Tag Archives: sugar

Junk Food | The Paleo Diet

While the title of this article may at first seem implausible (and somewhat scary), a new scientific study seems to show that an inborn preference for junk food is not only possible – it may be affecting more of us than ever could have possibly been imagined. For the first time in history, researchers for Obesity Society have identified two genetic variants, which help to change how the brain responds to high-calorie foods.1 2 While this is potentially terrible news for those of us who struggle to resist highly processed and manufactured foods – it also means there is possibly a way to stop this genetic variant from controlling our dietary choices. This could include changing how the brain processes junk food, changing how much people crave these foods, and even altering the brain’s dopamine system. There are even more potential treatments using this new information – including using gut hormones to act on dopamine brain cells.

To delve into further detail, researchers specifically found that two genetic variants – FTO and DRD2 – influenced brain activity related to the reward system. This occurred when subjects simply looked at pictures of high-calorie foods. As I’ve written previously, this is far from the first time neuroscience (or other scientific studies) have shown that some of our brains respond differently, to rewarding foods.3 4 5 6 7 8 9 10 11 In early 2014, for example, a study was published which showed that not only did some people crave chocolate (while others did not) – but that there was literally different brain activity, in the two groups.12

Asmaro D, Liotti M. High-caloric and chocolate stimuli processing in healthy humans: an integration of functional imaging and electrophysiological findings. Nutrients. 2014;6(1):319-41.

In another, similar study, researchers found that by altering dopamine receptors (specifically D2 receptors) – they could cure binge eating.13 Unfortunately for us, that ground breaking study was done on rats – not humans. However, this is further evidence that our brain plays a fundamental role in overeating and cravings. In fact, it may be the excess stimulation of the nucleus accumbens (the ‘pleasure center’ of the brain) from junk food, which leads to obesity.14 15 16 17 18 19 20

How does this relate to our current world? Well, 70% of the United States is overweight, with 30% of us now being obese.21 What accounts for all these extra pounds? Certainly, as shown by research from Yale scientists, a hyper-stimulatory environment and excess advertisement of junk food – is a large part of the problem.22 23 24 But this data is compounded by other research, which shows that extended access to high-fat and high-sugar food, results in behavioral and physiological changes – which are similar to those caused by illegal drugs.25 [26] While a large portion of these corresponding studies were conducted on rats, this does not mean that the results will not translate to humans. Like many areas of scientific research, we simply need more data.

Baik JH. Dopamine signaling in food addiction: role of dopamine D2 receptors. BMB Rep. 2013;46(11):519-26.

As I’ve covered previously, the neurobiology of sugar addiction is fascinating as well.27 28 The brain is bombarded with an overwhelming amount of chemicals and reward, when you consume junk food.29 30 31 32 Over time, this leads to a higher quantity of junk food needing to be consumed, to achieve the same rewarding effect.33 34 35 So even for those of us who are not genetically susceptible to the temptations of junk food, we can alter our brain’s preferences and reward receptors, to become just as likely to crave it.36 37 38 39 40

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

The good side of all this bad news? Your brain can also be positively impacted by food.41 42 43 44 45 46 A Paleo diet, which is full of nutrient dense foods, will help keep you satiated, and keep your brain from craving high sugar, nutritionally empty choices. Be sure to load your plate with wild-caught fish (high in brain-friendly omega-3 fatty acids), healthy fats (like avocados) and complete sources of protein (like grass fed beef). You may indeed be hardwired for junk food – but that doesn’t mean you have to give in to temptation. Adopting a Paleo diet is associated with many different health benefits – many of which work to counteract the negative effects of junk food.47 48 49 50 What this means, is that you can improve your health drastically, by simply changing what’s on your plate. Start eating a Paleo diet today, and watch your health soar!


1. Available at: http://www.sciencedaily.com/releases/2015/11/151105103957.htm. Accessed November 23, 2015.

2. Available at: http://www.newswise.com/articles/are-you-hardwired-to-enjoy-high-calorie-foods-research-links-genes-to-heightened-brain-reward-responses-to-foods-high-in-fat-and-sugar. Accessed November 23, 2015.

3. Fortuna JL. The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoactive Drugs. 2012;44(1):56-63.

4. Garber AK, Lustig RH. Is fast food addictive?. Curr Drug Abuse Rev. 2011;4(3):146-62.

5. Grimm O., Jacob M.J., Kroemer N.B., Krebs L., Vollstädt-Klein S., Kobiella A., Wolfensteller U., Smolka M.L. The personality trait self-directedness predicts the amygdala’s reaction to appetizing cues in fMRI. Appetite. 2012;58:1023–1029.

6. Macht M., Mueller J. Immediate effects of chocolate on experimentally induced mood states. Appetite.2007;49:667–674.

7. Kringelbach M.L. The human orbitofrontal cortex: Linking reward to hedonic experience. Nat. Rev. Neurosci. 2005;6:691–702.

8. Francis S.T., Head K., Morris P.G., Macdonald I.A. The effect of flavanol-rich cocoa on the fMRI response to a cognitive task in healthy young people. J. Cardiovasc. Pharm. 2006;47:S215–S220.

9. Small D.M., Zatorre R.J., Dagher A., Evans A.C., Jones-Gotman M. Changes in brain activity related to eating chocolate: From pleasure to aversion. Brain. 2001;124:1720–1733.

10. Kemmotsu N., Murphy C. Restrained eaters show altered brain response to food odor. Physiol. Behav.2006;87:323–329.

11.  Blechert J., Feige B., Hajcak G., Tuschen-Caffier B. To eat or not to eat? Availability of food modulates the electrocortical response to food pictures in restrained eaters. Appetite. 2010;54:262–268.

12. Asmaro D, Liotti M. High-caloric and chocolate stimuli processing in healthy humans: an integration of functional imaging and electrophysiological findings. Nutrients. 2014;6(1):319-41.

13. Halpern CH, Tekriwal A, Santollo J, et al. Amelioration of binge eating by nucleus accumbens shell deep brain stimulation in mice involves D2 receptor modulation. J Neurosci. 2013;33(17):7122-9.

14. Lawrence NS, Hinton EC, Parkinson JA, Lawrence AD. Nucleus accumbens response to food cues predicts subsequent snack consumption in women and increased body mass index in those with reduced self-control. Neuroimage. 2012;63(1):415-22.

15. Salamone JD, Cousins MS, Mccullough LD, Carriero DL, Berkowitz RJ. Nucleus accumbens dopamine release increases during instrumental lever pressing for food but not free food consumption. Pharmacol Biochem Behav. 1994;49(1):25-31.

16. Olausson P, Jentsch JD, Tronson N, Neve RL, Nestler EJ, Taylor JR. DeltaFosB in the nucleus accumbens regulates food-reinforced instrumental behavior and motivation. J Neurosci. 2006;26(36):9196-204.

17. Day JJ, Carelli RM. The nucleus accumbens and Pavlovian reward learning. Neuroscientist. 2007;13(2):148-59.

18. Pratt WE, Kelley AE. Nucleus accumbens acetylcholine regulates appetitive learning and motivation for food via activation of muscarinic receptors. Behav Neurosci. 2004;118(4):730-9.

19. Salamone JD, Correa M, Mingote S, Weber SM. Nucleus accumbens dopamine and the regulation of effort in food-seeking behavior: implications for studies of natural motivation, psychiatry, and drug abuse. J Pharmacol Exp Ther. 2003;305(1):1-8.

20. Demos KE, Heatherton TF, Kelley WM. Individual differences in nucleus accumbens activity to food and sexual images predict weight gain and sexual behavior. J Neurosci. 2012;32(16):5549-52.

21. Available at: http://www.cdc.gov/nchs/fastats/obesity-overweight.htm. Accessed November 23, 2015.

22. Yokum S, Gearhardt AN, Harris JL, Brownell KD, Stice E. Individual differences in striatum activity to food commercials predict weight gain in adolescents. Obesity (Silver Spring). 2014;22(12):2544-51.

23. Udo T, Weinberger AH, Grilo CM, et al. Heightened vagal activity during high-calorie food presentation in obese compared with non-obese individuals–results of a pilot study. Obes Res Clin Pract. 2014;8(3):e201-98.

24. Gearhardt AN, Roberto CA, Seamans MJ, Corbin WR, Brownell KD. Preliminary validation of the Yale Food Addiction Scale for children. Eat Behav. 2013;14(4):508-12.

25. Epstein DH, Shaham Y. Cheesecake-eating rats and the question of food addiction. Nat Neurosci. 2010;13(5):529-31.

26. Stockburger J., Schmälzle R., Flaisch T., Bublatzky F., Schupp H.T. The impact of hunger on food cue processing: An event-related brain potential study. Neuroimage. 2009;47:1819–1829.

27. Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

28. García-cáceres C, Tschöp MH. The emerging neurobiology of calorie addiction. Elife. 2014;3:e01928.

29. Norton P, Falciglia G, Gist D. Physiologic control of food intake by neural and chemical mechanisms. J Am Diet Assoc. 1993;93(4):450-4.

30. Wurtman RJ. Nutrients affecting brain composition and behavior. Integr Psychiatry. 1987;5(4):226-38.

31. Young SN. How to increase serotonin in the human brain without drugs. J Psychiatry Neurosci. 2007;32(6):394-9.

32. Wang GJ, Volkow ND, Telang F, et al. Exposure to appetitive food stimuli markedly activates the human brain. Neuroimage. 2004;21(4):1790-7.

33. Baik JH. Dopamine signaling in food addiction: role of dopamine D2 receptors. BMB Rep. 2013;46(11):519-26.

34. Lietti C.V., Murray M.M., Hudry J., le Coutre J., Toepel U. The role of energetic value in dynamic brain response adaptation during repeated food image viewing. Appetite. 2012;58:11–18.

35. Meule A. Are certain foods addictive?. Front Psychiatry. 2014;5:38.

36. Davis C, Curtis C, Levitan RD, Carter JC, Kaplan AS, Kennedy JL. Evidence that ‘food addiction’ is a valid phenotype of obesity. Appetite. 2011;57(3):711-7.

37. Reward systems and food intake: role of opioids. International Journal of Obesity. 2009;:S54.

38. Naleid AM, Grace MK, Chimukangara M, Billington CJ, Levine AS. Paraventricular opioids alter intake of high-fat but not high-sucrose diet depending on diet preference in a binge model of feeding. Am J Physiol Regul Integr Comp Physiol. 2007;293(1):R99-105.

39. Woolley JD, Lee BS, Fields HL. Nucleus accumbens opioids regulate flavor-based preferences in food consumption. Neuroscience. 2006;143(1):309-17.

40. Zhang M, Gosnell BA, Kelley AE. Intake of high-fat food is selectively enhanced by mu opioid receptor stimulation within the nucleus accumbens. J Pharmacol Exp Ther. 1998;285(2):908-14.

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

42. Bourre JM. Effects of nutrients (in food) on the structure and function of the nervous system: update on dietary requirements for brain. Part 1: micronutrients. J Nutr Health Aging. 2006;10(5):377-85.

43. Hill JO, Berridge K, Avena NM, et al. Neurocognition: the food–brain connection. Adv Nutr. 2014;5(5):544-6.

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

45. Galland L. The gut microbiome and the brain. J Med Food. 2014;17(12):1261-72.

46. Lachance L, Ramsey D. Food, mood, and brain health: implications for the modern clinician. Mo Med. 2015;112(2):111-5.

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

48. Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010;25(6):594-602.

49. 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.

50. 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.

Sweet Sugar Coconut Fat | The Paleo Diet
If you’ve popped into your local Starbucks lately, you’ve already seen it. The Christmas red cups are here!  As someone who is admittedly an absolute Christmas fanatic, I must say that the hint of the season’s festivities in the air brings a smile to my face and that happy, and coaxes the warm holiday aura.

But one thing that doesn’t sit quite right is thinking about the sizeable number of syrupy sweet holiday drinks we’re consuming as a whole, let alone the sheer size of each individual drink has gone from 12 oz to 16 oz to… a 31 oz!1

A ‘Grande,’ 2% milk, peppermint latte is a whopping 54g of sugar from Starbucks.2 Thinking about supersizing to the mega 31 oz? That’s a whole heck of a lot of sugar (nearly double)!

