Is that once in the whole study or several times? If it is a total of 6 days in 16 years then yes, that is ridiculous. You can expect people’s eating habits to change somewhat over such a long period of time.
I assume there must be other studies that found the same thing (low sodium is worse than moderate) because I keep hearing it over and over. If everyone is basing their facts off of one highly questionable study then something is wrong.
That is my understanding, but feel free to read the abstract (I linked it) and decide for yourself.
Edited to say that your well-founded scoffing highlights why physicians would not elect to buck longstanding clinical guidelines re salt consumption on the basis of a study such as this.
Actually, the ‘controversial’ finding is that there is a J-shaped relationship between sodium intake and mortality–modestly high at very low sodium levels, lower at moderate sodium levels, then higher still at high sodium levels.
I’ll mention here that since Sodium obviously has a “sweet” spot for health SOMEWHERE between zero and 8000 milligrams, correlations don’t give any info. The same is true of cholesterol, calories, blood sugar readings etc. Also, sodium intake itself correlates to intakes of other foods that may be health culprits. I believe for example, it has been found that food products targeting low income families tend to be higher in sodium.
Also, most, if not all of the “science” that lead to modern medical dietary guidelines were based on observational studies including estimates of nutrient intake from self reports.
In large, we are simply giving priority to poorly designed observational studies that suggested the prevailing view of modern medicine, over observational studies that suggested otherwise simply because they came first. Most were correlational, and dietary choices correlate to so many other factors that influence health that they were really bunk. The cholesterol model of heart disease has no foundation.
If anyone can find ANY controlled experiments that lead to the “current consensus” in the medical community, I would like to see them. The study offshoot from Framingham is not controlled, but it is better in most ways than any of the studies that lead to the current accepted sodium requirements, or the cholesterol model of heart disease.
Increased sodium intake was associated with greater increases in systolic blood pressure in individuals with hypertension (2.08 mm Hg change per g sodium increase) compared with individuals without hypertension (1.22 mm Hg change per g; pinteraction<0.0001). In those individuals with hypertension (6835 events), sodium excretion of 7 g/day or more (7060 [11%] of population with hypertension: hazard ratio [HR] 1.23 [95% CI 1.11-1.37]; p<0.0001) and less than 3 g/day (7006 [11%] of population with hypertension: 1.34 [1.23-1.47]; p<0.0001) were both associated with increased risk compared with sodium excretion of 4-5 g/day (reference 25% of the population with hypertension). In those individuals without hypertension (3021 events), compared with 4-5 g/day (18,508 [27%] of the population without hypertension), higher sodium excretion was not associated with risk of the primary composite outcome (≥ 7 g/day in 6271 [9%] of the population without hypertension; HR 0.90 [95% CI 0.76-1.08]; p=0.2547), whereas an excretion of less than 3 g/day was associated with a significantly increased risk (7547 [11%] of the population without hypertension; HR 1.26 [95% CI 1.10-1.45]; p=0.0009).
In other words, 4-5 grams is optimal if you have hypertension and there is no harm in Sodium intake up to 7 grams a day for people without hypertension. It supports the contention that a 3300 mg ceiling is harmfully low for people with and without hypertension. It also only includes urinary excretion, so the optimal level of intake for people with hypertension would be well over 4.0 grams per day. An hour of intense exercise results in about 1 gram of sodium excreted in sweat. Some is also lost in feces (not absorbed).
Here’s what the authors of the article I linked had to say regarding the study you excerpted:
“However, some scientists continue to produce and cite studies with paradoxical findings that conflict with the evidence base used to develop national and World Health Organization (WHO) guidelines on salt reduction.”
“The controversy arises from retrospective nonrandomized analyses of studies that include individuals who are already sick. Some such studies have found a U‐ or J‐shaped curve that can be explained by reverse causality (whereby BP may be low because of preclinical or prevalent diseases such as myocardial infarction or heart failure, which then lead to increased risk of premature death).”
