Tag Archives: carbohydrates


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.

Paleo dieters often wonder when the rest of the world will catch up.

Most of all, they wonder when mainstream nutritional science will finally validate what they experience every day: safe and natural weight loss; freedom from chronic illness; vibrant energy all day long.

But mainstream nutritional researchers remain divided on basic diet and health issues and many factors inhibit progress—especially toward understanding non-conventional approaches like Paleo.

Freighted with years of conventional wisdom, torn by conflicting agendas, and (like scientists in all disciplines) too frequently impervious to new ideas, these savants often run in place. Covering new ground sometimes only moves a few inches a year.

A new study by Professor Nita G. Forouhi and colleagues provides some understanding of the lack of consensus when it comes to diabetes, and what drives it.

The study itself is an overview or meta-analysis of several current dietary therapies for type 2 diabetes (T2D).[1]

The authors discuss several interventions, including pros and cons from different camps within the nutritional field. Forouhi is not afraid to show both sides of each debate, especially regarding low-carbohydrate diets.

The analysis acknowledges that dietary interventions can mitigate or even reverse T2D but admits up front that these interventions are both “controversial and difficult.”  

Paleo readers will quickly note how conventional Western dietary wisdom underlies much of the controversy.

Some highlights:


Questions about data and dietary guidelines

Intriguingly, the study notes that basic scientific nutritional data is subject to manipulation:  

Moreover, lack of transparency in the development of guidelines and bias in the primary nutritional studies can undermine the development of reliable dietary guidelines; recommendations for their improvement must be heeded.

The study continues further down …more investment is needed in good quality research with a greater focus on overcoming the limitations of existing research.”

This frank admission is important in the context of what follows—including the discussions of unconventional therapies like low-carb and ultra-low calorie diets.

And bear in mind that entrenched conventional ideas do bias the analysis throughout including the diet-heart hypothesis (bias against saturated fat), and the traditional low-fat-high fiber agenda including a strong bias in favor of whole grains.


Unexpected disagreement on foods

Participants agree that patients should avoid processed meats, sodium, trans fats, refined grains and sugars, as well as sugary drinks.

Surprisingly, fruits and vegetables are dismissed by some as desirable but too expensive for low- to middle- income populations. Other researchers recommend them, but only in the context of weight loss.  

Diets that rely on vegetables for fiber (instead of whole grains) are discarded as “difficult without further discussion.

As an aside, the study stops short of endorsing unprocessed red meat (and even fish) claiming more research is needed.


The low carbohydrate conundrum

Low carbohydrate diets are discussed extensively, but not all researchers endorse them—even though the study admits that they work.

Macronutrient ratios (fat to carbohydrates to protein) are acknowledged as important, but no consensus exists on therapeutic ratios. The American Heart Association is cited as insisting that no population-wide recommendations can be made and that all advice should be individualized.

The research cited by Forouhi shows no real agreement on what constitutes low-carb, or what type of carbs are best. Reducing grains and legumes appears broadly acceptable but different factions disagree on fruit consumption.  Refined carbs are discouraged, but most researchers insist on including whole grains.

Carbohydrate percentages in the analysis vary from ketogenic levels to 40% of calories, or more.

Some researchers think low-carb diets arent sustainable (or desirable) because they think people will eat too much protein, or too much saturated fat.  

Others claim that low-carb diets have no affect at all on diabetesdirectly contradicting the studys premise that such diets are recognized as therapeutic.

The study concludes that low-carb is controversial, but candidly admits it deserves further study.


Weight loss

The study emphasizes weight loss as therapeutic, endorsing it as a cornerstone of diabetes treatment.

The study emphasizes the success that bariatric surgery patients have with T2D due to caloric reduction and the resulting normalization of glucose levels. It explores ultra-low calorie diets that mimic this sudden, dramatic drop in total calories.

However, these diets are acknowledged as hard to sustain over time, and often include heavily processed, high sugar, liquid meal-replacements. The study notes and accepts the high sugar component as a tradeoff for the overall reduction in calories.

Note: The drug industry has also taken note of this bariatric surgery effect and is developing a new pill that coats the intestines to prevent caloric uptake. The goal is to mimic the surgerys blood glucose results for T2D patients.


Looking beyond weight loss  

Something the Forouhi seems to miss is that while sudden weight loss improves blood glucose markers, this may not be the whole story. Focusing on weight loss alone ignores the central issue that whole grains affect blood glucose levels the same way refined grains do. [2]

Even if a whole grain-based diet promotes overall weight loss, with all its acknowledged positive effects, the grains themselves will still promote insulin resistance, intestinal permeability, overall systemic inflammationand diabetes.

Most diabetics are unlikely to choose drastic surgery, with its likelihood of complications, or highly processed, unsatisfying sugar-based liquid diets. Instead, they should consider an inexpensive, low-impact, health-promoting low-carb diet like Paleo.


Paleo: the original low-carb, weight loss diet  

Following a sustainable, satiating Paleo Diet is easy (compared to surgery) and addresses the study’s major concerns:

  • High fiber: anyone on the Paleo Diet for over 30 days knows that vegetables provide MORE fiber than any type of grains.
  • Lower calories:  well-planned Paleo Diets (approximately 2/3 vegetables by volume) provide satiety from protein and healthy fats (like coconut, avocado, and olive oils) without exceeding sensible caloric guidelines. (Anyone can overeat on any diet, but Paleo makes this far less likely.)
  • Low carbohydrates: Paleo carb calories come from healthy, low-glycemic sources like sweet potatoes, squash, and non-starchy colorful vegetables.

Properly followed, Paleo is by definition a sustainable, low carb, high-fiber diet. Exactly what Forouhi’s analysis recommends and it has been demonstrated as therapeutic for Type 2 Diabetes many times [3].



  1. Dietary and nutritional approaches for prevention and management of type 2 diabetes, 6/13/2018, published in The BMJ by professors Nita G. Forouhi, Anoop Misra, Viswanathan Mohan, Roy Taylor, and director William Yancy, retrieved here
  2. The Paleo Diet, Revised, by Loren Cordain, Ph.D., Professor Emeritus, copyright 2002, 2011, published by John Wiley & Sons, Hoboken, NJ; electronic edition, page 48
  3. The Paleolithic Diet is the best bet for diabetes and other diseases by Loren Cordain, Ph.D., Professor Emeritus, published in The Insider, Vol. 5, Issue 12, retrieved here


Are you an athlete heading into the offseason, and feeling concerned about how best to avoid putting on those holiday pounds?

Or perhaps you’re just wondering how to avoid putting on those holiday pounds… period?

The athlete, weekend warrior, and desk jocky all have this one thing in common.

If we create an eating plan on the foundation of it being real, whole foods, we’re far less likely to pack on pounds at any time of year, regardless of training volume, tempting treats left in the office, or shorter periods of daylight making it easier to hit snooze and stay under the covers.

Let’s carry this into the heading of sports nutrition.

Much of the advice for what an athlete needs to be eating provided by running publications, triathlon blogs, or even the USDA for that matter, sways quite heavily towards the idea that at least a moderate or sometimes a high percentage of calories needs to come from carbohydrates.

Recommendations that 45-65% of calories should come from carbohydrates, 15-30% calories from protein, and 15-30% of calories from fat (1), or that we should stick with low-fat eating (2), only serve to further perpetuate the myth that anything more than a little bit of fat is bad for us.

What does this have to do with staying lean for off-season?


It’s all about consistency.

If your diet is comprised primarily of local, in-season produce, natural fat, wild fish, grassfed meat and game, and you eat in this manner year round, there’s little tweaking that needs to be done going from onseason to off.

The one variable that needs a bit of a shift is the amount of carbohydrates we choose to eat in the form of the starchier root vegetables, such as yams or sweet potatoes, as well as the higher glycemic fruits such as bananas or mangoes. This pertains more to the active or athletic category versus those who haven’t yet included physical activity as part of their daily routine.

It’s quite simple:  the more we move our bodies, the more it make sense for us to include these specific types of carbohydrates, strategically.

For example, if you’re getting ready for a summer time Ironman triathlon and you’re planning a five hour bike ride followed by a two hour run at race pace, you can bet you’ll need to include some yam with dinner the night before as well as some banana with the first meal you have after you’ve rehydrated and rested.

This applies even to those athletes who follow a keto-Paleo approach and are already quite fat adapted.

Remember, the goal is not to shut off our ability to use carbohydrates as a fuel but rather, to not rely on it solely.

On the other hand, regardless of whether we are considering the diet of an athlete during offseason, or a sedentary person, both aren’t going to need the high amount of starch recommended by the USDA (3).

The simple fact is that eating too much starch, sugar or carbohydrates in general (yes, this includes fruit) prevents us from becoming efficient at using fat as our primary fuel source and consequently, sets us up for increased chances of developing many health issues, including heart disease, breast cancer, and type 2 diabetes (4).

If we eat more fat, we’re more satiated.  We do a better job at absorbing nutrients from our food.   We bathe our brain in the very macronutrient it’s largely made of (fat).

And we’re not as hungry as often!


So what’s the

If we stay consistent with our eating year round, with a focus on eating real food, moving and adjusting the amount we consume by listening to our body’s hunger cues, we stay lean.