But what if we want to enjoy a taste of the season? Is there a way to do so without wreaking havoc to our blood sugar, our mood, and our guts? Yes.

And it’s not about finding a ‘more Paleo’ sweetener. Instead of focusing on sweet, do yourself a favor and instead focus on fat. Without sugar, you can forget about the blood sugar spike, ensuing crash, and craving pangs for another.

Long before we ever knew about putting butter in coffee, in the lofty Himalayan mountains a few cups of yak butter tea, or po cha, was a welcome respite from the cold, thin air.[3] Since neither butter nor coffee are part of a strict Paleo diet, why not put a spin on the Tibetan model and brew a hot cup with a healthy, Paleo approved fat?

Can you say let’s go nuts with coconuts? Tasty, warming, and a with a fantastic creamy texture to boot, the Paleo recipe below will satisfy your palate and leave you feeling energized and ready to face the hectic holiday season… without ever feeling like you’ve had to deprive yourself!

Paleoista’s Holiday Coconut Tea

(Serves 2)


  • Herbal tea, your preference; try peppermint, cinnamon or ginger to create the holiday flavor profile
  • ¼ cup coconut butter, at room temperature
  • Ground cinnamon, to taste


  1. Brew tea and let steep 3- 5 minutes.
  2. Remove tea leaves or bag and let cool slightly.
  3. Combine tea with coconut butter in blender and whiz to combine.
  4. Top with cinnamon and enjoy!


1. “Starbucks to Roll Out Biggest Drink Size Yet | Fox News.” Fox News. FOX News Network, 16 Jan. 2011. Web. 04 Nov. 2015.

2. “Peppermint Mocha.” Starbucks Coffee Company. Starbucks Coffee Company, n.d. Web. 04 Nov. 2015.

3. “Tea Tuesdays: Butter Up That Tea, Tibetan-Style.” NPR. NPR, n.d. Web. 04 Nov. 2015.

Quit Sugar | The Paleo Diet

Sugar – is there a more popular word for dieticians and nutritionists? Interestingly, economists have also been talking about the pure white stuff – but in a different context than the standard ‘insulin and cravings’ discussions. A new piece in The Atlantic discussed just how much money is spent on selling Americans sugar, every single day of our lives.1

Though nothing truly shocks me anymore, in the sleazy world of processed food marketing, I was a bit taken aback to realize that Kellogg’s spent $32 million on advertising their (truly awful) Pop Tarts last year. With that money, we could be helping to fix the obesity pandemic we are all collectively in, instead.2 3 4 5 70% of Americans are now overweight, and 30% of us are obese – couldn’t we allocate these funds better? I think so.6

But, instead, we get a new flavor of the Franken-Food that absolutely no one (let alone developing children) should eat for breakfast. Or any other time of day, for that matter. But the depressing statistics don’t end there. Last year, Coca-Cola spent over $250 million advertising their flagship sugar water. And for a quick science detour, remember that sugar has been shown to demonstrate a set of behaviors and parallel brain changes that are characteristic of addictive drugs.7 8 9 10

Brain Glucose Metabolusm

(a) Averaged images for DA D2 receptors (measured with [11C]raclopride) in a group of (i) controls (n=10) and (ii) morbidly obese subjects (n=10). (b) Results from SPM identifying the areas in the brain where D2 receptors availability was associated with brain glucose metabolism; these included the OFC, the CG and the DLPFC (region not shown in sagittal plane). (c) Regression slopes between D2 receptor availability (measured in striatum) and brain glucose metabolism in (i) CG and (ii) OFC in obese subjects. 10

Back to the money spent on sugar. Pepsi seems almost saint-like by comparison here, as they only spent $150 million advertising Gatorade last year. Keep in mind that all of the products listed so far (we’re at a total of $432 million at this point) are just brightly colored versions of sugar. This would almost be comical, if it weren’t destroying our collective health.11 12 13 14

I hope you’ve buckled up, because this is where things turn truly depressing. Did you know that our own government (who – obviously – should be looking out for our collective health) spent less than 0.5% of all agricultural subsidies on production of fruits and vegetables? You read that right – that’s less than 1%. Should less than 1% of any food-related funding be going to fruits and vegetables? Shouldn’t the majority of funding be going to fruits and vegetables? I feel like we are all in a bad Twilight Zone episode here.

And, while I wholeheartedly believe in freedom, liberty, and a free market economy, when you have 70% of the population overweight, and one in three people obese, you need to make some changes, and you need to have some oversight. It doesn’t take an advanced college degree, or even a high school diploma to see the problem here. As the old saying goes, numbers don’t lie.

I will leave you with one more staggering fact, which shows how truly disconnected we have become, from our Paleo ancestors. Fruits and vegetables are the only foods, which all nutrition experts can agree upon; we should be eating, ad libitum. But do you know what classification they have, by our own U.S. Department Of Agriculture? Their classification is only a brief two words: ‘specialty crops’.

Hopefully in your own personal, ongoing scientific experiment (that is your life), fruits and vegetables are not ‘specialty crops’. They should be part of your main course. I hope I’ve given you some real things to think about here. And remember – our children and future grandchildren are the ones who will suffer the most from this ludicrous sugar economy we are allowing to persist. Not us.

While it is easy to be complacent, apathetic, and not do anything, you have a voice. And what is a democracy, if not simply a collection of individual voices? Make your voice be heard, and tell the world where you stand on the true price of sugar.


1 Available at: http://www.theatlantic.com/health/archive/2015/09/the-money-spent-selling-sugar-to-americans-is-staggering/407350/. Accessed September 29, 2015.

2 Roth J, Qiang X, Marbán SL, Redelt H, Lowell BC. The obesity pandemic: where have we been and where are we going?. Obes Res. 2004;12 Suppl 2:88S-101S.

3 Swinburn BA, Sacks G, Hall KD, et al. The global obesity pandemic: shaped by global drivers and local environments. Lancet. 2011;378(9793):804-14.

4 Catenacci VA, Hill JO, Wyatt HR. The obesity epidemic. Clin Chest Med. 2009;30(3):415-44, vii.

5 Popkin BM, Adair LS, Ng SW. Global nutrition transition and the pandemic of obesity in developing countries. Nutr Rev. 2012;70(1):3-21.

6 Available at: http://www.toledoblade.com/Food/2015/06/23/70-of-Americans-overweight-or-obese-study-finds.html. Accessed September 29, 2015.

7 Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

8 Lustig RH. Fructose: it’s “alcohol without the buzz”. Adv Nutr. 2013;4(2):226-35.

9 Lustig RH. Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010;110(9):1307-21.

10 Volkow ND, Wang GJ, Fowler JS, Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philos Trans R Soc Lond, B, Biol Sci. 2008;363(1507):3191-200.

11 Puhl R, Brownell KD. Bias, discrimination, and obesity. Obes Res. 2001;9(12):788-805.

12 Brownell KD, Kersh R, Ludwig DS, et al. Personal responsibility and obesity: a constructive approach to a controversial issue. Health Aff (Millwood). 2010;29(3):379-87.

13 Vartanian LR, Schwartz MB, Brownell KD. Effects of soft drink consumption on nutrition and health: a systematic review and meta-analysis. Am J Public Health. 2007;97(4):667-75.

14 Brownell KD, Warner KE. The perils of ignoring history: Big Tobacco played dirty and millions died. How similar is Big Food?. Milbank Q. 2009;87(1):259-94.

Coca-Cola Sugar | The Paleo Diet

If your core business involves the mass production and distribution of sugary products with little nutritional value, times are tough. In the old days, prominent health institutions and regulatory governmental agencies looked upon sugar as relatively benign. Today, however, the science of sugar metabolism is much better understood and accordingly, those institutions and regulatory agencies are becoming increasingly fastidious regarding sugar.

The cat is out of the bag and it’s not going back. So if you’re in the sugar business, your most viable marketing strategies may well involve shifting consumer attention away from food and toward other aspects of healthy living, like exercise.

This seems to be the case with Coca-Cola, according to a story that broke earlier this week in The New York Times. A new nonprofit organization, the Global Energy Balance Network (GEBN), which collected $1.5 million in donations from Coke in 2014, promotes the idea that focusing on healthy food is the wrong approach to losing weight.1 Instead of food, dieters should be focusing on exercise.

In an astounding, you-have-see-it-for-yourself online video, GEBN’s vice president, Dr. Steven N. Blair, explains about obesity, “Most of the focus in the popular media and in the scientific press is that they’re eating too much, eating too much, eating too much, blaming fast food, blaming sugary drinks and so on. And there’s really virtually no compelling evidence that that in fact is the cause.”

While it’s true that no single food is solely responsible for obesity, the notion that sugar consumption doesn’t matter flies in the face of decades of nutritional science research. Even the big regulatory governmental agencies are now lining up against sugar and this isn’t happening for lack of “compelling evidence.”

After sitting on the sidelines for decades, both the U.S. and the U.K. governments are now aligning themselves with the published scientific literature and indicating that official warnings against excessive sugar consumption are forthcoming.

Last month in the U.K., the Scientific Advisory Committee on Nutrition (SACN), which advises Public Health England and other government agencies on nutrition, suggested that daily intake of sugar should be halved, from 10% to 5% of total calories, to reduce obesity and improve dental health.2

Here in the U.S., the USDA’s Dietary Guidelines for Americans are due for revision this year. The Dietary Guidelines Advisory Committee has already met and, after reviewing the published scientific literature, has determined that sugar should account for no more than 10% of total calories.3 Previously, the guidelines recommend against consuming “too much” sugar, but failed to quantify upper limits.

Finally, in March of this year, the World Health Organization issued an official communiqué stating that sugar should account for no more than 10% of total calories and that 5% would confer even greater health benefits.4 According to Dr. Francesco Branca, Director of WHO’s Department of Nutrition for Health and Development, “We have solid evidence that keeping intake of free sugars to less than 10% of total energy intake reduces the risk of overweight, obesity and tooth decay.”

Americans are drinking fewer soft drinks every year. In March, The Wall Street Journal reported that U.S. soft drink sales have declined every year for the past 10 years, representing a 14% decline since 2004.5 Are beverage giants trying to lull the public into believing that sugar plays no part in obesity?

Coca-Cola insists they partner with “the foremost experts in the fields of nutrition and physical activity,” but it’s curious that they seem to avoid funding groups that warn about sugar. In fact, since 2008, they have given upwards of $5.5 million to projects organized by two of GEBN’s founders, Dr. Blair and Gregory A. Hand, dean of the West Virginia University School of Public Health.6]

This story serves as a dramatic example of how corporate money can influence public opinion through purportedly independent, nonprofit organizations. We at The Paleo Diet would like to emphasize that exercise is indeed an important component of healthy lifestyles, but unfortunately exercise cannot compensate for unhealthy diets, particularly those high in processed, sugary foods.


1 O’Connor, Anahad. (August 9, 2015). Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets. The New York Times. Retrieved from http://well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shift-blame-for-obesity-away-from-bad-diets/?_r=0

2 The BBC. (July 17, 2015). Scientific experts: Sugar intake ‘should be halved’. Retrieved from http://www.bbc.com/news/health-33551501

3 O’Connor, Anahad. (February 19, 2015). Nutrition Panel Calls for Less Sugar and Eases Cholesterol and Fat Restrictions. The New York Times. Retrieved from http://well.blogs.nytimes.com/2015/02/19/nutrition-panel-calls-for-less-sugar-and-eases-cholesterol-and-fat-restrictions/?_r=1

4 Press Release. (March 4, 2015). WHO calls on countries to reduce sugars intake among adults and children. The World Health Organization. Retrieved from http://www.who.int/mediacentre/news/releases/2015/sugar-guideline/en/

5 Esterl, Mike. (March 26, 2015). Soft Drinks Hit 10th Year of Decline. The Wall Street Journal. Retrieved from http://www.wsj.com/articles/pepsi-cola-replaces-diet-coke-as-no-2-soda-1427388559

6 O’Connor, Anahad. (August 9, 2015). Coca-Cola Funds Scientists Who Shift Blame for Obesity Away From Bad Diets. The New York Times. Retrieved from http://well.blogs.nytimes.com/2015/08/09/coca-cola-funds-scientists-who-shift-blame-for-obesity-away-from-bad-diets/?_r=0

The Reality of Food Addiction: Recharged | The Paleo Diet

In one of my post popular articles, I dove deep into the mire of just why so many of us are addicted to food. This subject is fascinating on both a molecular and individual level.1, 2, 3, 4  There are so many factors which go into food addiction.5, 6, 7, 8, 9, 10, 11, 12, 13 And most of them go totally unnoticed, to most people.14, 15, 16, 17, 18, 19, 20, 21, 22 The pervasiveness of advertising, the purposely addictive nature of processed foods, and the stressful nature of modern life is just too much for most of us to stay healthy.23, 24, 25, 26, 27, 28, 29, 30, 31, 32 Of course, new research has emerged on this topic, since an entire calendar year has passed since I wrote my first piece on food addiction – and some of it is quite startling.33, 34, 35, 36, 37, 38, 39, 40,

The Reality of Food Addiction: Recharged | The Paleo Diet

Volkow, Nora D et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Philosophical Transactions of the Royal Society B: Biological Sciences 363.1507 (2008): 3191–3200. PMC. Web. 7 Aug. 2015.

