Tag Archives: The Paleo Diet

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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2.Axxya systems. Nutritionist Pro. //www.nutritionistpro.com/
3.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.
4.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.
5.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
6.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
7.//thepaleodiet.com/further-evidence-against-a-high-sodium-paleo-diet/
8.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
9.Jansson B. Human diet before modern times.   In: Sodium: “No!” Potassium: “Yes!”. Sodium increases and potassium decreases cancer risk.  Unpublished book manuscript, 1997, Chapter 2 pp. 1-20.
10.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.
11.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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15.Shaper AG. Communities without hypertension. In: Shaper AG, Hutt MSR, Fejfar Z eds. Cardiovascular disease in the tropics. London: British Medical Association. 1974:77-83.
16.Denton D. The hunger for salt: an anthropological, physiological and medical analysis. Chapter 27, Salt intake and high blood pressure in man. Primitive peoples, unacculturated societies: with some comparisons. Berlin: SpringVerlag, 1982, 556-578.
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18.Oberleithner H, Callies C, Kusche-Vihrog K, Schillers H, Shahin V, Riethmüller C, Macgregor GA, de Wardener HE. Potassium softens vascular endothelium and increases nitric oxide release. Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2829-34
19.Aaron KJ, Sanders PW. Role of dietary salt and potassium intake in cardiovascular health and disease: a review of the evidence. Mayo Clin Proc. 2013 Sep;88(9):987-95.
20.McDonough AA, Veiras LC, Guevara CA, Ralph DL. Cardiovascular benefits associated with higher dietary K<sup>+</sup> vs. lower dietary Na<sup>+</sup>: evidence from population and mechanistic studies. Am J Physiol Endocrinol Metab. 2017 Apr 1;312(4):E348-E356.
21.McDonough AA, Youn JH. Potassium Homeostasis: The Knowns, the Unknowns, and the Health Benefits. Physiology (Bethesda). 2017 Mar;32(2):100-111
22.Du S, Batis C, Wang H, Zhang B, Zhang J, Popkin BM. Understanding the patterns and trends of sodium intake, potassium intake, and sodium to potassium ratio and their effect on hypertension in China. Am J Clin Nutr. 2014 Feb;99(2):334-43.
23.Drewnowski A, Maillot M, Rehm C. Reducing the sodium-potassium ratio in the US diet: a challenge for public health. Am J Clin Nutr. 2012 Aug;96(2):439-44.
24.Fang Y, Mu JJ, He LC, Wang SC, Liu ZQ. Salt loading on plasma asymmetrical dimethylarginine and the protective role of potassium supplement in normotensive salt-sensitive asians. Hypertension. 2006 Oct;48(4):724-9
25.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.
26.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
27.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.
28.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.
29.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.
30.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.
31.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.
32.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.
33.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.
34.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.
35.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.
36.Kostyk AG, Dahl KM, Wynes MW, Whittaker LA, Weiss DJ, Loi R, Riches DW. Regulation of chemokine expression by NaCl occurs independently of cystic fibrosis transmembrane conductance regulator in macrophages. Am J Pathol. 2006 Jul;169(1):12-20.
37.Lang KS, Fillon S, Schneider D, Rammensee HG, Lang F. Stimulation of TNF alpha expression by hyperosmotic stress. Pflugers Arch. 2002 Mar;443(5-6):798-803.
38.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.
39.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
40.Binger KJ, Gebhardt M, Heinig M et al. High salt reduces the activation of IL-4- and IL-13-stimulated macrophages. J Clin Invest. 2015 Nov 2;125(11):4223-38
41.Min B, Fairchild RL. Over-salting ruins the balance of the immune menu.  J Clin Invest. 2015 Nov 2;125(11):4002-4.
42.Amara S, Tiriveedhi V. Inflammatory role of high salt level in tumor microenvironment (Review).  Int J Oncol. 2017 May;50(5):1477-1481
43.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
44.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.
45.Amara S, Whalen M, Tiriveedhi V. High salt induces anti-inflammatory MΦ2-like phenotype in peripheral macrophages. Biochem Biophys Rep. 2016 Sep;7:1-9
46.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
47.Davies RJ, Sandle GI, Thompson SM. Inhibition of the Na+,K(+)-ATPase pump during induction of experimental colon cancer. Cancer Biochem Biophys. 1991 Aug;12(2):81-94.
48.Thompson, Davies RJ.  A high potassium diet prevents transepithelial depolarization in experimental colon cancer. In: Vitamins and Minerals in the Prevention and Treatment of Cancer, (Maryce M. Jacobs, Ed.), CRC Press, Boston, 1991, p 263.
49.Fine BP, Hansen KA, Walters TR, Denny TN.  Dietary sodium deprivation inhibits cellular proliferation: evidence for circulating factor(s). In: Vitamins and Minerals in the Prevention and Treatment of Cancer, (Maryce M. Jacobs, Ed.), CRC Press, Boston, 1991, p 276.
50.Fine BP, Ponzio NM, Denny TN, Maher E, Walters TR. Restriction of tumor growth in mice by sodium-deficient diet. Cancer Res. 1988 Jun 15;48(12):3445-8.
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October has arrived in all its glory at The Paleo Diet and we have been harvesting our organic garden to create fresh, nutritious dishes.  After tending faithfully to our plants, we are reaping the rewards and sharing them with friends and family.  Many have asked for ideas and recipes for garden ingredients.  This month, we’ll be sharing our Fall Harvest recipes with our Paleo Diet followers.  Enjoy!

