Here's a big copy paste from Harvards school of public health:
www.hsph.harvard.edu/nutritionsource/salt/jama-sodium-study-flawed/index.html
A new study would have you believe that low-salt diets raise your risk of dying from heart disease—a surprising finding, and one that’s sure to grab headlines worldwide. The only problem is that the study’s conclusions are most certainly wrong.
In the study, published in the May 4, 2011, issue of the Journal of the American Medical Association (JAMA), European researchers followed 3,681 men and women for an average of about eight years. (1) They report that people with the lowest levels of sodium in their urine (a marker of salt intake) at the start of the study had a 56 percent higher risk of dying from cardiovascular disease than people with the highest levels. Equally unexpectedly, among the 2,096 participants who had normal blood pressure at the start of the study, urinary sodium appeared to have no effect on the development of high blood pressure over six and a half years.
Based on these findings, the study authors call into question recent estimates (2, 3) of the tens of thousands of heart attacks, strokes, and cardiac deaths that could be averted each year—and the billions of healthcare dollars that could be saved—by curbing Americans’ excessive salt intakes. Yet the study has several weaknesses, chief among them its modest size: With less than 4,000 participants—and only 84 deaths due to cardiovascular disease—the study is too small to support the authors’ sweeping conclusions.
Read about why cutting back on salt and sodium is a key to good health
Read about key studies that show the harmful effects of sodium on the heart
Furthermore, the study’s findings are inconsistent with a multitude of other studies conducted over the past 25 years that show a clear and direct relationship between high salt intakes and high blood pressure, and in turn, cardiovascular disease risk. (4–10)
“Take this study with a huge grain of salt, and then dispose of it properly,” says Dr. Walter Willett, chair of the Dept. of Nutrition at Harvard School of Public Health. “This study should not influence recommendations about sodium intake in any way.
Key problems that undermine the study’s conclusions include the following:
Unreliable measurement of sodium intake: The study investigators base their main findings on a single measurement of sodium collected at the start of the study specifically the amount of sodium that study participants excreted in their urine over a 24 hour period. Yet sodium excretion from just one day does not reflect people’s salt intake patterns over long periods of time. It’s weak science to use one-day sodium excretion to predict heart disease or mortality decades later.
Failure to account for key factors that influence sodium intake and heart disease risk: People who are taller (11) or more active (12) tend to have a lower risk of heart disease. They also tend to have higher sodium intakes, simply because they eat more food. Yet the JAMA study authors don’t account for differences in height, physical activity, and total calories. (13) This oversight could make it appear as though high sodium intakes protect against heart disease deaths, when in fact physical activity or height is responsible for the lowered risk.
Other weaknesses: There are other problems with the way that the investigators conducted the study, among them, missing or incomplete data from large numbers of participants. The study investigators, for example, could have accounted for incomplete urine samples by analyzing urinary sodium in relation to creatinine (another compound found in urine), but they did not.
The bottom line is that the researchers were trying to ask questions that their data are incapable of answering, and the study’s many methodological problems make its results unreliable. So the study’s findings do little to refute the strong evidence that cutting back on sodium would save lives.
Americans, on average, consume about 3,400 milligrams of sodium per day. Current U.S. recommendations call for a maximum of 2,300 milligrams of sodium a day (the amount found in a teaspoon of salt), and 1,500 milligrams of sodium (two-thirds of a teaspoon) for people who have high blood pressure or are at high risk of developing it. The latter group includes people who are over the age of 40, are African American, or have somewhat elevated blood pressure (prehypertension)—a group that includes almost 70 percent of adults in the United States. (14) A dash of prevention is worth a pound of cure: Since 90 percent of Americans will develop high blood pressure at some point in their lives, (15) it really makes sense for all of us to curb our sodium intake.