But perhaps most troublingly, many scientists are still trying to fight the notion that food addiction even exists.41, 42, 43 I’m alarmed, offended and angry about this continued hemming and hawing (no doubt influenced by industry) – and you should be too. In simplest terms, go ask the average person following a Standard American Diet (SAD) if they feel addicted to food. I would bet everything I own that their answer would be a resounding “yes.”44, 45 No one wants to be obese, and unquestionably some level of addiction is underlying our obesity pandemic.46, 47, 48, 49, 50, 51 52, 53, 54, 55 Certainly there are also other factors, which I’ve also written about, (like leptin resistance) that happen as a result of poor food choices compounded over time.56, 57, 58, 59, 60, 61, 62, 63, 64

The Reality of Food Addiction: Recharged | The Paleo Diet

Agrawal, Rahul, and Fernando Gomez-Pinilla. “‘Metabolic Syndrome’ in the Brain: Deficiency in Omega-3 Fatty Acid Exacerbates Dysfunctions in Insulin Receptor Signalling and Cognition.” The Journal of Physiology 590.Pt 10 (2012): 2485–2499. PMC. Web. 7 Aug. 2015.

The Reality of Food Addiction: Recharged | The Paleo Diet

Cai, Dongsheng, and Tiewen Liu. “Inflammatory Cause of Metabolic Syndrome via Brain Stress and NF-κB.” Aging (Albany NY) 4.2 (2012): 98–115. Print.

It is my generation who is now having to pay for all the poor choices made by prior ones, and now more than 66% of adults are overweight or obese.65 Four years ago researchers knew that “there are a number of shared neural and hormonal pathways…that may help researchers discover why certain individuals continue to overeat despite health and other consequences”.66 And yet, some scientists refuse to even acknowledge people are addicted to food! It is maddening.

The Reality of Food Addiction: Recharged | The Paleo Diet

Sturm, Roland, and Aiko Hattori. “Morbid Obesity Rates Continue to Rise Rapidly in the US.” International journal of obesity (2005) 37.6 (2013): 889–891. PMC. Web. 7 Aug. 2015.

The results of food addiction are happening here and now.67, 68 We see them every day on the way to work, at the store, in society, and even glamorized in popular media. Certainly, no one should be ‘fat shamed’ – but we shouldn’t be celebrating obesity either. Food addiction is just as sad as drug addiction – it is just destructive over a longer period of time, rather than acutely.69, 70, 71 As science shows, the same neurobiological pathways that are implicated in drug abuse also modulate food consumption.72, 73

The Reality of Food Addiction: Recharged | The Paleo Diet

Volkow, Nora D et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Philosophical Transactions of the Royal Society B: Biological Sciences 363.1507 (2008): 3191–3200. PMC. Web. 7 Aug. 2015.

The Reality of Food Addiction: Recharged | The Paleo Diet

Volkow, Nora D et al. “Overlapping Neuronal Circuits in Addiction and Obesity: Evidence of Systems Pathology.” Philosophical Transactions of the Royal Society B: Biological Sciences 363.1507 (2008): 3191–3200. PMC. Web. 7 Aug. 2015.

The Reality of Food Addiction: Recharged | The Paleo Diet

Baik, Ja-Hyun. “Dopamine Signaling in Food Addiction: Role of Dopamine D2 Receptors.” BMB Reports 46.11 (2013): 519–526. PMC. Web. 7 Aug. 2015.

Or how about the scientific paper which showed that Oreo cookies were as addictive as cocaine?74 Again, you will find some scientists hemming and hawing, but the reality, the way the science translates into our everyday lives, shows clear addiction. Do you feel like you need to eat the whole bag of broccoli? Obviously not. For most, vegetables are a chore. But it sure is easy to eat a whole box of Oreos! In fact, many find it hard not to.75 Does this sound addictive to you?

Then we have the case of researchers “curing binge eating” by modulating dopamine receptors.76 Why is this notable? Because by altering the brain’s response to rewarding food, we can stop the cravings/addiction! This really hammers home the point that food can be addictive, and that it is not just an innocent bystander that some people (66% of all adults, if you’re keeping track) can’t seem to stop consuming. If you wants to know more of the deep molecular mechanisms and psychology behind eating, I have also written on this very subject.

The Reality of Food Addiction: Recharged | The Paleo Diet

Green, Erin, and Claire Murphy. “Altered Processing of Sweet Taste in the Brain of Diet Soda Drinkers.” Physiology & behavior 107.4 (2012): 560–567. PMC. Web. 7 Aug. 2015.

And what is one of the most addictive, and least healthy habits in the world? Soda. The less soda you drink, the great weight loss you see.77, 78, 79 Even artificial sweeteners have shown rewarding mechanisms in the brain.80, 81, 82, 83, 84 Interestingly, new research has shown that a hormone deficiency in the brain may also be causing overeating.85, 86, 87 This is in addition to new research which shows that ‘bad’ genes may also play a role in overconsumption.88, 89, 90, 91, 92

Clearly, food addiction is a real problem, which needs to be fixed as soon as possible.93, 94 The future of (a healthy) human world…sort of depends on it. A Paleo diet is one of the best ways to go cold turkey, and stop food addiction in its tracks. By eating nutrient dense foods, sleeping soundly, and managing stress, we are taking proactive steps to avoiding food addiction and obesity.95, 96 97, 98, 99, 100




[1] Avena NM, Bocarsly ME, Hoebel BG. Animal models of sugar and fat bingeing: relationship to food addiction and increased body weight. Methods Mol Biol. 2012;829:351-65.

[2] Avena NM, Rada P, Hoebel BG. Sugar bingeing in rats. Curr Protoc Neurosci. 2006;Chapter 9:Unit9.23C.

[3] Rada P, Avena NM, Hoebel BG. Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell. Neuroscience. 2005;134(3):737-44.

[4] Blum K, Thanos PK, Gold MS. Dopamine and glucose, obesity, and reward deficiency syndrome. Front Psychol. 2014;5:919.

[5] Berridge KC. ‘Liking’ and ‘wanting’ food rewards: brain substrates and roles in eating disorders. Physiol Behav. 2009;97(5):537-50.

[6] Wise RA. Role of brain dopamine in food reward and reinforcement. Philos Trans R Soc Lond, B, Biol Sci. 2006;361(1471):1149-58.

[7] 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.

[8] 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.

[9] Swiecicki L, Scinska A, Bzinkowska D, et al. Intensity and pleasantness of sucrose taste in patients with winter depression. Nutr Neurosci. 2014.

[10] 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.

[11] Bellisle F, Drewnowski A. Intense sweeteners, energy intake and the control of body weight. Eur J Clin Nutr. 2007;61(6):691-700.

[12] Caffaro CE, Hirschberg CB. Nucleotide sugar transporters of the Golgi apparatus: from basic science to diseases. Acc Chem Res. 2006;39(11):805-12.

[13] Willett WC, Ludwig DS. Science souring on sugar. BMJ. 2013;346:e8077.

[14] Grant JE, Potenza MN, Weinstein A, Gorelick DA. Introduction to behavioral addictions. Am J Drug Alcohol Abuse. 2010;36(5):233-41.

[15] Greeno CG, Wing RR. Stress-induced eating. Psychol Bull. 1994;115(3):444-64.

[16] Soubry A, Murphy SK, Wang F, et al. Newborns of obese parents have altered DNA methylation patterns at imprinted genes. Int J Obes (Lond). 2013.

[17] Kerti L, Witte AV, Winkler A, Grittner U, Rujescu D, Flöel A. Higher glucose levels associated with lower memory and reduced hippocampal microstructure. Neurology. 2013;81(20):1746-52.

[18] Epstein DH, Shaham Y. Cheesecake-eating rats and the question of food addiction. Nat Neurosci. 2010;13(5):529-31.

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

[20] Walker RW, Dumke KA, Goran MI. Fructose content in popular beverages made with and without high-fructose corn syrup. Nutrition. 2014;30(7-8):928-35.

[21] Johnson PM, Kenny PJ. Dopamine D2 receptors in addiction-like reward dysfunction and compulsive eating in obese rats. Nat Neurosci. 2010;13(5):635-41.

[22] Yang Q. Gain weight by “going diet?” Artificial sweeteners and the neurobiology of sugar cravings: Neuroscience 2010. Yale J Biol Med. 2010;83(2):101-8.

[23] Popkin BM, Nielsen SJ. The sweetening of the world’s diet. Obes Res. 2003;11(11):1325-32.

[24] Brownell KD, Warner KE. The perils of ignoring history: Big Tobacco played dirty and millions died. How similar is Big Food?. Milbank Q. 2009;87(1):259-94.

[25] Sharma LL, Teret SP, Brownell KD. The food industry and self-regulation: standards to promote success and to avoid public health failures. Am J Public Health. 2010;100(2):240-6.

[26] Oliver KG, Huon GF, Zadro L, Williams KD. The role of interpersonal stress in overeating among high and low disinhibitors. Eat Behav. 2001;2(1):19-26.

[27] Copinschi G. Metabolic and endocrine effects of sleep deprivation. Essent Psychopharmacol. 2005;6(6):341-7.

[28] Harris JL, Bargh JA, Brownell KD. Priming effects of television food advertising on eating behavior. Health Psychol. 2009;28(4):404-13.

[29] Knutson KL, Spiegel K, Penev P, Van cauter E. The metabolic consequences of sleep deprivation. Sleep Med Rev. 2007;11(3):163-78.

[30] Andreyeva T, Long MW, Brownell KD. The impact of food prices on consumption: a systematic review of research on the price elasticity of demand for food. Am J Public Health. 2010;100(2):216-22.

[31] Gearhardt AN, White MA, Potenza MN. Binge eating disorder and food addiction. Curr Drug Abuse Rev. 2011;4(3):201-7.

[32] 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.

[33] Dimitrijević I, Popović N, Sabljak V, Škodrić-trifunović V, Dimitrijević N. Food addiction-diagnosis and treatment. Psychiatr Danub. 2015;27(1):101-6.

[34] Schulte EM, Avena NM, Gearhardt AN. Which foods may be addictive? The roles of processing, fat content, and glycemic load. PLoS ONE. 2015;10(2):e0117959.

[35] Meule A, Hermann T, Kübler A. Food addiction in overweight and obese adolescents seeking weight-loss treatment. Eur Eat Disord Rev. 2015;23(3):193-8.

[36] Hardman CA, Rogers PJ, Dallas R, Scott J, Ruddock HK, Robinson E. “Food addiction is real”. The effects of exposure to this message on self-diagnosed food addiction and eating behaviour. Appetite. 2015;91:179-84.

[37] Schulte EM, Joyner MA, Potenza MN, Grilo CM, Gearhardt AN. Current considerations regarding food addiction. Curr Psychiatry Rep. 2015;17(4):563.

[38] Piccinni A, Marazziti D, Vanelli F, et al. Food addiction spectrum: a theoretical model from normality to eating and overeating disorders. Curr Med Chem. 2015;22(13):1631-8.

[39] Pedram P, Sun G. Hormonal and dietary characteristics in obese human subjects with and without food addiction. Nutrients. 2015;7(1):223-38.

