Tag Archives: The Paleo Diet

Do you know what your blood pressure is? The American Heart Association (AHA) encourages everyone to know his or her key markers for heart health, which includes blood pressure. This has become increasingly important in the last few weeks as the American College of Cardiology (ACC) and the AHA, along with nine other health professional organizations and a panel of 21 scientists and health experts, have developed new blood pressure guidelines for the first time since 2003.

The new Blood pressure categories are as follows:

  • Normal: Less than 120/80 mm Hg;
  • Elevated: Systolic between 120-129 and diastolic less than 80;
  • Stage 1: Systolic between 130-139 or diastolic between 80-89;
  • Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg;
  • Hypertensive crisis: Systolic over 180 and/or diastolic over 120.

The top number of the measurement (systolic) indicates the amount of pressure against artery walls when the heart contracts, while the bottom number (diastolic) refers to the pressure when the heart is resting between beats.

The 2003 guidelines considered Stage 1 hypertension to be equal to or greater than 140/90, whereas now Stage 1 is measured as 130/80 or greater. Those who were previously diagnosed with pre-hypertension are now labeled as having elevated blood pressure.  This change will result in nearly half of the U.S. adult population (about 46 percent) having high blood pressure, with the greatest impact expected among younger people. Additionally, the prevalence of high blood pressure is expected to triple among men under age 45, and double among women under age 45, according to the guideline authors.

 

Why were the guidelines changed?

One reason for this change was that those who were previously diagnosed with pre-hypertension were at double the risk for a heart attack compared to someone with normal blood pressure. The new blood pressure classifications will allow clinicians to offer an earlier intervention, in the hopes of reducing the risks for cardiac events.

The new guidelines remind us that high blood pressure, in general, is not something we should ignore. It’s a major risk factor for heart disease, second perhaps only to smoking. However, most people with high blood pressure don’t even know they have it. The guidelines aim to aid in not only the prevention, but also in the early treatment of hypertension, in order to overcome this public health challenge.

Despite the alarming number of people who will now be labeled hypertensive, almost none of the newly labeled hypertensive people (those with systolic blood pressure between 130 and 140) should be placed on medications., Fortunately, most doctors will consider advising lifestyle changes, especially a low sodium diet and adequate exercise.

The Paleo Diet would be a more logical approach than a low sodium version of the modern diet for anyone seeking to lower high blood pressure or to maintain a healthy blood pressure.

 

Benefits of The Paleo Diet for Healthy Blood Pressure

Although The Paleo Diet is naturally low in sodium, it offers further benefits to achieving a healthy blood pressure. The Paleo Diet is higher in potassium, which has been linked to lower blood pressures. Potassium is also believed to have protective cardiovascular benefits that may be one factor contributing to the rarity of elevated blood pressures among huntergatherer populations.  Swiss chard, spinach, and avocados are examples of potassium rich foods.

The Paleo Diet consists of whole, unprocessed foods and is naturally low in sugar. The rise of modern disease can be linked to the evolution of the modern diet, consisting of heavily processed foods., In addition to the added sodium, processed foods are also preserved and their flavor is enhanced through the addition of refined sugar.  These added sugars, for which there are at least 56 different names , have also been linked to an increase in hypertension. ,    

We encourage you to know your blood pressure number and to follow The Paleo Diet for heart health.

 


References

1. “Understanding Blood Pressure Readings.” American Heart Association, November 2017, http://www.heart.org/HEARTORG/Conditions/HighBloodPressure/KnowYourNumbers/Understanding-Blood-Pressure-Readings_UCM_301764_Article.jsp#.Wk02OVQ-fOQ .

2. Whelton, Paul K., et al. “2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.” Journal of the American College of Cardiology (2017): 24430.

3. Chobanian, Aram V., et al. “The seventh report of the joint national committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report.” Jama289.19 (2003): 2560-2571.

4. Stamler, Jeremiah, Rose Stamler, and James D. Neaton. “Blood pressure, systolic and diastolic, and cardiovascular risks: US population data.” Archives of internal medicine 153.5 (1993): 598-615.

5. Whelton, Paul K., et al. “2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.” Journal of the American College of Cardiology (2017): 24430.

6. Whelton, Paul K., et al. “2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines.” Journal of the American College of Cardiology (2017): 24430.

7.  Collins, Rory, et al. “Blood pressure, stroke, and coronary heart disease: part 2, short-term reductions in blood pressure: overview of randomised drug trials in their epidemiological context.” The Lancet 335.8693 (1990): 827-838.

8. Go, Alan S., et al. “An effective approach to high blood pressure control: a science advisory from the American Heart Association, the American College of Cardiology, and the Centers for Disease Control and Prevention.” Hypertension63.4 (2014): 878-885.

9. Oliveria, Susan A., et al. “Hypertension knowledge, awareness, and attitudes in a hypertensive population.” Journal of general internal medicine 20.3 (2005): 219-225.

10. Appel LJ, Champagne CM, Harsha DW, et al. Effects of comprehensive lifestyle modification on blood pressure control: main results of the PREMIER clinical trial. JAMA. 2003;289:2083-93.

11. Diao, Diana, et al. “Pharmacotherapy for mild hypertension.” Sao Paulo Medical Journal 130.6 (2012): 417-418.

12. Jönsson, Tommy, et al. “Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study.” Cardiovascular diabetology 8.1 (2009): 35.

13. 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 Feb;81(2):341-54

14. Frassetto, Lynda A., et al. “Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet.” European journal of clinical nutrition 63.8 (2009): 947-955.

15. Cordain, Loren, et al. “Origins and evolution of the Western diet: health implications for the 21st century.” The American journal of clinical nutrition 81.2 (2005): 341-354.

16. Lanham-New, Susan A. “The balance of bone health: tipping the scales in favor of potassium-rich, bicarbonate-rich foods.” The Journal of nutrition 138.1 (2008): 172S-177S.

17. 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 Feb;81(2):341-54

18. Monteiro, Carlos Augusto, et al. “Increasing consumption of ultra-processed foods and likely impact on human health: evidence from Brazil.” Public health nutrition 14.1 (2010): 5-13.

19. Lustig, Robert H., Laura A. Schmidt, and Claire D. Brindis. “Public health: the toxic truth about sugar.” Nature 482.7383 (2012): 27-29.

20.  “The 56 Different Names for Sugar (Some Are Tricky)” June 3, 2017, https://www.healthline.com/nutrition/56-different-names-for-sugar .

21. Johnson, Richard J., et al. “Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease.” The American journal of clinical nutrition 86.4 (2007): 899-906.

22. Chen, Liwei, et al. “Reducing consumption of sugar-sweetened beverages is associated with reduced blood pressure: a prospective study among United States adults.” Circulation 121.22 (2010): 2398-2406.

 

 

 

The Paleo Diet is not anything new. It has been around for centuries. At its core, The Paleo Diet takes food back to its roots, sometimes literally. Whole foods, lean protein, organic and non-GMO foods are the basis of a paleo diet.

Going Paleo is a choice that will positively affect your entire life. By eliminating excess sugars, added preservatives, and processed foods, your diet is filled with nutrient- and mineral-rich sustenance.

But with all the research available on print and online, there are still many questions that sceptics of The Paleo Diet have. Here is a list of some of the most frequently asked questions and answers to help you understand The Paleo Diet.

References:

1. Eaton, S. B., L. Cordain and S. Lindeberg. Evolutionary Health Promotion: A Consideration of Common Counterarguments. Preventive Medicine. 2001. 34: 119-23.
2. Pinheiro, M. M., T. Wilson. Dietary Fat: The Good, the Bad, and the Ugly. Nutrition Guide for Physicians and Related Healthcare Professionals. 2017. 241-47.
3. Bernstein, A. M., et al., A Home-Based Nutrition Intervention to Increase Consumption of Fruits, Vegetables, and Calcium-Rich Foods in Community Dwelling Elders. Journal of the American Dietetic Association. 2002. 102(10): 1421-1427.
4. Hou, K. J., D. Lee, J. Lewis. Diet and Inflammatory Bowel Disease: Review of Patient-Targeted Recommendations. Clin Gastroenterol Hepatol. 2014. 12(10): 1592-1600.
5. Cordain, L. AARP The Paleo Answer: 7 Days to Lose Weight, Feel Great, Stay Young. 2012.
6. Masharani, U., et al. Metabolic and Physiologic Effects From Consuming a Hunter-Gatherer (Paleolithic)-Type Diet in Type 2 Diabetes. Eur J Clin Nutr. 2015. 69(8) 944-8.
7. Cordain, L., The Nutritional Characteristics of a Contemporary Diet Based Upon Paleolithic Food Groups. 2002. Jana 5(3): 15-24).
8. Poterba, M. J., S. F. Venti, D. A. Wise. The Asset Cost of Poor Health. The Journal of the Economics of Ageing. 2017. 9:172-84.
9. //thepaleodiet.com/bill-nye-science-guy. Accessed September 10, 2017.
10. //thepaleodiet.com/dr-cordain-responds-to-critics-of-a-recent-paleo-diet-study. Accessed September 10, 2017.

What is the Paleo Diet? That was my initial reaction to the term “The Paleo Diet” when I started working out at a CrossFit gym 10 years ago. A fellow gym member gave me a quick synopsis
of what it entailed, which was enough to get me intrigued. Going grain-free specifically, seemed to be just what I needed to improve my health.

Food was a huge part of my childhood. My father’s side of the family is Italian and we would all gather on Sunday for a feast starting with morning pastries, continuing to big plates of pasta
with bread, and ending with homemade pies and cookies. At home, our pantry was filled with sugar cereals, every imaginable type of packaged cookie, and a freezer full of microwaveable TV
dinners. My father owned and operated a Burger King, which we would get to eat every Friday night. Homemade dinner was whatever could be pulled together quickly, from a box, with the
occasional can of corn or green beans on the side. My mother likes to joke about when I was six, I asked if we could have a “normal” dinner like other families who ate fresh vegetables.

I was sick throughout my childhood. Starting with chronic ear infections as a baby, and graduating to chronic tonsillitis and strep throat during elementary school. I would be
prescribed antibiotics and about two weeks later would develop another infection. The solution was to have my tonsils removed. This certainly resolved the tonsillitis, but then lead to chronic
sinus infections throughout my teen years. Beginning when I was a teenager, I inherently knew that food was related to our health. However, I was operating on the paradigm of whole grains being the foundation.

I dabbled in various ways of eating through my 20’s, which could be described as low-fat, vegan-friendly, and then flexitarian – all aiming to follow the nutrition guidelines set forth by the
government. My grocery cart was filled with low sodium soups labeled healthy, and low-sugar wheat-based cereals, rounded out with whole grain breads. Once when I was living in Brooklyn,
after evaluating my purchases, the grocery cashier asked me if I was on a diet. I answered, “No, I just follow a healthy diet.”

Despite my attempts to eat nutritiously, I did not feel great. I had a bunch of symptoms, such as hypoglycemia, debilitating stomach pain, dizziness- sometimes leading to fainting, and
numbness and tingling in my limbs. Over the course of a few years, I endured a battery of tests from a variety of doctors, but no cause could be determined. And no solution for improvement
was suggested. Finally, in 2006 I learned about food sensitivities from my naturopath and I went on a strict protocol free of gluten, dairy, nightshades, eggs, and a host of other foods to
which a blood test revealed I was reacting to.

By eliminating these offenders from my diet, my energy and symptoms improved. However, I was disappointed to find out after six months of new eating habits my subsequent blood test
revealed I was reacting to the alternative grains I had been substituting for gluten. I took various supplements to support my digestion and continued my gluten-free diet thinking it was
the only thing I could do until I discovered the Paleo Diet about a year later.

It all began to make sense. Our modern diet, even when free of gluten and dairy (and with the use digestive supplements) doesn’t work with how our bodies run most efficiently. I’ve
embraced the Paleo Diet as a lifestyle and also as the nutritional foundation on which I am raising my daughter, who is seven.

I haven’t been completely disease free in the past decade. My pregnancy most likely triggered a reactivation of the Epstein-Barr virus (EBV) [1] that had been latent and lurking in my body. EBV is
the virus that usually causes the symptoms of mononucleosis [2]. Approximately 95 percent of people between the ages of 35 and 40 carry an inactive form of this infection [3]. Many of those
infected with mono never even develop symptoms upon initial infection– I was one of them. It is considered very rare to develop chronic EBV, which is diagnosable by blood test [4], and many doctors brush it off as an inconsequential illness. Although, I would argue it can be severely debilitating and has a negative impact on quality of life.

