TRUTHITION

Under Pressure: The Truth About Blood Pressure

Was salt not the bad guy after all?

October 22, 2024 Truthition Team

Introduction

In recent years, there have been numerous ongoing changes and debates in the medical community regarding what constitutes hypertension, i.e., high blood pressure. Current American Heart Association standards place prehypertension at a systolic range of 120-129 and a diastolic range of less than 80. It is important to know why this information should be accurate for the average person, as it is the reference point to which it is determined whether one should be inclined to take drugs for reducing blood pressure (such as beta blockers, diuretics, ACE inhibitors, and more) or if they should avoid them. Concerningly, there is evidence to suggest that drug companies have been deliberately trying to lower blood pressure guidelines to sell more of these drugs.

This article will shed light on this correlation and use evidence gathered from scientific resources to show what really is a healthy blood pressure level, the risks of medication, causes of high blood pressure, certain natural treatments that may work even more effectively than the drugs frequently prescribed to lower blood pressure, and debunk common myths about blood pressure to reveal the little-known science behind this topic.

Lowering Standards, Raising Profits

The official guideline range of hypertension has a history of change. More specifically, what constitutes high blood pressure has been steadily lowering over the years. What was initially classified as stage 1 hypertension, 160/90, has now dropped to 130/80-89. Despite a multitude of research to suggest that the latter range is closer to normal than “high”, the World Health Organization (WHO) and the federal National Institutes of Health have both been calling for a reduction of the numbers in these guidelines. There is evidence to suggest that these decisions may be financially motivated by drug companies. As stated in a 2005 article from The Seattle Times, "In May 2003, for example, an NIH panel recommended broader use of hypertension drugs at lower blood pressures. Nine of the 11 authors of the guidelines had ties to the drug companies."^[1]

To determine if current blood pressure guidelines are physiologically accurate, it is useful to look at where the guidelines originated from. The Framingham Heart Study is a famous study that analyzes patterns in families primarily in relation to cardiovascular health. The study began in 1948, recently passing its 75th year of continuous, multi-generational research, examining over 4,000 participants to determine risk factors for cardiovascular disease and, relevantly, its correlation with blood pressure. In January of 2000, there was a reevaluation of the data from the Framingham Heart study published in The Lancet that concluded the medical consensus of 140 mm Hg (now 130 mm Hg) systolic pressure being the cut-off value for high blood pressure was contradictory to the popular study that founded the cut-off value itself. Furthermore, the study states that “there is an age-dependent and sex-dependent threshold for hypertension. A substantial proportion of the population who would currently be thought to be at increased risk are, therefore, at no increased risk.”^[2,3]

^{https://academic.oup.com/eurheartj/article/21/20/1635/469051 [3]}

For reference, 140 mm Hg systolic pressure is now the current cut-off value for stage 2 hypertension according to the American Heart Association. Not only does the reevaluation discredit these guidelines, it also shows that the study data disproves the positive linear correlation between systolic blood pressure and mortality rates. This age and sex-dependent threshold for treating hypertension is found by using the formula provided in the reevaluation for ages up to 74:

For Men: 110 + (2/3)(age)

For Women: 104 + (5/6)(age)

This would mean that, for a 55-year-old man, the systolic cut-off value for hypertension is 146-147 mm Hg. This data suggests that there is more to these guidelines than typically assumed, and that older guidelines were likely more accurate before the recent reductions of these numbers. Moreover, instead of a linear correlation between higher mortality and higher systolic blood pressure as is currently used when establishing these guidelines, it is more accurate to say that there is a sharp increase in mortality upon reaching significantly higher blood pressure levels.

^{https://www.math.ucla.edu/~scp/publications/mortality.PDF [2]}

Pressure to be Healthy

As previously discussed, healthy blood pressure levels can vary according to age, sex, and numerous other variables. It was also shown that after a sharp point, between a systolic pressure of 170 to 180, only then does mortality begin to rise significantly. Another analysis of evidence from the Framingham Heart Study published in Open Heart further supports this.^[4]

The linear model commonly used to estimate the risks of high blood pressure is now shown to overestimate the risk in pressure based on provided data. Furthermore, this overestimation can put a significant portion of the population at risk who may not need or benefit from the treatment they are recommended.^[3] When using this data in clinical trials, as opposed to the linear models assumed in the previous discussion, one may see a significant benefit in reducing systolic pressure from 180 to 160, whereas there would be no benefit in reducing it from 160 to 140. As stated in the paper, “no randomized trial has ever demonstrated any reduction of the risk of either overall or cardiovascular death by reducing systolic blood pressure from our thresholds to below 140 mmHg.”^[3]

