Tag Archives: The Paleo Diet

Salt and CancerWhen I was in the middle of my academic career during the mid to late 1990’s (I retired from Colorado State University in December 2013,) I had the great pleasure of corresponding with Birger Jansson, Ph.D. at the University of Texas, M.D. Anderson Cancer Center in Houston, Texas. Dr. Jansson was a Professor in the Department of Biomathematics at the M.D. Anderson Cancer Center and worked as a biomathematician for the National Large Bowel Cancer Project (NLBCP) between 1973 and 1983 when President Nixon launched his war against cancer in the early 1970s. Birger was known internationally for his brilliant mathematical modeling of all types of cancer, but today he is perhaps best known for his epidemiological and review publications demonstrating how a high salt (sodium) diet promotes all types of cancer, whereas a high potassium diet impedes cancer (1-8).

My correspondence with Dr. Jansson came about from my interest in the reported low incidence of all types of cancers in hunter-gatherers (9-17) who were essentially salt free populations. From animal and tissue experiments, I had long suspected that salt added to diet acted as a promoter of various cancers whereas a high potassium intake retarded cancer development. My correspondence with Birger further confirmed the evidence I had compiled.

Almost exactly 20 years ago in May of 1997 (see attached PDF file), Birger sent me his unpublished and unedited book entitled, Sodium: “NO!” Potassium: “Yes!” Sodium increases and potassium decreases cancer risks. This book represented Birger’s scientific work, from 1981 to 1997, documenting the relationship between dietary sodium and potassium (1-8). The data from his book includes hundreds of scientific references from 1) epidemiological studies, 2) animal studies, 3) tissue studies, and a limited number of 4) randomized controlled human trials with various disease endpoints and markers.

Unfortunately, my correspondence with Birger ceased shortly after he sent me his unpublished and unedited book manuscript on May 10, 1997. I only recently discovered that Birger died (May 23, 1998) about a year to the date after our last correspondence at age 77 as a Professor Emeritus at the University of Texas, M.D. Anderson Cancer Center.

I am in a unique position, in that I probably have one of the few copies of Dr. Jansson’s unpublished book in existence. The book runs about 350 pages in length and is comprised of 10 chapters. My copy clearly was produced as a Xeroxed copy of Birger’s hand typed manuscript (one sided, double spaced pages) and spiral bound with plastic. From my correspondence with Birger (May 10, 1997), you can see that he was contemplating publication of his book in the popular literature, but unfortunately it never happened with his untimely death in 1998.

I have always felt a debt to this great scientist, and after consultation with my colleague Anthony Sebastian (M.D.) at the University of California, San Francisco, we concluded that Birger would have been happy to see that his unpublished book was finally made known to the scientific and world communities.

In this blog I have included a single chapter (Chapter II of Birger’s book), entitled “Human Diet Before Modern Times” that I thought would be of interest to the “Paleo Community” and to worldwide scientists as well. Enjoy!



1. Jansson B. Potassium, sodium, and cancer: a review. J Environ Pathol Toxicol Oncol. 1996;15(2-4):65-73

2. Jansson B. Dietary, total body, and intracellular potassium-to-sodium ratios and their influence on cancer. Cancer Detect Prev. 1990;14(5):563-5

3. Jansson B. Intracellular electrolytes and their role in cancer etiology. In Thompson JR, Brown BW, eds. Cancer modeling. New York: Marcel Dekker 1987:1-59.

4. Jansson B. Geographic cancer risk and intracellular potassium/sodium ratios. Cancer Detect Prev. 1986;9(3-4):171-94

5. Jansson B, Jankovic J. Low cancer rates among patients with Parkinson’s disease. Ann Neurol. 1985 May;17(5):505-9

6. Newmark HL, Wargovich MJ, Bruce VR, Boynton AL, Kleine LP, Whitfield JF. Jansson B, Cameron IL. Ions and neoplastic development. In: Mastromarino AJ, Brattain MG, eds. Large bowel cancer. Clinical and basic science research. Cancer Research Monographs, Vol 3, New York: Praeger Publisher 1985:102-129.

7. Jansson B. Geographic mappings of colorectal cancer rates: a retrospect of studies, 1974-1984. Cancer Detect Prev. 1985;8(3):341-8

8. Jansson B. Seneca County, New York: an area with low cancer mortality rates. Cancer. 1981 Dec 1;48(11):2542-6

9. Bulkley JL. Cancer among primitive tribes. Cancer 1927; 4:289-295.

10. Henson, WW. Cancer in Kafirs: suggested cause. Guy’s Hospital Gazette, March 26, 1904, 131-133

11. Hearsey H. The rarity of cancer among the aborigines of British Central Africa. Brit Med J, Dec 1, 1906, 1562-63.

12. Hildes JA, Schaefer O. The changing picture of neoplastic disease in the western and central Canadian Arctic (1950-1980). Can Med Assoc J 1984; 130:25-32.

13. Rabinowitch IM. Clinical and other observations on Canadian Eskimos in the Eastern Arctic. Can Med Assoc J 1936; 34:487-501.

14. Renner W. The spread of cancer among the descendants of the liberated Africans or Creoles of Sierre Leone. Brit Med J, Sept 3, 1910, 587-589.

15. Riveros M. First observation of cancer among the Pampidos (Chulupi) Indians of the Paraguayan Chaco. Int Surg 1970; 53:51-55.

16. Stefansson V. Cancer: Disease of Civilization? Hill and Wang, NY, 1960.

17. Urquhart JA. The most northerly practice in Canada. Can Med Assoc J. 1935;33:193-196.

Many people are skeptical whenever change is introduced. And the Paleo Diet, considered a disruptive diet by some, is no exemption. Many awful things have been said about this diet and it’s easy to get confused with what’s true and what’s not.

Contrary to these claims, The Paleo Diet has changed the lives of many people who were brave enough to try it out and discipline themselves to find the many great benefits of eating “caveman-style.”

Let’s debunk some of the common myths about The Paleo Diet. Who knows? One of the myths on this list may just be the very hurdle that’s been keeping you from leading a healthier lifestyle. So let’s get to the meat of it all, shall we?

Debunking the Biggest Myths About The Paleo Diet - infographic

In Part I of this series, we looked at the longstanding recommendations of many governmental health organizations to reduce dietary saturated fat and replace it with omega-6 fats. Doing so supposedly, these organizations claim, reduces cardiovascular disease (CVD) risk. As we saw in Part I, however, there is considerable controversy within the nutrition science community concerning this claim. There’s a case to be made for decreased saturated fat, but there’s also a case for decreased omega-6. Since the current science is far less black-and-white than the recommendations would lead you to believe, with Part II of this series, we’ll be looking at the debate from a paleolithic perspective, with the hope of gaining a broader and more balanced perspective on optimal consumption levels of both saturated and polyunsaturated fats.


Paleo PUFA Consumption

Although conclusive scientific studies are lacking, we can gain valuable insight by examining the diets of our Paleolithic ancestors. How much of these nutrients did they consume? How do current PUFA recommendations compare to PUFA consumption by our Paleolithic ancestors?

To know how much saturated fat and PUFAs they ate, we first must estimate how much total fat they ate. As always, Paleolithic diets varied based on geography and access to certain foods, but in general, our ancestors ate relatively more fat, more protein, and less carbohydrate, compared to contemporary diets. In 2000, Dr. Cordain and his colleagues estimated the following macronutrient ratios for Paleolithic diets:[1]

  • Fat: 28-58% of calories
  • Protein: 19-35% of calories
  • Carbohydrates: 22-40% of calories

They arrived at these estimates, in part, by analyzing the diets of 229 hunter-gather societies, assessing their specific foods, and measuring their ratios of plant to animal food consumption. The vast majority (73%) of these societies derived more than 50% of their calories from animal foods [2].

