a Cure?: The Story of Ketones. Second edition, Basic Health Publications, Inc, 2013.
  3. Bredesen, Dale E. The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline. Avery, an imprint of Penguin Random House, 2017.
  4. “Beating Alzheimer’s Disease? Anne Dredge’s ‘huge Improvements’ with Dale Bredesen Treatment.” RNZ, 21 Sept. 2018, https://www.rnz.co.nz/national/programmes/afternoons/audio/2018663546/beating-alzheimer-s-disease-anne-dredge-s-huge-improvements-with-dale-bredesen-treatment.
  5. Henderson, Samuel T., et al. “Study of the Ketogenic Agent AC-1202 in Mild to Moderate Alzheimer’s Disease: A Randomized, Double-Blind, Placebo-Controlled, Multicenter Trial.” Nutrition & Metabolism, vol. 6, 2009, p. 31. www.ncbi.nlm.nih.gov, doi:10.1186/1743-7075-6-31.
  6. “What to Know about the Stages of Alzheimer’s.” Mayo Clinic, https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/in-depth/alzheimers-stages/art-20048448.
  7. Kashiwaya, Yoshihiro, et al. “A Ketone Ester Diet Exhibits Anxiolytic and Cognition-Sparing Properties, and Lessens Amyloid and Tau Pathologies in a Mouse Model of Alzheimer’s Disease.” Neurobiology of Aging, vol. 34, no. 6, June 2013, pp. 1530–39. PubMed, doi:10.1016/j.neurobiolaging.2012.11.023.
  8. Newport, Mary. “What If There Was a Cure for Alzheimer’s Disease and No One Knew?  A Case Study by Dr. Mary Newport.” www.CoconutKetones.Com , Mary Newport, MD, 22 July 2008, http://coconutketones.com/wp-content/uploads/2016/09/whatifcure.pdf.
  9. Reger, Mark A., et al. “Effects of β-Hydroxybutyrate on Cognition in Memory-Impaired Adults.” Neurobiology of Aging, vol. 25, no. 3, Mar. 2004, pp. 311–14. DOI.org (Crossref), doi:10.1016/S0197-4580(03)00087-3.
  10. de la Monte, Suzanne M., and Jack R. Wands. “Alzheimer’s Disease Is Type 3 Diabetes–Evidence Reviewed.” Journal of Diabetes Science and Technology (Online), vol. 2, no. 6, Nov. 2008, pp. 1101–13.
  11. Schilling, Melissa A. “Unraveling Alzheimer’s: Making Sense of the Relationship between Diabetes and Alzheimer’s Disease 1.” Journal of Alzheimer’s Disease, vol. 51, no. 4, Jan. 2016, pp. 961–77. content.iospress.com, doi:10.3233/JAD-150980.
  12. Bredesen, Dale E. “Reversal of Cognitive Decline: A Novel Therapeutic Program.” Aging, vol. 6, no. 9, Sept. 2014, pp. 707–17. PubMed, doi:10.18632/aging.100690.
  13. Courchesne-Loyer, Alexandre, et al. “Stimulation of Mild, Sustained Ketonemia by Medium-Chain Triacylglycerols in Healthy Humans: Estimated Potential Contribution to Brain Energy Metabolism.” Nutrition, vol. 29, no. 4, Apr. 2013, pp. 635–40. ScienceDirect, doi:10.1016/j.nut.2012.09.009.

 

When it comes to brain fuel – glucose is king.[1] Glucose is the brain’s primary source of fuel and it is quite narrowly regulated inside our body as a result. This is referred to as glucose homeostasis.[2] There are two key players in this process – insulin and glucagon.[3] These two hormones are kept in balance so that our blood sugar remains stable. When we eat, the ratio of insulin to glucagon is high – which helps to facilitate many postprandial (after meal) processes in the body.[4]

The standard American diet is very high in glucose – meaning it’s high in carbohydrates like bread, pasta, baked goods, and juices.[5] While glucose is the king of brain (and body) fuel, we do also have the ability to fuel our brains with ketone bodies, which is part of why low carb diets are currently exploding in popularity.[6] Heck, even I got in on the action, and wrote a low carb cookbook. (Note that while the Paleo Diet is lower carbohydrate than the standard American diet, at www.thepaleodiet.com, Dr. Loren Cordain and the Editorial Board do not support extreme low-carbohydrate diets like the Ketogenic diet.)

