Tag Archives: Salt

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

 

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

1.”About Olives”. International Olive Council. Retrieved September 5, 2017.  //www.internationaloliveoil.org/estaticos/view/77-about-olives
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
12.Gleibermann L. Blood pressure and dietary salt in human populations. Ecol Food Nutr 1973;2:143-56
13.Dahl L. Possible role of salt intake in the development of hypertension. In: Cottier P. Bock KD eds. Essential hypertension: an international symposiu. Berlin: Springer-Verlag. 1960:53-65.
14.Froment A. Milon H, Gravier C. Relationship of sodium intake and arterial hypertension. Contribution of geographical epidemiology. Rev Epidemiol Sante Publique 1979;27:437-54.
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.
17.O’Donnell M1, Mente A, Rangarajan S et al. Urinary sodium and potassium excretion, mortality, and cardiovascular events. N Engl J Med. 2014 Aug 14;371(7):612-23.
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.
51.Davies RJ, Daly JM. Potassium depletion and malignant transformation of villous adenomas of the colon and rectum. Cancer. 1984 Mar 15;53(6):1260-4.

 

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.

New Studies on Salt: Adverse Influence Upon Immunity, Inflammation and Autoimmunity | The Paleo Diet

INTRODUCTION

The Paleo community clearly is not in complete agreement on all dietary issues. One of the more touchy topics is added dietary salt.  A number of popular (non-scientific/non-peer review) bloggers advocate the use of refined salt or various forms of sea salt added to recipes and meals.1 Highly salted meats such as bacon are wildly popular in the Paleosphere.2 Other concentrated, salty foods such as cheese, olives, canned sardines, tuna, anchovies, caviar, salted nuts, manufactured jerky, canned tomato paste, and other salted, processed foods frequently find their way into so-called Paleo diets. You will be hard pressed to find a Paleo diet cookbook anywhere that is completely free of added, salt – that is, except for one The Real Paleo Diet Cookbook (Houghton, Mifflin, Harcourt, New York, 2015).

I have written extensively on the health problems associated with added dietary salt – be it refined salt or sea salt. In the past two years startling, animal and human studies demonstrate that salt added to our diets doesn’t merely increase the risk for stroke, hypertension and heart disease,3, 4, 5, 6 but it also adversely affects immune function, promotes chronic inflammation and represents a previously unrecognized dietary factor in the pathogenesis of autoimmune diseases.7, 8, 9, 10, 11, 12

SODIUM CONSUMPTION: THE EVOLUTIONARY/ANTHROPOLOGICAL EVIDENCE

The USDA daily recommended intake of sodium is 2300 mg. However, it must be remembered that dietary sodium and dietary salt are not equivalent. 1 gram (1000 mg) of salt (NaCl) = 390 mg of sodium.  Hence 2300 mg of sodium would equal 5.9 grams of salt (NaCl).

In perhaps the most comprehensive study of hunter gatherers and non-westernized people worldwide, Denton demonstrated that their average dietary salt intake ranged from 0.6 grams to 2.9 grams of salt (NaCl) per day or 234 to 1131 mg of daily sodium.13 These numbers are derived from population wide urinary sodium excretion rates and are considerably lower than the USDA recommended value of 2300 mg sodium per day, and much lower than the wildly speculative values (3000 to 7000 mg sodium per day or 7.7 to 17.9 grams of daily salt) suggested by a non-scientific/non-peer review Paleo blogger.1

SODIUM CONSUMPTION: EVIDENCE FROM CONTEMPORARY, NON-PROCESSED FOODS

Consider Figure 1 below which demonstrates the sodium content of four contemporary Paleo foods: meat/seafoods (n=8), fruit (n=20) and vegetables (n=18). Note that meat/seafood averages 694 mg of sodium per 1000 kcal, vegetables 764 mg sodium per 1000 kcal and fruit 54 mg of sodium per 1000 kcal.

New Studies on Salt: Adverse Influence Upon Immunity, Inflammation and Autoimmunity | The Paleo Diet

Figure 1.  The Sodium Content of Contemporary Paleo Foods to Processed Foods.

Accordingly, contemporary Paleo diets averaging 55% to 66% of daily calories (range 2200 to 3000 kcal) from animal foods and the balance from plant foods would contain sodium intakes ranging from 1600 to 2200 mg.  These calculations show that unless processed foods containing added salt are consumed, it would be difficult to obtain the USDA 2300 mg recommendation for  daily sodium, and almost impossible to obtain a popular bloggers’ advice (3000 to 7000 mg sodium).1

If fruits were primarily consumed in lieu of vegetables for contemporary Paleo diets, the range of daily sodium intake would be lower still (900 to 1200 mg) which falls within the values of historically studied fully, non-westernized populations.13 With contemporary Paleo foods (fresh fruits, vegetables, meats, seafood, eggs, nuts etc.) and no added salt, you will be obtaining not only sufficient sodium intakes, but also therapeutically lower sodium intakes that are consistent with values that conditioned our species’ genome over millions of years of evolutionary wisdom.

Lowered, or no consumption of added, manufactured dietary salt will lessen your risk for hypertension, stroke and cardiovascular disease,3, 4, 5, 6 certain cancers,14, 15, 16 and now autoimmune and immune diseases, as well as multiple diseases involving chronic low level, systemic inflammation.7, 8, 9, 10, 11, 12

DIETARY SODIUM: ADVERSE EFFECTS UPON INFLAMMATION, IMMUNOLOGICAL FUNCTION AND AUTOIMMUNITY

I have now laid out the necessary foundation for the focus of this article. So, let’s get back into the topic at hand.

Unexpectedly, experimental studies in the past two years have provided powerful, new evidence that high salt diets cannot solely be related to hypertension, stroke , cardiovascular disease3, 4, 5, 6 and cancer,14, 15, 16 but also to diseases involving dysfunction of the immune system, chronic systemic inflammation and autoimmunity.7, 8, 9, 10, 11, 12

Let’s not forget that cardiovascular disease, cancer and autoimmune diseases cannot proceed without chronic, low level inflammation, or that the typical U.S diet is a high salt diet.17 Would it be surprising that the typical western diet which includes 70 % or more of its calories as salt laden processed foods17 and 10 to 12 grams of sodium per day5, 7, 17 might have any adverse effects upon the immune system and diseases of chronic inflammation?

The evolutionary discordance template18, 19 would predict that any recently introduced dietary elements found in concentrations many standard deviations above or below those which conditioned the human genome over 2 million years of evolutionary experience, might adversely impact contemporary health and well being. Indeed is the case for immunity, inflammation and autoimmunity.

ANALYSIS OF RECENT STUDIES

In April of 2013, before my recent retirement from CSU, I awoke to a flurry of emails from scientific colleagues around the world as well as from a few of my graduate students regarding two astounding papers that had just been published in the prestigious scientific journal, Nature.8, 9  These papers represented the first experimental evidence indicating that high salt diets fundamentally altered the immune system of experimental animals in a manner that promoted autoimmune disease.

Over the past decade, numerous studies (human, animal and tissue) have implicated a specific component of the immune system (Th17 or T Helper Cell 17) in a wide variety of autoimmune diseases.20, 21, 22, 23 The two papers on salt and autoimmunity published in Nature8, 9 were crucial, because for the first time empirical evidence demonstrated that high dietary intakes of salt were capable of up-regulating (increasing) Th17 cells in experimental animals and promoting autoimmunity.

OK – no big deal – these were just animal studies and until human studies were conducted, the link between dietary salt and the immune system, chronic low level inflammation and autoimmunity was tenuous.  The currency of science to demonstrate causality between diet and disease requires not just animal studies, but also tissue studies, epidemiological studies and most importantly experimental randomized controlled human trials.

