Prepare To Be Salt Struck

ASalt One good way of looking at salt, is to see it as an all purpose, metabolism enhancing, stress reducing, anti-inflammatory, disease protective, anxiolytic, anti-depressant. Now that was a mouthful, wasn’t it?

As a general rule, when dietary sodium is restricted, thyroid energy metabolism is interfered with. Another way of saying this is that insufficient salt intake, tends to promote a variety of biochemical changes, that can increase stress, promote inflammation, and encourage thyroid metabolism dysfunction, causing all sorts of disease symptoms.

Although it isn’t easy to find all of this information in one place, it is possible to put together a good case for the metabolically protective, stress lowering effects, of increasing salt consumption, by consolidating a number of biologically related pieces of the puzzle.

For starters, salt restriction alone, has been demonstrated to increase stress, for instance by increasing levels of the catecholamines, such as adrenaline and noradrenaline. Excessive exposure to stress, is something that is well known to interfere with metabolic function.

It’s important to understand, that an overly stressed, suppressed metabolism, shifts away from the efficient use of sugar, towards the increased release of fat from storage, as an alternative source of fuel.

Rising exposure to free fatty acids, in particular when they are increasingly polyunsaturated (PUFAs) in composition, is well known to cause inflammation, and in many different ways, to further promote stress and suppress thyroid function.

This kind of high stress scenario, can itself promote a greater loss of sodium, and is also associated with an additional rise in the release of the stress substances, including adrenaline. This can potentially create a vicious circle of stress.

When thyroid energy metabolism is under functioning, digestion tends to be impaired, which then allows for bacteria to feed and grow in number, and for greater absorption of bacterial toxins, like endotoxin, to enter into the blood stream. Digestive health and mental health are closely tied to each other, in both directions.

Bacterial endotoxin is directly inflammatory, and causes an increase in serotonin levels, and both of these stress substances, interfere with energy metabolism, and have been shown to increase symptoms of stress, anxiety and depression.

The more the thyroid system is interfered with, the more the stress system goes into action, and this means more adrenaline. More exposure to adrenaline and other mediators of stress, interferes with sleep, increases anxiety levels, and promotes many of the stress related diseases of inflammation. Improving sleep is important for healing, and this includes mood regulation issues in general.

Simply increasing salt intake is something which is known to be able to help prevent or reduce metabolic stress, and protect against inflammatory illness, in a multitude of ways.

Sufficient salt consumption can suppress adrenaline, raise body temperature, and improve sleep quality. Increasing body temperature, has alone been shown to be able to treat chronic and serious depression. More sodium can also help improve digestion, and this can result in the reduction of bacterial endotoxin exposure, thereby lowering secretion of serotonin and many other inflammatory stress related things that also cause metabolic issues and mood disorders.

Low serum sodium is connected with high HDL (the so called ‘good cholesterol’), which contrary to popular opinion, has been shown to rise in response to endotoxin exposure and excessive stress in general, and which rather than being an indicator of improved health, is actually associated with increased mortality.

It makes sense that increasing salt intake, by improving metabolism and lowering stress in general, can also improve overall cholesterol regulation, including helping with conversion of cholesterol into the protective steroid hormones, such as testosterone and progesterone.

Hyponatremia or low levels of sodium in the blood, activates the renin‐angiotensin‐aldosterone system (RAAS), and chronic activation of the RAAS, can be responsible for congestive heart failure, systemic hypertension, and chronic kidney disease.

Excessive exposure to angiotensin II and aldosterone promotes fibrosis, and the inflammatory milieu responsible for remodeling cardiovascular tissue seen in heart disease. A low sodium diet has been shown to cause aortic damage and to increase heart rate, even with reduced blood pressure.

Insufficient salt intake and the activation of the renin‐angiotensin‐aldosterone system (RAAS), interferes with blood sugar regulation, and promotes insulin resistance. Inhibition of this system by increasing salt intake, can improve blood sugar regulation and reduce the incidence of diabetes, as well as mortality from cardiovascular disease. Blood sugar issues, heart disease, suppressed thyroid, and depression and anxiety, often go together for metabolically explainable reasons.

