Amazoniac
Member
It's beyond me to read that the equivalent to 9 g (more like 8.6 g) of sodium intake used in an experiment is irrelevant. star, you must've not searched the forum to imply that such intake is rare around here: 1 tbsp of sea salt already provides about 5 g of it. The outliers are consuming more. And still, you think it would be completely impertinent for a pimp(ess) consuming 1-2 grams less than that? The person has to cross the equivalence for it to be meaningful? Such amount and 0.7 g are realistic and you're judging them useless, cultures go to further extremes:
- [Ch. 6] Sodium and Chloride - 'Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate' | Instituting the Medicines
But anyway, wow is balance?
What motived me to look into the effects of salt on digestion was Ramón's comment that extra calcium suppresses intestinal fermentation, then it occurred to me that salt should prevent microbial action in the upper gut, so both of them combined could give extensive protection. This is related to the increase in salt consumption when refrigeration wasn't available.
- [Ch. 6] Sodium and Chloride - 'Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate' | Instituting the Medicines
"Sodium and chloride are required to maintain extracellular volume and plamsa osmolality. Human populations have demonstrated the capacity to survive at extremes of sodium intake from less than 0.2 g (10 mmol)/day of sodium in the Yanomamo Indians of Brazil to over 10.3 g (450 mmol)/day in Northern Japan."
But anyway, wow is balance?
"The majority of ingested sodium chloride is excreted in the urine, provided that sweating is not excessive (Holbrook et al., 1984; Pitts, 1974). In humans who are at “steady-state” conditions of sodium and fluid balance and who have minimal sweat losses, the amount of sodium excreted in urine roughly equals intake. This phenomenon occurs due to the capacity of the normal human kidney to filter some 25,000 mmol of sodium each day and to reabsorb, by extremely precise mechanisms, 99 percent or more of the filtered load (Valtin and Schafer, 1995)."
"There are various systems and hormones that influence sodium and chloride balance, including the renin-angiotensin-aldosterone axis, the sympathetic nervous system, atrial natriuretic peptide, the [made-up] kallikrein-kinin system, various intrarenal mechanisms, and other factors that regulate renal and medullary blood flow. Angiotensin II, a potent vasoconstrictor, regulates the proximal tubule of the nephron to promote sodium and chloride retention and also to stimulate the release of aldosterone from the adrenal cortex (Valtin and Schafer, 1995). Aldosterone promotes the renal reabsorption of sodium in the distal tubule of the nephron by mineralocorticoid receptor-mediated exchange for hydrogen and potassium ions. With reduced salt intake, reduced blood volume, or reduced blood pressure, the renin-angiotensin-aldosterone axis is stimulated. When the renin-angiotensin-aldosterone system is less responsive, as with advancing age, there is a greater blood pressure reduction from a reduced intake of sodium chloride (Cappuccio et al., 1985; Weinberger et al., 1993a)."
"Renin is released from the juxtaglomerular cells of the kidney in response to a perceived reduction in blood volume, blood pressure, or tubular sodium concentration. As a result, renin induces the production of angiotensin II, which stimulates renal sodium reabsorption via a direct tubular effect, as well as by increasing the production of aldosterone. In cross-sectional studies, plasma renin activity is inversely associated with sodium intake; the relationship appears to be curvilinear with the greatest rise in plasma renin activity occurring below a sodium intake of 2.3 g (100 mmol)/day as estimated by urinary sodium excretion (see Figure 6-1). Furthermore, in clinical trials, most of which were brief (2 weeks or less) and had small sample sizes (< 50 participants), reduced sodium intake commonly led to a rise in plasma renin activity (Table 6-4)."
"Intrarenal mechanisms are also important for sodium and chloride homeostasis. These mechanisms include locally released prostaglandins, kinins, angiotensin, endothelial relaxing factor, and other less-well defined factors."
"When substantial sweating does not occur, total obligatory sodium losses are very small, up to 0.18 g/day or 8 mmol/day (Table 6-1) (Dahl, 1958). For this reason, in a temperate climate or even a tropical climate, acclimatized persons can survive on extremely low sodium intakes (Kempner, 1948; Oliver et al., 1975)."