Read more about how to preserve flavor and cut back on salt
Try these delicious low salt recipes from the Culinary Institute of America
Seventy-five percent of Americans’ sodium intake comes from processed foods. (16) That’s why the Institute of Medicine has called on the U.S. Food and Drug Administration to regulate the amount of salt and sodium allowed in processed foods. (10)
References
1. Stolarz-Skrzypek K, Kuznetsova T, Thijs L, et al. Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion. JAMA. 2011; 305:1777–85.
2. Palar K, Sturm R. Potential societal savings from reduced sodium consumption in the U.S. adult population. Am J Health PromotOpens in New Window. 2009; 24:49–57.
3. Bibbins-Domingo K, Chertow GM, Coxson PG, et al. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J MedOpens in New Window. 2010; 362:590–9.
4. Strazzullo P, D'Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJOpens in New Window. 2009; 339:b4567.
5. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJOpens in New Window. 1988; 297:319–28.
6. Cook NR, Cutler JA, Obarzanek E, et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJOpens in New Window. 2007; 334:885-8.
7. Cook NR, Obarzanek E, Cutler JA, et al. Joint effects of sodium and potassium intake on subsequent cardiovascular disease: the Trials of Hypertension Prevention follow-up study. Arch Intern MedOpens in New Window. 2009; 169:32–40.
8. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J MedOpens in New Window. 1997; 336:1117–24.
9. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J MedOpens in New Window. 2001; 344:3–10.
10. Institute of Medicine. Strategies to Reduce Sodium Intake in the United StatesOpens in New Window. Washington D.C.: National Academies Press. 2010. Accessed May 3, 2011.
11. Ferrie JE, Langenberg C, Shipley MJ, Marmot MG. Birth weight, components of height and coronary heart disease: evidence from the Whitehall II study. Int J EpidemiolOpens in New Window. 2006; 35:1532–42.
12. U.S. Dept. of Health and Human Services. 2008 Physical Activity Guidelines for AmericansOpens in New Window. 2008. Accessed May 3, 2010.
13. Willett W, Stampfer M. Implications of Total Energy Intake for Epidemiologic Analysis. in Willett W, Nutritional Epidemiology. New York: Oxford University Press, 1998: 273–301.
14. Application of lower sodium intake recommendations to adults—United States, 1999-2006. MMWR Morb Mortal Wkly RepOpens in New Window. 2009; 58:281–3.
15. Vasan RS, Beiser A, Seshadri S, et al. Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study. JAMAOpens in New Window. 2002; 287:1003–10.
16. Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the world: implications for public health. Int J EpidemiolOpens in New Window. 2009; 38:791–813.
Also, this Harvard article is strictly raising concerns about a May 2011 JAMA paper. The Scientific American 'End the War on Salt' article also relies on a "meta-analysis of seven studies" published in July, and talks of another 11-trial review of the effects of sodium-intake-reduction in 2004.
While the causes of too much salt are debated, I see fairly regularly the effects to too little salt.
In a hot climate (Southeastern U.S.), I'm often outdoors with sports teams or youth groups, and I see the effects of heat-related conditions regularly. These are prevented and treated with water and salt (electrolytes). [1] [2]
So yeah, too much salt may be a problem. Maybe not. But too little certainly is, and it's common in the active youth I observe.
Couple things here, and I say this with the utmost respect. Your anecdote is not "data", and even if it were, you've failed to prove any sort of causality of "too little salt". Salt is but one of many possible electrolytes, and and "heat related conditions" are not necessarily solved with salt; chances are dehydration clear and simple could also be the cause of the effects you're seeing.
A somewhat peripheral question, but if we all cut back on salt intake where are we going to get our dietary iodine from? I lived in Italy for several years, where salt is (was? might have changed) not iodized and I regularly saw people with huge goiters in the throat.
1. It's possible that we've reversed the causal association for all these years. You don't always get expansion of the extracellular fluid space with chronic kidney disease due to hypertension; with some tubulointerstitial diseases, you develop salt-wasting nephropathies. Perhaps these were the hypertensive patients who were referenced in the article, voraciously eating salt due to a deficiency caused by their kidney disease? I'd like to see more data before being willing to overturn dogma, but it's not the most outlandish idea I've heard all day. Still, the authors' conclusions are most likely wrong.
