This interesting study from Karolinska Institute, a diabetes center of very good reputation, concludes that there is an association between high salt intake and the incidence of Type 2 Diabetes and of LADA.
At the same time, it is very strangely written, and I am not quite sure what to make of it.
The study is solid, and is a retrospective study based on a questionnaire. It finds a strong association between each 2.5 grams of salt consumed daily and (a) a 43% increased incidence of Type 2 Diabetes; and (b) a 73% increased incidence of LADA. In fact, genotypes at high risk of LADA were FOUR times more likely to develop LADA if they consumed a "high " amount of salt (more than 8 grams per day), a shocking increase in risk.
This is where it becomes weird. The study concludes:
“We confirm an association between sodium intake and type 2 diabetes”
(that’s strong) and
“high sodium intake may be a risk factor for LADA, especially in carriers of high risk HLA genotypes.”
What the ??? They find a much higher risk factor for LADA, and a 4x increase in risk of LADA (!!!) for those consuming high amounts of sodium, but their conclusion is much stronger for Type 2 diabetes???
What do you make of this?
My suspicion: they are being influenced by the perception that T2 is a lifestyle issue (so they don’t doubt a lifestyle link here) while LADA is genetic (so they doubt the lifestyle link there).
I would just think it’s because it is nott exactly in line with the other models of LADA etiology… so it’s harder to make a slam dunk statement which would somewhat be like “it’s not autoimmune, it’s not really adult onset type 1, it’s just too much salt”
Wheras type 2 is already widely accepted to have a dietary component— so narrowing the focus on sodium… no big deal.
I’m not a researcher but I just suspect it’s harder to make bold statements that contradict other research even if it’s good evidence
While I don’t like the idea that any part of my diagnosis may have been something “I did to myself,” and thus tend to initially react to articles like this negatively and question their validity (a fault of mine I need to get past), I am truly curious why they think salt would increase incidence of LADA with it being an autoimmune response. Specifically, the article states, "Previous research* has suggested that excessive salt consumption may increase the risk of developing T2D, possibly through a direct effect on insulin resistance, and/or by promoting high blood pressure and weight gain."
If salt likely increases risk of T2 because of those effects listed, how does that translate into triggering an autoimmune disease?
This study is a retrospective study, not a causal study – so they can only observe correlations. If, for instance, there is a genotype that gets LADA more often and also increases your liking of salt, it’s not the salt that causes LADA. There can be a co-factor at play.
However, there is evidence of a steady increase in T1 and LADA rates over the past 40-50 years. So many (most?) epidemiologists believe that there are environmental factors at play.
I would also suggest that, as @MaryPat suggests, we don’t KNOW that LADA is purely genetic, in the same manner as we are now discovering many genetic factors to T2D.
I absolutely believe in environmental factors being a trigger for autoimmune diseases - I have lived it. My parents both carry genes for several autoimmune disorders, which they passed down to several of their children, but none of us had any of them triggered until we moved to a certain area and then bam. One after the other disease in several children. Our endocrinologist said she has never seen rates of autoimmune disorders anywhere else as high as that area.
Please! Do tell? Even privately. The suspense is killing me. I’ve always subscribed to the autoimmune trigger theory, but have never researched it. (Because sometimes just having an autoimmune problem or three in your life is enough. The why becomes unnecessary when obscured by the how of managing life.)
As a researcher, I always take correlational, retrospective studies with many… wait for it… grains of salt, because it’s just not a particularly informative or rigorous study design, as @Michel noted above. Retrospective correlations are weak science at best, and often end up not panning out in prospective and experimental studies. I still publish papers like that myself, but my findings are couched in a ton of mights/coulds/may influence/etc. Also, it’s definitely the case that to even publish a paper like that, ideally you should have theoretical backing for your finding (otherwise odds that you’re just capitalizing on some fluke of the data or a third variable association go up a lot), so I agree that the LADA stuff is probably be stated more cautiously because it is unexpected and without a theoretical explanation. Studies like this are best used as part of a much larger picture, so if they contribute to a growing trend of research findings across many samples and including more rigorous studies (which sometimes only happen after a preliminary study like this), that’s when science starts to take this stuff seriously.
One obvious (to me anyway) possibility here is that salt intake is a proxy for processed and restaurant-prepared foods (people rarely add as much salt to their foods as corporations and restaurants do), and those foods could confer risk in many other ways. Unless they controlled for that as well as the many other dietary factors likely correlated with salt intake, I would be extremely skeptical of these findings having much meaning.