[40] Karlsson HK, Tuominen L, Tuulari JJ, et al. Obesity is associated with decreased μ-opioid but unaltered dopamine D2 receptor availability in the brain. J Neurosci. 2015;35(9):3959-65.

[41] Hebebrand J, Albayrak Ö, Adan R, et al. “Eating addiction”, rather than “food addiction”, better captures addictive-like eating behavior. Neurosci Biobehav Rev. 2014;47:295-306.

[42] Ziauddeen H, Fletcher PC. Is food addiction a valid and useful concept?. Obes Rev. 2013;14(1):19-28.

[43] Barry D, Clarke M, Petry NM. Obesity and its relationship to addictions: is overeating a form of addictive behavior?. Am J Addict. 2009;18(6):439-51.

[44] Ogden J, Clementi C. The experience of being obese and the many consequences of stigma. J Obes. 2010;2010

[45] Fortuna JL. The obesity epidemic and food addiction: clinical similarities to drug dependence. J Psychoactive Drugs. 2012;44(1):56-63.

[46] Moreira PI. High-sugar diets, type 2 diabetes and Alzheimer’s disease. Curr Opin Clin Nutr Metab Care. 2013;16(4):440-5.

[47] Ford ES, Giles WH, Mokdad AH. Increasing prevalence of the metabolic syndrome among u.s. Adults. Diabetes Care. 2004;27(10):2444-9.

[48] Daly M. Sugars, insulin sensitivity, and the postprandial state. Am J Clin Nutr. 2003;78(4):865S-872S.

[49] Musselman LP, Fink JL, Narzinski K, et al. A high-sugar diet produces obesity and insulin resistance in wild-type Drosophila. Dis Model Mech. 2011;4(6):842-9.

[50] Lythgoe A, Roberts C, Madden AM, Rennie KL. Marketing foods to children: a comparison of nutrient content between children’s and non-children’s products. Public Health Nutr. 2013;16(12):2221-30.

[51] Gallagher EJ, Leroith D, Karnieli E. Insulin resistance in obesity as the underlying cause for the metabolic syndrome. Mt Sinai J Med. 2010;77(5):511-23.

[52] Gearhardt A, Roberts M, Ashe M. If sugar is addictive…what does it mean for the law?. J Law Med Ethics. 2013;41 Suppl 1:46-9.

[53] Johnson RK, Appel LJ, Brands M, et al. Dietary sugars intake and cardiovascular health: a scientific statement from the American Heart Association. Circulation. 2009;120(11):1011-20.

[54] Lustig RH, Schmidt LA, Brindis CD. Public health: The toxic truth about sugar. Nature. 2012;482(7383):27-9.

[55] Avena NM, Rada P, Hoebel BG. Evidence for sugar addiction: behavioral and neurochemical effects of intermittent, excessive sugar intake. Neurosci Biobehav Rev. 2008;32(1):20-39.

[56] Myers MG, Cowley MA, Münzberg H. Mechanisms of leptin action and leptin resistance. Annu Rev Physiol. 2008;70:537-56.

[57] Yates KF, Sweat V, Yau PL, Turchiano MM, Convit A. Impact of metabolic syndrome on cognition and brain: a selected review of the literature. Arterioscler Thromb Vasc Biol. 2012;32(9):2060-7.

[58] Singh RB, Gupta S, Dherange P, et al. Metabolic syndrome: a brain disease. Can J Physiol Pharmacol. 2012;90(9):1171-83.

[59] Tiehuis AM, Van der graaf Y, Mali WP, et al. Metabolic syndrome, prediabetes, and brain abnormalities on mri in patients with manifest arterial disease: the SMART-MR study. Diabetes Care. 2014;37(9):2515-21.

[60] Mauro C, De rosa V, Marelli-berg F, Solito E. Metabolic syndrome and the immunological affair with the blood-brain barrier. Front Immunol. 2014;5:677.

[61] Agrawal R, Gomez-pinilla F. ‘Metabolic syndrome’ in the brain: deficiency in omega-3 fatty acid exacerbates dysfunctions in insulin receptor signalling and cognition. J Physiol (Lond). 2012;590(Pt 10):2485-99.

[62] Cai D, Liu T. Inflammatory cause of metabolic syndrome via brain stress and NF-κB. Aging (Albany NY). 2012;4(2):98-115.

[63] Buijs RM, Kreier F. The metabolic syndrome: a brain disease?. J Neuroendocrinol. 2006;18(9):715-6.

[64] Zhu S, St-onge MP, Heshka S, Heymsfield SB. Lifestyle behaviors associated with lower risk of having the metabolic syndrome. Metab Clin Exp. 2004;53(11):1503-11.

[65] Available at: http://www.niddk.nih.gov/health-information/health-statistics/Pages/overweight-obesity-statistics.aspx. Accessed July 29, 2015.

[66] Zhang Y, Von deneen KM, Tian J, Gold MS, Liu Y. Food addiction and neuroimaging. Curr Pharm Des. 2011;17(12):1149-57.

[67] Kanoski SE, Davidson TL. Western diet consumption and cognitive impairment: links to hippocampal dysfunction and obesity. Physiol Behav. 2011;103(1):59-68.

[68] Sturm R, Hattori A. Morbid obesity rates continue to rise rapidly in the United States. Int J Obes (Lond). 2013;37(6):889-91.

[69] Schmidt LA. New unsweetened truths about sugar. JAMA Intern Med. 2014;174(4):525-6.

[70] Ruff JS, Suchy AK, Hugentobler SA, et al. Human-relevant levels of added sugar consumption increase female mortality and lower male fitness in mice. Nat Commun. 2013;4:2245.

[71] Blaisdell AP, Lau YL, Telminova E, et al. Food quality and motivation: a refined low-fat diet induces obesity and impairs performance on a progressive ratio schedule of instrumental lever pressing in rats. Physiol Behav. 2014;128:220-5.

[72] Blumenthal DM, Gold MS. Neurobiology of food addiction. Curr Opin Clin Nutr Metab Care. 2010;13(4):359-65.

[73] Volkow ND, Wang GJ, Fowler JS, Telang F. Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology. Philos Trans R Soc Lond, B, Biol Sci. 2008;363(1507):3191-200.

[74] Levy A, Salamon A, Tucci M, Limebeer CL, Parker LA, Leri F. Co-sensitivity to the incentive properties of palatable food and cocaine in rats; implications for co-morbid addictions. Addict Biol. 2013;18(5):763-73.

[75] Lenoir M, Serre F, Cantin L, Ahmed SH. Intense sweetness surpasses cocaine reward. PLoS ONE. 2007;2(8):e698.

[76] Halpern CH, Tekriwal A, Santollo J, et al. Amelioration of binge eating by nucleus accumbens shell deep brain stimulation in mice involves D2 receptor modulation. J Neurosci. 2013;33(17):7122-9.

[77] Chen L, Appel LJ, Loria C, et al. Reduction in consumption of sugar-sweetened beverages is associated with weight loss: the PREMIER trial. Am J Clin Nutr. 2009;89(5):1299-306.

[78] Drewnowski A, Bellisle F. Liquid calories, sugar, and body weight. Am J Clin Nutr. 2007;85(3):651-61.

[79] Malik VS, Pan A, Willett WC, Hu FB. Sugar-sweetened beverages and weight gain in children and adults: a systematic review and meta-analysis. Am J Clin Nutr. 2013;98(4):1084-102.

[80] Cantley LC. Cancer, metabolism, fructose, artificial sweeteners, and going cold turkey on sugar. BMC Biol. 2014;12:8.

[81] Suez J, Korem T, Zeevi D, et al. Artificial sweeteners induce glucose intolerance by altering the gut microbiota. Nature. 2014.

[82] Anton SD, Martin CK, Han H, et al. Effects of stevia, aspartame, and sucrose on food intake, satiety, and postprandial glucose and insulin levels. Appetite. 2010;55(1):37-43.

[83] Swithers SE. Artificial sweeteners produce the counterintuitive effect of inducing metabolic derangements. Trends Endocrinol Metab. 2013;24(9):431-41.

[84] Direct and indirect cellular effects of aspartame on the brain. European Journal of Clinical Nutrition. 2008;62(4):451.

[85] Zhiping P. Pang et al. Endogenous Glucagon-like Peptide-1 Suppresses High-Fat Food Intake by Reducing Synaptic Drive onto Mesolimbic Dopamine Neurons. Cell Reports, July 2015.

[86] Zumoff B. Hormonal abnormalities in obesity. Acta Med Scand Suppl. 1988;723:153-60.

[87] Wren AM. Gut and hormones and obesity. Front Horm Res. 2008;36:165-81.

[88] Nadia Micali, Alison E. Field, Janet L. Treasure, David M. Evans. Are obesity risk genes associated with binge eating in adolescence? Obesity, 2015; 23 (8): 1729.

[89] Stice E, Yokum S, Zald D, Dagher A. Dopamine-based reward circuitry responsivity, genetics, and overeating. Curr Top Behav Neurosci. 2011;6:81-93.

[90] Grimm ER, Steinle NI. Genetics of eating behavior: established and emerging concepts. Nutr Rev. 2011;69(1):52-60.

[91] Barry D, Clarke M, Petry NM. Obesity and its relationship to addictions: is overeating a form of addictive behavior?. Am J Addict. 2009;18(6):439-51.

[92] Fawcett KA, Barroso I. The genetics of obesity: FTO leads the way. Trends Genet. 2010;26(6):266-74.

[93] Gearhardt AN, Corbin WR. The role of food addiction in clinical research. Curr Pharm Des. 2011;17(12):1140-2.

[94] Pursey KM, Stanwell P, Gearhardt AN, Collins CE, Burrows TL. The prevalence of food addiction as assessed by the Yale Food Addiction Scale: a systematic review. Nutrients. 2014;6(10):4552-90.

[95] Kasim-karakas SE, Almario RU, Cunningham W. Effects of protein versus simple sugar intake on weight loss in polycystic ovary syndrome (according to the National Institutes of Health criteria). Fertil Steril. 2009;92(1):262-70.

[96] Van itallie TB. Dietary fiber and obesity. Am J Clin Nutr. 1978;31(10 Suppl):S43-52.

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

[98] 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.

[99] 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.

[100] Konner M, Eaton SB. Paleolithic nutrition: twenty-five years later. Nutr Clin Pract. 2010;25(6):594-602.

Soy, Sugar's Cohort in Causing Obesity | The Paleo Diet

Since the 1930s, the US government has been heavily subsidizing corn, soy, wheat, and other so-called staple crops. Subsequently, these foods have remained artificially cheap for decades, leading to enormously increased consumption.

For a new study, just published in PLOS One, scientists at UC Riverside compared the effects of diets high in soybean oil with those high in fructose and/or coconut oil. They concluded that soybean oil, when consumed at typical American consumption levels, causes significant liver damage and promotes obesity and diabetes even more so than fructose.1

“This was a major surprise for us—that soybean oil is causing more obesity and diabetes than fructose—especially when you see headlines everyday about the potential role of sugar consumption in the current obesity epidemic,” said Poonamjot Deol, the study’s lead scientist.2

This study is believed to be the first comparing the effects of unsaturated fat, saturated fat, and fructose on obesity, diabetes, insulin resistance and nonalcoholic fatty liver disease. While excessive sugar consumption has rightfully been criticized during the past several years, this study shows that industrial seed oils, particularly soybean oil, can be just as dangerous.

Soybean oil features prominently in many processed foods, especially margarine, salad dressings, and snack foods. It’s also the preferred cooking oil throughout the restaurant industry. In 2007, around 80 million tons of edible vegetable oils were produced globally, about half of which was soybean oil.3

Just how much money goes into keeping soy cheap and plentiful? Between 1995 and 2012, US soy subsidies totaled an astounding $27.8 billion, second only to corn, which amounted to $84.4 billion for the same period. In 2014, the US government replaced direct payments to farmers with Price Loss Coverage (PLC) and Agricultural Risk Coverage (ARC), but these new programs still cost taxpayers two-thirds as much as the direct payments did.4

Annual consumption of soybean oil increased from a miniscule 0.01 kg per person in 1909 to 11.2 kg in 1999.5 So what has been the impact on health? The UC Riverside scientists fed mice diets with 40% of calories coming from fat and supplemented those diets with fructose. Diet 1 consisted of 36 kcal% from coconut oil and 4 kcal% from soybean oil. Diet 2 consisted of 21 kcal% from coconut oil and 19 kcal% from soybean oil. These diets were formulated to mimic American consumption patterns with respect to saturated fat, soybean oil, and fructose.