EBV is known to damage mitochondria [5], the powerhouses of the body where energy [6], ATP is produced [7]. Fatigue is often the initial and major symptom when the virus is active. I had chalked my fatigue up to pregnancy and then the demands of motherhood. I also began to get sick all time, with a chronic sore throat, runny nose, leading to a lingering cough that would last for
over six weeks. I would get better and then two weeks later the cycle would start again, similar to the pattern I had as a child. Fortunately, over the past few years my immune system has
gotten the upper hand, and although the EBV will never go away, the Paleo Diet has been the core of how I manage it.

References

1 Fleisher, Gary, and Ronald Bolognese. “Persistent Epstein-Barr virus infection and pregnancy.” Journal of Infectious Diseases 147.6 (1983): 982-986.
2 Sumaya, Ciro Valent, and Yasmin Ench. “Epstein-Barr virus infectious mononucleosis in children.” Pediatrics 75.6 (1985): 1011-1019.
3 Schooley, R. T. “Epstein-Barr virus.” Current Opinion in Infectious Diseases 2.2 (1989): 267-271.
4 Okano, Motohiko, et al. “Proposed guidelines for diagnosing chronic active Epstein‐Barr virus infection.” American journal of hematology 80.1 (2005): 64-69.
5 Vernon, Suzanne D., et al. "Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr virus." BMC infectious diseases 6.1 (2006): 15.
6 Goldschmidt, Vivian. “What Are Mitochondria?.”
7 Myhill, Sarah, Norman E. Booth, and John McLaren-Howard. “Chronic fatigue syndrome and mitochondrial dysfunction.” International journal of clinical and experimental medicine 2.1 (2009)

I was recently interviewed by a reporter representing “The Academy of Nutrition and Dietetics” which was formerly known as “The American Dietetic Association (ADA)” http://www.eatright.org/.

This organization certifies registered dietitian nutritionists in the United States. University level nutrition students must have met academic and professional requirements including an earned bachelor’s degree with coursework approved by the Academy of Nutrition and Dietetics’ Accreditation Council for Education in Nutrition and Dietetics (ACEND).  

The official magazine of The Academy of Nutrition and Dietetics, is called “Food and Nutrition” https://foodandnutrition.org/ which reaches a readership of approximately 40,000 Registered Dieticians. Unfortunately, due to the length of my interview, the interview was not published in “Food and Nutrition” magazine.  Below is that interview in its entirety.

 

Dr. Cordain responds to the reporter’s questions:

Obviously, your questions are good ones and are of interest to the Registered Dietitian (RD) Community and to all people concerned about diet/health and well-being.   

I have written extensively about the “Paleo Diet” concept in high quality, peer-reviewed nutritional and medical journals including: The American Journal of Clinical Nutrition, The British Journal of Nutrition, The European Journal of Clinical Nutrition, The World Review of Nutrition and Dietetics, The Journal of Applied Physiology, Acta Opthalmolgica, The Archives of Dermatology, The Scandinavian Journal of Clinical Laboratory Investigation, Mayo Clinic Proceedings, Preventive Medicine, Nutrition and Metabolism, Proceedings of the National Academy of Sciences, Open Heart (1-39) and many other high impact factor, peer-reviewed journals.  Reprints of all of my scientific papers are available as free PDF downloads at my website: www.thepaleodiet.com.   

Additionally, I have written six popular books and cookbooks on The Paleo Diet Concept including: The New York Times Bestseller, The Paleo Diet, (2002, revised 2010) (1), The Paleo Diets for Athletes (2005, revised 2012 and co-authored with Joe Friel) (41), The Paleo Diet Cookbook (2011) (42), The Paleo Answer (2012) (43), The Real Paleo Diet Cookbook (2015) (44), and Real Paleo Fast and Easy (2016) (45).

 

Questions

What are the advantages of following a Paleo Diet?
As I originally conceived this way of eating in 2002 in The Paleo Diet (1), my intent was to mimic the food groups that our pre-agricultural ancestors ate by using contemporary foods (fresh fruits, fresh vegetables, fish, shellfish, grass produced meats, organ meats and poultry, freeranging eggs, nuts and certain healthful oils) commonly available at supermarkets.  As I have pointed out in all of my writings, clearly it would be impractical or impossible for modern people to only eat wild plant and animal foods.  Built into this diet was a behavioral crutch (the 85:15 rule) (1) which allowed people to occasionally “cheat” (1, 6, 41-45) but still obtain most of the nutritional and health advantages (1-3, 5, 8-31, 33, 35-39) of The Paleo Diet.

The nutritional advantages of following a diet comprised mainly of fresh fruits, fresh vegetables, fish, shellfish, grass produced meats and organ meats, freeranging poultry, freeranging eggs, nuts and certain healthful oils are readily apparent to any registered dietitian who has access to nutritional software.  I use Nutritionist Pro (http://www.nutritionistpro.com/) to analyze the nutritional characteristics of contemporary diets based upon ancestral food groups (16, 23).

The typical plant to animal food subsistence ratio in hunter gatherer diets ranges from about 35 to 45 percent plant food with the balance from animal food (2, 16, 23, 31).  Accordingly, when a modern, westernized person emulates the food groups in ancestral diets with contemporary foods, the diet becomes exceedingly rich in fresh fruits and vegetables (16, 23).  A recent (2017) report (40) from the Centers for Disease Control and Prevention (CDC) showed that just 12 percent of Americans eat the minimum daily fruit recommendation (1 ½ – 2 cups/day), and only nine percent of Americans consume the minimum daily vegetable recommendation (2-3 cups/day).  Hence, adoption of The Paleo Diet represents one of the best strategies to enrich the American diet with healthful fresh fruits and vegetables (1, 16, 23, 41-45).   

The Paleo Diet avoids or eliminates processed foods containing refined sugars, refined grains, refined vegetable oils, trans fatty acids, salt and added chemicals.  Because fresh fruits, fresh vegetables and nuts are consumed ad libitum as the carbohydrate source in lieu of refined sugars, refined grains and processed foods, The Paleo Diet is a low glycemic load diet (1, 16, 23) which promotes normalization of blood glucose, insulin and improvement in type 2 diabetes and the metabolic syndrome (46-55).

The Paleolithic diet is a lowsalt diet because it avoids or eliminates the highest salt sources in the American diet (bread, baked goods, cheese, processed meats, sandwiches, pizza, tacos, chips, condiments, etc.), and replaces these processed foods with unsalted, unadulterated fresh foods (fresh fruits, fresh vegetables, fish, shellfish, grass produced meats and organ meats, freeranging poultry, freeranging eggs, nuts and certain healthful oils).  The average U.S. diet (per day) contains 3,584 mg of sodium (Na+) and 2795 mg of potassium (K+) yielding a K+/Na+ ratio of 0.77 (56).   Few natural, unsalted foods maintain K+/Na+ ratios less than 1.00.  In fact, the K+/Na+ ratio in contemporary Paleo Diets ranges from 5.0 to 10.0 (16, 23, 30, 57, 58).  The high average U.S. daily sodium intake (3,584 mg) and low potassium intake (2795 mg) increases the risk for hypertension, stroke, cardiovascular disease (CVD) and gastric cancer.  By adopting a contemporary Paleo Diet, people will reduce their salt intake, increase their potassium intake (1, 41- 45) and reduce their risk for CVD, high blood pressure, stroke and stomach cancer.

In vivo (in the body) all foods are either net acid producing, netbase producing or neutral (59). The typical American diet is net acid producing because it contains high amounts of acid yielding cereal grains, salt, cheese, processed meats, processed foods and condiments (23, 57, 58), and low amounts of base yielding fruits and vegetables (40).  A net acid yielding diet increases the risk for osteoporosis, kidney stones, stroke and hypertension (1, 43, 57) whereas a net alkaline yielding diet, high in fresh fruits and vegetables reduces the risk for these diseases (60-62).  Hence, adoption of the contemporary Paleo Diet will result in a net base yielding diet and lessen the risk for osteoporosis, kidney stones, stroke and hypertension (1, 16, 23, 41-45).


What are the nutritional advantages of avoiding foods like dairy and legumes?
From an evolutionary perspective, the majority (65 to 70 percent) of the world’s adults are lactose intolerant (63, 64) and cannot drink milk without digestive discomfort because they lack the enzyme (lactase-phlorizin hydrolase) necessary to digest the sugar (lactose) present in the milk of mammals.  From an evolutionary perspective, this information indicates that milk and dairy products could not have been a component of the original adult diet that shaped the human genome until very recent times, (64).   

The human consumption of milk from a foreign species throughout our life is not without physiologic consequence, even if a person has inherited the gene (LCT) which codes for adult lactase persistence (64).  Fresh cow milk contains the full complement of enzymes and hormones that are present in cow blood (65).   

It had been assumed that these bioactive compounds in cow’s milk were degraded in the human gastrointestinal tract and that our immune systems ultimately prevented their entry into our bloodstreams.  Unfortunately, this model has been shown to be incorrect, as cow milk apparently elevates a key human hormone (IFG) known to affect insulin and glucose metabolism and promote various cancers (35, 66).  Other elements in cow’s milk are implicated in human cancer and disease including miRNAs (39) and stimulation of mTORC1-signaling (35).  Further, recent studies implicate prediabetes and type 2 diabetes with dairy intake in adults (67) and children (68).

Legumes (beans, lentils, peanuts etc.) contain high concentrations of various antinutrients including phytate, lectins, saponins, tannins and isoflavones, protease inhibitors, raffinose oligosaccharides, cyanogenetic glycosides and favism glycosides (43).  Without long term cooking or pressure cooking, these antinutrients remain active following ingestion by mammals and may disrupt gastrointestinal and immune function (43, 69, 70, 71).  Because of their antinutrient content, particularly phytates, legumes are low quality foods that are deficient in multiple nutrients (zinc, iron, magnesium, calcium) unavailable for human absorption (43, 71).  From an evolutionary perspective, until humanity was able to not only control fire, but to make fire at will (72), legumes would not have been a component of the diet that shaped our current genome until recent evolutionary times.

Why do you think there is such a strong following of this diet?
In this day and age of internet connectivity, people constantly correspond with their friends and neighbors about all things in their lives, including diet.  Like a loophole in tax laws, when they discover something that works, the information is passed along, and passed along and passed along again.   

The Paleo Diet works — it works to help people become healthier; to lower blood cholesterol levels, to lower blood pressure; to reduce body weight; to have more energy throughout the day; and to improve health and well-being.  This information has been substantiated in the scientific and medical literature for a decade (73-101)

Many athletes follow this diet and they do need carbs for fuel. What do you recommend for athletes in order to stay properly fueled?
All athletes do not compete in similar events.  The metabolic requirements of a sprinter, an 800 meter runner, a miler or a 5 or 10 K and marathon runner are completely different from a high jumper, a pole vaulter or a shot putter.  These athletes compete in events which have metabolic requirements that frequently overlap with team sports including soccer, basketball, football, baseball and tennis.  Hence it is unfair to suggest that all athletes need carbs for fuel at all times.

Endurance athletes who have previously trained their beta oxidation (fat) metabolic pathways have been shown to outperform athletes who solely utilize high carb diets (102).

Coconut and cauliflower are two very popular Paleo foods, but aren’t necessarily connected to the Paleolithic era. How do those connect within the Paleo diet? Are they healthy choices in the Paleo diet?
Hmm.  I disagree with you that coconut would not have been consumed by Paleolithic people (> 10,000 years ago).  The archaeological evidence shows that our Paleolithic ancestors occupied coastal areas in Africa and Asia where coconut trees grew.  There is no evidence to suggest otherwise that this plant food was exploited from the earliest of times.

Cauliflower on the other hand is a recent genetic permutation from broccoli which is a recent permutation from cabbage.  These three plants (cauliflower, broccoli, cabbage) have similar nutritional characteristics which differ little from their inherent genetic species.  Additionally, I never proclaimed that modern, domesticated versions of wild plant and animal foods should not be regular components of contemporary Paleo Diets.