Chimichurri Steak

Steak comes alive with the flavor of Paleo Chimichurri – a bright green Argentinian herb sauce. Pair it with a spicy cauliflower dish to make this a meal to remember!

Ingredients:
Makes 2 servings

  • 2 grass-fed beef top loin (strip) steaks, cut 1 inch thick
  • ½ teaspoon black pepper
  • 2 tablespoons extra virgin olive oil
  • 1 medium onion, halved lengthwise and thinkly sliced
  • ½ teaspoon crushed red pepper
  • 3 cloves garlic, minced
  • 1 10-ounce package fresh cauliflower florets
  • ¼ cup water
  • 1 tablespoon fresh lemon juice
  • ¼ cup Chimichurri Sauce

Sprinkle both sides of steaks with black pepper.  Grill steaks, covered, over medium heat 10 to 12 minutes for medium rare (145°F) or 12 to 15 minutes for medium (160°F), turning once halfway through grilling.  (Or cook steaks on a stove-top grill pan over medium heat.)

Meanwhile, in a large skillet heat oil over medium high-heat.  Add onion and crushed red pepper; cook 4 to 5 minutes or until onion softens and begins to brown. Add garlic; cook and stir 30 seconds or until fragrant.  Add cauliflower and the water; cover and cook 6 to 8 minutes or just until cauliflower is tender, stirring occasionally.  Uncover and cook 1 to 2 minutes more or until liquid has evaporated. Remove skillet from heat; stir in lemon juice.

Serve steaks with Chimichurri Sauce and cauliflower and a fresh green Paleo salad.

 

Chimichurri Sauce

Ingredients
Makes about 2 cups

  • 2 cups lightly packed fresh Italian parsley
  • 2 cups lightly packed cilantro
  • ½ cup lightly packed mint
  • ½ cup chopped shallots
  • 1 tablespoon minced garlic (6 cloves)
  • 1/3 cup red wine vinegar
  • 2 dried unsulfured apricots, finely chopped
  • 1/8 teaspoon crushed red pepper
  • ¾ cup extra virgin olive oil

In a food processor or blender combine all ingredients.  Process until ingredients are finely chopped and combined, scraping sides as necessary.  Use immediately or freeze in desired portions up to 3 months in tightly covered containers. 

*From: Real Paleo Fast and Easy by Loren Cordain PhD.  Get more great recipes at The Paleo Diet Store

Salad Dressing

Salad Dressing

Mid-Season Sprucing Up

The Paleo Diet’s 2017 organic vegetable garden is growing and thriving, which means a little tidying up is in order to ensure that all of the plants are happy and healthy.  Our veggies are spreading out and filling in every space available with their stems, leaves, and flowers.  Along with this comes the crowding out of others, so we have trimmed and thinned to keep everything flourishing with plenty of space to grow.  Our cucumbers plants have gotten much too large for our garden trough and we made the decision to transplant them into large pots that can be put on the ground in just the right sunny spot.  We are hopeful that they will still yield  plenty of delicious cukes to add to our fresh salads and Paleo dishes.  Now that the cucumbers have moved out, our spinach and other leafy greens are much happier and beginning to spread out and thrive.  