Mice on Diet 2, the high soybean oil diet, exhibited increased weight gain, adiposity, fatty liver, insulin resistance, and diabetes, compared to mice on Diet 1. The scientists believe the mechanisms behind these outcomes involve changes in gene expression. Diet 2, for example, caused significant global dysregulation of several genes, particularly cytochrome P450, related to diabetes, obesity, lipid metabolism, and cancer.

Fructose had less severe metabolic effects than did soybean oil, which was a surprise to the scientists. More importantly, they determined that fructose combined with soybean oil works synergistically to undermine health.

Fructose induced neither diabetes nor insulin resistance in this study, although it did induce obesity. The scientists point out that fructose and its metabolic impact are very hotly debated within the nutrition science community. Further research will yield a more evolved perspective on fructose, but this study stresses the importance of dietary context. In other words, fructose seems to be much more damaging when paired with unhealthy oils compared to healthy sources of fat.

Many people within the Paleo community are concerned about fructose, even going so far as to completely eliminate fruit from their diets. While this might be appropriate for some people, it’s probably unnecessary for others. The fat in the Paleo diet comes mostly from high-quality sources of saturated and monounsaturated fat, with minimal amounts of high-quality polyunsaturated fat. The current study shows how foods interact and why a holistic approach to diet is essential. If America is serious about reversing degenerative diseases, soybean oil must share the spotlight with sugar during the many ongoing national discussions about nutrition.



[1] Deol, P., et al. (July 2015). Soybean Oil Is More Obesogenic and Diabetogenic than Coconut Oil and Fructose in Mouse: Potential Role for the Liver. PLOS One, 10(7).

[2] University of California – Riverside. (2015, July 22). Soybean oil causes more obesity than coconut oil, fructose: Scientists found mice on high soybean oil diet showed increased levels of weight gain, diabetes compared to mice on a high fructose diet or high coconut oil diet. ScienceDaily.

[3] Rosillo-Calle, F. (2009). A global overview of vegetable oils, with reference to biodiesel. CEP/Imperial College, Luc Pelkmans, VITO and Arnaldo Walter, UNICAMP for IEA Bioenergy Task 40.

[4] Haspel, T. (February 18, 2014). Farm bill: Why don’t taxpayers subsidize the foods that are better for us? The Washington Post.

[5] Blasbalg, TL, et al. (March 2011). Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. The American Journal of Clinical Nutrition, 93(5).

Sugar and Alcohol: Your Liver Can’t Tell The Difference

Dr. David Unwin, Fellow of the Royal College of General Practitioners (FRCGP) together with fellow researchers recently completed a study showing low carb diets significantly reduce fatty liver, weight and blood sugar. Trialing a low carb approach over a year, they found rapid improvements in liver function among other positive effects.

“My interest in abnormal liver, and particularly GGT blood results began when I noticed that in our family practice of 9,000 patients well over a 1,000 had an abnormal GGT result,” said Dr. Unwin. “I could predict which patients would have lost weight -before they came into my consulting room from the improvement in GGT blood results alone- so began to wonder about raised GGT levels, Diabetes and non-alcoholic fatty liver disease (NAFLD): Was dietary carbohydrate a link?”

Before we get to the summary, let’s breakdown some of the statistics.

  • Approximately 30 million children and adults have diabetes in the United States. Out of that number, nearly 95% have type 2 diabetes according to the American Diabetes Association.1
  • The National Conference of State Legislatures (NCSL) reports obesity affects more than one-third of adults and 17% of youth in the United States. This equates to 78 million adults and 12 million children suffering from the obesity epidemic. As adopters of the Paleo diet well know, obesity increases risk for heart disease, type 2 diabetes, and cancer among other debilitating health conditions, like non-alcoholic fatty liver disease (NAFLD).2
  • The American Liver Foundation reports (NAFLD) affects up to 25% of Americans, where risk is directly correlated to being overweight or obese, having diabetes, high cholesterol or high triglycerides.3

As the cost of health care continues to skyrocket, Dr. Unwin has decreased his prescribing budget £15,000-£30,000 a year by prescribing a low carb diet to patients who in two years’ time decreased average blood sugar by 10% and is now below the national average in the UK4 and US.

“I would say sugar is definitely rather like alcohol for the liver, and would point out that starchy foods like bread and pasta are a rich source of glucose,” said Dr. Unwin.

Well, thankfully the Paleo diet is devoid of breads, pastas, grains, pseudo grains, and processed sugars. When we focus upon lean meats, fish, poultry, veggies, and fruits, nuts, and seeds in moderation, a Paleo prescription is the best, cost effective investment you can make for your health.

Summary* presented ahead of publication in Diabetes in Practice September 15, 2015.

Unwin DJ1, Cuthertson DJ2, Feinman R3, Sprung VS2 (2015) A pilot study to explore the role of a low-carbohydrate intervention to improve GGT levels and HbA1c. Diabesity in Practice 4 [in press]

1Norwood Surgery, Norwood Ave, Southport. 2Department of Obesity and Endocrinology, Institute of Ageing & Chronic Disease, University of Liverpool, UK. 3Professor of biochemistry and medical researcher at State University of New York Health Science Center at Brooklyn, USA.

Working title: Raised GGT levels, Diabetes and NAFLD: Is dietary carbohydrate a link?  Primary care pilot of a low carbohydrate diet

Abnormal liver function tests are often attributed to excessive alcohol consumption and/or medication without further investigation. However they may be secondary to non-alcoholic fatty liver disease (NAFLD). NAFLD is now prevalent in 20-30% of adults in the Western World. Considering the increased cardiovascular and metabolic risk of NAFLD, identification and effective risk factor management of these patients is critical.

Background Excess dietary glucose leads progressively to hepatocyte triglyceride accumulation (non-alcoholic fatty liver disease-NAFLD), insulin resistance and T2DM. Considering the increased cardiovascular risks of NAFLD and T2DM, effective risk-factor management of these patients is critical. Weight loss can improve abnormal liver biochemistry, the histological progression of NAFLD, and diabetic control. However, the most effective diet remains controversial.

Aim We implemented a low-carbohydrate (CHO) diet in a primary health setting, assessing the effect on serum GGT, HbA1c levels (as proxies for suspected NAFLD and diabetic control), and weight.

Design  69 patients with a mean  GGT of 77 iu/L (NR 0-50) and an average BMI of 34.4Kg/m2 were recruited opportunistically and advised on reducing total glucose intake (including starch), while increasing intake of  natural fats, vegetables and protein.

Method Baseline blood samples were assessed for GGT levels, lipid profile, and HbA1c. Anthropometrics were assessed and repeated at monthly intervals. The patients were provided monthly support by their general practitioner or practice nurse, either individually or as a group.

Results After an average of 13 months on a low-CHO diet there was a 46% mean reduction in GGT of 29.9 iu/L (95% CI= -43.7, -16.2; P<0.001), accompanied by average reductions in weight [-8.8Kg (95% CI= -10.0, -7.5; P<0.001)],and HbA1c [10.0mmol/mol (95% CI= -13.9, -6.2; P<0.001)].

Conclusions We provide evidence that low-carbohydrate, dietary management of patients with T2DM and/or suspected NAFLD in primary care is feasible and improves abnormal liver biochemistry and other cardio-metabolic risk factors. This raises the question as to whether dietary carbohydrate plays a role in the etiology of diabetes and NAFLD, as well as obesity. Over the study period and given a choice not a single patient opted to start antidiabetic medication, losing weight instead. This helps explain why our practice is the only one in the Southport and Formby CCG to have static diabetes drug costs for three years running.

*Note: The summary displayed above is not the official abstract from Diabetes in Practice.

David Unwin | The Paleo Diet

David Unwin is the senior partner and GP trainer at the Norwood Surgery, Southport, a seaside resort in the North West of England. He is an expert clinical adviser in diabetes for the Royal College of General Practitioners, and has a special interest in the Solution Focused psychological approach to the consultation. David lives on a farm with his wife, son and their sheep, turkeys, hens -and a very large pig!




[1] http://www.diabetes.org/diabetes-basics/statistics/infographics.html?loc=db-slabnav

[2] http://www.ncsl.org/research/health/obesity-statistics-in-the-united-states.aspx

[3] http://www.liverfoundation.org/abouttheliver/info/nafld/

[4] http://diabetesdietblog.com/2015/07/15/you-only-need-one-arrow-dr-unwin-proves-it-again/

A Brief History of the Contemporary Paleo Diet Movement | The Paleo Diet


In order to appreciate any concept, including the Paleo Diet, it is important to recognize its history and how it came to be. Most of you are aware that Paleo and particularly Paleo diets have recently become very hot, on trend topics.

These ideas have become household words in the past few years; however it hasn’t always been this way. Below is a graph from Google Trends for the words “ the Paleo diet” (Figure 1).  It’s fairly clear from Figure 1 that, except for the past four years, the Paleo diet was virtually unknown to all but dedicated fans. Fortunately, I’ve been in the middle of this worldwide movement from nearly its very beginnings. So, I can personally tell you how it all began and my involvement in it.

Google Trends | The Paleo Diet Over Time

Figure 1. Google Trends. 25 June 2015.

Last October, I approached my 64th birthday with just a little trepidation because I was part of the 60’s generation whose mantra was not to trust anyone over 30, and now I’m twice that age.  As I look back over my life, I can pinpoint a few key events which led me to discover and appreciate what is now almost universally known as the Paleo diet.

I came of age as a track and field athlete at the University of Nevada, Reno in the late 60s and early 70s, and as such was always interested in diet, fitness and athletic performance. Later as a lifeguard at Lake Tahoe, my friends and I read all of the now classic vegetarian diet/health books such as Francis Moore Lappe’s Diet for a Small Planet, Paivo Airola’s Are You Confused? and Dick Gregory’s Natural Diet for Folks Who Eat among others. I even attended a Dick Gregory lecture in Seattle and got to shake this famous comedian’s hand.

My lifeguard friends and I experimented with vegan diets, fasting, and all kinds of vitamins and supplements. Almost everyone seemed to own a juicer. Each summer, instead of shying away from the sun and using sunscreens, we all tried to get the deepest tans possible. We swam in Tahoe’s icy, invigorating, non-chlorinated waters, and decades before Vibram Five Fingers and Nike Frees were the rage, we ran barefoot in the sand along Sand Harbor’s pristine shoreline.

Those 20 memorable summers as a lifeguard at Tahoe heightened my awareness of the outdoor, natural world, sunshine, health, fitness and diet. As my lifeguarding days drew to a close in 1991, Lorrie and I had just begun to eat Paleo. Here’s how it began.


I completed my Ph.D. in exercise physiology at the University of Utah in the spring of 1981 and promptly hired as a young assistant professor in the Department of Health and Exercise Science at Colorado State University. For the first 5-10 years of my career, my research focused mainly upon how diet and exercise affected fitness and athletic performance. I still hadn’t discovered Paleo, but read widely and had a considerable interest in anthropology.

In the spring of 1987, I happened upon Boyd Eaton’s (M.D.) now classic scientific paper Paleolithic Nutrition: a Consideration of its Nature and Current Implications which was published two years earlier in the prestigious New England Journal of Medicine.7 This article made a lasting impression upon me and was the single factor which caused me to focus my research interests upon ancestral human diets from that point forward.

For me, one of the surprising points that Dr. Eaton made in a subsequent paper was that cereal grains were rarely or never consumed by pre-agricultural hunter-gatherers.6  In the days and months after reading Boyd’s groundbreaking paper,7 I became absolutely engrossed in studying ancestral human diets and voraciously read everything I could about the topic. At first, I simply filed all of these scientific papers and documents into a single file folder I labeled “Paleolithic Nutrition.” Early on I realized that this strategy wouldn’t work because of the enormous volume and diversity of topics that materialized.

As I read more and more, patterns began to emerge. Stone Age people did not drink milk or consume dairy products. So, I created a file folder labeled “Dairy.” They also didn’t eat cereal grains, so I created a single file folder called “Cereal Grains.” However, just like the single folder I had originally created for “Paleolithic Nutrition,” it soon became apparent that the topic of cereal grains and their potential for adversely affecting health was an enormous topic that ultimately would require a huge number of file folders.