“The most accurate technique to estimate usual dietary salt intake is the collection of multiple, high‐quality 24‐hour urine samples. A single urine sample is often used to estimate usual intake; however, this is also less accurate because of large day‐to‐day variation in dietary intake and because excretion varies widely even with a fixed salt intake. Several of the studies showing a J‐shaped relationship between salt intake and health outcomes rely on a single spot urine assessment to estimate each person’s long‐term usual sodium intake. Single spot urine sodium samples cannot accurately assess an individual’s usual salt intake, because sodium intake varies meal to meal and day to day and is also impacted by seasonal food availability.”
That is a long list of justifications of how we could be seeing paradoxical findings. It only provides conjecture about potential sources of error. For example, if a spot urine test produces a regression equation that predicts daily sodium intake accurately for a population, then the argument that spot urine tests are not accurate on an individual basis seems to be an overly aggressive attempt to de-legitimize. None of the conjectures counters the paradoxical research directly, they only point out limitations.
Yes, but that is the point. If one proposes a data-based argument to overthrow well-established clinical guidelines, the quality of that data needs to be very high.
And the contention that sick people don’t eat as much sodium because they are sick is also conjecture. You could take all of the foundational evidence supporting the blood cholesterol model of heart disease and argue conversely that people with heart disease have high cholesterol because it is the body’s way of trying to recover from endothelial tissue distress.
You could argue that people with high cholesterol are more likely to die of heart disease even if they are simply less likely to die from other factors first.
The data that lead to the clinical guidelines has all of the same limitations. For those who make the guidelines, the limitations of the paradoxical research should be important, but from the point of view of someone outside of the realm of those who make those guidelines-an objective scientist looking at the data, the guidelines carry no priority just because the data that lead to them came first.
Indeed. But the existence of plausible counterexplanations such as this is why even high-quality observational studies (and the ones discussed thus far have not been this) have to be interpreted cautiously, not simply accepted at face value.
No, I don’t think this is the case.
The guidelines have more going for them than the studies upon which they were originally based.
Please note that I am not in for a discussion of cholesterol. (I’m barely in for discussing sodium.)
If I may ask: Your wife–how does she feel about salt intake and HTN? What does she do vis a vis her own HTNive pts? (I’m assuming she a clinician and not a research cardiologist.)
She recommends limiting Sodium, trying to hit a goal of about 2000 mg/day, but she considers these patients to likely be from the subset of the population that is sodium sensitive. She also tells them to reduce or eliminate NSAID use which she finds can have a profound effect on blood pressure, and also to reduce sugar intake.
She says that most of the blood pressure management plan is already in place from the PCP by the time they are seeing a cardiologist and she tends to see more people who are over-medicated for blood pressure when they get to her.
It is apparently hard for patients to count sodium, so she says that docs typically recommend not eating foods with over 200 mg per serving.
On a side note, she was prescribed a statin for a cholesterol level in the 220s with a sparkling HDL to LDL ratio and excellent triglycerides. She stopped taking it after a month because she felt it was affecting her memory and she looked deeper into the emerging data on lipid profiles.
Wouldn’t surprise me if it turns out some individuals are more susceptible (genetically) to sodium’s effect on BP. Perhaps someday we’ll be able to discriminate (via genetic testing) between sodium responders and non-responders.
Just out of curiosity, what are the exceptions? My understanding is that saturated fats (i.e., no double bonds) cannot be cis or trans because they have no alkenes in the aliphatic tail.
You are right. I was thinking along a different line and made a mistake. I meant to say that natural saturated fatty acids are not mingled with trans fatty acids, (as hydrogenated saturated fats are) but there are a few oddball exceptions of naturally occurring benign or healthy trans fatty acids that are present in natural saturated fat sources.
Oh, yea, the one I was thinking about was CLA which is good for you and also vaccenic acid.