To add to what @cardamom said, these studies are done to find something promising to research further. One should only look at results such as these as interesting pieces of a puzzle, but never as the answer itself. For that you need different study tools. But if 5 studies like this all point to the same thing, then someone will get the bright idea to invest $2-3 million dollars and study it further.
No, absolutely! I meant, just seeing the title, I already would think, “not true!” just because of personal bias. After reading through this article, though, I do question the correlation. It just doesn’t seem to hold up to closer scrutiny (once I gave the article a chance and finally read it, lol).
Thank you so much for this interesting perspective as a researcher. We talk a lot at my house about the difference between correlation and causation, however I am very much not a scientist. And I don’t even think I took a “real” science class, um, ever. (Which is pretty embarrassing, because I teach college, albeit in the art field.)
But I wanted to thank you for pointing out the difference between the types of research, and making it understandable for the rest of us. I did wonder when I was reading the study if they had taken into consideration the type of diet that is high in salt, and the other lifestyle choices that might be made which with accompany that.
Not unlike @Pianoplayer7008 I am often heck-no-skeptical about studies that point at one thing which seems like way too easy of an explanation and which are not backed up by research. I guess it’s the idea that if you look hard enough, you can probably find something to support your point of you. From my place in Ludditeville (i.e. W/ oFB), I hear that’s becoming a problem these days.
@Michel, I couldn’t access the paper, are you sure it’s retrospective? If so, retrospective observational studies are some of the shakiest data out there. Imagine you’re a person who got sick – and then someone came along and asked you about a behavior that has been broadly labeled as unhealthy in our society. It’s just human nature to rack your brain and think of anything you might have done to have caused the condition, so people who get sick are more likely to exaggerate said unhealthy consumption relative to others who don’t have the condition.
So on that basis alone I’d say the study is limited in its conclusions.
On the other hand, there was a really fascinating article in the New York Times a few months ago suggesting we simply don’t understand salt physiology in the human body very well. So who knows how it might interact with, say, hunger signals in T2D or whatever…
“But urine tests suggested another explanation. The crew members were increasing production of glucocorticoid hormones, which influence both metabolism and immune function.”
@TiaG, I couldn’t access it either, I assumed it was from the questionnaire discussion in the ScienceDaily article that @MaryPat linked to – do you think I might have misinterpreted that?
I mean, a questionnaire could be given, say, daily or weekly, in which case it’s retrospective in the absolute sense (i.e. you say what you ate that week), or it could be a “food diary” in which you say what you ate after every single meal. Both of those do have limitations but they’re not as bad as the typical dietary retrospective study: given once and you’re asked to estimate how much of everything you ate over a six-month, or year-long period. Would be great to know which it is.
Her link worked for me. It is a good study as far as retrospective reviews go. It was done by a competent organization. It doesn’t appear to be over-reach. With that said, these types of studies are not definitive.
In research design, retrospective typically refers to that both the predictor and outcome are being collected after both have already occurred, in contrast to prospective data, in which the predictor data is collected initially and used to predict incidence of the outcome over time (so, new diagnoses of diabetes in the follow up period). Even in prospective studies, people are often asked to summarize behavior over some amount of time if self-report is used at all. Even studies using ecological momentary assessment or daily diary, in which people are asked once or multiple times a day about what they are doing, often ask people to report on experiences/behavior over the last period of assessment, not just what is happening right now. What’s different is that the data is used to predict future outcomes, not to try to explain what already happened. So it’s worth noting that just because a study is prospective, it is typically still correlational and not causal, but it at least establishes temporal precedence (i.e., the predictor came first), which is one of several requirements for causality. Experimental research is the only type of research that is causal in nature (and then still, only to the extent that it is done well and rarely definitively so), and many of the questions we are interested in do not lend themselves well to experimental research, because doing randomized controlled trials of lifestyle factors is often not feasible.
I’m nothing near a research scientist, I could best be describe as a person with a gut feeling. My gut feeling is that there is an agenda at work in this research. The agenda appears to be to prove that salt is bad but we already knew that.
Scare tactics are often used by nutritionist or anyone pushing an agenda. Does this research prove anything, it doesn’t appear so, but it for sure might scare someone.
