No Association Between Salt And Blood Pressure, Study Finds
time.com
time.com
1) All clinically treated hypertensive patients were excluded - that means if you have kidney or vascular disease (hypertension) and are being treated for it, you aren't counted here. Doctors WILL care about your salt intake if you have these conditions, as they should! It is very common to prescribe something called the DASH diet to lower sodium intake and increase potassium intake.
2) If you're healthy, it means your kidneys are healthy (simplifying). One of the purposes of the kidneys is to maintain homeostatic blood pressure by excreting a combination of salt and water. To put it simply, if you eat a huge load of NaCl, say in a dominoes pizza, your blood pressure WILL NOT be affected for a very long time. I'd guess 20 minutes or so after the salt enters your bloodstream. Which means these folks can't measure that blood pressure change by testing blood pressure yearly.
3) Either medical doctors or the press that listens to them have a nasty habit of taking treatments that often work for very sick people - morbidly obese, type 1 diabetics, bed-ridden centenarians - and applying it to normal healthy folks. I will go out on a limb and say that these unilateral recommendations are almost all BS, and should be ignored. If you're healthy: eating eggs will not affect your cholesterol, eating cheesecake will not give you diabetes, sitting in a chair will not misalign your spine. It would be prudent for you to be skeptical when you hear these claims, often on daytime television or on the internet.
I was confused but I think you mean "your blood pressure will only be affected for a short time".
You can parse what you said that way but your expression more readily reads [to me, an en-gb native] as saying that blood pressure changes will only appear a long time after salt intake.
I've read that salt has an almost immediate effect on blood pressure and so is used in some emergency treatments to increase blood pressure rapidly. I'd no idea of the mechanism of it though so the hint in 2) is welcome, thanks.
Salt does have an immediate effect on blood pressure, as you said, because of osmotic effects. Increased salt in the intravascular space will draw water from other areas into the vessels, thus increasing blood pressure. The kidney has both osmotic and pressure sensitivity.
Oh, that's also how it kills slugs! (Irrelevant remark; I've just put together two contexts containing "osmotic pressure").
2) See explanation in number 1.
3) I have not read the original paper, but the news article makes no mention of such inference.
I have to say that I think the premise that the human body must be excellent at maintaining NaCl levels perfect is sound. Sodium and chlorine are very active chemical elements. Having them in wrong levels probably throws every chemical reaction in the body out of whack. If I were to design a chemical machine that used NaCl, keeping the correct level would be a primary control. Evolution tends to get these things right, so our bodies probably do have excellent control mechanisms for this balance.
The study may have its own problems, but draws a conclusion I agree with, that the relationship between salt and blood pressure in healthy people may be overstated.
As for your point 3: I disagree. I think the news article makes a case that salt and blood pressure have no relationship, which isn't true. It is only true if, almost by definition, your salt / water regulation system is healthy.
Your point about maintaining NaCl levels is probably roughly correct, though I don't think it has been demonstrated per se.
It never states the inference directly, although as is common in mainstream media, the title of the piece is stronger than what is then told in the text. I think you may be getting too hung up on the title, and I understand the reason. Mainstream media often over-generalizes scientific findings, more so in the field of nutrition.
In the same vein you have a pet peeve with media behaviour, I have one with M.D. behaviour. One that may paint the overly generalized title in a kinder light:
Doctors often prescribe life-style changes: Eat less, eat better, exercise more, don't smoke, sleep well, sleep regularly, avoid stress. They fail at prioritizing, because they fail at recognizing that patients will never completely change their lifestyle. Willpower is a limited resource, and should be allocated as such.
The prioritization of lifestyle changes is important. If reducing salt intake is competing with reducing BMI, it should be a no-brainer that BMI reduction should come first. It is rarely the case. They are either presented as equally important changes or, since reducing salt intake is easier than shedding 20kg, doctors go for the easy goal.
The prioritization problem should be obvious. The closer to the root of problems you attack, the better the result you'll get. Salt intake is way way down the causal chain to health problems.
As such, blanket stating that you shouldn't care about salt in your diet may be good, if it leads to freeing willpower to do other lifestyle changes.
How active are the sodium and chlorine ions, which I assume is what you actually get since the salt is dissolved. Do they still have a major effect on most of the chemical reactions in the body? It's not like anyone is ingesting sodium metal.
Disclaimer: I have a physics degree but haven't taken chemistry or biology past high school, so I'm very ignorant here.
That only holds if the causal relationship does not affect health in any other way.
> The hypothesis being tested is "In good working condition, the human body maintains correct NaCl levels".
Maybe I'm misinterpreting things, but isn't maintaining correct NaCl levels is by definition part of a good working condition? Sounds a bit circular.
You're misinterpreting the definition of "good working condition". Good working condition, as I meant it means that it is operating as "designed" (no religious meaning intended), i.e. no malfunctions in any part are identified. It could be perfectly possible that, in good operating condition, the error margin on the NaCl control system allows for NaCl levels that cause hypertension. The hypothesis negates this possibility, and the hypothesis test seems to prove that the error margin on the body's NaCl level control keeps it narrow enough to exclude salt intake as a cause of hypertension (on healthy adults, of course).