Science typically moves slowly, but occasionally good ideas are rapidly pounced upon by scientists and researchers, thereby resulting in major leaps of knowledge.  Such was the case with salt and autoimmunity. Concurrent with the two animal studies on dietary salt and immune function,8, 9 came the first human study published by Zhou and colleagues, also in April of 2013.11 Their study showed that after a 7 day (short term) high salt diet (> 15  NaCl/day) compared to a lower salt (< 5 g NaCl/day), markers (CD14++ and CD16+) of pro-inflammatory immune responses increased.  CD14++ and CD16+ are molecules expressed on certain immune system cells called monocytes/macrophages. Normally, these cells produce pro-inflammatory cytokines (hormones) when bacterial infection occurs24, 25 or with autoimmune diseases.26, 27  Surprisingly, even a short term (7 day) high salt diet11 caused the human immune system to become inflamed, just as if it were being attacked by foreign pathogens24, 25 or during autoimmunity.26, 27

In the most powerful human study to date, Yi and colleagues have convincingly demonstrated that a high salt diet (12 g per day) promoted a pro-inflammatory immune response whereas a lower salt intake (6 g per day) reduced these effects and caused beneficial immune system changes. The sophistication and high scientific validity of this experiment occurred because it was conducted under metabolic ward conditions over a long (205 day) duration for a simulated spaceflight program (Mars520 Mission).7

With metabolic ward conditions, each and every meal or snack are exclusively provided to test subjects.  Consequently all nutrients (including sodium) are under strict control. During the experiment in an enclosed environment, daily salt intake was solely modified from 12 g/day to 9 g/day to 6 g/day for 50 + 10 days and then reversed back to 12 g/day for 30 days. During the high salt (12 g/day) stages of the experiment, the pro-inflammatory cytokines (localized hormones) IL-6 and IL-23 increased whereas the anti-inflammatory cytokine, IL-10 decreased. Further the high salt diet caused an expansion of white blood cells (monocytes) that occur during chronic inflammation, autoimmune diseases and cancer. On the low salt (6 g/day) diet, these deleterious immune system changes were reversed. Interestingly, during the high salt phase of this experiment, IL-17 was higher than during the low salt phase (P= 0.08). As I have mentioned earlier, numerous studies (human, animal and tissue) have implicated this specific component (Th-17) of the immune system in a wide variety of autoimmune diseases.20, 21, 22, 23

So, there you have it.  The most powerful and scientifically valid study in humans has indisputably demonstrated that a high salt diet promotes chronic inflammation and adversely affects the immune system.  Note that the high salt (12 g/day) phase of this experiment actually represents the normal (10-12 g/day) salt intake in the U.S.5, 7, 17 and that cardiovascular disease, cancer and autoimmune diseases cannot proceed without chronic inflammation.  It is not only irresponsible for certain Paleo bloggers1 to promote high salt diets, but potentially life threatening.

 

REFERENCES

[1] Kresser K. Shaking Up The Salt Myth: Healthy Salt Recommendations. May 4, 2012.

[2] Huntley T.  The Path to Culinary Bliss: Home Cured Bacon.

[3] Strazzullo P, D’Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJ. 2009 Nov 24;339:b4567. doi: 10.1136/bmj.b4567.

[4] 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.

[5] He FJ, MacGregor GA. A comprehensive review on salt and health and current experience of worldwide salt reduction programmes. J Hum Hypertens. 2009 Jun;23(6):363-84.

[6] Ando K, Kawarazaki H, Miura K, Matsuura H, Watanabe Y, Yoshita K, Kawamura M, Kusaka M, Kai H, Tsuchihashi T, Kawano Y. [Scientific statement] Report of the Salt Reduction Committee of the Japanese Society of Hypertension(1) Role of salt in hypertension and cardiovascular diseases. Hypertens Res. 2013 Dec;36(12):1009-19.

[7] 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.

[8] 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.

[9] 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.

[10] O’Shea JJ, Jones RG. Autoimmunity: Rubbing salt in the wound. Nature. 2013 Apr 25;496(7446):437-9.

[11] Zhou X1, 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. doi: 10.1371/journal.pone.0060332. Print 2013.

[12] van der Meer JW1, Netea MG. A salty taste to autoimmunity. N Engl J Med. 2013 Jun 27;368(26):2520-1.

[13] Denton D.  Salt intake and high blood pressure in man. Primitive peoples, unacculturated societies: with comparisons.  In: The Hunger for Salt, An Anthropological, Physiological and Medical Analysis. Springer-Verlag, New York, 1984, pp. 556-584).

[14] D’Elia L, Rossi G, Ippolito R, Cappuccio FP, Strazzullo P. Habitual salt intake and risk of gastric cancer: a meta-analysis of prospective studies. Clin Nutr. 2012 Aug;31(4):489-98.

[15] Ge S, Feng X, Shen L, Wei Z, Zhu Q, Sun J. Association between Habitual Dietary Salt Intake and Risk of Gastric Cancer: A Systematic Review of Observational Studies.  Gastroenterol Res Pract. 2012;2012:808120. doi: 10.1155/2012/808120. Epub 2012 Oct 22.

[16] Hu J, La Vecchia C, Morrison H, Negri E, Mery L; Canadian Cancer Registries Epidemiology Research Group. Salt, processed meat and the risk of cancer. Eur J Cancer Prev. 2011 Mar;20(2):132-9.

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

[19] Frassetto L1, 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.

[20] Burkett PR, Meyer Zu Horste G, Kuchroo VK. Pouring fuel on the fire: Th17 cells, the environment, and autoimmunity. J Clin Invest. 2015 Jun 1;125(6):2211-9.

[21] Ryu H, Chung Y. Regulation of IL-17 in atherosclerosis and related autoimmunity. Cytokine. 2015 Apr 15. pii: S1043-4666(15)00126-X. doi: 10.1016/j.cyto.2015.03.009. [Epub ahead of print]

[22] Li D, Guo B, Wu H, Tan L, Chang C, Lu Q. Interleukin-17 in systemic lupus erythematosus: A comprehensive review.  Autoimmunity. 2015 Apr 20:1-9. [Epub ahead of print]

[23] Patel DD , Lee DM, Kolbinger F, Antoni C. Effect of IL-17A blockade with secukinumab in autoimmune diseases. Ann Rheum Dis. 2013 Apr;72 Suppl 2:ii116-23. doi: 10.1136/annrheumdis-2012-202371. Epub 2012 Dec 19.

[24] Rietschel ET, Schletter J, Weidemann B, El-Samalouti V, Mattern T, Zähringer U, Seydel U, Brade H, Flad HD, Kusumoto S, Gupta D, Dziarski R, Ulmer AJ. Lipopolysaccharide and peptidoglycan: CD14-dependent bacterial inducers of inflammation. Microb Drug Resist. 1998 Spring;4(1):37-44.

[25] Scherberich JE1, Nockher WA. CD14++ monocytes, CD14+/CD16+ subset and soluble CD14 as biological markers of inflammatory systemic diseases and monitoring immunosuppressive therapy. Clin Chem Lab Med. 1999 Mar;37(3):209-13.

[26] Chuluundorj D, Harding SA, Abernethy D, La Flamme AC. Expansion and preferential activation of the CD14(+)CD16(+) monocyte subset during multiple sclerosis.  Immunol Cell Biol. 2014 Jul;92(6):509-17.

[27] Kawanaka N1, Yamamura M, Aita T, Morita Y, Okamoto A, Kawashima M, Iwahashi M, Ueno A, Ohmoto Y, Makino H. CD14+,CD16+ blood monocytes and joint inflammation in rheumatoid arthritis. Arthritis Rheum. 2002 Oct;46(10):2578-86.

Easy With That Salt Shaker: The Effect of Dietary Salt On Sleep | The Paleo Diet

INTRODUCTION

Got sleep? Fact is many of us have a problem sleeping. You probably fall into one category, either being unable to sleep, or not getting enough sleep. In actuality, “counting sheep” and staring at the clock may be the favorite pastimes of many adults. Poor sleep quality, and associated sleep disorders like insomnia remain at the foremost of global health issues. For many, a common solution to tiredness entails having a daily fix of caffeine. Yet, the negative effects of caffeine on the heart, as well as the importance of sleep in regulating chemical imbalances within the brain, cannot be overstated.1

Sleep disorders have long-term consequences. They increase the risk of chronic diseases such as cardiovascular conditions and diabetes, resulting in a dismal quality of life. In addition, this leads to a big hole in your wallet and great financial burden to the economy.2 Given the increasing prevalence of reduced sleep quality and its costs, finding hidden factors that affect sleep is required to improve public health. Many are aware of risk factors like alcohol and sugar consumption, but a possible risk factor that normally goes unmentioned may lie in the individual’s dietary salt intake.3

While devoted Paleo followers are conscious of reducing dietary salt, after reading Dr. Loren Cordain’s books, it is important to understand the scientific basis behind this premise. Let’s put together results from past research to connect the dots.