There’s no secret, trick or tweak.

As I always say, “Eat food and move”.

It truly is that simple.


(1)  “Carbohydrate Intake during Exercise.” Human Kinetics. N.p., n.d. Web. 17 Sept. 2017.

(2)  Fong, R.D. Bethany. “Benefits of Low-Fat Diet.” LIVESTRONG.COM. Leaf Group, 18 July 2017. Web. 17 Sept. 2017.

(3)  https://www.cnpp.usda.gov/sites/default/files/dietary_guidelines_for_americans/PolicyDoc.pdf

(4)  Howard, Jacqueline. “More Benefits to a High-fat Mediterranean Diet.” CNN. Cable News Network, 18 July 2016. Web. 17 Sept. 2017.


Big Brains Do Not Need Carbs | The Paleo Diet

Evolution. It is a complex and interesting process.1, 2, 3, 4, 5, 6, 7, 8, 9, 10 Whether you agree with Jerry Coyne or not, there is much fascination with what exactly has led us to the current bodies and brains which we inhabit.11, 12, 13, 14, 15, 16, 17, 18, 19, 20 Two weeks ago The Quarterly Review of Biology published a controversial paper entitled “The Importance of Dietary Carbohydrate in Human Evolution.”21 Its preceding press release22 added “Big Brains Needed Carbs,” ensuring the controversy-eager media would jump all over the publication, including the University of Sydney, home of the GI Foundation. Of course this media frenzy23, 24, 25 is without critical analysis, and is simply a regurgitation of the same story. So the researchers behind this paper argued that as humans evolved from our Paleolithic ancestry, we needed carbohydrates (particularly starch) in order to develop larger brains.

While certainly generating a large amount of buzz and receiving tremendous media attention, this scientific paper is severely flawed. Quite frankly, it is fairly baffling that it was able to survive the peer review process at all. There are a number of points that are incorrect, so without further ado, let’s delve into the details of exactly why we did not need starch, in order to help develop our current brains.

To start, researchers for the paper cite the use of fire as a key point in their argument. However, they incorrectly lead the reader into believing that the timeframe for humans using controlled fire was about 300,000-400,000 years ago, when they themselves contradict this with the statement that “the timing of widespread cooking is not known.” This is likely one misfire that should have been caught in the peer review process. In reality, our ancestors could only make fire in a controlled fashion, starting about 75,000 to 125,000 years ago.26, 27, 28, 29, 30, 31, 32, 33, 34 Hominid encephalization (enlargement of the brain), by contrast, began about 2 million years ago. 35, 36, 37

This is in addition to the researchers’ lack of scientific support for starch consumption compared with non-starchy vegetables, and the necessity of these foods in the human evolutionary process. And, if one were to veer to modern research, they would plainly see studies have proven a Paleo diet does not need to be high in starches or carbohydrates to vastly improve health.38, 39 Further, it is widely accepted that hepatic de novo gluconeogenesis (a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates) can provide brain and placental tissue with all the glucose required even on a carbohydrate free diet. The fact that previously published research by the paper’s author supports this,40 is a glaring inconsistency that is hard to reconcile.

Big Brains Do Not Need Carbs | The Paleo Diet

Figure 1: The Carnivore Connection hypothesis 1 and association with recent increased prevalence of insulin resistance (IR) and type 2 diabetes in susceptible (e.g., Pima Indian) and nonsusceptible (e.g., European) populations.

Suggesting early Homo acquired the capacity for endurance running as essential to exhaust prey is a weak assumption. This reference to persistence hunting, a method of hunting that utilizes the better thermoregulation of humans as compared to their prey, is only successful in a few select climates where thermoregulation is an issue. More importantly, the authors are clearly unaware of the research that measured the energetic cost of human running at different speeds.41 Researchers found, contrary to previous beliefs, individual humans do have optimal running speeds with respect to energetic cost, but it was also demonstrated “that the use of persistence hunting methods to gain access to prey at any running speed, even the optimum, would be extremely costly energetically, more so than a persistence hunt at optimal walking speed.” No starch is necessary for that. Even if the analysis on running efficiency were incorrect, and researchers proved persistence hunters did run at high intensities, the authors would need to explain the disconnect with their hypothesis with the fact that many present-day elite endurance athletes are succeeding on a low carbohydrate diet.

The fact is, our ancestors likely ate whatever they could – a fact, which is noted by modern Paleo diet researchers.42, 43 Current science supports the notion that dense acellular carbohydrates in the diet promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity.44 This is why modern Paleo diet research is conducted with the design of eliminating foods not available during the pre-agricultural period – rather than focusing on specific amounts and quantities of foods.

Big Brains Do Not Need Carbs | The  Paleo Diet

Spreadbury, Ian. “Comparison with Ancestral Diets Suggests Dense Acellular Carbohydrates Promote an Inflammatory Microbiota, and May Be the Primary Dietary Cause of Leptin Resistance and Obesity.” Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy 5 (2012): 175–189. PMC. Web. 19 Aug. 2015.

These researchers also fail to cite a very recent paper, which examined nuclear genome sequence data from Neandertals, Denisovans, and archaic anatomically modern humans.45 It was concluded “salivary amylase gene (AMY1) duplications were not observed in the Neandertal and Denisovan genomes, suggesting a relatively recent origin for the AMY1 copy number gains that are observed in modern humans. Thus, if earlier hominins were consuming large quantities of starch-rich underground storage organs, as previously hypothesized, then they were likely doing so without the digestive benefits of increased salivary amylase production.”

As you can see, there are a myriad of flaws in this paper. The conclusions reached by the authors contradict everything we know about uncooked starch metabolism in our gastrointestinal tract, the archaeological evidence for fire production, and the brain’s requirement for docosahexaenoic acid (DHA).46, 47 DHA was obtained by our ancestors, from animal foods – not starch – in order to synthesize nervous tissue.48, 49

Lastly, perhaps one of the most interesting flaws in this paper is that many scientific studies concluded chronically elevated blood sugar (which is directly influenced by carbohydrate consumption) is correlated with dementia.50 Certainly this is the exact opposite conclusion than the one reached by the paper’s authors, who would have you believe that we needed carbohydrates in order for our brains to thrive and develop.

Hopefully, it is clear we certainly did not need starch to develop our current brains, and in fact, too many carbohydrates (including starches) impair brain processes.51, 52, 53 The problem with this conclusion is not scientific – it is economic. For you see, it is quite easy to continually churn out starch-heavy foods and make a profit – as these foods are very cheap to produce. And, without an endorsement of carbohydrates, how could a company justify selling sugar water to us, en masse?54 Thanks to a diet rich in animal products and fat, you have a big enough brain to recognize the real scientific evidence and that unethical influences are at play here. Definitely some real food for thought.

Casey Thaler, B.A., NASM-CPT, FNS

Casey Thaler | The Paleo Diet TeamCasey Thaler, B.A., NASM-CPT, FNS is an NASM® certified personal trainer and NASM® certified fitness nutrition specialist. He writes for Paleo Magazine® and for PaleoHacks. He also runs his own nutrition and fitness consulting company, Eat Clean, Train Clean®. He is pursuing his Ph.D in Nutritional Biochemistry, hopefully from Harvard University.
Dr. Mark J. Smith

Dr. Mark J. Smith | The Paleo DietDr. Mark J. Smith graduated from Loughborough University of Technology, England, with a Bachelor of Science in PE & Sports Science and then obtained his teaching certificate in PE & Mathematics. As a top-level rugby player, he then moved to the United States and played for the Boston Rugby Club while searching the American college system for an opportunity to commence his Master’s degree. That search led him to Colorado State University where Dr. Smith completed his Masters degree in Exercise and Sport Science, with a specialization in Exercise Physiology. He continued his studies in the Department of Physiology, where he obtained his Doctorate. His research focused on the prevention of atherosclerosis (the build up of plaque in arteries that leads to cardiovascular disease); in particular, using low-dose aspirin and antioxidant supplementation.

Loren Cordain PhD, Professor Emeritus of Nutritional Science, Colorado State University, Fort Collins, Colorado

The Paleo Diet | Dr. Loren CordainDr. Loren Cordain is Professor Emeritus of the Department of Health and Exercise Science at Colorado State University in Fort Collins, Colorado. His research emphasis over the past 20 years has focused upon the evolutionary and anthropological basis for diet, health and well being in modern humans. Dr. Cordain’s scientific publications have examined the nutritional characteristics of worldwide hunter-gatherer diets as well as the nutrient composition of wild plant and animal foods consumed by foraging humans. He is the world’s leading expert on Paleolithic diets and has lectured extensively on the Paleolithic nutrition worldwide. Dr. Cordain is the author of six popular bestselling books including The Real Paleo Diet Cookbook, The Paleo Diet, The Paleo Answer, and The Paleo Diet Cookbook, summarizing his research findings.


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[2] Weinreich DM, Delaney NF, Depristo MA, Hartl DL. Darwinian evolution can follow only very few mutational paths to fitter proteins. Science. 2006;312(5770):111-4.