If that's true it's somewhat like making everybody wear glasses, whilst understating the risks to the folks who are actually sensitive.
This is how I learned that caffeine raises my blood pressure about 20 pts. One can of coke. Sigh. And every doctor I have says "oh that's not true, you'd have to drink like 35 cups of coffee". And I'd like to tell them "The more you talk, the less I respect your opinion". Off topic, but what is it about experts that make them spout off their book knowledge exactly when they're faced with contradicting evidence?
There's a lot of sugar in there too, which is also linked to high blood pressure.
But why would medical doctors apply those claims to normal people? Assuming they're not generally considered valid for those who are healthy.
For a med STUDENT you show quite a lot arrogance. You also misunderstand how studies works (All clinically treated hypertensive patients were excluded for a reason. Guess which?)
Can't believe you were upvoted since most of what you wrote is just self-serving and has absolutely no links with the study. (I read the original study too)
I'm criticizing Time magazine for making the claim that salt has no effect on blood pressure (or implying it), which is demonstrably not true.
My point is: if you're healthy, no, it isn't surprising that your body can regulate salt intake. If you aren't, it isn't surprising that doctors will want to keep track of how much salt you're eating.
> For a med STUDENT you show quite a lot arrogance.
I wish you hadn't said this, because I think it's unnecessary and diminishes the rest of your comment.
The problem is there's a lot more going on in the body than basic hydrostatic forces and in general the body is pretty good at maintaining homeostasis in the face of external perturbation. As one, very relevant example, the kidneys are constantly excreting both salt and fluid in opposition to various changes in blood pressure and chemistry.
We know there are patients who are sensitive to salt in their diets. Particularly those with decreased kidney function. This and some other studies are asking the question whether increased salt intake in otherwise healthy individuals leads to an increase in blood pressure. So far the answer seems to be a resounding ...maybe.
I trust Paul Bragg more than a biased health study.
The science is conflicted over a simple question of fact -- whether or not a trivially measurable short-term effect occurs when you eat one of the most common food additives in the world.
If we can't even answer THIS -- it seems like it should be incredibly easy to answer -- I don't see why people can claim anything at all about diets and macronutrients.
Nutrition science needs a fundamental breakthrough and I don't know where it's going to come from but I desperately hope it happens quickly. Because a lot of people are suffering and dying of poor nutrition and we don't know basic things about what's good and bad for us.
It's Great! Oops, No It Isn't: Why Clinical Research Can't Guarantee The Right Medical Answers
"The truth is, few people know the first thing about clinical research. The public reads about a medical research project that announces unbelievable results for a miraculous drug. Some years later, another investigation completely wipes out those initial favorable findings. Hormones Cut Women’s Risk of Heart Disease (San Francisco Chronicle, 1994) Hormones Don’t Protect Women from Heart Disease, Study Says (Washington Post, 2001) The people are confused because we do not understand the process behind these conflicting results. Our health, and in fact, our very lives are dependent on clinical trials, but we know little about them. This book explains the issues the public needs to be aware of when it comes to clinical research. It uncovers the problems in medical investigations that can not be overcome no matter how much care and diligence medical researchers bring to a research project. The basic premise that drives the writing is that it is impossible for medical researchers to guarantee that they can get all the right answers from a single study. No matter how good the investigators are, no matter how well a study is planned, no matter how carefully the plans are executed and no matter how conscientiously the results are analyzed and interpreted – the answer may still be wrong. The deck is stacked against medical researchers and the public – you – should be skeptical of the results no matter how impressive they seem on the surface."
So, is the difference that there isn't much consensus among scientists for nutrition, and if so, why not? It seems to me that a hypothesis like "salt consumption affects blood pressure" should be fairly straightforward to test.
Or is the difference that the public simply isn't aware of what the scientific consensus is regarding issues in nutrition?
So the whole high GI is bad thing taken to the extreme e.g. clean eating, is probably completely blown out of proportion. It's measured in a very isolated ring-fenced setting that most likely doesn't apply to how you eat food anyway. Put bluntly: don't fret too much about eating white rice instead of brown rice (especially if you're counting macros).
That is as inane as disregarding crash test dummy results because they take place in a controlled environment which is not the same as 'real life'.
Or it might not. Testable! Give subjects the same combinations of foods (maybe scaled by body weight) a set time before consuming the test food, and measure blood sugar delta.
In any case, it might be wrong but it's not silly.
Talking to them usually results in "more of this and less of that and exercise and being thorough and blah blah blah". That sounds a lot like "I have no real idea of what's going on, but something in this broad spectrum of measures is bound to eventually pay off". That's very different from an answer that one would expect from a true professional, which would be more along the lines of "In this long and complex chain of events, this point here is the one that you need to affect in order to experience the effect you're looking for".
And what goes for nutrition will work for drug interaction monitoring too.
ITYM people's conclusions will slowly adjust to accumulating evidence. The entire process is ultimately steered by experimental evidence.