DIETARY SALT AND THE BIG WHAMMY CORTISOL

Research studies have shown possible evidence between high dietary salt consumption and increased levels of the stress hormone cortisol.4 Furthermore, there appeared to be indication of metabolic syndrome. This group of conditions are characterized by risk factors including truncal obesity (where fat deposits around the waist line), low HDL cholesterol levels (which helps eliminate bad cholesterol from the body), hypertension and insulin resistance (which leads to hyperglycemia-high blood sugar)5.

This sounds like a lot, but let us put this in perspective. An individual diagnosed with metabolic syndrome doubles the risk of cardiovascular (heart) disease, while also quintupling the risk of diabetes. This should have set some alarms going off.

What exactly is cortisol, and how does it affect the body physiologically and psychologically? That answer will help you really understand where this is headed. Cortisol is a glucocorticoid hormone made in the adrenal cortex, near your kidneys.6 Aldosterone, which regulates sodium, is also made in the same area. Known as the key stress hormone in the body, the highest levels of cortisol are seen in the early part of the morning. A term coined as the “awakening response.” That feeling when you wake up excited and ready to start the day, yes thanks should go to cortisol. Cortisol helps your body in maintaining homeostasis. It keeps everything “A-okay” during and after exposure to stress.7 Regulation of cortisol takes place via the hypothalamic–pituitary–adrenal (HPA axis).

Cortisol acts on many parts of the body. In your immune system, cortisol exhibits weakening effects, while inhibiting the inflammatory process. It leaves you prone to developing infections.8 Cortisol encourages gluconeogenesis, basically it increases glucose/sugar production within the body.9 Makes sense right? In a stressful situation, your body needs energy.

In the brain, the memory zone, known as the hippocampus, has numerous cortisol receptors. Excess cortisol during stress has been shown to affect the hippocampus, through atrophy or wasting, resulting in severe memory loss.10 Evidence shows that cortisol affects the limbic system in the brain, which is responsible for mood and emotion.11

Cortisol prepares the body for a fight or flight response to stress, which explains the link between cortisol and insomnia. High levels of cortisol have been linked with a dysfunctional HPA axis, which helps regulate the sleep-wake circadian cycle. This affects sleep quality, and decreases slow-wave sleep aka deep sleep, and sleep time.12 Well the problem is that we need deep sleep. This is where human growth hormone is released, and where the body undergoes healing and repairs.13

Some evidence has shown the likelihood that cortisol also inhibits the production and release of melatonin, the sleep hormone, from the pineal gland.14 Adequate melatonin hormone is needed to induce good sleep. Melatonin and cortisol work inversely, think of it like a see-saw. Melatonin levels are naturally higher at night, but high cortisol levels at night leave melatonin unable to regulate this process.15

TIME TO CONNECT THE DOTS

Enough said. You may be thinking cortisol is pretty bad, but what does that have to do with dietary salt and sleep again. Well, it is a simple linear relationship. Dietary salt leads to increased cortisol levels, and these excess levels affect sleep. This means you can deduce dietary salt may affect sleep. Sounds simple right? Well in science, a hypothesis can be proposed, but a study must be carried out to provide answers.

A research study using a sample size of 20 individuals validated this hypothesis.16 In the study, significantly affected sleep quality, decreased deep sleep, resulting in frequent awakenings, alongside increased thirst. Given the small sample size of this study, further work is needed. Another study also confirmed the hypothesis that salt affects sleep.17

Yet another study shows that dietary salt increased the severity of the sleep disorder known as obstructive sleep apnea.18 With this condition, your airway narrows, decreasing oxygen availability, and leaving you with the inability to breathe for periods at a time.19

So now you have some science to back up your knowledge, when asked the real reason behind your decreased salt intake. Also remember that increased salt intake will make you wake up frequently to use the bathroom. As the body tries to get rid of the sodium, water goes out with it, leaving you thirsty and feeling dehydrated. As you place the almost empty salt shaker next to the empty wine glass, remember there is indeed a science behind this supposed madness.

Best wishes,

Obianuju Helen Okoye, M.D, M.B.A, M.S.-Epi

 

REFERENCES

[1] Harvard Medical School Division of Sleep Medicine. (2007, December 18). Under The Brain’s Control. Retrieved May 19, 2015, from //healthysleep.med.harvard.edu/healthy/science/how/neurophysiology

[2]<Grandner, M., Jackson, N., Gerstner, J., & Knutson, K. (2014). Sleep Symptoms Associated with Intake of Specific Dietary Nutrients. J Sleep Res, 23(1), 22–34. Retrieved June 22, 2015, from //www.ncbi.nlm.nih.gov/pmc/articles/PMC3866235/

[3] Ibid.

[4] Baudrand, R., Campino, C., Carvajal, C. A., Olivieri, O., Guidi, G., Faccini, G., . . . Cerda, J. (2014). High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Clin Endocrinol, 677–684. doi:10.1111/cen.12225

[5] National Health, Lung and Blood Institute. (2011, November 3). What Is Metabolic Syndrome? Retrieved June 23, 2015, from Metabolic Syndrome: //www.nhlbi.nih.gov/health/health-topics/topics/ms

[6]  Johns Hopkins Medicine. (2015). The Adrenal Glands. Retrieved June 23, 2015, from Health Library: //www.hopkinsmedicine.org/healthlibrary/conditions/endocrinology/adrenal_glands_85,P00399/

[7] Randall, M. (2011, February 3). The Physiology of Stress: Cortisol and the Hypothalamic-Pituitary-Adrenal Axis. Dartmouth Undergraduate Journal of Science. Retrieved June 24, 2015

[8] Ibid.

[9] Ibid.

[10] Ibid.

[11] Kandhalu, P. (2013, November 4). Berkley Scientific Journal, 18(1), 13-16. Retrieved June 22, 2015, from //bsj.berkeley.edu/wp-content/uploads/2013/11/04-FeaturesEffects-of-Cortisol_Preethi-KandhaluKim.pdf

[12] Kandhalu, P. (2013, November 4). Berkley Scientific Journal, 18(1), 13-16. Retrieved June 22, 2015, from //bsj.berkeley.edu/wp-content/uploads/2013/11/04-FeaturesEffects-of-Cortisol_Preethi-KandhaluKim.pdf

[13] National Sleep Foundation. (2006). Sleep-Wake Cycle: Its Physiology and Impact on Health. Washington DC. Retrieved May 15, 2015, from //sleepfoundation.org/sites/default/files/SleepWakeCycle.pdf

[14] Nikaidoa, Y., Aluru, N., McGuire, A., Park, Y., Vijayan, M., & Takemura, A. (2010, Jan). Effect of cortisol on melatonin production by the pineal organ of tilapia, Oreochromis mossambicus. Comp Biochem Physiol A Mol Integr Physiol, 155(1), 84-90. doi:10.1016/j.cbpa.2009.10.006

[15] Roden, M., Koller, M., Pirich, K., Vierhapper, H., & Waldhauser, F. (1993). The circadian melatonin and cortisol secretion pattern in permanent night shift workers. Am J Physiol, 265(1), R261-7. Retrieved June 24, 2015, from //ajpregu.physiology.org/content/265/1/R261

[16] Baudrand, R., Campino, C., Carvajal, C. A., Olivieri, O., Guidi, G., Faccini, G., . . . Cerda, J. (2014). High sodium intake is associated with increased glucocorticoid production, insulin resistance and metabolic syndrome. Clin Endocrinol, 677–684. doi:10.1111/cen.12225

[17] Grandner, M., Jackson, N., Gerstner, J., & Knutson, K. (2014). Sleep Symptoms Associated with Intake of Specific Dietary Nutrients. J Sleep Res, 23(1), 22–34. Retrieved June 22, 2015, from //www.ncbi.nlm.nih.gov/pmc/articles/PMC3866235/

[18] Pimenta, E., Stowasser, M., Gordon, R., Harding, S., Batlouni, M., Zhang, B., . . . Calhoun, D. (2013). Increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and hyperaldosteronism. Chest, 143(4), 978-83. Retrieved June 21, 2015, from 10.1378/chest.12-0802

[19] Pimenta, E., Stowasser, M., Gordon, R., Harding, S., Batlouni, M., Zhang, B., . . . Calhoun, D. (2013). Increased dietary sodium is related to severity of obstructive sleep apnea in patients with resistant hypertension and hyperaldosteronism. Chest, 143(4), 978-83. Retrieved June 21, 2015, from 10.1378/chest.12-0802

 

Add Salt and Stop Gaining Weight? | The Paleo Diet

“In a study that seems to defy conventional dietary wisdom, scientists have found that adding high salt to a high-fat diet actually prevents weight gain in mice.”1

So, after all this time, is adding salt to the diet not really as consequential as we thought?  Can we just douse our food with it, eat whatever foods we fancy and then magically stay lean and fit? Let’s investigate.