Both diabetes and cardiovascular disease have been shown to be connected to high stress, inflammation, and thyroid issues, including exposure to increased amounts of endotoxin and PUFAs. In patients with type 2 diabetes, lower urinary sodium excretion has been associated with increased all-cause mortality, and the highest mortality risks were observed in patients with the lowest sodium intake.

Apart from being able to promote hypertension, thyroid dysfunction has also been shown to be a cause of hyponatremia, and limiting water intake and increasing sodium, is known to be able to be an effective treatment for this, as well as even for cases of severe hyponatremia with epileptiform seizures.

Hyponatremia is able to cause sudden onset dementia, which again has been reversed by increasing serum sodium. It is probably no coincidence, that Alzheimer’s has also been shown to be an inflammatory disease, that is closely associated with hypo-metabolism and the substances of stress, including exposure to endotoxin and the breakdown products of the PUFAs. Again, dementia and mood dysregulation are closely tied together.

Stress and hypothyroidism is connected with iron dysregulation, and the relationship between inflammation, endotoxin exposure, iron excess, and dementia, is practically undeniable. Insufficient salt consumption is very likely to be an exacerbating factor.

Serum sodium levels in hyponatremia, are inversely correlated with many markers of inflammatory disease, including C-reactive protein and the inflammatory cytokines serum IL-6 and IL-1β, and it has been hypothesized that hyponatremia may be associated with inflammatory diseases in general.

Reduced serum sodium levels have also been inversely correlated with increased prostaglandin levels, involved in worsening congestive heart failure. In fact, reduced blood levels of sodium are considered a risk factor for mortality in critically ill patients, and there are many cases of hospital patients dying as a result of being given plain water, without first checking for hyponatremia.

Rather than being responsible for high blood pressure, sufficient salt intake can be something which helps to reduce hypertension, often resulting from stress and hypothyroidism issues, including the excessive release of adrenaline, cortisol, serotonin, and a number of related factors. Lack of salt can also cause a rise in cortisol and serotonin levels, and SSRI ‘anti-depressants’, which are intended to increase serotonin levels, have been shown to be able to cause hyponatremia and serotonin syndrome simultaneously, both of which are potentially life threatening. Not surprisingly, SSRIs have also been associated with worsening depression, anxiety and increased suicide.

Also related to this, over-activity of the HPA axis and high cortisol, seem to go together with significantly increased aldosterone levels in cases of depression. As mentioned earlier, aldosterone is known to rise as a result of sodium restriction.

Nitric oxide is another thing which rises during stress and when digestion and metabolism is suppressed, and excessive exposure has been found to be able to promote hypertension. Increased salt consumption has been shown to lower nitric oxide (which may be responsible for the temporary blood pressure lowering effects of salt restriction), and nitric oxide powerfully suppresses energy metabolism. This is another important factor driving inflammatory illness, including depression, anxiety and cancer.

There is a powerful connection between metabolic function, and the relationship between sodium and the other alkaline minerals, magnesium, potassium and calcium. The hypothyroid state is closely linked to the biological interactions between these minerals, and they have all been shown to play a part in mood instability issues.

One of the early things that happens when stress is high and thyroid energy metabolism is under functioning (when oxygen or glucose availability is interfered with, and ATP production is impeded), is that there is an impact upon proper sodium regulation in the body. This impacts upon alkaline mineral homeostasis in general, which can then go on to have stress increasing consequences. Providing enough sugar, and avoiding the stress promoting and inflammatory PUFAs is one way to help keep the minerals in balance.

High serum lactate levels, are another good indicator of stress and suppressed metabolic function, and in combination with low serum sodium levels, have been shown to be a significant predictor of mortality in necrotizing soft-tissue infections (NSTI), often involving sepsis and multisystem organ failure. Increased lactic acid (often combined with increased bacterial endotoxin exposure), is another driver of mood related issues, including anxiety and panic attacks.

