Tag Archives: keto

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.



  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.



  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.

Ketogenic diets are one of the hottest trends in wellness right now. This past year, I even wrote a keto cookbook. In fact, they have become so popular, that many variations of low carb diets are currently spearheading their way into the mainstream. While any focus on a healthier way of eating should be viewed as a positive, rather than a negative – the question remains: are carbohydrates really so bad? There is, of course – a complex scientific answer to this question.

First, we must look at the research. What does it say, what does it not say, and were the methods used to extract these conclusions properly conducted? Secondly – is there conclusive scientific evidence that the type of carbohydrates ingested, makes a difference? Third – is it possible that there is significant sensationalism around keto diets, which may tend to cloud the actual scientific data. Which in turn may be used to support their popularity? Lastly, is a Paleo Diet® actually worse for weight loss than a keto diet – or are there significant benefits to both approaches

To answer these questions, we must do a deep dive into the research of low carbohydrate diets. The newest study to gain widespread attention, focused only on 164 adults – not exactly a large enough sample pool, to say the least. While the media is quick to write attention grabbing headlines (i.e. “new study shows that low carb diets are better for weight loss”) the data rarely – if ever – supports these dramatic conclusions (1, 2, 3, 4, 5, 6, 7, 8, 9, 10).

This study is no different. While the results did show good outcomes for people following a low carbohydrate diet – the study did not come close to proving that all carbohydrate intake is bad. It also did not show that a diet filled with healthy carbohydrates cannot be just as good (if not better) for sustained weight loss. As has been shown in numerous scientific studies, higher carbohydrate diets consistently have better long-term success in terms of compliance (11, 12, 13, 14, 15, 16, 17, 18, 19, 20). In simpler terms, this means that those eating more carbohydrates have a much easier time adhering to a dietary protocol, over the course of years of eating.

This should not be shocking. While keto (and other low carb diets) do typically result in some short-term weight loss – this is sometimes just water weight. Secondly, almost without fail, people do eventually return to consuming carbohydrates (though sometimes it is in a diminished volume). Subsequently, they often do gain back the weight they may have lost (21, 22, 23, 24, 25, 26, 27, 28, 29, 30). Gary Taubes did an excellent job of analyzing and synthesizing nearly a century’s worth of research on this very topic, in his scientific tome Good Calories, Bad Calories.

A different study from earlier this year, showed that a low-carb diet and a low-fat diet both provided nearly identical results for dieters. This study followed 600 people over the course of a year and showed predictable results. The main takeaway from the sum of these studies is the conclusion that limiting sugar and eating high quality nutrient dense foods – a central tenant of The Paleo Diet – is the best strategy for long term weight loss (31, 32, 33, 34, 35, 36, 37, 38, 39, 40).

This means vegetables are the best foods to eat, along with high quality proteins, and anti-inflammatory fats. When it comes to a healthy diet (and especially fat loss) – the body’s delicate biochemistry and neurology must be prioritized. What foods provide the best hormonal response, along with limiting cravings and supporting brain health? Over and over again – the scientific research has pointed to the foods consumed when following a Paleo Diet (41, 42, 43, 44, 45, 46, 47, 48, 49, 50).

Another interesting aspect of these studies – they have highly variable results. For example, in the aforementioned study – one person lost a miraculous 60 pounds – while another gained 20. This shows the genetic variability inherent in all populations. It also illustrates that one specific diet is never going to be the solution for the entire population (51, 52, 53, 54, 55, 56, 57, 58, 59, 60).

Controlling leptin, ghrelin, blood sugar, and limiting consumption of empty calories – are all cornerstones of any healthy dietary approach. This is because scientific data has shown that these elements all quickly lead to rapid weight gain, if not properly controlled (61, 62, 63, 64, 65, 66, 67, 68, 69, 70). One fascinating study even showed that by modulating actual dopamine receptors (in this case, specifically the D2 receptors) – binge eating could be almost completely eliminated. This links in with other fascinating studies, which show that processed foods (like cookies) – may be as psychologically rewarding as hard drugs, like cocaine. It may appear shocking at first, but once the underlying neuronal circuitry is understood, there is truthfully very little difference between how the brain responds to these over-powering stimuli (71, 72, 73, 74, 75, 76, 77, 78, 79, 80).