The researchers hypothesized that fat and salt, both tasty and easy to overeat, would collectively increase food consumption and promote weight gain. They tested the hypothesis by feeding groups of mice different diets: normal or high-fat chow with varying levels of salt. To their surprise, the mice on the high-fat diet with the lowest salt gained the most weight.

But how can this be? Don’t we need to eat a diet lower in fat and salt, per USDA recommendations,2 in order to be as healthy as possible?

“Our findings, in conjunction with other studies, are showing that there is a wide range of dietary efficiency, or absorption of calories, in the populations, and that may contribute to resistance or sensitivity to weight gain”, says Michael Lutter, MD, PhD, co-senior study author and UI assistant professor of psychiatry.

Well, that certainly makes sense. Humans certainly are not all cut from the same cloth. We have to factor in genetic variability, and nature versus nurture, in terms of what we we’re fed growing up and whether our upbringing favored activity and exercise.

Furthermore, we need to consider what we are eating in the grand scheme of things. How does this affect our macronutrient ratios and consequently what is our body using for its fuel source? For example, if we eat a ‘healthy’ diet with many servings of natural fruit during the day, we provide our body with a constant, steady stream of carbohydrates. This prevents the body from tapping into stored fat which requires the body to put forth significantly more effort. If, however, we begin the process of becoming fat adapted, we force the body to do the latter and turn to fat as its primary fuel source.3

Many of us who are already in sync with the recommendations of a real Paleo diet are comfortable with the recommendation to eat a diet higher in fat. But, the mention of adding salt really throws us a curve ball! After all, added salt is linked to a host of negative side effects including high blood pressure, osteoporosis and kidney stones, stomach cancer, stroke, Menierre’s Syndrome, insomnia, motion sickness, asthma and exercise induced asthma.4

A brief glance at our colleagues, friends and family’s food habits, provide all the proof we need that the typical American is following a diet far too high in sodium. It’s a fair bet most could do with, at the very least, weaning off the salt, by cutting back on the salt shaker and simultaneously omitting processed foodstuffs. But, this begs the question, how should athletes balance their Paleo diets and replace electrolytes through sweat?

Rehydrating with pure water without also replenishing salts can be potentially fatal and lead to hyponatremia, a condition that can occur when the level of sodium in your blood is abnormally low. Drinking too much water during endurance sports causes the sodium in your body to become diluted. When this happens, your body’s water levels rise, and your cells begin to swell. This swelling can cause many health problems, from mild to life threatening.5 Other side effects may include lightheadedness, fatigue, headaches and constipation.

Moreover, on a low carb diet where the body becomes reliant on fat as its fuel, more salt is used in the process when insulin levels go down and the body starts shedding excess sodium and water along with it. On a high carb diet, insulin signals the cells to store fat and the kidneys to hold on to sodium, which is why people often get rid of excess bloat within a few days of low-carb eating.6

But again, if sodium is a crucial electrolyte in the body, how do we replace it? Presuming you’re following a healthy, high in fat, but void of refined, processed carbs and with adequate wild proteins and local veggies Paleo diet, adding a few pinches of salt to a recovery drink is permitted7 and may, in some instances, be a part of preventing weight gain. The general takeaway is not to simply add salt and watch the pounds melt away. Rather, train your body to become fat adapted in conjunction with following a real Paleo approach.

These findings “may lead to the developments of new anti-obesity treatments” and “may support continued and nuanced discussions of public policies regarding dietary nutrient recommendations.”

Let’s hope the new treatments go beyond a new pill or surgery, and the recommendations are evidenced by science versus the current guidelines deterring us as a society to truly follow a path to optimal health!

 

REFERENCES

[1] ScienceDaily. ScienceDaily, n.d. Web. 15 June 2015.

[2] “Dietary Guidelines.” Dietary Guidelines. N.p., n.d. Web. 15 June 2015.

[3] Volek, Jeff, Stephen D. Phinney, Eric Kossoff, Jacqueline A. Eberstein, and Jimmy Moore. The Art and Science of Low Carbohydrate Living: An Expert Guide to Making the Life-saving Benefits of Carbohydrate Restriction Sustainable and Enjoyable. Lexington, KY: Beyond Obesity, 2011. Print.

[4] “Sea Salt: Between the Devil and the Deep Blue Sea.” The Paleo Diet. N.p., 20 Apr. 2014. Web. 15 June 2015.

[5] “Hyponatremia.” – Mayo Clinic. N.p., n.d. Web. 15 June 2015.

[6] “Insulin’s Impact on Renal Sodium Transport and Blood Pressure in Health, Obesity, and Diabetes.” Insulin’s Impact on Renal Sodium Transport and Blood Pressure in Health, Obesity, and Diabetes. N.p., n.d. Web. 15 June 2015.

[7] Cordain, Loren, and Joe Friel. “Stages III, IV, V: Eating After Exercise.” The Paleo Diet for Athletes: The Ancient Nutritional Formula for Peak Athletic Performance. New York: Rodale, 2012. 56-57. Print.

Fish Roe and Caviar: Paleo? Yes and No | The Paleo Diet

INTRODUCTION

Unless you frequently eat at sushi bars or enjoy caviar with your champagne, most Americans have rarely if ever tasted fish roe (eggs). Worldwide, roe is not only consumed from just about any and all species of fish or aquatic animals that can be harvested or caught, but is considered a delicacy in most cultures and societies outside of the U.S.4, 33, 43 Table 1 below shows some of the more commonly consumed fish roe and aquatic animal eggs.

The Japanese are fond of almost all roe, particularly caviars such as salmon (Ikura), pollock (Tarako), flying fish (Tobiko),  herring (Kazunoko), mullet (Karasumi) and smelt (Masago).4, 33, 44 The Italian version of processed mullet roe is known as “Bottarga.”4, 25, 26, 28

Fish Roe and Caviar: Paleo? Yes and No

ROE VS. CAVIAR

I hate to split hairs, but a distinction must be made between roe and caviar. The commonly edible eggs of fish and other aquatic animals (sea urchins, squid, shrimp, lobster, scallops etc.) represent the mature ovaries of the females of these species. Roe, unlike chicken eggs, do not present themselves as a single distinct egg, but rather the eggs occur attached to one another in connective tissue called “skeins.”4 Roe skeins can be consumed in their raw (“green”) unadulterated state or processed in a manner that separates individual eggs from one another.

When salt is added to separated fish eggs (a procedure called “brining”) it yields a food product called “caviar” which may also be subject to other “curing” processes and added chemicals.4 In the U.S. only sturgeon caviar can be labeled as “caviar.”4 Other salted fish roe such as salmon must be labeled with the fish from which it was made. So, salted cured salmon roe becomes “salmon caviar.”4

Sturgeon caviar is one of the most expensive foods in the world with a one ounce (30 gram) tin costing between $50 and $75. High end Osetra sturgeon caviar runs about $12,000 a kilo or about $378 for an ounce. Surprisingly, much less expensive caviar from salmon, herring, squid and other species is nutritionally superior to sturgeon caviar, particularly in regard to omega 3 fatty acids.20, 34, 39, 40

SALT AND CAVIAR

Any and all caviars are by definition manufactured using salt.4 Accordingly, these processed foods would have been unavailable for consumption to our pre-agricultural ancestors. However there is little doubt that fresh, “green” unadulterated fish roe would have been relished.

Below in Table 2, you can see that fresh, non-processed fish roe represents a very low dietary source of sodium, whereas caviar is a concentrated source of sodium because of its processing with salt (NaCl).

Fish Roe and Caviar: Paleo? Yes and No | The Paleo Diet

The USDA recommended limit for daily sodium intake is 2,300 mg. Caviar eggs whether from sturgeon, salmon, herring or other species typically is packaged in 1 oz. (30 g) or 50 g (1.76 oz.) tins, but can be purchased in higher bulk quantities. Accordingly, a single 1 oz. (30 g) tin of caviar (on low end estimates) delivers a whopping 450 mg of sodium, whereas on high end values, it is more devastating still at 1162 mg of sodium.