Errr, I think we know these 'basic' things quite fine. Energy burned needs to be >= energy taken in. It's just complicated for other reasons.
There are a lot of incentives to stay unhealthy. There're the biological incentives (eating a shitload and packing on a few pounds is good if you're in the jungle and might not eat again for a few weeks), and the incredible cultural pressures that prey on those biological incentives (taco bell spends a lot of money to encourage you to make bad health decisions).
Salt, cholesterol, fat, carbs - these are distractions from being healthy. People who eat healthy amounts of reasonable food (although even then, there's that guy who ate twinkies for a year and managed to lose weight by keeping his calories in check) rarely suffer from poor nutrition.
Yeah, everyone knows that guy who was a vegan and ran every day for 40 years and keeled over at 45 from a heart problem. He's the exception.
Two people consuming the same quantity of energy and exerting the same number of joules on exercise equipment do not see identical or even necessarily related physiological effects. There are many, many factors - other nutrients, genetics, timing, the distribution of work over time (short intense exercise vs. long less intense exercise, etc.) and they all matter.
There are skinny people who have never been inside a gym. There are fat people who work harder than you. Obviously you can still influence your outcomes, but "energy out >= energy in" is a gross oversimplification.
Your basal metabolic rate is not much different from the guy next to you of similar age and weight, barring some extremely rare circumstance. I don't know what to tell you, other than that.
> Two people consuming the same quantity of energy and exerting the same number of joules on exercise equipment do not see identical or even necessarily related physiological effects. There are many, many factors - other nutrients, genetics, timing, the distribution of work over time (short intense exercise vs. long less intense exercise, etc.) and they all matter.
Exercise is probably the least important part in proper weight maintenance, because of all the reasons you listed. Most people promoting the 'calories calories calories' mantra will tell you the exact same thing.
Your diet, and specifically how much you're consuming (regardless of carbs/fats/salt/etc.) is critical, the rest is secondary.
> There are skinny people who have never been inside a gym. There are fat people who work harder than you. Obviously you can still influence your outcomes, but "energy out >= energy in" is a gross oversimplification.
Not really. Those skinny people are eating less (in aggregate) than the fat people, again barring some very rare metabolic condition. Guaranteed.
This is clearly some genetic thing - I was the same way; my nieces are the same way (one getting married in a size 2, that had to be taken in). Eats ice cream by the quart, as often as she can get it.
Folks, denial isn't an argument, so please say something instead of just clicking down. I've just mentioned all this not as a straw-man but because a claim of an absolute (Everybody who is skinny isn't eating much) can be disputed by a single counter-example. That's all.
>Not really. Those skinny people are eating less (in aggregate) than the fat people, again barring some very rare metabolic condition. Guaranteed.
Take a look at http://en.wikipedia.org/wiki/Basal_metabolic_rate#Causes_of_... to find actual measured differences. The #1 cause of differences in BMR is lean body mass. A body builder will therefore have a higher BMR than a fat guy of the same height and weight. Energy spent on short intense exercises that bulk you up will have a bigger impact on your weight than long less-intense exercise that doesn't.
It turns out that we can explain about 3/4 of the difference in BMR through known factors such as these. But 1/4 of the normal variation comes from unknown factors, and that variation can easily leave an individual using 10-15% more or less energy than would be otherwise expected. This is a pretty big difference!
Furthermore even if you were right about all of that, you would STILL be wrong! Among the other potential effects of exercise is appetite suppression. So if your goal is to eat less, the easiest route might be 45 minutes per day on a treadmill, and then paying attention to your appetite.
But about BMR: Lean body mass between two people of same height and weight can certainly make a difference, but people tends to overestimate how much of a difference it will make assuming weight stays relatively similar.
(Note that difference in lean body mass certainly can have very substantial effect when you ignore large differences in weight because that opens the door for much larger variations in lean body mass, but note that bronbron was explicitly talking about similar weight)
I'm an amateur power lifter. My lean body mass after abut 10 years of exercise is about 15kg higher than when I was pretty much the same weight but fat. If I'd stated lifting younger (I was about 30) or used steroids, or spent more time with a trainer early on learning the right way to train, I might have added substantially more, but people tend to overestimate how much muscle you can realistically add. My current weight and performance means I'm an advanced lifter, within the top 10% of gym goers easily.
I often see people think they need to add on huge amount of calories when they start exercising, but that's rarely true. My average calorie intake to maintain my weight including what I burn during 3+ intense weight sessions a week, at a weight of 106kg is about 2400. That is not estimated, but measured by tracking weight + intake in detail over periods of weeks. Subtract my exercise and some other activity, and that easily puts an upper bound on my BMR of 2000kcal/day, most likely more like 1800. A lot of kids freak out when they see those numbers, because they've looked at stories about steroid filled freaks of nature that eat 5000kcal+ a day and think you couldn't possibly add muscle at my intake...