So, is a high carb/low fat diet the holy grail to weight loss, or is the answer consuming no carbohydrates at all? As with most things, the truth lies somewhere in the middle. Moderate carbohydrate consumption (like the amount consumed in a healthy, properly implemented Paleo Diet) – seems to have the best long-term results (81, 82, 83, 84, 85, 86, 87, 88, 89, 90). This is not to say that low carbohydrate diets do not have their benefits – they do. But as Dr. Cordain has rightly pointed out, there can also be significant issues that may arise in long term implementations of ketogenic diets (91, 92, 93, 94, 95, 96, 97, 98, 99, 100).

In summary – neither approach is wrong, but carbohydrates (especially natural, low sugar forms) – are not bad. In fact, you will usually become very deficient in potassium, very quickly, if you do not consume at least some healthy carbohydrates. Of course, common sense wisdom like this (backed by strong science) – does not sell nearly as well as headlines like ‘lose 20 pounds quickly with the keto diet!’.

High quality protein, healthy fats, and low sugar carbohydrate consumption is really all you need to prioritize, to have a perfectly healthy diet. This is a simple, easy-to-remember paradigm, and it is applicable to anyone – no matter your age or gender. As always – don’t believe the hype. Carbohydrates won’t kill you, or absolutely cause you to gain weight. Sticking to whole, natural carbohydrates (which are low in sugar) is the best approach to a healthy diet. You can certainly experiment with a ketogenic diet, but it is not the only option for sustainable weight loss. For more reading on the fascinating topic of ketogenic diets, please read Dr. Cordain’s excellent piece.