2. There's a group at MGH doing a randomized clinical trial in which they are administering intravenous salt and measuring near-term blood pressure response. It's a one-off exposure, but it will be interesting to better nail down the relationship between serum sodium content and blood pressure via experiment rather than epidemiology.
"It's possible that we've reversed the causal association for all these years."
This is intriguing, because a similarly reversed causality was prevalent in the diagnosis and management of kidney stones for many years.
Perhaps this is TMI, but as a chronic kidney stone sufferer, I was told initially that I get too much calcium in my diet -- which builds up to cause the stones. Eventually, the doctors came around to the idea that I was actually secreting too much calcium into my bloodstream, and that secretion and consumption are not the same thing. In fact, I am losing more calcium than I consume, and I am losing much more than I should. Basically, I am deficient in calcium, even though my serum calcium levels are through the roof. (This phenomenon has underlying causes above and beyond the kidney disease; in fact, the kidney disease is most likely a secondary effect).
It's possible that we've reversed the causal association for all these years.
Another possibility: Cortisol. People under chronic stress produce more cortisol, and high cortisol levels act to inhibit urinary sodium loss. Maybe the people having heart attacks aren't eating more sodium; they're just retaining it better as a side effect of the stress which is killing them.
>But if the U.S. does conquer salt, what will we gain? Bland french fries, for sure. But a healthy nation? Not necessarily.
This week a meta-analysis of seven studies involving a total of 6,250 subjects in the American Journal of Hypertension found no strong evidence that cutting salt intake reduces the risk for heart attacks, strokes or death in people with normal or high blood pressure."
The article goes out of its way to dismiss the other impact of "French Fries" on health, obesity, and the role which salt plays in making manufactured food with low nutritional value habit forming.
The entire process of diagnosing people with hypertension needs a shake up. Managing blood pressure is such an important part of the human condition but the evidence as to what works and what doesnt can be confusing. Weight loss and stopping smoking works, but for exercise, cutting alchohol and cutting salt there are many conflicting reports.
Add in the fact that genetics plays such an important part, and the prevelence of White Coat Syndrome it's a shame that the medical world cannot make its mind up.
The confusion around hypertension is really annoying. I have a bit of white coat hypertension, and my BP is usually around 145/80 when measured by a medical professional, but is still around 132/80 when measured automatically. Getting it down to 120/80, or lower (where everyone else who I know in my age group is, and which seems to be the safest in the long term) is stubbornly impossible, despite exercise and a healthy diet. A 24 hour workup by a doctor seemed to point to stress-induced hypertension, but I was told that there's no need to treat it.
Is hypertension brought on by being stressed/awake less harmful than "intrinsic" hypertension? That seems to be the opinion by my physician. But it's maddening that these issues remain unresolved.
>>In May European researchers publishing in the Journal of the American Medical Association reported that the less sodium that study subjects excreted in their urine—an excellent measure of prior consumption—the greater their risk was of dying from heart disease. These findings call into question the common wisdom that excess salt is bad for you
<<
If I'm reading this correctly it is saying that people that urinate less sodium have higher chances of dying from heart disease. Then the author uses this as evidence that less sodium actually increase your chances of dying from heart disease.
If so then I would hypothesize that less sodium could simply mean that the body is no longer able to expunge it from the body and hence that is what is causing the heart disease.
"less sodium [output] could simply mean that the body is no longer able to expunge it from the body"
"the less sodium that study subjects excreted in their urine - an excellent measure of prior consumption"
These two statements seem mutually exclusive. If the amount of sodium a subject excretes is an excellent measure of prior consumption (ie, more out is demonstrably linked with more in, and less out = less in), then your hypothesis (less out may mean more retained, and therefore output can't be linked to input) cannot be true.