Schwarzenegger during his career as a bodybuilder was about my current weight when competing several seasons (he was heavier when he was a power lifter), but he probably had another approx. 15kg of lean body mass where I still have excess fat (if only I could magically transform my stomach fat and shift it to my chest and arms..).
That pretty much bounds the lean body mass difference for someone at around my current weight to around 30kg. I'm sure you could find someone with less lean body mass than I had when I was untrained if you went looking for really sickly people, but I was weak; you couldn't find many with more than Arnold without bumping the body weight up)
It's fairly normal to estimate about 12kcal per kg of extra lean body mass. The difference between untrained me 10 years ago and trained me today then adds up to only about 180kcal. And between untrained me 10 years ago and Arnold, about 360kcal/day.
Of course that's not nothing - 360kcal is a small/medium meal if you're careful. But very few find themselves towards the top of that range, so a difference that large at the same weight is likely not common (I was totally untrained and extremely sedentary when I started training), and if you do, your exercise will tend to dwarf the difference in basal metabolic rate. E.g. one of my workouts burns in the 500kcal range; I end up burning about 200kcal more per day on average. A top level bodybuilder will spend 3-5 times as long in the gym as me every week, maybe more (and on top of that, you are highly unlikely to get remotely close to Arnold level physique without steroids). But note also that this is before secondary effects: When I exercise, I am generally more active outside of the gym because I feel more energetic. I'll be more inclined to walk to/from the train station instead of taking the bus, or take a walk during lunch hour.
You can certainly find "mass monsters" amongst steroid using body builders today that have lean body mass way above that (e.g. Ronnie Coleman), but they are few and far between, and again the amount of exercise you'd put in makes the BMR relatively irrelevant.
if it were a small % of overweight people you might have a point, but the high % of overweight people in US in particular is certainly because of calories consumed >> calories burned.
i think the real tragedy is people looking for magical formulas, or giving up because 'its genetics'. further proof of that is that just about any dieting regiment works, the issue is that most people dont stick to them.
You say that like genetics has nothing to do with whether someone will stick to a diet or not ;)
Kidneys do not turn sugar into fat.
restrict carbs to a minimum and without a diet they will slowly lose the weight
That is a diet. They will lose weight if they consume fewer calories than they spend.
This nonsense is a great example of the awful ideas that people have about dietary science, and how poorly the truth is being communicated.
Make fat feel guilty about their weight and get them to continue eating sugar and corn syrup has only made the epidemic bigger in the last decades.
Controlling what you eat is the definition of implementing a diet, so doing that is not "without a diet".
Neither of which have any direct or consistent correlation to physical activity or food consumed. And that's the problem; everyone's body responds differently to a host of factors, and we don't understand the factors or the responses.
> Neither of which have any direct or consistent correlation to physical activity or food consumed.
is almost always bullshit. People who truthfully track their calories and err on the side of caution (did I eat 1 cup of yogurt or 1.5?) rarely end up surprised.
Sure, some people have thyroid conditions. If you do, you're the minority and you should get it treated. Otherwise, your body is pretty much the same as everyone else's with respect to metabolic rates (when age is factored in).
edit: I shouldn't even say "health" effects; just systemic effects period. Not only is nutrition not exclusively about weight loss, it isn't even about self-improvement. Rather, it's about a basic understanding of the construction and functioning of the human body.
Maintaining a healthy weight is the primary health problem for the vast majority of people concerned about their personal nutrition.
> Because a lot of people are suffering and dying of poor nutrition
In the developed world, they're mostly suffering and dying because of overconsumption (or reasonable consumption of really high-calorie food).
I'm not trying to say that I think it's as simple as 'put down the fork fatty!' or 'put the twinkie down!'.
I'm saying that instead of focusing on 'oh don't eat too many carbs' or 'lower your salt intake' as a silver bullet to 'why is our nutrition shit?', we should maybe be asking those harder questions: why is it so hard to put down the fork? how can we make it easier to be conscious of our caloric consumption?
It absolutely is the primary problem for most people concerned with nutritional issues in developed nations. Obesity (which is quickly becoming the epidemic it's made out to be) carries all sorts of nasty side-effects that are well documented.
Very long term, energy burned will be == energy taken in. If that's consistently out of balance by... say 100 Kcal/day, that's 0.2 lb/week every week or 10 lb/year or 100 lb/decade. How many 50-year-olds do you know who are 300 pounds heavier (or lighter) than they were at 20?
Not really, unless we're counting death. Most people gain weight as they get older.
> If that's consistently out of balance by... say 100 Kcal/day, that's 0.2 lb/week every week or 10 lb/year or 100 lb/decade. How many 50-year-olds do you know who are 300 pounds heavier (or lighter) than they were at 20?
You're phrasing that the wrong way. Your BMR changes depending on your current weight. If you weigh 180 pounds at 20 and you eat 2700 calories a day, eventually you'll reach a point where 2700 calories is what you require to maintain your body weight (probably somewhere in the 220-240 lb range).
To gain 300 pounds over 30 years would require you to constantly be consuming more and more as time goes on.
