Low sodium intake and cardiovascular health: an unanswered question. Response to: Letter from Dr N. Campbell, ‘Dissidents and dietary sodium. Concerns about the commentary by O’Donnell<i>et al.</i>’
Notice bibliographique
Résumé
‘An error does not become truth by reason of multiplied propagation, nor does the truth become error because nobody will see it’ [Mahatma Gandhi , All Men Are Brothers (2005 edition), Continuum - ISBN: 9780826417398]. The primary paper by Trinquart et al., upon which our invited commentary was based, is the evidentiary source demonstrating the polemic nature of researchers in the salt debate.1 Their findings are consistent with our anecdotal experience in this field, and also those of Dr Bruce Neal who, in an accompanying editorial reported their conclusions to ‘sound not too far from reality’.2 As an initial clarification, Dr Campbell (see this issue) repeatedly fails to make the distinction between reducing sodium intake in general and reducing sodium intake in the entire population to low levels (< 2.3 g/day). Dr Campbell’s recommendation that a sodium intake of under 1 g/day should be considered ‘normal’ intake cannot be taken seriously, as this intake is consumed by less than 1% of the population.3 We have never questioned the importance of lowering dietary sodium in those with high sodium intake (> 4-5 g/day), and in fact we have published large international studies reporting an increased risk of cardiovascular disease with high sodium intake.4,5 Neither do we question the positive relationship between sodium intake and blood pressure, which is curvilinear, and in fact have published the largest international study confirming the association between sodium intake and blood pressure.6 Whereas meta-analyses of sodium reduction clinical trials report a significant reduction in blood pressure in short-term trials, the reduction in blood pressure in trials longer than 6 months was non-significant in a recent meta-analysis of trials (Table 1), so the contention that longer-term trials have diminished blood pressure effect is not based on our opinion but derived from recent meta-analyses.7 There is activation of the renin–angiotensin–aldosterone system (RAAS) in both short- and longer-term trials of sodium reduction, the latter based on an updated meta-analysis (2013)8 of the one cited by Dr Campbell as reporting evidence of no effect on RAAS in long-term trials (2004).9 Our position, based on current evidence, is that there is adequate evidence to reduce high sodium intake to a moderate intake range, but insufficient data to support a further lowering of sodium intake to low levels in the entire population.10 Meta-analysis of clinical trials of sodium lowering on blood pressure, by duration of clinical trial CI, confidence interval. *Non-significant. Meta-analysis of clinical trials of sodium lowering on blood pressure, by duration of clinical trial CI, confidence interval. *Non-significant. Dr Campbell suggests that we should accept current guideline recommendations without question, even in the face of new information. Such an approach would mean that we would still be recommending widespread use of hormone replacement therapy in postmenopausal women. What Dr Campbell considers dissent is a necessary part of an evolving and dynamic scientific base, to guide clinical practice. As new information emerges old dogmas are challenged, and depending on the strengths of new and old evidence, guidelines may or may not change. This is particularly important for areas where the evidence base in imperfect, as it is for low sodium intake, where no study (observational or experimental) has reported a significantly lower risk of cardiovascular disease (CVD) in populations consuming a low sodium intake (< 2.3 g/day), compared with moderate (average) intake, and many report an increased risk of CVD and mortality. Dr Campbell focuses on the limitations of studies that report higher CV risk with low sodium intake, but ignores the fact that there are no primary studies reporting a significantly lower risk of CVD/mortality in general populations consuming a low sodium intake (compared with moderate intake). Before 2010, we accepted and promoted low sodium intake for CVD prevention, so our opinion has changed with changing information. As researchers, our main focus is conducting original research studies on the association of sodium intake and health. We advocate the conduct of a large randomized controlled trial of low sodium intake on health outcomes in different populations (e.g. general population, those with hypertension, heart failure) because there is considerable uncertainty about the feasibility and net clinical effects of low sodium intake, rather than stifling new research through claims of certainty. Dr Campbell is incorrect in stating that no scientific organization supports the view that the evidence base for low sodium intake is inadequate, and we would encourage him to read the 2013 Institute of Medicine committee report on this issue,11 which reported that there was insufficient evidence to support a recommendation for a low sodium intake. This was a committee comprising independent researchers (including the Chair) with no previous publications in the area, and researchers with diverging opinions. The question becomes why would different organizations reach different conclusions on the same evidence base, and what is the influence of researchers with fixed polarized positions on salt intake? A finding from the paper by Trinquart et al.1 was that selective referencing of studies was used by authors to support a particular position. Dr Campbell’s letter includes a number of examples, and one example is the referencing of studies criticizing use of formula-derived estimates for sodium intake. One study was a subgroup analysis (n = 120, 11% of entire cohort) of an international study we conducted to validate a formula-derived approach to estimating sodium intake from fasting morning urine.12 Unsurprisingly, some centres will find a lower or higher intraclass correlation (ICC) than