From table 2 above, you can see that if you are going to eat roe, a better strategy (sodium wise) would be to consume fresh or frozen fish eggs without added salt.

In the U.S. fresh roe (“green”) and frozen roe is considerably more difficult to obtain than salted caviar, but not impossible. Go online and you can see a substantial number of retailers offering unprocessed fresh or frozen roe without salt. So the bottom line with salted caviar is to eat it infrequently or as a treat – better yet eat non-salted roe if you can find it.

TASTE TEST OF THREE NON-STURGEON CAVIARS

As long as I am writing about the scientific merits or lack thereof caviar and fish roe, I thought that it might be useful for me to give you my taste test impressions of three caviars (whitefish, capelin, lumpfish) which I purchased from our local World Market store. Below are my taste impressions of these three items.

1. I started off my culinary caviar adventures with Pacific Plaza Imports “Golden Whitefish Caviar.”47

I bought a 50 g tin of this roe for $6.99 and carefully read the label which indicated the following items and their respective order: wild pasteurized whitefish roe, natural caramel coloring, truffle oil, water, tragacanth gum (as a stabilizer), salt, sodium benzoate (as a preservative).

Whew! That’s quite a list of non-Paleo ingredients. The label tells us that this whitefish caviar is harvested from a species known as Coregonus clupeaformis. By contrasting the slightly lower sodium content of this roe to capelin and lumpfish (Table 2) from the same company, I was expecting that my taste test would be somewhat positive or at least better than the capelin and lumpfish taste tests. Yuck! What a disappointment.

I gingerly picked out a clump of black whitefish caviar from the 50 g tin with a small hors d’oeuvres fork. Immediately, upon hitting my mouth, this tiny amount of roe sickened me with its overpowering salty taste to the point that I wanted to spit it out. It didn’t taste like any food I have ever eaten, but rather more like putting pure salt crystals on my tongue, but perhaps worse.

The fish oil seemed to cause the processed roe salt to permeate my tongue in a greater manner than salt itself.  This food was so excessively salty that I have little desire to ever again eat caviar. But waitFor this review, I had to sample capelin and lumpfish caviar which both contain considerably more salt than whitefish.

2. Lumpfish and Capelin Caviar.

I pop open the lids from the tins of both lumpfish and capelin caviar and prepare to dive into them with my hors d’oeuvres fork. After a brief taste (only a few caviar eggs of each), I simply cannot tolerate the overpowering salty queasiness this food brings on.

THERAPEUTIC HEALTH BENEFITS OF FRESH FISH ROE

Fish roes are one of the most concentrated food sources of long chain omega 3 fatty acids EPA (20:5n3) and DHA (22:6n3).3-5, 13, 14, 19,  20, 26, 28, 34, 38-40 In numerous animal experiments roe consumption has been shown to improve various markers of health and well being and to reduce morbidity and mortality.11, 21, 22, 33, 44, 46 Only a handful of human studies has evaluated roe consumption in regard to this food’s potential therapeutic health effects.3, 4 So, if you can find unsalted roe, it represents one of the best dietary sources of  healthful long chain omega 3 fatty acids.

The long chain omega 3 fatty acids found in roe are different from these beneficial fatty acids that you my get if you take fish oil or fish oil capsules. The omega 3 fatty acids (DHA and EPA) in fish roe are contained in phospholipids (structural fat) whereas EPA and DHA in fish oil are contained in the triglyceride (storage fat) fraction.48 A number of studies suggest that ingestion of EPA and DHA bound to phospholipids are more readily absorbed and better utilized than EPA and DHA bound to triglycerides.3, 48 – 52 Accordingly, some scientists propose that the omega 3 fatty acids (EPA and DHA) found in fish eggs39, 48 and krill oil48, 50, 52 are more effective in enriching our bloodstream with these healthy nutrients. Unfortunately, few human experimental trials3, 50 have shown this proposed effect, and the best evidence to date indicates the “jury may still be out” on this concept because of experimental and methodological issues.8, 27

Nevertheless, whether you consume fresh roe, krill oil, fish, fish oil, or fish oil capsules you will be doing your body a favor by ingesting long chain omega 3 fatty acids which reduce the risk of cardiovascular disease, cancer and other pro-inflammatory illnesses.

FISH ROE LECTINS AND ALLERGY

When most people in the Paleo diet community see the word, “lectin” it typically conjures up images of plant foods such as whole grains and legumes which contain lectins such as wheat germ agglutinin (WGA in wheat) and phytohemagglutinin (PHA in beans).

In experimental animals, both of these lectins have been shown to bypass the gut barrier and promote adverse physiological effects.53, 54 To date, these lectins have been scarcely studied in human tissue (in vitro) experiments  and almost never examined in living humans (in vivo studies).55

Rarely do Paleo dieters recognize that certain animal foods may also contain various antinutrients, including lectins. Starting in the late 1970s, fish roe from most species was discovered to be a significant source of certain lectins.56-59 As more recent work has confirmed, most fish roe lectins belong to a category of lectins called rhambose-binding lectins (RBLs).12, 16, 23, 32, 36, 37, 41, 42

The biological function of RBLs in fish eggs seems to primarily involve activation of innate immunity, host pathogen interaction and inflammatory reactions  in various fish tissues.32, 41, 42  Multiple RBLs (CSL1, 2 and 3) from chum salmon roe induced production of the pro-inflammatory cytokines (IL-1 β1, IL-2β2,  TNFα1 and IL-8) in fish macrophages.42 To date no experimental mammal, or human studies have determined if RBLs from fish roe interact with our immune systems to produce inflammation or undesired health effects.

However, substantial literature exists showing that fish roe consumption represents a common food allergen in humans, particularly children.7, 15, 24, 18, 29, 30, 31, 35 The primary allergen in fish roe is known as “ ß`- component”18, 29 and may cause severe anaphylactic reactions.

CONCLUSIONS

In the U.S., caviar is rarely eaten by the average consumer, whereas it is a common food item in Japan and other countries worldwide. Because caviar represents a concentrated salt source, it should be rarely consumed or avoided by regular Paleo dieters. If you can find it, fresh or frozen fish roe of any species represents one of the most concentrated dietary sources of the healthful, long chain, omega 3 fatty acids, EPA and DHA. Eat it if you can. However, if you experience an allergenic reaction – hives, itching skin, running nose, difficulty breathing, rashes, etc. – know that fish roe is a common dietary allergen, and the immunological flip side of allergy frequently involves autoimmunity.

 

REFERENCES

[1]Al-Holy, M., Wang, Y., Tang, J., & Rasco, B. (2005). Dielectric properties of salmon (Oncorhynchus keta) and sturgeon (Acipenser transmontanus) caviar at radio frequency (RF) and microwave (MW) pasteurization frequencies. Journal of Food Engineering, 70(4), 564-570.

[2]Al‐Holy , M. A., & Rasco, B. A. (2006). Characterization of salmon (Oncorhynchus keta) and sturgeon (Acipenser transmontanus) caviar proteins. Journal of food biochemistry, 30(4), 422-428.

[3]Bjørndal, B., Strand, E., Gjerde, J., Bohov, P., Svardal, A., Diehl, B. W., … & Berge, R. K. (2014). Phospholipids from herring roe improve plasma lipids and glucose tolerance in healthy, young adults. Lipids in health and disease, 13(1), 82.

[4]Bledsoe GE, Bledsoe CD, Rasco B. Caviars and fish roe products. Crit Rev Food Sci Nutr. 2003;43(3):317-56.

[5]Caprino F, Moretti VM, Bellagamba F, Turchini GM, Busetto ML, Giani I, Paleari MA, Pazzaglia M. Fatty acid composition and volatile compounds of caviar from farmed white sturgeon (Acipenser transmontanus). Anal Chim Acta. 2008 Jun 9;617(1-2):139-47.

[6]Chalamaiah M, Hemalatha R, Jyothirmayi T, Diwan PV, Bhaskarachary K, Vajreswari A, Ramesh Kumar R, Dinesh Kumar B. Chemical composition and immunomodulatory effects of enzymatic protein hydrolysates from common carp (Cyprinus carpio) egg. Nutrition. 2015 Feb;31(2):388-98.