Next, we need to estimate how macronutrients are distributed within the specific foods our ancestors ate. Figures 1 and 2 below compare the meat of wild animals with the meat of commercially raised animals. Figure 1 shows the percentage of calories from protein, fat, and carbohydrate (note that carbs are negligible in animal meat) whereas Figure 2 shows each type of fat as a percentage of total fat. We can assume, with a reasonable degree of certainty, that wild animals today are similar to those hunted and consumed by our ancestors, with respect to body composition.

Macronutrient Calories in Animal Foods

Figure 1. Percent of calories from macronutrients (protein, fat and carbohydrate) in wild and commercial animal foods.

Proportion of Fatty Acids in Animal Foods

Figure 2. Proportions of fatty acids in wild and commercial animal foods.


Examining these figures, two dominant trends emerge:

1. Wild meat is proportionally higher in protein and lower in fat compared to commercially raised meat.
2. The fat portion of wild meat is proportionally higher in PUFAs – both omega-6 and omega-3 – compared to commercial meat.

Additionally, we can say that grass-fed beef is closer to wild meat than grain-fed beef, but both grass-fed beef and grain-fed beef poorly approximate wild meat.

The above observations are based on data from the USDA Nutrient Database and are substantiated by numerous studies comparing wild and domesticated animals [3], [4], [5], [6], [7].

Additionally, scientists have recently extracted frozen, Paleolithic-era animal carcasses from the Siberian tundra. Tissue analyses of these carcasses further highlight the similarities between Paleolithic meat and modern wild meat, particularly with respect to n-6/n-3 ratios [8], [9].


The Ever-Important Omega Ratio

As we saw in part I, many RCTs, observational studies, and meta-analyses addressing omega-6 consumption fail to properly account for omega-3 consumption (and the n-6/n-3 ratio). For our Paleolithic ancestors, this ratio was approximately 1/1 (and probably no higher than 3/1) [10]. Today, however, the ratio approaches 20/1 for people consuming typical Western diets [11].

This disparity is critical to the entire debate about saturated fat and its replacement with omega-6. Recent studies show saturated fat isn’t a health menace, as previously believed [12][13][14][15]. On the other hand, our reliance on commercially raised meat has probably skewed our fat consumption by over-representing saturated fat and under-representing PUFAs. We’ve compensated by consuming large quantities of vegetable oils, which are rich in omega-6, but omega-3 consumption has fallen by the wayside.

The consequences of our dramatically elevated n-6/n-3 ratios include the following:[16]

  • Increased inflammation
  • Increased leptin and insulin resistance
  • Increased risk for diabetes
  • Increased weight gain and risk for obesity


Keeping it Real

Just as previous generations shunned saturated fat, we would be foolish to shun omega-6 completely. After all, omega-6 is an essential fatty acid (EFA), meaning our body requires it and can only obtain it from food. That being said, some sources of are better than others.

It’s easy to get good quality omega-6 from olive oil, avocados, nuts, and from certain animal foods. By following the Paleo Diet template, you’ll get a good balance of omega-6 and omega-3, plus a good distribution of SFAs, MUFAs, and PUFAs.

With respect to omega-6, our best advice would be to eliminate all vegetable and seed oils from your diet. These include, among others:

  • Soybean oil
  • Corn oil
  • Safflower oil
  • Sunflower oil
  • Canola oil
  • Grapeseed oil

The problem with these oils is they contain very high amounts of omega-6. Consuming them increases your n-6/n-3 ratio, while also introduces potentially dangerous free radicals.


Unstable Seed Oils

The industrial processing of vegetable seed oils involves high-heat and the use of various chemical solvents – a guaranteed recipe for free radical oxidation and lipid peroxidation [17].

Cooking with PUFA-rich oils creates lipid oxidation products known as alkenals, some of which are toxic [18].

Olive oil, which contains some PUFAs, but is mostly comprised of MUFAs, has been shown to be more heat-stable and better for cooking compared to vegetable oils [19],[20]. It’s best to avoid high-heat cooking with any oils, but those containing higher amounts of SFAs and MUFAs are more stable than those with higher amounts of PUFAs.



Saturated fat isn’t unhealthy, but it needn’t be over represented in our diets. Many health authorities recommend replacing saturated fat with omega-6, and although some studies support this recommendation, most fail to differentiate between omega-6 and omega-3. Replacing some saturated fat with PUFAs could be beneficial, particularly if doing so lowered the n-6/n-3 ratio. For most people, this would mean eliminating all vegetable seed oils, while increasing oily fish (omega-3) consumption.

It’s also important to recognize that meat from game animals is better than commercially raised meat, but since obtaining wild meat is impractical for most people, pasture-raised meat (grass-fed, etc.) should always be favored.

Don’t over complicate things too much. You don’t need to meticulously track your fat consumption. By following The Paleo Diet template and listening to your body, you’ll get a healthy mix.



[1] Cordain L, et al. (2000). Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition, 71(3). Retrieved from (link).

[2] Cordain L, et al. (2000). Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets. American Journal of Clinical Nutrition, 71(3). Retrieved from (link).

[3] Davidson B, et al. (Mar-Apr 2011). Meat lipid profiles: a comparison of meat from domesticated and wild Southern African animals. In Vivo, 25(2). Retrieved from (link).

[4] Rule DC, et al. (2002). Comparison of muscle fatty acid profiles and cholesterol concentrations of bison, beef cattle, elk, and chicken. J Anim Sci., 80(5). Retreived from (link).

[5] Cordain, et al. (Mar 2002). Fatty acid analysis of wild ruminant tissues: evolutionary implications for reducing diet-related chronic disease. Nature, 56(3). Retrieved from (link).

[6] Cordain, et al. (2001). Fatty acid composition and energy density of foods available to African hominids. Evolutionary implications for human brain development. World Rev Nutr Diet., 90. Retrieved from (link).

[7] Fine LB, et al. (2008). Comparison of lipid and fatty acid profiles of commercially raised pigs with laboratory pigs and wild-ranging warthogs. South African Journal of Science, 104. Retrieved from (link).

[8] Guil-Guerrero JL, et al. (2014). The Fat from Frozen Mammals Reveals Sources of Essential Fatty Acids Suitable for Palaeolithic and Neolithic Humans. PLoS One., 9(1). Retrieved from (link).

[9] Guil-Guerrero JL, et al. (2015). The PUFA-Enriched Fatty Acid Profiles of some Frozen Bison from the Early Holocene found in the Siberian Permafrost. Scientific Reports, 5. Retrieved from (link).

[10] Eaton SB, et al. (1998). Dietary intake of long-chain polyunsaturated fatty acids during the paleolithic. World Rev Nutr Diet., 83. Retrieved from (link).

[11] Simopoulos AP. (2016). An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity. Nutrients, 8(3). Retrieved from (link).

[12] Ruiz-Nunez, B., D.A.J. Dijck-Brouwer, and F.A.J. Muskiet, The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. Journal of Nutritional Biochemistry, 2016. 36: p. 1-20.

[13] Chowdhury, R., et al., Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk A Systematic Review and Meta-analysis. Annals of Internal Medicine, 2014. 160(6): p. 398-+.

[14] Astrup, A., et al., The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? American Journal of Clinical Nutrition, 2011. 93(4): p. 684-688.

[15] Hoenselaar, R., Saturated fat and cardiovascular disease: The discrepancy between the scientific literature and dietary advice. Nutrition, 2012. 28(2): p. 118-123.

[16] Simopoulos AP. (2016). An Increase in the Omega-6/Omega-3 Fatty Acid Ratio Increases the Risk for Obesity. Nutrients, 8(3). Retrieved from (link).

[17] Kanner J, et al. (2007). Dietary advanced lipid oxidation endproducts are risk factors to human health. Mol Nutr Food Res., 51(9). Retrieved from (link).

[18] Halvorsen BL, et al. (2011). Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements. Food Nutr Res., 55. Retrieved from (link).

[19] Halvorsen BL, et al. (2011). Determination of lipid oxidation products in vegetable oils and marine omega-3 supplements. Food Nutr Res., 55. Retrieved from (link).

[20] Silva L, et al. (2010). Oxidative stability of olive oil after food processing and comparison with other vegetable oils. Food Chemistry, 121(4). Retrieved from (link).