Anything else you would like to relay to dietetic professionals?
Always let the data speak for itself, and do not permit charismatic individuals or political organizations to interpret the data outside of scientific norms.


How would you like to be quoted?
Always let the data speak for itself.

 

References:

1.Cordain L.  The Paleo Diet, John Wiley & Sons, New York, NY, 2002 (revised 2010).

2.Cordain L, Brand Miller J, Eaton SB, Mann N, Holt SHA, Speth JD.  Plant to animal subsistence ratios and macronutrient energy estimations in world wide hunter-gatherer diets.  American Journal of Clinical Nutrition,  2000, 71:682-92.

3.Cordain L. (1999). Cereal grains: humanity’s double edged sword.  World Review of Nutrition and Dietetics, 84: 19-73.

4.Cordain L, Miller J, Mann N. (1999).  Scant evidence of periodic starvation among hunter-gatherers (letter). Diabetologia, 42: 383-84.

5.Mickleborough TD, Cordain L, Gotshall RW, Tucker A. A low sodium diet improves indices of pulmonary function in exercise-induced asthma. Journal of  Exercise Physiology Online 2000;3(2): http://www.css.edu/users/tboone2/asep/April2000.html

6.Cordain L, Melby CL, Hamamoto AE, O’Neill S, Cornier M, Barakat HA, Israel RG, Hill JO.  Influence of moderate chronic wine consumption on insulin sensitivity and other correlates of syndrome X in moderately obese women. Metabolism 2000;49:1473-78.

7.Gotshall RW, Mickleborough TD, Cordain L. Dietary salt restriction alters pulmonary function in exercise-induced asthmatics. Medicine and Science in Sports and Exercise, 2000;32:1815-19.

8.Cordain L, Watkins BA, Mann NJ. Fatty acid composition and energy density of foods available to African hominids: evolutionary implications for human brain development. World Review of Nutrition and Dietetics, 2001, 90:144-161.

9.Mickleborough TD, Gotshall RW, Rhodes J, Tucker A, Cordain L.  Elevating dietary salt exacerbates leukotrienes-dependent hyperpnea-induced airway obstruction in guinea pigs. J Appl Physiol 2001, 91:1061-66.

10.Mickleborough TD, Gotshall RW, Kluka E, Miller CW, Cordain L.  Dietary chloride as a possible determinant of the severity of exercise-induced asthma.  Eur J Appl  Physiol 2001;85:450-56.

11.Eaton SB, Strassman BI, Nesse RM, Neel JV, Ewald PW, Williams GC, Weder AB, Eaton SB 3rd, Lindeberg S, Konner MJ, Mysterud I, Cordain L.  Evolutionary health promotion. Prev Med 2002;34:109-118.

12.Eaton SB,  Cordain L.  Evolutionary Health Promotion. A consideration of common counter-arguments. Prev Med 2002;34:119-123.

13.Cordain L, Watkins BA, Florant GL, Kehler M, Rogers L, Li Y.  Fatty acid analysis of wild ruminant tissues: Evolutionary implications for reducing diet-related chronic disease. Eur J Clin Nutr, 2002;56:181-191.

14.Cordain L, Eaton SB, Brand Miller J, Mann N, Hill K.  The paradoxical nature of hunter-gatherer diets: Meat based, yet non-atherogenic. Eur J Clin Nutr 2002;56 (suppl 1):S42-S52.

15.Cordain L,  Eaton SB, Brand Miller J, Lindeberg S, Jensen C.  An evolutionary analysis of the etiology and pathogenesis of juvenile-onset myopia. Acta Opthalmolgica, 2002,80:125-135.

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

17.Cordain L, Lindeberg S, Hurtado M, Hill K, Eaton SB, Brand-Miller J. (2002). Acne vulgaris: A disease of civilization.  Archives of Dermatology,138: 1584-90.

18.Cordain L, Eades MR, Eades MD. (2003).  Hyperinsulinemic diseases of civilization: more than just syndrome X.  Comp Biochem Physiol Part A:136:95-112.

19.Lindeberg S, Ahren B, Cordain L, Nilsson-Ehle P, Vessby B, Nilsson A.  Determinants of serum triglycerides and high-density lipoprotein cholesterol in traditional Trobriand Islanders – the Kitava Study. Scand J Clin Lab Invest 2003;63:175-180.

20.Lindeberg S, Cordain L, Eaton B.  Biological and clinical potential of a Palaeolithic diet. J Nutr Environ Med 2003;13:149-160.

21.O’Keefe J.H., Cordain L.  Cardiovascular disease as a result of a diet and lifestyle at odds with our Paleolithic genome: how to become a 21st century hunter-gatherer. Mayo Clin Proc 2004;79:101-108.

22.Lindeberg S, Ahren B, Cordain L, Rastam L.  Serum uric acid in traditional Pacific Islanders and in Sweden. J Intern Med 2004; 255:373-378.

23.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.

24.Hoyt G, Hickey MS, Cordain L. Dissociation of the glycaemic and insulinaemic responses to whole and skimmed milk. Br J Nutr 2005;93:175-177.

25.Cordain, L. Implications for the role of diet in acne. Semin Cutan Med Surg 2005;24:84-91.

26.Cordain L., Hickey MS. Ultraviolet radiation represents an evolutionary selective pressure for the south-to-north gradient of the MTHFR 677TT genotype. Am J Clin Nutr 2006;84:1243.

27.Treloar V, Logan AC, Danby FW, Cordain L, Mann NJ. Comment on acne and glycemic index. J Am Acad Dermatol. 2008 Jan;58(1):175-7.

28.Ramsden CE, Faurot KR, Carrera-Bastos, P, Sperling LS, de Lorgeril M, Cordain L. Dietary fat quality and coronary heart disease  prevention: a unified theory based on evolutionary, historical, global and modern perspectives. Curr Treat Options Cardiovasc Med; 2009;11:289-301.

29.Eaton SB, Cordain L, Sparling PB, Cantwell JD.  Evolution, body composition and insulin resistance. Preventive Medicine,  2009;49:283-285.

30.Eaton SB, Konner MJ, Cordain L.  Diet-dependent acid load, Paleolithic nutrition, and evolutionary health promotion. Am J Clin Nutr 2010;91:295-97.

31.Remko S. Kuipers1, Martine F. Luxwolda1, D.A. Janneke Dijck-Brouwer1, S. Boyd Eaton, Michael A. Crawford, Cordain L, and Frits A.J. Muskiet.  Estimated macronutrient and fatty acid intakes from an East African Paleolithic diet.  Brit J Nutr , 2010 Dec;104(11):1666-87.

32.O’Keefe JH, Vogel R,  Lavie CJ, Cordain L.  Organic Fitness: Physical Activity Patterns Compatible with our Hunter Gatherer Genetic Legacy.  Physician and Sports Medicine 2010, 38 (4):11-18.   

33.Carrera-Bastos P, Fontes Villalba M, O’Keefe JH, Lindeberg S, Cordain L. The western diet and lifestyle and diseases of civilization. Res Rep Clin Cardiol 2011; 2: 215-235.

34.O’Keefe JH, Vogel R, Lavie CJ, Cordain L. Exercise Like a Hunter Gatherer: A Prescription for Organic Physical Fitness.  Prog Cardiovasc Dis. 2011;53:471-9.

35.Melnik BC, John SM, Carrera-Bastos P, Cordain L. The impact of cow’s milk-mediated mTORC1-signaling in the initiation and progression of prostate cancer. Nutr Metab (Lond). 2012 Aug 14;9(1):74. doi: 10.1186/1743-7075-9-74

36.Fontes-Villalba M, Carrera-Bastos P, Cordain L. African hominin stable isotopic data do not necessarily indicate grass consumption. Proc Natl Acad Sci U S A. 2013 Oct 22;110(43):E4055. doi: 10.1073/pnas.1311461110. Epub 2013 Sep 23.

37.Melnik BC, Schmitz G, John S, Carrera-Bastos P, Lindeberg S, Cordain L. Metabolic effects of milk protein intake strongly depend on pre-existing metabolic and exercise status. Nutr Metab (Lond). 2013 Oct 2;10(1):60. doi: 10.1186/1743-7075-10-60.

38.O’Keefe JH, Bergman N, Carrera-Bastos 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 Mar 22;3(1):e000325. doi: 10.1136/openhrt-2015-000325. eCollection 2016. Review.

39.Melnik BC, Kakulas F, Geddes DT, Hartmann PE, John SM, Carrera-Bastos P, Cordain L, Schmitz G. Milk miRNAs: simple nutrients or systemic functional regulators? Nutr Metab (Lond). 2016 Jun 21;13:42. doi: 10.1186/s12986-016-0101-2. eCollection 2016.

40.Lee-Kwan SH, Moore LV, Blanck HM, Harris DM, Galuska D. Disparities in State-Specific Adult Fruit and Vegetable Consumption — United States, 2015. MMWR Morb Mortal Wkly Rep 2017;66:1241–1247. DOI: http://dx.doi.org/10.15585/mmwr.mm6645a1

41.Cordain L, Friel J. The Paleo Diets for Athletes (2005, revised 2012), Rodale Inc., New York, NY.  

42.Cordain L, Stephenson N, Cordain L. The Paleo Diet Cookbook (2011), John Wiley & Sons, New York, NY

43.Cordain L. The Paleo Answer (2012), John Wiley & Sons, New York, NY

44.Cordain L. The Real Paleo Diet Cookbook (2015), Houghton Mifflin Harcourt, New York, NY.

45.Cordain L. Real Paleo Fast and Easy (2016), Houghton Mifflin Harcourt, New York, NY

46.Lindeberg S, Jönsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjöström K, Ahrén 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.

47.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. Aug;63(8):947-55

  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 doi: 10.1186/1475-2840-8-35

49.Boers I, Muskiet FA, Berkelaar E, Schut 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.

50.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.   

51.Manheimer EW, van Zuuren EJ, Fedorowicz Z, Pijl H.  Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. Am J Clin Nutr. 2015 Oct;102(4):922-32.

52.Pastore RL, Brooks JT1, Carbone JW2. et al. 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.   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 Aug;69(8):944-8.

54.Fontes-Villalba M, Lindeberg S, Granfeldt Y, Knop FK, Memon AA, Carrera-Bastos P, Picazo Ó, Chanrai M, Sunquist J, Sundquist K, Jönsson T. Palaeolithic diet decreases fasting plasma leptin concentrations more than a diabetes diet in patients with type 2 diabetes: a randomised cross-over trial. Cardiovasc Diabetol. 2016 May 23;15(1):80. doi: 10.1186/s12933-016-0398-1.

55.Otten J, Stomby A, Waling M, Isaksson A, Tellström A, Lundin-Olsson L, Brage S, Ryberg M, Svensson M, Olsson T. Effects of a Paleolithic diet with and without supervised exercise on fat mass, insulin sensitivity, and glycemic control: a randomized controlled trial in individuals with type 2 diabetes. Diabetes Metab Res R ev. 2016 May 27. doi: 10.1002/dmrr.2828. [Epub ahead of print]

56.Bailey RL, Parker EA, Rhodes DG, Goldman JD, Clemens JC, Moshfegh AJ, Thuppal SV, Weaver CM. Estimating sodium and potassium intakes and their ratio in the american diet: data from the 2011-2012 NHANES. J Nutr. 2016 Mar 9. pii: jn221184. [Epub ahead of print]

57.Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A. Diet, evolution and aging–the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr. 2001 Oct;40(5):200-13

58.Sebastian A, Frassetto LA, Sellmeyer DE, Morris RC Jr. The evolution-informed optimal dietary potassium intake of human beings greatly exceeds current and recommended intakes. Semin Nephrol. 2006 Nov;26(6):447-53

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60.van Breda SGJ, de Kok TMCM. Smart Combinations of Bioactive Compounds in Fruits and Vegetables May Guide New Strategies for Personalized Prevention of Chronic Diseases. Mol Nutr Food Res. 2017 Nov 6. doi: 10.1002/mnfr.201700597. [Epub ahead of print]

  1. Rodriguez-Casado A. The Health Potential of Fruits and Vegetables Phytochemicals: Notable Examples. Crit Rev Food Sci Nutr. 2016 May 18;56(7):1097-107.

62.Liu RH. Health-promoting components of fruits and vegetables in the diet. Adv Nutr. 2013 May 1;4(3):384S-92S.