Of course, it could also be the "excellent measure" which is incorrect - my point is simply that these two are contradictory.
IMO, one of the most overlooked variables in the great salt debate is potassium deficiency:
'The 2004 guidelines of the Institute of Medicine specify an RDA of 4700 mg of potassium for adults,[2] based on intake levels that have been found to lower blood pressure, reduce salt sensitivity, and minimize the risk of kidney stones. However, most Americans consume only half that amount per day.'
Personally, I think we have a potassium, weight, and pre-diabetic problem, not a salt problem.
Anecdotal, I know, but in my experience my blood pressure is directly correlated with alcohol consumption. I used to be a consumer of 2-3 beers daily. At this time, I was also running approximately 15 miles per week, and working out at the gym. I was about 20 lbs heavier and had borderline high blood pressure. One day I cut out the beer intake, pretty much completely. The 20 lbs have fallen off, blood pressure is normal to below, and I cut back my running to 3-5 miles per week. I crave salt and eat plenty of it with an otherwise healthyish diet(that didnt change)
I understand their position up until the point of The NEJM Feb 2010 study, where they are dismissive of it as "conjecture". Granted it's a computer simulated model but they are using valid data from the National Health and Nutrition Examination Survey and the Framingham Heart Study.
For (b), a lot of articles submitted here have nothing to do with tech or startups. That doesn't mean we wouldn't be interested in reading them. I think the HN community tends to know what the HN community wants to read more often than not.
[+] [-] bluena|14 years ago|reply
A new study would have you believe that low-salt diets raise your risk of dying from heart disease—a surprising finding, and one that’s sure to grab headlines worldwide. The only problem is that the study’s conclusions are most certainly wrong.
In the study, published in the May 4, 2011, issue of the Journal of the American Medical Association (JAMA), European researchers followed 3,681 men and women for an average of about eight years. (1) They report that people with the lowest levels of sodium in their urine (a marker of salt intake) at the start of the study had a 56 percent higher risk of dying from cardiovascular disease than people with the highest levels. Equally unexpectedly, among the 2,096 participants who had normal blood pressure at the start of the study, urinary sodium appeared to have no effect on the development of high blood pressure over six and a half years.
Based on these findings, the study authors call into question recent estimates (2, 3) of the tens of thousands of heart attacks, strokes, and cardiac deaths that could be averted each year—and the billions of healthcare dollars that could be saved—by curbing Americans’ excessive salt intakes. Yet the study has several weaknesses, chief among them its modest size: With less than 4,000 participants—and only 84 deaths due to cardiovascular disease—the study is too small to support the authors’ sweeping conclusions.
Read about why cutting back on salt and sodium is a key to good health
Read about key studies that show the harmful effects of sodium on the heart
Furthermore, the study’s findings are inconsistent with a multitude of other studies conducted over the past 25 years that show a clear and direct relationship between high salt intakes and high blood pressure, and in turn, cardiovascular disease risk. (4–10)
“Take this study with a huge grain of salt, and then dispose of it properly,” says Dr. Walter Willett, chair of the Dept. of Nutrition at Harvard School of Public Health. “This study should not influence recommendations about sodium intake in any way.
Key problems that undermine the study’s conclusions include the following:
Unreliable measurement of sodium intake: The study investigators base their main findings on a single measurement of sodium collected at the start of the study specifically the amount of sodium that study participants excreted in their urine over a 24 hour period. Yet sodium excretion from just one day does not reflect people’s salt intake patterns over long periods of time. It’s weak science to use one-day sodium excretion to predict heart disease or mortality decades later. Failure to account for key factors that influence sodium intake and heart disease risk: People who are taller (11) or more active (12) tend to have a lower risk of heart disease. They also tend to have higher sodium intakes, simply because they eat more food. Yet the JAMA study authors don’t account for differences in height, physical activity, and total calories. (13) This oversight could make it appear as though high sodium intakes protect against heart disease deaths, when in fact physical activity or height is responsible for the lowered risk. Other weaknesses: There are other problems with the way that the investigators conducted the study, among them, missing or incomplete data from large numbers of participants. The study investigators, for example, could have accounted for incomplete urine samples by analyzing urinary sodium in relation to creatinine (another compound found in urine), but they did not.