 

How the Body Manages Glucose

The nuts and bolts of how our brain handles glucose is actually very fascinating. To easily explain a very complex situation, it is best to start by describing the various different metabolic states which bring about different activity in the body and brain. For example, when we lack carbohydrates, our liver glycogen stores are rapidly used and fatty acids are then shuttled (from stored fat,) to provide energy via a process called oxidation.[7] These changes rapidly makes the body less reliant on glucose as it addresses the shortage.

Fatty acid oxidation allows the limited supply of glucose to be conserved for the brain – likely a mechanism developed to prevent starvation in our ancestors, during times of food scarcity.[8]

Think of this as a backup fuel system. Our body knows when one fuel is running low or not available, and switches to another energy supply. Taken to an extreme, when carbohydrates are low enough, for long enough, we go into ketosis.[9] The ‘keto flu’ – where we don’t feel very good after removing carbohydrates from our diet – is directly related to this switch in fuel systems.

On the flip side, if we have plenty of carbohydrates, our bodies will choose to store fat and rely on glucose for fuel since our ability to store carbohydrates is limited. This is also why marathon runners carb-load. They want to maximize this limited store and make sure more glucose is available for their bodies to draw upon as they step outside of a normal human activity range. Glycogen stores can be increased temporarily this way, but if you do this repeatedly – without burning the energy – you are very likely to gain weight instead.[10]

But when we really get into the details; how exactly does our brain sense glucose? and why is this important?

Essentially, there are neurons which detect the presence of glucose, and send signals to our brain, alerting the brain to its presence.[11] Since our brain controls our energy balance (as well as our hunger and satiety signaling processes) – the neurons which detect glucose are critically important.[12] But interestingly, these neurons are located outside the blood-brain barrier – not where you might expect.

 

What Happens to the Brain when Glucose Balance is Disrupted?

When glucose gets out of balance, diseases, obesity, and other conditions develop. But how does this happen, if we have glucose sensing neurons? In some cases, cells such as these neurons, can die and this is tightly related to brain disorders and degenerative brain conditions.[13] Also, neurotransmitter synthesis requires glucose, and our brain will simply have extreme issues if glucose levels (or regulation of glucose sensing) is disrupted.[14]

Glucose is actually shuttled from the blood to the brain through GLUT1 transporters on the surface of the brain which allows glucose to cross the blood-brain barrier.[15] This transport is carefully regulated and can be disrupted if the glucose-sensing neurons aren’t functioning appropriately. This can lead to serious issues.

Most glucose in the brain is used for ‘thinking’ and ‘processing’. These are broad terms, but essentially mean that without enough glucose in the brain, we can’t think properly, or process information. This disruption is similar to what is seen when alcohol is consumed, for example.

These processes (and glucose) are very critical for both learning and memory, and one can quickly see how glucose disruption and cell malfunction or cell death can greatly impair our brain’s critical processes.[16]

Glucose is in fact even more critical for other functions. For example, glucose can be used to synthesize glutamate, glycine, aspartate, and other important compounds. This is critical, as these compounds normally cannot easily gain entry directly into the brain, without glucose being used to synthesize them.[17] Another example of the importance of glucose, is autophagy. Autophagy is a greatly important process that “cleans out” dying or misfunctioning cells. It can be disrupted by poor glucose metabolism. In the simplest terms, think of it as recycling – but for the body.[18] Just as we recycle to provide better results for the earth – our body has internal mechanisms of recycling, for our own well-being. Glucose is also critical for metabolic coupling – where compounds made in one cell, can be used by a neighboring cell.[19] Think of it as similar to your neighbor borrowing a cup of sugar from you (though hopefully as a Paleo Dieter, you’re not keeping big bags of sugar in your kitchen.)

About 50 percent of all glucose in the body is used by the brain – which helps explain the ‘hangry’ state that we all experience.[20] If there isn’t glucose in the brain – neurotransmitters are not produced. This means neurons can’t talk to each other and helps explain our confusion and foul mood when our blood sugar gets very low.