Vitamin D: One of the Few Supplements Paleo Dieters May RequireOne of the most persuasive aspects of contemporary Paleo Diets is that you will not have to waste your hard earned dollars on supplements (1, 2).  Once you get going on this lifetime program of eating, except for Vitamin D and possibly fish oil, you will achieve all of the DRI’s recommended by governmental agencies from just the food you eat (1, 2).  Previously, I have extensively covered the calcium issue in a number of scientific publications (2-4), so in this blog, I want to re-emphasize the importance of vitamin D supplementation for health and well being.  As we come out of wintertime and into early Spring, the possibility exists that many of us may be vitamin D compromised or even Vitamin D deficient (5-11).

Why is this?  When we eat the foods that mother nature intended, why should we be deficient in any nutritional element?  Vitamin D is actually not a vitamin, but rather is a hormone naturally formed in our skins when we expose ourselves to the ultraviolet radiation of the sun.  In North America and in Europe, we receive scant little sunshine in the dead of winter, and consequently our body stores of this essential hormone become depleted as we go from Fall to Winter to early Spring (5-11).

Table 1 below lists the content of the 40 most concentrated sources of vitamin D in real, non-fortified foods.  Careful examination of this Table makes it clear that, except for salmon or fresh tuna (12), it is difficult or even impossible to achieve recommended vitamin D intakes (600 I.U. or greater per day) (10, 11) with real, non-fortified foods.

Table 1.  The 40 most concentrated sources of Vitamin D in real, non-fortified foods in the western diet.

Food 100 grams food Vit D I.U. kcal Vit D IU/kcal Vit D IU/100 kcal
Cod liver oil 100 10,000 902 11.09 1109
Catfish, Channel, Wild, Dry Heat 100 568 105 5.41 541
Tuna (bluefin), Fresh, wild, baked/broiled 100 920 184 5.00 500
Salmon, Coho (Silver), Wild,  Baked/Broiled 100 676 139 4.86 486
Salmon, Chinook (King), Wild, Baked 100 904 231 3.91 391
Fish eggs (roe), mixed species 100 484 143 3.38 338
Salmon, Sockeye, Wild Cooked Dry Heat 100 526 169 3.11 311
Oysters, Pacific, Steamed 100 320 163 1.96 196
Salmon, Atlantic Wild Baked 100 328 182 1.80 180
Halibut, Atlantic/Paciific, Baked 100 192 140 1.37 137
Salmon, Atlantic Farmed Baked 100 272 206 1.32 132
Mushrooms, Oyster raw 100 36 33 1.09 109
Herring 100 216 203 1.06 106
Tuna, (yellow fin/albacore), baked/broiled 100 140 139 1.01 101
Sardines in oil 100 193 208 0.93 93
Tuna, Canned in water 100 80 128 0.63 63
Mushrooms, Potabella raw 100 12 22 0.55 55
Mushrooms, Shiitake raw 100 18 34 0.53 53
egg yolks 100 187 351 0.53 53
Cod, Atlantic, Cooking dry heat 100 46 105 0.44 44
Beef, Kidney 100 68 159 0.43 43
Mackerel 100 104 262 0.40 40
Pork liver 100 52 134 0.39 39
Mushrooms, white 100 7 22 0.32 32
Beef liver 100 49 175 0.28 28
Cod, Pacific,  Cooking dry heat 100 24 85 0.28 28
Turkey liver 100 72 273 0.26 26
Salmon oil 100 177 902 0.20 20
Beef, Filet Mignon 100 36 211 0.17 17
Chicken liver 100 16 119 0.13 13
Pork loin 100 34 273 0.12 12
Lamb liver 100 16 139 0.12 12
Lamb, rib roast lean 100 24 232 0.10 10
Mushrooms, Enoki raw 100 4 44 0.09 9
Bacon 100 42 541 0.08 8
Catfish, Channel, Farmed, Dry Heat 100 10 144 0.07 7
Mussels 100 11.2 172 0.07 7
Pork kidney 100 8 151 0.05 5


At the top of the list for natural foods is cod liver oil, which at first appears to be a great source of vitamin D.  It is, but unfortunately it also contains high levels of vitamin A which competes with our bodies’ metabolism for vitamin D and may impair vitamin D metabolism (13).   A better choice is fish oil from the body of fish, rather than the liver.  It also contains vitamin D and the healthful long chain omega 3 fatty acids (EPA and DHA) without the higher concentrations of vitamin A which may impair vitamin D metabolism (13).  

But from an evolutionary perspective, fish oil whether derived from cod liver oil or only the body of fish, was known to have been consumed by the Vikings (circa 700s to 1100 AD) but was not commercially manufactured until relatively recent (200 – 300 years) times.

Accordingly, the Paleo Diet paradigm suggests that (as a species) if we consumed vitamin D from food, it must have come from other sources.  Table1 indicates that salmon is a concentrated source of vitamin D, and if we consume roughly ¼ pound of salmon or more per day (12), we may be able to achieve low level vitamin D balance.  But who do you know who eats a quarter pound or more of salmon a day (day in and day out) in the 21st century?

As you move on down the list of foods in Table 1 from salmon, it becomes increasingly obvious that with our modern tastes and diets, few people could achieve vitamin D balance on any normal diets before modern, fortified foods (milk, margarine and processed foods) were introduced in about the 1930’s and 1940’s.  Organ meats won’t do it, eggs won’t do it, shellfish won’t do it and meat won’t do it.  The obvious implications of Table 1 is that food never was or never could have been the primary source of the hormone, vitamin D, which is essential for optimal human health.  Before I leave this topic, let’s examine milk and dairy products.


Are Dairy Foods Good Sources of Vitamin D?

To even suggest that milk is a good source of vitamin D is a total stretch of the facts.  The Institute of Medicine Daily’s recommended intake for vitamin D is 600 IU per day for most people (14).  Although this advice represents a substantial increase from previous estimates, it still falls far short of human experimental evidence showing that at least 2,000 IU per day is required to keep blood levels of vitamin D at the ideal concentration of 30 ng/ml (6, 7, 10).  See Table 2 below.


Table 2.  Vitamin D Classifications in Blood.

Blood levels of vitamin D Category
less than 20 ng/ml Deficiency
21 to 29 ng/ml Insufficiency
greater than 30 ng/ml Sufficiency
60 ng/ml Maximal with sunlight exposure

An eight oz glass of raw milk (280 calories) straight from the cow without fortification gives you a paltry 3.6 IU of vitamin D.  At this rate, you’d have to drink a ridiculous 167 eight oz glasses of milk just to achieve the 600 IU daily recommendation.  Because most of the milk we drink is fortified with vitamin D, then an 8 oz glass typically yields 100 IU of this nutrient.   However, even with fortification, you would have to drink six 8 oz glasses (1,680 calories or ~ 75 % of your daily caloric intake) of milk to meet the daily requirement for vitamin D.  If you wanted to reach the 2,000 IU level as suggested by the world’s best vitamin D researchers, you would have to drink 20 eight oz glasses of fortified milk amounting to 5,600 calories.   No one in their right mind would drink 20 glasses of milk a day, even if they could.  

As you can see from these simple calculations, whether fortified or raw, milk is an abysmal source of vitamin D.   The best way to get your vitamin D is not by drinking milk, but rather by getting a little daily sun exposure as nature intended.


Sunlight Exposure

Lifeguards and other outdoor workers can achieve blood concentrations that top out at about 60 ng/ml.  But you really don’t need values this high. Most experts agree that values higher than 30 ng/ml will significantly reduce your risk for cancer and all of the other diseases associated with low vitamin D status (15-21).   The good news is that daily sunlight exposure in the summertime for short periods 15-30 minutes will rapidly boost your blood levels of vitamin D above 30 ng/ml.  Something that cannot be achieved with diet alone because almost all real foods, except salmon (12), that we commonly eat contain little or no vitamin D (Table 1).  


