Accidentally hit the quote button instead of edit there, but I was just adding some text from the last article linked above, since it mentions that high potassium foods can cause issues as well.cornivore wrote: ↑Sun Jan 20, 2019 10:14 pm• Maybe, then again, both could be safer together. Unless sodium absolutely had to be restricted, it may help prevent potassium levels from getting too high.
• For some people, extra sodium may interfere too much with potassium. As far as too little potassium goes, salt could perpetuate Hypokalemic Periodic Paralysis, so it seems that those need to be balanced together, or strange things can happen.Diets high in potassium have been associated with reducing hypertension and heart failure; however, optimal renin-angiotensin-aldosterone system inhibitor dosing is often limited by hyperkalemia, which can lead to life-threatening cardiac arrhythmias and increased mortality. Potassium binders are effective at reducing potassium levels. Although some use sodium as the potassium exchange ion, thus increasing sodium intake, a new potassium binder uses another exchange ion and therefore does not increase sodium intake. When treatment options require agents that may precipitate hyperkalemia, particularly in patients at high cardiorenal risk, drugs that do not add to the sodium load may be preferred . . .
• Hyperkalemia can also cause paralysis . . ., so either too low or high potassium can be an issue, and salt could either help with that or not (but staying within recommended intakes of those should be okay for most people, I presume).The goal of preventive treatment is to reduce the frequency and intensity of paralytic attacks. This may be achieved by avoidance of triggering factors, adherence to a diet low in sodium and carbohydrate and rich in potassium, and with the use of oral potassium supplementation.
Then there's this too. Review of case reports on hyperkalemia induced by dietary intake: not restricted to chronic kidney disease patients . . .A 52-year-old man with end-stage renal disease presented with ascending quadriplegia and dyspnea for 2 days. He had life-threatening hyperkalemia (9.0 mEq/L). His electrocardiogram showed typical features of hyperkalemia. His symptoms improved in 30 minutes and completely resolved in 5 hours after emergent treatment of hyperkalemia. He admitted eating large amounts of high potassium foods and taking ibuprofen in uncertain quantities... Hyperkalemia is a rare but treatable cause of acute flaccid paralysis that requires immediate treatment. Late diagnosis can delay appropriate treatment leading to cardiac arrhythmias and arrest.
That's what I was guessing when limiting my use of potassium chloride to 2000mg/day, to leave room for dietary potassium, but I'm trying not to eat much, or intermittently these days, so it should be okay either way. This is in contrast with what I'd read about most dietary supplements, like vitamin A, where you can get toxicity from supplements, but not food (unless maybe it's fortified with vitamins, or iodine, speaking of that again).Hyperkalemia is a metabolic disturbance of the potassium balance that can cause potentially fatal cardiac arrhythmias. Kidney dysfunction and renin-angiotensin-aldosterone system inhibiting drugs are notorious for their tendency to induce hyperkalemia by decreasing the excretion of potassium. The role of dietary potassium intake in inducing hyperkalemia is less clear. We review and analyze the common presentation, laboratory, and electrocardiogram (ECG) findings and therapeutic options associated with dietary-induced hyperkalemia, and find evidence for hyperkalemia development in non-renal impaired patients. Thirty-five case reports including 44 incidences of oral intake-induced hyperkalemia were assessed, 17 patients did not suffer from kidney dysfunction. Mean age was 49 ± 20 years. Mean potassium concentration was 8.2 ± 1.4 mEq/l, most frequently caused by abundant intake of fruit and vegetables (n = 17) or salt substitutes (n = 12). In patients with normal kidney function, intake of salt substitutes or supplements was the main cause of hyperkalemia. Main symptoms encompassed muscle weakness (29.5%), vomiting (20.4%), and dyspnea (15.9%). When ECGs were performed (n = 30), abnormalities were present in 86.7% of cases. Treatment involved administration of insulin (n = 22), sodium/calcium polystyrene sulfonate (n = 14), and/or calcium gluconate (n = 14). Forty patients fully recovered. Three, non-renal impaired, patients passed away. These results offer insight into the clinical aspects of dietary-induced hyperkalemia and suggest that the common assumption that dietary-induced hyperkalemia is a condition of renal impaired patients might be incorrect.
