True and true. And I also doubt a low K ratio is the source of all that ails us. Meat is source of potassium - nose to tail. Yes, I’d like to see something about K ratio of typical meat. Not farmed grain-fed but meat on the hoof. I’d especially like to see something on Pleistocene megafauna. There are studies on modern bison. I’ll do a doc search later after I get home from work.
True, and I agree it would have been helpful to include the Maasai and the Inuit for comparison. To the best of my knowledge - to date - our Pleistocene ancestors did not consume significant quantities of plant based nutrients for the simple reason there were few to consume. Even plants that they did consume were quite nutrient dilute. Some researchers claim otherwise, but I have yet to see convincing evidence. Nuts, for example, may have been a seasonal, occasional exception.
As would I. However, I’m really interested in responding to the OP question:
…if the Keto / Primal ? etc diets are derived from ancient human food habits, then why is there such a thing on upping the sodium and potassium intake. Ancient peoples don’t appear to have had access let alone the need to use copious amounts of salts.
Did our pre/Pleistocene ancestors really consume 4-6 grams of sodium per day, as you have stated above and in other numerous posts as the ideal amount based on the PURE study? Or did they eat a lot less sodium and more potassium? Is Moore correct that a natural, unprocessed human diet is rich in potassium and low in sodium? Did our pre-Holocene ancestors evolve to eat a diet rich in potassium and low in sodium? Has our love affair with sodium only begun since the Holocene? I’d like to find the answers to those questions if I can.
I think it’s quite plausible that if humans evolved in a low sodium high potassium metabolic environment - ie a higher K-factor - the reversal of that in the few thousand years since the advent of the Holocene might have a profound effect on metabolic function and health - maybe causative and/or aggravative.
That’s too bad. I find it lots easier to navigate than the USDA, from which it draws its data.
Let’s start with a general observation. Potassium occurs in a lot of foods, including meat, that our ancestors would have eaten. Yes, plants are the primary concentrators of potassium from the soil. But ruminants eat the plants and we eat the ruminants, so the potassium gets passed up the food chain even if in diminishing quantities. Our ancestors did not have to eat ‘fruits and veggies’ to get potassium.
I think the first question requiring an answer is how much potassium did Pleistocene megafauna contain and what was the K-factor for those animals? I don’t know if that question has a definitive answer or not, but I’m going to try to find one.
The following article is not directly relevant - although probably indirectly so - to the sodium/potassium ratio question. But it references lots of very interesting evolutionary/adaptive issues and contains many refs. It’s also a very interesting read. Lots of good stuff to know here. For example:
… Humans can earn tens of thousands of calories per hour hunting medium-sized animals, in contrast with the meager 1,431 calories from foraging plants . Human specialization for hunting large animals during the Pleistocene provided even bigger returns . Our fat stores and our hunting seem to go hand in hand.
Although it’s an interesting question, forgive me for not getting excited about it, until my earlier question about why they blame metabolic disease on a low potassium/sodium ratio is answered. Something sounds off about that idea, and until we know what it’s based on, I’m not going to get worked up about the rest. For all I know, they actually have good data and a plausible mechanism to explain how it works, but then so do the people who believe that metabolic disease is caused by hyperglycaemia and hyperinsulinaemia.
On the other hand, I think the more interesting question is how did consuming 4-6 grams of sodium per day become healthy (assuming it is). That’s a lot of sodium so there has to have been a reliable and steady source for a very long time during human evolution. Was that source meat and fat? If not, then what?
Well, the experience of modern-day carnivores is that almost all of them somehow get enough salt, without having to add much, if any, to their food.
As I mentioned, all traditional societies are very aware of where the salt licks are. You merely have to track the game to find them. I don’t see a problem with how our ancestors managed to get enough salt, however much they needed.
Why is there an assumption that 4-6 grams is not healthy?