Data from the CDC also supports the view that the risks of high blood pressure may be overstated: “although about 67% of people over 70 are hypertensive, about 0.04% between 65 and 74, 0.1% between 75 and 84, and 0.39% over 85 die each year due to their HBP (including hypertensive heart disease)”.^[4]

Moreover, for those with acute heart failure, there is a 2006 study performed within an in-hospital setting with over 48,600 patients. This study found that at lower systolic blood pressures there was actually a rise in mortality rates. At higher blood pressures, there was a decrease in in-hospital mortality rates.

^{Mortality rates in patients with acute heart failure [5]}

It is not just acute heart failure patients, either: another large study published in Oxford journal Age and Ageing was done on geriatric patients, also displaying a decrease in mortality risk with “higher-than-normal” blood pressures.^[6] Below is a table of the data from the study:

^{https://academic.oup.com/ageing/article/44/6/932/80958 [6]}

Using what has been gathered from previous evidence of the Framingham study, using the median age of 82, and taking into account that the subjects were mostly female:

High Systolic Blood Pressure Cutoff: 104 + (5/6)(82) = 172.3 mm Hg.

It’s quite interesting that it falls right within the range of lowest mortality overall—anything significantly below that appears to increase risk of death considerably, and anything above 180 mm Hg also has a moderately large rise in deaths. Unsurprisingly, one could conclude that 140/90 (i.e., stage 2 hypertension according to the AHA) is not a universal guideline to determine high blood pressure, contrary to common belief. Moreover, it was stated in the study that some of these individuals were using drugs to lower blood pressure, the most prominent being ACE inhibitors. If these drugs did what they are marketed to do, and assuming that lower blood pressure is actually healthier, why would there be so many deaths found in that group of people?

A study published in 2020 had the aim of evaluating if geriatric patients in the 70s-80s age range benefited from having their blood pressure artificially lowered below 140/90 via anti-hypertensive treatment. Given previous results, it should come as no surprise that the non-normalized blood pressure group in their 80s had a statistically significant lower risk of all-cause mortality. Interestingly, the patients aged 70-79 years did not have a notable difference in risk with or without artificially lowered blood pressure. However, in both of these groups, the group with “previous cardiovascular events” did have a substantial increase in mortality with artificially lowered blood pressures, in fact about a 55% higher risk per year.^[7]

A 2015 publication in Science Daily regarding a study performed by the University of Alabama Birmingham also states, “Compared to people with systolic blood pressure below 120 mmHg without treatment, hypertensive individuals on three or more blood pressure medications had a stroke risk of 2.5 times higher.”^[8] The article also provides great advice to reduce body fat and take part in physical activity to lower blood pressure; however, its recommendation to reduce salt intake is ineffective and potentially harmful, which will be discussed further in-depth later.

Some studies have found an increased risk of lung cancer with high dose usage of Angiotensin-Converting Enzyme (ACE) inhibitors, a common hypertension medication. For example, a Danish study published in Journal of the American Heart Association found that there was a moderately increased lung cancer risk for high overall doses of ACE inhibitors.^[9] A meta-analysis of 2400 records screened in 2022 also showed that there was a strong link between ACE inhibitors and lung cancer.^[10]

Beta blockers are another less common type of medication for high blood pressure. They block the effects of adrenaline on the body, causing the heart to beat slower and with less force, overall lowering pressure. A 21-year study with 37,581 obstructive sleep apnea patients concluded that for those who used beta blockers, CVD (cardiovascular disease) outcomes increased by 3.5% and all-cause mortality by 0.9% compared to those who did not use them.^[11]

Individuals should not be relying solely upon blood pressure medication — in fact, taking into consideration the data discussed in this article, it would not be a stretch to claim that at least the majority of those with hypertension should avoid blood pressure medication altogether.

Many doctors treat high blood pressure as a disease to be cured with medication. Accounting for the evidence above, it can be inferred that using many types of medication may have side effects including an increased risk of death. However, the root of the problem is not the high blood pressure, but rather other underlying issues that present the high blood pressure as a symptom of a disease, not the disease itself.