Summer means a bounty of fresh, crisp salads to beat the heat and keep us healthy and happy.  It is nearly impossible to find store bought salad dressings that comply with The Paleo Diet.  We’ve experimented over the years, and have come up with these 2 easy-to-make dressings made with fresh ingredients straight from The Paleo Diet garden.  Enjoy!

 

Spice of Life Balsamic Dressing

Ingredients:

Put all ingredients in a blender and puree on medium speed until well combined.  Refrigerate for up to 1 week.

 

Spice of Life Creamy Dressing and Veggie Dip

We changed up just 2 ingredients in the dressing and have found this to be a delicious dip for fresh veggies, or a creamy salad dressing for any combination of leafy greens.

Ingredients:

  • ½ cup Paleo Walnut Mayo*
  • 1 Tablespoon each: Fresh basil, spinach, german thyme, cilantro
  • 2 teaspoons Mrs. Dash Salt-Free Table Blend

Put all ingredients in a blender and puree on medium speed until well combined.  Refrigerate for up to 1 week.

 

* Paleo Walnut Mayo

from Real Paleo Fast and Easy p. 305

We go through a jar of this mayo per week in the Cordain kitchen, as it goes well with a variety of foods and spices. Our preference is to use walnut oil for a smooth, mellow taste.

Ingredients:
Makes about 3 ½ cups.

  • 1 large or extra-large egg, room temperature
  • 1 tablespoon dry mustard
  • 1 cup walnut oil, at room temperature

Crack egg into a tall, narrow glass jar (a wide-mouth pint canning jar works well).  Add a touch of lemon juice and dry mustard.

Carefully pour in oil.  Let egg settle down to the bottom of the jar, under the oil.

Insert an immersion blender and push it all of the way to the bottom of the jar. Turn power on high and let it run for 20 seconds without moving it.  The mayonnaise will start to form and rise to the top of the jar.  Slowly raise the blender until it reaches the top of the jar.  Use mayonnaise immediately or store in the refrigerator up to 1 week.    

Check out more pure Paleo recipes at The Paleo Diet store.

There is one all-encompassing and inescapable reason to adopt a Paleo Diet lifestyle – improved health. Early critics of the diet said there were no studies to back those claims. But in recent years, a growing body of new research has appeared showing better health in people of different ages, sex, and race. The evidence is mounting.

This month, our writers addressed just a few items on the growing list of benefits of the Paleo Diet. A list that Jane Dizon at least partially summarized in her monthly infographic.

Our feature article is a continuation of Dr. Cordain’s extensive research on the negative health effects of high salt consumption. The Paleo Diet is a low sodium diet, and it’s a good thing too, as the recent evidence that Dr. Cordain has been collecting against high salt consumption continues to mount.

Along with our feature piece, Marc Bubbs addresses the health benefits of periodic fasting for diabetics, Trevor Connor addresses Bill Nye’s recent claims that The Paleo Diet is unhealthy, and Nell Stephenson pushes the boundaries of the diet a little bit, telling you how to have your bacon and eat it, too.

We hope our new articles help make it a little easier for you to stay Paleo for the rest of your summer. Enjoy!

– The Paleo Diet Team


August’s Feature Article

Physiological Mechanisms: Underlying High Salt Diets and Cancer

By Loren Cordain, PhD, Professor Emeritus
Dr. Cordain continues his groundbreaking research into high-salt diets and their impact on our health. In this piece, responding to a reader’s question, Dr. Cordain addresses how salt consumption can contribute to cancer. This is not one to miss!


Other Articles for August

Fasting – Ancestral Cure for Diabetes?