You're also completely negating the fact that most people would (and probably do) have a 'reality check' once they get into the 200+ range, and reduce their caloric intake (though unfortunately most likely only to resume their high caloric intake once they've dropped in weight a little).
You're agreeing with the post then, that very long term it's pretty even.
Originally I thought the poster meant "it can't be that simple because otherwise everyone would be 500 pounds", but yes, over time it does become true.
I feel like you're trying to grind some axe relating to weight loss here, but in doing so you are obviously oversimplifying the field of nutrition.
In most developed nations (which, admittedly I assume HN is largely composed of), people have problems with overconsumption as opposed to underconsumption. You're right though, your ideal scenario is energy burned === energy taken in an appropriate weight range for your height and muscular stature.
> Even that basic question is more complicated than you're making it out to be.
It's really, really not.
> I feel like you're trying to grind some axe relating to weight loss here, but in doing so you are obviously oversimplifying the field of nutrition.
I'll repeat what I said in another comment: Maintaining a healthy weight is (or should be, at least) the primary concern of the vast majority of people concerned with their personal nutrition.
I guess that's the equivalent of Stroustrup's "If you understand int and vector you understand C++", for nutritionists.
MealSquares (http://mealsquares.com) will be sticking with the Cochrane Review conclusions for now, but of course we will update and inform our customers based on the recommendations with the strongest evidence behind them. It's interesting to note that Soylent 1.0 went with around 1g of salt/day and was forced to change this when people started getting dizzy. it will be interesting to see what they change it to.
1. http://books.nap.edu/openbook.php?record_id=18311&page=R1
2. http://www.nhs.uk/news/2011/11November/Pages/cochrane-review...
Salts are electrolytes. (Electrolytes are salts?) You need them in your body so that your nervous system can conduct signals and keep things going - like your heart.
We live. We grow. We hurt. We heal. We get sick. We recover. We age. We wear out. We die.
Rather that avoiding "omg sugar" or "omg salt" or "omg fat," we should just be eating well-rounded diets. Have some beef today. And some pork tomorrow. And some fish after that. Have some fruit. And veggies. And a bit of dessert. And a spoonful of honey. And some powdered sugar on that syrup'd French toast. Just don't eat large piles of stuff for a meal. And don't eat the same thing every day.
Life's gonna kill you. Just don't clog up your body with excessive amounts of the same thing and you probably won't die early.
You must eat fat (to obtain essential fatty acids). You must eat protein (to obtain essential amino acids). There are certain vitamins you must eat. And there are certain elements that you must consume.
The real question is how much of the required nutrients is enough and how much is too much?
What ratio of macronutrients (carbohydrates, protein, and fat) is ideal for maximizing health? Are there trade off for different ratios? For example, carbohydrates are not required for life, but most diets obtain a large portion of daily caloric intake from them. What percent of calories should be from carbohydrates?
Nobody yet knows what a well balanced diet is. In absence of that information, your advice is pretty good. Eat lots of different stuff.
Define well-rounded. ;) Isn't that what we're all trying to decide? We even have some people on here claiming McDonald's can be part of a balanced healthy diet.
> It's Time to End the War on Salt > http://www.scientificamerican.com/article/its-time-to-end-th...
This is why I hate the intersection of journalism, science, and the public.
Take Omega3 for example: It´s much healthier to reduce the content of Omega 6 in your diet than popping a couple of Omega 3 pills a day. This is so because our current diet has screwed up this optimal ratio [1]
Same applies to salt: The problem is not Sodium, but refined salt, that has a mineral composition so unbalanced that makes Sodium problematic.
Just eat unprocessed food.
[1] Optimal ratio Omega6/Omega3=around 1. Typical ratio in western diets: 15/1 http://www.sciencedirect.com/science/article/pii/S0753332202...
Think about what proving no association actually means. That would require proof of a negative, which is a widely recognized logical error, an impossible burden. To see why, imagine that I believe in Bigfoot and I will continue to believe until someone proves he doesn't exist. But no one can prove Bigfoot isn't hiding under some rock on a faraway planet, therefore I am justified in my belief. My belief is supported by an impossible evidentiary burden.
This is why scientists rely on the null hypothesis -- contradicting it requires positive evidence. Its opposite requires negative evidence.
What you have said above is horribly wrong and is exactly the point I am making. If it is true then I can prove anything I like just by designing a bad enough experiment.
For example, suppose I want to prove that the moon is made of green cheese. I can start with a null hypothesis that it IS made of green cheese. Then I can point my telescope in the wrong direction and find no evidence that it is not made of green cheese. Using your logic I am free to then conclude that my null hypothesis is true.
You cannot just make any null hypothesis you want and then when you fail to prove it untrue, claim it is true. If you want to make a positive claim about the null hypothesis (for example, claim there is no association between salt and blood pressure) then you have to test it directly with positive evidence in its own right.
> What you have said above is horribly wrong and is exactly the point I am making. If it is true then I can prove anything I like just by designing a bad enough experiment.