Interestingly, research has also shown a direct link between too much sugar (specifically fructose) – and premature aging. Other studies have shown that too much glucose can be linked to cognitive decline and memory issues.[21] This research is the most frequently cited when articles claim that ‘sugar can kill us’, or ‘sugar can cause Alzheimer’s’. Type 2 diabetes is of course known as the disease where our bodies simply become resistant to insulin – truly scary.

Glucose sensing in the brain is critically important, and a Paleo Diet® will keep glucose levels at normal, healthy levels – leading to much better brain health and a healthier life overall.

 

References

  1. Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587-97.
  2. Tups A, Benzler J, Sergi D, Ladyman SR, Williams LM. Central Regulation of Glucose Homeostasis. Compr Physiol. 2017;7(2):741-764.
  3. Kalra S, Gupta Y. The Insulin:Glucagon Ratio and the Choice of Glucose-Lowering Drugs. Diabetes Ther. 2016;7(1):1-9.
  4. Kalra S, Gupta Y. The Insulin:Glucagon Ratio and the Choice of Glucose-Lowering Drugs. Diabetes Ther. 2016;7(1):1-9.
  5. Sartorius K, Sartorius B, Madiba TE, Stefan C. Does high-carbohydrate intake lead to increased risk of obesity? A systematic review and meta-analysis. BMJ Open. 2018;8(2):e018449.
  6. Laffel L. Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes. Diabetes Metab Res Rev. 1999;15(6):412-26.
  7. Purdom T, Kravitz L, Dokladny K, Mermier C. Understanding the factors that effect maximal fat oxidation. J Int Soc Sports Nutr. 2018;15:3.
  8. Houten SM, Wanders RJ. A general introduction to the biochemistry of mitochondrial fatty acid β-oxidation. J Inherit Metab Dis. 2010;33(5):469-77.
  9. Miller VJ, Villamena FA, Volek JS. Nutritional Ketosis and Mitohormesis: Potential Implications for Mitochondrial Function and Human Health. J Nutr Metab. 2018;2018:5157645.
  10. Ma Y, Olendzki B, Chiriboga D, et al. Association between dietary carbohydrates and body weight. Am J Epidemiol. 2005;161(4):359-67.
  11. Burdakov D, Luckman SM, Verkhratsky A. Glucose-sensing neurons of the hypothalamus. Philos Trans R Soc Lond, B, Biol Sci. 2005;360(1464):2227-35.
  12. Routh VH. Glucose sensing neurons in the ventromedial hypothalamus. Sensors (Basel). 2010;10(10):9002-25.
  13. Hotchkiss RS, Strasser A, Mcdunn JE, Swanson PE. Cell death. N Engl J Med. 2009;361(16):1570-83.
  14. Bak LK, Schousboe A, Sonnewald U, Waagepetersen HS. Glucose is necessary to maintain neurotransmitter homeostasis during synaptic activity in cultured glutamatergic neurons. J Cereb Blood Flow Metab. 2006;26(10):1285-97.
  15. Morgello S, Uson RR, Schwartz EJ, Haber RS. The human blood-brain barrier glucose transporter (GLUT1) is a glucose transporter of gray matter astrocytes. Glia. 1995;14(1):43-54.
  16. Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587-97.
  17. Hertz L, Rothman DL. Glucose, Lactate, β-Hydroxybutyrate, Acetate, GABA, and Succinate as Substrates for Synthesis of Glutamate and GABA in the Glutamine-Glutamate/GABA Cycle. Adv Neurobiol. 2016;13:9-42.
  18. Glick D, Barth S, Macleod KF. Autophagy: cellular and molecular mechanisms. J Pathol. 2010;221(1):3-12.
  19. Steinman MQ, Gao V, Alberini CM. The Role of Lactate-Mediated Metabolic Coupling between Astrocytes and Neurons in Long-Term Memory Formation. Front Integr Neurosci. 2016;10:10.
  20. Mergenthaler P, Lindauer U, Dienel GA, Meisel A. Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends Neurosci. 2013;36(10):587-97.
  21. Calsolaro V, Edison P. Alterations in Glucose Metabolism in Alzheimer’s Disease. Recent Pat Endocr Metab Immune Drug Discov. 2016;10(1):31-39.