As for the observed risk curve, since two independent studies on large populations observed it and confirm each other, I tend to think it is valid. But you are right; the data are observational, and there may be confounders.
It would be interesting to use the same data collection methods on the sodium intake of modern-day carnivores, to see just how much sodium they are actually getting in a day. That would probably answer some of these questions, and probably stimulate fresh ones.
Not to mention that finding out how much sodium or potassium we’re getting in a day is impossible. You can get close – maybe – but not really. For instance, I had a drink of olive brine after my morning workout. How much potassium or sodium did I get? I just had some spaghetti squash in butter with beef heart and a beef hot dog, with some added salt, and a bit of sprinkle cheese. How much potassium and sodium were in there?
And I know that Michael is about to tell me all about his incredibly accurate scale and whatnot, but I refuse to measure anything. Sorry. Brings back years of measuring everything so I could keep my fat content below 10% by calories.
Edit: Sorry, got interrupted. I sous vided the beef heart at 160F for 24 hours. This allows me to eat the fat on the beef heart. If I use lower temperatures, the fat is inedible.
I tossed the liquid that was in the bag. Normally, I drink this. But this did not look that appetizing, and I was running late to take my daughter to the bus stop.
But tossing the liquid means I lost “something”, probably some sodium and potassium. How much? I have no idea.
My initial suspicion - not even an hypothesis - is that we’re currently eating more sodium and less potassium than we adapted to during our evolution. I suspect the closer one eats to a low carb - not even necessarily keto, just a lot lower than typical variations of SAD - the less sodium you need for health. I further suspect that low potassium intake is likely just as or possibly more significant than sodium intake. I also suspect that those of us eating keto or carnivore, which I think is much closer to our ancestral diet, requires less sodium than SAD. And I suspect sodium consumption increased in tandem with carb consumption only with the onset of the Holocene.
I will admit, I have no idea how much sodium I consumed on SAD, but I was a conscientious eater even then, following the dietary guidelines, and kept my sodium intake low. I did NOT have to toss down salt pre keto like I do now. In fact, I frequently bloated up after having a high sodium meal. I’m sure my sodium needs have gone up on keto and now carnivore.
And even will tossing down an extra 2 teaspoons a day of salt, not including what is in and on my food, my BP is still around 100/60. Without that salt, it drops.
That’s interesting… your BP drops even lower without salt. I’ve always had low BP and since going carnivore have noticed it’s even lower. Didn’t connect the two. Hmmm…
I guess I should ask why you increased sodium. Have you tried increasing potassium instead?
Let’s start at the beginning:
Body composition in Pan paniscus compared with Homo sapiens has implications for changes during human evolution
Robb Wolf on the Healthy Rebellion has mentioned several times that low salt can contribute to sleep issues. That is one of the things that’s improved since upping my salt. Much better sleep. That and my heart palpitations are gone.
I do take almost a 1/2!teaspoon of KCl mixed in with my salt, so I do get some extra K as well.