[7]Fujita, S., Shimizu, Y., Kishimura, H., Watanabe, K., Hara, A., & Saeki, H. (2012). In vitro digestion of major allergen in salmon roe and its peptide portion with proteolytic resistance. Food Chemistry, 130(3), 644-650.

[8]Ghasemifard S, Turchini GM, Sinclair AJ. Omega-3 long chain fatty acid “bioavailability”: a review of evidence and methodological considerations. Prog Lipid Res. 2014 Oct;56:92-108.

[9]Higuchi T, Shirai N, Suzuki H. Effects of dietary herring roe lipids on plasma lipid, glucose, insulin, and adiponectin concentrations in mice.J Agric Food Chem. 2006 May 17;54(10):3750-5.

[10]Higuchi T, Shirai N, Suzuki H. Effects of herring roe on plasma lipid, glucose, insulin and adiponectin levels, and hepatic lipid contents in mice. J Nutr Sci Vitaminol (Tokyo). 2008 Jun;54(3):230-6

[11]Higuchi T, Shirai N, Suzuki H. Effects of dietary herring roe lipids on plasma lipid, glucose, insulin, and adiponectin concentrations in mice. J Agric Food Chem. 2006 May 17;54(10):3750-5

[12]Hosono M, Kawauchi H, Nitta K, Takayanagi Y, Shiokawa H, Mineki R, Murayama K. Purification and characterization of Silurus asotus (catfish) roe lectin. Biol Pharm Bull. 1993 Jan;16(1):1-5.

[13]Intarasirisawat, R., Benjakul, S., & Visessanguan, W. (2011). Chemical compositions of the roes from skipjack, tongol and bonito. Food Chemistry, 124(4), 1328-1334.

[14]Kaitaranta JK, Linko RR. Fatty acids in the roe lipids of common food fishes. Comp Biochem Physiol B. 1984;79(3):331-4

[15]Kondo, Y., Kakami, M., Koyama, H., Yasuda, T., Nakajima, Y., Kawamura, M., … & Urisu, A. (2005). IgE cross-reactivity between fish roe (salmon, herring and pollock) and chicken egg in patients anaphylactic to salmon roe. Allergology International, 54(2), 317-323.

[16]Lam YW, Ng TB. Purification and characterization of a rhamnose-binding lectin with immunoenhancing activity from grass carp (Ctenopharyngodon idellus) ovaries.Protein Expr Purif. 2002 Dec;26(3):378-85.

[17]Ng TB, Lam YW, Woo NY. The immunostimulatory activity and stability of grass carp (Ctenopharyngodon idellus) roe lectin. Vet Immunol Immunopathol. 2003 Aug 15;94(3-4):105-12.

[18]Liu, Y. Y., Cao, M. J., Zhang, M. L., Hu, J. W., Zhang, Y. X., Zhang, L. J., & Liu, G. M. (2014). Purification, characterization and immunoreactivity of β′-component, a major allergen from the roe of large yellow croaker (Pseudosciaena crocea). Food and Chemical Toxicology, 72, 111-121.

[19]Méndez, E., Fernández, M., Pazo, G., & Grompone, M. A. (1992). Hake roe lipids: composition and changes following cooking. Food chemistry, 45(3), 179-181.

[20]Mol S, Turan S. Comparison of proximate, fatty acid and amino acid compositions of various types of fish roes. Int J Food Properties . Volume 11, Issue 3, 2008, 669-677.

[21]Moriya H, Hosokawa M, Miyashita K. Combination effect of herring roe lipids and proteins on plasma lipids and abdominal fat weight of mouse. J Food Sci. 2007 Jun;72(5):C231-4.

[22]Moriya, H., Kuniminato, T., Hosokawa, M., Fukunaga, K., Nishiyama, T. , Miyashita, K. (2007), Oxidative stability of salmon and herring roe lipids and their dietary effect on plasma cholesterol levels of rats. Fisheries Science, 73: 668–674.

[23]Ogawa T, Watanabe M, Naganuma T, Muramoto K. Diversified carbohydrate-binding lectins from marine resources. J Amino Acids. 2011;2011:838914. doi: 10.4061/2011/838914.

[24]Perez-Gordo M, Sanchez-Garcia S, Cases B, Pastor C, Vivanco F, Cuesta-Herranz J. Identification of vitellogenin as an allergen in Beluga caviar allergy. Allergy. 2008 Apr;63(4):479-80.

[25]Rosa A, Scano P, Atzeri A, Deiana M, Falchi AM. Potential anti-tumor effects of Mugil cephalus processed roe extracts on colon cancer cells. Food Chem Toxicol. 2013 Oct;60:471-8.

[26]Rosa, A., Scano, P., Melis, M. P., Deiana, M., Atzeri, A., & Dessi, M. A. (2009). Oxidative stability of lipid components of mullet (Mugil cephalus) roe and its product “bottarga”. Food chemistry, 115(3), 891-896.

[27]Salem N Jr, Kuratko CN. A reexamination of krill oil bioavailability studies. Lipids Health Dis. 2014 Aug 26;13:137.

[28]Scano P, Rosa A, Cesare Marincola F, Locci E, Melis MP, Dessì MA, Lai A. 13C NMR, GC and HPLC characterization of lipid components of the salted and dried mullet (Mugil cephalus) roe “bottarga”. Chem Phys Lipids. 2008 Feb;151(2):69-76

[29]Shimizu, Y., Oda, H., Seiki, K., & Saeki, H. (2015). Development of an enzyme-linked immunosorbent assay system for detecting β′-component (Onk k 5), a major IgE-binding protein in salmon roe. Food chemistry, 181, 310-317.

[30]Shimizu Y1, Kishimura H, Kanno G, Nakamura A, Adachi R, Akiyama H, Watanabe K, Hara A, Ebisawa M, Saeki H. Molecular and immunological characterization of β’-component (Onc k 5), a major IgE-binding protein in chum salmon roe. Int Immunol. 2014 Mar;26(3):139-47.

[31]Shimizu Y, Nakamura A, Kishimura H, Hara A, Watanabe K, Saeki H. Major allergen and its IgE cross-reactivity among salmonid fish roe allergy. J Agric Food Chem. 2009 Mar 25;57(6):2314-9.

[32]Shirai T, Watanabe Y, Lee MS, Ogawa T, Muramoto K. Structure of rhamnose-binding lectin CSL3: unique pseudo-tetrameric architecture of a pattern recognition protein. J Mol Biol. 2009 Aug 14;391(2):390-403.

[33]Shirai N, Higuchi T, Suzuki H. Effect of lipids extracted from a salted herring roe food product on maze-behavior in mice. J Nutr Sci Vitaminol (Tokyo). 2006 Dec;52(6):451-6

[34]Shirai, N., Higuchi, T., & Suzuki, H. (2006). Analysis of lipid classes and the fatty acid composition of the salted fish roe food products, Ikura, Tarako, Tobiko and Kazunoko. Food Chemistry, 94(1), 61-67.

[35]Tanaka K, Kondo Y, Inuo C, Nakajima Y, Tsuge I, Doi S, Yanagihara S, Yoshikawa T, Urisu A. Allergen analysis of sea urchin roe using sera from five patients. Int Arch Allergy Immunol. 2014;164(3):222-7

[36]Tateno H, Ogawa T, Muramoto K, Kamiya H, Saneyoshi M. Distribution and molecular evolution of rhamnose-binding lectins in Salmonidae: isolation and characterization of two lectins from white-spotted Charr (Salvelinus leucomaenis) eggs. Biosci Biotechnol Biochem. 2002 Jun;66(6):1356-65

[37]Terada T, Watanabe Y, Tateno H, Naganuma T, Ogawa T, Muramoto K, Kamiya H. Structural characterization of a rhamnose-binding glycoprotein (lectin) from Spanish mackerel (Scomberomorous niphonius) eggs. Biochim Biophys Acta. 2007 Apr;1770(4):617-29.

[38]Tocher DR, Sargent JR. Analyses of lipids and fatty acids in ripe roes of some Northwest European marine fish. Lipids. 1984 Jul;19(7):492-9.

[39]Wang, Q., Xue, C., Li, Z., & Xu, J. (2008). Analysis of DHA-rich phospholipids from egg of squid Sthenoteuthis oualaniensis. Journal of food composition and analysis, 21(4), 356-359.

[40]Wang, Q., Xue, Ch, Li, Z. J., & Xu, J. (2008). Phosphatidylcholine levels and their fatty acid compositions in squid egg: a comparison study with pollack roe and sturgeon caviar. Journal of Food Lipids, 15(2), 222-230.