[3] Wang HY, Chien HC, Osada N, et al. Rate of evolution in brain-expressed genes in humans and other primates. PLoS Biol. 2007;5(2):e13.

[4] Petersen RC, Caracciolo B, Brayne C, Gauthier S, Jelic V, Fratiglioni L. Mild cognitive impairment: a concept in evolution. J Intern Med. 2014;275(3):214-28.

[5] Bramble DM, Lieberman DE. Endurance running and the evolution of Homo. Nature. 2004;432(7015):345-52.

[6] Jablonski NG, Chaplin G. The evolution of human skin coloration. J Hum Evol. 2000;39(1):57-106.

[7] Aiello L. C., Wheeler P. 1995. The expensive-tissue hypothesis: the brain and the digestive system in human and primate evolution. Current Anthropology 36:199–221.

[8] Antón S. C., Snodgrass J. J. 2012. Origins and evolution of genus Homo: new perspectives. Current Anthropology 53:S479–S496.

[9] Crittenden A. N. 2011. The importance of honey consumption in human evolution. Food and Foodways 19:257–273.

[10] Kaplan H., Hill K., Lancaster J., Hurtado A. M. 2000. A theory of human life history evolution: diet, intelligence, and longevity. Evolutionary Anthropology 9:156–185.

[11] Wrangham R. W. 2007. The cooking enigma. Pages 308–323 in Evolution of the Human Diet: The Known, the Unknown, and the Unknowable, edited by P. S. Ungar. Oxford (United Kingdom): Oxford University Press.

[12] Wood B., Harrison T. 2011. The evolutionary context of the first hominins. Nature 470:347–352.

[13] Preuss TM, Cáceres M, Oldham MC, Geschwind DH. Human brain evolution: insights from microarrays. Nat Rev Genet. 2004;5(11):850-60.

[14] Leonard WR, Snodgrass JJ, Robertson ML. Effects of brain evolution on human nutrition and metabolism. Annu Rev Nutr. 2007;27:311-27.

[15] Northcutt RG. Changing views of brain evolution. Brain Res Bull. 2001;55(6):663-74.

[16] Hill RS, Walsh CA. Molecular insights into human brain evolution. Nature. 2005;437(7055):64-7.

[17] Cunnane SC. [Survival of the fattest: the key to human brain evolution]. Med Sci (Paris). 2006;22(6-7):659-63.

[18] Armelagos GJ. Brain evolution, the determinates of food choice, and the omnivore’s dilemma. Crit Rev Food Sci Nutr. 2014;54(10):1330-41.

[19] Gilbert SL, Dobyns WB, Lahn BT. Genetic links between brain development and brain evolution. Nat Rev Genet. 2005;6(7):581-90.

[20] Keverne EB. Epigenetics and brain evolution. Epigenomics. 2011;3(2):183-91.

[21] Karen Hardy, Jennie Brand-Miller, Katherine D. Brown, Mark G. Thomas, Les Copeland. The Importance of Dietary Carbohydrate in Human Evolution. The Quarterly Review of Biology, 2015; 90 (3): 251.

[22]Available at: //press.uchicago.edu/pressReleases/2015/August/150806_qrb_hardy_et_al_paleo_diet.html. Accessed August 18, 2015.

[23] Available at: //www.telegraph.co.uk/foodanddrink/foodanddrinknews/11798169/Did-cavemen-eat-carbs-Why-the-paleo-diet-could-be-wrong.html. Accessed August 16, 2015.

[24] Available at: //www.nytimes.com/2015/08/13/science/for-evolving-brains-a-paleo-diet-full-of-carbs.html. Accessed August 16, 2015.

[25] Available at: //www.geneticliteracyproject.org/2015/08/11/sorry-paleo-dieters-big-human-brain-needs-carbs-to-evolve/. Accessed August 16, 2015.

[26] James SR. Hominid use of fire in the Lower and Middle Pleistocene: A review of the evidence. Curr Anthropol. 1989;30:1–26.

[27] Clark JD, Harris JWK. Fire and its roles in early hominid lifeways. Afr Archaeol Rev. 1985;3:3–27.

[28] Gowlett JAJ, Harris JWK, Walton D, Wood BA. Early archaeological sites, hominid remains and traces of fire from Chesowanja, Kenya. Nature. 1981;294:125–129.

[29] Wrangham R. Catching Fire: How Cooking Made Us Human. New York: Basic Books; 2009.

[30] Wobber V, Hare B, Wrangham R. Great apes prefer cooked food. J Hum Evol. 2008;55:340–348.

[31] Karkanas P, et al. Evidence for habitual use of fire at the end of the Lower Paleolithic: Site-formation processes at Qesem Cave, Israel. J Hum Evol. 2007;53:197–212.

[32] Goren-Inbar N, et al. Evidence of hominin control of fire at Gesher Benot Ya’aqov, Israel. Science. 2004;304:725–727.

[33] Rowlett RM. Did the use of fire for cooking lead to a diet change that resulted in the expansion of brain size in Homo erectus from that of Australopithecus africanus? Science. 1999;284:741.

[34] Andre CC, Skinner AR, Schwarcz HP, Brain CK, Thackeray F. Further exploration of the first use of fire. PaleoAnthropology. 2010;2010:A1–A2.

[35] Leonard WR, Robertson ML, Snodgrass JJ, Kuzawa CW. Metabolic correlates of hominid brain evolution. Comp Biochem Physiol, Part A Mol Integr Physiol. 2003;136(1):5-15.

[36] Hofman MA. Encephalization in hominids: evidence for the model of punctuationalism. Brain Behav Evol. 1983;22(2-3):102-17.

[37] Foley RA, Lee PC. Ecology and energetics of encephalization in hominid evolution. Philos Trans R Soc Lond, B, Biol Sci. 1991;334(1270):223-31.

[38] Manheimer EW, Van zuuren EJ, Fedorowicz Z, Pijl H. Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. Am J Clin Nutr. 2015;

[39] Masharani U, Sherchan P, Schloetter M, et al. Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes. Eur J Clin Nutr. 2015;

[40] Brand-miller JC, Griffin HJ, Colagiuri S. The carnivore connection hypothesis: revisited. J Obes. 2012;2012:258624.

[41] Steudel-Numbers KL, Wall-Scheffler CM. Optimal running speed and the evolution of hominin hunting strategies. J Hum Evol. 2009 Apr;56(4):355-60. doi: 10.1016/j.jhevol.2008.11.002. Epub 2009 Mar 18.

[42] Boers I, Muskiet FA, Berkelaar E, et al. Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study. Lipids Health Dis. 2014;13:160.

[43] Spreadbury I. Comparison with ancestral diets suggests dense acellular carbohydrates promote an inflammatory microbiota, and may be the primary dietary cause of leptin resistance and obesity. Diabetes Metab Syndr Obes. 2012;5:175-89.

[44] Sayers K, Lovejoy CO. Blood, bulbs, and bunodonts: on evolutionary ecology and the diets of Ardipithecus, Australopithecus, and early Homo. Q Rev Biol. 2014;89(4):319-57.

[45] Perry GH, Kistler L, Kelaita MA, Sams AJ. Insights into hominin phenotypic and dietary evolution from ancient DNA sequence data. J Hum Evol. 2015;79:55-63.

[46] Bradbury J. Docosahexaenoic acid (DHA): an ancient nutrient for the modern human brain. Nutrients. 2011;3(5):529-54.

[47] Singh M. Essential fatty acids, DHA and human brain. Indian J Pediatr. 2005;72(3):239-42.

[48] Guil-guerrero JL, Tikhonov A, Rodríguez-garcía I, Protopopov A, Grigoriev S, Ramos-bueno RP. The fat from frozen mammals reveals sources of essential fatty acids suitable for Palaeolithic and Neolithic humans. PLoS ONE. 2014;9(1):e84480.

[49] Bourre JM. [Effect of increasing the omega-3 fatty acid in the diets of animals on the animal products consumed by humans]. Med Sci (Paris). 2005;21(8-9):773-9.

[50] Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540-8.

[51] De la Monte, S. M., & Wands, J. R. (2008). Alzheimer’s Disease Is Type 3 Diabetes–Evidence Reviewed. Journal of Diabetes Science and Technology, 2(6), 1101–1113.

[52] Molteni R, Barnard RJ, Ying Z, Roberts CK, Gómez-pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning. Neuroscience. 2002;112(4):803-14.

[53] Purnell JQ, Klopfenstein BA, Stevens AA, et al. Brain functional magnetic resonance imaging response to glucose and fructose infusions in humans. Diabetes Obes Metab. 2011;13(3):229-34.

[54] Available at: //well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shift-blame-for-obesity-away-from-bad-diets/. Accessed August 16, 2015.

The End of the Low-Fat Era? | The Paleo Diet

The year was 1977. The US Senate Select Committee on Nutrition and Human Needs, led by Senator George McGovern, issued the first Dietary Goals for Americans, thereby marking the beginning of the low-fat era of dietary nutrition, arguably the most misguided period of government-led nutrition ever. After 38 years, however, the low-fat era might officially end later this year.