Don’t Shoot the Messenger

There is a multitude of research to suggest that diseases like atherosclerosis are associated with high blood pressure. In fact, many scientific journals cite high blood pressure as the cause of atherosclerosis. For context, atherosclerosis is the buildup of plaque in the arteries that causes the arteries to narrow or clog. Many articles and studies cite high blood pressure as a direct cause of atherosclerosis, but this view fails to hold up to scrutiny.

High blood pressure is simply the heart beating harder, causing the arteries to undergo a greater amount of stress. Limbs require a certain amount of designated blood flow to keep them functioning. If, for some reason, the arteries were narrowed, perhaps due to arterial plaque caused by a separate disease, the heart would be required to pump harder and/or faster to provide the same amount of blood to keep the limbs alive and moving. It lacks sense that a heart pumping harder would cause arterial plaque; conversely, it appears logical that arterial plaque would cause the heart to pump harder. This flawed correlation is why hypertension is frequently considered a cause of CVD, even if it may not be true.

It may be stated that when hypertensive medication is used successfully, it can lower rates of mortality and CVD. Many trials have been published to demonstrate this. However, these trials largely ignore the fact that many of these medications have direct cardiovascular benefits that may treat the diseases which coexist with blood pressure. It doesn’t necessarily have to affect the blood pressure directly, but only treat the cardiovascular diseases it is associated with, subsequently lowering blood pressure. An October 2000 publication in the European Heart Journal states this clearly: “It is widely believed that randomized trials have proved that lowering blood pressure is beneficial. However, that is not true. All antihypertensive drugs have profound effects on the cardiovascular system, aside from their hemodynamic effect. How much, if any, of the observed risk relationship can be ascribed to the reduction in pressure and how much to the direct action of the drug on the cardiovascular system? Motivated by the belief in the linear relationship of risk to pressure, many automatically attribute the risk reduction to the pressure reduction, ignoring the direct action of the drugs on the target outcomes. Results from a multitude of clinical trials make it clear that such a simplistic view cannot be true. In fact, evidence is mounting (especially from more recent trials) that it is the direct effects that are producing most, if not all, of the benefit and that the accompanying blood pressure reduction may be just an inconsequential side effect.^[3]

Furthermore, a paper published in Journal of the American Heart Association in 2003 came to an interesting conclusion in regards to the ALLHAT study: “benefits beyond BP reduction had been attributed to some anti-hypertensive drug classes, ie, improved survival and reduced morbidity in persons with heart failure or left ventricular dysfunction treated with angiotensin-converting enzyme (ACE) inhibitors8 –10 and improved insulin sensitivity and lipid profiles with a-blocker treatment.”^[12]

One last statistic to emphasize the point: lisinopril (an ACE inhibitor) and amlodipine, a calcium-channel blocker, among other drugs, has been demonstrated to be less effective than chlorthalidone, a thiazide-type diuretic (or “water pill”) at preventing CVD while being considerably more expensive. For instance, lisinopril had 1.5% higher rates of combined CVD compared to chlorthalidone. Their conclusion was as follows: “Thiazide-type diuretics are superior in preventing 1 or more major forms of CVD and are less expensive. They should be preferred for first-step antihypertensive therapy.”^[13] Note that the mortality rates for these groups did not differ. This means that each medication is probably no more or less dangerous than another.

This further solidifies the argument that these medications are doing notably more than merely lowering blood pressure. If high blood pressure is not the cause of these diseases, could hypertension instead be a symptom of these diseases? To determine this, it may be useful to examine potential causes of high blood pressure.

The Pressure Cooker

One of the most common causes of hypertension, both short-term and long-term, is stress. Stress and powerful negative emotions have been consistently linked to higher blood pressures.^[14] Human bodies are biologically designed to induce stress via hormones such as cortisol and adrenaline, intentionally raising blood pressure to allow the limbs to move quicker, the brain to focus better, and to generally handle a stressful situation more effectively. Hypertension is a symptom of stress, whether chronic or acute.