63.Bayless TM,, Brown E, Paige DM. Lactase Non-persistence and Lactose Intolerance. Curr Gastroenterol Rep. 2017 May;19(5):23. doi: 10.1007/s11894-017-0558-9.

64.Cordain L, Hickey MS, and Kim K. Malaria and Rickets Represent Selective Forces for the Convergent Evolution of Adult Lactase Persistence. In: Biodiversity in Agriculture: Domestication, Evolution, and Sustainability, edited by P. Gepts, T.R. Famula, R.L. Bettinger et al. Published by Cambridge University Press. # Cambridge University Press 2012, pp 299-

65.Koldovský O. Hormones in milk. Vitam Horm. 1995;50:77-149.

66.Harrison S, Lennon R, Holly J3 Higgins JPT et al., Does milk intake promote prostate cancer initiation or progression via effects on insulin-like growth factors (IGFs)? A systematic review and meta-analysis. Cancer Causes Control. 2017 Jun;28(6):497-528.  

67.Hruby A, Ma J, Rogers G, Meigs JB, Jacques PF.  Associations of dairy intake with incident prediabeses or diabetes in middle-aged adults vary by both dairy type and glycemic status. J Nutr, Aug 2017, doi: 10.3945/jn.117.253401.

68.C Hoppe C, Molgaard C, Juul A & K F Michaelsen. High intakes of skimmed milk, but not meat, increase serum IGF-I and IGFBP-3 in eight-year-old boys. European Journal of Clinical Nutrition (2004) 58, 1211–1216 (2004)

69.Carbonaro M, Grant G, Cappelloni M, Pusztai A. Perspectives into Factors Limiting in Vivo Digestion of Legume Proteins:  Antinutritional Compounds or Storage Proteins? J. Agric. Food Chem., 2000, 48 (3), pp 742–749

70.Grant G, Dorward PM, Buchan WC, Armour JC, Pusztai A. Consumption of diets containing raw soya beans (Glycine max), kidney beans (Phaseolus vulgaris), cowpeas (Vigna unguiculata) or lupin seeds (Lupinus angustifolius) by rats for up to 700 days: effects on body composition and organ weights. Br J Nutr. 1995 Jan;73(1):17-29

71.Pusztai A, Clarke EM, King TP, Stewart JC.  Nutritional evaluation of kidney beans (Phaseolus vulgaris): chemical composition, lectin content and nutritional value of selected cultivars. J Sci Food Agric. 1979 Sep;30(9):843-8

72.Cordain L. http://thepaleodiet.com/ancestral-fire-production-implications-contemporary-paleo-diets/

2007

  1.   Lindeberg S, Jönsson T, Granfeldt Y, Borgstrand E, Soffman J, Sjöström K, Ahrén 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.

2008

  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.

2009

  1.   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. Aug;63(8):947-55
  2.   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 doi: 10.1186/1475-2840-8-35

2010

  1.   Jonsson T, Granfeldt Y, Erlanson-Albertsson C, Ahrén 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 doi: 10.1186/1743-7075-7-85.

2013

  1.   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

79.Clemens Z, Kelemen A, Fogarasi A, Tóth C. Childhood absence epilepsy successfully treated with the paleolithic ketogenic diet. Neurol Ther. 2013 Sep 21;2(1-2):71-6. doi: 10.1007/s40120-013-0013-2. eCollection 2013.

2014

80.Toth C, et al.  Type 1 diabetes mellitus successfully managed with the Paleolithic ketogenic diet. Int J Case Pep Images. 2014 5(10):699-703.

  1. 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.  

82.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 May;39(5):814-9  

  1.   Boers I, Muskiet FA, Berkelaar E, Schut 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.
  2.   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
  3.   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. J Clin Lipid. 2014 May; 8(3): 341.
  4.   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.   
  5.   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.

2015  

  1.   Manheimer EW, van Zuuren EJ, Fedorowicz Z, Pijl H.  Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. Am J Clin Nutr. 2015 Oct;102(4):922-32.
  2.   Pastore RL, Brooks JT1, Carbone JW2. et al. 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.
  3.   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 Aug;69(8):944-8.
  4.   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.  

2016

92.Talreja D, Talreja A, Talreja S, Choi H, Talreja R An Investigation of Plant-based, Mediterranean, Paleolithic, and Dash Diets. J Am Coll Cardiol Intv. 2016;9(4_S):S61-S61.  doi:10.1016/j.jcin.2015.12.195

93.Whalen KA, McCullough ML, Flanders WD, Hartman TJ, Judd S, Bostick RM. Paleolithic and Mediterranean diet pattern scores are inversely associated with biomarkers of inflammation and oxidative balance in adults. J Nutr. 2016 Apr 20. pii: jn224048. [Epub ahead of print]

94.Fontes-Villalba M, Lindeberg S, Granfeldt Y, Knop FK, Memon AA, Carrera-Bastos P, Picazo Ó, Chanrai M, Sunquist J, Sundquist K, Jönsson T. Palaeolithic diet decreases fasting plasma leptin concentrations more than a diabetes diet in patients with type 2 diabetes: a randomised cross-over trial. Cardiovasc Diabetol. 2016 May 23;15(1):80. doi: 10.1186/s12933-016-0398-1.

95.Otten J, Stomby A, Waling M, Isaksson A, Tellström A, Lundin-Olsson L, Brage S, Ryberg M, Svensson M, Olsson T. Effects of a Paleolithic diet with and without supervised exercise on fat mass, insulin sensitivity, and glycemic control: a randomized controlled trial in individuals with type 2 diabetes. Diabetes Metab Res R ev. 2016 May 27. doi: 10.1002/dmrr.2828. [Epub ahead of print]

96.Dolan C, Carillo A, Davies N, Markofski M.  Effects of an 8-week Paleo dietary intervention on inflammatory cytokines. 2016 American Physiological Society Conference, Inflammation, Immunity and Cardiovascular Disease, Westminster, CO, August 24-27, 2016, Poster Session II, 10.4, pp 40-41.

2017

97.Whalen KA, Judd S, McCullough ML, Flanders WD, Hartman TJ, Bostick RM. Paleolithic and Mediterranean Diet Pattern Scores Are Inversely Associated with All-Cause and Cause-Specific Mortality in Adults. J Nutr. 2017 Feb 8;:jn241919.

98.Blomquist C, Alvehus M, Burén J, Ryberg M, Larsson C, Lindahl B, Mellberg C, Söderström I, Chorell E, Olsson T. Attenuated Low-Grade Inflammation Following Long-Term Dietary Intervention in Postmenopausal Women with Obesity. Obesity (Silver Spring). 2017 May;25(5):892-900

99.Afifi L, Danesh MJ, Lee KM, Beroukhim K, Farahnik B, Ahn RS, Yan D, Singh RK, Nakamura M, Koo J, Liao W. Dietary Behaviors in Psoriasis: Patient-Reported Outcomes from a U.S. National Survey. Dermatol Ther (Heidelb). 2017 Jun;7(2):227-242

100.Manousou S, Stål M, Larsson C, Mellberg C, Lindahl B, Eggertsen R, Hulthén L, Olsson T, Ryberg M, Sandberg S, Nyström HF, A Paleolithic-type diet results in iodine deficiency: a 2-year randomized trial in postmenopausal obese women. Eur J Clin Nutr. 2017 Sep 13. doi: 10.1038/ejcn.2017.134. [Epub ahead of print]

101.Lee JE, Bisht B, Hall MJ, Rubenstein LM, Louison R, Klein DT, Wahls TL. A Multimodal, Nonpharmacologic Intervention Improves Mood and Cognitive Function in People with Multiple Sclerosis. J Am Coll Nutr. 2017 Mar-Apr;36(3):150-168.  

102.Heatherly AJ, Killen LG, Smith AF, Waldman HS, Hollingsworth A, Seltmann CL, O’Neal EK. Effects of ad libitum Low Carbohydrate High-Fat Dieting in Middle-Age Male Runners. Med Sci Sports Exerc. 2017 Nov 6. doi: 10.1249/MSS.0000000000001477. [Epub ahead of print]

 

As a wee lad of 11 during the summer of 1962, I remember an adventure with my father in his bright red, 1953 Studebaker Commander as we drove from Carson City, Nevada to Highway 341(the Comstock Highway), then up the canyon past Silver City, past Gold Hill and eventually arriving at our destination, the old Virginia City, Nevada refuse dump.  We spent an entire Saturday morning there digging for antique bottles.

Father and son had a great day together.  We uncovered two spectacular bottles that I have kept in my possession to this day.  The first bottle was dazzling, emerald green in color, tall (8 ½ inches), slender and with eight fluted sides (Figure 1). My Dad informed me that this was a “capers bottle.”  As a young boy, I had absolutely no idea what “capers” were, or where they came from, or even how they were used.  I only knew that the beauty and artistry of this bottle attracted my attention.  Later in the morning Dad and I discovered yet another capers bottle (Figure 2), that was shorter (6 ½ inch), more squat with an applied glass lip and a beautiful aquamarine blue color. Pictured below are the two capers bottles my father and I uncovered at the Virginia City dump 55 years ago.  

 

Figure 1.  Emerald green antique
Figure 2. Aquamarine blue antique capers bottle
circa 1880-90, Virginia City, NV, July 1962

Years later, I eventually decided upon a career in academia involving exercise, health and nutrition.  I am now retired, but find myself writing about the very topic of capers, and the ~ 130 to 150-year-old capers bottles that my father and I had dug up in Virginia City, Nevada, 55 years ago.   

Today, it is obvious to me that the capers in these beautiful bottles dated to (~1870-1890) came from the pickled immature, flower bud of a plant (Capparis spinosa) which commonly grows as a wild weed in the Mediterranean and Middle Eastern regions of the world, as the map below indicates (Figure 3). Frequently, capers are planted and harvested as a commercial, agricultural plant (19).  

Figure 3. Map of the indigenous distribution of the caper plant (Capparis species) (19)

From a historical perspective, the two antique capers bottles that made their way to the Virginia City refuse dump in the late 19th century were most likely manufactured and stuffed with pickled capers harvested in either Spain, Italy or Greece.  How these beautiful capers bottles found their way to Virginia City, Nevada in the late 19th century is less clear.  Did they cross the Atlantic to New York City packed in crates from a transport ship, only to be put on horses or trains to San Francisco and finally to Virginia City?  Or did they round Cape Horn on ships and arrive in San Francisco to be later transported to Virginia City by horse or train?

It seems likely that imported European capers were a food item that few Virginia City residents in the late 19th century could afford.  Hence, the capers bottles that my father and I uncovered in the old Virginia City refuse dump probably came from restaurant discards used for certain dishes on their menus.

 

The Caper Bud as a Condiment

Most experienced cooks and chefs are familiar with capers, as are many home cooks who typically sprinkle this item on smoked salmon (24).  Figure 4 below.

Figure 4. Smoked salmon with pickled, bottled capers.

Veteran chefs use capers as a spice or condiment to flavor a wide variety of recipes including: [1] Classic chicken Piccata, [2] Herb crusted leg of lamb with mint Gremolata, [3] Quick broiled barramundi fillets with Puttanesca sauce, [4] Sautéed chicken with olives, capers and lemons, [5] Roasted vegetables with caper vinaigrette, [6] Italian salsa Verde, [7] Smoked salmon with horseradish caper sauce, [8] Watercress citrus salad with olive-caper vinaigrette, [9] Radicchio salad with toasted hazelnuts and capers, [10] and Asparagus with shallot-caper vinaigrette (18).

When the immature caper flower bud is harvested from the bush, it is done according to the bud’s size.  The smallest sizes, up to 7-8 mm in diameter are referred to as, “non-pareil” and are considered to be the most desirable (24, 27).  Larger sizes including, capucines (8-9 mm), capotes ((9-11 mm), fines (11-13 mm), and grusas (14 + mm) are not as valued.  If the immature caper bud is not picked as it grows, its flowers produce a caper berry which is then pickled and served as a garnish for martinis or other drinks (26).