The bottom line is that the researchers were trying to ask questions that their data are incapable of answering, and the study’s many methodological problems make its results unreliable. So the study’s findings do little to refute the strong evidence that cutting back on sodium would save lives.
Americans, on average, consume about 3,400 milligrams of sodium per day. Current U.S. recommendations call for a maximum of 2,300 milligrams of sodium a day (the amount found in a teaspoon of salt), and 1,500 milligrams of sodium (two-thirds of a teaspoon) for people who have high blood pressure or are at high risk of developing it. The latter group includes people who are over the age of 40, are African American, or have somewhat elevated blood pressure (prehypertension)—a group that includes almost 70 percent of adults in the United States. (14) A dash of prevention is worth a pound of cure: Since 90 percent of Americans will develop high blood pressure at some point in their lives, (15) it really makes sense for all of us to curb our sodium intake.
Read more about how to preserve flavor and cut back on salt
Try these delicious low salt recipes from the Culinary Institute of America
Seventy-five percent of Americans’ sodium intake comes from processed foods. (16) That’s why the Institute of Medicine has called on the U.S. Food and Drug Administration to regulate the amount of salt and sodium allowed in processed foods. (10) References
1. Stolarz-Skrzypek K, Kuznetsova T, Thijs L, et al. Fatal and Nonfatal Outcomes, Incidence of Hypertension, and Blood Pressure Changes in Relation to Urinary Sodium Excretion. JAMA. 2011; 305:1777–85.
2. Palar K, Sturm R. Potential societal savings from reduced sodium consumption in the U.S. adult population. Am J Health PromotOpens in New Window. 2009; 24:49–57.
3. Bibbins-Domingo K, Chertow GM, Coxson PG, et al. Projected effect of dietary salt reductions on future cardiovascular disease. N Engl J MedOpens in New Window. 2010; 362:590–9.
4. Strazzullo P, D'Elia L, Kandala NB, Cappuccio FP. Salt intake, stroke, and cardiovascular disease: meta-analysis of prospective studies. BMJOpens in New Window. 2009; 339:b4567.
5. Intersalt: an international study of electrolyte excretion and blood pressure. Results for 24 hour urinary sodium and potassium excretion. Intersalt Cooperative Research Group. BMJOpens in New Window. 1988; 297:319–28.
6. Cook NR, Cutler JA, Obarzanek E, et al. Long term effects of dietary sodium reduction on cardiovascular disease outcomes: observational follow-up of the trials of hypertension prevention (TOHP). BMJOpens in New Window. 2007; 334:885-8.
7. Cook NR, Obarzanek E, Cutler JA, et al. Joint effects of sodium and potassium intake on subsequent cardiovascular disease: the Trials of Hypertension Prevention follow-up study. Arch Intern MedOpens in New Window. 2009; 169:32–40.
8. Appel LJ, Moore TJ, Obarzanek E, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J MedOpens in New Window. 1997; 336:1117–24.
9. Sacks FM, Svetkey LP, Vollmer WM, et al. Effects on blood pressure of reduced dietary sodium and the Dietary Approaches to Stop Hypertension (DASH) diet. DASH-Sodium Collaborative Research Group. N Engl J MedOpens in New Window. 2001; 344:3–10.
10. Institute of Medicine. Strategies to Reduce Sodium Intake in the United StatesOpens in New Window. Washington D.C.: National Academies Press. 2010. Accessed May 3, 2011.