[41]Watanabe Y, Shiina N, Shinozaki F, Yokoyama H, Kominami J, Nakamura-Tsuruta S, Hirabayashi J, Sugahara K, Kamiya H, Matsubara H, Ogawa T, Muramoto K. Isolation and characterization of l-rhamnose-binding lectin, which binds to microsporidian Glugea plecoglossi, from ayu (Plecoglossus altivelis) eggs.  Dev Comp Immunol. 2008;32(5):487-99.

[42]Watanabe Y, Tateno H, Nakamura-Tsuruta S, Kominami J, Hirabayashi J, Nakamura O, Watanabe T, Kamiya H, Naganuma T, Ogawa T, Naudé RJ, Muramoto K. The function of rhamnose-binding lectin in innate immunity by restricted binding to Gb3. Dev Comp Immunol. 2009 Feb;33(2):187-97.

[43]//en.wikipedia.org/wiki/Roe

[44]Shirai N, Higuchi T, Suzuki, H. A comparative study of lipids extracted from herring roe products and fish oil on plasma glucose and adipocytokine levels in ICR aged mice. Food Science and Technology Research, Vol. 14 (2008) No. 1, 25-31

[45]Nutritionist Pro Software, Version 4.7.0. Axxya Systems LLC. Redmond WA. //www.nutritionistpro.com/

[46]Bjørndal B, Burri L, Wergedahl H, Svardal A, Bohov P, Berge RK. Dietary supplementation of herring roe and milt enhances hepatic fatty acid catabolism in female mice transgenic for hTNFα. Eur J Nutr. 2012 Sep;51(6):741-53

[47]Pacific Plaza Imports Caviar label information. 1) Golden Whitefish Caviar, 2) Black Lumpfish Roe, 3) Black Capelin Roe. www.plazadecaviar.com

[48]Burri L, Hoem N, Banni S, Berge K. Marine omega-3 phospholipids: metabolism and biological activities. Int J Mol Sci. 2012 Nov 21;13(11):15401-19.

[49]Murru E, Banni S, Carta G. Nutritional properties of dietary omega-3-enriched phospholipids. Biomed Res Int. 2013;2013:965417. doi: 10.1155/2013/965417

[50]Ramprasath VR, Eyal I, Zchut S, Jones PJ. Enhanced increase of omega-3 index in healthy individuals with response to 4-week n-3 fatty acid supplementation from krill oil versus fish oil. Lipids Health Dis. 2013 Dec 5;12:178. doi: 10.1186/1476-511X-12-178.

[51]Rossmeisl M, Jilkova ZM, Kuda O, et al. Metabolic effects of n-3 PUFA as phospholipids are superior to triglycerides in mice fed a high-fat diet: possible role of endocannabinoids. PLoS One. 2012;7(6):e38834.

[52]Schuchardt JP, Schneider I, Meyer H, Neubronner J, von Schacky C, Hahn A. Incorporation of EPA and DHA into plasma phospholipids in response to different omega-3 fatty acid formulations–a comparative bioavailability study of fish oil vs. krill oil.  Lipids Health Dis. 2011 Aug 22;10:145. doi: 10.1186/1476-511X-10-145.

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

[54]Cordain L, Toohey L, Smith MJ, Hickey MS. Modulation of immune function by dietary lectins in rheumatoid arthritis. British Journal of Nutrition, 2000, 83:207-217.

[55]Kuzma JN, Cordain L. Ingestion of wheat germ in healthy subjects does not acutely elevate plasma wheat germ agglutinin concentrations. FASEB J 2010, 24:723.10 .

[56]Krajhanzl A, Horejsí V, Kocourek J.Studies on lectins. XLI. Isolation and characterization of a blood group B specific lectin from the role of the powan (Coregonus lavaretus maraena). Biochim Biophys Acta. 1978 Feb 15;532(2):209-14.

[57]Krajhanzl A, Horejsí V, Kocourek J. Studies on lectins. XLII. Isolation, partial characterization and comparison of lectins from the roe of five fish species. Biochim Biophys Acta. 1978 Feb 15;532(2):215-24.

[58]Nosek J, Krajhanzl A, Kocourek J. Studies on lectins. LVII. Immunofluorescence localization of lectins present in fish ovaries. Histochemistry. 1983;79(1):131-9.

[59]Krajhanzl A. Egg lectins of invertebrates and lower vertebrates: properties and biological function. Adv Lectin Res 1990; 3: 83-131.

Celtic Sea Salt | The Paleo Diet

Did you look into keltisch seasalt? (sic). I’ve read that it’s full of minerals and has the same balance between minerals and elements as our blood.

Willemieke Bakker on Sea Salt: Between the Devil and the Deep Blue Sea

Dr. Cordain’s Response:

“Celtic” sea salt, most commonly known as Sel gris or gray salt in French is harvested from seawater in the estuaries near the town of Guérande in France. As the tide comes in, seawater is first allowed to settle in clay silt ponds where the combined effects of wind and sun form a dense brine. The brine is then channeled to shallow salt pans dug in the native clay where it crystallizes via solar evaporation to form salt. The clay from the silt as well as from the salt pans impart Sel gris with its characteristic gray color. Sel gris is a coarse salt that is typically harvested with a moisture content of 15%, whereas most sea salts and commercially manufactured salt maintain moisture contents of less than 1%.

I know of no comprehensive, modern analysis of Sel gris, so it is difficult to determine if the harvesting of sea salt from the estuaries near Guérande affects the salt concentrations normally found in seawater. From a chemical perspective, there is no reason to expect that the relative concentrations of the dissolved elements normally found in sea water would be altered, unless the processing of Sel gris adds or subtracts elements. The salts in seawater are stable chemical compounds whose relative percentages are invariant.1, 2 The absolute weights of each of seawater’s dissolved salts will vary depending only upon the amount of moisture that is retained in Sel gris at harvest. Because Sel gris is typically harvested with a 15% moisture content, then the absolute weight of the dissolved salts will be about 85% of their equivalent amount in dry sea salt (<1 % moisture).

In the single account3 I am aware of, the following concentrations of dissolved salts were reported for Sel gris (100 grams):

  1. Sodium 34 grams
  2. Calcium 287 mg
  3. Potassium 109 mg
  4. Magnesium 34 mg
  5. Iron 11 mg,
  6. Manganese 1 mg
  7. Zinc 0.35 mg

Let’s take a look at these values and contrast them to normal dry (no moisture) sea salt or normal sea salt containing 15% moisture which is similar to Sel gris’ moisture content in the table below.

table1

We should first address a few important points:

  1. Does the data reported for Sel gris appear to be accurate?
  2. Is it possible that the addition of clay to sea salt increases its concentration of some minerals?
  3. Is it possible that evaporation of sea salt in clay pans could reduce the relative concentration of normal sea salts?
  4. Is Sel gris healthful and should it be a part of contemporary Paleo Diets?

To answer these questions we first must take a quick look at the minerals normally found in clays.4 Geologists have classified clay minerals into four groups:

  1. Kaolinite
  2. Illite
  3. Smectite
  4. Vermiculite

All clays are rich in iron (Fe) and magnesium (Mg).4 The principal cations in illites are potassium (K), calcium (Ca) and Mg; in smectites they are Ca, sodium (Na), Mg, Fe, Manganese (Mn) and zinc (Zn); in vermiculites the principle cation is Mg, but these compounds also contains significant quantities of Fe and Na. Accordingly, sea salts contaminated with residual clays during harvest might be expected to contain additional amounts of Na, Ca, Mg, Fe, Mn, Zn and/or K.

Indeed, if the reported Sel gris data is accurate, then the spreadsheet above confirms that Sel gris contains nearly 31% more salt (both sodium and chloride) than normal salt derived from sea water – definitely not a good thing health wise! Although some clays contain significant amounts of magnesium and potassium, the data above actually demonstrate Sel gris to maintain lower concentrations of both of these elements than normal sea salt. Regular sea salt represents a physiologically insignificant source of Ca and Fe, whereas the reported values for the reported Sel gris data are considerable higher. Whether these data are accurate or represent measurement errors is unknown. Although consumption of 100 grams of Sel gris delivers moderate quantities of Ca (287 mg) and Fe (11 mg), it does so at a terrible nutritional cost in terms of salt ingestion.   100 grams of Sel gris using reported data translates to 34 grams or 3400 mg of sodium. The United States Centers for Disease Control (CDC) recommends that we limit our sodium consumption to no more than 2300 mg per day.5

On paper, it may appear that Sel gris may be slightly more nutrient dense for a selected few mineral than normal sea salt, but the bottom line is that Sel gris, sea salt and common table salt all have undesirably high concentrations of NaCl (salt) which promote hypertension, osteoporosis, kidney stones, Menierre’s Syndrome (ear ringing), insomnia, motion sickness, asthma, and a variety of cancers.