  1. Obert J, Pearlman M, Obert L, Chapin S. Popular Weight Loss Strategies: a Review of Four Weight Loss Techniques. Curr Gastroenterol Rep. 2017;19(12):61.
  2. Ma Y, Pagoto SL, Griffith JA, et al. A dietary quality comparison of popular weight-loss plans. J Am Diet Assoc. 2007;107(10):1786-91.
  3. Jönsson T, Granfeldt Y, Ahrén B, et al. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. Cardiovasc Diabetol. 2009;8:35. Published 2009 Jul 16. doi:10.1186/1475-2840-8-35
  4. Manheimer EW, Van zuuren EJ, Fedorowicz Z, Pijl H. Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. Am J Clin Nutr. 2015;102(4):922-32.
  5. Strychar I. Diet in the management of weight loss. CMAJ. 2006;174(1):56-63.
  6. Soeliman FA, Azadbakht L. Weight loss maintenance: A review on dietary related strategies. J Res Med Sci. 2014;19(3):268-75.
  7. Champagne CM, Broyles ST, Moran LD, et al. Dietary intakes associated with successful weight loss and maintenance during the Weight Loss Maintenance trial. J Am Diet Assoc. 2011;111(12):1826-35.
  8. Sacks FM, Bray GA, Carey VJ, et al. Comparison of weight-loss diets with different compositions of fat, protein, and carbohydrates. N Engl J Med. 2009;360(9):859-73.
  9. Otten J, Stomby A, Waling M, et al. Benefits of a Paleolithic diet with and without supervised exercise on fat mass, insulin sensitivity, and glycemic control: a randomized controlled trial in individuals with type 2 diabetes. Diabetes Metab Res Rev. 2017;33(1)
  10. Pitt CE. Cutting through the Paleo hype: The evidence for the Palaeolithic diet. Aust Fam Physician. 2016;45(1):35-8.
  11. Hu T, Yao L, Reynolds K, et al. Adherence to low-carbohydrate and low-fat diets in relation to weight loss and cardiovascular risk factors. Obes Sci Pract. 2016;2(1):24-31.
  12. Alhassan S, Kim S, Bersamin A, King AC, Gardner CD. Dietary adherence and weight loss success among overweight women: results from the A TO Z weight loss study. Int J Obes (Lond). 2008;32(6):985-91.
  13. Mcclain AD, Otten JJ, Hekler EB, Gardner CD. Adherence to a low-fat vs. low-carbohydrate diet differs by insulin resistance status. Diabetes Obes Metab. 2013;15(1):87-90.
  14. Kitabchi AE, Mcdaniel KA, Wan JY, et al. Effects of high-protein versus high-carbohydrate diets on markers of β-cell function, oxidative stress, lipid peroxidation, proinflammatory cytokines, and adipokines in obese, premenopausal women without diabetes: a randomized controlled trial. Diabetes Care. 2013;36(7):1919-25.
  15. Mcclain AD, Otten JJ, Hekler EB, Gardner CD. Adherence to a low-fat vs. low-carbohydrate diet differs by insulin resistance status. Diabetes Obes Metab. 2013;15(1):87-90.
  16. Kouris A, Wahlqvist ML, Worsley A. Characteristics that enhance adherence to high-carbohydrate/high-fiber diets by persons with diabetes. J Am Diet Assoc. 1988;88(11):1422-5.
  17. Anderson JW, Gustafson NJ. Adherence to high-carbohydrate, high-fiber diets. Diabetes Educ. 1989;15(5):429-34.
  18. Astrup A, Meinert larsen T, Harper A. Atkins and other low-carbohydrate diets: hoax or an effective tool for weight loss?. Lancet. 2004;364(9437):897-9.
  19. Pekkarinen T, Kaukua J, Mustajoki P. Long-term weight maintenance after a 17-week weight loss intervention with or without a one-year maintenance program: a randomized controlled trial. J Obes. 2015;2015:651460.
  20. Elfhag K., Rössner S. Who succeeds in maintaining weight loss? A conceptual review of factors associated with weight loss maintenance and weight regain. Obesity Reviews. 2005;6(1):67–85. doi: 10.1111/j.1467-789X.2005.00170.x.
  21. Blomain ES, Dirhan DA, Valentino MA, Kim GW, Waldman SA. Mechanisms of Weight Regain following Weight Loss. ISRN Obes. 2013;2013:210524.
  22. Mcnay DE, Speakman JR. High fat diet causes rebound weight gain. Mol Metab. 2012;2(2):103-8.
  23. Turk MW, Yang K, Hravnak M, Sereika SM, Ewing LJ, Burke LE. Randomized clinical trials of weight loss maintenance: a review. J Cardiovasc Nurs. 2009;24(1):58-80.
  24. Mobbs CV, Mastaitis J, Yen K, et al. Low-carbohydrate diets cause obesity, low-carbohydrate diets reverse obesity: a metabolic mechanism resolving the paradox. Appetite. 2007;48(2):135-8.
  25. Lamont BJ, Waters MF, Andrikopoulos S. A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice. Nutr Diabetes. 2016;6:e194.