Over the course of the next seven or eight years, I collected more than 25,000 scientific papers and filled five large filing cabinets – each with hundreds of categories dealing with all aspects of Paleo diet and Paleo lifestyle. In 1994, I eventually mustered enough courage to telephone (no one used email then) the man who was responsible for my collection of articles on anything and everything related to Paleo. Dr. Eaton is a true gentleman and scholar in every sense of the word.  We spoke for almost an hour on that very first telephone call, and he gave me one of the greatest compliments of my life at the end of the conversation when he said, “It sounds to me like you know more about this than I do.”

Boyd and I eventually met in 1995, and two years later he invited me to speak with him at an international conference on fitness and diet organized by Dr. Artemis Simopoulos in Athens, Greece. Artemis was a wonderful hostess for the conference, and during my two week stay in Greece we had many conversations about diet and health. I mentioned that I had written a partially completed manuscript on the nutritional shortcomings of cereal grains. About a year later she asked me if I could complete the paper and submit it for publication in a scientific journal she edited.  I did, and that paper, Cereal Grains: Humanity’s Double Edged Sword, published in 199934 launched my published career in Paleo diets.

The Paleo Diet concept is now taken seriously in the scientific world thanks in part to Boyd Eaton’s pioneering work. There is no doubt in my mind that without Dr. Eaton’s influential 1985 New England Journal of Medicine paper,7 Paleo would continue to be an obscure word known mainly to anthropologists and would not have become the household term now recognized by millions. The Paleo Diet and Paleo lifestyle are clearly much larger than either my writings or Boyd Eaton’s. Hundreds if not thousands of scientists, physicians and people from all walks of life are responsible for creating this incredibly powerful idea that can be used to bring order and wisdom to dietary and lifestyle questions and issues.

Some of the key players who came before Dr. Eaton in the Paleo diet and lifestyle world require no introductions. Charles Darwin’s Origins of the Species was published in 1859 and started it all. It still amazes me that the most powerful idea in all of biology (evolution via natural selection) generally had not been applied to nutritional thought until 126 years later with Dr. Eaton’s classic paper.7  Theodosius Dobzhansky, a well-known Ukranian evolutionary biologist said, “Nothing in biology makes sense, except under the light of evolution.” Indeed, his statement could easily be reworked to “Nothing in nutrition makes sense, except under the light of evolution.5 A similar quote could also be applied to a multitude of lifestyle issues.

One way in which we can look at how and where the Paleo diet and Paleo lifestyle concepts arose would be to examine the contributions of a few of the key players who came both before and after Dr. Eaton’s landmark paper. Obviously, Charles Darwin started it all, but a number of noteworthy people had already recognized the value of ancestral dietary patterns decades before the publication of Boyd’s article.

Perhaps the very first book to achieve notoriety about non-western diets and disease was Weston Price’s Nutrition and Physical Degeneration, A Comparison of Primitive and Modern Diets and Their Effects, first published in 1939.23 Dr. Price, a U.S. dentist, extensively traveled the world in the 1920s and 30s and made detailed observations about diet and health in numerous non-westernized populations including Amazon Indians, Alaskan Eskimos, Australian Aborigines, Canadian Indians, Polynesians and African tribal populations among many others. This book is a real treasure and contains hundreds of photographs of non-westernized people in exquisite health taken in an era when modern processed foods were not universally available. Dr. Price noted that wherever and whenever modern diets were adopted by non-westernized cultures, their health declined. His statement was just as true then as it is today.

An intriguing aspect of early books like Dr. Price’s is that frequently the diet/health observations were correct but the underlying mechanisms about how diet and lifestyle specifically affected health were either unknown or poorly understood.  In the early part of the 20th century before population wide vaccination programs existed, tuberculosis remained a major public health problem responsible for millions of deaths worldwide.  In his book,23 Dr. Price noted that in Europe, heliotherapy (sunbathing) was being effectively used to treat tuberculosis. At the time and even decades later, these kinds of observations were commonly ridiculed by the “best medical minds” because they seemed ludicrous and had no known physiological basis. Let’s fast forward 65 years and put this 1930s observation under new light.

Discoveries made just in the past 5-7 years now show that sunlight exposure might be one of the best strategies to prevent or cure tuberculosis infections.10, 19, 27, 31, 35, 36  When you sunbathe, ultraviolet radiation from the sun causes vitamin D to be produced in your skin. The more sun you get, the more vitamin D is produced. Blood concentrations of vitamin D regulate the synthesis of a recently identified substance called cathelicidin which turns out to be one of the most potent antimicrobial (bacteria killing) peptides that our bodies produce. Cathelicidin shows specific killing activity against bacteria that cause tuberculosis,31, 35, 36 and epidemiological (population) studies confirm vitamin D insufficiency is a risk factor for tuberculosis.10, 19, 37  Most of us have been vaccinated against tuberculosis, so we really don’t need to worry about this disease.

Although Dr. Price’s book23 was advanced for its time, the evolutionary basis for optimal nutrition and healthy lifestyles still lay decades in the future. Other early popular books touching upon ancestral diets and health include:  Arnold DeVries’s Primitive Man and His Food (1952),4 Walter Voegtlin’s The Stone Age Diet (1975),30 Leon Chaitow’s, Stone Age Diet (1987),2 and Boyd Eaton’s The Paleolithic Prescription (1988).8

All of these books are long out of print and except for Boyd’s volume; these books simply fizzled and faded into obscurity because they didn’t have the bigger picture right. Without the evolutionary template correctly in place, these early books were incomplete and inconclusive.  At the time, scientists and the public at large still weren’t quite ready for Paleo diets and Paleo lifestyles.

Prior to the publication of Dr. Eaton’s 1985 paper,7 a few scientists had independently recognized the evolutionary underpinnings for healthful diets and lifestyle, but their work was published in obscure scientific journals that received little or no public notoriety.1, 25, 26, 28, 29, 32, 37 After publication of Boyd Eaton’s influential paper in the New England Journal of Medicine,7 a number of events ultimately set the stage for the worldwide recognition of the Paleo diet as well as the evolutionary basis for modern day Paleo lifestyles.


The basic foundation and logic for the Paleo diet concept lies in a recently recognized discipline called Darwinian Medicine. Following in the footsteps of Boyd’s landmark paper,7 came another revolutionary scientific publication in the Quarterly Review of Biology (1991) by Drs. George Williams and Randy Neese from the State University of New York at Stony Brook.33  The title of this paper was, “The Dawn of Darwinian Medicine.

As you can imagine from its title, it represented the very first scientific publication addressing how our ancestral evolutionary experience affects the manner in which we view and treat modern diseases. Although this paper is now more than 20 years old, its message is finally being filtered down to many physicians, their patients and the public at large.20

Here’s a quote from this paper that sums up Darwinian Medicine, “Human biology is designed for Stone Age conditions. Modern environments may cause many diseases.” Also, another enlightening quote that is totally relevant to this book: “it provides new insights into the causes of medical disorders.” For instance, cough, fever, vomiting, diarrhea, fatigue, pain, nausea and anxiety are widespread medical problems. Many orthodox physicians focus upon relieving short term distress by prescribing pharmaceuticals to block these responses. Darwinian Medicine would say these responses are not necessarily harmful, but rather signify the body’s effort to remedy a problem. In most situations coughing when you are sick is a natural and healthy response because it helps to purge disease causing microbes from your throat and lungs.

Similarly fever increases your body temperature which helps to destroy pathogens that have infected your body. Medications that suppress coughs and block fever may relieve symptoms but may actually prolong the illness. Obviously, certain extreme situations necessitate a balanced approach between our body’s evolutionary response to disease and modern medicine. For example, blocking fever can prevent febrile seizures and stopping vomiting can prevent severe dehydration.

The message is clear. We need to balance our hunter gatherer genetic legacy with the best technology of our modern world.


Having been a faculty member at a Division I Research University for 32 years, I can tell you that your personal experience with the Paleo diet and a dollar will buy you a single cup of coffee in the scientific community. In other words:  no matter how much weight you have dropped on the Paleo diet; no matter how much your blood chemistry has improved; nor how much better you feel, the medical and scientific community will, by and large, not listen to you. Your real world experiences have little or no traction in the academic community of science and medicine.   What they require is not your personal experience (anecdotal evidence), but rather experimental evidence based upon one of the following four scientific methods:  1) animal studies, 2) tissue or organ studies, 3) epidemiological [population] studies or 4) randomized controlled human trials.

When I first published The Paleo Diet in 2002 thousands of indirect experimental studies had supported its general principles in promoting weight loss, improving overall health and curing disease. For instance, a multitude of well controlled experimental studies had already confirmed beyond a shadow of a doubt that low glycemic load diets improved health and promoted weight loss. The Paleo diet is a low glycemic load diet.  Similarly, high protein diets were shown to be the most effective strategy to improve blood chemistry and help you lose weight. Yet again, the Paleo diet is a high protein diet.

Even in 2002, when The Paleo Diet first came into print, you would have been hard pressed to find a single nutritionist who would disagree with the notion that omega 3 fats improved health and well being in almost every conceivable way. Do I need to repeat myself? The Paleo diet is a diet rich in omega 3 fats.

By 2002 when my first book came into print, the thousands of scientific papers were independently verified that certain individual aspects of the Paleo diet normalized body weight and improved health and wellbeing. Nevertheless, at that time, not a single study had yet examined all of the combined nutritional characteristics of the Paleo diet.

Was a diet high in animal protein, omega 3 fats, monounsaturated fats, vitamins, minerals, phytochemicals, fiber and low in salt, refined sugars, cereal grains, dairy products, vegetable oils and processed foods healthy? Was it more healthful than the officially sanctioned USDA My Plate Diet or even the highly touted Mediterranean diet? The direct scientific answers to these questions had yet to be answered in 2002.

Fortunately, in the past eight years a number of scientists worldwide have dared to test contemporary versions of humanity’s original diet against supposed “healthful diets” as seen in Table 1 below.

One of the key figures behind this ground breaking research is my friend and colleague, Dr. Staffan Lindeberg (M.D., Ph.D.) from Lund University in Sweden. Staffan became interested in Paleo diets almost 25 years ago through his medical studies of the Kitavans,14-17 a non-westernized group of 2,250 people living on remote islands near Papua New Guinea. The Kitavans obtain virtually all of their food from either the land or the sea and have little contact with the modern world. Common western foods such as cereals, dairy, refined sugars, vegetable oils and processed foods are nearly absent from their diets.14-17 Predictably, these people represent the epitome of health compared to the average citizen living in the western world.  None of them are overweight, and heart disease and stroke are extremely rare. High blood pressure and type 2 diabetes are non-existent,14-17 and acne is not present among their children or teenagers.38 I doubt that you could round up a random group of 2,000 western people anywhere on the planet without encountering high rates of all of these diseases which are rare or not present in the Kitavans.

In the late 1990s I first began corresponding with Dr. Lindeberg on the then youthful internet.  We soon discovered that we had read almost all of the same scientific papers and were interested in almost all of the same diet/health topics. One study that stood out to both of us was an incredible experiment performed by Dr. Kerin O’Dea at the University of Melbourne and published in the Journal, Diabetes in 1984.21 In this study Dr. O’Dea gathered together 10 middle aged Australian Aborigines who had been born in the “Outback.” They had lived their early days primarily as hunter-gatherers until they had no choice but to finally settle into a rural community with access to western goods. Predictably, all 10 subjects eventually became overweight and developed type 2 diabetes as they adopted western sedentary lifestyles in the community of Mowwanjum in the northern Kimberley region of Western Australia.  However, inherent in their upbringing was the knowledge to live and survive in this seemingly desolate land without any of the trappings of the modern world.