Extra intake of salt can go a long way towards improving the regulation of all the alkaline minerals, protecting against deficiencies in (and preventing excessive wastage of) any of them, helping to guard against mood dysregulation and inflammatory illness in general. Sufficient intake of calcium and magnesium and potassium is still very important however, and many metabolic issues, including mood issues, can be prevented or reduced with an increased and balanced intake, from the right sources.

In any case, it appears that enough salt consumption is a very important factor, and it has been observed that loss of calcium and magnesium can be increased with sodium restriction, and insufficient sodium intake can continue to interfere with calcium and magnesium levels, even when calcium and magnesium intake is sufficient.

On the other hand, increasing magnesium has been shown to cure depression in a number of ‘treatment resistant’ cases, and hypertension has been proven to very often be the result of insufficient calcium intake.

Regardless, a large number of studies have shown that symptoms of depression and anxiety rise when metabolism is damaged in numerous different ways, and when the various stress substances (such as cortisol, nitric oxide, estrogen and serotonin) are increased because of the impact of the low energy or hypo-metabolic state.

Estrogen excess is closely associated with thyroid dysfunction and inflammation, as well as mood dysregulation, and it makes sense to see salt as an anti-estrogen substance in many ways, includung via protection against the inflammatory stress substances like bacterial endotoxin, via promotion of the anti-estrogen hormones, and simply via the up-regulation of energy system function in general.

I’m not a doctor or a nutritionist, but from what I have seen, it appears that adequate intake of salt, and the other important minerals, can help protect against metabolic dysfunction, and shift the body away from chronic sympathetic nervous system over-activity. Salt seems to also help protect against many of the inflammatory conditions (including diabetes, cancer and heart disease), which are all known to develop and worsen, because of damage to energy production systems, and excessive exposure to the defensive stress substances that play a big part in harming metabolism in the first place.

The combination of gradually increased consumption of simple sugar and salt (in the context of an appropriate anti-inflammatory, pro-metabolic diet and lifestyle) can be one of the significant things, that can lead to vast improvements in the biochemical, hormonal and nervous system related issues, which underlie the progression of many kinds of chronic diseases, or disturbances of the mind.

A diet with enough protein and other nutrients from milk, cheese and gelatinous meats, as well as plenty of sugar from sweet ripe fruits, fruit juice, honey and white sugar, has been shown to be a biologically reasonable approach to improving anxiety or depression and related inflammatory issues. Experimenting with gradually increasing salt intake (some say starting at 5 grams spread over the day), can potentially be the missing link to lowering stress and getting energy metabolism to start working again.

Salt cravings, as with sugar cravings, are very common, and can be one way to determine how much is needed at a particular time, however it is also possible that salt cravings can increase to compensate for other deficiencies, or because of increased stress in general. It’s important to be aware of the fact that metabolic issues can be complicated, and that blindly following one approach, without being aware of other possibilities, and without noticing changing symptoms and metabolic indicators, can be problematic. This is especially true in more serious circumstances, when metabolism is severely impeded. Keep in mind however, that much like with sugar, so called ‘high salt diets’ are very often high in problematic ingredients, like the PUFAs, that can be responsible for issues related to sodium homeostasis, many times incorrectly blamed on salt consumption.

A salty sugary drink, like for instance milk or orange juice with a few pinches of salt, and added sugar or honey, can, when taken during the day and before bed (or even when awakening during the night), help to improve sleep quality, which in and of itself, will likely alleviate many issues of stress and inflammation, which can have a powerful effect on mood states, and resilience to stressful life circumstances.

Have you experimented with increasing your salt intake?

See More Here

J Hypertens. 1993. Effect of dietary salt restriction on urinary serotonin and 5-hydroxyindoleacetic acid excretion in man. Sharma AM, et al.

J Card Fail. 2009. Long-term effects of dietary sodium intake on cytokines and neurohormonal activation in patients with recently compensated congestive heart failure. Parrinello G, et al.