  26. Maclean PS, Bergouignan A, Cornier MA, Jackman MR. Biology’s response to dieting: the impetus for weight regain. Am J Physiol Regul Integr Comp Physiol. 2011;301(3):R581-600.
  27. Iacovides S, Meiring RM. The effect of a ketogenic diet versus a high-carbohydrate, low-fat diet on sleep, cognition, thyroid function, and cardiovascular health independent of weight loss: study protocol for a randomized controlled trial. Trials. 2018;19(1):62.
  28. Obesity and Energy Balance: Is the Tail Wagging the Dog? J.C.K. Wells and M. Siervo in European Journal of Clinical Nutrition, Vol. 65, No. 11, pages 1173–1189; November 2011.
  29. Cornier MA. Is your brain to blame for weight regain?. Physiol Behav. 2011;104(4):608-12.
  30. Lean ME. Is long-term weight loss possible?. Br J Nutr. 2000;83 Suppl 1:S103-11.
  31. Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci. 2016;53(1):52-67.
  32. Delli bovi AP, Di michele L, Laino G, Vajro P. Obesity and Obesity Related Diseases, Sugar Consumption and Bad Oral Health: A Fatal Epidemic Mixtures: The Pediatric and Odontologist Point of View. Transl Med UniSa. 2017;16:11-16.
  33. Rippe JM, Angelopoulos TJ. Sugars, obesity, and cardiovascular disease: results from recent randomized control trials. Eur J Nutr. 2016;55(Suppl 2):45-53.
  34. Rippe JM, Angelopoulos TJ. Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding. Nutrients. 2016;8(11).
  35. Aller EE, Abete I, Astrup A, Martinez JA, Van baak MA. Starches, sugars and obesity. Nutrients. 2011;3(3):341-69.
  36. Dinicolantonio JJ, Berger A. Added sugars drive nutrient and energy deficit in obesity: a new paradigm. Open Heart. 2016;3(2):e000469.
  37. Malik VS, Popkin BM, Bray GA, Després JP, Hu FB. Sugar-sweetened beverages, obesity, type 2 diabetes mellitus, and cardiovascular disease risk. Circulation. 2010;121(11):1356-64.
  38. Carol S Johnston, Sherrie L Tjonn, Pamela D Swan, Andrea White, Heather Hutchins, Barry Sears; Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets, The American Journal of Clinical Nutrition, Volume 83, Issue 5, 1 May 2006, Pages 1055–1061.
  39. Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci. 2016;53(1):52-67.
  40. Yoshida Y, Simoes EJ. Sugar-Sweetened Beverage, Obesity, and Type 2 Diabetes in Children and Adolescents: Policies, Taxation, and Programs. Curr Diab Rep. 2018;18(6):31.
  41. Gómez-pinilla F. Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 2008;9(7):568-78.
  42. Wahl D, Cogger VC, Solon-biet SM, et al. Nutritional strategies to optimise cognitive function in the aging brain. Ageing Res Rev. 2016;31:80-92.
  43. Spencer, Sarah & Korosi, Aniko & Layé, Sophie & Shukitt-Hale, Barbara & Barrientos, Ruth. (2017). Food for thought: how nutrition impacts cognition and emotion. npj Science of Food. 1. 10.1038/s41538-017-0008-y.
  44. Volek JS, Sharman MJ, Love DM, et al. Body composition and hormonal responses to a carbohydrate-restricted diet. Metab Clin Exp. 2002;51(7):864-70.
  45. Yurko-mauro K, Alexander DD, Van elswyk ME. Docosahexaenoic acid and adult memory: a systematic review and meta-analysis. PLoS ONE. 2015;10(3):e0120391.
  46. Dauncey MJ. Nutrition, the brain and cognitive decline: insights from epigenetics. Eur J Clin Nutr. 2014;68(11):1179-85.
  47. Moore K, Hughes CF, Ward M, Hoey L, Mcnulty H. Diet, nutrition and the ageing brain: current evidence and new directions. Proc Nutr Soc. 2018;77(2):152-163.
  48. Gardener SL, Rainey-smith SR. The Role of Nutrition in Cognitive Function and Brain Ageing in the Elderly. Curr Nutr Rep. 2018;7(3):139-149.
  49. Lieberman HR. Nutrition, brain function and cognitive performance. Appetite. 2003;40(3):245-54.
  50. Burini, Roberto & Leonard, William. (2018). The evolutionary roles of nutrition selection and dietary quality in the human brain size and encephalization. 43. 19. 10.1186/s41110-018-0078-x.
  51. Stover PJ. Human nutrition and genetic variation. Food Nutr Bull. 2007;28(1 Suppl International):S101-15.
  52. Simopoulos AP. Genetic variation and nutrition. Biomed Environ Sci. 1996;9(2-3):124-9.
  53. Gibney MJ, Gibney ER. Diet, genes and disease: implications for nutrition policy. Proc Nutr Soc. 2004;63(3):491-500.
  54. Kalantarian S, Rimm EB, Herrington DM, Mozaffarian D. Dietary macronutrients, genetic variation, and progression of coronary atherosclerosis among women. Am Heart J. 2014;167(4):627-635.e1.