Dr. O’Dea requested these 10 middle aged subjects to revert to their former lives as hunter-gatherers for a seven week period. All agreed and traveled back into the isolated land from which they originated. Their daily sustenance came only from native foods that could be foraged, hunted or gathered. Instead of white bread, corn, sugar, powdered milk and canned foods, they began to eat the traditional fresh foods of their ancestral past: kangaroos, birds, crocodiles, turtles, shellfish, yams, figs, yabbies (freshwater crayfish), freshwater bream and bush honey.   At the experiment’s conclusion, the results were spectacular, but not altogether unexpected given what was known about Paleo diets, even then. The average weight loss in the group was 16.5 lbs; blood cholesterol dropped by 12% and triglycerides were reduced by a whopping 72%. Insulin and glucose metabolism became normal, and their diabetes effectively disappeared.

Dr. Lindeberg and I both realized that this type of experiment would probably never be repeated simply because the hunter-gatherer lifestyle is nearly extinct, and very few contemporary people have the knowledge or skills to live entirely off the land. Back in those early days of our friendship, we both had the same vision. This experiment should be conducted in a slightly different manner but not with westernized, former hunter-gatherers. Why not take a group of typically unhealthy westerners and put them on commonly available contemporary foods that mimic the nutritional characteristics of hunter-gatherer diets? Wow, what a great idea! We both knew that this experiment was precisely what Dr. Eaton had in mind with his inspirational paper way back in 1985.7


It took nearly 22 years for Dr. Eaton’s dream of experimentally testing modern day Paleo diets to come true, but it finally happened with the publication of a paper by Dr. Lindeberg’s research group in 2007.18 Staffan followed this publication with two additional papers in 200911 and 2010.13 Good ideas catch on, and two other independent research groups around the world followed suit with similar results – the first in 2008 by Dr. Osterdahl and co-workers at the Karolinska Institute in Sweden22 and the next in 2009 by my friend and colleague Dr. Lynda Frasseto (M.D.) from the University of California San Francisco School of Medicine.9

Although science may move slowly, it eventually does move forward as old ideas are replaced with new and better thoughts and information. I can assure you that this fundamental diet and lifestyle concept based upon evolutionary biology is not a fad and will not fade away.

In his first study in 200718 Dr. Lindeberg and associates placed 29 patients with type 2 diabetes and heart disease on either a Paleo diet or a Mediterranean diet based upon whole grains, low-fat dairy products, vegetables, fruits, fish, oils, and margarines. Note the Paleo diet excludes grains, dairy products, and margarines while encouraging greater consumption of meat and fish. After 12 weeks on either diet blood glucose tolerance (a risk factor for heart disease) improved in both groups, but was better in the Paleo dieters.

In a 2010 follow-up publication,18 of this same experiment the Paleo diet was shown to be more satiating on a calorie by calorie basis than the Mediterranean diet because it caused greater changes in leptin, a hormone which regulates appetite and bodyweight.

In the second ever study (2008) of Paleo diets, Dr. Osterdahl and co-workers put 14 healthy subjects on a Paleo diet. After only three weeks the subjects lost weight, reduced their waist size and experienced significant reductions in blood pressure, and plasminogen activator inhibitor (a substance in blood which promotes clotting and accelerates artery clogging). Because no control group was employed in this study, some scientists would argue that the beneficial changes might not necessarily be due to the Paleo diet. However, as you shortly will see, a better controlled experiment showed similar results.

In 2009, Dr. Frasetto and co-workers put nine inactive subjects on a Paleo diet for just 10 days.9 In this experiment, the Paleo diet was exactly matched in calories with the subjects’ usual diet.  Almost anytime people eat diets that are calorically reduced, no matter what foods are involved, they exhibit beneficial health effects. So the beauty of this experiment was that any therapeutic changes in the subjects’ health could not be credited to reductions in calories, but rather to changes in the types of food eaten. While on the Paleo diet either eight or all nine participants  experienced improvements in blood pressure, arterial function, insulin, total cholesterol, LDL cholesterol and triglycerides. What is most amazing about this experiment is how rapidly so many markers of health improved, and that they occurred in every single patient.

In an even more convincing recent (2009) experiment, Dr. Lindeberg and colleagues compared the effects of a Paleo diet to a diabetes diet generally recommended for patients with type 2 diabetes.11 The diabetes diet was intended to reduce total fat by increasing whole grain bread and cereals, low fat dairy products, fruits and vegetables while restricting animal foods. In contrast, the Paleo diet was lower in cereals, dairy products, potatoes, beans, and bakery foods, but higher in fruits, vegetables, meat, and eggs compared to the diabetes diet. The strength of this experiment was its cross over design in which all 13 diabetes patients first ate one diet for three months and then crossed over and ate the other diet for three months. Compared to the diabetes diet, the Paleo diet resulted in improved weight loss, waist size, blood pressure, HDL cholesterol, triglycerides, blood glucose and hemoglobin A1c (a marker for long term blood glucose control).    From an experimental design perspective, this trial represents a powerful example of the Paleo diet’s effectiveness in treating people with serious health problems.

From 2007 until 2010 only five experimental studies tested contemporary “Paleo” diets in humans (Table 1).  However since then, interest in experimentally testing these diets has grown concurrently (Table 1) with the general public’s explosive awareness of the Paleo Diet concept (Figure 1). Except for a single study, human trials testing modern day Paleo Diets have shown them to be therapeutic and generally more effective in reducing body weight and ameliorating symptoms of the metabolic syndrome (Table 1) than conventional western diets, type 2 diabetic diets, the Mediterranean diet, and the American Heart Association (AHA) diet (Table 1).   Further, contemporary “Paleo diets” are nutritionally more dense in the 13 vitamins and minerals most lacking in the typical U.S. diet when contrasted to the USDA my Plate recommendations,39, 40 the Mediterranean diet, and vegan/vegetarian diets.

Table 1.  Paleo Diet References: Direct Human/Animal Experimental and Epidemiological Studies in chronological order (oldest to most recent).



  1. 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.


  1. Jonsson T, Ahren B, Pacini G, Sundler F, Wierup N, Steen S, Sjoberg T, Ugander M, Frostegard J, Goransson Lindeberg S: A Paleolithic diet confers higher insulin sensitivity, lower C-reactive protein and lower blood pressure than a cereal-based diet in domestic pigs. Nutr Metab (Lond) 2006, 3:39.


  1. Lindeberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjostrom K, Ahren B: A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia 2007, 50(9):1795-1807.


  1. Osterdahl M, Kocturk T, Koochek A, Wandell PE: Effects of a short-term intervention with a paleolithic diet in healthy volunteers. Eur J Clin Nutr 2008, 62(5):682-685.


  1. Jönsson T, Granfeldt Y, Ahrén B, Branell UC, Pålsson G, Hansson A, Söderström M, Lindeberg S. 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
  2. Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC, Jr., Sebastian A: Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr 2009.


  1. Jonsson T, Granfeldt Y, Erlanson-Albertsson C, Ahren B, Lindeberg S. A Paleolithic diet is more satiating per calorie than a Mediterranean-like diet in individuals with ischemic heart disease. Nutr Metab (Lond). 2010 Nov 30;7(1):85


  1. Carter P, Achana F, Troughton J, Gray LJ, Khunti K, Davies MJ. A Mediterranean diet improves HbA1c but not fasting blood glucose compared to alternative dietary strategies: a network meta-analysis. J Hum Nutr Diet. 2014 Jun;27(3):280-97
  2. Jönsson T, Granfeldt Y, Lindeberg S, Hallberg AC.Subjective satiety and other experiences of a Paleolithic diet compared to a diabetes diet in patients with type 2 diabetes. Nutr J. 2013 Jul 29;12:105. doi: 10.1186/1475-2891-12-105.
  3. Ryberg M, Sandberg S, Mellberg C, Stegle O, Lindahl B, Larsson C, Hauksson J, Olsson T. A Palaeolithic-type diet causes strong tissue-specific effects on ectopic fat deposition in obese postmenopausal women. J Intern Med. 2013 Jul;274(1):67-76
  4. Frassetto LA, Shi L, Schloetter M, Sebastian A, Remer T. Established dietary estimates of net acid production do not predict measured net acid excretion in patients with Type 2 diabetes on Paleolithic-Hunter-Gatherer-type diets. Eur J Clin Nutr. 2013 Sep;67(9):899-903


  1. Fontes-Villalba M, Jönsson T, Granfeldt Y, Frassetto LA, Sundquist J, Sundquist K, Carrera-Bastos P, Fika-Hernándo M, Picazo Ó, Lindeberg S. A healthy diet with and without cereal grains and dairy products in patients with type 2 diabetes: study protocol for a random-order cross-over pilot study–Alimentation and Diabetes in Lanzarote–ADILAN.Trials. 2014 Jan 2;15:2. doi: 10.1186/1745-6215-15-2.
  2. Bisht B, Darling WG, Grossmann RE, Shivapour ET, Lutgendorf SK, Snetselaar LG, Hall MJ, Zimmerman MB, Wahls TL. A multimodal intervention for patients with secondary progressive multiple sclerosis: Feasibility and effect on fatigue. J Altern Complement Med. 2014 Jan 29. [Epub ahead of print]
  3. Mellberg C, Sandberg S, Ryberg M, Eriksson M, Brage S, Larsson C, Olsson T, Lindahl B. Long-term effects of a Palaeolithic-type diet in obese postmenopausal women: a 2-year randomized trial. Eur J Clin Nutr. 2014 Mar;68(3):350-7.
  4. Smith, M, Trexler E, Sommer A, Starkoff B, Devor S.teven (2014) Unrestricted Paleolithic Diet is associated with unfavorable changes to blood lipids in healthy subjects. Int J Exer Sci 2014, 7(2) : 128-139.
  5. Talreja D, Buchanan H, Talreja R, Heiby L, Thomas B, Wetmore J, Pourfarzib R, Winegar D. Impact of a Paleolithic diet on modifiable CV risk factors. Journal of Clinical Lipidology, Volume 8, Issue3, Page 341, May 2014.
  6. Boers I, Muskiet FA, Berkelaar E, Schur E, Penders R, Hoenderdos K, Wichers HJ, Jong MC. Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrom. A randomized controlled pilot-study. Lipids Health Dis. 2014 Oct 11;13:160. doi: 10.1186/1476-511X-13-160.
  7. Stomby A, Simonyte K, Mellberg C, Ryberg M, Stimson RH, Larsson C, Lindahl B, Andrew R, Walker BR, Olsson T. Diet-induced weight loss has chronic tissue-specific effects on glucocorticoid metabolism in overweight postmenopausal women. Int J Obes (Lond). 2014 Oct 28. doi: 10.1038/ijo.2014.188. [Epub ahead of print]
  8. Whalen KA, McCullough M, Flanders WD, Hartman TJ, Judd S, Bostick RM. Paleolithic and mediterranean diet pattern scores and risk of incident, sporadic colorectal adenomas. Am J Epidemiol. 2014 Dec 1;180(11):1088-97. doi: 10.1093/aje/kwu235. Epub 2014 Oct 17.
  9. Toth C, Clemens Z. Type 1 diabetes mellitus successfully managed with the Paleolithic ketogenic diet. Int J Case Pep Images. 2014 5(10):699-703.


  1. Talreja A, Talreja S, Talreja R,Talreja D. The VA Beach Diet Study: An investigation of  the effects  of plant-based, Mediterranean, Paleolithic, and Dash Diets on cardiovascular disease risk. J Am Coll Cardiol Intv. 2015;8(2_S):S41-S41.  doi:10.1016/j.jcin.2014.12.161
  2. Bligh HF, Godsland IF, Frost G, Hunter KJ, Murray P, MacAulay K, Hyliands D, Talbot DC, Casey J, Mulder TP, Berry MJ.Plant-rich mixed meals based on Palaeolithic diet principles have a dramatic impact on incretin, peptide YY and satiety response, but show little effect on glucose and insulin homeostasis: an acute-effects randomised study.Br J Nutr. 2015 Feb 28;113(4):574-84.
  3. London DS, Beezhold B. A phytochemical-rich diet may explain the absence of age-related decline in visual acuity of Amazonian hunter-gatherers in Ecuador. Nutr Res. 2015 Feb;35(2):107-17.
  4. Masharani U, Sherchan P, Schloetter M, Stratford S, Xiao A, Sebastian A, Nolte Kennedy M, Frassetto L. Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes. Eur J Clin Nutr. 2015 Apr 1. doi: 10.1038/ejcn.2015.39. [Epub ahead of print]
  5. Tóth, C, and Zsófia, C. “Gilbert’s Syndrome successfully treated with the Paleolithic ketogenic diet.” Am J Med Case Reports. 2015 3(4). http://pubs.sciepub.com/ajmcr/3/4/9/
  6. Pastore RL, Brooks JT, Carbone JW. Paleolithic nutrition improves plasma lipid concentrations of hypercholesterolemic adults to a greater extent than traditional heart-healthy dietary recommendations. Nutr Res. 2015; 35:474-479.