Arch Surg. 2007;142(9):840-846. Use of Admission Serum Lactate and Sodium Levels to Predict Mortality in Necrotizing Soft-Tissue Infections. Arezou Yaghoubian, MD; Christian de Virgilio, MD; Christine Dauphine, MD; et al

Journal Of Neuroscience Research, Volume95, Issue11Special Issue: Energy Metabolism and Neuron‐Glia Interactions in Brain: From Molecular Mechanisms to Novel Therapeutic Approaches, November 2017, Pages 2275-2285. Differential effects of energy deprivation on intracellular sodium homeostasis in neurons and astrocytes. Niklas J. Gerkau, Cordula Rakers, Gabor C. Petzold, Christine R. Rose.

Metabolism. 2011. Low-salt diet increases insulin resistance in healthy subjects. Garg R, et al.

Hypertension. 2013 Nov;62(5):836-43. Serum chloride is an independent predictor of mortality in hypertensive patients. McCallum L, Jeemon P, Hastie CE, Patel RK, Williamson C, Redzuan AM, Dawson J, Sloan W, Muir S, Morrison D, McInnes GT, Freel EM, Walters M, Dominiczak AF, Sattar N, Padmanabhan S.

FASEB Journal Vol. 31, No. 1_supplement April 2017. Low Sodium Intakes are Not Associated with Lower Blood Pressure Levels among Framingham Offspring Study Adults. Lynn L. Moore, Martha R. Singer, and M. Loring Bradlee

J Physiol Biochem. 2016 Dec;72(4):635-641. Aldosterone changes after consumption of a sodium-bicarbonated mineral water in humans. A four-way randomized controlled trial. Toxqui L, Vaquero MP.

PLoS One. 2017 May 8;12(5):e0177086. Low-sodium diet induces atherogenesis regardless of lowering blood pressure in hypertensive hyperlipidemic mice. Fernanda B. Fusco,Diego J. Gomes,Kely C. S. Bispo,Veronica P. Toledo,Denise F. Barbeiro,Vera L. Capelozzi,Luzia N. S. Furukawa,Ana P. P. Velosa,Walcy R. Teodoro,Joel C. Heimann,Eder C. R. Quintao,Marisa Passarelli,Edna R. Nakandakare,Sergio Catanozi

Intern Med. 2000 Dec;39(12):1075-8. Hyponatremia with increased plasma antidiuretic hormone in a case of hypothyroidism. Nakano M, Higa M, Ishikawa R, Yamazaki T, Yamamuro W.

Probl Endokrinol (Mosk). 1987 Jan-Feb;33(1):18-21. Russian. [Characteristics of the hydration status of patients with hypothyroidism]. Nazarov AN, Lobachik VI, Zhidkov VV, Borisov GI, Abrosimov SV.

Hormone and Metabolic Research 37(7):455-9 · July 2005. Aldosterone Inhibits Uncoupling Protein-1, Induces Insulin Resistance, and Stimulates Proinflammatory Adipokines in Adipocytes. Daniel Kraus, J Jäger, B Meier, M Fasshauer.

Endocrine Abstracts (2008) 15 P354. Hypo-osmolar hyponatremia and orthostatic hypotension as the chief symptom in primary hypothyroidism. Arif Ullah, Kamal Abouglila, Logan Thirugnanasothy & Helen Cooper.

International Journal of Hypertension Volume 2011, Article ID 685238, 8 pages. Role of the Renin-Angiotensin System and Aldosterone on Cardiometabolic Syndrome. P. Stiefel, A. J. Vallejo-Vaz, S. García Morillo, and J. Villar


Med Hypotheses. 2006;67(2):362-70. Rapid recovery from major depression using magnesium treatment. Eby GA, Eby KL.

J Clin Endocrinol Metab. 1991. Effects of sodium supplementation during energy restriction on plasma norepinephrine levels in obese women. Gougeon R, et al.

BMC PsychiatryDecember 2003, 3:15. The Renin-Angiotensin-Aldosterone system in patients with depression compared to controls – a sleep endocrine study. Harald Murck, Katja Held, Marc Ziegenbein, Heike Künzel, Kathrin Koch, Axel Steiger.