11. Ferrie JE, Langenberg C, Shipley MJ, Marmot MG. Birth weight, components of height and coronary heart disease: evidence from the Whitehall II study. Int J EpidemiolOpens in New Window. 2006; 35:1532–42.
12. U.S. Dept. of Health and Human Services. 2008 Physical Activity Guidelines for AmericansOpens in New Window. 2008. Accessed May 3, 2010.
13. Willett W, Stampfer M. Implications of Total Energy Intake for Epidemiologic Analysis. in Willett W, Nutritional Epidemiology. New York: Oxford University Press, 1998: 273–301.
14. Application of lower sodium intake recommendations to adults—United States, 1999-2006. MMWR Morb Mortal Wkly RepOpens in New Window. 2009; 58:281–3.
15. Vasan RS, Beiser A, Seshadri S, et al. Residual lifetime risk for developing hypertension in middle-aged women and men: The Framingham Heart Study. JAMAOpens in New Window. 2002; 287:1003–10.
16. Brown IJ, Tzoulaki I, Candeias V, Elliott P. Salt intakes around the world: implications for public health. Int J EpidemiolOpens in New Window. 2009; 38:791–813.
[+] [-] gojomo|14 years ago|reply
What would have been wrong with a clickable link (http://www.hsph.harvard.edu/nutritionsource/salt/jama-sodium...) and small salient excerpt?
Also, this Harvard article is strictly raising concerns about a May 2011 JAMA paper. The Scientific American 'End the War on Salt' article also relies on a "meta-analysis of seven studies" published in July, and talks of another 11-trial review of the effects of sodium-intake-reduction in 2004.
[+] [-] alttag|14 years ago|reply
In a hot climate (Southeastern U.S.), I'm often outdoors with sports teams or youth groups, and I see the effects of heat-related conditions regularly. These are prevented and treated with water and salt (electrolytes). [1] [2]
So yeah, too much salt may be a problem. Maybe not. But too little certainly is, and it's common in the active youth I observe.
1: http://en.wikipedia.org/wiki/Hyperthermia 2: http://en.wikipedia.org/wiki/Electrolyte
[+] [-] michaelcampbell|14 years ago|reply
[+] [-] ArbitraryLimits|14 years ago|reply
[+] [-] carbocation|14 years ago|reply
1. It's possible that we've reversed the causal association for all these years. You don't always get expansion of the extracellular fluid space with chronic kidney disease due to hypertension; with some tubulointerstitial diseases, you develop salt-wasting nephropathies. Perhaps these were the hypertensive patients who were referenced in the article, voraciously eating salt due to a deficiency caused by their kidney disease? I'd like to see more data before being willing to overturn dogma, but it's not the most outlandish idea I've heard all day. Still, the authors' conclusions are most likely wrong.
2. There's a group at MGH doing a randomized clinical trial in which they are administering intravenous salt and measuring near-term blood pressure response. It's a one-off exposure, but it will be interesting to better nail down the relationship between serum sodium content and blood pressure via experiment rather than epidemiology.
[+] [-] jonnathanson|14 years ago|reply
This is intriguing, because a similarly reversed causality was prevalent in the diagnosis and management of kidney stones for many years.
Perhaps this is TMI, but as a chronic kidney stone sufferer, I was told initially that I get too much calcium in my diet -- which builds up to cause the stones. Eventually, the doctors came around to the idea that I was actually secreting too much calcium into my bloodstream, and that secretion and consumption are not the same thing. In fact, I am losing more calcium than I consume, and I am losing much more than I should. Basically, I am deficient in calcium, even though my serum calcium levels are through the roof. (This phenomenon has underlying causes above and beyond the kidney disease; in fact, the kidney disease is most likely a secondary effect).
[+] [-] cperciva|14 years ago|reply
Another possibility: Cortisol. People under chronic stress produce more cortisol, and high cortisol levels act to inhibit urinary sodium loss. Maybe the people having heart attacks aren't eating more sodium; they're just retaining it better as a side effect of the stress which is killing them.