The Dietary Goals evolved into the Department of Health and Human Services’ (HHS) and Department of Agriculture’s (USDA) Dietary Guidelines for Americans, later represented as the Food Pyramid and, currently, as MyPlate. The Guidelines’ dominant theme has been that calories consumed should equal calories expended. And since fat has 9 calories per gram, compared to only 4 for both carbohydrates and protein, fat became typecast as the “bad guy” nutrient.

Furthermore, since saturated fat and dietary cholesterol have been thought to promote cardiovascular disease, the Guidelines have recommended restricting fat to less than 30% (revised to 35% in 2005) of total calories. Consequently, carbohydrates, particularly refined carbohydrates and added sugars, came to replace healthy fats in Americans’ diets.

USDA and HHS update the Guidelines once every five years and the next revision is forthcoming later this year. Historically, the Guidelines echo the Dietary Guidelines Advisory Committee (DGAC) report, written by appointed scientists who systematically review the scientific literature on nutrition. The current DGAC report, published earlier this year, features two monumental deviations from the current Guidelines.

First, as we previously reported, the DGAC no longer considers dietary cholesterol to be a “nutrient of concern.”1 Previously, they recommended limiting cholesterol to 300 mg/day, but now acknowledge, “available evidence shows no appreciable relationship between consumption of dietary cholesterol and serum cholesterol.”

Second, the DGAC recommends removing upper limits on total fat consumption with respect to total calories. “In low fat diets,” they write, “fats are often replaced with refined carbohydrates and this is of particular concern because such diets are generally associated with dyslipidemia.”2 Reducing total fat (replacing total fat with overall carbohydrates), they conclude, “does not lower cardiovascular disease risk.”

So what does all this mean? If USDA and HHS follow the DGAC’s recommendations, the low-fat era will finally end and, going forward, Americans will have more scientifically accurate information about fat and will likely embrace healthful, fatty foods more readily.


The DGAC recommendations are clear, but in making their final decision, the USDA and HHS also consider comments from the public, academics, advocacy groups, and industry. As such, two prominent scientists, Dr. David Ludwig and Dr. Dariush Mozaffarian, recently penned an article for the Journal of the American Medical Association in which they strongly endorsed lifting the total fat limits.3

Their article follows-up on a similar article they co-authored in 2010 about the previous Dietary Guidelines update. In their 2010 article, they recommended moving away from a nutrient-metrics approach, whereby specific nutrient targets are defined, and toward an approach emphasizing specific, healthy foods. They noted that the proportion of total energy from fat “appears largely unrelated to risk of cardiovascular disease, cancer, diabetes, or obesity” and that saturated fat “has little relation to heart disease within most prevailing dietary patterns.”4

We recently caught up with Dr. Mozaffarian to ask him about this extremely important story.

Q: What are your impressions about the progress made since your 2010 article with Dr. Ludwig? Are we moving in the right direction?

A: The 2015 DGAC report has made great strides in the right direction, with its major new focus on healthful, food-based, diet patterns. Now we must wait to see what the USDA and HHS do with this information in the final Guidelines—boldly move toward this modern evidence, or sit back and return to old conventions.

Assuming the USDA drops its limits on total fat consumption, how impactful do you think this could be?

This could have tremendous positive impact, especially if mirrored in other national policies e.g. food labeling, school lunch, feeding programs, and so on. Consumers and companies would be unshackled to allow focus on increasing healthy foods, including those higher in fat, and on reducing refined grains and sugars.

Would you care to comment on the Paleo diet from a nutritional perspective?

The main benefits of Paleo are recognizing the harms of refined grains, starches, and sugars, which dominate the food supply; and the (potential) focus on fruits, vegetables, nuts, and fish. But, if ‘Paleo’ leads one to high-meat diets, few benefits will be gained.

Dr. Mozaffarian makes a valid point. One of the largest misconceptions surrounding Paleo diets and lifestyles is that it promotes high-meat consumption without balance from other food groups. Dr. Cordain among the many other thought leaders in the scientific and lay communities continue to debunk this misconception. A real Paleo diet is a high-vegetable diet with moderate amounts of animal protein, including lean meat and fish high in omega-3, plus animal and vegetable sources of fat.

In our interview with Dr. Mozaffarian, he also noted that some vegetable oils “are extremely healthy, but are shunned by many Paleo aficionados.” While we respectfully disagree about the health impact of high-omega-6 vegetable oils, we strongly agree that proportional upper limits on total fat must be removed from the US Dietary Guidelines.

For nearly four decades, the US government has promoted high-carbohydrate, low-fat diets. Incidentally, a recent systematic review of the randomized controlled trials available to McGovern’s Committee back in 1977 determined there was no scientific basis for their restrictions on fat.[5] In other words, the low-fat era never should have happened. And with the 2015 Dietary Guidelines update, it should finally end.



[1] Dietary Guidelines Advisory Committee. (February 2015). Scientific Report of the 2015 Dietary Guidelines Advisory Committee.

[2] Ibid, Dietary Guidelines Advisory Committee.

[3] Dariush Mozaffarian and David S. Ludwig. (June 2015). The 2015 US Dietary Guidelines: Lifting the Ban on Total Dietary Fat. Journal of the American Medical Association, 313(24).

[4] Dariush Mozaffarian and David S. Ludwig. (August 2010). Dietary Guidelines in the 21st Century—a Time for Food. Journal of the American Medical Association, 304(6).

[5] Z Harcombe, JS Baker, SM Cooper, B Davies, N Sculthorpe, JJ DiNicolantonio and F Grace. (February 2015). Evidence from randomised controlled trials did not support the introduction of dietary fat guidelines in 1977 and 1983: a systematic review and meta-analysis. Open Heart, 2.

Forget the Macronutrient Ratios - You Are What You Were Designed to Eat

I’d be lying if I said I didn’t enjoy having this particular debate. Someone – not a fan of the Paleo Diet – points out that the diet’s higher protein content is proof that the diet is dangerous citing multiple studies linking higher protein to cancer, CVD, and all-cause mortality.1-3

I have this “dance” down pat. I simply shrug my shoulders and say, “Makes sense. Too bad vegetables are bad for us as well.” I get an incredulous look and a “How can you say that?” response. “Vegetables are a carbohydrate and so are jelly beans. And jelly beans are bad for you.” My frustrated opponent chastises me for drawing a ridiculous conclusion by lumping all carbohydrates together.

Gotcha! Almost invariably I’m able to point out that the high protein diets in their studies were based on processed meats like fast food hamburgers and bologna, not lean meats. “Aren’t you doing the same with all proteins?”

Its remarkable how much current literature and popular diets focus on nutrient ratios, from the “carbs are bad for you” Atkins diet to the 55-65% carbohydrate ratio of the popular food pyramid. It seems one of the hottest topic in nutrition today is the ideal ratio of carbohydrate to fat to protein.

But this debate can miss a very important point.

Throughout our entire evolution, our ancestors had no idea what carbohydrates, protein, and fats were. I am certain that when offered a mango, no hunter-gatherer ever muttered the words “No thanks, I’m watching my waistline. I don’t need the carbs right now.”

All they understood was what was edible and what was not.

The biography of Ishi – the last true North American hunter-gatherer – provides a great example of this awareness. Even while trying to adapt to western civilization, he refused to consume milk or butter. In his very limited English he explained that dairy “ruined his singing voice.”4

This is, in my opinion, one of the greatest strengths of the Paleo Diet. It doesn’t miss the point. While the Paleo Diet is lower than a Western diet in carbohydrates, it is not a low carb or a high protein/fat diet. That’s because not all carbohydrates, protein, and fats are made the same. A high protein or higher carbohydrate diet can be healthy or unhealthy depending on the foods.

The focus of the Paleo Diet is not on ratios, but on eating the foods we evolved to eat. The ratio is a by-product.

A healthy Paleo Diet in fact doesn’t have an ideal ratio.

In their 2009 review of plant-animal subsistence ratios of hunter gatherer societies, Dr. Cordain and his team were quick to point out that the plant-animal ratio varied greatly.5 Societies living close to the equator could get more than 55% of their calories from plant sources, while more polar societies (such as Eskimos) derived almost all of their calories from animal sources.

As a result, the macronutrient ratios could be vastly different. Hunter-gatherer societies ate anywhere between 22-40% carbohydrates, 19-35% protein, and 28-58% fat (though it’s worth pointing out that even those broad ranges are lower carbohydrate and higher protein/fat than the Western diet).6

So it’s somewhat ironic that despite showing such broad ranges, much of the early criticism of the Paleo Diet was over macronutrient ratios.

In 2002, Dr. Cordain described a sample one-day Paleo menu in one of his early reviews. His sample menu was 23% carbohydrate, 38% protein, and 39% fat.7 Those numbers have been cited repeatedly by critics of the diet.

But again, they missed the point.

The point of the review was not to establish exact macronutrient ratios. Dr. Cordain could have easily laid out a sample Paleo menu that was higher or lower in carbs, protein, or fat. The point was to show that the sample menu consisted of nutrient dense and healthier foods than a typical Western Diet.

Let me give a real world example of why focusing on ratios over foods can be so dangerous.

My wife recently told me about a friend of hers who describes himself as a “Paleo Diet fanatic.” He unfortunately has a habit of lecturing others on their food choices including my wife. Yet, a large portion of his diet consists of bacon, butter, and coconut oil. And he avoids fruit.