Unfortunately, behind a payway
Prehistoric animals and humans consumed a diet low in sodium but high in potassium, and thus, evolutionary forces fostered the development of physiologic systems that conserved sodium and excreted potassium. With the advent of civilized societies, food cooking and processing have greatly increased the sodium but decreased the potassium content of the diet. However, there has been little time for physiologic systems to adapt. The resulting excess of sodium has been implicated as an important factor in the development of hypertension and congestive heart failure. This traditional focus on sodium has ignored the potential role that an inadequate dietary intake of potassium might play in the degenerative diseases of the heart, brain and kidney. Yet dietary potassium may be as powerful a determinant of cardiovascular morbidity and mortality as dietary sodium. In experimental and clinical hypertension, an increased intake of potassium (without a change in dietary sodium) can reduce blood pressure, may suppress the activity of the sympathetic nervous and renin-angiotensin systems, and can prevent the development of vascular injury; conversely, potassium depletion has been associated with an increase in stroke and sudden death. In patients with chronic heart failure, potassium can modify both the mechanical and electrical properties of the heart, it can exert diuretic effects, and it can reduce the frequency and complexity of potentially lethal ventricular tachyarrhythmias. Given this central role, the effects of many pharmacologic interventions on the morbidity and mortality of patients with hypertension or chronic heart failure can be enhanced or diminished by the effect that these treatments might have on potassium homeostasis.(ABSTRACT TRUNCATED AT 250 WORDS)
The high sodium-low potassium environment of civilized people, operating on a genetic substrate of susceptibility, is the cardinal factor in the genesis and perpetuation of “essential” hypertension. The noxious effects begin in childhood, when habits of excess salt consumption are acquired at the family table, and are perpetuated by continuing habit and by increasing use of convenience and snack foods with artificially high concentrations of sodium and low levels of potassium. Present methods of food preparation leach out the protective potassium. Extradietary sodium chloride is a condiment not a requirement. Some primitive populations clearly preferred potassium chloride to sodium chloride. Chronic expansion of extracellular fluid volume induced by excess salt consumption causes the central and peripheral circulatory regulatory mechanisms to work at cross purposes, resulting in increased arterial pressure. The protective effect of potassium is dramatic and easily demonstrable in animals and man but its mechanism is not known. It cannot be entirely a direct effect on blood pressure because rats protected with extra potassium against a moderately high salt intake live much longer than control rats but have the same elevated blood pressures. In hypertension with a demonstrable “cause,” the high sodium-low potassium environment makes a bad matter worse. In nature, feral man and his forebears were not confronted with excessive sodium and deficient potassium; indeed, the reverse was the case. Evolution has provided powerful mechanisms for conserving sodium and eliminating potassium, but no efficient physiologic mechanisms for conserving potassium and eliminating excess sodium. Most laboratory animal “control” diets contain an amount of sodium that fully suppresses aldosterone secretion, and the same is true of the “average” diet of the American people. Inadequate attention to dietary sodium and potassium makes many studies in both animals and man of uncertain validity. Internally, essential hypertension is an exceedingly complex mosaic of physiologic interactions. Viewed from outside, it is a disorder for which genetic material sets the stage; excessive sodium precipitates it and perpetuates it. Extra salt makes all forms more rapidly progressive and accelerates the onset of terminal events; extra potassium is everywhere protective. When an entire population eats excessively of salt, hypertension will develop among those genetically susceptible, but epidemiologic studies of salt versus blood pressure will not show a relation of salt to hypertension. This is the saturation effect. Low sodium diets are therapeutically effective but generally regarded as an impossible or an unnecessary nuisance. Effective prevention programs must be instituted at as early an age as possible. The efficacy of a prophylactic/therapeutic low sodium-high potassium diet should be weighed against the uncertain hazards of a lifetime of pill taking.
Full study online:
My rationale for thinking why our paleolithic ancestors did not need ‘fruit, veggies, nuts’ to get a diet with a healthy K-factor as discussed by Passwater/Moore above.
I discovered this site searching for research papers. It’s an advocacy site but includes citations following articles. It does not look like it’s been updated recently, however. So… Various articles discuss some of the health issues claimed by Passwater/Moore as resulting from a sodium/potassium imbalance. Might be a start to answering your question. I’ve linked to the Beef Table:
PS: I’ll also mention that I’ve come across numerous studies and analyses that put the causation of many of the issues mentioned by Passwater/Moore to a high sodium to potassium ratio. I’ve linked a couple above for starters. I’ll link more as I encounter them and think them relevant and/or interesting.
I’ve only read through one study so far. It was certainly not done with people who eat low carb or keto. Can those results be trusted for our portion of the population?
This discussion got me curious about my potassium intake, so I did a little math. I am mostly carnivore. I eat about a 1.5 pounds of meat a day, plus a few eggs. I supplement with my salt mix (3:1 Salt to No Salt), and drink a Zip Fizz every other day for some vitamins. Normal vitamin supplements don’t agree with my stomach, but for some reason Zip Fizz does.