[+] [-] brudgers|14 years ago|reply
This week a meta-analysis of seven studies involving a total of 6,250 subjects in the American Journal of Hypertension found no strong evidence that cutting salt intake reduces the risk for heart attacks, strokes or death in people with normal or high blood pressure."
The article goes out of its way to dismiss the other impact of "French Fries" on health, obesity, and the role which salt plays in making manufactured food with low nutritional value habit forming.
http://www.sciencedaily.com/releases/2006/11/061101151027.ht...
[+] [-] DannoHung|14 years ago|reply
So... maybe the effort expended in reducing salt intake should instead be spent on increasing water as a beverage choice?
[+] [-] jdee|14 years ago|reply
Add in the fact that genetics plays such an important part, and the prevelence of White Coat Syndrome it's a shame that the medical world cannot make its mind up.
[+] [-] ern|14 years ago|reply
Is hypertension brought on by being stressed/awake less harmful than "intrinsic" hypertension? That seems to be the opinion by my physician. But it's maddening that these issues remain unresolved.
[+] [-] pradocchia|14 years ago|reply
"The (Political) Science of Salt", Gary Taubes. Science. 1998. 281: 5379; 898-907
http://web.archive.org/web/20060923051143/http://www.nasw.or...
[+] [-] greenyoda|14 years ago|reply
http://storyarchive.tumblr.com/post/9437438977/the-political...
[+] [-] brg|14 years ago|reply
http://www.foodnetwork.com/good-eats/good-eats-eat-this-rock...
Or for the brave: http://www.youtube.com/watch?v=0f62XQPBlTE
[+] [-] felipemnoa|14 years ago|reply
>>In May European researchers publishing in the Journal of the American Medical Association reported that the less sodium that study subjects excreted in their urine—an excellent measure of prior consumption—the greater their risk was of dying from heart disease. These findings call into question the common wisdom that excess salt is bad for you <<
If I'm reading this correctly it is saying that people that urinate less sodium have higher chances of dying from heart disease. Then the author uses this as evidence that less sodium actually increase your chances of dying from heart disease.
If so then I would hypothesize that less sodium could simply mean that the body is no longer able to expunge it from the body and hence that is what is causing the heart disease.
[+] [-] JacobAldridge|14 years ago|reply
"the less sodium that study subjects excreted in their urine - an excellent measure of prior consumption"
These two statements seem mutually exclusive. If the amount of sodium a subject excretes is an excellent measure of prior consumption (ie, more out is demonstrably linked with more in, and less out = less in), then your hypothesis (less out may mean more retained, and therefore output can't be linked to input) cannot be true.
Of course, it could also be the "excellent measure" which is incorrect - my point is simply that these two are contradictory.
[+] [-] Lost_BiomedE|14 years ago|reply
'The 2004 guidelines of the Institute of Medicine specify an RDA of 4700 mg of potassium for adults,[2] based on intake levels that have been found to lower blood pressure, reduce salt sensitivity, and minimize the risk of kidney stones. However, most Americans consume only half that amount per day.'
Personally, I think we have a potassium, weight, and pre-diabetic problem, not a salt problem.
[+] [-] e2daipi|14 years ago|reply
MoreOrLess: Is salt bad for you? 19 Aug 2011
http://itunes.apple.com/gb/podcast/more-or-less-behind-the-s...
Starts at about 00:45 up to 16:07.
[+] [-] S_A_P|14 years ago|reply
[+] [-] dr_|14 years ago|reply
[+] [-] pbhjpbhj|14 years ago|reply
[+] [-] alatkins|14 years ago|reply
[+] [-] gerggerg|14 years ago|reply
[+] [-] marshray|14 years ago|reply
[+] [-] crag|14 years ago|reply
[+] [-] lukifer|14 years ago|reply
b) This article doesn't have anything whatsoever to do with tech or startups.
[+] [-] PakG1|14 years ago|reply