How Much Salt, How Much Sugar?

How Much Salt, How Much Sugar?

Published on nirmukta.com on Oct 7, 2012

Food is one of the most important driving forces of evolution and is probably one of the most important causes for the modern day diseases. As our understanding of the modern diseases is growing, Dobzhansky’s famous statement, ‘nothing in biology makes sense except in the light of evolution’, is becoming truer. Over the past 10000 years, we have engineered a rapid evolution in our food and lifestyles, ‘producing’ our food in our own backyards. Processing of food, from the simple grinding to the more refined packaging, has weaned us away from natural foods such as vegetables, fish and meat towards mostly cereal based readymade foods. Such food processing has also brought in many additives to enhance taste and to make the food more palatable and likeable. Two such most important additives are the table salt and table sugar. Any consensus on the desired daily doses of these two inseparable additives of our modern diet has been elusive and is likely to remain so, considering the fact that there are many interests pulling in different directions – the health care industry, the Big Pharma, the food industry and the researchers burning their bulbs on their own or with corporate funding.

How Much Salt?

A little appetite for salt is well known, with even animals, particularly herbivores, going on long treks for salt-licks.[1] Sodium is an essential nutrient, being the principal cation of extracellular fluid and a major determinant of intravascular fluid volume, and maintenance of the volumes of these fluid compartments is very much vital to sustain the tissue perfusion and normal cellular metabolism.[1] Numerous stretch and chemoreceptors along the vascular bed that sense the blood volume and the sodium levels help in controlling the blood flow, cardiac output and renal functions.[1]

A natural diet made of greens and meat has a high potassium (K + )/sodium (Na + ) ratio of about 20:1 in herbivores and 5:1 in carnivores.[2] Our ancestral diet had at least 4 times more potassium, [3,4] with large amounts of potassium (>200 mmol/day) from vegetables, berries and meat and as little as 2–30 mmol of sodium per day.[4] That food was also rich in HCO3-yielding precursors like citrate, but contained little chloride. Human biological machinery evolved to process this high dietary potassium, our kidneys tending to excrete potassium and conserve sodium.[4] Kidneys respond to large load of sodium by conserving water and lack of sodium is managed by improved conservation.

Although addition of salt in our food has been in practice for more than 2000 years, [5] our consumption of sodium has increased manifold over the last 200 years, with salt (sodium chloride) being added at any stage before, during or after food-processing as well as before, during or after cooking.[2,4] During the same period, consumption of potassium and HCO3 – yielding substances has declined, and as a result, with the advent of the modern diet, both the K + /Na + and HCO3 – /Cl – ratio have become reversed.[4] But our kidneys that evolved to process the ancient diet remain largely unchanged, and the electrolytic mix of the modern diet is therefore mismatched to its genetically determined processing machinery.[4]

At present, the usual intake of sodium in developed societies ranges from about 100 mmol (2400 mg) to 225 mmol (5175 mg) per day.[1] Many isolated physically active population groups living in remote rural areas have been found to be living on less than 50 mmol (1150 mg) sodium per day and in these unacculturated societies, blood pressure is low and does not increase with age, and hypertension is uncommon.[1]

Even after several studies involving thousands of people, the question of our daily requirement of sodium chloride remains unanswered. Data from over 52,000 subjects have revealed that a 100 mmol rise in sodium intake led to only a modest rise in systolic blood pressure in the range of 1–3 mm Hg and diastolic blood pressure of 0–2 mmHg. On the other, a large series of intervention studies, in which salt was either withheld or supplemented, have shown that a reduction in sodium of approximately 100 mmol/day led to a reduction in systolic blood pressure of 4–5 mm Hg, and a fall in diastolic blood pressure of 1–3 mm Hg.[5] But too much restriction can be counter-productive, leading to marked reduction of the extracellular sodium space and intense activation of the vasoconstricting neuro-hormonal systems including activation of the renin- angiotensin-aldosterone axis, increased resistance to the metabolic actions of insulin etc.[1] Salt restriction at population level has been reported to produce a 1% decrease in blood pressure in normotensives, a 3.5% decrease in hypertensives, a significant increase in plasma renin, plasma aldosterone, plasma adrenaline and plasma noradrenaline, a 2.5% increase in cholesterol, and a 7% increase in triglyceride[6] and to increase the risk for cardiovasuclar disease, heart attacks, stroke, diabetes, and all cause mortality, while providing only a minimal reduction in blood pressure.[6-9] Accordingly, some authors have even termed sodium reduction at population level as “probably the largest delusion in the history of preventive medicine.”[9] Restriction of salt (1800mg/day) in patients with heart failure has also been reported to increase mortality.

What appears to be more important and useful is the reversal of the high sodium-potassium ratio of the present day diet, by reducing sodium chloride and increasing potassium rich vegetables and meat.[4,10-12]

How Much Sugar?

Refined sugar (sucrose, glucose+fructose) was never a part of our ancient diet. Our requirements of carbohydrates are also quite small [13] and we can get all that from our daily vegetables. Several papers have been published in recent years have blamed fructose as the biggest villain for the increasing epidemic of metabolic syndrome disorders such as obesity, type 2 diabetes, hypertension, vascular disease etc.,[14-19] and Lustig et al, in a comment published in Nature, dated Feb 2, 2012, have argued that such dangers to health justify controlling sugar like alcohol, by imposing higher taxes, limiting sales during school hours, and placing age limits on purchasing.[20]

Therefore, the conclusion is simple: Eat a little salt to taste and increae the consumption of vegetables, but avoid sugar completely.