"In nonsweating individuals living in a temperate climate who are in a steady-state of sodium and fluid balance, urinary sodium excretion is approximately equal to sodium intake (i.e., 90 to 95 percent of total intake is excreted in urine) (Holbrook et al., 1984; Pietinen, 1982). Obligatory urinary losses of sodium in adults are approximately 23 mg (1 mmol)/day (Dole et al., 1950)."
"Excretion of sodium in crap is minimal. When sodium intakes ranged from 0.05 to 4.1 g/day of sodium, only about 0.01 to 0.125 g (0.4 to 5.4 mmol)/day appeared in the stool (Dahl, 1958; Dole et al., 1950; Henneman and Dempsey, 1956). In a sodium balance study with three levels of intake, 1.5, 4.0, and 8.0 g (66, 174, and 348 mmol)/day (Allsopp et al., 1998), fecal sodium excretion increased as sodium intake rose. Still, fecal excretion of sodium was less than 5 percent of intake even at the highest level of sodium intake (Table 6-2)."
"Daily dermal losses of sodium have been reported to average less than 0.025 g (1.1 mmol)/day (Dahl, 1958; Dahl et al., 1955). In another study, estimated obligatory dermal losses of sodium ranged from 0.046 to 0.09 g (2 to 4 mmol)/day (Fregly, 1984). Sweat sodium loss depends on a number of factors, including: (1) the sweat rate, (2) sodium intake, and (3) heat acclimation (Allsopp et al., 1998). For these reasons, the sodium concentration in sweat varies widely. Most studies that measure sodium content of sweat are short-term (Table 6-3), and report sweat sodium concentrations rather than total sodium lost in sweat. Of note, in these studies intake data on dietary sodium was frequently not given. However, in the three studies where dietary sodium information was provided, dietary intakes were high (up to 8.7 g [378 mmol]/day)."
"One study provided detailed information on sweat losses at three levels of dietary sodium intake (Allsopp et al., 1998). Men were exposed to heat in an environmental chamber at 40°C (104°F) for 10 hours/day of the last 5 days of an 8-day experimental period. Sweat sodium loss, as well as fecal and urinary sodium losses, were progressively greater across the three levels of sodium studied (1.5 g [66 mmol], 4 g [174 mmol], or 8 g [348 mmol]/day) (see Table 6-2). By the eighth day, participants on the lowest sodium level were in sodium balance. Plasma aldosterone concentrations were significantly increased during the low sodium condition and significantly decreased during the high sodium condition. Earlier studies, including a 10-day pre-post study, reported similar reductions in sodium sweat loss following exercise in the heat over time (Kirby and Convertino, 1986), as well as decreased sweat sodium concentration with heat acclimation without exercise (Allan and Wilson, 1971)."
"In aggregate, available data indicate that wealthy, free-living individuals can achieve sodium balance following acclimation under a variety of conditions, including low sodium intake and extreme heat."
"There are various systems and hormones that influence sodium and chloride balance, including the renin-angiotensin-aldosterone axis, the sympathetic nervous system, atrial natriuretic peptide, the [made-up] kallikrein-kinin system, various intrarenal mechanisms, and other factors that regulate renal and medullary blood flow. Angiotensin II, a potent vasoconstrictor, regulates the proximal tubule of the nephron to promote sodium and chloride retention and also to stimulate the release of aldosterone from the adrenal cortex (Valtin and Schafer, 1995). Aldosterone promotes the renal reabsorption of sodium in the distal tubule of the nephron by mineralocorticoid receptor-mediated exchange for hydrogen and potassium ions. With reduced salt intake, reduced blood volume, or reduced blood pressure, the renin-angiotensin-aldosterone axis is stimulated. When the renin-angiotensin-aldosterone system is less responsive, as with advancing age, there is a greater blood pressure reduction from a reduced intake of sodium chloride (Cappuccio et al., 1985; Weinberger et al., 1993a)."