Caper plants and their various components (buds, mature flowers, leaves, seeds and roots) are a rich source of polyphenolics and antioxidants (11, 14, 16, 17, 20, 21).  Table 1 below demonstrates that pickled capers are the sixth most concentrated source of food antioxidants and the eighteenth richest food source of polyphenolics.  All food polyphenols are characterized by phenolic chemical structures which can deactivate reactive oxygen species (ROS) that may potentially damage our cells structure and function.  Accordingly, food polyphenolics with their associated antioxidant capacity are known to play a key role in the prevention of chronic disease including cancer, type 2 diabetes, heart disease, neurodegenerative diseases and osteoporosis (14, 28).

Specifically, fresh or dried caper (Capparis spinosa) parts (leaves, flower buds, mature flowers, seeds, roots, thorns and twigs) and their alcoholic extracts have been shown to have potent anti-inflammatory and inhibitive effects in both tissue (8, 15, 20, 23) and animal models of various diseases that are attributed to their high polyphenolic content (5, 6, 12, 13, 14, 20, 23, 25).  Additionally, caper plants contain other important bioactive compounds including glucosinolates, alkaloids, flavonoids, anthocyanins, lipids, vitamins and minerals known to have favorable health effects (1-4, 7, 9-10, 22).

Unfortunately, with virtually all of these studies, none of them employed the capers product eaten by real people (pickled capers, from bottles).  Rather, scientists tested the isolated, alcoholic extract of fresh caper parts: leaves, roots, flower buds or berries (5, 6, 8, 12, 13, 14, 15, 20, 23, 25).   Almost all people worldwide universally eat capers tainted with salt and vinegar from the pickling process, and rarely or never have the opportunity to eat fresh caper parts.   

 

Table 1.  The top 20 richest food sources of polyphenolics and antioxidants (17).

The Nutritional Downside of Capers

Capers are rarely or never consumed fresh (24, 26), apparently because when eaten raw they are considered “unpalatably bitter, but once cured in a vinegar brine or in salt, they develop an intense flavor that is all at once salty, sour, herbal, and slightly medicinal (27).” Capers are cured in one of three ways: [1] in a salt water brine with vinegar [the most common procedure], [2] in salt water brine only, or [3] with salt only.  The last method is costlier and available only in specialty stores in the U.S. (26).

Both wild and cultivated caper plants grow widely in the Mediterranean and Middle Eastern regions after the first rains of spring (April-May) and start disappearing during the beginning of cold weather (September-October) (19).  Hence, fresh caper buds are available to harvest seasonally for about 6 months in their indigenous geographic range.  Apparently, Mediterranean and Middle Eastern people reject fresh capers similar to raw olives and only consume them in their processed, salted state (24).  

Because capers are universally processed with salt, on a calorie by calorie basis, capers represent an incredibly high source of dietary sodium (Na+) compared to their potassium (K+) concentration.  Table 2 below lists the nutrients in processed capers.  Notice that just 23 kilocalories of capers contain an enormous amount of sodium (2,964 mg) that exceeds the recommended daily sodium intake of 2,300 mg (30) by 24 %.  To put this figure into proper perspective, 23 kilocalories of capers represents just 1/100 of our normal daily caloric intake.  Hence, if you were to eat pickled capers as your only daily food, you would consume a staggering amount (296,400 mg) of sodium.  The ratio of potassium to sodium (K+/Na+) in pickled capers is 0.01 whereas in fresh vegetables this ratio averages 46.68 (31) and in fresh fruit it averages 387.07 (31).  The average U.S. diet (per day) contains 3,584 mg of sodium (Na+) and 2795 mg of potassium (K+) yielding a K+/Na+ ratio of 0.77 (32).  In contemporary Paleo diets that mimic the nutritional characteristics of our ancestors, regular dietary K+/Na+ ratios of less than 1.00 are virtually impossible and in fact range from ~ 5.0 to ~ 10.0 (31, 33-35).

 

Table 2.  The nutrient values present in capers (29).

The consequence of a lifetime diet with a K+/Na+ ratios of less than 1.00 increases the risk of high blood pressure, stroke and cardiovascular disease (30, 36-38), increases the risk for autoimmune disease (39-42), increases the risk for immune dysfunction (43-48) and increases risk for cancer (49-55).

 

Conclusions   

When capers are eaten raw, they are considered “unpalatably bitter, but once cured in a vinegar brine or in salt, they develop an intense flavor that is all at once salty, sour, herbal, and slightly medicinal.”  (27).  The pickling of capers with salt, brine and vinegar transforms a once healthy, natural food that may reduce the risk for chronic disease into a highsalt food that increases the risk of developing cardiovascular disease, autoimmune disease, immune dysfunction and cancer.

 

References

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13.Mohebali N, Shahzadeh Fazeli SA, Ghafoori H, Farahmand Z, MohammadKhani E, Vakhshiteh F, Ghamarian A, Farhangniya M, Sanati MH . Effect of flavonoids rich extract of Capparis spinosa on inflammatory involved genes in amyloid-beta peptide injected rat model of Alzheimer’s disease. Nutr Neurosci. 2016 Oct 25:1-8.  

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20.Tlili N, Feriani A, Saadoui E, Nasri N, Khaldi A. Capparis spinosa leaves extract: Source of bioantioxidants with nephroprotective and hepatoprotective effects. Biomed Pharmacother. 2017 Mar;87:171-179

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22.Tlili N, Nasri N, Saadaoui E, Khaldi A, Triki S. Carotenoid and tocopherol composition of leaves, buds, and flowers of Capparis spinosa grown wild in Tunisia. J Agric Food Chem. 2009 Jun 24;57(12):5381-5.

23.Vahid H, Rakhshandeh H, Ghorbani A. Antidiabetic properties of Capparis spinosa L. and its components. Biomed Pharmacother. 2017 Aug;92:293-302. doi: 10.1016/j.biopha.2017.05.082.

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29.Nutritionist Pro Software.  USDA data base and other worldwide nutrient databases. Axxya Systems. http://www.nutritionistpro.com/

30.Centers for Disease Control and Prevention (CDC). Vital signs: food categories contributing the most to sodium consumption – United States, 2007-2008. MMWR Morb Mortal Wkly Rep. 2012 Feb 10;61(5):92-8.

31.Cordain L, Sebastian A. Aug 22, 2017.  The potassium to sodium ratio in fresh foods unadulterated with added salt. https://docs.google.com/spreadsheets/d/1bbKEmcI1IDO8nSvD–wwfzKnoDeAt_xam02DLeMioGQ/edit#gid=0

32.Bailey RL, Parker EA, Rhodes DG, Goldman JD, Clemens JC, Moshfegh AJ, Thuppal SV, Weaver CM. Estimating sodium and potassium intakes and their ratio in the american diet: data from the 2011-2012 NHANES. J Nutr. 2016 Mar 9. pii: jn221184. [Epub ahead of print]

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

34.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.

35.Frassetto L, Morris RC Jr, Sellmeyer DE, Todd K, Sebastian A. Diet, evolution and aging–the pathophysiologic effects of the post-agricultural inversion of the potassium-to-sodium and base-to-chloride ratios in the human diet. Eur J Nutr. 2001 Oct;40(5):200-13

36.McDonough AA, Veiras LC, Guevara CA, Ralph DL. Cardiovascular benefits associated with higher dietary K+ vs. lower dietary Na+: evidence from population and mechanistic studies. Am J Physiol Endocrinol Metab. 2017 Apr 1;312(4): E348-E356.

37.Mozaffarian D, Fahimi S, Singh GM, Micha R, Khatibzadeh S, Engell RE, Lim S, Danaei G, Ezzati M, Powles J, et al.  Global burden of diseases nutrition and chronic diseases expert group.

Global sodium consumption and death from cardiovascular causes. N Engl J Med. 2014 Aug 14;371(7):624-34

38.He FJ, Li J, Macgregor GA. Effect of longer-term modest salt reduction on blood pressure. Cochrane Database Syst Rev. 2013 Apr 30;(4):CD004937

39.Wu C, Yosef N, Thalhamer T, Zhu C, Xiao S, Kishi Y, Regev A, Kuchroo VK. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature. 2013 Apr 25;496(7446):513-7.  

40.Kleinewietfeld M, Manzel A, Titze J, Kvakan H, Yosef N, Linker RA, Muller DN, Hafler DA.  Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013 Apr 25;496(7446):518-22

41.Hucke S, Eschborn M, Liebmann M, Herold M, Freise N, Engbers A, Ehling P, Meuth SG, Roth J, Kuhlmann T, Wiendl H, Klotz L. Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity. J Autoimmun. 2016 Feb;67:90-101.  

42.Zostawa J, Adamczyk J, Sowa P, Adamczyk-Sowa M. The influence of sodium on pathophysiology of multiple sclerosis. Neurol Sci. 2017 Mar;38(3):389-398.  

43.Schatz V, Neubert P, Schröder A, Binger K, Gebhard M, Müller DN, Luft FC, Titze J, Jantsch J. Elementary immunology: Na+ as a regulator of immunity. Pediatr Nephrol. 2017 Feb;32(2):201-210.  

44.Hernandez AL, Kitz A, Wu C, Lowther DE, Rodriguez DM, Vudattu N, Deng S, Herold KC, Kuchroo VK, Kleinewietfeld M, Hafler DA. Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells. J Clin Invest. 2015 Nov 2;125(11):4212-22.  

45.Yi B, Titze J, Rykova M, Feuerecker M, Vassilieva G, Nichiporuk I, Schelling G, Morukov B, Choukèr A. Effects of dietary salt levels on monocytic cells and immune responses in healthy human subjects: a longitudinal study. Transl Res. 2015 Jul;166(1):103-10.  

46.Zhou X, Zhang L, Ji WJ, Yuan F, Guo ZZ, Pang B, Luo T, Liu X, Zhang WC, Jiang TM, Zhang Z, Li YM. Variation in dietary salt intake induces coordinated dynamics of monocyte subsets and monocyte-platelet aggregates in humans: implications in end organ inflammation. PLoS One. 2013 Apr 4;8(4):e60332.

47.Zhou X, Yuan F, Ji WJ, Guo ZZ, Zhang L, Lu RY, Liu X, Liu HM, Zhang WC, Jiang TM, Zhang Z, Li YM. High-salt intake induced visceral adipose tissue hypoxia and its association with circulating monocyte subsets in humans. Obesity (Silver Spring). 2014 Jun;22(6):1470-6.  

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50.Amara S, Alotaibi D, Tiriveedhi V. NFAT5/STAT3 interaction mediates synergism of high salt with IL-17 towards induction of VEGF-A expression in breast cancer cells. Oncol Lett. 2016 Aug;12(2):933-943

51.Amara S, Zheng M, Tiriveedhi V. Oleanolic acid inhibits high salt-induced exaggeration of warburg-like metabolism in breast cancer cells. Cell Biochem Biophys. 2016 Sep;74(3):427-34.

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53.Amara S, Ivy MT, Myles EL, Tiriveedhi V. Sodium channel γENaC mediates IL-17 synergized high salt induced inflammatory stress in breast cancer cells. Cell Immunol. 2016 Apr; 302:1-10

54.Amara S, Majors C, Roy B, Hill S, Rose KL, Myles EL, Tiriveedhi. Critical role of SIK3 in mediating high salt and IL-17 synergy leading to breast cancer cell proliferation. PLoS One. 2017 Jun 28;12(6):e0180097. doi: 10.1371/journal.pone.0180097

55.Cordain L. Physiological Mechanisms: Underlying High Salt Diets and Cancer. August 22, 2017.  https://thepaleodiet.com/physiological-mechanisms-underlying-high-salt-diets-cancer/

The holidays are a time for celebrating and feasting. There’s no reason you can’t enjoy some great meals and stick to your Paleo diet. It’s easy to lose sight of your health and nutrition goals this time of year. However, you don’t want to start the new year having to begin from scratch. Let’s look at some tips to maintain your healthy lifestyle and Paleo diet right through the holiday season.

 

Host Your Own Paleo-Friendly Dinner

The simplest way to make sure a meal is Paleo is to cook it yourself. If you have a partner or friends who can help, so much the better. Another option is to make it a potluck where everyone brings a dish. This isn’t always practical for traditional family celebrations but it can be fun for parties among like-minded friends. In this case, even people who don’t normally share the same diet can bring a dish that’s appropriate for the occasion.  