Salt be it in the form of Sel gris, sea salt or plain commercial salt is definitely not Paleo.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

References

1. Castro P, Huber M. Marine Biology, McGraw-Hill, 9th Ed., New York, NY, 2012.

2. Baseggio G. 1974. The composition of seawater and its concentrates. Proc. 4th Int. Symp. Salt Vol. 2, pp. 351-358. Northern Ohio Geological Society, Inc., Cleveland, OH.

3. Bitterman, M. Salted: A Manifesto On The World’s Most Essential Mineral With Recipes. Ten Speed Press, New York, 2010.

4. //earth.usc.edu/~dfarris/Mineralogy/17_ClayMinerals.pdf

5. Centers for Disease Control and Prevention (CDC). Vital signs: food categories contributing the most to sodium consumption – United States, 2007 – 2008, February 7, 2012.

Sea Salt | The Paleo Diet

One of the most gratifying rewards of having written The Paleo Diet in 2002 and having been involved in the Paleo movement from its very beginnings is that I receive numerous queries about various nutritional aspects of this lifelong way of eating. Clearly, I nor anyone else, have an inside track to all dietary questions that may arise about contemporary Paleo diets. However, I am happy to share with you the information I have compiled over more than 25 years of my research into this fascinating topic.

As the Paleo Diet gains traction and notoriety worldwide, it seems that part of the original idea has become partially diluted as more and more people discover and write about this lifetime nutritional program. I am flattered by the huge number of Paleo books and cookbooks released to market and available for purchase on Amazon, Barnes & Noble, and other outlets. These books and authors are a testament to the worldwide success and effectiveness of The Paleo Diet.

Unfortunaely, as I browse Paleo cookbooks and magazine recipes, I see that many authors have decided to add sea salt to their recipes, presumably in lieu of regular salt. Before I get into the scientific details let me make it clear from the beginning that neither sea salt nor conventional manufactured salt should be considered “Paleo,” as both were rarely or never consumed by our hunter gatherer ancestors, and both maintain nutritional qualities that adversely affect our health when consumed regularly.1

Sea salt contains high concentrations of sodium chloride (NaCl), just like manufactured salt. Sea salt is nothing more than evaporated sea water and can be mined from naturally occurring beds of rock salt or manufactured by solar evaporation of sea water. The salinity (concentration of all dissolved salts) in sea water is usually 35 parts per thousand (35 0/00), but varies somewhat in various oceans.

Salinity of Seawater | The Paleo Diet

The salinity of sea water near the mouth of a large fresh water river, like The Amazon, is lower, but the percentages of all salts in all sea water remains constant.2, 3
 

Salt Dissolved | The Paleo Diet

Dissolved Salts | The Paleo Diet

You can see from the Table 1 and Figure 2 that sea salt contains high concentrations of salt (NaCl) amounting to 85.62% of all the dissolved salts. Now let’s contrast sea salt to commercially manufactured table salt. Table Salt is refined sea salt, rock salt or lake salt in which almost all impurities are removed leaving pure NaCl. Most table salt is produced using vacuum pan refining and is typically 99.8 to 99.95 pure NaCl.4 Under US law, 2% of salt by weight can include the following additives:

1. Anti-caking agents (typically calcium silicate) are added to table salt.
2. Frequently iodine (a mineral that prevents goiter) is added to table salt in the form of potassium iodide (0.006% to 0.01%).
3. Along with stabilizers (sodium bicarbonate, sodium thiosulfate or dextrose) to prevent degradation of the iodine.

There is absolutely no doubt that the average American consumes excessive amounts of salt which in turn may adversely affect health and well being.1

Total Salt | The Paleo Diet

Sources of Salt | The Paleo Diet

From Table 2 and Figure 3, you can see that far and away, processed foods are the highest contributor (77%) of salt to the American diet. Because processed foods generally are not part of the contemporary Paleo Diet, you will not have to worry about salt – that is unless you add sea salt to your Paleo menu and Paleo recipes. And if you do so, you can see that the salt (NaCl) concentration of sea salt (85.62%) is not much better than manufactured salt (99.8%).

In Table 3, I have presented the top 10 food sources of salt in the U.S. Diet.5 Note that almost all of these high salt foods are not part of The Paleo Diet. If you decide to prepare your Paleo meals or recipes with sea salt, you will be changing a once healthful, low-salt Paleo diet with to high salt diet. The choice is yours, but know that sea salt is not healthier than conventional salt and in fact, may be worse.

Top 10 Salt Sources | The Paleo Diet

On paper, it appears that sea salt is more nutrient dense than table salt and may be nutritionally superior? Unfortunately both salts have undesirably high concentrations of salt (NaCl) as I have pointed out. Animal studies show sea salt to increase hypertension (high blood pressure) compared to table salt.6, 7

Many people including physicians and nutritionists assume that salt’s (NaCl) detrimental health effects occur only from the sodium ion (Na) contained within salt. Yet human experimental studies show the chloride anion is also responsible.8, 9 Chloride (Cl) yields a net acid load to kidney producing a slight metabolic acidosis that promotes high blood pressure, osteoporosis and kidney stones. These diseases along with stomach cancer and stroke are also associated with high salt consumption. Other less well recognized chronic illnesses known to be caused by a high salt diet include: Menierre’s Syndrome (Ear ringing), insomnia, motion sickness, asthma and exercise induced asthma.

Finally, an obscure fact in medical literature is dietary salt loading in even healthy subjects has been shown via MRI to:

  • Increase intracellular Sodium (Na)
  • Reduce intracellular Potassium (K)
  • Increase intracellular Calcium (Ca)
  • Decrease intracellular Magnesium (Mg) and reduce intracellular ph (increases acidity)10

All of these intracellular ionic changes are known to be associated with or promoters of a variety of cancers.11-13

Salt is definitely not Paleo, and neither is sea salt.

Cordially,

Loren Cordain, Ph.D., Professor Emeritus

 

References

1. 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
2. Castro P, Huber M. Marine Biology, McGraw-Hill, 9th Ed., New York, NY, 2012.
3. Baseggio G. 1974. The composition of seawater and its concentrates. Proc. 4th Int. Symp. Salt Vol. 2, pp. 351-358. Northern Ohio Geological Society, Inc., Cleveland, OH.
4. Kurlansky M. Salt, A World History. Penguin Books, NY, NY, 2002.
5. Centers for Disease Control and Prevention (CDC). Vital signs: food categories contributing the most to sodium consumption – United States, 2007 – 2008, February 7, 2012.
6. Dahl LK, Heine M. The enhanced hypertensogenic effect of sea salt over sodium chloride. Am J Cardiol. 1961 Nov;8:726-31
7. Dahl LK, Heine M. Effects of chronic excess salt feeding. Enhanced hypertensogenic effect of sea salt over sodium chloride. J Exp Med. 1961;113:1067-76
8. Kurtz I et al. Effect of diet on plasma acid-base composition in normal humans. Kidney Int 1983;24:670-80
9. Boegehold MA, Kotchen TA. Importance of dietary chloride for salt sensitivity of blood pressure. Hypertension. 1991 Jan;17(1 Suppl):I158-61.
10. Resnick et al. Intracellular ionic consequences of dietary salt loading in essential hypertension. J Clin Invest 1994;94:1269-76
11. Jansson B. Geographic cancer risk and intracellular potassium/sodium ratios. Cancer Detection and Prevention 1986; 9:171-94
12. Lee AH, Tannock IF. Heterogeneity of intracellular pH and of mechanisms that regulate intracellular pH in populations of cultured cells. Cancer Res. 1998 May 1;58(9):1901-8.
13. Mijatovic T et al. Cardiotonic steroids on the road to anti-cancer therapy. Biochim Biophys Acta. 2007 Sep;1776(1):32-57.

Affiliates and Credentials