Front Physiol. 2016 Mar 24;7:111. Reduced Dietary Sodium Intake Increases Heart Rate. A Meta-Analysis of 63 Randomized Controlled Trials Including 72 Study Populations. Graudal NA, Hubeck-Graudal T, Jürgens G.

Am J Med. 2017 Nov;130(11):1324.e7-1324.e13. Elevated High-Density Lipoprotein Cholesterol Is Associated with Hyponatremia in Hypertensive Patients. Israel A, Grossman E.

Swiss Med Wkly. 2012 Sep 17;142:w13669. Thyroid function and serum electrolytes: does an association really exist? Schwarz C, Leichtle AB, Arampatzis S, Fiedler GM, Zimmermann H, Exadaktylos AK, Lindner G.

Circ Res. 2005 Feb 4;96(2):252-60. Overexpression of inducible nitric oxide synthase in rostral ventrolateral medulla causes hypertension and sympathoexcitation via an increase in oxidative stress. Kimura Y, Hirooka Y, Sagara Y, Ito K, Kishi T, Shimokawa H, Takeshita A, Sunagawa K.

J Athl Train. 2010 Jul-Aug;45(4):364-71. Sweat Rates, Sweat Sodium Concentrations, and Sodium Losses in 3 Groups of Professional Football Players. Godek SF, Peduzzi C, Burkholder R, Condon S, Dorshimer G, Bartolozzi AR.

Nutr Metab Cardiovasc Dis. 2006 Mar;16(2):148-55. High- or low-salt diet from weaning to adulthood: effect on body weight, food intake and energy balance in rats. Coelho MS, Passadore MD, Gasparetti AL, Bibancos T, Prada PO, Furukawa LL, Furukawa LN, Fukui RT, Casarini DE, Saad MJ, Luz J, Chiavegatto S, Dolnikoff MS, Heimann JC.

Am J Hypertens. 2001 Feb;14(2):155-63. Effect of salt loading on nitric oxide synthase expression in normotensive rats. Ni Z, Vaziri ND.

American Journal of Hypertension, Volume 25, Issue 1, January 2012, Pages 1–15. Effects of Low-Sodium Diet vs. High-Sodium Diet on Blood Pressure, Renin, Aldosterone, Catecholamines, Cholesterol, and Triglyceride (Cochrane Review). Niels A. Graudal, Thorbjørn Hubeck-Graudal, Gesche Jürgens

Int J Sport Nutr Exerc Metab. 2005 Dec;15(6):641-52. Sweat and sodium losses in NCAA football players: a precursor to heat cramps? Stofan JR, Zachwieja JJ, Horswill CA, Murray R, Anderson SA, Eichner ER.

Korean J Pediatr. 2013 Dec;56(12):519-22. Inflammation and hyponatremia: an underrecognized condition? Park SJ, Shin JI.

Endocrinol Metab Clin North Am. 1994. Hypertension in thyroid disorders. Saito I, et al.

PLoS One. 2017 Jun 27;12(6):e0180067. Role of magnesium supplementation in the treatment of depression: A randomized clinical trial. Tarleton EK, Littenberg B, MacLean CD, Kennedy AG, Daley C.

Clinical Chemistry, Vol. 59, Issue 6June 2013. Inhibition of the Renin-Angiotensin System Reduces the Rise in Serum Aldosterone in Acute Coronary Syndrome Patients with Preserved Left Ventricular Function: Observations from the AVANT GARDE-TIMI 43 Trial. Jacob A. Udell, David A. Morrow, Eugene Braunwald, Karl Swedberg, Christoph Bode, Nader Rifai, Patrick C. Brunel, Margaret F. Prescott, Fang Ren, Elaine B. Hoffman, Benjamin M. Scirica

Iranian Journal of Psychiatry and Behavioral Sciences: 11 (4); e8013, June 11, 2017. Concurrent Serotonin Syndrome and Hyponatremia: A Case Report and Review. Forouzan Elyasi, Marzieh Azizi

Journal of Veterinary Internal Medicine, Volume33, Issue2March/April 2019, Pages 363-382. The renin‐angiotensin‐aldosterone system and its suppression. Marisa K. Ames, Clarke E. Atkins, Bertram Pitt.