 

Communicate Your Needs

If you’re attending a holiday dinner at someone else’s home, let them know about your dietary restrictions. People are getting increasingly used to accommodating different diets such as vegan, gluten-free and, yes, Paleo. Not all hosts are amenable to making special preparations for you. Your grandmother who’s been making the turkey with stuffing the same way for 50 years might not want to alter her recipe just for you. In these cases, politely refuse anything that isn’t suitable. If you know that the Paleo offerings will be limited, you can even bring something with you. The key is to communicate in a non-confrontational manner with people so it doesn’t look like you’re insulting their cooking or trying to convert them to your diet.

 

Strategic Compromises

It’s up to you whether to stay 100% compliant with your Paleo diet through the holidays or to make some exceptions. You might, for example, decide to compromise for one traditional family dinner and eat the non-Paleo stuffing, mashed potatoes, and dairy-rich desserts. Even then, you can always stick mainly to healthy foods and just take small samplings of everything else. Most holiday dinners contain lots of dishes and people are unlikely to notice the quantity of each item you consume. Whether you decide to stay true to your Paleo diet or compromise for certain occasions, stick to your decision and don’t feel guilty or apologize for it.

 

Stay Active

In addition to your diet, it’s important to keep up with exercise during the holidays. If you’re eating more than usual, you need to burn off those extra calories. Make sure you schedule workouts between all of your shopping, meals, and parties. If you don’t currently have a regular workout schedule, the holidays are a good time to start. Many people join gyms in January to keep their New Year’s resolutions but why not get a head start and join now?

 

Paleo-Friendly Holiday Foods

Popular holiday dishes cover a wide spectrum when it comes to healthiness and Paleo-friendliness. In many cases, it all depends on how you prepare the food. Here are some suggestions for food and snacks for the holidays.

  • Grass-fed Meat and Poultry -If you get your meats from organic sources, it’s suitable for a Paleo diet. Typical supermarket meats, however, are usually from grain-fed animals and don’t make the mark.
  • Stuffing – Many holiday meals are served with stuffing. Unfortunately, most stuffing is made with bread from grain flours. However, you can just as easily make stuffing with alternative ingredients such as mushrooms, almond flour, sweet potatoes, and other Paleo-friendly ingredients.
  • Sweet Potatoes – A delicious staple at all holiday meals. While white potatoes are not Paleo due to their starchiness and high-carb content, sweet potatoes are.
  • Veggies – Many vegetables are fine for a Paleo diet provided you don’t cover them with butter or sauces containing dairy. Squash, broccoli, avocado, cabbage, mushrooms, and cauliflower are some nutritious vegetables to serve at your holiday meals. Dressings and sauces made from oil and vinegar are Paleo-friendly, as is salsa and any sauces made from almonds, walnuts, and other nuts.
  • Dairy-free Pumpkin Pie – Pumpkins are a healthy and tasty food that’s often ruined with dairy and refined sugar. A pumpkin pie made with ingredients such as almond milk and sweet potatoes is just one example of a delicious Paleo dessert that’s perfect for the holidays.  

 

You Can Have a Healthy Holiday Season

These are some ways to get through the holidays with your Paleo diet and lifestyle intact. The specific strategies you employ depend on your circumstances, including your social obligations and how open the people around you are to healthy eating. No matter what your situation, there’s no reason that the holidays have to mean giving up on your goals and principles.

Introduction

From 2006 to 2017 a dramatic collapse occurred in the Northern Pacific Sardine population (extending from Baja California to British Columbia, Canada), amounting to a 95 % decline in the entire sardine population (Figure 1, Info graphic 1) (1-3).

Figure 1.   The Pacific sardine population (biomass in millions of tons) has declined 95 percent since 2006 and it is now below the minimum level required to support a commercial fishery (called the “cutoff”) (1, 3).

This fishery collapse caused biologists at the West Coast Region of the National Oceanic and Atmospheric Administration (NOAA) Fisheries to impose a moratorium on all commercial sardine fishing in the Northern Pacific Sardine population (including California, Oregon and Washington) for 2015, 2016, 2017 and then on through to June 30, 2018 (1-3) – a 4-year moratorium, which will likely be extended (2).

Accordingly, fresh Pacific sardines have disappeared entirely from U.S. supermarkets and fish dealers and elsewhere worldwide.  For any U.S. consumer wanting to purchase fresh sardines, you are now limited to a single high volume fish vendor in New York City (The Lobster Place: https://lobsterplace.com/) which imports “fresh” sardines seasonally from Spain.   

Only a single on-line U.S. merchant (https://wholey.com/sardines/) sells frozen sardines – also caught in Spanish waters.   These flash frozen fish retail at $64 for an 8-pound bag of sardines.  This cost is difficult to justify for frozen sardines when fresh salmon, mackerel or herring with comparable or superior omega 3 fatty acid concentrations are regularly available throughout the U.S.   

Infographic 1.

 

The current cost to import either “fresh” or flash frozen sardines from Spain or other Mediterranean countries to a select few U.S. markets represents an exorbitant expense when compared to other U.S. fresh, fatty fish such as salmon, mackerel and herring.  Hence, U.S. consumers now infrequently or never can purchase fresh or even flash frozen sardines at a reasonable cost.  The net result is that almost all U.S. consumers of sardines now have no choice but to eat canned sardines.

 

Canned Sardines

As The New York Times reported, the last sardine cannery in the U.S. closed its doors on April 18, 2010 in Prospect Harbor, Maine (4).  This action brought a final closure to our once thriving national, sardine packing industry which peaked during WWII and served as the backdrop of John Steinbeck’s gritty novel, “Cannery Row”.   

U.S. sardine canneries have been declining for 60 years and have now completely fallen victim to foreign competition because of: (1) less restrictive foreign fishing policies, (2) foreign disregard for U.S. consumer health and safety regulations, (3) foreign obliviousness to global environmental laws, and (4) low-cost foreign labor to process and can sardines.  The net result of these actions has been to produce an un-sustainable global sardine industry of unrestrained catches along with no international health or safety regulations for canned sardines and human health.

Excessive sardine catches during the same period in which natural environmental factors wax and wane to normally reduce sardine populations, creates an unsustainable situation which can eventually deplete or eliminate sardine populations (1-3).   Most marine biologists studying Pacific sardine populations understand the multitude of factors which operate synergistically to deplete sardine populations.  Unfortunately, my blog may be the first that you (most sardine consumers) have heard of this dismal situation for Pacific sardines.  

Marine biologists studying the collapse of Pacific sardine populations are well aware of this ecologic disaster, but unfortunately are generally unaware of the nutritional and health consequences of our reliance upon canned sardines in lieu of fresh sardines.

 

The Nutritional and Health Consequences of Eating Canned Sardines

Although the nutritional and health consequences of eating canned sardines versus eating fresh sardines may initially seem inconsequential, this viewpoint is flawed. For U.S. consumers who can’t purchase fresh sardines, this is a moot point.  Let’s examine the data.

 

Canned vs. Fresh Sardines
The canned sardines we consume in the U.S. actually are not a single fish species, but may represent one of 21 small marine fish species within the family (Clupeidae), that fall into the following four genera’s: Sardina, Sardinops, Sardinella, Dussumieria (5).  Frequently, lack of quality control in the global sardine canning industry results in numerous small fish being packed and labeled as “sardines” when in fact they are not sardines, but other species (5).

In order to understand why canned sardines may represent a nutritional and health risk for human consumption, it is necessary to follow the steps involved in catching wild sardines as they are processed and packed into the tinned cans we purchase at the supermarket.

After sardines are caught at sea, usually via encircling nets called purse seines, a number of processing steps may occur when the fish are intended for human consumption via canning.  Depending upon boat size, time at sea and distance to the cannery the sardines are put into brine tanks, which are either cooled or uncooled, or placed on ice.  If there is a local market for these seined fish, they can be sold as “fresh” sardines, as long as refrigerated conditions are maintained for a few days to a week.  Sometimes, sardines are flash frozen at sea and can then be marketed worldwide as “frozen”.

At the cannery, the sardines are normally washed, eviscerated and their heads removed.  The fish then are cooked, typically by deep-frying in soybean or olive oil or by steam-cooking, after which they are dried.  The sardines are then packed by hand into cans containing salt (brine), or (olive, sunflower or soybean oil with salt), or salt containing tomato, chili or mustard sauces.  The cans are sealed and then heated above the boiling point via pressure cooking (called retort cooking) for 2 to 4 hours. This process is employed to kill all bacteria including those that cause botulism.

 

Deleterious Nutritional and Health Effects from Consuming Canned Sardines

High Salt and Low Potassium Content in Canned Sardines
Table 1 below demonstrate how salt is nearly universally added to commercially canned sardines.  Fresh sardines like virtually all other unadulterated marine and fresh water fish contain  more potassium than sodium (8).  Notice that fresh sardines contain 4.04 times more potassium than sodium on a milligram by milligram basis compared to average processed sardines.  Conversely, canned sardines contain exceptionally higher sodium concentrations and lower potassium concentrations than fresh sardines.

Table 1.   Comparison of the sodium (Na+) and potassium (K+) concentrations between fresh and canned sardines (from citation 7) .

I have previously written about how a high salt (sodium) diet contributes to osteoporosis, hypertension, cardiovascular disease and exercise induced asthma (9-11).  More recently, high salt/sodium diets have been implicated in chronic inflammation (13-20) autoimmune disease (21-31), immune dysfunction (20, 21, 32-35) and cardiovascular disease from endothelial damage via glycocalyx dysfunction (36-39).  Given this information, it is irresponsible by the international fish canning industry to include added salt in canned sardines or any other canned fish product, particularly when these products can easily be manufactured without the addition of salt.

Decline in Vitamin and Mineral Content in Canned Sardines
In addition to their high salt content, canned sardines (because they are cooked twice at high temperatures during the canning process) maintain drastically reduced vitamin and mineral contents compared to their fresh counterparts. Table 2 below shows how B vitamins and  minerals decline with the canning process.  On average the canning of fresh sardines reduces vitamin B1 by 75 %, vitamin B2 by 51 %, vitamin B3 by 34 %, vitamin B6 by 50 % and vitamin B12 by 38 %.  Magnesium on average in canned sardines compared to fresh sardines is reduced by 44 %, zinc by 36 % and copper by 19 %.

Table 2.  The decline in nutrients between fresh and canned sardines.

 

The Formation of Oxidized Cholesterol by Products in Canned Sardines
Perhaps the least appreciated, but most important change in the nutritional quality of canned sardines (or any canned fish product) compared to their fresh counterpart is the formation of oxidized cholesterol by-products (40, 41).  Oxidized cholesterol by products are known to scientists as “oxysterols” and maintain multiple deleterious effects upon human health (42-46).  Oxysterols occur universally with the canning and processing of fish and seafood (40) and are associated with a multiplicity of chronic diseases including atherosclerosis (coronary heart disease), neurodegenerative diseases, inflammatory bowel diseases, and age related macular degeneration (40-46).

Canned fish and seafood products such as sardines (canned tuna, salmon, herring, shrimp, oysters etc.) are particularly susceptible to the formation of cholesterol oxides (oxysterols).  These fish and seafood products also contain high concentrations of long chain omega 3 fatty acids (docosahexaenoic acid [DHA], eicosapentaenoic acid [EPA] which have multiple beneficial health effects when they are consumed fresh.  Nevertheless, the long chain omega 3 fatty acids (DHA and EPA) found in canned fish and seafood are highly susceptible to thermal (heat) processing, and together with their endogenous cholesterol, yield highly toxic cholesterol oxide products (oxysterols) (40-46) that directly result from the retort cooking necessary to eliminate bacteria and botulism.  The very same process (retort cooking) which frees humanity from developing fatal botulism in canned foods, directly promotes chronic systemic inflammation via the synthesis of oxysterols that underlie heart disease, cancer, neurodegenerative diseases and inflammatory bowel diseases (40-46).     

Something as simple as eating canned sardines or canned tuna had never been considered to be a health risk, but the current evidence is undeniable, irrefutable and damning (40-46) particularly when canned sardines, fish and seafood are consumed on a regular basis.  Do yourself a favor, eat fresh fish, the way nature has always intended, and avoid the salt and cholesterol oxides found in the tainted products we call canned fish.