You obviously do not understand the null hypothesis. Under the null hypothesis, a claim is assumed to be false unless and until persuasive evidence shows otherwise. Only psychologists think a bad experiment contradicts the default assumption of no effect. Serious science must pass muster with other equally serious scientists, who will call out anyone trying to cheat.
> For example, suppose I want to prove that the moon is made of green cheese. I can start with a null hypothesis that it IS made of green cheese.
That is certainly not what "null hypothesis" means -- your utterly mistaken view asserts its opposite, the alternative hypothesis. Please learn anything at all about this topic before assuming you understand it.
> You cannot just make any null hypothesis you want and then when you fail to prove it untrue, claim it is true.
Honestly. Learn what it means before trying to discuss it.
http://en.wikipedia.org/wiki/Null_hypothesis
Quote: "In statistical inference of observed data of a scientific experiment, the null hypothesis refers to a general statement or default position that there is no relationship between two measured phenomena. Rejecting or disproving the null hypothesis – and thus concluding that there are grounds for believing that there is a relationship between two phenomena or that a potential treatment has a measurable effect – is a central task in the modern practice of science, and gives a precise sense in which a claim is capable of being proven false."
Try and find anything there that backs up this statement:
>> if positive evidence isn't present, then the default assumption is correct
Quoting from the same page:
"...it should be noted that the null hypothesis is never proved or established, but is possibly disproved, in the course of experimentation."
And again:
"We may, however, choose any null hypothesis we please, provided it is exact."
You need to learn about the null hypothesis. And science. The null hypothesis denies the reality of the asserted hypothesis until positive evidence supports it. How difficult is that? The default assumption is that there is no effect, no connection between a stated hypothesis and reality.
If I make the claim that Bigfoot exists, and then set out to test my claim using science, under the null hypothesis the default assumption is that Bigfoot does not exist. This means you have it exactly backwards.
> ... your insulting tone is not particularly conducive to ongoing discussion
A description is not an insult. Learn this difference also.
Learn about the null hypothesis. Discover that the null hypothesis cannot be used to make a positive claim or assertion, as you did earlier with your green cheese example. That is reserved to the alternative hypothesis, which is how pseudoscience works, i.e. make a claim and wait for someone else to disprove it with the impossible standard of "proof of a negative" or "absence of evidence":
1. "Salt intake was positively associated with SBP in men but not in women."
2. "Salt intake was not associated with SBP in either sex after multiple adjustments."
Also isn't this kind of journalism and article titles unethical? There should be some kind of regulatory board for articles in any media.
Anyone can write anything and can cause serious harm.
Doesn't that mean there is a causative effect, or are they saying it just a correlation? People with high blood pressure tend to eat more salt? Or if it is not statistically significant, why mention it at all?
Unless causality is clearly articulated, it never should be assumed. Also, it never would be stated if there was not statistically significant data supporting it - keeping in mind this is a Time article and not the original source [0] so you're dependent on the writer knowing what they're talking about as well.
[0]: http://ajh.oxfordjournals.org/content/early/2014/09/03/ajh.h...
The vast majority of the people complaining about the Big Soda ban don't buy big sodas, and those most enraged about the Buckyballs ban either already have them or would never want them. So the reaction has nothing to do with the products themselves, the rage is on a theoretical level, "I don't want government intruding in my private choices." But they already do this in a gazillion different ways, bigger, more important intrusions. The difference is that those are invisible. You know you can't value the risks in airplane safety or radiation leaks so you trust them to do it, but you think you can value the risks of a soda and hate that they try to do it for you.
I know you are thinking, "but I can resist soda; I understand the risks"-- never mind you don't even know the ingredients of soda, the point here is you are starting from you and multiplying by 6 billion.
When you say, "personal responsibility!" you are really saying "this is safe enough for it to be a question of personal responsibility." But you must ask yourself the question: how do you know Buckyballs and soda are safe enough for them to be about personal responsibility? Because "some other omnipotent entity" allowed them to exist. How do you know that Entity can be trusted? Because it even tries to ban silly things like Buckyballs and soda. The system is sound.
Isn't that a bit like saying that only African Americans are allowed to stand up to racism?
the rage is on a theoretical level
If individual liberty and personal responsibilities are only theories. I don't happen to agree.
But they already do this in a gazillion different ways
So because they get away with it in harder-to-grasp and harder-to-politically-oppose ways, we should just submit to all of it?
I know you are thinking, "but I can resist soda; I understand the risks"
You obviously have no idea what I'm thinking. I think about the bigger picture of a society of sheep that elects wolves to make all their decisions for them because the sheep are too busy watching the NFL and Miley Cyrus to be bothered to make decisions for themselves and take responsibility for those decisions. I ponder the paradox of a populace too stupid to decide whether or not to drink a soda but smart enough to elect angels who will protect them from themselves.
Because "some other omnipotent entity" allowed them to exist
You're totally and completely wrong yet again. I'm an atheist. How does that affect your rationalization of letting others use force to make the smallest decisions in life for you?
The argument to spell it out in a clearer way than the author is a reductio ad absurdum:
1) The system protects us from unsafe airline and car practices.