J Nutr Sci Vitaminol (Tokyo). 2005 Aug;51(4):265-70. Positive correlation between dietary intake of sodium and balances of calcium and magnesium in young Japanese adults–low sodium intake is a risk factor for loss of calcium and magnesium–. Nishimuta M, Kodama N, Morikuni E, Yoshioka YH, Matsuzaki N, Takeyama H, Yamada H, Kitajima H.

Diabetes Care. 2011 Mar;34(3):703-9. Dietary Salt Intake and Mortality in Patients With Type 2 Diabetes. Ekinci EI, Clarke S, Thomas MC, Moran JL, Cheong K, MacIsaac RJ, Jerums G.

Magnes Res. 2016 Mar 1;29(3):112-119. Magnesium and depression. Serefko A, Szopa A, Poleszak E.

Practical Laboratory Medicine, Volume 8, August 2017, Pages 30-33. An analysis of the relationship between serum cortisol and serum sodium in routine clinical patients. Eleanor McLaughlan, Julian H.Barth

American Journal of Hypertension, Volume 28, Issue 3, March 2015, Pages 362–371. Relationship Between Nutrition and Blood Pressure: A Cross-Sectional Analysis from the NutriNet-Santé Study, a French Web-based Cohort Study. Helene Lelong, Pilar Galan, Emmanuelle Kesse-Guyot, Leopold Fezeu, Serge Hercberg, Jacques Blacher

N Engl J Med. 1984 Feb 9;310(6):347-52. Prostaglandins in severe congestive heart failure. Relation to activation of the renin–angiotensin system and hyponatremia. Dzau VJ, Packer M, Lilly LS, Swartz SL, Hollenberg NK, Williams GH.

Diabetes Care. 2011. Endotoxemia is associated with an increased risk of incident diabetes. Pussinen PJ, et al.

Am J Med. 2013. Dietary sodium restriction: take it with a grain of salt. DiNicolantonio JJ, et al.

J Nutr Sci Vitaminol (Tokyo). 2003 Jun;49(3):201-9. Negative balance of calcium and magnesium under relatively low sodium intake in humans. Kodama N, Nishimuta M, Suzuki K.

PLoS One. 2017 Jun 7;12(6):e0178977. Hyponatremia and increased risk of dementia: A population-based retrospective cohort study. Mu-Chi Chung,Tung-Min Yu,Kuo-Hsiung Shu,Ming-Ju Wu,Chao-Hsiang Chang,Chih-Hsin Muo,Chi-Jung Chung.

Med Hypotheses. 2006;67(2):362-70. Rapid recovery from major depression using magnesium treatment. Eby GA, Eby KL.

Pflugers Arch. 2015 Mar;467(3):445-56. The biopsychology of salt hunger and sodium deficiency. Hurley SW, Johnson AK.

Am J Hypertens. 1997 Jul;10(7 Pt 1):720-7. Chronic salt overload increases blood pressure and improves glucose metabolism without changing insulin sensitivity. da Costa Lima NK, Lima FB, dos Santos EA, Okamoto MM, Matsushita DH, Hell NS, Heimann JC.

PLoS One. 2017 Dec 8;12(12):e0189099. Excessively low salt diet damages the heart through activation of cardiac (pro) renin receptor, renin-angiotensin-aldosterone, and sympatho-adrenal systems in spontaneously hypertensive rats. Okamoto C, Hayakawa Y, Aoyama T, Komaki H, Minatoguchi S, Iwasa M, Yamada Y, Kanamori H, Kawasaki M, Nishigaki K, Mikami A, Minatoguchi S.

J Hypertens. 2003 Jan;21(1):153-7. Nitric oxide production decreases after salt loading but is not related to blood pressure changes or nitric oxide-mediated vascular responses. Dishy V, Sofowora GG, Imamura H, Nishimi Y, Xie HG, Wood AJ, Stein CM.