Vitamin D Supplementation

For most of us, regular sunlight exposure is a luxury that is difficult or impossible to come by on a year round basis.  Obviously, our hunter gatherer ancestors, living at low to moderate latitudes did not have this problem.  Consequently, you will need to supplement your diet with vitamin D3 capsules.  If we look at the official governmental recommendation for vitamin D intake (between 400 and 600 IU), it is woefully inadequate.  This policy represents a complete failure in public health policy.  The most recent human experiments show that blood levels of 30 ng/ml could never be achieved with vitamin intakes between 400 and 600 IU (6, 7, 10, 11). 400 IU does not help improve insufficient blood concentrations of vitamin D one iota. In fact, a recent series of articles and reviews published in Nutrients demonstrated that the 600 IU recommendation was based on a misinterpretation of the data and was an order of magnitude too low. A meta-analysis of existing studies conservatively estimated daily needs of 1885, 2802 and 6235 IU for normal weight, overweight, and obese individuals respectively (22-24).

The majority of men, women and children in the U.S. maintain blood levels of vitamin D which are either deficient or insufficient (6-11).  Hence, one of the best strategies you can take with adopting The Paleo Diet is to supplement daily with vitamin D3 if you are unable to get sunshine on a regular basis. Most vitamin D experts agree that daily supplementation of at least 2,000 IU of vitamin D3 daily is necessary to achieve healthful blood levels of 30 ng/ml or greater.  


[1] Cordain L. The Paleo Answer. John Wiley & Sons, New York, NY, 2012.

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

[3] 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.

[4] O’Keefe JH, Bergman N, Carrera-Basto P, Fontes-Villalba M, DiNicolantonio JJ, Cordain L. Nutritional strategies for skeletal and cardiovascular health: hard bones, soft arteries, rather than vice versa.  Open Heart 2016;3: e000325. doi:10.1136/ openhrt-2015-000325 (in press).

[5] Binkley N, Novotny R, Krueger D, Kawahara T, Daida YG, Lensmeyer G, Hollis BW, Drezner MK. Low vitamin D status despite abundant sun exposure. J Clin Endocrinol Metab. 2007 Jun;92(6):2130-5.

[6] Holick MF, Chen TC: Vitamin D deficiency: a worldwide problem with health consequences. Am J Clin Nutr. 2008 Apr;87(4):1080S-6S.

[7] Hollis BW. Circulating 25-hydroxyvitamin D levels indicative of vitamin D sufficiency: implications for establishing a new effective dietary intake recommendation for vitamin D. J Nutr. 2005 Feb;135(2):317-22.

[8] Kumar J, Muntner P, Kaskel FJ, Hailpern SM, Melamed ML. Prevalence and associations of 25-hydroxyvitamin D deficiency in US children: NHANES 2001-2004. Pediatrics. 2009 Sep;124(3):e362-70.

[9] Melamed ML, Kumar J. Low levels of 25-hydroxyvitamin D in the pediatric populations: prevalence and clinical outcomes. Ped Health. 2010 Feb;4(1):89-97.

[10] Vieth R. Why the optimal requirement for vitamin D3 is probably much higher than what is officially recommended for adults. J Steroid Biochem Mol Biol 2004; 89-90:575-9.

[11] Bischoff-Ferrari HA. Optimal serum 25-hydroxyvitamin D levels for multiple health outcomes. Adv Exp Med Biol. 2008;624:55-71

[12] Lu Z, Chen TC, Zhang A, Persons KS, Kohn N, Berkowitz R, Martinello S, Holick MF. An evaluation of the vitamin D3 content in fish: Is the vitamin D content adequate to satisfy the dietary requirement for vitamin D? J Steroid Biochem Mol Biol. 2007 Mar;103(3-5):642-4. Epub 2007 Jan 30.

[13] Cannell JJ, Vieth R, Willett W, Zasloff M, Hathcock JN, White JH, Tanumihardjo SA, Larson-Meyer DE, Bischoff-Ferrari HA, Lamberg-Allardt CJ, Lappe JM, Norman AW, Zittermann A, Whiting SJ, Grant WB, Hollis BW, Giovannucci E.  Cod liver oil, vitamin A toxicity, frequent respiratory infections, and the vitamin D deficiency epidemic. Ann Otol Rhinol Laryngol. 2008 Nov;117(11):864-70.

[14] https://iom.nationalacademies.org/Reports/2010/Dietary-Reference-Intakes-for-Calcium-and-Vitamin-D.aspx

[15] Dobnig H, Pilz S, Scharnagl H, Renner W, Seelhorst U, Wellnitz B, Kinkeldei J, Boehm BO, Weihrauch G, Maerz W. Independent association of low serum 25-hydroxyvitamin d and 1,25-dihydroxyvitamin d levels with all-cause and cardiovascular mortality. Arch Intern Med. 2008 Jun 23;168(12):1340-9.

[16] Field S, Newton-Bishop JA. Melanoma and vitamin D. Mol Oncol. 2011 Feb 3. [Epub ahead of print]

[17] Forouhi NG, Luan J, Cooper A, Boucher BJ, Wareham NJ. Baseline serum 25-hydroxy vitamin D is predictive of future glycaemic status and insulin resistance: The MRC Ely prospective study 1990-2000. Diabetes. 2008 Oct;57(10):2619-25.

[18] Holick MF. Vitamin D and sunlight: strategies for cancer prevention and other health benefits. Clin J Am Soc Nephrol 2008;3:1548-54.

[19] Holick MF. Optimal vitamin d status for the prevention and treatment of osteoporosis. Drugs Aging. 2007; 24(12):1017-29.

[20] Plum LA, DeLuca HF. Vitamin D, disease and therapeutic opportunities. Nat Rev Drug Discov. 2010 Dec;9(12):941-55

[21] Sharief S, Jariwala S, Kumar J, Muntner P, Melamed ML. Vitamin D levels and food and environmental allergies in the United States: Results from the National Health and Nutrition Examination Survey 2005-2006. J Allergy Clin Immunol. 2011 Feb 15.

[22] Heaney, R., et al., Letter to Veugelers, P.J. and Ekwaru, J.P., A Statistical Error in the Estimation of the Recommended Dietary Allowance for Vitamin D. Nutrients 2014, 6, 4472-4475; doi:10.3390/nu6104472. Nutrients, 2015. 7(3): p. 1688-1690.

[23] Veugelers, P.J. and J.P. Ekwaru, A Statistical Error in the Estimation of the Recommended Dietary Allowance for Vitamin D. Nutrients, 2014. 6(10): p. 4472-4475.

[24] Veugelers, P.J., T.M. Pham, and J.P. Ekwaru, Optimal Vitamin D Supplementation Doses that Minimize the Risk for Both Low and High Serum 25-Hydroxyvitamin D Concentrations in the General Population. Nutrients, 2015. 7(12): p. 10189-10208.

Embracing Your Inner Paleo Chef | The Paleo Diet
It’s often said that meat made us human. Meat allowed for larger brains and greater intelligence, not to mention more time for pursuits other than chewing. So how did a species that ate relatively little meat 2.6 million years ago evolve into one that depended on meat and was radically transformed by its consumption?

Do we owe this success to fire and our learned ability to cook? Or does a more rudimental form of “cooking” deserve the credit? As every chef knows, you don’t just toss whole vegetables and large slabs of meat into the casserole. You have to slice and dice before turning on the fire. This sequence of processing food with tools before applying fire, which happens every time we cook, epitomizes the entire evolution of cooking.

Today’s chefs use knives, blenders, and other modern “processing tools,” but the “old-old school” chefs, to whom the entire human enterprise owes its existence, used crude stone tools to process meat, making it easier to chew and digest. This was and still is the beginning of cooking.


Chef Erectus

Around 1.8 million years ago, Homo erectus emerged on the Paleolithic scene. Homo erectus differed in many ways from earlier hominins, including his larger brain, shorter digestive tract, smaller jaws and teeth, reduced chewing muscles, and weaker bite force.