2) The system tries to ban toys and sodas.
3) Therefore, the system can protect us from anything that is bad.
The conclusion is clearly false, because lots of bad things still happen and you can't engineer a perfectly safe system. The omnipotent entity he refers is the the government, market, or whatever entity makes decisions you don't have to. In the full article there are lots of examples, from banking to whatever where the train of thought jumps from one type of savior to another, without ever pinning it down on the individual.
[And in the of long-distance airplane flights, the whole deep-vein-thrombosis thing does actually seem to be a documented problem, if a pretty rare one...]
The article sounds like a total yawn to me, that is, just old and obvious. So, I long understood: If eat some food with some table salt, that is, NaCl, then within an hour or so likely the salt concentration in blood will increase and then blood pressure will increase. But, the body has a system that regulates salt concentration; so, if the salt concentration is too high, then the body will lower the salt concentration, and the usual way is to flush out the extra salt in urine. So, net, likely within a few hours, the salt concentration will be back to where the body wants it. Typically, for reasonably healthy people, no biggie.
Somewhat separately there is a disease called hypertension which means high blood pressure, and such blood pressure can be dangerous, e.g., cause blood vessels to break and leak, say, in the brain -- not good. If a person has this disease, then extra salt that further increases blood pressure, even just for a few hours, can be not good. So, for such a person, a standard recommendation is to reduce input of salt: So, e.g., don't sit around eating salted peanuts, potato chips, etc.
But does eating salt cause the disease hypertension? Nope.
Then, bingo, presto, wonder of wonders, the mass media, always eager for getting eyeballs, often by grabbing people, by the heart, the gut, below the belt, always below the shoulders, never between the ears, comes out screaming about salt suggesting that salt, exploiting really simplistic thinking, is somehow bad. Or, since people are sensitive to suggestions or symptoms of danger, suggesting that salt is bad can get eyeballs.
Then companies that manufacture and want to sell food products, say, bread, may see a selling opportunity, lower the amount of salt in their products, and then scream on their product labels that their products are healthy because they are low salt.
We can see how the mass media and their food product advertising customers have a common interest: The media raises fears about salt, and the food companies scream that their products are healthy because they are low in salt. It's deliberate confusion and deception, that is, in a word, a scam, all in an attempt to get money from ordinary people.
This scam has been going on for decades. E.g., back in the 1980s I was in the house of some friends; they were in their 20s and in perfect health, with perfect weight, etc. The husband was a good athlete, and his wife was drop dead gorgeous. But the wife was cooking with low salt based on the scam, i.e., that salt would cause hypertension, which of course it would not.
Or, as in the title here, "No Association Between Salt And Blood Pressure", of course not. There never was any such association. Salt does not cause hypertension; there's never been any competent claim that salt did cause hypertension.
So, now Time gets another way to grab eyeballs -- debunk the scam that for at least three decades has had way too many people thinking the total nonsense that salt causes hypertension.
For the media, there's a pattern here: To get eyeballs, create a scam. Then, later, maybe decades later, to get more eyeballs, debunk the scam. Then continue with more scams -- there are many possible scams.
So, net, salt does not cause the disease hypertension, and the media likes to use scams to get eyeballs. Virginia, if you didn't already know this, then listen up and learn. I mean, by now, we expected something else?
"In response to controversy about the health effects of low sodium intake, the Institute of Medicine convened an expert committee to evaluate the evidence for a relation between sodium and health outcomes.4,5 The committee concluded that most evidence supports a positive relation between high sodium intake and risk of cardiovascular disease but that results from studies with health outcomes were insufficient to conclude whether low sodium intake (<2.3 g per day or <1.5 g per day, as recommended in current dietary guidelines6,7) is associated with an increased or reduced risk of cardiovascular disease in the general population. The committee found limited evidence that low salt intake may be associated with adverse health effects in some subgroups, including some patients with heart failure or other forms of cardiovascular disease, diabetes, or chronic kidney disease. Results from three studies, reported in this issue of the Journal, bear on this matter. The Prospective Urban Rural Epidemiology (PURE) study provides new evidence about the association between sodium and potassium intake, estimated from morning urine specimens, and blood pressure, death, and major cardiovascular events.8,9 The procedure for estimating electrolyte excretion was validated elsewhere.10 The PURE study included more than 100,000 adults sampled from the general population of 17 countries that varied in their economic development and acculturation to an urban lifestyle. Approximately 90% of the participants had either a high (>5.99 g per day) or moderate (3.00 to 5.99 g per day) level of sodium excretion; approximately 10% excreted less than 3.00 g per day, and only 4% had sodium excretion in the range associated with current U.S. guidelines for sodium intake (2.3 or 1.5 g per day).