As aforementioned, another cause of high blood pressure is clogging of the arteries, which is itself a symptom of any disease that may result in plaque buildup, such as CHD. Diseases like diabetes are also known to have a strong correlation with hypertension. Hyperinsulinemia (abnormally high insulin levels), commonly associated with type 2 diabetes, can cause hypertension. Insulin resistance may also be a cause.^[15]

Excess body fat, obesity, and a sedentary lifestyle also contribute to high blood pressure.^[16,17] In men and women, 26% and 28% of high blood pressure cases can be attributed to excess fat tissue or obesity, respectively.^[18] In many cases, high blood pressure may be treated simply by making lifestyle changes. This data further demonstrates that hypertension may not be a disease that causes symptoms itself, but conversely a symptom of other diseases and poor lifestyle habits. It is true that medication can help treat high blood pressure and perhaps even other diseases; however, it is far from the only, safest, or most effective method. Along with healthy dietary choices, regular exercise, and reducing stress, there are other effective methods to lower blood pressure, such as increasing potassium intake.

The Potassium Prescription

As discussed in previous sections, medications have several risks and should only be used if necessary. Fortunately, there are natural solutions to high blood pressure for those who truly need them. The most effective method for naturally lowering blood pressure may be simply increasing potassium intake: a randomized cross-over trial examining elderly hypertensive patients found that long-term potassium supplementation (4 months / 48mmol daily) was significantly effective for lowering blood pressure in the subjects compared to placebo. In the first month of taking 60mmol (~2,340mg) daily, the subjects had a BP of 160/89. Some of the subjects continued for 4 months of 48mmol (~1,872mg) daily and had their BP drop down to 147/83.^[19]

Even individuals whose blood pressures fall within medical guidelines can benefit from increasing potassium intake. A national survey performed by the CDC from 2017 to 2018 concluded that the average potassium intake of the U.S. population older than 2 years is 2,496mg,^[20] falling short of both the male and female Adequate Intake (AI) of 3,400mg and 2,600mg, respectively.

The consequences of widespread potassium deficiency are broad. In a study published in 1997, researchers analyzed blood and urine specimens of 11,600 people to determine risk factors for coronary heart disease and mortality. The researchers concluded that there was “an unexpectedly powerful protective relation of dietary potassium to all cause mortality.” ^[21]

With the significance of these improvements and protective effects, some may wonder how potassium, a mineral that is already in the food we consume, isn’t the first-line treatment for high blood pressure. Increasing potassium has little to no side-effects, especially compared to blood pressure medication; even high doses have not shown negative effects in studies, with the exception of increasing potassium intake in concurrence with drugs that artificially heighten blood potassium levels. Overall, high potassium doses over extended periods of time appear to be safer and more effective than traditional first-line treatment medication.

How To Get Your K Fix

There are numerous ways that people can get more potassium in their diet. Fruits, fruit juices, vegetables, and milk are among the best and easiest foods to implement. Bananas, potatoes, raisins, prunes, and coconut water contain high amounts of potassium. To consume an additional 1,900mg of potassium daily, it is viable to eat 4 large bananas, or 1 ¼ lbs potatoes, or a little over half a pound of raisins. Fruit juices, dairy, and vegetables are another option. 2 cups of orange juice nets 886mg of potassium. 2 cups of whole milk provide 644mg. Finally, one cup of chopped, fresh spinach packs 838mg.

Is It Salt’s Fault?

It is without question that there are many people, doctors included, who recommend restricting salt intake to treat high blood pressure. While salt restriction can indeed have a mild effect on blood pressure, its benefit is typically highly exaggerated and potentially dangerous. A 1998 meta-analysis on studies randomizing subjects with high and low-sodium diets concluded that for hypertensive individuals across 58 trials, reduced sodium intake lowered systolic blood pressure by an average of 3.9 mm Hg, and diastolic blood pressure by an average of 1.9 mm Hg. The mean consumption of sodium was 118 mmol—i.e., 2,700mg—per 24 hours.^[22] The same meta-analysis also examined 56 trials of reduced sodium intake on subjects with normal blood pressures. The mean reduced sodium intake was 160mmol, i.e., 3,678mg. This lowered blood pressure by 1.2mm Hg and .26 mm Hg on systolic and diastolic blood pressures, respectively.

For reference, the AHA currently recommends “no more than 2,300 mg a day and moving toward an ideal limit of no more than 1,500 mg per day for most adults,”^[23] with such recommendations being aimed at reducing hypertension and cardiovascular disease. The “reduced sodium intake” in the paper was 2.45x more than the “ideal limit” that the AHA recommends. In this meta-analysis, it did not significantly alter blood pressure. The authors concluded: “These results do not support a general recommendation to reduce sodium intake. Reduced sodium intake may be used as a supplementary treatment in hypertension.”