Between 2 and 3 million years ago, Africa was undergoing a dramatic drying trend, which resulted in new grassland habitats. Consequently, Homo erectus had larger foraging areas than his jungle-dwelling arboreal predecessors. In the words of University of Colorado paleoanthropologist Thomas Wynn, “Erectus has gone completely terrestrial — not climbing trees very much at all.”1

Homo erectus needed calories and plenty of them. Bigger brains require more calories as do the demands of travelling long distances searching for food. The modern human brain consumes 20 percent of the body’s at-rest energy, more than twice that of other primates.2 Less evolved primates, on the other hand, expend the bulk of their energy digesting low-calorie plant food. “You can’t have a large brain and big guts at the same time,” explains Leslie Aiello, an anthropologist and director of the Wenner-Gren Foundation in New York City.3

Homo erectus evolved because he ate meat, but what made this possible? Have you ever tried chewing raw meat? It’s extremely tedious and wholly unlike chewing cooked meat. Had Homo erectus already mastered the use of fire for cooking? Or was this technology still more than a million years from being discovered? If the latter, how was Homo erectus able to chew raw meat with such decidedly disadvantaged teeth?

The Homo Erectus School of Cooking

In his 2009 book, Catching Fire: How Cooking Made Us Human, Harvard anthropologist Richard Wrangham hypothesized that Homo erectus was already cooking with fire by 1.8 million years ago. Convincing evidence notwithstanding, most archaeologists, paleontologists and anthropologists think Wrangham was wrong. A more reasonable estimate for the beginning of fire-based cooking is 400,000 years ago.4

One thing is certain though. Before man learned to cook with fire, he learned to process meat with tools. On the difficulty of chewing raw meat, even Wrangham acknowledges, “It probably wouldn’t take [early man] long to realize you could pound the meat. To pound the meat they would have gotten more energy out of it.”5

But just how much energy did such tool processing save? This question was put to the test for a study recently published in Nature6. Harvard scientists Daniel Lieberman and Katherine Zink attached electrodes to volunteers’ faces to measure muscle activity while using force transducers between their molars to measure chewing force. They tested meat and root vegetables, including cooked samples, unprocessed samples, and sliced/pounded samples.

They found that slicing and pounding meat and vegetables results in 17% less chewing, equating to 2.5 million less chews per year. Lieberman and Zink concluded that tool processing, which is an early form of “cooking,” enabled Homo erectus to reap the benefits of meat. “If you are using less force and using fewer chews, you are, of course spending less time eating,” Zink explained. “And if you no longer need to maintain the big jaws and big teeth, it allows natural selection to choose for other performance benefits that improve fitness and survival.”7

We can say that Wrangham, Lieberman, and Zink are all correct. Cooking made us human because cooking enabled us to eat meat. And although Homo erectus probably didn’t cook with fire, he certainly used stone tools to slice and pound meat, making it easier to chew and digest. This is how the technology of cooking began, just as every cooked meal today begins with chopping, slicing, and dicing. So go ahead and embrace your inner Paleo chef. For if cooking truly made us human, then at our cores we are all chefs.


[1]  Choi, CQ. (November 11, 2009). Human Evolution: The Origin of Tool Use. LiveScience. Retrieved from http://www.livescience.com/7968-human-evolution-origin-tool.html

[2] Raichle, ME, et al. (August 6, 2002). Appraising the brain’s energy budget. Proceedings of the National Academies of Sciences, 99(16). Retrieved from http://www.pnas.org/content/99/16/10237.full

[3] Joyce, C. (August 2, 2010). Food For Thought: Meat-Based Diet Made Us Smarter. NPR. Retrieved from http://www.npr.org/2010/08/02/128849908/food-for-thought-meat-based-diet-made-us-smarter

[4] Roebroeks, W., et al. (2011). On the earliest evidence for habitual use of fire in Europe. Proceedings of the National Academy of Sciences, 108(13). Retrieved from http://www.pnas.org/content/108/13/5209.full

[5] Gorman, RM. (2007). Evolving Bigger Brains through Cooking: A Q&A with Richard Wrangham. Scientific American. Retrieved from http://www.scientificamerican.com/article/evolving-bigger-brains-th/

[6] Zink, KD and Lieberman, DE. (2016). Impact of meat and Lower Palaeolithic food processing techniques on chewing in humans. Nature. Retrieved from http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16990.html

[7] Netburn, D. (March 9, 2016). How raw meat — and our ancestors’ inability to chew it — changed the course of human evolution. LA Times. Retrieved from http://www.latimes.com/science/sciencenow/la-sci-sn-raw-meat-stone-tools-evolution-20160309-story.html


Stop Resisting! Leptin Resistance and Fat

There are undoubtedly many distinct variables, which each play a role, in the development of obesity.1, 2, 3, 4, 5 Whether it is too much sugar (usually leading to insulin resistance), too many calories, or simply a lack of exercise – obesity can result from a multitude of causative factors.6 7, 8, 9 However, one interesting variable that has come into light in the scientific community, is a hormone called leptin.10, 11, 12, 13 The rate of an individual’s leptin production is related to adiposity, but a large portion of the interindividual variability in plasma leptin concentration is independent of the percentage of body fat.14, 15 Obese individuals typically have large amounts of leptin,16, 17, 18 however, their brain usually cannot “see” their leptin, resulting in a state termed leptin resistance.19, 20, 21, 22

Stop Resisting! Leptin Resistance and Fat | The Paleo Diet

“The Role of Leptin in the Control of Insulin-glucose Axis.” Frontiers. N.p., n.d. Web. 22 Dec. 2014.

Stop Reisisting! Leptin Resistance and Fat | The Paleo Diet

“Obesity and Leptin Resistance.” Trends in endocrinology and metabolism: TEM 21.11 (2010)

Leptin is an adipocyte hormone that functions as the afferent signal in a negative feedback loop regulating body weight.23, 24, 25, 26 As researchers state, leptin also functions as a key link between nutrition and the function of most, if not all, other physiologic systems.27, 28, 29 How does this apply to you, and your quest to stay lean? Well, when an individual gains weight, their level of leptin increases.30, 31 The individual is then typically in a state of positive energy balance.32 Weight loss, in turn, typically leads to a state of negative energy balance.33 Interestingly, human beings appear to be multivariate, both in their sensitivity to leptin, and also how much leptin is produced by the body.34, 35

Stop Resisting! Leptin Resistance and Fat | The Paleo Diet

Paz-Filho G, Mastronardi C, Wong ML, Licinio J. Leptin therapy, insulin sensitivity, and glucose homeostasis. Indian J Endocr Metab 2012;16, Suppl S3:549-55

Since leptin is a key link between nutrition and just about every physiologic system, understanding leptin resistance, and possibly finding a way to intervene between insulin and leptin signaling, has become a major goal, in the science of finding a ‘cure’ for obesity.36, 37 A typical Western diet, which is usually extremely high in sugar, leads to excess insulin being secreted by the body.38 Chronically elevated insulin levels, help to block leptin’s negative feedback signal.39 This is how you get fat.

More specifically, researchers have posited that lack of available insulin receptor substrate 2, which is used by the leptin receptor (and can commonly be caused by hyperinsulinemia) may result in defective leptin signal transduction.40, 41 Interestingly, gender also plays a role in leptin levels, as women demonstrate markedly higher levels, compared to men.42 Even in the short term, changes in dietary carbohydrate intake induce changes in plasma leptin levels, which is also interesting, in regards to causative factors of obesity.43

Stop Resisting! Leptin Resistance and Fat |  The Paleo Diet

Nature.com. Nature Publishing Group, n.d. Web. 22 Dec. 2014.

Stop Resisting! Leptin Resistance and Fat | The Paleo Diet

Martínez de Morentin“‘Mens Sana In Corpore Sano’: Exercise and Hypothalamic ER Stress.” PLoS Biology 8.8 (2010): e1000464.