  55. Stover PJ. Influence of human genetic variation on nutritional requirements. Am J Clin Nutr. 2006;83(2):436S-442S.
  56. Bueno, N., De Melo, I., De Oliveira, S., & Da Rocha Ataide, T. (2013). Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: A meta-analysis of randomised controlled trials. British Journal of Nutrition, 110(7), 1178-1187. doi:10.1017/S0007114513000548
  57. Tay J, Thompson CH, Luscombe-marsh ND, et al. Long-Term Effects of a Very Low Carbohydrate Compared With a High Carbohydrate Diet on Renal Function in Individuals With Type 2 Diabetes: A Randomized Trial. Medicine (Baltimore). 2015;94(47):e2181.
  58. Wylie-rosett J, Aebersold K, Conlon B, Isasi CR, Ostrovsky NW. Health effects of low-carbohydrate diets: where should new research go?. Curr Diab Rep. 2013;13(2):271-8.
  59. Bartáková V, Kuricová K, Zlámal F, Bělobrádková J, Kaňková K. Differences in food intake and genetic variability in taste receptors between Czech pregnant women with and without gestational diabetes mellitus. Eur J Nutr. 2018;57(2):513-521.
  60. Xue Y, Li J, Yan L, Lu L, Liao FF. Genetic variability to diet-induced hippocampal dysfunction in BXD recombinant inbred (RI) mouse strains. Behav Brain Res. 2015;292:83-94.
  61. Ahima RS. Revisiting leptin’s role in obesity and weight loss. J Clin Invest. 2008;118(7):2380-3.
  62. Myers MG, Leibel RL, Seeley RJ, Schwartz MW. Obesity and leptin resistance: distinguishing cause from effect. Trends Endocrinol Metab. 2010;21(11):643-51.
  63. Friedman JM. Leptin and the regulation of body weigh. Keio J Med. 2011;60(1):1-9.
  64. Fleisch AF, Agarwal N, Roberts MD, et al. Influence of serum leptin on weight and body fat growth in children at high risk for adult obesity. J Clin Endocrinol Metab. 2007;92(3):948-54.
  65. Kalra SP. Circumventing leptin resistance for weight control. Proc Natl Acad Sci USA. 2001;98(8):4279-81.
  66. Scarpace PJ, Zhang Y. Elevated leptin: consequence or cause of obesity?. Front Biosci. 2007;12:3531-44.
  67. Weigle DS, Cummings DE, Newby PD, et al. Roles of leptin and ghrelin in the loss of body weight caused by a low fat, high carbohydrate diet. J Clin Endocrinol Metab. 2003;88(4):1577-86.
  68. Rohatgi KW, Tinius RA, Cade WT, Steele EM, Cahill AG, Parra DC. Relationships between consumption of ultra-processed foods, gestational weight gain and neonatal outcomes in a sample of US pregnant women. PeerJ. 2017;5:e4091.
  69. Poti JM, Braga B, Qin B. Ultra-processed Food Intake and Obesity: What Really Matters for Health-Processing or Nutrient Content?. Curr Obes Rep. 2017;6(4):420-431.
  70. Oginsky MF, Goforth PB, Nobile CW, Lopez-santiago LF, Ferrario CR. Eating ‘Junk-Food’ Produces Rapid and Long-Lasting Increases in NAc CP-AMPA Receptors: Implications for Enhanced Cue-Induced Motivation and Food Addiction. Neuropsychopharmacology. 2016;41(13):2977-2986.
  71. Berridge KC. ‘Liking’ and ‘wanting’ food rewards: brain substrates and roles in eating disorders. Physiol Behav. 2009;97(5):537-50.
  72. Wise RA. Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond, B, Biol Sci. 2006;361(1471):1149-58.
  73. Murray S, Tulloch A, Gold MS, Avena NM. Hormonal and neural mechanisms of food reward, eating behaviour and obesity. Nat Rev Endocrinol. 2014;10(9):540-52.
  74. Blum K, Gardner E, Oscar-berman M, Gold M. “Liking” and “wanting” linked to Reward Deficiency Syndrome (RDS): hypothesizing differential responsivity in brain reward circuitry. Curr Pharm Des. 2012;18(1):113-8.
  75. Swiecicki L, Scinska A, Bzinkowska D, et al. Intensity and pleasantness of sucrose taste in patients with winter depression. Nutr Neurosci. 2014.
  76. Kellerer M, Lammers R, Fritsche A, et al. Insulin inhibits leptin receptor signalling in HEK293 cells at the level of janus kinase-2: a potential mechanism for hyperinsulinaemia-associated leptin resistance. Diabetologia. 2001;44(9):1125-32.
  77. Bellisle F, Drewnowski A. Intense sweeteners, energy intake and the control of body weight. Eur J Clin Nutr. 2007;61(6):691-700.
  78. Caffaro CE, Hirschberg CB. Nucleotide sugar transporters of the Golgi apparatus: from basic science to diseases. Acc Chem Res. 2006;39(11):805-12.