By the way, here's another article about the importance of balancing fluid with those electrolytes: Dietary Influence on Body Fluid Acid-Base and Volume Balance: The Deleterious "Norm" Furthers and Cloaks Subclinical Pathophysiology
• Salt substitue (potassium chloride) is simply another option for the "all-important dietary potassium to sodium ratio", but you have to be careful with either one. I think they don't mention tempering its consumption as a food additive, because it doesn't taste as good as salt (or fruits and veggies), so it isn't ordinarily consumed at all. They say iodine is bitter too, and I don't think iodized salt tastes as good as pure salt, myself. Another name for kosher salt is kitchen salt, because it's often used in cooking (or most prepared food is boldly labled with 'sea salt' these days, perhaps for taste, but it seems like getting too much of that is supposed to be healthy somehow, or that's what people want to hear). Anyway, something I don't hear very often is that "indiscriminate Na restriction may have adverse effects on health": Dietary Salt (Sodium Chloride) Requirement and Adverse Effects of Salt Restriction in Humans...Abstract
The popular modern diet, characterized by an excess of animal protein and salt but insufficient in fruits, vegetables and water, is a poor fit for human physiological and homeostatic regulatory systems. Sustained net acid and sodium retention, coupled with an insufficient intake of cardiovascular protective potassium-rich foods and hydration in the modern diet can give rise to debilitating chronic organ dysfunction and ultimately, mortality. This holds true, especially in our aging population who are already facing inevitable decline in organ functional reserve. Importantly, in most cases, despite the mismatch and adverse effects to multiple organ systems, plasma electrolyte and acid-base parameters can, on the surface, be maintained within a "normal" reference range, primarily by activating (often maximally activating) compensatory homeostatic mechanisms. These diet-induced effects can thus be clinically silent for decades. Embodied in the chronic corrective homeostatic processes, however, are real risks for multiorgan damage. According to the Dietary Guideline Advisory Committee (DGAC), half of American adults have one or more chronic diseases that are preventable with dietary modification. Here, homeostasis of body fluid acid-base, sodium, potassium and water is examined. Our current dietary habits and their required regulatory adaptation, maladaptation and relevant physiology and pathophysiology are discussed. A framework of dietary modifications to avoid a propensity for maladaptation and thus lowers the risks of common modern diseases (primary prevention) and minimizes the risk of chronic and age-related disease progression (secondary prevention) is emphasized. Although there are other variables at play, a key to restoring the all-important dietary potassium to sodium ratio is greater consumption of vegetables/fruits and adopting salt temperance. Dietary and nutritional optimization is an under-emphasized area of health care that has an enormous potential to temper the epidemics of prevalent chronic diseases in modern society and improve population health.
• Ah, so there's more than iodine, and potassium, to consider with salt intake; calcium and magnesium too (especially if sodium is increased or reduced chronically . . . "strict and regimental Na restriction may have adverse effects on health", for example). They did a follow up study on this as well. Equilibrium intakes of calcium and magnesium within an adequate and limited range of sodium...Additionally, the negative balances of calcium and magnesium were observed under a relatively low sodium intake (100 mmol/d) even with the sufficient supply and intake of Ca and Mg into human body.
• Adequate intake would seem to be important, in general, as these nutrients are interdependent. For instance, if sodiuim affects magnesium, then . . .It is generally beleived that there are three levels of dietary intake of a nutrient: excess, adequate, and deficit. The border between excess and adequate is recognized as the upper limit, while the other border between adequate and deficit is termed the requirement.
To determine an upper limit and a requirement for a nutrient, it is necessary to understand the scientific evidence indicating quantitative information about the dietary intake and the signs and symptoms of excess or deficit of the nutrient...