References:

1. 1. Logan AG. Dietary Sodium Intake and its Relation to Human Health: A Summary of the Evidence. J Am Coll Nutr June 2006;25(3):165-169. Available at https://www.tandfonline.com/doi/10.1080/07315724.2006.10719528
   2. Dahl LK. Possible role of salt intake in the development of essential hypertension. Int. J. Epidemiol. October 2005;34(5):967-972. doi: 10.1093/ije/dyh317. Available at https://academic.oup.com/ije/article/34/5/967/645873
   3. Sebastian A, Frassetto LA, Sellmeyer DE, Morris Jr RC. The Evolution-Informed Optimal Dietary Potassium Intake of Human Beings Greatly Exceeds Current and Recommended Intakes. Seminars in Nephrology. November 2006;26(6):447-453. Abstract at https://pubmed.ncbi.nlm.nih.gov/17275582/
   4. Morris RC Jr, Schmidlin O, Frassetto LA, Sebastian A. Relationship and interaction between sodium and potassium. J Am Coll Nutr. 2006 Jun;25(3 Suppl):262S-270S. Available at https://pubmed.ncbi.nlm.nih.gov/16772638/
   5. Hollenberg NK. The Influence of Dietary Sodium on Blood Pressure. J Am Coll Nutr June 2006;25(suppl. 3):240S-246S. Available at https://pubmed.ncbi.nlm.nih.gov/16772635/
   6. Graudal NA, Hubeck-Graudal T, Jurgens G. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Cochrane Database of Systematic Reviews 2011, Issue 11. Art.No.: CD004022. DOI: 10.1002/14651858.CD004022.pub3. Available at https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD004022.pub3/full
   7. Stolarz-Skrzypek K, Kuznwtsova T, Thijs L, et al. Fatal and nonfatal outcomes, incidence of hypertension, and BP changes in relation to urinary sodium excretion. JAMA. 2011;305:1777-1785. Available at https://jamanetwork.com/journals/jama/fullarticle/899663
   8. Folkow B. On bias in medical research; reflections on present salt-cholesterol controversies. Scandinavian Cardiovascular Journal Aug 2011;45(4):194–197. Available at https://www.tandfonline.com/doi/10.3109/14017431.2011.588899?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
   9. Graudal N, Jürgens G. The sodium phantom. BMJ. 2011 Sep 27;343:d6119. doi: 10.1136/bmj.d6119. Available at https://www.bmj.com/content/343/bmj.d6119.full
   10. Cook NR et al. Joint effects of sodium and potassium intake on subsequent cardiovascular disease: the Trials of Hypertension Prevention follow-up study. Arch Intern Med. Jan 2009;169(1):32-40. Available at https://pmc.ncbi.nlm.nih.gov/articles/PMC2629129/
   11. Yang Q et al. Sodium and Potassium Intake and Mortality among US Adults: Prospective Data From the Third National Health and Nutrition Examination Survey. Arch Intern Med. 2011;171(13):1183- 1191. doi:10.1001/archinternmed.2011.257. Available at https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1106080
   12. Drewnowski A, Maillot M, Rehm C. Reducing the sodium-potassium ratio in the US diet: a challenge for public health. Am J Clin Nutr August 2012;96(2):439-444. Available at https://www.sciencedirect.com/science/article/pii/S0002916523028848?via%3Dihub
   13. Manninen AH. Metabolic Effects of the Very-Low-Carbohydrate Diets: Misunderstood ‘Villains’ of Human Metabolism. J Int Soc Sports Nutr. 2004;1(2):7–11. doi: 10.1186/1550-2783-1-2-7. Available at https://pmc.ncbi.nlm.nih.gov/articles/PMC2129159/
   14. Johnson RJ et al. Potential role of sugar (fructose) in the epidemic of hypertension, obesity and the metabolic syndrome, diabetes, kidney disease, and cardiovascular disease. Am J Clin Nutr. 2007;86(4):899-90. Available at https://www.sciencedirect.com/science/article/pii/S0002916523135052?via%3Dihub
   15. Rizkalla SW. Health implications of fructose consumption: A review of recent data. Nutrition and Metabolism 2010;7:82 doi:10.1186/1743-7075-7-82. Available at https://pmc.ncbi.nlm.nih.gov/articles/PMC2991323/
   16. Tappy L, Lê KA. Metabolic Effects of Sweetened Beverages: Pathophysiology and Mechanistic Insights. CMR e Journal December 2010;3(3):13-18. Available at https://www.myhealthywaist.org/cmrejournal/articles/vol3/v3i3a4.php
   17. 18. Tappy L. Q&A: ‘Toxic’ effects of sugar: should we be afraid of fructose? BMC Biology 2012;10:42 doi:10.1186/1741-7007-10-42. Available at https://bmcbiol.biomedcentral.com/articles/10.1186/1741-7007-10-42
   18. Lustig RH. Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol. J Am Diet Assoc. 2010;110:1307-1321. Available at https://www.lv-pharm.rs/wp-content/uploads/2018/01/Fructose-Metabolic-Hedonic-and-Societal-Parallels-with-Ethanol.pdf
   19. Lindeberg S. Paleolithic diets as a model for prevention and treatment of western disease. Am. J. Hum.Biol. March/April 2012;24(2):110–115. Available at https://onlinelibrary.wiley.com/doi/full/10.1002/ajhb.22218
   20. Lustig RH, Schmidt LA, Brindis CD. The Toxic Truth about Sugar. Nature. February 2012;482:27–29. doi:10.1038/482027a. Available at https://www.nature.com/articles/482027a