 

References

1.//usa.oceana.org/responsible-fishing/modern-day-pacific-sardine-collapse-how-prevent-future-crisis

2.Hill, K.T., P.R. Crone, J.P. Zwolinski. 2017. Assessment of the Pacific sardine resource in 2017 for U.S. management in 2017-18. Pacific Fishery Management Council, April 2017 Briefing Book, Agenda Item G.5.a, Portland, Oregon. 146 p. Available at: //www.pcouncil.org/wpcontent/uploads/2017/03/G5a_Stock_Assessment_Rpt_Full_ElectricOnly_Apr2017BB.pdf

3.//www.westcoast.fisheries.noaa.gov/fisheries/pelagic/pacific_sardine_landings.html

4.//www.nytimes.com/2010/04/04/us/04cannery.html

5.https://en.wikipedia.org/wiki/Sardine#Genera

6.FC Lago, B Herrero, JM Vieites, M Espiñeira. FINS methodology to identification of sardines and related species in canned products and detection of mixture by means of SNP analysis systems. Eur Food Res Technol, 232 (6), 2011: 1077-1086.

7.Nutritionist Pro, nutritional software. //www.nutritionistpro.com/

8.https://docs.google.com/spreadsheets/d/18gh7VCq2PYlYodY3hCj1KJe3uc3c2rUgrLLEGLcBALw/edit#gid=0

9.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.

10.Carrera-Bastos P, Fontes Villalba M, O’Keefe JH, Lindeberg S, Cordain L. The western diet and lifestyle and diseases of civilization. Res Rep Clin Cardiol 2011; 2: 215-235.

11.Gotshall RW, Mickleborough TD, Cordain L. Dietary salt restriction alters pulmonary function in exercise-induced asthmatics. Medicine and Science in Sports and Exercise, 2000;32:1815-19.

12.Jantsch J, Schatz V, Friedrich D et al. Cutaneous Na+ storage strengthens the antimicrobial barrier function of the skin and boosts macrophage-driven host defense. Cell Metab. 2015 Mar 3;21(3):493-501.  

13.Jantsch J, Schatz V, Friedrich D et al. Cutaneous Na+ storage strengthens the antimicrobial barrier function of the skin and boosts macrophage-driven host defense. Cell Metab. 2015 Mar 3;21(3):493-501.

14.Dmitrieva NI, Burg MB. Elevated sodium and dehydration stimulate inflammatory signaling in endothelial cells and promote atherosclerosis. PLoS One. 2015 Jun 4;10(6): e0128870. doi: 10.1371/journal.pone.0128870

15.Yi B, Titze J,  et al.  Effects of dietary salt levels on monocytic cells and immune responses in healthy human subjects: a longitudinal study. Transl Res. 2015 Jul;166(1):103-10.  

16.Zhou X,  et al.  Variation in dietary salt intake induces coordinated dynamics of monocyte subsets and monocyte-platelet aggregates in humans: implications in end organ inflammation. PLoS One. 2013 Apr 4;8(4):e60332.

17.Ip WK, Medzhitov R. Macrophages monitor tissue osmolarity and induce inflammatory response through NLRP3 and NLRC4 inflammasome activation. Nat Commun. 2015 May 11;6:6931.

18.Foss JD, Kirabo A, Harrison DG. Do high-salt microenvironments drive hypertensive inflammation? Am J Physiol Regul Integr Comp Physiol. 2017 Jan 1;312(1):R1-R4

19.Min B, Fairchild RL. Over-salting ruins the balance of the immune menu.  J Clin Invest. 2015 Nov 2;125(11):4002-4.

20.Amara S, Tiriveedhi V. Inflammatory role of high salt level in tumor microenvironment (Review).  Int J Oncol. 2017 May;50(5):1477-1481

21.Kleinewietfeld M, et al.  Sodium chloride drives autoimmune disease by the induction of pathogenic TH17 cells. Nature. 2013 Apr 25;496(7446):518-22

22.Schatz V, et al.  Elementary immunology: Na+ as a regulator of immunity. Pediatr Nephrol. 2017 Feb;32(2):201-210.  

23.Hernandez AL, et al. DA. Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells. J Clin Invest. 2015 Nov 2;125(11):4212-22.  

24.Wu C, et al. Induction of pathogenic TH17 cells by inducible salt-sensing kinase SGK1. Nature. 2013 Apr 25;496(7446):513-7.

25.Hucke S, et al.. Sodium chloride promotes pro-inflammatory macrophage polarization thereby aggravating CNS autoimmunity. J Autoimmun. 2016 Feb;67:90-101.  

26.Zostawa J, et al. The influence of sodium on pathophysiology of multiple sclerosis. Neurol Sci. 2017 M

27.Khalili H et al. Identification and characterization of a novel association between dietary potassium and risk of crohn’s disease and ulcerative colitis. Front Immunol. 2016 Dec 7;7:554. doi: 10.3389/fimmu.2016.00554. eCollection 2016.

27.Sigaux J, et al. Salt, inflammatory joint disease, and autoimmunity. Joint Bone Spine. 2017 Jun 23. pii: S1297-319X(17)30129-X. doi: 10.1016/j.jbspin.2017.06.003.

28.Sundstrom B et al.  Interaction between dietary sodium and smoking increases the risk for rheumatoid arthritis: results from a nested case-control study. Rheumatology 2015;54:487-493

29.Yang X et al.  Exacerbation of lupus nephritis by high sodium chloride related to activation of SGK1 pathway. Int Immunopharm 2015;29:568-573.

30.Krementsov DN et al.  Exacerbation of autoimmune neuroinflammation by dietary sodium is genetically controlled and sex specific. FASEB J 2017;29(8):3446-3457.

31.Jorg S et al.  High salt drives Th17 responses in experimental autoimmune encephalomyelitis without impacting myeloid dendritic cells. Exp Neurol 2016;279:212-222

32.Schatz V, et al.  Elementary immunology: Na+ as a regulator of immunity. Pediatr Nephrol. 2017 Feb;32(2):201-210.  

33.Grivennikov SI, Wang K, Mucida D et al. Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth. Nature. 2012 Nov 8;491(7423):254-8.

34.Safa K, et al.  Salt accelerates allograft rejection through serum- and glucocorticoid-regulated kinase-1-dependent inhibition of regulatory t cells. J Am Soc Nephrol. 2015 Oct;26(10):2341-7

35.Hernandez AL,  et al.  Sodium chloride inhibits the suppressive function of FOXP3+ regulatory T cells. J Clin Invest. 2015 Nov 2;125(11):4212-22

36.Oberleithner H, et al.  Plasma sodium stiffens vascular endothelium and reduces nitric oxide release. Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16281-16286.

37.Kusche-Vihrog K, Schmitz B, Brand E. Salt controls endothelial and vascular phenotype. Pflugers Arch. 2015 Mar;467(3):499-512

38.Ghimire K, et al. Nitric oxide: What’s new to NO? Am J Physiol Cell Physiol. 2016 Dec 14:ajpcell.00315.2016. doi: 10.1152/ajpcell.00315.2016. [Epub ahead of print]

39.Jeggle P, et al.  Aldosterone synthase knockout mouse as a model for sodium-induced endothelial sodium channel up-regulation in vascular endothelium. FASEB J. 2016 Jan;30(1):45-53.

40.Dantas NM, Sampaio GR, Ferreira FS, Labre Tda S, Torres EA, Saldanha T.  Cholesterol Oxidation in Fish and Fish Products. J Food Sci. 2015 Dec;80(12):R2627-39

41.Rodriguez-Estrada MT, Garcia-Llatas G, Lagarda MJ3 7-Ketocholesterol as marker of cholesterol oxidation in model and food systems: when and how. Biochem Biophys Res Commun. 2014 Apr 11;446(3):792-7.  

42.Otaegui-Arrazola A, Menéndez-Carreño M, Ansorena D, Astiasarán I. Oxysterols: A world to explore. Food Chem Toxicol. 2010 Dec;48(12):3289-303

43.Zarrouk A, Vejux A, Mackrill J, O’Callaghan Y, Hammami M, O’Brien N, Lizard G. Involvement of oxysterols in age-related diseases and ageing processes. Ageing Res Rev. 2014 Nov;18:148-62

44.Kulig W, Cwiklik L, Jurkiewicz P, Rog T, Vattulainen I. Cholesterol oxidation products and their biological importance. Chem Phys Lipids. 2016 Sep;199:144-160

45.Vejux A, Lizard G. Cytotoxic effects of oxysterols associated with human diseases: Induction of cell death (apoptosis and/or oncosis), oxidative and inflammatory activities, and phospholipidosis. Mol Aspects Med. 2009 Jun;30(3):153-70

46.Poli G, Biasi F, Leonarduzzi G. Oxysterols in the pathogenesis of major chronic diseases. Redox Biol. 2013 Jan 31;1:125-30

 

Our Paleolithic ancestors had to sprint to survive; to fend off predators or to hunt their prey. The “fight or flight” response (and thus sprinting) is one of our most primal survival mechanisms. It’s hardwired into our DNA. Today, we’ve unfortunately outsourced most of our daily movement to cars, trains, and escalators, and we remain sedentary most of the day. Our bodies adapted to this frequent high-intensity fight or flight response and may very well have learned to need it. Today, most people simply don’t get enough movement in their day and it comes at a steep cost for your health.

Over 400 million people around the world suffer from type-2 diabetes (T2D) and almost 50% of the current population in America is classified as pre-diabetic or diabetic [1,2].  While the standard American diet – calorie-dense, nutrient-poor, hyper-palatable processed foods – is an overwhelming culprit, physical inactivity also has a key role [3]. A recent 10-year follow-up study of intensive lifestyle modifications – which included regular exercise – lowered the incidence of diabetes (type-2) by 34% in highrisk adults, which was twice as effective as the standard metformin drug therapy [4 ].

Movement is an integral part of a Paleo lifestyle. If moderate intensity exercise supports improved blood sugar control, how would high-intensity movements like sprinting impact glycemic control? Children spend their days running around the house or playing games, yet as we get older we lose connection with this fundamental primal movement.

Can sprinting help to reverse type-2 diabetes? Interestingly, a growing body of research has investigated the effects of high-intensity interval training (HIIT) on T2D. (Note – Sprinting falls under the banner of HIIT training, as do sprints on a bike, Tabata-style workouts, etc.)

 

HIIT & Diabetes (Type-2)

The term high-intensity can scare people off, but the good news is that it’s relative to your own fitness level. For example, a recent study examined the effects of HIIT training (10 sets @60s x3 weekly) over eight weeks in 50-year old, non-active type-2 diabetics versus healthy controls. Researchers found the diabetic group significantly improved glucose control and insulin sensitivity, as well as pancreatic beta-cell function, and experienced significant loses in pro-inflammatory abdominal adiposity [5]. Post-menopausal women with T2D engaging in two sessions per week over 16 weeks (with no concomitant caloric reduction) experienced more significant reductions in belly-fat compared to traditional steady-state cardio [6]. Even just two weeks of HIIT training showed positive health benefits for people with T2D and improvements in insulin resistance from pre- to post-training period [7].

A recent meta-analysis of over 50 studies found a superior reduction in insulin resistance following HIIT compared to both control and steady-state training. Although it should be noted that continuous aerobic training is still highly effective at reducing insulin resistance. It has demonstrated results that are comparable to HIIT. It just requires a much greater time commitment. Another meta-analysis concluded… “exercise at higher intensity may offer superior fitness benefits and… optimize reductions in HbA1C% (a 3-month average of blood sugar control)” [8,9,10].

 

HIIT & Diabetes (Type-2) Risk Factors

Type-2 diabetics are at an increased risk of cardiovascular disease. The first study that was able to demonstrate improvements in cardiac structure and function, along with the greatest reduction in liver fat. It used HIIT training (2-3-minute intervals x5 over 12 weeks). The authors concluded,HIIT should be considered by clinical care teams as a therapy to improve cardiometabolic risk in patients with type 2 diabetes” [11].

 

HIIT & Time Efficiency

It looks like HIIT training may provide an effective strategy for reversing T2D, but the question remains; how do you get people to stick with it? Most people know exercise is good for them, but they decide (often subconsciously) not to engage in it.

Why? The number one reason is people say they “don’t have time.” No problem, HIIT training provides the perfect solution.

