Fake Health News: Low Salt is best! - Prescriptive Optimization

The FAKE HEALTH NEWS section of the blog originated from various material I presented to our Rotary club called the Bull session where the speaker quizzes different tables to extract money (for a good cause). This is one of the slides I put up:

Screen Shot 2018-08-05 at 2.25.32 PM

The red text is the correct, or false, statement in this case.

Salt is absolutely critical for optimal body function, yet it is also heavily maligned.

I mentioned in a post previously, that a great book for understanding salt physiology is The Salt Fix, and I will pull a couple clips from it to address a couple of the bullets in the slide above.

In fact, the stress on our kidneys mainly comes from having to conserve salt and reabsorb all of the 3.2 to 3.6 pounds of salt that we filter every day.43 This reabsorption requires us to use up adenosine triphosphate (ATP), the energy created from the food we ingest that’s utilized by our cells to facilitate many bodily functions. Our sodium pump uses approximately 70 percent of the basal energy expended by the kidneys,44 making a low-salt diet an energy hog and a tremendous stress to the kidneys. This is one way that low-salt diets can lead to weight gain, by slowly depleting our energy stores and leading us to become more sedentary.¹

Translation, to respond to low dietary salt intake, the kidneys must spend copious amounts of energy to retain salt passing through. Simply excreting salt is a free transaction energy wise, so appropriate amounts of salt in the diet allows the kidney to operate much more efficiently energetically speaking.

Scientific research suggests that the optimal range for sodium intake is 3 to 6 grams per day (about 1⅓ to 2⅔ teaspoons of salt) for healthy adults, not the 2,300 milligrams of sodium (less than 1 teaspoon of salt) per day that’s commonly advised. And some people need even more. ²

At the 1,500mg cited in the AHA materials, it is highly likely the kidneys will be called on to burn thru cellular energy to conserve all the salt they can. But, it isn’t simply an energy draining problem as we will see, there are other signals sent to compensate.

It is these other mechanisms that cause copious problems and consequences, represented very well by the image below.

salt taste ³

This shows that low salt changes your palate. By decreasing the salt (Na+) sensitivity you will consume more before you get that “too much salt” sensation, by design.

The image also shows how the final bullet from the quiz is addressed. Low salt causes cardiac stress via Angiotensin and Aldosterone.

AII has several very important functions:

Constricts resistance vessels (via AII [AT₁] receptors) thereby increasing systemic vascular resistance and arterial pressure

Stimulates sodium transport (reabsorption) at several renal tubular sites, thereby increasing sodium and water retention by the body

Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase sodium and fluid retention

Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary, which increases fluid retention by the kidneys

Stimulates thirst centers within the brain

Facilitates norepinephrine release from sympathetic nerveendings and inhibits norepinephrine re-uptake by nerve endings, thereby enhancing sympathetic adrenergic function

Stimulates cardiac hypertrophy and vascular hypertrophy⁴

Interpretation. Low salt causes a cascade of events that lead to cardiac stress via increased adrenergic stimulation which causes blood vessel constriction. It also causes cardiac hypertrophy, enlarging of the heart, as well as vascular resistance and arterial pressure increases. To me that sounds like it is not so good for the heart, how about to you?

Strong evidence is above that shows low salt causes unfavorable changes in cardiac physiology, and these changes are consistent with what many pharmaceuticals target.

Millions of people are on ACE inhibitors such as lisinopril or ARB drugs such as losartan or candesartan. Looking at the taste receptor image above, they act on angiotensin-converting enzyme and some angiotensin receptors respectively.

At this point we can see that there are two choices in how to prevent these cardiac consequences; (1) maintain adequate dietary salt intake or (2) medicate targets on the pathway activated by low salt. Enter the AHA and their low salt campaign, as they seem to be locked on to option 2. Why?

Let’s follow the AHA money trail from their own website:

⁵

Astra Zeneca contributes the most money of anybody on the list, 41%. Wikipedia has cataloged the medications they manufacture⁶, I selected the relevant ones to this conversation:

The following products are found on the AstraZeneca website.^[72] Generic drug names are given in parentheses following the brand name.

This list is incomplete; you can help by expanding it.

– Cardiovascular

Atacand (candesartan cilexetil)

Betaloc (metoprolol tartrate)

Brilinta/Brilique/Possia (ticagrelor)

Crestor (rosuvastatin; 2003 launch)

Inderal (propranolol)

Lexxel (enalapril/felodipine)

Logimax (felodipine/metoprolol)

Nif-Ten (nifedipine/atenolol)

Ramace (ramipril)

Seloken XL/Toprol-XL/Betaloc ZOC (metoprolol succinate extended-release)

Tenoretic (atenolol/chlortalidone)

Tenormin (atenolol)

Unimax (felodipine/ramipril)

Zestoretic (lisinopril/hydrochlorothiazide)

Zestril (lisinopril)

Quick and easy summary of where these work:

those generic names ending in ril (e.g. lisinopril) block the Angiotensin Converting Enzyme
candesartan works by blocking angiotensin II receptors, known as ARB’s
those ending in olol (e.g. atenolol) are beta blockers which work to blunt the effects of adrenergic stimulation via norepinephrine and epinephrine (adrenaline)

The commonality here is all these pharmaceutical targets being exploited are activated as a direct result of sodium deficiency.

Conclusion; low salt = massive opportunity for drug sales! The AHA’s low salt campaign appears to be helping their major contributor in a huge way.

I, as a pharmacist, have dispensed many of these prescriptions to people. I was trained on how beneficial these medications are, and they have many studies backing their effectiveness. I did not put all of this together from the causation side though until reading this passage from the Salt Fix:

As we’ve also seen, many people with normal blood pressure, prehypertension, and hypertension may even get a rise in their blood pressure if they restrict their salt intake.18 This is because when salt intake is severely limited, the body begins to activate rescue systems that avidly try to retain more salt and water from the diet. These rescue operations include the renin-angiotensin aldosterone system (well known for increasing blood pressure) and the sympathetic nervous system (well known for increasing heart rate).19 Clearly, this is the opposite of what you want to happen! ⁷

When I read that low salt activated this pathway that has been used to sell millions of prescriptions, my jaw dropped and I tossed my kindle to the other side of the couch. I hope I am wrong with drawing the parallels above but it seems pretty ominous.