By Marc Bubbs, ND, CISSN, CSCS
Is fasting the ancestral cure for diabetes? Read more from Marc Bubbs on this fascinating and exploding subject including whether fasting was a natural part of paleolithic lifestyles and recent evidence for its effects and potential benefits with diabetics.

Bill Nye – The Science Guy?

By Trevor Connor, M.S.
Does Bill Nye’s recent criticism of the Paleo Diet hold scientific weight? Read why the research doesn’t back up his claims about our ancestors and their diet. In this blog, Trevor Connor, M.S. addresses Bill Nye’s views on the Paleo Diet, as discussed in the Netflix show, Bill Nye Saves the World.

Nell’s Corner: National Bacon Lover’s Day August 20th

By Nell Stephenson, B.S.
Just about everyone loves bacon. But is it part of an authentic Paleo approach? Nell Stephenson answers both this important question and gives some guidelines on how to both choose and cook your bacon.

The Ultimate Benefits of Going Paleo

By Jane Dizon
Some people are skeptical about the Paleo diet, but the outstanding benefits for the people who have tried it are evidence that there is more to it than just a mere change in one’s food choice. If you’re looking to try out this proven diet, here are the ultimate reasons why you should go Paleo now.

Paleo Recipe Contest Winner

By The Paleo Diet Team
We had a contest in July and August for the best recipe submission from our readers. Congratulations to Kriag Menard, our winner. Give his recipe a try!


September at The Paleo Diet: Lean, Robust, and Anti-Inflammatory

In September, our writers will continue to guide you in terms of foods that are and aren’t Paleo, including recipes focused on fresh fall produce (you can never get enough fresh vegetables) and why you should avoid olives and cheese.

Pulling it all together, we report on two recent studies showing the anti-inflammatory effects of The Paleo Diet. Nell Stephenson, as a high-level triathlete, gives advice on how to stay lean in the off-season.

As always, our team appreciates your support for The Paleo Diet. We look forward to and encourage your feedback on our website and Facebook!

Thanks!
The Paleo Diet Team

At The Paleo Diet, we look forward to August when our local farmer’s markets are stocked with a plentiful array of fresh-picked produce. We love visiting the various vendors to pick up a bounty of heirloom tomatoes, squash, onions, peppers, lettuce, spinach, peaches, strawberries, melons, and just about anything that grows in our neck of the woods. Right through October, there is little need to visit our local grocery chain, as you can’t beat the freshness of our locally sourced foods. Wherever you reside, give your local growers your support and stock up on some delicious Paleo Diet foods. Give this versatile seasonal favorite from The Paleo Diet kitchen a try. Serve with your favorite fresh greens and some sliced seasonal fruit for an easy, nutritionpacked meal! For more delicious recipes, visit us at: www.thepaleodiet.com

 

Ingredients

  • 1 large 2-3 in diameter squash of your choice, or 4 large peppers
  • 1-pound of ground grass fed beef
  • 3 tablespoons of olive oil
  • ½ yellow onion, chopped
  • 1 cloves garlic, minced
  • ½ large bell pepper, seeds removed and chopped
  • 1 tablespoon of each: fresh thyme, basil, parsley, rosemary and cilantro, finely minced
  • ½ cup water

 

Preheat the oven to 400 degrees. Slice the squash in half lengthwise and scrape out seeds, leaving a 1-2 inch channel to fill later with the beef mixture. Set aside. Brown beef in fry pan on low heat, stirring to be sure the meat is cooked evenly. Heat 1 tablespoon olive oil in a separate medium sized sauté pan, setting aside the rest. Add onion and garlic and sauté on medium heat about 3 minutes. Add the chopped pepper and continue to sauté for an additional 3-5 minutes. Season evenly with fresh herbs and mix throughout the veggies. Add cooked veggies to meat mixture and mix thoroughly. Evenly coat the inside floor of a 1 or 2-inch baking dish with the remaining olive oil. Stuff squash or peppers with the meat mixture and place in baking dish. Add ½ cup water to bottom of dish and cover with foil. Cook for 20 minutes, or until the squash or peppers are tender. Serves up to 4 people.

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

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

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

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

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

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

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

 

References

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Debunking the Biggest Myths About The Paleo Diet - infographic

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