Sodium is, in fact, absolutely necessary for our bodies to function. Our bodies cannot synthesize it either, therefore it must be obtained from the diet. Despite the antagonistic view many hold against salt, higher sodium intake has been shown in studies to lower rates of cardiovascular death and hospitalization for congestive heart failure,^[24] reduce cardiovascular disease mortality and all-cause mortality rates,^[25,26] and improve potassium and magnesium retention.^[27] Sodium also balances water and electrolytes, and it is a requirement for every cell to function properly.^[28] It is necessary for numerous functions in the body, such as metabolic and nerve functions.

Why We Can’t Shake Salt Cravings

It has been shown that during salt depletion, the human body craves salty foods.^[29] In fact, many other animals have been shown to be able to pick their own diets for proper development and growth. Humans are no exception. An experiment on three infants in a hospital published in Chicago in October of 1928 suggests that human infants who have been recently weaned are able to successfully choose their own diets for proper human development and growth. There may be an instinctive desire for specific foods that have the nutrients their body knows they must obtain to survive. What the authors wrote regarding the infants’ salt consumption is interesting: “Salt they ate only occasionally, often spluttering, choking or even crying bitterly after getting it in the mouth but never trying to spit it out and frequently going back for more, with a repetition of the same spluttering, etc.”^[30] This begs the question: despite the fact that the children clearly did not like the taste, why did they keep going back for more? Either humans are born masochists, or more plausibly, their body instinctively recognized they needed salt in their diets. Note that no salt was added to any of the foods given to the toddlers. Naturally, the infants didn’t eat salt too often, as pure salt gives the body more than enough sodium even in what would be relatively small quantities.

It is easy to perform this experiment firsthand and return the same results. If one deliberately practices a very low-sodium diet, they will almost certainly find themself craving salt. Some people already do for health reasons and succumb to this craving on a daily basis. It is for these reasons provided that one may argue salt restriction is highly unphysiological.

Word of Caution

If, after reading all of the compiled research above regarding high blood pressure, medication risks, and potential solutions, you decide to quit your current medication, caution is advised. While it is safe to increase potassium intake and avoid sodium restriction, if you believe your blood pressure is too high, it is best to consult your doctor before quitting a medication, as ceasing use of medication abruptly has serious health risks. Additionally, every individual is different and there may be underlying issues that a doctor knows about you to better cater to your circumstances than this article can.

Turning the Pressure Down

Myths busted, science explained, and solutions provided—the research doesn’t lie. This article has touched on the history of dropping blood pressure guidelines, the truth that most people with clinical hypertension are not at risk, the popularly misled blame of hypertension as a disease rather than a symptom, the underlying causes of hypertension, the risks of hypertensive medication and how to treat high blood pressure safely and effectively with potassium, and why salt restriction is ineffective and dangerous. Deconstructing dogma and examining the data, there is a strong case to be made against the current medical recommendations for hypertensive individuals. Through challenging widely held beliefs and proposing a more nuanced point of view, Truthition aspires to spark a shift in perspective that leads to more personalized and effective approaches to health, improving individual outcomes and advancing the overall understanding of our bodies.

Citations

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[8] University of Alabama at Birmingham. "Blood pressure medications can lead to increased risk of stroke." ScienceDaily. ScienceDaily, 29 May 2015. .

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[10] Wu, Zhenchao, et al. “Association between Angiotensin-Converting Enzyme Inhibitors and the Risk of Lung Cancer: A Systematic Review and Meta-Analysis.” Nature News, Nature Publishing Group, 17 Nov. 2022, www.nature.com/articles/s41416-022-02029-5.

[11] Chen, Anthony, et al. “Impact of beta-blockers on mortality and cardiovascular disease outcomes in patients with obstructive sleep apnoea: A population-based cohort study in Target Trial Emulation Framework.” The Lancet Regional Health - Europe, vol. 33, Oct. 2023, p. 100715, https://doi.org/10.1016/j.lanepe.2023.100715.

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[13] Furberg, Curt D., et al. “Major Outcomes in High-Risk Hypertensive Patients Randomized to Angiotensin-Converting Enzyme Inhibitor or Calcium Channel Blocker vs Diuretic.” JAMA, American Medical Association, 18 Dec. 2002, jamanetwork.com/journals/jama/fullarticle/195626.