[1]Abrams, HL. The relevance of Paleolithic diet in determining contemporary nutritional needs. J Applied Nutr 1979;31: 43-59.

[2]Chaitow, L. Stone Age Diet. London, Macdonal & Co. (Publishers) Ltd., 1987.

[3]Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. Acne vulgaris: a disease of Western civilization. Arch Dermatol. 2002 Dec;138(12):1584-90.

[4]DeVries, A. Primitive Man and His Food. Chicago, Chandler Book Company, 1952.

[5]Dobzhansky T. Am Biol Teacher. 1973 March; 35:125-129.

[6]Eaton SB, et al. Stone agers in the fast lane: chronic degenerative diseases in evolutionary perspective. Am J Med 1988;84:739-49.

[7]Eaton SB, Konner M. Paleolithic nutrition. A consideration of its nature and current implications. N Engl J Med 1985;312:283-9.

[8]Eaton SB, Shostak M, Konner M. The Paleolithic Prescription. New York, Harper & Row, 1988.

[9]Frassetto LA, Schloetter M, Mietus-Synder M, Morris RC, Jr., Sebastian A: Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet. Eur J Clin Nutr 2009.

[10]Ho-Pham LT, Nguyen ND, Nguyen TT, Nguyen DH, Bui PK, Nguyen VN, Nguyen TV. Association between vitamin D insufficiency and tuberculosis in a Vietnamese population. BMC Infect Dis. 2010 Oct 25;10:306.

[11]Jönsson T, Granfeldt Y, Ahrén B, Branell UC, Pålsson G, Hansson A, Söderström M, Lindeberg S. 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

[12]Jonsson T, Ahren B, Pacini G, Sundler F, Wierup N, Steen S, Sjoberg T, Ugander M, Frostegard J, Goransson Lindeberg S: A Paleolithic diet confers higher insulin sensitivity, lower C-reactive protein and lower blood pressure than a cereal-based diet in domestic pigs. Nutr Metab (Lond) 2006, 3:39.

[13]Jonsson T, Granfeldt Y, Erlanson-Albertsson C, Ahren B, Lindeberg S. A Paleolithic diet is more satiating per calorie than a Mediterranean-like diet in individuals with ischemic heart disease. Nutr Metab (Lond). 2010 Nov 30;7(1):85

[14]Lindeberg S, Lundh B: Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J Intern Med 1993, 233(3):269-275.

[15]Lindeberg S, Nilsson-Ehle P, Terént A, Vessby B, Scherstén B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J Intern Med. 1994 Sep;236(3):331-40.

[16]Lindeberg S, Berntorp E, Carlsson R, Eliasson M, Marckmann P. Haemostatic variables in Pacific Islanders apparently free from stroke and ischaemic heart disease–the Kitava Study. Thromb Haemost. 1997 Jan;77(1):94-8.

[17]Lindeberg S, Eliasson M, Lindahl B, Ahrén B: Low serum insulin in traditional Pacific Islanders–the Kitava Study. Metabolism 1999, 48(10):1216-1219.

[18]Lindeberg S, Jonsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjostrom K, Ahren B: A Palaeolithic diet improves glucose tolerance more than a Mediterranean-like diet in individuals with ischaemic heart disease. Diabetologia 2007, 50(9):1795-1807.

[19]Nnoaham KE, Clarke A. Low serum vitamin D levels and tuberculosis: a systematic review and meta-analysis. Int J Epidemiol. 2008 Feb;37(1):113-9.

[20]Nesse RM, Stearns SC, Omenn GS. Medicine needs evolution. Science 2006;311:1071.

[21]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.

[22]Osterdahl M, Kocturk T, Koochek A, Wandell PE: Effects of a short-term intervention with a paleolithic diet in healthy volunteers. Eur J Clin Nutr 2008, 62(5):682-685.

[23]Price WA. Nutrition and physical degeneration; a comparison of primitive and modern diets and their effects. P.B. Hoeber, Inc., New York, 1939.

[24]Pritchard JK. How we are evolving. Sci Am. 2010 Oct;303(4):40-47.

[24]Shatin R. Man and his cultigens. Scientific Australian 1964;1:34-39

[26]Shatin R. The transition from food-gathering to food-production in evolution and disease. Vitalstoffe Zivilisationskrankheitein 1967;12:104-107.

[27]Talat N, Perry S, Parsonnet J, Dawood G, Hussain R. Vitamin d deficiency and tuberculosis progression. Emerg Infect Dis. 2010 May;16(5):853-5.

[28]Truswell AS. Diet and nutrition of hunter-gatherers. In: Health and disease in tribal societies. New York: Elsevier; 1977:213-21.

[29]Truswell AS. Human Nutritional Problems at Four Stages of Technical Development. Reprint. Queen Elizabeth College (University of London), Inaugural Lecture, May, 1972.

[30]Voegtlin, WL. The Stone Age Diet. New York, Vantage Press, 1975.

[31]Yamshchikov AV, Kurbatova EV, Kumari M, Blumberg HM, Ziegler TR, Ray SM, Tangpricha V. Vitamin D status and antimicrobial peptide cathelicidin (LL-37) concentrations in patients with active pulmonary tuberculosis. Am J Clin Nutr. 2010 Sep;92(3):603-11.

[32]Yudkin, J. Archaeology and the nutritionist. In: The Domestication and Exploitation of Plants and Animals, PJ Ucko, GW Dimbleby (Eds.), Chicago, Aldine Publishing Co, 1969, pp. 547-552.

[33]Williams GC, Nesse RM. The dawn of Darwinian medicine. Q Rev Biol. 1991 Mar;66(1):1-22.

[34]Cordain L. Cereal grains: humanity’s double edged sword. World Review of Nutrition and Dietetics. 1999;84:19-73.

[35]Afsal K, Harishankar M, Banurekha VV, Meenakshi N, Parthasarathy RT, Selvaraj P.Effect of 1,25-dihydroxy vitamin D3 on cathelicidin expression in patients with and without cavitary tuberculosis. Tuberculosis (Edinb). 2014 Dec;94(6):599-605.

[36]Selvaraj P. Vitamin D, vitamin D receptor, and cathelicidin in the treatment of tuberculosis. Vitam Horm. 2011;86:307-25.

[37]Abrams HL. A dischronic perview of wheat in hominid nutrition. J Appl Nutr 1978;30:41-43.

[38]Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. Acne vulgaris: A disease of civilization. Arch Dermatol. 2002;138: 1584-90.

[39]Cordain L. The nutritional characteristics of a contemporary diet based upon Paleolithic food groups. J Am Neutraceut Assoc 2002; 5:15-24.

[40]Cordain L, Eaton SB, Sebastian A, Mann N, Lindeberg S, Watkins BA, O’Keefe JH, Brand-Miller J. Origins and evolution of the western diet: Health implications for the 21st century. Am J Clin Nutr 2005;81:341-54.

Are Sugary Drinks Killing Your Liver? | The Paleo Diet

Everyone knows that increased sugar intake increases your risk for type 2 diabetes and obesity. The consumer market competes daily on how to cater to the average individual’s sweet tooth. In a society that loves the indulgence of super-sized drinks, it becomes easy to fall prey. Given the metabolism and breakdown of sugar takes place in the liver, it is no surprise excess sugar intake can lead to major liver problems.

According to a recent study conducted at Tufts University, and published in the Journal of Hepatology, drinking sugary drinks daily puts you at risk for non-alcoholic fatty liver disease.1 This condition can eventually lead to liver cirrhosis, just like with alcohol, in some cases liver cancer, and have the individual needing a liver transplant.2

In the study, 2,634 self-reported dietary questionnaires from mostly Caucasian middle-aged men and women enrolled in the National Heart Lunch and Blood Institute (NHLBI) Framingham Heart Study’s Offspring and Third Generation cohorts were analyzed. The sugary beverages listed on the questionnaires comprised of caffeinated and caffeine-free colas, other carbonated beverages with sugar, fruit punches, lemonade or other non-carbonated fruit drinks. Afterwards, a computed tomography (CT) scan was carried out on the participants to determine the quantity of fat in the liver and the authors of the current study used a previously defined cut-point to identify NAFLD.

Among the participants who drank sugar sweetened beverages, those who drank one or more sugar-sweetened beverage per day experienced a higher prevalence rate and had a 60% greater risk of NAFLD compared to people who said they drank no sugar-sweetened beverages. This association was still evident even after controlling for possible confounders, which could affect the results, such as age, sex, body mass index, calories and other risk factors. Basically, the more sugary beverage the people drank, the greater the risk. An estimated two thirds of the participants drank at least some fruit, cola or other sugary beverage, and over 10% drank the sugary beverage daily.

Between mislabeling, misleading advertisements, and chronic sugar addiction, it’s easy to understand why Dr. Cordain advocates eating your fruit whole rather than drinking commercial juices, which may be loaded with sugar.

About 20-30% of people living in the US has nonalcoholic fatty liver disease (NAFLD)3. The primary cause behind this condition remains relatively unknown. With NAFLD, in about 25% of the cases, there are no symptoms, with the fat accumulation in the liver only found from imaging results, when the liver has pretty much lost the sugar battle. Researchers have shown obesity increases a person’s risk for NAFLD, as well as a correlation between NAFLD and heart disease and type 2 diabetes.4 In other words, keep drinking that sugary beverage daily, and not only may you need a heart transplant, but you could have also traded in your heart and received a free serving of type 2 diabetes as well. Clearly not a fair or even worthy exchange.

The problem may lie in a part of sugar used in the beverages, known as fructose, and how it is processed within the body. When taken alone, fructose is poorly absorbed from the gastrointestinal tract, and it is almost completely cleared by the liver. While regular glucose blood concentration is with 5.5 mmol/L , that of fructose is about 0.01 mmol/L in peripheral blood.5

Both fructose and glucose follow different paths for absorption in the body. While glucose results in the release of insulin from the pancreas, fructose is unable to do so. Many cells lack the type of sugar transporter that takes fructose into the cell, unlike glucose. The breakdown of fructose mainly takes place in the liver, through a process known as phosphorylation, which avoids the rate-limiting phosphofructokinase step.6 While your body uses up glucose, for example the brain for energy, hepatic metabolism of fructose leads to the free fatty acids (FFAs), VLDL (the damaging form of cholesterol), and triglycerides, which get stored as fat. So, think of drinking that sugary beverage like you are drinking fat, because essentially that is what it ends up as.

Here in the Paleo world, it is safe to understand why we stay far away from commercial products such as sugar sweetened beverages. Not only do they provide empty calories, but there is the possibility of leaving your body in worse shape than imagined. Care for a liver transplant? I’ll pass, that refreshing glass of cold water sounds even better.



[1] Ma, J; Fox, CS; Jacques, PF; Speliotes, EK; Hoffmann, U; Smith, CE; Saltzman, E; and McKeown, NM. (2015, June 5). Sugar-Sweetened Beverage, Diet Soda, and Fatty Liver Disease in the Framingham Study Cohorts. Journal of Hepatology.

[2] Ibid.

[3] Ma, J; Fox, CS; Jacques, PF; Speliotes, EK; Hoffmann, U; Smith, CE; Saltzman, E; and McKeown, NM. (2014, April). Sugar-sweetened beverage intake is associated with fatty liver in the Framingham Offspring Study (267.3).  The FASEB Journal. 28(1).

[4] Cassidy, S., Hallsworth, K., Thoma, C., MacGowan, G., Hollingsworth, K., Day, C., . . . Trenell, M. (2015, Feb 13). Cardiac structure and function are altered in type 2 diabetes and non-alcoholic fatty liver disease and associate with glycemic control. Cardiovasc Diabetol, 14(23). doi:doi: 10.1186/s12933-015-0187-2.

[5] Bray, G. (2007). How bad is fructose?1,2. Am J Clin Nutr, 86(4), 895-896.

[6] Ibid.

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.

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