My meat is a mix of beef, pork, and chicken, so I took an average of their potassium content. I did use raw values. I don’t boil my meat, but I do understand some potassium is lost via cooking.
My potassium intake through food is about 1800-2000 mg a day. With my salt mix, I get another 1200 mg, so I’m somewhere around 3100 mg K/day. The days I have a Zip Fizz I am actually up around 4000 mg/day.
Using the same method for sodium intake, I am getting a little over 4g (4000 mg) a day. Without even realizing it, I’m pretty balanced between the two.
So… a few months or so ago, I upped my “salt” intake to the 2 teaspoons using my salt mix. I was getting muscle cramps, heart palpitations, and my sleep has been cruddy for years. Since I upped my intake, cramps, palpitations, and cruddy sleep are gone. I’m not thirsty all the time. I sleep through the night without having to get up to urinate. I’m realizing as I type this message, that when I upped my salt, I upped my potassium intake along with it. I guess that means I really can’t say what caused the improvements the increased salt, increased potassium, or both.
If what the articles say is true that the ratios should be skewed toward the potassium is true, and quantity shouldn’t matter, then upping the amount of salt mix I was taking shouldn’t have mattered. My ratios would have been the same.
Back to the one article I read, it seemed like most of the people in the study testing the Na:K were unhealthy already and eating crap high-carb diets. Food questionaires were used. (Need I say more on that? ) Again, does that really pertain to people keeping their insulin low on keto?
I shall end my ramblings here.
Thanks. We keto/carnivores are a small fringe, so I don’t expect much in ‘mainstream’ physiology to be based on studying us. I totally agree with you about FFQ based studies. That said, I just looked up the RDAs and ave consumption for both sodium and potassium.
In the US the sodium RDA is ~2300mg and in Canada ~1500mg. Average daily intakes for are 3400mg (US) and 2800mg (Can). For potassium the RDA (AI) in both US and Canada is 4700mg. Ave daily intake is 2800mg. The recommendations are max for sodium and min for potassium. So even the ‘mainstream’ recommends a 2:1 K-factor (US) and 3:1 K-factor (Can). Whereas actually consumed the K-factors are <1.
So getting back to the OP. Why are we keto/carnivore folks being told that we need to eat 4-6 grams of sodium per day? Well, if we actually ate the RDA for potassium or more that would be a ratio of 1. Is it plausible to think that our paleolithic ancestors consumed so much sodium? Or that they ‘supplemented’ one or the other to get to those quantities - eg the ‘salt lick’ idea? I think not. Looking at the sodium/potassium contents of various meats I suspect they consumed lots more potassium than sodium and had ratios of 3,4 or higher (@ctviggen and without weighing anything!). Of course, the meats we’re eating now (with the possible exception of ‘game’ meat) don’t contain the same amounts or ratios of potassium and sodium as the megafauna of the Pleistocene. So we can’t say for sure exactly what those amounts and ratiois were. But I think it’s reasonable to suspect they’re similar overall.
So the question then becomes, why did our more recent ancestors start consuming lots more sodium?
Because of study data that suggest that to be the healthiest range of sodium intake. (Granted, very few of the forty or fifty thousand people studied were likely to have been on a low-carb diet.)
U.S. dietary recommendations for sodium intake are pegged to what is thought to be a safe level for salt-sensitive hypotensives, who form a very small minority of the population. But those in charge of the dietary guidelines feel that the needs of that minority supersede those of the general population.
Do any of those references you read attempt to define “recent,” in this context? And I’d be curious to know, how do they know when the change actually occurred? I’m wondering what metric they could have used.
This sentence makes me automatically assume there is bias in the paper.
I would love to read the source for this information. How do they know this? Is it based on present day wildlife? Ancient bone composition?