the overall report and so selective emphasis on the best or the worst centre is not appropriate. In addition, the report from this one centre included individuals with incomplete collections of 24-h urine (which is an inherent limitation of 24-h urine collections), which would not be appropriate for a validation study, and the main analyses of the international validation study did not include such participants. The more appropriate reference reflection of the comparison of the single morning fasting urine with 24-h urine collection is the results of the main validation study (n = 1083), which reported an ICC of 0.71.13 Further, the association of sodium intake using our formula-derived estimates or the 24-h urinary estimates of sodium versus blood pressure was of similar strength. We have received no research funding from the food or salt industry, despite Dr Campbell’s repeated efforts to create such an impression. Each of us (including Dr Campbell) have presented at numerous scientific meetings, and participated in organizing committees, of organizations supported by the pharmaceutical, food or other industry. Current standards do not include these as potential conflicts of interest. Dr Yusuf has received no financial benefit from patents described by Dr Campbell, and none are related to dietary research. The patent for work done in the HOPE study has no relationship to salt or to any foods. The revenues were donated to create two chairs at McMaster University (one in Peace and Health and another in Diabetes) and to the Canadian Institutes of Health Research for the creation of the Canada HOPE scholarship which supported approximately 20 scholars from low-income countries to train at various universities in Canada. Dr Yusuf has derived no financial benefits from these patents. With respect to the food industry, from whom we have received no research funding, there is a legitimate debate on whether they should be included or excluded from the scientific discourse, as they are key participants in efforts to reduce high sodium intake. The ‘food policy’ meeting to which Dr. Campbell refers was organized by the Canadian Academy of Health Sciences and the World Heart Federation by a committee of experts, none of whom reported any links with the food industry. The portion of this meeting that focused on dietary sodium was stimulated by the findings of the Institute of Medicine expert panel on sodium intake in populations.11 Invitations were issued to speakers representing a diverse range of viewpoints, and included Dr. Campbell, and individuals recommended by him. He initially accepted the invitation, but shortly thereafter expressed reservations about the meeting, implying that he would withdraw unless certain conditions were met. The organizing committee concluded that his demands were unreasonable and were aimed at suppressing alternative views on the topic. Dr. Campbell then withdrew his agreement to be a speaker. The final group of speakers were required to declare any links they might have had to any industry or non-industry sources. The meeting concluded with a workshop of the speakers who had expressed a range of view-points and a summary was prepared including materials from all speakers (http://cahs-acss.ca/completed-projects/). (Personal communication, Dr. John Cairns). A report from the overall meeting was published in the Journal of the American College of Cardiology after extensive peer review.14 The fact is there is insufficient evidence to recommend low sodium intake for cardiovascular prevention, at this time. Our collective efforts should be directed at generating solid evidence from randomized controlled trials to inform sodium intake recommendations (and other dietary factors), and we would urge Dr Campbell to support, rather than stifle, such efforts.
Récupéré en direct depuis OpenAlex et désinversé. Les résumés ne sont pas conservés dans cette base de données : les index inversés représentent 8,6 Go des 9,3 Go de texte de la base, et le serveur dispose de 13 Go libres.
Comment cette classification a été obtenuedéplier
Prédiction machine sur la base complète
Imitation des enseignantsNi prévalence calibrée, ni vérité terrain. Validation humaine à venir. Le volet Gemma est une étiquette directe du modèle pour chaque travail de la base, lue sur la notice réduite au titre. Le volet Codex est un classifieur appris des 10 348 étiquettes directes de Codex et calibré sur les taux pondérés de l'échantillon; les champs sans appui suffisant ne portent aucun appel Codex. Le mode candidate est l'union des deux volets; le consensus est leur intersection. Ces sorties portent le statut machine_predicted_unvalidated et ne sont pas des étiquettes humaines.
Scores du classifieur distillé par catégorie (deux têtes)
| Catégorie | Codex | Gemma |
|---|---|---|
| Métarecherche | 0,006 | 0,043 |
| Méta-épidémiologie (sens strict) | 0,001 | 0,001 |
| Méta-épidémiologie (sens large) | 0,002 | 0,001 |
| Bibliométrie | 0,001 | 0,001 |
| Études des sciences et des technologies | 0,005 | 0,003 |
| Communication savante | 0,003 | 0,004 |
| Science ouverte | 0,002 | 0,002 |
| Intégrité de la recherche | 0,035 | 0,038 |
| Charge utile insuffisante (le modèle a refusé de juger) | 0,011 | 0,008 |
Scores machine (provisoires)
Les deux têtes enseignantes du modèle étudiant, lues sur ce travail. Un score ordonne la base pour la relecture; il n'affirme jamais une catégorie, et le statut de validation accompagne chaque rangée tel quel.
Scores de référence d'un modèle non mature (critères de maturité non atteints, 7 itérations). Un score ordonne; il n'affirme jamais une catégorie.
score_only:v0-immature-baseline · tel quel depuis la passe de notation : score_only signifie que le nombre peut ordonner les travaux, et qu'aucune étiquette de catégorie n'en découleClassification
machine, non validéePrédiction automatique; un appel candidat d’une seule source (Gemma direct ou Codex distillé), pas un consensus.
Le détail, modèle par modèle et score par score, se trouve en fin de page sous « Comment cette classification a été obtenue ».