Your hypothalamus contains a receptor for leptin, called LRb.44 Once leptin binds to this receptor, a cascade of biochemical signaling takes place.45 Orexigenic neuropeptides are downregulated, and anorexigenic neuropeptides are upregulated.46 Some of these neuropeptides include: neuropeptide Y, agouti-related peptide, melanin-concentrating hormone, corticotropin-releasing-hormone, and alpha-melanocyte-stimulating hormone, to name but a few.47 With basic logic, it would seem to make sense that by injecting leptin, we would be able to induce weight loss in humans. However, this has not been shown to work, further advancing the theory that it is leptin resistance, not lack of leptin, which is causing the problem of widespread obesity, in today’s population.48, 49

Stop Resisting! Leptin Resistance and Fat | The Paleo Diet

Martínez de Morentin“‘Mens Sana In Corpore Sano’: Exercise and Hypothalamic ER Stress.” PLoS Biology 8.8 (2010): e1000464.

Stop Resisting! Leptin Resistance and Fat | The Paleo Diet

“The Role of Leptin in the Control of Insulin-glucose Axis.” Frontiers. N.p., n.d. Web. 22 Dec. 2014.

Leptin-stimulated phosphorylation of Tyr(985) has been shown to promote a cellular leptin resistance, in obese subjects.50 Further, a multitude of features of the arcuate nucleus of the hypothalamus, may help to add to the level of cellular leptin resistance.51 Another factor, which is so overlooked by the general populace, is that circulating levels of leptin are influenced by sleep duration.52 Another commonly overlooked element to leptin resistance, is dietary fructose.53

Long term feeding of fructose has been shown to result in leptin resistance.54 This is yet another reason to leave fructose largely out of one’s diet. A Paleo Diet, which is rich with nutrients, fiber, protein and healthy fats, will not lead to leptin resistance, and may even help to reverse it. While the science of leptin is ever-evolving and changing, the tenets of a healthy lifestyle are not. Getting plenty of sleep, limiting stress, getting sunshine, and eating well – all tenets of a Paleo lifestyle – will result in a healthier, happier version of yourself!


[1] Furukawa S, Fujita T, Shimabukuro M, et al. Increased oxidative stress in obesity and its impact on metabolic syndrome. J Clin Invest. 2004;114(12):1752-61.

[2] 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.

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

[4] 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.

[5] Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and metabolism. Am J Clin Nutr. 2006;83(2):461S-465S.

[6] Keller KB, Lemberg L. Obesity and the metabolic syndrome. Am J Crit Care. 2003;12(2):167-70.

[7] Misra A, Khurana L. Obesity and the metabolic syndrome in developing countries. J Clin Endocrinol Metab. 2008;93(11 Suppl 1):S9-30.

[8] Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest. 2000;106(4):473-81.

[9] Dandona P, Aljada A, Bandyopadhyay A. Inflammation: the link between insulin resistance, obesity and diabetes. Trends Immunol. 2004;25(1):4-7.

[10] Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007;8(1):21-34.

[11] Friedman JM, Halaas JL. Leptin and the regulation of body weight in mammals. Nature. 1998;395(6704):763-70.

[12] Ahima RS. Revisiting leptin’s role in obesity and weight loss. J Clin Invest. 2008;118(7):2380-3.

[13] Enriori PJ, Evans AE, Sinnayah P, et al. Diet-induced obesity causes severe but reversible leptin resistance in arcuate melanocortin neurons. Cell Metab. 2007;5(3):181-94.

[14] Jéquier E. Leptin signaling, adiposity, and energy balance. Ann N Y Acad Sci. 2002;967:379-88.

[15] Huang KC, Lin RC, Kormas N, et al. Plasma leptin is associated with insulin resistance independent of age, body mass index, fat mass, lipids, and pubertal development in nondiabetic adolescents. Int J Obes Relat Metab Disord. 2004;28(4):470-5.

[16] Bravo PE, Morse S, Borne DM, Aguilar EA, Reisin E. Leptin and hypertension in obesity. Vasc Health Risk Manag. 2006;2(2):163-9.

[17] Carter S, Caron A, Richard D, Picard F. Role of leptin resistance in the development of obesity in older patients. Clin Interv Aging. 2013;8:829-44.

[18] Shah NR, Braverman ER. Measuring adiposity in patients: the utility of body mass index (BMI), percent body fat, and leptin. PLoS ONE. 2012;7(4):e33308.

[19] Myers MG, Leibel RL, Seeley RJ, Schwartz MW. Obesity and leptin resistance: distinguishing cause from effect. Trends Endocrinol Metab. 2010;21(11):643-51.

[20] Kalra SP. Circumventing leptin resistance for weight control. Proc Natl Acad Sci USA. 2001;98(8):4279-81.

[21] Carter S, Caron A, Richard D, Picard F. Role of leptin resistance in the development of obesity in older patients. Clin Interv Aging. 2013;8:829-44.

[22] Mark AL, Correia ML, Rahmouni K, Haynes WG. Selective leptin resistance: a new concept in leptin physiology with cardiovascular implications. J Hypertens. 2002;20(7):1245-50.

[23] Friedman JM. The function of leptin in nutrition, weight, and physiology. Nutr Rev. 2002;60(10 Pt 2):S1-14.

[24] Jönsson T, Olsson S, Ahrén B, Bøg-hansen TC, Dole A, Lindeberg S. Agrarian diet and diseases of affluence–do evolutionary novel dietary lectins cause leptin resistance?. BMC Endocr Disord. 2005;5(1):10.

[25] Air EL, Benoit SC, Clegg DJ, Seeley RJ, Woods SC. Insulin and leptin combine additively to reduce food intake and body weight in rats. Endocrinology. 2002;143(6):2449-52.

[26] Huang L, Li C. Leptin: a multifunctional hormone. Cell Res. 2000;10(2):81-92.

[27] Friedman JM. The function of leptin in nutrition, weight, and physiology. Nutr Rev. 2002;60(10 Pt 2):S1-14.

[28] Margetic S, Gazzola C, Pegg GG, Hill RA. Leptin: a review of its peripheral actions and interactions. Int J Obes Relat Metab Disord. 2002;26(11):1407-33.

[29] Ahima RS, Prabakaran D, Mantzoros C, et al. Role of leptin in the neuroendocrine response to fasting. Nature. 1996;382(6588):250-2.

[30] Guagnano MT, Romano M, Falco A, et al. Leptin increase is associated with markers of the hemostatic system in obese healthy women. J Thromb Haemost. 2003;1(11):2330-4.

[31] Phillips BG, Kato M, Narkiewicz K, Choe I, Somers VK. Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea. Am J Physiol Heart Circ Physiol. 2000;279(1):H234-7.

[32] Hall KD, Heymsfield SB, Kemnitz JW, Klein S, Schoeller DA, Speakman JR. Energy balance and its components: implications for body weight regulation. Am J Clin Nutr. 2012;95(4):989-94.

[33] Lemay V, Drapeau V, Tremblay A, Mathieu ME. Exercise and negative energy balance in males who perform mental work. Pediatr Obes. 2014;9(4):300-9.

[34] Ruhl CE, Everhart JE. Leptin concentrations in the United States: relations with demographic and anthropometric measures. Am J Clin Nutr. 2001;74(3):295-301.

[35] Plasma leptin levels are related to body composition, sex, insulin levels and the A55V polymorphism of the UCP2 gene. International Journal of Obesity. 2007;31(8):1311.

[36] Ozcan L, Ergin AS, Lu A, et al. Endoplasmic reticulum stress plays a central role in development of leptin resistance. Cell Metab. 2009;9(1):35-51.

[37] Mancour LV, Daghestani HN, Dutta S, et al. Ligand-induced architecture of the leptin receptor signaling complex. Mol Cell. 2012;48(4):655-61.

[38] Merat S, Casanada F, Sutphin M, Palinski W, Reaven PD. Western-type diets induce insulin resistance and hyperinsulinemia in LDL receptor-deficient mice but do not increase aortic atherosclerosis compared with normoinsulinemic mice in which similar plasma cholesterol levels are achieved by a fructose-rich diet. Arterioscler Thromb Vasc Biol. 1999;19(5):1223-30.

[39] Amitani M, Asakawa A, Amitani H, Inui A. The role of leptin in the control of insulin-glucose axis. Front Neurosci. 2013;7:51.

