Letters to the Editor
- Eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, the 2 main omega-3 long-chain polyunsaturated fatty acids of marine origin, have shown promise for the prevention of cardiovascular disease (CVD) outcomes in animal studies and epidemiologic studies.1 Although several recent trials have shown benefits, as summarized in Mayo Clinic Proceedings in 2019,2 2 randomized control trials published in late 2020 showed neutral results. The situation is summarized thoughtfully in a recent editorial by Farukhi et al, published in Mayo Clinic Proceedings,3 which cited our recent meta-analysis6 on the subject.
- We greatly appreciate the interest by Narasimhan and colleagues in the recent major meta-analysis by Bernasconi et al.1 In this article, we analyzed 40 studies, including more than 135,000 participants, and demonstrated that omega-3 therapy was associated with major reductions in fatal myocardial infarction (MI); (–35%), total MI (–13%), coronary heart disease (CHD) events (–10%), and CHD mortality (–9%). We further demonstrated a strong dosage effect in which higher doses of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were associated with fewer cardiovascular disease (CVD) outcomes.
- We appreciate Dr Snitker's interest in our recent editorial1 and his insightful comments regarding body fat (BF) and obesity. Additionally, we are aware of his clinical and research efforts in the area of obesity in children at the University of Maryland School of Medicine. Dr Snitker is correct that currently there is no definitive cutoff for percent BF in defining overweightness or obesity in men or women. In our efforts to simplify the message for readers, we referenced an easily accessible National Institutes of Health (NIH) publication2 that we thought was representative.
- We greatly appreciate the supportive input from Robinson regarding our commentary1 in Mayo Clinic Proceedings. Her recent meta-analysis2 regarding non–HDL-C and her well-written editorial3 on this topic were major resources for our work, and we completely agree with her conclusion that apolipoprotein (apo) B is not superior to non–HDL-C, especially in statin-treated patients.3–5 Therefore, we agree with her suggestions that current clinical trial evidence is lacking to suggest that treatment intensification based on apo B levels is superior to efforts targeted at LDL-C and non–HDL-C.
- To the Editor: We read with interest the review by Curtis and O'Keefe1 on the importance of autonomic tone as a potent cardiovascular risk factor. In their discussion of lifestyle interventions to improve autonomic function, exercise, social support, weight loss, smoking cessation, and stress reduction are among the listed items, prompting us to further tout a formal phase II cardiac rehabilitation and exercise training program as an effective and clinically proven mechanism for generating these specific lifestyle changes.
- In our recent publications demonstrating marked benefits on reducing levels of hostility1 as well as other adverse behavioral characteristics (especially depression and high levels of psychological distress2–6 we used nonspecific therapy with cardiac rehabilitation and exercise training. We agree with Mr Fogel that more specific psychological treatment aimed directly at reducing high levels of behavioral abnormalities, particularly in patients with more adverse profiles or persistently abnormal profiles after cardiac rehabilitation and exercise training, would likely result in more dramatic improvements than we have noted with our nonspecific and general treatment.