Both the keto diet and the paleo diet are all the rage right now, with many people choosing one or the other in an effort to change their eating habits, get healthier, and be better able to enjoy their lives. For many people, however, it can be difficult or even confusing to understand the differences between the two and how to manipulate their eating habits in order to achieve their goals. If you’re thinking about a drastic lifestyle change, consider how going paleo compares to going keto–and how those dietary changes can impact your life.

The Similarities

Both the keto diet and the Paleo Diet@ focus on reducing carbohydrate consumption. While the paleo diet aims at eating primarily the foods that would have been found in an earlier, caveman-era period of the human diet, the keto diet restricts carbs in an effort to send the body into ketosis, a state in which the body burns ketones for fuel. Ketones are derived from our fat stores. The carb restriction in both diets often leads to quick weight loss, especially early after making a dietary change. This carb restriction, however, often causes Keto and Paleo to be lumped into the same category–which can in turn be highly confusing for dieters. Both diets also restrict sugar and legumes and encourage dieters to consume diets high in animal protein and healthy fats.

The Differences

In order to choose the diet that’s right for you, it’s important to understand the key differences between keto and paleo.

Difference #1: Keto Relies Heavily on Macronutrient Balance

The keto diet works by keeping your body in that state of ketosis: the state at which, instead of burning carbohydrates for energy, the body swaps over and begins burning stored fat, instead. In order to maintain ketosis, it’s necessary to eat a diet high in healthy fats, moderate in protein, and extremely low in carbohydrates. The Paleo Diet, on the other hand, allows you to balance your macronutrients according to your personal needs.

Difference #2: The Paleo Diet Focuses on Removing Foods that are Hard to Digest

One of the key attributes of the paleo diet is its restriction of items like processed foods, dairy, and sugar, all of which can be difficult for the body to digest. Swapping to a paleo-based diet can help reduce inflammation throughout the body and lead to increased gut health. The keto diet, on the other hand, allows–and in some cases even encourages–full-fat dairy consumption.

Difference #3: The Paleo Diet Encourages Whole, Healthy Foods

The focus of the paleo diet is on eating whole, healthy foods that are good for your body and will give you the fuel you need to accomplish your daily tasks. The keto diet, on the other hand, primarily focuses on keeping your body in ketosis.

Difference #4: The Keto Diet is Unforgiving

Everyone ends up having a cheat day or a slip-up every now and then. That barbecue sauce turned out to have sugar in it that you weren’t anticipating; you didn’t know your soup had barley; you ended up eating a slice of birthday cake that wasn’t appropriate for your diet. On the keto diet, that means you’ll instantly fall out of ketosis and start over on your dietary approach. The paleo diet, on the other hand, doesn’t rely on a state that takes days or even weeks to achieve in order to meet your goal.

Which One is Right for You?

To learn more about the ketogenic diet and why we feel it is not a healthy diet for the long term, check out this thorough article by Dr. Loren Cordain.

For most people, the Paleo Diet is a great choice for improving overall health and sticking with a health-centered diet that will help reduce inflammation and make weight loss easier. The paleo diet doesn’t require regular counting and calculations; instead, it sets you up for success by providing you with a list of the foods that you should be avoiding and a list of the foods that can help you meet your dietary goals. The paleo diet also focuses heavily on removing highly processed foods that are difficult to digest, while many people who adhere to a keto diet choose to dodge some of the restrictions by consuming artificial sweeteners and other unhealthy dietary additions that can actually make it harder to lose weight.

The keto diet was originally intended to help manage a range of medical conditions, including epilepsy. The high-percentage weight loss is a side effect that many people enjoy, but it wasn’t its original intent. The paleo diet, on the other hand, takes people back to the diet that they were originally intended to eat, and brings a number of health benefits with it. By understanding the paleo diet more fully, you’ll discover that it can be a highly effective way to meet your dietary goals.  Most importantly, it is the diet you were intended to eat for a lifetime of optimum health.

 

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