His diet may be many things, but I wouldn’t personally call it Paleo. I’m unaware of any hunter-gatherer society that ate butter as a staple and gave the local fruit tree a wide berth.

When my wife asked her friend why he eats the way he does, his answer was all about macronutrients. Carbohydrates are bad for us because they cause cancer and all fats are good because they put us in ketosis.

Addressing both of those points fully is beyond the scope of this article, but let me give a cursory overview of carbohydrates and cancer to show why it’s so dangerous to make generalizations like that about macronutrients.

Cancer has been increasingly associated with elevated levels of the hormone Insulin-Like Growth Factor 1 (IGF-1), a potent promoter of growth and cell division.8-11 As its name implies, IGF-1 shares many commonalities with insulin. The pathways that raise insulin and insulin itself cause an increase in IFG-1 and lower its inhibitor Insulin-Like Growth Factor Binding Protein-3 (IGFBP-3).12, 13

If insulin raises IGF-1 and its common knowledge now-a-days that eating sugary foods spikes insulin, it’s easy to draw the conclusion that carbohydrates promote cancer.14

But that would be a mistake. A better way to determine how diet may influence both insulin and IGF-1 is to look at the glycaemic load – a measure of the ability of individual foods to raise blood sugar levels.15, 16 High glycaemic load foods have been linked to cancer in many studies.17-21

When we look at the glycaemic load of individual foods instead of carbohydrates in general we see a very different picture. For example, the fruits and vegetables promoted by the Paleo Diet all have a low glycaemic load despite being composed mostly of carbohydrates.16 Fruits and vegetables have certainly been shown to be protective against cancer.22

Likewise, foods on the Paleo-no fly list such as refined grains and soft drinks have a very high glycaemic load and may promote both IGF-123 and cancer.17-21 Interestingly, milk also has a low glycaemic load value but still strongly raises insulin and IGF-1.24

There are still many great discussions to have about the Paleo Diet. For example, the fact that most Palaeolithic foods don’t exist in the same form anymore, so how do we best approximate them? Likewise, should individuals eat different diets depending on whether they have more equatorial or polar heritages? Even macronutrient ratios are a good question to explore.

But all of these questions are the minutia not the focus. While addressing them we can never lose sight of the foundation – eat the foods we evolved to eat. Otherwise, we start snacking on sticks of butter and think it’s a good idea.

Trevor Connor | The Paleo DietTrevor Connor is Dr. Cordain’s last mentored graduate student and will complete his M.S. in HES and Nutrition from the Colorado State University this year and later enter the Ph.D. program. Connor was the Principle Investigator in a large case study, approximately 100 subjects, in which he and Dr. Cordain examined autoimmune patients following The Paleo Diet or Paleo-like diets.


1. Nilsson, L.M., et al., Low-carbohydrate, high-protein diet score and risk of incident cancer; a prospective cohort study. Nutrition Journal, 2013. 12: p. 10.

2. Pan, A., et al., Red Meat Consumption and Mortality Results From 2 Prospective Cohort Studies. Archives of Internal Medicine, 2012. 172(7): p. 555-563.


4. Kroeber, T., Ishi in two worlds; a biography of the last wild Indian in North America. 1961, Berkeley,: University of California Press. 255 p.

5. Cordain, L., et al., Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr, 2000. 71(3): p. 682-92.

6. McDowell, M.A., et al., Energy and macronutrient intakes of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, Phase 1, 1988-91. Adv Data, 1994(255): p. 1-24.

7. Cordain, L., The nutritional characteristics of a contemporary diet based upon Paleolithic food groups. Journal of the American Nutraceutical Association, 2002. 5(5): p. 15-24.

8. Safarinejad, M.R., N. Shafiei, and S. Safarinejad, Relationship of insulin-like growth factor (IGF) binding protein-3 (IGFBP-3) gene polymorphism with the susceptibility to development of prostate cancer and influence on serum levels of IGF-I, and IGFBP-3. Growth Hormone & Igf Research, 2011. 21(3): p. 146-154.

9. Yu, H. and T. Rohan, Role of the insulin-like growth factor family in cancer development and progression. Journal of the National Cancer Institute, 2000. 92(18): p. 1472-1489.

10. Christopoulos, P.F., P. Msaouel, and M. Koutsilieris, The role of the insulin-like growth factor-1 system in breast cancer. Mol Cancer, 2015. 14(1): p. 43.

11. Zhu, S., et al., Insulin-like growth factor binding protein-related protein 1 and cancer. Clin Chim Acta, 2014. 431: p. 23-32.

12. Cordain, L., The Paleo diet : lose weight and get healthy by eating the foods you were designed to eat. Rev. ed. 2011, Hoboken, N.J.: Wiley. xv, 266 p.

13. Attia, N., et al., The metabolic syndrome and insulin-like growth factor I regulation in adolescent obesity. Journal of Clinical Endocrinology & Metabolism, 1998. 83(5): p. 1467-1471.

14. Freedland, S.J., et al., Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. Prostate, 2008. 68(1): p. 11-9.

15. Runchey, S.S., et al., Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study. Eur J Clin Nutr, 2012. 66(10): p. 1146-52.

16. Foster-Powell, K., S.H. Holt, and J.C. Brand-Miller, International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr, 2002. 76(1): p. 5-56.

17. Augustin, L.S., et al., Dietary glycemic index and glycemic load, and breast cancer risk: a case-control study. Ann Oncol, 2001. 12(11): p. 1533-8.

18. Woo, H.D., et al., Glycemic index and glycemic load dietary patterns and the associated risk of breast cancer: a case-control study. Asian Pac J Cancer Prev, 2013. 14(9): p. 5193-8.

19. Sieri, S., et al., Dietary glycemic index and glycemic load and risk of colorectal cancer: results from the EPIC-Italy study. Int J Cancer, 2014.

21. Eslamian, G., et al., Higher glycemic index and glycemic load diet is associated with increased risk of esophageal squamous cell carcinoma: a case-control study. Nutr Res, 2013. 33(9): p. 719-25.

22. Block, G., B. Patterson, and A. Subar, FRUIT, VEGETABLES, AND CANCER PREVENTION – A REVIEW OF THE EPIDEMIOLOGIC EVIDENCE. Nutrition and Cancer-an International Journal, 1992. 18(1): p. 1-29.

23. Salmeron, J., et al., Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA, 1997. 277(6): p. 472-7.

24. Hoyt, G., M.S. Hickey, and L. Cordain, Dissociation of the glycaemic and insulinaemic responses to whole and skimmed milk. Br J Nutr, 2005. 93(2): p. 175-7.

Overkill Hypothesis: Why Eating Antelope is Preferable to 500 Squirrels

I recently had the pleasure of speaking with Eric Edmeades, author and Founder of WildFit, the fitness methodology training program informed by evolution. The grandson of Professor T.F. Dreyer who discovered the early hominid Florisbad skull in 1932, 1 Eric’s interest and business ventures in evolutionary biology were shaped by his grandfather’s exploration and research.

Together we discussed geoscientist Paul Martin of the University of Arizona “ Overkill Hypothesis ” which argues the Pleistocene extinction of large mammals worldwide was caused by overhunting by humans.2

We’ve made a contribution to this concept by developing 3rd order polynomial equations which allow one to predict total body calories of any mammal, if their weight is known. This procedure also allows for the calculation of total body fat calories and total body protein calories if one knows body weight. Hunter-gatherers must have intuitively known this phenomenon. In light of the hypothesis and optimal foraging theory, a large body of evidence indicates that larger and fatter animals generally were preferred by hunter-gatherers to smaller, leaner animals. We believe these physiological dictums are the reasons our Stone Age hunters frequently risked life and limb to kill very large mammals with nothing more than wooden spears.

A corollary to this phenomenon was originally written about extensively by my colleague and co-author, John Speth, a noted anthropologist from Michigan who is also a colleague of Martin.3 Speth’s idea has come to be known as “rabbit starvation” or “protein poisoning.” In the ethnographic and historical literature it was recognized that sole consumption of only lean protein without fat caused sickness and nausea to rapidly develop. The phenomenon was dubbed “rabbit starvation” because in the far North, both hunter-gatherers and frontiersmen (Lewis and Clark documented this phenomenon) knew that if small animals like rabbits were the sole food source, nausea, disease, weight loss and eventual death would result.4 Our research group has outlined the physiological mechanism involved and the dietary levels at which protein becomes toxic. It ranges between 35-40% of normal daily calories for most people.

This begs the question as to whether the Hadza, East Africa’s last remaining true hunter-gatherers, prefer a single Kudu or Gemsbok antelopes to 500 ground squirrels and why? The Hadza, unlike more northerly hunter-gatherers would generally always have had access year round to plant foods. Hence, sufficient dietary carbohydrate could in effect “dilute” excessive protein from small lean animals, so that small lean mammals could be consumed right up to the physiological protein ceiling without developing protein toxicity. This would provide the balance of calories stemming from either a fat or carbohydrate source. Except for some nuts and seeds, plant foods are generally poor sources of fat. Animal foods are poor sources of carbohydrate and are mixtures of protein and fat which scale to body weight via the 3rd order polynomial equations we developed.