Dr. Martin Gibala PhD, a world-renown expert in HIIT from McMaster University in Canada, recently compared the benefits of 3 minutes of exercise per week (yes… 3 minutes for the entire week!) versus the traditional recommendations of 150 minutes per week of exercise on fitness. His research team found that the HIIT group improved their fitness to the same degree as the continuous aerobic group after the 12-week intervention [12]. Looks like time is no longer an excuse (everyone has 3 minutes per week).

Sprinting is a fundamental primal movement. It’s deeply ingrained in our DNA, performed effortlessly when we’re children and the research supports its use (i.e HIIT) as an effective strategy for helping to reverse T2D symptoms and reduce cardiovascular disease risk. HIIT is time efficient, highly rewarding and best of all… it’s fun!

 

References

1. Retrieved from – //www.who.int/diabetes/global-report/en/
2. Menke A et al. Prevalence of and Trends in Diabetes Among Adults in the United States, 1988-2012. JAMA. 2015;314(10):1021-1029.
3. Woolf K et al. Physical activity is associated with risk factors for chronic disease across adult women’s life cycle. J Am Diet Assoc. 2008 Jun; 108(6):948-59.
4. Knowler et al. 10-year follow-up of diabetes incidence and weight loss in the Diabetes Prevention Program Outcomes Study. Diabetes Prevention Program Research Group. Lancet. 2009 Nov 14; 374(9702):1677-86.
5. Madsen S et al. High Intensity Interval Training Improves Glycaemic Control and Pancreatic β Cell Function of Type 2 Diabetes Patients. PLoS One. 2015 Aug 10;10(8):e0133286.
6. Maillard F et al. High-intensity interval training reduces abdominal fat mass in postmenopausal women with type 2 diabetes. Diabetes Metab. 2016 Dec;42(6):433-441.
7. Shaban N et al. The effects of a 2 week modified high intensity interval training program on the homeostatic model of insulin resistance (HOMA-IR) in adults with type 2 diabetes. J Sports Med Phys Fitness. 2014 Apr;54(2):203-9.
8. Jelleyman C et al. The effects of high-intensity interval training on glucose regulation and insulin resistance: a meta-analysis. Obes Rev. 2015 Nov;16(11):942-61.
9. Grace A et al. Clinical outcomes and glycaemic responses to different aerobic exercise training intensities in type II diabetes: a systematic review and meta-analysis.
10. Jung M et al. High-intensity interval training as an efficacious alternative to moderate-intensity continuous training for adults with prediabetes. J Diabetes Res. 2015;2015:191595.
11. Cassidy, S et al. High intensity intermittent exercise improves cardiac structure and function and reduces liver fat in patients with type 2 diabetes: a randomised controlled trial. Diabetologia 2016; 59(1): 56–66.
12. Gillen J et al. Twelve Weeks of Sprint Interval Training Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment. PlosONE April 26, 2016

 

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

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

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

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

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

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

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

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

 


It’s all about consistency.

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

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

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

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

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

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

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

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

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

And we’re not as hungry as often!

 


So what’s the
takeaway?

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

There’s no secret, trick or tweak.

As I always say, “Eat food and move”.

It truly is that simple.


References

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

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

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

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

 

Introduction

The olive tree (Olea europaea) is native to the Mediterranean basin and is cultivated in many other parts of the world.  The fruit of the olive tree is a drupe (a stone fruit) in which a hard inner seed is surrounded by a fleshy outer portion.  The olive has a low sugar content (2.6 – 6%) compared with other drupes (apricots, peaches, plum etc., which may contain 12% or more sugar).  Olives maintain a high oil content (12 – 30%) depending on the time of year and variety of olive harvested (1).  The olive fruit generally cannot be consumed directly from the tree because it contains a strong bitter component, oleuropein, which can be removed or lessened in concentrations by a series of processing techniques that vary considerably from region to region, but almost always involve treating the olives in brine or salt water.  Depending on local methods and customs, the fruit is first generally treated in sodium or potassium hydroxide (lye).  The olives are put into brine solutions and then rinsed in water.

Table olives are classified by the International Olive Council (IOC) into three groups according to the degree of ripeness achieved before harvesting (1):  

  1. Green olives are picked when they have obtained full size, but before the ripening cycle has begun; they are usually shades of green to yellow.
  2. Semi-ripe or turning-color olives are picked at the beginning of the ripening cycle, when the color has begun to change from green to multicolor shades of red to brown. Only the skin is colorful, as the flesh of the fruit lacks pigmentation at this stage, unlike that of ripe olives.
  3. Black olives or ripe olives are picked at full maturity when fully ripe. They are found in assorted shades of purple to brown to black. 

Green Olives

Green olives are processed in two principal ways: with fermentation (Spanish or Sevillian Type) and without fermentation (Picholine or American Type) (1).  

Spanish or Sevillian Type
The olives are treated in diluted lye solutions (sodium hydroxide or potassium hydroxide) to eliminate the oleuropein and transform sugars into form organic acids that aid in subsequent fermentation, and to also increase the permeability of the fruit. The lye concentrations vary from 2% to 3.5%, depending on the ripeness of the olives, the temperature, the variety, and the quality of the water. The olives remain in this solution until the lye has penetrated two thirds of the way through the flesh. The lye is then replaced by water, which removes any remaining residue, and the process is repeated, eliminating the oleuropein but keeping sufficient sugars which are necessary for subsequent fermentation.

Fermentation is carried out in inert containers in which the olives are covered with brine. The brine causes the release of the fruit cell juices, forming a culture medium suitable for fermentation. Brine concentrations are 9 – 10% to begin with, but rapidly drop to 5% because of the olive’s content of interchangeable water.

At first the contaminating Gram-negative bacteria multiply, but after a week and a half they disappear.  At a pH of 6 and upwards, lactobacilli develop until the Gram-negative bacteria disappear, and the brine attains a pH of 4.5. The lactobacilli produce lactic acid from the olive’s glucose, and when the fermentable sugars are spent, fermentation stops.

When properly fermented, olives keep for lengthy periods. The original brine is replaced and the olives are packed in barrels, tin or glass containers. Sometimes they are pitted or stuffed with anchovies, pimento, nuts and other food items. The most commonly consumed Spanish varieties are Manzanillo, Gordal and Moroccan Picholine (1).

Picholine Type
Olives belonging to the Picholine variety from Languedoc and Lucques in southern France are prepared in this manner, as are other varieties from Morocco and Algeria (1).  The bitter tasting oleuropein of the olives is removed by treating them in a 3 – 3.5 % lye solution (sodium or potassium hydroxide) until the lye has penetrated three-quarters of the way through the flesh. They are rinsed several times over the next day or two, and then placed into a 5 to 6% brine solution for two days. A second 7% brine solution is prepared, and acidity is corrected with citric acid (pH 4.5). After 8-10 days they are ready to be eaten and retain their intense green color. Before shipment, the olives are washed repeatedly, sorted, and packed in suitable containers in 5 to 6 % brine solutions (1).

 

Semi-Ripe Olives

Semi-ripe olives are harvested when their color is starting to change. They are picked before full maturity, when the flesh is quite firm and oil formation has not concluded.  Olives suitable for processing as green olives are selected as they enter the factory, then placed into brine at concentrations between 2.5 and 10 percent depending upon fruit size (1).

The olives are placed in large concrete tanks containing a 2 percent lye solution. When the olives are prepared for the market, they are placed in low-concentration lye and then washed in water that is injected with compressed air. Further treatments in dilute lye, each followed by aeration in water, facilitate penetration of the lye through the flesh to the pit. Next, the olives are washed to eliminate lye residue and lower the pH close to neutral. Solutions of 0.1 percent ferrous gluconate or lactate are often applied to California dark olives to enhance fruit darkening by oxidation.  After placement in brine for a few days, the olives are ready for canning. Heat processing in the form of temperature and pressure-controlled sterilization is fundamental to ensure the olives keep properly (1).

 

Ripe Olives

Ripe olives are harvested when the fruit is close to full ripeness, once it has attained the maximal color and oil content corresponding to the particular variety. The are many types of ripe olive processing techniques depending on local tastes.  Two of these are outlined below.

Black Olives in Brine
These olives are typical of eastern Mediterranean countries.  In Greece they are produced from the Conservolea variety, and in Turkey they are made from the Gemlik variety. The fruit is picked by hand when the fruit is black ripe, but before the olives over ripen. They have to be transported as quickly as possible to the processing plant where they are sorted, washed and immersed into tanks and vats containing an 8-10 % brine solution. At the start of fermentation, the tanks are tightly sealed to prevent the olives from being exposed to air. The brine stimulates the microbial activity for fermentation and also reduces the bitterness of the oleuropein. As the fermentation process takes over, if the brine solution drops below 6 %, it is increased back to 8-10% while homogenizing the brine solution with a pump.   

When the bitterness of the oleuropein has been sufficiently weakened, the fruit is sold. The olives’ color may fade during brining, but is later corrected by aerating the olives and by treating them with 0.1 percent ferrous gluconate or lactate to increase oxidation to make them a deeper black. Lastly, the olives are selected and packed into barrels, cans or jars which are filled with 8 percent brine. Theses olives are popular because of their slightly bitter taste and aroma.

They may also be packed in vinegar (25 percent of the brine volume); be heat processed and a little oil are then added to form a surface layer. The Kalamata olive variety from Greece is prepared in this way.

Black Olives in Dry Salt
Black olives in dry salt are also of Greek origin, and they are prepared using overripe olives of the Megaritiki variety. They are washed and placed in baskets with alternating layers of dry salt equivalent to 15 percent of the weight of the olives. The end product is not bitter, but salty, and it looks like a raisin.

 

Why Olives Are Not Paleo, But Olive Oil Is

From the information the International Olive Council has provided above (1), you can easily see that extensive processing is required to remove the bitter compound (oleuropein) from raw, fresh olives.  To make fresh olives edible requires massive additions of salt at nearly every stage of processing.   

Table 1 shows the high sodium (Na+) and low potassium (K+) content of processed olives.  A 500 kcal serving of green olives would supply you with 5,365 mg of Na+, whereas the same serving of jumbo black olives would give you 4,537 mg of Na+, and a 500 kcal serving of black olives would provide 3,196 mg of Na+.  The recommended daily intake of Na+ is 2300 mg for adult men and women (3-6).  Accordingly, even modest consumption of olives gives you way too much Na+ and not enough K+.

Table 1. Na+ and K+ content of olives (drupes) and olive oil (2)

Olives

Na+ mg/

1000 kcal

K+ mg/

1000 kcal

K+/Na+  

(mg/mg)

Green Olives

10731

290

0.027

Jumbo Black olives

9074

111

0.012

Black Olives

6391

70

0.011

Olive Oil

2.26

1.13

0.500

 

Now contrast the Na+ concentrations in a comparable 1000 kcal serving of olive oil to that found in whole olives.   A 1000 kcal serving of olive oil only contains 2.26 mg of Na+, or 4,748 times less Na+ than found in a 1000 kcal serving of green olives.

As I mentioned earlier, olives are member of the stone fruit (drupe) family.  Table 2 compares the Na+ and K+ concentrations of fresh drupes to processed olives.  Note that fresh drupes contain very low concentrations of Na+, comparable to olive oil, but additionally they  contain high concentrations of the health promoting ion K+.  A high K+/Na+ ratio is a universal characteristic of both wild and domesticated plant foods (7), and K+ is typically 5-10 times higher than Na+ in hunter gatherer diets (7-11).

Table 2. Na+ and K+ content of other drupes (stone fruit), including apricots, peaches, plums and nectarines (2)

  Drupes (stone fruits)

Na+ (mg)/

1000 kcal

K+ (mg)/

1000 kcal

K+/Na+ (mg/mg)

Apricot

21

5396

259.00

Nectarine

2

4568

2849.20

Peach

2

4872

2850.00

Plum

1

3413

2591.50

 

It is obvious that all olives contain much more Na+ than K+ (on average 18.5 times more Na+ than K+) compared to unadulterated, non-salted olive oil.  Clearly, the K+/Na+ ratios in processed olives lie far beyond the evolutionary normative values which conditioned our species’ genome (8-16).  Accordingly, it is not surprising that randomized controlled trials of salt consumption in humans as well as epidemiological studies (17-24) support the notion that added salt (be it sea salt or refined salt) from olives or any other processed food promotes cardiovascular disease, cancer, autoimmunity, chronic inflammation, immune system dysfunction, and ill health (17-51).

References

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