[40] Lustig RH. Childhood obesity: behavioral aberration or biochemical drive? Reinterpreting the First Law of Thermodynamics. Nat Clin Pract Endocrinol Metab. 2006;2(8):447-58.

[41] Isganaitis E, Lustig RH. Fast food, central nervous system insulin resistance, and obesity. Arterioscler Thromb Vasc Biol. 2005;25(12):2451-62.

[42] Hellström L, Wahrenberg H, Hruska K, Reynisdottir S, Arner P. Mechanisms behind gender differences in circulating leptin levels. J Intern Med. 2000;247(4):457-62.

[43] Dirlewanger M, Di vetta V, Guenat E, et al. Effects of short-term carbohydrate or fat overfeeding on energy expenditure and plasma leptin concentrations in healthy female subjects. Int J Obes Relat Metab Disord. 2000;24(11):1413-8.

[44] Bates SH, Kulkarni RN, Seifert M, Myers MG. Roles for leptin receptor/STAT3-dependent and -independent signals in the regulation of glucose homeostasis. Cell Metab. 2005;1(3):169-78.

[45] Banks AS, Davis SM, Bates SH, Myers MG. Activation of downstream signals by the long form of the leptin receptor. J Biol Chem. 2000;275(19):14563-72.

[46] Cowley MA, Smart JL, Rubinstein M, et al. Leptin activates anorexigenic POMC neurons through a neural network in the arcuate nucleus. Nature. 2001;411(6836):480-4.

[47] Münzberg H, Jobst EE, Bates SH, et al. Appropriate inhibition of orexigenic hypothalamic arcuate nucleus neurons independently of leptin receptor/STAT3 signaling. J Neurosci. 2007;27(1):69-74.

[48] Rahmouni K, Fath MA, Seo S, et al. Leptin resistance contributes to obesity and hypertension in mouse models of Bardet-Biedl syndrome. J Clin Invest. 2008;118(4):1458-67.

[49] Vasselli JR. The role of dietary components in leptin resistance. Adv Nutr. 2012;3(5):736-8.

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

[51] Håkansson ML, Hulting AL, Meister B. Expression of leptin receptor mRNA in the hypothalamic arcuate nucleus–relationship with NPY neurones. Neuroreport. 1996;7(18):3087-92.

[52] Spiegel K, Leproult R, L’hermite-balériaux M, Copinschi G, Penev PD, Van cauter E. Leptin levels are dependent on sleep duration: relationships with sympathovagal balance, carbohydrate regulation, cortisol, and thyrotropin. J Clin Endocrinol Metab. 2004;89(11):5762-71.

[53] Teff KL, Elliott SS, Tschöp M, et al. Dietary fructose reduces circulating insulin and leptin, attenuates postprandial suppression of ghrelin, and increases triglycerides in women. J Clin Endocrinol Metab. 2004;89(6):2963-72.

[54] Aijälä M, Malo E, Ukkola O, et al. Long-term fructose feeding changes the expression of leptin receptors and autophagy genes in the adipose tissue and liver of male rats: a possible link to elevated triglycerides. Genes Nutr. 2013;8(6):623-35.

Breathe Easy: The Paleo Fix for Bad Breath and Body Odor | The Paleo Diet

Nothing kills a conversation, business meeting or holiday party quicker than bad breath or body odor. If you’re following a Paleo Diet and experiencing improved health and performance, you may be stumped as to how your breath has suddenly taken a turn for the worst. While this isn’t the case for everyone, increased protein consumption can increase the likelihood of increased bacterial growth in the mouth. These bacteria produce volatile sulfur compounds (VSCs), the malodorous offenders that lead to bad breath.1,2 Furthermore, when it comes to body odor, studies have shown that the odor of non-meat eaters is considered “more attractive” than meat eaters!3

Does this mean you need to stop eating protein if you suffer from bad breath or body odor? Not at all, but you may need to make a few changes. Of course, your number 1 prevention should be maintain good dental hygiene. However, here are five tips you may not know that will help prevent the accumulation of foul-smelling VSCs and the dreaded B.O.:

Increase Cooling Foods

According to Traditional Chinese Medicine, excess heat in the body leads to symptoms of bad breath, foul–smelling stool, and mucous accumulation. Foods that increase heat in the body are chiefly proteins and grains, so if you’re a Paleo follower the high protein intake may be leading to excess heat, drying up your digestive tract and contributing to constipation, smelly stool, and bad breath.

The good news is it’s easy to bring your body back into balance­–start increasing your intake of cooling foods, such as radishes, cucumbers, celery, watermelon, cantaloupe, pears, and apples. The Paleo Diet after all focuses upon keep protein intake balanced with vegetables and fruits.

Add Fermented Foods

Studies show that dysbiosis or the overgrowth of ‘bad’ gut bacteria may be a key contributor to bad breath.4 Correct potential imbalances of ‘good’ to ‘bad’ gut flora by increasing your intake of Paleo-friendly fermented foods.

Be sure to eat fermented foods on a daily basis as part of a well-rounded Paleo Diet: raw cultured vegetables like sauerkraut and kimchee, natto miso, tamari sauce, kombucha tea, as well as polyphenol-rich green tea. Just double check you’re miso and tamari are free of added-salt!

Increase Your Chlorophyll Intake

While protein is the most nutrient dense food, containing the greatest concentrations of essential amino acids, fats, vitamins, minerals, and co-factors, you can’t forget your veggies!  Especially chlorophyll-rich green vegetables.

Chlorophyll is a green pigment found in algae and green plants, absorbing sunlight and converting it into energy. Green leafy veggies are loaded with chlorophyll, a powerful antioxidant and deodorizer that can be effective in your fight against bad breath and body odor.

Spinach and parsley pack the biggest chlorophyll punch, at approximately 24mg and 19mg respectively per half cup. Arugula, green beans, Chinese cabbage, broccoli, asparagus and zucchini are also great choices. Be sure to include a selection at every meal of the day.

Reduce Stress

In order to effectively reduce body odor, you need to get to the root of the problem. For many, this means reducing stress levels. The apocrine sweat glands increase their output in times of stress, in particular mental or emotional stress.5 The odorless, oily secretion then reacts with bacteria on your body to produce bad body odor.

If you have long, busy workdays or are under a great deal of stress, it could be the trigger that tips you over the ‘B.O.’ edge. To help reduce stress and activation of your sympathetic fight or flight nervous system, try eliminating coffee for two weeks, increasing your total sleep time, and trying some deep belly breathing to help blunt your overactive ‘sweat producing’ sympathetic nervous system.

Apply Herbal Anti-Microbials

If you’re experiencing consistently bad breath or body odour you can turn to herbal solutions. For bad breath, try gargling with peppermint oil, a potent anti-microbial that kills off harmful bacteria and leaves the breath fresh. Mix 1-2 drops with water and swish in your mouth for 30 seconds. For body odor, try adding tea tree or lavender essential oils to your skin. These natural anti-microbial oils kill bacteria and leave skin smelling fresh. Add a few drops to a damp cloth and dab onto your skin.

If you’re concerned about bad breath or body odor, there is no better time than now, before the holidays, to bring things back into balance. Try these five tips to knock out the unpleasant odors and ‘turn down the stink’ once and for all.


[1]Krespi YP et al. The relationship between oral malodor and volatile sulfur compound-producing bacteria. Otolaryngol Head Neck Sur 2006 Nov;135(5):671-6.

[2]T Imfeld. [Bad breath–aetiology, differential diagnosis and therapy]. Ther Umsch 2008 Feb;65(2):83-9.

[3]J Havlicek and P Lenochova. The Effect of Meat Consumption on Body Odor Attractiveness. Senses (2006) 31 (8): 747-752.

[4]Anjlkumar K and Monish A. Role of friendly bacteria in oral health – a short review. Oral Health Prev Dent. 2012;10(1):3-8

[5]C Calill, et al. Effects of stress hormones on the production of volatile sulfur compounds by periodontopathogenic bacteria. Braz Oral Res 2014 Jan-Feb;28(1).