[14] Gordon, Amie M., and Wendy Berry Mendes. “A large-scale study of stress, emotions, and blood pressure in daily life using a digital platform.” Proceedings of the National Academy of Sciences, vol. 118, no. 31, 29 July 2021, https://doi.org/10.1073/pnas.2105573118.

[15] Sowers, J R, and S Khoury. “Diabetes and hypertension: a review.” Primary care, vol. 18,3 (1991): 509-24.

[16] Hall, John E., et al. “Obesity, kidney dysfunction and hypertension: Mechanistic links.” Nature Reviews Nephrology, vol. 15, no. 6, 23 Apr. 2019, pp. 367–385, https://doi.org/10.1038/s41581-019-0145-4.

[17] Koenen, Mascha, et al. “Obesity, adipose tissue and vascular dysfunction.” Circulation Research, vol. 128, no. 7, 2 Apr. 2021, pp. 951–968, https://doi.org/10.1161/circresaha.121.318093.

[18] Schmieder, R E, and F H Messerli. “Does obesity influence early target organ damage in hypertensive patients?” Circulation, vol. 87, no. 5, May 1993, pp. 1482–1488, https://doi.org/10.1161/01.cir.87.5.1482.

[19] Fotherby, M D, and J F Potter. “Long-Term Potassium Supplementation Lowers Blood Pressure in Elderly Hypertensive Subjects.” International Journal of Clinical Practice, U.S. National Library of Medicine, June 1997, pubmed.ncbi.nlm.nih.gov/9287262/

[20] Hoy, M. Katherine. “Potassium Intake of the U.S. Population.” FSRG Dietary Data Briefs [Internet], U.S. National Library of Medicine, Sept. 2022, www.ncbi.nlm.nih.gov/books/NBK587683/.

[21] Tunstall-Pedoe, Hugh, et al. “Comparison of the Prediction by 27 Different Factors of Coronary Heart Disease and Death in Men and Women of the Scottish Heart Health Study: Cohort Study.” The BMJ, British Medical Journal Publishing Group, 20 Sept. 1997, www.bmj.com/content/315/7110/722.

[22] Graudal, N A et al. “Effects of sodium restriction on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride: a meta-analysis.” JAMA, vol. 279, 17 (1998): 1383-91. doi:10.1001/jama.279.17.1383

[23] “How Much Sodium Should I Eat per Day?” American Heart Association, 5 Jan. 2024, www.heart.org/en/healthy-living/healthy-eating/eat-smart/sodium/how-much-sodium-should-i-eat-per-day.

[24] Stolarz-Skrzypek, Katarzyna. “Fatal and nonfatal outcomes, incidence of hypertension, and blood pressure changes in relation to urinary sodium excretion.” JAMA, vol. 305, no. 17, 4 May 2011, p. 1777, https://doi.org/10.1001/jama.2011.574.

[25] O’Donnell, Martin J., et al. “Urinary sodium and potassium excretion and risk of cardiovascular events.” JAMA, vol. 306, no. 20, 23 Nov. 2011, https://doi.org/10.1001/jama.2011.1729.

[26] HORTON, R., & BIGLIERI, E. G. (1962). “Effect of Aldosterone on the Metabolism of Magnesium.” The Journal of Clinical Endocrinology & Metabolism, vol 22, no. 12, 1 December 1962, Pages 1187–1192, https://doi.org/10.1210/jcem-22-12-1187

[27] Cohen, Hillel W., et al. “Sodium intake and mortality in the NHANES II follow-up study.” The American Journal of Medicine, vol. 119, no. 3, Mar. 2006, https://doi.org/10.1016/j.amjmed.2005.10.042.

[28] Bernal, Antonio, et al. “Sodium Homeostasis, a Balance Necessary for Life.” National Library of Medicine, U.S. National Library of Medicine, 12 Jan. 2023, www.ncbi.nlm.nih.gov/pmc/articles/PMC9862583/.

[29] Beauchamp, GK, et al. “Experimental sodium depletion and salt taste in normal human volunteers.” The American Journal of Clinical Nutrition, vol. 51, no. 5, May 1990, pp. 881–889, https://doi.org/10.1093/ajcn/51.5.881.

[30] DAVIS, C. M. (1928). SELF SELECTION OF DIET BY NEWLY WEANED INFANTS. American Journal of Diseases of Children, 36(4). doi:10.1001/archpedi.1928.01920280002001