So, the second question to ask the Hadza would be, what would happen if they could only eat ground squirrels without access to plant foods? Have they experienced the nausea of excessive protein intake? I can tell you from personal experience that the phenomenon is real. In an experiment I performed upon myself, I ate only water packed tuna and skinless chicken breasts. After only two days I started to become nauseous and stopped the experiment on day three.

An interesting archaeological caveat to this concept comes from the fossil record of Neanderthals who almost exclusively targeted large mammals. Perhaps, it was because of the seasonal unavailability of plant foods (carbohydrates) in more northern latitudes and the protein toxicity of smaller animals. Plunging a wooden spear between the ribs of rhinos, mammoths, aurochs, and other animals alike becomes a much more sensible proposition if your life depends upon the higher fat/protein composition of large mammals.

Further, the best available most recent evidence indicates Neanderthals could not produce fire at will, but rather could control it only by gathering naturally occurring fire. This inference comes from European Neanderthal cave sites demonstrating the absence of fire during some winter periods in which the caves were occupied. Further no archaeological evidence exists showing that Neanderthals drilled objects — a first, foremost and necessary step involved in the accidental discovery of the technology required to make fire at will using a fire drill. Without the ability to make fire at will, entire groups (cereals, legumes, many underground storage roots and structures) of plant food (ergo carbohydrate) become unavailable, thereby physiologically forcing Neanderthals to become reliant upon large animals.

So, with this background information, I wonder if there could be confirmation by the Hadza that protein toxicity occurs in their world, or perhaps a year-round carbohydrate source that prevents “rabbit starvation.”


Loren Cordain, Ph.D., Professor Emeritus

The Paleo Diet | Dr. Loren CordainDr. Loren Cordain is Professor Emeritus of the Department of Health and Exercise Science at Colorado State University in Fort Collins, Colorado. His research emphasis over the past 20 years has focused upon the evolutionary and anthropological basis for diet, health and well being in modern humans. Dr. Cordain’s scientific publications have examined the nutritional characteristics of worldwide hunter-gatherer diets as well as the nutrient composition of wild plant and animal foods consumed by foraging humans. He is the world’s leading expert on Paleolithic diets and has lectured extensively on the Paleolithic nutrition worldwide. Dr. Cordain is the author of five popular bestselling books including The Paleo Diet, The Paleo Answer, and The Paleo Diet Cookbook, summarizing his research findings.



[1] “Florisbad Skull.” Wikipedia. Wikimedia Foundation, n.d. Web. 1 Mar. 2015.

[2] “Paul S. Martin.” Wikipedia. Wikimedia Foundation, n.d. Web. 1 Mar. 2015.

[3] Cordain L, Miller JB, Eaton SB, Mann N, Holt SH, Speth JD. Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. Am J Clin Nutr. 2000;71(3):682–692.

[4] Seidensticker, John. “Human Problems from a Rabbits Viewpoint.” Rabbits: The Animal Answer Guide. By Susan Lumpkin. N.p.: Nature, 2011. 185. Print.

Are You Eating Enough Carbs For Optimal Recovery?  | The Paleo Diet

While a low-carb Paleo diet is phenomenal for supporting weight loss and improving health if you are overweight, out of shape, or obese, not everyone is trying to lose weight.

For athletes training to achieve a personal best running a 10k, triathlon, or qualifying for the CrossFit Games, your eating strategy will not be one in the same.

Exercise is a catabolic process, triggering a release of stress hormones cortisol and adrenaline in order to raise blood sugars to fuel your activity. If you are exercising at a slow pace (less than 65% heart rate) your body has the time to use fat as a primary fuel source. However, as your exercise intensity increases your body quickly shifts to using muscle and liver glycogen (your body’s carb stores) to fuel exercise.

You have a limited capacity to store glycogen, which means after about 1-hour of training at a high intensity, you’ll likely have exhausted all your body’s glycogen stores.


The research is quite clear that if you start your next training session with low or sub-optimal glycogen status, you’ll significantly reduce your capacity to work and your performance will suffer. A recent study of athletes who consumed only 40% of their total calories as carbohydrates and performed “two-a-day” training sessions suffered a significant decrease in their performance during the 2nd session because they did NOT adequately replenish muscle glycogen stores.1

If you are training at high intensity and following a low-carb diet, you are treading a fine line. If your goal is to be fit and lean, this isn’t really a problem. However, if your goal is optimizing your performance potential, eventually you will exhibit signs of overtraining and exhaustion.

Overtraining happens when you train intensely for too long, without adequate rest periods or tapers built into your training regime. While you do want to push yourself to the edge to stimulate a training adaptation (‘over-reaching’), you don’t want to push yourself over the edge!

Short-term symptoms of inadequate glycogen repletion include fatigue, reduced work capacity during training, poor recovery and extended delayed onset muscle soreness (DOMS). Long-term symptoms are pronounced fatigue, reduced strength levels and increased muscular weakness.


The best way to replenish glycogen after training is to consume high-glycemic index (GI) carbs. High GI carbs enter the bloodstream quickly, allowing you to rapidly replenish glycogen stores in the first 30-60 minutes after training, when glycogen synthase enzyme activity is elevated and allows for optimal replenishment.2 Root vegetables make a great post-workout carb choice, especially if you bake them, which naturally raises the glycemic index of these foods, such as sweet potatoes, yams, yucca, plantains, carrots, beets, parsnips, etc.

If you are on the go and don’t have time to sit down for meal, try adding some dried fruit to your post-workout nutritional arsenal. Dried fruit is very high-glycemic, and while not ideal as a midday snack when sitting at your desk, it’s a great option after vigorous activity. Try 2-4 Medjool dates for 36-72g of carbs, or half a pack of dried mangos (1.5oz provides 36g of carbs).

The total amount of carbs you consume post-training depends on a few variables: your genetics, current body-fat percentage, training phase, etc. Aim for one gram of carbs per kilogram bodyweight in the first hour after exercise (divide your bodyweight in pounds by 2.2 to achieve your weight in kilograms).2,3 This can be repeated every two hours for up to 6 hours post-training for elite level trainees and sports that require two-a-day training, such as triathletes, Olympic weightlifters, and Ironman competitors.

In China, a recent study examined the effects of high-glycemic meals after exercise on performance in runners. The results showed athletes consuming high-GI meals post-training had significantly improved work capacity during their subsequent run four hours later.4 This highlights the importance for refilling your glycogen stores and ensuring your best performance in your next training session or race day.


Carbs directly replenish glycogen stores and after exercise your capacity to soak up carbs and top up glycogen is heightened. Research shows that if you wait several hours post-training you will reduce your glycogen repletion rate by as much as 50%!5 Not consuming enough carbs after exercise can also exacerbate inflammation, depress immunity, and lead to prolonged muscle soreness.6

If you’re already following a low-carb (LC) or very low-carb ketogenic (VLCK) diet you can still benefit by incorporating more carbs than normal post-training, without affecting your capacity to burn fat.7 For some, this may be the added boost you need to upgrade your performance. However, at higher intensity exercise the research shows a LC or VLCK diet does not likely support better performance.8

Remember, if you’re gearing up for a 10k run, triathlon, CrossFit Games or your competitive season, fatigue is directly related to muscle glycogen depletion when exercising at higher intensities. For optimal athletic performance, refuel with the right amount of carbs post-exercise and take your game to the next level.

Happy training!




1. Ivy JL et al. Muscle glycogen storage after different amounts of carbohydrate ingestion. J Appl Physiol. 1988 Nov;65(5):2018-23.

2. Jentjens R, Jeukendrup A. Determinants of post-exercise glycogen synthesis during short-term recovery. Sports Med. 2003;33(2):117-44.

3. Ivy JL1.Glycogen resynthesis after exercise: effect of carbohydrate intake. Int J Sports Med. 1998 Jun;19 Suppl 2:S142-5.

4. Wong SH et al. Effect of glycemic index meals on recovery and subsequent endurance capacity. Int J Sports Med. 2009 Dec;30(12):898-905.

5. Jentjens R, Jeukendrup A. Determinants of post-exercise glycogen synthesis during short-term recovery. Sports Med. 2003;33(2):117-44.

6. Flakell PJ et al. Postexercise protein supplementation improves health and muscle soreness during basic military training in Marine recruits. J Appl Physiol 2004;96:951-956.

7. Burke LM, Hawley JA, Angus DJ, et al. Adaptations to short-term high-fat diet persist during exercise despite high carbohydrate availability. Med Sci Sports Exerc 20002;34:83-91.

8. Antonio J, Kalman D, Stout S, et al. Essentials of Sports Nutrition and Supplements. International Society of Sports Nutritionists. Humana Press, NY 2008.

Carbs Wreck the Brain

It may come as a surprise to you that our brain handles the foods we ingest differently.1 Less of a surprise is the brain’s response to foods in obese individuals compared to healthy.2

Carbs and the Brain - Fig 1

Obesity (Silver Spring). Oct 2011; 19(10): 2019–2025.

Carbs and the Brain - Figure 2

Physiol Behav. Feb 17, 2013; 0: 122–128.