"Renin is released from the juxtaglomerular cells of the kidney in response to a perceived reduction in blood volume, blood pressure, or tubular sodium concentration. As a result, renin induces the production of angiotensin II, which stimulates renal sodium reabsorption via a direct tubular effect, as well as by increasing the production of aldosterone. In cross-sectional studies, plasma renin activity is inversely associated with sodium intake; the relationship appears to be curvilinear with the greatest rise in plasma renin activity occurring below a sodium intake of 2.3 g (100 mmol)/day as estimated by urinary sodium excretion (see Figure 6-1). Furthermore, in clinical trials, most of which were brief (2 weeks or less) and had small sample sizes (< 50 participants), reduced sodium intake commonly led to a rise in plasma renin activity (Table 6-4)."
"Intrarenal mechanisms are also important for sodium and chloride homeostasis. These mechanisms include locally released prostaglandins, kinins, angiotensin, endothelial relaxing factor, and other less-well defined factors."
"When substantial sweating does not occur, total obligatory sodium losses are very small, up to 0.18 g/day or 8 mmol/day (Table 6-1) (Dahl, 1958). For this reason, in a temperate climate or even a tropical climate, acclimatized persons can survive on extremely low sodium intakes (Kempner, 1948; Oliver et al., 1975)."
"In nonsweating individuals living in a temperate climate who are in a steady-state of sodium and fluid balance, urinary sodium excretion is approximately equal to sodium intake (i.e., 90 to 95 percent of total intake is excreted in urine) (Holbrook et al., 1984; Pietinen, 1982). Obligatory urinary losses of sodium in adults are approximately 23 mg (1 mmol)/day (Dole et al., 1950)."
"Excretion of sodium in crap is minimal. When sodium intakes ranged from 0.05 to 4.1 g/day of sodium, only about 0.01 to 0.125 g (0.4 to 5.4 mmol)/day appeared in the stool (Dahl, 1958; Dole et al., 1950; Henneman and Dempsey, 1956). In a sodium balance study with three levels of intake, 1.5, 4.0, and 8.0 g (66, 174, and 348 mmol)/day (Allsopp et al., 1998), fecal sodium excretion increased as sodium intake rose. Still, fecal excretion of sodium was less than 5 percent of intake even at the highest level of sodium intake (Table 6-2)."
"Daily dermal losses of sodium have been reported to average less than 0.025 g (1.1 mmol)/day (Dahl, 1958; Dahl et al., 1955). In another study, estimated obligatory dermal losses of sodium ranged from 0.046 to 0.09 g (2 to 4 mmol)/day (Fregly, 1984). Sweat sodium loss depends on a number of factors, including: (1) the sweat rate, (2) sodium intake, and (3) heat acclimation (Allsopp et al., 1998). For these reasons, the sodium concentration in sweat varies widely. Most studies that measure sodium content of sweat are short-term (Table 6-3), and report sweat sodium concentrations rather than total sodium lost in sweat. Of note, in these studies intake data on dietary sodium was frequently not given. However, in the three studies where dietary sodium information was provided, dietary intakes were high (up to 8.7 g [378 mmol]/day)."
"One study provided detailed information on sweat losses at three levels of dietary sodium intake (Allsopp et al., 1998). Men were exposed to heat in an environmental chamber at 40°C (104°F) for 10 hours/day of the last 5 days of an 8-day experimental period. Sweat sodium loss, as well as fecal and urinary sodium losses, were progressively greater across the three levels of sodium studied (1.5 g [66 mmol], 4 g [174 mmol], or 8 g [348 mmol]/day) (see Table 6-2). By the eighth day, participants on the lowest sodium level were in sodium balance. Plasma aldosterone concentrations were significantly increased during the low sodium condition and significantly decreased during the high sodium condition. Earlier studies, including a 10-day pre-post study, reported similar reductions in sodium sweat loss following exercise in the heat over time (Kirby and Convertino, 1986), as well as decreased sweat sodium concentration with heat acclimation without exercise (Allan and Wilson, 1971)."
"In aggregate, available data indicate that wealthy, free-living individuals can achieve sodium balance following acclimation under a variety of conditions, including low sodium intake and extreme heat."
What motived me to look into the effects of salt on digestion was Ramón's comment that extra calcium suppresses intestinal fermentation, then it occurred to me that salt should prevent microbial action in the upper gut, so both of them combined could give extensive protection. This is related to the increase in salt consumption when refrigeration wasn't available.
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