British Dietetic Association (BDA) | The Paleo Diet

It now seems that barely a day goes by without some individual or group attacking the Paleo Diet. The reason for this is certainly up for debate but because the diet eliminates grains, legumes and dairy, it should not be surprising that it is going to come under fire from companies and corporations that stand to lose financially the more popular and successful the Paleo Diet becomes. One might not expect, however, for organizations that, in their own words, “use the most up to date public health and scientific research on food, health and disease, which they translate into practical guidance to enable people to make appropriate lifestyle and food choices,” to do the same.

I’m British, and my father routinely sends me articles from the British media.  Last week, he sent me a short piece from the Daily Mail newspaper that reported on the British Dietetic Association (BDA) revealing its annual list of the Top 5 “Celebrity Diets” to avoid in 2015. A tagline contained in the graphic states, “Being famous does not make someone an expert on diet.” It appears the same can be said for being part of a large nutritional organization. Based upon “telephone calls and other contributing factors,” they ranked the Paleo Diet second in this list, being surpassed only by the Urine Therapy Diet! While there are indeed many celebrities (and, by the way, top professional athletes) that have adopted the Paleo Diet, calling it a “celebrity diet” clearly attempts to mislead the reader that the diet has no research and is simply a “dodgy fad diet.” After outlining the major tenants of the diet fairly accurately, they, then, provide the BDA Verdict:

“Jurassic fad!  A diet with fewer processed foods, less sugar and salt is actually a good idea, but unless for medical reason, there is absolutely no need to cut any food group out of your diet.  In fact, by cutting out dairy completely from the diet, without very careful substitution, you could be in danger of compromising your bone health because of a lack of calcium.  An unbalanced, time consuming, socially isolating diet, which this could easily be, is a sure-fire way to develop nutrient deficiencies, which can compromise health and your relationship with food.”

So, in the very first statement, the BDA does actually recognize that the Paleo Diet is beneficial by eliminating the processed foods typically found in most Western diets. However, they quickly move into the misconception that by removing certain foods from the diet (i.e., grains, legumes and dairy), “without very careful substitution,” one will likely suffer nutrient deficiencies.

Let us dwell on this statement for a moment.

This is a classic position from those that are against the Paleo Diet, and yet, it is so easy to demonstrate how wrong this thinking is. Certainly, for the general public that perhaps has little nutritional knowledge, the thought of completely removing a number of elements of what has been thrown at them as a must staple for so many years, may seem less than prudent. However, it is not difficult to run a nutritional analysis on any true Paleo meal that have these elements removed and realize that not only are there no deficiencies, but the nutrient density for the 13 nutrients most lacking in the US diet, compared to the USDA Food Plate (formerly the Pyramid) actually improves, including calcium!  And, there is absolutely no need for careful substitution, simply following the Paleo template that nature has served will provide this nutritional benefit. In spite of this, one should be aware of the hypocrisy of the BDA on this issue. Both the BDA and The Academy of Nutrition and Dietetics (formerly the American Dietetic Association) endorse vegan diets, which eliminate dairy, meat and fish. Accordingly, the BDA is simply hypocritical in their criticism of the Paleo Diet for eliminating dairy.

As I have previously stated in other writings, there are now hundreds of thousands of physicians, naturopaths, nutritionists, chiropractors, conditioning coaches, and other healthcare professionals who advocate for the Paleo Diet and rely on results for their businesses to be successful. As a consequence, millions of people have benefited from adopting this way of eating and it astounds me that the BDA would ignore this reality and instead portray the diet as a “fad celebrity” diet that will be short lived.

However, of even greater concern, is that an organization that claims to use the most up-to-date scientific research to form their positions, appears completely unaware that there are now 15 human experimental studies on the Paleolithic Diet that demonstrate a benefit to adopting this dietary template.1,2,3,4,5,6,7,8,9,10,11,12,13,14,15 In all clinical trials to date, the Paleo Diet outperforms the Food Plate, the Mediterranean Diet, and diabetic diets for a variety of clinical endpoints including weight loss and cardiovascular disease symptoms. There are also many more peer reviewed scientific papers that lend support to the Paleolithic Diet template with which the BDA might benefit from becoming a little more familiar when advising and educating their base.

Here are a few important points that can be found within the published research referenced above that I’m guessing would be unknown to the BDA. Simply put, humans have no whole grain dietary requirement. In fact, whole grains are one of the worst food groups in terms of their nutrient density for the 13 nutrients most lacking in the US diet and are poor sources of fiber compared to fresh fruits and vegetables. Around 5% of the UK (~3.25 million people) and US (~16 million people) populations have either celiac disease or gluten intolerance. Gluten containing grains increase intestinal permeability via the upregulation of zonulin (a protein that modulates the permeability of tight junctions between cells of the digestive tract), and this increased permeability promotes chronic low level inflammation, a universal characteristic underlying CVD, cancer and autoimmunity. Whole grains also contain phytate and other antinutrients, which impair divalent ion absorption. Further, wheat contains wheat germ agglutinin (WGA), which likely enters the systemic circulation (not in plasma but bound to formed elements) and can interact with the immune system. And 65% of the world’s people are lactose intolerant and have no ill effects from eliminating dairy from their diet.

Critics of the Paleo Diet need to understand a very important issue.  Unlike the vast majority of diets out there, no one person has formulated this diet.  It is based on the concept of evolutionary dietary selective pressure and all of the published research on the diet has attempted to examine the concept that following a diet that humans evolved with over a long period of time, may provide an optimal dietary template.  The vast majority of the published data and the clinical findings, to date, support this idea.  Any researcher I know in this field of evolutionary nutrition is more than open to being shown research to the contrary; but, respectfully, would request that the data shows that, not someone’s opinion.

I recently wrote a response to an article critical of the Paleo Diet written by Professor Sydney Finkelstein (@SydFinkelstein). I attempted to engage Professor Finkelstein to support the points in his article and counter my critique that used the published data.  However, his response simply stated that “to suggest that the science behind the diet is incontrovertible, or that questioning the Paleo prescription is an affront to logic, is ludicrous.” So here’s a really good example of my point. An initial critique of the Paleo Diet with no scientific support is rebutted with the published data and the comeback is to state that the “Paleo Police” are unhappy about “their” diet being questioned. For those of us involved in the research and clinical trenches, that could not be further from the truth; we would just like the counter arguments to have some published data supporting them or at least some substance with sound logic so that further research can be conducted based upon those arguments to help determine what may be an optimal diet for human health and performance.

Dr. Loren Cordain, the very founder of the modern Paleo Diet movement, demonstrated an example of being open minded when he changed his position on dietary saturated fats. Upon re-examining his initial work through the lens of the evolutionary template, he realized a different conclusion. And there is no evidence that that wouldn’t happen again if an argument or data showed a flaw in an original position or research finding. In his response to my critique of his article, Dr. Finkelstein, a professor of management, goes on to further state, “The truth is, it’s hard to know what the best solution is in most areas of life and in companies. But having one best way – one only way – is dangerous whether practiced by governments, academics, or corporate leaders. And yes, the Paleo Police are no different.” The question begs, however, is this logic, which may work well regarding strategic leadership and management, appropriate for nutritional science? As researchers in the Paleolithic nutrition field, we are examining a potential optimal dietary template and if the research continues to support this template, when it comes to nutrition, there actually may be one best way or perhaps some slight variations based upon one best template. Time will obviously tell, however; in the meantime, it only makes sense to make formulations based upon the current data of published research.

So, in closing, I would like to throw out a challenge to the BDA. In addition to obviously becoming familiar with the published research on Paleolithic nutrition, I challenge them to choose and analyze 21 meals (7 breakfasts, 7 lunches and 7 dinners) from Dr. Cordain’s The Paleo Diet Cookbook. Then, having done so, defend their position that the Paleo Diet is “an unbalanced… sure-fire way to develop nutrient deficiencies, which can compromise health.” I am very confident that it will be an impossible task.

Dr. Mark J. Smith

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


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