One prime example of this, is carbohydrates.3 One of the three main macronutrients, carbohydrates, especially the simple, man-made kind, are no doubt 21st-cenury man’s favorite dietary indulgence.4, 5 Do you crave broccoli? Hard to resist kale? I didn’t think so.6, 7, 8

However, replace the words “broccoli” and “kale” with “Reese’s Pieces” and “M&Ms” and we have a different situation altogether.9 The combination of sugar and fat, in just the right proportion (known in the food chemist field as ‘the bliss point’) is nigh-impossible to resist – quite literally.10, 11, 12 But even without the processed food industry, our brain handles carbohydrates in a very unique way.13, 14

Carbohydrates are either simple or complex.15 Whether they fall into one camp or the other, depends on their chemical structure.16 Simple carbs have one to two sugars, while complex carbohydrates contain three or more.17, 18 The standard dietary recommendation calls for 40-60% of your daily calories to come from carbohydrates.19 However, this is not a good idea.20, 21, 22, 23, 24

Our brain function’s dependency on carbohydrates is variable.25 Serotonin-releasing brain neurons are unique in the amount of neurotransmitter they release is normally controlled by food intake: carbohydrate consumption – acting via insulin secretion and the “plasma tryptophan ratio” – increases serotonin release; protein intake lacks this effect.26

This accounts for the “boost” we get when consuming carbs – and why we turn to them, day after day, to “make ourselves feel better,” after a long stressful day at work.27 Besides, the oft-repeated, anecdotal phrase “carbs make us fat,” stands up to science.28 In one study, a carbohydrate-restricted diet resulted in a significant reduction in fat mass and a concomitant increase in lean body mass in normal-weight men.29 Researchers posit this may be due to the reduced circulating insulin.30

The detrimental effects of carbohydrates are beginning to become clear.31, 32, 33

Carbs and The Brain - Figure 3

N Engl J Med 2013; 369:540-548. August 8, 2013.

Yet, many of the guiding sources for suggested carbohydrate intake for adults are at odds.34 This suggests very low-carbohydrate diets may not only be sustainable, but they may indeed be optimal.35, 36 Researchers point the likely finger at decreased transport of glucose across the brain, instead replaced by ketone bodies.37, 38

Carbs and the Brain - Figure 4

Biomed Res Int. 2014; 2014: 474296. Published online Jul 3, 2014.

Carbs and the Brain - Figure 5

Biomed Res Int. 2014; 2014: 474296. Published online Jul 3, 2014.

In some individuals, this can help with mental and behavioral detriments, such as obsessive-compulsive disorder and schizophrenia.39, 40, 41 Since the original “very low carbohydrate” diets were developed for treating epilepsy, this should come as no surprise.42

After eating carbohydrates, the level of the amino acid tryptophan in the brain goes up.43 This rise in brain tryptophan level follows from an increase in tryptophan transport into the brain, the consequence of an insulin-induced reduction in the blood levels of several amino acids that compete with tryptophan for brain uptake.44 This helps to explain, at least partially, why you may feel sleepy after a meal filled with large amounts of carbohydrates.45

One, as yet, untouched problem with carbohydrates and your brain, is an increased risk for dementia.46 Glycation is a big problem, and as sugar binds to protein in your body, you are now at an increased risk for developing dementia.47, 48, 49 What can you do to help control this? Quite simply, lower your carbohydrate intake.50 Instead, eat a diet rich in healthy fats, high in quality protein, and with enough quality carbohydrates to maintain activity levels.51, 52, 53 Quite simply, eat a Paleo Diet.


1. Leidy HJ, Lepping RJ, Savage CR, Harris CT. Neural responses to visual food stimuli after a normal vs. higher protein breakfast in breakfast-skipping teens: a pilot fMRI study. Obesity (Silver Spring). 2011;19(10):2019-25.

2. Cornier MA, Mcfadden KL, Thomas EA, et al. Differences in the neuronal response to food in obesity-resistant as compared to obesity-prone individuals. Physiol Behav. 2013;110-111:122-8.

3. Hevor TK. Some aspects of carbohydrate metabolism in the brain. Biochimie. 1994;76(2):111-20.

4. Siri PW, Krauss RM. Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Curr Atheroscler Rep. 2005;7(6):455-9.

5. Lavoie C. Gestational diabetes: poke, pee, and eat your carbs. Can Fam Physician. 2011;57(7):756-7, e239-40.

6. Imai S, Fukui M, Kajiyama S. Effect of eating vegetables before carbohydrates on glucose excursions in patients with type 2 diabetes. J Clin Biochem Nutr. 2014;54(1):7-11.

7. John JH, Ziebland S. Reported barriers to eating more fruit and vegetables before and after participation in a randomized controlled trial: a qualitative study. Health Educ Res. 2004;19(2):165-74.

8. Cordain L, Eaton SB, Sebastian A, et al. Origins and evolution of the Western diet: health implications for the 21st century. Am J Clin Nutr. 2005;81(2):341-54.

9. Gearhardt AN, Grilo CM, Dileone RJ, Brownell KD, Potenza MN. Can food be addictive? Public health and policy implications. Addiction. 2011;106(7):1208-12.

10. Gearhardt AN, Davis C, Kuschner R, Brownell KD. The addiction potential of hyperpalatable foods. Curr Drug Abuse Rev. 2011;4(3):140-5.

11. García-garcía I, Horstmann A, Jurado MA, et al. Reward processing in obesity, substance addiction and non-substance addiction. Obes Rev. 2014;

12. Davis C, Levitan RD, Kaplan AS, Kennedy JL, Carter JC. Food cravings, appetite, and snack-food consumption in response to a psychomotor stimulant drug: the moderating effect of “food-addiction”. Front Psychol. 2014;5:403.

13. Fernstrom JD, Wurtman RJ. Brain serotonin content: increase following ingestion of carbohydrate diet. Science. 1971;174(4013):1023-5.

14. Gómez-pinilla F. Brain foods: the effects of nutrients on brain function. Nat Rev Neurosci. 2008;9(7):568-78.

15. Englyst KN, Englyst HN. Carbohydrate bioavailability. Br J Nutr. 2005;94(1):1-11.

16. Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. The Molecular Composition of Cells. Available from: //www.ncbi.nlm.nih.gov/books/NBK9879/

17. Varki A. Biological roles of oligosaccharides: all of the theories are correct. Glycobiology. 1993;3(2):97-130.

18. Roberts KM, Noble EG, Hayden DB, Taylor AW. Simple and complex carbohydrate-rich diets and muscle glycogen content of marathon runners. Eur J Appl Physiol Occup Physiol. 1988;57(1):70-4.

19. Peterson CM, Jovanovic-peterson L. Randomized crossover study of 40% vs. 55% carbohydrate weight loss strategies in women with previous gestational diabetes mellitus and non-diabetic women of 130-200% ideal body weight. J Am Coll Nutr. 1995;14(4):369-75.

20. Gardner CD, Kiazand A, Alhassan S, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. 2007;297(9):969-77.

21. Kowalski LM, Bujko J. [Evaluation of biological and clinical potential of paleolithic diet]. Rocz Panstw Zakl Hig. 2012;63(1):9-15.

22. 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.

23. 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.

24. O’dea K. Marked improvement in carbohydrate and lipid metabolism in diabetic Australian aborigines after temporary reversion to traditional lifestyle. Diabetes. 1984;33(6):596-603.

25. Turner CE, Byblow WD, Stinear CM, Gant N. Carbohydrate in the mouth enhances activation of brain circuitry involved in motor performance and sensory perception. Appetite. 2014;80:212-9.

26. Wurtman RJ, Wurtman JJ. Brain serotonin, carbohydrate-craving, obesity and depression. Obes Res. 1995;3 Suppl 4:477S-480S.

27. Lemmens SG, Martens EA, Born JM, Martens MJ, Westerterp-plantenga MS. Lack of effect of high-protein vs. high-carbohydrate meal intake on stress-related mood and eating behavior. Nutr J. 2011;10(1):136.

28. Sinitskaya N, Gourmelen S, Schuster-klein C, Guardiola-lemaitre B, Pévet P, Challet E. Increasing the fat-to-carbohydrate ratio in a high-fat diet prevents the development of obesity but not a prediabetic state in rats. Clin Sci. 2007;113(10):417-25.

29. 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.

30. Slabber M, Barnard HC, Kuyl JM, Dannhauser A, Schall R. Effects of a low-insulin-response, energy-restricted diet on weight loss and plasma insulin concentrations in hyperinsulinemic obese females. Am J Clin Nutr. 1994;60(1):48-53.

31. Roberts RO, Roberts LA, Geda YE, et al. Relative intake of macronutrients impacts risk of mild cognitive impairment or dementia. J Alzheimers Dis. 2012;32(2):329-39.

32. Yaffe K, Blackwell T, Whitmer RA, Krueger K, Barrett connor E. Glycosylated hemoglobin level and development of mild cognitive impairment or dementia in older women. J Nutr Health Aging. 2006;10(4):293-5.