These results confirm that the level of Na intake is one of the factors that affects the requirements of Ca and Mg and that under an adequate Na status, the equilibrium intakes of Ca and Mg are lower than those determined when Na deficit and excess are included.
This may be because Na is stored in the bone physiologically as well as Ca and Mg. When Na is short in the blood stream, Na in the bone will be resorbed together with Ca and Mg, which inevitabley increases serum and urine Ca and Mg and decreases intestinal absorption of the two minerals. When Na intake is excess, renal excretion of Ca and Mg might be increased with that of Na . . .
• Magnesium, sodium, and iodine are among the nutrients found to influence nervous system function as well . . .There are several potential pathophysiologic mechanisms through which low dietary intake of magnesium could accelerate the loss of kidney function. There is extensive research demonstrating that low blood levels of magnesium, which in part is influenced by dietary intake, can lead to an inflammatory, atherogenic, and thrombotic response in the vasculature.
Our findings are supported by previous research demonstrating that other dietary patterns inclusive of magnesium are predictive of kidney disease risk. For instance, magnesium is a component of the equation for potential renal acid load, a measure of dietary acid load. Level of dietary acid load has been reported to be associated with markers of kidney disease in several studies of U.S. adults. Similarly, high intake of magnesium was one of the key nutrient targets of the Dietary Approaches to Stop Hypertension (DASH) diet and the DASH diet with reduced sodium, according to the design of the original trials. The DASH diet is low in dietary acid load and several recent studies have shown that following a DASH-style diet is significantly associated with kidney health. Also, nuts and legumes are two rich sources of magnesium, and their higher consumption, along with other vegetable sources of protein, may protect against the development of kidney disease possibly by favorably altering mineral metabolism.
In this urban population, lower dietary magnesium intake was independently associated with greater odds of rapid kidney function decline.
• The role of low acid load in vegetarian diet on bone health describes the roles of calcium and potassium there.The diet is directly connected not only with the physical status but also with the functioning of the brain and the mental status. The potentially beneficial nutrients with a protective effect on the nervous system function include amino acids (tryptophan, phenylalanine, tyrosine, taurine), glucose and vitamins C, E, D and beta-carotene, B group vitamins (vitamin B12, vitamin B6, vitamin B4, vitamin B1) and minerals (selenium, zinc, magnesium, sodium, iron, copper, manganese, iodine).
Over all, a plant based diet helps to keep these nutrients balanced (so they probably shouldn't be restricted). Adequate intake isn't necessarily the problem otherwise, and it seems that people are trying to restrict or supplement some nutrients in order to get away with excesses elsewhere (in an omnivorous diet), which doesn't work as well, I gather.Vegetarian and vegan diets contain low amounts of protein and calcium. For this reason they are supposed to cause low bone mineral density (BMD) and osteoporosis. But this is not the case, except for vegans with a particularly low calcium intake. The absence of osteoporosis or low BMD can be explained by the low acid load of these diets. Nutritional acid load is negatively correlated with bone mineral density (BMD) and positively with fracture risk. Low acid load is correlated with lower bone resorption and higher BMD. It is linked to high intake of potassium-rich nutrients, such as fruits and vegetables, as found in vegetarian diets. The total nutritional acid load, which not only depends on the potassium content of the nutrition, was recently assessed in several studies on vegetarian and vegan diets and was found to be very low or absent, while the diet of Western-style omnivores produces daily 50 to 70 mEq of acid. This might be an important factor for the protection of vegetarians from osteoporosis.
Most striking information came recently from a very large survey in non vegetarians (over 1 million patient years), which showed an increase in the risk of hip fracture when the intake of fruit and vegetables was below two servings/day, but no risk reduction in high consumers of fruit and vegetables. This observation is in line with the results of a 2-year supplementation study with fruit and vegetables, which did not reduce postmenopausal bone loss. Again, these subjects were not vegetarians. . .