J Nutr Sci Vitaminol (Tokyo). 2018;64(2):83-89. Dietary Salt (Sodium Chloride) Requirement and Adverse Effects of Salt Restriction in Humans. Nishimuta M, Kodama N, Yoshitake Y, Shimada M, Serizawa N.

J Physiol Anthropol. 2015 Jun 25;34:26. Salt intake and mental distress among rural community-dwelling Japanese men. Shimizu Y, Kadota K, Koyamatsu J, Yamanashi H, Nagayoshi M, Noda M, Nishimura T, Tayama J, Nagata Y, Maeda T.

Synapse, Volume27, Issue 1 September 1997 Pages 36-44. Thyroid hormones and the treatment of depression: An examination of basic hormonal actions in the mature mammalian brain. William Nolan Henley, Thomas Joseph Koehnle.

Hypertens Res. 1997 Mar;20(1):57-60. Restriction of dietary sodium may enhance nitric oxide production in rats. Nishimura M, Takahashi H, Nanbu A, Ohtsuka K, Yoshimura M. 

American Journal of Hypertension, Volume 25, Issue 7, July 2012, Pages 727–734. Dietary Sodium Intake and Cardiovascular Mortality: Controversy Resolved? Michael H. Alderman, Hillel W. Cohen

Minerva Psichiatr. 1992 Jul-Sep. Hyponatremia, cause of reversible dementia in the elderly. Pentimone F, et al.

JAMA. 2011;305(17):1777-1785. Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion. Katarzyna Stolarz-Skrzypek, MD, PhD; Tatiana Kuznetsova, MD, PhD; Lutgarde Thijs, MSc; et al.

Trends Pharmacol Sci. 2011 Dec;32(12):734-9. Renin-angiotensin-aldosterone system and glucose homeostasis. Luther JM, Brown NJ.

Br Med J (Clin Res Ed). 1986 Jan 18;292(6514):168-70. Treatment of hyponatraemic seizures with intravenous 29.2% saline. Worthley LI, Thomas PD.

BMC Medicinevolume 15, Article number: 144 (2017). The renin–angiotensin system: a possible new target for depression. João Vian, Círia Pereira, Victor Chavarria, Cristiano Köhler, Brendon Stubbs, João Quevedo, Sung-Wan Kim, André F. Carvalho, Michael Berk & Brisa S. Fernandes

Curr Opin Endocrinol Diabetes Obes. 2010 Jun;17(3):199-204. Aldosterone and Inflammation. Gilbert KC, Brown NJ.

The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 6, 1 June 2003, Pages 2376–2383. Aldosterone: Direct Effects on and Production by the Heart. Perrin C. White.

Atherosclerosis. 2008 Oct;200(2):410-6. Dietary salt restriction increases plasma lipoprotein and inflammatory marker concentrations in hypertensive patients. Nakandakare ER, Charf AM, Santos FC, Nunes VS, Ortega K, Lottenberg AM, Mion D Jr, Nakano T, Nakajima K, D’Amico EA, Catanozi S, Passarelli M, Quintão EC.

Diabetology & Metabolic Syndromevolume 6, Article number: 90 (2014). The involvement of aldosterone on vascular insulin resistance: implications in obesity and type 2 diabetes. Thiago Bruder-Nascimento, Marcondes AB da Silva & Rita C Tostes.

Hydration State Controls Stress Responsiveness and Social Behavior. Eric G. Krause, Annette D. de Kloet, Jonathan N. Flak, Michael D. Smeltzer, Matia B. Solomon, Nathan K. Evanson, Stephen C. Woods, Randall R. Sakai and James P. Herman.

Physiol Behav. 2011 Jul 6;103(5):453-8. Low dietary sodium is anxiogenic in rats. Leshem M.


Image: Rakkard: “A salt with a deadly weapon”

You may also like...

Leave a Reply

Your email address will not be published. Required fields are marked *

Please "like" us:Already liked? You can close this