Across this broad range of populations, the relation between sodium excretion and blood pressure was positive but nonuniform: it was strong in participants with high sodium excretion, modest in those in the moderate range, and nonsignificant in those with low sodium excretion. The authors concluded from the findings that a very small proportion of the worldwide population consumes a low-sodium diet and that sodium intake is not related to blood pressure in these persons, calling into question the feasibility and usefulness of reducing dietary sodium as a population-based strategy for reducing blood pressure. There was also an interaction between sodium excretion and potassium excretion: high sodium excretion was more strongly associated with increased blood pressure in persons with lower potassium excretion. The authors suggested that the alternative approach of recommending high-quality diets rich in potassium might achieve greater health benefits, including blood-pressure reduction, than aggressive sodium reduction alone. After a mean of 3.7 years of follow-up, the composite outcome of death and cardiovascular events occurred in 3317 participants (3.3%). As compared with those who had a moderate level of sodium excretion, those with a higher or lower level of sodium excretion had an increased risk of cardiovascular-disease outcomes.
The authors attempted to rule out residual confounding or reverse causation as explanations for their findings by showing that participants with a low level of sodium excretion had a similar mean INTERHEART Modifiable Risk Score and higher intake of fruit and vegetables, as compared with those with a moderate level of sodium excretion, and that more than 90% of the cohort was free of antecedent cardiovascular disease. The findings were not altered by the exclusion of participants with prior cardiovascular disease, cancer, or use of blood-pressure medication, by the exclusion of outcome events occurring in the first 2 years of observation, or by adjustment for all identifiable confounders.
The major weaknesses of the PURE study, inherent in its study design and scope, include the absence of direct measurement of 24-hour urinary excretion on multiple occasions, which is the accepted model for assessing electrolyte intake, and the lack of an intervention component to assess the direct effects of altering sodium and potassium intake on blood pressure and cardiovascular-disease outcomes, thus making it impossible to establish causality. Nevertheless, this large study does provide evidence that both high and low levels of sodium excretion may be associated with an increased risk of death and cardiovascular-disease outcomes and that increasing the urinary potassium excretion counterbalances the adverse effect of high sodium excretion. These provocative findings beg for a randomized, controlled outcome trial to compare reduced sodium intake with usual diet. In the absence of such a trial, the results argue against reduction of dietary sodium as an isolated public health recommendation.
The authors of the third article, from the Global Burden of Diseases Nutrition and Chronic Diseases Expert Group (NutriCode),11 used modeling techniques to estimate global sodium consumption and its effect on cardiovascular mortality.12 The investigators quantified global sodium intake on the basis of published surveys from 66 countries and used a hierarchical Bayesian model to estimate global sodium consumption. They then estimated the effects of sodium on blood pressure in a meta-analysis of 107 published trials and estimated the effects of systolic blood pressure on cardiovascular mortality by combining the results of two large international pooling projects that included individual-level data. They found a strong linear relationship between sodium intake and cardiovascular events and estimated that 1.65 million cardiovascular deaths in 2010 were attributable to excess sodium consumption. The NutriCode investigators should be applauded for a herculean effort in synthesizing a large body of data regarding the potential harm of excess salt consumption. However, given the numerous assumptions necessitated by the lack of high-quality data, caution should be taken in interpreting the findings of the study. Taken together, these three articles highlight the need to collect high-quality evidence on both the risks and benefits of low-sodium diets."
EAT FOOD THAT TASTES GOOD. STAY AWAY FROM PROCESSED FOOD. GET OFF YOUR ASS AS MUCH AS POSSIBLE. THAT IS ALL!
/rant
I say that based on my personal experience:
A nurse in the clinic checked my BP (as a routine) when I went to get checked for some eye infection. And she was shocked that it was 170/100 (normal is 120/80).
It was shocking for her (and of course me) because: I was 25 I looked healthy and lean (not too thin). I showed/experienced no signs of hyper tension.
My eating habits, was to go on a Frozen Prepared Food diet (for lunch and dinner) because that was the cheapest tasty food I could afford along with cereals for breakfast, for about 3 months before my BP was checked.
I dropped this diet since that day, reduced salt intake considerably. And it took about 9 months for my BP to come down to normal levels, without any medication, and with a little extra exercising.
I'd have taken this article with a pinch of salt. But, I have cut down on salt intake. So I prefer to not take it :)
Since anything that cuts processed salt considerably almost assuredly improves those other metrics, I'm not sure why you believe your anecdotal evidence is so convincing.
btw, my diet, even though had a lot of frozen food, wasn't loaded with carbs, and was sufficient in protein.
Back to the point: When doctors I trust say that I'm better off cutting salt and sodium intake, I'll cut down on it. And because its the trusted doctors that say so, I consider it as non Anecdotal Evidence
A terrible article from Time magazine going against what a lot of institutions doing research are saying. Not like this is controversy to get eyeballs or perhaps a study backed by industry to confuse people.
And suddenly there are a lot of experts on nutrition and diet on a startup forum.
I started eating out more often because of this, which is not low on Sodium, but its not as loaded as it is in the frozen foods.
Anyone who thinks there's an ounce of truth in the Time article, try living on a frozen food only diet (at your own risk) for a few months.
Check your blood pressure regularly. if after 3 or 6 months, your BP remains the same, Salt and Frozen Food industry would be ready to pay you millions to publicize your anecdotal test.