33. Crane PK, Walker R, Hubbard RA, et al. Glucose levels and risk of dementia. N Engl J Med. 2013;369(6):540-8.

34. Manninen AH. Metabolic effects of the very-low-carbohydrate diets: misunderstood “villains” of human metabolism. J Int Soc Sports Nutr. 2004;1(2):7-11.

35. Krebs NF, Gao D, Gralla J, Collins JS, Johnson SL. Efficacy and safety of a high protein, low carbohydrate diet for weight loss in severely obese adolescents. J Pediatr. 2010;157(2):252-8.

36. Galletly C, Moran L, Noakes M, Clifton P, Tomlinson L, Norman R. Psychological benefits of a high-protein, low-carbohydrate diet in obese women with polycystic ovary syndrome–a pilot study. Appetite. 2007;49(3):590-3.

37. Klepper J, Diefenbach S, Kohlschütter A, Voit T. Effects of the ketogenic diet in the glucose transporter 1 deficiency syndrome. Prostaglandins Leukot Essent Fatty Acids. 2004;70(3):321-7.

38. Paoli A, Bianco A, Damiani E, Bosco G. Ketogenic diet in neuromuscular and neurodegenerative diseases. Biomed Res Int. 2014;2014:474296.

39. Kraft BD, Westman EC. Schizophrenia, gluten, and low-carbohydrate, ketogenic diets: a case report and review of the literature. Nutr Metab (Lond). 2009;6:10.

40. Barañano KW, Hartman AL. The ketogenic diet: uses in epilepsy and other neurologic illnesses. Curr Treat Options Neurol. 2008;10(6):410-9.

41. O’rourke DA, Wurtman JJ, Wurtman RJ, et al. Aberrant snacking patterns and eating disorders in patients with obsessive compulsive disorder. J Clin Psychiatry. 1994;55(10):445-7.

42. Levy RG, Cooper PN, Giri P. Ketogenic diet and other dietary treatments for epilepsy. Cochrane Database Syst Rev. 2012;3:CD001903.

43. Spring B. Recent research on the behavioral effects of tryptophan and carbohydrate. Nutr Health. 1984;3(1-2):55-67.

44. Fernstrom JD. Carbohydrate ingestion and brain serotonin synthesis: relevance to a putative control loop for regulating carbohydrate ingestion, and effects of aspartame consumption. Appetite. 1988;11 Suppl 1:35-41.

45. Afaghi A, O’connor H, Chow CM. High-glycemic-index carbohydrate meals shorten sleep onset. Am J Clin Nutr. 2007;85(2):426-30.

46. Cukierman-yaffe T, Gerstein HC, Williamson JD, et al. Relationship between baseline glycemic control and cognitive function in individuals with type 2 diabetes and other cardiovascular risk factors: the action to control cardiovascular risk in diabetes-memory in diabetes (ACCORD-MIND) trial. Diabetes Care. 2009;32(2):221-6.

47. Sasaki N, Fukatsu R, Tsuzuki K, et al. Advanced glycation end products in Alzheimer’s disease and other neurodegenerative diseases. Am J Pathol. 1998;153(4):1149-55.

48. Münch G, Schinzel R, Loske C, et al. Alzheimer’s disease–synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts. J Neural Transm. 1998;105(4-5):439-61.

49. Takeuchi M, Yamagishi S. Possible involvement of advanced glycation end-products (AGEs) in the pathogenesis of Alzheimer’s disease. Curr Pharm Des. 2008;14(10):973-8.

50. Gasior M, Rogawski MA, Hartman AL. Neuroprotective and disease-modifying effects of the ketogenic diet. Behav Pharmacol. 2006;17(5-6):431-9.

51. Frassetto LA, Schloetter M, Mietus-synder M, Morris RC, Sebastian A. Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr. 2009;63(8):947-55.

52. 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.

53. 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.

Cholesterol | The Paleo Diet

Dr. Kim A. Williams, the President-Elect of the American College of Cardiology, recently published an essay, “Vegan Diet, Healthy Heart?” which has sparked passionate debate.1 “I didn’t know it would create such a firestorm of everything from accolades to protests,” said Williams.2 His essay describes how his LDL cholesterol level dropped from 170 to 90 within six weeks of adopting a vegan diet. He now encourages patients with diabetes, hypertension, coronary artery disease, and high cholesterol to consider going vegan.

By now, most people recognize the distinction between HDL, the so-called “good cholesterol,” and LDL, “bad cholesterol.” The distinction regarding LDL particle size, however, is just as important, but not universally known. LDL varies by particle size—small and large—and only small particle LDL should be labeled “bad.” Small, dense LDL particles tend to accumulate within the arteries, contributing to arterial plaque.3 Conversely, large, buoyant LDL particles float through the bloodstream and are far less likely to accumulate. Observational studies suggest small-particle LDL predicts heart disease at more than three times the rate of large-particle LDL.4

Neither William’s essay nor the response published in The New York Timesmentioned anything about this important distinction between small and large particle LDL. Most healthy individuals have predominantly higher proportions of large-particle LDL and for these people diets lower in carbohydrates and higher in fat have been shown to promote healthier blood cholesterol levels.5 Some people, however, are genetically predisposed to a phenotype characterized by a predominance of small-particle LDL and for these people diets lower in fat and higher in carbohydrates may promote healthier blood cholesterol levels.6

The Paleo Diet, of course, includes animal foods, some of which contain significant amounts of saturated fat. Dr. Williams stops short of recommending vegan diets for everyone, but readers of his essay might wrongly suppose the Paleo Diet promotes unhealthy blood cholesterol levels and that vegan diets, which are typically lower in saturated fat and higher in carbohydrates, are healthier. This might be true if not for the fact that size does matter regarding LDL—and bigger is better. Research shows that dietary carbohydrates, particularly simple sugars and starches with high glycemic indexes, increase small-particle LDL.7 From a cholesterol perspective, these are the foods to avoid. Saturated fat, on the other hand, increases only large-particle LDL, which is benign.8

And what about Paleo foods like eggs, which contain higher amounts of dietary cholesterol? Dr. Williams wrote about switching to a “cholesterol-free” vegan diet, implying that dietary cholesterol negatively impacts blood cholesterol. The scientific literature, however, doesn’t support this implication. Clinical studies show dietary cholesterol actually reduces small-particle LDL and only increases large-particle LDL, the benign variety, while also increasing HDL, thus promoting proper LDL/HDL ratios.9 Furthermore, according to a recent review, “current epidemiologic data have clearly demonstrated that increasing concentrations of dietary cholesterol are not correlated with increased risk for cardiovascular disease.”sup>10 There’s no reason, therefore, to forgo animal foods. The Paleo Diet naturally promotes healthy blood cholesterol levels.

Christopher James Clark, B.B.A.
Nutritional Grail

Christopher James Clark | The Paleo Diet TeamChristopher James Clark, B.B.A. is an award-winning writer, consultant, and chef with specialized knowledge in nutritional science and healing cuisine. He has a Business Administration degree from the University of Michigan and formerly worked as a revenue management analyst for a Fortune 100 company. For the past decade-plus, he has been designing menus, recipes, and food concepts for restaurants and spas, coaching private clients, teaching cooking workshops worldwide, and managing the kitchen for a renowned Greek yoga resort. Clark is the author of the critically acclaimed, award-winning book, Nutritional Grail.


1. Williams, Kim. (July 21, 2014). CardioBuzz: Vegan Diet, Healthy Heart? MedPage Today. Retrieved August 8, 2014.

2. O’Connor, Anahad. (August 6, 2014) Advice From a Vegan Cardiologist. The New York Times. Retrieved August 8, 2014.

3. Voros, S., et al. (November 2013). Apoprotein B, small-dense LDL and impaired HDL remodeling is associated with larger plaque burden and more noncalcified plaque as assessed by coronary CT angiography and intravascular ultrasound with radiofrequency backscatter: results from the ATLANTA I study. Journal of the American Heart Association, 2(6). Retrieved August 8, 2014 from //www.ncbi.nlm.nih.gov/pubmed/24252842

4. Lamarche, B., et al. (January 1997). Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Québec Cardiovascular Study. Circulation, 95(1). Retrieved August 8, 2014 from //www.ncbi.nlm.nih.gov/pubmed/8994419

5. Krauss, RM. (February 2001). Atherogenic lipoprotein phenotype and diet-gene interactions. Journal of Nutrition, 131(2). Retrieved August 8, 2014 from //www.ncbi.nlm.nih.gov/pubmed/11160558

6. Ibid.

7. Siri, PW., et al. (November 2005). Influence of dietary carbohydrate and fat on LDL and HDL particle distributions. Current Artherosclerosis Reports, 7(6). Retrieved August 8, 2014 from //www.ncbi.nlm.nih.gov/pubmed/16256003

8. Dreon, DM., et al. (May 1998). Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. American Journal of Clinical Nutrition, 67(5). Retrieved August 8, 2014 from //ajcn.nutrition.org/content/67/5/828.short

9. Fernandez, ML., Calle, M. (November 2010). Revisiting dietary cholesterol recommendations: does the evidence support a limit of 300 mg/d? Current Artherosclerosis Reports 12(6). Retrieved August 8, 2014 from //www.ncbi.nlm.nih.gov/pubmed/20683785

10. Ibid.

Affiliates and Credentials