  79. Willett WC, Ludwig DS. Science souring on sugar. BMJ. 2013;346:e8077.
  80. Grant JE, Potenza MN, Weinstein A, Gorelick DA. Introduction to behavioral addictions. Am J Drug Alcohol Abuse. 2010;36(5):233-41.
  81. Lindeberg S, Jönsson T, Granfeldt Y, et al. A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia. 2007;50(9):1795-807.
  82. Klonoff DC. The beneficial effects of a Paleolithic diet on type 2 diabetes and other risk factors for cardiovascular disease. J Diabetes Sci Technol. 2009;3(6):1229-32.
  83. Kowalski LM, Bujko J. [Evaluation of biological and clinical potential of paleolithic diet]. Rocz Panstw Zakl Hig. 2012;63(1):9-15.
  84. Gotsis E, Anagnostis P, Mariolis A, Vlachou A, Katsiki N, Karagiannis A. Health benefits of the Mediterranean Diet: an update of research over the last 5 years. Angiology. 2015;66(4):304-18.
  85. Tosti V, Bertozzi B, Fontana L. Health Benefits of the Mediterranean Diet: Metabolic and Molecular Mechanisms. J Gerontol A Biol Sci Med Sci. 2018;73(3):318-326.
  86. Romagnolo DF, Selmin OI. Mediterranean Diet and Prevention of Chronic Diseases. Nutr Today. 2017;52(5):208-222.
  87. Widmer RJ, Flammer AJ, Lerman LO, Lerman A. The Mediterranean diet, its components, and cardiovascular disease. Am J Med. 2015;128(3):229-38.
  88. Ma Y, Olendzki B, Chiriboga D, et al. Association between dietary carbohydrates and body weight. Am J Epidemiol. 2005;161(4):359-67.
  89. Wal JS, Mcburney MI, Moellering N, Marth J, Dhurandhar NV. Moderate-carbohydrate low-fat versus low-carbohydrate high-fat meal replacements for weight loss. Int J Food Sci Nutr. 2007;58(4):321-9.
  90. Sasakabe T, Haimoto H, Umegaki H, Wakai K. Association of decrease in carbohydrate intake with reduction in abdominal fat during 3-month moderate low-carbohydrate diet among non-obese Japanese patients with type 2 diabetes. Metab Clin Exp. 2015;64(5):618-25.
  91. Reddy ST, Wang CY, Sakhaee K, Brinkley L, Pak CY. Effect of low-carbohydrate high-protein diets on acid-base balance, stone-forming propensity, and calcium metabolism. Am J Kidney Dis. 2002;40(2):265-74.
  92. High protein diet brings risk of kidney stones. BMJ. 2002;325(7361):408.
  93. Macdonald HM, New SA, Fraser WD, Campbell MK, Reid DM. Low dietary potassium intakes and high dietary estimates of net endogenous acid production are associated with low bone mineral density in premenopausal women and increased markers of bone resorption in postmenopausal women. Am J Clin Nutr. 2005 Apr;81(4):923-33.
  94. New SA, MacDonald HM, Campbell MK, Martin JC, Garton MJ, Robins SP, Reid DM. Lower estimates of net endogenous non-carbonic acid production are positively associated with indexes of bone health in premenopausal and perimenopausal women. Am J Clin Nutr. 2004 Jan;79(1):131-8
  95. Willi SM, Oexmann MJ, Wright NM, Collop NA, Key LL Jr. The effects of a high-protein, low-fat, ketogenic diet on adolescents with morbid obesity: body composition, blood chemistries, and sleep abnormalities. Pediatrics. 1998 Jan;101(1 Pt 1):61-7.
  96. Wynn E, Krieg MA, Lanham-New SA, Burckhardt P. Postgraduate Symposium: Positive influence of nutritional alkalinity on bone health. Proc Nutr Soc. 2010 Feb;69(1):166-73.
  97. Cicero AF1, Benelli M2, Brancaleoni M3, Dainelli G3, Merlini D3, Negri R3. Middle and long-term impact of a very low-carbohydrate ketogenic diet on cardiometabolic factors: A multi-center, cross-sectional, clinical study. High Blood Press Cardiovasc Prev. 2015 Dec;22(4):389-94.
  98. Clifton PM, Condo D, Keogh JB. Long term weight maintenance after advice to consume low carbohydrate, higher protein diets–a systematic review and meta-analysis. Nutr Metab Cardiovasc Dis. 2014 Mar;24(3):224-35.
  99. Bielohuby M, Matsuura M, Herbach N, et al. Short-term exposure to low-carbohydrate, high-fat diets induces low bone mineral density and reduces bone formation in rats. J Bone Miner Res. 2010;25(2):275-84.
  100. Carol S Johnston, Sherrie L Tjonn, Pamela D Swan, Andrea White, Heather Hutchins, Barry Sears; Ketogenic low-carbohydrate diets have no metabolic advantage over nonketogenic low-carbohydrate diets, The American Journal of Clinical Nutrition, Volume 83, Issue 5, 1 May 2006, Pages 1055–1061, https://doi.org/10.1093/ajcn/83.5.1055.
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